Shock (Rags)
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Transcript of Shock (Rags)
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Pediatric Shock
Recognition and Classification
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Introduction
Shock is a syndrome of cardiovascular
dysfunction cause inability of circulatory
system to provide adequate oxygen and
nutrient to meet the metabolic demands
of vital organs.
Oxygen delivery (DO2 ) is less than
Oxygen Consumption (< VO2)
Untreated this leads to metabolic
acidosis, organ dysfunction and death
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Shock
Transition between life and death
Failure to oxygenate & nourish the body
adequately
Mortality > 20%
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Hemodynamics
MyocardialContractility
Stroke Volume Preload
Cardiac Output Afterload
BloodPressure Heart Rate
Systemic VascularResistance
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Oxygen Delivery
Oxygen delivery = Cardiac Output x ArterialOxygen Content
(DO2 = CO x CaO2)
Art Oxygen Content = Oxygen content of theRBC + the oxygen dissolved in plasma
(CaO2 = Hb X SaO2 X 1.34 + (.003 X PaO2)
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Defending the blood pressure
Neural Sympathetic
Baroreceptors
Carotid Body
Aortic Arch
Volume receptors
Right Atrium
Pulmonary vascular
Chemoreceptors
Aortic and carotid
Medullary
Cerebral ischemic
response
Humoral
Adrenal medulla
Catecholamines
Hypothalamopituitaryresponse
Adrenocorticotropichormone
Vasopressin Renin-angiotensin-
aldosterone system
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Cardiovascularfunction
Cardiac Output
Clinical Assessment
peripheral perfusion, temperature, capillary refill, urine
output, mentation, acid-base status
CO = HR x SV
HR responds the quickest
SV is a function of three variables
preload, afterload, and myocardial contractility
A noncompliant heart cannot increase SV
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Stroke Volume
Preload (LVEDV)
Reflects patients volume status
CVP or PCWP
Afterload The resistance to ventricular ejection
Two variables:
vascular tone and transmural pressure
Myocardial Contractility (squeeze)
Many factors including coronary perfusion, baselinemyocardial function, use of cardiotonic medications
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Pathophysiology
&
Biochemistry in shock
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Pathophysiology
Shock affects mitochondria first
Without oxygen mitochondria convert
fuels to lactate lactic acid
Failure of the krebs cycle
Oxygen is the final electron accepter to form
water
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Lactic Acid
Early shock
Skeletal muscle and splanchnic organs 1st
affected
Lactic acid production
Resuscitation
Pyruvate delivery from glycolysis canoverwhelm Krebs cycle
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Systemic Response
Decreased vascular wall tension
increases sympathetic stimulation
(blocked in sepsis)
Increased epi, norepi, corticosteroids, renin,and glucagon
Increased glycogenolysis and lipolysis
Increased glucose and FFAs to TCA can
overwhelm it
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Immune Response
Neutrophil and macrophage activation
due to hypoxia
Enzymatic organ damage
Capillary plugs causing micro ischemia
TNF and Interleukins released
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Cardiac Physiology
Inflammatory actions of TNF, Interleukins,
and NO decrease contractility
Acidosis can decrease contractility but effect
is minimal
Gregg Phenomenon Contractile strength decreases with decreased
coronary perfusion
Decreased coronary perfusion in shock
Decreased workload due to lower SVR
Very minimal cardiac ischemia even in severe
shock
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Classification of Shock
COMPENSATED blood flow is normal or increased and may be
maldistributed; vital organ function ismaintained
UNCOMPENSATED microvascular perfusion is compromised;
significant reductions in effective circulating
volume
IRREVERSIBLE inadequate perfusion of vital organs;
irreparable damage; death cannot berevented
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Classification:
Hypovolumic
Cardiogenic
Obstructive
Distributive
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Hemodynamic Variables in
Different Shock States
or Septic: LateOr Septic: Early
Or Or Or Distributive
Or Obstructive
Or Cardiogenic
Or Hypovolemic
CVPWedgeMAPSVRCO
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Clinical Presentation
Early diagnosis requires a high index
of suspicion
Diagnosis is made through the
physical examination focused on
tissue perfusion
Abject hypotension is a late and
premorbid sign
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Initial Evaluation: Physical
Exam Findings of Shock
Neurological: Fluctuatingmentalstatus, sunken fontanels
Skin and extremities: Cool, pallor,mottling, cyanosis, poor cap refill, weak
pulses, poor muscle tone.
Cardio-pulmonary: Hyperpnoea,tachycardia.
Renal: Scant, concentrated urine
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Evaluation
Early Signs of Shock
sinus tachycardia
delayed capillary refill
fussy, irritable Late Signs of Shock
bradycardia
altered mental status (lethargy, coma)
hypotonia, decreased DTRs
Cheyne-Stokes breathing
hypotension is a very late sign
Lower limit of SBP = 70 + (2 x age in years)
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Cardiovascular Assessment
Heart Rate
Too high: 180 bpm forinfants, 160 bpm forchildren >1year old
Blood Pressure Lower limit of SBP =
70 + (2 x age inyears)
Peripheral Pulses
Present/Absent
Strength (diminished,normal, bounding)
Skin Perfusion Capillary refill time
Temperature
Color
Mottling
CNS Perfusion
Recognition ofparents
Reaction to pain
Muscle tone Pupil size
Renal Perfusion
UOP >1cc/kg/hr
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Neonate in Shock:
Include in differential:Congenital adrenal hyperplasia
Inborn errors of metabolism
Obstructive left sided cardiac lesions:
Aortic stenosis
Hypo plastic left heart syndrome
Coarctation of the aorta
Interrupted aortic arch
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Hypovolemic Shock
Clinically, history of vomiting/diarrhea or
trauma/blood loss
Signs of dehydration: dry mucousmembranes, absent tears, decreased skin
turgor
Hypotension, tachycardia without signs ofcongestive heart failure, CRT delayed.
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Hemorrhagic Shock
Most common cause of shock (due to
trauma)
Patients present with an obvious history
(but in child abuse history may be
misleading)
Site of blood loss obvious or concealed
(liver, spleen, intracranial, GI, long bone
fracture)
Hypotension, tachycardia and pallor
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SIRS/Sepsis/Septic shock
Mediator release:
exogenous & endogenous
Maldistribution
of blood flow
Cardiac
dysfunction
Imbalance ofoxygen
supply anddemand
Alterations in
metabolism
Septic Shock
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Septic Shock: Warm Shock
Early, compensated, hyperdynamic state
Clinical signs Warm extremities with bounding pulses,
tachycardia, tachypnea, confusion.
Physiologic parameters widened pulse pressure, increased cardiac
ouptut and mixed venous saturation, decreasedsystemic vascular resistance.
Biochemical evidence: Hypocarbia, elevated lactate, hyperglycemia
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Septic Shock: Cold Shock
Late, uncompensated stage with drop incardiac output.
Clinical signs Cyanosis, cold and clammy skin, rapid thready
pulses, shallow respirations.Physiologic parameters
Decreased mixed venous sats, cardiac outputand CVP, increased SVR, thrombocytopenia,oliguria, myocardial dysfunction, capillary leak
Biochemical abnormalities Metabolic acidosis, hypoxia, coagulopathy,
hypoglycemia.
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Cold Shock rapidly progresses to mutiorgansystem failure or death if untreated.
Multi-Organ System Failure: Coma, ARDS, CHF,Renal Failure, Ileus or GI hemorrhage, DIC.
More organ systems involved, worse theprognosis
Septic Shock
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Cardiogenic
ShockEtiology:
Dysrhythmias
Infection (myocarditis)
Metabolic
Obstructive
Drug intoxication
Congenital heart disease
Trauma
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Cardiogenic Shock
Differentiation from other types of shock:
History
Exam:
Enlarged liver
Gallop rhythm
Murmur
Cold extremitis, altered mental status, oliguria.
Tachypnea
tachycardia
CXR:
Enlarged heart, pulmonary venous congestion
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Distributive Shock
Due to an abnormality in vascular tone leading to
peripheral pooling of blood with a relative
hypovolemia.
Etiology
Anaphylaxis
Drug toxicity
Neurologic injury
Early sepsis
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Obstructive Shock
Mechanical obstruction to ventricular outflow.
Etiology: Congenital heart disease, massivepulmonary embolism, tension pneumothorax,
cardiac tamponade.
Inadequate C.O. in the face of adequate preload
and contractility
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Dissociative Shock
Inability of Hemoglobin molecule to give up theoxygen to tissues.
Etiology: Carbon Monoxide poisoning,methemoglobinemia, dyshemoglobinemias.
Tissue perfusion is adequate, but oxygen releaseto tissue is abnormal.
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Differential Diagnosis of Shock
Hypovolemic Hemorrhage
Fluid loss
Drugs
Distributive Anaphylactic
Neurogenic
Septic
Cardiogenic Myocardial dysfunction
Dysrrhythmia
Congenital heartdisease
Obstructive Pneumothorax,
CardiacTamponade,Aortic Dissection
Dissociative Heat, Carbon
monoxide, Cyanide
Endocrine
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Recognition and Classification
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Initial Management of Shock
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Final Thoughts
Recognize compensated shock quickly- have a
high index of suspicion, remember tachycardia is
an early sign. Hypotension is late and ominous.
Gain access quickly- if necessary use an
intraoseous line.
Fluid, fluid, fluid - Administer adequate amounts of
fluid rapidly. Remember ongoing losses.
Correct electrolytes and glucose problems quickly.
If the patient is not responding the way you think
he should, broaden your differential, think about
different types of shock.
References Recommended
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References, RecommendedReading, and
Acknowledgments Uptodate: Initial Management ofShock in Pediatric patients
Nelsons Textbook of Pediatrics
Some slides based on works by Dr.
Lou DeNicola and Dr. Linda Siegel for
PedsCCM
American Heart Association PALS
guidelines