Diagnosis &

Management of Shock
F. Heru Irwanto
Dept. of Anesthesiology and Critical Care, Dr. Moh.
Hoesin General Hospital
Shock: Inadequate perfusion
resulting in O
2
debt at cellular level


DEFINITIONS
Early Phase
Preservation of Cardiac Output
Catecholamine release - increase HR, enhanced
contractility
Sympathetic stimulation - increase
SVR, Arterial pressure
Venoconstriction - increase preload
Common
Pathophysiology
Later Phase
Failure of compensatory mechanisms
Reduction in cardiac output,
arterial pressure
Microcirculation - sludging,
rouleaux formation
Common Pathophysiology
Cellular dysfunction
DO
2
and energy substrate reduction - anaerobic metabolism,
systemic acidosis (myocardial,
smooth muscle depressant), organ failure
Marked decrease VO
2
, may
indicate irreversible shock
Common
Pathophysiology
Hemorrhagic/Hypovolemic
Cardiogenic
Obstructive (tension
pneumothorx, cardiac
tamponade)
Distributive (SIRS, septic,
high output failure, spinal
cord injury, anaphylactic)


Etiologic Classification
of Shock
Type PAP CO SVR
hemorrhagic decr decr incr
cardiogenic incr decr incr
distributive n, n, decr
decr incr,
decr
obstructive incr decr incr
Hemodynamic
Classification of Shock
Pathophysiology
Volume deficit - decr. BP, CO
Compensatory Mechanisms
Catecholamine, sympathetic
stimulation
Interstitial fluid entry into
intravascular compartment
Hemorrhagic Shock
Clinical Presentation
Early Phase
Tachycardia, narrow pulse
pressure, may exhibit orthostatic
changes in HR/AP
Healthy patient with 25-30% loss may exhibit only
these signs
Hemorrhagic Shock
Later Phase
Cool moist skin, hypotensive,
anxious, disoriented, oliguric
KEY: EARLY RECOGNITION
Hemorrhagic Shock
Management
Therapeutic Goals
Correct Hypotension, thereby
normalizing cellular perfusion,
reducing acidemia
Increase SaO
2
, thereby
increasing DO
2



Hemorrhagic Shock
Restoration of intravascular volume
Fluid administered should replace
fluid lost
Initial Management:
Crystalloids :Ringers
Colloids ( 5% alb., hetastarch) do
not increase survival and are costly
W.B. PRBC, when indicated
Hemorrhagic Shock
Urine output (0.5 - 1.0 ml/kg/hr)
acceptable renal perfusion
Reversal of lactic acidosis (normal pH)
improved perfusion
Normal mental status
adequate cerebral perfusion
Parameters of Adequate
Resuscitation
Pathophysiology
AMI- 10-15% cardiogenic shock
Mortality > 80%
Decreased CO, Arterial pressure
Neurohumoral compensatory
mechanisms can be deleterious:
> venoconstriction - >preload
Cardiogenic Shock
> SVR > afterload
> HR > VO
2

< Arterial Press < coronary perfusion
All contribute to extension of infarct and
morbid progression of cardiogenic shock
Cardiogenic Shock
Prognostic Parameters
Group PAEDP CI Mortality
I > 29 100%
II < 29 ->15 < 2 92%
III < 29 < 2 63%
IV < 15 > 2 13%
PAEDP=mm Hg, CI=L/M
2
/min.
PAEDP : Pulmonary Artery End Diastolic Press.
CI : Cardiac Index

Cardiogenic Shock
Clinical Presentation
Hypotension - < 90 syst.,
Cool diaphoretic skin, dyspnea,
disorientation, oliguria
Cardiogenic Shock
Management Principles
Primary Goal: Improve myocardial function
Decrease O
2
consumption (VO
2
)
Intubation, sedation, analgesia
Increase O
2
delivery (DO
2
)
Optimize CI, Hb. (SaO
2
)


Cardiogenic Shock
Management Methods
Pharmacologic Manipulation
Preload . morphine, nitro, lasix, volume
Cardiac contractility - inotropes,
chronotropes, vasopressors
Afterload (PVR,SVR) - nitro, beta-blockers
Cardiogenic Shock
Interventional Therapy
Intraaortic Balloon Pump (IABP)
or Counterpulsation
IABP + Early CABG (12-16 hr.
post AMI)
Left Ventricular Assist Device
(LVAD)
Cardiogenic Shock
Pathophysiology
Peripheral vascular dilatation
disproportionate to existing
intravascular volume
Septic/Systemic inflammatory
shock(SIRS), anaphylaxis,
spinal shock
Distributive Shock
Etiology
Gram neg bacteria (gm. neg rods)
Most common (E. coli, 31% all cases)
Incidence - 12.8%/1000 hosp. adm.
Mortality
25%; 30-50% if shock present
30% if Resp./GI/unkn. Source
15% if Biliary/GU/GYN source
Septic Shock
Endotoxin
A complex lipopolysaccharide in the
cellular wall of gram negative rods
Probably the causative agent
Experimental endotoxin shock produces changes like
those seen in patients (fever, hypotension, DIC,
complement activation, leukocytosis)
Septic Shock
Clinical Presentation
Early Phase
Vasodilatation, CO normal or high, fever,
agitation/confusion, hyperventilation
Often, fever and hyperventilation are
the earliest signs.
Hypotension may not be present.
Septic Shock
Late Phase
CO decreased, hypotension,
vasoconstriction, impaired perfusion,
decreased level of consciousness,
oliguria, DIC
Atypical Presentation
Elderly/debilitated Fever, respiratory
alkalosis, confusion, hypotension
Septic Shock
Management
Fluid resuscitation
Pressure support
After adequate volume restored
Dopamine (5-10 ug/kg/min)
Dobutamine (5-20ug/kg/min)
Airway management
Septic Shock
Management
Surgical drainage (abscess, infected
organ (gangrenous gallbladder, bowel)
Antibiotics

Septic Shock
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