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2. Introduction
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Review the current view on
etiology, pathophysiology and
management of shock with
emphasis on pharmacotherapy.
Daniel Game, M.D.
O. D. Polk, Jr., M.D.
Wayne Davis, M.D.
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3. Topics of Discussion
Pathophysiology of Shock
Types of Circulatory Shock
Management of Shock
Inotropic Agents
Vasodilators
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4. Shock
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Term “choc” – French for “push” or
impact was first published in 1743
by the physician LeDran
Belief – symptoms arose from fear
or some other form of altered
cerebral function
Crile in 1899 showed that
replacement of blood volume
decreased mortality experimentally
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5. Determinants of Shock
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Inadequate tissue perfusion
Sustained loss of effective circulatory
blood volume
Breakdown of cellular metabolism
and microcirculatory homeostasis
Hypoperfusion of peripheral tissue
that leads to a diminutive
transcapillary exchange function
Disproportion between VO2 and DO2
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7. Pathophysiology of
Shock
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Shock develops with inadequate
capillary perfusion by decreased
Cardiac Output following heart
attack (cardiogenic shock) or
blood/volume loss (hypovolemic
shock)
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13. Question
Which one of the folowing is the most common cause of severe
Lactic acidosis (blood lactate concentration >5 mmol/L)?
a.
b.
c.
d.
e.
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Ethanol intoxication
Severe liver disease
Circulatory shock
Ischemic bowel
Acute asthma
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14. Management of Shock
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Shock begins when DO2 to the
cells is inadequate to meet
metabolic demand
The major therapeutic goals in
shock therefore are sufficient
tissue perfusion and oxygenation
Early diagnosis remains a major
problem
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16. Hemodynamic Characteristics in
Different Types of Shock
Type
Preload
CO
PVR
SVR
Hemmorrhagic
Anaphylactic
/
Cardiogenic
Septic
(Hyperdynamic)
Septic
(Hypodynamic)
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17. Question
The wavefrom shown in this figure was observed while
attempting to advance a pulmonary arterial catheter, with the
Balloon inflated, from the proximal pulmonatry artery to a
“wedged” position.
Which one of the following best explains the terminal
portion of the depicted waveform?
W
a. Pulmonary hypertension
h
b. Mitral regurgitation
i
c. Severe left ventricular dysfunction
c
d. Obstruction of the catheter tip
h
e. Pericardial www.indiandentalacademy.com
tamponade
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18. Inotropic Agents and
Vasodilators
Vasoactive drugs are an important
pharmacologic defense in the
treatment of shock.
May be required to support BP in the
early stages of shock.
These agents may be needed to:
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Enhance CO through the use of inotropic
agents
Increase SVR through the use of
vasopressors
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19. Effects of Inotropic
1
Agents and Vasodilators
Drug
Epinephrine
Receptor
CO
SVR
α1 ,β1, (β2)
Norepinephrine α1, β1
Dose Range
0.02 – 0.5
0-
0.05 – 0.5
Dopamine
β2, DR, (α)
2 -12
Dobutamine
β1 , β2
2 - 12
Dopexamine
β1, β2, DR
Vasopressin
Angiotensin III
Amrinone
PDI
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00-
0.9 - 5
5 - 20
5 -10
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(µg/kg/min)
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20. Effects of Inotropic
2
Agents and Vasodilators
Drug
CO
SVR
Dose Range
Nifedipine
0-
0.5 - 10
Nitroglycerin
0-
3-5
Nitroprusside
0-
0.5 - 5
Prostacyclin
10 - 40
(µg/kg/min)
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21. Dopamine
An endogenous precursor of norepinephrine with
multiple dose-related effects
Low Dose (0.5 - 3 mg/kg/min)
Positive inotropic effects
High Dose (>20 mg/kg/min)
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Enhanced blood flow to renal and
splanchnic beds
Moderate Dose (5 -10 mg/kg/min)
β2 and dopaminergic (DR) effects
α-actions (vasoconstriction)
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