TY - JOUR
T1 - ECG changes in experimental acute pulmonary hypertension with and without hypoxia
AU - Ahmad, Masood
AU - Blomqvist, C. Gunnar
AU - Mullins, Charles B.
N1 - Funding Information:
*From the Pauline and Adolph Weinberger Laboratory for Cardiopulmonary Research, Department of Internal Medicine, University of Texas Southwestern Medical School at Dallas, Dallas, Texas. This study was supported by grants from the NHLI (HL 14187 and HL 06296) and from NASA (NGR-012-151). tFellow in cardiology supported by NHLI training Grant HL 05812. **Established Investigator of the American Heart Association and Associate Professor of Medicine and Physiology, UTSMS. STeaching Scholar, American Heart Association and Associate Professor of Medicine and Chief of Clinical Cardiology, UTSMS. Reprint requests to: Charles B. Mullins, M.D., Cardiopulmonary --D-710, 5323 Harry Hines Boulevard, Dallas, Texas 75235.
PY - 1974
Y1 - 1974
N2 - Recent clinical studies of pulmonary embolism indicate that typical ECG changes of acute right ventricular overload become evident only with severe pulmonary hypertension. The present study was performed to determine whether less obvious yet consistent ECG changes are present during mild and moderate pulmonary hypertension and to what extent hypoxia modifies the ECG response. Three series of experiments were performed; each employed 6 dogs. The orthogonal ECG (McFee system) was recorded at 3 levels of pulmonary artery (PA) mean pressures: control, 20 and 40 mm Hg in closed-chest dogs with and without hypoxia. Mean arterial pO2 was 53 mm Hg in the hypoxic series. Pulmonary hypertension was induced by means of a PA balloon catheter. Right ventricular (RV) volumes were determined from biplane cineangiograms in a separate series. The ECG analysis was performed utilizing digital computer techniques. No significant ECG changes were produced by a mean PA pressure of 20 mm Hg despite a 17% increase in RV end-diastolic volume above control values. At 40 mm Hg and a 45% increase in RV volume, dogs in the series without hypoxia showed a small but significant posterior shift of the initial QRS vector. Hypoxic dogs demonstrated directionally similar but more prominent changes with significant posterior displacement of both early and late QRS vectors and posterior-superior ST displacement. Thus, this study confirmed clinical data suggesting that the ECG is an insensitive indicator of acute RV pressure overload. ECG changes present at high PA pressures were accentuated by hypoxia.
AB - Recent clinical studies of pulmonary embolism indicate that typical ECG changes of acute right ventricular overload become evident only with severe pulmonary hypertension. The present study was performed to determine whether less obvious yet consistent ECG changes are present during mild and moderate pulmonary hypertension and to what extent hypoxia modifies the ECG response. Three series of experiments were performed; each employed 6 dogs. The orthogonal ECG (McFee system) was recorded at 3 levels of pulmonary artery (PA) mean pressures: control, 20 and 40 mm Hg in closed-chest dogs with and without hypoxia. Mean arterial pO2 was 53 mm Hg in the hypoxic series. Pulmonary hypertension was induced by means of a PA balloon catheter. Right ventricular (RV) volumes were determined from biplane cineangiograms in a separate series. The ECG analysis was performed utilizing digital computer techniques. No significant ECG changes were produced by a mean PA pressure of 20 mm Hg despite a 17% increase in RV end-diastolic volume above control values. At 40 mm Hg and a 45% increase in RV volume, dogs in the series without hypoxia showed a small but significant posterior shift of the initial QRS vector. Hypoxic dogs demonstrated directionally similar but more prominent changes with significant posterior displacement of both early and late QRS vectors and posterior-superior ST displacement. Thus, this study confirmed clinical data suggesting that the ECG is an insensitive indicator of acute RV pressure overload. ECG changes present at high PA pressures were accentuated by hypoxia.
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U2 - 10.1016/S0022-0736(74)80019-1
DO - 10.1016/S0022-0736(74)80019-1
M3 - Article
C2 - 4822534
AN - SCOPUS:0015997462
SN - 0022-0736
VL - 7
SP - 109
EP - 114
JO - Journal of Electrocardiology
JF - Journal of Electrocardiology
IS - 2
ER -