COVID-19-associated heart failure: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
Presumed pathophysiologic mechanisms for the development of new or worsening heart failure in patients with COVID-19 include:<ref name="pmid32219357">{{Cite pmid|32219357}}</ref> <ref name="pmid32360242">{{Cite pmid|32360242}}</ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref> | *Presumed pathophysiologic mechanisms for the development of new or worsening heart failure in patients with COVID-19 include:<ref name="pmid32219357">{{Cite pmid|32219357}}</ref> <ref name="pmid32360242">{{Cite pmid|32360242}}</ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref> | ||
**Acute exacerbation of chronic heart failure | **Acute exacerbation of chronic heart failure | ||
Revision as of 13:52, 25 June 2020
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Synonyms and keywords:
Overview
- Patients with chronic heart failure (HF) may be at higher risk of developing severe COVID-19 infection due to the advanced age and the presence of multiple comorbidities.
- Both de novo acute heart failure and acute decompensation of chronic heart failure can occur in patients with COVID-19.
Classification
Pathophysiology
- Presumed pathophysiologic mechanisms for the development of new or worsening heart failure in patients with COVID-19 include:[1] [2] [3] [4] [5]
- Acute exacerbation of chronic heart failure
- 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
Differentiating ((Page name)) from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications, and Prognosis
Diagnosis
Diagnostic Study of Choice
History and Symptoms
Physical Examination
Laboratory Findings
- Cardiac Troponins:
- Elevated cardiac troponin levels suggest the presence of myocardial cell injury or death.
- Cardiac troponin levels may increase in patients with chronic or acute decompensated HF.[6]
- 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 transthoracic (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
- ↑ PMID 32219357 (PMID 32219357)
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