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Core Lecture Series:
Shock
Eric M. Wilson, MD
September 22, 2009
Definition
• A physiologic state characterized by
– Inadequate tissue perfusion
• Clinically manifested by
– Hemodynamic disturbances
– Organ dysfunction
Pathophysiology
• Imbalance in oxygen supply & demand
• Conversion from aerobic to anaerobic
metabolism
• Insult initiates neuroendocrine &
inflammatory mediator reponses
Pathophysiology
• Hemodynamics maintained
Compensated
• Continued hypoTN-> tissue
injury; reversible
w/resuscitation
Decompensation
• Cont’d volume loss /
inadequate resuscitation ->
hypoperfusion, cell injurydeath
Irreversible phase
Shock:
Compensatory Mechanisms
• Neural response
• Hormonal response
Neural Response
- Decreased filling pressures lead to
decreased output from left atrial stretch
receptors to the vasomotor center of the
medulla.
- Decreased frequency of impulses from the
Carotid and aortic arch baroreceptors to
the vasomotor center of the medulla.
- Result
- Increased sympathetic output.
- Inhibition of the vagal center
Neural Response:
Effects on cardiovascular function
• Larger arterioles constrict
– Increases blood pressure
• Smaller arterioles dilate
– Lowers capillary hydrostatic pressure resulting in fluid
shift from interstitial space into intravascular space
• Vasoconstriction minimal in brain & heart & most
intense in peripheral tissues
Pathophysiology:
Neuroendocrine Response
α1 & β1
Gluconeogenesis
Insulin resistance
Glycogenolysis
Lipolysis
The hormonal response to
injury and shock
Hormones with increased release
Epinephrine
Β-endorphin
Norepinephrine
Growth Hormone
Dopamine
Prolactin
Glucagon
Somatostatin
Renin
Eicosanoids
Angiotensin II
Histamine
AVP (ADH)
Kinins
ACTH
Serotonin
Cortisol
Interleukin 1
Aldosterone
TNF
Hormones with decreased
release
Insulin
Estrogen
Testosterone
Thyroxine
T3
TSH
FSH
LH
IGF
Pathophysiology
• Cellular physiology
– Tissue hypoxia -> decrease generation of ATP
anaerobic glycolysis
– Pyruvate lactate  decrease in pH 
Intracellular metabolic acidosis
– Cell membrane pump dysfunction
• Na & H2O in  cellular swelling; K out
• Resultant systemic physiology
– Cell death & end organ dysfunction
– MSOF & death
Pathophysiology
• Shock
– Initial signs of organ dysfunction
– Tachycardia
– Tachypnea
– Metabolic acidosis
– Oliguria
– Cool & clammy skin
Pathophysiology
• End organ dysfunction
– Progressive irreversible dysfunction
– Oliguria, anuria
– Progressive acidosis & depressed CO
– Agitation, obtundation, & coma
– Patient death
Classification
•
•
•
•
Hypovolemic/Hemorrhagic
Cardiogenic
Vasodilatory/Septic
Neurogenic
Distributive
Hypovolemic Shock
• Results from decreased preload
• Etiologic classes
– Hemorrhage: trauma, GI bleed, ruptured
aneurysm
– Fluid loss: diarrhea, vomiting, burns
Hypovolemic Shock
Hemorrhagic Shock
Parameter
I
II
III
IV
Blood loss (ml)
<750
750–1500
1500–2000
>2000
Blood loss (%)
<15%
15–30%
30–40%
>40%
Pulse rate (beats/min)
<100
>100
>120
>140
Blood pressure
Normal
Normal
Decreased
Decreased
Respiratory rate (bpm)
14–20
20–30
30–40
>35
Urine output (ml/hour)
>30
20–30
5–15
Negligible
Normal
Anxious
Confused
Lethargic
CNS symptoms
Elderly – blood thinners, meds masking compensatory responses to bleeding
(beta-blockers)
Hemorrhagic Shock:
Treatment
• Control the source of blood loss
• Intravenous volume resuscitation
– Crystalloid solutions
– If shock state is uncorrected after 2L,
transfuse blood
Cardiogenic Shock
• Inadequate blood flow to vital organs due
to inadequate cardiac output despite
normal intravascular volume status
Pump Failure
Cardiogenic Shock:
Causes
•
•
•
•
•
MI
Arrhythmias
Cardiomyopathy
Myocarditis
Mechanical
– Acute mitral regurgitation
– Acute aortic insufficiency
– Ventricular septal defect
Cardiogenic Shock:
Treatment
• Maintain adequate oxygenation
• Judicious fluid administration to avoid
pulmonary edema
• Correct electrolyte abnormalities
• Treat dysrhythmias – reduce heart rate
• Inotropic agents
• Intra-aortic balloon counterpulsation
Cardiogenic Shock:
Intra-aortic balloon pump
-Improves coronary blood flow
-Decreases afterload
-Decreases myocardial oxygen demand
Vasodilatory Shock
• Hypotension from failure of vascular
smooth muscle to constrict
• Vasodilation
• Causes
– Sepsis
– Anaphylaxis
– Systemic inflammation
Vasodilatory Shock
SIRS
2 or more of the following:
Temp >38 or <36
HR > 90
RR > 20
WBC > 20K
>10% bands
Sepsis
SIRS in the presence of suspected or documented infection
Severe Sepsis
Sepsis with hypotension, hypoperfusion, or organ dysfunction
Septic Shock
Sepsis with hyotension unresponsive to volume resuscitation,
and evidence of hypoperfusion or organ dysfunction
MODS
Dysfunction of more than one organ
Vasodilatory Shock:
Treatment
•
•
•
•
•
Treat source of infection
Maximize intravascular volume status
Intubation, if necessary
Vasopressors
Immune modulators
– Activated protein C (Xigris)
• Promotes fibrinolysis
• Inhibits thrombosis & inflammation
Neurogenic Shock
• Usually caused by an
injury to the spinal cord
• Not caused by an
isolated brain injury
Neurogenic Shock:
Clinical Presentation
•
•
•
•
•
Hypotension
Bradycardia
Sensory loss
Motor paralysis
Warm, dry skin
Neurogenic Shock:
Pathophysiology
• Hypotension
– Loss of sympathetic tone to arterial system resulting
in decreased systemic vascular resistance
– Loss of sympathetic tone to venous system resulting
in pooling of blood in venous capacitance vessels
with decreased cardiac filling and diminished cardiac
output
• Bradycardia
– Loss of sympathetic input from spinal cord
– Tonic parasympathetic input to heart unopposed
leading to bradycardia
Neurogenic Shock:
Pathophysiology
• Sensory loss
– Loss of efferent communication from the sensory
organs to the brain
• Motor paralysis
– Loss of afferent communication from the brain to the
voluntary muscles
• Warm, dry skin
– Loss of sympathetic input to sweat glands leads to
failure to produce sweat
– Failure of peripheral vasoconstriction maintains flow
of warm blood to periphery and “warm skin”
Neurogenic Shock:
Treatment
• Fluid replacement
• Pressor agents to restore vascular tone
once volume status restored
Obstructive Shock
• Reduced filling of the right side of the
heart resulting in decreased cardiac output
• Tension pneumothorax
– Increased intrapleural pressure secondary to
air accumulation
• Pericardial tamponade
– Increased intrapericardial pressure precluding
atrial filling secondary to blood accumulation
Distinguishing Types of Shock
Shock
Hypovolemic
Septic
Cardiogenic
Neurogenic
CVP/
PCWP
CO
SVR
Which of the following is an appropriate definition of the
shock state?
A. Low blood pressure
B. Low cardiac output
C. Low circulating volumes
D. Inadequate tissue perfusion
E. Abnormal vascular resistance
In cases of hemorrhagic shock, what initial alteration in blood
pressure is seen?
A. Increase in systolic pressure
B. Decrease in systolic pressure
C. Increase in diastolic pressure
D. Decrease in diastolic pressure
Class II shock – decrease in pulse pressure, which is
generally related to increase in diastolic component, which in
turn is related to elevation of catecholamines produced by
neural response to shock