(Stroke. 1996;27:140-142.)
© 1996 American Heart Association, Inc.
Articles |
Influence of the Intra-Aortic Balloon Pump on the Transcranial Doppler Flow Pattern in a Brain-dead Patient
From the Critical Care Unit (J. van der N.) and the Department of Anaesthesia (A.J.B.), St Michael's Hospital, Toronto, Canada.
Correspondence to J. van der Naalt, Department of Neurology, University Hospital Groningen, PO Box 30.001, 9700 RB Groningen, Netherlands.
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Abstract |
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Background Confirmation of clinical brain death with transcranial Doppler (TCD) has been described. With the introduction of mechanical assist devices, it is important to know how these devices influence TCD measurements.
Case Description A patient who fulfilled the clinical criteria for brain death after cardiac arrest is described. An intra-aortic balloon pump (IABP) was necessary to maintain hemodynamic stability. A TCD examination was performed as an adjunct to the clinical diagnosis of brain death. A pattern of reversal of blood velocity typical of brain death was observed. With the IABP functioning, an increase of mean forward flow velocity without appreciable increase in the net flow velocities was seen. The results of the TCD measurements with the IABP functioning are not in concordance with values reported in the literature that confirm the clinical diagnosis of brain death.
Conclusions Application of TCD in a patient with an IABP could lead to false interpretation of results if the TCD mean velocities are not registered with the IABP on standby or if the net flow velocities are not calculated.
Key Words: brain death • intra-aortic balloon pump • ultrasonics
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Introduction |
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Since the introduction of transcranial Doppler ultrasound monitoring (TCD) in 1982 by Aaslid et al,1 a large number of reports have been published on its clinical use. Confirmation of the clinical diagnosis of brain death with TCD has been described.2 3 4 5
Advances in cardiac intensive care now make use of mechanical assist devices that not only influence extracranial but also intracranial blood flow,6 7 and it is important to know how these devices influence the intracranial blood flow velocity measurements.
In this case report, we describe the influence of the intra-aortic balloon pump (IABP) on cerebral blood flow in a patient who had fulfilled the clinical criteria for brain death as defined by the current Canadian guidelines.8
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Case Report |
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A 49-year-old man was admitted to the hospital with progressive unstable angina pectoris. Coronary angiography demonstrated severe, diffuse three-vessel coronary artery disease. Coronary artery bypass grafting was performed successfully, and the patient was transferred back to the intensive care unit. Within hours after the operation, the patient became hemodynamically unstable and suffered an asystolic cardiac arrest. After internal cardiac massage and resuscitation, an immediate reoperation revealed a thrombosed graft, which was replaced with a new vein graft. Postoperatively, the patient required inotropic support and an IABP to maintain hemodynamic stability. After cardiac arrest, the patient remained comatose with fixed and dilated pupils, areflexia, and no response to painful stimuli, although no sedation had been administered since surgery. Neurological examination 2 days after cardiac arrest showed that the patient fulfilled all the clinical criteria for brain death. The etiology was assumed to be severe global cerebral ischemia at the time of the cardiac arrest. A TCD examination of the cerebral circulation was performed as an adjunct to the clinical diagnosis of brain death.
During the TCD assessment, the patient had a sinus rhythm of 120 with a systolic pressure of 74 mm Hg, a diastolic pressure of 40 mm Hg, and a mean arterial blood pressure of 51 mm Hg. The augmented pressure from the IABP was 74 mm Hg. The cardiac index was 2.39. Arterial blood gas values were pH 7.41, PaCO2 32 mm Hg, and PaO2 68 mm Hg. The hemoglobin concentration was 88 g/L. The patient's temperature was 36.3°C. Adrenaline, noradrenaline, and dobutamine were being infused at high doses. The IABP was on 1:1 support. There were no gross metabolic abnormalities, and his neurological condition had not changed during the previous 24 hours.
TCD studies were performed with a 2-MHz pulsed Doppler probe
(Medasonics-CDS). Standard technique was used to insonate and identify
arteries (Aaslid et al1 ). Net flow velocities could be
determined by calculating the difference between the forward mean flow
(F) and the reversed mean flow (R) velocities, and the direction of
flow index (DFI) was calculated as DFI=1-(R/F). TCD
recordings of both left and right middle cerebral and internal
carotid arteries showed a characteristic pattern of flow reversal
during diastole (Fig 1
) as described in
brain death. The TCD pattern consisted of sharp, peaked
systolic forward flow with dissociation of
diastolic forward flow and reversal of flow in early and
late diastole. The mean flow velocity was 16 cm/s, with a
net flow velocity of 3.3 cm/s (DFI, 0.25). With the IABP on standby,
the mean flow decreased and especially the late diastolic
forward and reversed flow became less prominent. The mean flow velocity
decreased to 9 cm/s (Fig 2), with no appreciable change
in net flow velocity or DFI. This typical TCD pattern remained
unaltered during the measurement period of approximately 1 hour. Soon
afterward, the patient became cardiologically instable and died.
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Discussion |
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The IABP is used to reduce myocardial oxygen demand by augmenting coronary blood flow with afterload reduction of the left ventricle. An increase in mean arterial pressure is noted. The effect of the IABP on cerebral blood flow is less clear. In patients with various cardiac disorders, increased diastolic cerebral flow has been found, including five patients with IABPs.6 However, as the balloon was deflated, reversal of flow in late diastole has been reported without the development of neurological deficits.7
Normally, forward cerebral blood flow is detected in both systole and diastole with TCD. As intracranial pressure increases, characteristic changes in flow pattern are described.9 The typical TCD pattern in brain death consists of three stages: oscillating or biphasic flow, systolic spike flow, and no flow. With increasing intracranial pressure, diastolic flow ceases and systolic peaks become more sharp. As cerebral perfusion pressure approaches zero, there is collapse of blood vessels during diastole, and so absent or reversed diastolic flow can be demonstrated. This diastolic backflow can show various velocity profiles, depending on individual cerebral perfusion pressure fluctuations.10 When total luminal collapse occurs, a small degree of antegrade flow during systole is possible because of the compliance of the arteries. With increasing intracranial pressure, only systolic spikes are seen, and finally no flow is detected.
Not only the flow pattern but also the duration of the pattern is important. Transient reversal of flow in diastole in patients who subsequently survived is reported in patients in the first minutes after acute subarachnoid hemorrhage11 and in metabolically compromised comatose patients.12
In addition to the occurrence and duration of the oscillating flow pattern, the evaluation of net flow in brain death is important. Oscillatory flow does not necessarily imply net zero flow. Net flow velocities can be determined by calculating the difference between the positive and the negative mean velocity values. No recovery, however, has been observed in clinically brain-dead patients with a net flow velocity below 10 cm/s13 or a mean velocity below 10 cm/s and a net flow index below 0.8 during a 30-minute period.14 In our patient, the mean flow velocity was increased above 10 cm/s with the IABP functioning, whereas the mean flow velocity was below 10 cm/s with the IABP on standby. No appreciable difference in the net flow velocity or DFI was seen with the IABP on standby or functioning. The TCD patterns were unaltered during repeated measurements after approximately 1 hour.
In this case report, anterograde systolic and retrograde diastolic flow patterns characteristic for brain death were seen. Despite the assumed high intracranial pressure, the IABP could induce alterations in the pattern of blood flow velocity measurements, resulting in an increase of the mean flow velocity without a significant increase in net flow velocities. This means that in a patient with an IABP who is clinically brain-dead the IABP has to be on standby to allow a proper determination of the actual mean flow velocities. Net flow velocities have to be calculated. The typical TCD pattern has to be detectable for at least 30 minutes.
TCD is a noninvasive technique, permitting repeatable bedside assessment of cerebral blood flow velocity. However, when using TCD in a brain-dead patient, one should be aware of the influence of the IABP on cerebral blood flow velocity measurements to prevent incorrect interpretation of results in the application of a new technique to confirm the clinical diagnosis of brain death.
Received June 8, 1995; revision received October 17, 1995; accepted October 17, 1995.
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References |
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