**3. Etiology and pathophysiology**

Acute coronary syndrome (ACS) leading to ischemia and left ventricular (or right ventricular) failure is the leading cause of CS and represents around 80% of CS cases (8% of those are caused by mechanical complications of AMI such as ventricular septal rupture, free wall rupture, papillary muscle rupture and acute mitral regurgitations) [7].

The pathophysiology of ischemia leading to CS is illustrated as a vicious cycle in **Figure 1**. AMI may lead to severe left ventricular (LV) dysfunction and pump failure. The hypotension that accompanies CS leads to the release of inflammatory cytokines and catecholamines leading to increased contractility, which in turn leads to increased myocardial oxygen demand that

To differentiate CS from other types of shock, the following general hemodynamic measures can be used with the help of echocardiography or pulmonary artery catheterization (**Table 1**).

**Hypovolemic Obstructive**

Usually unchanged

**PE Tamponade**

**Cardiogenic Distributive (e.g.** 

or unchanged

resistance; CI, cardiac index; CO, cardiac output.

**septic shock)**

Unchanged or

But might be

CS is the second most common type of circulatory shock representing 16% of patients presenting with shock [3]. CS complicates up to 8.6% of patients with ST segment elevation myocardial infarction (STEMI) and about 2.5% of patients with non-ST segment elevation myocardial infarction (NSTEMI), and remains one of the leading causes of death in patients presenting with acute myocardial infarction (AMI) [4]. Despite the advancement in the medical and technological management, CS carries a poor prognosis with high morbidity

PCWP, pulmonary capillary wedge pressure, LVEDP, left ventricular end diastolic pressure; SVR, systematic vascular

**Table 1.** General hemodynamic measures to differentiate between cardiogenic shock and other types of shock.

AMI is the most common cause of CS, and patients with AMI older than 75 years tend to pres-

Acute coronary syndrome (ACS) leading to ischemia and left ventricular (or right ventricular) failure is the leading cause of CS and represents around 80% of CS cases (8% of those are caused by mechanical complications of AMI such as ventricular septal rupture, free wall

The pathophysiology of ischemia leading to CS is illustrated as a vicious cycle in **Figure 1**. AMI may lead to severe left ventricular (LV) dysfunction and pump failure. The hypotension that accompanies CS leads to the release of inflammatory cytokines and catecholamines leading to increased contractility, which in turn leads to increased myocardial oxygen demand that

and mortality (40–60% of patients with CS will die within 6 months) [5–7].

ent more frequently with CS than patients younger than 75 [2–4, 8].

rupture, papillary muscle rupture and acute mitral regurgitations) [7].

**3. Etiology and pathophysiology**

**2. Epidemiology**

PCWP/LVEDP

142 Interventional Cardiology

SVR

CI/CO

**Figure 1.** The vicious cycle of cardiogenic shock. SV, stroke volume; CO, cardiac output; LVEDP, left ventricular end diastolic pressure; MCS, mechanical circulatory support.

causes worsening of the ischemia and shock state. The increase in catecholamines also causes peripheral vasoconstriction that in turn leads to an increase in the afterload, worsening the ischemia and the shock state [2].

CS also occurs in the absence of coronary artery disease; those etiologies represent around 20% of CS cases. The non-ACS-related CS patients tend to do slightly better than those with ACS [7]. Those conditions may include hypertrophic cardiomyopathy, end stage heart failure, acute fulminant myocarditis, severe valvular stenosis, and acute valvular regurgitation secondary to trauma or infection. CS complicates about 10% of patients presenting with Takotsubo cardiomyopathy and carries a poorer prognosis than the rest of Takotsubo cardiomyopathy population [1, 9, 10].

CS could also occur secondary to right ventricular (RV) dysfunction and failure secondary to RV ischemia, acute pulmonary embolism, pulmonary hypertension (PH) and others [2, 11, 12].

The right ventricle is affected in nearly 50% of inferior STEMI patients, however, RV infarction leading to CS occurs in approximately 5% of CS cases caused by AMI; despite that, it carries high mortality similar to that of LV failure. RV failure leads to decreased transpulmonary delivery of LV preload and intraventricular dependence, which in turn may lead to decreased LV filling. The RV end diastolic pressure in CS secondary to RV failure is usually very high, exceeding 20 mmHg [2, 11–13].

**Figure 2** summarizes the most common causes of CS.

**Figure 2.** The most common causes of cardiogenic shock. (A) ACS represents 80% of CS cases, (B) non-ACS etiologies, which represent 20% of CS causes. ACS, acute coronary syndrome; LV, left ventricle; RV, right ventricle; HCM, hypertrophic cardiomyopathy; ADHF, acute decompensated heart failure; CMP, cardiomyopathy; PE, pulmonary embolism; PAH, pulmonary arterial hypertension.
