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Patient - shock
This is a mind map about the patient-shock. Symptoms include pale or purple complexion, clammy limbs, slow pulse, oliguria, lack of consciousness, low blood pressure, etc.
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Patient - shock
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- Outline
shock
concept
It is a variety of strong therapeutic factors that act on the body to cause acute microcirculatory failure. It is characterized by microcirculation disorders, insufficient return flow to important organs and cell function and metabolism disorders. The resulting systemic critical pathological process.
Overview of classic symptoms
Pale or cyanotic complexion, clammy limbs, slow pulse, oliguria, indifferent mind, and low blood pressure
Cause
blood and fluid loss
Burns are associated with pain and fluid loss
Trauma is associated with pain and blood loss
Infect
allergy
acute heart failure
strong mental stimulation
Changes in cellular metabolism and organ dysfunction
Cell metabolism disorder
Insufficient oxygen supply, enhanced glycolysis
Insufficient energy, sodium pump failure
local acidosis
cell damage
changes in cell membrane
Mitochondrial changes
changes in lysosomes
vital organ failure
Acute renal dysfunction—shock kidney
(Insufficient renal perfusion) functional failure organic failure
Acute respiratory failure—shock lung
(respiratory membrane damage)
cardiac dysfunction
Coronary artery function reduced blood flow
Acidosis or hyperkalemia has a depressive effect on myocardium
myocardial inhibitory factor
intramyocardial DIC
Cytotoxicity inhibits myocardial function
Pathophysiological basis of shock prevention and treatment
Cause prevention and treatment
Pathogenesis prevention and treatment
correct acidosis
Expand blood volume
Rational use of vasoactive drugs
Prevention and treatment of cell damage
Use of humoral factor antagonists
Prevent and treat organ failure
Staging and pathogenesis of shock
Ischemic shock (compensated)
The changing characteristics of microcirculation
There is spasm of blood all over the body, and the Yang force in front of the capillaries increases significantly. Blood flow slows down, blood flow is limited Fortunately, the circuit is closed, the movement and movement are short-circuited and misfired, and tissue perfusion is reduced.
Microcirculation obstacle mechanism
Sympathetic-adrenomedullary system excitement
Vasoconstrictor substances
Compensatory significance of microcirculatory changes
Muscular venules and venules contract, and the hepatic blood reservoir contracts, rapidly and briefly increasing blood return to the heart. volume, called “autotransfusion”
The front resistance of capillaries is greater than the rear resistance (arteries are greater than veins), and tissue fluid flows back into the blood, which is called "autoinfusion"
blood redistribution
Increased myocardial contractility and increased peripheral resistance
clinical manifestations
Pale face, cold limbs, cold sweat, thin pulse, decreased pulse pressure, irritability Note: blood pressure changes, can be normal or reduced
Stasis-hypoxic phase (compensatory phase may be missing)
Characteristics of changes in microcirculation
Spasm of arterioles and posterior arterioles is reduced, venules dilate, and blood flows into the capillary network, Increased resistance at the venous end (posterior resistance is greater than anterior resistance), microcirculatory blood stasis
Stasis mechanism of microcirculation
Ischemia and hypoxia cause acidosis, which leads to reduced vascular responsiveness to catecholamines
Ischemia and hypoxia lead to increased production of local blood-expanding substances
Due to the effect of endotoxin (intestinal bacteria entering the bloodstream), LPS can cause vasodilation through multiple pathways
Blood rheology changes (related to white blood cells)
decompensation
clinical manifestations
Blood progressively decreases and various manifestations increase to varying degrees
Refractory period of shock (irreversible period)
DIC (disseminated vascular coagulation) formation
Hemoconcentration, increased blood viscosity, and blood in a hypercoagulable state
Acidosis
The role of septic shock toxins
The role of septic shock toxins and traumatic shock tissue factor entering the blood
vital organ failure
Classification
Classification by cause
hemorrhagic shock
burn shock
septic shock
anaphylactic shock
cardiogenic shock
neurogenic shock
According to the initial stage of shock
hypovolemic shock
vasogenic shock
subtopic
The basis for achieving effective perfusion
Need enough blood
Requires normal vasomotor function
Requires normal heart pump function
Vasoconstrictor substances: catecholamines, angiotensin②, vasopressin, TXA2 (thromboxane), endothelin
Vasodilator substances: histamine, kinin, adenosine, PG12 (prostacyclin), NO (endothelium-derived relaxing factor
Concept of microcirculation: The blood circulation in the microblood chapter between arterioles and venules is the blood The smallest functional unit for metabolic exchange of substances between tissues