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 < 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 PaO2 100 mmHg Partial Pressure Hgb 15 gm/100 mL Hemoglobin SaO2 97% Oxygen Saturation + + O2 bound to Hgb O2 in plasma

DO2=Cardiac Output x 1.34 (Hgb x SaO2) + Pa02 x 0.003 Oxygen Delivery DO2=Cardiac Output x 1.34 (Hgb x SaO2) + Pa02 x 0.003 O2O2O2O2O2O2 Oxygen Express O2O2O2O2O2O2 Ca02

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 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

Cardiac Output x x Preload Afterload Contractility x Stroke Volume Heart Rate Cardiac Output O2 Content Resistance x x O2 Delivery Arterial Blood Pressure

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

Inadequate Fluid Volume (decreased preload) Hypovolemic Shock: Inadequate Fluid Volume (decreased preload)

Hypovolemic Shock: Causes Fluid depletion internal external Hemorrhage

Pump Malfunction (decreased contractility) Cardiogenic Shock: Pump Malfunction (decreased contractility)

Cardiogenic Shock: Causes Electrical Failure Mechanical Failure Cardiomyopathy metabolic anatomic hypoxia/ischemia

Abnormal Vessel Tone (decreased afterload) 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)

Decreased Pump Function Septic Shock Decreased Pump Function Decreased Volume Abnormal Vessel Tone

Cardiac Output C.O.=Heart Rate x Stroke Volume Preload- volume of blood in ventricle Afterload- resistance to contraction Contractility- force applied

Clinical Assessment Heart rate Peripheral circulation Pulmonary capillary refill pulses extremity temperature Pulmonary End organ perfusion brain kidney

Improving Stroke Volume: Therapy for Cardiovascular Support Preload Volume Inotropes Contractility Vasodilators Afterload

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

Assessment of Circulation

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

Assessment of Circulation

OBSTRUCTIVE SHOCK OBSTRUCTED FLOW

Obstructive Shock: Causes Pericardial tamponade Pulmonary embolism Pulmonary hypertension

Hemodynamic Assessment of Shock

Goals of Resuscitation Overall goal: increase O2 delivery decrease demand O2 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: O2 delivery progressive respiratory fatigue/failure energy shunted from vital organs afterload

Airway Management Early intubation provides: O2 delivery and content controlled ventilation which: reduces metabolic demand allows C.O. to vital organs

Therapy Vagolysis Heart Rate  Chromotropy

Fluid Choices Colloid Crystalloid Tastes Great ! Less Filling

Crystalloids Hypotonic Fluids (D5 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 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 1o deficit is water and/or electrolytes Good in initial resuscitation to restore extracellular volume Hypertonic solutions however, may act as plasma volume expanders

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

Colloids Albumin Hepatic production MW = 69,000 80% of COP Serum t1/2: 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 type of deficit Based on: urgency of repletion pathophysiology of condition plasma COP Tastes Great ! Less Filling

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

 ß Alpha-Beta Meter Dopamine Epinephrine Norepinephrine Dobutamine  ß Dopamine Epinephrine Dobutamine Norepinephrine Neosynephrine

Inotropes

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 NO pressors Yes NO

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 Dobutamine or Milrinone Dopamine and/or norepinephrine adequate MAP Dobutamine or Milrinone CO 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! Anonymous