MindMap Gallery Pathophysiology of shock content
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shock
Glossary
Shock means that under the action of strong pathogenic factors such as severe blood loss and fluid loss, infection, and trauma, the effective circulating blood volume is sharply reduced, and tissue blood perfusion is seriously insufficient, causing cell ischemia and hypoxia, resulting in the failure of important life organs. , systemic critical pathological process of metabolic disorder or structural damage.
Causes and Classification
Classification according to the cause of shock
Hemorrhagic shock, traumatic shock, burn shock, septic shock, cardiogenic shock, neurogenic shock, anaphylactic shock
Classification according to the initiating stage of shock
common basis for shock
Effective irrigation volume
enough blood
normal vasomotor function
normal heart pump function
hypovolemic shock
Decreased blood volume
vasogenic shock
Peripheral vasodilation and increased vascular bed capacity
cardiogenic shock
Heart pump dysfunction, sharp reduction in cardiac output
development mechanism
Structure and Regulation of Microcirculation
Glossary: Microcirculation refers to the blood circulation of microvessels between arterioles and venules. It is the most basic structure of the circulatory system and the smallest functional unit for metabolic exchange of substances between blood and tissue cells.
structure
seven units
Arterioles, posterior arterioles, precapillary sphincters, true capillaries, direct pathways, arteriovenous junctions, and venules
three paths
Roundabout pathway, direct pathway, arteriovenous short circuit
two gates
Anterior gate: precapillary resistance
Post-gate: post-capillary resistance
adjust
Perfusion is mainly regulated by neurohumoral fluids
Sympathetic innervation of arterioles and venules
Arterio-venous regulation of body temperature
Staging of shock and changes in microcirculation
installment
compensatory period
Shock stage 1 (microcirculatory ischemic hypoxic stage)
Microcirculation and tissue perfusion characteristics
Less perfusion and less flow, less perfusion and less flow, severe microcirculation ischemia and hypoxia
The mechanism of microcirculatory tissue disorder
The sympathetic-adrenomedullary system is excited and catecholamines are released into the blood in large quantities.
Secondary to the initiating mechanism, various other humoral factors are produced in the body
Compensatory significance of microcirculatory changes
Helps maintain arterial pressure in early stage of shock
Increased blood return to the heart, increased cardiac output, and increased total peripheral resistance
Helps maintain blood supply to the heart and brain
clinical manifestations
Pale face, cold limbs, cold sweat, thin pulse, decreased pulse pressure, decreased urine output, irritability
Treatment principles
Eliminate the causes of shock as early as possible and inhibit the conditions for the development of lesions
decompensation period
Shock stage 2 (microcirculatory congestion and hypoxia stage)
Perfusion characteristics
Perfusion but little flow, perfusion greater than flow, tissue congestion and hypoxic state
The mechanism of microcirculatory stasis
acidosis
Local metabolite effects
Endotoxic effects
Changes in blood rheology
Consequences of microcirculatory congestion
The effective circulating blood volume decreases sharply, plasma extravasation, hemoconcentration, and reduced peripheral resistance lead to a decrease in cardiac and cerebral blood perfusion and dysfunction.
clinical manifestations
Weak heartbeat, dull heart sounds, apathy and transition to coma; oliguria or even anuria; weak and rapid pulse, collapsed veins, cyanosis of the skin, and mottling may appear
Treatment principles
Correct acidosis to increase vascular responsiveness to active drugs
Infusion to expand blood volume and replace lost blood volume
Unblock microcirculation
Refractory period
Shock stage 3 (microcirculatory failure stage)
Perfusion characteristics
No irrigation, no flow
Significant decrease in microvascular reactivity
Capillary no-reflow phenomenon
Occurrence of DIC
DIC is a complication of late stage shock
The mechanism of DIC formation
Changes in blood rheology
Activation of the coagulation system
PGI2/TXA2 imbalance
Decreased monocyte-macrophage system function
Impact and consequences of DIC
Aggravate microcirculatory disorders and further reduce cardiac return volume
Cause bleeding and reduce blood volume
Increase vascular permeability and aggravate microvasomotor dysfunction
aggravation of acute organ failure
vital organ dysfunction
Renal dysfunction, cardiac dysfunction, pulmonary dysfunction, brain dysfunction, digestive tract and liver dysfunction, multiple organ dysfunction syndrome
Prevention and control
Pathology prevention and treatment
Actively prevent and treat primary diseases causing shock
pathogenesis treatment
correct acidosis
Expand blood volume
Rational use of vasoactive drugs
Prevent and treat organ failure
antagonist humoral factor