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2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
2013 Pediatric Subspecialty Boot Camp_SHOCK
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2013 Pediatric Subspecialty Boot Camp_SHOCK

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  • Teacher’s GuideReferenced above: Watson RS et al. The epidemiology of severe sepsis in children in the United States, Am J Respir Crit Care Med 2003; 167:695. Bone, RC. Toward an epidemiology and natural history of SIRS (systemic inflammatory response syndrome). JAMA 1992: 268:3452.
  • Teachers’ Guide:(This represents hypovolemic shock.)Example questions and examples of acceptable answers: What is your assessment?15 year-old post-operative patient with sudden tachycardia and borderline low blood pressure with impaired peripheral perfusion. Suggests hypovolemic shock.2) What stage of shock? Compensated … for now, given his lack of hypotension by strict definition. Given rapidity of onset, be extremely cautious for rapid decline.3) What classification of shock? If uncertain, what additional information would you want to obtain to decide?Hypovolemic shock, likely due to blood loss related to surgery; less likely septic shock (though you would be suspicious of this given the nature of his wounds) due to his physical exam findings. What is your initial management.Again, ABCDs, fluid resuscitation with 20 ml/kg crystalloid as needed to restore perfusion and blood pressure. Ensure a type and screen/cross match has been done and order PRBCs to the bedside in the event that bleeding continues. Stat baseline hemoglobin/hematocrit with repeat every 4 hrs until stable.MAIN TEACHING POINT: Hypovolemic shock is often first manifest by tachycardia and decreased peripheral perfusion. Hypotension is a late finding and indicates uncompensated shock.
  • Teachers’ Guide:(This represents cardiogenic shock.)Example questions and examples of acceptable answers: What is your assessment? 4 mo old with subacute onset of decreased desire to feed, emesis in setting of viral symptoms and possibly decreased urine output. Afebrile on exam with tachycardia and signs of hypoperfusion and liver distension and gallop. Suggests cardiogenic shock.2) What stage of shock? Answer is unclear given lack of available BP reading, but exam with impaired perfusion (and weak cry possibly indicating altered mental status) would suggest progression toward uncompensated shock.3) What classification of shock? If uncertain, what additional information would you want to obtain to decide?Likely cardiogenic, given decreased desire to feed, emesis, impaired perfusion, distended liver, and S4. Additional information could be gained through CXR looking for cardiac enlargement and pulmonary edema, stat echo, lactate, possibly chemistry looking for acidosis due to hypoperfusion and electrolyte imbalances due to emesis, +/- BNP. What leads your differential for the etiology?Given recent viral illness, viral cardiomyopathy possible cause. What is your initial management?ABCDs, continuing to monitor blood pressure closely and ensuring sufficient access, 10 ml/kg bolus (repeated with caution and constant monitoring for worsening heart failure, as needed) to restore perfusion if altered mental status or other signs of end organ dysfunction. Stat cardiac echo (or at least bedside ultrasound). Dopamine stat to the bedside. Stat cardiology consultation.MAIN TEACHING POINT: Cardiogenic shock is marked by decreased peripheral perfusion due to decreased cardiac output. Despite increased preload in cardiogenic and obstructive shocks, fluid boluses may be needed to restore perfusion if signs of end organ dysfunction. Howerver, because patient may worsen with these boluses the volume should be small and re-evaluation should occur after each intervention.
  • Transcript

    • 1. PEDIATRIC SHOCK Ayse Akcan Arikan Texas Children’s Hospital Pediatric Critical Care Section Fellows Bootcamp 2013
    • 2. Objectives • By the end of this workshop, the learner will be able to: • Differentiate between septic and cardiogenic shock states according to clinical assessment and evaluation • Generate a therapeutic/diagnostic plan according to institutional and SCCM guidelines where applicable
    • 3. What is shock? a. BP less than 5th percentile of age normal b. Uncontrolled fluid loss/blood loss c. Tachycardia and hypotension d. Acidosis and increased lactate e. Signs of organ dysfunction with decreased UOP, altered mental status, etc.
    • 4. Pediatric Shock • Definition – what it is and what it is not • Pathophysiology • Recognition – early is key! • Management- guidelines • Case scenarios • Ask for references, and you shall receive
    • 5. Pump Fluid Pipes Site of exchange
    • 6. Pediatric shock • Cellular pathology • Has nothing to do with blood pressure (until very late), cardiac output, heart rate • Inability to meet the metabolic demands (=oxygen) of the tissue – or inability of the cell to use oxygen • Supply-demand imbalance
    • 7. What is shock? • A hemodynamic abnormality that leads to inability to meet tissue metabolic demands. • Dynamic, progressive. • A systemic reduction in tissue perfusion  decreased tissue O2 delivery. • A shift to anaerobic metabolism • Less efficient – 20-fold less ATP generated • Leads to lactic acidosis • Over time, progresses to, • Cell membrane ion pump dysfunction • Cellular edema, leakage of cells’ contents • Inadequate regulation of intracellular pH • Cell death, organ failure, cardiac arrest, and death.
    • 8. Pediatric shock • Dynamic process • Progressive • Changing physiology* • Requires bedside management • Oxygen debt • Energy uncoupling
    • 9. Vocabulary • CO –cardiac output • CI cardiac index – CO indexed to BSA • SVR, SVRI - systemic vascular resistance • PVR,PVRI – pulmonary vascular resistance • MAP – mean arterial pressure • CVP – central venous pressure • SV – stroke volume • PAP – pulmonary artery pressure • DO2 – oxygen delivery • VO2 – oxygen consumption
    • 10. Vocabulary - II • CO – cardiac output: volume of blood ejected by the heart in one minute 4-8 L/min • Heart rate • Stroke volume • Contractility • Afterload • Preload • SVR = MAP – CVP / CO
    • 11. Oxygen Delivery – DO2 • Oxygen delivery= CO X CaO2 (Arterial oxygen content) • CO=Heart rate X Stroke volume • Stroke volume depends on preload, afterload and contractility •Arterial Oxygen content (CaO2) = Hb x Sa02 x 1.34 +(0.003 x Pa02)
    • 12. Oxygen Consumption – VO2 • VO2 = CO x (CaO2 – CvO2) • Under normal conditions DO2 >> VO2 (physiological reserve) – this is why you can exercise and don’t die 
    • 13. Oxygen delivery – consumption imbalance in shock
    • 14. Shock pathophysiology • Oxygen delivery DO2 < oxygen demand VO2
    • 15. OXYGEN DELIVERY CARDIAC OUTPUT X ARTERIAL OXYGEN CONTENT Cardiac Output Arterial oxygen content Heart rate Stroke Volume Preload Afterload Contractility Hemoglobin Oxygen Saturation Partial pressure of oxygen dissolved in plasma
    • 16. Oxygen extraction ratio= (SaO2-SmvO2)/Sa SmvO2 = mixed venous oxygen saturations ScvO2 = upper extremity line
    • 17. Shock – signs and symptoms • Evidence of end organ hypoperfusion • Decreased urine output • Altered mental status • Poor peripheral perfusion • Metabolic dysfunction • Lactic acidosis • Altered metabolic demands
    • 18. Shock: Feel the feet, look at the neck • Tachycardia? - Non-specific, but early • Skin changes? - Prolonged cap refill (vasoconstriction) with compensated shock. Flash refill with early distributive shock and with irreversible shock. • Pallor? – If Hb is fine, is your patient acidotic • Impaired mental status? – Fussy, irritable? Sleepy? • Oliguria? – When was the last diaper? • Hypotension? – You have missed the ball  • Widened pulse pressure (>40 mmHg)? - distributive shock, aortic insufficiency, AVMs?
    • 19. Compensatory Mechanisms • Baroreceptors-In aortic arch and carotid sinus, low MAP cause vasoconstriction, increases BP, CO and HR • Chemoreceptors- Respond to cellular acidosis, results in vasoconstriction and respiratory stimulation • Renin Angiotensin Aldosterone - Decreased renal perfusion leads to angiotensin causing vasoconstriction and aldosterone causing salt and water retentions • Humoral Responses-Catecholamines • Autotransfusion-Reorientation of extravascular fluid
    • 20. Stages of Shock • Compensated Shock: • Cardiac output (HR x SV) and systemic vascular resistance (peripheral vasoconstriction) work to keep BP within normal limits. • Tachycardia; decreased pulses & cool extremities in cold shock; flushing and bounding pulses in warm shock; oliguria; may have mild lactic acidosis • Uncompensated Shock: • Compensatory mechanisms are overwhelmed. • Hypotension, altered mental status; increased lactic acidosis • Generally quick progression to cardiac arrest. • Irreversible Shock: • Irreversible organ damage, cardiac arrest, death.
    • 21. • Compensated • Uncompensated • Irreversible Act quickly Think slowly DEATH
    • 22. Types of shock •Hypovolemic •Hemorrhagic •Cardiogenic •Distributive •Septic* •Obstructive
    • 23. Classifications of Shock • Hypovolemic Shock • Decreased preload due to internal or external losses. • Distributive Shock • Decrease in SVR, with abnormal distribution of blood flow  functional hypovolemia, decreased preload. • Typically, NL or  CO. • Cardiogenic Shock • “Pump failure.”  CO, systolic function. • Obstructive Shock • Outflow from left or right side of heart physically obstructed.
    • 24. © 2009 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins. Published by Lippincott Williams & Wilkins, Inc. 2 Table 2. Clinical practice parameters for hemodynamic support of pediatric and neonatal septic shock: 2007 update from the American College of Critical Care Medicine *. Brierley, Joe; Carcillo, Joseph; Choong, Karen; Cornell, Tim; DeCaen, Allan; Deymann, Andreas; Doctor, Allan; Davis, Alan; Duff, John; Dugas, Marc- Andre; Duncan, Alan; Evans, Barry; Feldman, Jonathan; Felmet, Kathryn; Fisher, Gene; Frankel, Lorry; Jeffries, Howard; Greenwald, Bruce; Gutierrez, Juan; Hall, Mark; Han, Yong; Hanson, James; Hazelzet, Jan; Hernan, Lynn; Kiff, Jane; Kissoon, Niranjan; Kon, Alexander; Irazusta, Jose; Lin, John; Lorts, Angie; Mariscalco, Michelle; Mehta, Renuka; Nadel, Simon; Nguyen, Trung; Nicholson, Carol; Peters, Mark; Okhuysen-Cawley, Regina; Poulton, Tom; Relves, Monica; Rodriguez, Agustin; Rozenfeld, Ranna; Schnitzler, Eduardo; Shanley, Tom; Skache, Sara; Skippen, Peter; Torres, Adalberto; von Dessauer, Bettina; Weingarten, Jacki; Yeh, Timothy; Zaritsky, Arno; Stojadinovic, Bonnie; Zimmerman, Jerry; Zuckerberg, Aaron Critical Care Medicine. 37(2):666-688, February 2009. DOI: 10.1097/CCM.0b013e31819323c6 Table 2. American College of Critical Care Medicine hemodynamic definitions of shock
    • 25. Type of shock Mechanism of circulatory failure Signs and symptoms Interventions Hypovolemic Volume depletion absolute or relative, CO ↓, SVR ↑ Tachycardia, diminished pulses, sunken eyes and fontanels, oliguria, prolonged cap refill time Crystalloid bolus 20 ml/kg until hemodynamics improve, reassess after each bolus, blood products in hemorrhagic shock Cardiogenic CO ↓, SVR ↑ Tachycardia, diminished pulses, hepatomegaly, JVD Inotropic agents dopamine, dobutamine, epinephrine, milrinone Small volume boluses 5-10 ml/kg might be administered carefully while monitoring response Get echo early Consider PGE
    • 26. Type of shock Mechanism of circulatory failure Signs and symptoms Interventions Distributive Anaphylactic Neurogenic CO ↑, then ↓, SVR ↓↓ Angioedema, respiratory distress, stridor, wheezing, early hypotension Start adrenergic support while giving fluids, obtain vascular access early, supratherapeutic doses of inotropes might be required CO normal, SVR ↓ Hypotension in the absence of tachycardia Support SVR with vasopressors, phenylephrine might be required, give fluids as necessary Obstructive Preload ↓, CO ↓, SVR normal to ↑ Tachycardia, hypotension, JVD, tracheal deviation if pneumothorax, equalization of pressures with elevated CVP if invasive monitoring in place Rapidly fatal if underlying process not recognized and reversed, fluid boluses should be given while preparation is made for emergent drainage
    • 27. Type of shock Mechanism of circulatory failure Signs and symptoms Interventions Septic “Warm shock” CO ↑, SVR↓ Tachycardia, bounding pulses, warm extremities with hypotension, hyperpnoea, altered mentation Crystalloid boluses of 20 ml/kg repeat until hemodynamics stable, first choice agents vasopressors (dopamine or norepinephrine) “Cold shock” CO ↓, SVR ↑ (60% of pediatric cases) Tachycardia, poor peripheral perfusion, diminished pulses, hyperpnoea, altered mentation Crystalloid boluses of 20 ml/kg, repeat until hemodynamics stable, early inotropic support with dopamine or epinephrine might be required, echocardiography might be useful to guide therapy CO ↓, SVR ↓ Tachycardia, diminished pulses, with hypotension, hyperpnoea, altered mentation Crystalloid boluses of 20 ml/kg repeat until hemodynamics stable, early inotropic support with dopamine or epinephrine might be required, echocardiography might be useful to guide therapy
    • 28. © 2009 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins. Published by Lippincott Williams & Wilkins, Inc. 2 Table 3. Clinical practice parameters for hemodynamic support of pediatric and neonatal septic shock: 2007 update from the American College of Critical Care Medicine *. Brierley, Joe; Carcillo, Joseph; Choong, Karen; Cornell, Tim; DeCaen, Allan; Deymann, Andreas; Doctor, Allan; Davis, Alan; Duff, John; Dugas, Marc-Andre; Duncan, Alan; Evans, Barry; Feldman, Jonathan; Felmet, Kathryn; Fisher, Gene; Frankel, Lorry; Jeffries, Howard; Greenwald, Bruce; Gutierrez, Juan; Hall, Mark; Han, Yong; Hanson, James; Hazelzet, Jan; Hernan, Lynn; Kiff, Jane; Kissoon, Niranjan; Kon, Alexander; Irazusta, Jose; Lin, John; Lorts, Angie; Mariscalco, Michelle; Mehta, Renuka; Nadel, Simon; Nguyen, Trung; Nicholson, Carol; Peters, Mark; Okhuysen-Cawley, Regina; Poulton, Tom; Relves, Monica; Rodriguez, Agustin; Rozenfeld, Ranna; Schnitzler, Eduardo; Shanley, Tom; Skache, Sara; Skippen, Peter; Torres, Adalberto; von Dessauer, Bettina; Weingarten, Jacki; Yeh, Timothy; Zaritsky, Arno; Stojadinovic, Bonnie; Zimmerman, Jerry; Zuckerberg, Aaron Critical Care Medicine. 37(2):666-688, February 2009. DOI: 10.1097/CCM.0b013e31819323c6 Table 3. Threshold heart rates and perfusion pressure mean arterial pressure-central venous pressure or mean arterial pressure-intra-abdominal pressure for age
    • 29. What is the goal of shock treatment ? •Optimizing oxygen content of the blood •Improving volume and distribution of cardiac output •Reducing oxygen demand •Correcting metabolic derangements
    • 30. Treatment • Overall goal: Normalization of tissue perfusion and homeostasis • A - airway • Secure, patent • Oxygen administration – 100% FiO2 (except in some cases of cardiogenic shock) • B - breathing • Decrease WOB, intubation-mechanical ventilation may be necessary (decrease oxygen consumption) • C - circulation • Improve cardiac output • Ensure adequate preload – FLUIDS!!!
    • 31. Treatment - II • Have I mentioned fluids? • Give lots of fluids – fast! • Then – give some more –up to 200 ml/kg may be required • REASSESS! (After every step/intervention) • Pay attention to hepatomegaly, JVD, rales, worsening respiratory distress – if your patient is not responding to the fluids, reconsider your diagnosis • Once you reach 60 ml/kg, consider starting vasoactive infusions –more on this later
    • 32. Treatment - III • D – “derangements” • Correct metabolic abnormalities – hypoglycemia, hypocalcemia, etc • Etiology specific treatment •DO NOT DELAY ANTIBIOTICS FOR ANY REASON IF YOU SUSPECT SEPTIC SHOCK ! • Source control • Consider transfusion of PRBCs
    • 33. Assessing efficacy of treatment • Blood pressure: Normal * • Quality of central and peripheral pulses: Strong, distal pulses equal to central pulses. • Skin perfusion: Warm, with capillary refill 1-2 seconds. • Mental status: Normal.  Urine output: >1 mL/kg per hour, once effective circulating volume is restored.
    • 34. Sepsis • High mortality despite improvements • KID database : 4.2% in all-comers, 2.3% in previously healthy, 7.8% in chronically ill • Guidelines are not effective unless protocol driven • Early intervention is critical – no delay is acceptable. • Every hour spent without reversing shock increases OR of mortality
    • 35. SIRS SEPSIS SEVERE SEPSIS SEPTIC SHOCK T > 38.5 or < 36 Tachycardia Tachypnea  WBC  SIRS + Infection (suspected or proven) SEPSIS + CV dysfunction or ARDS or ≥ 2 organ failures SEPSIS + CV dysfunction despite >40 ml/kg in 1 hr 2 of the above 4
    • 36. Early Goal-directedTherapy
    • 37. Pediatrics 2003; 112:793 Early Resuscitation
    • 38. © 2009 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins. Published by Lippincott Williams & Wilkins, Inc. 2 Figure 1. Clinical practice parameters for hemodynamic support of pediatric and neonatal septic shock: 2007 update from the American College of Critical Care Medicine *. Brierley, Joe; Carcillo, Joseph; Choong, Karen; Cornell, Tim; DeCaen, Allan; Deymann, Andreas; Doctor, Allan; Davis, Alan; Duff, John; Dugas, Marc-Andre; Duncan, Alan; Evans, Barry; Feldman, Jonathan; Felmet, Kathryn; Fisher, Gene; Frankel, Lorry; Jeffries, Howard; Greenwald, Bruce; Gutierrez, Juan; Hall, Mark; Han, Yong; Hanson, James; Hazelzet, Jan; Hernan, Lynn; Kiff, Jane; Kissoon, Niranjan; Kon, Alexander; Irazusta, Jose; Lin, John; Lorts, Angie; Mariscalco, Michelle; Mehta, Renuka; Nadel, Simon; Nguyen, Trung; Nicholson, Carol; Peters, Mark; Okhuysen-Cawley, Regina; Poulton, Tom; Relves, Monica; Rodriguez, Agustin; Rozenfeld, Ranna; Schnitzler, Eduardo; Shanley, Tom; Skache, Sara; Skippen, Peter; Torres, Adalberto; von Dessauer, Bettina; Weingarten, Jacki; Yeh, Timothy; Zaritsky, Arno; Stojadinovic, Bonnie; Zimmerman, Jerry; Zuckerberg, Aaron Critical Care Medicine. 37(2):666-688, February 2009. DOI: 10.1097/CCM.0b013e31819323c6 Figure 1. Algorithm for time sensitive, goal-directed stepwise management of hemodynamic support in infants and children. Proceed to next step if shock persists. 1) First hour goals-Restore and maintain heart rate thresholds, capillary refill MAP]-central venous pressure [CVP]) for age, central venous O2 saturation >70%, and CI >3.3, 2 in pediatric intensive care unit (PICU). Hgb, hemoglobin; PICCO, pulse contour cardiac output; FATD, femoral arterial thermodilution; ECMO, extracorporeal membrane oxygenation; CI, cardiac index; CRRT, continuous renal replacement therapy; IV, intravenous; IO, interosseous; IM, intramuscular.
    • 39. TCH Shock Protocol
    • 40. Definitions • Pressor-increases SVR, and therefore BP • Inotrope-Increases contractility, SV • Chronotrope- increases HR • Lusitrope- improves diastolic relaxation, SV • Vasodilator- decreases SVR, afterload • “Inodilator”
    • 41. TCH BOOTCAMP Shock II – Cardiogenic shock
    • 42. Pump Fluid Pipes Site of exchange
    • 43. • Tachycardia • Tachypnea • Hx of sweating/tiring with feeds • Vomiting, feeding intolerance • Fussiness • Gallop • Hepatomegaly • Rales • Decreased UOP • Cardiomegaly • Altered mentation • “Septic” newborn ! • Cyanosis
    • 44. VENTRICULAR FUNCTION CURVES NORMALAND FAILING LV
    • 45. Cardiogenic shock • Electrical failure • Mechanical failure • Myocarditis • Cardiomyopathy • Anatomic • Obstructive • Congestive • Ischemic • Trauma
    • 46. Cardiogenic shock • Anatomic • Left sided obstructive = ductal dependent systemic flow  IAA, critical AS, HLHS, etc  HCM* • Congestive • large L R shunts • Acute valvular regurgitation • Ductal dependent pulmonary blood flow • Parallel circulation – TGA-IVS • Obstructed pulmonary flow – TAPVR, obstructed
    • 47. Ischemic Heart Disease in Children • ALCAPA • Anomalous Left Coronary Artery arising from the Pulmonary Artery • Kawasaki Disease • Aneurysms • Other vasculitis
    • 48. Treatment • Support the failing pump • Decrease oxygen consumption/metabolic demand • Intubation*, mechanical ventilation • Sedation, NMB • Prevention of fever, stress • Consider bolus 5-10 ml/kg • Consider PGE • Echo early
    • 49. Treatment - II • Optimize contractility • Correct metabolic derangements • Inotropic support • Afterload reduction • Decongestion • Address the underlying cause – surgery? • Mechanical support • ECMO • Implantable devices, VAD, EXCOR, etc
    • 50. Type of shock Mechanism of circulatory failure Signs and symptoms Interventions Hypovolemic Volume depletion absolute or relative, CO ↓, SVR ↑ Tachycardia, diminished pulses, sunken eyes and fontanels, oliguria, prolonged cap refill time Crystalloid bolus 20 ml/kg until hemodynamics improve, reassess after each bolus, blood products in hemorrhagic shock Cardiogenic CO ↓, SVR ↑ Tachycardia, diminished pulses, hepatomegaly, JVD Inotropic agents dopamine, dobutamine, epinephrine, milrinone Small volume boluses 5-10 ml/kg might be administered carefully while monitoring response Get echo early Consider PGE
    • 51. Question • 13 month old patient with DCM, HR 180 (sinus), CVP 25 mm Hg, BP 55/24, lactate 4->8, SvO2 50%, cap refill of 5 seconds, best choice of action is: a. Epinephrine gtt b. Milrinone gtt c. Phenylephrine gtt d. NS bolus 20 ml/kg e. Esmolol (B-blocker) for HR control
    • 52. Question • 12 year old female presents with fever, tachycardia, right flank pain, WBC count is elevated. Vital signs are HR 155, RR 35, BP 124/73, T 102. She is somnolent. Working diagnosis is sepsis secondary to pyelonephritis. What is the next most appropriate intervention? A. Renal US B. Normal saline bolus C. Antibiotics D. Vasopressor infusion E. Urinalysis
    • 53. Question • 12 year old female presents with fever, tachycardia, right flank pain, WBC count is elevated. Vital signs are HR 110, RR 25, BP 124/83, T 102. She is AAO x 3 and is . Working diagnosis is sepsis secondary to pyelonephritis. What is the next most appropriate intervention? A. Renal US B. Normal saline bolus C. Antibiotics D. Vasopressor infusion E. Urinalysis
    • 54. Case 1 • 15-year-old male is just transferred to 11 WT from PICU, POD #3 from partial small bowel resection after multiple gunshot wounds to the abdomen. The nurse calls an RRT because his HR has increased in the last hour from 90 to 130, despite pain score of 1/10 on morphine drip. On exam, he is afebrile, HR is 140, BP 80/50. Cap refill is >3 seconds in his cool extremities and pulses are 1+. • What is your assessment? • What is the stage of shock? • What is the classification of shock? • What is your initial management?
    • 55. Case 2 • 6-year-old previously healthy girl is transferred from West Campus ER with fever, bloody diarrhea x 1 day. She’s had no urine x 24 hrs and is becoming harder to awaken. On exam, her HR is 152, BP 72/32, temp 103. She’s sleepy but arousable. She’s flushed with capillary refill <1 second. • What is your assessment? • What is the stage of shock? • What is the classification of shock? • What is your differential for the etiology? • What is your initial management? If a higher level of care is needed, how would you obtain it?
    • 56. Case 3 • 4-month-old boy former premie, presents to ED with decreased po x 2 days with 2 times daily emesis, following what sounds like viral URI. Urine output has been 3 wet diapers daily. He is afebrile with HR 180; BP has not been obtained. He has a weak cry, is mottled with 3-second capillary refill, pulses 1+ in all extremities. Liver is palpable 4 cm below RCM. S4 is present without murmur. • What is your assessment? • What is the stage of shock? • What is the classification of shock? • What is your differential for the etiology? • What is your initial management?
    • 57. What is the end goal for resuscitation ? • Mixed venous sats • Lactate clearance • Traditional clinical variables – UOP, perfusion, pulses, CVP • Combination of all three with common sense
    • 58. Minimize variationEarly Resuscitation Intensive Care Med 2008; 34:1065
    • 59. Intensive Care Med 2008; 34:1065 Minimize variationEarly Resuscitation
    • 60. • crashingpatient.com • ccmtutorials.com • cvphysiology.com • learnhemodynamics.com* • library.med.utah.edu

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