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__NOTOC__ | |||
{{COVID-19 associated Heart Failure}} | |||
'''For patient information, click [[Xyz (patient information)|here]]''' | |||
{{CMG}}; {{AE}} {{Mitra}} | |||
{{SK}} | |||
==[[Heart Failure overview|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. | |||
==[[Heart Failure historical perspective|Historical Perspective]]== | |||
==[[Heart Failure classification|Classification]]== | |||
==[[Heart Failure 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> | |||
**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) | |||
==[[Heart Failure causes|Causes]]== | |||
==[[Heart Failure differential diagnosis|Differentiating Heart Failure from other Diseases]]== | |||
==[[Heart Failure epidemiology and demographics|Epidemiology and Demographics]]== | |||
==[[Heart Failure risk factors|Risk Factors]]== | |||
==[[Heart Failure screening|Screening]]== | |||
==[[Heart Failure natural history, complications and prognosis|Natural History, Complications and Prognosis]]== | |||
==Diagnosis== | |||
[[COVID-19-associated heart failurediagnostic study of choice|Diagnostic study of choice]] | [[COVID-19-associated heart failure history and symptoms|History and Symptoms]] | [[COVID-19-associated heart failure physical examination|Physical Examination]] | [[COVID-19-associated heart failure laboratory findings|Laboratory Findings]] | [[COVID-19-associated heart failure electrocardiogram|Electrocardiogram]] | [[COVID-19-associated heart failure x ray|X-Ray Findings]] | [[COVID-19-associated heart failure echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[COVID-19-associated heart failure CT scan|CT-Scan Findings]] | [[COVID-19-associated heart failure MRI|MRI Findings]] | [[COVID-19-associated heart failure other imaging findings|Other Imaging Findings]] | [[COVID-19-associated heart failure other diagnostic studies|Other Diagnostic Studies]] | |||
====Electrocardiography (ECG)==== | |||
| [[Xyz x ray|X-Ray Findings]] | |||
====Chest x-ray (CXR)==== | |||
*The Chest x-ray may show evidence of: | |||
**Cardiomegaly | |||
**Pulmonary congestion | |||
**Increased pulmonary vascular markings. | |||
*Signs of pulmonary edema may be obscured by underlying respiratory involvement and ARDS due to COVID-19. | |||
| [[Heart Failure echocardiography and ultrasound|Echocardiography and Ultrasound]] | |||
====Echocardiography==== | |||
*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.<ref name="pmid32391912">{{Cite pmid|32391912}}</ref> | |||
*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 an underlying ischemia | |||
| [[Heart Failure CT scan|CT-Scan Findings]] | [[Heart Failure MRI|MRI Findings]] | [[Heart Failure other imaging findings|Other Imaging Findings]] | [[Heart Failure other diagnostic studies|Other Diagnostic Studies]] | |||
====Cardiac biomarkers==== | |||
*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.<ref name="pmid20863950">{{Cite pmid|20863950}}</ref> | |||
*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.<ref name="pmid28062628">{{Cite pmid|28062628}}</ref> | |||
**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.<ref name="pmid32293449">{{Cite pmid|32293449}}</ref> <ref name="pmid32232979">{{Cite pmid|32232979}}</ref> | |||
**However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases.<ref name="pmid18298480">{{Cite pmid|18298480}}</ref> <ref name="pmid16442916">{{Cite pmid|16442916}}</ref> <ref name="pmid28322314">{{Cite pmid|28322314}}</ref> <ref name="pmid23837838">{{Cite pmid|23837838}}</ref> <ref name="pmid21478812">{{Cite pmid|21478812}}</ref> | |||
**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. | |||
==Treatment== | |||
[[Heart Failure medical therapy|Medical Therapy]] | |||
*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. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref> | |||
*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.<ref name="pmid24251454">{{Cite pmid|24251454}}</ref> | |||
*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.<ref name="pmid12656651">{{Cite pmid|12656651}}</ref> | |||
| [[Heart Failure interventions|Interventions]] | [[Heart Failure surgery|Surgery]] | [[Heart Failure primary prevention|Primary Prevention]] | [[Heart Failure secondary prevention|Secondary Prevention]] | [[Heart Failure cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Xyz future or investigational therapies|Future or Investigational Therapies]] | |||
==Case Studies== | |||
[[Xyz case study one|Case #1]] | |||
[[Category: (name of the system)]] | |||
==[[Heart Failure overview|Overview]]== | ==[[Heart Failure overview|Overview]]== | ||
Revision as of 12:05, 25 June 2020
Template:COVID-19 associated Heart Failure For patient information, click here
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mitra Chitsazan, M.D.[2]
Synonyms and keywords:
Template:COVID-19 associated Heart Failure
For patient information, click here
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3]; Associate Editor(s)-in-Chief: Mitra Chitsazan, M.D.[4]
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.
Historical Perspective
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 Heart Failure 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 | Electrocardiogram | X-Ray Findings | Echocardiography and Ultrasound | CT-Scan Findings | MRI Findings | Other Imaging Findings | Other Diagnostic Studies
Electrocardiography (ECG)
Chest x-ray (CXR)
- The Chest x-ray may show evidence of:
- Cardiomegaly
- Pulmonary congestion
- Increased pulmonary vascular markings.
- Signs of pulmonary edema may be obscured by underlying respiratory involvement and ARDS due to COVID-19.
| Echocardiography and Ultrasound
Echocardiography
- 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.[6]
- 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 an underlying ischemia
| CT-Scan Findings | MRI Findings | Other Imaging Findings | Other Diagnostic Studies
Cardiac biomarkers
- 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.[7]
- 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.[8]
- 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.[9] [10]
- However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases.[11] [12] [13] [14] [15]
- 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.
Treatment
- 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. [16]
- 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.[17]
- 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.[18]
| Interventions | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies
Case Studies
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.
Historical Perspective
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 Heart Failure 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 | Electrocardiogram | X-Ray Findings | Echocardiography and Ultrasound | CT-Scan Findings | MRI Findings | Other Imaging Findings | Other Diagnostic Studies
| Physical Examination | Laboratory Findings | Electrocardiogram
Electrocardiography (ECG)
- There is no specific electrocardiographic sign 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
Chest x-ray (CXR)
- The Chest x-ray may show evidence of:
- Cardiomegaly
- Pulmonary congestion
- Increased pulmonary vascular markings.
- Signs of pulmonary edema may be obscured by underlying respiratory involvement and ARDS due to COVID-19.
| Echocardiography and Ultrasound
Echocardiography
- 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.[6]
- 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 an underlying ischemia
| CT-Scan Findings | MRI Findings | Other Imaging Findings | Other Diagnostic Studies
Cardiac biomarkers
- 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.[7]
- 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.[8]
- 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.[9] [10]
- However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases.[11] [12] [13] [14] [15]
- 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.
Treatment
- 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. [16]
- 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.[17]
- 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.[18]
| Interventions | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies
Case Studies
- ↑ 1.0 1.1 PMID 32219357 (PMID 32219357)
Citation will be completed automatically in a few minutes. Jump the queue or expand by hand - ↑ 2.0 2.1 PMID 32360242 (PMID 32360242)
Citation will be completed automatically in a few minutes. Jump the queue or expand by hand - ↑ 3.0 3.1 PMID 32186331 (PMID 32186331)
Citation will be completed automatically in a few minutes. Jump the queue or expand by hand - ↑ 4.0 4.1 PMID 30625066 (PMID 30625066)
Citation will be completed automatically in a few minutes. Jump the queue or expand by hand - ↑ 5.0 5.1 PMID 32140732 (PMID 32140732)
Citation will be completed automatically in a few minutes. Jump the queue or expand by hand - ↑ 6.0 6.1 PMID 32391912 (PMID 32391912)
Citation will be completed automatically in a few minutes. Jump the queue or expand by hand - ↑ 7.0 7.1 PMID 20863950 (PMID 20863950)
Citation will be completed automatically in a few minutes. Jump the queue or expand by hand - ↑ 8.0 8.1 PMID 28062628 (PMID 28062628)
Citation will be completed automatically in a few minutes. Jump the queue or expand by hand - ↑ 9.0 9.1 PMID 32293449 (PMID 32293449)
Citation will be completed automatically in a few minutes. Jump the queue or expand by hand - ↑ 10.0 10.1 PMID 32232979 (PMID 32232979)
Citation will be completed automatically in a few minutes. Jump the queue or expand by hand - ↑ 11.0 11.1 PMID 18298480 (PMID 18298480)
Citation will be completed automatically in a few minutes. Jump the queue or expand by hand - ↑ 12.0 12.1 PMID 16442916 (PMID 16442916)
Citation will be completed automatically in a few minutes. Jump the queue or expand by hand - ↑ 13.0 13.1 PMID 28322314 (PMID 28322314)
Citation will be completed automatically in a few minutes. Jump the queue or expand by hand - ↑ 14.0 14.1 PMID 23837838 (PMID 23837838)
Citation will be completed automatically in a few minutes. Jump the queue or expand by hand - ↑ 15.0 15.1 PMID 21478812 (PMID 21478812)
Citation will be completed automatically in a few minutes. Jump the queue or expand by hand - ↑ 16.0 16.1 PMID 31129923 (PMID 31129923)
Citation will be completed automatically in a few minutes. Jump the queue or expand by hand - ↑ 17.0 17.1 PMID 24251454 (PMID 24251454)
Citation will be completed automatically in a few minutes. Jump the queue or expand by hand - ↑ 18.0 18.1 PMID 12656651 (PMID 12656651)
Citation will be completed automatically in a few minutes. Jump the queue or expand by hand