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hypovolemic-shock

Hypovolemic Shock: Pathogenesis, Complications, and Clinical Findings
Authors: Dean Percy Miranda Schmidt Reviewers: Yan Yu Tristan Jones Frank Spence* Ben Campbell Ayaaz Sachedina* * MD at time of publication
Progressive ↓ in level of consciousness
Pulseless Electrical Activity
Acute Kidney Injury
↑ Reabsorption of salt and water in the kidney
Oliguria
(↓ urine output)
    Inflammation (pancreatitis, cirrhosis, post-operative, etc.)
Inflammatory mediators ­ vessel permeability and fluid leaks out
Trauma
Ruptured vessels leak fluid into potential spaces
Hemorrhagic losses
(GI bleed, postpartum hemorrhage, etc.)
↓ Intravascular volume
↓ Venous return to the heart
↓ Cardiac output (blood pumped from the heart)
Hypovolemic Shock
↓ Oxygen delivery to tissues due to low blood volume
Insufficient organ perfusion
Non-Hemorrhagic losses
(dehydration, GI losses, skin losses / burns, renal losses, etc.)
         ‘Third Spacing’ of fluid
(fluid located outside the intravascular or intracellular space; large collections can occur in the pelvis, thorax, GI tract, long bones of children, intra-abdominally, retroperitoneally)
P = Q x R; less ‘flow’ in the vessels (Q), with vessels not constricting enough to maintain resistance (R)à pressure (P) will drop
↓ Blood Pressure
Caution: young, healthy individuals can maintain blood pressure during circulatory collapse with ­ cardiac output and ­ vasoconstriction; do not use blood pressure as an indicator of shock severity in children
Carotid sinus baroreceptors sense low blood pressure ↓ Carotid sinus inhibition of sympathetic nervous system Release of sympathetic catecholamines (epinephrine and
↓ Pressure in venous circulation
Brain
Heart
Kidneys
↓ Blood in the right internal jugular vein
↓ Oxygen delivery to the brain
↓ Myocardial contractility (from lactic acidosis)
↓ Blood flow to kidneys
↓ Jugular Venous Pressure
                                        Catecholamines bind to beta-1 receptors in the sinoatrial node of the heart
Beta-1 receptor activation causes ↑ heart rate
Tachycardia
norepinephrine)
Catecholamines bind to and stimulate alpha-1 receptors in peripheral vessels
Vasoconstriction of peripheral vessels
↓ Blood flow to peripheral tissue
Catecholamines bind to and stimulate beta receptors in sweat glands
Diaphoresis
(sweating)
In all body tissues
Inadequate oxygen delivery
↓ ATP production
↑ Anaerobic metabolism
↓ Body temperature
Impaired neurological functioning
Renal ischemia
Activation of the renin-angiotensin aldosterone system
↓ Glomerular filtration rate
↓ Clearance of lactic acid by the kidney
↑ Lactic acid production
↓ Rate of activity of clotting enzymes
Lactic Acidosis
Unknown mechanism
Coagulopathy Hypothermia
             Trauma Triad of Death
           ↑ Capillary Cold, mottled refill time extremities
   Legend:
 Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
 Complications
 Published January 24, 2013, updated December 4, 2022 on www.thecalgaryguide.com