Transcript SHOCK - Emory University Department of Pediatrics

SHOCK
NGA B. PHAM, MD, FAAP
CRITICAL CARE MEDICINE
CHILDREN’S HEALTHCARE OF ATLANTA
EGLESTON
2006
Objectives
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Review basic physiologic aspects of shock
Define shock and its different categories
Describe management of shock
What is Shock?
Pathophysiology of shock
Oxygen
Demand > Supply
Definition of Shock
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Inadequate tissue perfusion to meet tissue
demands
Usually result of inadequate blood flow
and/or oxygen delivery
Shock is not a blood pressure
diagnosis
Determinants of Oxygen Delivery
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Oxygen
Delivery = Content x Cardiac output
Determinants of Oxygen Delivery
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Oxygen content = 1.34 (Hgb x SaO2) + (PaO2 x
0.003)
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SaO2: Oxygen saturation
Hgb: Hemoglobin concentration
PaO2: partial pressure Oxygen in plasma
To improve Oxygen content
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Increase Hemoglobin concentration
Increase saturation
Determinants of Oxygen Delivery
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Cardiac output
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C.O. = Heart rate x stroke volume
To improve Cardiac output
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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
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Respiratory failure
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Tachypnea
Decreased compliance
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Pulm edema, pulm infiltrate, etc.
Increased resistance
Diaphragm fatigue
Central vs peripheral
 Demand >> supply
 Inadequate O2 delivery
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Secondary Organ Dysfunction
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CNS – altered mental status
Renal insufficiency – pre-renal
Coagulation abnormalities – DIC
Hepatic/GI dysfunction – bowel ischemia
Endocrine – Calcium, hypo-adrenalism,
vasopressin
Classification of Shock
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Hypovolemic Shock (#1 cause world wide)
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Cardiogenic Shock
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Pump failure, obstructive, L-R shunt
Distributive Shock
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Dehydration, hemorrhagic
Neurogenic
Anaphylaxis
Septic Shock – All of the above
Classification of Shock
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Compensated
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Uncompensated
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Organ perfusion is maintained
Circulatory failure with end organ dysfunction
Irreverisble
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Irreparable loss of essential organs
Mechanical Requirements for
Adequate Tissue Perfusion
Fluid
 Pump
 Vessels
 Flow
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Hypovolemic Shock
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#1 cause of death world wide
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Gastroenteritis
Hemorrhagic – Trauma, GI bleed
Diagnosis of Hypovolemic Shock
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Early
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Increase HR
Decrease perfusion
Normal BP, decrease pulse pressure
Late
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Sign increase HR
Sign decrease perfusion
Decrease BP
End organ dysfunction
Pathophysiology of
Hypovolemic Shock
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Decrease intravascular volume
Compensation – increase endogenous
catecholamines
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Increase HR – increase C.O., O2 delivery
Increase SVR – increase BP (esp diastolic)
Compensation for <15% dehydration
Cardiogenic Shock
Pump failure/malfunction
(decreased contractility)
Cardiogenic Shock
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Electrical Failure
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Arrhythmias
Mechanical failure
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Cardiomyopathy
Metabolic – acidosis
Anatomic
Hypoxia/ischemia
Obstruction
Cardiogenic Shock
Symptoms
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Tachycardia
Tachypnea
Respiratory distress
Mental status change
Cool extremities
Poor perfusion
Signs of dehydration
Cardiogenic Shock
Obstruction of Flow
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Causes
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Pericardial tamponade
Pulmonary embolism
Pulmonary hypertension
Cardiogenic Shock
Obstruction of Flow
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Causes
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Pericarditis
Post-traumatic
Post-cardiac surgery
Complication of central line placement
Recognition
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Cardiac tamponade
Tachycardia
Low C.O., narrow pulse pressure (inc. diastole)
Inc. CVP, JVD
PULSUS PARADOXUS (>10mmHg)
Muffled heart sounds (??rub)
NO RALES
Distributive Shock
 Abnormal
vessel tone
(decreased afterload)
Distributive Shock
Vasodilitation
Venous Pooling
Decreased Afterload
Maldistribution of regional blood flow
Distributive Shock
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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
Septic Shock
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Terminology in Sepsis
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Infection = response to micro organism
Bacteremia = bug in blood
Systemic Inflammatory Response Syndrome
(SIRS)
T>38, <36
 Increase HR
 Increase RR, paCO2<32
 WBC>12,000, <4,000, >10% bands
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Septic Shock
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Terminology in Sepsis
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Sepsis = SIRS as response to a known
infection
Severe sepsis = Sepsis + organ dysfunction
Septic Shock = Sepsis + inadequate oxygen
delivery
Multiple Organ Dysfunction Syndrome (MODS)
– organ dysfunction that requires intervention
Septic Shock
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Components of Septic shock
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Decreased volume
Decreased pump function
Abnormal vessel tone
Septic Shock
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Therapy for Caridovascular Support
Preload
Volume
Contractility
Inotropes
Afterload
Vasodilators
Septic Shock
Etiologies
 Inflammatory: too much, too little
 Coagulation pathway: DIC-bleeding, procoagulant, microthombosis
 Multiple organ system failure
Recognition of Septic Shock
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Early – warm shock – similar to
neurogenic shock
Late – Cold shock – similar to
cardiogenic shock
Diagnosis of Septic Shock
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Establish presence of infection
Inc. HR, normal or dec. BP & perfusion
Latic acidosis
Muti-organ dysfunction
Early vs Late Septic Shock
Early
Late
Heart rate
Tachycardia
Tachycardia/
bradycardia
Blood pressure
Normal
decreased
Peripheral
Perfusion
Warm/cool
Cool
Dec./inc. pulses Dec. pulses
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
Treatment Strategies in
Shock
Principles of Resuscitation
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Increase Oxygen Delivery\
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Increase Oxygen content
Increase Cardiac output
Increase blood pressure
Decrease Demand
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Sedation/analgesia
Intubation
Initial Treatment in Shock
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Airway
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Supplemental oxygen, intubation
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Carefull with cardiovascular collapse post intubation due to
positive thoracic pressure decrease venous return
Breathing
Circulation
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Intravenous access – go early, go IO
Volume expansion (40cc/kg NS, repeat prn)
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Carefull with cardiogenic shock (5cc/kg then reassess)
Optimize cardiac function, oxygenation
Restoration of Circulation
Volume
Fluids, fluids, fluids
Crystalloids vs Colloids
Restoration of Circulation
Volume
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Crystalloids
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NS is the fluid of choice, availability
Rapid redistribution out of intravascular space
– capillary leak
Restoration of Circulation
Volume
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Colloids: albumin, blood
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Albumin
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Worsening of edema due to cap leak in early
sepsis
Blood
Great volume expanders
 Side effects: with massive transfusion >1.5 blood
volumes
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Risk of infection
Dilutional thrombocytopenia and factors V & VIII
Calcium binding hemodynamic instability (citrate)
Restoration of Circulation
Volume – Fluid Choices
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Based on:
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Type of deficit
Urgency of repletion
Pathophysiology of shock
Restoration of Circulation
Volume – Fluid Choices
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Crystalloids for initial resuscitation
Colloids/PRBC’s to replace blood loss
Treatment of Shock
Cardiac Support
Alpha
Dopamine
Beta
Epinephrine
Norepinephrine
Neosynephrine
Dobutamine
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
Phosphodiesterase
inhibitor
0.5 – 0.75
Inotrope
vasodilation
“New” Therapies in Septic Shock
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Vasopressin
Steroids
Activated protein C (Xigris) in Septic Shock
New” “ Therapies in Septic Shock
Vasopressin
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Unclear mechanism of action
Bridging vascular instability in high
exogenous catecholamines requirement
septic shock, therefore decrease side
effects of toxic dosage of catecholamines
Also shows greater blood flow diversion
from non-vital to vital organs
New” “ Therapies in Septic Shock
Vasopressin
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Dosage 0.01 – 0.04U/min up to 0.08U/min
New” “ Therapies in Septic Shock
Steroids
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Hypo-adrenalism: abnormal
hypothalamus-pituitary-adrenal axis
At risk of adrenal insufficiency – in the
presence of catecholamine requirement
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Fluid refractory shock
Normal BP, cold shock
Low BP, cold shock
Dosage – stress dose
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Hydrocortisone 150 mg/m2 ivp
New” “ Therapies in Septic Shock
Steroids
Glucocorticoid function – immune response
 Fall in circulating lymphocytes
 Inhibits neutrophils migration to the
inflammatory sites
 Inhibits macrophages secretion
 Promotes eosinophilic apoptosis
 Modulates cytokines production
New” “ Therapies in Septic Shock
Steroids
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Glucocorticoid function – Cardiovascular
Modulate vascular reactivity to angiotensin
II and to catecholamines -Not fully
understood mechanism
Modulate vascular permeability and
production of NO and other vasodilator
factor
INCREASE IN BLOOD PRESSURE
New” “ Therapies in Septic Shock
Steroids
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Glucocorticoid production in stress
Maintain homeostasis
Normalize vascular reactivity
Modulate inflammatory response
New” “ Therapies in Septic Shock
Activated Protein C (Xigris)
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Recombinant Human Activated Protein C
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Prevent DIC cascade with antithrombotic
activity by inhibiting factors Va & VIIIa
May exerts anti-inflammatory effects by
inhibiting TNF and by blocking leukocytes
adhesions
Side effects
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Bleeding
Pediatric trial terminated early (03/04) due to
no benefit to known risk of bleeding