This is the fifth installment of our 8-part series on cardiovascular complications in patients with COVID-19. In this installment, we will discuss heart failure in patients with COVID-19.
A 60-year-old woman presents to the emergency department with complaints of shortness of breath that started in the early morning hours and progressively worsened throughout the day. Additional presenting symptoms include chest tightness, cough for 1 week, and hearing a “crackling” and “fluid” when laying down.
The patient tested positive for COVID-19. The initial troponin level is within normal limits. N terminal pro–brain natriuretic peptide (NT-proBNP) is elevated at 1254 pg/mL and D-dimer is critical at 0.85 µg/mL. Glucose is slightly elevated at 127 mg/dL and creatinine is 1.1 mg/dL respectively. All other laboratory results are normal.
An electrocardiogram (ECG) demonstrates sinus tachycardia at a rate of 118 beats per minute with a new left bundle branch block when compared with previous ECGs. Chest radiograph reveals early pulmonary edema. Computed tomography angiography (CTA) with and without contrast shows no evidence of pulmonary embolus but acute bilateral pulmonary edema is present. Transthoracic echocardiogram reveals a left ventricular ejection fraction (LVEF) of 20% to 25% and a mildly dilated left ventricle and atrium. Previous transthoracic echocardiogram performed 6 months prior to this admission revealed an EF of 50% to 55% and a normal left ventricle and atrium.
Significant Medical History
The patient’s medical history includes chronic heart failure with preserved ejection fraction (HFpEF), viral cardiomyopathy, hypothyroidism controlled with medication, tachycardia, mixed anxiety, and depressive disorder, and obesity. She is currently taking diltiazem daily for hypertension.
The patient is obese with a BMI of 35. She appears anxious and is in mild respiratory distress. She has labored breathing. Her oxygen saturation is 91% on room air but she is able to maintain an oxygen saturation of 100% on 2 L/min supplemental oxygen via nasal cannula. Regular rhythm with an elevated heart rate at 118 beats per minute is noted upon cardiac auscultation. Bilateral crackles are noted in lung bases anterior and posterior.
Diagnosis and Treatment
The patient is diagnosed with acute decompensated heart failure (HF) with pulmonary edema and COVID-19 infection. She is treated with intravenous furosemide for diuresis. Diltiazem is discontinued per cardiology and the patient is started on metoprolol extended release, lisinopril, and hydralazine/isosorbide dinitrate secondary to left ventricular systolic dysfunction. Enoxaparin is started at 40 mg subcutaneous daily for venous thromboembolism (VTE) prophylaxis.
The patient demonstrates symptom improvement 3 days after admission at which point she is transitioned from intravenous furosemide to oral furosemide and discharged with metoprolol extended release 12.5 mg daily, lisinopril 10 mg daily, and hydralazine/isosorbide dinitrate 37.5 mg/20 mg daily with close cardiology follow-up.
Patients with chronic HF are at increased risk of decompensated HF requiring hospitalization when infected with SARS-CoV-2. One study found a 42.9% prevalence of pre-existing HF in critically ill patients with COVID-19.1 Further, COVID-19 increases a patient’s risk for developing new-onset HF by 23% to 33%.2 The mechanism by which COVID-19 causes new-onset or worsening HF is not completely understood; however, current theories include a direct effect of the viral particles on the myocardium or indirect causes such as hypoxia, cytokine release, volume overload, renal failure, stress, or overwhelming critical illness.3
Recommended Diagnostic/Laboratory Tests4
|Lung computed tomography|
|White blood cell count, brain natriuretic peptides, troponin, creatine kinase, transaminase, bilirubin, myoglobin, creatinine, lactate dehydrogenase, D-dimer|
Interstitial thickening and alveolar edema in lung bases are consistent with HF.4 With COVID-19 pneumonia, diffuse interstitial and alveolar edema may be noted without preferential distribution to the lung bases, or chest radiography may be normal.4
Lung Computed Tomography
In HF, lung computed tomography (CT) typically shows congestion predominantly in the central and basal lung, cardiac enlargement, and basal pleural effusions that are larger at the right lung bases.4 In COVID-19 disease, lung CT typically shows bilateral, diffuse ground-glass opacities, reticular patterns, air bronchograms, bilateral consolidation areas, and lobular interstitial thickening.4
Electrocardiogram in HF and COVID-19 may reveal sinus tachycardia and arrhythmia. As many as 75% of COVID-19 patients will have an abnormal ECG regardless of HF status.4
Transthoracic echocardiography should be considered in all patients with HF and suspected or confirmed COVID-19 to assess the extent of myocardial injury and to detect any other causes of worsening HF.4 Transthoracic echocardiography should also be considered in patients with no pre-existing cardiac disease who are exhibiting signs of left ventricular systolic dysfunction such as dyspnea, tachycardia, and edema.4
White blood cell count is typically normal in patients with HF alone but may be normal or decreased with a decreased lymphocyte count in patients with COVID-19.4 Increased mortality is associated with decreased lymphocytes; thus, lymphocyte count should be monitored daily.4
Brain natriuretic peptides (BNP) may be elevated in patients with HF and COVID-19. Elevated BNP in patients with COVID-19 and no history of HF suggest impairment of cardiac function but is not diagnostic of new-onset HF.3,4
Troponin may be increased in HF; however, an increased troponin level in the presence of COVID-19 is associated with an increased risk of major complications and poor prognosis.3,4
A large majority of critically ill patients with COVID-19 will demonstrate elevated lactate dehydrogenase and D-dimer levels consistent with increased inflammation and thrombogenicity. As with troponin, increased levels of these markers are associated with higher mortality rates.4 Other inflammatory markers that may be used include C-reactive protein, erythrocyte sedimentation rate, ferritin, interleukin-6, and fibrinogen.4
Biomarkers of end-organ damage should be measured upon admission and as indicated by a worsening clinical course. These include transaminase and bilirubin for the liver, serum creatinine for the kidneys, and myoglobin and creatine kinase for skeletal muscle.4
Hospital admission is typically recommended for all patients with HF (acute and chronic) and concomitant COVID-19 because of the increased risk for pulmonary complications.2,4 Medications for HF should be continued or initiated as per current American College of Cardiology guideline-directed medical therapy (GDMT).5
Fluid status should be assessed on all patients to determine the need for pharmacologic therapy. If the patient is exhibiting decompensated HF, treatment should include diuretics, vasodilators, and inotropes as indicated.4
Patients with decompensated HF and stable HF who have COVID-19 should be treated symptomatically and careful consideration should be given for treatment with antiviral drugs as many antivirals can negatively interact with medications prescribed for HF.4 The antiviral medications favipiravir and remdesivir do not appear to interact with medications currently used for GDMT in HF.4 Favipiravir is not commercially available in the US but suggested dosing is 600 mg three times daily for no more than 14 days.4 Remdesivir dosing is 200 mg intravenously on the first day, then 100 mg intravenously once daily for up to 10 days. Patients receiving remdesivir should be monitored closely for QT prolongation.3,4
Some patients with tachycardia should be treated with a beta-blocker for heart rate control. While there is no evidence to guide beta-blocker selection, findings from experimental studies suggest that carvedilol may have an increased benefit as it has demonstrated anticytokine properties.4
Oxygen therapy should be considered in patients with an oxygen saturation of less than 93% on room air with a target of 95% or greater. Patients who do not respond to standard oxygen therapy can be titrated up using an air-entrainment mask (Venturi mask), OxyMask, or mask with reservoir bag.4 If the patient does not improve within 1 to 2 hours, endotracheal intubation and mechanical ventilation should occur with a low tidal volume setting (6-8 mL/kg of ideal body weight) and low-level platform pressure (<30 cmH2O) to prevent lung injury.4
Heart failure and COVID-19 are both associated with an increased risk for thromboembolic events. Anticoagulation should be considered in hospitalized patients with COVID-19 for VTE prophylaxis.3 To date no anticoagulant agent has proven superior to the other (heparin, low-molecular-weight heparin, warfarin, or direct oral anticoagulants) for VTE prophylaxis.3,4
Ideally, admission should occur for all patients who have concomitant HF and COVID-19; however, in the case of hospital bed shortages, it may be appropriate to closely monitor stable patients at home using available telemedicine tools.4 Once a patient is discharged from the hospital, they should be advised to follow up with cardiology or the provider managing their HF and continue HF medications per GDMT.5
Christy L. McDonald Lenahan, DNP, FNP-BC, ENP-C, CNE, is an advanced practice registered nurse in family and emergency medicine who works for an emergency medicine and hospitalist staffing agency. She is also an associate professor at the University of Louisiana at Lafayette and teaches in the masters and doctoral programs.
Frances Stueben, DNP, RN, CHSE, is an assistant professor and simulation program coordinator at the University of Louisiana at Lafayette. She teaches in the graduate and undergraduate nursing programs.
Deedra Harrington, DNP, MSN, APRN, ACNP-BC, is associate professor at the College of Nurse and Allied Health Professions, University of Louisiana at Lafayette. Dr Harrington is an advanced practice registered nurse-acute care who works with an inpatient cardiology intensivist group in Louisiana.
To read the first article in this series, on management of NSTEMI/STEMI in patients with COVID-19, click here. To read the second article on venous thromboembolism management in patients with COVID-19, click here. To read the third article on atrial fibrillation and other dysrhythmias in patients with COVID-19, click here. To read the fourth article on acute pericarditis, myopericarditis, and perimyocarditis in patients with COVID-19, click here.
1. Arentz M, Yim E, Klaff L, Lokhandwala S, Riedo FX, Chong M, Lee M. Characteristics and outcomes of 21 critically ill patients with COVID-19 in Washington state. JAMA. 2020;323(16):1612-1614. doi:10.1001/jama.2020.4326
2. Ranard LS, Fried JA, Abdalla M, et al. Approach to acute cardiovascular complications in COVID-19 infection. Circ Heart Fail. 2020;13(7):e007220. doi:10.1161/CIRCHEARTFAILURE.120.007220
3. Basu-Ray I, Almaddah Nk, Adeboye A, et al. Cardiac manifestations of coronavirus (COVID-19). In: StatPearls [Internet]. StatPearls Publishing; 2021 Jan-. Accessed September 8, 2021. https://www.ncbi.nlm.nih.gov/books/NBK556152/
4. Zhang Y, Coats AJS, Zheng Z, et al. Management of heart failure patients with COVID-19: a joint position paper of the Chinese Heart Failure Association & National Heart Failure Committee and the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2020;22(6):941-956. doi:10.1002/ejhf.1915
5. Maddox TM, Lanuzzi JL, Allen LA, et al. 2021 Update to the 2017 ACC Expert Consensus Decision Pathway for Optimization of Heart Failure Treatment: answers to 10 pivotal issues about heart failure with reduced ejection fraction: a report of the American College of Cardiology Solution Set Oversight Committee. JACC. 2021;77(6):772-810.