shock2

SHOCKEmergency pediatric – PICU division

Pediatric Department

Medical Faculty, University of Sumatera Utara – H. Adam Malik Hospital

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Definition

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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

PathophysiologyPathophysiology

Delivery of Oxygen (DO2):

DO2 = Cardiac output (CO) x Arterial oxygen content (CaO2)

CO = Heart Rate (HR) x Stroke Volume (SV)

CaO2= Hb x SaO2 x 1,39

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CO = Cardiac OutputSVR = Systemic Vascular resistanceSV = Stroke VolumeHR = Heart Rate

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Clinical Manifestation

Clinical Sign Compensated Uncompensated Irreversible

Heart rateSystolic BPPulse volumeCapillary refillSkinRespiratory rateMental state

Tachycardia +NormalNormal/reducedNormal/increasedCool,paleTachypnoea +Mild agitation

Tachycardia ++Normal or fallingReduced +Increased +Cool,mottledTachypnoea ++LethargicUncooperative

Tachycardia /bradicardiaPlummeting Reduced ++Increased ++Cold,deathly paleSighing respirationReact only to pain orunresponsive

Three phases: compensated, uncompensated, irreversible

Management

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• Intubation & mechanical ventilation• Fluid resuscitation• Vasoactive infusion

• Intubation & mechanical ventilation• Fluid resuscitation• Vasoactive infusion

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FUNCTIONAL CLASSIFICATION

• Hypovolemia• Cardiogenic• Obstructive• Distributive• Septic• Endocrine

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HYPOVOLEMIC SHOCK

• A decrease in intra vascular blood volume to such an extent that effective tissue perfusion can not be maintain

• Most common cause of shock in infants & children• Etiology:

– Hemorrhage– Plasma loss– Fluid & electrolyte loss

• Hypovolemia ↓ preload ↓ SV ↓ CO

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CLINICAL MANIFESTATION:• Tachycardia• Skin mottling• Prolonged capillary refill• Cool extremities• ↓ UOP• Hypotensive• Lethargy / comatose

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THERAPY• Adequate oxygenation and ventilation• Rapid volume replacement reestablish circulation:

– Crystalloid: 20 ml/kg shock persist 20 ml/kg– Hemorrhagic: transfusion

Continuous monitoring of HR, arterial BP, CVP, UOP Continuous monitoring of HR, arterial BP, CVP, UOP

Shock (+)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

Ventricular filling pressure rises without evidence of improvement in cardiovascular performance

Discontinue fluid resuscitation

Inotropic agent (+)

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REFRACTORY SHOCK:

– Unrecognized pneumothorax / pericardial effusion– Intestinal ischemia– Sepsis– Myocardial dysfunction– Adrenal cortical insufficiency– Pulmonary hypertension

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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:– Temp. >38,5 C or < 36 C– Tachycardia– Tachypnea– WBC ↑ / ↓ or >10% immature neutrophils

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• Sepsis: SIRS + documented infection• Severe sepsis: Sepsis + end organ dysfunction• Septic shock: Sepsis with hypotension despite adequate fluid

resuscitation

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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

ECMORefractory shockStart cardiac output measurement and direct fluid, inotrope, vasopressor, vasosilator,

and hormonal therapies to attain normal MAP-CBP and CI > 3.3 and < 6.0 L/min/m 2

Persistent Catecholamine-resistant shock

Add vasodilator or type III PDE inhibitor with volume loading

Normal Blood Pressure Cold ShockSVC O2 Sat < 70%

Low Blood Pressure Cold ShockSVC O2 Sat < 70%

Titrater volume resuscitationand epinephrine

Low Blood Pressure Warm ShockSVC O2 Sat < 70%

Titrater volume and norepinephrine

60 min Draw baseline cortisol level Then give hydrocortisone

Draw baseline cortisol level or perform ACTH stim test. Do not give hydrocortisone

Not at risk ?

Catecholamine-resistant shock resistant

Observe in PICUTitrate epinephrine for cold shock, norepinephrine for warm shock to

Normal MAP-CVP difference for age and SVCO2 saturation > 70%

Establish central venous access, begin dopamine orDobutamine therapy and establish arterial monitoring

Push 20 cc/kg isotonic saline or colloid boluses up to and Over 60 cc/kg correct hypoglycemia and hypocalcemia

Fluid responsive*

15 min

Recognize decreased mental status and perfusion.Maintain airway and establish acces according to PALS guidelines

0 min5 min

At risk of adrenal insufficiency ?

Fluid refractory-dopamine/dobutamine resistant shock

Fluid refractory shock**

THANK YOU

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