Shock/Hypotension

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Shock/Hypotension
Clinical Presentation and Pharmacological
Treatment of Shock/Hypotension
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Introduction

• Review the current view on clinical presentation
  and management of shock with emphasis on
  pharmacotherapy.
• O. D. Polk, Jr., M.D. Assistant Professor of
  Medicine Pulmonary Critical Care Medicine

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Topics of Discussion

• Clinical Presentation
• 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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SHOCK - DEFINITION

• A profound and widespread reduction in the
  effective delivery of oxygen and other nutrients
  to tissues leads first to reversible and then, if
  prolonged, to irreversible cellular injury.

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SHOCK-NEW CONCEPTS

• Shock is probably the most common and important
  problem in critical care medicine.
• Cardiogenic shock represents one of the most
  important complications of IHD, the number one
  cause of mortality in the US.
• Hypovolemic and/or extracardiac obstructive shock
  are major contributors to trauma-associated
  morbidity and mortality.
• Septic shock is the 13th most frequent cause of
  death in the US.
• Shock causes or contributes to multiple organ
  dysfunction syndrome (MODS), organ failure, and
  death.

Parillo JE 1999
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MORTALITY FROM SHOCK

• Septic Shock
• 35 to 40 within one month
• Cardiogenic Shock
• 60 to 90
• Hypovolemic Shock
• Highly variable

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STAGES OF SHOCK

• Preshock
• Shock
• 20 to 25 reduction of EBV
• Fall in CI to lt2.5
• Activation of mediators
• End-organ dysfunction
• Urine output decline
• Restlessness evolves into agitation, obtundation,
  and coma
• Acidosis further decreases CO and alters cellular
  metabolic processes
• Multiple organ system failure proceeds to cause
  the demise of the patient

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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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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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Cardiogenic Shock

• Myopathies
• Infarction involving gt40 of LV
• Dilated cardiomyopathies
• Myocardial depression of sepsis
• Arrhythmias
• Atrial fibrillation/flutter
• Ventricular fibrillation
• Bradyarrhythmias/Heart Block
• Mechanical abnormalities
• Valvular defects
• Ventricular aneurysm

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Obstructive Shock

• Pulmonary Embolism
• Cardiac Tamponade
• Pneumothorax

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Common Features of Shock

• Hypotension
• Systolic BP lt90 mmHg
• Drop systolic BP gt40 mmHg
• Cool, clammy skin
• Oliguria
• Objective measure of intravascular volume
  depletion
• Change in Mental Status
• Metabolic acidosis

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Other Signs of Hypovolemia

• Tachycardia
• Orthostatic hypotension
• Poor skin turgor
• Absent axillary sweat
• Dry mucous membranes

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Management of Shock

• Shock begins when DO2 (delivery of oxygen) 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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ShockInitial Diagnostic Steps

• History and Physical
• Laboratory
• CBC
• Coags
• ABGs
• Biochemical profile
• Lactate
• EKG
• Chest x-ray

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ShockInitial Management

• Venous access
• Central venous catheter
• Arterial catheter
• EKG monitoring
• Pulse oximetry
• Hemodynamic support (MAPlt60 mmHg)
• Fluid Challenge
• Vasopressors for patients unresponsive to fluids

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Complicated Shock

• Pulmonary Artery Catheterization done to measure
• Cardiac output
• Filling pressures
• Echocardiography done to look at
• Pericardial fluid
• Cardiac function (non-invasively)
• Valve or shunt abnormalities

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Hemodynamic Characteristics in Different Types of
Shock
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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
1
Drug Receptor CO SVR Dose Range
0
0 -
(mg/kg/min)
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Effects of Inotropic Agents and Vasodilators
2
Drug CO SVR Dose Range
(mg/kg/min)
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Dopamine An endogenous precursor of
norepinephrine withmultiple dose-related effects

• Low Dose (0.5 - 3 µg/kg/min)
• Predominantly dopaminergic (DR) effects
• Enhanced blood flow to renal and splanchnic beds
• Moderate Dose (5 -10 µg/kg/min)
• Positive inotropic effects (?1)
• High Dose (gt10 µg/kg/min)
• a-actions (vasoconstriction)

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Indications for Selected Vasoactive Drugs
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ComplicationsVasopressors and Inotropic Agents

• Hypoperfusion
• Dysrhythmias
• Myocardial ischemia
• Local effects
• Skin necrosis
• Hyperglycemia
• Unique drug interactions/contraindications
• Pheochromocytoma
• Avoid dobutamine in the setting of IHSS
• Patients receiving MAO Inhibitors

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Reference
Pharmacotherapy of Shock. In The Pharmacologic
Approach to the Critically Ill Patient, 3rd ed.
Williams Wilkins,1994, pp 1104 1121.