ECG changes in experimental acute pulmonary hypertension with and without hypoxia

Masood Ahmad, C. Gunnar Blomqvist, Charles B. Mullins

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)109-114
Number of pages6
JournalJournal of Electrocardiology
Volume7
Issue number2
DOIs
StatePublished - 1974
Externally publishedYes

Fingerprint

Pulmonary Hypertension
Electrocardiography
Pulmonary Artery
Dogs
Pressure
Hypoxia
Ventricular Pressure
Pulmonary Embolism
Stroke Volume
Thorax
Catheters

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

ECG changes in experimental acute pulmonary hypertension with and without hypoxia. / Ahmad, Masood; Blomqvist, C. Gunnar; Mullins, Charles B.

In: Journal of Electrocardiology, Vol. 7, No. 2, 1974, p. 109-114.

Research output: Contribution to journalArticle

Ahmad, Masood ; Blomqvist, C. Gunnar ; Mullins, Charles B. / ECG changes in experimental acute pulmonary hypertension with and without hypoxia. In: Journal of Electrocardiology. 1974 ; Vol. 7, No. 2. pp. 109-114.
@article{18da9c7d835f404d8ed6c8600838ae61,
title = "ECG changes in experimental acute pulmonary hypertension with and without hypoxia",
abstract = "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.",
author = "Masood Ahmad and Blomqvist, {C. Gunnar} and Mullins, {Charles B.}",
year = "1974",
doi = "10.1016/S0022-0736(74)80019-1",
language = "English (US)",
volume = "7",
pages = "109--114",
journal = "Journal of Electrocardiology",
issn = "0022-0736",
publisher = "Churchill Livingstone",
number = "2",

}

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.

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.

UR - http://www.scopus.com/inward/record.url?scp=0015997462&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0015997462&partnerID=8YFLogxK

U2 - 10.1016/S0022-0736(74)80019-1

DO - 10.1016/S0022-0736(74)80019-1

M3 - Article

VL - 7

SP - 109

EP - 114

JO - Journal of Electrocardiology

JF - Journal of Electrocardiology

SN - 0022-0736

IS - 2

ER -