Making Sense of Shock

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Making Sense of Shock

• J. Brassard
• MaineGeneral Medical Center

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ShockDefinitions

• Low BP associated with clinical signs of tissue
  hypoperfusion
• Inadequate tissue O2 delivery for existing
  metabolic demands
• DO2 oxygen delivery
• VO2 oxygen consumption
• DO2 C.O. x CaO2 x 10
• VO2 C.O. x (CaO2- CmvO2) x 10
• CaO2 (Hb x SaO2 x 1.36) (PaO2 x 0.003)

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Shockclinical signs

• Skin mottling
• Diaphoresis
• Tachycardia
• Altered mental status
• Increased respiratory rate
• Categorize shock based on cause

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Shockhypovolemic/ hemorrhagic

• Most common cause post trauma/ injury
• Establishment of IV access is important
• Normal 70 kg male has 5L circulating volume
• ATLS criteria
• I lt 15- few clinical signs/ symptoms
• II 15-30- tachycardia, tachypnea, decr. PP
• III 30-40- measurable fall in BP
• IV gt 40- immediately life threatening

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Shock Cardiogenic(myocardial, valvular,
dysrhythmias)

• Most common origin due to AMI (5-10)
• Most common cause of death in AMI (50-80)
• SHOCK trial registry 1160 CS patients
• 75 LV failure
• 8 acute MR
• 5 ventriculoseptal rupture
• 3 RV infarct
• 2 tamponade/ free wall rupture

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Shockcardiogenic

• Signs oliguria, AMS, extremity mottling, JVD,
  rales
• Definition decreased C.O., evidence of tissue
  hypoperfusion despite adequate intravascular
  volume
• SBP lt 90 mm Hg, C.I. lt 2.2 L/min/m2, PCWP gt 15
  mm Hg

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Shockcardiogenic

• Approx. 90 develop CS post hospital admission
• 75 within 1st 24 hours
• Both systolic and diastolic dysfunction
• Mostly associated with anterior infarct
• RX ASA, B-blockers, nitrates
• Inotropic agents
• IABP
• Reperfusion (interventional cath, thrombolysis,
  CABG)

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Shock cardiogenic RV infarct

• Seen in up to 30 IMI patients
• R precordial leads ST elevation (RV4)
• Hypotension, JVD, clear lung fields
• Better prognosis as RV function returns to normal
  with time
• RX increase preload (IVF)
• Mortality reperfusion- 2, no reperf.- 58

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Shockcardiogenic Acute MR

• Associated with IMI
• Ischemia/ infarction of post papillary muscle
• Rupture occurs 2-7 days post MI
• Dramatic presentation pulm edema, early systolic
  murmur (soft due to low C.O.)
• Dx Echo
• RX surgical repair/ replacement of MV

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Shock cardiogenicventricular septal rupture

• Pansystolic murmur, parasternal thrill, L-R
  intracardiac shunt (stepup in SaO2 RA- RV)
• Dramatic large v-waves (similar to MR)
• Dx Echo
• RX operative repair (within 48 hrs)

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Shock cardiogenicfree wall rupture

• Usually within 1st week post AMI
• Risk may be increased by thrombolytic use
• Catastrophic event- pericardial tamponade and PEA
• Classic setting elderly, hypertensive female

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Shockdistributive/ vasodilatory

• Vasoconstriction is the normal vascular
  response
• DX occurs with failure of vascular smooth muscle
  (VSM) to contract
• May be common pathway for longstanding, severe
  shock of any cause

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Shockdistributive

• Cytokine cascade
• Triggering of external receptors on VSM causes
  increased Calcium conc. in cytosol
• Myosin
• Phosphorylation VSM contraction
• Dephosphorylation no contraction
• Resting membrane potential with hyperpolarization
  of potassium channel (NO, acidosis) prevents
  calcium from entering cell

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Shockdistributive

• Sepsis- most common cause
• In U.S.
• gt 400,000 cases of sepsis/ yr
• gt 200,000 cases of septic shock/ yr
• gt 100,000 deaths/ yr

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Shockother causes

• Flow obstructive shock
• Massive PE
• Pericardial tamponade
• Severe valvular stenosis
• Atrial myxoma
• Anaphylactic shock
• Neurogenic shock

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Shockneurogenic

• Spinal chord injury- loss of sympathetic tone
• Often associated with mechanism of injury leading
  to concurrent hypovolemic shock
• Classic picture hypotension without tachycardia
  (normal pulse pressure)

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Septic Shocktreatment

• Volume resuscitation to increase C.O. and DO2
• Main complication of volume tissue edema
• 1 L crystalloid expands IVV only 250 ccs
• Typical 4-8 Liters isotonic fluids over 24 hrs
• Venous access (central)
• Vasopressor agents

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Septic Shockr-activated protein C

• NEJM, March 2001, Vol 344, pp 699-709
• Xigris (Drotrecogin alfa)- recombinant human APC
• Dosed at 24 mcg/kg/hr for 96 hrs
• Inhibits inflammatory coagulation cascade,
  promotes fibrinolysis
• Prior studies showed dose-dependent reduction in
  plasma d-dimer, IL-6 levels
• Primary end point all cause deaths at 28 days
  post initiation of infusion

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Septic Shockr-APC
Absolute mortality reduct. Relative risk mortality reduct.
Overall (n 1690) 6 19
APACHE II 25-53 (n 817) 13 29
APACHE II 3-24 (n 873) 0 1