{"version":1,"type":"rich","provider_name":"Libsyn","provider_url":"https:\/\/www.libsyn.com","height":90,"width":600,"title":"Approach to Shock","description":"Do we recognize shock early enough?\r\nHow do we prioritize our interventions?\r\nHow can we tell whether we’re making our patient better or worse?\r\n \r\nWorld wide, shock is a leading cause of morbidity and mortality in children, mostly for failure to recognize or to treat adequately.\r\nSo, what is shock?\r\n\r\nSimply put, shock is the inadequate delivery of oxygen to your tissues.  That’s it.  Our main focus is on improving our patient’s perfusion.\r\n\r\nOxygen delivery to the tissues depends on cardiac output, hemoglobin concentration, the oxygen saturation of the hemoglobin you have, and the environmental partial pressure of oxygen.\r\nAt the bedside, we can measure some of these things, directly or indirectly.  But did you notice that blood pressure is not part of the equation?  The reason for that is that blood pressure is really an indirect proxy for perfusion – it’s not necessary the ultimate goal.\r\nThe equation here is a formality:\r\n\r\nDO2 = (cardiac output) x [(hemoglobin concentration) x SaO2 x 1.39] + (PaO2  x 0.003)\r\n\r\n \r\n \r\nShock CAN be associated with a low blood pressure, but shock is not DEFINED by a low blood pressure.\r\n \r\n \r\nCompensated Shock: tachycardia with poor perfusion.  A child compensates for low cardiac output with tachycardia and a increase in systemic vascular resistance.\r\n \r\n \r\nDecompensated Shock: frank hypotension, an ominous, pre-arrest phenomenon.\r\n \r\nShock is multifactorial, but we need to identify a primary cause to prioritize interventions.\r\n \r\n \r\nHow they "COHDe": Cardiogenic, Obstructive, Hypovolemic, and Distributive.\r\n \r\nCardiogenic Shock\r\nAll will present with tachycardia out of proportion to exam, and sometimes with unexplained belly pain, usually due to hepatic congestion.  The typical scenario in myocarditis is a precipitous decline after what seemed like a run-of-the-mill URI.\r\nCardiogenic shock in children can be from congenital heart disease or from acquired etiologies, such as myocarditis.  Children, like adults, present in cardiogenic shock in any four of the following combinations: warm, cold, wet, or dry.\r\n"Warm and Dry"\r\nA child with heart failure is “warm and dry” when he has heart failure signs (weight gain, mild hepatomegaly), but has enough forward flow that he has not developed pulmonary venous congestion.  A warm and dry presentation is typically early in the course, and presents with tachycardia only.\r\n"Warm and Wet"\r\nIf he worsens, he becomes “warm and wet” with pulmonary congestion – you’ll hear crackles and see some respiratory distress.  Infants with a “warm and wet” cardiac presentation sometimes show sacral edema – it is their dependent region, equivalent to peripheral edema as we see in adults with right-sided failure.\r\n“Warm” patients – both warm and dry and warm and wet -- typically have had a slower onset of their symptoms, and time to compensate partially. Cool patients are much sicker.\r\n"Cold and Dry”\r\nA patient with poor cardiac output; he is doing everything he can to compensate with increased peripheral vascular resistance, which will only worsen forward flow.  Children who have a “cold and dry” cardiac presentation may have oliguria, and are often very ill appearing, with altered mental status.\r\n"Cold and Wet"\r\nThe sickest of the group, this patient is so clamped down peripherally that it is now hindering forward flow, causing acute congestion, and pulmonary venous back-up.  You will see cool, mottled extremities.\r\nCardiogenic Shock: Act\r\nUse point-of-care cardiac ultrasound:\r\nGood Squeeze? M-mode to measure fractional shortening of the myocardium or anterior mitral leaflet excursion.\r\nPericardial Effusion? Get ready to aspirate.\r\nVentricle Size? Collapsed, Dilated,\r\nCareful with fluids -- patients in cardiogenic shock may need small aliquots, but go quickly to a pressor to support perfusion\r\nPressor of choice: epinephrine, continuous IV infusion: 0.1 to 1 mcg\/kg\/minute.  Usual adult starting range will end up being 1 to 10 mcg\/min.\r\nAvoid norepinephrine, as it increases systemic vascular resistance, may affect afterload\r\nJust say no to dopamine: increased mortality when compared to epinephrine\r\n \r\nObstructive Shock\r\nMostly one of two entities: pulmonary embolism or cardiac tamponade.\r\nPulmonary embolism in children is uncommon – when children have PE, there is almost always a reason for it – it just does not happen in normal, healthy children without risk factors.\r\nChildren with PE will either have a major thrombophilic comorbidity, or they are generously sized teenage girls on estrogen therapy.\r\nTamponade -- can be infectious, rheumotologic, oncologic, or traumatic.  It’s seen easily enough on point of care ultrasound.  If there is non-traumatic tamponade physiology, get that spinal needle and get to aspirating.\r\nObstructive Shock: Act\r\nPulmonary embolism (PE) with overt shock: thrombolyse; otherwise controversial.  PE with symptoms: heparin.\r\nTamponade: if any sign of shock, pericardiocentesis, preferentially ultrasound-guided.\r\n \r\nHypovolemic Shock\r\nThe most common presentation of pediatric shock; look for decreased activity, decreased urine output, absence of tears, dry mucous membranes, sunken fontanelle.  May be due to obvious GI losses or simply poor intake.\r\nRapid reversal of hypovolemic shock: may need multiple sequential boluses of isotonic solutions. Use 10 mL\/kg in neonates and young infants, and 20 mL\/kg thereafter.\r\nHypovolemic Shock: Act\r\nTip: in infants, use pre-filled sterile flushes to push fluids quickly.  In older children, use a 3-way stop cock in line with your fluids and a 30 mL syringe to "pull" fluids, turn the stop cock, and "push them into the patient.\r\nTitrate to signs of perfusion, such as an improvement in mental status, heart rate, capillary refill, and urine output.\r\nWhen concerned about balancing between osmolality, acid-base status, and volume status, volume always wins.  Our kidneys are smarter than we are, but they need to be perfused first.\r\n \r\nDistributive Shock\r\nThe most common cause of distributive shock is sepsis, followed by anaphylactic, toxicologic, adrenal, and neurogenic causes.  Septic shock is multifactorial, with hypovolemic, cardiogenic, and distributive components.\r\nChildren with sepsis come in two varieties: warm shock and cold shock.\r\nDistributive Shock: Act\r\nWarm shock is due to peripheral vascular dilation, and is best treated with norepinephrine.\r\nCold shock is due to a child’s extreme vasoconstriction in an attempt to compensate.  Cold shock is the most common presentation in pediatric septic shock, and is treated with epinephrine.\r\nEarly antibiotics are crucial, and culture everything that seems appropriate.\r\n \r\nShock: A Practical Approach\r\n \r\n"How FAST you FILL the PUMP and SQUEEZE"\r\nSometimes things are not so cut-and-dried.  We'll use a practical approach to diagnose and intervene simultaneously.\r\nLook at 4 key players in shock: heart rate, volume status, contractility, and systemic vascular resistance.\r\nHow FAST you FILL the PUMP and SQUEEZE\r\nFirst, we look at heart rate -- how FAST?\r\nLook at the heart rate – is it sinus?  Could this be a supraventricular tachycardia that does not allow for enough diastolic filling, leading to poor cardiac output?  If so, use 1 J\/kg to synchronize cardiovert.  Conversely, is the heart rate too slow – even if the stroke volume is sufficient, if there is severe bradycardia, then cardiac output  -- which is in liters\/min – is decreased.  Chemically pace with atropine, 0.01 mg\/kg up to 0.5 mg, or use transcutaneous pacing.\r\nIf the heart rate is what is causing the shock, address that first.\r\nNext, we look at volume status.\r\nHow FAST you FILL the PUMP and SQUEEZE\r\nLook to FILL the tank if necessary.  Does the patient appear volume depleted?  Try a standard bolus – if this improves his status, you are on the right track.\r\nNow, we look at contractility.\r\nHow FAST you FILL the PUMP and SQUEEZE\r\nIs there a problem with the PUMP?  That is, with contractility?  Is this in an infarction, an infection, a poisoning?  Look for signs of cardiac congestion on physical exam.  Put the probe on the patient’s chest, and look for effusion.  Look to see if there is mild, moderate, or severe decrease in cardiac contractility.  If this is cardiogenic shock – a problem with the pump itself -- begin pressors.\r\nAnd finally, we look to the peripheral vascular resistance.\r\nHow FAST you FILL the PUMP and SQUEEZE\r\nIs there a problem with systemic vascular resistance – the SQUEEZE?\r\nLook for signs of changes in temperature – is the patient flushed?  Is this an infectious etiology?  Are there neurogenic or anaphylactic concerns?  After assessing the heart rate, optimizing volume status, evaluating contractility, is the cause of the shock peripheral vasodilation?  If so, treat the cause – perhaps this is a distributive problem due to anaphylaxis.  Treat with epinephrine. The diagnosis of exclusion in trauma is neurogenic shock.  Perhaps this is warm shock, both are supported with norepinephrine.  All of these affect systemic vascular resistance – and the shock won’t be reversed until you optimize the peripheral squeeze.\r\n \r\nSummary\r\nThe four take-home points in the approach to shock in children\r\n\r\nTo prioritize your innterventions, remember how patients COHDe: Cardiogenic, Obstructive, Hypovolemic, and Distributive. Your patient's shock may be multifactorial, but mentally prioritize what you think is the MAIN case of the shock, and deal with that first.\r\nTo treat shock, remember: How FAST You FILL The PUMP and SQUEEZE: Look at the heart rate – how FAST.  Look at the volume status – the FILL.  Assess cardiac contractility – the PUMP, and evaluate the peripheral vascular tone – the SQUEEZE.\r\nIn pediatric sepsis, the most common type is cold shock – use epinephrine (adrenaline) to get that heart to increase the cardiac output. In adolescents and adults, they more often present in warm shock, use norepinephrine (noradrenaline) for its peripheral squeeze to counteract this distributive type of shock.\r\nRapid-fire word association:\r\n\r\n\r\nEpinephrine for cardiogenic shock\r\nIntervention for obstructive shock\r\nFluids for hypovolemic shock\r\nNorepinephrine for distributive shock\r\n\r\n\r\nReferences\r\nAgha BS, Sturm JJ, Simon HK, Hirsh DA. Pulmonary embolism in the pediatric emergency department. Pediatrics. 2013 Oct;132(4):663-7.\r\nDellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013; 41:580-637.\r\nJaff MR et al. for the American Heart Association Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation; American Heart Association Council on Peripheral Vascular Disease; American Heart Association Council on Arteriosclerosis, Thrombosis and Vascular Biology. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation. 2011; Apr 26;123(16):1788-830.\r\nLevy B et al. Comparison of norepinephrine-dobutamine to epinephrine for hemodynamics, lactate metabolism, and organ function variables in cardiogenic shock. A prospective, randomized pilot study. Crit Care Med. 2011; 39:450.\r\nMicek ST, McEvoy C, McKenzie M, Hampton N, Doherty JA, Kollef MH. Fluid balance and cardiac function in septic shock as predictors of hospital mortality. Crit Care. 2013; 17:R246.\r\nOsman D, Ridel C, Ray P, et al. Cardiac filling pressures are not appropriate to predict hemodynamic response to volume challenge. Crit Care Med. 2007; 35:64-8.\r\nVentura AM, Shieh HH, Bousso A, Góes PF, de Cássia F O Fernandes I, de Souza DC, Paulo RL, Chagas F, Gilio AE. Double-Blind Prospective Randomized Controlled Trial of Dopamine Versus Epinephrine as First-Line Vasoactive Drugs in Pediatric Septic Shock. Crit Care Med. 2015;43(11):2292-302.\r\n\r\nThis post and podcast are dedicated to Natalie May, MBChB, MPHe, MCEM, FCEM for her collaborative spirit, expertise, and her super-charged support of #FOAMed.  You make a difference.  Thank you.\r\n\r\n\r\nUndifferentiated Shock\r\nPowered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP","author_name":"Pediatric Emergency Playbook","author_url":"http:\/\/pemplaybook.org\/","html":"