Hypocapnia reduces the T wave of the electrocardiogram in normal human subjects

Abstract

During voluntary hyperventilation in unanesthetized humans, hypocapnia causes coronary vasoconstriction and decreased oxygen (O 2) supply and availability to the heart. This can induce local epicardial coronary artery spasm in susceptible patients. Its diagnostic potential for detection of early heart disease is unclear. This is because such hypocapnia produces an inconsistent and irreproducible effect on electrocardiogram (ECG) in healthy subjects. To resolve this inconsistency, we have applied two new experimental techniques in normal, healthy subjects to measure the effects of hypocapnia on their ECG: mechanical hyperventilation and averaging of multiple ECG cycles. In 15 normal subjects, we show that hypocapnia (20 Ϯ 1 mmHg) significantly reduced mean T wave amplitude by 0.1 Ϯ 0.0 mV. Hypocapnia also increased mean heart rate by 4 beats/min without significantly altering blood pressure, ionized calcium or potassium levels, or the R wave or other features of the ECG. We therefore provide the first unequivocal demonstration that hypocapnia does consistently reduce T wave amplitude in normal, healthy subjects. coronary circulation; carbon dioxide; angina DURING VOLUNTARY HYPERVENTILATION in unanesthetized humans, hypocapnia causes coronary vasoconstriction and decreased oxygen (O 2 ) supply and availability to the heart. Thus cardiac catheterization studies show that voluntary hyperventilation [to partial pressure levels of carbon dioxide in arterial blood (Pa CO 2 ) of 20 mmHg] increases coronary vascular resistance by 17% (47), decreases coronary blood flow by 30% (47), and increases the affinity of hemoglobin for O 2 by 25% (35). During voluntary hyperventilation, hypocapnia can induce local epicardial coronary artery spasm in single or multiple vessels with associated ST displacement, both in susceptible patients with voluntary hyperventilation syndrome (but without symptoms of heart disease) (15, 24) and in the rare group of patients with Prinzmetal's variant angina (29,59).It is unclear whether this effect has any diagnostic potential for early coronary heart disease. This is because numerous studies in healthy subjects report that hypocapnia produces only inconsistent decreases in the amplitude of the ECG T wave that are not reproducible in every subject (5,6,8,16,20,22,30,49,54,58).Such inconsistency is not surprising because of the methodological difficulties inherent with voluntary hyperventilation in the variability of inflation volumes achieved and of the duration, level, and stability of hypocapnia. Variability in movement of the body surface (and its attached electrodes) relative to the heart with each inflation introduces a crucial artifact that alone might explain this inconsistency. These difficulties are compounded by the lack of a standardized procedure for ECG analysis during hyperventilation. It is unclear precisely how many ECG complexes were measured, how they were selected, and what was their precise relationship to the inflation cycle (6,16,58,60).We have therefore applied two novel ap...

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“…We found similarly small or no such changes in the resting heart rate and blood pressure in previous studies with pre-oxygenation and hypocapnia. 16−18,20 …”

“…We maintained hypocapnia at the mean PetCO 2 level of 20 ± 0 mmHg (the lowest level of hypocapnia that can be safely induced that causes paraesthesiae without causing hypocapnic tetany). 16,20,22,23 After 15 min of hypocapnia, mechanical hyperventilation was switched off and patients were instructed to inhale 60% oxygen maximally, exhale maximally, inhale maximally and then breath-hold (Table 2, order 4). Only at the end of the day were patients told how long they had breath-held in each session.…”

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“…While this disparity may tend to contradict a major role of lung stretch receptors, two factors may explain these results. First, a recent paper by Rutherford et al (40) proposes an additional tachy-cardic effect due to hypocapnic coronary vasoconstriction. Second, blunting of the chemosensory response to hypoxia during hypocapnia could be expected to result in a decreased reflex bradycardia; therefore a smaller V E may act to withdraw parasympathetic tone and cause HR to rise to the same extent as during isocapnia.…”

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