Keywords
Autotriggering - cardiogenic oscillation - ventilator
Spurious auto-triggering of ventilator can create confusion in mechanical ventilatory
management of patients and confounds the diagnosis of brain death.
We describe a 35-year-old man with multiple gunshot injuries to abdomen, cervical
spine and thigh was brought to hospital after many hours of critical delay. The patient
had a cardiac arrest while on the way from another hospital. On arrival in emergency
department, trachea was intubated and immediate fluid resuscitation measures were
taken. Focused Assessment with Sonography in Trauma (FAST) ultrasound was positive
for blood; emergency laparotomy was done.
Patient was shifted to Intensive Care Unit (ICU) with Glasgow Coma Score (GCS) of
E1VTM1, pupils mid-dilated sluggishly reacting to light. The patient was ventilated using
Detex Ohmeda – Engstrom Care station on Synchronized Intermittent Mandatory Ventilation
(SIMV) mode with a tidal volume of 550 ml, positive end-expiratory pressure (PEEP)
of 6 cm H2O, pressure trigger sensitivity of -2 cm H2O, fraction of inspired concentration of oxygen (FiO2) at 0.5, ventilatory rate of 14 breaths/min and pressure support of 15 cm H2O.
Once the patient was stabilized, we decided to put him on continuous positive airway
pressure (CPAP) mode with a pressure support of 15 cms of H2O, trigger of − 0.25 cm H2O, FiO2 of 0.5 and PEEP of 5 cm H2O on Day 3. Patient was maintaining gases on this mode with respiratory rate of 25/min.
GCS of patient was still E1VTM1, pupils became fixed, dilated, coughing and gag reflex were absent but haemodynamic
parameters were stable. But with no brain stem reflexes, it was confounding as to
how he could maintain his respiratory drive? Then, apnoea test was performed that
was negative for respiratory drive. Ventilation was reinitiated on CPAP mode with
trigger of − 0.25 cm of H2O that again started triggering spontaneous breaths [Figure 1]. The trigger was increased to -1 cm H2O from -0.25 cms H2O. We observed that there was no triggering from the patient, only cardiogenic oscillations
were seen on airway pressure and flow waveform [Figure 2]. So, it was inferred that the ventilator was being auto-triggered due to cardiogenic
oscillations that was being misinterpreted by us as patient’s spontaneous effort.
Figure 1: The ventilator being triggered at a trigger sensitivity of -0.25 cms of H2O. All the breaths are being sensed as patients own spontaneous efforts
Figure 2: The ventilator not being triggered at a trigger sensitivity of -1.0 cms of H2O. Only cardiac oscillatory waves are being shown on airway pressure and flow waveforms.
Spontaneous Minute ventilation being shown is from the previous respiratory cycle
So, this case highlights the role of cardiogenic oscillation in auto-triggering the
ventilator and mimicking spontaneous breaths. Airway pressure and flow waveforms identified
this auto-trigerring. Raising the trigger sensitivity abolished this auto-trigerring
and was confirmed by apnoea test.
The most probable mechanism of cardiogenic oscillation induced auto-triggering is
change in volume of beating heart causing an intra-thoracic pressure change that moves
air in and out of the lungs. The movement of the heart may cause displacement with
consequent compression or expansion of the adjacent lung, resulting in movement of
gas at the airway.[1] The magnitude of the cardiogenic oscillation increases significantly with high cardiac
output, high filling pressures, large cardiothoracic ratio and low resistance of the
respiratory system.[2]
There are many clinical implications of auto-triggering caused by cardiogenic oscillation
in ICU. Patients appear to breath spontaneously that possibly leads to a mistaken
decision to wean them from mechanical ventilation, raising false hope of recovery
among patient’s family members. The determination of brain death may not be appropriate.
It will prolong the ICU stay and confound the brain-death determination, adding to
the financial costs of ICU care and delay in organ donation or may even abort this
opportunity.[3]
In conclusion, auto-triggering caused by cardiogenic oscillation must be anticipated.
Spontaneous breaths can be distinguish from auto-triggering by adjusting trigger sensitivity,
careful monitoring of the graphs on the ventilator display. Spontaneous breaths should
be eliminated by temporal hyperventilation or by test administration of sedatives/muscular
relaxants. Auto-triggering can be prevented by triggering sensitivity adjustment,
use of pressure triggering because it is usually less prone to noise than flow triggering
and changing to intermittent mandatory ventilation (IMV) mode.
