Arrhythmias – ClinCaseQuest

Lyme disease

Tatyana Zaikina — Fri, 22 Dec 2023 13:20:42 +0000

Tatyana Zaikina

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.

Clinical picture	Treatment of choice	Alternative treatment
Erythema migrans	Doxycycline 100 mg 2 times a day orally (PO) for 10 days or Amoxicillin 500 mg 3 times a day PO for 14 days or Cefuroxime 500 mg 2 times a day PO for 14 days	Azithromycin 500 mg once a day p/o for 5-10 days
Damage to the nervous system	Ceftriaxone 2 g once a day IV for 14-21 days or Cefotaxime 2 g 3 times a day IV for 14-21 days or Benzylpenicillin sodium salt 2.4 g every 4-6 hours IV or IV for 14-21 days
Heart damage (without clinical manifestations of myopericarditis, without arrhythmia, without AV block II or III degree, without block I degree with PR interval ≥0.3 sec.)	Doxycycline 100 mg 2 times a day orally (p/o) for 14-21 days or Amoxicillin 500 mg 3 times a day p/o for 14-21 days or Cefuroxime 500 mg 2 times a day p/o for 14-21 days	Azithromycin 500 mg once a day p/o
Heart damage (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.)	Ceftriaxone 2 g once a day IV for 14-21 days or Cefotaxime 2 g 3 times a day IV for 14-21 days or Benzylpenicillin sodium salt 2.4 g every 4-6 hours IV or IV for 14-21 days
Damage to the joints	Doxycycline 100 mg 2 times a day orally (PO) for 28 days or Amoxicillin 500 mg 3 times a day PO for 28 days or Cefuroxime 500 mg 2 times a day PO for 28 days
Borreliosis lymphocytoma	Doxycycline 100 mg 2 times a day orally (PO) for 14 days or Amoxicillin 500 mg 3 times a day PO for 14 days or Cefuroxime 500 mg 2 times a day PO for 14 days
Chronic atrophic acrodermatitis	Doxycycline 100 mg 2 times a day orally (p/o) for 21-28 days or Amoxicillin 500 mg 3 times a day p/o for 21-28 days or Cefuroxime 500 mg 2 times a day p/o for 21-28 days

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:

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
Official site of the Centers for Disease Control and Prevention. https://www.cdc.gov/lyme/treatment/index.html

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Counseling of a patient with symptomatic bradycardia – OSCE guide

Tatyana Zaikina — Thu, 21 Dec 2023 12:21:28 +0000

Tatyana Zaikina

Clinical case simulator “An interrupted symphony”

The onset of the consultation

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

Clarification of the main complaint

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

Comprehensive assessment

Assess other symptoms to get a comprehensive picture

Medical history

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

History of life

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

Find out if the patient has previously been diagnosed with a rhythm and/or conduction disorder
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
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
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
Find out if the patient has recently had an infectious disease and if the patient has been bitten by a tick
Find out if the patient has a drug or food intolerance and how it manifests itself
Find out if the patient has bad habits – drinking alcohol, drugs, smoking
Determine whether the patient’s blood relatives have had cardiovascular disease, including rhythm and/or conduction disorders
Find out the patient’s marital status, living conditions
Clarify whether the patient works, his profession, working conditions, the presence of harmful occupational factors

Objective examination

Assessment of the patient’s general condition
Conducting a general inspection
Evaluation of the constitution
Estimation of the degree of obesity
Skin and mucous membranes
Evaluation of thyroid glands
Assessment of peripheral lymph nodes
Assessment of respiratory organs
Evaluation of the cardiovascular system
Assessment of abdominal organs
Evaluation of organs of the genitourinary system

Laboratory examination

Blood analysis for electrolytes
Blood test for thyroid hormones and TSH
Clinical blood count (if needed)
Coagulogram (if necessary)
Blood test for creatinine and urea (if needed)
Blood test for troponin- I (if necessary)
Blood test for IgM and IgG antibodies to Borrelia (if necessary)
PCR for Borrelia burgdorferi DNA detection (if necessary)
Assessment of blood pH (if necessary)
Genetic testing (if needed)
Toxicological screening (if necessary)

Diagnostic tests

Electrocardiography in 12 leads
Transthoracic echocardiography
Ambulatory ECG monitoring (if necessary)
ECG test with dosed exercise (if necessary)
Coronary angiography (if necessary)
MRI of the heart (if necessary)
Positron emission tomography (if necessary)
Electrophysiological examination (if necessary)
Polysomnography (if necessary)

Making a clinical diagnosis

Identification of the underlying disease
Indication of the nature of the conduction disturbance that caused the bradycardia
Indication of comorbid pathology

Specialist consultations

Cardiologist
Cardiac surgeon
Arithmologist
Rheumatologist
Neuropathologist _
Endocrinologist
Nephrologist
Geneticist
Infectious Disease Specialist

Treatment

Emergency therapy
Long-term therapy (permanent cardiac stimulation)

Explain the procedure for cardiac stimulation

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

Consulting and support

Inform the patient about the disease
Explain to the patient the possible causes of the disease
Inform the patient of the symptoms that may occur with the identified disease
Discuss the results of the examinations with the patient
Explain to the patient the possible consequences of the disease
Educate the patient about available treatments
Help the patient understand the risks and benefits of different treatments
Answer the patient’s questions
Provide an explanation of the extent of monitoring during and after treatment
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

Clinical assessment
Instrumental assessment
Control over side effects of therapy

End of consultation

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

Key communication skills

Active listening
Summing up
Selection of indicative signs

Join our Simulation Training to gain clinical experience

Reflections	Explore the patient’s perception of the current problem	“What do you think could have caused these symptoms?” “Do you have any ideas about why these symptoms appeared?”
Concern	Explore the patient’s current concerns	“Is there something specific that’s been bothering you?” “How do you usually manage your daily activities?” “Is there anything else you feel we should talk about?”
Expectation	Ask what the patient hopes to gain from the consultation	“How can I assist you during today’s consultation?” “What are you hoping to achieve from today’s appointment?” “In your opinion, what would be the most suitable approach moving forward?”

System	Symptoms
General manifestations	fever, weight change, fatigue, sweating, general weakness
Respiratory	shortness of breath, cough, sputum discharge, wheezing, hemoptysis, pleural chest pain
Cardiovascular	chest pain, shortness of breath, swelling of the lower extremities, heart failure
Gastrointestinal	dyspepsia, nausea, vomiting, dysphagia, abdominal pain, stool disorders
Genitourinary	oliguria, polyuria, nocturia, pain during urination
Neurological	vision changes, motor or sensory disturbances, headache, paresis, plegia
Locomotor	pain in the chest wall, bone pain, trauma
Skin	rashes, ulcers, hemorrhages, petechiae, bruises, hemorrhages, neoplasms

Inform the patient about the disease	“Mr./Ms. [Last Name], I would like to inform you of your diagnosis. You have a significant slowing of the heart rate, known as bradycardia. Bradycardia results from a malfunction of the heart’s conduction system, such as sinus node weakness syndrome or atrioventricular block. With sinus node weakness syndrome, the generation or conduction of electrical impulses to the atria is disrupted, leading to a slower heart rate. With atrioventricular block, electrical impulses are generated normally but may be significantly delayed or completely blocked from reaching the ventricles. Due to inadequate oxygen and nutrient supply, all organs and systems suffer, particularly the brain and heart.”
Explain to the patient the possible causes of the disease	“There are various reasons for conduction system disorders of the heart, categorized as internal (cardiac) or external (extracardiac). Common causes include myocardial ischemia, elevated blood potassium levels, certain medications, or central nervous system damage. Less frequent causes include hypothermia, hypothyroidism, myocardial inflammation, and sleep apnea syndrome. Additional examinations will be needed to pinpoint the specific cause of your bradycardia, enabling us to determine the most effective treatment.”
Inform the patient of the symptoms that may occur with the identified disease	“Bradycardia may often be asymptomatic, but significant slowing of the heart rate can lead to noticeable complaints. Mild cases may cause feelings of fatigue, weakness, or reduced tolerance to physical exertion. Severe cases can result in shortness of breath, chest pain, or even loss of consciousness due to impaired blood supply to the heart and brain.”
Discuss the results of the examinations with the patient	“Mr./Ms. [Last Name], I want to share the results of your examinations with you. Electrocardiography revealed a significant slowing of the heart rate, stemming from impaired electrical impulse conduction through the heart. Blood tests showed normal laboratory parameters. To assess your heart’s blood supply, we conducted a coronary angiography, which revealed minor cholesterol deposits in your blood vessels, but they do not significantly affect blood flow to the heart. Do you have any questions about the information I’ve provided?”
Explain to the patient the possible consequences of the disease	“The severity of the consequences of bradycardia depends on the heart rate. Heart rates above 50 beats per minute typically do not result in negative consequences. However, heart rates below 50 beats per minute may lead to decreased blood pressure, altered consciousness, and heart ischemia, which pose significant health risks.”
Educate the patient about available treatments	“I’d like to discuss the treatment options for bradycardia. If your bradycardia is asymptomatic or mildly symptomatic, observation may suffice without intervention. However, in cases of life-threatening symptoms like loss of consciousness or chest pain, treatment is necessary. Initial treatment often involves atropine to improve electrical impulse conduction in the heart. If atropine is ineffective, other medications like epinephrine or dopamine may be used. Electrical cardiostimulation is commonly employed if medications are ineffective. If bradycardia is due to a reversible cause, temporary transcutaneous cardiostimulation may be sufficient until normal heart rhythm is restored. For irreversible cases, permanent pacemaker implantation is recommended. A pacemaker generates electrical impulses, ensuring the heart beats at the correct rate.”
Help the patient understand the risks and benefits of different treatments	“Although electrical cardiostimulation is generally safe when performed by experienced medical professionals, there is a small risk of complications such as infection or bleeding at the electrode insertion site, perforation of the heart, or electrode displacement. However, we will take all necessary precautions to minimize these risks.”
Answer the patient’s questions	“If you have any questions about the causes, symptoms, diagnosis, or treatment of your condition, please don’t hesitate to ask. It’s essential that you understand your condition and the next steps in your care.”
Provide an explanation of the extent of monitoring during and after treatment	“Monitoring your condition is crucial for timely assessment and correction of any changes and evaluating treatment effectiveness. We will monitor your general condition, blood oxygen saturation, blood pressure, and heart rate. Pulse oximetry will assess blood oxygen saturation, while blood pressure monitoring helps evaluate heart function. Electrocardiography will monitor heart rhythm. Regular follow-ups with your family doctor and arrhythmologist are essential for ongoing monitoring and pacemaker assessment.”
Schedule regular check-ups and follow-up to assess the effectiveness of treatment and changes in the patient’s condition	“After discharge, it’s important to monitor your well-being. Keep a diary noting any changes in symptoms, pulse, or blood pressure. Regular visits to your family doctor for electrocardiogram monitoring and arrhythmologist appointments, initially every 4-6 weeks and later every 6-12 months, are recommended. Modern pacemakers may include remote monitoring systems, enabling your doctor to assess pacemaker function remotely and detect any issues.”

H-Hypoxia	hypoxia	shortness of breath, tachypnea, cyanosis, low blood oxygen saturation
H-Hydrogen ion	excess hydrogen ions (acidosis)	low QRS amplitude on the ECG
H-Hypokalemia	hypokalemia	hypokalemia, flat T waves on the ECG, the appearance of a U wave
H- Hyperkalemia	hyperkalemia	hyperkalemia, high-amplitude T waves on the ECG, widening of QRS complexes
H-Hypothermia	hypothermia	staying in conditions of low temperatures, low body temperature
T-Tension pneumothorax	tension pneumothorax	progressive difficulty breathing, shortness of breath, tachypnea, cyanosis, X-ray signs of air accumulation in the pleural cavity
T- Tamponade	cardiac tamponade	Beck’s triad – enlargement of jugular veins, deafness of heart sounds, hypotension; fluid accumulation in the pericardial cavity
T-Toxins	toxins	As a rule, a prolonged QT interval is registered on the ECG; neurological symptoms may be observed
T-Thrombosis	thrombosis (myocardial infarction)	increased markers of myocardial necrosis, ECG signs of acute myocardial ischemia, angiographic confirmation of coronary artery occlusion

Interval R-R
Interval R-R	ms sec mm
Pulse	beats / min
Q-T measured
Q-T measured	ms sec mm
Corrected Interval QT

Categories of diagnostic criteria	ACMP (right ventricle) Updated criteria based on ITF modified diagnostic criteria 2010	ACMP (left ventricle) New Padua Diagnostic Criteria
I. Morphological abnormalities of the ventricles	Echo, MRI, or angiography: Major criteria: • RV regional akinesia, dyskinesia, or aneurysm plus one of the following: – global dilatation of the RV (increase in EDV of the RV in accordance with the indexing for age, sex and PPT) according to the data of the imaging study when compared with the nomogram – global contractile dysfunction of the RV (decrease in RV EF in accordance with the nomogram for age and gender) Minor criterion: • Regional akinesia of the pancreas, dyskinesia, or aneurysm of the free wall of the pancreas	Echo, MRI, or angiography: *Major criterion:* • Global contractile dysfunction (decrease in LVEF according to echocardiography or decrease in global longitudinal deformity of the LV when compared with the nomogram for age, sex and PPT), with or without LV dilatation (increase in LV EDV, indexed to age, sex and PPT) according to imaging research – echocardiography or MRI. Minor criterion: • Regional hypokinesia or akinesia of the free wall of the LV and / or IVS
II. Structural myocardial abnormalities	MRI criterion: *Major criterion* • Transmural contrast delay (fibrosis pattern in one or more pancreatic segments, mandatory confirmation in two orthogonal projections – along the short and long axis). For EMB (limited indications): *Major criterion* • Fibrous myocardial replacement in one or more samples, with or without fatty infiltration	MRI criterion: *Major criterion* • Subepicardial or median LV fibrosis (striae pattern, stripes of fibrosis in one or more LV segments according to the “bovine eye” scheme, necessarily in two orthogonal projections) with localization in the septum and / or free LV wall (except for the junction points of the IVS with the ventricles)
III. Depolarization anomalies	*Major criterion* • Inversion of T waves in the right precordial leads (V1, V2, V3) in the absence of complete RBBB (in persons with full pubertal development) *Minor criteria* • Inversion of T waves in the right precordial leads (V1 and V2) in persons with full pubertal development in the absence of complete RBBB • Inversion of T waves in the right precordial leads (V1, V2, V3 and V4) in persons with full puberty with complete RBBB	*Minor criterion* • T-wave inversion in the left precordial leads (V4-V6) in the absence of complete LBBB
IV. Repolarization anomalies	*Major criterion* • Inversion of T waves in the right precordial leads (V1, V2, V3) in the absence of complete RBBB (in persons with full pubertal development) precordial leads (V1, V2, V3 and V4) in persons with full pubertal development in the presence of complete RBBB Minor criterion • Inversion of T waves in the left precordial leads (V4-V6) in the absence of complete LBBB	*Minor criteria* • T-wave inversion in the right precordial leads (V1 and V2) in persons with full pubertal development in the absence of complete RBBB • T-wave inversion in the right precordial leads (V1, V2, V3 and V4) in persons with full pubertal development in the presence of complete RBBB *Small criterion* • T-wave inversion in the left precordial leads (V4-V6) in the absence of complete RBBB
V. Ventricular arrhythmias	*Major criterion* • Frequent ventricular premature beats (VES> 500 per day), persistent or unstable ventricular tachycardia with LBBB morphology *Minor criterion* •Frequent ventricular extrasystoles (> 500 per day), unstable or sustained ventricular tachycardia of LBBB morphology with the lower axis (pattern of ectopic substrate of the RV outflow tract)	*Minor criterion* • Ventricular premature beats (VES> 500 in 24 h), persistent or unstable ventricular tachycardias with RBBB morphology (excluding the “fascicular pattern”)
VI. Family history (heredity) / genetics	*Major criteria* • ACMP was confirmed in first-line relatives with diagnostic criteria • ACMP confirmed histopathologically at autopsy or intraoperatively in a first-line relative • Identification of a pathogenic or possibly pathogenic mutation associated with ACMP in the examined patient *Minor criteria* • History of ACMP in a first-line family member when it is not possible to determine if the relative’s phenotype meets the diagnostic criteria • Premature sudden death (under the age of 35) with suspected CMP in a first-line relative • ACMP confirmed by histopathological or diagnostic criteria in second-line family members

Arrhythmias – ClinCaseQuest

Lyme disease

Counseling of a patient with symptomatic bradycardia – OSCE guide

Symptomatic bradycardia

Corrected QT Interval Bazett’s formula online calculator

Corrected Interval Q-T

Arrhythmogenic cardiomyopathy

Aetiology

Epidemiology

Pathophysiology

Symptoms

Physical examination

Diagnosis

Diagnostic criteria for arithmogenic cardiomyopathy of the right ventricle new “padua criteria”

Diagnostic Criteria of Arrhythmogenic Right Ventricle Cardiomyopathy (DIAGNOSTIC CRITERIA ITF 2010).

I. Global and regional dysfunction and structural alterations

Major

Minor

II. Tissue characterization

Major

Minor

III. Depolarization abnormalities

Major

Epsilon wave in right precordial leads (V1-V3)

Minor

IV. Repolarization abnomalies

Major

Minor

V. Ventricular arrhythmias

Major

Minor

VI. Family history and genetics

Major

Minor

Algorithm for diagnostics of acmp according to new 2020 criteria.

Molecular genetics

Differential diagnosis:

Management

Antiarrhythmics

Radiofrequency ablation

Implantable cardioverter defibrillators

Cardiac Transplantation

Unconsciousness and ECG changes in a patient with comorbidities