k13 - shock ped
DESCRIPTION
Emergency MedicineTRANSCRIPT
Shock in pediatric
EM1-K13
Shock
A state of circulatory dysfunction that fails to provide sufficient oxygen and nutritions to meet the metabolic needs of vital organs and peripheral tissues
Oxygen Delivery
DO2 = CaO2 x COCaO2 = (Hgb x 1.34 x SaO2) + (0.003 x PaO2)CO = HR x SV
Decreased DO2 - GlucoseDecreased ATP production
Loss of membrane integrity
K efflux, Na influx
Ca influx
Formation of damaging free radicals
Increases Nitric Oxide production
Activates proteases
Damages mitochondria
Damage cellular contents
Elaborated inflammatory mediators (eg, IL-1B, Tumor Necrosis Factor-α)
Microvascular thrombosis and loss of vascular integrity
Further edema formation
Cell death
Cellular edema
Pathophysiology of hypoxic-ischemic injury
Multiple system organ failure
Death
Disturbance cellular homeostasis
TachycardiaCool extremitiesProlonged capillary refillWeak peripheral pulsesNormal blood pressure
Depressed mental statusDecreased urine outputMetabolic acidosisTachypneaWeak central pulses
©Compensated
©Inadequate end organ perfusion
©Decompensated
Sign of shock state & progress
Hypotension
Major categories of shock
Hypovolemic
The most common type; circulating intravascular blood volume decrease; decrease in preload; decrease CO
Cardiogenic
Heart rate abnormalities (heart block, ventricular, supraventricular tachycardia), decreased myocardial contractility
Distributive
Relative uncommon; maldistribution of tissue blood flow due to decreased systemic vascular resistance,
ObstructiveExtrinsic force acting on intrathoracic structures (great vessels, ventricle)
Etiology and typical presentation of
Hypovolemic ShockEtiology Diarrhea
Blood loss (traumatic)
Presentation
Tachycardia Narrowed pulse
pressure Delayed capillary refill Cool extremities Late stages:
hypotension
Etiology and typical presentation of
Cardiogenic ShockEtiology CHD, cardiomyopathies, myocarditis, coronary infark
Dysrhytmia Acidosis, hypoxic-ischemic,
poisoning, metabolic disorders Prolonged shock Sepsis
Presentation
Bradycardia/tachycardia Gallop Barely perceptible pulses Cardiomegaly Rales
Etiology and typical presentation of
Distributive ShockEtiology Early septic Shock
Anaphylaxis Toxic ingestion Spinal/ epidural anesthesia Head/spinal cord injuries
Presentation Flush appearance Warm extremities Bounding pulses Tachycardia Wide pulse pressure Capillary refill may be
instantaneous
Etiology and typical presentation of
Obstructive ShockEtiology · CHD (Aortic stenosis/
coarctation)· Tension pneumothorax· Hemopneumothorax· Pericardial effusion
Presentation
· Tachycardia· Cool extremities· Delayed capillary refill· Narrow pulse pressure· Distended neck veins, distant
heart tones, asymmetric breath sounds
Evaluation of shock
· Assesment of Airway, breathing and circulation
· Blood glucose· History and physical examination
Assesment of airway, breathing and circulation
Airway · Airway patencyBreathing · Respiratory rate
· Respiratory pattern· Work of breathing (respiratory
distress)· Continuous pulse oxymetry
Circulation · Bradycardia· Tachycardia· Rhythm abnormalities· Central and distal pulse· Capillary refill (normal : complete
between 2 to 3 seconds)· Hypotension (late finding)
Normal respiratory rates in children
Age Respiratory rate (breaths/minute)
Newborn-1 year
30-60
1-3 years 25-403-12 years 20-30>12 years 12-20
Normal heart rates in children
Age Heart rate (beats/minute)
Newborn 80-200< 2 years 80-1802-10 years 60-150>10 years 60-100
Neonatal blood pressurebased on birth weight
Lower limit of systolic blood pressure by age
Age Systolic blood pressure (mm Hg)
Newborn 60< 1 years 701-10 years 70 + (age in years x 2) > 10 years 90
Blood glucose
· Bedside assessment· Infant are vulnerable to hypoglycemia· Hypoglycemia may result
severe/permanent neurologic disability
History and Physical Examination
· History· Serial assessment of vital signs, mentation,
and perfusion· Fever (serious infection?), hypothermia
(sepsis?)· The lung fields auscultation (rales :
hypervolemia?)· Gallop rhythm (underlying heart disease,
hypervolemia)· Palpation of liver edge below the costal
margin (hypervolemia, cardiac failure?)· Purpuric or petechial rashes (infectious?)· Secondary survey (injuries?)
1. ABC’s of life support2. Vascular access3. Fluid resuscitation 4. Inotropic-Vasoactive5. Control acidosis6. Monitoring, laboratory studies,
CXR7. Treat the underlying cause
Management of shock
ABC’s of life support
· Open airway· Suction· High Concentration O2· Assist ventilation (as needed)· Control bleeding· Shock position· Keep warm
· Use isotonic crystalloid solution (eg, lactated Ringer’s solution or normal saline) or 5 % albumine.
· Fluid boluses, 20 mL per kg, severe : 40-60 ml/kg, max 200 ml/kg rapidly until the shock is resolved (delivered in 5-10 minutes)
· Observing for signs of fluid overload (increased work of breathing, rales, gallop rhythm, or hepatomegaly)
· Use a glucose-containing solution to only treat documented hypoglycemia
· Correct hypocalcemia· Insufficient data to recommendation or
against using hypertonic saline for shock associated with head injuries or hypovolemia
Fluid resuscitation
Inotropes-Vasoactive agents is use if shock requiring pharmacologic improvement of cardiac contractility function or decompensated shock refractory to volume expansion alone
Inotropes-Vasoactive
Inotropes/Vasoactive AgentsDopamine 1-5 mcg/kg/min: dopaminergic; 5-15
mcg/kg/ min: more beta-1; 10-20 mcg/kg/min: more alpha-1
Dobutamine 2.5-15 mcg/kg/min; mostly beta-1, some beta-2
Epinephrine 0.05-0.1 mcg/kg/ min: mostly beta-1, some beta-2; >0.1 to 0.2 mcg/ kg/min: alpha-1
Nor-epinephrine 0.05-0.2mcg/kg/ min; Use up to 1mcg/kg/min; only alpha and beta-1
Milrinone 50mcg/kg load then 0.375-0.75 mcg/kg/min; Phosphodiesterase inhibitor; results in increased inotropy and peripheral vasodilation (greater effect on pulmonary vasculature)
Control acidosis
· Metabolic acidosis may become evident as child’s condition worsen
· Na Bic no longer routinely recommended because the use of Na Bic may increase intracellular acidosis
· Fluid resuscitation, vasoactive infusion and adequate ventilation/oxygenation are the main management
· Tromethamine /THAM given slowly (3-5 ml/kg) may use in extreme condition (i.e. pH < 7)
Monitoring, lab studies, and CXR
· Monitoring HR, BP continuously· Clinical evaluations/5 min until the patient is
stable· Urine output monitoring with an indwelling
catheter· Lab : ABG, serum electrolytes, glucose, Ca
levels, CBC, PT/PTT, blood type/cross match, and culture
· Evaluate ET tube position, heart size, and pulmonary status by CXR
Treat the underlying cause
· Trauma: ongoing bleeding may need to be addressed surgically
· Myocardial failure: inotropic medications· Sepsis: isolated and treat the infectious
organism with appropriate AB’s