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Hemorrhagic Shock
Richard E. Klabunde, Ph.D.
Associate Professor of Physiology
Department of Biomedical Sciences
Ohio University College of Osteopathic Medicine
Learning Objectives
General Definition of
Hemorrhagic Shock
A clinical syndrome resulting from
decreased blood and oxygen perfusion
of vital organs resulting from a loss of
blood volume.
Hemorrhagic Shock
(Initial Uncompensated Responses)
Blood
Loss
CVP
Frank-Starling
Mechanism
PA
SV
CO
SV
EDV (Preload)
LV
Press
B
LV Vol
5
15%
25%
50
Compensated
100
I
II
35%
III
45%
IV
60%
Decompensated
Transfusion
0
0
Time (hours)
(Adapted from Guyton & Crowell, 1961)
Compensatory Mechanisms
Baroreceptor reflexes
Circulating vasoconstrictors
Chemoreceptor reflexes
Reabsorption of tissue fluids
Renal reabsorption of sodium and water
Activation of thirst mechanisms
Cerebral ischemia
Hemapoiesis
8
Arterial Baroreceptors
Arterial Pressure Pulse
Receptor Firing
100
Receptor
Firing Rate
(% max) 50
Carotid Sinus
Decreased
MAP &
Pulse Press
200
100
MAP (mmHg)
Klabunde, RE, Cardiovascular Physiology Concepts, Lippincott Williams & Wilkins, 2004
Autonomic Responses to
Baroreceptor Activity
Klabunde, RE, Cardiovascular Physiology Concepts, Lippincott Williams & Wilkins, 2004
10
-20
-40
Intact
Carotid sinus only
Aortic arch only
No baroreceptors
-60
(Adapted from A.J. Edis, 1971)
11
Cardiopulmonary Baroreceptors
Baroreceptor Reflexes
Klabunde, RE, Cardiovascular Physiology Concepts, Lippincott Williams & Wilkins, 2004
13
14
15
Vol
B
Press
Hemorrhage decreases
blood volume and
decreases CVP (AB)
Peripheral venous
constriction decreases
venous compliance (BC),
which increases CVP and
shifts blood volume toward
heart
Increased CVP increases
ventricular preload and
force of contraction (FrankStarling mechanism)
16
Humoral Compensatory
Mechanisms
Klabunde, RE, Cardiovascular Physiology Concepts, Lippincott Williams & Wilkins, 2004
17
Importance of Humoral
Compensatory Mechanisms
Chemoreceptor Reflexes
Peripheral chemoreceptors
Carotid bodies
Aortic bodies
Central chemoreceptors
Medulla (associated with cardiovascular
control centers)
19
FM = K A [( PC PT ) ( C T )]
22
Cerebral Ischemia
Decompensatory Mechanisms
Progressive Shock
Cardiogenic Shock
Impaired coronary perfusion causing myocardial
hypoxia, systolic and diastolic dysfunction,
arrhythmias
Sympathetic Escape
Loss of vascular tone (SVR) causing progressive
hypotension and organ hypoperfusion
Increased capillary pressure causing increased fluid
filtration and hypovolemia
Cerebral Ischemia
Loss of autonomic outflow due to severe cerebral
hypoxia
24
Metabolic Acidosis
Rheological
Increased microvascular viscosity
Microvascular plugging by leukocytes and platelets
Intravascular coagulation
Decompensatory Mechanisms
(Cardiogenic Shock and Sympathetic Escape)
Cardiac
Output
Inotropy
+
Coronary
Perfusion
Sympathetic
Vasoconstriction
Arterial
Pressure
Tissue
Hypoxia
Vasodilation
26
Time-Dependent Changes in
Cardiac Function
0 2
Hours after
Hemorrhage
4
4.5
Cardiac
Output
5
5.2
Precipitous fall in
cardiac function
occurred after 4 hours
of severe hypotension
0
5
10
Left Atrial Pressure (mmHg)
(adapted from Crowell et al., 1962)
27
Hemorrhagic
Shock
Septic
Shock
CV Origin
Cardiac
Volume
Vascular
Cardiac
Output
Vascular
Resistance
Blood
Volume
Management
Mechanical
Inotropes
Vasopressors
Vasodilators
IV Fluids/Blood
Vasopressors
IV Fluids
Antibiotics
Vasopressors
Inotropes
28
Resuscitation Issues
Resuscitation fluids
30