Cardiogenic shock

Cardiogenic shock is the leading cause of death for patients with myocardial infarction in the hospital.

In 50% of patients with cardiogenic shock develops within the first days of myocardial infarction, 10% - in the pre-hospital and 90% - in the hospital. In myocardial infarction with a Q wave (or myocardial infarction with ST elevation), the incidence of cardiogenic shock is approximately 7%, an average of 5 hours after the onset of symptoms of myocardial infarction.

In myocardial infarction without Q wave, cardiogenic shock develops in 2.5-2.9%, on average after 75 hours. Thrombolytic therapy reduces the incidence of cardiogenic shock. Mortality of patients with cardiogenic shock in the hospital is 58-73%, with revascularization, the mortality rate is 59%.

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What causes cardiogenic shock?

Cardiogenic shock is a consequence of necrosis of about 40% of the left ventricular myocardium and therefore is rarely compatible with life. The prognosis is somewhat better if the shock is caused by a rupture of the papillary muscle or interventricular septum (with timely surgical treatment), since the magnitude of necrosis in these cases is usually less. However, in the “narrow” sense, cardiogenic shock is considered shock due to left ventricular dysfunction (“true” cardiogenic shock). Most often, cardiogenic shock develops during anterior myocardial infarction.

In recent years, data have been obtained that many patients with cardiogenic shock have a necrosis rate of less than 40%, many have no increase in total peripheral vascular resistance and no signs of stagnation in the lungs. It is believed that in these cases ischemia and systemic inflammatory reactions play a major role. There is reason to believe that the early administration of nitrates, beta-blockers, morphine and ACE inhibitors in patients with myocardial infarction plays a significant role in the development of cardiogenic shock. These drugs can increase the likelihood of cardiogenic shock due to the "vicious circle": a decrease in blood pressure - a decrease in coronary blood flow - an even greater decrease in blood pressure, etc.

There are three main forms of shock in myocardial infarction.

Reflex cardiogenic shock develops as a result of an insufficient compensatory increase in vascular resistance in response to a stressful situation caused by the entry of nociceptive impulses into the central nervous system and a disturbance in the physiological balance between the tone of the sympathetic, parasympathetic divisions of the autonomic nervous system.

As a rule, it is manifested by the development of collapse or severe arterial hypotension in patients with myocardial infact against the background of uncropped pain syndrome. Therefore, it is more correct to regard it as a collaptoid state, which is accompanied by bright clinical symptoms in the form of pallor of the skin, excessive sweating, low blood pressure, increased heart rate and a small filling of the pulse.

Reflex cardiogenic shock is usually short-lived, quickly relieved by adequate pain relief. Sustained recovery of central hemodynamics is easily achieved by administering small vasopressor drugs.

Arrhythmic cardiogenic shock is caused by hemodynamic disorders as a result of the development of paroxysmal tachyarrhythmias or bradycardia. It is caused by impaired heart rhythm or cardiac conduction, leading to severe central hemodynamic disorders. After stopping these disorders and restoring sinus rhythm, the pumping function of the heart quickly normalizes and the effects of shock disappear.

A true cardiogenic shock is caused by a sharp decrease in the pumping function of the heart due to extensive myocardial damage (necrosis of more than 40% of the mass of the left ventricular myocardium). In such patients, a hypokinetic type of hemodynamics is observed, often accompanied by symptoms of pulmonary edema. Pulmonary congestion occurs when the pulmonary capillary wedge pressure is 18 mmHg. Art., moderate manifestations of pulmonary edema - at 18-25 mm Hg. Art. Bright clinical manifestations - at 25-30 mm Hg. Art., with more than 30 mm Hg. Art. - a classic picture. Usually signs of cardiogenic shock appear within a few hours after the onset of myocardial infarction.

Symptoms of cardiogenic shock

Symptoms cardiogenic shock - sinus tachycardia, decrease blood pressure, dyspnea, cyanosis, integument pale, cold and humid (usually cold clammy sweat), disturbance of consciousness, decreased urine output of less than 20 ml / h. It is advisable to conduct an invasive hemodynamic control: intra-arterial blood pressure measurement and determination of seizure pressure in the pulmonary artery.

The classic definition of cardiogenic shock is “a decrease in systolic blood pressure less than 90 mm Hg. Art. Within 30 min in combination with signs of peripheral hypoperfusion. " V. Menon JS and Hochman (2002) give the following definition: “cardiogenic shock is inadequate peripheral perfusion with adequate intravascular volume, regardless of the level of blood pressure”.

Hemodynamically, in cardiogenic shock, there is a decrease in cardiac index of less than 2.0 l / min / m ² (from 1.8-2.2 l / min / m ² ) in combination with an increase in the filling pressure of the left ventricle more than 18 mm Hg. Art. (from 15 to 20 mm of mercury.), if there is no concomitant hypovolemia.

A decrease in blood pressure is already a relatively late sign. First, a decrease in cardiac output causes reflex sinus tachycardia with a decrease in pulse BP. At the same time, vasoconstriction begins, first of the skin vessels, then of the kidneys, and finally of the brain. Due to vasoconstriction, normal blood pressure can be maintained. The deterioration of perfusion of all organs and tissues, including the myocardium, is progressively increasing. In severe vasoconstriction (especially against the background of the use of sympathomimetics), a noticeable decrease in blood pressure is often auscultatory, while intra-arterial blood pressure, as determined by arterial puncture, is within normal limits. Therefore, if invasive blood pressure control is impossible, it is better to be guided by palpation of large arteries (carotid, femoral), which are less susceptible to vasoconstriction.

[7], [8], [9], [10], [11], [12], [13]

How is cardiogenic shock diagnosed?

• severe arterial hypotension (systolic blood pressure below 80 mmHg; in patients with hypertension — a decrease of more than 30 mmHg); decrease in pulse pressure to 30 mm Hg. Art. And below;
• shock index more than 0.8;

* Shock index is the ratio of heart rate and systolic blood pressure. Normally, its average value is 0.6-0.7. With shock, the index value can reach 1.5.

• clinical signs of impaired peripheral circulation;
• oliguria (less than 20 ml / h);
• retardation and confusion (there may be a short period of excitement).

The development of cardiogenic shock is also characterized by a decrease in cardiac output (cardiac index less than 2-2.5 l / min / m2) and an increased filling of the left ventricle (more than 18 mmHg), a wedging capillary wedge pressure of more than 20 mmHg. Art.

Treatment of cardiogenic shock

With a cardiogenic shock picture unfolded, the probability of survival is almost zero with any method of treatment, death usually occurs within 3-4 hours. With less pronounced disorders of hemodynamics, if you carry out drug treatment of cardiogenic shock, and the probability of success is no more than 20-30%. There is evidence that thrombolytic therapy does not improve the prognosis for cardiogenic shock. Therefore, the issue of the use of thrombolytics in cardiogenic shock is not finally resolved (the pharmacokinetics and the effect of these drugs in shock are unpredictable). In one study, the administration of streptokinase was effective in 30% of patients with cardiogenic shock — among these patients, the mortality was 42%, but the overall mortality remained high — about 70%. However, if there is no possibility of coronary angioplasty or coronary artery bypass surgery, thrombolytic therapy is indicated.

Ideally, it is necessary to start intra-aortic balloon counterpulsation as early as possible (this procedure allows you to quickly stabilize hemodynamics and maintain the state of relative stabilization for a long time). Against the background of counterpulsation, coronary angiography is performed and myocardial revascularization is attempted: coronary angioplasty (CAP) or coronary artery bypass surgery (CABG). Naturally, the possibility of a complex of such events is extremely rare. When conducting the CAP, it was possible to reduce the overall mortality rate to 40-60%. In one study, among patients with successful recanalization of the coronary arteries and restoration of coronary blood flow, mortality averaged 23% (!). Carrying out urgent CABG can also reduce mortality in cardiogenic shock to about 50%. It is estimated that early revascularization in cardiogenic shock can save lives in 2 out of 10 treated patients younger than 75 years old (SHOCK study). However, such a modern “aggressive” treatment requires the early hospitalization of patients in a specialized cardiac surgery unit.

In terms of practical public health, the following tactics for managing patients with cardiogenic shock are acceptable:

With a sharp decrease in blood pressure Norepinephrine infusion to increase blood pressure above 80-90 mm Hg. Art. (1-15 µg / min). After that (and with less pronounced hypotension in the first place) it is advisable to switch to the introduction of dopamine. If to maintain blood pressure at about 90 mm Hg. Art. Dopamine infusion is sufficient at a rate of no more than 400 µg / min, dopamine has a positive effect, expanding the vessels of the kidneys and abdominal organs, as well as the coronary and cerebral vessels. With a further increase in the rate of dopamine administration, this positive effect gradually disappears, and at an injection rate higher than 1000 µg / min, dopamine already causes only vasoconstriction.

If it is possible to stabilize blood pressure using small doses of dopamine, it is advisable to try to connect dobutamine (200–1000 μg / min) to treatment. In the future, the rate of administration of these drugs is regulated by the reaction of blood pressure. Perhaps the additional appointment of phosphodiesterase inhibitors (milrinone, enoximon).

If there are no pronounced wheezing in the lungs, many authors recommend to evaluate the reaction to the introduction of fluid in the usual manner: 250-500 ml for 3-5 minutes, then 50 mg every 5 minutes, until signs of increased stagnation in the lungs appear. Even with cardiogenic shock, approximately 20% of patients have a relative hypovolemia.

Cardiogenic shock does not require the appointment of corticosteroid hormones. In the experiment and in some clinical studies revealed a positive effect from the use of glucose-insulin-potassium mixture.