What is cardiogenic shock, emergency care for the victim. Arrhythmogenic shock

14.01.2011 14308

Cardiogenic shock is the most serious hemodynamic complication of myocardial infarction. Characterized by an extremely high mortality rate, which reaches 80-90% with true shock, and 100% with areactive shock, this complication occurs in acute myocardial infarction in 10-25% of cases.
Diagnostic criteria cardiogenic shock on DGE:
decrease in systolic blood pressure below 80 mm Hg. (for patients with arterial hypertension 100-110 mmHg);
low (less than 20-25 mmHg) pulse pressure;
the presence of “peripheral microcirculatory syndrome”: pallor, cyanosis, sweating, decreased body temperature;
oliguria, anuria.
In the work of an emergency physician, the following classification of cardiogenic shock can be used:
1. Reflex cardiogenic shock or collapse.
It is characterized by a decrease in cardiac output as a result of suppression of the pumping function of the myocardium and a decrease in vascular tone by reflex influence from the damage zone. With this form of shock, a clear positive effect can be achieved with adequate pain relief (Morphine or neuroleptanalgesia). (See “Treatment of uncomplicated myocardial infarction”).

2. Arrhythmogenic tachysystolic and bradysystolic cardiogenic shock.
Elimination of the heart rhythm disturbance usually leads to the disappearance of signs of shock. Untimely or insufficient therapeutic measures for reflex shock can lead to its transformation into true shock, both in the case of arrhythmogenic and reflex shock.
3. True cardiogenic shock.
As a rule, it develops with necrosis of 40% or more muscle mass heart, as well as with repeated large-focal infarctions. Therapeutic measures include the use of non-glycoside inotropes (Fig. 7).

Treatment

Dopamine is administered in a dose of 200 mg in 400 ml of isotonic solution or 5% glucose. Administration rates ranging from 5 to 15 mcg/kg*min provide a positive inotropic effect without causing vasoconstriction and the risk of dangerous arrhythmias.
Dobutamine, unlike Dopamine, has a more powerful inotropic effect, has a weak effect on heart rate, and reduces wedging pressure in the pulmonary artery. It is administered at a dose of 250 mg in 500 ml of isotonic solution or 5% glucose at an initial rate of 2.5 mcg/kg*min. The maximum rate of administration is 15 mcg/kg*min.
Persistent hypotension below 60 mm Hg. against the background of the administration of inotropic drugs, it gives grounds to add Noradrenaline to therapy (the rate of administration in combination with Dopamine is no more than 8-10 mcg/min).
Experience clearly shows that the severity of cardiogenic shock depends not only on the volume of myocardial damage, but also lies in direct proportion to the duration of the period from the moment of its manifestations to the start of active therapy. Thus, the timely detection of signs of shock and the fastest possible correction of blood pressure are the primary task for the emergency physician. The most effective way to compensate for blood circulation during acute myocardial infarction (up to 6 hours, sometimes up to 12 hours) is to restore coronary blood flow, which can be achieved by prehospital stage by systemic thrombolysis in a specialized team or team intensive care.
4. Areactive cardiogenic shock.
Clinically characterized by the lack of effect from the use of increasing doses of pressor amines.
Separately, cardiogenic shock should be considered, resulting from the spread of myocardial infarction to the right ventricle (occurs in approximately 20-25% of cases of myocardial infarction of lower localization). It develops as a result of right ventricular failure through the mechanism of hypovolemic shock and requires active plasma replacement therapy: rapid intravenous fractional (200 ml) infusion of Polyglyukin until a positive hemodynamic effect is obtained, or until signs of left ventricular failure appear.
Self-hospitalization of patients with complicated forms of myocardial infarction by linear teams is allowed only in cases of providing assistance on the street and in public places. During transportation, it is necessary to continue oxygen inhalation and drug therapy as indicated.

During development arrhythmogenic cardiogenic shock therapy is aimed at stopping rhythm disturbances and maintaining adequate blood pressure levels. For this purpose, a vein is punctured and sympathomimetics are started intravenously. The maximum adequate SBP is 110 mm Hg. Art. (a greater increase leads to an increase in the load on the myocardium, and a decrease in SBP to 100 mm Hg and below leads to a violation of the MCB).

In order to quickly restore the rhythm in the presence of tachyarrhythmias that threaten the patient’s life, EIT is performed. It is dangerous to use AAP in this case, since they themselves sometimes lead to a decrease in myocardial contractility. If CABG is associated with cardiac arrhythmia, then, as a rule, within the next hour after the rhythm is restored, blood pressure itself returns to a satisfactory level. In case of arrhythmogenic CABG, the main task is to timely assess the threat of rhythm disturbance and promptly stop it.

During development true cardiogenic shock(as a result of impaired myocardial contractility) and a decrease in SVR, there is always a compensatory reaction from the vessels, leading to spasm. In CABG this reaction is so pronounced that it leads to disruption of the MCB. The introduction of vasopressors (dopamine, norepinephrine), which increase vascular tone, in this case is often unsuccessful: such therapy disrupts the MCB to a greater extent, which further increases the load on the myocardium. The main emphasis in the treatment of true CABG is on improving cardiac output and blood flow.

Since true cardiogenic shock develops in 99% of cases with MI, then the first thing to do is to relieve pain and restore normal blood flow through the blocked coronary artery(restore the function of the “hibernating” myocardium) through early systemic thrombolysis or PCCA. Thrombolysis relatively rarely leads to complete elimination of the thrombus that caused MI, but the administration of a fibrinolytic additionally leads to a decrease in the total thrombogenic potential of the blood, improvement in blood fluidity, MCB and the state of the intact myocardium.

With the prevalence in clinical picture of cardiogenic shock signs of pulmonary circulation overload (pulmonary artery wedge pressure more than 18 mm Hg and mean blood pressure less than 65 mm Hg) dopamine, dobutamine (which has similar inotropic, but weak chronotropic effects, can reduce afterload) is administered as initial therapy and norepinephrine. The choice of vasopressor depends on the severity of the MI and the patient's response. Thus, dopamine is usually used initially, which has little effect on heart rate (tachycardia may be useful for patients with bradycardia, but unfavorable for patients with MI).

Dopamine(having inotropic and vasoactive effects) increases cardiac output and blood pressure (with a minimal increase in afterload) to an adequate level (mean blood pressure should exceed 70 mm Hg) by reducing systemic hypotension by stimulating adrenergic receptors - beta 1 (cardiac, increasing the contractility of the intact myocardium) and beta 2 (vasodilating and reducing OPS). Dopamine in small doses can increase renal blood flow.

Dopamine(40 ml of a 1% solution in 400 ml of rheopolyglucin) is first administered intravenously at a rate of 2.5-5-10 mcg/kg-min, necessary to control blood pressure and depending on which symptoms predominate: renal hypoperfusion or pulmonary congestion. If no effect is obtained (no increase in blood pressure), norepinephrine is administered intravenously (1-2 ml of 0.2% solution in 200-400 ml of 5% glucose solution) at an initial rate of 2 mcg/kg-min, then increasing it to 10- 20 mcg/kg-min to achieve a mean blood pressure of 70 mm Hg. Art.

For the same purpose you can use anticholinesterase drugs(amrinone, milrinone at an initial dose of 50 mcg/kg for 10 minutes, then at a rate of 0.375-0.75 mcg/kg-min), which quickly and significantly increase the contractility of the heart. When blood pressure rises to normal level(or subnormal), a combination of dopamine with peripheral vasodilators is justified, which further increases the stroke volume and reduces the LV filling pressure.

All vasopressors in large doses can cause ischemic vasoconstriction. The gastrointestinal mucosa and liver are especially sensitive to it (renal vasoconstriction appears only with very large doses of vasopressors). Severe hypotension (SBP less than 50 mm Hg) is associated with decreased pressure-dependent blood flow in the heart and brain (with subsequent myocardial depression and cerebral ischemia).

When dopamine, norepinephrine and rapid fluid infusion turned out to be ineffective in restoring perfusion, adrenaline (the drug of last choice) is used. If it does not give a positive effect (the patient is resistant to standard therapy), then they prescribe large doses GKS (mandatory component complex therapy KS).

Positive effect of glucocorticosteroids is associated with an improvement in MCB, stabilization of lysosamal membranes, a decrease in the effect of catecholamines on vascular smooth muscle (reduction of OPS), and peripheral vasodilation. Prednisolone is administered (intravenous bolus at a dose of 90-150 mg) or solumedrol (30 mg/kg body weight, repeating injections every 4-6 hours for 48 hours), which can enhance the effect of catecholamines. GCS can also be useful in cases of the often concomitant complication of CABG - the development of adrenal insufficiency.

This condition refers to current pathological processes that directly affect a sharp decrease in heart rate.

Arrhythmogenic shock can be primary and secondary and can occur against the background of tachycardia and blockade of 2 and 3 degrees.

This condition requires immediate attention medical assistance, and therapy will be effective only after the heart rhythm is restored.

Arrhythmogenic shock is a type of circulatory disorder with reduced cardiac output occurring against the background of an imbalance of heart rhythms:

ventricular paraxysmal tachycardia;
paroxysms of flutter;
atrial fibrillation.

A rapid increase in heart rate against this background entails a shortening of diastole, a decrease in ventricular filling and a decrease in cardiac output.

The shock clinic is manifested by tachycardia, decreased systolic blood pressure and pulse pressure, as well as signs of hypoperfusion.

Such shock is rare, mainly in patients with a large focus of myocardial infarction. The tachycardic form of atrial flutter is most often observed. There are also cases when arrhythmogenic shock occurs together with pulmonary edema.

Impaired blood supply as a result arrhythmogenic shock, leads to inadequate blood supply to organs and tissues.

Symptoms

Among distinctive features and symptoms of shock are noted:

rapid pulse (which is difficult to feel);
impaired consciousness;
decrease in diuresis by 20 ml;
blood oxidation due to low bicarbonate concentration.

The general condition also changes:

The skin becomes pale, with a blue tint.
Sticky sweat appears on the skin.
Broken veins.
Lethargy.
Loss of strength.

Reasons

Usually, and most often in practice, shock occurs against a background of prolonged pain (several hours). Knowing the reason is more important than the type itself pathological process. It is often obvious after reviewing the patient's medical history.

Some conditions of a patient in shock may indicate various serious complications.

Common reasons are:

Myocardial infarction.
Cardiac tamponade.
Pulmonary embolism.
Prolonged bed rest.
Pancreatitis.

Arrhythmogenic shock can often occur for no apparent reason. To determine the exact “culprit” that provoked the pathology, doctors begin an immediate examination of the patient. They give him an X-ray of the sternum, an ECG, and examine blood gases. At good performance results, the probable cause may be drug overdose, rare infections, obstructive shock.

ECG registration is important. The tactics are independent of the type of tachycardia, but in all cases electrical cardioversion is indicated.

Acute pancreatitis can give serious complications. - the most dangerous consequence of this disease.

The causes and symptoms of toxic shock are described in detail.

Despite the fact that donor material is checked for compatibility before blood transfusion, sometimes it happens that the recipient's body rejects the donor's blood. In this case it happens blood transfusion shock. This topic details the symptoms of this condition and treatment methods.

Treatment

To begin with, anesthesia is given, in some cases this stabilizes the dynamics. Next, oxygen and oxygen therapy is needed. If necessary, a catheter is inserted to monitor hemodynamics. At the stages of treatment there are such points as:

pharmacological treatment of arrhythmia;
administering medications through a vein;
performing actions that reduce peripheral resistance;
balloon counterpulsation.

In some cases, they resort to surgical intervention - coronary bypass surgery.

Coronary artery bypass surgery

Treatment of shock involves medications and other more serious measures. We are talking about defibrillation and electrical stimulation. If antiarrhythmic drugs are relevant, a certain dosage of 1% Mezaton is added.

In case of arrhythmogenic shock developed against the background of bradysystole, immediate administration of diluted Isoproterenol is carried out. It is used intravenously and for a long time. Successful treatment it is quite possible if all measures have been taken to alleviate the patient’s condition and to stop all pathological processes in the body.

The treatment tactics for patients with this pathology have their own characteristics. Help must be provided quickly, since the disease is considered serious. Patients with an attack of arrhythmogenic shock are not transportable. As soon as the team relieves the severity of this serious condition, it is advisable to place the person in the intensive care unit.

All treatment occurs according to the standard scheme, if there are no concomitant serious illnesses internal organs:

Examination of the patient.
Measurement of pulse and blood pressure.
Palpation of the peritoneum.
Electrocardiography (if possible).
Installation of a dropper (glucose, Polyglucin, sodium chloride).
Constant monitoring of blood pressure, heart muscle contractions, appearance skin.

If certain indicators occur, medications are administered exclusively intravenously. In this case, it is worth taking into account the medications that the patient has taken over the past 48 hours.

If the accelerated idioventricular rhythm has a picture of shock, it is not arrhythmogenic.

Success will only occur with early diagnosis and timely initiation of treatment for arrhythmogenic shock. Intensive therapy gives positive results in patients. Thanks to the “quick setting” of the state and current illness, the risk of complications due to shock is significantly reduced. This is especially true for its areactive manifestations.

Video on the topic

– this is an extreme degree of manifestation of acute heart failure, characterized by a critical decrease in myocardial contractility and tissue perfusion. Symptoms of shock: drop in blood pressure, tachycardia, shortness of breath, signs of centralized blood circulation (pallor, decreased skin temperature, appearance of congestive spots), impaired consciousness. The diagnosis is made based on the clinical picture, ECG results, and tonometry. The goal of treatment is to stabilize hemodynamics and restore heart rhythm. As part of emergency therapy, beta blockers, cardiotonics, narcotic analgesics, oxygen therapy.

ICD-10

R57.0

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 recorded in countries with high rates of cardiovascular pathology, poorly developed preventive medicine, lack of high-tech medical care.

Reasons

The development of the syndrome is based on a sharp decrease in LV contractility and a critical decrease in cardiac output, which is accompanied by circulatory failure. A sufficient amount of blood does not enter the tissue, symptoms of oxygen starvation develop, blood pressure levels decrease, and a characteristic clinical picture appears. CABG 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 with large-focal transmural infarctions 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 tissue, since the remaining intact cardiomyocytes compensate for the function of dead myocardial cells.
Myocarditis. Shock, leading to 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 damage to cardiomyocytes by infectious toxins, the formation of anticardiac antibodies.
Poisoning with cardiotoxic poisons. Such substances include clonidine, reserpine, cardiac glycosides, insecticides, and organophosphorus compounds. An overdose of these drugs causes a weakening of cardiac activity, a decrease in heart rate, and a drop in cardiac output to levels at which the heart is unable to provide required level blood flow
Massive pulmonary embolism. Blockage of large branches of the pulmonary artery by a thrombus - pulmonary embolism - is accompanied by impaired 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.
Cardiac tamponade. Cardiac tamponade is diagnosed with pericarditis, hemopericardium, aortic dissection, and chest injuries. The accumulation of fluid in the pericardium complicates the work of the heart - this causes disruption of blood flow and shock phenomena.

Less commonly, pathology develops with papillary muscle dysfunction, ventricular septal defects, myocardial rupture, cardiac arrhythmias and blockades. Factors that increase the likelihood of cardiovascular accidents are atherosclerosis, old age, diabetes mellitus, chronic arrhythmia, hypertensive crises, excessive physical activity in patients with cardiogenic diseases.

Pathogenesis

The pathogenesis is due to 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 during certain time. Deterioration of perfusion causes the development of compensatory and adaptive reactions. The body's reserves are used to supply blood to vital organs: the heart and brain. Other structures (skin, limbs, skeletal muscles) experience 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, and the retention of sodium and water ions in the body. Diuresis decreases to 0.5 ml/kg/hour or less. The patient is diagnosed with oliguria or anuria, liver function is disrupted, and multiple organ failure occurs. On late stages acidosis and cytokine release provoke excessive vasodilation.

Classification

The disease is classified according to pathogenetic mechanisms. At the prehospital stages, it is not always possible to determine the type of CABG. In a hospital setting, the etiology of the disease plays a role decisive role in the choice of therapy methods. Misdiagnosis in 70-80% of cases ends in the death of the patient. The following types of shock are distinguished:

Reflex– violations are caused by a severe pain attack. It is diagnosed when the volume of the lesion is small, since the severity of the pain syndrome does not always correspond to the size of the necrotic lesion.
True Cardiogenic– a consequence of acute MI with the formation of a voluminous necrotic focus. The contractility of the heart decreases, which reduces cardiac output. A characteristic complex of symptoms develops. The mortality rate exceeds 50%.
Areactive– most dangerous species. Similar to true CS, pathogenetic factors are more pronounced. Doesn't respond well to therapy. Mortality – 95%.
Arrhythmogenic– prognostically favorable. It is the result of rhythm and conduction disturbances. Occurs with paroxysmal tachycardia, AV blockade of the third and second degree, complete transverse blockade. After the rhythm is restored, the symptoms disappear within 1-2 hours.

Pathological changes develop stepwise. Cardiogenic shock has 3 stages:

Compensation. Decreased cardiac output, moderate hypotension, weakened perfusion in the periphery. Blood supply is maintained by centralizing the circulation. The patient is usually conscious, clinical manifestations are moderate. There are complaints of dizziness, headache, heart pain. 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. Blood pressure level is critically low. There are no irreversible changes, but there are minutes left before they develop. The patient is in stupor or unconscious. Due to the weakening of renal blood flow, urine formation is reduced.
Irreversible changes. Cardiogenic shock enters the terminal stage. It is characterized by an intensification of existing symptoms, severe coronary and cerebral ischemia, and the formation of necrosis in the internal organs. Disseminated intravascular coagulation syndrome develops, and a petechial rash appears on the skin. Internal bleeding occurs.

Symptoms of cardiogenic shock

In the initial stages, cardiogenic pain syndrome is expressed. The location and nature of the sensations are similar to a heart attack. The patient complains of squeezing pain behind the sternum (“as if the heart is being squeezed in the palm of your hand”), spreading to left shoulder blade, arm, side, jaw. There is no irradiation on the right side of the body.

Complications

Cardiogenic shock is complicated by multiple organ failure (MOF). The functioning of the kidneys and liver is impaired, side effects are observed digestive system. 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 rescue measures taken are ineffective. Symptoms of MODS are spider veins on the skin, vomiting “coffee grounds,” the smell of raw meat on the breath, swelling of the jugular veins, anemia.

Diagnostics

Diagnosis is carried out on the basis of physical, laboratory and instrumental examination. When examining a patient, a cardiologist or resuscitator notes external signs diseases (pallor, sweating, marbling of the skin), assesses the state of consciousness. Objective diagnostic measures include:

Physical examination. Tonometry determines a decrease in blood pressure below 90/50 mmHg. Art., pulse rate less than 20 mm Hg. Art. On initial stage hypotension may be absent due to the inclusion of compensatory mechanisms. Heart sounds are muffled, moist fine rales are heard in the lungs.
Electrocardiography. A 12-lead ECG reveals characteristic features myocardial infarction: decreased amplitude of the R wave, displacement of the S-T segment, negative T wave. Signs of extrasystole and atrioventricular block may be observed.
Laboratory research. The concentration of troponin, electrolytes, creatinine and urea, glucose, and liver enzymes is assessed. The level of troponins I and T increases already in the first hours of AMI. Sign of developing renal failure- increased concentrations of sodium, urea and creatinine in plasma. The activity of liver enzymes increases with the reaction of the hepatobiliary system.

When carrying out diagnostics, it is necessary to distinguish cardiogenic shock from dissecting aortic aneurysm and vasovagal syncope. With aortic dissection, the pain radiates along the spine, persists for several days, and is wave-like. With syncope, there are no serious changes on the ECG, and there is no history of pain or psychological stress.

Treatment of cardiogenic shock

Patients with acute heart failure and symptoms state of shock are urgently hospitalized in a cardiology hospital. The ambulance team responding to such calls must include a resuscitator. At the prehospital stage, oxygen therapy is provided, central or peripheral venous access is provided, and thrombolysis is performed according to indications. In the hospital, treatment started by the emergency medical team continues, which includes:

Drug correction of disorders. To relieve pulmonary edema, loop diuretics are administered. Nitroglycerin is used to reduce cardiac preload. Infusion therapy is carried out in the absence of pulmonary edema and CVP below 5 mm Hg. Art. The infusion volume is considered sufficient when this figure reaches 15 units. Antiarrhythmic drugs (amiodarone), cardiotonics, narcotic analgesics, steroid hormones. Severe hypotension is an indication for the use of norepinephrine through a perfusion syringe. For persistent heart rhythm disturbances, cardioversion is used; for severe respiratory failure– IVL.
High-tech assistance. When treating patients with cardiogenic shock, high-tech methods such as intra-aortic balloon counterpulsation, artificial ventricle, and balloon angioplasty are used. The patient receives an acceptable chance of survival with timely hospitalization in a specialized cardiology department, where the equipment necessary for high-tech treatment is available.

Prognosis and prevention

The prognosis is unfavorable. Mortality is more than 50%. This indicator can be reduced in cases where 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%. Survival rate is significantly higher among patients who underwent surgery, aimed at restoring the patency of damaged coronary vessels.

Prevention consists of preventing the development of MI, thromboembolism, severe arrhythmias, myocarditis and heart injuries. For this purpose, it is important to undergo preventive courses of treatment, maintain a healthy and active image life, avoid stress, follow the principles healthy eating. When the first signs of a cardiac catastrophe occur, an ambulance must be called.

A deadly complication of myocardial infarction is true cardiogenic shock, which causes death in 90% of cases. The pathological process is based on an acute and sudden cessation of blood flow in most organs and tissues of the body, which leads to irreversible changes in cellular structures.

Vascular collapse can occur against the background of different types of acute conditions (during bleeding, sepsis, thromboembolism): cardiogenic shock is an acute cardiac pathology, most often occurring with infarction of the left ventricle.

Acute coronary syndrome (ACS) has typical clinical manifestations; first aid for cardiogenic shock involves intensive resuscitation measures, and the consequences depend on the degree of damage to vital organs and body systems.

Shock Heart Options

Shock is a typical syndrome characteristic of large quantity dangerous pathological conditions and requiring emergency medical care. Cardiogenic shock, the classification of which distinguishes several types of acute situations, occurs in cardiac pathology. The following forms of cardiogenic shock are possible:

true (cardiogenic shock during myocardial infarction);
CABG due to severe arrhythmia;
reflex;
areactive cardiogenic shock.

The severity of the coronary circulation disturbed by the infarction has great prognostic significance for survival:

average;
heavy;
areactive.

Cardiogenic shock of any stage is characterized by a sudden and pronounced decrease in blood pressure and cessation of blood flow, which is manifested by a variety of symptoms and signs indicating a life-threatening pathology.

Causal factors of acute condition

Any types and variants of cardiogenic shock occur when the main function of the heart is disrupted: cessation of pump operation leads to a lack of oxygenated blood in the vessels. All causes of cardiogenic shock can be divided into 2 groups:

Impaired systolic function of the heart

The most common causative factor is myocardial infarction. In addition, the following pathological options are possible:

severe myocarditis;
heart surgery;
rupture of the heart muscle;
toxic effects of drugs or alcoholic beverages.

Acute mechanical overload of the left ventricle

Stopping the flow of blood into the aorta can occur due to the following factors:

acute cardiac failure at the level of the mitral or aortic valve;
infective endocarditis;
surgical intervention;
congenital heart defects, which most often cause cardiogenic shock in children;
interventricular defect;
acute aneurysm in the wall of the left ventricle;
spherical thrombus in the atrium;
acute arrhythmia with original violation coronary blood flow.

Whatever the causative factor, it is important to understand how cardiogenic shock develops and progresses: the pathogenesis of a life-threatening condition determines the symptoms of the disease and indicates the outcome of coronary pathology. Due to a complete or partial stop of the pump in the chest, the cardiac output (the amount of blood sent to the tissues) sharply decreases, which leads to the formation of a vicious circle: the less blood is pumped, the worse the supply to vital organs and the less supply to the heart muscle. The state of shock becomes irreversible when total ischemia occurs in the cellular structures of the heart, brain and major internal organs.

Symptoms and signs of coronary disorders

For quick diagnosis and effective primary care you need to know the criteria for cardiogenic shock:

a sudden and catastrophic drop in systolic blood pressure below 80-60 mm Hg. Art.;
rapid pulse, which is very difficult to detect on the wrist;
frequent and shallow breathing;
changes in consciousness up to a coma;
severe pallor of the skin;
significant decrease or absence of urine.

Extensive vascular collapse does not always develop immediately and with lightning speed. It is advisable to detect signs of cardiogenic shock before the onset of irreversible symptoms, which is especially important in the case of myocardial ischemia. The most common manifestations of a dangerous pathology are:

burning increasing pain in the chest area;
irritability, psycho-emotional agitation with a feeling of fear;
skin cyanosis, pallor and severe sweating;
apathy and severe weakness associated with a drop in blood pressure;
tachycardia, arrhythmia and rapid breathing.

Cardiogenic shock, the symptoms of which indicate a severe and areactive stage of the disease, is almost impossible to cure, therefore timely diagnosis initial forms of an acute pathological condition and detection of moderate severity of coronary disorders is the only chance to save a person’s life.

Emergency assistance

Effective treatment of cardiogenic shock depends on the severity of the acute coronary syndrome and the speed of delivery of the sick person to the cardiac intensive care unit of a specialized hospital. Great value For prognosis, emergency care for cardiogenic shock, carried out by a doctor in the resuscitation team, is essential.

The specialist will perform the following mandatory tasks:

Providing effective pain relief;
Removing emotional arousal;
Correction of respiratory disorders (oxygen mask, provision of artificial ventilation if necessary);
Drug therapy aimed at increasing blood pressure and preventing irreversible changes in the organs and tissues of the body.

In addition to the IV and constant measurement of vascular tone, the doctor will administer intravenous medications to maintain the functioning and ensure the correct rhythm of the heart, means to improve vascular blood flow and correct metabolic disorders.

The main task of the emergency resuscitation team doctor is to prevent irreversible circulatory disorders in vital organs and deliver the patient to the cardiac intensive care unit as quickly as possible.

Complications and consequences

Discovered in time acute pathology and correctly provided emergency care for cardiogenic shock does not at all guarantee against the following frequently occurring types of complications:

respiratory failure (shock lung - shortness of breath, swelling in the lung tissue, severe metabolic and vascular disorders);
acute renal pathology (shock kidney - absence or extremely low amount of urine, necrotic damage in the tissues of the excretory system);
liver failure with death of some liver cells;
the occurrence of acute ulcers and erosions in the stomach, which lead to bleeding;
the appearance of small blood clots in the vascular bed;
necrotic changes in soft tissues limbs (gangrene), which occurs due to lack of blood flow in small vessels legs and arms.

The most dangerous complication of a sudden heart attack or acute cardiac pathology with disruption of general blood flow in the body is cardiogenic shock. Rendering emergency care in this condition, it should be as quickly as possible, but even with timely admission to the cardiac intensive care unit, the probability of survival is about 10%. Optimal prevention of an extremely dangerous complication and prevention of the disabling consequences of a state of shock is regular examination by a doctor, treatment of heart disease and following the recommendations of a specialist to prevent myocardial infarction.

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Reasons

The causes of cardiogenic shock occur inside the heart or in the surrounding vessels and membranes.

TO internal reasons include:

Acute left ventricular myocardial infarction, which is accompanied by long-term unrelieved pain syndrome and the development of severe weakness of the heart muscle due to a large area of necrosis. The spread of the ischemic zone to the right ventricle significantly aggravates the shock.
Paroxysmal types of arrhythmias with high pulse frequency during fibrillation and ventricular fibrillation.
Complete heart block due to the inability to conduct impulses from the sinus node to the ventricles.

External causes are considered:

Various inflammatory or traumatic injuries pericardial sac (the cavity in which the heart lies). As a result, an accumulation of blood (hemopericardium) or inflammatory exudate occurs, compressing the outside of the heart muscle. Under such conditions, reductions become impossible.
Pneumothorax (air in pleural cavity due to lung rupture).
The development of thromboembolism in the large trunk of the pulmonary artery disrupts blood circulation through the pulmonary artery, blocks the functioning of the right ventricle, and leads to tissue oxygen deficiency.

Mechanisms of pathology development

The pathogenesis of the appearance of hemodynamic disturbances differs depending on the form of shock. There are 4 varieties.

Reflex shock - caused by the body's reaction to severe pain. In this case, there is a sharp increase in the synthesis of catecholamines (substances similar to adrenaline). They cause spasm of peripheral blood vessels and significantly increase the resistance of the heart. Blood accumulates at the periphery, but does not nourish the heart itself. The energy reserves of the myocardium are quickly depleted, and acute weakness develops. This variant of the pathology can occur with a small area of infarction. It has good treatment results if pain is quickly relieved.
Cardiogenic shock (true) - associated with damage to half or more of the muscle mass of the heart. If even part of a muscle is excluded from work, this reduces the strength and volume of blood ejection. With significant damage, the blood coming from the left ventricle is not enough to nourish the brain. It does not enter the coronary arteries, the supply of oxygen to the heart is disrupted, which further impairs the ability of myocardial contraction. The most severe variant of the pathology. Reacts poorly to therapy.
Arrhythmic form - impaired hemodynamics is caused by fibrillation or rare contractions of the heart. Timely application antiarrhythmic drugs, the use of defibrillation and electrical stimulation makes it possible to cope with such pathology.
Areactive shock - most often occurs with repeated heart attacks. The name refers to the body's lack of response to therapy. In this form, hemodynamic disturbances are accompanied by irreversible tissue changes, accumulation of acid residues, and slagging of the body with waste substances. With this form, death occurs in 100% of cases.

Depending on the severity of shock, all described mechanisms take part in the pathogenesis. The result of the pathology is a sharp decrease in the contractility of the heart and severe oxygen deficiency of the internal organs and brain.

Clinical manifestations

Symptoms of cardiogenic shock indicate the manifestation of impaired blood circulation:

the skin is pale, the face and lips have a grayish or bluish tint;
cold, sticky sweat is released;
hands and feet are cold to the touch;
varying degrees of impairment of consciousness (from lethargy to coma).

When measuring blood pressure, low numbers are detected (the upper one is below 90 mm Hg), the typical difference with the lower pressure is less than 20 mm Hg. Art. Pulse on radial artery not detectable, difficult to detect when sleepy.

When pressure drops and vasospasm occurs, oliguria (low urine output) occurs, leading to complete anuria.

Classification

Classification of cardiogenic shock according to the severity of the patient’s condition involves three forms:

Clinical manifestations	1st degree	2nd degree (moderate)	3rd degree (heavy)
Duration of shock	less than 5 hours	from 5 to 8 hours	more than 8 hours
Blood pressure in mm Hg. Art.	at the lower limit of normal 90/60 or up to 60/40	upper at 80-40, lower – 50-20	not defined
Tachycardia (beats per minute)	100–110	up to 120	dull tones, threadlike pulse
Typical symptoms	weakly expressed	left ventricular failure predominates, pulmonary edema is possible	pulmonary edema
Response to treatment	good	slow and unstable	absent or short-term

Diagnostics

Diagnosis of cardiogenic shock is based on typical clinical signs. Much harder to determine the real reason shock. This must be done to clarify the regimen of upcoming therapy.

At home, the cardiology team performs an ECG study to determine the signs of an acute heart attack, the type of arrhythmia or blockade.

In a hospital setting, ultrasound of the heart is performed according to emergency indications. The method allows you to detect a decrease in the contractile function of the ventricles.

Based on x-ray of organs chest it is possible to establish pulmonary embolism, altered contours of the heart due to defects, pulmonary edema.

As treatment progresses, doctors in the intensive care or resuscitation room check the degree of oxygen saturation of the blood, the functioning of internal organs using general and biochemical tests, and take into account the amount of urine excreted.

How to provide first aid to a patient

Help for cardiogenic shock from loved ones or passers-by may include: call as soon as possible"Ambulance" full description symptoms (pain, shortness of breath, state of consciousness). The dispatcher can send a specialized cardiology team.

As first aid, you should remove or untie your tie, unfasten your tight collar, belt, and give Nitroglycerin for heart pain.

Goals of first aid:

elimination of pain syndrome;
maintaining blood pressure with medications at least at the lower limit of normal.

To do this, the ambulance administers intravenously:

painkillers from the group of nitrates or narcotic analgesics;
drugs from the group of adrenergic agonists are used carefully to increase blood pressure;
with sufficient pressure and pulmonary edema fast-acting diuretics are needed;
oxygen is given from a cylinder or pillow.

The patient is urgently taken to the hospital.

Treatment

Treatment of cardiogenic shock in the hospital continues the therapy started at home.

The algorithm of actions of doctors depends on a quick assessment of the functioning of vital organs.

Insertion of a catheter into the subclavian vein for infusion therapy.
Determination of the pathogenetic factors of the shock state - the use of painkillers in case of continued pain, antiarrhythmic drugs in the presence of a disturbed rhythm, elimination of tension pneumothorax, cardiac tamponade.
Lack of consciousness and own respiratory movements - intubation and transition to artificial ventilation using a breathing apparatus. Correction of oxygen content in the blood by adding it to the breathing mixture.
Upon receipt of information about the onset of tissue acidosis, add sodium bicarbonate solution to the therapy.
Installation of a catheter in bladder to control the amount of urine excreted.
Continuation of therapy aimed at increasing blood pressure. To do this, Norepinephrine, Dopamine with Reopoliglucin, and Hydrocortisone are carefully administered by drip.
The administered fluid is monitored; when pulmonary edema begins, it is limited.
To restore the impaired coagulating properties of blood, Heparin is added.
Lack of response to the applied therapy requires an urgent solution to the operation of intra-aortic counterpulsation by introducing a balloon into the descending aortic arch.

The method allows you to maintain blood circulation before performing coronary angioplasty, inserting a stent, or deciding whether to perform coronary artery bypass surgery according to vital indications.

The only way to help with areactive shock may be an emergency heart transplant. Unfortunately, current state Healthcare development is still far from this stage.

International symposiums and conferences are devoted to the organization of emergency care. Government officials are being asked to increase spending to bring cardiac specialty care closer to the patient. Early start treatment plays vital role in preserving the life of the patient.

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Reasons

The cause of cardiogenic shock is a violation of myocardial contractility (acute myocardial infarction, hemodynamically significant arrhythmias, dilated cardiomyopathy) or morphological disorders (acute valvular insufficiency, ventricular septal rupture, critical aortic stenosis, hypertrophic cardiomyopathy).

The pathological mechanism for the development of cardiogenic shock is complex. Violation of myocardial contractile function is accompanied by a decrease in blood pressure and activation of the sympathetic nervous system. As a result, the contractile activity of the myocardium increases, and the rhythm becomes more frequent, which increases the heart’s need for oxygen.

A sharp decrease in cardiac output causes a decrease in blood flow in the renal arteries. This leads to fluid retention in the body. The increasing volume of circulating blood increases the preload on the heart and provokes the development of pulmonary edema.

Long-term inadequate blood supply to organs and tissues is accompanied by the accumulation of under-oxidized metabolic products in the body, resulting in the development of metabolic acidosis.

Species

According to the classification proposed by Academician E.I. Chazov, the following forms of cardiogenic shock are distinguished:

Reflex. Conditioned sharp drop vascular tone, which leads to a significant drop in blood pressure.
True. The main role belongs to a significant decrease in the pumping function of the heart with a slight increase in peripheral total resistance, which, however, is not enough to maintain an adequate level of blood supply.
Areactive. Occurs against the background of extensive myocardial infarction. The tone of peripheral blood vessels sharply increases, and microcirculation disorders manifest themselves with maximum severity.
Arrhythmic. Deterioration of hemodynamics develops as a result of significant disturbances in heart rhythm.

Signs

The main symptoms of cardiogenic shock:

a sharp decrease in blood pressure;
thread-like pulse (frequent, weak filling);
oligoanuria (decrease in the amount of urine excreted to less than 20 ml/h);
lethargy, even to the point of coma;
pallor (sometimes marbling) of the skin, acrocyanosis;
decreased skin temperature;
pulmonary edema.

Diagnostics

The diagnostic scheme for cardiogenic shock includes:

coronary angiography;
chest x-ray (concomitant pulmonary pathology, dimensions of the mediastinum, heart);
electro- and echocardiography;
computed tomography;
blood test for cardiac enzymes, including troponin and phosphokinase;
arterial blood gas analysis.

Treatment

Emergency care for cardiogenic shock:

check airway patency;
install intravenous catheter wide diameter;
connect the patient to a cardiac monitor;
deliver humidified oxygen through a face mask or nasal catheters.

After this, measures are taken to find the cause of cardiogenic shock, maintain blood pressure, and cardiac output. Drug therapy includes:

analgesics (allow relief of pain);
cardiac glycosides (increase the contractile activity of the myocardium, increase the stroke volume of the heart);
vasopressors (increase coronary and cerebral blood flow);
phosphodiesterase inhibitors (increase cardiac output).

If indicated, other medications are also prescribed (glucocorticoids, volemic solutions, β-blockers, anticholinergics, antiarrhythmic drugs, thrombolytics).

Prevention

Prevention of the development of cardiogenic shock is one of the most important measures in the treatment of patients with acute cardiopathology; it consists of rapid and complete relief of pain and restoration of heart rhythm.

Possible consequences and complications

Cardiogenic shock is often accompanied by the development of complications:

acute mechanical damage to the heart (rupture of the interventricular septum, rupture of the left ventricular wall, mitral insufficiency, cardiac tamponade);
severe left ventricular dysfunction;
right ventricular infarction;
disturbances of conductivity and heart rhythm.

Mortality in cardiogenic shock is very high - 85-90%.

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Causes of shock

According to the leading starting factor, we can distinguish following types shock:

1. Hypovolemic shock:

Hemorrhagic shock (with massive blood loss).
Traumatic shock (combination of blood loss with excessive pain impulses).
Dehydration shock (excessive loss of water and electrolytes).

2. Cardiogenic shock is caused by a violation of myocardial contractility (acute myocardial infarction, aortic aneurysm, acute myocarditis, rupture of the interventricular septum, cardiomyopathies, severe arrhythmias).

3. Septic shock:

Action of exogenous toxic substances(exotoxic shock).
The action of bacteria, viruses, endotoxemia due to massive destruction of bacteria (endotoxic, septic, infectious-toxic shock).

4. Anaphylactic shock.

Mechanisms of shock development

Common to shock are hypovolemia, impaired rheological properties blood, sequestration in the microcirculation system, tissue ischemia and metabolic disorders.

In the pathogenesis of shock, the following are of primary importance:

Hypovolemia. True hypovolemia occurs as a result of bleeding, loss of plasma and various forms of dehydration (primary decrease in blood volume). Relative hypovolemia occurs at a later date during deposition or sequestration of blood (in septic, anaphylactic and other forms of shock).
Cardiovascular failure. This mechanism is primarily characteristic of cardiogenic shock. The main reason is a decrease in cardiac output associated with impaired contractile function of the heart due to acute myocardial infarction, damage to the valvular apparatus, arrhythmias, pulmonary embolism, etc.
Activation of the sympathetic-adrenal system arises as a result increased emissions adrenaline and norepinephrine and causes centralization of blood circulation due to spasm of arterioles, pre- and especially post-capillary sphincters, and opening of arteriovenous anastomoses. This leads to impaired organ circulation.
In the zone microcirculation Spasms of pre- and post-capillary sphincters, an increase in arteriovenous anastomoses, and blood shunting, which sharply disrupt tissue gas exchange, continue to increase. There is an accumulation of serotonin, bradykinin and other substances.

Violation of organ circulation causes the development of acute renal and liver failure, shock lung, dysfunction of the central nervous system.

Clinical manifestations of shock

Decrease in systolic blood pressure.
Decreased pulse pressure.
Tachycardia.
Reduced diuresis to 20 ml per hour or less (oligo- and anuria).
Impaired consciousness (excitement is possible at first, then lethargy and loss of consciousness).
Poor peripheral circulation (pale, cold, clammy skin, acrocyanosis, decreased skin temperature).
Metabolic acidosis.

Stages of diagnostic search

The first stage of diagnosis is to identify signs of shock based on its clinical manifestations.
The second stage is to establish the possible cause of shock based on medical history and objective signs (bleeding, infection, intoxication, anaphylaxis, etc.).
The final stage is to determine the severity of shock, which will allow us to develop patient management tactics and the scope of emergency measures.

When examining a patient at the site of development of a threatening condition (at home, at work, on the street, in a vehicle damaged as a result of an accident), the paramedic can only rely on data from an assessment of the state of the systemic circulation. It is necessary to pay attention to the nature of the pulse (frequency, rhythm, filling and tension), depth and frequency of breathing, and blood pressure level.

The severity of hypovolemic shock in many cases can be determined using the so-called Algover-Burri shock index (AI). By the ratio of pulse rate to systolic blood pressure, the severity of hemodynamic disorders can be assessed and even approximately determined the amount of acute blood loss.

Clinical criteria for the main forms of shock

Hemorrhagic shock as a variant of hypovolemic shock. It can be caused by both external and internal bleeding.
In case of traumatic external bleeding, the location of the wound is important. Heavy bleeding accompanied by injuries to the face and head, palms, soles (good vascularization and low-fat lobules).

Symptoms. Signs of external or internal bleeding. Dizziness, dry mouth, decreased diuresis. The pulse is frequent and weak. Blood pressure is reduced. Breathing is frequent and shallow. Increase in hematocrit. The rate of blood loss is of decisive importance in the development of hypovolemic hemorrhagic shock. A decrease in blood volume by 30% within 15-20 minutes and a delay in infusion therapy (up to 1 hour) lead to the development of severe decompensated shock, multiple organ failure and high mortality.

Dehydration shock (DS). Dehydration shock is a variant of hypovolemic shock that occurs with profuse diarrhea or repeated indomitable vomiting and is accompanied by severe dehydration of the body - exicosis - and severe electrolyte disturbances. Unlike other types of hypovolemic shock (hemorrhagic, burn), direct loss of blood or plasma does not occur during the development of shock. The main pathogenetic cause of DS is the movement of extracellular fluid through the vascular sector into the extracellular space (into the intestinal lumen). With severe diarrhea and repeated profuse vomiting, the loss of body fluid can reach 10-15 liters or more.

DS can occur with cholera, cholera-like variants of enterocolitis and other intestinal infections. A condition characteristic of DS can be detected at high intestinal obstruction, acute pancreatitis.

Symptoms. Signs intestinal infection, profuse diarrhea and repeated vomiting in the absence of high fever and other manifestations of neurotoxicosis.
Signs of dehydration: thirst, haggard face, sunken eyes, significant decrease in skin turgor. Characterized by a significant drop in skin temperature, frequent shallow breathing, and severe tachycardia.

Traumatic shock. The main factors in this shock are excessive pain impulses, toxemia, blood loss, and subsequent cooling.

The erectile phase is short-lived and characterized by psychomotor agitation and activation of basic functions. Clinically, this is manifested by normo- or hypertension, tachycardia, tachypnea. The patient is conscious, excited, euphoric.
The torpid phase is characterized by psycho-emotional depression: indifference and prostration, a weak reaction to external stimuli. The skin and visible mucous membranes are pale, cold sticky sweat, rapid thready pulse, blood pressure below 100 mm Hg. Art., body temperature is reduced, consciousness is preserved.

However, at present, the division into erectile and torpid phases is losing its meaning.

According to hemodynamic data, there are 4 degrees of shock:

I degree - no pronounced hemodynamic disturbances, blood pressure 100-90 mm Hg. Art., pulse up to 100 per minute.
II degree - blood pressure 90 mm Hg. Art., pulse up to 100-110 per minute, pale skin, collapsed veins.
III degree - blood pressure 80-60 mm Hg. Art., pulse 120 per minute, severe pallor, cold sweat.
IV degree - blood pressure less than 60 mm Hg. Art., pulse 140-160 per minute.

Hemolytic shock. Hemolytic shock develops from transfusions of incompatible blood (group or Rh factors). Shock can also develop when large volumes of blood are transfused.

Symptoms. During or shortly after a blood transfusion, headache, pain in lumbar region, nausea, bronchospasm, fever. Blood pressure decreases, the pulse becomes weak and frequent. The skin is pale and moist. There may be convulsions and loss of consciousness. Hemolyzed blood and dark urine are noted. After recovery from shock, jaundice and oliguria (anuria) develop. On the 2-3rd day, shock lung with signs of respiratory failure and hypoxemia may develop.

In case of Rh conflict, hemolysis occurs at a later date, and clinical manifestations are less pronounced.

Cardiogenic shock. Most common cause Cardiogenic shock is myocardial infarction.

Symptoms. Pulse is frequent and small. Impaired consciousness. Decrease in diuresis less than 20 ml/hour. Severe metabolic acidosis. Symptoms of peripheral circulatory disorders (skin pale cyanotic, moist, collapsed veins, decreased temperature, etc.).

There are four forms of cardiogenic shock: reflex, “true”, arrhythmogenic, areactive.

The cause of the reflex form of cardiogenic shock is a response to pain mediated through baro- and chemoreceptors. Mortality with erectile shock exceeds 90%. Heart rhythm disturbances (tachy- and bradyarrhythmias) often lead to the development of an arrhythmogenic form of cardiogenic shock. Most dangerous paroxysmal tachycardia(ventricular and to a lesser extent supraventricular), atrial fibrillation, complete atrioventricular block, often complicated by MES syndrome.

Infectious-toxic shock. Infectious-toxic shock is mainly a complication purulent-septic diseases, approximately 10-38% of cases. It is caused by the penetration into the bloodstream of a large number of toxins of gram-negative and gram-positive flora, damaging systems microcirculation and hemostasis.
There is a hyperdynamic phase of ITS: an initial (short-term) “hot” period (hyperthermia, activation of the systemic circulation with an increase in cardiac output with a good response to infusion therapy) and a hypodynamic phase: a subsequent, longer “cold” period (progressive hypotension, tachycardia, significant resistance Exo- and endotoxins, proteolysis products have a beneficial effect on intensive therapy. toxic effect on the myocardium, lungs, kidneys, liver, endocrine glands, reticuloendothelial system. A pronounced disturbance of hemostasis is manifested by the development of acute and subacute disseminated intravascular coagulation syndrome and determines the most severe clinical manifestations of toxic-infectious shock.

Symptoms. Clinical picture consists of symptoms of the underlying disease (acute infectious process) and symptoms of shock (drop in blood pressure, tachycardia, shortness of breath, cyanosis, oliguria or anuria, hemorrhages, hemorrhages, signs of disseminated intravascular coagulation).

Diagnosis of shock

Clinical assessment
Sometimes lactate is detected in the blood, a deficiency of bases.

Diagnosis is primarily clinical, based on evidence of inadequate tissue perfusion (stunning, oliguria, peripheral cyanosis) and evidence of compensatory mechanisms. Specific criteria include stupor, heart rate >100/min, respiratory rate >22, hypotension, or 30 mmHg. drop in baseline blood pressure and diuresis<0,5 мл/кг/ч. Лабораторные исследования в пользу диагноза включают лактат >3 mmol/l, base deficiency, and PaCO 2<32 мм рт. Однако ни один из этих результатов не является диагностическим и каждый оценивается в общем клиническом контексте, в т.ч. физические признаки. В последнее время, измерение сублингвального давления РСO 2 и ближней инфракрасной спектроскопии были введены в качестве неинвазивных и быстрых методов, которые могут измерять степень шока, однако эти методы до сих пор не подтверждены в более крупном масштабе.

Diagnosis of the cause. Knowing the cause of shock is more important than classifying the type. Often the cause is obvious or can be discovered quickly based on the history and physical examination, using simple testing techniques.

Chest pain (with or without shortness of breath) suggests MI, aortic dissection, or pulmonary embolism. A systolic murmur may indicate ventricular rupture, atrial septal rupture, or mitral valve regurgitation due to acute MI. A diastolic murmur may indicate aortic regurgitation due to aortic dissection involving the aortic root. Cardiac tamponade can be judged by the jugular vein, muffled heart sounds and paradoxical pulsation. Pulmonary embolism is severe enough to cause shock, usually causes a decrease in O2 saturation, and is more common in characteristic situations, including. with prolonged bed rest and after surgery. Tests include ECG, troponin I, chest x-ray, blood gases, lung scan, spiral CT, and echocardiography.

Abdominal or back pain suggests pancreatitis, rupture of an abdominal aortic aneurysm, peritonitis, and in women of childbearing age, rupture of an ectopic pregnancy. A pulsatile mass in the midline of the abdomen suggests an abdominal aortic aneurysm. A tender adnexal mass on palpation suggests an ectopic pregnancy. Testing usually includes a CT scan of the abdomen (if the patient is unstable, bedside ultrasound may be used), a complete blood count, amylase, lipase and, for women of childbearing age, a urine pregnancy test.

Fever, chills, and focal signs of infection suggest septic shock, especially in immunocompromised patients. Isolated fever depends on medical history and clinical conditions and may indicate heatstroke.

In several patients the cause is unknown. Patients who do not have focal symptoms or signs suggestive of a cause should have an ECG, cardiac enzymes, chest x-ray, and blood gas studies. If the results of these tests are normal, the most likely causes are drug overdose, obscure infections (including toxic shock), anaphylaxis, and obstructive shock.

Prognosis and treatment of shock

If left untreated, shock is fatal. Even with treatment, mortality from cardiogenic shock after MI (60% to 65%) and septic shock (30% to 40%) is high. The prognosis depends on the cause, pre-existing or complication of the disease, the time between onset and diagnosis, as well as the timeliness and adequacy of therapy.

General guidance. First aid is to keep the patient warm. Monitor external hemorrhages, check the airway and ventilation, and provide respiratory assistance if necessary. Nothing is given by mouth, and the patient's head is turned to one side to avoid aspiration if vomiting occurs.

Treatment begins at the same time as the assessment. Additional O 2 is delivered through the mask. If shock is severe or ventilation is inadequate, intubation of the airway with mechanical ventilation is necessary. Two large (16- to 18-gauge) catheters are inserted into separate peripheral veins. A central venous line or intraosseous needle, especially in children, provides an alternative when peripheral venous access is not available.

Typically, 1 L (or 20 ml/kg in children) of 0.9% saline is infused over 15 minutes. For bleeding, Ringer's solution is usually used. If clinical parameters do not return to normal levels, the infusion is repeated. Smaller volumes are used for patients with signs of high right-sided pressure (eg, distension of the jugular veins) or acute myocardial infarction. This strategy and volume of fluid administration should probably not be used in patients with signs of pulmonary edema. In addition, infusion therapy against the background of the underlying disease may require monitoring of central venous pressure or blood pressure. Bedside ultrasound of the heart to evaluate the contractility of the vena cava.

Critical illness monitoring includes ECG; systolic, diastolic and mean blood pressure, intra-arterial catheter is preferred; control of breathing rate and depth; pulse oximetry; installation of a permanent renal catheter; monitoring body temperature, and assessing clinical condition, pulse volume, skin temperature and color. Measurement of central venous pressure, pulmonary arterial pressure, and thermodilution of cardiac output using the balloon tip of a pulmonary artery catheter may be useful in the diagnosis and initial treatment of patients with shock of undetermined or mixed etiology or with severe shock, especially with oliguria or pulmonary edema. Echocardiography (bedside or transesophageal) is a less invasive alternative. Serial measurements of arterial blood gases, hematocrit, electrolytes, serum creatinine, and blood lactate. Sublingual CO 2 measurement, when available, is a non-invasive monitoring of visceral perfusion.

All parenteral drugs are given intravenously. Opioids are generally avoided because they can cause blood vessels to dilate. However, severe pain can be treated with morphine 1 to 4 mg intravenously over 2 minutes and repeated over 10 to 15 minutes if necessary. Although cerebral hypoperfusion may be concerning, sedatives or tranquilizers are not prescribed.

After initial resuscitation, specific treatment is aimed at the underlying disease. Additional supportive care depends on the type of shock.

Hemorrhagic shock. In hemorrhagic shock, surgical control of bleeding is the first priority. Intravenous resuscitation accompanies, rather than precedes, surgical control. Blood products and crystalloid solutions are used for resuscitation, however, packed red blood cells and plasma are considered first in patients who will require a 1:1 mass transfusion. Lack of response usually indicates insufficient volume or an unrecognized source of bleeding. Vasopressor agents are not indicated for the treatment of hemorrhagic shock if cardiogenic, obstructive, or distributive causes are also present.

Distribution shock. Distributive shock with profound hypotension after initial fluid resuscitation with 0.9% saline can be treated with inotropes or vasopressors (eg, dopamine, norepinephrine). Parenteral antibiotics should be used after blood samples are collected for culture. Patients with anaphylactic shock do not respond to fluid infusion (especially if accompanied by bronchospasm), they are shown epinephrine, and then epinephrine infusion.

Cardiogenic shock. Cardiogenic shock caused by structural abnormalities is treated surgically. Coronary thrombosis is treated either by percutaneous intervention (angioplasty, stenting), if a multi-vessel lesion of the coronary arteries is detected (coronary artery bypass grafting) or thrombolysis. For example, tachyform of atrial fibrillation, ventricular tachycardia are restored by cardioversion or medications. Bradycardia is treated by implantation of a percutaneous or transvenous pacemaker; atropine can be given intravenously in up to 4 doses over 5 minutes while awaiting pacemaker implantation. Isoproterenol may sometimes be prescribed if atropine is ineffective, but is contraindicated in patients with myocardial ischemia due to coronary artery disease.

If pulmonary artery occlusion pressure is low or normal, shock after acute MI is treated with volume expansion. If the pulmonary artery catheter is not in place, infusions are carried out with caution, while auscultation of the chest is performed (often accompanied by signs of overload). Shock after right ventricular infarction is usually accompanied by partial volume expansion. However, vasopressor agents may be necessary. Inotropic support is most preferred in patients with normal or above-normal filling. Tachycardia and arrhythmia sometimes occur during dobutamine administration, especially at higher doses, which requires a dose reduction of the drug. Vasodilators (eg, nitroprusside, nitroglycerin), which increase venous capacitance or low systemic vascular resistance, reduce stress on the damaged myocardium. Combination therapy (eg, dopamine or dobutamine with nitroprusside or nitroglycerin) may be more beneficial but requires frequent ECG and pulmonary and systemic hemodynamic monitoring. For more severe hypotension, norepinephrine or dopamine may be given. Intraballoon counterpulsation is a valuable method for temporarily relieving shock in patients with acute myocardial infarction.

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