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Core Lecture Series - Shock Daniel J. Riskin, MD September 9, 2007

Shock 2.ppt

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Core Lecture Series -Shock

Daniel J. Riskin, MD

September 9, 2007

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Outline

Definition

Epidemiology

Physiology

Classes of Shock

Clinical Presentation

Management

Controversies

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Definition

 A physiologic state characterized by

Inadequate tissue perfusion

Clinically manifested by

Hemodynamic disturbances

Organ dysfunction

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Epidemiology

Mortality

Septic shock – 35-40% (1 month mortality)

Cardiogenic shock – 60-90%

Hypovolemic shock – variable/mechanism

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Pathophysiology

Imbalance in oxygen supply and demand

Conversion from aerobic to anaerobicmetabolism

 Appropriate and inappropriate metabolic andphysiologic responses

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Pathophysiology

Cellular physiology

Cell membrane ion pump dysfunction

Leakage of intracellular contents into the

extracellular space Intracellular pH dysregulation

Resultant systemic physiology

Cell death and end organ dysfunction

MSOF and death

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Physiology

Characterized by three stages

Preshock (warm shock, compensated shock)

Shock End organ dysfunction

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Physiology

Compensated shock

Low preload shock – tachycardia,

vasoconstriction, mildly decreased BP Low afterload (distributive) shock – peripheral

vasodilation, hyperdynamic state

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Pathophysiology

Shock

Initial signs of end organ dysfunction

Tachycardia

Tachypnea

Metabolic acidosis

Oliguria Cool and clammy skin

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Physiology

End Organ Dysfunction

Progressive irreversible dysfunction

Oliguria or anuria

Progressive acidosis and decreased CO

 Agitation, obtundation, and coma

Patient death

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Classification

Schemes are designed to simplify complex

physiology

Major classes of shock

Hypovolemic

Cardiogenic

Distributive

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Hypovolemic Shock

Results from decreased preload

Etiologic classes

Hemorrhage - e.g. trauma, GI bleed, rupturedaneurysm

Fluid loss - e.g. diarrhea, vomiting, burns, third

spacing, iatrogenic

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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 Decreased Decreased Decreased

Respiratory rate (bpm) 14 –20 20 –30 30 –40 >35

Urine output (ml/hour) >30 20 –30 5 –15 Negligible

CNS symptoms Normal Anxious Confused Lethargic

Crit Care. 2004; 8(5): 373 –381. 

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Cardiogenic Shock

Results from pump failure

Decreased systolic function

Resultant decreased cardiac output

Etiologic categories

Myopathic

 Arrhythmic Mechanical

Extracardiac (obstructive)

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Distributive Shock

Results from a severe decrease in SVR

Vasodilation reduces afterload

May be associated with increased CO

Etiologic categories

Sepsis

Neurogenic / spinal Other (next page)

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Distributive Shock

Other causes

Systemic inflammation – pancreatitis, burns

Toxic shock syndrome Anaphylaxis and anaphylactoid reactions

Toxin reactions – drugs, transfusions

 Addisonian crisis Myxedema coma

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Distributive Shock

Septic 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

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Clinical Presentation

Clinical presentation varies with type and

cause, but there are features in common

Hypotension (SBP<90 or Delta>40) Cool, clammy skin (exceptions – early

distributive, terminal shock)

Oliguria Change in mental status

Metabolic acidosis

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Evaluation

Done in parallel with treatment!

H&P – helpful to distinguish type of shock

Full laboratory evaluation (including H&H,cardiac enzymes, ABG)

Basic studies – CxR, EKG, UA

Basic monitoring – VS, UOP, CVP, A-line Imaging if appropriate – FAST, CT

Echo vs. PA catheterization

CO, PAS/PAD/PAW, SVR, SvO2

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Treatment

Manage the emergency

Determine the underlying cause

Definitive management or support

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Manage the Emergency

Your patient is in extremis – tachycardic,

hypotensive, obtunded

How long do you have to manage this?

Suggests that many things must be done at

once Draw in ancillary staff for support!

What must be done?

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Manage the Emergency

One person runs the code!

Control airway and breathing

Maximize oxygen delivery

Place lines, tubes, and monitors

Get and run IVF on a pressure bag

Get and run blood (if appropriate) Get and hang pressors

Call your senior/fellow/attending

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Determine the Cause

Often obvious based on history

Trauma most often hypovolemic (hemorrhagic)

Postoperative most often hypovolemic(hemorrhagic or third spacing)

Debilitated hospitalized pts most often septic

Must evaluate all pts for risk factors for MI and

consider cardiogenic

Consider distributive (spinal) shock in trauma

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Determine the Cause

What if you’re wrong? 

85 y/o M 4 hours postop S/P sigmoid resectionfor perforated diverticulitis is hypotensive on a

monitored bed at 70/40

Likely causes

Best actions for the first 5 minutes?

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Definitive Management

Hypovolemic – Fluid resuscitate (blood or

crystalloid) and control ongoing loss

Cardiogenic - Restore blood pressure(chemical and mechanical) and prevent

ongoing cardiac death

Distributive – Fluid resuscitate, pressors for

maintenance, immediate abx/surgical control

for infection, steroids for adrenocortical

insufficiency

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Controversies

IVF Resuscitation

Limited resuscitation in penetrating trauma

Use of hypertonic saline resuscitation in trauma Endpoints for prolonged resuscitation

Pressors

Best pressors for distributive shock Monitoring

Most appropriate timing and use for PA

catheterization or intermittent echocardiogram

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Cases