Apnea testing for the diagnosis of brain death.

Neurologische Universitätsklinik, Erlangen, Germany.
Acta Neurologica Scandinavica (Impact Factor: 2.47). 01/2006; 112(6):358-69. DOI: 10.1111/j.1600-0404.2005.00527.x
Source: PubMed

ABSTRACT A review is given on various methods, preconditions and pitfalls of apnea testing for the diagnosis of brain death.
An extensive medical data base search was implemented by information gathered from books and our own experience with more than 2000 apnea tests.
While testing for apnea (AT) is considered indispensable worldwide, recommendations and handling differ. Rather than relying on elapsed time, a specific target value for the partial arterial pressure of carbon dioxide (PaCO2) should be aimed at being the maximum physiological stimulus for respiration. Methodological points are elaborated upon in detail for apneic oxygenation and hypoventilation.
AT is an indispensable element of diagnosing brain death. Although with proper handling and adequate precautions AT is safe, it should be performed as a last resort. An international agreement on target values for the PaCO2 is desirable.

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    ABSTRACT: The apnea test (AT) is essential to confirming the diagnosis of brain death, but critical complications can occur if the AT is maintained over a long period. To minimize the AT period, we used end-tidal carbon dioxide (ETCO2) monitoring because ETCO2 is closely correlated with partial pressure of arterial carbon dioxide (PaCO2). The aim of the present study is to evaluate the usefulness of ETCO2 monitoring during apnea testing.
    Korean journal of anesthesiology. 09/2014; 67(3):186-92.
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    Journal of Taibah University Medical Sciences. 01/2013; 8(1):1–6.
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    ABSTRACT: The aim of this study was to elucidate the magnitude of variations in oxygenation indices and the pattern of hemodynamic changes in response to the net effect of tracheal apneic oxygenation (AO) with a view to define the safe time limit of its application. After obtaining Animal Research Ethics Committee approval, AO was applied in 12 piglets for 40 min. Arterial (a) and mixed venous (v) blood samples for oxygen (O2) and carbon dioxide (CO2) tension (PaO2/PvO2, PaCO2/PvCO2), O2 saturation (SaO2/SvO2), pHa, base excess (BEa), and bicarbonate (HCO3a) determination and for alveolar O2 tension (PAO2), PaO2/FiO2 and PaO2/PAO2 ratio, arterial-mixed venous O2 content (AVDO2), and O2 extraction ratio (O2ER) estimation were collected on anesthesia induction, 10, 20, 30, and 40 min during AO and 10 and 20 min after reconnection to the ventilator. Concomitant hemodynamic data were obtained. Besides PvO2 and PAO2, AO adversely influenced PaO2 (248-113 mmHg), PaCO2 (35-145 mmHg), PvCO2, PaO2/FiO2, and PaO2/PAO2 in a time-depended fashion, whereas SvO2, AVDO2, and O2ER were minimally affected. P(a - v)CO2 was reversed throughout AO. Acid-base status derangement, consisting of HCO3a elevation, BEa widening, and acidemia (pH 6.9) maximized 40 min after AO. During AO, heart rate, systemic and pulmonary circulation pressures, and cardiac output were progressively elevated, whereas systemic vascular resistance was reduced. All the studied parameters reverted almost to baseline within the 20-min period of ventilator reconnection. Tracheal AO for 40 min ensures acceptable blood oxygenation, promotes notable hypercapnic acidosis, and consequent transient hemodynamic alterations, which are almost completely reversible after reconnection to the ventilator.
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