**Applications**

Canadian Association of Interventional Cardiology-Association Canadienne de Cardiologie

**2**(1):22


d'intervention. Journal of the American College of Cardiology. 2015;**65**(19):e7-26

futile. International Journal of Academic Medicine. 2016;

Journal of Medicine. 2018;**378**(21):1965-1975

8 Advances in Extra-corporeal Perfusion Therapies

and Lung Transplantation. 2012;**31**(1):9-15

controversies. BMC Anesthesiology. 2014;**14**:65

[15] Hill S, Hejal R, Bowling SM, Firstenberg MS. Neurologic complications in patients receiving extracorporeal membrane oxygenation for influenza H1N1: Morbid but not

[16] Combes A, Hajage D, Capellier G, Demoule A, Lavoué S, Guervilly C, et al. Extracorporeal membrane oxygenation for severe acute respiratory distress syndrome. New England

[17] Schmid C, Philipp A, Hilker M, Rupprecht L, Arlt M, Keyser A, et al. Venovenous extra

[18] Tulman DB, Stawicki SPA, Whitson BA, Gupta SC, Tripathi RS, Firstenberg MS, et al. Veno-venous ECMO: A synopsis of nine key potential challenges, considerations, and

corporeal membrane oxygenation for acute lung failure in adults. The Journal of Heart

**Chapter 2**

**Provisional chapter**

**Cardiogenic Shock**

**Cardiogenic Shock**

Additional information is available at the end of the chapter

Additional information is available at the end of the chapter

DOI: 10.5772/intechopen.76688

Cardiogenic shock (CS) is an end-organ hypoperfusion associated with heart failure. Any reason impairing acute left ventricular (LV) or right ventricular (RV) function may cause CS. The only way to avoid CS is to provide early reperfusion in myocardial infarction (MI) patients. CS is characterized by permanent or transient rearrangement of the entire circulatory system. According to the current IABP-SHOCK II trial, 74% of the patients with CSMI are treated with norepinephrine, 53% of them with dobutamine, 26% of them with epinephrine, 4% of them with levosimendan, and 4% of them with dopamine. Percutaneous circulatory support devices such as intra-aortic balloon pump (IABP), LV assist device (LVAD), or extracorporeal life support (ECLS) create treatment options for selected patients such as CS, cardiopulmonary resuscitation, or high-risk pPCI and CABG. Extracorporeal Life Support Organization (ELSO, 2017) evaluated that the use of ECLS/VA-ECMO should be considered when the mortality risk exceeds 50% despite optimal conventional treatment in case of acute severe heart or pulmonary failure, whereas it should be assessed as a primary indication when it exceeds 80%. Early and effective revascularization is the best treatment option for CS. Thus, the organizations on the national and global basis will play the most effective role for the short- and long-term

**Keywords:** cardiogenic shock, multiple organ failure, inotropes, left ventricular assist

Cardiogenic shock (CS) is one of the most important issues dealt by cardiologists today and still needs solutions. Prevention, accurate diagnosis, urgent intervention, effective support for heart failure, and multi-organ failure (MOF) are what this endeavor involves [1]. More than 90% of patients arriving at the hospital with acute myocardial infarction (MI) are likely

> © 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

© 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use,

distribution, and reproduction in any medium, provided the original work is properly cited.

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

Fevzi Sarper Türker

Fevzi Sarper Türker

**Abstract**

survival of patients.

devices

**1. Introduction**

**Chapter 2 Provisional chapter**

#### **Cardiogenic Shock Cardiogenic Shock**

Fevzi Sarper Türker Fevzi Sarper Türker

Additional information is available at the end of the chapter Additional information is available at the end of the chapter

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

**Abstract**

Cardiogenic shock (CS) is an end-organ hypoperfusion associated with heart failure. Any reason impairing acute left ventricular (LV) or right ventricular (RV) function may cause CS. The only way to avoid CS is to provide early reperfusion in myocardial infarction (MI) patients. CS is characterized by permanent or transient rearrangement of the entire circulatory system. According to the current IABP-SHOCK II trial, 74% of the patients with CSMI are treated with norepinephrine, 53% of them with dobutamine, 26% of them with epinephrine, 4% of them with levosimendan, and 4% of them with dopamine. Percutaneous circulatory support devices such as intra-aortic balloon pump (IABP), LV assist device (LVAD), or extracorporeal life support (ECLS) create treatment options for selected patients such as CS, cardiopulmonary resuscitation, or high-risk pPCI and CABG. Extracorporeal Life Support Organization (ELSO, 2017) evaluated that the use of ECLS/VA-ECMO should be considered when the mortality risk exceeds 50% despite optimal conventional treatment in case of acute severe heart or pulmonary failure, whereas it should be assessed as a primary indication when it exceeds 80%. Early and effective revascularization is the best treatment option for CS. Thus, the organizations on the national and global basis will play the most effective role for the short- and long-term survival of patients.

DOI: 10.5772/intechopen.76688

**Keywords:** cardiogenic shock, multiple organ failure, inotropes, left ventricular assist devices

### **1. Introduction**

Cardiogenic shock (CS) is one of the most important issues dealt by cardiologists today and still needs solutions. Prevention, accurate diagnosis, urgent intervention, effective support for heart failure, and multi-organ failure (MOF) are what this endeavor involves [1]. More than 90% of patients arriving at the hospital with acute myocardial infarction (MI) are likely

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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 the pathogenesis and persistence of CS.

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

Cardiogenic Shock

13

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

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 pul-

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,

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

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

and left bundle branch block are risk factors for the development of CS [12].

explains that all or some of these changes are completely reversible.

along with correct intervention.

**2.3. Causes**

monary congestion.

**2.4. Risk identification**

**3. Physiopathology**

**3.1. Left ventricle**

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].
