Original article
Confounding factors in brain death: Cardiogenic ventilator autotriggering and implications for organ transplantation

https://doi.org/10.1016/j.iccn.2012.03.003Get rights and content

Summary

Brain death is characterised by a flaccid, areflexic neurological examination; fixed, dilated and midpoint pupils and total absence of intrinsic respiratory drive. A non-reversible clinical state or brain lesion must also be identified. Integral to brain death diagnosis is loss of respiratory drive. Following terminal brainstem herniation, a cardiovascular hyperdynamic state often occurs. This hyperdynamic state causes cyclical volume displacement within the chest in phase with the cardiac cycle, causing oscillations in gas flow patterns and may be reflected in ventilator airway pressure and flow waveforms. When these flow/pressure waveform oscillations meet or exceed ventilator flow or pressure trigger sensitivity, ventilator breaths may be triggered in the total absence of intrinsic respiratory drive. In a patient with no apparent neurological function who is still triggering ventilator breaths, detailed analysis of ventilator pressure/flow waveforms in context with neurological assessment findings can identify cardiac autotriggering in a brain-dead patient. Undetected, cardiogenic ventilator autotriggering results in prolonged ICU stay and potential loss of transplantable organs. Collaborative practice and aggressive surveillance to determine loss of all neurologic function and evaluate possible autotriggering in this population is paramount and can minimise ICU stay, reduce costs of care, decrease family stress and facilitate recovery of transplantable organs.

Implications for clinical practice

  • Delay in brain death determination may prolong the ICU experience for patients’ families.

  • Possible confusion about brain death determination on the part of family members and clinicians’ consequent to cardiac autotriggering may raise false hope of recovery.

  • Time required for ICU care and brain death determination consequent to cardiac autotriggering add to financial costs of ICU care possibly exceeding £3000.00 per day.

  • Longer ICU management times for potential donors due to ventilator autotriggering increases risk of losing potentially transplantable organs consequent to refractory haemodynamic instability.

  • Apparent triggered ventilations consequent to cardiogenic oscillation may lead to the mistaken evaluation that terminal brainstem herniation has not occurred and delay appropriate, mechanism-specific care.

  • Time intervals between the terminal event of final brainstem death and final declaration of death by neurologic criteria are of particular concern. Formal brain death protocols may take as long as 6–24 hours, creating a delay between occurrence of final, terminal loss of brain/brainstem function and pronouncement of brain death.

Section snippets

Introduction: brain death: clinical findings and consequences

Brain death is characterised by loss of all function in the brain and brain stem including apnoea, loss of consciousness, unresponsive state, absent cough, gag, corneal, oculovestibular and oculocephalic reflexes. Unresponsiveness to assessment of cranial nerve function is also required for determination of death by neurologic criteria (Arbour, 2009, Arbour, 2005, Hills, 2010, Wijdicks et al., 2010, Wijdicks, 2001). Preceding brain death, patients are mechanically ventilated in critical care

Cardiogenic oscillation and cardiopulmonary physiology

A proposed mechanism for cardiogenic oscillation is outlined here. During systole and cardiac contraction, volume reduction of the heart and net volume outflow from the chest with stroke volume are counter-balanced with cyclical displacement (compression/expansion) of compliant lung tissue. This displacement of compliant, air-filled lung tissue may cause gas movement within the patient–ventilator system which may be sufficient to generate regular oscillations in ventilator pressure and flow

Discussion

Cardiogenic oscillation and ventilator autotriggering delayed or aborted brain death protocols as illustrated here. Clinical implications are multiple. First, delay in brain death determination and prolonging the ICU experience for patients’ families. Second, possible confusion about brain death determination on the part of family members and clinicians including raising false hope of recovery. Third, time required for ICU care and brain death determination add to financial costs of ICU care.

Conclusions

A patient with a catastrophic metabolic or structural brain injury with fixed, dilated and midpoint pupils and a flaccid, areflexic neurological examination may over breathe the ventilator set rate due to significant cardiogenic oscillation in ventilator pressure and flow waveforms. This may be more common than is realised and missed even by experienced clinicians. To identify this, the clinician must conduct a physical assessment to determine the presence or absence of intrinsic respiratory

Acknowledgement

I thank Patrick Cunningham, RN, CCRN for his assistance in initiating evaluation of the patient described in case two for ventilator autotriggering.

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