**3. Physiopathology**

CS is characterized by permanent or transient rearrangement of the entire circulatory system. The primary cause of many CS instances is the failure of LV pump function, but other components of the circulatory system, inadequate compensation, or additional defects can also contribute to this condition. The fact that surviving patients demonstrate improved functionality explains that all or some of these changes are completely reversible.

#### **3.1. Left ventricle**

The degree of LV myocardial dysfunction usually initiates CS. In most cases, it is not severe. Left ventricular dysfunction reflects newly onset irreversible damage, reversible ischemia, and previous infarct-related injury in CS. Myocardial injury causes systolic and diastolic dysfunction. Low blood pressure helps by reducing afterload due to the unique position of the heart even though it causes damage at the same time by impairing the coronary blood flow. It can lead to an increase in ischemia and cell death at the border and remote zone of the infarct area. Reduction in coronary perfusion causes deterioration in perfusion of the heart and other vital organs by causing a decline in cardiac output (CO). Metabolic impairments occur inside and outside of the infarct region. Hypoperfusion leads to catecholamine discharge, resulting in an increase in contractility and peripheral blood flow, while, at the same time, increased contractility causes increased oxygen demand on the part of the myocardium, as well as arrhythmia and myocardial toxic effects [13]. Systemic inflammation may play a limiting role in peripheral vascular compensatory response or may only be considered as an epiphenomenon. Revascularization makes the ischemia disappear, but increased CO or LV ejection fraction (LVEF) could not be shown as a benefit of revascularization. Revascularization significantly increases the quality of life as well as survival rates [14, 15].

as that of shock secondary to LV dysfunction. The benefit of revascularization was similar in the SHOCK registry for patients with primarily RV dysfunction and those with primarily LV

Cardiogenic Shock

15

http://dx.doi.org/10.5772/intechopen.76688

Hypoperfusion of the extremities and vital organs is a sign of CS. MI-induced CO reduction and persistence of ischemia both result in the release of catecholamines leading to constriction of the peripheral arteries and, thus, affecting the maintenance of perfusion to the vital organs. Attempts to improve peripheral and coronary circulation at the expense of elevation in afterload by increasing the levels of vasopressin and angiotensin II at the beginning of MI and shock will subsequently lead to impairment in myocardial functions. The continuation of neurohormonal cascade activation will also increase acute pulmonary edema while attempting to improve perfusion by causing water and salt retention. The reflex increase of systemic vascular resistance (SVR) mechanism is not fully effective. The SHOCK trial showed that SVR was at mean levels during CS despite vasopressor treatment and that in some cases it was even as low as in a septic shock [23]. Sepsis was suspected in 18% of the cohort of the SHOCK trial, 74% of which developed positive bacterial cultures. SVR was lower in these patients, and low SVR preceded the clinical diagnosis of infection and culture positivity by days [23]. Findings and observations of MI may cause systemic inflammatory response syndrome (SIRS). Inappropriate vasodilation as part of SIRS results in impaired perfusion of the intestinal tract leading to the transmigration of bacteria and sepsis. As the duration of shock increases, so the

Sometimes, the medications given can contribute to the development of CS. Numerous medications such as beta-blockers, angiotensin-converting enzyme inhibitors, and morphine were associated with the development of shock. The early use of these treatments contributes in a small way to increase the risk of CS. However, given the large patient population receiving this treatment, the number of incidents it causes significant [25, 26]. The timing of CS (early after medication initiation) in the placebo-controlled, randomized trials of β-blockage and angiotensin-converting enzyme inhibition combined with their mechanisms of action indi-

Diuretics may also contribute to the development of post-MI shock [14]. The earliest effect of ischemia is usually a reduction in LV compliance. MI may cause pulmonary edema before a drop occurs in CO. The redistribution of intravascular volume to the lungs causes a clear decline in the volume of circulating plasma before heart failure. High-dose diuretics administered subsequently further reduce plasma volume. Low diuretic dose coupled with low-dose nitrates and positional measures to decrease preload (e.g., seated position with legs down) should be attempted in patients with MI and pulmonary edema to avoid precipitating shock. Excessive volume loading in patients with RV infarction may also cause or contribute to shock.

For MI, giving aspirin and heparin routinely along with antithrombotic treatment is recommended. Since emergency coronary artery bypass grafting (CABG) therapy can be required

cates that they may contribute to the development of CS in those at high risk.

dysfunction [20].

possibility of SIRS increases [24].

**4. Treatment**

**4.1. Supportive treatment**

Vasoconstrictors and inotropic agents are able to correct CO and peripheral circulation temporarily, but they do not break this vicious cycle. Although rapid intra-aortic balloon pump (IABP) application improves ischemia transiently and supports the circulation, it is not the final solution. Correcting coronary occlusion through surgery or PCI will break the vicious cycle and increase survival.

In the light of CS's complex pathophysiology, the cause of shock in many cases is a severe impairment in contractility and moderate disruption in the LVEF [16]. LVEF was found approximately 30% in the SHOCK trial [17]. In terms of LVEF value, the SHOCK trial obscures many post-MI studies in which LVEF decreases with or without heart failure. The LVEF in this study generally does not indicate that the magnitude of myocardial damage causes CS, although it is measured in patients with inotropic and/or IABP support. LVEF is the same in the acute phase of CS, and 2 weeks later, its functional status is different [18]. Even when there are conditions in which there is no serious mitral regurgitation and the LV is preserved, CS still develops in some patients [19]. LVEF is a prognostic indicator in patients who end up with shock. The size of the LV is small or normal in about half of patients with CS [19]. LV dilatation is an adaptive mechanism of failure in order to provide stroke volume in the early phase. LV dilatation in the chronic phase may be maladaptive. The LV end-diastolic volume was shown to increase slightly to 15 mL as a result of the serially performed echo within the first 2 weeks in the survivors of CS [18].

#### **3.2. Right ventricle**

The RV may cause or contribute to CS. Shock based on the dominance of the RV occurs in 5% of CSMI cases. RV insufficiency may limit CO, ventricular interdependence, or both of them by decreasing LV filling. The treatment of patients with RV dysfunction and shock focuses not on reducing CO and on maintaining adequate right heart filling pressure in order to provide adequate LV preload in the conventional sense. However, in these patients, there is usually a very high RV end-diastolic pressure above 20 mmHg due to RV dysfunction [20]. The increase in RV end-diastolic pressure shifts the interventricular septum to the left via mechanical pressure, thus impairing the functions by reducing the filling [21]. This means that aggressive fluid resuscitation in RV dysfunction is actually the incorrect method. Inotropic therapy should be initiated if it persists despite optimization of RV end-diastolic pressure in the CS secondary to the RV. Maintaining RV end-diastolic pressures between 10 and 15 mmHg provides the best CO [22]. Inhaled nitric oxide (NO) may be useful in reducing pulmonary vascular resistance and promoting forward flow. Shock secondary to RV dysfunction has a mortality rate as high as that of shock secondary to LV dysfunction. The benefit of revascularization was similar in the SHOCK registry for patients with primarily RV dysfunction and those with primarily LV dysfunction [20].

Hypoperfusion of the extremities and vital organs is a sign of CS. MI-induced CO reduction and persistence of ischemia both result in the release of catecholamines leading to constriction of the peripheral arteries and, thus, affecting the maintenance of perfusion to the vital organs. Attempts to improve peripheral and coronary circulation at the expense of elevation in afterload by increasing the levels of vasopressin and angiotensin II at the beginning of MI and shock will subsequently lead to impairment in myocardial functions. The continuation of neurohormonal cascade activation will also increase acute pulmonary edema while attempting to improve perfusion by causing water and salt retention. The reflex increase of systemic vascular resistance (SVR) mechanism is not fully effective. The SHOCK trial showed that SVR was at mean levels during CS despite vasopressor treatment and that in some cases it was even as low as in a septic shock [23]. Sepsis was suspected in 18% of the cohort of the SHOCK trial, 74% of which developed positive bacterial cultures. SVR was lower in these patients, and low SVR preceded the clinical diagnosis of infection and culture positivity by days [23].

Findings and observations of MI may cause systemic inflammatory response syndrome (SIRS). Inappropriate vasodilation as part of SIRS results in impaired perfusion of the intestinal tract leading to the transmigration of bacteria and sepsis. As the duration of shock increases, so the possibility of SIRS increases [24].

Sometimes, the medications given can contribute to the development of CS. Numerous medications such as beta-blockers, angiotensin-converting enzyme inhibitors, and morphine were associated with the development of shock. The early use of these treatments contributes in a small way to increase the risk of CS. However, given the large patient population receiving this treatment, the number of incidents it causes significant [25, 26]. The timing of CS (early after medication initiation) in the placebo-controlled, randomized trials of β-blockage and angiotensin-converting enzyme inhibition combined with their mechanisms of action indicates that they may contribute to the development of CS in those at high risk.

Diuretics may also contribute to the development of post-MI shock [14]. The earliest effect of ischemia is usually a reduction in LV compliance. MI may cause pulmonary edema before a drop occurs in CO. The redistribution of intravascular volume to the lungs causes a clear decline in the volume of circulating plasma before heart failure. High-dose diuretics administered subsequently further reduce plasma volume. Low diuretic dose coupled with low-dose nitrates and positional measures to decrease preload (e.g., seated position with legs down) should be attempted in patients with MI and pulmonary edema to avoid precipitating shock. Excessive volume loading in patients with RV infarction may also cause or contribute to shock.
