Cardiogenic shock (CABG) is a serious 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 an extreme terminal stage in the development of left ventricular failure, an acute disturbance in cardiac activity, which often inevitably results in the death of the patient.
Types of disease
In the pathogenesis of cardiogenic shock, in the first place is the inhibition of systolic function of the heart, which leads to a depletion of 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 contractility, these types of cardiogenic shock are distinguished:
- reflex shock associated with a strong irritant, often a sharp pain;
- true CABG, caused by direct damage to the heart muscle during a heart attack or acute myocarditis, tamponade of the heart, rupture of the papillary muscles or destruction of the valves of the left ventricle;
- arrhythmic variant of CABG, which develops with ventricular fibrillation or tachycardia, idioventricular rhythm, transverse blockade or severe bradyisystole;
- reactive CABG associated with multifactorial damage to the heart, for example, with myocardial infarction and hemodynamically significant arrhythmias.
The classification traditional for cardiogenic shock was developed and presented in 1971 by the Soviet cardiologist and academician E.I. Chazov. And to highlight the clinical variant of shock is very important, because it gives information about the prognosis for the patient. For example, reflex shock has a mortality rate of 10% and is relatively easy to correct.
With true shock, mortality is about 20-35% in the first 4 hours of occurrence, and 40-60% during further treatment of myocardial infarction. With the arrhythmic and areactive variant, the probability of death of the patient is 80-100%, if it is not possible to stop arrhythmia or eliminate at least one cause of cardiogenic shock, the cause.
Clinical picture
Cardiogenic shock is an acute condition caused by traumatic, ischemic, arrhythmic or combined myocardial damage. It develops due to the influence of factors that directly or indirectly inhibit the myocardial contractility. The result of this effect is a sharp decrease in blood volume, which is pushed 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 transmural infarction, affecting more than 50% of the muscle of the left ventricle (LV). This part of the heart is not involved in the contraction, and therefore ventricular systole becomes less effective. For example, normally LV expels 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 lacks nutrients and oxygen, and there is no outflow of blood from the small pulmonary circle. Then, in a large circle, the pressure due to a sharply decreased systolic ejection fraction drops significantly, and in the pulmonary circle 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 constantly deteriorating.
Symptoms
The symptomatic picture of true cardiogenic shock caused by myocardial infarction is revealed quickly and is a chain of events, each of which aggravates the patient’s condition. Initially, in the acute period of a heart attack, the patient is disturbed for 20 minutes or more by a strong burning or pressing pain behind the sternum, after which a feeling of shortage of air quickly builds up, mental agitation appears, and fear of death and panic develop. Almost immediately, the skin becomes wet, perspiration appears on the forehead, the face turns pale, the pink color of the lips gives way to pale, and then cyanotic (cyanotic).
Shortness of breath and acrocyanosis
Far from the heart parts of the body, feet, lower 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 significantly weakens. Due to the increase in hypoxia, the patient’s condition rapidly worsens, he cannot sit on his own, falls on his side or on his back, neuropsychic excitement passes, inhibition develops, apathy. He cannot speak, closes his eyes, breathes heavily and often, clings to his heart.
Pulmonary hypertension
When breathing, due to rapidly developing pulmonary edema, moist rales appear on the background of decreased renal blood flow and pulmonary hypertension. Then a dry cough develops, a feeling of suffocation, after which a white foam clears its throat. This symptom is a signal of high pressure in the pulmonary artery, due to which blood plasma flows into the alveolar cavities, and gas exchange in the lungs is even more reduced. Because of this, the oxygen content in the blood drops even more, and the signs of cardiogenic shock are aggravated, the patient ceases to respond to calls to him.
Hemoptysis
Later, as the swelling increases, red blood cells enter the pulmonary alveoli due to a further increase in pressure in the pulmonary artery. Then a wet cough with whitish foam is replaced by a cough with pink sputum (stained with blood). The patient's bubbling breathing gives the impression 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, the patient quickly faints. Then breathing is inhibited, and shortness of breath is replaced by a state of bradypnea, the frequency of inspirations and expirations decreases to 10-15 per minute or lower.
Terminal stage of shock
Respiration gradually becomes superficial and later completely stops after the development of asystole or ventricular fibrillation. The patient dies (clinical death). The time from the moment of heart attack development to death is very short, although it depends on the development of fatal arrhythmias. Without arrhythmia, CABG can occur 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, lateral blockade, idioventricular rhythm or electromechanical dissociation, as well as with 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 in the intensive care unit. It is possible that with myocardial infarction or cardiogenic shock, the symptoms will not be correctly interpreted by the patient's family members. However, the price of the error here is minimal, since assistance with these conditions is provided by 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 care. It is impossible to help the patient without narcotic anesthesia, cardiotonic drugs , oxygen therapy with antifoam agents , 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 in conditions of SMP and OITR gives the patient a good chance of survival.
Prehospital diagnosis
In a condition such as cardiogenic shock, the diagnosis is based on the detection of myocardial infarction or a factor that could provoke a decrease in systolic function of the heart: hemodynamically significant arrhythmia, poisoning with cardiotropic poisons, wound and tamponade of the heart, pulmonary embolism, myocarditis, rupture of the papillary muscles of the left ventricle, destruction of the mitral cusp or aortic valve with endocarditis. Primary diagnosis is based on assessing the patient's condition, identifying the dynamics of the development of the disease and worsening well-being, electrocardiography data, blood pressure measurements, pulse oximetry.
These studies are appropriate at the prehospital stage and represent the minimal set of measures that will clarify the cause of the shock and act etiotropically. In particular, an ECG in 100% of cases will reveal 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 the syndromic diagnosis (shock of unspecified etiology). Then the infusion of cardiotonics is established, oxygen therapy, narcotic anesthesia, anticoagulant treatment, hemodynamic unloading of the pulmonary circulation are carried out.
Prehospital emergency care
Without medications, an oxygen inhaler and narcotic painkillers, it’s difficult to help the patient with anything. At the same time, it is very difficult to give unambiguous and devoid of conventions recommendations to people without a medical education and experience in managing critical health conditions. Therefore, the only recommendation is to quickly seek medical help for the development of myocardial infarction, any acute respiratory or consciousness disturbances.
The main factor that determines the prognosis for cardiogenic shock is emergency care. The SMP algorithm involves 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 with 100% oxygen 8-12 liters per minute with ethanol as an antifoam agent;
- narcotic analgesia by "Morphine" or neurolepanalgesia "Droperidolum" with "Fentanyl";
- anticoagulant therapy with Heparin, Enoxaparin, or Fragmin intravenously;
- hemodynamic discharge with blood pressure above 100 \ 60 mmHg (short-acting nitrate infusion, urosemide 40 mg osmotic diuretic intravenously);
- stopping arrhythmias (“Atropine” or percutaneous pacemaker in case of bradyarrhythmia, “Novokainamid” or “Amiodarone” in case of tachyarrhythmia, defibrillation);
- resuscitation in case of clinical death of the patient;
- emergency hospitalization in the ICTR.
The indicated stages are rarely possible in arrhythmic or reactive shock due to the rapid death of the patient. But in the case of a true or reactive CABG, they allow you to compensate for health problems and begin evacuation. In the ICU of a hospital hospital with a heart attack with stable hemodynamics, it is possible to recanalize the coronary artery and restore the contractility of a certain area of the affected myocardium.
It should be understood that cardiogenic shock is a serious complication of a heart attack, and there are a lot of insurmountable difficulties in treating it 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 to adequately respond to drug intake and stabilize hemodynamics. In this situation, strict implementation of the emergency care algorithm may not have an effect in stopping shock and saving the patient.