SHOCK Emergency pediatric – PICU division Pediatric Department Medical Faculty, University of Sumatera Utara – H. Adam Malik Hospital 1

Definition 2 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 (DO 2 ): DO 2 = Cardiac output (CO) x Arterial oxygen content (CaO 2 ) CO = Heart Rate (HR) x Stroke Volume (SV) CaO 2 = Hb x SaO 2 x 1,39 3

Blood Pressure COSVPreload Myocard Contractility AfterloadHRSVR 4 CO = Cardiac Output SVR = Systemic Vascular resistance SV = Stroke Volume HR = Heart Rate

5 Clinical Manifestation Clinical SignCompensatedUncompensatedIrreversible Heart rate Systolic BP Pulse volume Capillary refill Skin Respiratory rate Mental state Tachycardia + Normal Normal/reduced Normal/increased Cool,pale Tachypnoea + Mild agitation Tachycardia ++ Normal or falling Reduced + Increased + Cool,mottled Tachypnoea ++ Lethargic Uncooperative Tachycardia /bradicardia Plummeting Reduced ++ Increased ++ Cold,deathly pale Sighing respiration React only to pain or unresponsive Three phases: compensated, uncompensated, irreversible

Management 6 Intubation & mechanical ventilation Fluid resuscitation Vasoactive infusion Intubation & mechanical ventilation Fluid resuscitation Vasoactive infusion

7 FUNCTIONAL CLASSIFICATION Hypovolemia Cardiogenic Obstructive Distributive Septic Endocrine

8 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

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

10 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 Shock (+)

11 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 (+)

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

13 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

14 CLINICAL MANIFESTATION Tachycardia Hypotensive Diaphoretic Oliguria Acidotic Cool extremities Altered mental status Hepatomegaly Jugular venous distension Rales Peripheral edema

15 THERAPY ↑ Tissue oxygen supply ↓ Tissue oxygen requirements Correct metabolic abnormalities Preload should be optimized Myocardial contractility: inotropic agent  cathecholamine: norepinephrine, epinephrine, dopamine & dobutamine

16 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

17 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

18 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

19 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

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

21 MANAGEMENT: Early recognition Antibiotics appropriate with microbiological examination Initial fluid resuscitation 20 ml/kg boluses over 5-10 minutes up to ml/kg in the first hour Inotropic / vasopressor  refractory to fluids Mechanical ventilation  refractory shock Hydrocortisone Glycemic control Blood transfusion

ECMO Refractory shock Start 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 Shock SVC O 2 Sat < 70% Low Blood Pressure Cold Shock SVC O 2 Sat < 70% Titrater volume resuscitation and epinephrine Low Blood Pressure Warm Shock SVC O 2 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 PICU Titrate epinephrine for cold shock, norepinephrine for warm shock to Normal MAP-CVP difference for age and SVCO 2 saturation > 70% Establish central venous access, begin dopamine or Dobutamine 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 min 5 min At risk of adrenal insufficiency ? Fluid refractory-dopamine/dobutamine resistant shock Fluid refractory shock**

THANK YOU 23