PEM Playbook – Approach to Shock
Originally published at Pediatric Emergency Playbook on June 1,
2016 – Visit to listen to accompanying podcast. Reposted with permission.
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Do we recognize shock early enough?
How do we prioritize our interventions?
Are we making our patient better or worse?
World wide, shock is a leading cause of morbidity and mortality in children, mostly for failure to recognize or to treat adequately.
So, what is shock?
Simply put, shock is the inadequate delivery of oxygen to your tissues. That’s it. Our main focus is on improving our patient’s perfusion.
Oxygen 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.
At the bedside, we can measure some of these things, directly or indirectly. Did you notice, however, 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.
The equation here is a formality:
DO2 = (cardiac output) x [(hemoglobin concentration) x SaO2 x 1.39] + (PaO2 x 0.003)
Shock CAN be associated with a low blood pressure,
but shock is not DEFINED by a low blood pressure.
Compensated Shock: tachycardia with poor perfusion. A child compensates for low cardiac output with tachycardia and a increase in systemic vascular resistance.
Decompensated Shock: frank hypotension, an ominous, pre-arrest phenomenon.
Shock is multifactorial, but we need to identify a primary cause to prioritize interventions.
How they “COHDe”: Cardiogenic, Obstructive, Hypovolemic, and Distributive.
All 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.
Cardiogenic 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.
“Warm and Dry”
A 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.
“Warm and Wet”
If he worsens, he becomes “warm and wet” with pulmonary congestion – you’ll hear crackles and seesome 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.
“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.
“Cold and Dry”
A 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.
“Cold and Wet”
The 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.
Cardiogenic Shock: Act
Good Squeeze? M-mode to measure fractional shortening of the myocardium or anterior mitral leaflet excursion.
Pericardial Effusion? Get ready to aspirate.
Ventricle Size? Collapsed, dilated, or normal.
Careful with fluids — patients in cardiogenic shock may need small aliquots, but go quickly to a pressor to support perfusion.
Pressor of choice: epinephrine, continuous IV infusion: 0.1 to 1 mcg/kg/minute. The usual adult starting range will end up being 1 to 10 mcg/min.
Avoid norepinephrine, as it increases systemic vascular resistance, may affect afterload.
Just say no to dopamine: increased mortality when compared to epinephrine.
Mostly one of two entities: pulmonary embolism or cardiac tamponade.
Pulmonary 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.
Children with PE will either have a major thrombophilic comorbidity, or they are generously sized teenage girls on estrogen therapy.
Tamponade — 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.
Obstructive Shock: Act
Pulmonary embolism (PE) with overt shock: thrombolyse; otherwise controversial. PE with symptoms: heparin.
Tamponade: if any sign of shock, pericardiocentesis, preferentially ultrasound-guided.
The 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.
Rapid 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.
Hypovolemic Shock: Act
Tip: 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 stopcock, and “push them into the patient.
Titrate to signs of perfusion, such as an improvement in mental status, heart rate, capillary refill, and urine output.
When 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.
The 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.
Children with sepsis come in two varieties: warm shock and cold shock.
Distributive Shock: Act
Warm shock is due to peripheral vascular dilation, and is best treated with norepinephrine.
Cold 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.
Early antibiotics are crucial, and culture everything that seems appropriate.
Shock: A Practical Approach
“How FAST you FILL the PUMP and SQUEEZE”
Sometimes things are not so cut-and-dried. We’ll use a practical approach to diagnose and intervene simultaneously.
Look at 4 key players in shock: heart rate, volume status, contractility, and systemic vascular resistance.
How FAST you FILL the PUMP and SQUEEZE
First, we look at heart rate — how FAST?
Look 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.
If the heart rate is what is causing the shock, address that first.
Next, we look at volume status.
How FAST you FILL the PUMP and SQUEEZE
Look 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.
Now, we look at contractility.
How FAST you FILL the PUMP and SQUEEZE
Is 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.
And finally, we look to the peripheral vascular resistance.
How FAST you FILL the PUMP and SQUEEZE
Is there a problem with systemic vascular resistance – the SQUEEZE?
Look 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.
The four take-home points in the approach to shock in children:
- To prioritize your interventions, 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.
- To 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.
- In 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.
- Rapid-fire word association:
- Epinephrine for cardiogenic shock
- Intervention for obstructive shock
- Fluids for hypovolemic shock
- Norepinephrine for distributive shock
Jaff 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.
Levy 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.
Ventura 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.
This 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.
Powered by #FOAMed — Tim Horeczko, MD, MSCR, FACEP, FAAP
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