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Definition
Shock is an acute, complex state of
circulatory dysfunction that results in
failure to deliver sufficient amounts of
oxygen and other nutrients to meet
tissue metabolic demands
Pathophysiology
Delivery of Oxygen (DO2):
DO2 = Cardiac output (CO) x Arterial oxygen content (CaO 2)
CO = Heart Rate (HR) x Stroke Volume (SV)
CaO2= Hb x SaO2 x 1,39
CO = Cardiac Output
SVR = Systemic Vascular resistance
SV = Stroke Volume
HR = Heart Rate
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Clinical Manifestation
Three phases: compensated, uncompensated, irreversible
Clinical Sign
Compensated
Heart rate
Systolic BP
Pulse volume
Capillary refill
Skin
Respiratory rate
Mental state
Tachycardia +
Normal
Normal/reduced
Normal/increased
Cool,pale
Tachypnoea +
Mild agitation
Uncompensated
Tachycardia ++
Normal or falling
Reduced +
Increased +
Cool,mottled
Tachypnoea ++
Lethargic
Uncooperative
Irreversible
Tachycardia
/bradicardia
Plummeting
Reduced ++
Increased ++
Cold,deathly pale
Sighing respiration
React only to pain or
unresponsive
Management
FUNCTIONAL CLASSIFICATION
Hypovolemia
Cardiogenic
Obstructive
Distributive
Septic
Endocrine
HYPOVOLEMIC
SHOCK
CLINICAL MANIFESTATION:
Tachycardia
Skin mottling
Prolonged capillary refill
Cool extremities
UOP
Hypotensive
Lethargy / comatose
THERAPY
Adequate oxygenation and ventilation
Rapid volume replacement reestablish circulation:
Crystalloid: 20 ml/kg shock persist 20 ml/kg
Hemorrhagic: transfusion
Shock (+)
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CVP:
< 10 mmHg fluid infusion until preload is reach
>10 mmHg indication: flow-direct thermo dilution
pulmonary artery catheter and/or echocardiogram
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REFRACTORY SHOCK:
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CARDIOGENIC SHOCK
The pathophysiologic state in which abnormality of cardiac
function is responsible for the failure of the cardiovascular system
to meet the metabolic needs of tissue
Depressed CO
Etiology: Heart rate abnormalities, Cardiomyopathies/carditis,
Congenital heart disease, Trauma
Myocardial dysfunction is frequently a late manifestation of shock
of any etiology
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CLINICAL MANIFESTATION
Tachycardia
Hypotensive
Diaphoretic
Oliguria
Acidotic
Cool extremities
Altered mental status
Hepatomegaly
Jugular venous distension
Rales
Peripheral edema
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THERAPY
Tissue oxygen supply
Tissue oxygen requirements
Correct metabolic abnormalities
Preload should be optimized
Myocardial contractility: inotropic agent cathecholamine:
norepinephrine, epinephrine, dopamine & dobutamine
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OBSTRUCTIVE SHOCK
Caused by inability to produce adequate CO despite normal
intravascular volume & myocardial function
Causative factor:
Acute pericardial tamponade
Tension pneumothorax
Pulmonary / systemic hypertension
Congenital / acquired outflow obstruction
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CARDIAC TAMPONADE
Hemodinamically significant cardiac compression accumulation
pericardial contents that evoke & defeat compensatory mechanism
Physical examination:
Pulsus paradoxus
Narrowed pulse pressure
Pericardial rub
Jugular venous distension
Definitive treatment: removed pericardial fluid or air surgical drainage /
pericardiocentesis
Medical management:
Blood volume expansion maintain venoarterial gradients
Inotropic agent
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DISTRIBUTIVE SHOCK
Results from maldistribution of blood flow to the tissue
May be seen with anaphylaxis, spinal / epidural
anesthesia, disruption of spinal cord, inappropriate
administration vasodilatory medication
Treatment:
Reversal underlying etiology
Vigorous fluid administration
Vasopressor infusion
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SEPTIC SHOCK
Contains many elements of the other types of shock discussed
previously (hypovolemic, cardiogenic, and distributive shock)
SIRS (Systemic Inflammatory Response Syndrome): non specific
inflammatory response
Modified criteria for SIRS:
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MANAGEMENT:
Early recognition
Antibiotics appropriate with microbiological examination
Initial fluid resuscitation 20 ml/kg boluses over 5-10
minutes up to 40-60 ml/kg in the first hour
Inotropic / vasopressor refractory to fluids
Mechanical ventilation refractory shock
Hydrocortisone
Glycemic control
Blood transfusion
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0 min
5 min
15 min
Observe in PICU
Not at risk ?
Refractory shock
ECMO
THANK
YOU
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