Critical Care

Beyond ATLS: What the Manual Doesn't Tell You

All these factors coalesce in the trauma bay to create a downward spiral of shock where life-saving interventions wrestle with each other as the patient circles the drain.

A 28-year-old male presents to your trauma bay already intubated, with multiple stab wounds to his chest and right upper extremity. He is hypotensive and tachycardic. An emergent right-sided tube thoracostomy produces no blood and no rush of air, but the patient is now gurgling around the endotracheal tube. An emergent introducer catheter is placed for additional access, and he is induced and re-intubated for concern for tube dislodgement. The patient then codes. A resuscitative thoracotomy is performed immediately, only to find no hemopericardium and a clean thorax. What went wrong?

Guidelines Are Guidelines

While trauma algorithms are a valuable tool to drive performance during high pressure or time-limited situations, and while both the Eastern Association for the Surgery of Trauma and Western Trauma Association algorithms would have supported the described treatment and resuscitation of this patient, it is important to remember that guidelines are just that — guidelines. They must always be interpreted within a deeper understanding of context. Could this particular patient's cardiac arrest have been avoided? Without a fuller appreciation for the physiology and evidence behind certain procedural and pharmacologic trauma interventions, algorithms have the potential to be dangerous.

The patient's resuscitative thoracotomy revealed no hemothorax, hemopericardium, or significant thoracic injury. Without a clear cause for the patient's decline, the only suspects left in this case of hypovolemic shock were the hemodynamic and pharmacologic interventions of the trauma management. The goal of this article is to shed light on 3 specific interventions that have profound effects on the physiology of trauma patients.

Induction Agent for RSI

The critically ill trauma airway is a delicate balancing act whereby the expected physiologic derangements of intubation are complicated by severe hemorrhage and catecholamine depletion. Induction creates hypotension, vasodilatation, and a loss of sympathetic surge that could be disastrous for a trauma airway.

The philosophy of rapid sequence intubation (RSI) is structured upon the assumption that the patient is not physiologically optimized or prepared for the insult of intubation. However, poor volume status, fluctuating respiratory system compliance, and derangements of intrathoracic pressures complicate the hemodynamics of RSI induction and paralysis when applied to critically ill trauma patients. All these factors coalesce in the trauma bay to create a downward spiral of shock where life-saving interventions wrestle with each other as the patient circles the drain.

Emergency physicians must choose a sedation agent for RSI that has a stable hemodynamic profile, such as ketamine or etomidate. However, there is still some debate over the ideal agent for trauma patients in shock.

A 2016 study showed that an institutional switch from etomidate to ketamine for RSI in trauma produced no significant benefits in terms of mortality, length-of-stay, ventilator-free, or vasopressor-free days.6 With the risks of elevated intracranial pressure debunked by recent meta-analyses and systematic reviews from both emergency medicine and neuro-critical care literature, the choice for ketamine induction would seem reasonable for its sympathomimetic effects.7,8

However, both anesthesia and emergency medicine literature has questioned ketamine's efficacy in the context of the catecholamine-depleted patient.10 Another 2016 study prospectively enrolled trauma patients induced with ketamine and separated them into low or high shock index groups. Defined by the heart rate over the systolic blood pressure, a high shock index (> 0.9) predicts mortality and need for transfusion.11 The study found that high shock index patients intubated with ketamine maintained a significantly higher pulse rate and were unable to augment their systolic blood pressures when compared to the low shock index cohort. Though further trials of high shock index trauma patients need to be performed, the findings suggest that catecholamine-depleted patients may not mount the anticipated sympathomimetic effects of ketamine.

Positive Pressure Ventilation

As the patient hangs in the precipice of hemodynamic collapse, pre-oxygenation becomes an art when the standard practice of non-rebreather (NRB) and nasal cannula is not able to overcome shunt physiology.3 When standard nasal cannula and NRB fail to achieve nitrogen washout and the patient remains hypoxemic, the emergency physician must consider using either noninvasive ventilation (NIV) or invasive ventilation to overcome the atelectatic alveoli.

Positive pressure ventilation (whether invasive or noninvasive) creates unfavorable conditions for the function of the right side of the heart because preload, or venous return, is impeded by high intrathoracic pressures.4 Using either high PEEP or a tension pneumothorax as an example, elevated intrathoracic pressure prevents the pressure head of the vena cava from flowing into the right atrium. Furthermore, PEEP at lung volumes above functional residual capacity creates higher pulmonary vascular resistance, increasing the pressure against which the right ventricle ejects.5 Though many factors influence the effects of noninvasive or invasive on the pulmonary vascular resistance, the general effect is increased resistance.

In contrast, the left heart may benefit from the elevated intrathoracic pressure. Left ventricular wall stress is lessened with increased intrathoracic pressure. Additionally, the pressure differential of the thorax in comparison to the lesser pressure of the systemic circulation creates a decreased afterload for the left heart upon which to eject.5 The physiologic effects of positive pressure in the trauma patient cannot be overlooked.


With multiple life-saving resuscitative measures ongoing at once, it is unclear to what extent the ACLS and ATLS paradigms should factor into decision-making, particularly when the patient loses pulses. The topic of chest compressions in the setting of traumatic arrest does not have robust data to support it. Though conducted with animal data, one study showed that traumatic mechanisms of arrest (specifically, hypovolemia and cardiac tamponade) do not benefit from external chest compressions. Arterial pressure transducers in bleeding baboons showed that diastolic blood pressures (ie, the pressure perfusing the myocardium) dropped after starting external chest compressions. Conversely, a medically-induced (ie, barbiturate-induced) cardiac arrest benefited from external chest compressions with an augmentation of both the systolic and diastolic arterial pressure tracings.12

Using end-tidal CO2 outcomes as a proxy for resuscitation, a 2016 study by the University of Maryland's Shock Trauma Center showed no difference between open vs. closed chest compressions. Though there is an obvious effect on end-tidal CO2 when an open chest is only ventilating one lung, the current data on whether closed chest compressions offer benefit in trauma is unclear. Another recent study looked at the utility of transthoracic echocardiography to prognosticate traumatic cardiac arrest. They found that lack of pericardial effusion or lack of cardiac motion on echo could obviate the need to proceed with resuscitative thoracotomy for open compressions and hemorrhage control.14


The trauma patient in severe shock has multifaceted physiologic derangements. Life-saving interventions often perturb hemodynamics in ways that work simultaneously with and against resuscitative goals. Given the lack of randomized, prospective data on the critically ill trauma patient, the physiologic data and a deeper understanding of heart-lung interactions are the best tools we have in the trauma bay.


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  2. Burlew CC, Moore EE, Moore FA, et al. Western Trauma Association critical decisions in trauma: resuscitative thoracotomy. J Trauma Acute Care Surg. 2012;73(6):1359-1363.

  3. Hayes-bradley C, Lewis A, Burns B, Miller M. Efficacy of Nasal Cannula Oxygen as a Preoxygenation Adjunct in Emergency Airway Management. Ann Emerg Med. 2016;68(2):174-180.

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  5. Luecke T, Pelosi P. Clinical review: Positive end-expiratory pressure and cardiac output. Crit Care. 2005;9(6):607-621.

  6. Upchurch CP, Grijalva CG, Russ S, et al. Comparison of Etomidate and Ketamine for Induction During Rapid Sequence Intubation of Adult Trauma Patients. Ann Emerg Med. 2017;69(1):24-33.e2.

  7. Zeiler FA, Teitelbaum J, West M, Gillman LM. The ketamine effect on intracranial pressure in nontraumatic neurological illness. J Crit Care. 2014;29(6):1096-1106.

  8. Cohen L, Athaide V, Wickham ME, Doyle-waters MM, Rose NG, Hohl CM. The effect of ketamine on intracranial and cerebral perfusion pressure and health outcomes: a systematic review. Ann Emerg Med. 2015;65(1):43-51.e2.

  9. Zsigmond EK, Kelsch RC, Kothary SP. Rise in plasma free-norepinephrine during anesthetic induction with ketamine. Behav Neuropsychiatry. 1974;6(1-12):81-84.

  10. Sprung J, Schuetz SM, Stewart RW, Moravec CS. Effects of ketamine on the contractility of failing and nonfailing human heart muscles in vitro. Anesthesiology. 1998;88(5):1202-1210.

  11. Miller M, Kruit N, Heldreich C, et al. Hemodynamic Response After Rapid Sequence Induction With Ketamine in Out-of-Hospital Patients at Risk of Shock as Defined by the Shock Index. Ann Emerg Med. 2016;68(2):181-188.e2.

  12. Luna GK, Pavlin EG, Kirkman T, Copass MK, Rice CL. Hemodynamic effects of external cardiac massage in trauma shock. J Trauma. 1989;29(10):1430-1433.

  13. Bradley MJ, Bonds BW, Chang L, et al. Open chest cardiac massage offers no benefit over closed chest compressions in patients with traumatic cardiac arrest. J Trauma Acute Care Surg. 2016;81(5):849-854.

  14. Inaba K, Chouliaras K, Zakaluzny S, et al. FAST ultrasound examination as a predictor of outcomes after resuscitative thoracotomy: a prospective evaluation. Ann Surg. 2015;262(3):512-518.