Emergency pediatric – PICU division Pediatric Department ...

SHOCK

Emergency pediatric – PICU division

Pediatric Department

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

1

Definition

Shock is an acute, complex state of

circulatory dysfunction that results in

failure to deliver sufficient amounts of

2

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 (CaO2)

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

CaO2= Hb x SaO2 x 1,39

3

Blood CO

SV

Preload

Myocard

Contractility

Blood

PressureAfterloadHR

SVR

4

CO = Cardiac Output

SVR = Systemic Vascular resistance

SV = Stroke Volume

HR = Heart Rate

Clinical Manifestation

Clinical Sign Compensated Uncompensated Irreversible

Heart rate

Systolic BP

Pulse volume

Capillary refill

Tachycardia +

Normal

Normal/reduced

Normal/increased

Tachycardia ++

Normal or falling

Reduced +

Increased +

Tachycardia

/bradicardia

Plummeting

Reduced ++

Three phases: compensated, uncompensated, irreversible

5

Capillary refill

Skin

Respiratory rate

Mental state

Normal/increased

Cool,pale

Tachypnoea +

Mild agitation

Increased +

Cool,mottled

Tachypnoea ++

Lethargic

Uncooperative

Reduced ++

Increased ++

Cold,deathly pale

Sighing respiration

React only to pain or

unresponsive

Management

• Intubation & mechanical ventilation

• Fluid resuscitation

• Vasoactive infusion

6

• Vasoactive infusion

FUNCTIONAL CLASSIFICATION

• Hypovolemia

• Cardiogenic

• Obstructive

7

• Distributive

• Septic

• Endocrine

HYPOVOLEMIC SHOCK

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

• Most common cause of shock in infants & children

• Etiology:

– Hemorrhage

– Plasma loss

8

– Plasma loss

– Fluid & electrolyte loss

• Hypovolemia � ↓ preload � ↓ SV � ↓ CO

CLINICAL MANIFESTATION:

• Tachycardia

• Skin mottling

• Prolonged capillary refill

• Cool extremities

• ↓ UOP

9

• ↓ 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

10Continuous monitoring of HR, arterial BP, CVP, UOP Continuous monitoring of HR, arterial BP, CVP, UOP

Shock (+)Shock (+)

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

11

Ventricular filling pressure rises without evidence of improvement

in cardiovascular performance

Discontinue fluid resuscitation

Inotropic agent (+)

REFRACTORY SHOCK:

– Unrecognized pneumothorax / pericardial effusion

– Intestinal ischemia

– Sepsis

– Myocardial dysfunction

12

– Adrenal cortical insufficiency

– Pulmonary hypertension

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

13

� Depressed CO

• Etiology: Heart rate abnormalities, Cardiomyopathies/carditis,

Congenital heart disease, Trauma

• Myocardial dysfunction is frequently a late manifestation of

shock of any etiology

CLINICAL MANIFESTATION

• Tachycardia

• Hypotensive

• Diaphoretic

• Oliguria

• Acidotic

• Cool extremities

14

• Cool extremities

• Altered mental status

• Hepatomegaly

• Jugular venous distension

• Rales

• Peripheral edema

THERAPY

• ↑ Tissue oxygen supply

• ↓ Tissue oxygen requirements

• Correct metabolic abnormalities

• Preload should be optimized

15

• Preload should be optimized

• Myocardial contractility: inotropic agent ���� cathecholamine:

norepinephrine, epinephrine, dopamine & dobutamine

OBSTRUCTIVE SHOCK

• Caused by inability to produce adequate CO despite normal

intravascular volume & myocardial function

• Causative factor:

– Acute pericardial tamponade

16

– Tension pneumothorax

– Pulmonary / systemic hypertension

– Congenital / acquired outflow obstruction

CARDIAC TAMPONADE

• Hemodinamically significant cardiac compression � accumulation

pericardial contents that evoke & defeat compensatory mechanism

• Physical examination:

– Pulsus paradoxus

– Narrowed pulse pressure

– Pericardial rub

17

– 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

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

18

• Treatment:

– Reversal underlying etiology

– Vigorous fluid administration

– Vasopressor infusion

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

19

– Temp. >38,5 C or < 36 C

– Tachycardia

– Tachypnea

– WBC ↑ / ↓ or >10% immature neutrophils

• Sepsis: SIRS + documented infection

• Severe sepsis: Sepsis + end organ dysfunction

• Septic shock: Sepsis with hypotension despite adequate fluid

20

• Septic shock: Sepsis with hypotension despite adequate fluid

resuscitation

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

21

• Inotropic / vasopressor ���� refractory to fluids

• Mechanical ventilation ���� refractory shock

• Hydrocortisone

• Glycemic control

• Blood transfusion

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

Fluid refractory-dopamine/dobutamine resistant shock

Fluid refractory shock**

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/m2

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 resuscitation

and epinephrine

Low Blood Pressure Warm ShockSVC O2 Sat < 70%

Titrater volume and

norepinephrine

60 minDraw baseline cortisol level

Then give hydrocortisone

Draw baseline cortisol level or perform

ACTH stim test. Do not give hydrocortisone

Not at risk ?At risk of adrenal insufficiency ?

THANK YOUTHANK YOUTHANK YOUTHANK YOU

23