COVID-19 is caused by infection with the SARS-CoV-2. The principal target cells for the virus to infect are the epithelial cells of the respiratory tract, but viral RNA has also been found in other tissues, such as the cardiac tissue. Most patients with this condition remain asymptomatic, some can present with mild respiratory symptom, and few can have more severe presentations such as cardiogenic shock. Cardiovascular manifestations of COVID-19 are variable, and they may include arrhythmias, heart failure, and myocarditis. Data regarding the etiology, epidemiology, and management approach of cardiogenic shock in COVID-19 are limited at this time. To date, one of the most common described causes of cardiogenic shock in COVID-19 patients is acute coronary syndrome. About 50% of the patients that present to the hospital with ST-segment elevation myocardial infarction (STEMI), and test positive for SARS-CoV-2, develop cardiogenic shock, increasing mortality significantly in these patients. In the group of patients with STEMI, positive SARS-CoV-2 test, and cardiogenic shock, 75% die. However, it is important to note that during the peak of the pandemic, a 40% decrease in acute myocardial infarctions and delays in presentation to the hospitals have been reported. This fact may alter significantly the incidence of cardiogenic shock in patients positive for SARS-CoV-2. Because of delayed presentations, the incidence of acute myocardial infarctions with severe hemodynamic alterations have increased. In an Italian study analyzing data from intensive care units, the rate of myocardial infarction with complications, such as cardiogenic shock, increased during the first week after the initial lockdown. Data may vary from country to country. Numbers may vary now as patients start to come back to the hospitals in a timely manner. It is possible that the increased rate of cardiogenic shock related to myocardial infarction during the peak of the pandemic could be related to prolonged ischemia and progressive myocardial dysfunction due to delayed presentation.
Multiple causes can explain why patients with COVID-19 develop cardiogenic shock. The ones that have been more frequently described in the literature are acute fulminant myocarditis, stress-mediated cardiomyopathy, coronary artery thrombosis, and pulmonary thromboembolism. All of these may occur even in the absence of comorbid conditions. Because there are many possible etiologies of cardiogenic shock in COVID-19 patients, a thorough history, physical exam, and proper assessment of the lab data are needed to properly address the underlying condition.
COVID-19 can induce a systemic hypercoagulable state that may present as cardiogenic shock due to coronary thrombosis or pulmonary thromboembolism. The increased thromboembolic risk may also explain the risk of developing myocardial infarction, although the complete mechanism is not fully understood. Patients aged more than 65, with diabetes, hypertension, and/or dyslipidemia, are at increased risk.
Stress-related cardiomyopathy in patients infected with SARS-CoV-2 is likely related to adrenergic surge secondary to the inflammatory process, sepsis, hypoxemia, or myocardial infection with the virus of concern. A combination of factors is the most likely mechanism. Other mechanisms that may explain myocardial injury in patients with COVID-19 include elevated right ventricular afterload due to respiratory acidosis, and oxygen supply/demand mismatch.
In general, any inciting event that evolves into cardiogenic shock is characterized by profound depression of the cardiac contractility, which causes reduced cardiac output, leading to decreased blood pressure, which causes further coronary ischemia with concomitant further reduction in the myocardial contractility. Endothelial dysfunction could lead to increased risk of myocardial infarction and heart failure due to thrombosis, coagulopathy, and low nitric oxide levels. Release of tumor necrosis factors and various interleukins may account for the decreased adrenergic sensitivity and decreased contractility of the cardiac muscle, leading to death if not treated appropriately.
There is no separate approach described for patients with cardiogenic shock and COVID-19. The same standard protocols used for any patient with cardiogenic shock are used. Initial protocol should include an ECG, chest radiography, laboratory tests (complete blood counts, complete metabolic panel, creatine kinase, troponin, pro-BNP, lactic acid, blood gas, and blood cultures). ECG can vary from sinus tachycardia, bigeminy, atrial arrhythmias, or significant ST-T changes. Performing early transthoracic echocardiography is crucial in all COVID patients with hypotension/cardiogenic shock to assess for left and right ventricle function, wall motion abnormalities, valvular abnormalities, and pericardial effusion. Coronary angiography and right-sided heart catheterizations may be appropriate based on clinical presentation. (1-3) If there is clinical suspicion for myocarditis, an endomyocardial biopsy can also be considered (Figure 9-1).
Diagnostic algorithm in cardiogenic shock.
Therapeutics and Complications
Overall, the basic approach of management includes general routine measures, such as inotropes/vasopressors and mechanical ventilation, for cardiovascular and pulmonary support; systemic corticosteroids; and anticoagulation in certain cases. Corticosteroids are particularly useful in patients with myocarditis as they can reduce the infiltration of WBCs into the cardiac tissue, decreasing cardiac symptoms. In cases of acute coronary thrombosis, management should be directed toward percutaneous revascularization. An early invasive approach is usually recommended, but fibrinolysis can be considered in cases where percutaneous coronary intervention cannot be performed in a timely manner. In cases of pulmonary thromboembolism, management may also include thrombolysis or percutaneous management (in case thrombolysis is contraindicated). Patients who have an increasing pressor requirement or clinical deterioration should be evaluated for temporary mechanical circulatory support including venoarterial-extracorporeal membrane oxygenation (VA-ECMO) and percutaneous ventricular assist device. It is also key to manage the viral infection accordingly to provide comprehensive management.
In patients with the ‘’wet and cold’’ presentation, the vasoactive agent of choice is norepinephrine; an inotropic agent can be added, but this should be assessed on a case-by-case basis. In patients with the ‘’cold and dry-euvolemic’’ presentation, dopamine and norepinephrine can also be used, along with an inotropic agent (case-by-case consideration). (4-5) The hemodynamic effects of the most commonly used inotropes and inodilators are presented in Table 9-2.
TABLE 9-2Hemodynamic Effects of the Most Common Inotropes and Inodilators Used in Cardiogenic Shock ||Download (.pdf) TABLE 9-2 Hemodynamic Effects of the Most Common Inotropes and Inodilators Used in Cardiogenic Shock
|Medication ||Hemodynamic Effects |
|Dopamine ||Increases cardiac output |
|Norepinephrine ||Increases systemic vascular resistance and cardiac output |
|Phenylephrine ||Increases systemic vascular resistance |
|Vasopressin ||Increases systemic vascular resistance |
|Epinephrine ||Increases systemic vascular resistance and cardiac output |
|Dobutamine ||Increases cardiac output, decreases systemic vascular resistance |
|Milrinone ||Increases cardiac output, decreases systemic vascular resistance |
|Isoproterenol ||Increases cardiac output, decreases systemic vascular resistance |
Cases when myocardial infarction is complicated with cardiogenic shock in the setting of COVID-19, the patient’s recovery becomes more challenging. Therefore, constant monitoring and a proper surveillance strategy of the hemodynamics and lab data are important (Figure 9-2).
Hemodynamic monitor using an arterial line (LIDCO).
Constant monitoring of blood pressure, heart rate, respiratory rate, pulse oximetry, and temperature is the cornerstone in patients with cardiogenic shock. These patients should be managed in a critical care setting. Continuous monitoring of the arterial blood pressure and central venous pressure is also needed. A Swan-Ganz catheter for hemodynamic monitoring should be considered in cases complicated by cardiogenic shock. Periodical monitoring of the lactic acid and mixed venous oxygen saturation levels are appropriate to assess how effective the interventions have been in the patient under concern. Urine output should be monitored at least every 2 hours. If urine output is decreased, it is likely because of renal hypoperfusion, which is related to increased mortality. Furthermore, complete blood counts, electrolyte levels, markers of the liver and renal function tests, and lactate and coagulation studies should be done at least every 12 hours. Particularly, lactic acid levels have been described as important markers with prognostic value.
Prognosis and Long-Term Follow-Up
Patients that undergo percutaneous coronary intervention, without bleeding complications and no increased bleeding risk, should be continued on dual antiplatelet therapy. The medical team should be watchful for bleeding complications in these cases. The palliative care team should be on-board in patients with poor prognoses to have a complete interdisciplinary team taking care of the patients and supporting family members. Future directions in the management of COVID-19–related cardiogenic shock are geared not only toward management approaches but also toward monitoring and prognostic values that will provide a better understanding of this challenging condition (Figure 9-3).
Sequential management of cardiogenic shock.