shock (rags)

7/31/2019 Shock (Rags)

1/39

Pediatric Shock

Recognition and Classification


2/39

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


3/39

Shock

Transition between life and death

Failure to oxygenate & nourish the body

adequately

Mortality > 20%


4/39

Hemodynamics

MyocardialContractility

Stroke Volume Preload

Cardiac Output Afterload

BloodPressure Heart Rate

Systemic VascularResistance


5/39

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)


6/39

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


7/39

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


8/39

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


9/39

Pathophysiology

&

Biochemistry in shock


10/39

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


11/39

Lactic Acid

Early shock

Skeletal muscle and splanchnic organs 1st

affected

Lactic acid production

Resuscitation

Pyruvate delivery from glycolysis canoverwhelm Krebs cycle


12/39

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


13/39

Immune Response

Neutrophil and macrophage activation

due to hypoxia

Enzymatic organ damage

Capillary plugs causing micro ischemia

TNF and Interleukins released


14/39

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


15/39

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


16/39

Classification:

Hypovolumic

Cardiogenic

Obstructive

Distributive


17/39

Hemodynamic Variables in

Different Shock States

or Septic: LateOr Septic: Early

Or Or Or Distributive

Or Obstructive

Or Cardiogenic

Or Hypovolemic

CVPWedgeMAPSVRCO


18/39

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


19/39

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


20/39

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)


21/39

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


22/39

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


23/39


24/39

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.


25/39

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


26/39

SIRS/Sepsis/Septic shock

Mediator release:

exogenous & endogenous

Maldistribution

of blood flow

Cardiac

dysfunction

Imbalance ofoxygen

supply anddemand

Alterations in

metabolism

Septic Shock


27/39

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


28/39

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.


29/39

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


30/39

Cardiogenic

ShockEtiology:

Dysrhythmias

Infection (myocarditis)

Metabolic

Obstructive

Drug intoxication

Congenital heart disease

Trauma


31/39

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


32/39

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


33/39

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


34/39

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.


35/39

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


36/39

Recognition and Classification


37/39

Initial Management of Shock


38/39

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


39/39

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

shock (rags)

Documents