Shock Comprehensive


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Shock Comprehensive

  1. 1. NEONATAL SHOCK and HYPOTENSION Steven M. Donn, M.D. Professor of Pediatrics Director, Neonatal-Perinatal Medicine C.S. Mott Children’s Hospital University of Michigan Health System
  2. 2. SHOCK <ul><li>A complex clinical syndrome caused by an acute failure of circulatory function and characterized by inadequate tissue and organ perfusion. </li></ul>
  3. 3. CONSEQUENCES OF SHOCK <ul><li>Inadequate oxygen and substrate delivery </li></ul><ul><li>Inadequate metabolic waste removal </li></ul><ul><li>Cellular dysfunction and death </li></ul><ul><li>May involve isolated organs or entire organism </li></ul>
  4. 4. PATHOPHYSIOLOGY OF SHOCK <ul><li>Decreased cardiac output </li></ul><ul><li>Diminished vascular integrity </li></ul><ul><li>Inability of blood to carry out necessary functions </li></ul>
  5. 5. CARDIAC OUTPUT <ul><li>Product of: </li></ul><ul><li>heart rate X stroke volume </li></ul><ul><li>Neonatal CO depends more on HR than SV </li></ul><ul><li>Compromised at high or low HR </li></ul>
  6. 7. Stroke Volume To increase cardiac output Increase stroke volume or Increase heart rate or Increase both
  7. 8. STROKE VOLUME <ul><li>Preload </li></ul><ul><li>Afterload </li></ul><ul><li>Contractility </li></ul>
  8. 9. PRELOAD <ul><li>Corresponds to myocardial end-diastolic fiber length </li></ul><ul><li>Determined by volume of blood filling ventricles during diastole </li></ul><ul><li>Increases in preload increase SV up to a maximum, beyond which SV falls (Starling’s Law) </li></ul>
  9. 10. Preload Equals End Diastolic Volume Stroke volume
  10. 11. AFTERLOAD <ul><li>Force that the myocardium generates during ejection against systemic and pulmonary vascular resistances </li></ul><ul><li>Reduction in afterload increases SV </li></ul>
  11. 12. Stroke volume Afterload is End-systolic Wall Stress or Resistance
  12. 13. Effects of changes in afterload on Frank-Starling curves. A shift from A to B occurs with increased afterload, and from A to C with decreased afterload. 100 Stroke volume (mL) LVEDP (mmHg) 50 0 0 10 20
  13. 14. CONTRACTILITY <ul><li>Semi-quantitative measure of ventricular function </li></ul><ul><li>Increased contractility increases SV if both preload and afterload are unchanged </li></ul>
  14. 15. ALTERING CARDIAC OUTPUT <ul><li>Clinically significant alterations in preload, afterload, and contractility can be achieved by use of vasoactive drugs, inotropic agents, or changes in blood volume. </li></ul>
  15. 16. BLOOD FLOW TO TISSUES AND ORGANS <ul><li>Influenced by local vascular beds </li></ul><ul><li>Controlled by local and central vasoregulation </li></ul><ul><li>Pressure-passive with loss of autoregulation </li></ul><ul><li>Biochemical mediators different for each bed and poorly understood </li></ul>
  16. 17. BLOOD FACTORS <ul><li>Fetal hemoglobin </li></ul><ul><li>Temperature </li></ul><ul><li>pCO 2 </li></ul><ul><li>pH </li></ul><ul><li>Oxygen extraction </li></ul>
  17. 18. INADEQUATE TISSUE PERFUSION <ul><li>Pump problem </li></ul><ul><li>Inadequate volume </li></ul><ul><li>Abnormalities in vascular beds </li></ul><ul><li>Flow restriction </li></ul><ul><li>Inadequate oxygen-release </li></ul>
  18. 19. HYPOTENSION <ul><li>Blood pressure lower than the expected reference range </li></ul><ul><li>On first day of life: </li></ul><ul><li>MAP ≈ GA (??) </li></ul>
  20. 21. TISSUE OXYGEN DELIVERY <ul><li>Influenced more by cardiac output and blood flow than by BP </li></ul><ul><li>“ Statistically abnormal” BP may not be pathologic. </li></ul><ul><li>Hypotension is not synonymous with shock. </li></ul>
  21. 22. MORTALITY AND MORBIDITY <ul><li>Shock is a major cause of neonatal mortality and morbidity. </li></ul><ul><li>Because shock accompanies other primary conditions, specific figures are not available. </li></ul>
  22. 23. CAUSES OF NEONATAL SHOCK <ul><li>Hypovolemic acute blood, fluid/electrolyte loss </li></ul><ul><li>Distributive sepsis, vasodilators, myocardial depression, endothelial injury) </li></ul><ul><li>Cardiogenic cardiomyopathy, heart failure, arrhythmia, myocardial ischemia </li></ul><ul><li>Obstructive tension pneumothorax, cardiac tamponade </li></ul><ul><li>Dissociative severe anemia, methemoglobinemia </li></ul>
  23. 24. RISK FACTORS <ul><li>Umbilical cord accident </li></ul><ul><li>Placental abnormalities </li></ul><ul><li>Fetal/neonatal hemolysis </li></ul><ul><li>Fetal/neonatal hemorrhage </li></ul>
  24. 25. RISK FACTORS (2) <ul><li>Maternal infection </li></ul><ul><li>Maternal anesthesia/hypotension </li></ul><ul><li>Intrauterine/intrapartum asphyxia </li></ul>
  25. 26. RISK FACTORS (3) <ul><li>Neonatal sepsis </li></ul><ul><li>Air leak syndromes </li></ul><ul><li>Lung overdistention </li></ul><ul><li>Cardiac arrhythmia </li></ul>
  26. 27. CLINICAL MANIFESTATIONS <ul><li>Prolonged capillary refill </li></ul><ul><li>Tachycardia </li></ul><ul><li>Mottling of skin </li></ul><ul><li>Cool extremities </li></ul><ul><li>Decreased urine output </li></ul>
  27. 28. STAGES OF SHOCK <ul><li>Compensated </li></ul><ul><li>Uncompensated </li></ul><ul><li>Irreversible </li></ul>
  28. 29. COMPENSATED SHOCK <ul><li>Perfusion to vital organs preserved </li></ul><ul><li>Minimal or absent derangement of vital signs (HR, RR, BP, Temp) </li></ul><ul><li>Increased angiotension, vasopressin, catecholamine release </li></ul><ul><li>Decreased spontaneous activity </li></ul><ul><li>Pallor, tachycardia, cool skin, prolonged capillary refill </li></ul>
  29. 30. UNCOMPENSATED SHOCK <ul><li>Delivery of oxygen and nutrients becomes marginal or inadequate </li></ul><ul><li>Anaerobic metabolism -> lactic acid </li></ul><ul><li>Decreased myocardial contractility </li></ul><ul><li>Release of chemical mediators, enzymes, histamine, cytokines, xanthine oxidase (free radicals), PAF, bacterial toxins </li></ul>
  30. 31. UNCOMPENSATED SHOCK (2) <ul><li>Decreased oxidative phosphorylation </li></ul><ul><li>Failure of Na + -K + pump </li></ul><ul><li>Disrupted capillary endothelium </li></ul><ul><li>Plasma protein leak </li></ul><ul><li>Decreased oncotic pressure </li></ul>
  31. 32. UNCOMPENSATED SHOCK (3) <ul><li>Sluggish blood flow, platelet adhesion, DIC </li></ul><ul><li>Falling BP, very prolonged capillary refill, tachycardia, cold skin, tachypnea, oliguria/anuria </li></ul>
  32. 33. IRREVERSIBLE SHOCK <ul><li>Retrospective diagnosis </li></ul><ul><li>Major vital organs extensively damaged </li></ul><ul><li>Death despite circulatory restoration </li></ul>
  33. 34. WORK-UP <ul><li>Hct, electrolytes, glucose, cultures </li></ul><ul><li>Blood gases (preferably arterial) </li></ul><ul><li>Mixed venous blood gas (reflects oxygen extraction and waste products at tissue level) </li></ul><ul><li>Plasma lactate, pyruvate </li></ul><ul><li>Specific studies to rule out both causes and sequelae </li></ul>
  34. 35. IMAGING STUDIES <ul><li>Chest radiograph </li></ul><ul><li>Echocardiogram/Doppler flow </li></ul><ul><li>Other, as clinically indicated </li></ul>
  35. 37. TREATMENT <ul><li>Initiate supportive measures immediately </li></ul><ul><li>Secure airway, provide oxygen, PPV </li></ul><ul><li>Achieve vascular access </li></ul><ul><li>Infuse volume </li></ul>
  36. 38. TREATMENT (2) <ul><li>Determine type of shock </li></ul><ul><li>Insert bladder catheter </li></ul><ul><li>Measure hourly urine output </li></ul>
  38. 40. HYPOVOLEMIC SHOCK <ul><li>Most common cause of shock in the newborn </li></ul><ul><li>Key to successful resuscitation is early recognition and controlled volume expansion </li></ul><ul><li>Blood volume: 80-85 mL/kg </li></ul>
  39. 41. HYPOVOLEMIC SHOCK (2) <ul><li>Volume Depletion: </li></ul><ul><li>Compensated 25% </li></ul><ul><li>Uncompensated 25-40% </li></ul><ul><li>Irreversible > 40% </li></ul>
  40. 42. HYPOVOLEMIC SHOCK (3) <ul><li>Initial fluid: 20 mL/kg </li></ul><ul><li>Replaces 25% of blood volume </li></ul><ul><li>Repeat if circulatory insufficiency persists. </li></ul>
  41. 43. HYPOVOLEMIC SHOCK (4) <ul><li>Once half of the blood volume is replaced, titrate further fluid against CVP or clinical parameters. </li></ul><ul><li>Crystalloid v. colloid controversy: most recent reports favor crystalloid. </li></ul><ul><li>Whole blood or reconstituted components for hemorrhage </li></ul>
  42. 44. CARDIOGENIC SHOCK <ul><li>Most commonly after asphyxia, structural heart problem, arrhythmia </li></ul><ul><li>Myocardial ischemia reduces contractility and causes papillary muscle dysfunction and tricuspid valvular insufficiency. </li></ul>
  43. 45. CARDIOGENIC SHOCK (2) <ul><li>Clinical findings: peripheral edema, hepatomegaly, cardiomegaly, murmur </li></ul><ul><li>Initiate treatment with inotrope (with or without peripheral vasodilators) </li></ul><ul><li>Treat arrhythmia, structural disease </li></ul><ul><li>Avoid volume overload </li></ul>
  44. 46. DISTRIBUTIVE SHOCK <ul><li>Most common form is septic shock </li></ul><ul><li>Cardiac output may be normal, even elevated, but unable to be adequately delivered to tissues because of microcirculatory abnormalities. </li></ul>
  45. 47. DISTRIBUTIVE SHOCK (2) <ul><li>Early compensated phase </li></ul><ul><ul><li>Increased cardiac output </li></ul></ul><ul><ul><li>Decreased systemic vascular resistance </li></ul></ul><ul><li>Cardiovascular performance deteriorates. </li></ul><ul><li>Normal relationship between CO and SVR breaks down leading to intractable hypotension/shock. </li></ul>
  46. 48. DISTRIBUTIVE SHOCK (3) <ul><li>Little cardiac reserve </li></ul><ul><li>Survival depends on maintenance of hyperdynamic circulatory state. </li></ul><ul><li>Treat underlying condition(s). </li></ul>
  47. 49. DISTRIBUTIVE SHOCK (4) <ul><li>Early treatment: </li></ul><ul><li>volume expansion </li></ul><ul><li>Later treatment: </li></ul><ul><li>inotropes, with or without peripheral vasodilators </li></ul><ul><li>Look for evidence of organ damage and treat accordingly. </li></ul>
  48. 50. <ul><li>MECHANISMS OF INJURY: SEPTIC SHOCK </li></ul>
  49. 51. VOLUME EXPANDERS <ul><li>Saline </li></ul><ul><li>Albumin (5%) </li></ul><ul><li>Plasma </li></ul><ul><li>Lactated Ringer’s </li></ul><ul><li>Whole blood </li></ul><ul><li>Blood products </li></ul>
  50. 52. VASOACTIVE DRUGS Constrictors <ul><li>Dopamine </li></ul><ul><li>Dobutamine </li></ul><ul><li>Epinephrine </li></ul><ul><li>Norepinephrine </li></ul><ul><li>Vasopressin </li></ul>
  51. 53. VASOACTIVE DRUGS Dilators <ul><li>Isoproterenol </li></ul><ul><li>Nitroprusside </li></ul><ul><li>Phentolamine </li></ul><ul><li>Amrinone </li></ul><ul><li>Milrinone </li></ul>
  52. 54. AGENTS USED TO TREAT NEONATAL SHOCK Never administer intra-arterially 0.05-1 mcg/k/g/min IV Norepinephrine Vasocative drugs Afterload reducer 1-20 mcg/kg/min IV Phentolamine Afterload reducer 0.5-8 mcg/kg/min IV Nitroprusside Never administer intra-arterially 0.05-0.5 mcg/kg/min IV Isoproterenol Afterload reducer 0.1-0.5 mg/kg IV q3-6h Hydralazine Never administer intra-arterially 0.05-1 mcg/kg/min IV Epinephrine Never administer intra-arterially 5-20 mcg/kg/min IV Dobutamine Never administer intra-arterially 5-20 mcg/kg/min IV Dopamine Use O Neg 10-20 mL/kg IV Reconstituted blood products Limited availability 10-20 mL/kg IV Whole blood products Inexpensive, available 10-20 mL/kg/ IV Isotonic glucose Inexpensive, available 10-20 mL/kg IV Lactated Ringer solution Expensive 10-20 mL/kg IV Plasma Expensive 10-20 mL/kg IV Albumin (5%) Inexpensive, available 10-20 mL/kg IV Isotonic sodium Volume expanders Comments Dosage Agent Agent Type
  53. 55. DOPAMINE <ul><li>Endogenous catecholamine </li></ul><ul><li>Precursor of norepinephrine </li></ul><ul><li>Affects all three determinants of cardiovascular function </li></ul><ul><li>Major action from increased contractility and peripheral vascular resistance </li></ul>
  54. 56. DOPAMINE <ul><li>Beneficial renal effects </li></ul><ul><ul><li>Increased RPF and GFR </li></ul></ul><ul><ul><li>Increased hypoxic threshold of renal tubular cells </li></ul></ul><ul><ul><li>Increased Na and free water clearance </li></ul></ul><ul><li>Endocrine effects </li></ul><ul><ul><li>Decreased prolactin </li></ul></ul><ul><ul><li>Decreased TRH </li></ul></ul>
  55. 57. DOPAMINE <ul><li>Prolonged clearance in renal or hepatic dysfunction </li></ul><ul><li>Adverse effects </li></ul><ul><ul><li>Excessive increased afterload </li></ul></ul><ul><ul><li>Ectopic beats </li></ul></ul><ul><ul><li>Tachycardia </li></ul></ul><ul><ul><li>Hyponatremia </li></ul></ul><ul><ul><li>Vasoconstriction (peripheral, pulmonary) </li></ul></ul><ul><ul><li>Extravasation/soft tissue injury </li></ul></ul>
  56. 58. DOPAMINE DOSING <ul><li>Low 1-5 mcg/kg/min (renal) </li></ul><ul><li>Medium 5-10 mcg/kg/min (cardiac) </li></ul><ul><li>High 10-20 mcg/kg/min (SVR) </li></ul>
  57. 59. DOBUTAMINE <ul><li>Synthetic catecholamine </li></ul><ul><li>Greater inotropic activity </li></ul><ul><li>Increased C.O. through increased SVR </li></ul><ul><li>Most effective dose: 5-15 mcg/kg/min </li></ul><ul><li>May decrease pulmonary vascular resistance </li></ul>
  58. 60. DOBUTAMINE <ul><li>Adverse effects: </li></ul><ul><ul><li>Systemic hypo- or hypertension </li></ul></ul><ul><ul><li>Ectopic beats </li></ul></ul><ul><ul><li>Ventricular tachycardia and other tachyarrhythmias </li></ul></ul><ul><li>Contraindications: </li></ul><ul><ul><li>IHSS </li></ul></ul><ul><ul><li>Atrial Fibrillation </li></ul></ul>
  59. 61. BIPYRIDINES <ul><li>Non-sympathomimetic agents </li></ul><ul><li>Newer class of inotropes </li></ul><ul><li>Function as phosphodiesterase inhibitors </li></ul><ul><ul><li>Amrinone </li></ul></ul><ul><ul><li>Milrinone </li></ul></ul>
  60. 62. BIPYRIDINES <ul><li>Cardiac relaxation </li></ul><ul><li>Decreased PVR and SVR </li></ul><ul><li>Dilation of coronary arteries </li></ul><ul><li>Decreased afterload </li></ul><ul><ul><li>C.O. increased by improving contractility without increasing myocardial oxygen consumption </li></ul></ul>
  61. 63. BIPYRIDINES <ul><li>Possess inotropic and vasodilating properties </li></ul><ul><li>Milrinone 10-30 times more potent than amrinone </li></ul><ul><li>Major complication is hypotension </li></ul><ul><li>Side effects: </li></ul><ul><ul><li>Thrombocytopenia (dose-related) </li></ul></ul><ul><ul><li>Supraventricular and ventricular dysrhythmias </li></ul></ul>
  62. 64. PRESSOR-RESISTANT HYPOTENSION <ul><li>Insufficiency of hypothalamic-pituitary axis or adrenal glands </li></ul><ul><li>Prolonged activation of sympathetic nervous system and exogenous catecholamines: </li></ul><ul><ul><li>Down-regulation of CV adrenergic receptors </li></ul></ul><ul><ul><li>Desensitization of CVS to catecholamines </li></ul></ul>
  63. 65. PRESSOR-RESISTANT HYPOTENSION <ul><li>Genomic effects </li></ul><ul><ul><li>Steroid-responsive element on genes of adrenergic receptors </li></ul></ul><ul><ul><li>Increased sensitivity to catecholamines </li></ul></ul><ul><li>Non-Genomic effects </li></ul><ul><ul><li>Inhibition of catecholamine metabolism </li></ul></ul><ul><ul><li>Increased cytosolic calcium availability in myocardial and vascular smooth muscle cells </li></ul></ul>
  64. 66. PRESSOR-RESISTANT HYPOTENSION <ul><li>Defined by the instability of the cardiovascular status and severity of capillary leak syndrome in the critically ill infant </li></ul><ul><li>Not defined by establishing arbitrary dose limits for the pressor treatment </li></ul>
  65. 67. ASSESSING BLOOD PRESSURE <ul><li>TREAT THE BABY </li></ul><ul><li>Numbers are guidelines </li></ul><ul><li>Assess key elements of tissue oxygen delivery: </li></ul><ul><ul><li>Heart rate </li></ul></ul><ul><ul><li>Central venous pressure </li></ul></ul><ul><ul><li>Capillary refill </li></ul></ul><ul><ul><li>Urine output </li></ul></ul><ul><ul><li>Acid-base status </li></ul></ul>
  66. 68. INTRACTABLE SHOCK <ul><li>If volume expanders and vasoactive/inotropic drugs do not correct shock, glucocorticoids may be effective. </li></ul><ul><li>Steroids rapidly up-regulate cardiovascular adrenergic receptor expression and serve as hormone replacement therapy if adrenal insufficiency exists. </li></ul>
  67. 69. FURTHER CARE <ul><li>Complications and prognosis are related to both underlying causes and injuries sustained during period of inadequate tissue perfusion. </li></ul><ul><li>Neurodevelopmental screening and follow-up, including imaging, BAER, and others is indicated. </li></ul>