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297418
Shock
Descripción
Doctorate Pathology Mapa Mental sobre Shock, creado por melian.yates el 23/10/2013.
Sin etiquetas
pathology
pathology
doctorate
Mapa Mental por
melian.yates
, actualizado hace más de 1 año
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Creado por
melian.yates
hace casi 11 años
35
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Resumen del Recurso
Shock
Types
Cardiogenic
Failure of the heart to pump properly
Causes:
Death of Cardiac muscle
Ex. Disease of blood vessels
Thrombosis
Arrhythmia
Obstruction of blood flow leaving heart
Ex. PTE (Pulmonary thromboembolism)
Primary Cardiac Disease
Ex. DCM, HCM
DCM: Dogs
HCM: Cats
Cardiomegaly
Tricuspid valve dysplasia
Myocardial fibrosis
Decrease in SV & CO
Hypovolemic
Shock due to reduced circulating blood volume
Causes:
Blood Loss
Haemorrhage
Blood volume = 7% of BW
Ex. 5kg Cat: 5 *.07 = 0.35L = 350mL blood
Fluid loss
Vomiting, Diarrhea, Burns
Hypotension & Hypoperfusion
Recovery possible under certain circumstances
If caught early => Fluid Therapy
Can lose 10% of fluid volume
Blood Maldistribution
Blood pools in peripheral tissues due to a decrease in peripheral resistance in blood vessels
Blood volume is unchanged, but the VASCULAR SPACE increases so that effective circulating blood volume decreases
Types:
Neurogenic Shock
Damage to CNS (usually spinal cord)
Loss of autonomic signals to smooth muscle in blood vessel walls
Vasodilation
Blood pooling in veins
Need resistance to keep blood flowing
Anaphylactic Shock
Food
Pollen
Bee stings
Mast cell degranulation
Histamine
Leaky dilated blood vessels
Drop in BP & Reduced perfusion
Hypovolemia & Hypoperfusion
Oedema
Septic Shock
Most common form of maldistributive shock
Mediated by vascular & inflammatory mediators in response to bacterial & fungal infection
Trigger: Gram -ve Bacteria => LPS (Endotoxin)
Binds TLR4 & CD14 (Monocyte derived cells: Dendritic cells & Macrophages)
Cytokine release: IL-1 & IL -6
Factor XII
Coagulation
Thrombosis +
Low Dose:
Activation of Macrophages, Endothelial cells & Complement
Medium Dose:
Raised TNF & IL-1 => Pyrexia
High Dose:
Vasodilation, Hypotension, Reduced myocardial contractility (Reduced CO) & Hypoperfusion
BV injury (release of too many cytokines)
=> DIC
Pooling, stagnation, Hypoxia
Stages
1) Compensated
Increase in CO & Vasoconstriction to maintain BP & tissue oxygenation
Tachycardia
Via Stimulation of SNS
Adrenaline
Control of H2O balance
GRF drops => Increase H2O absorption
RAAS
ADH
2) Progressive
Compensatory Mechanisms cannot cope with prolonged or severe drop in blood volume
Hypoperfusion & Cell injury
Low O2 => Cell metabolism shifts to Anaerobic respiration
Lactic Acid production & reduced ATP
Cell membrane damage, Lysosomal enzyme release
=> Tissue Necrosis
ATP needed to maintain cellular membranes
3) Irreversible
Mechanisms aimed at Vasoconstriction are overwhemled
Widespread Vasodilation & Organ failure
Clincal Features
Hypotension
Weak pulse & Tachycardia
Hyperventilation
Decreased urine production
Peripheral vasoconstriction (During compensation)
Lesions
Congestion & pooling of blood
Oedema & Haemorrhage
Petechial
Ecchymotic
Thromobosis (Microscopic)
Coagulation cascade
Cellular Necrosis (Microscopic)
Ex. Myocardial cells, Neurons, Hepatocytes, Renal Tubules
Recursos multimedia adjuntos
Cardiomegaly (image/png)
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