Cardiogenic Shock


cardiogenic shockCardiogenic shock is a syndrome caused by a severe insufficiency of the heart pump manifested by the inability to provide the necessary oxygen and tissue nutrients and to remove metabolic activity product of metabolism. The main condition that leads to cardiogenic shock is the acute myocardial infarction in which necrosis is over 40% of the muscle mass of the left ventricle.

In AMI, shock usually appears at 6-8 hours after the onset, but it is possible to install and after 1-2 days by extending the myocardial necrosis or by the AMI complications such as ventricular aneurysm, ventricular septal rupture (rupture of the wall that separates the two ventricles) and ventricular wall rupture. Other causes of cardiogenic shock are: diseases of the heart valves, especially aortic and mitral, intra-atrial thrombosis (formation of the clots with fairly large volume inside the atria), myocarditis, and dilated hypertrophic cardiomyopathy, arrhythmias with large increases in ventricular rate.

Myocardial area affected of necrosis becomes akinetic (no more participating in heart contractions, becomes inert) and part of the myocardium that surrounds the necrosis is dyskinetic (contractions are weak). To produce cardiogenic shock, necrosis should contain 40-70% of left ventricular mass. Ventricular systolic function is reduced due to the emergence of these myocardial akinetic and dyskinetic areas and the amount of blood pumped during each systoles in the arterial system is greatly reduced; decreases, thereby, the flow-beat and by extension the cardiac output. In infarcted myocardial region over time, it is reproduced scarring with a more reduced surface area than originally allocated to the coronary artery infarction.

The scar shows a diastolic dysfunction, not dilating properly during diastole, increasing the left ventricle filling pressure. Increasing the filling pressure of the left ventricle, the blood from the left atrium flows into the left ventricle with difficulty during diastole, causing a stagnation of blood in the pulmonary veins with increasing hydrostatic pressure in these veins. When the hydrostatic pressure in the pulmonary veins exceeds a certain value appears the pulmonary edema with great seriousness.

In the early stages, the body tries to compensate deficits installed through following mechanisms:

  • It produces vasoconstriction in the abdominal organs territory, muscular and cutaneous, blood flow is redistributed to the heart and brain (vital organs). This redirection of blood is needed because it is known that the cardiac output is low and the minimum amount of blood ejected by the left ventricle during systole must provide the oxygen and energy substances in the first place the vital organs (brain, heart).

  • Increases the blood levels of catecholamine’s (adrenaline) mainly downloaded from the adrenal glands, which result in increased heart rate (sinus tachycardia) with regular rhythm and arterial vasoconstriction to prevent hypotension by reducing cardiac output.

  • Unaffected areas of the left ventricle contract more strongly, leading in time to their hypertrophy.

  • Increased muscle mass of these healthy areas of the left ventricle. This compensatory hyper-contractility is a direct result of the occurrence of myocardial akinetic and dyskinetic areas we discussed above. Myocardial hypertrophy the secondary compensatory hyper-contractility has a positive effect, to maintain the cardiac output to acceptable parameters, and a negative effect by increasing the local demands for oxygen and energy substrate (glucose). These increased demands on reduced demands caused by the existence of a low cardiac output. This produces a vicious circle.

When the clearing mechanisms are insufficient, the shock becomes decompensated, emphasizing the hypotension and myocardial ischemia with the possible expansion of the zone of myocardial necrosis, the extremities become cold and cyanotic, irrigation of blood to the brain decreases sharply with installing a characteristic symptoms of: confusion, disorientation, agitation, coma, decreased urine output less than 20ml/h through decreased renal perfusion, and driving rhythm disorders occur the secondary ischemic myocardial ischemia and intestinal digestive disorders, increases blood viscosity and platelet aggregation. Excess lactic acid builds up, leading to metabolic acidosis (low blood pH). It is important to note that paraclinical and laboratory data indicate disturbances preceding cardiogenic shock.

Increased levels of serum enzymes CK, CK-MB, LDH, and SGOT suggest setting up an acute myocardial infarction. Due to the sub-renal blood perfusion increases serum levels of urea, creatinine and uric acid, and urine output is <20ml/h (oliguria).

Acidosis (low blood pH) can have double cause. Whether, due to pulmonary blood stasis, increases the blood pressure in the pulmonary capillaries above 18mmHg thus resulting the transfer of capillary pulmonary interstitium and alveoli, severely disrupting the O2-CO2 exchange between the lungs and the outside environment. The body tries to compensate by increasing dyspnea and respiratory amplitude (polypnea, tachypnea) but after a while respiratory muscles become tired and such compensatory mechanisms become ineffective. This will lead to an increase in the partial pressure of CO2 in arterial blood, a decrease in the partial pressure of O2 and a decrease in blood oxygen saturation, respiratory acidosis parameter which indicates installation.

A second cause of acidosis is represented by cellular metabolic activity, especially muscular, in terms of contribution the tissue of oxygen decreased, due to lower cardiac output in cardiogenic shock. Glucose required in metabolized energy performance in anaerobiosis conditions, resulting in a high amount of lactic acid in advanced stages, it cannot be neutralized by the body’s own buffer systems. It installs thereby metabolic acidosis. Cardiac index falls below 2.2 l/min/m2, the venous pressure is increased, and the blood pressure falls below normal. Mortality among patients with secondary cardiogenic shock myocardial infarction depends on many factors, but we can say that is between 80-85%.

Therapeutic measures are divided into cardiogenic shock in preventive measures and therapeutic measures addressed to the specific setting of myocardial infarction in a time interval as small as its production, and curative measures, correction of hypovolemia (low blood volume circulating) if it exists, through administration of 10% glucose up to normalization of the parameters, the administration of furosemide and dobutamine in the case of intravenous infusion in acute pulmonary edema, the administration of oxygen 4-6 l/min per tube or mask, correction of acidosis and hypokalemia through management of the sodium bicarbonate iv, normalization of cardiac output and pressure in the left ventricle at the end of diastole through operational administration of dopamine, dobutamine, norepinephrine.


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