Biomedical subjects

W P Santamore

Publications and source records attributed to W P Santamore.

At least 19 recordsLinked to original sources

PubMed1992

Virtual real-time digital processing of hemodynamic data.

At present, the majority of cardiac catheterization laboratories acquire and store hemodynamic data in analog form. To examine the possibility of performing complex analysis of digital data during the catheterization procedure, we examined whether virtual real-time digital (fast Fourier) analysis improves the accuracy of clinical data. We compared digital filtering of fluid manometry during the right heart catheterization with 10-Hz and 250-Hz analog filters. Using the simultaneously acquired micromanometry as the "gold standard," we found that analog filtering is associated with a greater error and time delay than digital filtering. This study demonstrates that digital hemodynamic data analysis performed during cardiac catheterization can improve the quality of data obtained during right heart catheterization, with the results available within seconds. More extensive use of computers in the cardiac catheterization laboratory may be useful for both clinical and research purposes.

Atrial Function, Right↗

PubMed1992

Computer simulation of the effects of ventricular interdependence on indices of left ventricular systolic function.

The influence of ventricular interdependence on cardiovascular function has been convincingly demonstrated. In the intact cardiovascular system ventricular interdependence is always present, and thus measures of cardiac function include the contribution of ventricular interdependence (VI). A cardiovascular system model is presented and used to discuss how VI affects selected indices of left ventricular (LV) systolic function. Indices of LV function studied were the ejection fraction, stroke work, peak time derivative of ventricular pressure (dP/dT) and the LV end-systolic pressure-volume relationship. The effects of right ventricular (RV) volume through systolic VI on these indices are conveniently studied by comparing the model responses to pulmonary artery (PA) and vena caval (VC) occlusions; both PA and VC occlusion reduce LV volume, but the RV volume is increased by PA but reduced by VC occlusions. Through systolic VI the increase in RV volume with PA occlusion shifted the LV end-systolic pressure-volume relationship to the left and thus affected measures of LV maximum elastance. The LV ejection fraction, peak dP/dT and stroke work were all augmented by the increase in RV volume associated with the PA occlusion. Experimental studies comparing the responses to PA and VC occlusions are in broad agreement with the results described here. Systolic VI also shifted the cardiac function curve, a global measure of cardiac function, to the left. The results thus suggest that commonly used indices of LV systolic function are dependent on RV function and do not solely reflect LV function.

Cardiac Volume↗

PubMed1992

Differential effects of positive end expiratory pressure and cardiac tamponade on left-right ventricular mechanical function in the dog.

OBJECTIVE: The aim was to examine the hypothesis that an increased coupling occurs between the ventricles during tamponade via a ventricular-pericardial-ventricular interaction, but that ventricular coupling would be unaltered or reduced with positive end expiratory pressure (PEEP). METHODS: An in situ arrested, canine heart preparation was used. Changes in left and right ventricular pressure (dPl, dPr) and volume (dVl, dVr) caused by increasing the volume of the other ventricle were measured at normal and at matched levels of raised pericardial pressures (Pp) caused by 20 cm H2O PEEP and by tamponade. RESULTS: With PEEP, the coupling between the ventricles was unaltered when compared to control. With tamponade, dPl/dPr, dVl/dPr, dPr/dPl, and dVr/dPl increased significantly (p less than 0.05) by 0.21 (SEM 0.03, unitless), 0.45(0.04) ml.mm Hg-1, 0.18(0.03), and 0.28(0.04) ml.mm Hg-1 respectively. CONCLUSIONS: Augmented ventricular interdependence occurs during tamponade but not with PEEP, which may help to explain the different haemodynamic patterns observed under these conditions.

Animals↗

PubMed1992

Positive end-expiratory pressure potentiates the severity of canine right ventricular ischemia-reperfusion injury.

Positive end-expiratory pressure (PEEP) increases right ventricular (RV) afterload and oxygen demands. However, whether increased RV oxygen demands with high levels of PEEP can potentiate the severity of RV ischemic damage is unknown. In 20 anesthetized, closed-chest dogs randomly assigned to 0 cmH2O PEEP (ZEEP; n = 10) or 15 cmH2O PEEP (PEEP; n = 10), RV blood flow (radioactive microspheres) and segmental shortening (ultrasonic crystals) were determined during 90 min ischemia and 120 min reperfusion while mean aortic pressure was maintained above 90 mmHg. The in vivo RV area at risk (gentian violet) and area of necrosis (triphenyltetrazolium chloride) were assessed. After application of 15 cmH2O PEEP, pulmonary vascular resistance increased by 75% (P less than 0.05). During ischemia, the RV rate-pressure product remained greater with PEEP (2,403 +/- 174 mmHg.beat.min-1) than with ZEEP (1,909 +/- 94 mmHg.beat.min-1; P less than 0.05), indicating higher oxygen demands with PEEP. The area at risk from ischemia relative to RV free wall tended to be greater with PEEP (68.5 +/- 2.4%) than with ZEEP (60.0 +/- 3.9%; P = 0.08), and collateral blood flow in this risk zone was significantly lower during ischemia with PEEP (9.0 +/- 1.7 ml.min-1 x 100 g-1) than with ZEEP (18.3 +/- 3.6 ml.min-1 x 100 g-1; P less than 0.05). Accordingly, PEEP extended RV necrosis in the area at risk from 21.8 +/- 5.3% (ZEEP) to 58.1 +/- 8.4% (PEEP; P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Platelet amplification of vasospasm.

Platelets may accentuate vasoconstriction in stenotic arteries capable of vasomotion. We examined the interaction of platelets, stenosis, and arterial vasoconstriction in normal and stenotic arteries with intact endothelium. Beagle carotid arteries (n = 38) were isolated, removed, and placed in an in vitro perfusion system. Platelet-rich plasma (PRP) or platelet-poor plasma (PPP) were perfused through the arteries under constant pressure (100 mmHg) and a fixed distal resistance. In intact arteries without a stenosis, angiotensin II (ANG II) decreased luminal diameter without altering flow during PRP perfusion. After creating an intraluminal stenosis, vasoconstriction produced by ANG II resulted in near total cessation of flow. During PRP perfusion, this effect was amplified, demonstrating suppression of flow at significantly (P less than 0.05) lower concentrations of ANG II (PRP, ED50 = 0.03 +/- 0.01 x 10(-8) M) compared with arteries perfused with PPP (PPP, ED50 = 2.7 +/- 0.8 x 10(-8) M). This accentuated vasoconstrictor response in the presence of platelets was not blocked by SKF 96148 (a thromboxane A2 antagonist) but was abolished by ketanserin (a 5-HT2-serotonergic blocker). This increased sensitivity to vasoconstriction was not due to significant platelet plugging inasmuch as no cyclic flow reductions were observed, aspirin (acetylsalicylic acid) did not prevent this accentuated vasoconstrictor response, and adventitial administration of nitroglycerin restored flow to baseline levels. These studies illustrate that 1) platelets amplify the effect of vasoconstrictors in stenotic arteries, 2) this amplification of vasoconstriction is primarily due to platelet release of serotonin, and 3) the amplification occurs in the absence of significant platelet plugging and endothelial damage.

Animals↗

PubMed1992

Importance of intraluminal pressure on hemodynamics and vasoconstriction responses of stenotic arteries.

BACKGROUND: Clinical and morphological studies clearly indicate that most human coronary artery stenoses are capable of vasomotion. Variable ischemic thresholds, ischemia unrelated to work load, and variant angina further show the presence and importance of vasoconstriction in coronary artery stenosis. Despite the importance of vasoconstriction, the effect of intraluminal pressure on the hemodynamic response to vasoconstrictors has not yet been examined. Intraluminal pressure is a primary determinant of vessel size and the force opposing vasoconstriction. Accordingly, we examined the effects of intraluminal pressure on the hemodynamic response to norepinephrine (NE)-induced vasoconstriction. METHODS AND RESULTS: In canine carotid arteries perfused with physiological salt solution, pressures at the proximal and distal ends of the artery, as well as flow, were continuously recorded. We altered intraluminal pressure using three diverse interventions: changes in perfusion pressure, decreasing distal resistance, and collaterals. In normal, nonstenotic arteries, NE decreased the external vessel diameter but did not reduce flow. Perfusion pressure changes did not affect the ED50 of the NE-diameter relation. After an intraluminal stenosis was created, NE-induced constriction decreased flow. The threshold concentration of NE needed to decrease flow decreased as the perfusion pressure decreased (38.5 +/- 17.9, 2.3 +/- 1.3, and 0.12 +/- 0.1 x 10(-7) mol/l for 125, 100, and 75 mm Hg of perfusion pressure, respectively; p less than 0.05). Lowering distal resistance decreased stenotic pressure and decreased the threshold NE concentration from 5.4 +/- 1.9 to 0.34 +/- 0.2 x 10(-7) mol/l (p less than 0.05), and increasing stenotic pressure with collaterals increased the threshold NE concentration from 2.6 +/- 1.4 to 7.5 +/- 4.6 x 10(-7) mol/l (p less than 0.05). CONCLUSIONS: In stenotic arteries, interventions that lowered the intraluminal pressure decreased the threshold NE concentration needed to decrease flow, and interventions that raised the intraluminal pressure increased the threshold NE concentration. This pressure-dependent constrictor sensitivity affects the vasomotor tone and is important in pathophysiology of ischemia occurring with hypotension (low perfusion pressure) or mild increase in myocardial oxygen demand (low distal arteriolar resistance). The results also suggest that collaterals, by maintaining stenotic pressure, could decrease the constrictor sensitivity and prevent ischemia.

Animals↗

PubMed1992

Dynamic cardiomyoplasty acutely impairs left ventricular diastolic function.

In patients with congestive heart failure, medical treatment has a high rate of mortality and morbidity, and transplantation is limited by the availability of donor hearts. Dynamic cardiomyoplasty is being investigated as surgical therapy to improve left ventricular function in these patients. To evaluate the early postoperative effects of this procedure on left ventricular diastolic function, we studied seven dogs through the use of sonomicrometry and micromanometry in a canine model of dynamic cardiomyoplasty. Left ventricular diastolic parameters were determined before wrapping the latissimus dorsi muscle (baseline), after latissimus dorsi muscle wrap but without stimulation, and with synchronous left ventricular contraction-latissimus dorsi muscle stimulation. End-diastolic pressure was increased in both conditions after latissimus dorsi muscle wrap (without stimulation, 5 +/- 1; with stimulation, 6 +/- 2 mm Hg; p < 0.05) compared with baseline (3 +/- 2 mm Hg). The peak rate of diastolic pressure decay was greater at baseline (1560 +/- 370 mm Hg/sec) than after latissimus dorsi muscle wrap, both without (1260 +/- 330 mm Hg/sec, p < 0.01) and with (1120 +/- 420 mm Hg/sec, p < 0.01) stimulation. The constant of pressure decay was prolonged both without (53 +/- 10 seconds, p < 0.05) and with (62 +/- 11 seconds, p < 0.01) latissimus dorsi muscle stimulation compared with the baseline (38 +/- 5 seconds). Compared with baseline (0.2 +/- 0.2 cm-2), the constant of passive chamber stiffness increased after the latissimus dorsi muscle was wrapped around the heart (1.6 +/- 0.7 cm-2, p < 0.05) and with stimulation (2.1 +/- 1.0 cm-2, p < 0.01). The maximal diastolic filling rate (baseline, 18.1 +/- 6.7; without stimulation, 16.6 +/- 8.9; with stimulation, 16.6 +/- 4.1 cm2/sec, not significant) and end-diastolic short-axis area (baseline, 7.3 +/- 2.3; without stimulation, 7.4 +/- 2.1; with stimulation, 7.5 +/- 2.3 cm2, not significant) were similar among the three conditions. The latissimus dorsi muscle wrap prolonged relaxation and increased left ventricular passive stiffness. Synchronous latissimus dorsi muscle stimulation with left ventricular contraction did not improve diastolic function in this model. The results suggest that in the early postoperative period, dynamic cardiomyoplasty impairs diastolic function.

Animals↗

PubMed1992

Effects of dynamic cardiomyoplasty on indices of left ventricular systolic and diastolic function in a canine model of chronic heart failure.

The effects of cardiomyoplasty were evaluated with multiple-gated equilibrium radionuclide angiocardiography and catheterization in a canine model of chronic heart failure. Doxorubicin was administered to 12 dogs at a dose of 1 mg/kg/wk intravenously for 10 weeks. Left ventricular ejection fraction was reduced from a mean of 53.6% +/- 3.4% to 33.5% +/- 2.3% preoperatively. Two dogs died of presumed arrhythmia during this period. Cardiomyoplasty with the left latissimus dorsi muscle was performed on 10 dogs. The muscle was wrapped around both the left and right ventricles. Five dogs died of infection or arrhythmia after the operation. Postoperatively the muscle remained unstimulated for 2 weeks to allow adhesion to the heart. After this period, the latissimus dorsi muscle was conditioned by a progressive stimulation protocol. After the muscle was conditioned, multiple-gated equilibrium radionuclide angiocardiography studies showed that left ventricular global ejection fraction was 18.4% +/- 7.2% at 0 volts (nonstimulation), 26.2% +/- 3.7% at 5-volt stimulation (p less than 0.05), and 31.0% +/- 5.4% at 10-volt stimulation (p less than 0.05). Regional ejection fractions in low lateral, apical, and low septal regions at 5 volts and 10 volts were higher than those at 0 volts (p less than 0.05). Regional wall motion (percent radial shortening) of the low lateral region was higher than that during nonstimulation (p less than 0.05). Peak emptying rate was 2.07 +/- 0.95 end-diastolic counts per second at 0-volt, 3.10 +/- 0.67 at 5-volt, and 3.34 +/- 0.89 at 10-volt stimulation (p less than 0.05). Peak filling rate was 1.81 +/- 0.52 end-diastolic counts per second at 0-volt, 2.67 +/- 1.18 at 5-volt, and 3.11 +/- 0.65 at 10-volt stimulation (p less than 0.05). Cardiac catheterization data showed a nonsignificant increase in left ventricular rate of pressure rise with increasing voltage (1302 +/- 355 mm Hg/sec at 0 volts, 1450 +/- 413 mm Hg/sec at 5 volts, and 1568 +/- 455 mm Hg/sec at 10 volts). Left ventricular systolic pressures were unchanged. End-diastolic pressures decreased (11.2 +/- 1.48 mm Hg at 0 volts, 10.4 +/- 2.30 mm Hg at 5 volts, and 9.6 +/- 1.52 at 10 volts; p less than 0.05). These data show that cardiomyoplasty can improve indices of systolic and diastolic function in a canine model of chronic heart failure.

Animals↗

PubMed1991

Dynamics of coronary occlusion in the pathogenesis of myocardial infarction.

In most coronary artery stenoses in humans, lumen size decreases in response to acute vasoconstriction, reduced aortic pressure or passive collapse. Because the effects of vasoconstriction and plaque rupture with thrombus formation are additive, in some cases total cessation of flow may result from only minimal obstruction by thrombus. This hypothesis was investigated with use of a previously developed model of the coronary circulation in which the pressure drop across and flow through an arterial stenosis were determined by standard hemodynamic equations. The vessel wall was assumed to be composed of pliable and rigid sections, as is the case in most arterial stenoses in humans. The computer analysis was conducted for a rigid stenosis and for a dynamic stenosis in which proximal artery constriction and distal collapse were simulated. Plaque rupture with subsequent thrombus formation was simulated as a decrease in lumen area without effect on the arterial wall. Compared with a dynamic stenosis, a rigid stenosis required a significantly larger thrombus for vessel occlusion. Thrombus formation equal to the nonobstructed area of the lumen was required to occlude a rigid vessel; a 60% stenotic vessel required a 40% plaque rupture with thrombus formation for occlusion. However, for a dynamic stenosis, if vasoconstriction and passive collapse were simulated, small plaque ruptures led to vessel occlusion: a 60% stenotic vessel required only a 12% plaque rupture with thrombus formation for occlusion. This analysis indicates that even mild coronary lesions may be responsible for myocardial infarction, suggesting that vasomotion may be a very important element in the pathogenesis of most myocardial infarcts.

Computer Simulation↗

PubMed1991

Variable non-linearity in end systolic pressure-volume relationships results from interaction between end diastolic and developed pressure-volume relations.

OBJECTIVE: The aim was to determine the contributions of diastolic pressure to the shape of the relationship of total systolic left ventricular pressure with volume (pressure-volume relationship). STUDY DESIGN: The pressure-volume relationship was approximated (by least squares fit) to a parabola P = aV2 + bV + C. Non-linearity was indicated by values "a" significantly different from zero. Negative values indicated concavity to the volume axis, positive values convexity to the volume axis. MATERIALS: Langendorff perfused rabbit hearts (n = 8) with intraventricular balloon were used. Balloon pressure was measured for varying balloon volumes. RESULTS: The total systolic pressure-volume relationship was concave towards the volume axis at 2.4 mM extracellular calcium ions concentrations ([Cae++]) a = -47.2 (SD 5.4), p less than 0.05. It was nearly linear at [Cae++] = 0.6 mM; a = -0.8(5.8), p greater than 0.05. It was convex at [Cae++] = 0.3 mM; a = 25.3(4.0), p less than 0.01. The diastolic pressure-volume relationship was always convex: a = 30.1(6.7), 33.5(7.6), 42.2(6.6) for [Cae++] = 2.4, 0.6, and 0.3 mM respectively. When these diastolic values were subtracted from the total pressures, pressure-volume curves for developed pressure were obtained which were always concave: a = -76.9(10.2), -33.5(3.7), -16.3(2.9) for [Cae++] = 2.4, 0.6, and 0.3 mM. CONCLUSIONS: The true systolic pressure-volume relationship of the left ventricle is not linear but concave to the volume axis. The slope is therefore variable and not an index of contractility. Apparently linearity or convexity is due to inappropriate addition of the diastolic pressure-volume properties.

Animals↗

PubMed1991

Importance of endothelial function in stenotic haemodynamic responses.

STUDY OBJECTIVE: The aim was to examine endothelium mediated flow dependence in a dynamic stenosis. DESIGN: The coronary circulation was modelled as a proximal compliant stenosis and a fixed distal resistance. Pressures and flow were calculated using standard haemodynamic equations. Within the stenosis, the vessel wall was composed of normal and rigid sections, and the normal section dilated proportionally with flow. From this theoretical analysis, three perfusion pressures (150, 100, and 75 mm Hg) and two distal resistances (high and low) were examined. MAIN RESULTS: In a stenotic artery (93% area reduction) with high flow dependence, decreasing distal resistance increased flow substantially. At 75 mm Hg perfusion pressure, flow increased from 40.8 to 81.6 ml.min-1. With moderate flow dependence, flow increases were attenuated. Without flow dependence, flow increases were smaller, and at low perfusion pressure, flow paradoxically decreased (39.0 to 0.0 ml.min-1) when distal resistance decreased. Vasoconstriction responses with and without flow dependence were analysed. In a stenotic artery, vasoconstrictors caused a concentration dependent decrease in flow. Without flow dependence, the flow dose-response curve was shifted to the left: a lower level of arterial vasoconstriction resulted in a greater flow decrease. CONCLUSIONS: The theoretical analysis shows significantly different flow responses to decreasing distal resistance and to vasoconstriction depending on endothelial function. Endothelial dysfunction may be important in the pathophysiology of angina pectoris.

Arterial Occlusive Diseases↗

PubMed1991

Comparative significance in systolic ventricular interaction.

STUDY OBJECTIVE: The aim was to measure the systolic coupling between the ventricles and to determine the relative importance of ventricular interaction in the pressure development of each ventricle. DESIGN: Acute studies were done in dogs to measure the changes in right and left ventricular pressures (dPr, dPl) caused by sudden changes in left ventricular pressure (dPl') with release of an aortic constriction, and sudden changes in right ventricular pressure (dPr') with release of a pulmonary artery constriction, respectively. The instantaneous cross talk gain [dPr/dPl' (Klr) or dPl/dPr' (Krl)] was calculated during the ejection phase. The potential systolic pressure generated by the contralateral ventricle was evaluated as the cross talk gain multiplied by the contralateral systolic developed pressure. EXPERIMENTAL MATERIAL: Studies were done in eight random source dogs (12-18 kg), anaesthetised with sodium pentobarbitone. MEASUREMENTS AND MAIN RESULTS: The maximal Klr was lower than the maximal Krl, at 0.09 (SD 0.05) v 0.25 (0.06), and the mean Klr also was lower than the mean Krl, at 0.04 (0.02) v 0.10 (0.03), p less than 0.05. The potential right ventricular pressures developed by the left ventricle [maximum 10.3(5.6), mean 4.8(2.7) mm Hg] were not significantly different from the potential left ventricular pressures developed by the right ventricle [maximum 8.8(2.7), mean 3.4(0.7) mm Hg]. However, the ratio between the potential transmitted pressure and the measured developed pressure was greater in the right ventricle [maximum 39.0(21.1), mean 17.8(8.9)%] than in the left ventricle [maximum 11.1(7.1)%, p less than 0.05; mean 3.9(1.5)%, p less than 0.01]. This suggests that about 20-40% of the right ventricular systolic pressure may result from the left ventricle and about 4-10% of the left ventricular systolic pressure may result from right ventricle. CONCLUSIONS: Although the pressure coupling was greater in right to left ventricular interaction, right ventricular pressure generation may be more dependent on the left ventricle. Systolic ventricular interaction may be more important for right ventricular systolic function. Further, the parameters of right ventricular systolic function currently used may be considerably affected by the left ventricle.

Animals↗

PubMed1991

Hemodynamic consequences of ventricular interaction as assessed by model analysis.

Because of close anatomic association, the pressure and volume in one ventricle can directly influence the pressure and volume in the opposite ventricle. To examine the importance of ventricular interdependence in controlling the circulation, we developed a computer model in which ventricular interdependence could be turned on and off. Left ventricular chamber contractility, as judged by maximal elastance (Emax), was enhanced on the order of 10% as a result of ventricular interaction, whereas right ventricular Emax was affected by as much as 60% under physiological conditions. With increases in systemic vascular resistance, ventricular interaction caused a smaller stroke volume (SV) decrease than with no interaction. For canine data (SV = 21.4 ml), doubling systemic vascular resistance decreased SV by 3.7 without ventricular interdependence, 3.5 with diastolic ventricular interdependence, and 3.3 ml with diastolic and systolic ventricular interdependence. In contrast, with increases in pulmonary vascular resistance, ventricular interaction caused a greater decrease in SV than with no interaction present. Decreasing left ventricular free wall elastance or right ventricular free wall elastance decreased SV. Diastolic ventricular interdependence reduced the SV changes, whereas systolic ventricular interdependence accentuated the SV changes with alterations in right and left ventricular free-wall elastance. The results of the present simulation demonstrate the importance of ventricular interdependence in the observed responses of the right ventricle to volume overload, pressure overload, and ischemia.

Animals↗

PubMed1991

Significant left ventricular contribution to right ventricular systolic function.

To examine the importance of systolic ventricular interdependence on right ventricular function, we used a unique electrically isolated right ventricular free wall preparation. Double-peaked waveforms for right ventricular pressure and pulmonary arterial blood flow occurred over a wide range of pacing intervals between the left and right ventricles. One component of the waveforms could be directly related to right ventricular free wall contraction, whereas the other component was directly related to left ventricular and septal contraction. For left ventricular pressure, the left ventricular component was significantly larger than the right ventricular free wall component (92.7 +/- 3.2 vs. 7.3 +/- 3.2% peak-to-peak value, P less than 0.01). For right ventricular pressure, the left ventricular and septal component was significantly greater than the right ventricular component (63.5 +/- 10.9 vs. 36.5 +/- 10.9% peak-to-peak value, P less than 0.05). Similarly, for pulmonary arterial blood flow, the left ventricular component was significantly greater than the right ventricular component. When right ventricular free wall pacing stopped in diastole, 68 +/- 4% of right ventricular systolic pressure and 80 +/- 4% of pulmonary flow were obtained in the subsequent beat. The results of this study indicate that left ventricular contraction is very important for right ventricular developed pressure and volume outflow.

Animals↗

PubMed1991

Does tortuosity in cerebral arterioles impair down-autoregulation in hypertensives and elderly normotensives? A hypothesis and computer model.

A mathematical model of pressure/flow relationships in straight and tortuous intracerebral arterioles is presented. Using this model, it is predicted that patients with severe tortuosity would never be able to tolerate an appreciable decrease in MAP. This morphological alteration may explain the inability of a few hypertensive and normotensive elderly patients to tolerate periods of mild reductions in blood pressure. The alkaline phosphatase histochemical staining technique is potentially an excellent method of establishing the identity of deep white matter signal alterations seen on MRI because of its ability to trace the vascular supply from the brain surface to the lesion.

Aging↗

PubMed1990

Left ventricular pressure effects on right ventricular pressure and volume outflow.

Massive destruction of the right ventricular free wall has been shown to cause only mild hemodynamic alterations. Further, the derivative of right ventricular (RV) pressure (P) is broad or double peaked, with one peak occurring coincidentally with peak left ventricular (LV) dP/dt. Both observations suggest a direct LV assistance to RV function. Since the ventricles contract nearly simultaneously, the relative contribution of LV to RV pump function has been difficult to determine. This LV assistance was quantified in six canine experiments using a unique electrically isolated RV preparation. While on total cardiopulmonary bypass, the RV free wall was electrically isolated from the remainder of the heart. This preparation allowed for wide variations in the timing interval between RV and LV contractions. Double-peaked waveforms for RVP and pulmonary flow (RVF) occurred over a wide range (0 to 300 ms) of pacing intervals between the RV and LV. One derivative peak always followed RV contraction for RVP and RVF (r = 0.971 +/- .011, P less than 0.01: r = 0.972 +/- .012, p less than 0.01; respectively). The second derivative peak was unrelated to the RA-RV pacing interval (r = 0.297 +/- .191, P greater than 0.5 RVP; 4 = 0.237 +/- .278, P greater than 0.5 RVF), but corresponded to the maximal LVP rise. Additionally, the magnitude of the two derivative peaks was similar when the ventricles contracted synchronously. When RV contraction preceded or followed LV contraction, the derivative peak associated with LV contraction was significantly greater (P less than 0.05, range 2.1 +/- 0.6 to 6.7 +/- 1.6 for RVP; P less than 0.05 range 1.9 +/- 0.4 to 6.7 +/- 1.5 for RVF) than the derivative associated with RV contraction. These data demonstrate a normally present, large LV assistance to RV contraction and may help to explain the RV response to myocardial infarction.

Animals↗

PubMed1990

Effect of acute cardiac tamponade on left ventricular pressure-volume relations in anaesthetised dogs.

STUDY OBJECTIVE: The aim was to determine whether depressed myocardial contractility is responsible for the decline in stroke volume that occurs with cardiac tamponade. DESIGN: Left ventricular contractile performance was assessed before and after beta adrenergic blockade using the end systolic pressure-volume relation, the left ventricular dP/dtmax-end diastolic volume relation, and the left ventricular stroke work-end diastolic volume relation during acute cardiac tamponade in dogs. EXPERIMENTAL MATERIAL: In eight pentobarbitone anaesthetised dogs (15.7-24.8 kg), transducer tipped and volume impedance catheters were positioned in the left ventricle. Through a median sternotomy incision, a pericardial catheter was inserted to produce varying stages of cardiac tamponade. By the use of transient bicaval occlusions, variably loaded pressure-volume loops were recorded. MEASUREMENTS AND RESULTS: Incremental tamponade reduced mean arterial pressure from 105(SEM 3) to 89(2) mm Hg (mild tamponade), 75(2) mm Hg (moderate tamponade), and 59(10) mm Hg (severe tamponade). The slope of the end systolic pressure-volume relation was 6.3(1.2) mm Hg.ml-1 at baseline and increased slightly to 7.7(1.8), 8.5(1.3), and 9.2(1.5) mm Hg.ml-1 with the progressive levels of tamponade (NS). The role of autonomic reflexes was assessed by repeating the tamponade sequence after beta adrenergic blockade with 10 mg of metoprolol intravenously. The slope of the end systolic pressure-volume relation was reduced by metoprolol, at 4.9(1.0) mm Hg.ml-1 (p less than 0.01), but was not significantly altered by the sequence of tamponade following beta blockade [5.6(0.9), 6.0(1.0), and 5.5(7.0) mm Hg.ml-1, respectively (NS)]. Neither were changes found indicative of depressed contractile function with progressive tamponade in the slopes of the left ventricular dP/dtmax-end diastolic volume and stroke work-end diastolic volume relations. CONCLUSIONS: Left ventricular contractility was not altered during acute cardiac tamponade in an anaesthetised, closed chest canine model. Depressed left ventricular contractile function was not responsible for the observed haemodynamic deterioration.

Acute Disease↗

PubMed1990

Effects of increased pericardial pressure on the coupling between the ventricles.

STUDY OBJECTIVE: The mechanical coupling between the ventricles occurs directly through the myocardium (ventricular-ventricular coupling) and indirectly through the pericardium (ventricular-pericardial-ventricular coupling). We postulated that the magnitude of ventricular-pericardial-ventricular coupling would increase at high pericardial pressures, while ventricular-ventricular coupling would be unaltered. DESIGN: Canine hearts were removed and placed in cold cardioplegic solution. Balloons were inserted into each ventricle and the left and right ventricular pressure (dP1, dPr) and volume (dV1, dVr) changes caused by increasing the pressure and volume of the other ventricle and by increasing pericardial pressure (dPp) were measured. EXPERIMENTAL MATERIALS: Hearts from 10 random source dogs, weight 12.5-18 kg, were used. MEASUREMENT AND MAIN RESULTS: At control pericardial pressure levels, the magnitude of the pericardial-ventricular interactions was greater than the ventricular-ventricular interactions: dP1/dPp was significantly greater than dP1/dPr, at 0.71 (SEM 0.04), n = 6, v 0.18 (0.03), p less than 0.01, and dV1/dPp was significantly greater than dV1/dPr, at -0.83 (0.09) v -0.24 (0.06), p less than 0.05. Raising the pericardial pressure increased the mechanical coupling between the ventricles: dP1/dPr approximately, dV1/dPr approximately, dPr/dP1 approximately, and dVr/dP1 approximately increased significantly (p less than 0.05) by 0.48 (0.03), 0.67 (0.13), 0.38 (0.05), and 0.61 (0.09) respectively. This increased coupling occurred through pericardial pressure changes. If pericardial pressure was maintained constant, the coupling between the ventricles was unaltered. This same pattern was observed in four in situ experiments. For these experiments, at the raised pericardial pressure levels, dP1/dPr increased, from 0.51 (0.03) to 0.79 (0.01), p less than 0.05, if pericardial pressure was allowed to vary, but was unaltered with a constant pericardial pressure, at 0.42 (0.03) v 0.44 (0.04), p greater than 0.5. CONCLUSIONS: Ventricular interdependence was increased with raised pericardial pressure and this increased coupling was due primarily to an increased ventricular-pericardial-ventricular coupling. This increased coupling may help to explain the paradoxical pulse observed in cardiac tamponade.

Animals↗