SHOCK IN CHILDREN

1. SHOCK IN CHILDREN

2. Definition Circulatory system failure to supply oxygen and nutrients to meet cellular metabolic demands

3. Other Definitions • Blood Pressure BP = CO x SVR • Cardiac Output CO = SV X HR • Vascular Tone (SVR) • Regulated by several mechanisms

4. Oxygen Delivery • DO2 = CO x CaO2 x 10 • Remember: CO depends on HR, preload, afterload, and contractility • CaO2 = Hgb x 1.34 x SaO2 + (PaO2 x 0.003) • Remember: hemoglobin carries more than 99% of oxygen in the blood under standard conditions

5. Hemodynamics Textbook of Pediatric Advanced Life Support, 1988

6. 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 Hypothalamopituitary response Adrenocorticotropic hormone Vasopressin Renin-angiotensin-aldosterone system Defending the blood pressure

7. Cardiovascular function • 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. Stroke Volume • Preload (LVEDV) • Reflects patient’s volume status • CVP or PCWP • Starling curve • Afterload • The resistance to ventricular ejection • Two variables: • vascular tone and transmural pressure • Myocardial Contractility (“squeeze”) • Many factors including coronary perfusion, baseline myocardial function, use of cardiotonic medications

9. Classification of Shock • COMPENSATED • blood flow is normal or increased and may be maldistributed; vital organ function is maintained • UNCOMPENSATED • microvascular perfusion is compromised; significant reductions in effective circulating volume • IRREVERSIBLE • inadequate perfusion of vital organs; irreparable damage; death cannot be prevented

10. Other Classifications • Hypovolemic or Hemorrhagic • Cardiogenic • Obstructive • Distributive

11. Cardiovascular Changes in Shock TypePreload AfterloadContractility Cardiogenic  Hypovolemic  No change Distributive  Septic early  late 

12. Evaluation • Regardless of the cause: ABC’s • First assess airway patency, ventilation, then circulatory system • Respiratory Performance • Respiratory rate and pattern, work of breathing, oxygenation (color), level of alertness • Circulation • Heart rate, BP, perfusion, and pulses, liver size • CVP monitoring may be helpful

13. Evaluation • Early Signs of Shock • sinus tachycardia • delayed capillary refill • fussy, irritable • Late Signs of Shock • bradycardia • altered mental status (lethargy, coma) • hypotonia, decreased DTR’s • Cheyne-Stokes breathing • hypotension is a very late sign • Lower limit of SBP = 70 + (2 x age in years)

14. Heart Rate Too high: 180 bpm for infants, 160 bpm for children >1year old Blood Pressure Lower limit of SBP = 70 + (2 x age in years) Peripheral Pulses Present/Absent Strength (diminished, normal, bounding) Skin Perfusion Capillary refill time Temperature Color Mottling CNS Perfusion Recognition of parents Reaction to pain Muscle tone Pupil size Renal Perfusion UOP >1cc/kg/hr Cardiovascular Assessment

15. Treatment Airway management • Always provide supplemental oxygen • Endotracheal intubation and controlled ventilation is suggested if respiratory failure or airway compromise is likely • elective is safer and less difficult • decrease negative intrathoracic pressure • improved oxygenation and O2 delivery and decreased O2 consumption • can hyperventilate if necessary

16. Treatment Circulation • Based on presumed etiology • Rapid restoration of intravascular volume • PIV-if unstable you have 60-90 seconds • I.O. if less than 4-6 years old • Central venous catheter • Use isotonic fluid: NS, LR, or 5% albumin • PRBC’s to replace blood loss or if still unstable after 60cc/kg of crystalloid • anemia is poorly tolerated in the stressed, hypoxic, hemodynamically unstable patient

17. Vasoactive/Cardiotonic Agents • Dopamine • 1-5 mcg/kg/min: dopaminergic • 5-15 mcg/kg/min: more beta-1 • 10-20 mcg/kg/min: more alpha-1 • may be useful in distributive shock • Dobutamine • 2.5-15 mcg/kg/min: mostly beta-1, some beta-2 • may be useful in cardiogenic shock • Epinephrine • 0.05-0.1 mcg/kg/min: mostly beta-1, some beta-2 • > 0.1 to 0.2 mcg/kg/min: alpha-1

18. Vasoactive/Cardiotonic Agents • Norepinephrine • 0.05-0.2mcg/kg/min: only alpha and beta-1 • Use up to 1mcg/kg/min • Milrinone • 50mcg/kg load then 0.375-0.75mcg/kg/min: phosphodiesterase inhibitor; results in increased inotropy and peripheral vasodilation (greater effect on pulmonary vasculature) • Phenylephrine • 0.1-0.5mcg/kg/min: pure alpha

19. Hypovolemic • # 1 cause of death in children worldwide • Causes • Water Loss (diarrhea, vomiting with poor PO intake, diabetes, major burns) • Blood Loss (obvious trauma; occult bleeding from pelvic fractures, blunt abdominal trauma, “shaken baby”) • Low preload leads to decreased SV and decreased CO. • Compensation occurs with increased HR and SVR

20. Hypovolemic Shock • Mainstay of therapy is fluid • Goals • Restore intravascular volume • Correct metabolic acidosis • Treat the cause • Degree of dehydration often underestimated • Reassess perfusion, urine output, vital signs... • Isotonic crystalloid is always a good choice • 20 to 50 cc/kg rapidly if cardiac function is normal • NS can cause a hyperchloremic acidosis

21. Treatment Solution Na+ Cl- K+ Ca++ Mg++ Buffer NS 154 154 0 0 0 None LR 130 109 4 3 0 Lactate Plasmalyte 140 98 5 0 3 Acetate & Gluconate • Inotropic and vasoactive drugs are not a substitute for fluid, however... • Can have various combinations of hypovolemic and septic and cardiogenic shock • May need to treat poor vascular tone and/or poor cardiac function

22. Hemorrhagic Shock • Treatment is PRBCs or whole blood • Treat the cause if able (stop the bleeding) • Transfuse if significant blood loss is known or if patient unstable after 60cc/kg crystalloid • In an emergency can give group O PRBCs before cross matching is complete or type specific non-cross-matched blood products

23. Cardiogenic • Low CO and high systemic vascular resistance • Result of primary cardiac dysfunction: • A compensatory increase in SVR occurs to maintain vital organ function • Subsequent increase in LV afterload, LV work, and cardiac oxygen consumption • CO decreases and ultimately results in volume retention, pulmonary edema, and RV failure

24. Congenital heart disease Arrhythmias Ischemic heart disease Myocarditis Myocardial injury Acute and chronic drug toxicity Late septic shock Infiltrative diseases mucopolysaccharidoses glycogen storage diseases Thyrotoxicosis Pheochromocytoma Cardiogenic ShockEtiologies

25. Cardiogenic Shock • Initial clinical presentation can be identical to hypovolemic shock • Initial therapy is a fluid challenge • If no improvement or if worsens after giving volume, suspect cardiogenic shock • Usually need invasive monitoring, further evaluation, pharmacologic therapy • Balancing fluid therapy and inotropic support can be very difficult. • Call an intensivist and/or a cardiologist

26. Obstructive Shock • Low CO secondary to a physical obstruction to flow • Compensatory increased SVR • Causes: • Pericardial tamponade • Tension pneumothorax • Critical coarctation of the aorta • Aortic stenosis • Hypoplastic left heart syndrome

27. Obstructive Shock • Initial clinical presentation can be identical to hypovolemic shock • Initial therapy is a fluid challenge • Treat the cause • pericardial drain, chest tube, surgical intervention • if the patient is a neonate with a ductal dependent lesion then give PGE • Further evaluation, invasive monitoring, pharmacologic therapy, appropriate consults

28. Distributive Shock • High CO and low SVR (opposite of hypovolemic, cardiogenic, and obstructive) • Maldistribution of blood flow causing inadequate tissue perfusion • Due to release of endotoxin, vasoactive substances, complement cascade activation, and microcirculation thrombosis • Early septic shock is the most common form

29. Distributive Shock • Goal is to maintain intravascular volume and minimize increases in interstitial fluid (the primary problem is a decrease in SVR) • Use crystalloid initially • Additional fluid therapy should be based on lab studies • Can give up to 40cc/kg without monitoring CVP • Vasoactive/Cardiotonic agents often necessary • Treat the cause (i.e.. antimicrobial therapy)

30. Distributive ShockEtiologies • Anaphylaxis • Anaphylactoid reactions • Spinal cord injury/spinal shock • Head injury • Early sepsis • Drug intoxication • Barbiturates, Phenothiazines, Antihypertensives

31. Metabolic IssuesAcid-Base • Metabolic acidosis develops secondary to tissue hypoperfusion • Profound acidosis depresses myocardial contractility and impairs the effectiveness of catecholamines • Tx: fluid administration and controlled ventilation • Buffer administration • Sodium Bicarbonate 1-2meq/kg or can calculate a 1/2 correction = 0.3 x weight (kg) x base deficit • hyperosmolarity, hypocalcemia, hypernatremia, left-ward shift of the oxyhemoglobin dissociation curve

32. Metabolic IssuesElectrolytes • Electrolytes • Calcium is important for cardiac function and for the pressor effect of catecholamines • Hypoglycemia can lead to CNS damage and is needed for proper cardiovascular function • Check the BUN and creatinine to evaluate renal function • Hyperkalemia can occur from renal dysfunction and/or acidosis

33. Metabolic IssuesSpecial Topics Congenital adrenal hyperplasia • Infant presents in shock, usually in the second week of life, typically a boy, with metabolic acidosis, hyponatremia, hypoglycemia, and hyperkalemia Hyperammonemia • mild elevations are common with shock • levels > 1000 are consistent with inborn errors of metabolism • consider Reye Syndrome, toxins, hepatic failure

34. Other Studies • Look for etiology of shock • Evaluate hemoglobin, hematocrit, and platelet count • Should be followed as these values may drop after fluid resuscitation • Shock from any etiology can lead to DIC and end organ damage • CBC, PT, INR, PTT, Fibrinogen, Factor V, Factor VIII, D-dimer, and/or FDPs • Check LFT’s, follow CNS and pulmonary status

35. Other Studies II • Think about inborn errors of metabolism • Lactate and pyruvate • Ammonium, LFTs • Plasma amino acids, urine organic acids • Urinalysis with reducing substances • Urine tox screen

36. Conclusion • Goal of therapy is identification, evaluation, and treatment of shock in its earliest stage • Initial priorities are for the ABC’s • Fluid resuscitation begins with 20cc/kg of crystalloid or 10cc/kg of colloid • Subsequent treatment depends on the etiology of shock and the patient’s hemodynamic condition • Successful resuscitation depends on early and judicious intervention