Shock in the Pediatric Patient: or Oxygen Doesn’t Go Where

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Transcript Shock in the Pediatric Patient: or Oxygen Doesn’t Go Where

Shock in the Pediatric Patient: or Oxygen Don’t Go Where the Blood Won’t Flow!

James D. Fortenberry MD FAAP, FCCM Medical Director, PICU Division of Critical Care Medicine Children’s Healthcare of Atlanta

Objectives

  

Define shock and its different categories Review basic physiologic aspects of shock Describe management of shock including:

oxygen supply and demand

fluid resuscitation

crystalloid vs. colloid controversy

vasopressor support

Definition of Shock

   

Uncontrolled blood or fluid loss Blood pressure less than 5th percentile for age Altered mental status, low urine output, poor capillary refill None of the above

Definition of Shock

An acute complex pathophysiologic state of circulatory dysfunction which results in a failure of the organism to deliver sufficient amounts of oxygen and other nutrients to satisfy the requirements of tissue beds

SUPPLY

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DEMAND

Definition of Shock

  

Inadequate tissue perfusion to meet tissue demands Usually result of inadequate blood flow and/or oxygen delivery

Shock is not a blood pressure diagnosis!!

Characteristics of Shock

 

End organ dysfunction:

reduced urine output

 

altered mental status poor peripheral perfusion Metabolic dysfunction:

 

acidosis altered metabolic demands

Essentials of Life

    

Gas exchange capability of lungs Hemoglobin Oxygen content Cardiac output Tissues to utilize substrate

Arterial Oxygen Content

100 mm Hg Hgb 15 gm/100 mL Hemoglobin SaO 2 97% Oxygen Saturation O 2 bound to Hgb + + PaO 2 100 mmHg Partial Pressure O 2 in plasma

Oxygen Delivery

DO 2=Cardiac Output x 1.34 (Hgb x SaO 2 ) + Pa0 2 x 0.003

Oxygen Express

O 2 O 2 O 2 O 2 O 2 O 2 Ca0 2 O 2 O 2 O 2 O 2 O 2 O 2

Cardiac Output

The volume of blood ejected by the heart in one minute 4 - 8 liters / minute

Cardiac Output

C.O.=Heart Rate x Stroke Volume

 

Heart rate Stroke volume:

Preload- volume of blood in ventricle

Afterload- resistance to contraction

Contractility- force applied

Cardiac Output

C.O.=Mean arterial pressure (MAP) - CVP/SVR

   

To improve CO: MAP CVP SVR

Preload Afterload Contractility Stroke Volume x Heart Rate O 2 Content x Cardiac Output x Resistance O 2 Delivery

Classification of Shock

   

Hypovolemic

dehydration,burns, hemorrhage

Distributive

septic, anaphylactic, spinal

Cardiogenic

myocarditis,dysrhythmia Obstructive

tamponade,pneumothorax

Compensated

organ perfusion is maintained Uncompensated

Circulatory failure with end organ dysfunction Irreversible

Irreparable loss of essential organs

Mechanical Requirements for Adequate Tissue Perfusion

   

Fluid Pump Vessels Flow

Hypovolemic Shock:

Inadequate Fluid Volume (decreased preload)

Hypovolemic Shock: Causes

 

Fluid depletion

 

internal external Hemorrhage

 

internal external

Cardiogenic Shock:

Pump Malfunction (decreased contractility)

Cardiogenic Shock: Causes

Electrical Failure Mechanical Failure

 

Cardiomyopathy metabolic

 

anatomic hypoxia/ischemia

Distributive Shock

Abnormal Vessel Tone (decreased afterload)

Distributive Shock

Vasodilation Venous Pooling Decreased Preload Maldistribution of regional blood flow

Distributive Shock:

   

Causes

Sepsis Anaphylaxis Neurogenesis (spinal) Drug intoxication (TCA, calcium, Channel blocker)

Septic Shock Decreased Volume Decreased Pump Function Abnormal Vessel Tone

Cardiac Output

C.O.=Heart Rate x Stroke Volume

 

Heart rate Stroke volume:

Preload- volume of blood in ventricle

Afterload- resistance to contraction

Contractility- force applied

Clinical Assessment

   

Heart rate Peripheral circulation

capillary refill

 

pulses extremity temperature Pulmonary End organ perfusion

 

brain kidney

Improving Stroke Volume:

Therapy for Cardiovascular Support

Preload Contractility Volume Inotropes Afterload Vasodilators

Septic Shock

Early (“Warm”) Decreased peripheral vascular resistance Increased cardiac output Late (“Cold”) Increased peripheral vascular resistance Decreased cardiac output

Assessment of Circulation

Early Late Heart rate Blood pressure Peripheral circulation Tachycardia Tachycardia/ Bradycardia Normal Decreased Warm/Cool Decreased/ Increased pulses Cool Decreased pulses

Heart Rate and Perfusion Pressure (MAP-CVP) Parameters by Age

Age Term newborn < 1 < 2 < 7 < 15 Heart Rate MAP-CVP 120-180 55 120-180 120-160 120-160 90-140 60 65 65 65

Assessment of Circulation

Early Late End-organ: Skin Brain Kidneys Decreased cap refill Irritable, restless Oliguria Very decreased cap refill Lethargic, unresponsive Oliguria, anuria

OBSTRUCTIVE SHOCK

OBSTRUCTED FLOW

Obstructive Shock: Causes

  

Pericardial tamponade Pulmonary embolism Pulmonary hypertension

Hemodynamic Assessment of Shock

Type of Shock Preload Afterload Contractility Cardiogenic Hypovolemic Septic Early Late Obstructive

              

Cardiac Output

    

Distributive

   

Goals of Resuscitation

Overall goal:

 

increase O 2 delivery decrease demand O 2 content Cardiac output

Treatment

Sedation/analgesia Blood pressure

Principles of Management

  

A: Airway

patent upper airway B: Breathing

adequate ventilation and oxygenation C: Circulation

optimize

 

cardiac function oxygenation

Act quickly, Think slowly.

Greek Proverb

Airway Management

Patients in shock have:

  

O 2 delivery progressive respiratory fatigue/failure energy shunted from vital organs

afterload

Airway Management

Early intubation provides:

 

O 2 delivery and content controlled ventilation which:

 

reduces metabolic demand allows C.O. to vital organs

Therapy

Vagolysis Chromotropy Preload Heart Rate  Stroke Volume Afterload Contractility Volume CVP Vasodilators Vasoconstrictors Correct acidosis hypoxia hypoglycemia Inotropic agents

Colloid

Fluid Choices

Crystalloid

Crystalloids

Hypotonic Fluids (D 5 1/4 NS)

 

No role in resuscitation Maintenance fluids only

Fluids, Fluids, Fluids

 

Key to most resuscitative efforts Give generously and reassess

Crystalloids

Isotonic Fluids

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Intravascular volume expansion Hauser:

crystalloids rapidly redistribute Lethal animal model

 

NS = good resuscitative fluid 4x blood volume to restore hemodynamics

Crystalloids

Isotonic Fluids

2 trauma studies

crystalloids = colloids but:

 

4x amount longer time to resuscitation

Crystalloids

Complications

Under-resuscitation

 

renal failure Over-resuscitation

pulmonary edema

peripheral edema

Crystalloids

Summary Crystalloids less effective than equal volume of colloids

  

Preferred when 1 o and/or electrolytes deficit is water Good in initial resuscitation to restore extracellular volume Hypertonic solutions however, may act as plasma volume expanders

Fluid Transport

Oncotic pressure (tendency to pull unit) Hydrostatic pressure (tendency to drive unit) Capillary

Colloids

Albumin

   

Hepatic production MW = 69,000 80% of COP Serum t 1/2 : 18 hours endogenous 16 hours exogenous

Colloids

Hydroxyethyl Starch (Hespan)

Synthetic

  

Derived from corn starch Average MW = 69,000 Stable, nonantigenic

 

Used for volume expansion Renal excretion

 

t 1/2 2-67 hours 90% gone in 42 days

Colloids

Hydroxyethyl Starch (Hespan)

     

Greater in COP than albumin Longer duration of action 0.006% adverse reactions No effect on blood typing Prolongs PT, PTT and clotting times Dosage

20 ml/Kg/day

max 1500 ml/day

Fluid Choices

Based on:

   

type of deficit urgency of repletion pathophysiology of condition plasma COP

Fluid Choices

 

Crystalloids for initial resuscitation PRBC’s to replace blood loss

Fluid Management in Pediatric Septic Shock

  

Emphasis on the golden hour Early aggressive use of fluids may improve outcome Titrate-Reassess!

Clinical Practice Parameters, Carcillo et al., CCM, 2002

Alpha-Beta Meter

Dopamine Epinephrine

ß

Inotropes

Agent Site of action Dopamine Dopaminergic

 

Dose (

g/kg/min) 1-3 5-10 Dobutamine

 

and

 

11-20 1-20 Epinephrine



0.05-1.0

Norepinephrine



0.05-1.0

Nitroprusside Milrinone Vasodilator Arterial > venous PDE inhibitor 0.5-1.0

0.5-0.75

Effects Renal vasodilator Inotrope Vasoconstriction Increase PVR Inotrope Vasodilation Inotrope Tachycardia Profound vasoconstriction Inotrope Vasodilation Inotrope Vasodilator

Dopamine Activity

0.5-5.0 mcg/kg/min - dopaminergic receptors 2.0-10 mcg/kg/min - beta receptors (inotrope) 10-20 mcg/kg/min - alpha and beta receptors Over 20 mcg/kg/min - alpha receptors (pressors)

A Rational Approach to Shock in the Pediatric Patient

Shock / Hypotension Volume Resuscitation Signs of adequate circulation Adequate MAP Yes NO NO pressors

A Rational Approach to Pressor Use in the PICU

Signs of adequate circulation Adequate MAP NO Dopamine Inadequate MAP Dopamine and/or Norepinephrine

A Rational Approach to Pressor Use in the PICU

Dopamine and/or norepinephrine adequate MAP CO Dobutamine or Milrinone Inadequate MAP low C.O.

tachycardia epinephrine phenylephrine??

“New” Therapies in Septic Shock

  

Steroids Vasopressin Activated Protein C (Xigris) in septic shock

Management of Pediatric Septic Shock: The Golden Hour

 

First 15 minutes Emphasis on response to volume

Clinical Practice Parameters, Carcillo et al., CCM, 2002

Patients don’t suddenly deteriorate, healthcare professionals suddenly notice!

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