Biomedical Engineering Reference
In-Depth Information
ity, and epileptiform discharges [56-61]. Figure 7.6 shows example traces of EEG
signals during various phases of the experiment. Figure 7.6 (top) shows an EEG dur-
ing hypothermic recovery, whereas Figure 7.6 (bottom) shows an EEG during
normothermic recovery. First of all, a very distinct evolution of the EEG waveforms
after CA is evident, beginning with an isoelectric period, followed by the period with
spikes and burst suppression, and continuous activity in the subsequent phases. The
difference between hypothermic and normothermic EEG is not so obvious by visual
examination alone. This is why a more objective quantitative, or qEEG, approach is
needed to provide a measurable, serial analysis that follows the trends in the signal
evolution.
7.4.1 Experimental Model of CA, Resuscitation, and Neurological Evaluation
We have developed a CA animal model using the rat. This model produces gradu-
ated levels of brain injury by controlling the duration of asphyxial CA. In this model,
different physiological parameters, short-term and long-term neurobehavioral out-
comes, EEG recovery, and postmortem histological results are measured [9, 53,
62-65]. Briefly, rats are endotracheally intubated and mechanically ventilated at 50
breaths per minute (Harvard Apparatus model 683, South Natick, Massachusetts)
with 1.0% Halothane in N 2 /O 2 (50%/50%). Ventilation is adjusted to maintain
physiological pH, pO 2 , and pCO 2 . A body temperature of 37.0
0.5°C is maintained
throughout the experiment. Venous and arterial catheters are inserted into the femo-
ral vessels to continuously monitor mean arterial pressure (MAP), intermittently
sample arterial blood gas (ABG), and administer fluid and drugs. After 5 minutes of
baseline recording, vecuronium 2 mg/kg is infused and the inhaled anesthetic is dis-
continued for 5 minutes to reduce residual effects of the anesthetics on the EEG sig-
nals [8]. No sedative or anesthetic agents are subsequently administered throughout
the remainder of the experiment to avoid confounding effects on EEGs [66]. CA is
initiated via asphyxia by cessation of mechanical ventilation after neuromuscular
blockade for a period of 7 minutes. CA is defined by pulse pressure
±
10 mm Hg and
asystole. Cardiopulmonary resuscitation (CPR) is performed with resumption of
ventilation and oxygenation (100% FIO 2 ), infusion of epinephrine (0.005 mg/kg),
NaHCO 3 (1 mmol/kg), and sternal chest compressions (200/min) until ROSC with
<
Hypothermia
I II
III
IV
V
IQ
VI
VII
VIII
1
2
4
12
24
48
72
Hour
Normothermia
I II
III
IV
V
VI
VII
VIII
IQ
IQ
2 4 12 24 48 72 Hour
Figure 7.6 IQ for hypothermia and normothermia over 72-hour period. The various phases of the
experiment are as follows: I: beginning of the experiment, II: cardiac arrest and resuscitation, III: early
recovery phase, IV: late recovery phase, V-VIII: intermittent recordings during the 72-hour recovery
period. ( From: [64]. © 2006 Elsevier B. V. Reprinted with permission.)
1
 
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