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SHOCK
NGA B. PHAM, MD, FAAPCRITICAL CARE MEDICINE
CHILDRENS HEALTHCARE OF ATLANTA
EGLESTON2006
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Objectives
Review basic physiologic aspects of shock
Define shock and its different categories Describe management of shock
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What is Shock?
Pathophysiology of shock
Oxygen
Demand > Supply
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Definition of Shock
Inadequate tissue perfusion to meet tissuedemands
Usually result of inadequate blood flowand/or oxygen delivery
Shock is not a blood pressurediagnosis
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Determinants of Oxygen Delivery
Oxygen
Delivery = Content x Cardiac output
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Determinants of Oxygen Delivery
Oxygen content = 1.34 (Hgb x SaO2) + (PaO2 x0.003)
SaO2: Oxygen saturation
Hgb: Hemoglobin concentration PaO2: partial pressure Oxygen in plasma
To improve Oxygen content
Increase Hemoglobin concentration
Increase saturation
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Determinants of Oxygen Delivery
Cardiac output
C.O. = Heart rate x stroke volume
To improve Cardiac output Increase Heart rate
Increase Stroke Volume
Preload volume of blood in the ventricle
Afterload resistance to contraction
Contractility force applied
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Secondary Organ Dysfunction
Respiratory failure
Tachypnea
Decreased compliance
Pulm edema, pulm infiltrate, etc.
Increased resistance
Diaphragm fatigue
Central vs peripheral
Demand >> supply
Inadequate O2 delivery
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Secondary Organ Dysfunction
CNS altered mental status
Renal insufficiency pre-renal
Coagulation abnormalities DIC Hepatic/GI dysfunction bowel ischemia
Endocrine Calcium, hypo-adrenalism,
vasopressin
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Classification of Shock
Hypovolemic Shock (#1 cause world wide)
Dehydration, hemorrhagic
Cardiogenic Shock Pump failure, obstructive, L-R shunt
Distributive Shock
NeurogenicAnaphylaxis
Septic Shock All of the above
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Classification of Shock
Compensated Organ perfusion is maintained
Uncompensated Circulatory failure with end organ dysfunction
Irreverisble
Irreparable loss of essential organs
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Hypovolemic Shock
#1 cause of death world wide
Gastroenteritis
Hemorrhagic Trauma, GI bleed
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Diagnosis of Hypovolemic Shock
Early Increase HR
Decrease perfusion
Normal BP, decrease pulse pressure
Late Sign increase HR
Sign decrease perfusion Decrease BP
End organ dysfunction
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Pathophysiology of
Hypovolemic Shock
Decrease intravascular volume
Compensation increase endogenouscatecholamines
Increase HR increase C.O., O2 delivery
Increase SVR increase BP (esp diastolic)
Compensation for
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Cardiogenic Shock
Pump failure/malfunction(decreased contractility)
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Cardiogenic Shock
Electrical Failure
Arrhythmias
Mechanical failure
Cardiomyopathy
Metabolic acidosis
Anatomic
Hypoxia/ischemia
Obstruction
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Cardiogenic Shock
Symptoms
Tachycardia
Tachypnea
Respiratory distress Mental status change
Cool extremities
Poor perfusion Signs of dehydration
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Cardiogenic Shock
Obstruction of Flow
Causes
Pericardial tamponade
Pulmonary embolism
Pulmonary hypertension
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Cardiogenic Shock
Obstruction of FlowCardiac tamponade
Causes Pericarditis Post-traumatic Post-cardiac surgery Complication of central line placement
Recognition Tachycardia Low C.O., narrow pulse pressure (inc. diastole) Inc. CVP, JVD PULSUS PARADOXUS (>10mmHg) Muffled heart sounds (??rub) NO RALES
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Distributive Shock
Abnormal vessel tone
(decreased afterload)
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Distributive Shock
Vasodilitation Venous Pooling
Decreased Afterload
Maldistribution of regional blood flow
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Distributive Shock
Neurogenic or Anaphylactic Shock
Diminished or absent sympathetic tone
Reduce peripheral vascular tone Peripheral pooling of blood volume
Inadequate venous return
Decreased perfusion, acidosis,hypotension
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Septic Shock
Terminology in Sepsis
Infection = response to micro organism
Bacteremia = bug in blood
Systemic Inflammatory Response Syndrome(SIRS)
T>38,
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Septic Shock
Terminology in Sepsis
Sepsis = SIRS as response to a knowninfection
Severe sepsis = Sepsis + organ dysfunction
Septic Shock = Sepsis + inadequate oxygendelivery
Multiple Organ Dysfunction Syndrome (MODS) organ dysfunction that requires intervention
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Septic Shock
Components of Septic shock
Decreased volume
Decreased pump function
Abnormal vessel tone
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Septic Shock
Therapy for Caridovascular Support
Preload Volume
Contractility Inotropes
Afterload Vasodilators
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Septic Shock
Etiologies
Inflammatory: too much, too little
Coagulation pathway: DIC-bleeding, pro-coagulant, microthombosis
Multiple organ system failure
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Recognition of Septic Shock
Earlywarm shock similar toneurogenic shock
LateCold shock similar tocardiogenic shock
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Diagnosis of Septic Shock
Establish presence of infection
Inc. HR, normal or dec. BP & perfusion
Latic acidosis Muti-organ dysfunction
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Early vs Late Septic Shock
Early Late
Heart rate Tachycardia Tachycardia/
bradycardia
Blood pressure Normal decreased
Peripheral
Perfusion
Warm/cool
Dec./inc. pulses
Cool
Dec. pulses
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Early vs Late Septic Shock
Early Late
End-organ: skin Dec. cap refill Very dec. cap
Refill
Brain Irritable,restless
Lethargic,unresponsive
Kidneys Oliguria Oliguria, anuria
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Treatment Strategies in
Shock
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Principles of Resuscitation
Increase Oxygen Delivery\
Increase Oxygen content
Increase Cardiac output
Increase blood pressure
Decrease Demand
Sedation/analgesia
Intubation
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Initial Treatment in Shock
Airway
Supplemental oxygen, intubation
Carefull with cardiovascular collapse post intubation due topositive thoracic pressure decrease venous return
Breathing
Circulation
Intravenous access go early, go IO
Volume expansion (40cc/kg NS, repeat prn) Carefull with cardiogenic shock (5cc/kg then reassess)
Optimize cardiac function, oxygenation
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Restoration of Circulation
Volume
Fluids, fluids, fluidsCrystalloids vs Colloids
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Restoration of Circulation
Volume
Crystalloids
NS is the fluid of choice, availability
Rapid redistribution out of intravascular space
capillary leak
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Restoration of Circulation
Volume
Colloids: albumin, bloodAlbumin
Worsening of edema due to cap leak in early
sepsis Blood
Great volume expanders
Side effects: with massive transfusion >1.5 blood
volumes Risk of infection Dilutional thrombocytopenia and factors V & VIII
Calcium binding hemodynamic instability (citrate)
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Restoration of Circulation
Volume Fluid Choices
Based on:
Type of deficit
Urgency of repletion
Pathophysiology of shock
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Restoration of Circulation
Volume Fluid Choices
Crystalloids for initial resuscitation
Colloids/PRBCs to replace blood loss
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Treatment of Shock
Cardiac Support
Alpha Dopamine Beta
Epinephrine
Norepinephrine DobutamineNeosynephrine
I t
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Inotropes
Agent Site of Action Dose
Mcg/kg/min
Effects
Dopamine Dopaminergic
Beta
Alpha > Beta
1-3
5-10
11-20
Renal vasodilation
Inotrope/vasoconstriction
Increase perip. Vasc. resistance
Dobutamine Beta 1 & 2 1-20 Inotrope
Vasodilation
Epineprhine Beta > alpha 0.05 1.0 Inotrope, vasoconstriction
Tachycardia
Norepinephrine Alpha > beta 0.05 1.0 Profound vasoconstriction
inotrope
Nitroprusside Vasodilator
(art > venous)
0.5 1.0 Vasodilation
Milranone Phosphodiesteraseinhibitor
0.5 0.75 Inotrope
vasodilation
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New Therapies in Septic Shock
Vasopressin
Steroids
Activated protein C (Xigris) in Septic Shock
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New Therapies in Septic Shock
Vasopressin
Unclear mechanism of action
Bridging vascular instability in highexogenous catecholamines requirementseptic shock, therefore decrease sideeffects of toxic dosage of catecholamines
Also shows greater blood flow diversion
from non-vital to vital organs
S S
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New Therapies in Septic Shock
Vasopressin
Dosage 0.01 0.04U/min up to 0.08U/min
N Th i i S i Sh k
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New Therapies in Septic Shock
Steroids
Hypo-adrenalism: abnormalhypothalamus-pituitary-adrenal axis
At risk of adrenal insufficiency in the
presence of catecholamine requirement Fluid refractory shock
Normal BP, cold shock
Low BP, cold shock Dosage stress dose
Hydrocortisone 150 mg/m2 ivp
N Th i i S ti Sh k
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New Therapies in Septic Shock
Steroids
Glucocorticoid function immune response
Fall in circulating lymphocytes
Inhibits neutrophils migration to theinflammatory sites
Inhibits macrophages secretion
Promotes eosinophilic apoptosis Modulates cytokines production
N Th i i S ti Sh k
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New Therapies in Septic Shock
Steroids
Glucocorticoid function Cardiovascular
Modulate vascular reactivity to angiotensinII and to catecholamines -Not fullyunderstood mechanism
Modulate vascular permeability andproduction of NO and other vasodilator
factor
INCREASE IN BLOOD PRESSURE
N Th i i S ti Sh k
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New Therapies in Septic Shock
Steroids
Glucocorticoid production in stress
Maintain homeostasis
Normalize vascular reactivity
Modulate inflammatory response
N Th i i S ti Sh k
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New Therapies in Septic Shock
Activated Protein C (Xigris)
Recombinant Human Activated Protein C Prevent DIC cascade with antithrombotic
activity by inhibiting factors Va & VIIIa
May exerts anti-inflammatory effects byinhibiting TNF and by blocking leukocytesadhesions
Side effects Bleeding Pediatric trial terminated early (03/04) due to
no benefit to known risk of bleeding