Shock is a condition in which the cardiovascular system fails to perfuse tissues adequately
An impaired cardiac pump, circulatory system, and/or volume can lead to compromised blood flow to tissues
Inadequate tissue perfusion can result in:
generalized cellular hypoxia (starvation)
widespread impairment of cellular metabolism
tissue damage organ failure
death
Diagnosis of Shock
PATHOPHYSIOLOGY OF SHOCK SYNDROME
Impaired tissue perfusion occurs when an imbalance develops between cellular oxygen supply and cellular oxygen demand.
All Types of shock eventually result in impaired tissue perfusion & the development of acute circulatory failure or shock syndrome.
PATHOPHYSIOLOGY OF SHOCK SYNDROME
Cells switch from aerobic to anaerobic metabolism
lactic acid production
Cell function ceases & swells
membrane becomes more permeable
electrolytes & fluids seep in & out of cell
Na+/K+ pump impaired
mitochondria damage
cell death
COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS)-Adrenal Response
COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS)-Adrenal Response
SNS - Hormonal: Renin-angiotension system
Decrease renal perfusion
Releases renin angiotension I
angiotension II potent vasoconstriction &
releases aldosterone adrenal cortex
sodium & water retention
COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS)-Adrenal Response
SNS - Hormonal: Antidiuretic Hormone
Osmoreceptors in hypothalamus stimulated
ADH released by Posterior pituitary gland
Vasopressor effect to increase BP
Acts on renal tubules to retain water
COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS)-Adrenal Response
Decreased blood flow to the tissues causes cellular hypoxia
Anaerobic metabolism begins
Cell swelling, mitochondrial disruption, and eventual cell death
If Low Perfusion States persists:
IRREVERSIBLE DEATH IMMINENT!!
Stages of Shock
Initial stage - tissues are under perfused, decreased CO, increased anaerobic metabolism, lactic acid is building
Compensatory stage - Reversible. SNS activated by low CO, attempting to compensate for the decrease tissue perfusion.
Progressive stage - Failing compensatory mechanisms: profound vasoconstriction from the SNS ISCHEMIA Lactic acid production is high metabolic acidosis
Irreversible or refractory stage - Cellular necrosis and Multiple Organ Dysfunction Syndrome may occur
DEATH IS IMMINENT!!!!
Pathophysiology Systemic Level
Net results of cellular shock:
systemic lactic acidosis
decreased myocardial contractility
decreased vascular tone
decrease blood pressure, preload, and cardiac output
Clinical Presentation: Generalized Shock
Vital signs
Hypotensive:(may be WNL or due to compensatory mechanism) < 90 mmHg
MAP < 60 mmHg
Tachycardia: Weak and Thready pulse
Tachypneic-blow off CO2 Respiratory alkalosis
Hypovolemic Shock
blood VOLUME problem
Cardiogenic Shock
blood PUMP problem
Distributive Shock [septic;anaphylactic;neurogenic]
blood VESSEL problem
Hypovolemic Shock
Loss of circulating volume “Empty tank ”
decrease tissue perfusion general shock response
ETIOLOGY:
Internal or External fluid loss
Intracellular and extracellular compartments
Most common causes:
Hemmorhage
Dehydration
Hypovolemic Shock: External loss of fluid
Fluid loss: Dehydration
Nausea & vomiting, diarrhea, massive diuresis, extensive burns
Blood loss:
trauma: blunt and penetrating
BLOOD YOU SEE
BLOOD YOU DON’T SEE
Hypovolemic Shock: Internal fluid loss
Loss of Intravascular integrity
Increased capillary membrane permeability
Decreased Colloidal Osmotic Pressure
(third spacing)
S/S vary depending on severity of fluid loss:
15%[750ml]- compensatory mechanism maintains CO
15-30% [750-1500ml- Hypoxemia, decreased BP & UOP
30-40% [1500-2000ml] -Impaired compensation & profound shock along with severe acidosis
40-50% - refactory stage:
loss of volume= death
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