Cardiogenic shock is a state of end-organ hypoperfusion due to cardiac failure. It is a type of circulatory shock resulting from severe impairment of ventricular pump function characterized by a systolic blood pressure <80 mm Hg without inotropic or vasopressor support (or <90 mm Hg with inotropic or vasopressor support) for at least 30 minutes; low cardiac output of <2 L/min/m² (not related to hypovolemia, dysrhythmia, hypoxemia, acidosis or atrioventricular block); and tissue hypoperfusion manifested by oliguria (<30 mL/hr), peripheral vasoconstriction or altered mental status.¹ Cardiogenic shock carries a high mortality rate; the good news is that recent U.S. observational data suggest that the in-hospital mortality from cardiogenic shock has improved from 49 percent to 37 percent over the past 15 years.² It is my hope that by reading this article, your understanding of cardiogenic shock, emergency department recognition, and management will help contribute to further improvements in survival.

Assessment

Assessment of end-organ perfusion, volume status, and cardiac contractility is essential in the early recognition and management of cardiogenic shock. Cardiogenic shock occurs when the reduced contractility of the ventricle impairs mean arterial pressures and cardiac output, which results in decreased end-organ perfusion. One of the reasons cardiogenic shock is challenging to recognize in the emergency department is that only about 25 percent of patients who develop cardiogenic shock are not in an obvious shock state when they initially present to the emergency department.³ Many patients will present in occult shock or pre-cardiogenic shock. Identifying this and initiating treatment are key to preventing full-blown cardiogenic shock and death. Patients with heart failure may have a lower baseline systolic blood pressure due to heart failure medications, which can make the diagnosis of cardiogenic shock difficult. Assessment for impaired end-organ perfusion in these patients can aid in the identification of occult cardiogenic shock. At the bedside, this involves assessment of the skin (mottling, cool temperature to palpation, prolonged capillary refill), mental status, and urine output. Of note, most patients with cardiogenic shock will have cool extremities compared to most adult patients with septic shock, who will have warm extremities from vasodilatory shock.⁴ An elevated lactate is suggestive of poor end-organ perfusion although the specificity is poor.⁵ A rough estimation of cardiac contractility can be gleaned from a quick point-of-care ultrasound assessment (≥1/3 the diameter of the left ventricle [LV] between systole and diastole is normal) as part of a global LV function assessment.⁷

A subset of patients with pre-cardiogenic shock are those with sympathetic crashing acute pulmonary edema (SCAPE), an extreme state of rapidly progressive acute pulmonary edema in which a sympathetic surge results from decreased systemic perfusion.⁶ This leads to further increases in afterload resulting in cardiovascular collapse if left untreated.

Not all patients with cardiogenic shock are volume overloaded. They may be hypovolemic, euvolemic, or hypervolemic. Determining volume status will guide whether they require diuresis or volume replacement. Volume status ultrasound assessment includes measuring LV size, jugular venous distention, and inferior vena cava size and collapsibility (diminished respiratory variation).⁷ A careful fluid bolus/infusion may be required if a patient is in cardiogenic shock and deemed to be intravascularly volume depleted.

Emergency Department Management

The goals of emergency department management of cardiogenic shock should be thought of in the context of the ultimate goal of definitive mechanical treatment or temporary mechanical circulatory support. Determining the cause of cardiogenic shock is essential to optimize management.

A simple way to think of the underlying cause of cardiogenic shock is to think of four categories:

1. Cardiac ischemia (most common cause)⁸
2. Mechanical causes (such as severe aortic stenosis, endocarditis, valve rupture, free wall rupture)
3. Acute myocarditis
4. Progressive nonischemic end-stage chronic heart failure

Patients in whom you identify cardiac ischemia as the primary cause of cardiogenic shock require emergency cardiac catheterization. Those with a mechanical cause may require emergency cardiac surgery in the operating room. Those with severe acute myocarditis may benefit from temporary mechanical circulatory support, such as an Impella machine, and those with progressive nonischemic end-stage chronic heart failure may benefit from temporary mechanical circulatory support or palliation.⁹

The patient in cardiogenic shock from severe aortic stenosis deserves special attention, as any decrease in afterload, by administering nitroglycerin or ACE inhibitors for example, may be catastrophic. Particular attention should be paid to the heart rate when starting and titrating inotropes so as to avoid tachycardia. Diastolic blood pressure should be targeted slightly higher than normal to help ensure adequate forward flow. The aortic stenosis causes the left ventricle to chronically generate high pressures to overcome the high afterload. This leads to LV hypertrophy requiring higher coronary perfusion pressures. Careful maintenance of a slightly elevated diastolic blood pressure (ideally guided by an arterial line) is important to ensure adequate coronary perfusion. On the other hand, if the diastolic blood pressure is very high, there is some evidence to suggest that nitroprusside may be beneficial.¹⁰

The aim of emergency department management of the patient in whom you have identified cardiogenic shock should be to stabilize them to provide safe transport to the cardiac catheterization lab (if the underlying cause is cardiac ischemia), operating room (if the underlying cause is a mechanical surgical cardiac lesion) or ICU for temporary mechanical circulatory support if necessary. It is advisable to involve your interventional cardiologist, cardiovascular surgeon and/or intensivist early to plan for any definitive mechanical intervention that may be required.

Mechanical circulatory support methods include intra-aortic balloon pump, percutaneous ventricular assist devices (Impella, Tandem Heart) and veno-arterial extracorporeal membrane oxygenation. Patients with poor LV function (<25 percent) and severe hemodynamic compromise refractory to medical therapies should be considered for one of these interventions as a bridge to definitive surgical therapy or bridge to recovery. Unfortunately, there are no robust randomized control trials showing a significant mortality benefit for any of these temporary mechanical circulatory support interventions in patients with cardiogenic shock.^11–13

Here, I outline four simple emergency department stabilization strategies:

Optimize oxygenation with carefully titrated noninvasive positive-pressure ventilation (NIPPV) and avoid endotracheal intubation if possible (as sudden removal of respiratory drive may lead to cardiovascular collapse). NIPPV reduces work of breathing and decreases intrathoracic muscle use, thereby reducing oxygen consumption. It has the additional benefit of decreasing preload and afterload, thus improving forward flow and end-organ perfusion. One common pitfall is overshooting positive-pressure ventilation in the patient with right ventricular failure, which increases right ventricular afterload and decreases cardiac output.¹⁴

Maintain sufficient cardiac, kidney, and brain perfusion with vasopressors. The first-line medication is norepinephrine, and the second-line medication is vasopressin to target a mean arterial pressure of 65–80.¹⁵

Improve cardiac contractility with inotropes such as dobutamine or milrinone. Both of these agents are inotropes and vasodilators. A recent randomized control trial showed no significant difference in in-hospital survival and major cardiac outcomes with dobutamine versus milrinone in patients in cardiogenic shock.¹⁶ The decision to use one drug or the other should be based on several factors. If the clinical situation is such that the drug would need to be turned off quickly, dobutamine is a shorter-acting drug and would be preferred.¹⁷ If the patient has recently taken a Beta-blocker, milrinone is preferred, as dobutamine is a Beta-1 and -2 agonist. If the underlying cause is acute cardiac ischemia, dobutamine may be a better choice, as milrinone may worsen cardiac ischemia.18 The starting dose of dobutamine is 2–5 mcg/kg/min followed by a maintenance infusion at 2–10 mcg/kg/min. The starting dose of milrinone is 0.125–0.25 mcg/kg/min followed by a maintenance infusion of 0.125–0.75 mcg/kg/min.^16,18

Optimize volume status as needed with crystalloid or diuretics.

Next time you are faced with a patient who presents to the emergency department in cardiogenic shock, take into consideration the following: a careful bedside clinical assessment including point-of-care ultrasound; early involvement of consultants; identification of the underlying cause; and stabilization via careful titration of NIPPV, vasopressors, and inotropes so that a patient is safe to be transported for definitive care. Taking these steps will maximize your patient’s chances of survival of this challenging condition that carries a high mortality rate.

Special thanks to Dr. Bourke Tillman and Dr. Tarlan Hedayati for their expert contributions to the EM Cases podcast that inspired this article.

References

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