Cardiogenic shock

Introduction to cardiogenic shock Cardiogenic shock is the extreme manifestation of heart pump failure. Due to cardiac dysfunction, it is unable to maintain its minimum cardiac output, resulting in a decrease in blood pressure, severely insufficient blood supply to important organs and tissues, and systemic microscopy. Circulatory dysfunction, resulting in a series of pathophysiological processes characterized by ischemia, hypoxia, metabolic disorders and important organ damage. basic knowledge The proportion of illness: 7% to 10% (the incidence of cardiogenic shock in patients with acute myocardial infarction is 7% to 10%) Susceptible people: no specific population Mode of infection: non-infectious Complications: disseminated intravascular coagulation acute renal failure arrhythmia stress ulcer

Cause of cardiogenic shock

Myocardial contractility is extremely reduced (15%):

Including large area myocardial infarction, acute fulminant myocarditis (such as viral, diphtheria and a few rheumatic myocarditis, etc.), primary and secondary cardiomyopathy (the former includes dilated, restrictive and hypertrophic cardiomyopathy; Including various infections, thyrotoxicosis, hypothyroidism), familial storage diseases and infiltration (such as hemochromatosis, glycogen storage disease, mucopolysaccharidosis, amyloidosis, connective tissue disease), family hereditary Diseases (such as muscular dystrophy, hereditary ataxia), drug and toxicity, allergic reactions (such as radiation, doxorubicin, alcohol, quinidine, expectorant, imipenem, etc.), myocardial damage Inhibitory factors (such as severe hypoxia, acidosis, drugs, toxins), drugs (such as calcium channel blockers, beta blockers, etc.), advanced valvular heart disease, severe arrhythmia (such as ventricular flutter or tremor ), as well as the end-stage performance of various heart diseases.

Ventricular ejection disorder (9%):

Including large or multiple large-area pulmonary infarction (the source of the embolus includes thrombus from the body vein or right heart cavity, amniotic fluid embolism, fat plug, air embolism, tumor thrombus and right heart endocarditis, or tumor shedding, etc.) , papillary muscle or chordae rupture, severe heart valve insufficiency caused by valve perforation, severe aortic or pulmonary stenosis (including valvular, valvular or subvalvular stenosis).

Ventricular filling disorder (20%):

Including acute pericardial tamponade (acute fulminant exudative pericarditis, pericardial hemorrhage, aortic sinus aneurysm or aortic dissection into the pericardial cavity, etc.), severe second, tricuspid stenosis, atrial tumor (common such as mucus Tumor) or spherical thrombus incarcerated in the atrioventricular mouth, intraventricular space-occupying lesions, restrictive cardiomyopathy.

Mixed type (5%):

That is, the same patient can have two or more causes at the same time, such as acute myocardial infarction complicated by interventricular septal perforation or papillary muscle rupture. The cause of cardiogenic shock is both myocardial contractility reduction factor and ventricular septal perforation or nipple. Hemodynamic disturbance caused by muscle rupture, such as shock caused by rheumatic activity in patients with severe rheumatic mitral stenosis and aortic regurgitation, both myocardial contractility and rhythm caused by rheumatic myocarditis Hemodynamic disorders caused by ejection disorders and filling disorders.

Low-stasis syndrome after open heart surgery (5%):

Most patients are due to the inability of the heart to adapt to the increased preload after surgery. The main causes include poor heart function, myocardial damage caused by surgery, subendocardial hemorrhage, or myocardial degeneration before surgery, necrosis, and correction of cardiac surgery. , arrhythmia, some anatomical changes caused by surgery, such as left ventricular outflow tract obstruction after artificial spherical aortic valve replacement, and low blood volume caused by cardiac output decreased sharply and shock.

Pathogenesis

In the development of acute myocardial infarction and cardiogenic shock, the imbalance of myocardial oxygen supply and demand is the central link of pathological changes. If this contradiction cannot be solved in time, the infarct size will continue to expand and the pumping capacity will be more and more Poor, eventually leading to irreversible shock, can cause the following changes in acute myocardial infarction:

Cardiac infarction

The myocardial contractility is reduced, and the cardiac output is reduced. It is well known that the maintenance of effective blood circulation mainly depends on the coordination between the three functions of cardiac blood discharge, blood volume and vascular bed volume, and any one of the factors may lead to effective blood circulation. Insufficient volume leads to the occurrence and development of shock, and cardiac pumping failure is the leading cause and key factor for cardiogenic shock.

It has been confirmed that the degree of cardiac output reduction is directly related to the infarct size. When the infarct size exceeds 40% of the left ventricular muscle, shock is very likely to occur at this time. If the infarct size is <30%, shock is less likely to occur. The heart pump function is positively correlated with the range of myocardial necrosis. Patients with acute myocardial infarction should maintain normal blood output and maximize the use of the Frank-Starling principle. The left ventricular end-diastolic pressure (LVEIDP) must be appropriately increased. It is generally considered that the most suitable LVEDP is 14 ~18mmHg, a few can reach 20mmHg, but when LVEDP is excessively increased, more than 25mmHg, it will go to the opposite side of things - causing pulmonary congestion, when it exceeds 30mmHg, it can produce acute pulmonary edema, when the body can not maintain enough by increasing LVEDP The cardiac output, cardiac output index <2.0L / (min · m2), there will be clinical manifestations of insufficient organ and tissue perfusion; plus necrotic and severely damaged myocardium in the ventricular contraction, not only do not participate in contraction, And can cause movement inconsistency, or even bulging outward, resulting in so-called contradictory movement phenomenon, which will further aggravate the cardiac hemodynamic disorder; if the papillary muscles are combined at the same time When insufficiency, chordal rupture complications mitral regurgitation, and ventricular septal perforation, cardiac output can be further reduced, the occurrence and development of shock.

2. The occurrence and development of microcirculatory disorders

Microcirculation refers to the microcirculation between the arterioles and venules. It is distributed in various organs and tissues of the whole body. Its functional status directly affects the nutrient metabolism and function of tissue cells, although the structure of microcirculation in different organs and tissues is not The same, but the basic structure is similar, including micro-arteries, posterior micro-arteries, anterior capillaries, true capillaries, venules and arteriovenous short-circuit and other microscopic blood vessels. Under normal circumstances, blood flow from the arterioles, posterior micro-arteries The anterior capillary channel continuously flows, the flow rate is faster, and only 20% of the true capillary network is in the open state of blood flow, and the rest is in the closed state, so its potential capacity is very impressive. Once fully open, a large amount of blood will be Stasis in the capillary network can lead to a sharp decrease in effective blood volume and aggravate the occurrence and development of shock.

When various heart diseases cause a sharp decrease in cardiac output, it will affect microcirculation perfusion, leading to the occurrence and development of microcirculatory dysfunction. Now, taking acute myocardial infarction and cardiogenic shock as an example, briefly describe the cardiogenic shock. The change of the cycle.

(1) Changes in microvascular smooth muscle tone: In acute myocardial infarction, due to a sharp decrease in cardiac output, arterial pressure is reduced, baroreceptors can be stimulated by the aortic arch and carotid sinus, and the reflex sympathetic-adrenal medulla system increases the release of catecholamines. , causing strong contraction of microvessels, especially the arterioles, posterior micro-arteries and anterior capillaries contraction more obvious; plus myocardial infarction, severe pain in the anterior region and high mental tension, making the sympathetic nerves highly excited, further Increased contraction of peripheral blood vessels, in addition, catecholamine release, decreased blood volume and decreased cardiac output can activate the renin-angiotensin system (RAS), an increase in angiotensin II, leading to strong contraction of blood vessels; Hypothalamic synthesis and release of vasopressin reflex inhibition is weakened, resulting in increased release of pituitary vasopressin, leading to vasoconstriction; thromboxane A2 produced by platelets in early shock, vascular endothelin release, can also cause vasoconstriction, within appropriate limits This mechanism is protective, it can increase arterial pressure and protect important organs. Blood perfusion, but the vasoconstriction is too high. On the one hand, the vascular resistance increases, which can aggravate the post-load of the heart, increase the myocardial oxygen consumption, and expand the myocardial infarction range. On the other hand, the anterior capillary arteries contract vigorously and permanently, which can cause capillary The vascular network is hypoxic, and most of the blood is not connected to the capillary via the arteriovenous network. The whole microcirculation perfusion is greatly reduced, the organs and tissues are not supplied with blood, and the ischemia and hypoxia are If hemodynamics is not corrected in time, with the development of shock, serotonin, histamine, prostaglandin E2 (PGE2), endorphin (endorphin) and bradykinin release increased vasoactive substances, the body Under anaerobic metabolism, lactic acid production increases, and acidic metabolites accumulate. These substances all relax the anterior capillaries of the capillaries; at the same time, the reactivity of the blood vessels to the vasoactive substances such as catecholamines gradually decreases, resulting in a large opening of the capillary network. The venule smooth muscle is less sensitive to hypoxia and vasoactive substances and is still in a contracted state. Therefore, the blood is stagnant in the hair. In the blood vessel network, the blood volume and effective blood volume are further reduced, which can aggravate the process of shock on the one hand, and on the other hand, a large amount of blood stasis in the capillary network can cause congestion and hypoxia, and stagnant blood makes the capillary static. The pressure is increased, and the permeability of the tube wall is increased due to lack of oxygen. When the hydrostatic pressure exceeds the blood osmotic pressure, the plasma will extravasate into the interstitial space, causing blood to concentrate, sticky and easy to coagulate, which can further reduce the effective Blood volume and blood flow to the heart, cardiac output is further reduced, in addition, blood concentration plus capillary endothelial cell damage, red blood cell agglutination and platelet aggregation and release of thromboxane A2 simultaneously activate the internal coagulation process, can produce diffuse intravascular coagulation ( DIC), in the late stage of shock, vascular smooth muscle does not respond to various vasoactive substances, vascular tension is significantly reduced, microthrombus is formed extensively in capillaries, especially at the proximal vein end, blood perfusion stops, and microcirculation is in a state of exhaustion. Shock is often difficult to reverse.

(2) changes in hemodynamics and vascular resistance: most hemorrhagic hemodynamics are characterized by low-grade high-resistance shock, ie cold shock or vasoconstriction shock, because of cardiogenic shock Sympathetic gods are often in a state of high excitement, adrenal cortex, medulla and pituitary hyperfunction, catecholamine secretion and release increased, alpha receptor excitability predominates, causing severe contraction of small arteries and anterior capillaries, peripheral vascular resistance increases, and cardiac output Reduced, its clinical features are pale skin, wet and cold, sweating, skin temperature reduction, more conscious disturbance, oliguria or urinary closure, lower blood pressure, weak pulse, small pulse pressure, increased peripheral vascular resistance, severely reduced cardiac output A small number of cardiogenic shock can be characterized by low-grade and low-resistance shock, also known as vasodilatation shock or warm shock. As for high-grade and low-resistance shock, it is extremely rare in cardiogenic shock, and low-row and low-resistance shock produces it. Unclear mechanism may be the predominance of 2 receptor excitability, arteriovenous shunt, histamine, bradykinin vasodilator polypeptide and serotonin and other vasodilators More release, while catecholamines, angiotensin II, vasopressin and other vasoactive substances secrete and release relatively less, so that vasodilator reflexes predominate, so that peripheral blood vessels can not produce a corresponding generation of decreased cardiac output Compensatory contraction, it is also believed that due to decreased cardiac output, left ventricular end-diastolic pressure is increased, myocardial and ventricular wall tension is increased, muscle fiber elongation is stimulated, and sympathetic nerves are reflexively inhibited by vagal afferent fibers, causing peripheral blood vessels to dilate. The resistance is reduced, that is, Bezoid-Jarisch reflex. Another method is that the ischemic myocardium bulges during systole, stimulating the extension receptor in the myocardium, causing central inhibition of sympathetic tone through the afferent fibers of the autonomic nerve, resulting in Peripheral vascular resistance is reduced, its clinical features are warm, rosy, not pale, cold or less sweat, slightly reduced urine output, mild disturbance of consciousness, normal or low peripheral vascular resistance, moderately decreased cardiac output, this type of shock The prognosis is better, and in addition, there is an intermediate type between the above two types.

(3) Blood redistribution: After the occurrence of shock, due to the reduction of effective blood volume, in order to ensure the blood supply of important organs such as heart, brain and kidney, the body must reduce the blood supply to the secondary organs and redistribute and adjust the blood flow in the body. The earliest tissues and organs that reduce blood supply are the skin, limbs and skeletal muscles, followed by organs such as the gastrointestinal tract, kidney, lung and liver. The persistent low blood supply can cause the above-mentioned organ dysfunction. In addition, the body accelerates between tissues. The fluid enters the capillaries to increase microcirculation perfusion and effective blood volume, but can lead to a decrease in functional extracellular fluid and affect cell function. In the late stage of shock, a large amount of blood stagnates in the capillaries plus diffuse intravascular coagulation microthrombus. The formation of extensive hemorrhage, increased capillary permeability, extravasation of plasma, further reduction of effective blood volume, organ ischemia, and hypoxia are more serious, resulting in irreversible pathological changes.

(4) Hemorheological changes: In cardiogenic shock, due to the significant reduction in cardiac output, microcirculation blood flow is slow, with the development of shock, blood stasis in the capillaries, blood hydrostatic pressure rises, plus Upper capillary endothelial cells are damaged by ischemia, hypoxia, and increased permeability, leading to extravasation of plasma, concentration of blood, increased hematocrit, decreased pH, increased blood viscosity and easy coagulation.

(5) Disseminated intravascular coagulation (DIC): In the late stage of shock, the microcirculation blood flow is slow, the blood is concentrated, and the red blood cells are deformed, so that the damaged capillary endothelium is more prone to fibrin deposition and platelet aggregation, forming microthrombus, and occurs more frequently. At the capillary end of the capillary, the blood stasis and plasma extravasation in the capillaries can be further aggravated, and the blood flow and cardiac output are further reduced. Disseminated intravascular coagulation (DIC) consumes a large amount of blood coagulation factors, which can cause clotting factor deficiency. Bleeding; in DIC, fibrin degradants are released into the blood in large quantities, which promotes the conversion of plasminogen to plasmin. The latter has a strong anticoagulant effect, which can further aggravate the bleeding phenomenon. If bleeding occurs in important organs, the prognosis is worse. In addition, DIC can aggravate tissue cell and capillary damage, increase or rupture of lysosomal membrane permeability in tissue cells, release lysosomal hydrolase, which can lead to autolysis and tissue necrosis, organ function Further damaged.

3. Cell damage, metabolic changes and acid-base imbalance

(1) Cell damage: shock caused by decreased blood volume, insufficient tissue perfusion, ischemia, hypoxia and acidosis, etc., can cause cell damage, even necrosis, if not corrected in time, eventually become irreversible shock and inevitably die, Cell damage during shock is mainly manifested in the following aspects:

1 Cell membrane damage: In the early stage of shock, the cell membrane mainly showed increased permeability, increased intracellular Na and water content, and K efflux, and activated Na-K-ATPase, which increased the consumption of triphosphate adenosine and aggravated cell energy deficiency. Lead to cell membrane damage; metabolic acidosis can directly damage the function and structure of the cell membrane, while cell shock during hypoxia, hypoxia can affect mitochondrial respiratory function, dysfunction of cytochrome oxidase system, can produce more oxygen free radicals, plus A large amount of lactic acid produced during shock, increased proteolytic activity and inflammatory factors, activation of neutrophils and macrophages can promote the production of oxygen free radicals. Excessive oxygen free radicals are another cause of further damage to the cell membrane. For important reasons, the cell membrane in the late stage of shock is destroyed, eventually leading to cell death.

2 mitochondrial damage: cytotoxicity and endotoxin and other toxic substances in shock can directly inhibit various mitochondrial respiratory enzymes; ischemia leads to mitochondrial synthesis of adenosine triphosphate cofactors such as coenzyme A, adenosine and other internal and environmental Changes can affect cell energy supply, and excessive oxygen free radicals produced during shock also directly damage mitochondria. Early mitochondrial damage in shock is mainly caused by decreased mitochondrial respiratory function and adenosine triphosphate synthesis, followed by matrix particle reduction. Or disappear, and finally the lumen of the sac is dilated and the mitochondria collapse.

3 lysosomal rupture: lysosome contains a variety of enzymes, including cathepsins, polypeptide enzymes, phosphatases, etc. These enzymes have no active effect before they are released, and once released, they are active and can be digested and decomposed into cells. Various macromolecular substances, especially proteinaceous substances, can cause direct damage to lysosomes due to tissue ischemia, hypoxia and endotoxin during shock, plus oxygen free radicals for peroxidation of lysosomal membrane phospholipids The action can cause lysosomal damage, rupture, and activation of the complement component in the blood during shock, which can stimulate the release of lysosomal enzyme from neutrophils. This enzyme can not only destroy the lysosomal membrane, but also destroy the cell membrane and mitochondrial membrane. Integrity, direct damage to vascular endothelial cells and vascular smooth muscle cells, can lead to extravasation of blood, hemorrhage, platelet aggregation, can induce disseminated intravascular coagulation, early shock mainly lysosomal swelling, loss of particles and increased release of enzymes, Following the lysosomal membrane damage, destruction, eventually leading to lysosomal rupture, lysosomes of various tissue cells in the body can be damaged during shock, especially The lysosomal damage of the liver, intestine, spleen and other organs is particularly prominent. In short, shock and damage can be caused to various tissues and cells of the body during shock. If the shock cannot be corrected in time, the cell damage will progress as the disease progresses. Aggravation or even necrosis can eventually lead to irreversible shock.

(2) Metabolic changes: hyperbolism of glycogen and fat during shock, due to cellular ischemia, hypoxia, increased anaerobic metabolism, increased acid products such as lactic acid, pyruvic acid, and liver function damage to lactic acid utilization and transformation Reduced ability, decreased glomerular filtration rate, impaired acid function, accumulation of acidic metabolites in the body, can cause metabolic acidosis, due to tissue damage, destruction, excessive release of intracellular potassium ions; cell membrane sodium pump function is impaired, Lead to the increase of sodium ions into the cells, and a large amount of potassium ions in the cells, coupled with impaired renal function, oliguria, hyperkalemia, which can cause severe arrhythmia, and potassium deficiency in cardiomyocytes Myocardial contractility is further reduced, which can aggravate the process of shock.

(3) Acid-base imbalance: early shock due to reduced blood volume, hypoxia and lactate, reflex caused by accelerated breathing, excessive carbon dioxide emissions, can produce respiratory alkalosis; late respiratory center excitability and shock The formation of the lungs, the breathing becomes shallow, and carbon dioxide retention can cause respiratory acidosis.

Cardiogenic shock prevention

As soon as possible to diagnose the disease that can cause shock and timely treatment, is the most effective measure to prevent shock, because acute myocardial infarction is the most common cause of cardiogenic shock, so early prevention and treatment of coronary heart disease risk factors (such as hyperlipidemia , hypertension, diabetes and smoking) have certain clinical significance in preventing the occurrence of cardiogenic shock. SPRINT study shows: diabetes, angina pectoris, peripheral vascular or cerebrovascular disease, old myocardial infarction, women, etc. are all patients with acute myocardial infarction Risk factors for shock, if these six factors are present at admission, the probability of shock is 25%, and high-risk patients with shock in acute myocardial infarction should have early PTCA.

Cardiogenic shock complications Complications, disseminated intravascular coagulation, acute renal failure, arrhythmia, stress ulcer

Shock lung

The formation of shock lungs is related to a variety of factors:

(1) Insufficient pulmonary capillary perfusion causes type I alveolar cells and capillary endothelial cells to swell, and the air-blood flow barrier of the lungs is thickened.

(2) The alveolar capillary endothelium is damaged, the permeability is increased, and interstitial edema is caused in the case of pulmonary congestion.

(3) Diffuse intravascular coagulation occurs in the pulmonary circulation.

(4) A large amount of endotoxin in the intestine acts on the lungs through the blood; severe trauma, infection, inappropriate infusion and infusion of blood, unreasonable oxygen supply, etc. may also be related to "shock lung".

2. Shock kidney

Shock can directly affect the blood perfusion of the kidney, causing renal functional and organic lesions, leading to a decrease in urine output, which can cause acute renal failure in severe cases, and acute renal failure in turn directly exacerbates shock.

3. Cardiovascular complications

Severe shock can occur in the course of disseminated intravascular coagulation, and the corresponding clinical manifestations, chest pain, chest tightness, chest tightness and cardiogenic shock.

4. Arrhythmia

89.3% of patients with shock have an arrhythmia, showing sinus tachycardia, supraventricular tachycardia, atrial premature contraction, ventricular premature contraction, ventricular fibrillation, and conduction block.

5. Nervous system complications

When the mean arterial pressure drops below 50mmHg (6.67kPa), the cerebral perfusion flow is insufficient, which can cause brain tissue damage and dysfunction. For example, the brain circulation cannot be re-established in a short time, and cerebral edema will continue to develop, such as the average artery. If the pressure continues to drop or fall too long (more than 5 to 10 minutes), it can cause brain cell damage, necrosis and brain failure.

6. Gastrointestinal complications

Hepatic blood flow is reduced during shock, liver function is impaired, hepatic lobular necrosis can occur, and severe hepatic necrosis can be developed to eventually lead to liver failure. In cardiogenic shock, gastrointestinal tract perfusion is insufficient, which can not only cause digestion. Absorption dysfunction can also cause mucosal edema, hemorrhage, necrosis, complicated with stress ulcers and acute hemorrhagic enteritis.

7. Disseminated intravascular coagulation (DIC)

Cardiogenic shock is easy to cause slow blood flow, stagnant blood flow, easy to lead to thrombosis, and even microthrombus formation, myocardial microvascular embolization during DIC, degeneration and necrosis of myocardial cells, myocardial rupture and acute myocardial infarction have been diseased According to the Institute of Science, hemorrhage, shock, multiple microthrombus formation, and multiple microvascular hemolysis can occur.

Symptoms of cardiogenic shock Common symptoms Shock coma consciousness Fuzzy weakness Arrhythmia Pulse is weak or even not... Slow response, unconsciousness, cardiogenic respiratory distress, circulatory failure

Clinical staging

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

(1) Early shock: As the body is under stress, catecholamines are secreted into the blood, and the sympathetic nerves are excitatory. Patients often show irritability, fear and nervousness, but they are conscious, pale or pale or slightly blemishes. The limbs are wet and cold, sweating, heart rate is increased, there may be nausea, vomiting, blood pressure is still normal or even slightly increased or slightly lower, but the pulse pressure becomes smaller and the urine volume is slightly reduced.

(2) mid-shock: if the early stage of shock can not be corrected in time, the symptoms of shock are further aggravated, the patient's expression is indifferent, the response is slow, the consciousness is blurred or unclear, the whole body is weak, the pulse is weak or unable to reach, and the heart rate often exceeds 120. Times / min, systolic pressure <80mmHg (10.64kPa), and even not measured, pulse pressure <20mmHg (2.67kPa), pale, cyanosis, skin cold, cyanosis or marble-like changes, less urine (<17ml / h) or no urine.

(3) late stage of shock: symptoms of disseminated intravascular coagulation (DIC) and multiple organ failure may occur. The former may cause extensive bleeding of the skin, mucous membranes and internal organs; the latter may manifest as acute kidney, liver and brain and other important organs. Symptoms of dysfunction or failure, such as acute renal failure, may be characterized by oliguria or urinary closure, blood urea nitrogen, creatinine progressively increased, uremia, metabolic acidosis, etc., urine specific gravity, protein may appear Urine and cast, etc., pulmonary failure can be characterized by progressive dyspnea and cyanosis, oxygen can not relieve symptoms, shallow breathing and irregular, both lungs can be heard and fine voice and respiratory sounds are reduced, resulting in acute respiratory distress Symptoms of the syndrome, brain dysfunction and failure can cause coma, convulsions, limb paralysis, pathological nerve reflexes, pupil size, cerebral edema and respiratory depression. Liver failure can cause jaundice, liver damage and bleeding tendency. Even coma.

2. Shock degree division

According to the severity of shock, it can be roughly divided into light, medium, heavy and extremely severe shock.

(1) mild shock: the patient's consciousness is clear, but irritability, pale, dry mouth, sweating, heart rate >100 beats / min, strong pulse rate, limbs are still warm, but the limbs are slightly cramped, cold, Systolic blood pressure 80mmHg (10.64kPa), urine output is slightly reduced, pulse pressure <30mmHg (4.0kPa).

(2) Moderate shock: pale, indifferent expression, cold limbs, cyanosis at the extremities, systolic pressure at 60-80mmHg (8 ~ 10.64kPa), pulse pressure <20mmHg (2.67kPa), significantly reduced urine output (<17ml /h).

(3) Severe shock: ambiguity, confusion, unresponsiveness, pale complexion, cyanosis, cold limbs, cyanosis, marble-like changes in the skin, heart rate >120 beats/min, low heart sound, weak pulse or a little After the pressure disappears, the systolic pressure drops to 40-60 mmHg (5.32-8.0 kPa), and the urine volume is significantly reduced or urinary closure.

(4) Extremely severe shock: unconsciousness, coma, shallow and irregular breathing, cyanosis of the lips, cold limbs, weak pulse or suffocation, low heart sound or single tone rhythm, systolic blood pressure <40mmHg (5.32 kPa), no urine, can have a wide range of subcutaneous, mucosal and visceral bleeding, and signs of multiple organ failure.

It must be pointed out that the division of the clinical stage and severity of the above shock is artificial, and they are not one-size-fits-all, and may have a transitional type, which can only serve as a reference for judging the condition in clinical work.

3. Other clinical manifestations

Because of the different causes of cardiogenic shock, in addition to the clinical manifestations of shock mentioned above, there are corresponding medical history, clinical symptoms and signs. Taking acute myocardial infarction as an example, this disease occurs mostly in the middle-aged and elderly people, often with severe pain in the precordial area. Sustained for several hours, with nausea, vomiting, sweating, severe arrhythmia and cardiac insufficiency, and even acute brain insufficiency can produce signs of stroke, including signs of mild to moderate enlargement of the heart sounds, first heart sounds low blunt There may be a third or fourth heart sound running through the horse; if the papillary muscle is insufficiency or chordae rupture, rough systolic reflux murmur may occur in the apical region; concurrent ventricular septal perforation is in the left sternal border There is a loud systolic murmur between the 3 and 4 ribs, and the wet lungs can be heard at the bottom of the lungs.

Cardiac shock examination

Laboratory inspection

Blood routine

Leukocytosis, usually in (10 ~ 20) × 10 ⁹ / L (10000 ~ 20000 / mm ³ ), neutrophils, eosinophils decreased or disappeared, hematocrit and hemoglobin increased often suggest blood concentration, concurrent In disseminated intravascular coagulation, the platelet count is progressively reduced, and the clotting time is prolonged.

2. Urine routine and renal function tests

Reduced urine output, proteinuria, red blood cells, white blood cells and casts, and acute renal failure, urine relative density (specific gravity) from initial high to low and fixed at 1.010 ~ 1.012, blood urea nitrogen and creatinine increased, The urine/creatinine ratio is often reduced to 10, the urine osmotic pressure is lowered, the urine/blood osmotic pressure ratio is <1.5, the urine/blood urea ratio is <15, and the urine sodium can be increased.

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

Serum sodium can be low, serum potassium levels are different, serum potassium can be significantly increased during oliguria, metabolic acidosis and respiratory alkalosis change in early shock, shock, acidosis and respiratory in the late stage Acidosis, blood pH lowers, oxygen partial pressure and oxygen saturation decrease, carbon dioxide partial pressure and carbon dioxide content increase, normal blood lactic acid content is 0.599 ~ 1.78mmol / L (5.4 ~ 16mg / dl), if raised to 2 ~4mmol / L indicates mild hypoxia, microcirculation is basically good, the prognosis is better; if the blood lactate content > 4mmol / L indicates that the microcirculation has been exhausted, has been in moderate anoxic; if > 9mmol / L indicates micro The circulation has been depleted, there is severe hypoxia, and the prognosis is poor. In addition, blood free fatty acids are often significantly increased during severe shock.

4. Serum enzymology

Acute myocardial infarction with cardiogenic shock, serum aspartate aminotransferase (aspartate aminotransferase, AST/GOT), lactate dehydrogenase (LDH) and its isoenzyme LDH 1, creatine phosphokinase (CPK) and Its isoenzyme CPK-MB is significantly increased, especially in the latter, its sensitivity and specificity are extremely high, reaching 100% and 99%, respectively. The increase and duration of the increase help to determine the extent and severity of infarction, shock In the late stage, if liver function damage is complicated, alanine aminotransferase (ALT; alanine aminotransferase, GPT) may be elevated and the corresponding liver function test is abnormal.

5. Myocardial myosin light chain and myoglobin and myocardial specific troponin assay

In the acute myocardial infarction, the cardiac myosin light chain was increased. The human myocardium light chain I (LCI) was mainly measured, and its normal value was (3.7±0.9) g/L [(3.7±0.9). )ng/ml], blood, urinary myoglobin content increased, the normal value of Chinese serum myoglobin is 0.585 ~ 5.265nmol / L (10 ~ 90ng / ml), the increase is positively correlated with the infarct size, and serum Enzymological changes are early, with high sensitivity and specificity. Cardiac troponin (cT-nT, cTnI) is a very high marker for early diagnosis of myocardial infarction. Normal human cardiac troponin I (cTnI) The normal value is <4g/L, the acute myocardial infarction can be significantly increased from 3 to 6h, often exceeding 165g / L; the normal value of cardiac troponin T (cTnT) <1ng / L, acute myocardial infarction or myocarditis, necrosis often Can be significantly increased.

6. Examination of disseminated intravascular coagulation (DIC)

In the late stage of shock, DIC is often complicated. In addition to the progressive decline in platelet count and abnormal platelet function (such as platelet adhesion and aggregation dysfunction, clot retraction defects, etc.), the following changes may be made: prothrombin time prolongation, fibrinogen Often reduced, thrombin clotting time and normal control plasma compared with > 3s, whole blood clotting time more than 10min, coagulation factors I, II, V, VIII, X, XII are reduced, because DIC is often accompanied by secondary fibrinolysis Invasive, the following tests can be used to indirectly explain the existence of DIC, including shortening of the dissolution time of whole blood clots (no dissolution in normal people within 72 hours), determination of fibrin (original) degradation products (FDP), commonly used in clinical practice such as plasma The protamine sub-agglutination test (3P test) is positive, the Fi test (ie, the determination of fibrin degradation products) has a normal reference value of less than 1:8, and has a diagnostic value when it is greater than 1:16. In addition, it can be used as a citrated red blood cell. Agglutination inhibition immunoassay, ethanol gel test, etc., DIC are often positive.

7. Hemorheological examination

When the shock is slow, the blood flow rate is slow, the effective blood volume is reduced, the blood stasis in the capillaries, and the plasma extravasation, blood concentration and viscosity increase, so the whole blood and / or plasma specific viscosity is often increased, when combined with DIC In the initial stage, it is in a state of hypercoagulation, and then it can be converted to low-coagulation when fibrinolysis is carried out.

8. Inspection of microcirculation perfusion

Commonly used indicators in clinical are:

(1) Temperature difference between skin and anus: The temperature of skin and anus is measured separately. Under normal circumstances, the former is 0.5 °C lower than the latter. When the skin contracts, the skin temperature is significantly reduced, and the anus temperature does not decrease or even increase. The temperature difference between the two increases. When the temperature difference is >1.5 °C, it often indicates that the shock is severe; when it is greater than 3 °C, it indicates that the microcirculation is in a state of severe exhaustion.

(2) fundus and nail wrinkles examination: fundus examination can be seen small arteriolar spasm and venule dilatation, retinal edema can occur in severe cases, nail wrinkles are usually in the nameless nail wrinkles, under the optical microscope with special cold light source, observe with the naked eye Subcutaneous tissue microvascular arrangement, morphology and response to stimulation and pressurization, shock patients due to vasoconstriction, so the number of tuberculosis of the nail fold microvascular is significantly reduced, disordered arrangement, slow blood flow, microthrombus formation, blood cells often aggregate It is formed into small granules and even aggregates into flocs. When the nails are pressurized and relaxed, the filling time of blood flow in the capillaries is prolonged.

(3) Hematocrit examination: When the hematocrit of peripheral peripheral blood is 0.03 vol (3 vol%) higher than that of central venous blood, it indicates that there is significant contraction of peripheral blood vessels.

The above-mentioned index measurement of microcirculation has reference value for judging the severity of microcirculation disorder during shock and rational selection of vasoactive drugs.

Film degree exam

1. ECG and heart vector chart check

Electrocardiogram is helpful for the diagnosis of acute myocardial infarction and cardiogenic shock. Typical cases often have pathological Q wave, ST segment elevation and T wave inversion and its evolution. It must be pointed out that there are 20% to 30% acute myocardial infarction. There may be no pathological Q wave (no Q-wave myocardial infarction), so it should be combined with clinical manifestations and serum enzymology and cardiac troponin and other related tests to make a diagnosis. It is generally believed that the specificity and sensitivity of electrocardiogram for the diagnosis of acute myocardial infarction are About 80%, it is very helpful to estimate the location, extent and progression of the disease. Therefore, in the case of shock for unknown reasons, ECG should be routinely performed to rule out myocardial infarction.

The heart vector diagram can change the QRS ring in acute myocardial infarction, and the ST vector and T ring changes. The QRS ring changes mainly show that the starting vector will point to the opposite direction of the infarct; the ST vector appears as the QRS ring. Closed, the 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 is mainly represented by the opposite of the maximum vector and the QRS maximum average vector or QRS- The angle of T increases, the length/width ratio of T ring is <2.6:1, the speed of T-ring centrifugation and the center of the heart branch are equal, and the heart vector diagram can be used as an auxiliary test only when the electrocardiogram is difficult to diagnose.

2. Echocardiography and Doppler ultrasonography

Regardless of M-mode or two-dimensional echocardiography, the amplitude of ventricular wall motion in patients with acute myocardial infarction is often reduced or contradictory, while the infarcted area of the myocardium often has compensatory exercise enhancement. When combined with ventricular atrial tumor, papillary muscle function Incomplete, chordae rupture or ventricular septal perforation, there are often characteristic ultrasound signs in real time, at this time pulse Doppler or continuous Doppler can detect abnormal turbulence or turbulence signals, diagnosis of interventricular septal perforation and acute Mitral regurgitation is helpful. The application of late-color Doppler flow imaging technology combined with two-dimensional echocardiography can detect abnormal blood flow in real time and semi-quantitative estimation of interventricular septal perforation. And the size of the mitral regurgitation is of great value in the diagnosis of some complications of acute myocardial infarction. In addition, echocardiography can be used to measure cardiac function non-invasively, which is also helpful for assessing the condition.

3. Radionuclide myocardial imaging

Myocardial imaging is a technique that directly displays myocardial morphology using certain radionuclides or their markers. There are two types of myocardial imaging methods depending on the imaging agent used: one is capable of concentration in normal myocardium and reflects functionality. The radionuclide of myocardial tissue such as 131(131Cs), 201(201Tl), etc., such as myocardial blood flow damage, myocardial necrosis or scar tissue formation, there is no function of absorbing such radionuclides, the lesions show It is a radioactive "cold zone" without radionuclide, so it is called "cold zone imaging", and the other is just the opposite, it can be taken up by fresh infarcted myocardial tissue, while normal myocardium is not developed, such as 90mTc-pyrophosphate Salt, etc., shows a radioactive "hot zone" in the lesion, so it is called "hot zone imaging". The radionuclide myocardial imaging can directly show the location, size and shape of the infarct area, showing that the lesion is more intuitive, and it is ECG and enzymology. An important supplement to the examination, in addition, through the nuclear angiography and blood pool imaging, can still evaluate the state of cardiac function.

4. X-ray inspection

In particular, counting photography and selective ventricular angiography are helpful for estimating the condition of myocardial infarction. Emergency coronary angiography is not only valuable for determining coronary artery disease associated with myocardial infarction, but also for thrombolytic therapy, percutaneous coronary balloon. Dilatation and coronary artery bypass grafting provide data. In addition, bedside chest X-ray examination can also detect pulmonary congestion, pulmonary edema signs to evaluate cardiac function status, differential diagnosis such as pulmonary infarction, myocarditis, cardiomyopathy, mainX(CT)CT(UFCT)

5.

1970(Swan-Ganz)()

(1)

X(PCWP)PCWPX

1

(2)

(PCWP)(LVEDP)()()PCWP(LAP)LVEDPPCWPPCWP(PAEDP)-1.69mmHg-5.96mmHgPCWP

PCWPFrank-StalingPCWP612mmHgLVEDP010mmHgPCWPLVEDP15mmHgLVEIDP1520mmHgFrank-Starling24mmHgPCWP<18mmHg;1820mmHg;2l25mmHg;2630mmHg;>30mmHg

Swan-GanzFick(5ml10ml)(0)(CI)<2.2L/(min·m2);CI<2.0L/(min·m2)PCWPCI>3.5L/(min·m2)

(+l/3)75mmHg;30mmHg6070mmHg4050mmHg;7080mmHg8090mmHg100110mmHg()

(CVP)CVPPCWP2030mmHgCVP34cmH20CVP!PCWPCVPCVPCVP

(3)()()

A.12ml

B.Swan-GanzX30cmSwan-Ganz()(0.81.2ml)(PCWP)(PAWP)30cm05ml10ml

LVEDPPCWPMLVEDP=21.6(QC/A2E) 1.1(mmHg)PCWP=18.8(QC/A2E) 1.8(mmHg)QCORSQC(ms)A2EEPCWPPCWP=18.8(QB/S2O) 1.8(mmHg)QBQRSBS2OO

diagnosis

1.<80mmHg80mmHg<100mmHg

2.

3.<20ml

4.

5.(CI)<2.0L/(min·m2)(PCWP)>18mmHg(CVP)>12cmH2O>1400dyn·s·cm-5

Differential diagnosis

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