pharmacotherapy of shock
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Pharmacotherapy of Shock
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Introduction
Review the current view on etiology, pathophysiology and management of shock with emphasis on pharmacotherapy.
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Topics of Discussion
Pathophysiology of Shock Types of Circulatory Shock Management of Shock
Inotropic Agents Vasodilators
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Shock
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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Determinants of Shock
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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Hemodynamic States of Shock Hyperdynamic State Hypodynamic State Related to:
Cardiac Output (CO) Systemic Vascular Resistance
(SVR)
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Pathophysiology of Shock 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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Mediators of Shock
Toxins Endotoxins
Oligo- and polypeptides Complement Factors Opiods TNF, Interleukins
Fatty Acid Derivatives Arachidonic acid metabolites
Varia Calcium
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Main Classes of Shock
Hypovolemic Shock Distributive Shock Cardiogenic Shock Obstructive Shock
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Hypovolemic Shock
Hemorrhagic/Traumatic Dehydrative Burn
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Distributive Shock
Septic Anaphylactic/
Anaphylactoid Neurogenic
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Obstructive Shock
Pulmonary Embolism Cardiac Tamponade Pneumothorax
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Question
Which one of the folowing is the most common cause of severeLactic acidosis (blood lactate concentration >5 mmol/L)?
a. Ethanol intoxicationb. Severe liver diseasec. Circulatory shockd. Ischemic bowele. Acute asthma
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Management of Shock
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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Pulmonary Artery Catheter Waveforms
Right Atrium Right Ventricle Pulmonary Artery PCWP
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Hemodynamic Characteristics in Different Types of Shock
Type Preload CO PVR SVR
Hemmorrhagic
Anaphylactic
Cardiogenic
Septic (Hyperdynamic)
Septic (Hypodynamic)
/
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QuestionThe wavefrom shown in this figure was observed whileattempting to advance a pulmonary arterial catheter, with the Balloon inflated, from the proximal pulmonatry artery to a “wedged” position.
Which one of the following bv
Which one of the following best explains the terminal portion of the depicted waveform?
a. Pulmonary hypertensionb. Mitral regurgitationc. Severe left ventricular dysfunctiond. Obstruction of the catheter tipe. Pericardial tamponadewww.freelivedoctor.com
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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: Enhance CO through the use of inotropic
agents Increase SVR through the use of
vasopressors
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Effects of Inotropic Agents and Vasodilators
Epinephrine 0.02 – 0.5
Norepinephrine 0 - 0.05 – 0.5
Dopamine DR 2 -12
Dobutamine 2 - 12
Dopexamine DR 0 - 0.9 - 5
Vasopressin Angiotensin III 5 - 20
Amrinone PDI 5 -10
Drug Receptor CO SVR Dose Range
0 -
(g/kg/min)
1
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Effects of Inotropic Agents and Vasodilators
Nifedipine 0 - 0.5 - 10
Nitroglycerin 0 - 3 - 5
Nitroprusside 0 - 0.5 - 5
Prostacyclin 10 - 40
2
Drug CO SVR Dose Range
(g/kg/min)
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Dopamine An endogenous precursor of norepinephrine with
multiple dose-related effects
Low Dose (0.5 - 3 mg/kg/min) 2 and dopaminergic (DR) effects Enhanced blood flow to renal and
splanchnic beds Moderate Dose (5 -10 mg/kg/min)
Positive inotropic effects High Dose (>20 mg/kg/min)
-actions (vasoconstriction)
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