Comparison of submaximal cardiovascular step test response to a maximal aerobic performance task.
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Atrial volume, pressure, and heart rate are considered the most important modulators of atrial natriuretic peptide (ANP) release, although their relative role is unknown. Continuous positive-pressure breathing in normal humans may cause atrial pressure and atrial volume to go in opposite directions (increase and decrease, respectively). We utilized this maneuver to differentially manipulate atrial volume and atrial pressure and evaluate the effect on ANP release. Effective filling pressure (atrial pressure minus pericardial pressure) was also monitored, because this variable has been proposed as another modulator of ANP secretion. We measured right atrial (RA) pressure, RA area, esophageal pressure (reflection of pericardial pressure), and RA and peripheral venous ANP in seven healthy adult males at rest and during continuous positive-pressure breathing (19 mmHg for 15 min). Continuous positive-pressure breathing decreased RA area (mean +/- SE, *P less than 0.05) 13.6 +/- 1.1 to 10.5 +/- 0.8* cm2, increased RA pressure 4 +/- 1 to 16 +/- 1* mmHg, increased esophageal pressure 2 +/- 1 to 12 +/- 1* mmHg, and increased effective filling pressure 2 +/- 0 to 4 +/- 1* mmHg. RA ANP increased from 67 +/- 17 to 91 +/- 18* pmol/l and peripheral venous ANP from 43 +/- 4 to 58 +/- 6* pmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)
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The left ventricular-arterial coupling relationship was used in patients with long-term mitral regurgitation to test the hypothesis that the low impedance left atrial contribution to left ventricular ejection obscures an impairment in left ventricular-arterial coupling and forward left ventricular pump efficiency. Twenty-two control patients and 26 patients with long-term mitral regurgitation were studied. Micromanometer left ventricular pressures and radionuclide angiograms for left ventricular volumes were acquired over a range of loading conditions. Left ventricular-arterial coupling was assessed by the ratio of left ventricular chamber elastance, E(es), to total arterial elastance, E(a). Forward left ventricular pump efficiency was calculated as the ratio of forward left ventricular stroke work to the corresponding pressure-volume area. There was a progressive decrease in E(es) in the patients with long-term mitral regurgitation (p < 0.001), but there was no significant difference in E(a) in comparison to the control patients. Consequently, E(es)/E(a) demonstrated a progressive decrease (p < 0.001). Although the efficiency of performing total left ventricular stroke work was only reduced when left ventricular contractile function was severely impaired (p < 0.001), there was a progressive reduction in left ventricular pump efficiency for performing forward left ventricular stroke work in the patients with long-term mitral regurgitation (p < 0.001). Further, normalized left ventricular stroke work was reduced for any left ventricular-arterial coupling ratio in the patients with long-term mitral regurgitation compared with the control patients. These data indicate that despite the outward evidence for normal left ventricular ejection in patients with long-term mitral regurgitation, a progressive deterioration in left ventricular contractile state leads to impaired left ventricular-arterial coupling and to an impairment in the efficiency of performing forward left ventricular stroke work. Once the left ventricle begins to dilate in patients with long-term mitral regurgitation, the progressive deterioration in left ventricular-arterial coupling and pump efficiency suggests that an earlier consideration of mitral valve surgery may be warranted to preserve left ventricular contractile function.
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This pilot study was undertaken to characterize age-related alterations in airway and metabolic beta 2-adrenergic receptor response using terbutaline as a probe. A single dose of terbutaline 0.007 mg/kg was administered subcutaneously to 10 young (range 20-35 yrs) and 10 elderly (range 60-73 yrs) men and women with asthma. beta-Receptor function was assessed by serial pulmonary function tests, heart rate, blood pressure, plasma potassium, glucose, insulin, and catecholamine levels, and in vitro 3', 5'-cyclic adenosine monophosphate (cAMP) production of pure T lymphocytes. The trend was for lung beta 2-receptor response (bronchodilation) and T lymphocyte cAMP production to be lower in elderly than in young asthmatics, but differences did not reach statistical significance. Elderly subjects' beta 1-adrenergic receptor responsiveness (systolic blood pressure) was also dampened. These data suggest that T lymphocyte stimulation does reflect pulmonary beta 2-receptor response. Whether elderly asthmatics require and tolerate higher dosages of parenteral terbutaline than younger asthmatics deserves further study.
Between April 5, 1984 and May 9, 1987, 24 patients underwent heart-lung transplantation for a variety of vascular and pulmonary diseases. Graft procurement being usually distant, the cardiopulmonary protection used was based on a simple hypothermic flush technique performed in donors prepared with prostacyclin. There was no primary graft deficiency and no intra-operative death. 17 patients are alive after a follow-up period of 1 to 41 months. The actuarial survival rate at 1 year was 77 p. 100. Late mortality was mainly due to cytomegalovirus infections. Immunosuppression relied on cyclosporine A and azathioprine with peri-operative use of antilymphocyte serum and corticosteroids. Early graft rejection episodes were treated with bolus intravenous methylprednisone. These episodes were detected from combined clinical, radiological, spirometric and histological data. Transbronchial lung biopsy was the reference examination for an objective diagnosis of lung rejection. In this series there was only one case of obliterative bronchiolitis (4 p. 100). This must be credited to the strategy used to detect rejection which seems to be the main factor of occurrence of this dangerous complication.
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OBJECTIVES: The purpose of this study was to serially evaluate the response and variability of the end-systolic pressure-volume relation, the left ventricular end-diastolic volume-peak positive first derivative of left ventricular pressure (dP/dt) relation and the left ventricular end-diastolic volume-stroke work relation in the development of progressive left ventricular dysfunction. BACKGROUND: Evaluation of systolic performance of the failing left ventricle may be enhanced by using relatively load-insensitive measures of left ventricular performance. The end-systolic pressure-volume, left ventricular end-diastolic volume-peak positive dP/dt and left ventricular end-diastolic volume-stroke work relations adequately define left ventricular performance under multiple loading conditions, but efficacy has not been fully assessed in the failing heart, particularly in the intact circulation. METHODS: Fourteen dogs underwent instrumentation and rapid pacing to heart failure. Variably loaded pressure-volume beats were produced by inferior vena cava occlusion. The dogs were evaluated at baseline and at three progressively more severe levels of left ventricular dysfunction. RESULTS: There was a progressive increase in left ventricular volumes at end-diastole ([mean value +/- SE] 60 +/- 28 to 73 +/- 29 ml, p < 0.001) and end-systole (39 +/- 19 to 61 +/- 27 ml, p < 0.001) during the 3 weeks of rapid pacing and a progressive decline in peak positive dP/dt (1,631 +/- 410 to 993 +/- 222 mm Hg/s, p < 0.001) and ejection fraction (37 +/- 8% to 16 +/- 11%, p < 0.001). There was a corresponding decline in the slope of each of the three relations: for end-systolic pressure-volume, 6.3 +/- 2.2 to 2.8 +/- 0.7 (p < 0.05); for left ventricular end-diastolic volume-stroke work, 61.9 +/- 9.1 to 26.5 +/- 2.4 (p < 0.05); and for left ventricular end-diastolic volume-peak positive dP/dt, 47.1 +/- 13.6 to 20.31 +/- 6.8 (p < 0.05). There was also a corresponding increase in position volumes: for end-systolic pressure-volume, 33.6 +/- 3.9 to 61.2 +/- 6.6 ml (p < 0.05); for left ventricular end-diastolic volume-stroke work, 46.2 +/- 3.6 to 89.3 +/- 7.6 ml (p < 0.05); and for left ventricular end-diastolic volume-peak positive dP/dt, 29.1 +/- 19.1 to 68.6 +/- 25.9 ml (p < 0.05). The relative degree of change in each of the three relations was similar as more severe heart failure developed. The coefficients of variation for position were significantly less than the variation for slopes. The response of volume intercepts was heterogeneous. For left ventricular end-diastolic volume-stroke work, the intercept increased as ventricular performance decreased. The intercept of the end-systolic pressure-volume relation was significantly more variable than the left ventricular end-diastolic volume-stroke work relation and did not change with progressive heart failure. The intercept for left ventricular end-diastolic volume-peak positive dP/dt was highly variable and showed no consistent changes as left ventricular function declined. CONCLUSIONS: All three relations consistently describe changes in left ventricular performance brought about by tachypacing. Evolution of left ventricular dysfunction causes a decline in slope and a rightward shift of these relations. The position of the relation is the most sensitive and least variable indicator of left ventricular systolic performance.
Twenty-four mongrel dogs were divided into two equal groups to determine the effects of orally administered amiodarone on left ventricular function. Measurements of left ventricular function included left ventricular contractility as denoted by maximum rate of rise of left ventricular pressure (dP/dtmax), cardiac index (CI), left ventricular stroke work index (LVSWI), and peripheral vascular resistance (PVR). Left ventricular function was measured in 6 of the 12 animals in Group 1 before and after 14 days of amiodarone administered orally; the remaining animals served as controls. The dP/dtmax was reduced from 2,855 to 1,291 mm Hg/sec (p less than 0.01), and LVSWI fell from 1.6 to 0.74 gm-m/beat/kg (p less than 0.05) in the 6 animals given amiodarone. The 12 animals in Group 2 underwent 30 minutes of ischemic arrest. Six animals in Group 2 underwent 30 minutes of ischemic arrest. Six animals were given amiodarone orally for 14 days prior to cardiopulmonary bypass and ischemic arrest; the other 6 served as controls. Before cardiopulmonary bypass, the dogs administered amiodarone had significantly greater depression of dP/dtmax (p less than 0.01) and LVSWI (p less than 0.05). Thirty minutes of ischemia produced significant depression of left ventricular function in all animals in Group 2. However, a significantly greater reduction in dP/dtmax and LVSWI occurred in those animals receiving amiodarone. Furthermore, 4 of the 6 dogs receiving amiodarone were unable to sustain sufficient cardiac output following cardiopulmonary bypass to permit long-term survival (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Interatrial septum pacing (IASP) reduces interatrial conduction time and consequently may interfere with atrioventricular delay (AVD) optimization. We studied 14 patients with an implanted BEST Living system device able to measure peak endocardial acceleration (PEA) signal. The aims of our study were to compare the (1) optimal AVD (OAVD) in right atrial appendage pacing (RAAP) and IASP, and (2) OAVD derived by the PEA signal versus OAVD derived by Echo/Doppler evaluation of the left ventricular filling time (LVFT) and cardiac output (CO). Measurements were performed in DDD VDD modes Eight patients (group A) had RAAP and six patients (group B) had IASP. In group A, OAVD measured by LVFT, CO, and PEA was 185 +/- 23 ms, 177 +/- 19 ms, and 192 +/- 23 ms in DDD and 147 +/- 19 ms, 135 +/- 27 ms, and 146 +/- 20 ms in VDD, respectively. OAVD measured by LVFT, CO, and PEA was significantly longer in DDD mode than in VDD (P < 0.01, P < 0.01, P < 0.001). In group B, OAVD measured by LVFT, CO, and PEA was 116 +/- 19 ms, 113 +/- 10 ms, and 130 +/- 30 ms in DDD and 106 +/- 16 ms, 96 +/- 15 ms, and 108 +/- 26 ms in VDD, respectively. No statistical differences were observed between DDD and VDD. Significant correlations between OAVDs PEA derived and OAVDs LVFT and CO derived were observed (r = 0.71, r = 0.69, respectively). When new techniques of atrial stimulation, as IASP, are used an OAVD shorter and similar in VDD and DDD has to be considered. The BEST Living system could provide a valid method to ensure, in every moment, the exact required OAVD to maximize atrial contribution to CO.
We compared hemodynamics, ventricular function, and force-frequency relationships in six open-chest and six closed-chest anesthetized mice (FVB/N strain). Left ventricular (LV) pressure was measured with a 1.8- or 1.4-Fr Millar catheter placed via the right carotid artery and the LV apex in the closed- and open-chest state, respectively. Pacing was performed with electrodes placed either directly on atrial appendages (open chest) or with a 1-Fr bipolar catheter via the jugular vein (closed chest). Closed-chest animals had greater spontaneous heart rate (267 +/- 106 vs. 147 +/- 27 beats/min), LV systolic (81 +/- 14 vs. 48 +/- 9 mmHg) and diastolic pressures (11.2 +/- 4.8 vs. 5.6 +/- 2.4 mmHg), and maximal rise (+ dP/dtmax: 6,208 +/- 2,519 vs. 3,682 +/- 671 mmHg/s) and fall in pressure development (-dP/dtmax: -6,094 +/- 2,386 vs. -3,001 +/- 399 mmHg/s). LV systolic pressure (98 +/- 18 vs. 52 +/- 11 mmHg), + dP/dtmax (9,240 +/- 2,459 vs. 5,777 +/- 2,473 mmHg/s), and -dP/dtmax (-8,375 +/- 2,551 vs. -3,753 +/- 1,170 mmHg/s) were significantly higher when animals were matched at a heart rate of 420 beats/min in closed-chest vs. open-chest animals. Biphasic force-frequency relationships were seen in all animals, but the critical heart rate was greater in the closed- than open-chest animals (432 +/- 42 vs. 318 +/- 42 beats/min). We conclude that 1) there are significant differences between invasive indexes of systolic and diastolic function between the closed- and open-chest preparations, 2) there is a biphasic force-frequency relationship in the anesthetized mouse, and 3) dP/dtmax can be used to assess the cardiovascular phenotype.
The importance of right ventricular (RV) function in maintaining global cardiac performance is the focus of this discussion. The physiological determinants of normal right ventricular function will be discussed, with particular emphasis on the afterload and contractility characteristics of the right ventricle. Numerous clinical conditions have been shown to affect RV performance. These conditions include positive-pressure ventilation, ischemia, pulmonary hypertension, and cardiac surgery. Present methods for the perioperative evaluation of RV function include angiography, radionuclide techniques, thermodilution techniques, echocardiography, and magnetic resonance imaging. Traditional modalities for the treatment of RV dysfunction consist of pharmacological interventions (i.e., vasodilators and inotropes) and/or mechanical assist devices. Newer pharmacological strategies for the treatment of RV failure and associated pulmonary hypertension include the phosphodiesterase fraction III inhibitors and the prostaglandins, specifically PGE1. In summary, the accurate evaluation of perioperative RV performance combined with new treatment options will ensure maximal preservation of RV performance.
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