**2. Diagnosis and causes**

#### **2.1. Definition**

CS is an end-organ hypoperfusion associated with heart failure. In terms of the hemodynamic parameters used in the definition of CS, it is characterized by a systolic blood pressure of 80–90mmHg, a cardiac index below 1.8L min−1 m−2 without support and below 2.0–2.2L min−1 m−2 with support, a mean arterial baseline under 30 mmHg, and a pulmonary capillary wedge pressure of 15 or >18 mmHg [9].

#### **2.2. Diagnosis**

However, it is not necessary to measure these parameters in order to make the diagnosis of CS. Hypotension is not observed at the start in one-fourth of the patients diagnosed with CSMI. In this case, the diagnosis is made according to the clinical findings of organ hypoperfusion including extremity coldness, oliguria, and changes in mental condition such as agitation. It is imperative to distinguish MI-related complications, from primarily mechanical complications. The main complications are ventricular septal defect, free wall, and papillary muscle rupture developing after MI. Usually, if it is the first MI event and there is no anterior involvement, it should be considered that mechanical complications may have occurred. First of all, diagnosing CSMI should begin by quickly obtaining a 12-lead ECG (STEMI) and examining the clinical findings with respect to CS. In rare instances, the diagnosis of NSTEMI can be made based on the clinical criteria and troponin levels. Performing a rapid echocardiography (ECHO) before PCI may discount these complications, and, at the same time, the detection of any pre-angiographic valve disease may alter the revascularization approach. Bleeding, infection, and/or intestinal ischemia may also cause shock in cases of MI. In these situations, patient survivability depends on being skeptical and makes a rapid diagnosis along with correct intervention.

#### **2.3. Causes**

to survive [2]. CS occurs in approximately 5–8% of inpatients with ST-elevation myocardial infarctions (STEMI) and has a mortality rate of more than 30% [1]. CS is caused by end-organ hypoperfusion due to impaired cardiac pump function. Although CS-related mortality has declined significantly over the past decade, it continues to remain high, especially in cases of its coexistence with ischemic heart disease. Acute coronary syndrome (ACS) is still the most common cause of CS despite significant advances that have been made in its diagnosis and treatment. The most successful form of treatment is primary percutaneous coronary intervention (pPCI), which is carried out as rapidly as possible [3]. The recent research has suggested that the peripheral vasculature and neurohormonal and cytokine systems also play a role in

In cases where CS complicates MI (CSMI), only one in two patients survives after 1 year [4, 5]. In a large study including 5782 patients, CSMI had developed in 2.5% of the patients with STEMI before admission to hospital, in 4.3% of them on the first day of hospitalization, and in 2.3% of them afterward [6]. For non-STEMI (NSTEMI) patients, these ratios were 1.2% for each condition [6]. Mortality rates were 45.7% before the hospitalization, 32.8% in the early period, and 54.1% in the late period [7]. Of 1422 CSMI patients, in the SHOCK Trial Registry, a shock is developed following left ventricular failure in 78.5% of them, acute mitral insufficiency in 6.9% of them, acute ventricular septal defect in 3.9% of them, right ventricular failure in 2.8% of them, cardiac tamponade in 1.4% of them, and other reasons in 6.7% of them [8].

CS is an end-organ hypoperfusion associated with heart failure. In terms of the hemodynamic parameters used in the definition of CS, it is characterized by a systolic blood pressure of 80–90mmHg, a cardiac index below 1.8L min−1 m−2 without support and below 2.0–2.2L min−1 m−2 with support, a mean arterial baseline under 30 mmHg, and a pulmonary capillary wedge

However, it is not necessary to measure these parameters in order to make the diagnosis of CS. Hypotension is not observed at the start in one-fourth of the patients diagnosed with CSMI. In this case, the diagnosis is made according to the clinical findings of organ hypoperfusion including extremity coldness, oliguria, and changes in mental condition such as agitation. It is imperative to distinguish MI-related complications, from primarily mechanical complications. The main complications are ventricular septal defect, free wall, and papillary muscle rupture developing after MI. Usually, if it is the first MI event and there is no anterior involvement, it should be considered that mechanical complications may have occurred. First of all, diagnosing CSMI should begin by quickly obtaining a 12-lead ECG (STEMI) and examining the clinical findings with respect to CS. In rare instances, the diagnosis of NSTEMI can be made based on the clinical criteria and troponin levels. Performing a rapid echocardiography (ECHO) before PCI may discount these complications, and, at the same time, the

the pathogenesis and persistence of CS.

12 Advances in Extra-corporeal Perfusion Therapies

**2. Diagnosis and causes**

pressure of 15 or >18 mmHg [9].

**2.1. Definition**

**2.2. Diagnosis**

Anything that impairs acute left ventricular (LV) or right ventricular (RV) function may cause CS. In cases of acute myopericarditis, tako-tsubo, and hypertrophic cardiomyopathy, shock may present with ST elevation in which cardiac markers are released without coronary artery disease. Stress-induced cardiomyopathy, also known as apical ballooning or tako-tsubo cardiomyopathy, is a syndrome of acute LV dysfunction after emotional or respiratory distress leading to CS in 4.2% of cases [10]. Chordal rupture caused by degenerative diseases and trauma and acute valvular insufficiency caused by endocarditis may also cause CS. Severe aortic insufficiency (regurgitation) or coronary involvement developing as a result of aortic dissection may cause CS. Stress occurring in cases of severe aortic or mitral stenosis can cause shock. Cardiac tamponade and massive pulmonary embolism may cause shock without pulmonary congestion.

#### **2.4. Risk identification**

The only way to avoid CS is to provide early reperfusion in MI patients. In a randomized trial, CS occurred less frequently compared to PCI in STEMI patients treated with thrombolytic therapy within the first 2 hours of symptom onset before hospitalization (1.3 vs. 5.3%, p = 0.032) [11]. Low blood pressure and accelerated heart rhythm in patients admitted to hospital suggest shock. Advanced age, anterior MI, hypertension, diabetes mellitus, multivessel coronary artery disease, previous MI or angina, or being diagnosed with heart failure, STEMI, and left bundle branch block are risk factors for the development of CS [12].
