Emergent Care / Stabilization:
Cardiogenic shock (CS) is an end-organ hypoperfusion disease.

For the patient presenting with CS, consider performing a rapid chart review scanning for risk factors. Look for signs of hypoperfusion during the physical examination. Obtain an ECG and use point-of-care ultrasound (POCUS) to rapidly identify the etiology.

Resuscitation begins with managing airway, breathing, and circulation (ABC). Be prepared to intubate or apply noninvasive positive-pressure ventilation (NIPPV) versus high-flow nasal cannula (HFNC) in the appropriate setting. Apply continuous cardiac monitoring, obtain intravenous (IV) line access, and administer judicious IV fluids (often isotonic crystalloids), inotropes, and vasopressors to restore tissue perfusion. An arterial line may be required to obtain an accurate blood pressure.

Investigate the cause of the CS to guide management and disposition. Prompt cardiology consultation is recommended because definitive care is often percutaneous coronary intervention (PCI). If the patient is not a candidate for PCI, a shock team should be activated to help determine the grade of CS per the Society for Cardiovascular Angiography and Intervention (SCAI) and to facilitate discussion on individualized hemodynamic support.

Diagnosis Overview:
Cardiogenic shock is sustained multiorgan hypoperfusion stemming from low cardiac output despite the presence of adequate circulating volume.

Classic criteria used to establish the diagnosis include:

1. Consistent hypotensive state (≥ 30 minutes) with systolic blood pressure of < 90 mm Hg or requirement of vasoactive drugs.
2. Normal or elevated cardiac filling pressures (left ventricular end-diastolic pressure > 18 mm Hg and/or right ventricular end-diastolic pressure > 10-15 mm Hg).
3. Severely reduced cardiac output (< 1.8 L/min/m² and < 2.2 L/min/m² without and with support, respectively).
4. Markers of severe organ dysfunction including lactate > 2.0 mmol/L, and urine output < 30 mL/hour.

However, cardiogenic shock is more often a clinical diagnosis based on rapid clinical evaluation of the patient. The SCAI has published a 5-tier shock stage that has been endorsed by the American College of Cardiology (ACC), American College of Emergency Physicians (ACEP), and American Heart Association (AHA).

• Stage A is a patient at risk of CS but not currently experiencing signs or symptoms of CS.
• Stage B is a patient who has hemodynamic instability without hypoperfusion.
• Stage C is classic CS. The patient has hypoperfusion and requires 1 intervention (pharmacological or mechanical) beyond volume resuscitation.
• Stage D is a patient who is failing to respond to the initial support strategy to restore perfusion.
• Stage E is actual or impending circulatory collapse.

Symptoms and signs of cardiogenic shock include lightheadedness, altered mental status, cool extremities or clammy skin, dyspnea, rales, elevated jugular pressure (JVP), and narrow pulse pressure. The most prominent physical examination findings include low blood pressure that remains uncorrected with volume replacement and tachycardia. Frequently, the patient will present with pulmonary edema and low blood pressure. However, if the patient has chronic heart failure, some of these symptoms may be absent due to the body adapting to the chronic nature of the pathology.

Etiologies for cardiogenic shock include cardiomyopathy (primarily due to acute myocardial ischemia (AMI) / infarction or dilated cardiomyopathy), arrhythmia (including tachyarrhythmias such as sustained ventricular tachycardia and severe bradyarrhythmias such as complete heart block), and mechanical causes (eg, severe aortic or mitral valve disease, severe ventricular septal defects, and left ventricular free wall rupture). Typically, severe depression of myocardial contractility leads to decreased cardiac output and low blood pressure and worsens coronary ischemia. The pathophysiology leading to shock includes the compensatory increase in systemic vascular resistance to compensate for inadequate stroke volume and hypotension, which further exacerbates the issue. Systemic inflammation has also been theorized to play a role by release of interleukins (ILs), tumor necrosis factors (TNFs), and nitric oxide.

The timeline in which a patient can develop CS can be acute or subacute. In AMI, the median time for the development of CS is 6 hours from emergency department (ED) arrival.

Risk factors:

• Previous myocardial ischemia with:
  • Sinus tachycardia or bradycardia
  • Systolic blood pressure < 120 mm Hg
  • A long duration of symptoms before treatment
• Congestive heart failure
• Diabetes (Type 1, Type 2)
• Advanced age
• Female sex
• Exposure: Immune checkpoint inhibitor toxicity

Treatment includes establishing adequate circulation with inotropes (eg, dopamine or dobutamine), vasopressors (eg, norepinephrine), and/or mechanical support (eg, intra-aortic balloon pump or left ventricular assist device) as well as treatment of the underlying cause (eg, revascularization for ischemia, pacemaker placement for severe bradycardia, or surgical intervention for severe valvular disease, ventricular septal defect, or free wall rupture). Extracorporeal membrane oxygenation (ECMO) is a consideration for the decompensated cardiogenic shock patient. Venoarterial ECMO is used in this situation.