The onset of the consultation

1. Wash hands and put on PPE if necessary.
2. Introduce yourself to the patient by stating your name and role.
3. Confirm the patient’s last name, first name, and date of birth.
4. Explain what the examination will involve using language the patient can understand.
5. Get consent for consultation.
6. Adequately expose the patient for examination.
7. Ask the patient if he is in pain before proceeding with the clinical examination.

Clarification of the main complaint

8. Use open-ended questions to explore the patient’s complaints
9. Details of the main complaint
10. Analyze the patient’s thoughts, fears, and expectations
11. Summarize the patient’s complaints

Comprehensive assessment

12. Assess other symptoms to get a comprehensive picture

Medical history

13. Find out when and how the chest pain first appeared; what, according to the patient, could have caused its appearance (pay special attention to psychological or physical stress); specify whether the patient sought medical help, if so, to whom and what was the end of his appeal, if not, then specify why the patient did not seek medical help; whether he took medical drugs on his own or as prescribed by a doctor, if so, whether the nature of complaints changed against the background of treatment 
14. In the case of hospitalization for chest pain, read the extract from the patient’s medical history, pay attention to the established clinical diagnosis, the results of laboratory or instrumental examinations, the treatment and recommendations after discharge

15. If the patient has previously undergone laboratory or instrumental examinations for current complaints, analyze their results and indicate important findings
16. Find out what prompted the patient to contact you
17. Exclude other causes of chest pain by asking the patient clarifying questions

History of life

18. The accuracy of the presence of previously diagnosed cardiovascular diseases in the patient, in particular myocardial infarction, stroke, rhythm disorders, cardiomyopathy, angina pectoris, arterial hypertension
19. Find out whether the patient suffers from mental health disorders, such as depression, anxiety, or schizophrenia, which are risk factors for the development of Takotsubo syndrome
20. Determine whether the patient has chronic diseases, in particular diabetes, bronchial asthma, and chronic obstructive pulmonary disease, which are risk factors for the development of Takotsubo syndrome
21. Determine whether the patient is taking medications that stimulate the sympathetic nervous system (eg, beta 2-adrenergic receptor agonists, alpha 1-adrenergic receptor agonists, serotonin and norepinephrine reuptake inhibitors, epinephrine)
22. Determine whether the patient is abusing psychotropic substances (eg, cannabis, cannabinoids)
23. Find out whether the menstrual function is preserved; if not, find out the time of menopause and whether the patient is taking hormone replacement therapy
24. Check whether the patient has undergone surgery
25. Find out if the patient had any injuries, find out how the recovery period went
26. Find out whether the patient has a drug intolerance and specify how it manifests itself
27. Find out whether the patient has bad habits – drinking alcohol, narcotic substances, smoking
28. Find out the family status of the patient, living conditions, and psychological problems in the family; find out if there were any blood relatives of the patient with cardiovascular diseases
29. Find out whether the patient works, his profession, conditions, and nature of work, and whether the work is related to physical or psychological overload

Objective examination:

30. Assessment of the patient’s general condition (satisfactory, moderate, severe, very severe).
31. General examination of the patient:

• Consciousness, the position of the patient, gait, and posture.
• Physique, type of constitution, height, weight, body mass index.
• Skin and visible mucous membranes (color, rash, scars, scratches), elasticity and moisture of the skin, condition of skin derivatives, and development of subcutaneous adipose tissue.
• Pastiness, edema.
• Lymph nodes.
• Muscular system: development of muscles, their tone, presence of atrophy, soreness.
• Joints: examination, palpation, measurement of limbs and joints, determination of the degree of joint mobility.
• Examination of the head, face, and neck with an assessment of the state of the thyroid gland.

32. Research of organ systems

• Research of respiratory organs
• Research of circulatory organs.
• Research of digestive organs.
• Examination of the urinary system

33. Assessment of the probability of Takotsubo syndrome

Laboratory tests

34. Clinical blood count with leukocyte formula and calculation of ESR (erythrocyte sedimentation rate)
35. Biochemical blood analysis (total protein, creatinine, urea, alanine aminotransferase, aspartate aminotransferase, glucose, alkaline phosphatase, uric acid, bilirubin with fractions)
36. Blood electrolytes (K+ and Na+)
37. Lipid profile
38. Coagulogram
39. Blood test for troponin I / T
40. Blood test for creatine phosphokinase (CK)
41. Blood analysis for brain natriuretic peptide ( BNP ) or the N-terminal precursor of brain natriuretic peptide ( NT – pro-BNP )
42. Assessment of thyroid gland function (thyroid-stimulating hormone-TSH) (according to indications)
43. Urine analysis with sediment microscopy (as indicated)
44. Pregnancy test for patients of childbearing age (according to indications)

Instrumental diagnostic tests

45. Electrocardiography
46. Transthoracic echocardiography
47. Coronarography
48. Ventriculography
49. MRI of the heart
50. CT angiography of coronary arteries

Making a clinical diagnosis

51. Carrying out differential diagnosis
52. Assessment of diagnostic criteria
53. Determination of the anatomical variant
54. Definition of complications
55. Making of clinical diagnosis

Specialist consultations

56. Cardiologist
57. Interventional cardiologist
58. Radiologist
59. Psychotherapist
60. Psychiatrist
61. Endocrinologist
62. Narcologist
63. Gynecologist
64. Doctor of physical and rehabilitation medicine

Purpose of treatment

65. Supportive therapy
66. Treatment of complications
67. Prevention of relapse

Consulting and support

68. Informing the patient about the disease
69. Discussion of research results with the patient
70. Explanation to the patient of the possible cause of the disease
71. Explanation to the patient of possible symptoms that may occur during the disease
72. Explanation to the patient of the possible consequences of the disease
73. Explaining the available treatment methods, informing the patient about the risks and benefits of different treatment methods
74. Answers to the patient’s questions
75. Explanation of the scope of monitoring during and after treatment
76. Appointment of regular checks and controls to assess the effectiveness of treatment and changes in the patient’s condition

End of consultation

77. Summarize the data and ask the patient if anything important has been missed
78. Inform the patient about further tactics
79. Thank the patient
80. Dispose of PPE properly and wash hands

Key communication skills

• Active listening
• Summing up
• Selection of indicative signs

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The onset of the consultation

1. Wash hands and put on PPE if necessary.
2. Introduce yourself to the patient by stating your name and role.
3. Confirm the patient’s last name, first name, and date of birth.
4. Explain what the examination will involve using language the patient can understand.
5. Get consent for consultation.
6. Adequately expose the patient for examination.
7. Ask the patient if he is in pain before proceeding with the clinical examination.

Examination for Takotsubo syndrome is conducted when characteristic clinical symptoms and objective signs of this condition are present.

Typical clinical symptoms of Takotsubo syndrome include:

1. Symptoms of myocardial ischemia (chest pain)
2. Symptoms of heart failure (shortness of breath, sensation of air hunger)
3. Symptoms of cerebral hypoperfusion (dizziness, loss of consciousness)

Clarification of the main complaint

8. Use open-ended questions to explore the patient’s complaints
9. Details of the main complaint
10. Analyze the patient’s thoughts, fears, and expectations
11. Summarize the patient’s complaints

• Use open-ended questions to explore the patient’s complaints
• Details of the main complaint

The most common complaint of a patient with Takotsubo syndrome is chest pain. To detail this complaint, follow this algorithm:

• Localization: find out where it hurts
• Onset: find out how the pain started – suddenly or gradually
• Nature: Ask the patient to describe how he/she feels the pain.
• Irradiation: Find out if the pain is spreading
• Accompanying symptoms: find out if there are other symptoms that accompany the pain
• Dynamics over time: Determine whether the pain has changed over time
• Factors that make the pain worse or worse: Find out if there is anything that makes the pain worse or worse

“Can you show me precisely where it hurts?”

“Could you describe this pain?”

Is this pain constant or intermittent?

“How long does the pain typically last?“

“Does the pain radiate to other areas?“

“What typically triggers the onset of this pain?“

“What measures provide relief from this pain?“

“Are there any other symptoms accompanying the pain?”

To detail the complaint of chest pain, we recommend using the SOCRATES questionnaire. An example survey is given below.

Some elements of the SOCRATES acronym can be used to detail a complaint of shortness of breath.

Analyze the patient’s thoughts, fears, and expectations

A key component of history taking involves exploring the patient’s thoughts, concerns, and expectations to gain insight into how they currently perceive their condition, their worries, and what they anticipate from the consultation.

The exploration of thoughts, concerns, and expectations should be flexible throughout the consultation, responding to cues from the patient. This approach ensures that your consultation remains patient-oriented rather than formulaic.

It’s important to structure the analysis of thoughts, fears, and expectations in a way that feels natural during your consultation.

Summarize the patient’s complaints

Summarize what the patient told you about his complaint. This allows you to check how correctly you understood the patient’s complaints and gives the patient the opportunity to correct any inaccurate information.

When you have concluded, ask the patient if there is anything else you missed. Periodically, as the consultation progresses, summarize intermediate results.

Comprehensive assessment

12. Screen for symptoms of damage to other organs and systems

A comprehensive assessment includes a brief survey of the patient for symptoms of other systems that may or may not be related to the chief complaint. This comprehensive examination also helps identify symptoms that the patient may have forgotten to mention.

Deciding which symptoms to inquire about depends on the presenting complaint and your level of experience.

Here are some examples of symptoms that you might inquire about for each system:

Medical history

13. Find out when and how the chest pain first appeared; what, according to the patient, can cause its appearance (pay special attention to psychological or physical stress experienced); specify whether the patient sought medical help, if so, to whom and what was the end of his application, if not, then specify why he did not seek help; whether he took medical drugs on his own or as prescribed by a doctor, if so, whether the nature of the complaints changed against the background of treatment 

“When did the chest pain start for you?”

“What do you think might have caused it to start?”

“Did you seek medical assistance?”

14. In the case of hospitalization for chest pain, read the extract from the patient’s medical history, pay attention to the established clinical diagnosis, the results of laboratory or instrumental examinations, the treatment and recommendations after discharge

15. If the patient has previously undergone laboratory or instrumental examinations for current complaints, analyze their results and indicate important findings
16. Find out what prompted the patient to contact you

“What made you decide to reach out to me?”

17. Exclude other causes of existing symptoms by asking the patient clarifying questions

“Did you have a fever?”

“Is the chest pain accompanied by nausea or the urge to vomit?”

Other causes of chest pain:

• Acute coronary syndrome (ACS)

Acute coronary syndrome is characterized by complaints of intense chest pain radiating to the left arm, left shoulder, left scapula, neck, and epigastrium, lasting more than 20 minutes, not relieved by taking nitrates, and often accompanied by shortness of breath, a feeling of fear, and increased sweating. The pain syndrome in ACS is very similar to the pain syndrome in Takotsubo syndrome, which creates significant difficulties for differential diagnosis.

• Acute myocarditis

Clinical symptoms such as chest pain, shortness of breath, and palpitations are characteristic of both Takotsubo syndrome and myocarditis. The pain syndrome in myocarditis is very similar to the pain syndrome in Takotsubo syndrome, which makes it challenging to differentiate these two conditions based solely on this criterion. However, it should be noted that myocarditis is characterized by the presence of a recently acquired infectious disease, which is not typically associated with Takotsubo syndrome. Conversely, in Takotsubo syndrome, the onset of pain is often preceded by psychological or physical stress.

• Angina

Angina is characterized by chest pain radiating to the left arm, left shoulder, left shoulder blade, neck, and epigastrium. However, in angina, the pain typically lasts up to 20 minutes and subsides with rest or after taking nitrates. In contrast, in Takotsubo syndrome, the pain persists for a longer duration and is not relieved by nitrates.

• Thromboembolism of the pulmonary artery

For thromboembolism of the pulmonary artery and Takotsubo syndrome, chest pain often accompanied by shortness of breath and a sensation of breathlessness is characteristic. The nature of the pain in both conditions is anginal, posing a challenge for differential diagnosis. Considering that the primary cause of pulmonary embolism (PE) is typically deep vein thrombosis in the lower extremities, it’s essential to consider typical symptoms such as unilateral pain and swelling of the affected lower limb, along with an increase in its size.

• Dissecting aneurysm of the aorta

Patients with a dissecting aortic aneurysm typically present with sudden, excruciating, tearing chest pain that radiates to the neck, back, and lower limbs, often in a migratory pattern. While the pain in Takotsubo syndrome can also be intense, it is typically not as severe as in a dissecting aortic aneurysm.

• Acute pericarditis

The clinical presentation of acute pericarditis shares many similarities with that of Takotsubo syndrome, as both conditions typically involve chest pain and shortness of breath. However, acute pericarditis is distinguished by chest pain that worsens when lying down and improves when sitting, a characteristic not seen in Takotsubo syndrome. Additionally, acute pericarditis often occurs as a complication of an infectious disease, leading to symptoms such as fever and other signs of inflammation.

• Gastroesophageal reflux

Pain associated with gastroesophageal reflux typically develops gradually and is characterized by a burning sensation localized in the central part of the chest. This discomfort is often accompanied by symptoms such as heartburn, nausea, and a sour taste in the mouth, all of which typically alleviate after taking antacids. Unlike Takotsubo syndrome, dyspeptic symptoms are not a hallmark feature of gastroesophageal reflux.

• Gastric ulcer disease

In peptic ulcer disease, pain is frequently localized behind the sternum or in the epigastrium, typically occurring approximately 40 minutes after eating. This discomfort tends to diminish or disappear following the administration of antacids and is often accompanied by symptoms such as nausea and a sour taste in the mouth. Such a pain pattern is not characteristic of Takotsubo syndrome.

• Diseases of the biliary tract

These conditions are typified by the emergence of dull pain behind the sternum or in the epigastrium, typically occurring approximately 1 hour after consuming food, particularly fatty or fried fare. This discomfort is often coupled with nausea, the urge to vomit, and a bitter taste in the mouth. Conversely, chest pain in Takotsubo syndrome is not influenced by dietary intake, and dyspeptic symptoms are generally absent.

• Spontaneous pneumothorax

In spontaneous pneumothorax, intense chest pain abruptly arises, exacerbating with deep breathing, and is accompanied by pronounced shortness of breath. The aggravation of chest pain during inhalation is not a characteristic feature of Takotsubo syndrome.

• Diseases of the neuromuscular system and musculoskeletal system

Chest pain resulting from neuromuscular and musculoskeletal system disorders typically worsens with significant body movements such as turning, bending, or raising the arm, a feature not commonly associated with Takotsubo syndrome.

• Pain in herpes zoster

The pain in herpes zoster typically manifests as a constant burning sensation, often preceding the appearance of a characteristic vesicular rash. It may persist for some time after the rash disappears and is localized along the affected nerve pathway.

Learn more about the specific details of detailing chest pain as the main complaint and taking a patient’s medical history regarding chest pain by visiting the following link:

Other causes of shortness of breath:

• Bronchial asthma

Shortness of breath in bronchial asthma typically manifests as attack-like episodes with an expiratory character. It is often accompanied by wheezing, a sensation of chest tightness, and coughing, often resulting in the discharge of a small amount of glassy viscous sputum. These episodes tend to occur in the early morning hours and are typically relieved by the inhalation of a short-acting β2-agonist.

• Chronic obstructive pulmonary disease

Shortness of breath in chronic obstructive pulmonary disease (COPD) typically has a constant and progressive nature. It is often accompanied by a cough productive of mucus or sputum, particularly in the morning upon waking up.

• Pneumonia

Shortness of breath in pneumonia is often accompanied by an elevated body temperature, symptoms of intoxication, cough with productive sputum, and sometimes chest pain.

• Lung tumor

Shortness of breath associated with lung tumors typically exhibits a constant and progressive nature, often accompanied by hemoptysis, chest pain, coughing, and symptoms of tumor intoxication such as fatigue, weakness, weight loss, and loss of appetite.

• Thromboembolism of the pulmonary artery

Shortness of breath associated with pulmonary embolism typically arises suddenly, often without a known cause. It can be so severe that it impedes the patient’s ability to speak. Additionally, it is accompanied by chest pain of a coronary or pleural nature, hemoptysis, dizziness, or even loss of consciousness. Symptoms of deep vein thrombosis of the lower extremities may also be present.

• Arrhythmia

Tachyarrhythmias, particularly atrial fibrillation, frequently manifest with shortness of breath, palpitations, heart irregularities, and other symptoms indicative of hemodynamic impairment, such as sweating, dizziness, and possibly loss of consciousness. Because rhythm disturbances are typically paroxysmal, shortness of breath also tends to occur in episodes.

• Anemia

Severe anemia often presents with shortness of breath exacerbated by minimal physical exertion, accompanied by rapid heartbeat, angina pectoris-like pains, dizziness, pronounced weakness, and increased fatigue.

• Adiposity

Excess weight often leads to shortness of breath due to increased strain on the cardiovascular system, typically manifesting during physical exertion. In cases of significant excess weight, shortness of breath may even occur at rest.

• Panic attack

Shortness of breath is just one of the symptoms experienced during a panic attack. It typically occurs suddenly and is often accompanied by feelings of fear, anxiety, nausea, palpitations, dry mouth, sweating, and dizziness, which can be unexpected and uncontrollable.

• Hyperventilation

Shortness of breath is the primary symptom of hyperventilation syndrome. Patients commonly describe it as a sudden sensation of breathing dissatisfaction and a feeling of air deprivation. Due to the underlying cause of hyperventilation syndrome, shortness of breath is often accompanied by feelings of anxiety, panic, numbness, and tingling.

• Gastroesophageal reflux disease

Shortness of breath is a relatively rare symptom of gastroesophageal reflux disease and arises due to the prolonged exposure of acidic stomach contents to the respiratory tract, typically after eating, while lying down, or when bending forward. Suspect gastroesophageal reflux disease when more specific symptoms are present, such as heartburn, belching, and discomfort when swallowing food.

History of life

18. The accuracy of the presence of previously diagnosed cardiovascular diseases in the patient, in particular myocardial infarction, stroke, rhythm disorders, cardiomyopathy, angina pectoris, arterial hypertension
19. Find out whether the patient suffers from mental health disorders, such as depression, anxiety, or schizophrenia, which are risk factors for the development of Takotsubo syndrome
20. Determine whether the patient has chronic diseases, in particular diabetes, bronchial asthma, and chronic obstructive pulmonary disease, which are risk factors for the development of Takotsubo syndrome
21. Determine whether the patient is taking medications that stimulate the sympathetic nervous system (eg, beta 2-adrenergic receptor agonists, alpha 1-adrenergic receptor agonists, serotonin and norepinephrine reuptake inhibitors, epinephrine)
22. Determine whether the patient is abusing psychotropic substances (eg, cannabis, cannabinoids)
23. Find out whether the menstrual function is preserved; if not, find out the time of menopause and whether the patient is taking hormone replacement therapy
24. Check whether the patient has undergone surgery
25. Find out if the patient had any injuries, find out how the recovery period went
26. Find out whether the patient has a drug intolerance and specify how it manifests itself
27. Find out whether the patient has bad habits – drinking alcohol, narcotic substances, smoking
28. Find out the family status of the patient, living conditions, and psychological problems in the family; find out if there were any blood relatives of the patient with cardiovascular diseases
29. Find out whether the patient works, his profession, conditions, and nature of work, and whether the work is related to physical or psychological overload

Objective examination:

30. Assessment of the patient’s general condition (satisfactory, moderate, severe, very severe).
31. General examination of the patient:

• Consciousness, the position of the patient, gait, and posture.
• Physique, type of constitution, height, weight, body mass index.
• Skin and visible mucous membranes (color, rash, scars, scratches), elasticity and moisture of the skin, condition of skin derivatives, and development of subcutaneous adipose tissue.
• Pastiness, edema.
• Lymph nodes.
• Muscular system: development of muscles, their tone, presence of atrophy, soreness.
• Joints: examination, palpation, measurement of limbs and joints, determination of the degree of joint mobility.
• Examination of the head, face, and neck with an assessment of the state of the thyroid gland.

32. Research of organ systems

• Research of respiratory organs
• Organs of blood circulation.
• Research of digestive organs.
• Examination of the urinary system.

Assess for objects or equipment on or around the patient that may provide useful information about the patient’s medical history and current clinical condition.

It should be noted that physical findings depend on the severity of Takotsubo syndrome.

In patients with a severe course of Takotsubo syndrome, signs of heart failure can be detected, including wet wheezing in the lungs and tachypnea. During auscultation of the heart, tachycardia, an additional pathological third heart sound, as well as a systolic murmur over the apex of the heart due to obstruction of the outflow tract of the left ventricle and mitral regurgitation are often detected. Additionally, patients with Takotsubo syndrome often exhibit a decrease in blood pressure and low pulse pressure.

In patients with a mild course of Takotsubo syndrome, physical findings are typically unchanged.

Assessment of the probability of Takotsubo syndrome

33. Assessment of the probability of Takotsubo syndrome

The probability of Takotsubo syndrome is assessed in patients presenting with chest pain and/or shortness of breath in the absence of ST-segment elevation on the ECG, particularly those hospitalized in intensive care units.

The InterTAK (The International Takotsubo Diagnostic Criteria) diagnostic scale is utilized to assess the likelihood of Takotsubo syndrome. A score of >70 points on this scale indicates a high probability (approximately 90%) of Takotsubo syndrome, whereas a sum of points ≤70 points suggests a low or moderate probability.

With a high probability of Takotsubo syndrome, urgent transthoracic echocardiography is recommended. For cases with a low or moderate probability of Takotsubo syndrome, coronary angiography is recommended. This procedure allows for definitive differentiation between Takotsubo syndrome and acute myocardial infarction.

Laboratory tests

34. Clinical blood count with leukocyte formula and calculation of ESR (erythrocyte sedimentation rate)
35. Biochemical blood analysis (total protein, creatinine, urea, alanine aminotransferase, aspartate aminotransferase, glucose, alkaline phosphatase, uric acid, bilirubin with fractions)
36. Blood electrolytes (K+ and Na+)
37. Lipid profile
38. Coagulogram
39. Blood test for troponin I / T
40. Blood test for creatine phosphokinase (CK)
41. Blood analysis for brain natriuretic peptide ( BNP ) or the N-terminal precursor of brain natriuretic peptide (NT – pro-BNP )
42. Assessment of thyroid gland function (thyroid-stimulating hormone-TSH) (according to indications)
43. Urine analysis with sediment microscopy (as indicated)
44. Pregnancy test if the patient is of childbearing age (as indicated)

• Clinical blood count with leukocyte formula and calculation of ESR (erythrocyte sedimentation rate)

Clinical blood count, including the leukocyte count and calculation of the erythrocyte sedimentation rate (ESR), is one of the mandatory laboratory tests conducted in routine clinical practice for somatic patients.

• Biochemical blood analysis (total protein, creatinine, urea, alanine aminotransferase, aspartate aminotransferase, glucose, alkaline phosphatase, uric acid, total bilirubin with its fractions)

The biochemical analysis of blood, which includes measurements of total protein, creatinine, urea, alanine aminotransferase (ALT), aspartate aminotransferase (AST), glucose, alkaline phosphatase, uric acid, and total bilirubin with its fractions, is one of the mandatory laboratory examination methods performed in routine clinical practice for somatic patients.

• Blood electrolytes (K+ and Na+)

Blood analysis for electrolytes (potassium and sodium) is a mandatory laboratory method of examination carried out in routine clinical practice for patients with cardiovascular diseases to diagnose electrolyte disorders.

• Lipid profile

Lipid profile is a mandatory laboratory test for adult patients with cardiovascular diseases to diagnose lipid metabolism disorders.

• Coagulogram

Coagulation profile is a mandatory laboratory test for adult patients with cardiovascular diseases to diagnose disorders of the blood coagulation system.

• Blood test for troponin I / T

“Takotsubo syndrome” is a condition characterized by transient myocardial dysfunction, often triggered by emotional or physical stressors. While troponin levels can be elevated in Takotsubo syndrome, the degree of elevation is typically modest compared to that seen in acute myocardial infarction. It’s important to note that the elevation in troponin levels observed in Takotsubo syndrome is often disproportionate to the extent of regional myocardial dysfunction detected on imaging studies such as echocardiography.

• Blood test for creatine phosphokinase (CK)

Creatine phosphokinase (CK) is indeed an early marker of myocardial necrosis. In Takotsubo syndrome, its levels may show a moderate elevation, typically disproportionate to the extent of regional myocardial dysfunction detected on echocardiography.

• Blood analysis for brain natriuretic peptide ( BNP ) or the N-terminal precursor of brain natriuretic peptide (NT–proBNP )

B-type natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) are indeed markers of heart failure. In Takotsubo syndrome, their levels are often significantly elevated due to the overstretching of cardiomyocytes caused by the condition’s hemodynamic stress.

Appointment of instrumental methods of examination

45. Electrocardiography
46. Transthoracic echocardiography
47. Coronarography
48. Ventriculography
49. MRI of the heart
50. CT angiography of coronary arteries

• Electrocardiography

Electrocardiography (ECG) is a mandatory method of examination of patients with suspected Takotsubo syndrome. The most characteristic ECG signs include elevation of the ST segment in the precordial leads, elevation of the ST segment in the AVR lead, diffuse inversion of the T wave, prolongation of the QT interval, rarely depression of the ST segment.

Some experts note that the elevation of the ST segment in the dept. V1-V3 in combination with elevation of the ST segment in the dept. AVR is a characteristic feature of Takotsubo syndrome.

• Transthoracic echocardiography

Transthoracic echocardiography is a mandatory method of examination of patients with suspected Takotsubo syndrome. Moreover, it is diagnostically significant in patients with a high probability of Takotsubo syndrome according to the InterTAK scale.

Echocardiographic signs of Takotsubo syndrome include a decrease in the ejection fraction of the left ventricle, akinesis of the apical segments of the myocardium of the left ventricle in combination with hyperkinesis of the basal part, apical dilatation of the myocardium of the left ventricle, sometimes obstruction of the outflow tract of the left ventricle.

It should be noted that these signs are transitory in nature.

• Coronarography

Coronary angiography indeed serves as a vital diagnostic tool to distinguish Takotsubo syndrome from acute myocardial infarction, particularly in patients with a low or moderate probability of Takotsubo syndrome according to the InterTAK scale.

In individuals with Takotsubo syndrome, coronary angiography typically reveals either normal coronary arteries or coronary arteries with non-obstructive stenosis (defined as stenosis <50%). This absence of significant coronary artery disease further supports the diagnosis of Takotsubo syndrome, helping to differentiate it from acute myocardial infarction.

• Ventriculography

Ventriculography provides an assessment of the morphology and function of the left ventricle. In patients with Takotsubo syndrome, transient dysfunction and dilatation of the mid and apical segments of the left ventricle occur, resulting in a heart shape resembling that of an octopus.

• MRI of the heart

MRI of the heart is an informative examination method that allows differentiation between Takotsubo syndrome and myocarditis. Characteristic MRI signs of Takotsubo syndrome include transmural edema in regions with reduced local myocardial contractility and myocardial scarring, while the basal parts of the left ventricle remain normal.

• CT angiography of coronary arteries

CT angiography of the coronary arteries is an alternative examination method for stable patients contraindicated for cardiac MRI. It is performed to rule out significant coronary stenosis.

• Assessment of thyroid gland function (thyroid-stimulating hormone-TSH) (according to indications)

A blood test for thyroid-stimulating hormone is conducted when there is suspicion of thyroid dysfunction, which can contribute to mental health disorders and potentially act as a trigger for the development of Takotsubo syndrome.

• General urine analysis with sediment microscopy (as indicated)

A complete urine analysis with sediment microscopy is conducted when there is suspicion of kidney and/or urinary system damage.

• Pregnancy test if the patient is of childbearing age (as indicated)

It is advisable to conduct a pregnancy test for female patients of childbearing age with Takotsubo syndrome. This helps in selecting appropriate drug therapy tactics, considering that some medications used to treat Takotsubo syndrome are contraindicated during pregnancy due to their teratogenic effects.

Making a clinical diagnosis

51. Carrying out differential diagnosis

In clinical practice, it is often necessary to differentiate Takotsubo syndrome from acute coronary syndrome (ACS), acute myocarditis, as well as diseases accompanied by chest pain, in particular, angina pectoris, pulmonary embolism, dissecting aortic aneurysm, acute pericarditis, and others.

Clinical symptoms, objective data, ECG signs of Takotsubo syndrome, and acute coronary syndrome have a lot in common, which causes certain difficulties for differential diagnosis.

Both Takotsubo syndrome and acute coronary syndrome are characterized by complaints of intense radiating chest pain lasting more than 20 minutes and often accompanied by shortness of breath.

Levels of markers of myocardial necrosis, in particular troponin I/T and CK, are increased in both cases, but in Takotsubo syndrome this increase is insignificant compared to patients with acute myocardial infarction.

On the ECG of a patient with Takotsubo syndrome and a patient with ACS, ST-segment elevation and T-wave inversion can often be detected.

Echocardiography of a patient with Takotsubo syndrome and a patient with ACS revealed a decrease in the ejection fraction of the left ventricle and a local violation of myocardial contractility. However, patients with Takotsubo syndrome are characterized by akinesis of the apical segments of the myocardium of the left ventricle in combination with hyperkinesis of the basal part, which leads to apical ballooning of the left ventricle. In addition, these changes are transient and disappear within 3 weeks.

Coronary angiography definitively distinguishes Takotsubo syndrome from acute coronary syndrome. In Takotsubo syndrome, coronary arteries typically appear normal, without evidence of stenosis or hemodynamically insignificant stenosis (<50%). In contrast, acute coronary syndrome is characterized by acute occlusion of the arterial lumen.

Takotsubo syndrome develops in 90% of cases in women over the age of 50, whereas acute myocarditis most often affects young people without gender dominance.

Takotsubo syndrome in most cases is preceded by severe stress, while myocarditis is an infectious disease.

Clinical symptoms such as chest pain, shortness of breath, and palpitations are characteristic of both Takotsubo syndrome and myocarditis.

Blood troponin levels are elevated in both Takotsubo syndrome and myocarditis. However, in Takotsubo syndrome, this increase is insignificant and disproportionate to the area of ​​the affected myocardium, while in myocarditis, troponin is usually significantly increased and correlates with the area of ​​myocardial damage.

The level of brain natriuretic peptide is often elevated in Takotsubo syndrome and is usually elevated in myocarditis.

On the ECG of a patient with cardiomyopathy and myocarditis, changes in the ST segment and inversion of the T wave can often be detected. Unlike Takotsubo syndrome, myocarditis is also characterized by conduction disturbances and arrhythmias.

Echocardiography is important for differential diagnosis. Thus, in Takotsubo syndrome, swelling of the apical segments of the myocardium with intact basal sections is determined, which is not characteristic of myocarditis.

Myocardial edema can often be detected on MRI of the heart in Takotsubo syndrome and myocarditis. However, in the acute stage of Takotsubo syndrome, unlike myocarditis, there is no late accumulation of gadolinium.

Both angina and Takotsubo syndrome are characterized by radiating chest pain. However, in angina, the pain typically lasts up to 20 minutes and subsides with rest or after taking nitrates, whereas in Takotsubo syndrome, the pain persists longer and is not alleviated by nitrates.

The ECG of a patient with angina is usually normal or shows ST-segment depression, whereas patients with Takotsubo syndrome often show ST-segment elevation and T-wave inversion.

In patients with angina pectoris, the levels of markers of myocardial necrosis are normal, while in patients with Takotsubo syndrome, they are elevated.

A coronary angiography of a patient with angina usually shows significant stenosis of the coronary arteries, whereas in Takotsubo syndrome the coronary arteries are either intact or with insignificant stenosis.

Chest pain and shortness of breath are characteristic symptoms of both pulmonary embolism and Takotsubo syndrome. The chest pain in both conditions is anginal in nature.

Blood troponin levels may be mildly elevated in both pulmonary embolism and Takotsubo syndrome.

ECG in patients with pulmonary embolism and Takotsubo syndrome often shows sinus tachycardia, T-wave inversion. Pulmonary embolism is characterized by the classic S _I Q _III T _III   pattern, while Takotsubo syndrome is characterized by ST-segment elevation in the precordial leads.

Echocardiography is essential for differential diagnosis. In Takotsubo syndrome, ballooning of the apical segments of the myocardium of the left ventricle with intact basal sections is observed, while in pulmonary artery thromboembolism, akinesia or hypokinesia of the free wall of the right ventricle with preserved contractility of the apex of the right ventricle (McConnell’s sign), 60/60 sign, dilatation and dysfunction of the right ventricle, and acute tricuspid regurgitation may occur.

Patients with a dissecting aortic aneurysm typically describe sudden, excruciating, tearing pain in the chest, which often radiates to the neck, back, and lower limbs and may be migratory. Although the pain in Takotsubo syndrome is intense, it typically does not reach the same level. Physical examination of a patient with a dissecting aortic aneurysm may reveal asymmetry of the pulse and blood pressure in the extremities compared to the other side. In cases where the aortic valve is involved, a diastolic murmur over the aorta and a high pulse pressure may be detected.

On the ECG of a patient with a dissecting aortic aneurysm, as in a patient with Takotsubo syndrome, ST- segment elevation can often be detected, however, in Takotsubo syndrome, ST-segment elevation is visualized in the precordial leads, while in aortic dissection involving the right coronary artery – in leads II, III, AVF.

Echocardiography and chest X-ray have important diagnostic value. On echocardiography and chest X-ray, in the case of aortic arch dissection, dilatation of the affected part of the aorta is revealed, which is not the case with Takotsubo syndrome.

Acute pericarditis is characterized by chest pain that intensifies when lying down and diminishes when sitting up, a feature not typically observed in Takotsubo syndrome. Additionally, patients with acute pericarditis often present with a history or ongoing symptoms of an infectious disease, including fever, respiratory symptoms, and others, which are not commonly associated with Takotsubo syndrome.

Clinical blood analysis of a patient with acute pericarditis reveals signs of an inflammatory process, which is not the case with Takotsubo syndrome.

On the ECG of a patient with acute effusion pericarditis, as in a patient with Takotsubo syndrome, ST -segment elevation, and T-wave inversion can often be detected, however, in Takotsubo syndrome, these changes are visualized in the precordial leads, while in acute pericarditis, ST-segment elevation is diffuse.

Echocardiography is important for differential diagnosis. Thus, in Takotsubo syndrome, ballooning of the apical segments of the myocardium of the left ventricle with intact basal sections is determined, while in pericarditis – thickening and compaction of the pericardial leaves, free fluid in the pericardium, signs of diastolic dysfunction.

52. Assessment of diagnostic criteria

Diagnostic criteria are used to establish a clinical diagnosis. Among the existing criteria, the diagnostic criteria of the Mayo Clinic are of the greatest practical importance:

• transient dyskinesia of the middle segments of the left ventricle; local violation of the contractility of the myocardium, which goes beyond the blood supply of one epicardial artery;
• absence of obstructive coronary artery disease or angiographic signs of acute plaque rupture;
• the appearance of new changes on the ECG (elevation of the ST segment and/or inversion of the T wave) or a moderate increase in the level of troponins;
• absence of pheochromocytoma or myocarditis.

In addition to the Mayo Clinic diagnostic criteria, you can use the Takotsubo International Diagnostic Criteria:

• patients with transient dysfunction of the left ventricle in the form of apical, mid-ventricular, basal or focal dilatation; in some cases, the right ventricle is involved in the process; the area of ​​the affected myocardium goes beyond the area of ​​blood supply by one epicardial artery;
• an emotional, physically, or combined trigger preceding the onset of symptoms, but not necessarily;
• neurological disorders (subarachnoid hemorrhage, stroke/transient ischemic attack, convulsions), in particular, pheochromocytoma can serve as a trigger for Takotsubo syndrome;
• the appearance of new changes on the ECG (elevation/depression of the ST segment, inversion of the T wave, prolongation of the QT interval), in rare cases the ECG remains normal;
• a moderate increase in the level of cardiac biomarkers (troponin, CPK) in most cases; a significant increase in the level of BNP and NT-proBNP;
• severe coronary artery disease does not exclude the diagnosis of Takotsubo syndrome;
• absence of signs of infectious myocarditis;
• menopausal women are most often affected.

As well as the criteria of the Heart Failure Association and the European Community:

• transient regional myocardial contractility disorder of the left and right ventricle, which often, but not always, develops as a result of experienced emotional or physical stress;
• the area of ​​the affected myocardium goes beyond the area of ​​blood supply by one epicardial artery and often leads to circular dysfunction of the involved segments of the ventricles;
• absence of obstructive coronary artery disease, including acute plaque rupture, thrombus formation, coronary artery dissection, or other diseases that could explain transient left ventricular dysfunction (eg, hypertrophic cardiomyopathy, viral myocarditis);
• new and reversible changes on the ECG (elevation/depression of the ST segment, inversion of the T wave, prolongation of the QT interval, complete blockade of the left leg of the bundle of His) during the acute phase (3 months);
• significant increase in the level of BNP and NT-proBNP during the acute phase;
• moderate increase in the level of cardiac troponin;
• restoration of the systolic function of the left ventricle, confirmed by MRI of the heart, in dynamics from 3 to 6 months.

53. Determination of the anatomical variant

To date, there are several anatomical variants of Takotsubo syndrome: apical or typical (75-80%), mid-left ventricular (10-20%), basal or inverted (5%), biventricular (<0.5%), focal (very rarely).

54. Definition of complications

When formulating a clinical diagnosis, it is necessary to indicate the complications that have arisen in the patient, in particular, arrhythmias, heart failure, thromboembolic complications.

55. Making of clinical diagnosis

Here is an example of the formulation of the diagnosis in Takotsubo syndrome:

Takotsubo syndrome, apical variant. Ventricular polymorphic polytopic extrasystole, class III according to Laun. ACS-pulmonary edema.

Specialist consultations

56. Cardiologist

Given that Takotsubo syndrome is a cardiovascular condition, consulting with a cardiologist for timely diagnosis and appropriate treatment is essential.

57. Interventional cardiologist

Considering that Takotsubo syndrome must be differentiated from acute coronary syndrome, it is recommended to perform coronary angiography, which necessitates the involvement of an interventional cardiologist.

58. Radiologist

A radiologist is an important member of a multidisciplinary medical team, involved in the implementation of imaging methods of research when Takotsubo syndrome is suspected, particularly magnetic resonance imaging of the heart.

59. Psychotherapist

Patients with a confirmed diagnosis of Takotsubo syndrome and mental health disorders are recommended to be referred to a psychotherapist, considering that stress, depression, and anxiety are triggers for the development of Takotsubo syndrome.

60. Psychiatrist

Patients with a confirmed diagnosis of Takotsubo syndrome and symptoms of mental disorders are recommended to be referred to a psychotherapist, considering that some of these disorders, including depression, anxiety disorder, and schizophrenia, are factors in the development of Takotsubo syndrome. Additionally, if a depressed patient is taking serotonin and norepinephrine reuptake inhibitors, a psychiatrist should consider replacing them with other drugs, as serotonin and norepinephrine reuptake inhibitors can also trigger the development of Takotsubo syndrome.

61. Endocrinologist

Given the established association between hormonal disorders and Takotsubo syndrome, consultation with an endocrinologist is recommended if symptoms of an endocrine disease are present.

62. Narcologist

If a patient with suspected Takotsubo syndrome is suspected of using psychotropic substances, they should be referred to a narcologist for consultation. This is because some substances, such as cannabis, cannabinoids, and amphetamines, can provoke the development of Takotsubo syndrome.

63. Gynecologist

Considering that Takotsubo syndrome most often occurs in women during menopause, consulting a gynecologist to determine treatment tactics can be beneficial as part of the comprehensive therapy for such patients.

64. Doctor of physical and rehabilitation medicine

A physical and rehabilitation medicine physician plays an important role in maintaining the physical well-being of patients with Takotsubo syndrome, assisting them in their recovery process.

Purpose of treatment

65. Supportive therapy
66. Treatment of complications
67. Prevention of relapse

• Supportive therapy

Patients with Takotsubo syndrome require inpatient treatment, the main goal of which is to maintain hemodynamics until normal left ventricular function is restored and to prevent complications. As a rule, supportive treatment lasts several weeks.

Patients with signs of lung congestion, but without hypotension, are prescribed diuretics and nitrates to reduce venous return to the heart. Additionally, ACE inhibitors, ARB II, and beta-blockers are prescribed to help alleviate congestion, reduce myocardial load, and regulate blood pressure.

Patients with unstable hemodynamics require urgent echocardiography to diagnose obstruction of the left ventricular outflow tract. If signs of obstruction are detected, the administration of beta-blockers and IV fluid infusion is recommended, while inotropic drugs are contraindicated. Inotropes such as dopamine, dobutamine, milrinone, and levosimendan are indicated for patients without signs of left ventricular outflow tract obstruction. In severe cases, mechanical circulatory support is necessary, including extracorporeal membrane oxygenation for patients with left ventricular outflow tract obstruction or intra-aortic balloon counterpulsation for patients without obstruction.

An essential aspect of treating patients with Takotsubo syndrome is the prevention of thromboembolic complications, particularly when there is a large area of akinesis or hypokinesis in the myocardium of the left ventricle. To mitigate this risk, anticoagulant therapy is typically prescribed for a duration of 3 months.

• Treatment of complications

The most prevalent complications of Takotsubo syndrome include acute heart failure, left ventricular outflow tract obstruction, arrhythmias, and thromboembolic events.

For acute heart failure, refer to the previously outlined therapy. In cases of arrhythmias or thromboembolic complications, treatment should be administered following established guidelines.

• Prevention of relapse

Considering the high incidence of mental health disorders among Takotsubo syndrome patients, such as depression, anxiety disorders, and substance use, it’s crucial to address these conditions to prevent relapse.

Certain experts advocate for the prolonged use of beta-blockers to mitigate sympathetic nervous system tone, which can serve as adjunctive therapy for anxiety disorders. Retrospective analyses of extensive international registries have shown a beneficial effect of ACE inhibitors, ARBs, and calcium channel antagonists.

Consulting and support:

68. Informing the patient about the disease
69. Discussion of research results with the patient
70. Explanation to the patient of the possible cause of the disease
71. Explanation to the patient of possible symptoms that may occur during the disease
72. Explanation to the patient of the possible consequences of the disease
73. Explaining the available treatment methods, informing the patient about the risks and benefits of different treatment methods
74. Answers to the patient’s questions
75. Explanation of the scope of monitoring during and after treatment
76. Appointment of regular checks and controls to assess the effectiveness of treatment and changes in the patient’s condition

End of consultation

77. Summarize the data and ask the patient if anything important has been missed
78. Inform the patient about further tactics

Hospitalization to a specialized cardiology hospital is recommended for a comprehensive examination and selection of optimal treatment tactics. Obtain the patient’s Informed Voluntary Consent for diagnosis and treatment, and agree to the Patient’s Informed Voluntary Consent for processing personal data.

79. Thank the patient
80. Dispose of PPE properly and wash hands

Key communication skills

• Active listening
• Summing up
• Selection of indicative signs

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Lyme disease is an infectious disease caused by the spirochete Borrelia burgdorferi, which is transmissible during a tick bite.

Prevalence

Lyme disease is the most common transmissible disease in the northern hemisphere, affecting thousands of people each year. For example, about 40 cases of Lyme disease per 100 thousand population are registered in the USA every year. Outbreaks of infection are usually registered in the spring-autumn period.

Etiology

The causative agent of Lyme disease is the spirochete Borrelia burgdorferi, which enters the human body when bitten by an ixodid tick.

Pathogenesis

When a spirochete enters the body, the following occurs:

• the immune system of an infected person destroys the spirochete or
• The spirochete remains viable and causes erythema migrans, a skin lesion characteristic of Lyme disease or
• the spirochete spreads for several weeks through the lymphatics or blood.

After entering the bloodstream, the spirochete shows a distinct tropism to the skin, heart, central nervous system (CNS), joints, and eyes.

Clinical picture

The interval between a tick bite and the appearance of the first symptoms of the disease is usually from 7 to 14 days, but in some cases it can increase to several months.

In the course of Lyme disease, early and late periods are conventionally distinguished. The early period consists of an early localized stage and an early disseminated stage.

The early localized stage is characterized by fever and migrating erythema at the site of the tick bite. Gradually increasing in diameter over several days (usually more than 5 cm in diameter), the center of the spot becomes lighter, resembling a “target” or “bull’s eye”. Erythema migrans is accompanied by an increase in local temperature, but rarely itches or hurts. Erythema migrans persists for several days or weeks, then disappears, leaving behind pigmentation or scaling.

In one-third of patients, the disease ends on its own at this stage, and in two-thirds, it turns into a disseminated one, which is characterized by the appearance of signs of damage to the nervous system, heart, joints, and eyes.

The early disseminated stage develops 3-12 weeks after the primary infection and is characterized by the appearance of general weakness, fever, muscle pain, neurological symptoms, joint, eye, and cardiac symptoms.

When the central nervous system is affected, patients complain of a severe headache, neck stiffness; facial asymmetry occurs when the facial nerve is damaged; when peripheral nerves are affected, there is a shooting pain, numbness and tingling in the hands and feet.

Lyme arthritis is accompanied by the appearance of severe pain and swelling of mainly large joints, periodic muscle and tendon pain.

Heart damage in Lyme disease is characterized by the development of myocarditis or myopericarditis. Patients complain of chest pain, shortness of breath, heart rhythm and/or conduction disturbances. Often patients with Lyme carditis have a violation of AV conduction. The degree of AV block can rapidly progress from first-degree AV block to complete AV block.

A rare skin manifestation of early Lyme borreliosis is the so-called borreliosis lymphocytoma – a single bluish-red nodular formation that can be localized on the earlobe, near the nipple or in the scrotum.

Late-stage Lyme disease occurs months or years after the onset of the disease. At the late stage of the disease, patients develop aseptic meningitis, Bell’s palsy, impaired cognitive functions, and arthritis. In addition, chronic atrophic acrodermatitis often occurs – a slowly progressive skin lesion with the appearance of blue-red spots mainly on the extensor surfaces of the distal parts of the limbs and subsequent skin atrophy.

Classification

Depending on the period of the disease, the following are distinguished: early (localized and disseminated stages) and late period.

The early period of Lyme Borreliosis is characterized by the development of migratory erythema at the site of tick suction and spread of infection, which is manifested by the development of benign lymphocytoma of the skin, damage to the nervous system (neuritis of the facial nerve, polyradiculopathy, acute meningoencephalitis), heart (myocarditis with AV conduction disorders), and joints.

The late period of Lymboreliosis is characterized by various organ lesions of autoimmune genesis, in particular, recurrent arthritis of mainly large joints, chronic encephalomyelitis, dilated cardiomyopathy, chronic atrophic acrodermatitis.

Depending on the stage of the disease, the following are distinguished: early localized, early disseminated, late stage.

Depending on the variant of the course, they are distinguished: acute (lasts up to 3 months), subacute (lasts from 3 to 6 months), chronic course (lasts more than 6 months).

Depending on the predominant clinical symptoms, the following are distinguished: skin, joint, cardiac, neurological, mixed forms.

Depending on the severity, the following are distinguished: mild, moderate, and severe.

A mild course of lymoborreliosis is characterized by a moderately pronounced intoxication syndrome, an increase in body temperature up to 38 0 ^C , the presence of migratory erythema in the absence of damage to the nervous system, heart or joints.

A moderately severe course of lymoborreliosis is characterized by a pronounced intoxication syndrome, an increase in body temperature to 38-39 ⁰ C, the presence of migratory erythema, minor damage to the nervous system, heart or joints.

A severe course of lymoborreliosis is characterized by a pronounced intoxication syndrome, an increase in body temperature above 39 ⁰ C, moderate or severe damage to the nervous system (meningitis) or heart (AV-blockade II-III stage, pronounced myocarditis).

Diagnostics

The diagnosis of Lyme borreliosis is established on the basis of a characteristic clinical picture, anamnestic data and serological confirmation.

When analyzing the results of a serological test, it is important to take into account the dynamics of the serological response to infection.

During the first 2-4 weeks from the moment of the tick bite in patients with erythema migrans, the result of the serological test may be false-negative. In this case, in the case of a high probability of Lyme disease, it is recommended to repeat the serological examination after 4-6 weeks.

A positive result of a test for the presence of antibodies can indicate both an active infectious process and a transferred infection, because both classes of immunoglobulins can persist in the blood serum for months and even years.  

In some cases, a Borrelia antibody test result may be false-positive due to the presence of cross-reactive antibodies to other microbes or an autoimmune disease. That is why it is appropriate to conduct a serological examination only in case of high probability of Lyme disease.

In view of the above, the following two-level procedure is recommended for serological confirmation of the diagnosis:

• Stage 1: Enzyme immunoassay (IFA) or immunofluorescence assay (IFA) to determine the titer of IgG and/or IgM

• Stage 2: Western blotting, which is carried out in case of a positive or doubtful result of a blood test for antibody titer

To identify the DNA of the causative agent, polymerase chain reaction (PCR) is performed, however, according to existing recommendations, it is of secondary importance in the diagnosis of Lyme borreliosis.

In addition to laboratory confirmation of Lyme disease, patients undergo additional examination methods depending on clinical symptoms.

In case of heart damage, it is advisable to conduct electrocardiography, transthoracic echocardiography, blood test for troponin-I and others. In patients with Lyme carditis, signs of myopericarditis, heart rhythm and/or conduction disturbances are found.

When joints are affected, in some cases, it is advisable to perform an arthrocentesis followed by an examination of the synovial fluid. In patients with Lyme arthritis, the synovial fluid is usually inflammatory, with cell counts ranging from 500 to 98,000/μl. In adult patients, the fluid should also be checked for crystals to rule out gout and pseudogout. Detection of B. burgdorferi DNA in synovial fluid is not a reliable test for active joint infection in Lyme disease.

In the case of damage to the central nervous system, in particular, when meningitis is suspected, a lumbar puncture is performed followed by analysis of the cerebrospinal fluid. In patients with meningitis caused by Lyme disease, analysis of the cerebrospinal fluid (CSF) often shows moderate pleocytosis (< 1000 cells/μl) with a predominance of lymphocytes. Patients with meningitis usually have an elevated protein concentration (>50 mg/dL) but a normal glucose level (45-80 mg/dL). Oligoclonal bands specific for B burgdorferi may be present.

Differential diagnosis

Depending on the clinical manifestations, Lyme disease is differentiated into the following conditions:

• Ankylosing spondylitis and rheumatoid arthritis

• Contact dermatitis

• Gout and pseudogout

• Annular granuloma

• Prion diseases

• Bell’s palsy

• Chronic fatigue syndrome (myalgic encephalomyelitis)

• Fibromyalgia

• Juvenile rheumatoid arthritis

• Systemic lupus erythematosus (SLE)

• Other diseases transmitted by ticks

Specialist consultations

In some cases, in particular when it is necessary to exclude other causes of existing complaints, there is a need to consult related specialists, such as a rheumatologist, dermatologist, cardiologist, neurologist, psychotherapist.

Treatment

The main goals of treatment are to eliminate the symptoms and signs of infection, prevent the development of complications and relapses of active infection.

For this, patients with confirmed Lyme disease are prescribed antibiotic therapy. The drugs of choice are doxycycline, amoxicillin, cefuroxime axetil. In case of intolerance to doxycycline and beta-lactams, azithromycin is used.

Drug therapy of erythema migrans

The duration of antibiotic therapy for patients with erythema migrans depends on the selected drug: doxycycline is prescribed at a dose of 100 mg 2 times a day for 10 days, amoxicillin is prescribed at a dose of 500 mg 3 times a day for 14 days or cefuroxime axetil at a dose of 500 mg 2 times for day for 14 days. In case of intolerance to doxycycline or beta-lactams, azithromycin is used for 5-10 days.

Antibiotic therapy of other clinical manifestations of Lyme disease has certain features.

Drug therapy of acute neurological manifestations

In patients with meningitis associated with Lyme disease, cranial neuropathy, radiculoneuropathy, or other manifestations of peripheral nervous system involvement, intravenous ceftriaxone, cefotaxime, penicillin G, or oral doxycycline should be used instead of other antimicrobial agents. The recommended duration of antibiotic therapy is 14–21 days.

Drug therapy of carditis

Outpatient treatment is indicated for patients: without clinical manifestations of myopericarditis, without arrhythmia, without II or III degree AV blockade, without I degree blockade with a PR interval ≥0.3 seconds. Outpatients with heart damage are prescribed oral antibacterial drugs: doxycycline, amoxicillin, cefuroxime, azithromycin.

Inpatient treatment is indicated for patients: with clinical manifestations of myopericarditis, with arrhythmias, with II or III degree AV block, with I degree AV block with a PR interval ≥0.3 sec. Inpatient patients with heart damage are prescribed parenteral antibacterial drugs: ceftriaxone in IV, cefotaxime IV, benzylpenicillin IV or IV. After the appearance of positive dynamics, it is possible to switch to oral antibiotics.

The duration of antibiotic therapy for Lyme carditis should be 14-21 days.

For patients with symptomatic bradycardia due to heart damage in Lyme disease that is not amenable to medical treatment, temporary electrical cardiostimulation is recommended.

Drug therapy of arthritis

Patients with Lyme arthritis are prescribed doxycycline, amoxicillin, or cefuroxime. The duration of antibiotic therapy for joint damage should be 28 days.

Borreliosis lymphocytoma

Antibiotic therapy with doxycycline, amoxicillin or cefuroxime for 14 days is recommended for patients with borreliosis lymphocytoma.

Chronic atrophic acrodermatitis

Antibiotic therapy with doxycycline, amoxicillin or cefuroxime for 21-28 days is recommended for patients with chronic atrophic acrodermatitis.

Tactics in case of ineffectiveness of antibiotic therapy

Patients who have persistent or recurrent nonspecific symptoms such as fatigue, pain, or cognitive impairment after recommended Lyme disease treatment, but who do not have objective evidence of reinfection or treatment failure, should not be given additional courses of antibiotic therapy.

Evidence of persistent infection or ineffectiveness of treatment is the preservation of objective signs of disease activity, such as arthritis, meningitis, or neuropathy.

Prevention

Individual protection measures

Persons at risk of infection should take personal protective measures to reduce the risk of being bitten by ticks and contracting the pathogens they transmit. To do this, when going to an area with a high probability of contact with ticks, it is recommended to wear light-colored clothes with long sleeves and pants, tuck your pants into socks or high shoes, and conduct a thorough check of your clothes and body after returning.

Use of repellents to prevent tick bites

For the prevention of tick bites, it is recommended to use products containing N,N-diethyl-meta-toluamide (DEET), picaridin, ethyl 3-(Nn-butyl-N-acetyl) aminopropionate (IR3535), oil of lemon eucalyptus (OLE), p-methane-3,8-diol (PMD), 2-undecanone or permethrin.

Removal of attached ticks

Given that the length of time a tick is attached to the skin is an extremely important predictor of developing Lyme disease (the likelihood of Lyme disease increases significantly after 36-48 hours), immediate removal of the attached tick is recommended. This is best done with clean, fine-tipped tweezers (or similar device) inserted between the body of the tick and the skin.

It is not advisable to burn the attached tick (with a match or other thermal intervention) or to use harmful chemicals or petroleum products to detach it.

After removing the tick, it is recommended to carry out a study to identify its species. But at the same time, it is not advisable to test the removed tick for B. Burgdorferi, because the presence or absence of this microorganism is not a reliable sign of the presence of infection.

Antibiotic prophylaxis

It is recommended to prescribe prophylactic antibiotic therapy for adults and children within 72 hours after removal of a high-risk tick.

The patient is prescribed a single dose of doxycycline at a dose of 200 mg for adults or 4.4 mg/kg (up to 200 mg) for children.

A tick bite is considered high-risk if it meets the following three criteria: the removed tick belongs to the Ixodes species; the bite occurred in a highly endemic area; the tick was attached for ≥36 hours.

If the tick bite is not high-risk, observation is recommended.

Post-Treatment Lyme Disease Syndrome ( PTLDS )

Post-treatment Lyme disease syndrome (PTLDS) is characterized by the presence of persistent (more than 6 months) symptoms (pain, fatigue, difficulty thinking) after the end of Lyme disease treatment.

The cause of this syndrome is unknown. Some experts believe that Borrelia burgdorferi can trigger an “autoimmune” reaction, causing symptoms that persist even after the infection has cleared. Other experts suggest that PTLDS is the result of a persistent but difficult-to-detect infection. Finally, some believe that the symptoms of PTLDS are due to other causes unrelated to Borrelia burgdorferi infection.

Unfortunately, there is no specific treatment for PTLDS. Studies have shown that long-term outcomes are no better for patients who receive additional long-term antibiotic treatment than for patients who receive placebo. Prolonged antibiotic treatment of Lyme disease is associated with serious, sometimes fatal, complications.

Patients with PTLDS usually improve over time, but this may take many months.

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Resources:

1. Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA), American Academy of Neurology (AAN), and American College of Rheumatology (ACR): 2020 Guidelines for the Prevention, Diagnosis and Treatment of Lyme Disease. Clinical Infectious Diseases, Volume 72, Issue 1, 1 January 2021, Pages e1-e48. https://doi.org/10.1093/cid/ciaa1215
2. Official site of the Centers for Disease Control and Prevention. https://www.cdc.gov/lyme/treatment/index.html

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The onset of the consultation

1. Wash hands and put on PPE if necessary.
2. Introduce yourself to the patient by stating your name and role.
3. Confirm the patient’s last name, first name and date of birth.
4. Explain what the examination will involve using language the patient can understand.
5. Get consent for consultation.
6. Adequately expose the patient for examination.
7. Ask the patient if he is in pain before proceeding with the clinical examination.

Clarification of the main complaint

8. Use open-ended questions to explore the patient’s complaints
9. Details of the main complaint
10. Analyze the patient’s thoughts, fears, and expectations
11. Summarize the patient’s complaints

Comprehensive assessment

12. Assess other symptoms to get a comprehensive picture

Medical history

13. Find out when and how complaints first appeared; specify the possible reason for the appearance of these complaints; detailed identification of the circumstances that preceded bradycardia, for example, stress, physical exertion, taking medication or food; did the patient seek medical help, if so, to whom and how did his appeal end, if not, then specify why he did not seek medical help; whether the patient took medical drugs independently or as prescribed by the doctor, if so, whether the nature of the complaints changed
14. In case of a history of hospitalization due to symptomatic bradycardia, read the extract from the patient’s medical history, pay attention to the established clinical diagnosis, the results of the laboratory or instrumental examinations, the treatment and recommendations after discharge
15. If the patient has previously undergone laboratory or instrumental examinations for current complaints, analyze their results and indicate important findings
16. Find out what prompted the patient to contact you
17. Exclude other causes of existing complaints by asking the patient clarifying questions

History of life

18. Clarify whether the patient has previously been diagnosed with cardiovascular diseases, in particular myocardial infarction, angina pectoris, cardiomyopathy, congenital heart defects, myocarditis

19. Find out if the patient has previously been diagnosed with a rhythm and/or conduction disorder
20. Find out whether the patient suffers from infiltrative diseases, in particular sarcoidosis, hemochromatosis, amyloidosis; systemic diseases of connective tissue, such as rheumatoid arthritis, scleroderma, systemic lupus erythematosus; endocrine diseases, in particular hypothyroidism; neurological diseases accompanied by increased intracranial pressure
21. Find out if the patient has had previous surgical interventions, including prosthetic heart valves, coronary artery bypass grafting, Maze procedure, and find out how the post-operative period was
22. Find out whether the patient is taking medications, in particular digoxin, beta-adrenergic blockers, calcium channel antagonists, antiarrhythmics, potassium, magnesium, calcium preparations; specify the doses of the drugs
23. Find out if the patient has recently had an infectious disease and if the patient has been bitten by a tick
24. Find out if the patient has a drug or food intolerance and how it manifests itself
25. Find out if the patient has bad habits – drinking alcohol, drugs, smoking
26. Determine whether the patient’s blood relatives have had cardiovascular disease, including rhythm and/or conduction disorders
27. Find out the patient’s marital status, living conditions
28. Clarify whether the patient works, his profession, working conditions, the presence of harmful occupational factors 

Objective examination

29. Assessment of the patient’s general condition
30. Conducting a general inspection
31. Evaluation of the constitution  
32. Estimation of the degree of obesity
33. Skin and mucous membranes
34. Evaluation of thyroid glands
35. Assessment of peripheral lymph nodes
36. Assessment of respiratory organs
37. Evaluation of the cardiovascular system
38. Assessment of abdominal organs
39. Evaluation of organs of the genitourinary system

Laboratory examination

40. Blood analysis for electrolytes
41. Blood test for thyroid hormones and TSH
42. Clinical blood count (if needed)
43. Coagulogram (if necessary)
44. Blood test for creatinine and urea (if needed)
45. Blood test for troponin- I (if necessary)
46. Blood test for IgM and IgG antibodies to Borrelia (if necessary)
47. PCR for Borrelia burgdorferi DNA detection (if necessary)
48. Assessment of blood pH (if necessary)
49. Genetic testing (if needed)
50. Toxicological screening (if necessary)

Diagnostic tests

51. Electrocardiography in 12 leads
52. Transthoracic echocardiography
53. Ambulatory ECG monitoring (if necessary)
54. ECG test with dosed exercise (if necessary)
55. Coronary angiography (if necessary)
56. MRI of the heart (if necessary)
57. Positron emission tomography (if necessary)
58. Electrophysiological examination (if necessary)
59. Polysomnography (if necessary)

Making a clinical diagnosis

60. Identification of the underlying disease
61. Indication of the nature of the conduction disturbance that caused the bradycardia
62. Indication of comorbid pathology

Specialist consultations

63. Cardiologist
64. Cardiac surgeon
65. Arithmologist
66. Rheumatologist
67. Neuropathologist _
68. Endocrinologist
69. Nephrologist
70. Geneticist
71. Infectious Disease Specialist

Treatment

72. Emergency therapy
73. Long-term therapy (permanent cardiac stimulation)

Explain the procedure for cardiac stimulation

74. Check the patient’s understanding of the reason for the procedure
75. Check the patient’s understanding of the procedure
76. Inform about the stages of the procedure
77. Tell about the risks and complications
78. Carry out work on mitigating fears
79. Suggest an additional source of information

Consulting and support

80. Inform the patient about the disease
81. Explain to the patient the possible causes of the disease
82. Inform the patient of the symptoms that may occur with the identified disease
83. Discuss the results of the examinations with the patient
84. Explain to the patient the possible consequences of the disease
85. Educate the patient about available treatments
86. Help the patient understand the risks and benefits of different treatments
87. Answer the patient’s questions
88. Provide an explanation of the extent of monitoring during and after treatment
89. Schedule regular check-ups and follow-up to assess the effectiveness of treatment and changes in the patient’s condition

Monitoring the effectiveness of treatment

90. Clinical assessment
91. Instrumental assessment
92. Control over side effects of therapy

End of consultation

93. Summarize the data and ask the patient if anything important has been missed
94. Inform the patient about further tactics
95. Thank the patient
96. Dispose of PPE properly and wash hands

Key communication skills

97. Active listening
98. Summing up
99. Selection of indicative signs

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The beginning of the consultation

1. Wash hands and put on PPE if necessary.
2. Introduce yourself to the patient by stating your name and role.
3. Confirm the patient’s last name, first name, and date of birth.
4. Explain what the examination will involve using language the patient can understand.
5. Get consent for consultation.
6. Adequately expose the patient for examination.
7. Ask the patient if he is in pain before proceeding with the clinical examination.

Symptoms of bradycardia typically manifest when the heart rate falls below 50 beats per minute, often indicating signs of hypoperfusion in critical organs such as the brain and heart.

Clinical signs may include:

• Symptoms indicative of cerebral hypoperfusion (e.g., dizziness, blurred vision, loss of consciousness).
• Manifestations of compromised cardiac perfusion (e.g., chest pain, dyspnea, sensation of air insufficiency, diminished tolerance to physical exertion).
• General symptoms suggestive of inadequate blood supply to other organs and systems (e.g., weakness, heightened fatigue).

Clarification of the main complaint

8. Use open-ended questions to explore the patient’s complaints
9. Details of the main complaint
10. Analyze the patient’s thoughts, fears, and expectations
11. Summarize the patient’s complaints

• Use open-ended questions to explore the patient’s complaints
• Details of the main complaint

The most common complaints of a patient experiencing bradycardia often involve dizziness and potential loss of consciousness.

To further investigate complaints of dizziness, consider the following algorithm:

1. Circumstances preceding the onset of dizziness: Inquire about recent physical activity, body position changes, emotional stressors, food or drink consumption, and medication intake.
2. Onset: Determine if the dizziness occurs suddenly or develops gradually.
3. Description: Prompt the patient to articulate the sensations experienced during the episode of dizziness.
4. Intensity: Ask the patient to rate the severity of their dizziness on a scale from 0 to 10.
5. Associated symptoms: Inquire about any additional symptoms accompanying the dizziness.
6. Duration: Establish whether the dizziness occurs periodically or persists continuously.
7. Aggravating or alleviating factors: Identify any factors that exacerbate or relieve the intensity of dizziness, particularly changes in body position.

“Could you describe what happened before you started feeling dizzy?”

“Does the dizziness come on suddenly or does it develop gradually?”

“Can you please explain what sensations you experience when you feel dizzy?”

“On a scale from 0 to 10, how would you rate the severity of your dizziness?”

“Are there any other symptoms that occur along with the dizziness?”

“Does the dizziness occur constantly or does it happen periodically?”

“Are there any factors that make the dizziness worse or better?”

If the main complaint of your patient is an episode of loss of consciousness, follow this algorithm:

• Circumstances preceding loss of consciousness: physical activity, prolonged standing, change in body position, emotional stress, intake of food or medication, intense cough.
• Start: Find out if any symptoms preceded the loss of consciousness (dizziness, visual disturbances, sweating, nausea, palpitations, shortness of breath).
• Concomitant symptoms: Ask the person who witnessed the fainting episode if the fainting episode was accompanied by other symptoms (including convulsions, involuntary defecation or urination).
• Duration: Ask the witness about the duration of the episode of unconsciousness.
• Factors contributing to faster recovery of consciousness: horizontal position of the body, use of medication.

“Tell me what you were doing before you lost consciousness?”

“Tell me, was loss of consciousness preceded by dizziness, sweating, nausea, palpitations, shortness of breath?”

“How long was the patient unconscious?”

“Was the episode of unconsciousness accompanied by other symptoms?”

“Was there anything that helped you to restore the consciousness of the patient?”

Analyze the patient’s thoughts, fears, and expectations

A key component of history-taking is exploring the patient’s thoughts, concerns, and expectations to gain insight into how the patient currently perceives their condition, their concerns, and what they expect from the consultation.

The exploration of thoughts, concerns, and expectations should be fluid throughout the consultation in response to cues from the patient. This will help to make your consultation patient-oriented, rather than formulaic.

It is essential to structure the analysis of thoughts, fears, and expectations so that it sounds natural in your consultation.

Summarize the patient’s complaints

Summarize the patient’s complaint to ensure understanding and provide an opportunity for the patient to correct any inaccuracies. After summarizing, ask if there’s anything else the patient would like to add or clarify. Throughout the consultation, periodically summarize intermediate findings

Comprehensive assessment

12. Screen for symptoms of damage to other organs and systems

A comprehensive assessment involves briefly surveying the patient for symptoms of other systems, which may or may not be related to the chief complaint. This approach can help identify symptoms the patient may have overlooked.

Here are some examples of symptoms to monitor for each system:

Medical history

13. Find out when and how complaints first appeared; specify the possible reason for the appearance of these complaints; did the patient seek medical help, if so, to whom and how did his appeal end, if not, then specify why he did not seek medical help; whether the patient took medical drugs independently or as prescribed by the doctor, if so, whether the nature of the complaints changed

“When did you first experience these symptoms?”

“What do you think might be causing these symptoms?”

“Have you consulted a healthcare professional about this issue?”

14. In case of a history of hospitalization due to symptomatic bradycardia, read the patient’s medical history, pay attention to the established clinical diagnosis, the results of the laboratory or instrumental examinations, the treatment and recommendations after discharge
15. If the patient has previously undergone laboratory or instrumental examinations for current complaints, analyze their results and indicate important findings
16. Find out what prompted the patient to contact you

“What led you to reach out to me?”

“What prompted you to seek my assistance?”

17. Exclude other causes of existing complaints by asking the patient clarifying questions

“Do you experience shortness of breath or a sensation of air hunger?”

“Are you experiencing any chest pain?”

Other causes of dizziness:

• Cerebrovascular disorders

Dizziness is a relatively common symptom of impaired blood flow to the brain, but it’s not the only one. Alongside dizziness, patients typically report numbness or weakness in one side of the body, difficulty understanding speech or speaking, double vision, unsteadiness while walking, loss of balance, or coordination problems. Patients with impaired cerebral circulation often have a medical history of hypertension, rhythm disturbances (such as atrial fibrillation), diabetes mellitus, and dyslipidemia. Neurological examination may reveal deficits such as hemiparesis or hemiplegia, sensory or motor aphasia, nystagmus, facial asymmetry, deviation of the tongue from the midline, inability to perform the thumb-nose test, instability in Romberg’s sign, among others. Blood pressure and heart rate typically remain normal or may show slight increases.

• Hypoglycemia

Patients experiencing hypoglycemia often report severe hunger, pronounced weakness, and increased sweating alongside dizziness. They typically have a history of taking hypoglycemic medications, prolonged fasting, or engaging in excessive physical activity. These patients may appear agitated, with cold, clammy skin, and the doctor may observe tachycardia and a moderate increase in blood pressure. The initial agitation can rapidly transition to central nervous system depression, leading to loss of consciousness.

• Arterial hypertension

Dizziness commonly accompanies high blood pressure. Additionally, patients with arterial hypertension often report a throbbing or aching headache, nausea, and visual disturbances like flickering. During the physical examination, the doctor typically observes elevated blood pressure readings ≥140/90 mm Hg and often notes tachycardia.

• Arterial hypotension

Dizziness can manifest as a symptom of both high and low blood pressure. Patients with hypotension also commonly experience pronounced weakness, lethargy, drowsiness, and reduced tolerance to physical exertion. These patients often have a history of taking vasodilators, diuretics, experiencing repeated vomiting, diarrhea, bleeding, or adhering to a diet with limited salt and water intake. During the physical examination, the doctor may observe pallor of the skin, increased sweating, cold extremities, and a decrease in blood pressure ≤90/60 mm Hg, accompanied by reduced urine output.

• Anemia

Dizziness is a common symptom of chronic anemia. Alongside dizziness, patients with anemia often report persistent pronounced weakness, increased fatigue, palpitations, shortness of breath, brittle nails and hair, pain in the tongue, and alterations in food preferences and taste. In their medical history, patients may mention dietary changes, avoidance of animal protein, gastrointestinal diseases, gastrointestinal surgeries, pregnancy, chronic hemorrhoidal bleeding, or prolonged menstruation. Physical examination typically reveals pallor of the skin and mucous membranes, tachycardia, a small, frequent pulse, and a functional systolic murmur.

• Meniere’s disease

Characteristic symptoms of Ménière’s disease include systemic dizziness, tinnitus, and progressive hearing loss. Typically, these symptoms occur in an episodic manner, often in the morning or at night, triggered by psychological or physical stressors. During an episode, patients may experience nausea, vomiting, and coordination disturbances. The duration of these episodes can range from a few minutes to several days, with the average being several hours.

Other reasons for episodes of loss of consciousness:

• Vasovagal syncope

Vasovagal syncope is a type of reflex syncope triggered by severe stress (such as fear, pain, the sight of blood, or medical procedures) or prolonged standing in an upright position. It typically develops gradually and is often preceded by symptoms like dizziness, visual disturbances, nausea, and increased sweating. During a vasovagal syncope episode, patients may experience involuntary movements, hypotension, and a decrease in heart rate. The duration of the episode usually does not exceed 1 minute, and patients typically regain consciousness spontaneously.

• Situational syncope

Situational syncope is another type of reflex syncope that occurs due to a sudden increase in intra-abdominal pressure, such as during a forceful cough, defecation, urination, or after eating a large meal. Similar to vasovagal syncope, situational syncope tends to develop gradually, with preceding symptoms like dizziness, nausea, and visual disturbances. During the episode, the patient may exhibit pallor, bradycardia, and hypotension. Situational syncope episodes typically last no more than 1 minute, and patients often regain consciousness spontaneously.

• Carotid sinus syndrome

Carotid sinus syndrome is characterized by hypersensitivity of the carotid sinus, often triggered by actions like a sharp turn of the head, wearing a tight collar, or shaving the neck. Before losing consciousness, patients may experience symptoms such as visual dimming and dizziness. During an episode of carotid syncope, marked pallor of the skin, along with a decrease in heart rate and blood pressure, is typically observed.

• Syncope due to orthostatic hypotension

Syncope due to orthostatic hypotension, on the other hand, occurs when there is a sudden drop in blood pressure upon moving from a horizontal to a vertical position. This type of syncope is commonly seen in the elderly and in individuals taking medications like diuretics, vasodilators, and antidepressants. Patients may also have hypovolemia due to conditions such as bleeding, repeated diarrhea, or vomiting. Diagnosis involves measuring blood pressure in both horizontal and vertical positions. A difference in systolic pressure of ≥20 mm Hg and/or diastolic pressure of ≥10 mm Hg upon changing positions suggests orthostatic hypotension. Unlike carotid sinus syndrome, patients with syncope due to orthostatic hypotension typically exhibit tachycardia rather than bradycardia.

• Syncope due to cerebrovascular disease

Syncope resulting from cerebral ischemia is typically accompanied by various neurological symptoms, including speech disorders, facial asymmetry, hemiparesis or hemiplegia, meningeal symptoms, ataxia, and others.

History of life

18. Clarify whether the patient has previously been diagnosed with cardiovascular diseases, in particular myocardial infarction, angina pectoris, cardiomyopathy, congenital heart defects, myocarditis
19. Find out if the patient has previously been diagnosed with a rhythm and/or conduction disorder
20. Find out whether the patient suffers from infiltrative diseases, in particular sarcoidosis, hemochromatosis, amyloidosis; systemic diseases of connective tissue, such as rheumatoid arthritis, scleroderma, systemic lupus erythematosus; endocrine diseases, in particular hypothyroidism; neurological diseases accompanied by increased intracranial pressure
21. Find out if the patient has had previous surgical interventions, including prosthetic heart valves, coronary artery bypass grafting, Maze procedure, and find out how the post-operative period was
22. Find out if the patient is taking medications, including digoxin, beta-adrenergic blockers, calcium channel antagonists, antiarrhythmics, psychoactive drugs, clonidine, potassium, magnesium, calcium drugs; specify the doses of the drugs
23. Find out if the patient has recently had an infectious disease and if the patient has been bitten by a tick
24. Find out if the patient has a drug or food intolerance and how it manifests itself
25. Find out if the patient has bad habits – drinking alcohol, drugs, smoking
26. Determine whether the patient’s blood relatives have had cardiovascular disease, including rhythm and/or conduction disorders
27. Find out the patient’s marital status, living conditions
28. Clarify whether the patient works, his profession, working conditions, the presence of harmful occupational factors 

Objective examination

29. Assessment of the patient’s general condition

30. Conducting a general inspection
31. Evaluation of the constitution  
32. Estimation of the degree of obesity
33. Skin and mucous membranes
34. Evaluation of thyroid glands
35. Assessment of peripheral lymph nodes
36. Assessment of respiratory organs
37. Evaluation of the cardiovascular system
38. Assessment of abdominal organs
39. Evaluation of organs of the genitourinary system

Assess for objects or equipment on or around the patient that may provide useful information about the patient’s medical history and current clinical condition.

The key, and sometimes the only, objective sign of symptomatic bradycardia is a slowing of the heart rate (HR) to less than 60 beats per minute.

In the case of a moderate decrease in heart rate, blood pressure remains normal, but with a significant decrease in heart rate, hypotension often occurs.

With a significant decrease in heart rate, acute heart failure may occur with the appearance of moist rales in the lungs, tachypnea, and cyanosis.

In the case of a disruption of the blood supply to the brain, a disturbance of consciousness is often observed.

Additionally, during the physical examination, it is important to pay attention to signs of a disease that has led to a decrease in heart rate.

Thus, additional III or IV heart sounds, gallop rhythm, systolic noise of mitral regurgitation, paradoxical splitting of the II sound, congestive rales in the lungs can suggest coronary heart disease.

In patients with myocarditis, weakening of the I heart tone, an additional III heart tone is often detected, and in those with congestion alongside myocarditis, an accent of the II tone is heard over the pulmonary artery, wet fine-vesicular rales, and swelling of the lower extremities.

In patients with restrictive cardiomyopathy, the systolic murmur of mitral regurgitation, weakening of the first heart sound, wet, small bubbling rales in the lungs, ascites, edema of the lower extremities, hepatomegaly, and swelling of the jugular veins can be detected in the late stages of the disease.

Endocarditis may be indicated by the detection during a physical examination of a characteristic skin shade similar to coffee with milk, systolic or diastolic regurgitation noise over the affected valve, Osler nodules (painful, red nodules on the fingers and toes), Janeway spots (painless hemorrhagic spots on the palms and soles), hepato- and splenomegaly.

In patients with sarcoidosis, skin changes such as erythema nodosum, papular or spot-papular rashes, small ulcers, generalized lymphadenopathy, moist rales in the lungs, hepatomegaly, and enlargement of the parotid salivary gland can be observed.

Bronze skin shade, ascites, swelling of the lower extremities, and signs of liver cirrhosis may indicate hemochromatosis.

Rheumatoid arthritis should be suspected in patients with signs of inflammation and deformation of the metacarpophalangeal and proximal interphalangeal joints.

Discoloration of the skin of the fingers and toes, thickening and atrophy of the skin, formation of radial wrinkles around the mouth, ulcers on the tips of the fingers, and telangiectasia may indicate scleroderma.

Dry skin, hair loss, hoarseness of voice, facial swelling, and hypotonia can indicate hypothyroidism.

Laboratory examination

40. Blood analysis for electrolytes (required)

41. Blood test for thyroid hormones and TSH (required)
42. Clinical blood count (if needed)
43. Coagulogram (if necessary)
44. Blood test for creatinine and urea (if needed)
45. Blood test for troponin- I (if necessary)
46. Blood test for IgM and IgG antibodies to Borrelia (if necessary)
47. PCR for Borrelia burgdorferi DNA detection (if necessary)

48. Assessment of blood pH (if necessary)
49. Genetic testing (if needed)
50. Toxicological screening (if necessary)

• Blood test for electrolytes (required )

A blood test for potassium, calcium, and magnesium levels is a crucial laboratory assessment in patients presenting with symptomatic bradycardia to diagnose electrolyte imbalances. Hypokalemia, hyperkalemia, hypercalcemia, and hypermagnesemia are recognized causes of significant bradycardia.

• Blood test for thyroid hormones and TSH ( required )

A blood test for thyroid hormones and TSH is a crucial laboratory assessment in patients with symptomatic bradycardia, as hypothyroidism frequently manifests with a slow heart rate and conduction disturbances.

• Clinical blood test (if needed)

Clinical blood count is not typically considered mandatory for patients presenting with symptomatic bradycardia. However, it becomes necessary as part of pre-procedural preparations for pacemaker implantation.

• Coagulogram (if necessary)

A coagulogram is indeed included in the list of laboratory tests performed on patients with symptomatic bradycardia before a permanent cardiac pacing procedure to assess blood coagulation activity.

• Blood test for creatinine and urea (if needed)

Blood tests for creatinine and urea are indeed included in the list of laboratory tests performed in patients with symptomatic bradycardia before the procedure of permanent cardiac pacing.

• Blood test for troponin- I (if necessary)

A blood test for troponin-I is indeed performed in patients with symptomatic bradycardia when myocardial ischemia is suspected.

• Blood test for IgM and IgG antibodies to Borrelia (if necessary)

A blood test for IgM and IgG antibodies to Borrelia is indeed performed in patients with symptomatic bradycardia when Lyme disease is suspected.

• PCR for Borrelia burgdorferi DNA detection (if necessary)

Additionally, PCR for Borrelia burgdorferi DNA detection may be necessary in certain cases.

• Assessment of blood pH level (if necessary)

Assessment of blood pH level is also important in patients with symptomatic bradycardia, especially when metabolic acidosis is suspected, as it can contribute to bradycardia.

• Genetic testing (if needed)

Genetic testing for SCN5A and TRPM4 gene mutations may be needed in patients with symptomatic bradycardia, particularly when there is suspicion of a hereditary component to the rhythm or conduction disorder, especially in patients under the age of 50 who are experiencing symptoms.

• Toxicological screening (if necessary)

Toxicological screening is indeed indicated for suspected bradycardia induced by the action of a toxic substance or drug. For instance, when an overdose of cardiac glycosides is suspected, determining the level of digoxin in the blood is essential. Other tests aimed at detecting toxic substances in the body exist, but they typically require the involvement of a toxicologist.

Diagnostic tests

51. Electrocardiography in 12 leads (required)

52. Transthoracic echocardiography (mandatory)
53. Ambulatory ECG monitoring (if necessary)
54. ECG test with dosed exercise (if necessary)
55. Coronary angiography (if necessary)
56. MRI of the heart (if necessary)
57. Positron emission tomography (if necessary)
58. Electrophysiological examination (if necessary)
59. Polysomnography (if necessary)

• Electrocardiography in 12 leads ( required )

Electrocardiography (ECG) in 12 leads is indeed a crucial method of examination for all patients with symptomatic bradycardia.

The primary causes of symptomatic bradycardia typically involve sinus node weakness syndrome and atrioventricular conduction disorders.

Manifestations of sinus node weakness syndrome encompass various abnormalities such as persistent sinus bradycardia, ectopic atrial bradycardia, sinoatrial block of different degrees, pacemaker migration, sinus node arrest with a pause lasting more than 3 seconds, bradysystolic form of atrial fibrillation, tachy-brady syndrome, and chronotropic incompetence.

ECG signs of persistent sinus bradycardia manifest as a sustained reduction in heart rate to less than 50 beats per minute.

Figure 1. Atrial fibrillation. Image sourced from litfl.com internet resource. https://litfl.com/sinus-bradycardia-ecg-library

ECG signs of second-degree sinoauricular block include periodic loss of the PQRST complex, with the duration of the pause equal to the sum of two or more normal RR complexes of the underlying rhythm. During these pauses, substitute complexes originating from the AV node or ventricles may appear.

Figure 2. Second-degree sinoauricular block. Image sourced from litfl.com internet resource. https://litfl.com/sinoatrial-exit-block-ecg-library

ECG signs of complete sinoauricular block include the complete cessation of sinus rhythm with the appearance of a replacement rhythm, typically originating from the AV node.

Figure 3. Complete sinoauricular block. Image from litfl.com internet resource. https://litfl.com/sinus-node-dysfunction-sick-sinus-syndrome

ECG signs of pacemaker migration include a gradual change in the shape and polarity of the P wave from cycle to cycle.

Figure 4. Migration of the pacemaker. Image https://therapy.odmu.edu.ua/ecg-online-course/wandering-pacemaker

ECG signs of tachy-brady syndrome include alternating episodes of acceleration and deceleration of the heart rate.

Figure 5. Tachy-brady syndrome. Image from litfl.com internet resource. https://litfl.com/sinus-node-dysfunction-sick-sinus-syndrome

ECG signs of Mobitz I second-degree AV block include progressive lengthening of the PQ interval with periodic loss of QRS complexes.

Figure 6. Second-degree AV block II, Mobitz I. Image from the internet resource litfl.com. https://litfl.com/av-block-2nd-degree-mobitz-i-wenckebach-phenomenon

ECG signs of Mobitz II second-degree AV block include stable prolongation of the PQ interval with periodic loss of QRS complexes.

Figure 7. Second-degree AV-block, Mobitz II. Image from litfl.com internet resource. https://litfl.com/av-block-2nd-degree-mobitz-ii

ECG signs of third-degree AV block include complete dissociation of atrial and ventricular waves, with the atrial contraction frequency significantly exceeding the frequency of ventricular activation.

Figure 8. Third-degree AV block. Image from litfl.com internet resource. https://litfl.com/av-block-3rd-degree-complete-heart-block

• Transthoracic echocardiography (mandatory)

Transthoracic echocardiography is a crucial examination method for all patients presenting with symptomatic bradycardia. It aids in identifying myocardial structural abnormalities that could contribute to heart rate slowing, assessing left ventricular systolic function, and diagnosing potentially reversible causes of cardiac conduction disturbances.

• Ambulatory ECG monitoring (if necessary)

Ambulatory ECG monitoring is recommended when there’s a need to confirm the direct relationship between ECG changes and clinical manifestations.

• ECG test with dosed exercise (if necessary)

An ECG test with dosed exercise is conducted for patients who develop bradycardia during or immediately after physical activity. If symptoms arise during exercise, it may suggest a cardiac cause, while post-exercise bradycardia could indicate a reflex mechanism.

• Coronary angiography (if necessary)

Coronary angiography is indicated for patients with suspected ischemic causes of bradycardia or those with a significant family history.

• MRI of the heart (if necessary)

MRI of the heart is performed to investigate suspected inflammatory or infiltrative heart diseases contributing to bradycardia.

• Positron emission tomography (if necessary)

Positron emission tomography aids in complex cases by detecting myocardial inflammation foci.

• Electrophysiological examination (if necessary)

Electrophysiological examination serves as an adjunct when non-invasive methods fail to record bradycardia. It’s particularly useful for identifying sinus node dysfunction or pinpointing the site of impaired AV conduction.

• Polysomnography (if necessary)

Polysomnography is conducted for patients experiencing nocturnal bradycardia episodes, often associated with obstructive sleep apnea syndrome.

Differential diagnosis

Diagnosing symptomatic bradycardia typically isn’t challenging, but determining its cause can be more complex.

Common causes include acute myocardial ischemia, overdose of medications like cardiac glycosides, beta-blockers, and calcium channel antagonists, hyperkalemia, hypothermia, and hypoxia.

Acute myocardial ischemia presents with chest pain radiating to the left arm, scapula, or epigastrium. Elevated myocardial necrosis markers (troponin-I/T, CK-MB), along with characteristic ECG changes (ST segment elevation/depression, pathological Q wave, T wave inversion), are observed. Heart conduction issues often accompany ischemia affecting the lower left ventricular wall, considering the shared vascular supply.

Glycoside intoxication manifests as dyspeptic symptoms (anorexia, nausea, vomiting, diarrhea), visual disturbances (yellowish perception), and pulse slowing to asystole. ECG findings include ventricular extrasystoles, PQ interval prolongation, pacemaker migration, and trough-like ST segment depression. Suspected cases warrant digoxin-level assessment.

Beta-adrenergic blockers or calcium channel antagonist overdose leads to sinus and AV node depression with a substitute rhythm. Symptoms range from mild fatigue to dizziness and syncope. Detailed history-taking aids in diagnosis.

Hyperkalemia occurs in severe renal impairment, ACE inhibitor/sartan use, potassium supplements, aldosterone receptor blockers, rhabdomyolysis, metabolic acidosis, and sepsis. Diagnosis involves serum potassium assessment, and ECG may show high-amplitude T waves and intraventricular conduction abnormalities.

Hypothermia-induced bradycardia arises from prolonged cold exposure, typically exhibiting Osborne waves on the ECG.

Hypoxia, with blood oxygen saturation below 95%, presents with headache, dizziness, pallor, rapid breathing, and impaired memory and attention. Pulse oximetry is the primary diagnostic tool. Identifying the underlying cause of hypoxia – cardiovascular or respiratory diseases, anemia, vasculitis, altitude exposure, suffocation, drowning – is crucial. The effectiveness of oxygen therapy in restoring normal heart rhythm confirms the link between hypoxia and AV conduction slowing.

Making a clinical diagnosis

60. Identification of the underlying disease
61. Indication of the nature of the conduction disturbance that caused the bradycardia
62. Indication of comorbid pathology

• Identification of the underlying disease

Given that bradycardia is typically a manifestation or complication of an underlying disease, it’s crucial to first specify the primary diagnosis and then the associated rhythm disturbance. This approach aligns with existing classifications and ensures clarity in diagnosis.

• Indication of the nature of the conduction disturbance that caused the bradycardia

When identifying the conduction disturbance causing bradycardia, denote its type and degree: first-, second-, or third-degree sinoauricular block or atrioventricular block.

• Indication of comorbid pathology

In formulating the clinical diagnosis, specify any comorbid conditions according to established classifications.

Specialist consultations

63. Cardiologist
64. Cardiac surgeon
65. Arithmologist
66. Rheumatologist
67. Neuropathologist _
68. Endocrinologist
69. Nephrologist
70. Geneticist
71. Infectious Disease Specialist

A cardiologist serves as the primary specialist overseeing the management of bradycardia. They lead the diagnostic and treatment process, conducting thorough examinations, taking medical histories, prescribing treatment protocols, monitoring patient progress, and making necessary adjustments.

• Cardiac surgeon

Consultation with a cardiac surgeon becomes necessary when bradycardia is suspected to be induced by myocardial ischemia or a heart defect. The cardiac surgeon performs surgical corrections for these conditions, which can help alleviate bradycardia.

• Arithmologist

Given that pathological heart rate slowing often stems from sinus node weakness syndrome or AV conduction disturbances, an arrhythmologist’s assistance is invaluable. They determine the nature of existing rhythm or conduction disorders, including through electrophysiological studies, and if required, perform pacemaker implantation.

• Rheumatologist

If collagenosis is suspected as the cause of bradycardia, consulting a rheumatologist is necessary. Through additional laboratory or instrumental examinations, this specialist can confirm or rule out autoimmune connective tissue pathology.

• Neurologist

A neurologist’s consultation is necessary if a neurogenic cause of bradycardia is suspected, particularly due to central nervous system injuries or tumors leading to increased intracranial pressure. Additionally, since symptomatic bradycardia often coincides with alterations in mental status, a neurologist aids in differential diagnosis, especially against acute cerebral circulation disruptions.

• Endocrinologist

If hypothyroidism is suspected as the cause of symptomatic bradycardia, consultation with an endocrinologist is warranted.

• Nephrologist

Hyperkalemia is a common cause of slow heart rate, particularly in patients with severe renal impairment, necessitating consultation with a nephrologist.

• Geneticist

When hereditary conduction system disorders are suspected, especially if symptoms manifest before the age of 50 and progress over time, genetic consultation is essential.

• Infectious Disease Specialist

Consultation with an infectious disease specialist is advisable if an infectious disease is suspected as the cause of symptomatic bradycardia, such as Lyme disease or diphtheria.

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Treatment

72. Emergency therapy
73. Long-term therapy (permanent cardiac stimulation)

• Emergency therapy

When administering emergency care to a patient with symptomatic bradycardia, it’s crucial to adhere to the following algorithm of actions:

1. Ensure the patency of the respiratory tract.
2. Initiate oxygen therapy for hypoxemia (blood oxygen saturation <90%).
3. Monitor heart rate and blood pressure.
4. Establish intravenous access.
5. Consider potential causes of symptomatic bradycardia (discontinue drugs and, if possible, administer their antidotes; perform myocardial revascularization in acute ischemia; correct hyperkalemia).

In case of the development of hypotension, impaired consciousness, symptoms of acute heart failure, or myocardial ischemia, medical treatment is indicated:

• Administer atropine in a dose of 0.5-1.0 mg IV, with the possibility of repeated administration every 3-5 minutes if necessary (maximum dose – 3 mg).
• If atropine is ineffective, consider using dopamine at a dose of 5-20 μg/kg/min. or epinephrine at a dose of 0.02-0.2 μg/kg/min. IV drip.

If drug treatment proves ineffective, electrocardiostimulation is indicated, with preference given to temporary transvenous cardiostimulation. If transvenous cardiostimulation is not feasible, transcutaneous cardiostimulation may be considered.

It’s worth noting that administering aminophylline in a dose of 250 mg IV as a bolus is recommended for patients with second or third-degree AV block occurring against the backdrop of an acute lower myocardial infarction.

In cases of overdose with calcium channel antagonists, consider administering a 10% solution of calcium chloride in a dose of 1-2 g every 10-20 minutes intravenously or as an intravenous infusion at a rate of 0.2-0.4 ml/kg/h; alternatively, a 10% solution of calcium gluconate can be given in a dose of 3-6 g every 10-20 minutes intravenously or as an intravenous infusion at a rate of 0.6-1.2 ml/kg/h.

For beta-adrenergic blocker overdose, glucagon may be used at a dose of 3-10 mg IV as an infusion at a rate of 3-5 mg/h.

In cases of digoxin overdose, consider administering digibind at a rate of 1 vial to bind 0.5 mg of digoxin in the blood.

Patients with a transplanted heart or those with sinus node weakness syndrome due to spinal cord injury may benefit from aminophylline at a dose of 6 mg/kg, dissolved in 100-200 ml of physiological solution IV drip over 20-30 minutes, or theophylline 300 mg IV followed by oral administration at a dose of 5-10 mg/kg.

ACLS Bradycardia Algorithm

• Long-term therapy (permanent cardiac stimulation)

The choice of long-term therapy for patients with sinus node weakness syndrome depends on the presence of bradycardia symptoms:

• Observation is indicated for asymptomatic patients with sinus bradycardia or sinus pauses caused by sinus node syndrome, vagotonia, or nocturnal sleep apnea syndrome. Continuous cardiac stimulation may cause more harm than good in these cases.
• Symptomatic patients with bradycardia caused by sinus node syndrome are indicated for continuous pacing to increase heart rate and improve symptoms.

The choice of cardiac stimulation type depends on the frequency of necessary stimulation and the presence of concomitant pathology:

• For infrequent stimulation or in the presence of severe concomitant pathology, single-chamber ventricular cardiostimulation is advisable.
• If frequent stimulation is necessary, and there is no severe concomitant pathology with normal AV conduction, single-chamber atrial cardiostimulation is recommended.
• If frequent stimulation is necessary without severe concomitant pathology but with impaired AV conduction, two-chamber cardiostimulation is recommended.

Long-term therapy for patients with AV conduction disorders depends on the severity of the blockade and bradycardia symptoms:

• Asymptomatic patients with first-degree AV block or Mobitz type I second-degree AV block are observed; continuous cardiac stimulation may not be beneficial.
• Symptomatic patients with first-degree AV block or Mobitz type I second-degree AV block may consider permanent pacing.
• Symptomatic patients with Mobitz type II second-degree AV block and third-degree AV block are recommended for permanent cardiac stimulation.

The choice of cardiac stimulation type depends on the required frequency of stimulation and concomitant pathology:

• For infrequent stimulation or severe concomitant pathology, single-chamber ventricular cardiostimulation is advisable.
• For frequent stimulation without severe concomitant pathology, single-chamber ventricular cardiostimulation is recommended, especially for patients with a permanent form of atrial fibrillation.
• For frequent stimulation without severe concomitant pathology and without a permanent form of atrial fibrillation, two-chamber cardiostimulation is recommended.

Explain the procedure for cardiac stimulation

74. Check the patient’s understanding of the reason for the procedure

• “Do you understand the reason for performing this procedure on you?”
• “Do you understand the importance of carrying out this procedure for you?”

75. Check the patient’s understanding of the procedure

“Did you understand the procedure?”

76. Inform about the stages of the procedure

“I would like to explain to you what electrical cardiostimulation is and how it is performed. Electrical cardiac stimulation is a medical procedure aimed at normalizing the heart rhythm. Before conducting electrical cardiostimulation, you will be given a sedative and painkiller so that you feel comfortable and do not have any unpleasant sensations. After that, the surgeon will make a small skin incision under your collarbone and insert a special electrode into the subclavian vein. Under X-ray control, the doctor will lead this electrode to your heart and fix it in the right place. Then the surgeon will make a small pocket under your skin on the chest where a special pacemaker device will be located. This device will generate electrical impulses that will be conducted through the electrode to your heart. Thanks to this, your heart will contract in the correct rhythm. During the entire procedure and for some time after it, an experienced medical staff will be by your side, who will carefully monitor your condition.”

77. Talk about the risks and complications

“This procedure is quite safe, but sometimes patients may experience complications, for example, hematoma in the area of the formed subcutaneous pocket, infection, or displacement of the electrode. However, we will do everything possible to minimize the risk of their development.”

78. Do the work of mitigating fears

• “This procedure is routine for our clinic.”
• “This procedure is constantly performed in our department.”

79. Suggest an additional source of information

“You can learn more about the cardiac pacing procedure by reading the information in this booklet“

Consulting and support

80. Inform the patient about the disease
81. Explain to the patient the possible causes of the disease
82. Inform the patient of the symptoms that may occur with the identified disease
83. Discuss the results of the examinations with the patient
84. Explain to the patient the possible consequences of the disease
85. Educate the patient about available treatments
86. Help the patient understand the risks and benefits of different treatments
87. Answer the patient’s questions
88. Provide an explanation of the extent of monitoring during and after treatment
89. Schedule regular check-ups and follow-up to assess the effectiveness of treatment and changes in the patient’s condition

Monitoring the effectiveness of treatment

90. Clinical assessment

The effectiveness of treatment is clinically assessed by evaluating both subjective symptoms reported by the patient and objective parameters of the body’s functioning. Effective treatment should alleviate or significantly reduce symptoms associated with insufficient organ and system blood supply due to bradycardia. These symptoms may include fatigue, decreased tolerance to physical activity, dizziness, fainting, chest discomfort, and shortness of breath.

91. Studies to assess the presence of bradycardia

Objective assessment of bradycardia severity requires regular electrocardiography and, if necessary, daily Holter ECG monitoring. These tests provide valuable information about heart rhythm patterns and any fluctuations in heart rate over time.

92. Control over side effects of therapy

Following pacemaker implantation, patients should be monitored for potential side effects or complications. Common complications include discomfort or pain at the implantation site, hematoma formation, infection at the pacemaker site, systemic infection, allergic reactions to pacemaker materials, and impaired wound healing. Patients should be educated about these potential side effects and instructed to seek immediate medical attention if they experience any symptoms suggestive of these complications. Early detection and intervention are crucial for managing complications effectively.

End of consultation

93. Summarize the data and ask the patient if anything important has been missed
94. Inform the patient about further tactics

Hospitalization in a specialized cardiology hospital is recommended for a comprehensive examination and the selection of optimal treatment strategies. Ensure the patient’s Informed Voluntary Consent for diagnosis and treatment and obtain agreement for processing personal data.

95. Thank the patient
96. Dispose of PPE properly and wash hands

Key communication skills

97. Active listening
98. Summing up
99. Selection of indicative signs

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Сообщение Counseling of a patient with symptomatic bradycardia – OSCE guide появились сначала на ClinCaseQuest.

Symptomatic bradycardia occurs when the heart rate drops below 50 beats per minute.

Most often, a significant slowing of the heart rate stems from dysfunction in the heart’s conduction system, particularly high-degree blockages. These blockages can result from impaired impulse generation in the sinoatrial node or disrupted conduction from the sinoatrial node to the atria (sinoauricular) or ventricles (atrioventricular).

A notable decrease in heart rate often leads to compromised blood supply to organs and systems, especially the heart and brain. This can contribute to the development of acute heart failure, myocardial ischemia, and impaired mental status.

Causes of occurrence

1. Internal Causes:
   • Idiopathic degenerative fibrosis (most common).
   • Myocardial ischemia.
   • Myocarditis (especially associated with Lyme disease, diphtheria, and rheumatic fever) and pericarditis.
   • Cardiomyopathy.
   • Infiltrative diseases (such as sarcoidosis, hemochromatosis, and amyloidosis).
   • Collagen disorders (rheumatoid arthritis, scleroderma, systemic lupus erythematosus).
   • Congenital heart defects.
   • Genetic mutations (e.g., SCN5A, TRPM4, and others).
   • Surgical interventions on the heart (such as heart valve replacement, Maze procedure, aorto-coronary bypass, and others).
   • Heart irradiation.
2. External Causes:
   • Medications (such as digoxin, beta-blockers, calcium channel antagonists, ivabradine, clonidine, reserpine, class I and III antiarrhythmic drugs, antidepressants, narcotic drugs, lithium drugs, cannabinoids, cimetidine).
   • Vagotonia (during night sleep, endotracheal aspiration, strong cough, urination, and other activities).
   • Hypersensitivity of the carotid sinus.
   • Endocrine disorders (e.g., hypothyroidism).
   • Electrolyte disturbances (including hyperkalemia, hypokalemia, hypercalcemia, hypermagnesemia).
   • Hypothermia, hypoxemia, hypercapnia, anorexia, acidosis.
   • Neurological disorders (such as trauma or tumor of the central nervous system accompanied by increased intracranial pressure).
   • Obstructive sleep apnea syndrome.
   • Chest injury.

Clinical presentation

Most patients with sinus bradycardia are asymptomatic.

Symptoms typically arise when the heart rate drops below 50 beats per minute.

The clinical presentation of symptomatic bradycardia can vary, ranging from mild fatigue, dizziness, and reduced tolerance to physical exertion, to hypotension, signs of acute heart failure, chest discomfort, and loss of consciousness.

Medical history

Careful collection of anamnestic data is crucial for determining the cause of bradycardia.

• Inquire about the onset and nature of symptoms, including factors that may have triggered them such as stress, physical exertion, medication, or food intake.
• Determine if the patient sought prior medical assistance and if so, the outcome of the consultation.
• Assess if the patient self-administered any medications and whether this affected the nature of their symptoms.
• Review any prior hospitalizations for symptomatic bradycardia, focusing on clinical diagnoses, laboratory or instrumental findings, treatment, and post-discharge recommendations.
• Analyze previous laboratory or instrumental examinations related to the current complaints for relevant findings.
• Understand the patient’s motivation for seeking your assistance.
• Rule out alternative causes of symptoms through targeted questioning.
• Ascertain any history of cardiovascular diseases, including myocardial infarction, angina pectoris, cardiomyopathy, congenital heart defects, and myocarditis.
• Determine if the patient has been diagnosed with rhythm or conduction disorders previously.
• Inquire about any infiltrative diseases, connective tissue disorders, endocrine diseases, or neurological conditions associated with increased intracranial pressure.
• Obtain information on previous surgical procedures, particularly those involving prosthetic heart valves, aorto-coronary bypass, or the Maze procedure, and inquire about postoperative recovery.
• Document current medication use, including doses, especially medications such as digoxin, beta-blockers, calcium channel blockers, antiarrhythmics, and electrolyte supplements.
• Investigate recent infectious diseases or tick bites.
• Assess the patient’s family history of cardiovascular disease, including rhythm or conduction disorders.

Physical examination

The primary objective sign of symptomatic bradycardia is a heart rate (HR) slower than 60 beats per minute, which may be the sole indicator in some cases.

When the heart rate moderately decreases, blood pressure typically remains within normal limits. However, a significant drop in heart rate often leads to hypotension.

A substantial reduction in heart rate can manifest with signs of acute heart failure, including moist wheezing in the lungs, tachypnea, and cyanosis.

Diminished blood supply to the brain may result in altered consciousness.

Furthermore, during physical examination, it is essential to search for signs indicative of the underlying disease causing the bradycardia.

Additional examination methods

Plan of laboratory examination methods:

• Blood analysis for electrolyte levels.
• Thyroid hormone and TSH blood tests.
• Complete blood count.
• Coagulation profile (coagulogram).
• Blood tests for creatinine and urea levels.
• Troponin-I blood test.
• Blood tests for IgM and IgG antibodies to Borrelia (Lyme disease).
• PCR for detection of Borrelia DNA.
• Assessment of blood pH.
• Genetic testing.
• Toxicological screening

Plan of instrumental survey methods :

• Electrocardiography (ECG) in 12 leads.
• Transthoracic echocardiography.
• Ambulatory ECG monitoring (Holter monitoring).
• ECG stress test.
• Coronary angiography.
• Cardiac magnetic resonance imaging (MRI).
• Positron emission tomography (PET scan).
• Electrophysiological study.
• Polysomnography (sleep study).

Laboratory tests that should be performed in patients with cardiac conduction disorders include a blood test for electrolytes, a blood test for the level of thyroid hormones, a blood test for troponin-I/T when acute myocardial ischemia is suspected, and a serological test for Borrelia antibodies when suspected for Lyme disease, determination of the blood pH level in case of suspicion of metabolic acidosis, determination of the level of digoxin in the blood in case of suspicion of glycoside intoxication.

• Electrocardiography in 12 leads

ECG in 12 leads is essential for evaluating all patients with symptomatic bradycardia. If characteristic changes are not evident on resting ECG, ambulatory ECG monitoring is advisable.

Persistent sinus bradycardia is diagnosed when the heart rate remains below 50 beats per minute persistently (see Figure 1).

Figure 1. Persistent sinus bradycardia. Image from litfl.com internet resource. https://litfl.com/sinus-bradycardia-ecg-library

Manifestations of sinus node weakness syndrome include: persistent sinus bradycardia, ectopic atrial bradycardia, sinoatrial blockade of various degrees, pacemaker migration, sinus node arrest with a pause lasting more than 3 seconds, bradysystolic form of atrial fibrillation, tachy-brady syndrome, chronotropic incompetence, isorhythmic dissociation .

AV blocks are characterized by prolongation of the PQ interval with or without loss of ventricular complexes.

• ECG with dosed exercise

A timed exercise ECG may be beneficial for patients experiencing symptoms of bradycardia during or immediately after exercise. Appearance of bradycardia symptoms during exercise typically indicates cardiac pathology, whereas occurrence immediately after physical activity suggests a reflex mechanism.

Additionally, an ECG test with dosed physical load is essential to detect chronotropic incompetence, a manifestation of sinus node weakness syndrome. An inadequate chronotropic response of the sinus node (less than 80% of the expected maximum heart rate) during exercise is indicative of sinus node dysfunction.

• Visualizing examination methods

Echocardiography is recommended for all patients with symptomatic bradycardia to assess for possible structural heart disease, evaluate left ventricular systolic function, and diagnose any underlying causes that may have led to cardiac conduction abnormalities

• Coronary angiography or CT angiography is recommended if coronary heart disease is suspected.

• MRI 

MRI of the heart is highly informative for diagnosing myocardial inflammation or fibrosis, particularly in patients under 60 years of age, where suspicion of such conditions arises.

• Genetic testing

In most cases, heart conduction disorders arise due to age-related or structural changes in the heart’s conduction system. However, mutations in genes such as SCN5A, TRPM4, and LMNA can also be responsible for heart blocks. Current understanding suggests that mutations in these genes lead to a progressive conduction system disease, particularly in young patients under the age of 50, even with structurally normal hearts and without signs of skeletal myopathy.

As a result, genetic testing is recommended for young patients under 50 with progressive conduction system disease.

• Polysomnography

Polysomnography is recommended for patients experiencing nocturnal episodes of bradycardia, which may be potentially associated with episodes of nocturnal sleep apnea. Hypoxemia, commonly observed in sleep apnea, can increase vagal nerve tone and contribute to the development of bradycardia.

• Electrophysiological research

An electrophysiological study is conducted in patients when the cause of bradycardia cannot be identified through non-invasive methods.

Differential diagnosis

Standard electrocardiography is typically adequate for diagnosing heart conduction disturbances, although differentiation of potential underlying causes may be necessary.

To aid in the memorization of the main causes of bradycardia, an English-language mnemonic called ‘Hs/Ts’ is often used. This mnemonic represents the initial letters of pathological conditions associated with significant slowing of the heart rate.

The most common causes of life-threatening bradycardia include hyperkalemia, myocardial ischemia, and overdose with cardiac glycosides, beta-blockers, and calcium channel antagonists.

Now, let’s delve deeper into the causes of dysfunction in the heart’s conduction system, which are associated with significant slowing of the heart rate.

Sinus node weakness syndrome

Sinus node weakness syndrome is a condition characterized by dysfunction in the normal functioning of the sinus node, resulting in bradycardia and the potential development of heart failure.

This syndrome encompasses various manifestations, including:

• Persistent sinus bradycardia
• Ectopic atrial bradycardia
• Sinoatrial block of varying degrees
• Rhythm driver migration
• Sinus node arrest with pauses lasting more than 3 seconds
• Atrial fibrillation with a low ventricular contraction frequency (bradysystolic form)
• Tachy-brady syndrome (alternating episodes of tachycardia and bradycardia)
• Chronotropic incompetence (the heart’s inability to increase heart rate in response to increased activity or demand, often indicated by failure to reach 80% of expected heart rate reserve during exercise)
• Isorhythmic dissociation (where the frequency of atrial depolarization is lower than that of ventricular depolarization).

Clinical presentation

Sinus node weakness syndrome predominantly affects the elderly population, but it can also occur in individuals of all age groups.

Symptoms of sinus node weakness syndrome arise from decreased cardiac output and hypoperfusion of internal organs.

The clinical presentation of sinus node weakness syndrome can vary widely, ranging from mild fatigue, dizziness, and shortness of breath during physical exertion to reduced exercise tolerance, chest pain, and sudden loss of consciousness (Morganhi-Adams-Stokes syndrome).

Diagnostics

• ECG

The primary method for diagnosing sinus node weakness syndrome is through an ECG.

ECG findings indicative of second-degree sinoatrial block include periodic loss of the PQRST complex, with the duration of the pause equal to the sum of two or more normal RR complexes of the main rhythm (see Figure 2). Substitute complexes from the AV node or ventricles may appear during these pauses.

Figure 2. Second-degree sinoatrial block. Image sourced from the internet resource litfl.com. Accessed on https://litfl.com/sinoatrial-exit-block-ecg-library

Complete sinoatrial block is characterized by a complete cessation of impulse conduction from the sinus node to the right atrium. Instead of a sinus rhythm, a substitute rhythm typically arises on the ECG, originating from secondary or tertiary pacemaker centers, most commonly the AV node (see Figure 3).

Figure 3. Complete sinoatrial block. Image sourced from the internet resource litfl.com. https://litfl.com/sinus-node-dysfunction-sick-sinus-syndrome

Rhythm driver migration refers to the gradual movement of the pacemaker site. This phenomenon is characterized by a gradual change in the shape and polarity of the P wave from cycle to cycle, as recorded on the ECG (see Figure 4).

Figure 4. Migration of the pacemaker. Image https://therapy.odmu.edu.ua/ecg-online-course/wandering-pacemaker

Tachy-brady syndrome is characterized by alternating episodes of tachycardia and bradycardia (Figure 5).

Figure 5. Tachy-brady syndrome. Image from litfl.com internet resource. https://litfl.com/sinus-node-dysfunction-sick-sinus-syndrome

Isorhythmic dissociation is characterized by a slower atrial depolarization originating from the sinus node or ectopic atrial region compared to ventricular depolarization originating from the AV node, His bundle, or ventricular region.

Atrioventricular blockade

Atrioventricular block refers to a partial or complete interruption of impulses’ conduction from the atria to the ventricles.

There are three degrees of AV block:

1. First-degree AV block is characterized by slightly slowed conduction through the AV node, but each atrial impulse reaches the ventricles.
2. Mobitz I, or second-degree AV block, involves progressive deterioration of conduction through the AV node with periodic blockade of atrial impulses.
3. Mobitz II, or second-degree AV block, features persistent significant slowing of conduction through the AV node with periodic blockade of atrial impulses.
4. Third-degree, or complete, AV block is characterized by complete cessation of atrial impulse transmission to the ventricles.

Symptomatic bradycardia commonly occurs in patients with second- and third-degree AV block.

Clinical Presentation:

The clinical presentation of second-and third-degree AV block can vary, ranging from mild fatigue, dizziness, reduced exercise tolerance, and dyspnea during physical exertion to loss of consciousness (Morganhi-Adams-Stokes syndrome).

Morganhi-Adams-Stokes syndrome results from cerebral ischemia due to a sudden decrease in cardiac output. Symptoms typically appear 3-10 seconds after blood circulation ceases, last several minutes, and generally do not lead to acute neurological complications

Diagnostics

• ECG

 Mobitz I, or second-degree AV block, is characterized by a progressive lengthening of the PQ interval on the ECG, leading to periodic loss of QRS complexes (see Figure 6).

Figure 6. Second-degree AV block, Mobitz I. Image sourced from litfl.com. https://litfl.com/av-block-2nd-degree-mobitz-i-wenckebach-phenomenon

         Mobitz II degree II AV block is characterized by persistent prolongation of the PQ interval with periodic loss of QRS complexes (Figure 7).

Figure 7. Second-degree AV block, Mobitz II. Image sourced from litfl.com internet resource. https://litfl.com/av-block-2nd-degree-mobitz-ii

Third-degree AV block is characterized by complete dissociation of atrial and ventricular waves on the ECG, with the atrial contraction frequency significantly exceeding the frequency of ventricular activation (see Figure 8).

Figure 8. Third-degree AV block. Image sourced from litfl.com internet resource. https://litfl.com/av-block-3rd-degree-complete-heart-block

Action algorithm for symptomatic bradycardia

1. Maintain airway patency.
2. Provide oxygen therapy in cases of hypoxemia.
3. Monitor heart rate and blood pressure.
4. Establish intravenous access.
5. Identify and address potential causes of symptomatic bradycardia (discontinue medications and administer antidotes if available, consider myocardial revascularization for ischemic heart disease, and correct electrolyte imbalances such as hyperkalemia).
6. Initiate drug treatment if hypotension, altered mental status, acute heart failure, or chest discomfort persists despite initial measures.
7. Administer 0.1% atropine solution intravenously at a dose of 1.0 mg, with repeated doses every 3-5 minutes if necessary (maximum total dose: 3 mg).
8. If atropine is ineffective, consider dopamine infusion at a rate of 5-20 μg/kg/min or epinephrine infusion at a rate of 0.02-0.2 μg/kg/min.
9. If medical treatment is ineffective, consider percutaneous pacing.
10. Note that atropine is contraindicated in patients after heart transplantation. In such cases, or in the presence of AV block due to acute myocardial ischemia, consider administering an infusion of aminophylline at a dose of 6 mg/kg or theophylline at a dose of 300 mg intravenously.

It should be noted that atropine is contraindicated in patients after heart transplantation. In such cases, as well as in instances of AV blockade occurring against the background of acute myocardial ischemia, it is advisable to administer an infusion of aminophylline at a dose of 6 mg/kg or theophylline at a dose of 300 mg intravenously.

Specific therapy is used for heart conduction disturbances caused by drug overdose:

• In cases of overdose with calcium channel antagonists:
  • Calcium chloride can be administered intravenously at a dose of 1-2 g every 10-20 minutes, or as an IV infusion at a dose of 0.2-0.4 ml/kg/h.
  • Alternatively, calcium gluconate can be administered intravenously at a dose of 3-6 g every 10-20 minutes, or as an IV infusion at a dose of 0.6-1.2 ml/kg/hour.
• In cases of overdose with calcium channel antagonists or beta-blockers:
  • Glucagon can be administered intravenously at a dose of 3-10 mg as an IV drip, at a rate of 3-5 mg/h.
  • Intravenous insulin therapy can also be considered at a dose of 0.5 IU/kg/hour.
• In cases of digoxin overdose:
  • Digibind can be administered at a dose of 1 vial to bind 0.5 mg of digoxin.

Electrocardiostimulation

Temporary electrocardiostimulation is indicated for symptomatic patients with bradycardia if medical treatment fails to improve symptoms.

For long-term therapy of symptomatic bradycardia, including sinus node weakness syndrome, second-degree AV block (Mobitz type II), and third-degree AV block, permanent cardiostimulation is recommended.

The choice of cardiac stimulation type depends on the required stimulation frequency and the presence of concomitant pathology:

• For infrequent stimulation needs or in the presence of severe concomitant pathology, single-chamber ventricular cardiostimulation is advised.
• For frequent stimulation needs without severe concomitant pathology and normal AV conduction, single-chamber atrial cardiostimulation is recommended.
• For frequent stimulation needs without severe concomitant pathology but with impaired AV conduction, two-chamber cardiostimulation is recommended.

Prognosis:

With appropriate treatment, the prognosis for patients undergoing electrocardiostimulation is generally favorable. However, outcomes may vary depending on the underlying cardiac condition and any associated comorbidities.

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Resources:

1. 2021 ESC Guidelines on cardiac pacing and cardiac resynchronization therapy developed by the Task Force on cardiac pacing and cardiac resynchronization therapy of the European Society of Cardiology (ESC) with the special contribution of the European Heart Rhythm Association (EHRA). European Heart Journal. 2021; 00: 1-94. doi:10.1093/eurheartj/ehab364
2. 2018 ACC/AHA/HRS Guideline on the evaluation and management of patients with bradycardia and cardiac conduction delay: executive summary. Circulation. 2019; 140: 333-381. DOI: 10.1161/CIR.0000000000000627.

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Opening the consultation

1. Wash your hands and don PPE if appropriate
2. Introduce yourself to the patient including your name and role
3. Confirm the patient’s name and date of birth
4. Explain the reason for the consultation
5. Obtain consent for counseling and care

Ensure the correct position of the patient, lying with his head slightly raised, to reduce the load on the myocardium, limit physical activity and provide psychological peace.

Confirm the patient’s name and date of birth using the next questions:

Availability of a defibrillator

6. Provide the availability of a defibrillator
7. Start ECG monitoring

When caring for a patient with suspected acute myocardial infarction, a defibrillator should be available to the patient as early as possible, which may be needed for immediate defibrillation if necessary!

As soon as possible, it is necessary to start ECG monitoring, and provide constant monitoring of vital signs.

If the patient is unconscious or unresponsive, start a basic life support (BLS) algorithm in accordance with resuscitation guidelines.

Presenting complaint

Use open questioning to explore the patient’s presenting complaint

• “What’s brought you in to see me today?”
• “What`s brought you along today?“
• “What`s brought you here?“
• “Tell me about the issues you’ve been experiencing.”
• “Can you tell me what seems to be bothering you?”
• “What seems to be the problem?”
• “What can I do for you?“

History of presenting complaint

Take additional information about the patient’s chest pain using the abbreviation SOCRATES. It is important to determine the time of onset of chest pain, its nature, localization, duration, irradiation, the effectiveness of nitroglycerin, provoking factors, comparison of this pain syndrome with previous ones.

SOCRATES

The SOCRATES acronym is a useful tool for exploring each of the patient’s presenting symptoms in more detail. It is most commonly used to explore pain, but it can be applied to other symptoms, although some of the elements of SOCRATES may not be relevant to all symptoms.

8. Site: ask where the pain is
9. Onset: clarify when the pain first started and if it came on suddenly or gradually
10. Character: ask the patient to describe how the pain feels
11. Radiation: ask if the pain moves anywhere else
12. Associated symptoms: ask if there are any other associated symptoms
13. Time course: ask how the pain has changed over time
14. Exacerbating or relieving factors: ask if anything makes the pain worse or better
15. Severity: ask how severe the pain is on a scale of 0-10

Be polite, use for questions “Can you tell me…?” or “Can you describe…?”

For example:

• “Can you tell me where it hurts?”
• “Can you tell me what your pain is like?”
• “Can you tell me where she works?”
• “Can you tell me what your symptoms are?”

Adjectives for pain

Shortness of breath can accompany cardiac pain. For the assessment of shortness of breath ask the patient “Have you had any shortness of breath?“

Past medical history

16. Screen for conditions that may be associated with chest pain
17. Ask about other medical diagnoses and previous surgical history
18. Ask if the patient has any allergies and if so, clarify what kind of reaction they had to the substance

Cardiovascular risk factors

When taking a cardiovascular history it’s essential that you identify risk factors for cardiovascular disease as you work through the patient’s history (e.g. past medical history, family history, social history).

Important cardiovascular risk factors include:

• Hypertension
• Hyperlipidemia
• Diabetes
• Family history of cardiac disease
• Smoking

If the patient has a medical condition, you should gather more details to assess how well controlled the disease is and what treatment(s) the patient is receiving. It is also important to ask about any complications associated with the condition including hospital admissions.

Examples of relevant medical conditions

Cardiovascular disease:

• Hypertension
• Hyperlipidemia
• Angina
• Myocardial infarction
• Obesity
• Chronic kidney disease
• Atrial fibrillation
• Stroke
• Peripheral vascular disease
• Rheumatic fever

Respiratory disease:

• Pneumonia
• Pneumothorax
• Pulmonary embolus

Gastrointestinal disease:

• Gastro-oesophageal reflux
• Oesophageal spasm

Drug history

19. Ask the patient is currently taking any prescribed medications or over-the-counter remedies
20. Ask the patient if they’re experiencing any side effects from their medication

Medication examples

Medications commonly prescribed to patients with medical conditions relevant to chest pain:

• Anticoagulants (e.g. pulmonary embolism)
• Antiplatelets (e.g. coronary artery disease)
• Statins (e.g. coronary artery disease)
• Glyceryl trinitrate spray (e.g. angina, oesophageal spasm)
• Calcium channel blockers (e.g. hypertension)
• ACE inhibitors (e.g. hypertension)
• Antibiotics (e.g. pneumonia)
• Colchicine (e.g. pericarditis)

Physical examination

21. Assessment of general condition and vital functions according to the ABCDE algorithm
22. Visual assessment of the color of the skin, the presence of swelling of the cervical veins, and edema.
23. Assessment of the state of the cardiovascular system.
24. Assessment of the state of the respiratory system.
25. Pulse oximetry to determine blood oxygen saturation (normal ≥ 95%).
26. Oxygen therapy (supporting saturation over 94-95%).

Assessment of the general condition and vital functions according to the ABCDE algorithm (A – airway patency, B – breathing, C – blood circulation, D – impaired state of consciousness, E – additional information);

Visual assessment of the color and moisture of the skin, the presence of swelling of the cervical veins, edema;

Assessment of the state of the cardiovascular and respiratory system of the patient.

Check the patient’s respiratory rate:

The normal respiratory rate is 12-20 breaths per minute. Patients with ACS may have tachypnea in an attempt to increase myocardial tissue oxygenation.

Check the patient’s oxygen saturation (SpO2):

The normal SpO₂ range is 94-98% in healthy individuals and 88-92% in COPD patients at high risk of CO₂ retention.

Hypoxemia may occur due to heart failure and secondary pulmonary edema.

Oxygen therapy at a saturation of 95% is carried out with humidified oxygen using a mask or through a nasal catheter at a rate of 3-5 l/min.

Auscultation of the lung sounds

Wheezing or crepitus on auscultation may be a sign of pulmonary edema due to impaired cardiac function. If the patient is conscious, sit him upright. To increase oxygen saturation, a mask with an oxygen flow rate of 15 liters can be used. If the patient has COPD and a history of CO₂ retention, switch to a Venturi mask as soon as possible and properly titrate oxygen.

A decrease in air intake from both sides indicates the need for emergency care.

Pulse

Assess the patient’s pulse:

• Tachycardia is a common sign of ACS.
• Bradycardia is a late sign and often precedes cardiac arrest.

Blood pressure

Assess the patient’s blood pressure:

• Patients may have hypertension due to increased sympathetic activity and pain.
• Hypotension is a late sign and means heart failure.

Auscultation of heart sounds

Identification of pathological heart murmurs.

If the patient has a reduced level of consciousness, review the patient’s medications for drugs that can cause a decrease in the level of consciousness (eg, opioids, sedatives, anxiolytics, insulin, oral hypoglycemic drugs).

Intravenous access

27. Intravenous access
28. Starting the infusion of Ringer’s lactate solution

Peripheral vein catheterization (providing intravenous access); initiation of Ringer’s lactate solution.

Registration of a 12-channel ECG

29. Recording ECG
30. Assess the presence/absence of pathological ST-elevation according to formal STEMI criteria;
    • Exclusion of other causes of benign ST-elevation in the presence of such ST-elevation – to exclude a possible non-coronary or acute coronary origin: early ventricular repolarization syndrome, left ventricular aneurysm, secondary ST-changes in LVH, recording artifacts, and others;
    • Assessment of additional ECG patterns and conditions that may be caused by critical coronary artery occlusion (STEMI-equivalents) – in the absence of ST-elevation – make sure that there are no other signs of coronary artery occlusion (STEMI equivalents);
31. Identification of the localization of myocardial ischemia

Assess for the presence of right ventricular myocardial infarction

ECG recording and evaluation must be carried out within at least 8-10 minutes (from first medical contact to diagnosis)!

ECG recording should not be given priority over providing emergency care if necessary (resuscitation)!

After the ECG recording an assessment should made of the presence of ST segment elevation and other ECG patterns associated with critical occlusion of the coronary arteries.    

  Pathological ST segment elevation is considered:

• new ST segment elevation in two consecutive limb leads ≥0.1 mV (≥1 mm)
• elevation
  • ≥0.2 mV in men ≥40 years old, ≥0.25 mV in men <40 years old in leads V2-V3,
  • ≥1.5 mV in women (≥ 1.5 mm) in leads V2-V3.
• In patients with inferior wall myocardial infarction (ST-segment elevation in II, III, AVF), it is recommended to record the right precordial leads (V3R and V4R) to exclude ST-segment elevation, which indicates right ventricular myocardial infarction.

In patients with inferior wall myocardial infarction (ST-segment elevation in II, III, AVF), it is recommended to record the right precordial leads (V3R and V4R) to exclude ST-segment elevation, which indicates right ventricular myocardial infarction.

When evaluating elevation, if there is elevation in II, III, avF leads, and if there is elevation in V4R, do not prescribe nitroglycerin!

If ST segment depression is detected in leads V₁-V₃, additionally take an ECG in V₇-V₉

Patients with STEMI usually have acute chest pain and sustained (>20 minutes) ST-segment elevation.

ST-elevation is a sign of complete occlusion of the epicardial coronary artery by a thrombus, which causes immediate myocardial death in the affected area of ​​the myocardium::

• Anterior: V1-V4
• Lower: II, III, aVF
• High lateral: I, aVL
• Low lateral: V5, V6
• Posterior: dominant R wave in V1-3 with ST depression in V1-3 (mirror image of anterior MI)

In the absence of characteristic ECG signs against the background of clinical manifestations of ACS, it is necessary to repeat the ECG registration with an interval of 20-30 minutes, paying attention to the presence of sharp T waves, which may precede ST segment elevation;

Once the electrodes are positioned and the wires are properly attached, the patient should be covered with a sheet for moral purposes.

However, traditional STEMI criteria often fail us, as more than 30% of cases of acute coronary occlusion are misclassified and interpreted. In addition, the STEMI/NSTEMI paradigm depends on ST elevation as defined by millimeter criteria, however, many occlusive myocardial infarctions (OMIs) do not have ST elevation at all.

In the current paradigm of STEMI and NSTEMI, 25–30% of patients with STEMI have an unrecognized acute total occlusion (OMI) on delayed angiography (24 hours after symptom onset) and is twice as high in patients with STEMI without OMI (MI without occlusion or NOMI). Conversely, 15–35% of catheter labs are activated through probable STEMI criteria that are false positive and unsupported by angiographic assessments of causative coronary artery disease.

«NSTEMI» – 25% false negative (skipping occlusions with 2x mortality)
«STEMI» – 15-35%  false positive (iatrogenic harm and waste of resources)

Assessment of additional ECG patterns and conditions that may be accompanied by critical coronary artery occlusion

ECG signs suggestive of coronary artery occlusion in the absence of ST-elevation have long been known. They are called “STEMI equivalents”:

• LBBB combined with Sgarbosa’s original/modified criteria
• Posterior MI
• ST-elevation in aVR
• Pattern De Winter
• Wellens Syndrome
• Sharp T waves
• Pacemaker rhythm combined with Sgarbosa’s original/modified criteria

It is also known that so-called benign (non-ischemic) ST-elevation can occur, for example:

• syndrome of early repolarization of the ventricles;
• recording artifacts simulating ST segment elevation;
• secondary ST changes against the background of LV myocardial hypertrophy, LBBB;
• imitation of ST deviations due to the superimposition of waves of atrial fibrillation/trembling, etc.

The algorithm for differential diagnosis depends on the presence (Table 2.) or absence of ST segment elevation (Table 3.), which meets the STEMI criteria.

Table 2. ST-elevation meeting STEMI criteria

Table 3. Absence of ST-elevation that meets STEMI criteria

A complex display of the discussed algorithm is presented in the images:

Therefore, ECG data can recognize coronary occlusion without ST-segment elevation (“STEMI equivalents”), and also be able to distinguish ST-elevation in acute coronary occlusion from elevation due to other causes (early ventricular repolarization syndrome, ST artifacts, subacute stage acute myocardial infarction, that is, with conditions that do not require thrombolysis or emergency coronary angiography.

Express test for the determination of cardiac troponin, myoglobin, creatine phosphokinase-MB, if possible

32. The timing of the increase in markers of myocardial damage
33. Analysis of other causes that may lead to increased markers of myocardial necrosis

The timing of the increase in markers of myocardial necrosis is presented in the table. It should be noted that the levels of Myoglobin and creatine phosphokinase, the creatine phosphokinase-MB (CPK-MB) isoform, are the first to increase.

Other causes of increased markers of myocardial necrosis

There are many causes of elevated troponin levels, including:

• Myocardial infarction
• Tachy/bradyarrhythmias
• Aortic dissection
• Severe aortic valve disease
• Hypertrophic cardiomyopathy
• Severe respiratory failure
• Severe anemia
• Coronary spasm
• Heart failure
• Takotsubo cardiomyopathy
• Sepsis
• Kidney failure
• Stroke
• Subarachnoid hemorrhage

Preliminary diagnosis

34. Criteria for ACS with ST-segment elevation (STEMI)
35. STEMI Equivalents
36. Localization
37. Killip score

Classification of acute heart failure Killip

Interpretation:

* From Khot 2003 who combined class III/IV due to the relatively smaller number of patients in class IV (0.3% of patients).

** From Killip 1967. This classification was developed as early as the 1960s, before being introduced into the clinical practice of reperfusion therapy (thrombolytics, PCI); however, since then, several studies have shown that the Killip classification still predicts mortality for both STEMI and NSTEMI. However, there is certainly a significant decrease in mortality compared to the original study.

Drug therapy (basic)

38. Acetylsalicylic acid
39. Anticoagulant
40. Nitroglycerin
41. Beta-blocker
42. Administering solutions as needed
43. Pain relief
44. Midozalom administration for cocaine-induced STEMI
45. Concomitant therapy as needed

Evaluation of the door-balloon time (the choice of further reperfusion strategy aimed as soon as possible to restore the coronary blood flow in the infarct-dependent artery)

46. Primary PCI
47. Hospital thrombolysis followed by PCI

Evaluation of the door-balloon time (the choice of further reperfusion strategy aimed as soon as possible to restore the coronary blood flow in the infarct-dependent artery)

• Primary PCI
• Hospital thrombolysis followed by PCI

If the criteria for ACS are met, the patient should be taken to the nearest reperfusion center as soon as possible!

When providing medical care to a patient with acute coronary syndrome with ST-segment elevation or its equivalent, the distance to the center of percutaneous coronary intervention is assessed.

The optimal method of reperfusion therapy for ACS with ST-segment elevation is percutaneous coronary intervention (PCI). Primary PCI should be performed as early as possible, preferably within 60-90 minutes (in high-risk cases in patients with large anterior myocardial infarction, preferably no later than 60 minutes). If it is impossible to transport the patient to the PCI center within 60-90 minutes, pre-hospital thrombolysis is recommended in the absence of contraindications.

If the time from the onset of pain is less than 90 minutes and the time to transport the patient to the center is <120 minutes, the patient should be immediately transported to the PCI center without prior thrombolysis.

Scheme of patient with STEMI transportation (ACS with ST-segment elevation)

Algorithm for providing assistance at the prehospital stage

• An initial PCI is warranted within the first 3-24 hours.
• Don’t forget the golden hour rule.
• Reperfusion of the balloon door is desirable in less than 60 minutes.
• Total ischemic time – the time from symptom onset to reperfusion – preferably less than 120 minutes.

Call the nearest reperfusion center

48. Activation of the intervention team of the reperfusion center

If the patient meets STEMI criteria or STEMI equivalents, then the patient is a priority patient requiring immediate notification to the nearest reperfusion heart center to allow the hospital to prepare.

In some countries, there is a verbal statement called “STEMI ALERT” indicating that the patient meets the criteria for acute coronary syndrome with ST-segment elevation (STEMI).

Based on the report of the emergency doctor, the doctor on the duty at the hospital, who is also responsible for communication with the emergency medical service, informs and activates the team of interventional cardiologists.

P2Y12 receptor inhibitor prescription depending on the chosen strategy of reperfusion therapy

49. Choice of P2Y12 inhibitor for medical care

P2Y12 receptor inhibitors: pharmacological properties

The use of P2Y12 antagonists in acute coronary syndrome (ACS) has potential advantages: reduction in the incidence of intraprocedural and postprocedural stent thrombosis, and reduction of periprocedural myocardial infarction.

Clopidogrel, prasugrel, or ticagrelor are the most commonly used P2Y12 receptor antagonists.

Clopidogrel is an irreversible P2Y12 receptor antagonist. The onset of action is dose-dependent (loading dose 600 mg versus loading dose 300 mg) with onset 2-6 hours later. This dynamic makes clopidogrel less effective in preventing stent thrombosis before PCI.

Prasugrel is another irreversible oral P2Y12 antagonist. Its onset of action is faster compared to clopidogrel (30 minutes – 4 hours versus 2-6 hours).

Ticagrelor is a reversible oral P2Y12 antagonist that, unlike clopidogrel and prasugrel, does not require in vivo conversion to an active metabolite.

Therefore, the onset of action is much faster (30 minutes – 2 hours). Ticagrelor has been approved for use in patients with ACS (both NSTEMI and STEMI).

Loading dosage of ticagrelor 180 mg.

Carrying out thrombolytic therapy as needed

50. Criteria for selecting patients for thrombolytic therapy
51. Evaluation of success criteria for fibrinolytic therapy
52. Choice of the drug for thrombolysis
53. Assessment of absolute contraindications for thrombolysis
54. Assessment of relative contraindications for thrombolysis

Prehospital thrombolysis

Criteria for selecting patients for thrombolytic therapy:

• diagnosis of STEMI (ACS with ST-segment elevation);
• symptoms onset 12 hours;
• lack of opportunities for providing PCI within up to 90 minutes from the first medical contact with the patient to the introduction of the balloon;
• absence of contraindications to thrombolysis;
• availability of informed consent of the patient.

An important criterion for the success of fibrinolytic therapy is the reduction of ST-segment elevation by at least 50% within 60-90 minutes from the start of fibrinolytic administration.

Before the introduction of streptokinase and alteplase, a bolus of heparin 5000 IU IV is recommended.

If fibrinolytic therapy is necessary, preference is given to fibrin-specific drugs.

Contraindications for thrombolysis:

It is necessary in the first 24 hours from the onset of symptoms of myocardial infarction to transfer the patient after fibrinolytic therapy to the hospital with PCI opportunities.

Transportation to the nearest reperfusion center

55. Analysis of delays in the medical care of a patient with acute coronary syndrome
56. Monitoring of vital signs during the transfer
57. Pain management as needed
58. Reporting in the emergency department of the hospital during the patient’s hospitalization

A generalized algorithm for transporting a patient with ST-segment elevation ACS is presented below.

Note: EMS – emergency medical service, PCI – percutaneous coronary intervention

Every patient with ACS with ST-segment elevation after receiving emergency care at the prehospital stage should be immediately admitted to the hospital.

At the same time, hospitalization in a healthcare facility with the possibility of emergency percutaneous coronary intervention (PCI) is an absolute priority. Unfortunately, this possibility is not always available, and sometimes patients are admitted to healthcare facilities without this possibility.

When transporting patients, it is recommended to carefully monitor all vital signs, and, most importantly, to record a series of ECGs – preferably every 15 minutes (rather than an hour or two), if possible, perform a troponin test. Hospital physicians should be notified that the arrival of such a patient is being prepared so that they can activate the entire reperfusion center team and prepare the catheter laboratory for intervention. When hospitalized in a hospital, it is necessary to continue to record ECG series and evaluate troponin in dynamics, if possible, perform an Echo-ECG.

In the management of the patient with ST-segment elevation, delay reduction is critical, as early reperfusion is critical and has been proven to improve the prognosis of these patients.

• Patient delay – the delay between the onset of symptoms and the initial medical contact.
• The delay between initial medical contact and diagnosis – is the time required to record the first ECG. The goal should be to get this delay down to 10 minutes or less – preferably 8 minutes.
• System delay – the delay between the initial medical contact and reperfusion therapy (initial medical contact before the guidewire is inserted into the infarct-dependent artery).
  • If the reperfusion strategy has chosen primary percutaneous intervention, then the goal should be to reduce system delay to ≤90 min, and in high-risk cases with large anterior infarction and symptoms within 2 hours, this time should be reduced to less than 60 min).
  • If reperfusion therapy is fibrinolysis, the goal is to reduce this delay (primary medical contact to the needle) to ≤30 min.
• Total ischemic time. From the patient’s point of view, the delay between the onset of symptoms and the provision of reperfusion therapy (either onset of fibrinolysis, or insertion of a guidewire into an infarct-dependent artery) is a total ischemic time that should be minimized as much as possible (preferably less than 120 minutes).

The graphic scheme of time delays is shown in the figure:

When reporting in relation to the patient to the duty cardiologist of the emergency medical center in the emergency department of the hospital during the patient’s hospitalization:

• Complaints of the patient;
• Data of the physical examination at the time of FMC and during transportation;
• Identified ECG changes;
• Provision of ECG archives recorded during FMC and transportation of the patient to the hospital;
• Amount of care provided and patient response to the treatment;
• Provision of relevant records of the patient’s medical history.
  

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• Opening the consultation

Wash your hands and don PPE if appropriate

Introduce yourself to the patient including your name and role

Confirm the patient's name and date of birth

Explain the reason for the consultation

Obtain consent for counseling and care

• Availability of a defibrillator

Provide the availability of a defibrillator

Start ECG monitoring

• Presenting complaint

Use open questioning to explore the patient’s presenting complaint

• History of presenting complaint

Site: ask where the pain is

Onset: clarify when the pain first started and if it came on suddenly or gradually

Character: ask the patient to describe how the pain feels

Radiation: ask if the pain moves anywhere else

Associated symptoms: ask if there are any other associated symptoms

Time course: ask how the pain has changed over time

Exacerbating or relieving factors: ask if anything makes the pain worse or better

Severity: ask how severe the pain is on a scale of 0-10

• Past medical history

Screen for conditions that may be associated with chest pain

Ask about other medical diagnoses and previous surgical history

Ask if the patient has any allergies and if so, clarify what kind of reaction they had to the substance

• Drug history

Ask the patient is currently taking any prescribed medications or over-the-counter remedies

Ask the patient if they’re experiencing any side effects from their medication

• Physical examination

Assessment of general condition and vital functions according to the ABCDE algorithm

Visual assessment of the color of the skin, the presence of swelling of the cervical veins, and edema

Assessment of the state of the cardiovascular system

Assessment of the state of the respiratory system

Pulse oximetry to determine blood oxygen saturation (normal ≥ 95%)

Oxygen therapy (supporting saturation over 94-95%)

• Intravenous access

Intravenous access

Starting the infusion of Ringer's lactate solution

• Registration of a 12-channel ECG

Recording ECG

Assess the presence/absence of pathological ST-elevation according to formal STEMI criteria

Exclusion of other causes of benign ST-elevation in the presence of such ST-elevation – to exclude a possible non-coronary or acute coronary origin: early ventricular repolarization syndrome, left ventricular aneurysm, secondary ST-changes in LVH, recording artifacts, and others

Assessment of additional ECG patterns and conditions that may be caused by critical coronary artery occlusion (STEMI-equivalents) – in the absence of ST-elevation - make sure that there are no other signs of coronary artery occlusion (STEMI equivalents)

Identification of the localization of myocardial ischemia

Assess for the presence of right ventricular myocardial infarction

• Express test for the determination of cardiac troponin, myoglobin, creatine phosphokinase-MB, if possible

The timing of the increase in markers of myocardial damage

Analysis of other causes that may lead to increased markers of myocardial necrosis

• Making preliminary diagnosis

Criteria for ACS with ST-segment elevation (STEMI)

STEMI Equivalents

Localization

Killip score

• Drug therapy (basic)

Acetylsalicylic acid

Anticoagulant

Nitroglycerin

Beta-blocker

Administering solutions as needed

Pain relief

Midozalom administration for cocaine-induced STEMI

Concomitant therapy as needed

• Evaluation of the door-balloon time (the choice of further reperfusion strategy aimed as soon as possible to restore the coronary blood flow in the infarct-dependent artery)

Primary PCI

Hospital thrombolysis followed by PCI

• Call the nearest reperfusion center

Activation of the intervention team of the reperfusion center

• P2Y12 receptor inhibitor prescription depending on the chosen strategy of reperfusion therapy

Choice of P2Y12 inhibitor for medical care

• Carrying out thrombolytic therapy as needed

Criteria for selecting patients for thrombolytic therapy

Evaluation of success criteria for fibrinolytic therapy

Choice of the drug for thrombolysis

Assessment of absolute contraindications for thrombolysis

Assessment of relative contraindications for thrombolysis

• Transportation to the nearest reperfusion center

Analysis of delays in the medical care of a patient with acute coronary syndrome

Monitoring of vital signs during the transfer

Pain management as needed

Reporting in the emergency department of the hospital during the patient's hospitalization

Total

Result:

Total: 0 / 62

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Additional materials:

Literature:

1. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. European Heart Journal (2018) 39 (2), 119-177. doi:10.1093/eurheartj/ehx393.
2. 2017 ESC focused update on dual antiplatelet therapy in coronary artery disease developed in collaboration with EACTS: The Task force for dual antiplatelet therapy in coronary artery disease of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS). European Heart Journal, V.39, Issue 3, 14 January 2018, Pages 213-260, https://doi.org/10.1093/eurheartj/ehx419.
3. Continuum of care for acute coronary syndrome: optimizing treatment for ST-elevation myocardial infarction and non-elevation acute coronary syndrome. W. Brian Gibler, Judy M. Racadio et al. EMCREG-International Monograph February. Critical Pathways in Cardiology (2018), V.17, №3.
4. 2019 ESC/EAS Guidelines for the management of dyslipidemias: lipid modification to reduce cardiovascular risk. European Heart Journal, Volume 41, Issue 1, January 2020,p. 111-188. doi: 10.1093/eurheartj/enz455.
5. 1. Meyers HP, Bracey A, Lee D, Lichtenheld A, Li WJ, Singer DD, Kane JA, Dodd KW, Meyers KE, Thode HC, Shroff GR, Singer AJ, Smith SW. Comparison of the ST-Elevation Myocardial Infarction (STEMI) vs. NSTEMI and Occlusion MI (OMI) vs. NOMI Paradigms of Acute MI. J Emerg Med. 2021 Mar;60(3):273-284. doi: 10.1016/j.jemermed.2020.10.026. Epub 2020 Dec 9. PMID: 33308915.
6. Meyers PH, Weingart S, Smith SW. The OMI Manifesto. Dr Smith’s ECG blog 2018
7. Alblaihed L. The DIFOCCULT Trial: Time to Change from STEMI/NSTEMI to OMI/NOMI? REBEL EM
8. H. Pendell Meyers, Alexander Bracey, Daniel Lee, Andrew Lichtenheld, Wei J. Li, Daniel D. Singer, Zach Rollins, Jesse A. Kane, Kenneth W. Dodd, Kristen E. Meyers, Gautam R. Shroff, Adam J. Singer, Stephen W. Smith, Accuracy of OMI ECG findings versus STEMI criteria for diagnosis of acute coronary occlusion myocardial infarction, IJC Heart & Vasculature, Volume 33, 2021, 100767, https://doi.org/10.1016/j.ijcha.2021.100767

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Сообщение Emergency care of a patient with chest pain – Acute Coronary Syndrome with ST-segment elevation and equivalents /OSCE guide появились сначала на ClinCaseQuest.

The low-voltage electrocardiogram (ECG) is associated with various cardiac and noncardiac conditions as well as lead wire reversals and other electronic equipment problems. Low-voltage QRS in the ECG creates problems with continuous cardiac monitoring, such as false lethal arrhythmia alarms at central monitoring stations, and general false alarms, thus contributing to alarm fatigue. The low-voltage ECG may be associated with physiological, anatomical features and conditions.

Diagnostic criteria

The QRS has low voltage when:

• The amplitudes of all the QRS complexes in the limb leads are < 5 mm; or
• The amplitudes of all the QRS complexes in the precordial leads are < 10 mm

Low voltage of the QRS amplitude can be defined according to the criteria depicted in Table.
Table: Criteria for ECG voltage measurement

Mechanisms

Low voltage is produced by:

• The “damping” effect of increased layers of fluid, fat or air between the heart and the recording electrode
• Loss of viable myocardium
• Diffuse infiltration or myxoedematous involvement of the heart

Causes

• Fluid: Pericardial effusion; Pleural effusion
• Fat: Obesity
• Air: Chronic obstructive pulmonary disease, or COPD, Emphysema; Pneumothorax; Subcutaneous emphysema
• Infiltrative / Connective Tissue Disorders
  • Myxoedema – Severe hypothyroidism
  • Infiltrative myocardial diseases — i.e. restrictive cardiomyopathy due to Infiltrative/restrictive diseases such as amyloid cardiomyopathy, sarcoidosis, haemochromatosis
  • Constrictive pericarditis
  • Scleroderma
• Loss of viable myocardium:
  • Massive myocardial damage/infarction
  • Previous massive MI
  • End-stage dilated cardiomyopathy

Note! If the gain indicated at the left of the ECG is turned down accidentally, the voltage will be falsely low (pseudo low voltage). The indicator should be set to 10 mm amplitude.

Low ECG QRS voltage in limb leads with normal QRS precordial amplitudes, or LQRSV in limb leads with high QRS complexes in the precordial leads with poor R-wave progression (“Goldberger triad”) 3 have been described in patients with dilated cardiomyopathy.

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Cardiac causes of LQRSV

• Multiple myocardial infarctions due to cancellations and diminished electromotive force generation;
• LQRSV and QRS notches are seen in conjunction with severe post–myocardial infarction dysynergy
• Infiltrative cardiomyopathies (amyloidosis), which occurs despite the marked cardiac hypertrophy or dilatation
• Myocarditis is associated with LQRSV attributed to the ailing myocytes, although extracardiac influences may also contribute to the LQRSV
• Reduction of QRS voltage (not necessarily LQRSV) follows reduction of cardiac volumes due to various pathologies, hemorrhage, or hypovolemia (“Brody effect”).
• Pulmonary congestion and/ or peripheral edema (PERED) may contribute to LQRSV (vide infra).
• Extensive skin burns may lead to hypovolemia and cause LQRSV, although associated hypoalbuminemia may contribute (vide infra).
• An increased hematocrit leads to LQRSV because of the reduction in disparity of electrical resistivity of the intracardiac blood mass and the surrounding myocardium, which attenuates the radial depolarization forces, as per the Brody effect.

Pericardial causes of LQRSV

 The mechanism purported to be that of a short-circuiting of the heart’s potentials as they are transmitted to the body surface;

• the intrapericardial pressure, like in tamponade, as the primary reason, along with the inflammation. However, the delays in recovery of LQRSV after pericardiocentesis or alleviation of tamponade suggest that the effects on the ECG in pericarditis/pericardial effusion/tamponade are multifactorial.
• Electrical alternans, in the presence of a large pericardial effusion, often with impending tamponade, is attributed to a swinging motion of the heart, with a 2-beat or varying periodicity.
• Thickening of the pericardium in constrictive pericarditis is associated with LQRSV20; however, pericardiectomy only partially restores the QRS amplitude, suggesting that the underlying myocardium is contributing to the LQRSV.

Extracardiac causes of LQRSV

The pathology of the organs and tissues surrounding the heart impacts the transfer of the heart’s potential to the body surface with resultant LQRSV.

Patients with chronic obstructive lung disease may show LQRSV, particularly in the limb leads, because of an increased heart/chest wall distance from lung hyperinflation, which, if not offset, would be expected to augment QRS potentials by way of an increased electrical impedance.

Pneumopericardium, pneumomediastinum, and pneumothorax, particularly left-sided, are associated with LQRSV. Pulmonary edema and bronchopulmonary “lavage” result in LQRSV because of decreased lung impedance by way of increased water content. Pneumonia, with extensive pulmonary infiltrates, and adult respiratory distress syndrome (“wet lung”) are expected to lead to similar ECG findings, although nothing to this effect has been described heretofore. Pleural effusion, particularly left-sided and in the absence of congestive heart failure, causes LQRSV with an inverse relationship between the extent of the effusion and the amplitude of QRS complexes. Extensive subcutaneous emphysema, with retro pneumoperitoneum and mediastinal emphysema, is associated with LQRSV. Change in the position of the heart and its relationship with the chest wall, and certain ECG leads must be influential in LQRSV in some of the above-discussed conditions. Obesity is linked to reversible LQRSV.

Although LQRSV is rarely found in hypothyroidism in the absence of pericardial effusion, it has been suggested that hypothyroidism per se contributes to LQRSV.

Sepsis, certain drugs (eg, nonsteroidal anti-inflammatory drugs and the antidiabetic thiazolidinediones [unpublished data]), cor pulmonale, perioperative fluid load administration, even in the presence of normal left ventricular function, chronic renal failure, particularly during the predialytic state, congestive heart failure, hepatic cirrhosis, and numerous other conditions result in reversible LQRSV.

Hypoalbuminemia and resultant PERED must be the mechanism of LQRSV noted invariably in children with kwashiorkor, rather than “myocardial atrophy,” although low cardiac volumes and decreased cardiac thickness and mass may contribute to the LQRSV. Peripheral edema also decreases the amplitude of P waves and T waves, and the duration of P waves, QRS complexes, and QT intervals; such changes have enormous clinical implications for the diagnosis, management, and follow-up of patients with broad categories of cardiac and noncardiac diseases and, in addition, impact the signal-averaged electrocardiogram and T-wave alternans, with major consequences on the reproducibility and clinical relevance of such measurements.

Causes of low voltage based on the mechanism:

Previously Andrew O. Usoro et al. reported that the mortality rate in individuals with LQRSV was almost twice that in those without LQRSV (51.1 vs 23.5 events per 1,000 person-years, p <0.01).

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Literarure:

1. Cyrille NB, Goldsmith J, Alvarez J, Maurer MS. Prevalence and prognostic significance of low QRS voltage among the three main types of cardiac amyloidosis. The American journal of cardiology. 2014;114(7):1089-1093.
2. Mussinelli R, Salinaro F, Alogna A, Boldrini M, Raimondi A, Musca F, Palladini G, Merlini G, Perlini S. Diagnostic and prognostic value of low QRS voltages in cardiac AL amyloidosis. Ann Noninvasive Electrocardiol. 2013;18(3):271-280.
3. Carroll JD, Gaasch WH, McAdam KP. Amyloid cardiomyopathy: characterization by a distinctive voltage/mass relation. The American journal of cardiology. 1982;49(1):9-13.
4. Madias JE. Low QRS voltage and its causes. J Electrocardiol. 2008;41(6):498–500. doi:10.1016/j.jelectrocard.2008.06.021.
5. Andrew O. Usoro, Natalie Bradford, Amit J. Shah, Elsayed Z. Soliman. Risk of Mortality in Individuals With Low QRS Voltage and Free of Cardiovascular Disease. Arrhythmias and conduction disturbances. 2014; Vol. 113(9): P.1514-1517. DOI:https://doi.org/10.1016/j.amjcard.2014.02.006
6. Kamath SA, Meo Neto Jde P, Canham RM, Uddin F, Toto KH, Nelson LL, Kaiser PA, de Lemos JA, Drazner MH. Low voltage on the electrocardiogram is a marker of disease severity and a risk factor for adverse outcomes in patients with heart failure due to systolic dysfunction. Am Heart J. 2006 Aug;152(2):355-61. doi: 10.1016/j.ahj.2005.12.021. PMID: 16875922. https://pubmed.ncbi.nlm.nih.gov/16875922/
7. Hannibal Gerard B. Interpretation of the Low-Voltage ECG. AACN Adv Crit Care (2014) 25 (1): 64–68.https://doi.org/10.4037/NCI.0000000000000001

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Stephen Smith’s formula for Subtle Anterior STEMI online Calculator

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Сообщение Low electrocardiographic QRS voltage (LQRSV) появились сначала на ClinCaseQuest.

Stephen Smith’s formula for Subtle Anterior STEMI use in chest pain patients presenting with an ECG that is non-diagnostic but suspicious for anterior MI.

NB! Before using this calculator, make sure the EKG shows ≥1 mm ST elevation (STE) in ≥1 of the precordial leads V2-V4.

If it shows any one of the following, then it is NOT normal variant, and is very likely to be LAD occlusion; such cases were excluded from the study as “obvious” MI:

• >5 mm STE.
• Non-concave STE.
• Inferior reciprocal changes ST in II, III, aVF, V6.
• Anterior ST depression.
• Terminal QRS distortion in V2 or V3:

• Q waves in any of V2 to V4.
• Any T wave inversion from V2 to V6.

Both benign early repolarization and STEMI cause ST elevation. The challenge is to differentiate the two entities.

Some patients present with subtle ECG changes nondiagnostic for STEMI but still have 100% coronary artery occlusion and benefit from acute percutaneous coronary intervention (PCI).

Using the equation in such cases can lead to timely cath lab activation, or more intensive evaluation.

Stephen Smith’s formula for the diagnosis of “Insidious” anterior ST-segment elevation acute myocardial infarction (4 variables) includes:

• Interval QTc with Bazett correction, msec
• Amplitude of QRS in lead V2, mm
• Amplitude of the R wave in lead V4, mm
• ST segment elevation 60 ms after the J-point in lead V3 mm

Formula:

• STE – ST-elevation 60 ms after the J-point in lead V3, in mm;
• QTc – QT interval corrected relative to heart rate, in ms (according to automatic ECG analysis);
• RV4 – the amplitude of the R wave in lead V4, in mm;

Interpretation of 3-component formula results:

• Indicators ≥23.4, probably there is PNA occlusion.
• Indicators 22-23.4 – the value does not reach the diagnostic threshold of 23.4, but there is a possibility that the patient has PNA occlusion.
• Indicators <23.4, low probability of PNA occlusion, possible benign early ventricular repolarization.

Interpreting the results of the 4-component formula:

• Scores ≥18.2 are likely to be for anterior STEMI (sensitivity 83.3%, specificity 87.7%, and diagnostic accuracy 85.9%).
• Scores <18.2 are likely to indicate early benign repolarization.

Smith’s 4-variable formula is more sensitive than the 3-variable version of the formula.

NB! The authors specifically excluded patients with obvious MI. Using the calculator in cases that were excluded in the study may lead to a wrong result.

Tips for ECG interpretation:

1). Measure STE at 60 ms in lead V3:

ST elevation at 60 ms after the J-point in lead V3, relative to the PR segment.

• Measure STE 60 ms (1½ small box after J point).
• The baseline is the PR segment.
• In this example, STE 60 = 4 mm.

2). Measure amplitude of R wave in V4:

In this example, RV4 = 9 mm.

3). Calculate the QTc: QTc is simply read from the computerized interpretation (uses Bazett’s formula).

Conclusion

Activation of a cath lab team is appropriate in patients with a positive Smith formula in the appropriate clinical context. At the very least, this result should prompt the command of the heart team to carry out repeated ECG recordings, the so-called serial ECG, and echocardiography.

The Smith Formula is best used to identify patients with LAD occlusion, which was initially considered a normal option for early repolarization.

If the Smith formula (4-variable) is negative for STEMI, proceed with caution if STEMI is still suspected.

References:

1. Smith SW, Khalil A, Henry TD, et al. Electrocardiographic differentiation of early repolarization from subtle anterior ST-segment elevation myocardial infarction. Ann Emerg Med. 2012;60(1):45-56.e2. https://pubmed.ncbi.nlm.nih.gov/22520989/
2. Driver BE, Khalil A, Henry T, Kazmi F, Adil A, Smith SW. A new 4-variable formula to differentiate normal variant ST segment elevation in V2-V4 (early repolarization) from subtle left anterior descending coronary occlusion – Adding QRS amplitude of V2 improves the model. J Electrocardiol. 2017;50(5):561-569. https://www.sciencedirect.com/science/article/abs/pii/S0022073617301073
3. Bozbeyoğlu E, Aslanger E, Yıldırımtürk Ö, et al. A tale of two formulas: Differentiation of subtle anterior MI from benign ST segment elevation. Ann Noninvasive Electrocardiol. 2018;:e12568. https://onlinelibrary.wiley.com/doi/epdf/10.1111/anec.12568

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Сообщение Stephen Smith’s formula for Subtle Anterior STEMI online Calculator появились сначала на ClinCaseQuest.

• Bazett’s formula The formula should be used in patients with a heart rate of 60 to 100 beats per minute. In cases of tachycardia or bradycardia, the values may not be correct.
• For heart rate below 60 or above 100 beats per minute, the adjusted QT interval should be calculated by the Framingham formula.

Normal values of Corrected QT: 320-430 for men and 320-450 for women.

• Bazett’s formula The formula should be used in patients with a heart rate of 60 to 100 beats per minute. In cases of tachycardia or bradycardia, the values may not be correct.
• For heart rate below 60 or above 100 beats per minute, the adjusted QT interval should be calculated by the Framingham formula.

Normal values of Corrected QT: 320-430 for men and 320-450 for women.

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Сообщение Corrected QT Interval Bazett’s formula online calculator появились сначала на ClinCaseQuest.

Fig. 1. Coronary arteries. First diagonal artery (D1) (pointer – yellow arrow).

Culprit’s arteries

• Occlusion of the first diagonal branch (D1) of the left anterior descending artery (LAD) can cause isolated ST elevation in I and aVL.
• Occlusion of the left circumflex artery can cause ST-segment elevation in I, aVL along with leads V5-6.

Clinical relevance

Very often, high lateral infarctions (STEMI) are not diagnosed on time even by experienced emergency doctors due to the non-contiguous nature of ST-segment elevation on the electrocardiogram (ECG).

Sign of the South African flag on the ECG

With occlusion of D1 (LAD-D1), on the ECG are revealed the following changes (Fig. 2):

• ST-elevation: leads I, aVL, V2
• ST depression: Leads III (and inferior leads).

ST-elevation is predominantly localized in leads I, aVL +/- V2, but not in other anterior leads.

Reciprocal ST depression and/or T-wave inversion in inferior leads, most pronounced in lead III.

Fig. 2. South Africa Flag sign on ECG (ST Elevation: Leads I, aVL, V2, ST Depression: Leads III (and inferior leads aVF)).

Algorithm for identifying the feature of the “South Africa Flag sign” on the ECG

Littmann L. offers a simple step-by-step algorithm that can help emergency physicians identify the typical ST-segment abnormalities seen in high lateral STEMI.

The author uses a three-step approach:

Step 1: understand the ST vector in high lateral STEMI.

In high lateral infarction, the ST vector is directed towards the armpit and is usually directed from 0 ° to -90 ° in the frontal plane. 6 ECG leads are grouped in this area, which can inherit a high lateral ST vector. 0 ° corresponds to lead I, -30 ° corresponds to aVL, -60 ° corresponds to a mirror image of lead III, and -90 ° corresponds to a mirror image of lead aVF. Located on the left and above the center of the heart, the projection of lead V2 in the frontal plane is also directed towards the armpit. Therefore, the morphology of complexes in V2 often resembles the morphology in lead aVL. Based on Fig. 3, it is easy to recognize why STEMI-D1 is characterized by ST elevation in leads I, aVL, and V2, and ST depression in leads III and aVF.

Fig. 3. ST-elevation vector in high lateral myocardial infarction with occlusion of the first diagonal branch (D1) of the left anterior descending artery (LAD) (yellow arrow, blue zone). The ST vector points to leads I, aVL, V2 and forms a mirror image in III and aVF leads.

Therefore, any D1-LAD occlusion causes ST-elevation in lead I, aVL, lead III mirroring, which represents ST depression in lead III and lead V2. Since they are not contiguous in the 4 × 3 12-lead ECG format registration, it is very easy to skip these changes. And since it also causes ST-depression in lead III and aVF, which are adjacent, it is easy to mistake an ST-segment elevation patient for a non-ST-elevated myocardial infarction.

Step 2: recognize the electrocardiographic “South African flag sign”.

Most electrocardiographs record 12-lead ECGs in a 4 × 3 format. With this display, the location of ST-segment deviation resembles the image of the South African flag with ST-elevation in the upper left panel (lead I) and in the two middle panels in the second and third columns (leads aVL and V2, respectively) and ST-depression in the lower-left panel (lead III ).

In fig. 4 shows a case where STEMI can be accurately identified and therefore easier to remember the South African flag pattern. It also demonstrates that the prominent ST-elevation seen in V2 should be a frontal plane rather than a horizontal ST vector reflection because there is absolutely no corresponding ST elevation in leads V1 and V3, the two contiguous chest’s leads.

Fig. 4. The South Africa Flag sign on the ECG. In the most common 12-lead 4×3 ECG format, the most significant ST abnormalities resemble the shape of the South African flag.

The South Africa Flag sign on the ECG has a green middle zone that resembles a “Y”. Leads I and III occupy the upper and lower limb Y. Lead aVL occupies the intersection of two limbs Y, and lead V2 unites the upper and lower parts of Y. Thus, all of these leads coincide, and the elevation ST depression in lead I, aVL, V2, and ST depression in lead III match the South African flag. Therefore, to recognize D1-LAD occlusion, Littmann described one specific 12-lead ECG feature called the flag of South Africa. This flag of South Africa can be easily recognized, which can minimize the chances of missing a D1-LAD occlusion.

Step 3: recognize a more subtle high lateral STEMI.

High lateral STEMI is often not diagnosed early because ST depression seen in leads III and aVF is mistaken for inferior ischemia. However, it should be borne in mind that ST depression in any lead can be a reflection of ST elevation in the mirrored leads. Even when ST elevation is quite mild, if it is localized in leads I, aVL, and V2, ST depression in the inferior leads should probably be considered reciprocal (Fig. 5).

Fig. 5. South Africa Flag sign on the ECG.

Conclusions

Identification of the sign of the South African flag on the ECG can improve the timely diagnosis of high lateral myocardial infarctions that are not diagnosed in time due to the non-contiguous nature of ST segment elevation on the electrocardiogram, which will allow timely reperfusion therapy for this group of patients.

Reference

1. Durant E., Singh A. Acute first diagonal artery occlusion: a characteristic pattern of ST elevation in noncontiguous leads. Am J Emerg Med. 2015; 33: 1326.e3-5
2. Littmann L. South African flag sign: a teaching tool for easier ECG recognition of high lateral infarct. The American Journal of Emergency Medicine. 2016;34(1), P107-109.
3. G Rajendran, S Mahalingam, R Kagne, B Nathan, The South African flag sign—an electrocardiographic sign to predict the culprit artery, QJM: An International Journal of Medicine, 2021.
4. Monica Monaghan, Shiva Sreenivasa A Red Flag ECG Circulation. 2020;142:1871–1874

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https://clincasequest.hospital/course/interrupted-symphony/ The onset of the consultation Wash hands and put on PPE if necessary. Introduce…

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Symptomatic bradycardia

Symptomatic bradycardia occurs when the heart rate drops below 50 beats per minute. Most often,…

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