Approximately 5% to 10% of patients with COVID-19 infection require intensive care unit (ICU) admission and, of those, up to 67% develop shock.1 Distributive, cardiogenic, obstructive, and hypovolemic shock have all been observed in patients infected with COVID-19.1 Shock can be characterized by systemic hypotension (systolic BP <90 mm Hg or mean arterial pressure <65 mm Hg), organ hypoperfusion, and abnormal cellular oxygen metabolism.1
Cardiogenic shock in patients with COVID-19 can be caused by severe right or left ventricular failure.1 Left ventricular failure can be secondary to myocarditis, ST-elevation myocardial infarction, or worsening underlying cardiovascular disease.1 Right ventricular failure may occur secondary to pulmonary embolism or acute cor pulmonale from hypoxia, hypercapnia, and/or high mean airway pressures.1 In addition to medical management of the underlying COVID-19 infection, prompt recognition and management of cardiogenic shock and underlying pathophysiology is critical to reducing the risk for death and promoting optimal outcomes.
Table 2. Recommended Diagnostic/Laboratory Tests1,2,3
|CBC, comprehensive metabolic panel, troponin, brain natriuretic peptide, and lactate level|
Baseline complete blood cell count (CBC) and comprehensive metabolic panel should be obtained initially and subsequently every 12 to 24 hours to monitor electrolyte status and end-organ function.2 Troponin levels will be elevated in the presence of myocardial injury. Myocardial injury can occur secondary to coronary occlusion, supply-demand mismatch, and myocarditis.2,4 Brain-type natriuretic peptide will be elevated in the presence of acute decompensated heart failure.2 Lactate levels will be elevated with tissue hypoperfusion and anerobic metabolism.2
The 12-lead ECG may show evidence of ST-segment elevation or ST-segment depression.2 ST-segment elevation in 2 or more contiguous leads is diagnostic for ST-segment elevation myocardial infarction (STEMI). Patients with myocarditis may have nonspecific ST-segment and T-wave abnormalities.5
Coronary angiography is diagnostic for underlying coronary disease and can identify precise lesions precipitating coronary injury and shock.2 If culprit lesions are identified, a reperfusion strategy can be initiated. Data regarding intracardiac pressures, valvular function, and structural impairments can also be identified with angiography.
Transthoracic echocardiogram will provide information regarding left and right ventricular function, chamber size, presence of pericardial effusions, valvular function, outflow obstructions, and wall motion abnormalities.1
Management and Treatment
Fluid resuscitation in cardiogenic shock is only indicated in the presence of preload insufficiency.2 Evaluation of volume status and preload responsiveness should be conducted prior to administration of fluid boluses.2 Conservative boluses of crystalloids (250-500 mL) can be considered if the patient is determined to be volume contracted and/or preload responsive.2
Oxygenation and Ventilation
Respiratory support is aimed at maintaining adequate oxygenation and ventilation. Oxygen should be titrated to keep blood oxygen saturation levels above 90%.2 Invasive mechanical ventilation is indicated when noninvasive methods of oxygenation are inadequate.2 When mechanically ventilating patients with cardiogenic shock, lung protective strategies (tidal volumes 5-7 mL/kg of ideal body weight) should be employed.2 Monitoring of oxygenation and ventilation status can be accomplished with peripheral oxygen saturation, end-tidal CO2 monitors, and arterial blood gasses.
Vasopressor and Inotropic Support
Vasopressor support is indicated for patients who have persistent hypotension (mean arterial pressure <65 mm Hg) in the absence of volume contraction.2 Vasopressive agents should be titrated with the goal of achieving a mean arterial pressure of >65 mm Hg. Norepinephrine is generally considered as the first-line agent and is associated with fewer dysrhythmias than other vasoactive agents.1-3 Vasopressin may be a better option in patients with right ventricular failure as it causes less pulmonary vasoconstriction.2 Other inotropic agents such as dobutamine or epinephrine may be considered in patients with continued evidence of hypoperfusion.1
Renal Replacement Therapy
Acute kidney injury occurs in approximately 13% to 28% of patients experiencing cardiogenic shock.3 Of those, approximately 20% will require renal replacement therapy.3 Initiation of renal replacement therapy should be considered for patients who have stage 2 kidney injury (elevated serum creatinine ≥2x baseline and urine output <0.5 mL/kg per hour for ≥12 hours), life-threatening changes in fluid/electrolyte balance, and/or acid-base balance.3 Continuous renal replacement therapy is better tolerated than intermittent hemodialysis in patients with cardiogenic shock.3 Patients with hemodynamic instability do not tolerate the hemodynamic shifts that occur with intermittent hemodialysis.2,3
Mechanical Circulatory Support Devices
Mechanical circulatory support (MCS) devices2,6 are alternative or adjunctive options to consider for patients with cardiogenic shock. Inotropic therapy can be associated with arrhythmia, increased myocardial oxygen demand, and decreased peripheral perfusion and microcirculation, which can further compromise end-organ perfusion.2 Mechanical circulatory support can offer substantial cardiovascular support and can be a bridge to interventional strategies and/or improved cardiac contractile function. Early implementation of MCS, prior to the initiation of inotropes, has been associated with improved survival rates.2,6 Options for MCS devices include intra-aortic balloon pump therapy, Impella® axial flow pumps, TandemHeart® left atrial-to-femoral arterial ventricular assist devices, and venous-arterial extracorporeal membrane oxygenation (ECMO).2
Hemodynamic and laboratory monitoring can help guide therapy and evaluate response to therapy. Continuous intra-arterial pressure monitoring is indicated with hemodynamic instability and high prevalence of vasopressor use.3 Pulmonary artery catheters can provide valuable information about volume status, vascular resistance, cardiac output, and oxygen supply/demand balance.2,3 Other surrogates to monitor end-organ perfusion include lactate levels, urine output, creatinine levels, liver function test, and mental status.2,3
In cases of cardiogenic shock caused by acute coronary occlusion resulting in STEMI, emergent coronary reperfusion is indicated.3 Strategies for coronary reperfusion include percutaneous intervention (PCI), thrombolytic therapy, and coronary artery bypass grafting (CABG).3 Early invasive strategy with PCI is the preferred method of reperfusion for all suitable patients when services are available.3 If PCI cannot be completed in a timely fashion, thrombolytic therapy can be considered. Risks, benefits, and anticipated time delay to angiography should be considered when making determinations about the appropriateness of thrombolytic therapy. In cases of triple-vessel or left-main disease, CABG revascularization may be appropriate.
Anti-inflammatory therapy can be considered when myocarditis is the underlying pathophysiology causing cardiogenic shock. Management guidelines for COVID-19 myocarditis are still evolving.7 Because hyper-inflammation and cytokine release are likely responsible for the myocardial injury leading to myocarditis, anti-inflammatory therapy can be considered. Data supporting the use of anti-inflammatory therapy with COVID-19 myocarditis is limited, but some case reports have shown favorable outcomes with steroid therapy.7 First-line therapy for hemodynamically stable myocarditis/pericarditis includes aspirin or nonsteroidal anti-inflammatory drugs (NSAIDS) plus colchicine.8 Low-dose corticosteroids are second-line therapy. Until more empirical data is available, the decision to use anti-inflammatory therapy in cases of COVID-19 myocarditis with cardiogenic shock should be made on an individualized case-by-case basis.
Prompt recognition and treatment are imperative for optimal outcomes. Correcting the hypoperfusion and treating the underlying condition(s) are a priority when patients initially present with cardiogenic shock. Once stabilized, a more in-depth diagnostic evaluation will help guide medical management in the longer term. Patients with COVID-19 myocarditis may need supportive care and time for inflammatory processes to resolve. Follow-up care for patients with underlying coronary artery disease will require chronic care management of underlying disease processes and any complications, such as heart failure, which may arise.
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.
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.
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. To read the fifth article on heart failure in patients with COVID-19, click here.
- Fox S, Vashisht R, Siuba M, Dugar S. Evaluation and management of shock in patients with COVID-19. Cleve Clin J Med. 2020;10.3949/ccjm.87a.ccc052. doi:10.3949/ccjm.87a.ccc052
- Vahdatpour C, Collins D, Goldberg S. Cardiogenic shock. J Am Heart Assoc. 2019;8(8):e011991. doi:10.1161/JAHA.119.011991
- van Diepen S, Katz JN, Albert NM, et al. Contemporary Management of Cardiogenic Shock: A Scientific Statement from the American Heart Association. Circulation. 2017;136(16):e232-e268. doi:10.1161/CIR.0000000000000525
- Janardhanan R. Myocarditis with very high troponins: risk stratification by cardiac magnetic resonance. J Thorac Dis. 2016;8(10): E1333-E1336. doi:10.21037/jtd.2016.10.60
- Sharif N, Dehghani P. Emergency files: acute pericarditis, myocarditis, and worse! Can Fam Physician. 2013;59(1):39-41.
- Basir MB, Schreiber TL, Grines CL, et al. Effect of early initiation of mechanical circulatory support on survival in cardiogenic shock. Am J Cardiol. 2017; 119:845-851. doi:10.1016/j.amjcard.2016.11.037
- Sawalha K, Abozenah M, Kadado AJ, et al. Systematic review of COVID-19 related myocarditis: insights on management and outcome. Cardiovasc Revasc Med. 2021;23:107-113. doi:10.1016/j.carrev.2020.08.028
- Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. Eur Heart J. 2015;36(42):2921-2964. doi:10.1093/eurheartj/ehv31