Cardiogenic shock is an extreme manifestation of acute heart failure, characterized by a critical decrease in myocardial contractility and tissue perfusion. Symptoms of shock: falling blood pressure, tachycardia, shortness of breath, signs of centralization of blood circulation (pallor, decrease in skin temperature, the appearance of stagnant spots), impaired consciousness. The diagnosis is made on the basis of the clinical picture, ECG results, tonometry. The purpose of treatment is to stabilize hemodynamics, restore heart rhythm. As part of emergency therapy, beta-blockers, cardiotonics, narcotic analgesics, and oxygen therapy are used.
ICD 10
R57.0 Cardiogenic shock
General information
Cardiogenic shock (CS) is an acute pathological condition in which the cardiovascular system is unable to provide adequate blood flow. The required level of perfusion is temporarily achieved due to the depleted reserves of the body, after which the decompensation phase begins. The condition belongs to class IV heart failure (the most severe form of cardiac dysfunction), mortality reaches 60-100%. Cardiogenic shock is more often registered in countries with high rates of cardiovascular pathology, poorly developed preventive medicine, lack of high-tech medical care.
Causes
The development of the syndrome is based on a sharp decrease in LVF contractility and a critical decrease in minute ejection, which is accompanied by circulatory insufficiency. The tissues do not receive enough blood, symptoms of oxygen starvation develop, blood pressure decreases, and a characteristic clinical picture appears. CS can aggravate the course of the following coronary pathologies:
- Myocardial infarction. It is the main cause of cardiogenic complications (80% of all cases). Shock develops mainly in large-focal transmural infarcts with the release of 40-50% of the heart mass from the contractile process. It does not occur in myocardial infarctions with a small volume of affected tissues, since the remaining intact cardiomyocytes compensate for the function of dead myocardial cells.
- Myocarditis. Shock resulting in the death of the patient occurs in 1% of cases of severe infectious myocarditis caused by Coxsackie viruses, herpes, staphylococcus, pneumococcus. The pathogenetic mechanism is the defeat of cardiomyocytes by infectious toxins, the formation of anticardial antibodies.
- Poisoning with cardiotoxic poisons. Such substances include clonidine, reserpine, cardiac glycosides, insecticides, organophosphorus compounds. With an overdose of these drugs, there is a weakening of cardiac activity, a decrease in heart rate, a drop in minute volume to indicators at which the heart is unable to provide the necessary level of blood flow.
- Massive TELA. Blockage of large branches of the pulmonary artery by a thrombus – thromboembolism PA – is accompanied by a violation of pulmonary blood flow and acute right ventricular failure. Hemodynamic disorder caused by excessive filling of the right ventricle and stagnation in it leads to the formation of vascular insufficiency.
- Tamponade of the heart. Cardiac tamponade is diagnosed with pericarditis, hemopericardium, aortic dissection, chest injuries. The accumulation of fluid in the pericardium makes it difficult for the heart to work ‒ this causes a violation of blood flow and shock phenomena.
Less often, pathology develops with papillary muscle dysfunction, ventricular septal defects, myocardial rupture, cardiac arrhythmias and blockades. Factors that increase the likelihood of cardiovascular catastrophes are atherosclerosis, old age, the presence of diabetes mellitus, chronic arrhythmia, hypertensive crises, excessive physical exertion in patients with cardiogenic diseases.
Pathogenesis
The pathogenesis is caused by a critical drop in blood pressure and subsequent weakening of blood flow in the tissues. The determining factor is not hypotension as such, but a decrease in the volume of blood passing through the vessels for a certain time. Deterioration of perfusion causes the development of compensatory and adaptive reactions. The reserves of the body are directed to providing blood to vital organs: the heart and brain. The remaining structures (skin, limbs, skeletal muscles) are experiencing oxygen starvation. Spasm of peripheral arteries and capillaries develops.
Against the background of the described processes, activation of neuroendocrine systems occurs, the formation of acidosis, the retention of sodium and water ions in the body. Diuresis is reduced to 0.5 ml/kg/hour or less. The patient is diagnosed with oliguria or anuria, liver function is disrupted, multiple organ failure occurs. In the later stages, acidosis and cytokine release provoke excessive vasodilation.
Classification
The disease is classified by pathogenetic mechanisms. At the prehospital stages, it is not always possible to determine the type of CS. In a hospital setting, the etiology of the disease plays a crucial role in the choice of therapy methods. An erroneous diagnosis in 70-80% of cases ends in the death of the patient. The following shock variants are distinguished:
- Reflex – the disorders are caused by a severe pain attack. It is diagnosed with a small lesion volume, because the severity of the pain syndrome does not always correspond to the size of the necrotic focus.
- True cardiogenic is a consequence of acute MI with the formation of a voluminous necrotic focus. The contractility of the heart decreases, which reduces the minute volume. A characteristic complex of symptoms develops. Mortality exceeds 50%.
- Areactive is the most dangerous variety. It is similar to true CS, pathogenetic factors are more pronounced. It does not respond well to therapy. The mortality rate is 95%.
- Arrhythmogenic – prognostically favorable. It is the result of a violation of rhythm and conduction. Occurs with paroxysmal tachycardia, AV blockades of the III and II degrees, complete transverse blockades. After the rhythm is restored, the symptoms disappear within 1-2 hours.
Pathological changes develop stepwise. Cardiogenic shock has 3 stages:
- Compensation. Decrease in minute volume, moderate hypotension, weakening of perfusion at the periphery. Blood supply is maintained due to the centralization of blood circulation. The patient is usually conscious, the clinical manifestations are moderate. There are complaints of dizziness, headache in the heart. At the first stage, the pathology is completely reversible.
- Decompensation. There is a developed symptom complex, blood perfusion in the brain and heart is reduced. The blood pressure level is critically low. There are no irreversible changes, but minutes remain before their development. The patient is in sopor or unconscious. Due to the weakening of the renal blood flow, the formation of urine decreases.
- Irreversible changes. Cardiogenic shock passes into the terminal stage. It is characterized by an increase in the existing symptoms, pronounced coronary and cerebral ischemia, the formation of necrosis in internal organs. Disseminated intravascular coagulation syndrome develops, petechial rash appears on the skin. Internal bleeding occurs.
Symptoms
In the initial stages, cardiogenic pain syndrome is expressed. The localization and nature of sensations are similar to a heart attack. The patient complains of compressive pain behind the sternum (“as if the heart is being squeezed in the palm of the hand”), spreading to the left shoulder blade, arm, side, jaw. There is no irradiation on the right side of the body.
Respiratory insufficiency is manifested by a complete or partial loss of the ability to breathe independently (cyanosis, respiratory rate less than 12-15 per minute, anxiety, fear of death, inclusion of auxiliary muscles in the breathing process, retraction of the wings of the nose). With the development of alveolar pulmonary edema, white or pinkish foam is released from the patient’s mouth. A person takes a forced sitting position, leaning forward and resting his hands on a chair.
There is a decrease in systolic blood pressure below 80-90 mm Hg, pulse – up to 20-25 mm Hg. Pulse is thready, weak filling and tension, tachycardia up to 100-110 beats / minute. Sometimes the heart rate drops to 40-50 beats/min. The patient’s skin is pale, cold and moist to the touch. General weakness is expressed. Diuresis is reduced or completely absent. Against the background of shock, a violation of consciousness occurs, a sopor or coma develops.
Complications
Cardiogenic shock is complicated by multiple organ failure (MOF). The work of the kidneys and liver is disrupted, reactions from the digestive system are noted. Systemic organ failure is a consequence of untimely provision of medical care to the patient or a severe course of the disease, in which the measures taken to save the patient are ineffective. Symptoms of MOF are vascular asterisks on the skin, vomiting of “coffee grounds”, the smell of raw meat from the mouth, swelling of the jugular veins, anemia.
Diagnostics
Diagnostics is carried out on the basis of physical, laboratory and instrumental examination data. When examining a patient, a cardiologist or resuscitator notes the external signs of the disease (pallor, sweating, marbling of the skin), assesses the state of consciousness. Objective diagnostic measures include:
- Physical examination. With tonometry, a decrease in blood pressure below 90/50 mm Hg is determined, the pulse index is less than 20 mm Hg. At the initial stage of the disease, hypotension may be absent, due to the inclusion of compensatory mechanisms. The heart tones are deaf, moist, small-bubbly wheezes are heard in the lungs.
- Electrocardiography. An ECG in 12 leads reveals characteristic signs of myocardial infarction: a decrease in the amplitude of the R wave, an offset of the S-T segment, a negative T wave. There may be signs of extrasystole, atrioventricular blockade.
- Laboratory test. The concentration of troponin, electrolytes, creatinine and urea, glucose, liver enzymes is evaluated. The level of troponins I and T increases already in the first hours of AMI. A sign of developing renal insufficiency is an increase in the concentration of sodium, urea and creatinine in plasma. The activity of liver enzymes increases with the reaction of the hepatobiliary system.
When conducting diagnostics, cardiogenic shock should be distinguished from delaminating aortic aneurysm, vasovagal syncope. When the aorta is dissected, the pain radiates along the spine, persists for several days, has a wave-like character. With syncope, there are no serious changes on the ECG, in the anamnesis – pain or psychological stress.
Treatment
Patients with acute heart failure and signs of shock are urgently hospitalized in a cardiology hospital. At the prehospital stage, oxygen therapy is performed, central or peripheral venous access is provided, and thrombolysis is performed according to indications. The hospital continues the treatment, which includes:
- Medical correction of violations. Loop diuretics are administered to relieve pulmonary edema. To reduce cardiac preload, nitroglycerin is used. Infusion therapy is performed in the absence of pulmonary edema and CVP below 5 mm Hg. The volume of infusion is considered sufficient when this indicator reaches 15 units. Antiarrhythmic drugs (amiodarone), cardiotonics, narcotic analgesics, steroid hormones are prescribed. Severe hypotension is an indication for the use of norepinephrine through a perfusion syringe. In case of persistent cardiac arrhythmias, cardioversion is used, in case of severe respiratory insufficiency, a ventilator is used.
- High-tech assistance. In the treatment of patients with cardiogenic shock, such high-tech methods as intra-aortic balloon contrapulsation, artificial ventricle, balloon angioplasty are used. The patient gets an acceptable chance to survive with timely hospitalization in a specialized cardiology department, where the equipment necessary for high-tech treatment is present.
Prognosis and prevention
The prognosis is unfavorable. The mortality rate is more than 50%. It is possible to reduce this indicator in cases when first aid was provided to the patient within half an hour from the onset of the disease. The mortality rate in this case does not exceed 30-40%. The survival rate is significantly higher among patients who underwent surgical intervention aimed at restoring the patency of damaged coronary vessels.
Prevention consists in preventing the development of MI, thromboembolism, severe arrhythmias, myocarditis and heart injuries. To this end, it is important to undergo preventive treatment courses, lead a healthy and active lifestyle, avoid stress, and follow the principles of a healthy diet. When the first signs of a cardiac catastrophe occur, an ambulance team is required.
