Volumes and Compliances Measured Simultaneously in the Right and Left Ventricles of the Dog

Laks, Michael M.; Garner, Daniel; Swan, H. J. C.

doi:10.1161/01.res.20.5.565

Cited by 156 publications

(67 citation statements)

References 9 publications

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“…The time required for determination of each P-V relation was less than 30 sec. Total study time from removal of the heart to completion was less than 40 min, thus avoiding changes in wall stiffness secondary to rigor mortis (10)(11). At the completion of study, the right ventricle, atria, and great vessels were trimmed away and the LV was weighed to the nearest gram.…”

mentioning

confidence: 99%

Early Increase in Left Ventricular Compliance after Myocardial Infarction

Forrester¹,

Diamond²,

Parmley³

et al. 1972

J. Clin. Invest.

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160

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A B S T R A C T The left ventricular (LV) pressurevolume (P-V) relationship is a resultant of several determinants, including initial ventricular volume, geometry, and wall stiffness. A quantitative index of one of these determinants, LV wall stiffness, was developed from a mathematical analysis of the isolated P-V relationship. Since this relationship was exponential, stiffness (dP/dV) could be expressed by the equation dP/dV = aP + b, where a and b are constants. The a constant, termed the passive elastic modulus, was independent of both pressure and volume, was modified only slightly by changes in geometry, and thus was primarily affected by changes in wall stiffness. LV wall stiffness was assessed by determination of the passive elastic modulus in eight normal canine hearts and in five hearts 1 hr after acute myocardial infarction. The value of the passive elastic modulus for the normal canine LV was found to be 0.099 ±0.006 cc'. In the five infarcted hearts there was a modest, but statistically insignificant, shift of the P-V curves from control, such that for the same pressure the infarcted hearts contained greater volume. However, the passive elastic modulus decreased 41% to 0.057 +0.006 cc' (P < 0.001). Thus, although LV wall stiffness may increase later in the course of myocardial infarction, it is concluded that it was significantly decreased 1 hr after infarction. Calculation of the passive elastic modulus provided a sensitive means of detecting such changes, whereas P-V curves alone were generally insensitive.Abstract presented at 20th Annual Scientific Session,

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mentioning

confidence: 99%

Early Increase in Left Ventricular Compliance after Myocardial Infarction

Forrester¹,

Diamond²,

Parmley³

et al. 1972

J. Clin. Invest.

Self Cite

160

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“…After reversal of the disease process, left ventricular end-diastolic pressure returned to normal, and in one animal a marked enhancement of the Starling ventricular function curve was demonstrated. However, increases in right ventricular filling within the physiologic range have been shown to shift the pressure-volume curve of the left ventricle so that a given left ventricular volume is associated with a higher left ventricular pressure.7 8 It is thus possible that the elevated left ventricular pressures in right heart failure may simply reflect a change in the pressure-volume characteristics of the left ventricle, rather than a depression of left ventricular contractility.…”

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confidence: 99%

Effects of Chronic Right Ventricular Volume and Pressure Loading on Left Ventricular Performance

et al. 1971

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SUMMARYThe effects of chronic right ventricular (RV) distension on left ventricular (LV) funiction were assessed in dogs 3 weeks after pressure and volume loading of the RV lhad been produced by the emplacement of a constricting band around the pulmonary artery and the creation of tricuspid insufficiency. This resulted in ascites, RV hypertrophy and dilatation, an increase in RV end-diastolic pressure (EDP), and a reduction of RV and LV norepinephrine concentrations. Peak LV pressure, wall stress, and dp/dt were measured during isovolumic beats at LVEDP's of 1 to 20 mm Hg, and comparisons at matched EDP's were made among the normal, sham-operated, and RV stressed dogs. Under these circumstances, LV function appeared to be depressed appreciably. The effects of RV volume loading on the pressure-volume curve of the LV in the potassium-arrested heart were assessed in a separate group of dogs. The pressure-volume curve of the LV was shifted so that any given LV volume was associated with a higher LV pressure. Thus, when peak pressure and wall stress were related to LV end-diastolic volume rather than to LVEDP, the relationship did not appear to differ from normal; peak dp/dt and peak VCE, however, remained depressed. This depression may represent a decrease in LV contractility consequent to the chronic RV stress or may reflect alterations in LV geometry. Thus, when the RV is subjected to a chronic flow and pressure load, assessment of LV function may be unreliable when indices of contractility are employed that require measurements of LVEDP.

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“…1). This entire procedure was completed in 45 min or less to avoid postmortem compliance changes which may occur beyond this time interval in normal hearts (13), as well as in hearts with infarction.1 After the compliance study the left ventricle was excised and weighed. Volume data for the compliance curves were normalized to a ventricular weight of 100 g.…”

Section: Methodsmentioning

confidence: 99%

Experimental myocardial infarction

Hood¹,

Bianco²,

Kumar³

et al. 1970

J. Clin. Invest.

169

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A B S T R A C T Compliance of the infarcted left ventricle was studied in dogs 3-5 days after occlusion of the left anterior descending coronary artery. Compliance was assessed from postmortem pressure-volume curves and from pressure-length measurements (mercury-in-silastic segment length gauges) made both in vivo and postmortem. Postmortem pressure-volume curves showed reduced compliance compared to sham-operated animals. Postmortem pressure-length curves of infarcted and adjacent normal myocardium indicated that the diminished total compliance could be attributed to an increase in stiffness of the infarcted area. This was confirmed by in vivo end-diastolic pressure-length changes produced by transient aortic occlusion. The infarcted area was akinetic, showing neither contraction nor aneurysmal bulging. In addition, anesthetized dogs with infarcts, when compared with sham-operated animals, had similar left ventricular end-diastolic volumes (indicator dilution method), but higher left ventricular enddiastolic pressures. Taken with previous observations, which show that systolic aneurysmal bulging is uniformly present at the onset of ischemia, these results indicate that stiffening of the ischemic myocardium occurs during the first 5 days after infarction, and show that elevation of left ventricular filling pressure does not necessarily signify ventricular dilatation. The results also suggest a mechanism whereby ventricular performance may improve during recovery from acute myocardial infarction.

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Volumes and Compliances Measured Simultaneously in the Right and Left Ventricles of the Dog

Cited by 156 publications

References 9 publications

Early Increase in Left Ventricular Compliance after Myocardial Infarction

Early Increase in Left Ventricular Compliance after Myocardial Infarction

Effects of Chronic Right Ventricular Volume and Pressure Loading on Left Ventricular Performance

Experimental myocardial infarction

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