COVID-19-associated heart failure: Difference between revisions
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===Physical Examination=== | ===Physical Examination=== | ||
*Physical examination of patients with acute heart failure is usually remarkable for: | |||
**Crackles on auscultation | |||
**Distended jugular veins | |||
**Lower extremity edema | |||
===Laboratory Findings=== | ===Laboratory Findings=== |
Revision as of 21:21, 29 June 2020
For COVID-19 frequently asked inpatient questions, click here
For COVID-19 frequently asked outpatient questions, click here
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mitra Chitsazan, M.D.[2]Mandana Chitsazan, M.D. [3]
Synonyms and keywords:
Overview
- Both de novo acute heart failure and acute decompensation of chronic heart failure can occur in patients with COVID-19.
- Patients with chronic heart failure may be at higher risk of developing severe COVID-19 infection due to the advanced age and the presence of multiple comorbidities.
Historical perspective
Classification
- Heart Failure in COVID-19 may be classified similarly to heart failure from other causes.
- In general, HF can be classified based on:
- The pathophysiology of heart failure:
- systolic vs diastolic
- left-sided vs right-sided
- The duration of symptoms:
- acute vs chronic
- The underlying physiology based on left ventricular ejection fraction (LVEF):
- Heart failure with reduced ejection fraction (HFrEF) vs heart failure with mid-range ejection fraction (HFmrEF) and heart failure with preserved ejection fraction (HFpEF),
- The severity of heart failure (i.e., the New York Heart Association Class I-IV)
- The stage of congestive heart failure (i.e., AHA Class A,B,C,D)
- The pathophysiology of heart failure:
- Acute heart failure has two forms:
- Newly-arisen (“de novo”) acute heart failure
- Acutely decompensated chronic heart failure (ADCHF)
Pathophysiology
- Presumed pathophysiologic mechanisms for the development of new or decompensated heart failure in patients with COVID-19 include:[1] [2] [3] [4] [5]
- Acute exacerbation of chronic heart failure caused by precipitating factors
- Acute myocardial injury (which in turn can be caused by several mechanisms)
- Stress cardiomyopathy (i.e., Takotsubo cardiomyopathy)
- Impaired myocardial relaxation resulting in diastolic dysfunction [i.e., Heart failure with preserved ejection fraction (HFpEF) ]
- Right-sided heart failure, secondary to pulmonary hypertension caused by hypoxia and acute respiratory distress syndrome (ARDS)
Causes
- Acute myocardial injury
- Acute coronary syndromes
- Myocarditis
- Hypertensive crisis
- Arrhythmias: Tachycardia or severe bradycardia
- Stress-induced cardiomyopathy
- Circulatory failure:
- Acute pulmonary embolism
- Pericardial tamponade
Differentiating ((COVID-19 associated heart failure)) from other Diseases
In patients with COVID-19 infection, acute heart failure should be differentiated from other diseases presenting with dyspnea and/or tachypnea. The differentials include the following:
- Pneumonia
- ARDS
- Myocarditis/pericarditis
- Acute pulmonary embolism
Epidemiology and Demographics
- In one study, acute heart failure was seen in 4.1% of patients with acute cardiac injury.
- In a retrospective study on study 191 COVID-19 patients in Wuhan, China, the incidence of heart failure was 23% (52% in non-survivors vs 12% in survivors).
Risk Factors
Screening
- There is insufficient evidence to recommend routine screening for heart failure in COVID-19 patients.
- Routine measurement of natriuretic peptides and/or cardiac troponins have not been recommended in the absence of a high index of suspicion for HF on the clinical grounds.
Natural History, Complications, and Prognosis
Diagnosis
Diagnostic Study of Choice
History and Symptoms
- The most common symptoms of acute heart failure in COVID-19 patients are:
- New or worsening dyspnea: may overlap with dyspnea caused by concomitant respiratory involvement and ARDS due to COVID-19
- Peripheral edema
- Confusion and altered mentation
- Orthopnea
- Palpitations
- Paroxysmal nocturnal dyspnea
- Cool extremities
- Cyanosis
- Dizziness
- Syncope
- Fatigue
- Hemoptysis
Physical Examination
- Physical examination of patients with acute heart failure is usually remarkable for:
- Crackles on auscultation
- Distended jugular veins
- Lower extremity edema
Laboratory Findings
- Cardiac Troponins:
- Natriuretic Peptides:
- Natriuretic peptides (BNP/NT-proBNP) are released from the heart in response to increased myocardial stress and are quantitative markers of increased intracardiac filling pressure.[7]
- Elevated BNP and NT-proBNP are of both diagnostic and prognostic significance in patients with heart failure.
- Increased BNP or NT-proBNP levels have been demonstrated in COVID-19 patients.
- Increased NT-proBNP level was associated with worse clinical outcomes in patients with severe COVID-19.[8] [9]
- However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases.[10] [11] [12] [13] [14]
- Therefore, routine measurement of BNP/NT-proBNP has not been recommended in COVID-19 patients, unless there is a high suspicion of HF based on clinical grounds.
Electrocardiogram
- There is no specific electrocardiographic finding for acute heart failure in COVID-19 patients.
- The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors, such as ischemia, myocarditis, and arrhythmias.
- These ECG findings may include:
- Low QRS Voltage
- Left ventricular hypertrophy
- Left atrial enlargement
- Left bundle branch block
- Poor R progression
- ST-T changes
X-ray
- An x-ray may be helpful in the diagnosis of heart failure. Findings on an x-ray suggestive of heart failure include:
- Cardiomegaly
- Pulmonary congestion
- Increased pulmonary vascular markings.
- However, signs of pulmonary edema may be obscured by underlying respiratory involvement and ARDS due to COVID-19.
Echocardiography or Ultrasound
- A complete standard transthoracicechocardiography (TTE) has not been recommended in COVID-19 patients considering the limited personal protective equipment (PPE) and the risk of exposure of additional health care personnel.[15]
- To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
- In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
- Cardiac point-of-care ultrasound (POCUS)
- Focused cardiac ultrasound study (FoCUS)
- Critical care echocardiography
- Cardiac ultrasound can help in assessing the following parameters:
- Left ventricular systolic function (ejection fraction) to distinguish systolic dysfunction with a reduced ejection fraction (<40%) from diastolic dysfunction with a preserved ejection fraction.
- Left ventricular diastolic function
- Left ventricular structural abnormalities, including LV size and LV wall thickness
- Left atrial size
- Right ventricular size and function
- Detection and quantification of valvular abnormalities
- Measurement of systolic pulmonary artery pressure
- Detection and quantification of pericardial effusion
- Detection of regional wall motion abnormalities/reduced strain that would suggest underlying ischemia.
CT scan
MRI
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
- Acute heart failure in the setting of COVID-19 is generally treated similarly to acute heart failure in other settings. These may include:
- Fluid restriction
- Diuretic therapy
- Vasopressors and/or inotropes
- Ventricular assisted devices and extracorporeal membrane oxygenation (ECMO)
- Beta-blockers should not be initiated during the acute stage due to their negative inotropic effects.[16]
- Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) should be used with caution in patients with acute heart failure due to their effect on fluid and sodium retention.[17]
- Patients with chronic heart failure are recommended to continue their previous guideline-directed medical therapy, including beta-blockers, ACEI or ARB, and mineralocorticoid receptor antagonists. [18]
References
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