Cardiogenic shock

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

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

In non-Q-wave myocardial infarction, cardiogenic shock develops in 2.5-2.9%, on average after 75 hours. Thrombolytic therapy reduces the incidence of cardiogenic shock. The mortality rate of patients with cardiogenic shock in 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 is therefore 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 extent of necrosis in these cases is usually less. However, in the "narrow" sense, cardiogenic shock is considered to be shock due to dysfunction of the left ventricle ("true" cardiogenic shock). Most often, cardiogenic shock develops with anterior myocardial infarction.

In recent years, data have been obtained that many patients with cardiogenic shock have a necrosis value of less than 40%, many do not have an increase in total peripheral vascular resistance and there are no signs of pulmonary congestion. It is believed that in these cases, ischemia and systemic inflammatory reactions play a major role. There is reason to believe that early administration of nitrates, beta-blockers, morphine and ACE inhibitors to 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 a "vicious circle": decreased blood pressure - decreased coronary blood flow - 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 insufficient compensatory increase in vascular resistance in response to a stressful situation caused by the flow of nociceptive impulses into the central nervous system and a violation of the physiological balance between the tone of the sympathetic and parasympathetic divisions of the autonomic nervous system.

As a rule, it manifests itself by the development of collapse or sharp arterial hypotension in patients with myocardial infarction against the background of uncontrolled pain syndrome. Therefore, it is more correct to regard it as a collapse-like condition, which is accompanied by vivid clinical symptoms in the form of pale skin, increased sweating, low blood pressure, increased heart rate and low pulse filling.

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

Arrhythmic cardiogenic shock is caused by hemodynamic disturbances as a result of the development of paroxysmal tachyarrhythmias or bradycardia. It is caused by disturbances in cardiac rhythm or cardiac conduction, leading to pronounced disturbances in central hemodynamics. After these disturbances are stopped and sinus rhythm is restored, the pumping function of the heart quickly normalizes and the symptoms of shock disappear.

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 left ventricular myocardial mass). Such patients have a hypokinetic type of hemodynamics, often accompanied by symptoms of pulmonary edema. Congestive phenomena in the lungs appear at a pulmonary capillary wedge pressure of 18 mm Hg, moderate manifestations of pulmonary edema - at 18-25 mm Hg, pronounced clinical manifestations - at 25-30 mm Hg, at more than 30 mm Hg - a classic picture. Usually, signs of cardiogenic shock appear several hours after the onset of myocardial infarction.

Symptoms of cardiogenic shock

Symptoms of cardiogenic shock are sinus tachycardia, decreased blood pressure, dyspnea, cyanosis, pale, cold and moist skin (usually cold clammy sweat),impaired consciousness, decreased diuresis to less than 20 ml/h. It is advisable to perform invasive hemodynamic monitoring: intra-arterial blood pressure measurement and determination of pulmonary artery wedge pressure.

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

Hemodynamically, in cardiogenic shock, a decrease in the cardiac index of less than 2.0 l/min/m2 ⁽ from 1.8-2.2 l/min/m2 ⁾ is observed in combination with an increase in the filling pressure of the left ventricle of more than 18 mm Hg (from 15 to 20 mm Hg), if there is no concomitant hypovolemia.

A decrease in blood pressure is a relatively late sign. At first, a decrease in cardiac output causes reflex sinus tachycardia with a decrease in pulse pressure. At the same time, vasoconstriction begins, first in the skin vessels, then in the kidneys and, finally, in the brain. Due to vasoconstriction, normal blood pressure can be maintained. Perfusion of all organs and tissues, including the myocardium, progressively worsens. With pronounced vasoconstriction (especially against the background of sympathomimetics), auscultation often reveals a noticeable decrease in blood pressure, while intra-arterial blood pressure, determined by arterial puncture, is within normal limits. Therefore, if invasive blood pressure monitoring is impossible, it is better to rely on palpation of large arteries (carotid, femoral), which are less susceptible to vasoconstriction.

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How is cardiogenic shock diagnosed?

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

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

• clinical signs of peripheral circulatory disorders;
• oliguria (less than 20 ml/h);
• lethargy and confusion (there may be a short period of agitation).

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 increased filling of the left ventricle (more than 18 mm Hg), pulmonary capillary wedge pressure more than 20 mm Hg.

Treatment of cardiogenic shock

In the case of a full-blown picture of cardiogenic shock, the probability of survival is practically zero with any method of treatment, death usually occurs within 3-4 hours. In less pronounced hemodynamic disorders, if drug treatment of cardiogenic shock is carried out, 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 question of the use of thrombolytics in cardiogenic shock has not been finally resolved (the pharmacokinetics and action of these drugs in shock are unpredictable). In one study, the introduction of streptokinase was effective in 30% of patients with cardiogenic shock - among these patients, the mortality rate was 42%, but the overall mortality remained high - about 70%. Nevertheless, if coronary angioplasty or coronary artery bypass grafting is not possible, thrombolytic therapy is indicated.

Ideally, it is necessary to start intra-aortic balloon counterpulsation as early as possible (this procedure allows for rapid stabilization of hemodynamics and maintaining a state of relative stabilization for a long time). Against the background of counterpulsation, coronary angiography is performed and an attempt at myocardial revascularization is made: coronary angioplasty (CAP) or coronary artery bypass grafting (CABG). Naturally, the possibility of carrying out a complex of such measures is extremely rare. When CAP was performed, it was possible to reduce overall mortality to 40-60%. In one study, among patients with successful recanalization of the coronary arteries and restoration of coronary blood flow, mortality averaged 23% (!). Urgent CABG also allows for a reduction in mortality in cardiogenic shock to approximately 50%. It has been calculated that early revascularization in cardiogenic shock allows saving lives in 2 out of 10 treated patients under 75 years of age (SHOCK study). However, such modern “aggressive” treatment requires early hospitalization of patients in a specialized cardiac surgery department.

In practical healthcare conditions, the following tactics for managing patients with cardiogenic shock are acceptable:

In case of a sharp decrease in blood pressure, infusion of norepinephrine until blood pressure increases above 80-90 mm Hg (1-15 mcg/min). After this (and in case of less pronounced hypotension, first of all), it is advisable to switch to dopamine administration. If dopamine infusion at a rate of no more than 400 mcg/min is sufficient to maintain blood pressure at a level of about 90 mm Hg, dopamine has a positive effect, dilating 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 administration rate higher than 1000 mcg/min, dopamine already causes only vasoconstriction.

If it is possible to stabilize blood pressure with small doses of dopamine, it is advisable to try to add dobutamine (200-1000 mcg/min) to the treatment. Subsequently, the rate of administration of these drugs is adjusted according to the blood pressure reaction. Additional administration of phosphodiesterase inhibitors (milrinone, enoximone) is possible.

If there are no pronounced rales in the lungs, many authors recommend assessing the response to fluid administration using the standard method: 250-500 ml over 3-5 minutes, then 50 mg every 5 minutes until signs of increased congestion in the lungs appear. Even with cardiogenic shock, approximately 20% of patients have relative hypovolemia.

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