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Shock. William Lawson, MD Division of Allergy, Pulmonary, and Critical Care Medicine. Outline for Today. Definition Ramifications Physiologic determinants Classification Approach to the patient with shock Treatment strategies. Definition. Shock is not:

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shock

Shock

William Lawson, MD

Division of Allergy, Pulmonary, and Critical Care Medicine

outline for today
Outline for Today
  • Definition
  • Ramifications
  • Physiologic determinants
  • Classification
  • Approach to the patient with shock
  • Treatment strategies
definition
Definition
  • Shock is not:
    • an absolute blood pressure measurement
    • an independent diagnosis
  • Shock is:
    • a physiologic state in which significant, systemic reduction in tissue perfusion results in decreased tissue oxygen delivery
ramifications of shock
Ramifications of Shock
  • Can lead to irreversible cell and tissue injury ultimately resulting in:
    • end-organ damage
    • multi-system organ failure
    • death
  • Mortality from shock remains high:
    • cardiogenic shock from AMI - 60-90%
    • septic shock - 35-40%
    • hypovolemic shock - varies depending on disease state
physiologic determinants
Physiologic Determinants

P = CO * SVR

MAP – CVP = CO * SVR

P = change in pressure

MAP = mean arterial pressure

CVP = central venous pressure

CO = cardiac output

SVR = systemic vascular resistance

physiologic determinants1
Physiologic Determinants

CO = HR * SV

CO = cardiac output

HR = heart rate

SV = stroke volume

physiologic determinants2
Physiologic Determinants

O2 consumption = O2 Delivery – O2 Return

VO2 = CO(CaO2-CvO2)

VO2 = CO*1.34*Hgb*(SaO2-SvO2)

CO = cardiac output

CaO2 and CvO2 = arterial and mixed venous oxygen content

SaO2 and SvO2 = arterial and mixed venous oxygen saturation

classification of shock
Classification of Shock
  • Hypovolemic
  • Cardiogenic
  • Distributive (vasodilatory)
hypovolemic shock
Hypovolemic Shock
  • Results from decreased preload
  • Preload is one of the determinants of stroke volume
  • Thus, when preload drops, cardiac output drops
hypovolemic shock1
Hypovolemic Shock
  • Hemorrhage – examples include:
    • Trauma
    • GI bleed
    • Ruptured aneurysm
  • Fluid losses – examples include:
    • Diarrhea
    • Vomiting
    • Burns
    • Third spacing of fluid
cardiogenic shock
Cardiogenic Shock
  • Results from pump failure
  • Manifested as decreased cardiac output
  • Four broad categories (examples given):
    • Cardiomyopathies
      • Myocardial infarction
      • Dilated cardiomyopathy
    • Arrhythmias
      • Both tachycardic and bradycardic
cardiogenic shock1
Cardiogenic Shock
  • Mechanical
    • Valvular stenoses or insufficiencies
  • Obstructive/extracardiac
    • Pulmonary embolism
    • Tension pneumothorax
    • Pericardial tamponade
distributive shock
Distributive Shock
  • Also referred to as vasodilatory shock
  • Results from a severe decrease in SVR
  • Examples include:
    • septic shock
    • systemic inflammatory response syndrome (SIRS)
    • anaphylaxis
    • neurogenic shock
    • Addisonian crisis
profiles of shock states
Profiles of Shock States

Note: This table represents “classic” shock states; in reality, mixed states may be present or parameters may vary depending on evolution of shock.

common features of shock
Common Features of Shock
  • Hypotension
  • Cool, clammy skin
  • Oliguria
  • Altered mental status
  • Metabolic acidosis
evaluation of the patient in shock
Evaluation of the Patient in Shock
  • Primary
    • History
    • Physical Examination
    • Laboratory
    • Radiographic
  • Secondary
    • pulmonary artery catheterization
    • echocardiography
pulmonary artery catheterization
Pulmonary Artery Catheterization
  • Allows measurement of:
    • vascular pressures including PCWP
    • CO by thermodilution
    • calculation of SVR and PVR
    • mixed venous oxygen saturation (SvO2)
  • Most cases of shock can be managed without a PA catheter
  • Debate ongoing on utility and safety of PA catheter
management of the patient in shock
Management of the Patient in Shock
  • Shock is an emergency state:
    • initial focus is on ABC’s of resuscitation
      • airway, breathing, circulation
  • Adequate venous access
    • central venous access not always required, but often necessary
  • Optimization of volume status
  • Identification of cause of shock and directed therapy
management hypovolemic shock
Management - Hypovolemic Shock
  • Volume replacement key for all causes of hypovolemic shock
    • nonhemorrhagic: crystalloid fluid replacement
    • hemorrhagic: crystalloid fluid replacement and blood product replacement
  • Directed therapy to correct the cause of hypovolemic shock
management cardiogenic shock
Management - Cardiogenic Shock
  • General points for cardiogenic shock
    • PA catheter commonly used
    • vasopressor support (specific discussion later) often needed
    • may need intra-aortic balloon pump
    • hypotension may or may not be present
    • identification of type of cardiogenic shock critical for optimal management
management cardiogenic shock1
Management - Cardiogenic Shock
  • Myocardial infarction
    • most common cause of cardiogenic shock
    • directed therapy for MI
      • aspirin, heparin, glycoprotein IIb/IIIa inhibitors, revascularization
  • Pulmonary embolism
    • most common cause of obstructive shock
    • avenues available to rapidly resolve clot burden
      • thrombolysis, interventional radiology directed clot extraction, surgical embolectomy
management distributive shock
Management - Distributive Shock
  • Identification of cause and directed therapy
    • e.g. Addisionian crisis - steroid replacement
  • Septic shock
    • most common form of distributive (vasodilatory) shock
    • early and aggressive fluid replacement is important and often underutilized
    • vasopressor support often required
management distributive shock1
Management - Distributive Shock
  • Septic shock (continued)
    • identification of infectious site/source and guided therapy (antibiotics and drainage)
    • steroid replacement with concomitant relative adrenal insufficiency
    • optimal glucose control
    • recombinant human activated protein C (drotrecogin alfa activated)
    • attention to support of each organ system
pharmacological therapy of shock
Pharmacological Therapy of Shock
  • Goals:
    • Increase CO to restore normal hemodynamics
    • Increase blood pressure and redistribute blood flow to vital organs (brain).
  • Pharmacological agents used depend on clinical and physiological parameters of shock and type of shock.
    • Agents used are primarily adrenergic receptor agonists
physiological actions of adrenergic receptors

Receptor type

Receptor action (relative to hemodynamics)

α1

Arterial vasoconstriction

Increased myocardial contractility (minor)

α2

Constriction of venous capacitance (major)Feedback inhibition of norepinephrine release at sympathetic fibers

β1

Increased myocardial contractility (inotropy)

Increased heart rate (chronotropy)

β2

Relaxation of vascular smooth muscle (skeletal muscle)

(Relaxation of bronchial smooth muscle)

D1

Relaxation of splanchnic vascular smooth muscleRelaxation of renal vascular smooth muscle

D2

Inhibition of norephinephrine uptake at sympathetic fibers

Physiological actions of adrenergic receptors
receptor pharmacology

Activity at

receptors

α

β1

β2

D

Dopamine

++/+++

++++

++

++++

Dobutamine

+

++++

++

0

Epinephrine

++++

++++

+++

0

Isoproteronol

0

+++

+++

0

Norepinephrine

+++

+++

+

0

Phenylephrine

++/+++

0

0

0

Receptor pharmacology
dopamine
Dopamine
  • Pharmacodynamics
    • Low and moderate doses – primarily binds dopaminergic and β1 receptors
    • Higher doses – α1 receptors stimulated
  • Clinical effects
    • Increase heart rate (chronotropy) and contractility (inotropy)
    • Increase SVR by arteriolar vasoconstriction (higher doses).
dopamine1
Dopamine
  • Clinical application
    • Most commonly used vasopressor
      • common starting dose – 5 μg/kg/min
    • Cardiogenic or distributive shock (shock of any etiology)
  • Adverse effects
    • Tachyarrhythmias, excessive tachycardia
    • Precipitate myocardial ischemia
    • Excessive vasoconstriction (digital ischemia)
    • Nausea and vomiting (central effects)
dobutamine
Dobutamine
  • Pharmocodynamics
    • Primarily stimulates β1 receptors
    • Lesser binding to β2 and α receptors
  • Clinical effects
    • Increase CO (primarily inotropic effect)
    • SVR without significant change or a decline
    • Starting dose – 2-5 μg/kg/min
dobutamine1
Dobutamine
  • Clinical application
    • Cardiogenic shock and congestive heart failure
      • Common starting dose – 2-5 μg/kg/min
    • Sometimes used in distributive shock (when CO is normal or low which can occur in septic shock)
  • Adverse effects
    • Tachycardia and tachyarrhythmias
    • Myocardial ischemia
epinephrine
Epinephrine
  • Pharmacodynamics
    • Extremely potent, high affinity binding of all α and β receptors.
  • Clinical effects
    • Increase CO
    • Increase SVR by vasoconstriction
      • High doses cause prominent vasoconstriction
epinephrine1
Epinephrine
  • Clinical applications
    • Refractory shock of all types – starting at 0.2 μg/kg/min
    • Cardiopulmonary resuscitation – 1 mg IV push
    • Anaphylaxis – 0.2-0.5 ml of 1:1000 dilution subcutaneously
  • Adverse effects
    • Excessive vasoconstriction
    • Tachycardia and tachyarrhythmias
    • Myocardial ischemia
    • Hyperglycemia
isoproteronol
Isoproteronol
  • Pharmacodynamics
    • β1 and β2 receptor agonist
    • No α effects
  • Clinical effects
    • Increased CO
    • Decreased SVR
    • Variable effect on blood pressure
isoproteronol1
Isoproteronol
  • Clinical application
    • Not useful for shock because of prominent β2 effect and lack of α – may decrease MAP
    • Rare uses to increase heart rate (as in Torsade de Pointes)
norepinephrine
Norepinephrine
  • Pharmacodynamics
    • β1, α1, α2 receptor agonist
    • Low doses (< 0.03 μg/kg/min) have prominent β1 effect
    • Higher doses (> 0.06 μg/kg/min) stimulate α receptors
  • Clinical effects
    • Increase CO
    • Increase SVR
norepinephrine1
Norepinephrine
  • Clinical applications
    • Distributive shock
    • Profound, refractory shock of any type
  • Adverse effects
    • Excessive vasoconstriction
    • Arrhythmia
    • Myocardial ischemia
phenylephrine
Phenylephrine
  • Pharmacodynamics
    • α1 and α2 receptor agonist
    • Lacks β effect
  • Clinical effects
    • Increased SVR
    • Starting dose - 30 μg/min
phenylephrine1
Phenylephrine
  • Clinical application
    • Distributive shock (especially if very high heart rate or history of tachyarrhythmia)
    • Less commonly used than norepinephrine
  • Adverse effects
    • Excessive vasoconstriction
    • Reflex bradycardia
nonadrenergic vasopressors and inotropes
Nonadrenergic Vasopressors and Inotropes
  • Vasopressin
    • antidiuretic hormone (ADH) analoge
    • can be used as a second line pressor agent
    • recent studies suggest a relative deficiency of ADH in sepsis
    • often added at a fixed rate of 0.04 units/min
nonadrenergic vasopressors and inotropes1
Nonadrenergic Vasopressors and Inotropes
  • Phosphodiesterase inhibitors
    • amrinone and milrinone
    • have inotropic and vasodilatory actions
    • effects are similar to dobutamine
    • used in cardiac failure
summary
Summary
  • Treat shock as an emergency
  • Remember the physiology that governs shock - your goal in treatment is to intervene appropriately to help correct the variable that is driving the shock state.
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