Hemorrhagic shock is what causes

Microcirculation (ischemia congestion disseminated intravascular coagulation) of microcirculation blood perfusion less than the life of an important organ because of asphyxia and metabolic functions in various types of obstacles is the common shock of shock-cycle changes can be broadly That is, for the three-cycle ischemia microcirculation congestion period and the microcirculation of blood coagulation

(A) of micro-circulation ischemia (hypoxic ischemic period)

Micro-cycle changes in this period was characterized by: ① after the micro-micro-artery artery and capillary sphincter contraction before the micro-irrigation cycle dramatically reduce traffic pressure on the lower; ② micro-and small vein vein of catecholamine less sensitive contraction lighter; ③ arteriovenous anastomosis Support may have different degrees of blood from the open-artery anastomosis with the arteriovenous directly into the small veins

Microcirculation ischemia caused a critical change is sympathetic - adrenomedullin system strongly excited different types of shock can be caused by different mechanisms sympathetic - adrenomedullin shock and cardiac shock when cardiac output and reduce arterial blood pressure Can be reduced through the arch sinus reflex sympathetic to - excited adrenomedullin system in the majority of endotoxin shock endotoxin can directly stimulate the sympathetic - adrenomedullin system make it a strong excitement

Sympathetic excited about the release of catecholamines on the cardiovascular system to increase the overall effect is to make the total peripheral resistance and increased cardiac output increase but different organs of the reaction vessel by a difference in the skin of the abdominal organs and kidney is rich in blood vessels due to sympathetic shrink Vascular and disposable fiber α receptor and thus take advantage of the sympathetic catecholamine more excited when these parts of the arteries-arteries and veins of small capillaries including former Red muscle contraction which have taken place in the artery because of micro-fiber sympathetic vasoconstrictor distribution of the capillary Vascular before catecholamines sphincter of the response of the strongest so that they contracted the most strong resistance before the result was significantly higher capillary micro-irrigation cycle of capillary flow dramatically reduced the average blood pressure decreased by only a small amount of blood straight Jie Tong Road and a few really into the capillaries Micro-vein small vein organizations so serious hypoxic ischemic brain vascular sympathetic vasoconstrictor fiber distribution of at least α-density low-calibre can be no significant changes in coronary Although there are also sympathetic innervation and β receptor α sympathetic but excited And catecholamines are more activities to strengthen the heart by raising the level of metabolism that vasodilative metabolites in particular the increase in adenosine coronary expansion

Sympathetic excited and can reduce blood volume activation of the renin - angiotensin - Ⅱ angiotensin-aldosterone system and have a stronger role in the vasoconstrictor, including the contraction of the coronary

Besides the increase in catecholamine stimulation can produce more platelet thromboxane A2 (thromboxane A2, TXA2) and TXA2 also have a strong role in the vasoconstrictor



Hemorrhagic shock



Figure 1 microcirculation model of the development process

1. Normal circumstances

⑴ arteriovenous anastomosis with the closure of the

⑵ only 20% of capillary blood perfusion rotation and opening up

⑶ capillaries open and close the capillaries before sphincter contraction and relaxation of the regulation

2. Microcirculation ischemia

⑴ sympathetic excitement and adrenaline secretion of norepinephrine increase in small arteries after artery-artery-capillary before sphincter contraction

⑵ arteriovenous anastomosis with blood by the open-artery directly into the small veins

⑶ capillary blood perfusion less than hypoxia

3. Microcirculation of blood stasis

⑴ small and micro-artery contraction artery anastomosis with arteriovenous still in the open state of the capillary into the blood is still very small

⑵ due to hypoxia histamine bradykinin hydrogen ions and other substances increased after Shu-vascular arteries and capillaries sphincter relaxation before the opening capillary blood vessels to expand into the volume of capillary blood flow is slow

⑶ sympathetic excited because epinephrine and norepinephrine secretion increased (and possibly the role of histamine) to enable small and micro-vein capillary veins shrink after the results of increased resistance to blood stasis telangiectasia

4. Microcirculation of blood coagulation

⑴ due to hypoxia organizations serious acid poisoning capillary wall damage and increased permeability of capillary blood flow stasis concentrated other blood coagulation results in increased microcirculation produced disseminated intravascular coagulation

⑵ due to more heavy-thrombosis hypoxia and metabolic barriers lysosomal rupture cells from the tissue necrosis serious organ dysfunction

⑶ because of clotting blood coagulation factor (such as the prothrombin fibrinogen, etc.) and platelet consumption by a large number of fibrin degradation products also increased to reduce blood coagulation; damaged vessel wall and then extensive bleeding occurred

And TXA2 also have a strong role in the vasoconstrictor

There are lysosomal enzyme - myocardial inhibitor system in the shock stage Ⅰ microcirculation in the incidence of ischemic also played a role mainly due to shock when the pancreas reduced blood flow caused by irrigation of ischemia and hypoxia and acidosis can pancreatic Exocrine cells rupture and release of lysosomal cathepsin decomposition of the latter to generate protein and myocardial inhibitory factor (myocardial depressant factor, MDF) MDF small peptides into the blood after contraction in addition to cause myocardial weakened inhibition mononuclear phagocytes Phagocytosis outside the system can make visceral abdominal contraction of the small blood vessels so as to further increase the weight of these parts microcirculation of ischemic

This issue's main clinical manifestations are: skin pale limbs Jueleng a cold sweat urine output decreased because of peripheral resistance can not increase significantly reduce systolic blood pressure and diastolic blood pressure has increased the pulse of small-speed pulse pressure decreases; clear consciousness, such as irritability

Micro-cycle changes in this period have a certain significance of compensatory skin and abdominal organs, and other small artery contraction can increase peripheral resistance in order to maintain blood pressure can reduce the number of tissues and organs of blood flow to ensure that the heart and brain and other vital organs of the blood supply; capillary ago Resistance increased capillary fluid pressure to reduce tissue fluid entered the blood plasma to increase the capacity of other arteriovenous open vein anastomosis with the contraction capacity of narrow vein (some 70% of normal blood in the veins) can speed up and increase output but also conducive to Huixin blood pressure The maintenance of heart and brain and the blood supply because most of tissues and organs because of microcirculation to lack of blood perfusion in hypoxia will lead to the further development of shock if early detection of positive timely rescue added output to reduce the drama of the stress response can be quickly Improve microcirculation and restore blood pressure to prevent further deterioration of shock and Turning the Tide

At this time the mechanism of micro-cycle changes can be summarized as follows (Figure 2):

(B) microcirculation congestion period (congestion period of hypoxia)

In a shock through the cycle of ischemia such as failure to improve microcirculation early for emergency treatment due to the ongoing and serious vascular Shu hypoxia local materials (such as histamine bradykinin acid adenosine, etc.) after the number of arterioles and capillaries Sphincter relaxation before expand micro-cycle capacity to shock the development of congestion-congestion period of this cycle of micro-circulation is characterized by: ① after the arteries and capillaries-before sphincter relaxation (a result of local acidosis catecholamine response to lower) open a large number of capillaries Was not the side of the capsule-shaped expansion (pool of blood-forming) expansion of micro-circulation volume; ② micro-and small vein vein of local acidosis catecholamine still greater tolerance to shrink (histamine can make hepatopulmonary Vein, such as micro-and small vein shrinkage) after the resistance increased capillary blood flow -slow; ③ microvascular wall of plasma leakage increased permeability of blood stasis; ④ concentrated blood cells as blood pressure increases red blood cell plot of platelet aggregation interleukin impaction Adhesion and aggregation, and other changes in hemorheology microcirculation blood flow can slow down or even stop the ⑤ microcirculation congestion due to increased pressure on Circulating the blood into the micro-less (At this point small and micro-artery artery is still in effect due to sympathetic Contraction) due to massive siltation in the blood-circulating Huixin output to reduce cardiac output further reduce the shock of increased development



Hemorrhagic shock



Figure 2 hypoxic ischemic mechanism of micro-cycle changes

As a result of these micro-cycle changes in the microcirculation Although the plot but a large number of arterial blood flow irrigation will be reduced even more patients from the pale skin color gradually cyanosis especially because I-chen and fingertip vein to flow and cardiac output decrease more patients intravenous wilt depression Filling slow arterial pressure decreased pulse pressure on the small clock speed; heart and brain due to insufficient supply of blood and reduce the ATP generation performance for the weakening of the heart contraction (lower heart sounds) or indifferent expression of consciousness can occur unclear serious heart and kidney failure that lung function Is the critical state of shock should immediately lift the rescue of small vasospasm rehydration of oxygen to correct acid poisoning to clear the microcirculation and prevent disseminated intravascular coagulation when the mechanism of micro-cycle changes can be summarized as follows (Figure 3):

Hemorrhagic shock



Figure 3 congestion period of hypoxia-cycle changes in the mechanism

(C) microcirculation of blood coagulation (disseminated intravascular coagulation)

Microcirculation from the congestion phase of the development cycle for the micro-coagulation is the shock of the deteriorating performance of its features are: microcirculation congestion on the basis of the microcirculation (especially micro-capillary veins vein small vein) fibrin thrombosis And often focal or diffuse bleeding due to severe hypoxic cells caused necrosis

Disseminated intravascular coagulation and the shock of the extremely close contact on disseminated intravascular coagulation caused pathological changes and how it can cause shock or add to the development of in shock, "disseminated intravascular coagulation," a chapter here again discussed the outline How to summarize the shock caused disseminated intravascular coagulation

1. Stress response to increased blood coagulation of the cause of shock (such as burn wounds bleeding, etc.) and the shock itself is a strong stimulus can cause stress and excitement of pituitary sympathetic - adrenal cortex activities to strengthen the blood Platelet and clotting factor in the increase of platelet aggregation and adhesion to strengthen the capacity of blood coagulation provide the necessary material foundation

2. Clotting factor and the activation of the release of some cause shock (such as trauma burns, etc.) can make their own clotting factor release and activation of the damage such as the organization can release a large number of organizations thromboplastin start of exogenous clotting process; large Burned large number of red blood cells to destroy the red blood cell membrane phospholipid destruction of red blood cells and release of the ADP process to promote blood coagulation

3. Microcirculation hypoxia local histamine bradykinin, such as lactic acid number of these substances on the one hand telangiectasia congestion caused increased permeability of the slow flow of blood viscosity increase red blood cell concentration is conducive to thrombosis; On the other hand damage capillary Vascular endothelial cells exposed collagen activate clotting factor Ⅻ and the platelet adhesion and aggregation

4. Hypoxia engulfed the single-cell nuclear systems can not function timely removal of thrombin and thrombin yuan fibrin results in the role of these factors caused disseminated intravascular coagulation

Disseminated intravascular coagulation event will microcirculation more serious shock condition further deteriorated this is because: ① wide range of microvascular obstruction microcirculation to further increase output further reduce Huixin; ② clotting substances that Deplete the secondary fibrinolysis activation And other factors cause bleeding so that reduced blood volume; ③ soluble fibrin polymer and its products, such as cracking can be swallowed up by the closed-cell system so that the toxins from the intestine can not be fully cleared

As disseminated intravascular coagulation and the occurrence of microcirculation congestion due to the continuous increase of blood pressure lowering of the body caused by micro-irrigation cycle of the severe shortage of general flow of hypoxia and acidosis will also become increasingly serious; serious acid poisoning also can Cell membrane rupture within the lysosomes release of lysosomal enzyme (such as hydrolyzed protein Meideng) and cause some shock (such as endotoxin, etc.) so that cells can be serious and irreversible damage to the heart and brain, including the The various metabolic functions of vital organs are more serious obstacles (in detail later) that gave cause great difficulties for the current period is also known as the refractory period of shock