hemorrhagic shock
Introduction
Introduction to hemorrhagic shock A large number of blood loss caused by shock called hemorrhagic shock (hemorrhagic shock), common in bleeding caused by trauma, peptic ulcer bleeding, esophageal variceal rupture, bleeding caused by obstetrics and gynecology diseases, etc., whether shock occurs after blood loss depends not only on blood loss The amount also depends on the speed of blood loss. Shock is often caused by rapid, large (more than 30 to 35% of total blood) blood loss without timely replenishment. basic knowledge The proportion of illness: 0.005% Susceptible people: no special people Mode of infection: non-infectious Complications: thrombosis, acute renal failure, cerebral thrombosis, disturbance of consciousness
Cause
Causes of hemorrhagic shock
Microcirculation ischemic period:
The characteristics of this microcirculation change are: 1 micro-arterial, posterior micro-arterial and capillary sphincter contraction, microcirculation perfusion flow decreased sharply, pressure decreased; 2 venules and venules were less sensitive to catecholamines, and contraction was lighter; 3 arteriovenous anastomosis may have different degrees of openness, blood from the arterioles through the arteriovenous anastomosis directly into the venules. The key change that causes microcirculatory ischemia is the sympathetic nervous-adrenal medullary system. Different types of shock can cause sympathy through different mechanismsthere is a decrease in cardiac output during adrenal medullary shock and cardiogenic shock. Arterial blood pressure reduction can excite the sympathetic-adrenal medulla system through sinus arch reflex; in most endotoxic shock, endotoxin can directly stimulate sympathetic sympathy - the adrenal medullary system is strongly excited.
Sympathetic excitation:
The total effect of increased catecholamine release on the cardiovascular system is to increase peripheral total resistance and increase cardiac output, but the response of blood vessels in different organs is very different. The skin, abdominal cavity and kidney blood vessels are rich in sympathy. The vasoconstrictor fibers dominate, and the alpha receptors have an advantage. Therefore, when the sympathetic nerves are excited and the catecholamines increase, the small arteries, venules, arterioles, and capillary anterior red muscles of these sites contract. The sympathetic vasoconstrictor fibers are most densely distributed, and the anterior capillaries of the capillaries are the most reactive to catecholamines, so they contract most strongly. As a result, the anterior capillary resistance is significantly increased, the microcirculation perfusion flow is drastically reduced, and the mean blood pressure of the capillaries is markedly Reduced, only a small amount of blood flows through the direct pathway and a few true capillaries into the venules, venules, and tissue, resulting in severe ischemic hypoxia. The cerebral vascular symphyseal vasoconstriction fibers are least distributed, and the alpha receptor density is also low. There can be no obvious changes, although the coronary arteries also have sympathetic innervation, there are also and . Body, but it has increased sympathetic nerve activity and catecholamine activity by strengthening the heart, improving metabolism so that vasodilator metabolites increased adenosine especially the coronary artery.
Sympathetic excitability and reduced blood volume can also activate the renin-angiotensin-aldosterone system, while angiotensin II has a strong vasoconstrictor effect, including contraction of the coronary arteries.
In addition, increased catecholamines can also stimulate platelets to produce more thromboxane A2 (TXA2), while TXA2 also has a strong vasoconstrictor effect.
1, normal situation
(1) Arteriovenous anastomosis is closed.
(2) Only 20% of the capillaries are open in turn, with blood perfusion.
(3) The opening and closing of capillaries is regulated by the relaxation and contraction of the anterior capillaries of the capillaries.
2. Microcirculation ischemic period
(1) Sympathetic excitation and adrenaline, norepinephrine secretion increased, small arteries, arterioles, posterior micro-arteries, contraction of the anterior capillaries.
(2) The arteriovenous anastomosis is open, and the blood flows directly from the arteriole to the venule.
(3) Insufficient blood perfusion of capillaries, tissue hypoxia.
3, microcirculation congestion
(1) The arterioles and arterioles are contracted, the arteriovenous anastomosis is still open, and the blood entering the capillaries is still very small.
(2) Due to hypoxia, histamine, bradykinin, hydrogen ion and other vasodilators increase, post-arterioles and capillaries sphincter relax, capillaries open, blood vessels expand, and blood flow into capillaries is slow.
(3) Due to sympathetic excitation, the secretion of adrenaline and norepinephrine is increased (possibly with the action of histamine), the venules and venules are contracted, and the post-capillary resistance is increased, resulting in capillary dilation and congestion.
4, microcirculation coagulation period
(1) Due to severe hypoxia, acidosis, capillary wall damage and permeability, blood in the capillaries is concentrated, blood flow is stagnant; in addition, blood coagulation is increased, resulting in disseminated intravascular blood vessels in the microcirculation Coagulation.
(2) Due to the formation of microthrombus, more severe hypoxia and metabolic disorders, intracellular lysosomal rupture, tissue cell necrosis, causing severe dysfunction in various organs.
(3) Due to coagulation, coagulation factors (such as prothrombin, fibrinogen, etc.) and platelets are consumed in large quantities, fibrin degradation products are increased, and blood coagulability is reduced; the blood vessel wall is damaged again, followed by extensive bleeding.
TXA2 also has a strong vasoconstrictor effect.
In addition, the lysosomal hydrolase-myocardial inhibitor system also plays a role in the development of stage I microcirculation ischemia. In shock, ischemia, hypoxia and acid are mainly caused by decreased blood perfusion of the pancreas. Poisoning can rupture the lysosomes of pancreatic exocrine cells and release cathepsin, which can decompose tissue proteins to produce myocardial depressant factor (MDF). After the small molecule peptide MDF enters the bloodstream, it causes myocardial contraction. The weakening of the force inhibits the phagocytic function of the mononuclear phagocytic system, and also causes the small blood vessels of the abdominal viscera to contract, thereby further aggravating the ischemia of microcirculation in these areas.
The main clinical manifestations of this period are: pale skin, cold limbs, cold sweat, and reduced urine output; because of increased peripheral resistance, systolic blood pressure can be not significantly reduced, while diastolic blood pressure is increased, pulse pressure is reduced, and pulse rate is fine. Conscious, irritated, and so on.
The microcirculation changes in this period have certain compensatory significance. The small arteries such as skin and abdominal organs contract, which can increase the peripheral resistance to maintain blood pressure, and reduce the blood flow of these tissues and organs to ensure the blood of important organs such as the heart and brain. Supply; increased capillary anterior resistance, reduced capillary hydrostatic pressure, promotes tissue fluid into the blood vessels to increase plasma volume; in addition, arteriovenous anastomosis is open, venous contraction reduces the venous volume (normally about 70% of blood is in the vein) It can speed up and increase the amount of blood returning to the heart. It is also conducive to the maintenance of blood pressure and blood supply to the heart and brain. However, due to the lack of oxygen in most tissues and organs due to insufficient perfusion of microcirculation arterial blood, it will lead to further development of shock, such as early detection. Active rescue, timely replenishment of blood volume, reduce the stress response of the drama, can quickly improve the microcirculation and restore blood pressure, prevent shock from further deterioration, and turn to safety.
Microcirculation congestion period:
In the cyclical ischemic period of shock, if the rescue is not early and the microcirculation is improved, local vasoactive substances (such as histamine, kinin, lactate, adenosine, etc.) may be caused by persistent and severe hypoxia. Increased, posterior micro-arterial and capillary sphincter relaxation, microcirculation capacity expansion, congestion, development into shock microcirculation congestion, the characteristics of microcirculation changes in this period are:
1 After the arterioles and capillaries sphincter relaxation (due to local acidosis, reduced reactivity to catecholamines), capillaries are largely open, and some are irregular lateral cystic expansion (micro-blood pool formation), and the microcirculation volume is enlarged. ;
2 venules and venules are more tolerant to local acidosis, and catecholamines can still cause contraction (histamine can also contract the venules and venules of the liver, lungs, etc.), and the post-capillary resistance increases, making the microcirculation Slow blood flow;
3 microvascular wall permeability increased, plasma oozing, stagnant blood flow;
4 due to blood concentration, increased hematocrit, red blood cell aggregation, white blood cell impaction, platelet adhesion and aggregation and other changes in blood rheology, can make microcirculation blood flow slow or even stop;
5 due to microcirculation congestion, increased pressure, less arterial blood entering the microcirculation (the small arteries and arterioles are still in a contracted state due to sympathetic nerves), due to a large amount of blood deposition in the microcirculation, the amount of blood return to the heart, Further reduce the cardiac output and increase the development of shock.
Mechanism of microcirculation changes during ischemic hypoxia
Due to the above microcirculation changes, although a large amount of blood accumulates in the microcirculation, the arterial blood perfusion flow will be further reduced, and the patient's skin color will gradually become pale due to paleness, especially the mouth and fingertips, because the venous return flow and cardiac output are more Reduced, the patient's vein collapsed, the filling was slow; the arterial pressure was significantly reduced, the pulse pressure was small, and the pulse was fine; the heart and brain were reduced due to insufficient blood supply, and the ATP production was reduced, but the heart contraction was weakened (low heart sound), and the expression was indifferent or conscious. Unclear, severe heart, kidney, lung failure, which is a critical state of shock, should be immediately rescued, rehydration, relieve small blood vessels, give oxygen, correct acidosis, to clear microcirculation and prevent disseminated blood vessels Internal coagulation.
Microcirculation coagulation period:
The development from the hemorrhagic phase of the microcirculation to the microcirculation coagulation phase is a manifestation of the deterioration of shock. It is characterized by the presence of fibers in the microcirculation (especially the capillary veins, venules, venules) on the basis of microcirculation congestion. Protein thrombosis, and often focal or diffuse hemorrhage; tissue cells degeneration and necrosis due to severe hypoxia.
Disseminated intravascular coagulation is closely related to shock. The pathological changes caused by disseminated intravascular coagulation and how it causes shock or exacerbation of shock have been discussed in the chapter on disseminated intravascular coagulation. Here, we briefly summarize how shock causes disseminated intravascular coagulation.
1. Stress response increases blood coagulability, causing shock causes (such as trauma, burns, bleeding, etc.) and shock itself is a strong stimulus that can cause stress, sympathetic excitation and pituitary-adrenal gland Enhanced cortical activity, increased blood platelets and clotting factors, enhanced platelet adhesion and aggregation, providing the necessary material basis for blood clotting.
2, the release and activation of clotting factors, and some causes of shock (such as trauma, burns, etc.) can release and activate clotting factors themselves, for example, damaged tissue can release a large amount of tissue thromboplastin, start exogenous Sexual coagulation process; large area burns destroy a large number of red blood cells, and the phospholipids and red blood cells in the red blood cell membrane destroy the released ADP, which promotes the blood coagulation process.
3, microcirculatory disorders, tissue hypoxia, local histamine, kinins, lactic acid, etc., on the one hand cause capillary dilation and congestion, increased permeability, slow blood flow, increased blood erythrocyte viscosity, there are Conducive to thrombosis; on the other hand damage capillary endothelial cells, expose gelatin, activate factor XII and cause platelet adhesion and aggregation.
4. Hypoxia reduced the function of mononuclear phagocytic system, and could not clear thrombin enzyme, thrombin and fibrin in time. As a result, disseminated intravascular coagulation occurred under the above factors.
Once disseminated intravascular coagulation occurs, the microcirculatory disorder will be more severe and the shock condition will worsen because:
1 extensive microvascular obstruction further aggravates microcirculatory disorders, further reducing the amount of blood returning;
2 coagulation substance consumption, secondary activation of fibrinolysis and other factors cause bleeding, thereby reducing blood volume;
3 Soluble fibrin multimers and their cleavage products can block the mononuclear phagocytic system, thus preventing endotoxin from the intestines from being sufficiently eliminated.
Due to the occurrence of disseminated intravascular coagulation and the increasing aggravation of microcirculation, the systemic hypoxia and acidosis will become more and more serious due to the severe deficiency of systemic microcirculation perfusion caused by blood pressure reduction; severe acidosis It can rupture the lysosomal membrane in the cell, release lysosomal enzymes (such as proteolytic enzymes, etc.) and certain shock drivers (such as endotoxin), which can cause serious or irreversible damage to the cells, thus The functional metabolic disorders of the important organs, including the heart and the brain, are also more serious (detailed), which causes great difficulty in treatment, so this period is also called the refractory period of shock.
Prevention
Hemorrhagic shock prevention
1. Actively prevent infection.
2, do a good job of on-site treatment of trauma, such as timely hemostasis, analgesia, heat preservation and so on.
3, patients with blood loss or excessive fluid loss (such as vomiting, diarrhea, hemoptysis, gastrointestinal bleeding, a lot of sweating, etc.) should promptly replenish or transfuse blood.
Complication
Hemorrhagic shock complications Complications thrombosis acute renal failure cerebral thrombosis disturbance
As with traumatic shock, hemorrhagic shock is complicated by DIC (diffuse intravascular coagulation), and severe cases can cause death. Therefore, patients with shock need to be rescued in time.
Disseminated intravascular coagulation (DIC) is a syndrome, not an independent disease, extensive fibrin deposition and platelets in capillaries, arterioles, and venules under various pathogenic factors. Aggregation, the formation of a wide range of microthrombotic, leading to circulatory function and other visceral dysfunction, consumptive coagulopathy, secondary fibrinolysis, shock, hemorrhage, embolism, hemolysis and other clinical manifestations. Used to be called low fibrinogen blood Defibrination, comsumptive coagulopathy, recently considered to be constiptive thrombohemorrhagic disordors, but the most commonly used is still disseminated intravascular coagulation. Acute DIC, onset Rapid, rapid development. Common clinical symptoms are as follows:
1, bleeding: light can only have a few skin bleeding points, severe cases can be seen in a wide range of skin, mucosal ecchymosis or hematoma, typically large skin ecchymosis, visceral bleeding, bleeding at the wound site.
2, thrombosis related performance:
(1) skin thromboembolism: the most common, fingertip, toe, nose, auricle skin blemishes, skin plaque hemorrhagic necrosis, dry necrosis.
(2) renal thrombosis: oliguria, anuria, azotemia and other acute renal failure are the most common manifestations.
(3) Pulmonary thrombosis: difficulty breathing, purpura, hemoptysis, severe acute lung failure may occur.
(4) Gastrointestinal thrombosis: gastrointestinal bleeding, nausea, vomiting and abdominal pain.
(5) cerebral thrombosis: irritability, lethargy, disturbance of consciousness, coma, convulsions, cranial nerve palsy and limb paralysis.
3, shock: acral chills, bruising, oliguria and blood pressure decreased, DIC caused by vascular endothelial injury is more common.
4, hemolysis: due to microvascular disease, red blood cells through mechanical damage, deformation and rupture and hemolysis, clinically may have jaundice, anemia, hemoglobin.
5, the symptoms of the primary disease.
Symptom
Hemorrhagic shock symptoms Common symptoms Blood presents concentrated pulmonary wedge pressure (P... Peripheral vein filling venous oxygen saturation... Serum sodium increased shock
Insufficient capacity beyond the compensatory function will present a comprehensive symptom of shock.
The blood output from the heart is reduced, and although the surrounding blood vessels contract, the blood pressure still drops. Reduced tissue perfusion, promotes anaerobic metabolism, and increases lactic acid and metabolic acidosis. Redistribution of blood flow allows brain and heart supply to be maintained. Further contraction of blood vessels can cause cellular damage. Damage to vascular endothelial cells results in loss of body fluids and proteins, aggravating hypovolemia. Multiple organ failure will eventually occur. The intestinal mucosa is impaired in the defense of antibodies derived from the intestine caused by hemorrhagic shock, and is likely to be an important pathogenesis of pneumonia and other infectious complications. The lethal dose of blood loss has an ability to cross-tolerate the attack on endotoxin. The lethal dose of blood loss can protect against lethal endotoxin challenge.
Examine
Hemorrhagic shock test
The examination of this disease mainly depends on physical examination and experimental examination:
1, physical examination
Detailed medical history and strict physical examination of the patient, the general lack of vascular content and the compensatory response of adrenal energy are reflected by these indicators.
2, experimental inspection
The experimental test is different from the physical examination because the body fluid movement is not very obvious in a short time after acute blood loss. It is difficult to reflect through the blood test indicators. If the blood loss process is slightly longer, the body fluid movement will gradually increase, and the blood will be presented. Concentration, manifested as increased hemoglobin, increased hematocrit, increased ratio of urea nitrogen to creatinine, if the process of blood loss is longer, the amount of blood loss is larger, especially the loss of free water gradually increases, and serum sodium increases, therefore, Accurate estimates of blood loss are based on laboratory blood tests.
Diagnosis
Diagnosis and diagnosis of hemorrhagic shock
In many cases, it is not too difficult to diagnose bleeding. Both medical history and physical signs can reflect the lack of vascular content and the compensatory response of adrenal energy. However, experimental testing is not entirely true. Because in the short time after acute blood loss, body fluid movement is not very obvious, it is difficult to reflect through blood test indicators. If the process of blood loss is slightly longer and the body fluid movement is gradually increased, the blood will be concentrated, which is manifested by increased hemoglobin, increased hematocrit, and increased ratio of urea nitrogen to creatinine. If the process of blood loss is long, the amount of blood loss is large, especially the loss of free water is gradually increased, and serum sodium is also increased. In short, the amount of blood loss in shock should be fully estimated, and it is often estimated that the clinical is insufficient.
When the blood loss is large, causing severe low-volume shock, and it is difficult to grasp the actual and regular changes in the clinical, especially if the rehydration therapy is difficult to show positive effects, it should be considered that the central venous catheter or pulmonary artery can be placed. Catheter for invasive hemodynamic monitoring. Central venous pressure (CVP) and pulmonary wedge pressure (PCWP) were reduced by central manometry, cardiac output was reduced, venous oxygen saturation (SVO2) was reduced, and systemic vascular resistance was increased.
