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Pathophysiology-Shock
Pathophysiology - The mind map of shock refers to the ischemic deficiency of tissue cells caused by a sharp increase in effective circulating blood volume and a serious lack of tissue perfusion under the influence of strong pathogenic factors such as severe blood loss and fluid loss, trauma, and infection. Systemic pathological process of oxygen, functional/metabolic disorders of various organs and structural damage.
Edited at 2023-10-27 15:05:37
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Pathophysiology-Shock
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shock
installment
Early shock/shock compensatory stage/ischemic hypoxic stage
1. Characteristics of microcirculatory changes
Less perfusion and less flow, less perfusion than flow, and the tissue is in a state of ischemia and hypoxia
Continuous contraction of small blood vessels throughout the body (especially arterioles, posterior arterioles and precapillary sphincter) → anterior resistance > posterior resistance → closure of true capillaries, blood reflux through direct pathways and open arteriovenous anastomoses → tissue perfusion The traffic is obvious↓
2. Mechanism of microcirculatory changes
(1) Sympathetic nerve excitation: direct excitation/indirect excitation of decompression reflex → a large amount of catecholamines are released into the blood → α receptor effect (constriction of small blood vessels in the skin, viscera, and kidneys), β receptor effect (microcirculation arteriovenous short circuit opening)
(2) Release of vasoconstrictor humoral factors: AngII, ADH, TXA2, endothelin (ET), LT
3. Compensatory significance of microcirculatory changes
(1) Conducive to the maintenance of arterial blood pressure: ① auto-blood transfusion, auto-infusion ② → blood return volume ↑; ② CO↑ → heart rate ↑, myocardial contractility ↑, blood return volume ↑; ③TPR↑
(2) Conducive to blood redistribution → ensuring blood supply to the heart and brain
4. Main clinical manifestations
Pale complexion, clammy limbs, thin and rapid pulse, decreased urine output; but still conscious and with obvious difference in pulse pressure↓
(Blood pressure ↓ is actually not obvious, so it has more early diagnostic significance than blood pressure ↓)
Progressive stage of shock/decompensated stage of reversible shock/congestive hypoxic stage
1. Characteristics of microcirculatory changes
Perfusion but little flow, perfusion greater than flow, the tissue is in a state of congestion and hypoxia
Contractility of arterioles, posterior arterioles, and precapillary sphincter ↓ or even expansion → A large amount of blood pours into the true capillary network → Although the venules are dilated, the outflow resistance is ↑ → Anterior resistance < posterior resistance → Capillaries are open ↑, and blood is stagnated in the venules in loop
2. Mechanism of microcirculatory changes
(1) Mechanism of microvascular dilation (despite continued excitation of the sympathetic-adrenal medullary system)
① Acidosis: massive accumulation of lactic acid → metabolic acidosis → sensitivity of vascular smooth muscle to catecholamines↓
②Generation of blood vessel dilating substances↑: histamine, adenosine, bradykinin, NO
(2) Mechanism of blood stasis
①Leukocyte adhesion to venules →outflow tract resistance↑
②Capillary permeability↑→Plasma extravasation, hemoconcentration, blood viscosity↑
3. Decompensation and the creation of a vicious cycle (impact on the body)
(1) The amount of blood returned↓ and the formation of a vicious cycle
① A large number of microcirculatory vascular beds are opened and blood is stagnant → The effective circulating blood volume is sharply reduced, and the return blood volume↓→CO↓, BP↓→The sympathetic-adrenal medullary system is more excited→The blood perfusion is further↓, and the tissue hypoxia becomes more severe. serious;
② Stop autoinfusion and autologous blood transfusion → restore blood volume ↓↓;
③Capillary permeability↑→blood viscosity
(2) Cardio-cerebral blood perfusion↓
Progressive mean arterial pressure ↓ (<50mmHg) → loss of autoregulation
4. Main clinical manifestations
① Progressive blood pressure ↓ → rapid pulse, venous collapse; ② Insufficient perfusion of coronary arteries and cerebral vessels → weak heartbeat, apathy or even coma;
③ Renal blood flow ↓ → Oliguria or even anuria; ④ Increased coolness of the skin, cyanosis, and mottling may occur
Shock refractory stage/DIC stage/irreversible decompensation stage/microcirculatory failure stage
1. Characteristics of microcirculatory changes
No irrigation, no flow
Paralytic dilation of microvessels, large capillary openings, microcirculation thrombosis → blood flow stops, and capillary no-reflow may occur
2. Mechanism of microcirculatory changes
(1) Paralytic dilation of microvessels
①Acidosis→H competitively inhibits the binding of Ca2 to troponin;
②iNOS activation→NO↑→cGMP↑→Ca2 ↓
③KATP opening on vascular smooth muscle cells→membrane hyperpolarization→voltage-dependent calcium channels are inhibited→Ca2 influx↓
(2) Formation of DIC
①Activation of coagulation system
a. Severe hypoxia/acidosis/endotoxin damages vascular endothelial cells → massive release of tissue factor → activates the extrinsic coagulation pathway;
b. Endothelial cells are damaged → expose subendothelial collagen → activate the intrinsic coagulation pathway;
c. Massive destruction of RBC → release of ADP → promote platelet aggregation
②Stress response→Procoagulant substances↑
③TXA2-PGI2 imbalance: endothelial cell damage → PGI2 production ↓; platelet activation → TXA2 production ↑
④ Changes in blood rheology: slowed blood flow, hemoconcentration, blood viscosity ↑ → blood hypercoagulability
⑤Phagocytosis function of monocyte macrophage system↓
3. Serious consequences
①Microthrombosis → blood vessel obstruction and organ infarction;
②Hemorrhage; ③Microvascular permeability↑
4. Main clinical manifestations
(1) Circulatory failure: refractory progressive hypotension (vasopressors are ineffective), weak and rapid pulse, reduced CVP, superficial vein collapse (difficulty in intravenous infusion)
(2) Concurrent DIC
(3) Capillary no-reflow phenomenon: massive blood transfusion and fluid replenishment → blood pressure rises, but sometimes capillary blood flow still cannot be restored
(4) Vital organ dysfunction/failure
Cellular changes (cellular molecular mechanisms)
Common basis for organ dysfunction
1. Cell membrane damage: permeability↓, changes in membrane phospholipid microenvironment, cAMP↓ leading to signal transduction disorders
2. Mitochondria damage: It is the first organelle to change during shock; it can initiate cell apoptosis.
3. Lysosomal damage: release related lysosomal enzymes → cell autolysis, damage organelles, promote the occurrence of DIC, and produce myocardial depressant factor (MDF)
Pathophysiological basis of prevention and treatment
(1) Etiological prevention and treatment
(2) Pathogenesis prevention and treatment
1. Improve microcirculation - the central link in treating shock
(1) Expand blood volume (principle of fluid replenishment)
① During the ischemic period of microcirculation, fluids should be replenished promptly and as early as possible;
② During the microcirculatory stasis period, "replenish as much as you need";
③The total amount of fluid replacement must be correctly estimated → PAWP (the best indicator for monitoring shock infusion) and CVP can be used as monitoring indicators if possible, and Hct is controlled at 35%~40%
(2) Rational use of vasoactive drugs
(3) Correct acidosis and electrolyte imbalance
2. Prevent and treat cell damage: stabilize membranes, scavenge free radicals, and replenish energy.
3. Antagonize the harmful effects of inflammatory mediators
5. Others: such as metabolic support therapy, improving oxygen supply
4. Prevent and treat organ dysfunction and failure
Body metabolism and functional changes
Metabolic disorders
substance metabolism disorder
(1) Features: reduced oxygen consumption, enhanced glycolysis, increased decomposition/reduced synthesis of fat and protein (septic autocatabolism)
(2) Clinical manifestations: (early) transient hyperglycemia and glycosuria, increased free fatty acids and ketone bodies in the blood, increased serum urea nitrogen levels, increased urinary nitrogen excretion → negative nitrogen balance
Electrolyte and acid-base balance disorders
(1) Hypoxia leads to glycolysis ↑ Liver function ↓ causing lactic acid to be unable to be converted into glucose Renal function ↓ causing lactic acid to be unable to be excreted from the body → lactic acid ↑ → AG increased metabolic acidosis → myocardial contractility ↓, smooth muscle of blood vessel walls is sensitive to catecholamines Sex↓→CO↓、BP↓
(2) Breathing deepens and accelerates → Respiratory alkalosis ① (early stage) → Respiratory acidosis (late stage shock lung)
(3) Hyperkalemia
organ dysfunction
(1) Pulmonary dysfunction (shock lung) (most common)
1. Early stage of shock: hypocapnia, respiratory alkalosis
2. Late stage of shock: progressive hypoxemia & dyspnea - ARDS/Shock Pulmonary (see "Pulmonary Insufficiency")
3. Reasons why the lungs are easily damaged: ① The lungs are filters for systemic blood; ② Activated neutrophils in the blood adhere to the endothelial cells of the small pulmonary vessels; ③ The lungs are rich in macrophages, which can produce TNF, etc. pro-inflammatory mediators
4. Mechanism: ① DIC formation in small pulmonary blood vessels; ② Damage to respiratory membrane → pulmonary edema and hyaline membrane formation; ③ Alveolar surfactant ↓ → Alveolar collapse
(2) Renal dysfunction (shock kidney)
1. Early stage of shock - acute functional renal failure (reversible): ① Sympathetic nerve ( ) → renal vasoconstriction; ② Renal ischemia → RASS ( ) → AngⅡ → renal vasoconstriction; ③ADS, ADH↑
2. Late stage of shock - organic renal failure (irreversible)
(3) Heart dysfunction
1. Cardiogenic shock is accompanied by primary cardiac dysfunction; early heart failure is also uncommon in non-cardiogenic shock (compensation effect)
2. The mechanism of cardiac dysfunction when non-cardiogenic shock develops to a certain stage
① Sympathetic nerve ( ) → myocardial contractility ↑ → myocardial oxygen consumption ↑ → myocardial contractility ↓;
② Sympathetic nerve ( ) → heart rate ↑ → diastolic duration ↓ → coronary blood flow ↓;
③Metabolic acidosis and hyperkalemia;
④Active factors (such as inflammatory mediators, MDF) increase myocardial contractility ↓;
⑤Bacterial toxins;
⑥Intramyocardial DIC affects the nutritional blood flow of the myocardium and causes focal necrosis.
(4) Brain dysfunction
1. Early stage of shock: no obvious obstacles (compensation)
2. Late stage of shock: severe ischemia and hypoxia of brain tissue → cerebral edema and increased intracranial pressure
(5) Gastrointestinal dysfunction
1. Early stage of shock: stress ulcer
2. Bacterial translocation (see below)
(6) Liver dysfunction
1. Reason
① When bacteria translocate, the bacteria and toxins absorbed into the blood first act on the liver (can cause direct damage) → Kupffer cells activate and secrete inflammatory mediators to damage liver cells;
② The liver has high purine oxidase content and is prone to ischemia-reperfusion injury.
2. Liver dysfunction → blocked lactic acid metabolism → accelerated acidosis
(7) Immune system dysfunction
1. Early stage of shock: immune system is activated
2. Late stage of shock: immune system is suppressed
(8) Multiple organ dysfunction syndrome
Overview
definition
It refers to the ischemia and hypoxia of tissue cells, functional/metabolic disorders of various organs and Systemic pathological process of structural damage
Cause
Hypovolemic shock: hemorrhagic shock, fluid loss shock/collapse
septic shock
Anaphylactic shock: Type I hypersensitivity reaction
Classification
severity
Mild: less than 20% of total body blood volume (<800ml for adults), in the compensatory stage of shock
Moderate 20~40% of whole body blood volume (800~1600ml for adults) Can be corrected with timely treatment
Severe: more than 40% of total body blood volume (>1600ml in adults) refractory shock, prone to MODS
Hemodynamic characteristics
Low-discharge, high-resistance shock (low power
Features
CO↓, cardiac index↓, total peripheral resistance (TPR)↑, CVP↓
clinical manifestations
Cold shock: mean arterial pressure ↓ is not obvious, pulse pressure difference is significant ↓ → urine output is obvious ↓,
Pale and clammy skin, rapid pulse, and indifferent expression
mechanism
① Toxins directly damage the myocardium
②Severe infection → Sympathetic-adrenal medullary system ( ) → Vasoconstrictor substance ↑
The cause is seen in
Hypovolemic shock, cardiogenic shock, traumatic shock, most septic shocks
High-discharge, low-resistance shock (high motility
Features
CO↑, cardiac index↑, TPR↓, CVP↑
clinical manifestations
Warm shock: Slightly low blood pressure, poor pulse pressure↑, significant arterial blood oxygen difference↓, blood flow↑→warm and dry skin, fast and strong pulse
mechanism
①β receptor activation
② Vasodilator substance ↑, KATP ( ) → peripheral blood vessel dilation
The cause is seen in
A small number of septic shock, anaphylactic shock, neurogenic shock
Low discharge and low resistance type
Features
CO↓, cardiac index↓, TPR↓
clinical manifestations
Mean arterial pressure, systolic blood pressure, and diastolic blood pressure are all↓
mechanism
Ventricular end-diastolic volume↑→stimulate ventricular wall stretch receptors→reflexively inhibit the sympathetic center
The cause is seen in
Various types of late stage shock (decompensation)
The initial stage of shock
Common links in shock
Decreased blood volume, increased vascular bed volume, and sharp decrease in cardiac output
hypovolemic shock
Mechanism: acute blood volume↓→insufficient venous return, CO↓, blood pressure↓→baroreceptor negative feedback↓→sympathetic nerve excitement→peripheral vasoconstriction, tissue perfusion↓
Clinical manifestations (three lows and one high): low CVP/CO/BP, high TPR
Examples: hemorrhagic shock, fluid loss shock, burn shock
Hematogenous shock (distributive)
Mechanism: Vasoactive substances ↑→ Small blood vessels, especially small blood vessels in the abdominal viscera, dilate and vascular bed volume ↑ → A large amount of blood is stagnated in the dilated small blood vessels → Effective circulating blood volume ↓
Examples: septic shock, anaphylactic shock, neurogenic shock
cardiogenic shock
Mechanism: Myocardial origin/non-myocardial origin (extracardiac obstruction) → Heart pump failure → CO acute ↓ → Effective circulating blood volume ↓
Examples: massive acute myocardial infarction, acute cardiac tamponade, pulmonary hypertension
obstructive shock
Mechanism: Blood flow channels are blocked
Examples: restrictive cardiomyopathy, tension pneumothorax, massive pulmonary embolism, aortic dissection