MindMap Gallery Pathophysiology-Shock
Pathophysiology-Shock, summarizes the mechanisms, changes in metabolic function, Common shock, etc. It is recommended to study by yourself with the textbook. I hope this mind map will be helpful to you!
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This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
This is a mind map about plant asexual reproduction, and its main contents include: concept, spore reproduction, vegetative reproduction, tissue culture, and buds. The summary is comprehensive and meticulous, suitable as review materials.
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shock
Note
↑
increase/expand/activate/promote
↓
reduce/shrink/suppress
concept
Cause—effective circulating blood volume↓—insufficient tissue perfusion—ischemia and hypoxia—structural and functional damage
Cause
Classification
The mechanism
microcirculatory mechanism
capillaries
Arterioles, posterior arterioles, precapillary sphincter (anterior resistance vessels), true capillaries, venules
Direct access, arteriovenous short circuit
adjust
Neurohumoral regulation-Jiaoshen marrow, AngII, VP, TXA2, ET
Blood vessels ↓
Local vasoactive substances - histamine, kinin, adenosine, PGI2, endorphins, TNF, NO
Acidic metabolite (lactic acid) - sensitivity of blood vessels to vasoconstrictor substances↓
Blood vessels ↑
installment
Ischemic phase - compensatory phase (early stage of shock)
Features
Less perfusion and less flow, less perfusion than flow, tissue ischemia and hypoxia
Small blood vessels ↓ (>anterior resistance vessels)
mechanism
↑Renal-medullary system—catecholamines↑
α—Small blood vessels↓
β
Arteriovenous short circuit opening
Peripheral—tissue perfusion↓
Pulmonary-venous blood oxygenation↓
↑Heart
Vasoconstrictor substances↑
Angiotensin II (AngII)
Vasopressin VP
Thromboxane A2 (TXA2), endothelin ET, leukotrienes LTs
Compensatory significance
maintain arterial blood pressure
Blood volume returned↑
Autologous infusion - obvious contraction of anterior resistance vessels - capillary hydrostatic pressure ↓ - interstitial fluid infiltration
Autotransfusion - contraction of blood storage organs
Cardiac output↑
Peripheral resistance↑
Maintain blood supply to heart and brain
clinical manifestations
Thin pulse, pulse pressure↓
Fluctuating blood pressure
Pale face, clammy limbs
Urine volume↓
Conscious and restless
Congestion phase - reversible decompensation phase
Features
Perfusion but little flow, perfusion greater than flow, tissue congestion and hypoxia
mechanism
Microvessel↑
Acidosis—vascular sensitivity to catecholamines↓
Vasodilator substances↑
blood stasis
Leukocyte adhesion to venules—outflow resistance↑
Hemoconcentration
Vasodilator substances-permeability↑-plasma extravasation
Decompensation and vicious cycle
Blood volume returned↓↓
Self-infusion stopped
Heart and brain blood supply↓
clinical manifestations
Blood pressure and pulse pressure continue↓
Heart blood supply↓
delirious - coma
Cerebral blood supply↓—central dysfunction
Oligouria and anuria
Kidney blood supply↓
Cyanosis or mottling
Deoxyhemoglobin↑
Failure stage - irreversible stage/refractory stage/DIC stage
Features
No irrigation, no flow
mechanism
microvascular paralytic dilation
DIC formation
Hypercoagulability
↑Coagulation system
endothelial injury
TXA2-PGI2 imbalance
Endothelial damage—TXA2↑, PGI2↓—platelet aggregation, small blood vessels↓
clinical manifestations
Circulatory failure—refractory hypotension
Concurrent DIC
organ dysfunction
cellular molecular mechanisms
Cell damage (sequentially)
1 cell membrane
Ion pump abnormality (Na pump, Ca pump)
Na, Ca influx, K outflow↑—cell edema
2mitochondria
ATP↓
3 lysosomes
Lysosomal enzyme release
4 cell death
↑Inflammatory cells-inflammatory mediators↑
Changes in metabolic function
Substance metabolism disorder
Hypermetabolism, acute phase protein synthesis
electroacidity disorder
Acid replacement (hyperlactatemia)
Early - infection, trauma - respiratory ↑ - respiratory alkali (early shock diagnosis)
Late stage-shock lung-acidic breathing
hyperkalemia
Hypoxia-ATP↓-Na pump↓-blood K↑
Acid-H-K exchange↑
organ dysfunction
Shock lung-ARDS
shock kidney
Cross-renal medullary system-catecholamine-kidney A↓
renal aldehyde system
AngII-kidney A↓
ADH, aldosterone↑-sodium and water retention, urine output↓
Liver dysfunction
Common shock
hemorrhagic shock
Blood loss >20% within 15 minutes - cardiac output, mean arterial pressure MAP↓
septic shock
pathogenic microbial infection
cause
Direct damage to blood vessels/myocardium
Stimulate inflammation-SIRS
Cytokines, vasoactive substances-blood vessels↑, permeability↑
High dynamic shock (warm shock)
high metabolism
High power cycle - high discharge and low resistance
mechanism
renal medullary system
Catecholamines↑-↑β-cardiac output↑
Vasodilator substance↑-Peripheral blood vessels↑-Peripheral resistance↓
Low dynamic shock (cold shock)
Low power cycle - low exhaust, high resistance
mechanism
Pathogen toxins/acidosis/inflammatory mediators-direct ↓cardiac-cardiac output↓
Strong excitement of the renal medullary system - vasoconstrictor substance ↑ - peripheral blood vessels ↓ - peripheral resistance ↑
anaphylactic shock
Type I allergic reaction, accompanied by urticaria, respiratory and digestive tract allergies, acute onset
Blood vessels ↑
Permeability↑
cardiogenic shock
Cardiac pump dysfunction-cardiac output↓-blood pressure in early stage of shock↓↓
>Low discharge high resistance type
Low discharge and low resistance type