Cardiogenic shock (CS) is a complex condition characterized by end-organ hypoperfusion due to a decline in cardiac output resulting from a primary cardiac disorder. Clinically, CS can present with a broad spectrum of hemodynamic phenotypes. However, the unifying characteristic is inadequate cardiac output requiring pharmacologic and/or mechanical circulatory support.

CS is a leading indication for admission to a contemporary cardiac intensive care unit (CICU). Investigators with the Critical Care Cardiology Trials Network characterized the demographics, diagnoses, and outcomes of more than 3,000 consecutive admissions to tertiary CICUs across the United States and Canada and found that the primary indications for CICU care were respiratory insufficiency (26.7) and shock (21.1).1 Intravenous vasoactive medications, invasive hemodynamic monitoring, and mechanical ventilation were required in 58.2 of patients, and those admitted with CS had a 30.6 mortality rate.1 The presence of acute noncardiovascular illnesses such as acute kidney injury or acute respiratory failure has been associated with increased inhospital mortality and longer length of stay in the CICU.2

Optimal management of CS in the CICU first requires careful investigation into its etiology. The most common causes of CS remain acute myocardial infarction followed by acute on chronic heart failure (Table 1). Diagnostic and management strategies for these specific etiologies of CS are reviewed elsewhere in this issue. Regardless of the etiology, CS is frequently complicated by multiorgan system dysfunction that requires a multidisciplinary approach to care in an intensive care setting. Initial goals of treatment are to achieve euvolemia and hemodynamic stabilization to optimize end-organ perfusion to avoid or minimize multiorgan system dysfunction. Prevention and management of multiorgan system dysfunction is paramount to achieve favorable outcomes in CS. In a retrospective cohort study over a 15-year period (20002014), Vallabhajosyula and colleagues found that 31.9 of admissions for CS due to acute myocardial infarction were complicated by multiorgan failure. The presence of multiorgan failure was associated with an odds ratio of 2.23 (95 CI, 2.192.27) for higher in-hospital mortality, greater resource utilization, and fewer discharges to home.3

Table 1.

Etiologies of cardiogenic shock.

Acute coronary syndrome
  • Mechanical complication of acute myocardial infarction
Acute or chronic heart failure
Acute heart failure
  • Myocarditis
  • Takotsubo
  • Peripartum
  • Thyroid disorder
Valvular disease
  • Native valve stenosis or regurgitation
  • Prosthetic valve malfunction
Uncontrolled arrhythmia
Cardiac tamponade
Myocardial contusion
Left ventricular outflow obstruction
Acute pulmonary embolism
  • Right ventricular failure


Hemodynamic instability and metabolic derangements are inherent in the pathophysiology of CS. Therefore, invasive monitoring of not only systemic arterial pressures but also measures of end-organ perfusion are important to properly identify the etiology of the shock state. The pulmonary artery (PA) catheter is a vital diagnostic tool widely available in a critical care setting that can aid in appropriate identification of the presence and type of CS as well as guide therapy.

The concept of cardiac catheterization was first introduced in 1929 when Werner Forssmann introduced a catheter into his own heart and proved that it was feasible. Since then, many iterations of catheters have been developed that can be introduced into the right side of the heart and measure pressure in pulmonary arteries.46 However, it was Drs. William Ganz and H.J.C. Swan who developed the floating balloon-tipped PA catheter in 1970 that could be inserted at the bedside without the use of fluoroscopy.7 Since its first iteration, the Swan-Ganz catheter has undergone further modifications including the placement of a thermistor coil for measurement of cardiac output by thermodilution, infusion ports for drug delivery, and pacing function for right ventricular pacing.

The routine use of Swan-Ganz catheters in clinical practice in acutely ill patients in an ICU has been controversial. Early after its introduction, the catheter was widely adopted and used especially in patients post myocardial infarction (MI) for hemodynamic monitoring. Although instrumental in understanding the hemodynamics in acute MI patients, their routine use came with its own set of adverse events. In 1987, Gore et al. reported in a retrospective observational study that PA catheters were associated with increased mortality and morbidity in patients with acute MI and hypotension and/or congestive cardiac failure.8 These results prompted further randomized clinical trials examining the utility of PA catheters. Several studies performed in high-risk surgical patients and those with acute lung injury showed that use of PA catheters in these populations was associated with increased mortality.911

The Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE) trial was conducted in hospitalized patients with decompensated chronic heart failure. This trial randomized patients to therapy guided by clinical assessment in conjunction with the PA catheter versus clinical assessment alone. ESCAPE showed no difference in mortality between the two groups. Moreover, use of the PA catheter in this trial was associated with more adverse events.12 However, ESCAPE has been criticized for its multiple potential confounders, including the possibility that appropriate use in CS patients in particular may have shown overall benefit.

A retrospective cohort study conducted by Hernandez and colleagues showed that although use of PA catheters has declined over the past decade, its use in patients admitted with CS was associated with lower mortality.13 Rossello et al. also reported lower short- and long-term mortality associated with using a PA catheter in patients with CS.14 Use of PA catheters also allows for continuous evaluation of the hemodynamic response to therapeutic manipulations to optimize filling pressures and cardiac output. However, their use does carry risks for procedural complications, infections, pulmonary infarction, pulmonary hemorrhage, and the potential for inaccurate data collection and interpretation.15 Therefore, invasive hemodynamic monitoring should be incorporated to complement clinical assessment and other available markers of tissue perfusion such as measures of arterial lactate, kidney and liver function, mental status, and urine output.


Initial pharmacologic management of CS should include a review of the medications and discontinuing those that may be contributing to hypotension and negative inotropy. For example, in patients on guideline-directed medical therapy (GDMT) for chronic heart failure, this may require discontinuation of all or part of their GDMT regimen. Discontinuation of GDMT in this population portends a worse prognosis. Compelling data from the OPTIMIZE-HF (Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure) registry show that beta blocker withdrawal in patients hospitalized for acutely decompensated heart failure is associated with worse mortality (HR: 2.3; 95 CI, 1.24.6, P .013).16 Tran and colleagues assessed over 5,000 patients admitted for acute decompensated heart failure and found that patients who had GDMT discontinued during the hospital admission had increased mortality (HR 1.30; 95 CI, 1.021.66).17 In patients with CS due to acute MI, early initiation of beta blockers and renin-angiotensin-aldosterone system inhibitors prior to complete resolution of CS was associated with an increased 30-day mortality.18


Inotropes increase the cardiac contractility and output in CS. Vasopressors increase vascular tone and therefore augment systemic vascular resistance to increase blood pressure. Commonly used vasopressors and inotropes are outlined in Table 2. Dobutamine and milrinone are the main inotropes used in a contemporary CICU, and both result in increased myocardial contractility albeit through different mechanisms. Norepinephrine, epinephrine, dopamine, and vasopressin are commonly used vasopressors in cases of CS with hypotension. Despite their widespread availability, a Cochrane meta-analysis of inotropes and vasopressor use in CS did not find conclusive evidence to recommend one particular agent over another.19 The American Heart Association (AHA) consensus scientific statement on the management of CS also notes that insufficient evidence exists to guide the selection of pharmacologic therapies.20 Therefore, use of inotropic and vasopressor agents should be guided by available hemodynamic data and clinician judgment.

Table 2.

Inotropic and vasopressor drugs commonly used in cardiogenic shock.

Dobutamine 1 agonist 2.520 mcg/kg/min
Milrinone Phosphodiesterase 3 inhibitor 0.1250.5 mcg/kg/min
Epinephrine Mixed , agonist 0.011 mcg/kg/min
Norepinephrine Mixed , agonist (> ) 0.011 mcg/kg/min
Vasopressin V1 receptor in vascular smooth muscle 0.020.04 units/min
Dopamine Dopamine at low dose; increasing and agonist at higher doses 0.520 mcg/kg/min



Adjunctive nonpharmacologic therapies have a role in the critical care management of CS. Acute heart failure and CS are often characterized by increased intracardiac filling pressures due to sodium and fluid retention by the kidneys resulting from neurohormonal activation. Diuretics are the mainstay of therapy to reduce congestion. However, impaired absorption, decreased renal blood flow, and proteinuria can lead to diuretic resistance. In turn, worsening congestion can lead to multiorgan dysfunction, including acute renal failure, which further propagates this vicious cycle.33 Acute right ventricular failure can also manifest with worsening congestion associated with right ventricular distention, increased ventricular interdependence, decreased left ventricular filling, and worsening of shock and end-organ failure.34 In such situations, ultrafiltration may be a viable option to decrease vascular congestion.

Ultrafiltration describes the process of solvent-free fluid transport across a semipermeable membrane driven by the pressure gradient across the membrane. Ultrafiltration can be used in isolation to achieve volume control or can be combined with diffusion, as is done with dialysis to achieve both solute and volume control.35 With the development of newer simplified devices, ultrafiltration can be achieved with minimal extracorporeal volume, thus minimizing hemodynamic instability.

In theory, ultrafiltration appears advantageous over pharmacologic diuresis because it does not lead to neurohumoral activation, significant hypokalemia, or hypomagnesemia, and the rate and amount of fluid removed can be precisely controlled. Several randomized trials were conducted to assess the benefit of ultrafiltration over diuretics. Although some of the trials showed greater reduction in heart failure symptoms and weight loss with ultrafiltration compared to diuretics,36,37 the results were not consistent across all the trials. A greater increase in serum creatinine was seen, reflecting possible renal tubular injury and other adverse effects, thereby questioning the benefit of ultrafiltration over diuretics.38,39 Unfortunately, these trials excluded patients on inotropic or vasoactive agents, effectively excluding patients in CS. Currently, there are no large randomized trial data to test the benefit of ultrafiltration in CS. In a retrospective study conducted by Li et al. among post-cardiac surgery patients in CS with acute kidney failure, continuous venovenous hemofiltration was associated with better in-hospital and long-term survival.40

Mechanical Ventilation

Mechanical ventilation may be required in cases of CS due to acute hypoxemia, increased work of breathing, decreased level of consciousness requiring airway protection, or overall hemodynamic instability. Despite the high prevalence of respiratory failure requiring mechanical ventilation, there is a paucity of data to support a particular mode of ventilation or physiologic targets for oxygenation or ventilation in CS. Clinicians must be mindful of the interactions between positive pressure ventilation on left and right ventricular hemodynamics as well as the optimal agents for analgesia and sedation in CS.


CS is a complex heterogeneous disorder of ineffective cardiac output associated with high mortality and often complicated by multiorgan system dysfunction. Rapid identification of the etiology of CS aided by invasive hemodynamic data are critical to optimal management. The lack of high-quality data in the field of CS demands coordination of care across multiple disciplines in order to improve patient outcomes. Management of CS remains a high research priority to address the multiple gaps in knowledge.


  • Cardiogenic shock (CS) is a complex heterogeneous disorder of inadequate end-organ perfusion caused by inadequate cardiac output and is associated with a high mortality rate.
  • CS is frequently complicated by multiorgan system dysfunction that requires a multidisciplinary approach using both pharmacologic and nonpharmacologic therapies.
  • Limited data exist to guide the selection of pharmacologic therapies for CS. Therefore, clinical judgment and appropriate application of hemodynamic data are critical to improve patient outcomes.