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Professional Reference articles are designed for health professionals to use. You may find one of our health articles more useful. Cardiogenic shock occurs when there is failure of the pump action of the heart, resulting in a decrease in cardiac output causing reduced end-organ perfusion. Cardiogenic shock can be defined as the presence of the following despite adequate left ventricular filling pressure :.

Cardiogenic shock most commonly occurs as a complication of acute myocardial infarction MI. Cardiogenic shock is most often caused by acute MI, particularly affecting the anterior wall of the heart. Shock is due to an inability to perfuse vital organs and tissues adequately.

Cardiogenic Shock - Developments and Treatment Strategies

The skin, brain, heart and kidneys are usually most severely affected by this. The symptoms and signs can present abruptly or develop insidiously over the course of many hours. See separate Acute Myocardial Infarction Management article. Did you find this information useful? We'd love to send you our articles and latest news by email, giving you the best opportunity to stay up to date with expert written health and lifestyle content.

By clicking 'Subscribe' you agree to our Terms and conditions and Privacy policy. Thanks for your feedback. Percutaneous coronary intervention: cardiogenic shock. Szymanski FM, Filipiak KJ ; Cardiogenic shock - diagnostic and therapeutic options in the light of new scientific data. Anaesthesiol Intensive Ther. Casella G, Savonitto S, Chiarella F, et al ; Clinical characteristics and outcome of diabetic patients with acute myocardial infarction.

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Crit Care Med. J Am Coll Cardiol. Epub Feb Unverzagt S, Wachsmuth L, Hirsch K, et al ; Inotropic agents and vasodilator strategies for acute myocardial infarction complicated by cardiogenic shock or low cardiac output syndrome. Cochrane Database Syst Rev.

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. 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.

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 ]. 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. 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.

Cardiogenic Shock Diagnosis | Temple Health

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 significantly increases the quality of life as well as survival rates [ 14 , 15 ]. 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.

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Correcting coronary occlusion through surgery or PCI will break the vicious cycle and increase survival. 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 RV may cause or contribute to CS. 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. 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.

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. 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. SVR was lower in these patients, and low SVR preceded the clinical diagnosis of infection and culture positivity by days [ 23 ]. 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 ].

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. Excessive volume loading in patients with RV infarction may also cause or contribute to shock.

Cardiogenic Shock: Diagnosis and Tests

For MI, giving aspirin and heparin routinely along with antithrombotic treatment is recommended. Since emergency coronary artery bypass grafting CABG therapy can be required depending on the results of coronary angiography, clopidogrel therapy may be delayed to the period after emergency angiography.

There are indications of clopidogrel in all patients who are to undergo PCI, and this will be useful in MI patients with shock depending on the information obtained from non-shock MI patients. The use of vasodilators including negative inotropes and nitroglycerin should be avoided. The arterial oxygen and pH levels should be kept within normal limits in order to minimize the ischemia. Intensive insulin therapy improves survival in critically ill patients with hyperglycemia and is a recommended course of action in complicated MI [ 27 ]. An easy indication should be established in order to initiate mechanical ventilation with mask or endotracheal intubation.

Positive end-expiratory pressure reduces preload and afterload. Mechanical ventilation also reduces respiratory workload. There has been a decline in the use of PA catheters following the controversy caused by a prospective observational study suggesting that PA catheters are associated with poor outcome [ 28 ].

The use of PA catheters in severely hypotensive patients with MI can be performed according to patient [ 27 ]. At present, many clinics do not prefer PA catheter for CS treatment anymore. According to the German-Austrian CSMI guideline, dobutamine should be preferred as an inotrope option, norepinephrine as a vasopressor option, and levosimendan over phosphodiesterase III inhibitors in case of refractiveness to catecholamines [ 29 ].