What Is the Treatment for Cardiogenic Shock?

Cardiogenic shock refers to a group of syndromes that cause a significant decrease in cardiac output and cause severe acute peripheral circulatory failure due to the extreme decrease in cardiac function. Cardiogenic shock is the extreme manifestation of cardiac pump failure. Due to the failure of cardiac drainage, the blood pressure cannot be maintained due to the failure to maintain its minimum cardiac output. The blood supply to important organs and tissues is severely insufficient, causing systemic microcirculatory dysfunction. As a result, a series of pathophysiological processes characterized by ischemia, hypoxia, metabolic disorders and important organ damage. The mortality rate of this disease is extremely high, domestic reports are 70% to 100%, timely and effective comprehensive rescue can increase patient survival rate.

Basic Information

English name

cardiogenic shock

Visiting department

Cardiology

Common locations

heart

Common causes

Extremely reduced myocardial contractility, ventricular ejection disorder, ventricular filling disorder, low exhaust syndrome after open heart surgery

Common symptoms

Ischemia, hypoxia, metabolic disorders, important organ damage

Contagious

no

Causes of cardiogenic shock

1. Extremely reduced myocardial contractility

Including large-scale myocardial infarction, acute fulminant myocarditis (viral, diphtheria, and a few rheumatic myocarditis, etc.), primary and secondary cardiomyopathy (the former includes dilated, restricted, and hypertrophic cardiomyopathy; the latter Including various infections, thyrotoxicosis, cardiomyopathy caused by hypothyroidism), familial storage diseases and infiltration (hemochromatosis, glycogen storage disease, mucopolysaccharidosis, amyloidosis, connective tissue disease), family Hereditary diseases (muscular dystrophy, hereditary ataxia), pharmacological and toxic allergic reactions (radiotherapy and myocardial damage caused by doxorubicin, alcohol, quinidine, antimony, emmetine, etc.), myocardium Inhibitors (severe hypoxia, acidosis, drugs, infectious toxins), drugs (calcium channel blockers, -blockers, etc.), advanced heart valve disease, severe arrhythmia (ventricular flutter or fibrillation), and various End-stage manifestations of heart disease.

Ventricular ejection disorder

Including massive or multiple large-area pulmonary infarction (the emboli are derived from thrombus, amniotic fluid, fat plugs, air emboli, tumor thrombi, right endocardial neoplasia or tumor shedding, etc. from the body vein or right heart cavity), Rupture of the papillary muscles or chordae, severe heart valve insufficiency caused by valve perforation, severe aortic or pulmonary stenosis (including supravalvular or subvalvular stenosis).

3. Ventricular filling disorder

Including acute pericardial tamponade (acute fulminant exudative pericarditis, pericardial hemorrhage, aortic sinus tumor or aortic dissection hematoma breaking into the pericardial cavity, etc.), severe mitral and tricuspid valve stenosis, and atrial tumors (common such as mucus Tumor) or spherical thrombus incarcerated in the atrioventricular port, intraventricular space occupying lesions, restricted cardiomyopathy, etc.

4.hybrid

That is, there can be two or more causes in the same patient at the same time, such as acute myocardial infarction complicated by ventricular septal perforation or papillary muscle rupture. The cause of cardiogenic shock is both myocardial contractility and ventricular septal perforation or papillary muscle. Hemodynamic abnormalities caused by fracture. Another example is the shock caused by rheumatic activity in patients with severe rheumatic mitral stenosis and aortic valve insufficiency. There are both factors that reduce myocardial contractility due to rheumatic myocarditis and hemodynamics due to ventricular ejection and filling disorders. Learn disorder factors.

5. Low exhaust syndrome after open heart surgery

Most patients are caused by the inability of the heart to adapt to the increased preload after surgery. The main reasons include poor cardiac function, damage to the myocardium during surgery, subendocardial bleeding or preexisting myocardial degeneration and necrosis, incomplete correction of cardiac surgery, and arrhythmia. Certain anatomical changes caused by surgery, such as obstruction of left ventricular outflow tract and low blood volume after artificial spherical aortic valve replacement, cause a sharp decrease in cardiac output and shock.

Clinical manifestations of cardiogenic shock

Clinical staging

According to the occurrence and development of cardiogenic shock, it can be roughly divided into early, middle and late periods.

(1) In the early stage of shock, because the body is in a stress state, a large amount of catecholamine is secreted into the blood, and the excitability of sympathetic nerves is increased. Patients often show irritability, fear, and nervousness, but they are sober, complexion, or pale or slightly cyanose, The extremities are damp and cold, sweating, and the heart rate increases, and may have nausea and vomiting. Normal blood pressure may even increase slightly or slightly, but the pulse pressure becomes smaller and the urine output slightly decreases.

(2) If the shock is not corrected early in the middle stage of shock, the symptoms of shock will be further aggravated, the patient's expression is indifferent, the reaction is slow, the consciousness is weak, the whole body is weak, the pulse is weak or unable to reach, the heart rate often exceeds 120 times / minute, and the contraction Pressure <80mmHg (10.64kPa), even pulse pressure <20mmHg (2.67kPa), pale pale hair, wet or cold skin, or marble-like changes, less urine output (<17mL / h) or no urine.

(3) In the later stage of shock, symptoms of disseminated intravascular coagulation (DIC) and multiple organ failure may occur. The former can cause extensive bleeding of the skin, mucous membranes and internal organs; the latter can be manifested as the corresponding symptoms of acute organ dysfunction or failure such as acute kidney, liver and brain. Such as acute renal failure can be manifested as oliguria or urinary occlusion, blood urea nitrogen creatinine increased progressively, and produce symptoms such as metabolic acidosis of uremia; fixed proportion of urine, proteinuria and cast can appear. Pulmonary failure can be manifested by progressive dyspnea and cyanosis, oxygen insufficiency can relieve symptoms, shallow and regular breathing, snoring and reduced respiratory sounds can be heard at the bottom of both lungs, and signs of acute respiratory distress syndrome can occur. Brain dysfunction and failure can cause signs of coma, convulsions, limb paralysis, pathological neuroreflexes, varying pupil sizes, cerebral edema, and respiratory depression. Liver failure can cause jaundice, liver damage, bleeding tendency, and even coma.

2. Shock Degree Division

According to the severity of shock, it can be roughly divided into mild, moderate, severe and extremely severe shock.

(1) Patients with mild shock are clear-headed but irritable, pale, dry mouth, sweating, heart rate> 100 beats / minute, strong pulse rate, warm limbs, but slightly cyanotic and cold limbs, systolic blood pressure 80mmHg (10.64kPa), slightly reduced urine output, pulse pressure <30mmHg (4.0kPa).

(2) Mild shock, pale face, indifferent expression, chills in extremities, cyanosis of extremities, systolic blood pressure of 60-80mmHg (8-10.64kPa), pulse pressure <20mmHg (2.67kPa), urine output decreased significantly (<17mL / h).

(3) Severe shock , unconsciousness, blurred consciousness, unresponsiveness, pale hair cyanosis, cold cyanosis of limbs, marble-like changes in skin, heart rate> 120 beats / min, dull heart sounds, weak pulses or slight pressure Disappeared, systolic blood pressure decreased to 40-60 mmHg (5.32 to 8.0 kPa), urine output decreased significantly, or urine was closed.

(4) Very severe shock , unconsciousness, coma, shallow and irregular breathing, cyanosis of lips and skin, cold limbs, very weak or impaired pulse, dull or monophonic heart sound, systolic blood pressure <40mmHg (5.32kPa ), No urine, there may be extensive bleeding of the skin and mucous membranes and internal organs, and signs of multiple organ failure appear.

3. Other clinical manifestations

Due to the different etiology of cardiogenic shock, in addition to the clinical manifestations of shock described above, there are other clinical manifestations. Taking acute myocardial infarction as an example, this disease mostly occurs in middle-aged and elderly people, often with severe pain in the precardiac area, which can last for several hours, with nausea, vomiting, sweating, severe arrhythmia and heart dysfunction, even due to acute cerebral insufficiency Can produce signs of stroke. Physical signs include a mild to moderate expansion of the heart dullness, a low first heart sound, and a third or fourth heart sound galloping rhythm; if the papillary muscle dysfunction or chordae rupture is complicated, a rough systolic period may appear in the apical area Reflux murmurs; those with concomitant ventricular septal perforation in the 3rd and 4th intercostal space of the left margin of the sternum have a loud systolic murmur, and moist sounds can be heard at the bottom of both lungs.

Cardiogenic shock test

Blood routine

Leukocytosis, generally at (10-20) × 10 ⁹ / L (10000-20,000 / mm ³ ), increased neutrophils, decreased or disappeared eosinophils, and increased hematocrit and hemoglobin often indicate blood concentration. In the presence of disseminated intravascular coagulation, the platelet count decreased progressively, and the coagulation time was prolonged.

2. Urine routine and renal function tests

Urine volume decreases, proteinuria, red blood cells, white blood cells, and casts can appear. When acute renal failure is complicated, the relative density (specific gravity) of urine changes from an initial high to a low and is fixed at 1.010 to 1.012. Blood urea nitrogen and creatinine increase, and urine The ratio of creatinine / blood creatinine is often reduced to 10, the osmotic pressure of urine is reduced, so that the urinary / blood osmotic pressure ratio is less than 1.5, and the urinary / blood urea ratio is less than 15, which may increase the sodium in urine.

3. Serum electrolyte acid-base balance and blood gas analysis

Serum sodium can be low, serum potassium can vary, serum potassium can be significantly increased during oliguria, and metabolic acidosis and respiratory alkalosis can occur early in shock. In the middle and late stages of shock, metabolic acidosis is often accompanied by respiratory acidosis, blood pH decreases, oxygen partial pressure and blood oxygen saturation decrease, carbon dioxide partial pressure and carbon dioxide content increase, and the normal blood lactic acid content is 0.599 to 1.78mmol / L (5.4 ~ 16mg / dL), if it rises to 2 ~ 4mmol / L, it indicates mild hypoxia, the microcirculation is basically good, and the prognosis is good; if the blood lactic acid content is> 4mmol / L, it means that the microcirculation has been exhausted and is already in Moderate hypoxia; if> 9mmol / L, microcirculation has failed, severe hypoxia, and poor prognosis. In addition, during severe shock, blood free fatty acids often increase significantly.

4. Serum enzyme test

In patients with acute myocardial infarction and cardiogenic shock, serum aspartate aminotransferase (AST / GOT), lactate dehydrogenase (LDH) and its isoenzyme LDH1, phosphocreatine kinase (CPK) and its The isoenzymes CPK-MB were significantly increased, especially the latter, whose sensitivity and specificity were extremely high, reaching 100% and 99%, respectively. The increase and duration of the increase were helpful for judging the scope and severity of infarction. Late shock If the liver function is complicated, alanine aminotransferase (ALT, alanine aminotransferase, GPT) can be increased and the corresponding liver function test abnormal.

5. Determination of myocardial myosin light chain, myoglobin and cardiac specific troponin

Myocardial myosin light chain is increased during acute myocardial infarction. Humans mainly measure myocardial myosin light chain I (LCI). The normal value is (3.7 ± 0.9) µg / L [(3.7 ± 0.9) ng / ml], The blood and urine myoglobin content increased, and the increase was positively correlated with the infarct size, and it was earlier than the serum enzyme change, which has very high sensitivity and specificity. The cardiac troponin (cT-nT, cTnI) measurement It is a very specific marker for early diagnosis of myocardial infarction. Normal myocardial troponin I (cTnI) has a normal value of <4µg / L, and acute myocardial infarction can increase significantly within 3 to 6 hours, often exceeding 165µg / L; myocardium Troponin T (cTnT) normal value <1ng / L, acute myocardial infarction or myocarditis, necrosis can often increase significantly.

6. Examination of disseminated intravascular coagulation (DIC)

DIC is often complicated by advanced shock. In addition to the progressive decline in platelet count and related platelet dysfunctions (such as platelet adhesion and aggregation dysfunction, blood clot retraction defects, etc.), the following changes can be made: prolonged prothrombin time, fibrinogen Often reduced, thrombin clotting time is> 3s compared with normal control plasma, whole blood clotting time is more than 10 minutes, and coagulation factors , , , , , are all reduced, because DIC is often accompanied by secondary fibers Hyperlysis, the following tests can be done to indirectly explain the existence of DIC, including shortening the dissolution time of whole blood clots (no dissolution within 72 hours in normal people), determination of fibrin (proto) degradation products (FDP), commonly used clinically such as The plasma protamine side agglutination test (3P test) is positive. The normal reference value of the Fi test (that is, the determination of fibrin degradation products) is less than 1: 8. When it is greater than 1:16, it has diagnostic value. In addition, it can also be used for tanned red blood cell agglutination inhibition immunoassay, ethanol gel test, etc., DIC is often positive.

7. Hemorheology

The blood flow is slow during shock, the effective blood volume is reduced, blood stagnation in capillaries, and plasma extravasation, blood concentration and viscosity increase, so the determination of whole blood and / or plasma specific viscosity often increases. When combined with DIC, the initial state was hypercoagulation, and then it became hypocoagulation when fibrinolysis was increased.

8. Inspection of microcirculation perfusion

Clinically used indicators are:

(1) The temperature difference between the skin and the anus Skin vasoconstriction, the skin temperature significantly decreases, and the anus temperature does not decrease or even increases, which makes the temperature difference between the two increase. The temperature of the skin and the anus is measured separately. Under normal circumstances, the former is 0.5 ° C lower than the latter. Right and left, when the temperature difference is> 1.5 ° C, it usually means that the shock is severe; when it is greater than 3 ° C, it means that the microcirculation is already in a state of exhaustion.

(2) Fundus and nail wrinkle examination Fundus examination reveals arteriolar spasm and venous dilatation, and retinal edema may occur in severe cases. The nail wrinkle examination is usually performed on an unnamed nail wrinkle under a light microscope illuminated by a special cold light source. Tissue microvascular arrangement, morphology, and response to stimulation and compression. Due to vasoconstriction in shock patients, the number of tube ridges in the nail veins is significantly reduced, the arrangement is disordered, the blood flow is slow, and microthrombosis may occur. Blood cells often aggregate into small particles, and even aggregate into floc, and pressurize on the nails. After relaxation, we can see that the blood flow filling time in the capillaries is prolonged.

(3) Hematocrit examination When the hematocrit of peripheral peripheral blood is 0.03vol (3vol%) higher than that of central venous hematocrit, it indicates that peripheral blood vessels have contracted significantly.

The measurement of the above indicators of microcirculation is of reference value for judging the severity of microcirculation disorders during shock and the reasonable selection of vasoactive drugs.

9. ECG and ECG examination

Electrocardiogram is helpful for the diagnosis of acute myocardial infarction complicated by cardiogenic shock. The typical person often has pathological Q wave, ST segment elevation and T wave inversion. It must be pointed out that 20% to 30% of patients with acute myocardial infarction may have no pathological Q wave (no Q wave myocardial infarction), so the diagnosis should be made in conjunction with clinical manifestations and serum enzymes and cardiac troponin. It is generally believed that the specificity and sensitivity of the electrocardiogram for the diagnosis of acute myocardial infarction are about 80%, which is of great help in estimating the location, extent and evolution of the disease. Therefore, in case of shock of unknown cause, routine electrocardiogram should be performed to rule out myocardial infarction.

Cardiac vector diagrams may show changes in the QRS ring during acute myocardial infarction, and changes in the ST vector and T ring. The changes in the QRS ring are mainly reflected by the starting vector pointing in the opposite direction of the infarct region; the appearance of the ST vector is shown by the QRS ring. Closed, its end point does not return to the starting point, the line from the start point to the end point of the QRS ring is the direction of the ST vector, and points to the infarct area; the change of the T ring mainly manifests in the direction where the maximum vector is opposite to the maximum average vector of QRS or QRS- The T angle increases, and the T-ring length / width ratio is less than 2.6: 1. The T-ring centrifugal branch runs at the same speed as the homing branch. The ECG can only be used as an auxiliary examination when it is difficult to diagnose the ECG.

10. Echocardiography and Doppler

Regardless of M-mode or two-dimensional echocardiography, it can often be found that the amplitude of the ventricular wall movements affected by acute myocardial infarction is reduced or contradictory, and the myocardium in the non-infarcted area often has compensatory movement enhancement; when combined with ventricular wall tumors, papillary muscles Insufficient function, tendon cord rupture or ventricular septal perforation often have characteristic ultrasound signs. At this time, pulse Doppler or continuous Doppler can detect abnormal turbulence or turbulence signals, and diagnose ventricular septal perforation and acute mitral. Incomplete valve closure is helpful. The application of color Doppler flow imaging technology combined with two-dimensional echocardiography can detect abnormal blood flow beams in real time, and can semi-quantitatively estimate ventricular septal perforation and mitral The magnitude of valve counterflow is of great value in the diagnosis of some complications of acute myocardial infarction. In addition, non-invasive measurement of cardiac function through echocardiography is also helpful in assessing the condition.

11. Radionuclide myocardial imaging

Myocardial imaging is a technique that uses some radionuclides or their markers to directly display myocardial morphology. There are two types of myocardial imaging methods due to the different imaging agents: one is the concentration of normal myocardium and reflects functional Radionuclide of myocardial tissue such as cesium ¹³¹ ( ¹³¹ Cs), plutonium ²⁰¹ ( ²⁰¹ Tl), etc. If local myocardial blood flow is impaired, myocardial cell necrosis or scar tissue formation, there is no function to absorb such radionuclide The radioactive "cold zone", which shows no radionuclide, is called "cold zone imaging". The other is exactly the opposite. It can be taken up by fresh infarcted myocardial tissue, but normal myocardium is not developed, such as ^90m Tc. -Pyrophosphate, etc., shows a radioactive "hot zone" at the site of the lesion, so it is called "hot zone imaging". The nuclide myocardial imaging can directly show the location, size and morphology of the infarcted zone, showing the lesions more intuitively. It is an important supplement for enzymology and other tests. In addition, it is still possible to evaluate the cardiac function status through radionuclide angiography and blood pool imaging.

12.X-ray inspection

In particular, wave counting photography and selective ventricular angiography can help to estimate the condition of myocardial infarction. Emergency coronary angiography is not only of great value in determining coronary lesions associated with myocardial infarction, but also for thrombolytic therapy, percutaneous coronary balloon Dilatation and coronary bypass surgery provide information. In addition, bedside X-ray chest examination can also detect the signs of pulmonary congestion and pulmonary edema to evaluate the state of cardiac function and the differential diagnosis such as pulmonary infarction, myocarditis, cardiomyopathy, aortic dissection and complications, such as the discovery of pneumonia It also helps to a certain extent. In recent years, through other imaging technologies, such as computer computed tomography, tomography (CT), ultra high-speed CT (UFCT), magnetic resonance and digital subtraction cardiovascular angiography, etc., Complications and the identification of cardiogenic shock from other causes are helpful.

13. Hemodynamic monitoring

A floating catheter with a balloon at the top was successfully developed in 1970, which overcomes the main limitations of classic right heart catheterization, makes intubation simpler and safer, and can be monitored at the bedside. It can diagnose and treat myocardial infarction and pump failure (especially left Heart failure and cardiogenic shock) have played a role and have been widely used in clinical practice in recent years.

Cardiogenic shock diagnosis

1. Severe basic heart disease (extensive myocardial infarction, myocarditis, tamponade, arrhythmia, mechanical valve failure, etc.).

2. Typical clinical manifestations of shock (hypotension, oliguria, altered consciousness, etc.).

3. After active volume expansion treatment, hypotension and clinical symptoms did not improve or worsen.

4. Hemodynamic indicators meet the following typical characteristics

(1) The mean arterial pressure is <8KPa (60mmHg).

(2) The central venous pressure is normal or high.

(3) The left ventricular end-diastolic filling pressure or pulmonary capillary wedge pressure is elevated.

(4) Cardiac output is extremely reduced.

Differential diagnosis of cardiogenic shock

Acute myocardial infarction and cardiogenic shock are sometimes associated with acute pericarditis, especially acute non-specific pericarditis, acute cardiac tamponade, acute pulmonary embolism, aortic dissection, and certain acute abdominal conditions such as acute pancreatitis and peptic ulcer , Acute cholecystitis, cholelithiasis and other diseases for identification.

Cardiogenic shock complications

Respiratory failure

The formation of shock lungs is related to many factors: insufficient capillary perfusion in the lungs causes swelling of type alveolar cells and capillary endothelial cells, thickening of the air-blood flow barrier in the lungs; damage to the alveolar capillary endothelium, and increased permeability. Interstitial edema caused by pulmonary congestion; disseminated intravascular coagulation occurs in the pulmonary circulation; large amounts of endotoxins in the intestine act on the lungs through the blood; severe trauma, infection, improper infusion and infusion of stock blood, unreasonable oxygen supply, etc. , May also be related to "shock lung".

2. Renal failure

Shock can directly affect the blood perfusion of the kidney, cause renal functional and organic lesions, lead to decreased urine output, and can cause acute renal failure in severe cases, which in turn directly aggravates shock.

3. Cardiovascular complications

Severe shock can cause myocardial infarction during the course of disseminated intravascular coagulation, and produce corresponding clinical manifestations, such as chest pain, chest tightness, chest tightness, and cardiogenic shock.

4. Arrhythmia

In the electrocardiogram of shock patients, various arrhythmias occurred in 89.3%. Sinus tachycardia, supraventricular tachycardia, preatrial contraction, preventricular contraction, ventricular fibrillation, and conduction block were seen.

5. Neurological complications

When the mean arterial pressure drops below 50 mmHg, insufficient cerebral perfusion flow can cause damage to brain tissue and dysfunction. If the cerebral circulation cannot be re-established in a short time, cerebral edema will continue to develop, such as the mean arterial pressure continues to decrease or If the fall time is too long (more than 5-10 minutes), it can cause brain cell damage, necrosis and brain failure.

6. Gastrointestinal complications

Liver blood flow is reduced during liver shock, liver function is impaired, and hepatic lobular central necrosis can occur, which can progress to massive liver necrosis, eventually leading to liver failure. In cardiogenic shock, insufficient perfusion of the gastrointestinal tract can not only cause digestion Absorption dysfunction can also cause mucosal edema, hemorrhage, necrosis, concurrent stress ulcers and acute hemorrhagic enteritis.

7. Diffuse intravascular coagulation (DIC)

Cardiogenic shock can easily lead to slow systemic blood flow, stagnant blood flow, and easily cause thrombosis, even microthrombosis. Microvascular embolism in the myocardium, myocardial cell degeneration and necrosis, myocardial rupture and acute myocardial infarction have been diseased during DIC. It is confirmed by physical science that bleeding, shock, multiple microthrombosis, and multiple microangiopathy hemolysis can occur clinically.

Cardiogenic shock treatment

Treatment principle

Once the diagnosis of acute myocardial infarction with cardiogenic shock is established, the basic treatment principles are as follows:

(1) Absolute bed rest immediately inhale oxygen immediately, effectively relieve pain, establish intravenous drug delivery channels as soon as possible, conduct ECG monitoring and establish necessary hemodynamic monitoring as quickly as possible, indwelling urinary tubes to observe urine volume, and actively treat symptomatically and Strengthen supportive care.

(2) Expansion of blood volume If there is a low blood volume state, expand blood volume first. If combined with metabolic acidosis, 5% sodium bicarbonate should be given in time to correct water and electrolyte disorders. According to the cardiac function status and hemodynamic monitoring data, the infusion volume and infusion speed were estimated. Under normal circumstances, the total daily fluid replacement should be controlled at 1500 ~ 2000mL.

(3) Use of vasoactive drugs After replenishing blood volume, if shock is still not relieved, vasoactive drugs should be considered. Commonly used drugs include dopamine, dobutamine, m-hydroxylamine, norepinephrine, nitroglycerin, and sodium nitroprusside.

(4) Minimize the scope of myocardial infarction to save dying and severe ischemic myocardium. These measures include intravenous and / or intracoronary thrombolytic therapy, emergency percutaneous coronary angioplasty (PTCA) and coronary bypass surgery. Surgery.

(5) Active treatment of complications such as arrhythmia and prevention of brain, lung, liver and other important organ failure, prevention and treatment of secondary infections.

(6) At the same time or in the case of ineffective treatment with other drugs, conditionally units can use mechanical assisted circulation, such as intra-aortic balloon counterpulsation, left ventricular assist pump or double-ventricular assist pump, and even perform artificial heart and heart transplantation. Surgery, etc.

2. General treatment

(1) Analgesics must be closely observed when applying analgesics. Patients' blood pressure may rise after analgesia, but they must be aware of possible side effects caused by these drugs, including hypotension, nausea, vomiting, respiratory depression, hypoxia and increased carbon dioxide tension, and heartbeat. Wait too slowly. When applying analgesics, sedatives such as diazepam and phenobarbital can be used as appropriate, which can not only strengthen the efficacy of analgesics, but also reduce the tension and psychological burden on patients.

(2) Oxygen supply Patients with acute myocardial infarction should routinely inhale oxygen and keep the airway open to correct hypoxemia and maintain normal or near-normal partial pressure of oxygen, which is conducive to reducing the scope of infarction and improving myocardial function.

(3) Volume expansion therapy (supplementing blood volume) Shock patients have hypovolemia (including absolute or relative deficiency), and about 20% of patients with acute myocardial infarction due to vomiting, sweating, fever, use of diuretics, and eating less, etc. As a result, the blood volume is absolutely insufficient. An intravenous infusion channel should be established first to quickly replenish effective blood volume to ensure cardiac output, which is one of the key measures to correct shock.

3. Vasoactive drugs and positive inotropic drugs

(1) Vasoactive drugs mainly refer to two categories of vasodilators and vasoconstrictors: one class dilates blood vessels and the other class vasoconstrictors. The two functions are very different, but they are widely used in the treatment of shock.

(2) Positive inotropic drugs Pump failure caused by acute myocardial infarction is mainly based on the application of morphine or pethidine and diuretics. Vasodilators can also be used to reduce the pre- and post-load of the heart. If pump failure is still difficult to control after the above treatments, non-digitalis positive inotropic drugs can be considered. However, some people think that if the heart is enlarged and other drugs are not effective, fast-acting digitalis preparations can also be used as appropriate.

4. Some progress in drug treatment of shock

In recent years, new anti-shock drugs have been continuously introduced, coupled with the in-depth understanding of shock, a new understanding of the anti-shock effect of certain drugs.

(1) Naloxone Many neuropeptides play a role in mediating cardiovascular responses in a variety of shock states. -endorphin levels in the blood increase during shock, it inhibits cardiovascular function through the central opioid receptor, and reduces blood pressure; naloxone is an opioid blocker, so it can reverse the shock state.

(2) Fructose 1,6-diphosphate Fructose 1,6-diphosphate is an important intermediate in glucose metabolism. It can promote the rebuilding of high-energy groups in cells and can be used as an adjuvant therapy for cardiogenic shock.

(3) Angiotensin-converting enzyme inhibitors (ACEI) Application of angiotensin-converting enzyme inhibitors can antagonize the aforementioned effects of angiotensin II. Commonly used preparations include captopril, enalapril and the like.

5.Mechanical auxiliary circulation

At present, the most widely used in domestic is aortic balloon counterpulsation (IABP). Its principle is to insert an inflatable balloon catheter into the thoracic aorta and use the QRS wave of the patient's electrocardiogram to trigger the counterpulsation, so that the balloon is in systole Exhaust to reduce aortic systolic pressure and cardiac afterload; diastolic balloon inflation significantly increases aortic diastolic pressure, increases coronary diastolic perfusion, improves myocardial oxygen supply and promotes collateral circulation to reduce myocardium Necrotic area and improved cardiac function. If internal aortic balloon counterpulsation is performed after the medical treatment fails or the shock is quite severe, the rescue time is often lost. At present, intra-aortic balloon counterpulsation has become one of the important measures to maintain the circulation before, during and after emergency PTCA and coronary bypass surgery.

6. Etiology treatment

Etiological treatment is a key measure for the reversal of cardiogenic shock, such as emergency percutaneous coronary angioplasty (PTCA) and coronary bypass surgery (CABG) for acute myocardial infarction. These new measures have opened a new era for the treatment of myocardial infarction. .

7. Prevention and treatment of complications and vital organ failure

Early prevention and treatment of complications and vital organ failure is also one of the important measures for the treatment of cardiogenic shock. The combined water, electrolyte and acid-base balance imbalance should be treated accordingly. If secondary infection occurs, clinically, respiratory infection and urinary tract infection are the most common, and appropriate antibiotics should be selected for treatment according to bacterial drug sensitivity tests.

Cardiogenic shock prognosis

The cardiogenic shock hospital mortality rate is mostly above 80%. In recent years, various early coronary reperfusion and blood pressure maintenance measures have been carried out to reduce the mortality rate, but cardiogenic shock is still the main cause of hospital deaths in patients with acute myocardial infarction. In recent years, in the treatment of acute myocardial infarction, due to timely detection of fatal arrhythmia and effective treatment, the number of deaths from arrhythmia has been greatly reduced, and pump failure has become the main cause of death.