Late hemodynamic changes in percutaneous mitral valvuloplasty

Percutaneous mitral valvuloplasty (PMV) was performed in 57 patients with mitral stenosis. Twenty-three women and 34 men (mean age 28 +/- 10 mean +/- SD) were included in the study. A single-balloon (trefoil or bifoil) technique was used in 49 patients and a double-balloon (trefoil + monofoil) technique in eight. After a 3-month follow-up period, right- and left-sided cardiac catheterization was repeated. In the single-balloon group there was improvement in the mitral valve gradient (16.10 +/- 5.99 to 4.41 +/- 2.03 mm Hg), mean left atrial pressure (22.65 +/- 6.13 to 9.76 +/- 3.01 mm Hg), and mitral valve area (0.89 +/- 0.22 to 1.95 +/- 0.46 cm2/m2). Mean pulmonary artery pressure and mean pulmonary wedge pressure decreased to 19.33 +/- 4.19 mm Hg and 10.73 +/- 2.60 mm Hg from 32.94 +/- 7.90 mm Hg and 21.49 +/- 5.98 mm Hg. Cardiac output increased to 6.86 +/- 0.56 L/min from 5.57 +/- 0.66. All improvements were statistically significant (p less than 0.001). In the double-balloon study group, mitral valve gradient (23.75 +/- 2.77 to 4.50 +/- 1.94 mm Hg), mean left atrial pressure (31.63 +/- 3.57 to 9.50 +/- 1.94 mm Hg), mean pulmonary artery pressure (44.00 +/- 6.36 to 18.88 +/- 7.10), and mean pulmonary wedge pressure (29.25 +/- 3.73 to 10.25 +/- 1.85 mm Hg) all improved significantly (p less than 0.001). Mitral valve area and cardiac output increased from 0.89 +/- 0.15 to 2.44 +/- 0.44 cm2/m2 (p less than 0.001) and from 5.46 +/- 0.76 to 7.15 +/- 0.52 L/min (p less than 0.002), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of hydralazine on mouth occlusion pressure and ventilatory response to hypercapnia in patients with chronic obstructive pulmonary disease and pulmonary hypertension

Hydralazine has been shown to increase minute ventilation (VE) in patients with chronic obstructive pulmonary disease and pulmonary hypertension. The mechanism by which hydralazine produces this effect has not been defined. We investigated the effects of orally administered hydralazine on hypercapnic ventilatory response (delta VE/delta PaCO2) and central respiratory drive (delta P0.1/delta PaCO2) as well as the effects on hemodynamics, ventilation, and gas exchange in 10 male patients (mean age, 59 +/- 2 yr). The patients had a severe degree of chronic air-flow obstruction (FEV1, 1.07 +/- 0.08 L) and mild pulmonary hypertension (mean pulmonary artery pressure, 25 +/- 4 mm Hg). After hydralazine, the slope of delta VE/delta PaCO2 increased by 177% (p less than 0.005), and the slope of delta P0.1/delta PaCO2 increased by 145% (p less than 0.05). Resting ventilation increased from 14.8 +/- 1.0 to 17.1 +/- 1.4 L/min (p less than 0.02), primarily as a result of increased respiratory frequency. After hydralazine, PaO2 increased from 66 +/- 4 to 70 +/- 3 mm Hg (p less than 0.05) at rest and from 54 +/- 3 to 59 +/- 3 mm Hg (p less than 0.02) during exercise. PaCO2 decreased from 46 +/- 3 to 42 +/- 3 mm Hg (p less than 0.001) at rest and from 50 +/- 3 to 45 +/- 3 mm Hg (p less than 0.001) during exercise. No change was seen in the dead space to tidal volume ratio or the degree of venous admixture. Mean pulmonary artery pressure and total pulmonary resistance both at rest and during exercise were unchanged after hydralazine.(ABSTRACT TRUNCATED AT 250 WORDS)     

Long-term effects of hydralazine on ventilation and blood gas values in patients with chronic obstructive pulmonary disease and pulmonary hypertension

Hydralazine has been shown to increase minute ventilation, alveolar ventilation, and arterial partial pressure of oxygen (PaO2) after short-term administration in patients with chronic obstructive pulmonary disease and pulmonary hypertension. The effects of orally administered hydralazine on ventilation and blood gas values were evaluated after six to 18 months of treatment in 10 male patients who had demonstrated an increase in minute ventilation after 24 hours of treatment. Hydralazine was administered at a dose of 200 mg per day during the initial 24 hours and in doses ranging from 40 mg per day to 200 mg per day during long-term therapy. Following 24 hours of treatment, a statistically significant increase in minute ventilation, alveolar ventilation, and PaO2, and reduction in arterial partial pressure of carbon dioxide (PaCO2) were seen both at rest and during exercise. After six to 18 months of hydralazine therapy, the increase in minute ventilation at rest persisted when compared with the pre-hydralazine value (15.3 +/- 1.3 liters/minute versus 13.1 +/- 1.1 liters/minute; p less than 0.05). The improvement in PaO2 at rest continued relative to the pre-hydralazine value (70.9 +/- 3.2 mm Hg versus 65.1 +/- 3.0 mm Hg, p less than 0.05) as did the PaO2 during exercise (60.3 +/- 3.5 mm Hg versus 53.3 +/- 2.0 mm Hg; p less than 0.05). The reduction in PaCO2 at rest persisted compared with the pre-hydralazine value (41.2 +/- 2.4 mm Hg versus 47.0 +/- 3.0 mm Hg; p less than 0.05) as did the PaCO2 during exercise (44.0 +/- 2.8 mm Hg versus 48.0 +/- 2.8 mm Hg; p less than 0.05). No significant changes in minute ventilation, PaO2, or PaCO2 were seen at rest or during exercise, when re-measured after six to 18 months in an age- and sex-matched control group of 10 patients who did not receive hydralazine. These results demonstrate that the short-term effects of hydralazine on ventilation and blood gas values persisted after six to 18 months of treatment in this sample of patients, some of whom received doses less than 200 mg per day.     

Pressure controlled inverse ratio ventilation in severe adult respiratory failure

Thirty-one patients with severe respiratory failure who were failing volume controlled conventional ratio ventilation were placed on pressure controlled inverse ratio ventilation (PC-IRV) for a total of 4,426 patient-hours. The PC-IRV resulted in a reduction of minute ventilation from 22 +/- 1.0 L/min (mean +/- SEM) to 15 +/- 0.7 L/min. Peak inspiratory pressure (PIP) was reduced from 66 +/- 2.3 cm H2O to 46 +/- 1.6 cm H2O and positive end expiratory pressures (PEEP) from 15 +/- 1.0 cm H2O to 2.5 +/- 0.5 cm H2O. Mean airway pressure increased from 30 +/- 1.7 cm H2O to 35 +/- 1.7 cm H2O. Oxygenation (PaO2) improved from 69 +/- 4.0 mm Hg to 80 +/- 4.5 mm Hg. The PaCO2 and arterial pH were not significantly changed. There were no significant changes in mean hemodynamic pressures. A lung compromise index (FIO2.PIP.10/PaO2) retrospectively distinguished between successful and unsuccessful PC-IRV episodes. These data suggest that PC-IRV can be successfully and safely implemented in critically ill patients with severe respiratory failure over prolonged periods of time resulting in significant improvement in oxygenation at lower minute volume, peak airway pressure and PEEP requirements.     

Determinants of delayed improvement in exercise capacity after percutaneous transvenous mitral commissurotomy

BACKGROUND: Percutaneous transvenous mitral commissurotomy (PTMC) results in short-term hemodynamic and symptomatic improvements. We have previously shown that the immediate symptomatic relief is related to the improvement in excessive exercise ventilation. The exercise capacity, however, does not improve in the short term but does improve gradually over several months. The pathophysiologic basis for the delayed improvement in exercise capacity has not been fully evaluated. METHODS: To elucidate the determinants of improvement in exercise capacity late after PTMC, maximal ergometer exercise with respiratory gas analysis and exercise hemodynamic measurements were performed in 22 patients with symptomatic mitral stenosis before, immediately after, and 7 months after PTMC. RESULTS: Mitral valve area increased from 0.9 +/- 0.2 cm(2) to 1.7 +/- 0.4 cm(2) after PTMC (P <.01). Significant improvements were observed in symptoms, cardiac output at peak exercise (6.6 +/- 1.5 L/min vs 8.6 +/- 1.9 L/min, P <.01), and mean pulmonary artery pressure at peak exercise (54.1 +/- 15.6 mm Hg vs 42.3 +/- 9.5 mm Hg, P <.01) immediately after PTMC. Excessive exercise ventilation, as assessed by the slope of the regression line between expired minute ventilation and carbon dioxide output (VE-VCo(2)), decreased significantly from 38.2 +/- 8.2 to 33.3 +/- 4.9 (P <.01). There were no significant changes in peak oxygen uptake (from 17.5 +/- 3.2 mL/kg per minute to 17.9 +/- 3.6 mL/kg per minute) immediately after PTMC. At 7 months, improved mitral valve area, symptoms, cardiac output at peak exercise, mean pulmonary artery pressure at peak exercise, and VE-VCo(2) were unchanged compared with values immediate after PTMC. Significant improvement was observed in peak oxygen uptake (19.7 +/- 3.0 mL/kg per minute [P <.01 compared with pre-PTMC or immediate post-PTMC values]). The increase in exercise cardiac output or the decrease in pulmonary artery pressure was not correlated with the late improvement in peak oxygen uptake. The short- or long-term improvements in VE-VCo(2), however, were significantly correlated with the late improvement in peak oxygen uptake. CONCLUSIONS: Our results suggest that ventilatory improvement, not increased exercise cardiac output, contributed at least in part to the late improvement in exercise capacity after PTMC.     

Improvement in exercise capacity and exercise hemodynamics 3 months after double-balloon, catheter balloon valvuloplasty treatment of patients with symptomatic mitral stenosis

Clinical status, exercise treadmill performance, and hemodynamics were determined in 24 patients with symptomatic mitral stenosis before catheter balloon valvuloplasty (CBV) and at 3 months follow-up. Hemodynamic determinations at rest showed that mitral CBV performed by the double-balloon technique resulted in significant immediate decreases in mean pulmonary arterial wedge pressure (28 +/- 7 to 16 +/- 5 mm Hg, p less than .01), mean pulmonary arterial pressure (41 +/- 11 to 33 +/- 10 mm Hg, p less than .05), and mitral valve gradient (16 +/- 7 to 6 +/- 3 mm Hg, p less than .01), and significant increases in cardiac output (4.3 +/- 1.1 to 5.0 +/- 1.4 liters/min, p less than .01). Mitral valve area increased from 1.0 +/- 0.3 to 2.2 +/- 0.7 cm2 (p less than .01). The mitral valve area was unchanged (2.0 +/- 0.7 cm2, p = NS) at 3 months. The lower pulmonary arterial wedge pressure, pulmonary arterial pressure, and mitral valve gradient persisted at 3 month follow-up catheterization. Clinical examinations showed that before CBV, 21 of 24 patients were in New York Heart Association functional class III or IV; 3 months after CBV, 22 patients were in class I or II. Before CBV, the mean exercise treadmill time was 5.9 +/- 3.2 min and it had increased to 9.8 +/- 2.9 min (p less than .01) by the 3 month follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)     

Systemic to pulmonary bronchial blood flow in mitral stenosis

We measured systemic to pulmonary bronchial blood flow [Qbr(s-p)] during total cardiopulmonary bypass in 15 patients with mitral stenosis and elevated pulmonary venous pressure (group A, mean pulmonary wedge pressure = 22.2 +/- 5.4 mm Hg, mean +/- SD) and in 15 patients with coronary artery diseases and normal pulmonary venous pressure (group B). Qbr(s-p) is the volume of blood accumulating in the left side of the heart in the absence of pulmonary and coronary flows. This blood was vented through a cannula introduced into the left atrium and measured. Qbr(s-p) was 76.3 +/- 13.9 ml/min (2.18 +/- 0.37 percent of extracorporeal circulation pump flow) and 22.3 +/- 2.1 (0.63 +/- 0.15) in group A and B, respectively (p less than 0.01). During total cardiopulmonary bypass, pulmonary venous pressure is approximately atmospheric pressure, and no differences in systemic blood pressure, extracorporeal circulation pump flow, and airways pressure were observed between group A and B. Therefore, vascular resistance through the bronchial vessels draining into the pulmonary circulation is reduced in patients with mitral stenosis and elevated pulmonary venous pressure.     

Effects of exercise on transmitral gradient and pulmonary artery pressure in patients with mitral stenosis or a prosthetic mitral valve: a Doppler echocardiographic study

Doppler echocardiography was used to determine changes in transmitral gradient and pulmonary artery pressure after exercise in 12 patients with mitral stenosis and 11 patients with a prosthetic mitral valve. The mean transmitral gradient in the mitral stenosis group was 9 +/- 7 mm Hg at rest and increased to 17 +/- 8 mm Hg after exercise. In patients with a prosthetic mitral valve, exercise resulted in an increase in mean transmitral gradient from 5 +/- 2 to 8 +/- 3 mm Hg. Calculated pulmonary artery systolic pressure increased with exercise from 41 +/- 19 to 70 +/- 32 mm Hg in the mitral stenosis group and from 28 +/- 8 to 39 +/- 15 mm Hg in patients with a prosthetic valve. Exercise Doppler echocardiographic evaluation of changes in transmitral gradient and pulmonary artery systolic pressure was found to be technically simple and an important addition to the noninvasive evaluation of patients with mitral valve disease.     

Lung mechanics and gas exchange during pressure-control ventilation in dogs. Augmentation of CO2 elimination by an intratracheal catheter.

Increased awareness of pressure-related injury to the alveolar-capillary interface has renewed interest in modes of ventilation that limit alveolar distention such as pressure-controlled ventilation (PCV). We examined respiratory system mechanics and gas exchange during PCV in six dogs. Our data conformed to the predictions of our single-compartment mathematical model of respiratory dynamics during PCV (J Appl Physiol 1989; 67:1081-92). For a fixed pressure (Pset) and inspiratory time fraction (Tl/Ttot) (15 cm H2O and 0.3, respectively), minute ventilation (VE) reached a well-defined plateau as frequency (f) increased from 10 to 50 breaths/min and tidal volume (VT) fell progressively. Concomitantly, the physiologic dead-space fraction (VD/VT) increased from 0.50 +/- 0.04 to 0.85 +/- 0.04, and arterial PCO2 (PaCO2) rose from 39 +/- 4 to 76 +/- 12 mm Hg. At a fixed combination of frequency, applied pressure, and Tl/Ttot (40 breaths/min, 15 cm H2O, and 0.3), VE did not change when we introduced fresh gas continuously from an intratracheal catheter. However, PaCO2 and VD/VT fell progressively as catheter flow increased from zero to 14 L/min (60 +/- 12 to 40 +/- 12 mm Hg and 0.83 +/- 0.03 to 0.25 +/- 0.14 mm Hg, respectively). We conclude that during PCV at a fixed Pset and Tl/Ttot increasing frequency caused VT to fall and VE to reach a plateau. Declining VT was associated with a rise in PaCO2 because of a subsequent fall in alveolar ventilation. Insufflating fresh gas by an intratracheal catheter increased alveolar ventilation and improved CO2 elimination by washing out the anatomic dead space.(ABSTRACT TRUNCATED AT 250 WORDS)     

The usefulness of dobutamine in the assessment of the severity of mitral stenosis

Patients with mitral stenosis often require supine exercise in order to increase their heart rate and cardiac output to assess the severity of their valvular obstruction during cardiac catheterization. We substituted dobutamine for exercise in 14 patients with suspected mitral stenosis. The dobutamine infusion was started at 5 micrograms/kg/min and was increased to 10, 15, and 20 micrograms/kg/min every 3 minutes as tolerated. The heart rate increased from 84 +/- 4 to 123 +/- 7 bpm (p less than 0.001), the cardiac index increased from 2.4 +/- 0.2 to 3.4 +/- 0.2 L/min/m2 (p less than 0.001), and the mean pulmonary artery pressure increased from 27 +/- 3 to 30 +/- 2 mm Hg (p less than 0.02). The pulmonary wedge pressure of 19 +/- 2 mm Hg and the mitral valve index of 0.8 +/- 0.1 cm2/m2 remained unchanged, but the left ventricular end-diastolic pressure decreased from 11 +/- 2 to 6 +/- 2 mm Hg (p less than 0.02). The hemodynamic response during the infusion of dobutamine identified a subgroup of patients with more severe mitral stenosis. Thus, the administration of dobutamine is useful in the evaluation of the severity of mitral valve obstruction during catheterization.     

Effect of nitroglycerin on the pulmonary venous gradient in patients after mitral valve replacement

Because the equality of the pulmonary artery wedge pressure and left atrial pressure has been questioned in patients with mitral valve disease and pulmonary hypertension, this study examined how vasomotor activity in the pulmonary capacitance vessels might contribute to a discrepancy between these pressures. The difference between the pulmonary wedge and left atrial pressures (designated as the pulmonary venous gradient) was measured after nitroglycerin administration in nine patients who had pulmonary hypertension (mean pulmonary artery pressure 40 mm Hg) after mitral valve replacement. Five minutes after sublingual nitroglycerin, 0.4 mg, the mean pulmonary wedge pressure decreased from 19 +/- 2 to 13 +/- 2 mm Hg (p less than 0.005), exceeding the decrease in left atrial pressure (15 +/- 2 to 11 +/- 2 mm Hg; p less than 0.005). Pulmonary blood flow increased from 4.6 +/- 0.4 to 4.9 +/- 0.4 liters/min (p less than 0.005). The decrease in mean pulmonary venous gradient from 4.0 +/- 0.8 to 1.7 +/- 0.6 mm Hg (p less than 0.025) was attributed to nitrate-mediated pulmonary venodilation. The ratio of venous gradient to blood flow, an index of pulmonary venous tone, decreased after nitroglycerin from 0.9 +/- 0.2 to 0.4 +/- 0.1 (p less than 0.01). These data indicate that reversible pulmonary vasoconstriction contributes to elevation of the pulmonary wedge pressure above the left atrial pressure in patients with chronic mitral valve disease and pulmonary hypertension and that nitroglycerin may produce pulmonary venodilation decreasing the pulmonary venous gradient.     

Importance of the "atrial kick" in determining the effective mitral valve orifice area in mitral stenosis

Atrial fibrillation with a rapid ventricular response in patients with mitral stenosis (MS) is often accompanied by pulmonary congestion and reduced cardiac output owing to a diminished diastolic filling period and the loss of the end-diastolic left ventricular (LV) pressure increment. To test the hypothesis that loss of atrial contraction (atrial kick) also results in a decrease in effective mitral valve orifice area, 6 patients with pure, isolated MS were studied in sinus rhythm during atrial pacing and simultaneous atrioventricular pacing. Atrial pacing at 140 beats/min caused no significant change from baseline in cardiac output or mitral valve area, but there was a decrease in LV end-diastolic volume and ejection fraction as well as an increase in left atrial pressure and mean diastolic gradient. Simultaneous atrioventricular pacing (to eliminate atrial kick) induced a decrease in cardiac output (4.4 +/- 0.9 vs 5.2 +/- 0.8 liters/min at 110 beats/min, 4.2 +/- 0.9 vs 5.1 +/- 0.9 liters/min at 140 beats/min; p less than 0.05) and LV end-diastolic volume (77 +/- 27 vs 93 +/- 29 ml at 110 beats/min, 54 +/- 17 vs 65 +/- 19 ml at 140 beats/min; p less than 0.05), an increase in left atrial pressure (28 +/- 3 vs 20 +/- 5 mm Hg at 110 beats/min, 30 +/- 4 vs 25 +/- 5 mm Hg at 140 beats/min; p less than 0.05), and a decrease in mitral valve area (1.2 +/- 0.4 vs 1.4 +/- 0.5 cm2 at 110 beats/min, 1.2 +/- 0.4 vs 1.4 +/- 0.4 cm2 at 140 beats/min; p less than 0.05). Thus, loss of atrial kick may cause pulmonary congestion and reduced cardiac output in patients with MS, partly because of a decrease in effective mitral valve area.     

Percutaneous transluminal balloon dilatation of the mitral valve in pregnancy

Pregnancy can cause life threatening complications in women with mitral stenosis, and there is a substantial risk of fetal death if valvotomy under cardiopulmonary bypass is required. A patient is described in whom pulmonary oedema developed after delivery of her first child by caesarean section 13 months previously. Subsequent cardiac catheterisation showed severe mitral stenosis (valve area 0.96 cm2, valve gradient 12 mm Hg, pulmonary artery pressure 30/16 mm Hg). Before valvotomy could be performed the patient again became pregnant and presented in pulmonary oedema at twenty two weeks' gestation. Medical treatment was unsuccessful and she underwent percutaneous transluminal balloon dilatation of the mitral valve. This increased the valve area to 1.78 cm2 and reduced the transmitral gradient to 6 mm Hg. The procedure was uncomplicated, and she remained symptom free on no medication. She delivered vaginally at 37 weeks' gestation. Percutaneous transluminal balloon dilatation of the mitral valve is a safe and effective alternative to mitral valvotomy in pregnancy.     

Percutaneous transluminal balloon dilatation of the mitral valve in pregnancy.

Pregnancy can cause life threatening complications in women with mitral stenosis, and there is a substantial risk of fetal death if valvotomy under cardiopulmonary bypass is required. A patient is described in whom pulmonary oedema developed after delivery of her first child by caesarean section 13 months previously. Subsequent cardiac catheterisation showed severe mitral stenosis (valve area 0.96 cm2, valve gradient 12 mm Hg, pulmonary artery pressure 30/16 mm Hg). Before valvotomy could be performed the patient again became pregnant and presented in pulmonary oedema at twenty two weeks' gestation. Medical treatment was unsuccessful and she underwent percutaneous transluminal balloon dilatation of the mitral valve. This increased the valve area to 1.78 cm2 and reduced the transmitral gradient to 6 mm Hg. The procedure was uncomplicated, and she remained symptom free on no medication. She delivered vaginally at 37 weeks' gestation. Percutaneous transluminal balloon dilatation of the mitral valve is a safe and effective alternative to mitral valvotomy in pregnancy.     

Balloon dilation of mitral stenosis in adult patients: postmortem and percutaneous mitral valvuloplasty studies

Preliminary reports have documented the utility of percutaneous balloon valvuloplasty of the mitral valve in adult patients with mitral stenosis, but the mechanism of successful valve dilation and the effect of mitral valvuloplasty on cardiac performance have not been studied in detail. Accordingly, mitral valvuloplasty was performed in five postmortem specimens and in 18 adult patients with rheumatic mitral stenosis, using either one (25 mm) or two (18 and 20 mm) dilation balloons. Postmortem balloon dilation resulted in increased valve orifice area in all five postmortem specimens, secondary to separation of fused commissures and fracture of nodular calcium within the mitral leaflets. In no case did balloon dilation result in tearing of valve leaflets, disruption of the mitral ring or liberation of potentially embolic debris. Percutaneous mitral valvuloplasty in 18 patients with severe mitral stenosis (including 9 with a heavily calcified valve) resulted in an increase in cardiac output (4.3 +/- 1.1 to 5.1 +/- 1.5 liters/min, p less than 0.01) and mitral valve area (0.9 +/- 0.2 to 1.6 +/- 0.4 cm2, p less than 0.0001), and a decrease in mean mitral pressure gradient (15 +/- 5 to 9 +/- 4 mm Hg, p less than 0.0001), pulmonary capillary wedge pressure (23 +/- 7 to 18 +/- 7 mm Hg, p less than 0.0001) and mean pulmonary artery pressure (36 +/- 12 to 33 +/- 12 mm Hg, p less than 0.01). Left ventriculography before and after valvuloplasty in 14 of the 18 patients showed a mild (less than or equal to 1+) increase in mitral regurgitation in five patients and no change in the remainder.(ABSTRACT TRUNCATED AT 250 WORDS)     

Arterial oxygenation and pulmonary function with Saralasin in chronic lung disease

During our earlier saralasin infusion study in hypertensive patients, we found a drug-induced rise in arterial oxygen tension (PaO2) associated with unchanged mixed venous PO2 or the PaCO2 and unrelated to cardiopulmonary hemodynamic changes. To test the hypothesis that saralasin improved pulmonary mechanics, blood gases, lung mechanics, lung volumes, diffusing capacity, and distribution of ventilation were analyzed and cardiac output (CO) measured in 12 normotensive men with chronic pulmonary disease before and during a 2 1/2 hour infusion of Saralasin (5 micrograms/kg/min). The PaO2 increased from a mean of 63 +/- 3 (SEM) to 70 +/- 3 mm Hg (p less than 0.001), while the CO decreased from 6.81 +/- 0.52 L/min to 6.18 +/- 0.48 L/min (p less than 0.005). The change in (delta)CO correlated with delta PaO2 (r = -0.67, p less than 0.05). Total systemic vascular resistance rose from 1,201 +/- 134 to 1,353 +/- 147 dynes X sec X cm5 (p less than 0.001). The PaCO2 and other measurements remained unchanged. We conclude that saralasin raised the PaO2 not by changing pulmonary function or mechanics, but by redistributing pulmonary blood flow and improving the ventilation-perfusion relationship.     

Pulmonary outcomes of off-pump vs on-pump coronary artery bypass surgery in a randomized trial

STUDY OBJECTIVES: Comparison of pulmonary outcomes after off-pump coronary artery bypass (OPCAB) vs on-pump coronary artery grafting with cardiopulmonary bypass (CABG/CPB).Study design: We examined preoperative and postoperative respiratory compliance, fluid balance, hemodynamics, arterial blood gases, chest radiographs, spirometry, pulmonary complications, and time to extubation in a prospective trial of 200 patients randomized to OPCAB vs CABG/CPB performed by one surgeon. RESULTS: One CABG/CPB patient and two OPCAB patients required mitral valve repair or replacement and were withdrawn. After three crossovers from CABG/CBP to OPCAB and one crossover from OPCAB to CABG, 97 CABG/CPB patients and 100 OPCAB patients remained. There were no significant preoperative demographic differences between groups. Postoperative compliance was reduced more after OPCAB than after CABG/CPB (- 15.4 +/- 10.7 mL/cm H(2)O vs - 11.2 +/- 10.1 mL/cm H(2)O [mean +/- SD]; p = 0.007), associated with rotation of the heart into the right chest to perform posterolateral bypasses (p < 0.001) and the concomitant increased fluid requirements necessary to maintain hemodynamic stability during rotation of the heart. In addition to higher intraoperative fluid intake (4,541 +/- 1,311 mL vs 3,585 +/- 1,033 mL, p < 0.0001), OPCAB patients had higher intraoperative fluid balance (3,903 +/- 1,315 mL vs 1,772 +/- 1,373 mL, p < 0.0001), and higher postoperative pulmonary arterial diastolic pressure (15.0 +/- 5.5 mm Hg vs 11.8 +/- 5.2 mm Hg, p < 0.0001) and central venous pressure (10.4 +/- 4.5 mm Hg vs 8.4 +/- 4.7 mm Hg, p < 0.0001). Despite lower compliance, immediate postoperative Pao(2) on fraction of inspired oxygen of 1.0 (275 +/- 97 torr vs 221 +/- 92 torr, p = 0.001) was higher after OPCAB and extubation was earlier (p = 0.001). Postoperative chest radiographs, spirometry, mortality, reintubation, or readmission for pulmonary complications were not different between groups. CONCLUSIONS: Compared to CABG/CPB, OPCAB was associated with a greater reduction in postoperative respiratory compliance associated with increased fluid administration and rotation of the heart into the right chest to perform posterolateral grafts. OPCAB yielded better gas exchange and earlier extubation but no difference in chest radiographs, spirometry, or rates of death, pneumonia, pleural effusion, or pulmonary edema.     

Hypoxemic threshold for lung ventilation in the toad

The relationship between the activity of the buccal force pump, expressed as the time integral of positive buccal pressure, and PaO2 was investigated in conscious toads, Bufo marinus, unidirectionally ventilated at a high flow rate (240-260 ml/min). The high ventilatory flow rate meant that PaO2 was largely independent of the animal's ventilatory activity so that the relationship between pulmonary ventilation and PaO2 was effectively open-loop. The hypoxemic threshold (PaO2) for lung ventilation was 54.2 mm Hg in hypocapnia (PaCO2 = 4.7 +/- 0.3 mm Hg), 82.6 mm Hg in normocapnia (PaCO2 = 11.6 +/- 0.2 mm Hg), and 137.9 mm Hg in hypercapnia (PaCO2 = 20.1 +/- 0.1 mm Hg). Unidirectional ventilation with 20% O2 in N2, a condition in which the toads were normoxic but hypocapnic, stopped pulmonary ventilation cycles. Taken with existing evidence that hyperoxia stops pulmonary ventilation even under conditions in which PaCO2 is elevated this suggests that hypoxic and hypercapnic stimuli summate to drive lung ventilation in the toad. Bilateral denervation of the carotid labyrinths decreased pulmonary ventilation in absolute terms, but did not reduce the proportionate increase in pulmonary ventilation in response to normocapnic hypoxia, suggesting that chemoreceptors within the carotid labyrinth may contribute to, but are not solely responsible for, the hypoxemic ventilatory drive.     

Pathogenesis of congestive state in chronic obstructive pulmonary disease. Studies of body water and sodium, renal function, hemodynamics, and plasma hormones during edema and after recovery.

BACKGROUND. The pathogenesis of salt and water accumulation in patients with chronic obstructive pulmonary disease is unclear and may differ from that in patients with congestive heart failure due to myocardial disease. This study was undertaken to investigate some of the mechanisms involved. METHODS AND RESULTS. Hemodynamics, water and electrolyte spaces, renal function, and plasma hormone concentrations were measured in nine patients with edema due to chronic obstructive pulmonary disease and in six patients after recovery. Mean cardiac output (3.8 +/- 0.26 l/min.m2) was normal, but right atrial (11 +/- 1 mm Hg) and mean pulmonary arterial (41 +/- 3 mm Hg) pressures were increased. Mean pulmonary arterial wedge pressure (11 +/- 1 mm Hg) was normal. Pulmonary vascular resistance (8.6 +/- 1.3 mm Hg.min.m2/l) was increased, but systemic vascular resistance (19.3 +/- 1.3 mm Hg.min.m2/l) and mean arterial pressure (83 +/- 4 mm Hg) were low. All patients were hypoxemic (PaO2, 40 +/- 2 mm Hg) and hypercapnic (PaCO2, 60 +/- 2 mm Hg). There was a significant increase in total body water (+21%), extracellular volume (+45%), plasma volume (+45%), blood volume (+88%), and exchangeable sodium (+38.2%). Renal plasma flow was severely reduced (-63.2%), but glomerular filtration rate was only mildly decreased (-32%). Significant increases were seen in plasma norepinephrine (3.5-fold normal), renin activity (7.6-fold normal), vasopressin (twice normal), atrial natriuretic peptide (9.4-fold normal), growth hormone (10.7-fold normal), and cortisol (1.9-fold normal). After recovery, the PaO2 increased (50 +/- 3 mm Hg) and PaCO2 fell (45 +/- 4 mm Hg), and the patients became free from edema. All the body compartments returned toward normal, although they did not entirely reach normal values. Renal plasma flow increased significantly, and glomerular filtration became normal. Right atrial and pulmonary arterial pressures and pulmonary vascular resistance decreased (p less than 0.01). Cardiac output decreased but not significantly. Blood pressure increased but not significantly. However, systemic vascular resistance increased significantly to a normal value. CONCLUSIONS. We conclude that patients with edema due to chronic obstructive pulmonary disease have severe retention of salt and water, reduction in renal blood flow and glomerular filtration, and neurohormonal activation similar to that seen in patients with edema due to myocardial disease. However, unlike the latter, in chronic obstructive pulmonary disease cardiac output is normal, and systemic vascular resistance and arterial blood pressure are low. This probably is due to the vasodilator properties of hypercapnia. The consequent low arterial blood pressure may be the stimulus for the neurohormonal activation and retention of salt and water.     

Benefits of intraoperative echocardiography in the surgical management of hypertrophic cardiomyopathy.

OBJECTIVES. The purpose of this study was to determine the role of intraoperative echocardiography in planning the site and extent of myectomy and in ensuring adequate control of the left ventricular outflow tract gradient. BACKGROUND. Although intraoperative echocardiography has been found to be beneficial in patients undergoing valve repair, its impact on surgical decisions in patients undergoing septal myectomy for hypertrophic cardiomyopathy has not been described. METHODS. In 50 patients undergoing septal myectomy over a 5-year period, epicardial echocardiography was performed before cardiopulmonary bypass to establish the extent of outflow tract obstruction, locate its site and plan the myectomy. In 30 patients, transesophageal echocardiography was also used to corroborate data on outflow tract anatomy and examine the mitral valve. RESULTS. In 40 patients (80%) the initial myectomy resulted in a reduction of the maximal outflow tract gradient from 88 +/- 45 to 24 +/- 11 mm Hg, measured by epicardial continuous wave Doppler echocardiography. Ten patients (20%) were shown by postbypass intraoperative echocardiography to have an unsatisfactory result, based on a persistent gradient > 50 mm Hg (n = 7) or persistent mitral regurgitation of greater than moderate severity (n = 3). The postbypass two-dimensional echocardiogram was then used to direct the surgeon toward the most likely site of continued obstruction, and cardiopulmonary bypass was reinstituted to permit further myectomy (n = 9) or mitral valve repair (n = 1). After the second or subsequent period of cardiopulmonary bypass, the outflow tract gradient (26 +/- 14 mm Hg) was substantially reduced and was not significantly different from the postbypass gradient (24 +/- 11 mm Hg) in the group with initial surgical success. At postoperative follow-up (20 +/- 37 weeks), the maximal measured outflow tract gradient (22 +/- 21 mm Hg) showed no difference between patients with immediate surgical success and those requiring a second period of cardiopulmonary bypass for further resection. CONCLUSIONS. Intraoperative echocardiography proved a useful tool to guide the site and extent of septal myectomy, leading to more adequate surgical resection and to persistence of satisfactory control of the outflow tract obstruction into the early follow-up period.