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PubMed2003

Responses of chronically hypoxic rat hearts to ischemia: KATP channel blockade does not abolish increased RV tolerance to ischemia.

Chronic hypoxia may precondition the myocardium and protect from ischemia-reperfusion damage. We therefore examined the recovery of left and right ventricular function after ischemia and reperfusion (15 min each) in isolated blood-perfused working hearts from normoxic (Norm) and hypoxic (Hypo; 14 days, 10.5% O(2)) adult rats. In addition, the mRNA expression of hypoxia-inducible factor (HIF)-1alpha and the protein expression of endothelial nitric oxide synthase (eNOS) were measured. Postischemic left ventricular function recovered to 66 +/- 6% and 67 +/- 5% of baseline in Norm and Hypo, respectively. In contrast, postischemic right ventricular function was 93 +/- 2% of baseline in Hypo vs. 67 +/- 3% in Norm (P < 0.05). Improved postischemic right ventricular function in Hypo (93 +/- 2% and 96 +/- 2% of baseline) was observed with 95% O(2) or 21% O(2) in the perfusate, and it was not attenuated by glibenclamide (5 and 10 micromol/l) (86 +/- 4% and 106 +/- 6% recovery). HIF-1alpha mRNA and eNOS protein expression were increased in both left and right hypoxic ventricles. In conclusion, postischemic right, but not left, ventricular function was improved by preceding chronic hypoxia. ATP-sensitive K(+) channels are not responsible for the increased right ventricular tolerance to ischemia after chronic hypoxia in adult rat hearts.

ATP-Binding Cassette Transporters↗
PubMed2002

Effect of partial left ventriculectomy on left and right ventricular volumes and function as assessed with electron beam tomography: preliminary results.

Our objective was to determine if left ventricular reduction surgery affects left and right ventricular volumes and function. Twenty-three patients with end-stage heart failure underwent contrast-enhanced electron beam tomographic function studies before and twice after partial left ventriculectomy (PLV). The PLV was combined with other cardiosurgical procedures in 20 of 23 patients. Left and right ventricular enddiastolic volume (LVEDV, RVEDV), stroke volume (LVSV, RVSV), ejection fraction (LVEF, RVEF), and enddiastolic diameter (LVEDD, RVEDD) were determined by manual tracing of endo- and epicardial borders at enddiastole and endsystole. Patients were scanned 31 days (+/-34) before and 18 days (+/-13) and 8 months (+/-4) after PLV. Mean pre- and early and late postoperative values for LVEDV, LVSV, LVEF, and LVEDD were 387.9 ml (+/-125.5 ml), 255.6 ml (+/-79.3 ml; p<0.01), and 253.7 ml (+/-97.8 ml; p<0.05), 79.7 ml (+/-25.2 ml), 74.8 ml (+/-17.9; n.s.), and 79.1 ml (+/-26.5 ml; n.s.), 21.6% (+/-7.3%), 31.9% (+/-13.4%; p<0.05), and 34.1% (+/-14.1%; p<0.05), and 72.0 mm (+/-10.6 mm), 64.3 mm (+/-8.5 mm; p<0.05), and 63.5 mm (+/-9.4 mm; p<0.05), respectively. Mean pre- and postoperative values for RVEDV, RVSV, RVEF, and RVEDD were 177.7 ml (+/-72.8 ml), 172.4 ml (+/-59.2 ml; n.s.), and 178.9 ml (+/-60.8 ml; n.s.), 60.3 ml (+/-21.6 ml), 68.8 ml (+/-19.9 ml; n.s.), and 78.3 ml (+/-25.3 ml; n.s.), 38.1% (+/-15.4%), 43.7% (+/-16.3%; p<0.05), and 45.1% (+/-11.2%; n.s.), and 50.4 mm (+/-10.9 mm), 48.1 mm (+/-8.7 mm; n.s.), and 48.5 mm (+/-9.8 mm; n.s.), respectively. The PLV may induce a significant early reduction of left ventricular volumes and improvement of biventricular function; however, our results must be judged carefully as the majority of patients in this study underwent additional cardiosurgical procedures, the contributory effect of which on the overall outcome remains unclear.

Aged↗
PubMed1995

Effects of ductus arteriosus occlusion on pulmonary artery pressure during in utero ventilation in fetal sheep.

Seven fetal sheep were prepared to study the short-term effects of in utero ventilation and ductus arteriosus occlusion on pulmonary artery pressure and on fetal right ventricular function assessed using the right atrial pressure-right ventricular stroke volume relationship. Nine days post-surgery (140 days gestation), blood gas and haemodynamic values were obtained before and during in utero ventilation with 100% O2, and during ventilation with the ductus arteriosus occluded. Oxygen content increased significantly from 7.2 to 14.5 ml dl-1 with ventilation and remained elevated at 14.4 ml dl-1 with ventilation with the ductus arteriosus occluded. In utero ventilation produced a left to right atrial pressure gradient and depression of the right atrial pressure-right ventricular stroke volume relationship. Ductus arteriosus occlusion during in utero ventilation reduced the left to right atrial pressure gradient, and along with a decrease in pulmonary artery pressure, resulted in an upward shift of the right atrial pressure-right ventricular stroke volume relationship, but only to the preventilation level. This study indicates that the fetal right atrial pressure-right ventricular stroke volume relationship is significantly altered, both by changes in the left to right atrial pressure gradient and by changes in pulmonary artery pressure seen with in utero ventilation and subsequent ductus arteriosus occlusion.

Animals↗
PubMed1987

Factors that exaggerate the deleterious effects of pulmonary insufficiency on the right ventricle after tetralogy repair. Surgical implications.

Postoperative cardiac catheterization data of 74 patients with pulmonary insufficiency after tetralogy repair were analyzed. Two groups were identified: Group A, 26 patients with normal right ventricular function (ejection fraction 95% +/- 5.5%, end-systolic volume 110% +/- 17% of predicted normal) and Group B, 48 patients with right ventricular dysfunction (ejection fraction 80% +/- 18% [p less than 0.001], and end-systolic volume 218% +/- 75% of predicted normal [p less than 0.001]). There was no significant difference between the two groups with respect to frequency of previous palliative procedures, age at operative repair, operative techniques, methods of myocardial protection, and follow-up period. Right ventricular dysfunction in Group B was associated with significant distal pulmonary stenosis (right ventricle-pulmonary artery pressure gradient 28 +/- 13 torr in Group A versus 55 +/- 20 torr in Group B, p less than 0.001), moderate pulmonary regurgitation (regurgitant fraction 18% +/- 11% in Group A versus 32% +/- 10% in Group B, p less than 0.001), and large transannular outflow patch (ratio of patch diameter to descending aorta diameter 1.31 +/- 0.16 in Group A versus 2.50 +/- 0.28 in Group B, p less than 0.001). Pulmonary valve insertion was performed in 42 patients in Group B. Eighteen had subsequent cardiac catheterization. Right ventricular function recovered completely (end-systolic volume 122% +/- 24%, and ejection fraction 92% +/- 7% of predicted) in five of six patients (83%) who had valve insertion within the first 2 years after tetralogy repair. In contrast, right ventricular function remained abnormal in all 12 patients who had valve insertion later than 2 years after tetralogy repair (p less than 0.05). Patients with residual pulmonary stenosis and/or a large transannular outflow patch are at risk for the development of right ventricular dysfunction from pulmonary insufficiency after tetralogy repair. Early correction of these residual lesions and control of pulmonary insufficiency may prevent long-term deterioration in right ventricular function.

Adolescent↗
PubMed1987

Effect of the left ventricle on the right ventricle.

The importance of the once-obscure right ventricle is becoming evident. Even in disorders that primarily affect the left ventricle, the once-considered-passive conduit has proved essential for maintenance of normal cardiac output. In coronary artery disease, the function of the right ventricle is affected by both its circulation and the after-load placed on it by dysfunction of the left ventricle. In congestive heart failure, right ventricular function relates to functional capacity, whereas left ventricular function does not, and right ventricular ejection fraction is a useful prognostic guide in these patients. In mitral and aortic valvular disease, the role of the right ventricle is only now becoming evident, and the precise interplay of all factors has yet to be explained. In systemic hypertension, it is likely that the pulmonary circulation is affected by the same humoral factors that elevate systemic pressures.

Coronary Disease↗
PubMed1992

Left ventricular involvement in right ventricular dysplasia.

Right ventricular dysplasia, a heart muscle disease of unknown cause, anatomically characterized by variable replacement of myocardial muscle with adipose or fibroadipose tissue, is usually considered a selective disorder of the right ventricle. However, concomitant left ventricular involvement has been noted in a few cases. The aim of this study was to evaluate the prevalence and characteristics of left ventricular involvement in right ventricular dysplasia, as well as possible progression of the disease. Thirty-nine patients with right ventricular dysplasia were studied by M-mode and two-dimensional echocardiography; 28 of them also underwent cardiac catheterization, and in 25 endomyocardial biopsy was performed. On first examination the left ventricle was normal in 25 patients, whereas in the remaining 14 right ventricular abnormalities were associated with left ventricular involvement, characterized by asynergic areas (12 patients) or diffuse mild hypokinesis (two patients). During follow-up (27 patients, 84.1 +/- 66.1 months) 10 patients showed worsening of right ventricular function; in nine the appearance or worsening of left ventricular abnormalities was observed. Five patients died (four in congestive heart failure and one suddenly). Results of postmortem examination (available in two patients) showed atrophy of myocells and a massive fatty and fibrous infiltration of the right ventricular wall, associated with degenerative changes and fibrosis of the left ventricle. In conclusion, right ventricular dysplasia may be associated with left ventricular involvement and the disorder appears to be progressive in some instances.

Adult↗
PubMed1989

[Function of the right ventricle in patients with mitral valve diseases].

To investigate right ventricular function in mitral valve disease, biplane cineventriculograms of the right and left ventricle were performed in 96 patients-35 with mitral stenosis, 26 with mitral regurgitation, 12 with combined mitral valve disease, 14 with mitral stenosis and tricuspid regurgitation, and nine with mitral regurgitation and tricuspid regurgitation, compared to 18 normals (N). Right ventricular enddiastolic volume index was moderately elevated in patients with mitral stenosis and concomitant tricuspid regurgitation (111.6 +/- 35.3 ml/m2, no significance compared to N: 95.9 +/- 21.8 ml/m2) and with mitral regurgitation and tricuspid regurgitation (107.9 +/- 45.1 ml/m2, no significance compared to N). A reduced right ventricular ejection fraction (RVEF less than or equal to 50%) was found in 40 of the 96 patients. Right ventricular ejection fraction was frequently reduced in patients with mitral regurgitation and tricuspid regurgitation (46.7% +/- 15.1%) and significantly reduced in patients with combined mitral valve disease (45.0 +/- 17.6%, compared to N: 58.0 +/- 7.1%, p less than 0.01). No significant correlations were found between right ventricular ejection fraction and left ventricular enddiastolic volume or left ventricular ejection fraction in patients with mitral valve disease. Moreover, right ventricular ejection fraction did not correlate with systolic pulmonary artery pressure, mean pulmonary artery pressure or mean pulmonary capillary wedge pressure. Local wall motion (mean systolic shortening) was determined for the anterior, anteroapical, and inferior segment in the RAO-projection and for the right ventricular free wall in the LAO-projection. 63% of the patients (n = 25) with reduced right ventricular function (RVEF less than of equal to 50%) showed local wall motion abnormalities, preferably in the anterior segment of the RAO- projection (48%) and the right ventricular free wall (30%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

The effects of phenylephrine on right ventricular performance in patients with pulmonary hypertension.

Pulmonary hypertension causes right ventricular ischemia and failure as a result of increased afterload combined with reduced coronary blood flow. Increasing coronary driving pressure by raising aortic pressure with phenylephrine has been shown to reverse right ventricular ischemia from pulmonary hypertension in animals. Since vasodilators often fail to reduce afterload, we tested whether raising the coronary driving pressure would improve right ventricular function in man. Ten patients with pulmonary hypertension had hemodynamics and right ventricular coronary driving pressure measured before and 10 minutes after a steady state was reached with a phenylephrine infusion titrated to raise aortic pressure by 25 percent. Phenylephrine caused a significant (p less than .01) increase in mean aortic pressure (84 to 108 mm Hg) and right ventricular coronary driving pressure (46 to 69 mm Hg). In response, there was a significant (p less than .01) rise in mean pulmonary artery pressure (58 to 67 mm Hg), right ventricular end-diastolic pressure (10 to 16 mm Hg) and wedge pressure (5 to 9 mm Hg), and an insignificant fall in cardiac output (3.26 to 3.09 L/min) and pulmonary artery O2 saturation (57 to 49 percent). Although phenylephrine increased right ventricular coronary driving pressure, it worsened right ventricular function as manifest by a rise in end-diastolic pressure and fall in cardiac output. Any benefit of raising right ventricular coronary driving pressure may have been offset by alpha vasoconstriction of right ventricular coronary blood flow and/or pulmonary arterial vasoconstriction. Phenylephrine does not appear to be a useful therapy of right ventricular failure from pulmonary hypertension in patients who fail vasodilators.

Adult↗
PubMed1997

Effects of mechanical left ventricular support on right ventricular diastolic function.

BACKGROUND: Previous studies have shown that left ventricular (LV) unloading alters right ventricular (RV) systolic mechanics, but the effects of LV assist device (LVAD) support on RV diastolic function have not been examined in intact subjects. METHODS: Seven closed-chest, sedated dogs were studied after placement of a LVAD and 27 myocardial markers; in four animals, a right coronary artery occluder was placed to induce acute RV free wall ischemia. Data were recorded with the LVAD off and LVAD on before (control) and during RV ischemia. Assessment of RV diastolic function included RV myocardial relaxation (time constant of isovolumic pressure decay [tau]), RV chamber stiffness (slope of the end-diastolic pressure-volume relation), and RV filling dynamics (peak filling rate and mean filling rate during early diastole). RESULTS: During control, full LVAD support did not alter RV tau (104 +/- 67 msec LVAD off versus 109 +/- 49 msec LVAD on, p > 0.50), RV diastolic stiffness (0.56 +/- 0.31 versus 0.51 +/- 0.25 mm Hg/ml, p > 0.20), peak filling rate (107 +/- 51 versus 119 +/- 82 ml/sec, p > 0.35) or mean filling rate during early diastole (32 +/- 28 versus 27 +/- 18 ml/sec, p > 0.40). With right coronary artery occlusion, RV tau rose to 136 +/- 33 msec (p < 0.001), and RV diastolic stiffness fell to 0.29 +/- 0.13 mm Hg/ml (p < 0.005), but there was no change in RV filling rates (p > 0.20). With mechanical LV support during acute RV ischemia, there was no additional change in RV tau, diastolic stiffness, or filling dynamics (p > 0.20). CONCLUSIONS: In intact animals, RV ischemia impaired RV relaxation and decreased chamber stiffness, but there was no change in RV filling rates. Mechanical LV support, during the control state and with RV ischemia, did not affect RV diastolic performance.

Animals↗
PubMed1994

Right ventricular end-systolic pressure-volume relation during propofol infusion.

The effects of propofol on right ventricular function were studied in 11 ICU patients who needed sedation for acute respiratory failure or neurological diseases. Right ventricular function was studied using a thermodilution method at patients' bedside. Right ventricular ejection fraction (RVEF), cardiac output (CO), right ventricular end-diastolic volume (RVEDV), right ventricular end-systolic volume (RVESV), right ventricular end-systolic pressure (RVESP) and pulmonary capillary wedge pressure (PCWP) were obtained from a modified Swan-Ganz catheter. Calculation of right ventricular end-systolic pressure-volume relation (ESPVR) allowed to assess changes in right ventricular inotropic state. A baseline ESPVR was obtained before propofol infusion: RVESP = 0.21 RVESV + 2.4, r = 0.83, P < 0.0001. Then, patients were given an induction dose of 1 to 2.5 mg.kg-1 propofol over 1 min followed by a continuous infusion of 3 mg.kg-1.h-1. During propofol infusion heart rate, mean arterial pressure, PCWP, CO, systemic vascular resistance and RVEF significantly decreased. No change in RVEDV and RVESV was observed. ESPVR was significantly altered with a dramatic decrease in the slope of the relation: RVESP = 0.12 RVESV + 6.9 (P < 0.001 from baseline). Dobutamine was used in five patients with clinically significantly cardiac dysfunction and restored the slope of the ESPVR to the baseline value: RVESP = 0.22 RVESV + 6.3 (NS from baseline). In the study patients, propofol altered the inotropic state of the right ventricle.

Anesthesia, Intravenous↗
PubMed2003

Greater impairment of right ventricular systolic function in patients with anterior myocardial infarction because of the extent of proximal lesions.

The present study examined the influence of the extent of the ischemic area on right ventricular (RV) systolic function and the relation between the RV global and regional systolic function in patients with anteroseptal myocardial infarction (MI). Biplane right ventriculography was performed in 15 subjects as the control group, and 46 patients with anteroseptal MI as the MI group. Three dimensions of the RV (the long axis dimension [LA], the anterior-posterior dimension [AP] and the septum-free wall dimension [SF]) were examined to assess regional function The MI group had a larger right ventricular end-systolic volume index and lower right ventricular ejection fraction than the control group. The more proximal the coronary lesion, the lower was the ejection fraction of the RV in the MI group. The MI group had lower percent shortening (% shortening) of the SF than the control group, but there were no significant change in the % shortening of AP and LA between the groups. The results suggest that the degree of impairment of RV systolic function depends on the extent of the infarcted area, and that the impairment is mainly from a reduction in the %shortening of the SF.

Aged↗
PubMed2005

Long term complications in single and dual chamber pacing are influenced by surgical experience and patient morbidity.

OBJECTIVE: To determine how short and long term complication rates after pacemaker implantation are influenced by patient morbidity, operator experience, and choice of pacing system. DESIGN: Retrospective analysis of 1884 patients who received VVI (n = 610), VDD (n = 371), or DDD devices (n = 903) between 1990 and 2001. Follow up period was 64 (34) months. The influence of age, sex, coronary artery disease, myocardial infarction, reduced left ventricular (LV) function, right ventricular (RV) dilatation, atrial fibrillation, device type, and operator experience on operation time and complication rate were analysed. RESULTS: Operation time was prolonged in patients with coronary artery disease, inferior myocardial infarction, reduced LV function, and RV dilatation. Implantation of DDD pacemakers prolonged operation time, particularly among operators with a low or medium level of experience. The overall complication rate was 4.5%. Sixty seven per cent of these complications occurred within the first three months. Complication rate was increased by age, reduced LV function, and RV dilatation. Implantation of DDD systems led to a higher complication rate (6.3%) than implantation of VVI (2.6%) or VDD pacemakers (3.2%). These differences were present only among operators with a low or medium level of experience. CONCLUSIONS: Operation time and complication rate increased with age, impaired LV function, and RV dilatation. Complication rates were higher with DDD than with VVI or VDD implantation and were excessive among inexperienced but not experienced operators.

Age Factors↗
PubMed1992

Right ventricular volumes and hemodynamics after successful orthotopic heart transplantation. A comparison to coronary artery disease using thermodilution.

Only few data exist concerning right ventricular function in the chronic stage after cardiac transplantation. Therefore, we investigated hemodynamic and right ventricular volumetric data by a computerized thermodilution Swan-Ganz catheter in 17 patients (median age: 53, range: 18-63 yr) at a median of 24 (4 to 44) months after cardiac transplantation during rest and supine bicycle exercise. Myocardial biopsy showed grade one or less according to the classifications of Billingham. Sixteen patients with coronary artery disease, but without prior myocardial infarction, served for comparison. While angiographic left ventricular ejection fraction was nearly identical in transplant recipients [77 (60-92)%, median (range)] and in patients with coronary artery disease [78 (64-94)%], right ventricular ejection fraction was lower (p < 0.001) in patients after cardiac transplantation [37 (16-58)%] as compared to patients with coronary artery disease [56 (46-62)%]. In transplant recipients right atrial pressure was significantly higher both at rest [10 (2-18) mmHg] and exercise [18 (8-30) mmHg] than in patients with coronary artery disease [5 (1-11) and 8 (3-18) mmHg]. Pulmonary capillary wedge pressure behaved similar in both groups. To further evaluate reasons for right ventricular impairment, a correlation analysis was performed. This showed a negative correlation between right ventricular ejection fraction and the time interval after transplantation (p < 0.0002). However, there was no correlation between right ventricular ejection fraction and acute rejection or a rejection score. In conclusion, right ventricular function may be severely altered in transplant recipients, in contrast to an only slight impairment of left ventricular function.

Adolescent↗
PubMed1996

Mid-term results of pulmonary thromboendarterectomy for chronic thromboembolic pulmonary hypertension.

BACKGROUND: In patients with chronic thromboembolic pulmonary hypertension, acute and striking decreases of pulmonary artery pressures and vascular resistance can be achieved by pulmonary thromboendarterectomy. In this study, the long-term effects of pulmonary thromboendarterectomy on hemodynamic indices and right ventricular function were investigated. METHODS: Sixty-five patients (31 women and 34 men; mean age, 47 +/- 17 years; range, 19 to 69 years; New York Heart Association [NYHA] functional class II, n = 3; class III, n = 38; class IV, n = 24) were reassessed 13 to 48 months (mean, 27 months) after pulmonary thromboendarterectomy. Measurements are reported as mean +/- standard deviation. RESULTS: All patients reported a significant improvement of symptoms: 46 patients were in NYHA functional class I, 16 patients in class II, and 3 patients in class III. Mean pulmonary vascular resistance was significantly reduced compared with preoperative and postoperative values (preoperative: 1,015 +/- 454 dynes.s.cm-5; postoperative: 322 +/- 154 dynes.s.cm-5; follow-up: 198 +/- 72 dynes.s.cm-5; p < 0.001 versus preoperative; p < 0.025 versus postoperative). Concomitantly, cardiac index was significantly increased compared with preoperative values (preoperative: 2.0 +/- 0.7 L.min-1.m-2; follow-up: 2.9 +/- 0.5 L.min-1.m-2; p < 0.001). Significant reductions of right ventricular dimensions and recovery of right ventricular function could be demonstrated radiologically and echocardiographically. In 3 patients (preoperative NYHA class IV, NYHA class III at follow-up) with proven coagulation abnormalities, pulmonary vascular resistance was moderately increased at follow-up compared with postoperative measurements. CONCLUSIONS: In patients with chronic thromboembolic pulmonary hypertension, a persistent decrease of pulmonary vascular resistance and improvement of right ventricular function and NYHA functional status can be achieved by pulmonary thromboendarterectomy.

Adult↗
PubMed2007

Thoracic epidural anesthesia impairs the hemodynamic response to acute pulmonary hypertension by deteriorating right ventricular-pulmonary arterial coupling.

OBJECTIVE: Thoracic epidural anesthesia is increasingly used in critically ill patients. This analgesic technique was shown to decrease left ventricular contractility, but effects on right ventricular function have not been reported. A deterioration of right ventricular performance may be clinically relevant for patients with acute pulmonary hypertension, in which right ventricular function is an important determinant of outcome. In the present study, we tested the hypothesis that thoracic epidural anesthesia decreases right ventricular contractility and limits its capacity to tolerate pulmonary hypertension. DESIGN: Prospective, placebo-controlled study using an established model of acute pulmonary hypertension. SETTING: University hospital laboratory. SUBJECTS: A total of 14 pigs (mean weight, 35 +/- 2 kg). INTERVENTIONS: After instrumentation with an epidural catheter, biventricular conductance catheters, a pulmonary flow probe, and a high-fidelity pulmonary pressure catheter, seven pigs received thoracic epidural anesthesia and seven pigs served as control. Hemodynamic measurements were performed in baseline conditions and after induction of pulmonary hypertension via hypoxic pulmonary vasoconstriction (Fio2 of 0.15). MEASUREMENTS AND MAIN RESULTS: Ventricular contractility was assessed using load- and heart rate-independent variables. Right ventricular afterload was characterized with instantaneous pressure-flow measurements. In baseline conditions, thoracic epidural anesthesia decreased left but not right ventricular contractility. In untreated animals, pulmonary hypertension was associated with an increase in right ventricular contractility and cardiac output. Pretreatment with thoracic epidural anesthesia completely abolished the positive inotropic response to acute pulmonary hypertension. As a result, ventriculo-vascular coupling between the right ventricle and pulmonary-arterial system deteriorated, and cardiac output was significantly lower in animals with thoracic epidural anesthesia than in untreated controls during hypoxia-induced pulmonary hypertension. CONCLUSIONS: Thoracic epidural anesthesia inhibits the native positive inotropic response of the right ventricle to increased afterload and deteriorates the hemodynamic effects of acute pulmonary hypertension.

Acute Disease↗
PubMed1992

Effects of milrinone on systemic capacitance vessels in relation to venous return and right ventricular pump function.

To investigate the effect of milrinone (MIL) on systemic capacitance vessels, we measured the mean circulatory filling pressure (MCP) in anesthetized open chest dogs. We measured hemodynamic parameters (a) at baseline blood volume (BV), (b) immediately after bloodletting (5 ml/kg), and (c) immediately after dextran injection (5 ml/kg). These measurements were taken in a control group (n = 8) and in a MIL group (n = 8), where MIL (100 + 2.5 micrograms/kg/min) was administered i.v. The extra volume (EV) was obtained by extrapolating the straight line that was fit to the MCP-BV plot. MIL significantly decreased the EV, from 22.8 +/- 1.0 to 19.1 +/- 0.4 ml/kg, indicating that MIL dilates the systemic capacitance vessels. MIL shifted the right ventricular output curve to the left and upward and shifted the venous return curve to the left and rotated it clockwise. Thus, venous return was increased by decreasing the resistance to venous return and by improving right ventricular pump function. Next we evaluated the effects of MIL (100 micrograms/kg) on systemic capacitance and resistance vessels from changes seen in the MCP and the total peripheral resistance (TPR), respectively. In the untreated dogs, MIL decreased TPR significantly without affecting MCP. In dogs pretreated with total spinal anesthesia or phenoxybenzamine, MIL significantly decreased both MCP and TPR. This suggests that the intrinsic venodilator action of MIL is modified by the baroreflex in untreated animals. MIL decreased the MCP and TPR elevated previously by norepinephrine. One would, therefore, predict that MIL would dilate the systemic capacitance vessels in patients with congestive heart failure.

Anesthesia, Spinal↗
PubMed1991

Functional tricuspid regurgitation following replacement of the mitral valve.

In this series, the effect of replacement of the mitral valve was examined in 86/900 (9.6%) patients who had developed moderate functional tricuspid regurgitation, secondary to rheumatic mitral valvar disease. These patients were subdivided according to the severity of pulmonary hypertension and impairment of right ventricular function. Forty-six patients presented with severe pulmonary hypertension and 40 patients had moderate pulmonary hypertension (mean main pulmonary arterial pressure: 78 +/- 14 mmHg vs 41 +/- 6 mmHg; P less than 0.05). The latter had more advanced disease, greater impairment of right ventricular function and dilatation of the right heart chambers. Functional tricuspid regurgitation regressed in 38/42 survivors with severe pulmonary hypertension and persisted or progressed significantly in 22/34 survivors with impaired right ventricular function despite successful replacement of the mitral valve. The latter underwent replacement of the tricuspid valve (n = 16) or tricuspid annuloplasty (n = 6), at a mean interval of 44 +/- 4.4 months after replacement of the mitral valve, which resulted in 8/22 (23.5%) early deaths. Functional tricuspid regurgitation is more likely to persist in patients with advanced right ventricular failure. Tricuspid valvar competence should be restored in these patients at initial replacement of the mitral valve.

Adult↗
PubMed1984

Characterization of the human right ventricular pressure-volume relation: effect of dobutamine and right coronary artery stenosis.

Right ventricular function was assessed in 15 patients using right ventricular pressure-volume loops. Right ventricular pressure using a micromanometer-tipped catheter, thermodilution cardiac output and gated blood pool scintigrams were simultaneously obtained. To help isolate the right ventricle, a slant hole collimator was used. The measurements were repeated during dobutamine infusion, which was titrated so there was minimal change in systemic pressure and heart rate. The right ventricular pressure-volume loop resembles the usual left ventricular loop except that the isovolumic contraction phase is often not as distinct, and right-sided ejection may continue well beyond right ventricular peak systolic pressure. Systolic but not diastolic function improved with dobutamine administration. There was no significant difference in right ventricular systolic function (ejection fraction, stroke work index, stroke volume index and cardiac index) or in end-diastolic volume index between patients without (Group I) and with (Group II) significant right coronary artery stenosis. However, there was a small but significant difference in right ventricular end-diastolic pressure (5.3 +/- 2.5 and 8.1 +/- 1.8 mm Hg [p less than 0.05]) for Group I and II, respectively. Thus, the right ventricular pressure-volume loop can be used to graphically display right ventricular function and improvement in contractility with dobutamine. The right ventricular isovolumic contraction phase and ejection phase differ from those in the usual left ventricular loop. Although there was a small difference in right ventricular end-diastolic pressure in patients with and without right coronary artery stenosis, the right ventricular pressure-volume loop did not provide additional discriminatory information between these two groups of patients.

Adult↗