Shock

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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
• Hypodynamic
• 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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Clinically

• Hypotension.
• Poor Tissue Perfusion with Anaerobic Metabolism
  and lactate production.
• Poor Renal Perfusion will cause a Decrease in
  Urine Output.
• Poor Cerebral Perfusion will cause an and
  Altered Mental status.
• Other clinical parameters depend on Etiology.
  E.g. Warm Extremities in Septic Shock vs Cold
  Clammy Extremites in Cardiogenic shock.

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Mediators of Shock

• Toxins
• Endotoxins
• Oligo- and polypeptides
• Complement Factors
• Opiods
• TNF, Interleukins
• Fatty Acid Derivatives
• Arachidonic acid metabolites
• Other

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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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Obstructive Shock

• Pulmonary Embolism
• Cardiac Tamponade
• Pneumothorax

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Distributive Shock

• Septic
• Anaphylactic/ Anaphylactoid
• Neurogenic

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Systemic inflammatory response syndome (SIRS)

• Evidence of is indicated by at least two of the
  following
• 1. Fever or hypothermiaCore body temperature of
  greater than or equal to 38ºC or less than or
  equal to 36ºC
• 2. Tachypneagreater than or equal to 20 breaths
  per minute or need for mechanical ventilation for
  an acute process
• 3.. Tachycardiaheart rate greater than or equal
  to 90 beats per minute, unless the patient has a
  preexisting tachycardia
• 4. White blood cell countgreater than or equal
  to 12,000 cells/mm3 or less than or equal to
  4,000 cells/mm3, or greater than 10 bands on
  differential

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Sepsis Continued

• Sepsis is SIRS due to a presumed or known site of
  infection.
• Severe sepsis is sepsis with an acute associated
  organ failure.
• Septic shock, a subset of severe sepsis, is
  defined as a persistently low mean arterial blood
  pressure despite adequate fluid resuscitation.
• Refractory septic shock is a persistently low
  mean arterial blood pressure despite vasopressor
  therapy and adequate fluid resuscitation

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A sepsis-induced organ failure is indicated by
one of the following criteria

• Cardiovascular dysfunctionmean arterial pressure
  less than or equal to 60 mm Hg, the need for
  vasopressors to maintain this blood pressure in
  the face of adequate intravascular volume
  (central venous pressure greater than 8 or
  pulmonary artery occlusion pressure greater than
  12), or after an adequate fluid challenge has
  been given
• Respiratory organ failurean arterial oxygen
  pressure/fraction of inspired oxygen ratio less
  than 250 in the absence of pneumonia or less than
  200 in the presence of pneumonia
• Renal dysfunctionurine output less than 0.5
  mL/kg/hr for 1 hour in the face of adequate
  intravascular volume or after an adequate fluid
  challenge
• Hematologic dysfunctionthrombocytopenia with
  80,000 platelets/mm3, a 50 drop in the previous
  3 days, or a prothrombin-INR greater than 1.2
  that cannot be explained by liver disease or
  concomitant warfarin usage
• Unexplained metabolic acidosisa pH less than
  7.30 and a plasma lactate greater than 1.5 times
  the upper limit of normal for the laboratory

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Addition of Thermodilution Cardiac Output
Ganz Swan Am J Cardiol 197229,241.
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Pulmonary Artery Catheter Waveforms
Right Atrium Right Ventricle Pulmonary Artery
PCWP
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PA Cath Measured Parameters

• Central Venous Pressure
• Pulm Artery Occlusion Pressure (Wedge Pressure)
• Pulmonary Artery Pressures
• Cardiac Output (CCO) nl 4 - 8.0 L/min
• Mixed Venous Saturation

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Calculated Parameters

• Systemic Venous Resistance (SVR)
• Pulmonary Vascular Resistance (PVR)
• Stroke Volume (SV) nl 60 - 100 ml
• SV CO/HR x 1000
• Arterial Venous O2 Content Difference

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Calculating Ventricular Volume
CI HR x REF
SVI REF
RVEDVI

• RVEDVI - right ventricular end-diastolic volume
  index
• nl 60 - 100 ml/m2
• SVI - stroke volume index
• REF - right ventricular ejection fraction

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Hemodynamic Characteristics in Different Types of
Shock
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Example
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? a.
Pulmonary hypertension b. Mitral
regurgitation c. Severe left ventricular
dysfunction d. Obstruction of the catheter
tip e. Pericardial tamponade
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An Alternative to the Pulmonary Artery
Catheter Type Natriuretic Peptide
Maesel et al N Engl J Med 2002347,161-167
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B Type Natriuretic Peptide

• Useful for distinguishing Congestive Heart
  Failure from non cardiac cause of dyspnea.
• Values of gt than 100pcg/ml is 83.4 Sensitive
  for diagnosing CHF.
• Values of lt than 50pcg/ml is 96 Specific in
  excluding dyspnea as being secondary to CHF.
• Correlates with CHF more accurately than
  history and physical exam.

Maesel et al N Engl J Med 2002347,161-167
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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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Inotropic Agents

• 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.
• Maintain vital organ tissue perfusion.

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Effects of Inotropic Agents and Vasodilators
1
Drug Receptor CO SVR Dose Range
0 -
(?g/kg/min)
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Effects of Inotropic Agents and Vasodilators
Drug CO SVR Dose Range
(?g/kg/min)
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Dopamine An endogenous precursor of
norepinephrine withmultiple dose-related effects

• Low Dose (0.5 - 3 mcg/kg/min)
• ?2 and dopaminergic (DR) effects
• Enhanced blood flow to renal and splanchnic beds
• Moderate Dose (5 -10 mcg/kg/min)
• Positive inotropic effects
• High Dose (10-20 mcg/kg/min)
• ?-actions (vasoconstriction)

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Xigris for Sepsis

• Recombinant human activated protein C (rhAPC
  drotrecogin alfa
• RhAPC is a molecule that targets the cascade of
  inflammation and coagulopathy characteristic of
  sepsis through its antithrombotic,
  profibrinolytic, and anti-inflammatory
  properties.

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New Therapies for Septic Shock

• Xigris use limited by cost.
• 7 000 dollars for the usual 4 day treatment.
• 6 improvement in Mortality
• This means we need to spend 666 666.00 (2/3 of
  a million dollars) to save a single life.
• Is it worth it? Ask Dr. Nalamati.

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Monitoring of Resusitation in Sepsis.

• Inclusion criteria included.
• 2 of 4 SIRS Criteria
• SBP lt90 after 25ml/kg IVF and/or a lactate of
  gt4mmol/l
• Then Randomized to Standard therapy vs
  Interventional Group.

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Standard Care

• CVP, Pulse Oximetry, Urine Cath, Art. Line.
• CVP gt 8-12mm Hg
• MAP gt65mm Hg
• Urine Output gt 0.5ml/kg/hr

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Treatment group

• Standard Care (25ml/kg/IVF)
• If Central Venous Oxygen saturation was less than
  70
• 1. Transfused Blood until Hctgt30
• 2. If HTN Vasodilators until MAP lt65m Hg
• 3. Dobutamine if above failed to raise Mixed
  Venous Oxygen Saturation.
• 4. If above still failed Mech Ventilation and
  Sedatives

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Results

• All Patient Standard Therapy Mortality was 46.5
• All Patient Treatment Group was 38
• Septic Shock Standard Therapy Mortality was 56.8
• Septic Shock Treatment Group was 38.

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Treatment Differences in First 6hrs
Pressor use did not substantially differ.
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Comments

• Impressive study in ER Setting
• Majority of difference was Correction of any
  Anemia and Early Administration of More IV Fluids
  and Blood.
• Dobutamine may indicated in Cardiogenic Shock.
  Patients received Dobutamine in this trial did so
  only after Volume resusitation (see above) and
  Central Venous Oxygen Saturation remained low
  indicating they had some underlying Cardiac
  Dysfunction.