Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3793_Библиотеки_им_академика_М_И_Перельмана

Before the recent emphasis on time to treatment and primary PCI, the incidence of cardiogenic shock had remained unchanged for over 25 years, with approximately 8% of patients with ST elevation myocardial infarction (STEMI) with non-STEMI

baroreceptor activity due to hypotension increases sympathetic outflow and reduces vagal tone. This increases heart rate, myo­cardial contractility, venous tone, and arterial vasoconstriction. Vasoconstriction is most pronounced in the skeletal, splanchnic, and cutaneous vascular beds to redistribute cardiac output to the coronary, renal, and cerebral circulations. An increase in the ratio of precapillary to postcapillary resistance decreases capillary hydrostatic pressure, facilitating movement of interstitial fluid into the vascular compartment. Increased catecholamine levels and decreased renal perfusion lead to renin release and angiotensin production. Elevated angiotensin levels stimulate peripheral vasoconstriction and aldosterone synthesis. Aldosterone increases sodium and water retention by the kidney, raising blood volume. Release of antidiuretic hormone from the posterior pituitary by baroreceptor stimulation also increases water retention. Local autoregulatory mechanisms that decrease arteriolar resistance and increase regional blood flow are stimulated by hypoxia, acidosis, and accumulation of vasoactive metabolites (e.g., adenosine).

Troponin and creatine kinase levels are high, may peak late because of prolonged washout or ongoing necrosis, and can rise secondarily with infarct extension. Lactic acidosis, hypoxemia, and mixed venous oxygen desaturation are usually present.