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Biomedical subjects

K Childs

Publications and source records attributed to K Childs.

4 recordsLinked to original sources
PubMed1992

Effects of physical stress on complete blood count and venous blood gas profile of individuals with sickle cell trait.

The association between sickle cell trait (SCT) and adverse effects of exercise has been controversial. While individuals with SCT are at higher risk of sudden death, the mechanism for this outcome remains to be elucidated. In order to shed light on this controversy, we have monitored venous blood count and blood gas parameter values in normal and SCT subjects during treadmill exercise. White and red blood cell counts and hemoglobin changed significantly over time in both the SCT and normal groups, with peak exercise values different from pre-exercise or post-exercise values. Red blood cell counts showed significant group-time interaction; increase in count during exercise was accentuated in SCT subjects. All blood gas parameters showed significant changes over time in both groups. O2 content was significantly higher in SCT than AA at all time intervals. O2 saturation, pO2 and CO binding to hemoglobin showed significant group-time interaction. Furthermore, O2 saturation for the combined groups was significantly greater at peak exercise and at rest than before exercise. It is possible that treadmill exercise causes microvascular shunting in SCT subjects, leading to a decrease in the peripheral utilization of oxygen.

Adult↗
PubMed1991

Differences in QRS configuration during unipolar pacing from adjacent sites: implications for the spatial resolution of pace-mapping.

To examine the spatial resolution of unipolar pace-mapping, 12 lead electrocardiograms (ECGs) recorded during pacing from each of the poles of a quadripolar catheter (5 mm interelectrode distance) were examined. Unipolar pacing was performed from each of the poles at late diastolic threshold, twice threshold and 10 mA at a cycle length of 500 ms. In 15 patients, pacing was performed at the right ventricular apex and in 14 at various left ventricular sites. Pacing from the distal catheter pole at threshold (index ECG) was used to simulate the site of origin of ventricular tachycardia, and all other ECGs were compared with the index ECG. Electrocardiograms were evaluated by two independent observers for 1) minor configuration differences (notch, new small component, change in the amplitude of individual components or change in QRS shape); 2) major differences in configuration (new large component, marked change in the amplitude of an existing component or two minor changes); and 3) peak to peak changes in amplitude. Minor differences in configuration were seen in a mean 2.4 +/- 1.9, 4.6 +/- 2.4 and 4.4 +/- 2.9 leads during pacing at 5, 10 and 15 mm from the distal electrode (index site). Major differences in configuration were seen in a mean of 0.3 +/- 0.5, 2.1 +/- 2.1 and 3.7 +/- 2.3 leads during pacing at 5, 10 and 15 mm from the index site. Differences in amplitude were seen in a mean of 3.1 +/- 2.2, 5.6 +/- 2.5 and 6.8 +/- 3.0 leads per ECG during pacing at 5, 10 and 15 mm from the index ECG pacing site, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1991

Monophasic action potential duration during programmed electrical stimulation.

UNLABELLED: To examine changes in monophasic action potential duration (APD) with a pacing protocol similar to that used during electrophysiological testing, action potentials were recorded in vivo from the left ventricular apical endocardium of 12 normal mongrel dogs. The atrioventricular node was ablated and the dogs paced from the anterior right ventricle at a baseline cycle length of 1000 ms between interventions. Mean steady-state APD (APDss) was 266 +/- 7 ms at a pacing cycle length (PCL) of 1000 ms. Two pacing protocols were used. The first consisted of a sudden acceleration in pacing from a cycle length of 1000 ms to one between 300 and 600 ms. The second consisted of an 8-beat train at a cycle length of 400 ms followed by a premature beat at a coupling interval of 280 ms followed by a pause. The inter-train pause varied between 1 second and 32 seconds. With a sudden acceleration in pacing rate, steady-state values for APD at the faster PCLs were significantly smaller than APDss at 1000 ms with a change to cycle lengths of 600 ms (247 +/- 29 ms), 500 ms (229 +/- 21 ms), 400 ms (220 +/- 17 ms), and 300 ms (203 +/- 31 ms; P less than 0.01 for all comparisons). The time constant of the change in APD was shorter at a PCL of 300 ms (14.9 +/- 0.8 s) than 600 ms (20.3 +/- 4.7 s; P less than 0.05). With drive train pacing and incorporating an inter-train pause, the percent drop in steady-state APD compared to APD for the first train ranged from 10.1% with a 1-second inter-train pause to 2.1% with a 32-second pause. The difference in APD between the first drive train and drive trains after at least 3 minutes of pacing when APD had stabilized was not significant for an inter-train pause exceeding 8 seconds. IN CONCLUSION: (1) with a sudden acceleration in pacing rate, endocardial APD in vivo decreases exponentially. The faster the new rate, the shorter the new steady-state APD and the shorter the time constant. (2) When pacing using an 8-beat drive train and an inter-train pause, there is a decremental shortening in APD for pause lengths shorter than 16 seconds. Thus, while performing programmed stimulation using a pause, a conditioning period of at least 2 minutes should be used prior to diastole scanning to allow APD to achieve a steady state.

Action Potentials↗