A 64-year-old man was transported to the emergency department by ambulance due to a progressively worsening shortness of breath over the past two weeks. He also noticed swelling in his legs. The patient reports feeling breathless when climbing stairs or walking more than two blocks. Approximately one month ago, he suffered an ST-elevation myocardial infarction, which required the implantation of a stent in the left anterior descending artery.

On physical examination, elevated jugular venous pressure was noted, along with bilateral lower extremity edema. Lung auscultation revealed bilateral crepitation in the basal regions. A chest X-ray showed bilateral pleural effusion and the presence of Kerley B lines.

Pulmonary edema

Acute pulmonary edema is a life-threatening emergency that requires immediate medical intervention. It is characterized by secondary shortness of breath and hypoxia, resulting from fluid accumulation in the lungs, which disrupts gas exchange.

Acute heart failure (HF) typically manifests as “acute decompensated heart failure” (ADHF), secondary chronic heart failure (CHF), or de novo heart failure. The most severe complications of acute heart failure are acute pulmonary edema and cardiogenic shock. According to the EuroHeart Failure Survey II, 37% of patients hospitalized with heart failure presented with de novo acute heart failure, and 16% had acute pulmonary edema.

Acute pulmonary edema has a high mortality rate, requiring urgent care and often hospitalization. The one-year mortality rate for patients hospitalized with acute pulmonary edema is as high as 40%.

The most common causes of acute pulmonary edema include myocardial ischemia, arrhythmias (e.g., atrial fibrillation), acute valvular dysfunction, and fluid overload. Other contributing factors can include pulmonary embolism, anemia, and renal artery stenosis. Non-adherence to treatment plans and adverse drug effects may also precipitate pulmonary edema.

General practitioners are typically familiar with the classic presentation of acute pulmonary edema—severe dyspnea, distress, pallor, sweating, tachycardia, and decreased peripheral perfusion. However, in primary care settings, the clinical manifestations of acute heart failure may be less pronounced or atypical (e.g., delirium or falls in the elderly), making timely diagnosis more challenging.

Pulmonary edema is the accumulation of fluid in the interstitial space and air spaces of the alveoli, impairing normal gas exchange.

Types of Pulmonary Edema

1. Cardiogenic Pulmonary Edema
   This occurs due to a sharp increase in left ventricular filling pressure and left atrial volume, leading to increased pulmonary capillary pressure.
   • Atrial Outflow Obstruction
     Pulmonary edema can result from mitral stenosis or, more rarely, from conditions like atrial myxoma, thrombosis of a prosthetic valve, or a congenital membrane in the left atrium (e.g., cor triatriatum). Mitral stenosis, often a consequence of rheumatic fever, gradually causes pulmonary edema. Other factors commonly accompany mitral stenosis in acute pulmonary edema, such as reduced left ventricular filling caused by tachycardia in arrhythmias (e.g., atrial fibrillation) or fever.
   • Causes of Left Ventricular Dysfunction:
     • Ischemic heart disease
     • Hypertension
     • Acute and chronic heart valve disease (e.g., aortic stenosis, aortic regurgitation, mitral regurgitation)
     • Dilated cardiomyopathy
     • Metabolic conditions (e.g., hypothyroidism)
     • Myocarditis
     • Myocardial toxins (e.g., alcohol, cocaine, chemotherapeutic agents such as doxorubicin, trastuzumab)
     • Ventricular hypertrophy
     • Outflow obstruction
     • Left ventricular diastolic dysfunction (ischemia and infarction can cause diastolic dysfunction in addition to systolic dysfunction). Similarly, myocardial injury can cause systolic or diastolic dysfunction.
   • Arrhythmias
     Tachysystolic atrial fibrillation and ventricular tachycardia can precipitate pulmonary edema.
   • Non-Compliance with Dietary or Medication Guidelines
     Failure to adhere to dietary salt restrictions or prescribed medications (e.g., diuretics) can lead to fluid retention and pulmonary edema.
2. Non-Cardiogenic Pulmonary Edema
   Pulmonary edema with normal pulmonary artery pressure (≤ 18 mm Hg).
   • Causes include:
     • Acute respiratory distress syndrome (ARDS)
     • High-altitude pulmonary edema (HAPE)
     • Opioid overdose
     • Hypoxia, shortness of breath, and dry cough due to altitude exposure in cases of altitude sickness.

Symptoms

• Sudden onset of severe shortness of breath.
• Anxiety and a feeling of drowning.
• Profuse sweating.
• Patients with a gradual onset of symptoms (e.g., over 24 hours) often report dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea.
• Cough is a common symptom. Pink, frothy sputum may occur in severe cases. Occasionally, hoarseness (Ortner’s sign) can result from compression or recurrent paralysis of the laryngeal nerve by an enlarged left atrium, as seen with mitral stenosis.
• Chest pain should raise suspicion for acute ischemia, myocardial infarction, or aortic dissection with acute aortic regurgitation causing pulmonary edema.

Physical Examination

• Tachypnea and tachycardia are often present. Patients may adopt an upright position (orthopnea) and become agitated or confused. They usually appear anxious, with profuse sweating.
• Hypertension is commonly seen in the hyperadrenergic state.
  Hypotension indicates severe left ventricular (LV) systolic dysfunction and the possibility of cardiogenic shock.
• Cool extremities may signal low cardiac output and poor peripheral perfusion.
• Lung auscultation typically reveals fine crackles (rales), often starting in the lung bases. As the condition worsens, the crackles progress toward the upper lung fields. Wheezing may also be present. Jugular venous distention may indicate increased right heart pressures.
• Heart auscultation can aid in diagnosing acute valvular disorders that manifest with pulmonary edema:
  • Aortic stenosis is associated with a crescendo-decrescendo systolic murmur, best heard at the upper sternal border, radiating to the carotid arteries.
  • Acute aortic regurgitation presents with a short, soft diastolic murmur.
  • Acute mitral regurgitation produces a loud systolic murmur, best heard at the apex or lower left sternal border. In the context of ischemic heart disease, this may indicate acute myocardial infarction with rupture of the mitral valve chordae.
• Rust-colored sputum may result from ruptured pulmonary capillaries due to increased hydrostatic pressure.
• Pallor or mottled skin can result from peripheral vasoconstriction, low cardiac output, and blood shunting to the central circulation in patients with poor LV function and increased sympathetic tone. Mottled skin is an independent predictor of increased in-hospital mortality.
• In patients with concomitant right ventricular failure, hepatomegaly, hepatojugular reflux, and peripheral edema may be observed.
• Severe acute pulmonary edema may be associated with altered mental status, often due to hypoxia or hypercapnia. Although acute pulmonary edema is typically associated with hypocapnia, hypercapnia and respiratory acidosis can occur in patients with severe or underlying chronic obstructive pulmonary disease (COPD).

Differential Diagnosis

• Pneumonia
• Diffuse opacification of lung fields due to atelectasis without fluid accumulation

Additional Examination Methods

• Chest X-ray
  Signs of increased left atrial pressure, Kerley B lines, and pleural effusion.
• Echocardiography
  • Reduced or preserved left ventricular ejection fraction (LVEF)
  • Valvular abnormalities, chordal or papillary muscle rupture
  • Mitral regurgitation
  • Aortic stenosis

Causes of Acute Pulmonary Edema

Cardiogenic pulmonary edema must be distinguished from pulmonary edema caused by damage to the alveolar-capillary membrane, which can result from various etiologies. Damage to this barrier may occur in several direct lung injuries (such as pneumonia, aspiration pneumonitis, toxin inhalation, radiation exposure, drowning, or fat embolism) as well as in indirect lung injuries (such as sepsis, shock, multiple blood transfusions, acute pancreatitis, or anaphylactic shock).

The most common cause of heart failure is myocardial dysfunction, which can arise due to one or more of the following factors:

• Hypertension (present in over 60% of patients with heart failure)
• Ischemic heart disease (present in over 50% of patients with heart failure)
• Idiopathic dilated cardiomyopathy (seen in approximately 10% of patients with heart failure)
• Diabetes mellitus
• Excessive alcohol consumption
• Obesity
• Drug toxicity

Other cardiac causes of heart failure include arrhythmias, valvular dysfunction, and pericardial disease.

Non-cardiac causes of heart failure include hypovolemia (due to dehydration or hemorrhage), pulmonary embolism, and conditions associated with increased cardiac output (such as anemia, sepsis, and thyrotoxicosis).

Cardiogenic pulmonary edema is defined as pulmonary edema caused by elevated capillary hydrostatic pressure, which is secondary to increased pulmonary venous pressure. It reflects the accumulation of low-protein fluid in the pulmonary interstitium and alveoli as a result of cardiac dysfunction.

Stages of Development of Pulmonary Edema

The progression of fluid accumulation in acute pulmonary edema can be described in three physiological stages:

Stage 1
In the initial stage, increased pressure in the pulmonary artery leads to the stretching and opening of small pulmonary vessels. At this stage, gas exchange is not significantly impaired and may even slightly improve. This is due to the redistribution of blood flow within the lungs, enhancing perfusion in certain areas.

Stage 2
In stage 2, fluid and colloids begin to move from the pulmonary capillaries into the pulmonary interstitium. Initially, the lymphatic system compensates by increasing lymphatic outflow to efficiently remove the excess fluid. However, continued fluid filtration can overwhelm the drainage capacity of the lymphatic system. Fluid first accumulates in the compliant interstitial compartments, especially around large vessels in dependent zones (such as the perivascular tissue).

At this stage, the accumulation of fluid in the interstitium can start to affect the function of small airways, leading to mild hypoxemia. However, the hypoxemia is usually not severe enough to cause significant tachypnea. Any tachypnea that does occur is mainly due to the stimulation of juxtapulmonary capillary (J-type) receptors, which are unmyelinated nerve endings near the alveoli. These receptors are involved in reflexes that regulate respiration and heart rate.

Stage 3
In the final stage, as fluid filtration continues and the loose interstitial space becomes filled, excess fluid crosses into the alveolar spaces. The interstitial space can accommodate up to approximately 500 mL of fluid. Once the interstitial capacity is exceeded, fluid moves across the alveolar epithelium into the alveoli. At this stage, gas exchange is noticeably impaired, vital capacity and other lung volumes are significantly reduced, and hypoxemia becomes more pronounced. This is when patients typically experience more severe respiratory distress and worsening oxygenation.

Diagnostics

Laboratory tests and imaging are essential for evaluating patients with cardiogenic pulmonary edema. The following diagnostic tools are commonly used:

Complete Blood Count (CBC)
A CBC is useful for detecting severe anemia and may reveal signs of sepsis or infection, particularly if there is a significantly elevated white blood cell count.

Serum Electrolytes
Measuring serum electrolytes is important because patients with chronic heart failure often take diuretics, making them prone to electrolyte imbalances, especially hypokalemia and hypomagnesemia. Patients with chronic renal failure are at high risk for hyperkalemia, particularly if they are not undergoing regular hemodialysis.

Blood Urea Nitrogen (BUN) and Creatinine Levels
These tests assess kidney function, which is crucial for evaluating the patient’s potential response to diuretics and identifying any underlying renal failure.

Pulse Oximetry
Pulse oximetry is used to assess hypoxia, providing insight into the severity of acute pulmonary edema. It is also helpful for monitoring the patient’s response to supplemental oxygen therapy and other treatments.

Arterial Blood Gas (ABG) Analysis
ABG analysis offers a more precise measurement of oxygen saturation compared to pulse oximetry. While the decision to initiate mechanical ventilation is usually based on clinical findings, ABG results may be considered in more complex cases.

Electrocardiography (ECG)
An ECG can detect acute tachyarrhythmias or bradyarrhythmias, as well as signs of acute myocardial ischemia or myocardial infarction, which may be contributing factors to pulmonary edema.

Chest Radiography (X-ray)
A chest X-ray helps differentiate cardiogenic pulmonary edema from other pulmonary causes of severe dyspnea. Key features of cardiogenic pulmonary edema on a chest X-ray include:

• Enlarged heart (cardiomegaly)
• Redistribution of blood flow
• Kerley B lines (indicative of interstitial edema)
• Edema in the basal parts of the lungs (contrasted with diffuse edema)
• Absence of air bronchograms
• Presence of pleural effusion, particularly bilateral and symmetrical, which is more common in acute presentations of chronic heart failure

Table: Differential Diagnosis of Acute Shortness of Breath and Causes of Acute Pulmonary Edema

Table: Differential Diagnosis of Acute Pulmonary Edema

Echocardiography

Bedside echocardiography in patients with decompensated congestive heart failure (CHF) is an essential diagnostic tool for determining the etiology of pulmonary edema. This imaging modality can assess left ventricular (LV) systolic and diastolic function, as well as evaluate valvular function and pericardial disease.

The identification of new wall motion abnormalities may suggest an acute myocardial infarction. Echocardiography is particularly valuable in diagnosing the mechanical causes of pulmonary edema, including the following conditions:

• Acute rupture of the papillary muscle
• Acute ventricular septal defect
• Cardiac tamponade
• LV rupture
• Valve vegetation leading to acute severe mitral or aortic regurgitation

Treatment

The management of both acute heart failure and acute pulmonary edema is primarily based on clinical experience rather than randomized controlled trials.

The algorithm for providing medical care can be conditionally divided into two stages:

1. Pre-Hospital Care: This involves immediate assistance to stabilize the patient before they reach the hospital.
2. Hospital Care: This stage focuses on comprehensive treatment and monitoring of the patient after admission.

While there are various clinical guidelines for treating acute pulmonary edema, the general principles across these guidelines remain consistent. The goals of therapy for acute pulmonary edema include:

• Improving oxygenation
• Maintaining adequate blood pressure to ensure perfusion of vital organs
• Reducing excess extracellular fluid

Additionally, it is crucial to address the underlying cause of the condition or mitigate its impact on the patient’s status.

Drugs Used in Treatment

The medications commonly used in the management of acute pulmonary edema include nitrates, diuretics, morphine, and inotropes. Some patients may also require ventilatory support.

Strongest Evidence

Nitrates and noninvasive ventilation have the strongest evidence for efficacy in treating acute pulmonary edema. Diuretics are indicated only for patients with fluid overload; furosemide should be administered slowly via intravenous infusion. The most common causes of cardiogenic pulmonary edema include excessive venous return (fluid overload), increased systemic vascular resistance (e.g., after exercise), and left ventricular dysfunction, which can involve contractility disorders, rhythm disturbances, and frequency issues.

Continuous use of morphine is not recommended due to its potential adverse effects. Oxygen should be administered only in cases of hypoxemia.

Inotropic agents should be initiated only when hypotension is present with reduced organ perfusion. In such cases, dobutamine is usually the first-line treatment.

Table. Treatment of acute pulmonary edema

Nitrates

The mechanism of action of nitrates involves the relaxation of smooth muscle, leading to the dilation of veins and a consequent reduction in preload at low doses. At higher doses, nitrates also cause the dilation of arterioles, which results in decreased preload and blood pressure. In the coronary arteries, this dilation enhances coronary blood flow. Collectively, these actions improve oxygenation and decrease the workload on the heart.

In clinical practice, nitrates are often prescribed sublingually. Intravenous infusions of nitroglycerin are also used, as this route allows for rapid onset of action and precise dose titration.

Advantages of using nitro preparations for acute pulmonary edema:

• Fast and reliable reduction of preload.
• Medium to high doses decrease systemic vascular resistance (afterload), helping to maintain or improve stroke volume and cardiac output.
• Various routes of administration: sublingual and intravenous.
• Short duration of action and rapid metabolism (approximately 60 mcg per minute).

Therefore, nitroglycerin is considered a first-line medication during both the pre-hospital and early hospital stages for patients with acute pulmonary edema.

Contraindications: The use of nitrates should be avoided if the patient has taken phosphodiesterase inhibitors (e.g., sildenafil, vardenafil, tadalafil) within the last 48 hours, as these medications are commonly prescribed for erectile dysfunction and pulmonary hypertension. Additionally, avoid the intravenous administration of eprostenol or treprostinil, which are used in the treatment of pulmonary hypertension.

Nitrates are also not recommended for patients with myocardial infarction of the inferior wall or for those suspected of having an ST-segment elevation myocardial infarction affecting the right ventricle, as these patients require adequate preload for the right ventricle. Moreover, nitrates should not be used in patients with aortic stenosis, hypotension, or acute mitral insufficiency.

Recommended Modes of Use of Nitro Preparations

In the conducted studies, a high efficacy of sublingual administration of nitroglycerin at a dose of 0.4 mg every 5 minutes was demonstrated until the onset of a pronounced clinical effect. The administration of the drug according to this regimen is recognized as equivalent to intravenous administration of nitroglycerin at a rate of 60 μg/min.

Diuretics

The use of furosemide is not recommended at the pre-hospital stage. Pulmonary edema is more commonly related to volume distribution rather than volume overload; therefore, furosemide does not provide improvement in most patients.

The administration of furosemide can lead to increased afterload due to vasoconstriction and decreased renal blood flow. In some patients, this may result in a significant drop in cardiac output and systemic pressure, potentially increasing the risk of fatal arrhythmias.

An incorrect diagnosis of chronic congestive heart failure, coupled with excessive diuresis, can lead to complications and fatalities. This is because the use of furosemide:

• Reduces preload through increased diuresis, but has a delayed effect.
• Causes an initial negative hemodynamic response, characterized by increased systemic vascular resistance, decreased stroke volume, and reduced cardiac output.
• Can be detrimental when administered to patients with severe cardiogenic pulmonary edema in the first minutes of medical assistance.

Diuretics are indicated only for patients who exhibit signs of fluid overload. Intravenous administration of furosemide in doses of 40 to 80 mg is preferred. Higher doses may be required for patients already on oral diuretics or those with chronic kidney disease. The initial bolus can be administered slowly via intravenous infusion and repeated after 20 minutes if necessary. Following the bolus, a continuous intravenous infusion can be considered, starting at a rate of 5–10 mg per hour. Higher doses have been associated with better results in alleviating dyspnea but also with worsening renal function and increased hospitalizations in intensive care units. However, this association likely reflects the presence of more severe comorbidities and underlying diseases that contribute to the development of acute pulmonary edema. An indwelling urinary catheter should be placed to monitor urine output volume.

Recommended Dosage Regimens of Furosemide

*The bioavailability of the oral preparation of furosemide (frusemide) is approximately half that of the intravenous form.

Morphine

Morphine was traditionally part of the treatment regimen for acute pulmonary edema due to its ability to reduce shortness of breath. It also lowers sympathetic nervous system activity, which may help alleviate anxiety and distress associated with dyspnea.

However, the use of morphine carries several side effects, including respiratory and central nervous system depression, decreased cardiac output, and hypotension. Approximately one-third of patients experience nausea, and morphine can increase the risk of aspiration, especially when continuous positive airway pressure (CPAP) is needed, due to its suppression of the respiratory center. Furthermore, its use in acute pulmonary edema has been linked to a higher incidence of mechanical ventilation, intensive care unit admissions, and mortality.

In the absence of high-quality data from randomized trials, current evidence suggests that morphine may cause harm in this context. As a result, it is no longer recommended for routine use in acute pulmonary edema.

However, administration of morphine may be justified in patients with persistent, intense chest pain that is resistant to nitrates. In such cases, low doses of morphine (1–2.5 mg) may help facilitate the tolerability of invasive ventilation; close monitoring for sedation is essential.

Ventilation Support

The first step in improving ventilation for patients with acute pulmonary edema is to ensure they are in a sitting position, which helps reduce the ventilation-perfusion mismatch.

Oxygen Therapy:
Oxygen is not recommended for routine use in patients without hypoxemia because hyperoxemia can lead to vasoconstriction, decreased cardiac output, and increased short-term mortality. Administering oxygen to a patient who is asphyxiating without hypoxemia may mask clinical deterioration and delay necessary treatment. Supplemental oxygen and assisted ventilation should only be used if oxygen saturation falls below 92%.

When necessary, oxygen should be administered to achieve a target oxygen saturation of 92–96% (with a guideline of 94–98% from the Ministry of Health of Ukraine). Depending on the clinical scenario, oxygen titration can be performed using various delivery devices, including:

• Up to 4 L/min via nasal cannulas
• 5–10 L/min via a face mask
• 15 L/min via a non-rebreather mask
• High-flow nasal cannulas with a fraction of inspired oxygen greater than 35%

For patients with chronic obstructive pulmonary disease (COPD), the target oxygen saturation is 88–92%, and a Venturi mask with inspired oxygen set at 28% is recommended.

Noninvasive Ventilation:
If the patient experiences respiratory distress, acidosis, or hypoxia despite supplemental oxygen, noninvasive ventilation is indicated. There is no significant clinical advantage of bi-level positive airway pressure (BiPAP) over continuous positive airway pressure (CPAP), so the choice of ventilation mode may depend on the specific characteristics of the care center and local availability. Noninvasive ventilation should be initiated with 100% oxygen, with recommended initial settings of 10 cm H2O for CPAP and 10/4 cm H2O (positive inspiratory pressure/expiratory positive airway pressure) for BiPAP. Contraindications to noninvasive ventilation include hypotension, potential pneumothorax, vomiting, and altered levels of consciousness.

Intubation:
If persistent hypercapnia, hypoxemia, or acidosis occurs despite noninvasive ventilation, intubation should be considered. Other indications for intubation include signs of physical exhaustion, decreased level of consciousness, or cardiogenic shock. Endotracheal intubation is indicated only in a limited number of cases and carries significant risks and complications. After intubation, continuous suctioning is often required, and ventilation may be challenging. Additionally, positive pressure ventilation can exacerbate hypotension.

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Inotropes

Intravenous inotropic drugs are indicated for acute pulmonary edema when the patient exhibits hypotension, leading to reduced organ perfusion. Their use is limited to this clinical situation in critically ill patients, as they are associated with longer hospital stays and increased mortality. In cases of left ventricular dysfunction accompanied by hypotension, the first-line therapy is the intravenous infusion of dobutamine.

It is important to note that, in addition to its positive inotropic effects, dobutamine has peripheral vasodilator properties, which can exacerbate hypotension and may necessitate treatment with vasopressors. Additionally, dobutamine can induce arrhythmias and is contraindicated in patients with ventricular arrhythmias or tachysystolic forms of atrial fibrillation.

Another inotrope, milrinone, can also increase cardiac output and improve peripheral perfusion. However, it should be reserved for the short-term treatment of severe heart failure that has not responded to other therapies. Caution is advised with milrinone, as it may increase mortality in acute exacerbations of chronic heart failure.

Inotropes and vasopressors are critical in the management of acute heart failure.

Follow-up

Once the patient’s condition is stabilized, the underlying cause of acute pulmonary edema should be identified and treated. This includes reviewing the patient’s medications to determine if any, such as nonsteroidal anti-inflammatory drugs, verapamil, or diltiazem, may have contributed to the condition. Careful additional monitoring is also recommended, including daily weight monitoring, measurement of serum electrolytes, and assessment of renal function.

After stabilizing a patient with acute cardiogenic pulmonary edema, the goal of therapy is to improve long-term outcomes. If a preserved left ventricular ejection fraction is detected during echocardiography, primary attention should be paid to treating any concomitant diseases. This includes:

• Treating hypertension with antihypertensive drugs.
• Reducing pulmonary congestion and peripheral edema with diuretics.
• Controlling heart rate in cases of atrial fibrillation.

If there is evidence of reduced ejection fraction and chronic heart failure, ACE inhibitors, beta-blocker titration, and the use of drugs affecting mineralocorticoid receptors should be considered.

It is advisable to start ACE inhibitors 24-48 hours after the patient’s condition stabilizes, provided the patient is hemodynamically stable. Caution should be exercised when using ACE inhibitors in patients with hypotension or renal insufficiency, with close monitoring of blood pressure and renal function. Beta-blockers should be titrated from low doses as soon as the patient reaches a euvolemic state before discharge from the hospital. Mineralocorticoid receptor antagonists, such as spironolactone, are best initiated soon after discharge, with close monitoring of blood pressure, serum potassium, and renal function.

Recommendations for the Patient

• Lifestyle Changes:
  • Smoking: Complete cessation.
  • Diet: Follow cardiological recommendations, limiting salt intake.
  • Fluid Restriction: Maximum of 2 liters per day (1.5 liters per day with pronounced CHF).
  • Alcohol: No more than one unit per day.
  • Physical Activity: Individualized rehabilitation program.
• Diagnostics:
  • Echocardiography: Mandatory for all patients after acute pulmonary edema.
  • Basic Cardiological Studies: ECG, lipid profile, glucose assessment, renal function assessment, including calculation of GFR.
  • Other Tests: Liver function, thyroid function, iron content, and clinical blood analysis.
• Monitoring:
  • Self-monitoring of symptoms, weight, and blood pressure.
  • Regular examinations by a general practitioner (frequency determined by the severity and manifestations of CHF):
    • Monitor symptoms, weight, blood pressure, and cardiorespiratory status.
    • Manage risk factors and concomitant diseases (especially coronary heart disease, diabetes, COPD, impaired kidney function, sleep apnea, obesity, depression, osteoarthritis).
    • Assess mental state and control available medications (which can be used as emergency aid in case of recurrent acute pulmonary edema).
    • Monitor pathology (urea, creatinine, electrolytes, and clinical blood analysis).
• Medications that Improve Prognosis and Symptoms:
  • ACE Inhibitors: Angiotensin II receptor blockers can be used in patients with CHF who are intolerant to ACE inhibitors.
  • Beta-blockers: Indicated for patients with systolic heart failure; COPD is not a contraindication for prescribing beta-blockers (e.g., bisoprolol, carvedilol, metoprolol, nebivolol).
  • Furosemide: For symptoms of fluid overload.
  • Spironolactone: To be added if symptom control is insufficient.
  • Digoxin: Considered for patients with concomitant atrial fibrillation or as an adjunct therapy for severe CHF inadequately controlled by the aforementioned drugs.
• Medications to Use with Caution:
  • Contraindicated: Verapamil and diltiazem, NSAIDs or cyclooxygenase-2 inhibitors, corticosteroids.
• Vaccinations: Influenza, pneumococcus, COVID-19.
• Device Therapy for Patients with Moderate to Severe CHF: (To be assessed and recommended by a cardiologist if appropriate):
  • Cardiac resynchronization therapy (e.g., if QRS is greater than 120 ms).
  • Implanted cardioverter-defibrillator.

Conclusion

Clinical guidelines emphasize the lack of evidence supporting currently available treatments. There are also concerns about the effectiveness and safety of these treatments. Therefore, in recent years, there has been a shift toward favoring nitrates and noninvasive ventilation as first-line treatments. However, opioids and diuretics may still play a positive role in some patients.

References:

• 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC) https://academic.oup.com/eurheartj/article/37/27/2129/1748921
• Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. European Heart Journal, Volume 37, Issue 27, 14 July 2016, Pages 2129–2200, https://doi.org/10.1093/eurheartj/ehw128
• Purvey M, Allen G. Managing acute pulmonary oedema. Aust Prescr. 2017;40(2):59-63. doi:10.18773/austprescr.2017.012  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5408000/
• Acute cardiogenic pulmonary oedema. In: eTG complete [Internet]. Melbourne: Therapeutic Guidelines Limited; 2016. www.tg.org.au
• Coons JC, McGraw M, Murali S. Pharmacotherapy for acute heart failure syndromes. Am J Health Syst Pharm 2011;68:21-35. 10.2146/ajhp100202 [PubMed]
• Andrew Baird. Acute pulmonary oedemaю. Management in general practice. Australian Family Physician Vol. 39, No. 12, 2010:  910-914.

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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 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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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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Date

Student name

Group, faculty

---

• 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

Reset

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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.

Loading...

Email (indicate if you want the results to be sent to your email)

Date

Student name

Group, faculty

---

• 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

Reset

Additional materials:

Register on our website right now to have access to more learning materials!

Register

Subscribe to our pages:

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• Instagram
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Acute Pulmonary Edema: Emergency Care Algorithm – Should We Remove or Redistribute the Fluid?

October 5, 2024

Case Presentation: A 64-year-old man was transported to the emergency department by ambulance due to…

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March 24, 2024

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March 1, 2024

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December 22, 2023

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December 21, 2023

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Сообщение Interactive OSCE Checklist – Emergency care of a patient with chest pain – Acute Coronary Syndrome with ST-segment elevation and equivalents 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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