- Email: [email protected]
The use of left ventricular cineangiographic volume and the first time derivative in the quantitation of left atrial function
ABSTRACTS
sion in the d-thyroxin group (8.13 f 0.064 g/mmz) when compared with the control group (6.16 -+ 0.30) (P < 0.05). In addition dp/dt at L,,, was increased from 25.2 + 1.4 (control) to 52.7 +- 5.7 g/mm2/sec (d-bhyroxin
treated) (P < 0.01). Thus d-thyroxin increases myocardial contractibi1it.y. Since this effect, occurs in the absence of an increased metabolic rate, d-thyroxin may have clinical application as a chronic inotropic agent.
The Use of Left Ventricular Cineangiographic Volume and the First Time Derivative in the Quantitation of Left Atrial Function KARL E. HAMMERMEISTER, Baltimore, Mary/and
MD and JAMES R. WARBASSE,
MD
The contribution of left atria1 contraction to left ventricular filling and mitral valve blood flow was examined quantitatively by calculation with a digital computer of instantaneous left ventricular volume and the first, time derivative (dv/dt) (which, during diastole, represents mitml valve flow). The increment in left ventricular volume contributed by atria1 systole (s~V), stroke volume, end-diastolic volume, and dv/dt were determined in 12 normal subjects and 5 patients with atria1 fibrillation. In the normal group atria1 systole increased left, ventricular volume by an averagd of 17.8 f 3.8 ml or 21.7 _t 4.6% of stroke volume (average end-diastolic volume = 132 f 22 ml). Mitral valve flow reached a maximum of 409 -t 102 ml/set early in d&stole, then fell to a low of 45 It 61 ml/set just before atrial systole; however, with atria.1 contraction,
the rate of mitral valve flow increased to 175 + 47 ml/set. To measure the passive filling of the left ventricle that occurs in the absence of atria1 systole but during the same diastolic time interval, left ventricular volume and dv/dt were measured in the group with atria1 fibrillation at the average time intervals determined for normal patients (i.e., a.trial contra.ction began 0.135 f 0.049 set before enddiastole). In atria1 fibrillation, nV was only 4.2 +- 4.4 ml (end-diastolic volume = 203 + 43 ml) or 3.7 + 3.8y0 of stroke volume. Mitral valve flow peaked at 572 +- 24 ml/set in early diastole, but was only 36 * 46 ml/set at a time corresponding t,o atria1 systole. These measurements indicate that. atria1 syst,ole contributed about 18% to cardiac output and increased mitral valve flow rate to 43% of the peak flow rate.
Mechanism of the Hepatojugular Reflux Test PAUL HAMOSH,
Washington,
MD and JAY N. COHN,
MD, FACC
D. C. return to the heart was maintained constant did not abolish the increase ‘in right atrial pressure following abdominal compression. Mechanical pressure on the heart by cephalad displacement of the diaphragm produced t(he hepatojugular reflux in the dog in heart failure with an open abdomen. Left ventricular circumference measured by a mercury-inrubber gauge increased during abdominal compression in the intact dog without change in LVEDP. In heart failure, however, left ventricular circumference was unchanged or actually decreased during abdominal compression while right atria1 pressure and LVEDP increased sharply. We conclude that the mechanism responsible for the hepatojugular reflux is compression or deformation of a distended, noncompliant ventricle by the rising diaphragm.
The hepatojugular reflux is a clinical sign frequently found in heart failure. An increase in right atria1 pressure during abdomina.1 compression is thought to be caused by inability of the ventricles to increase output to match an augmented venous return. In anesthetized intact dogs, abdominal compression did not produce elevation of right atrial pressure or left ventricular end-diastolic pressure (LVEDP). Heart failure was induced by a combination of volume overload. propranolol and pentobarbital infusion. The heart failure preparation responded to a#bdominal compression with a prompt increase in right atria1 pressure and LVEDP. Opening the chest did not significantly alter the response. Diversion of inferior vena caval flow t’o a reservoir from which venous
Myocardial Digoxin Binding: Relation to Hemodynamic Status and Serum Magnesium CARLOS E. HARRISON, Jr., MD, FACC/KHALIL and ARNOLD L. BROWN, Jr., MD Rochester, Minnesota
G. WAKIM,
Depletion of sodium or potassium alters binding of 3Hdigoxin to myocardium, presumably through affecting glycoside t,ransport by sarcoplasmic sodium and potassiumstimulated and magnesiumdependent adenosine triphospha-
100
MD
tase. Because other investigators have reported enha,nced toxicity of digitalis glycosides in magnesium-deficient states, we investigated the effect, of acute depletion of serum magnesium on myocardial binding of “H-digoxin. Accordingly, 25 dogs underwent Kiil hemodialysis; 16 were dia-
The American Journal of CARDIOLOGY
sion in the d-thyroxin group (8.13 f 0.064 g/mmz) when compared with the control group (6.16 -+ 0.30) (P < 0.05). In addition dp/dt at L,,, was increased from 25.2 + 1.4 (control) to 52.7 +- 5.7 g/mm2/sec (d-bhyroxin
treated) (P < 0.01). Thus d-thyroxin increases myocardial contractibi1it.y. Since this effect, occurs in the absence of an increased metabolic rate, d-thyroxin may have clinical application as a chronic inotropic agent.
The Use of Left Ventricular Cineangiographic Volume and the First Time Derivative in the Quantitation of Left Atrial Function KARL E. HAMMERMEISTER, Baltimore, Mary/and
MD and JAMES R. WARBASSE,
MD
The contribution of left atria1 contraction to left ventricular filling and mitral valve blood flow was examined quantitatively by calculation with a digital computer of instantaneous left ventricular volume and the first, time derivative (dv/dt) (which, during diastole, represents mitml valve flow). The increment in left ventricular volume contributed by atria1 systole (s~V), stroke volume, end-diastolic volume, and dv/dt were determined in 12 normal subjects and 5 patients with atria1 fibrillation. In the normal group atria1 systole increased left, ventricular volume by an averagd of 17.8 f 3.8 ml or 21.7 _t 4.6% of stroke volume (average end-diastolic volume = 132 f 22 ml). Mitral valve flow reached a maximum of 409 -t 102 ml/set early in d&stole, then fell to a low of 45 It 61 ml/set just before atrial systole; however, with atria.1 contraction,
the rate of mitral valve flow increased to 175 + 47 ml/set. To measure the passive filling of the left ventricle that occurs in the absence of atria1 systole but during the same diastolic time interval, left ventricular volume and dv/dt were measured in the group with atria1 fibrillation at the average time intervals determined for normal patients (i.e., a.trial contra.ction began 0.135 f 0.049 set before enddiastole). In atria1 fibrillation, nV was only 4.2 +- 4.4 ml (end-diastolic volume = 203 + 43 ml) or 3.7 + 3.8y0 of stroke volume. Mitral valve flow peaked at 572 +- 24 ml/set in early diastole, but was only 36 * 46 ml/set at a time corresponding t,o atria1 systole. These measurements indicate that. atria1 syst,ole contributed about 18% to cardiac output and increased mitral valve flow rate to 43% of the peak flow rate.
Mechanism of the Hepatojugular Reflux Test PAUL HAMOSH,
Washington,
MD and JAY N. COHN,
MD, FACC
D. C. return to the heart was maintained constant did not abolish the increase ‘in right atrial pressure following abdominal compression. Mechanical pressure on the heart by cephalad displacement of the diaphragm produced t(he hepatojugular reflux in the dog in heart failure with an open abdomen. Left ventricular circumference measured by a mercury-inrubber gauge increased during abdominal compression in the intact dog without change in LVEDP. In heart failure, however, left ventricular circumference was unchanged or actually decreased during abdominal compression while right atria1 pressure and LVEDP increased sharply. We conclude that the mechanism responsible for the hepatojugular reflux is compression or deformation of a distended, noncompliant ventricle by the rising diaphragm.
The hepatojugular reflux is a clinical sign frequently found in heart failure. An increase in right atria1 pressure during abdomina.1 compression is thought to be caused by inability of the ventricles to increase output to match an augmented venous return. In anesthetized intact dogs, abdominal compression did not produce elevation of right atrial pressure or left ventricular end-diastolic pressure (LVEDP). Heart failure was induced by a combination of volume overload. propranolol and pentobarbital infusion. The heart failure preparation responded to a#bdominal compression with a prompt increase in right atria1 pressure and LVEDP. Opening the chest did not significantly alter the response. Diversion of inferior vena caval flow t’o a reservoir from which venous
Myocardial Digoxin Binding: Relation to Hemodynamic Status and Serum Magnesium CARLOS E. HARRISON, Jr., MD, FACC/KHALIL and ARNOLD L. BROWN, Jr., MD Rochester, Minnesota
G. WAKIM,
Depletion of sodium or potassium alters binding of 3Hdigoxin to myocardium, presumably through affecting glycoside t,ransport by sarcoplasmic sodium and potassiumstimulated and magnesiumdependent adenosine triphospha-
100
MD
tase. Because other investigators have reported enha,nced toxicity of digitalis glycosides in magnesium-deficient states, we investigated the effect, of acute depletion of serum magnesium on myocardial binding of “H-digoxin. Accordingly, 25 dogs underwent Kiil hemodialysis; 16 were dia-
The American Journal of CARDIOLOGY