Cardiogenic shock (CS) is the most severe complication of myocardial infarction or acute damage to the heart muscle. It includes a sharp inhibition of the pumping function of the myocardium, accompanied by a drop in blood pressure and the development of pulmonary hypertension. This is the extreme terminal stage in the development of left ventricular failure, an acute disturbance in cardiac activity, which often inevitably ends in the death of the patient.
Types of disease
In the pathogenesis of cardiogenic shock in the first place is the inhibition of the systolic function of the heart, which leads to impoverishment of the blood supply. And the development of such a complication occurs in several ways. For example, with a reflex effect, with a significant weakening of the heart muscle, with the development of hemodynamically significant arrhythmias, or with combined myocardial damage. According to the indicated violations of contractilityallocate such variants of cardiogenic shock:
- reflex shock associated with a strong stimulus, often a sharp pain;
- True CABG caused by direct damage to the heart muscle in myocardial infarction or acute myocarditis, cardiac tamponade, papillary muscle rupture, or left ventricular valve destruction;
- arrhythmic variant of CABG that develops with ventricular fibrillation or tachycardia, idioventricular rhythm, transverse block or severe bradysystole;
- Reactive CABG associated with multifactorial heart disease, such as myocardial infarction and hemodynamically significant arrhythmia.
Traditional classification for cardiogenic shock was developed and presented in 1971 by the Soviet cardiologist and academician E. I. Chazov. And highlighting the clinical variant of shock is very important, because it provides information about the prognosis for the patient. For example, reflex shock has a mortality rate of 10% and is relatively easy to correct.
In true shock, mortality is about 20-35% in the first 4 hours of onset, and 40-60% during further therapy for myocardial infarction. In the arrhythmic and areactive variants, the probability of death of the patient is 80-100% if it is not possible to stop the arrhythmia or eliminate at least one cause that caused cardiogenic shock.
Clinical picture
Cardiogenic shock is an acute condition caused by traumatic, ischemic, arrhythmic or combined damage to the myocardium. It develops due to the impactfactors that directly or indirectly inhibit myocardial contractility. The result of this influence is a sharp decrease in blood volume, which is pushed out by the left ventricle to the periphery, which leads to a drop in blood pressure, impaired microcirculation, an increase in pressure in the pulmonary artery and pulmonary edema.
Hypotension
Shock of cardiogenic origin begins with myocardial damage. In this publication, the true variant of shock is considered as an example to demonstrate symptoms and clinical signs. It begins with a transmural infarct involving more than 50% of the left ventricular (LV) muscle. This part of the heart does not participate in the contraction, and therefore the ventricular systole becomes less effective. For example, normally the LV pushes out more than 70% of the blood volume from its cavity, but with extensive necrosis, this volume drops below 15%.
As a result of the fall in systolic volume, the periphery receives less nutrients and oxygen, and there is no outflow of blood from the small pulmonary circle. Then, in the large circle, the pressure drops sharply due to the sharply reduced systolic ejection fraction, and in the pulmonary circle it increases significantly. Against the background of developing pulmonary edema, the efficiency of breathing decreases, the blood is even less saturated with oxygen, and the patient's condition is continuously deteriorating.
Symptoms
The symptomatic picture of true cardiogenic shock caused by myocardial infarction unfolds quickly and is a chain of events, each ofwhich, one after the other, aggravates the patient's condition. Initially, in the acute period of a heart attack, the patient is worried for 20 minutes or more by severe burning or pressing pain behind the sternum, after which the feeling of lack of air quickly increases, mental excitement appears, fear of death, panic develops. Almost immediately, the skin becomes moist, perspiration appears on the forehead, the face turns pale, the pink color of the lips is replaced by pale, and then bluish (cyanotic).
Dyspnea and acrocyanosis
Parts of the body distant from the heart, feet, legs and hands quickly become cold, acquire a pale or cyanotic color, severe shortness of breath develops with a respiratory rate of more than 35-40 per minute, the heart rate increases, but the pulse on the peripheral arteries weakens significantly. Due to the increase in hypoxia, the patient's condition rapidly worsens, he cannot sit on his own, falls on his side or back, neuropsychic excitation disappears, lethargy and apathy develop. He cannot speak, closes his eyes, breathes heavily and quickly, holds his heart.
Pulmonary hypertension
When breathing due to rapidly developing pulmonary edema against the background of a decrease in renal blood flow and pulmonary hypertension, moist rales appear. Then a dry cough develops, a feeling of suffocation, after which white foam is coughed up. This symptom is a signal of high pressure in the pulmonary artery, due to which blood plasma leaks into the alveolar cavities, and gas exchange in the lungs is further reduced. Because of this, the oxygen content in the blood drops even more, and signs of cardiogenic shockaggravated, the patient ceases to respond to calls to him.
Hemoptysis
Later, as edema increases, erythrocytes enter the alveoli of the lung due to a further increase in pressure in the pulmonary artery. Then a wet cough with a whitish foam is replaced by a cough with pink sputum (stained with blood). The patient's breathing is bubbling, it seems that there is a large amount of fluid in his lungs. And if for some reason qualified medical care was not provided for cardiogenic shock, then the patient quickly loses consciousness. At the same time, breathing is depressed, and shortness of breath is replaced by a state of bradypnea, the frequency of inhalations and exhalations decreases to 10-15 per minute and below.
Terminal shock
Respiration gradually becomes shallow and later completely stops after the development of asystole or ventricular fibrillation. The patient dies (clinical death). The time from the moment of development of a heart attack to death is very short, although it depends on the development of fatal arrhythmias. Without arrhythmia, CABG can proceed in 40-60 minutes, although this time is highly dependent on the initial volume of myocardial damage. With the rapid development of asystole, ventricular fibrillation, transverse blockade, idioventricular rhythm or electromechanical dissociation, as well as ventricular tachycardia, death can occur suddenly.
The actions of others
It is very important at the first signs of a heart attack to seek medical help and hospitalize the patient inintensive care unit. It is possible that in myocardial infarction or cardiogenic shock, the symptoms will not be correctly interpreted by the patient's family members. However, the cost of a mistake here is minimal, since assistance in these conditions is provided according to a similar algorithm.
It is important to remember that the appearance of pain in the heart of a pressing and burning character with shortness of breath, acute respiratory failure and loss of consciousness, regardless of whether others understand the cause of the origin of these symptoms, are reasons for seeking emergency medical help. It is impossible to help the patient without narcotic pain relief, cardiotonic drugs, oxygen therapy with defoamers, nitrates and osmotic diuretics. Without treatment, he will certainly die in any variant of the course of CABG, while therapy according to the standard algorithm under the conditions of the SMP and NICU gives the patient a good chance of survival.
Prehospital diagnostics
In a condition such as cardiogenic shock, diagnosis is based on the detection of myocardial infarction or a factor that could provoke a drop in systolic function of the heart: hemodynamically significant arrhythmia, poisoning with cardiotropic poisons, injury and tamponade of the heart, pulmonary embolism, myocarditis, rupture of the papillary muscles of the left ventricle, destruction of the leaflet of the mitral or aortic valve in endocarditis. Primary diagnosis is based on assessing the patient's condition, identifying the dynamics of the disease and deterioration of he alth, electrocardiography data, blood pressure measurement, pulse oximetry.
These studies are relevant at the prehospital stage and represent the minimum set of measures that will clarify the cause of shock and act etiotropically. In particular, ECG in 100% of cases will reveal a hemodynamically significant arrhythmia and in 98-100% will show the presence of transmural myocardial infarction. Although, in such a condition as cardiogenic shock, emergency care is provided even at the stage of syndromic diagnosis (shock of unspecified etiology). Then cardiotonic infusion is established, oxygen therapy, narcotic pain relief, anticoagulant treatment, hemodynamic unloading of the pulmonary circulation is carried out.
Prehospital emergency care
Without drugs, an oxygen inhaler and narcotic painkillers, it is difficult to do anything to help the patient. At the same time, it is very difficult to give unambiguous and unconditional recommendations to people without medical education and experience in stopping critical he alth conditions. Therefore, the only recommendation is to quickly seek medical help in the development of myocardial infarction, any acute respiratory or consciousness disorders.
The main factor that determines the prognosis in cardiogenic shock is emergency care. The SMP algorithm assumes the establishment of adequate prehospital intensive care. For this purpose, the following drugs and treatments are prescribed:
- intravenous cardiotonic therapy ("Dopamine" or "Dobutamine");
- oxygen therapy 100% oxygen 8-12 liters per minute withethyl alcohol as defoamer;
- narcotic pain relief with "Morphine" or neurolepanalgesia "Droperidol" with "Fentanyl";
- anticoagulant therapy with "Heparin", "Enoxaparin" or "Fragmin" intravenously;
- hemodynamic unloading at blood pressure above 100\60 mmHg (short-acting nitrate infusion, osmotic diuretic "Furosemide 40 mg" intravenously);
- arrythmia relief ("Atropine" or transcutaneous pacing for bradyarrhythmia, "Novocainamide" or "Amiodarone" for tachyarrhythmia, defibrillation);
- resuscitation in case of clinical death of a patient;
- Emergency admission to the ICU.
The indicated stages in case of arrhythmic or areactive shock are rarely possible due to the rapid death of the patient. But in the case of true or reactive KSh, they allow compensating for he alth disorders and proceeding with evacuation. In the intensive care unit of a hospital hospital with a heart attack with stable hemodynamics, it is possible to perform coronary artery recanalization and restore the contractility of a certain area of the affected myocardium.
It should be understood that cardiogenic shock is the most severe complication of a heart attack, in the treatment of which there are a lot of insurmountable difficulties at the prehospital and hospital stages. The essence of drug therapy is to influence the processes in the patient's body. In the case of severe shock, he does not have functional reserves left to adequately respond to the intake of the drug and stabilize hemodynamics. In this situation, strict implementation of the emergency care algorithmmay not be effective in relieving shock and saving the patient.
