Decrease In Pulmonary Wedge Pressure Research Articles

Chronic obstructive pulmonary disease: a slowly progressive cardiovascular disease masked by its pulmonary effects?

Chronic obstructive pulmonary disease: a slowly progressive cardiovascular disease masked by its pulmonary effects?

Clinical and Hemodynamic Effects of CPAP-Therapy in Patients with Cardiogenic Pulmonary Edema

Objective: to evaluate the clinical and hemodynamic effects of CPAP-therapy in the treatment of alveolar cardiogenic pulmonary edema (CPE) in patients with acute myocardial infarction (AMI). Subjects and methods. The open-labeled prospective study included 22 patients (19 males; mean age, 59.2±5.8 years) with CPE that had complicated the course of AMI. Despite the drug and oxygen therapies of CPE for 30 minutes, progressive respiratory and left ventricular failures were an indication for the initiation of CPAP-therapy (7.3±1.2 cm H2O) that was performed, by employing REM-Star apparatuses (Respironics, USA) and Ultra Mirage facial masks (ResMed, Australia). Oxygen, 2 l/min (FiO2 = 40%), was delivered through the mask circuit. Central hemodynamic parameters were measured before and 60 and 180 minutes after the initiation of CPAP-therapy, by using a Swan-Ganz thermodilution cathether (HANDS OFF, model AH-05000-H, ARROW, USA). Arterial and mixed venous blood gas composition was rapidly determined on an automatic gas analyzer (Rapidlab 348, Bayer, USA). Results. Cyanosis and acrocyanosis disappeared and the number of congestive moist rales reduced in the lung in 19 (86.4%) patients during 30-min CPAP-therapy. The patients’ oxygen status changed: the value of PaO2 significantly increased (82.5±2.5 versus 57.4±4.2 mm Hg at the baseline;p<0.05); SaO2 reached the normal values 60 minutes following CPAP-therapy. There was an increase in the cardiac index (3.1±0.2 versus 2.3±0.1 l/min/m2 at the baseline; p<0.05), a decrease in pulmonary wedge pressure (14.4±21 versus 23.6±2.1 mm Hg at the baseline; p<0.05), and synchronism of right and left cardiac performance. Conclusion. CPAP-therapy optimizes treatment of patients with CPE-complicated AMI, results in the normalization of the arterial blood gas composition, significantly diminishes hydrostatic pulmonary capillary pressure, and promotes the synchronism of the right and left hearts.

Effect of β-blockade on the haemodynamic responses of levosimendan and dobutamine in the treatment of low-output heart failure

The novel calcium sensitiser, levosimendan (LS), and the β-adrenoceptor agonist dobutamine (DO), both improve cardiac haemodynamics in patients withsevere low-output heart failure (HF). However, co-administration of β-blockers may influence the action of these inotropic agents. In a multicentre, randomised, double-blind trial in patients with severe low output HF (n = 203), the haemodynamic effects of LS and DO infusions over 24 hours were compared. The influence of concomitant β-blocker therapy (37% in the LS and 39% in the DO groups) were analysed separately. Patients were given either LS (loading dose of 24 μg/kg over 10 min followed by a continuous infusion of 0.1 μg/kg/min), or DO (continuous infusion of 5 μg/kg/min). The infusion rates were doubled if the cardiac index did not increase by ≥ 30% after 2 hours of treatment. The use of β-blockers had significant effects on the increase in cardiac output and the decrease in pulmonary wedge pressure (P = 0.01 and P = 0.03, respectively) (Fig. ​(Fig.1).1). β-blockade attenuated the effect of DO but did not reduce the effects of LS. There was even a slight trend for improved haemodynamic benefits of LS in patients under β-blockade. These findings suggest that LS may be successfully combined with β-blockers to treat patients with low-output heart failure. Figure 1 Mean changes in cardiac output (CO) and pulmonary capillary wedge pressure (PCWP) in patients given LS (β- n = 69 and β+ n = 33) and DO (β- n = 67 and β+ n = 28).

Partial left ventriculectomy with mitral valve preservation in the treatment of patients with dilated cardiomyopathy

Objective: This study reports initial results of partial left ventriculectomy performed with preservation of the mitral valve in the treatment of 27 patients with idiopathic dilated cardiomyopathy. Methods: Patients were in New York Heart Association class III or IV. Partial ventriculectomy was performed as an isolated procedure in four patients and associated with mitral annuloplasty in 23 patients. There were four hospital deaths (14.8%) and the remaining patients were followed for 11.2 ± 6 months. Results: Decrease of left ventricular diastolic diameter (81.8 ± 8.7 to 68.5 ± 7.6 mm, p < 0.001) and improvement of left ventricular wall shortening (12% ± 3.1% to 18.1% ± 3.9%, p < 0.001) were demonstrated by echocardiography after the operation. Left ventricular radioisotopic angiography showed reduction of diastolic volume (495 ± 124 ml to 352 ± 108 ml, p < 0.001) and increase of ejection fraction (17.7% ± 4.6% to 23.7% ± 8.8%, p < 0.001). Right-sided heart catheterization demonstrated improvement of stroke index (24.3 ± 7.7 ml/m 2 to 28.3 ± 7.6 ml/m 2, p < 0.01) and decrease of pulmonary wedge pressure (23.2 ± 8.8 mm Hg to 17 ± 7 mm Hg, p < 0.01). Similar results were documented at 6 and 12 months of follow-up. Functional class improved from 3.6 ± 0.5 to 1.4 ± 0.6 ( p < 0.001). However, seven patients died at midterm follow-up because of heart failure progression or arrhythmia-related events, and survival rate was 59.2% ± 9.4% from 6 to 24 months of follow-up. Conclusions: Partial left ventriculectomy performed with preservation of the mitral valve improves left ventricular function and congestive heart failure in patients with dilated cardiomyopathy. Nevertheless, the high incidences of heart failure progression and arrhythmia-related deaths observed after this procedure preclude its wide clinical application. (J Thorac Cardiovasc Surg 1998;115:800-7)

Coronary flow and left ventricular diastolic function in aortic regurgitation

An abnormal coronary perfusion pressure is probably the major determinant of altered myocardial perfusion in aortic regurgitation; ventricular hypertrophy and diastolic function may also be involved. This study was undertaken to investigate the respective roles of these two variables. Using multiplane transesophageal echocardiography, we evaluated the coronary Doppler flow velocity in the proximal left anterior descending coronary artery in 15 patients with aortic regurgitation before and immediately after valve replacement. The ratios of diastolic:systolic velocity integral and early:late diastolic velocity integral were correlated against coronary perfusion pressure, pulmonary wedge pressure and Doppler echocardiographic indices of left ventricular diastolic function. Patients were compared with 10 subjects without valvular diseases. Aortic regurgitation was associated with a reduction of the coronary diastolic:systolic velocity integral ratio and increment in the early:late diastolic velocity integral ratio. The latter correlated positively with early:late diastolic ratio of mitral flow velocity, pulmonary wedge pressure and left ventricular mass index. Soon after valve replacement, a decrease in pulmonary wedge pressure and a rise in coronary perfusion pressure were seen. Both the echo-Doppler parameters related to diastolic function and the systodiastolic distribution of coronary flow returned to normal. This indicates that diastolic dysfunction rather than left ventricular mass may be related to a disordered myocardial perfusion. In aortic regurgitation, a relationship exists between diastolic ventricular function and coronary flow phasic distribution. Valve replacement improves the former and normalizes the latter. Echo-Doppler parameters of diastolic dysfunction identify patients with worse coronary perfusion and might represent an additional criterion in the preoperative evaluation of patients with aortic regurgitation.

Hemodynamic Mechanisms of the Effect of Nitroglycerin in Patients with Acute Myocardial Infarction

We studied the hemodynamic response to intravenous nitroglycerin (NTG) in 40 patients with and without acute heart failure (hemodynamic subsets I-IV) during acute myocardial infarction. Hemodynamic measurements were performed by right heart catheterization. The results showed that NTG response influenced mainly the preload and to a lesser extent the afterload, however these changes were dependent on initial hemodynamic status. The changes in mean arterial pressure and cardiac index were predominantly related to pretreatment pulmonary wedge pressure and slightly to systemic vascular resistance. Response to NTG could be predicted with 85% probability as a decrease of pulmonary wedge pressure, with 58% probability as a decrease in mean arterial pressure and cardiac index, and with 32% probability as an increase in cardiac index and a decrease in systemic vascular resistance. These results indicate that NTG therapy could have optimal results in patients with elevated pulmonary wedge pressure and normal cardiac index, while in the subsets with low mean arterial pressure or low cardiac index potentially deleterious decrease in these values could occur. Therefore the optimal condition for use of intravenous nitroglycerin in the patients with acute heart failure is isolated pulmonary congestion.

The placebo effect in heart failure

Many patients who are enrolled in controlled clinical trials of new drugs for the treatment of heart failure show favorable hemodynamic and clinical responses to placebo therapy. This “placebo effect” results from both the creation of a supportive therapeutic environment and the spontaneous improvement that is commonly seen when measurements of symptoms and cardiac function are repeated frequently over long intervals of time. Three months of treatment with a placebo produces a reduction in symptoms in 25% to 35% of patients, an increase in cardiac output and a decrease in pulmonary wedge pressure, and an increase in exercise tolerance of up to 90 to 120 seconds. Physicians commonly seek to maximize the “placebo effect”, since the goal of treatment in the clinical setting is to improve the quality of the patient's life. On the other hand, clinical investigators seek to minimize the “placebo effect,” since the goal of a research study is to test the hypothesis that the new drug is superior to a placebo.

Intravenous isosorbide-5-mononitrate in the treatment of acute myocardial infarction

The action of isorsorbide-5-mononitrate (IS-5-MN) infusion (range 6.0 to 10.0 mg/hour) was studied in 24 patients with and without acute heart failure (hemodynamic subsets I to IV) during acute myocardial infarction. Hemodynamic measurements were performed by right-sided cardiac catheterization. Intravenous IS-5-MN demonstrated significant hemodynamic effects compared with baseline values. In subsets I and II, a decrease in pulmonary wedge pressure (PWP) and in cardiac index (CI), without significant changes in heart rate, mean arterial pressure or systemic vascular resistance index were demonstrated. In subsets III and IV, a major increase in CI and a decrease in systemic vascular resistance index, as well as a decrease in PWP were found. Again no changes occurred in mean arterial pressure and heart rate. The dosage was similar in subsets I to IV (8.0, 7.9, 7.8 and 7.3 mg/hour); thus, the differences in the responses could not be attributed to dosage. It appears that several different patterns of hemodynamic IS-5-MN action exist, assuming that IS-5-MN operates on preload and afterload levels. The action of IS-5-MN mechanisms seems to be dependent on an initial hemodynamic subset. No patient had any deleterious hemodynamic effects. A decrease in CI in subsets I and II was not of clinical importance with these dosages. No nitrate tolerance during 9.0 hours of continuous therapy appeared. The duration of the time needed to restore baseline values after IS-5-MN discontinuation demonstrated the following: a decrease in CI in subsets I and II lasting an average of 2.2 hours; a decrease in PWP in subsets II and IV lasting an average of 4.2 hours; and an increase in CI in subsets III and IV maintained at an average of 3.8 hours. No signs of a rebound hemodynamic phenomenon were found in any patient.

Nitrate tolerance in heart failure: Differential venous, pulmonary and systemic arterial effects

The hemodynamic profile of tolerance to intravenous nitroglycerin was studied in 9 patients with New York Heart Association Class III to IV congestive heart failure. After rapid dosage build-up to the maximal tolerated dose (decrease in pulmonary wedge pressure to 10 mm Hg or systolic blood pressure to 90 mm Hg), nitroglycerin (525 ± 548 μg/min) was administered at a constant continuous intravenous infusion for a total of 24 hours. The extent of nitrate tolerance at 24 hours was calculated as the percentage loss of the benefit achieved at time of peak effect of nitroglycerin. Tolerance had a different time course and magnitude in the venous, arterial and pulmonary circulations. At 24 hours, right atrial pressure and pulmonary vascular resistance returned to control values in most patients, while 40 to 50% of the effect on systemic vascular resistance, cardiac index and pulmonary wedge pressure was maintained. These findings emphasize the importance of precise definitions in studies relating to nitrate tolerance.

Long-term beta-blockade in dilated cardiomyopathy. Effects of short- and long-term metoprolol treatment followed by withdrawal and readministration of metoprolol.

To evaluate the short- and long-term effects of beta-adrenergic blockade (metoprolol) as well as the reaction to withdrawal and readministration of metoprolol in severe heart failure, 33 patients (25 men and eight women; mean age, 47.6 +/- 14.0 years) with dilated cardiomyopathy were studied by right and left heart catheterization, right ventricular biopsy, two-dimensional and Doppler echocardiography, and external pulse recordings. Twenty-six of 33 patients survived more than 6 months, and 24 of the 26 patients improved their functional class (from mean 3.3 to 1.8, p less than 0.0001). These 24 patients were subjected to withdrawal of metoprolol until the number of symptoms increased and deterioration occurred as observed noninvasively (group 1, n = 16), whereas the eight patients did not deteriorate during a 12-month period (group 2). During long-term treatment with metoprolol, there was an increase in ejection fraction from 0.24 to 0.42 (p less than 0.0001), whereas there was a decrease in the left ventricular (LV) end-diastolic dimension (from 7.3 to 6.4 cm, p less than 0.0001), in the grade of mitral regurgitation (from 1.7 to 0.4, p less than 0.0001), and in the grade of tricuspid regurgitation (from 0.6 to 0.05, p less than 0.007). There was a decrease in pulmonary wedge pressure (from 23.8 to 10.7 mm Hg, p less than 0.0001), LV end-diastolic pressure (from 24.1 to 13.4 mm Hg, p less than 0.002), and systolic vascular resistance (from 1,782 to 1,499 dynes/sec/cm, p less than 0.04). There was an increase in systolic blood pressure (from 116 to 132 mm Hg, p less than 0.003), cardiac index (from 2.17 to 2.58 l/min/m2, p less than 0.005), and LV stroke work index (from 31 to 65 g.m/m2, p less than 0.0001). During withdrawal of metoprolol, the heart rate and left atrial dimension increased (p less than 0.0001), whereas ejection fraction decreased (p less than 0.0001). The 12 (of 16) patients in group 1 who survived the withdrawal period had metoprolol readministered, and subsequently, ejection fraction increased (from 0.23 to 0.33, p less than 0.002). Patients had a low number of ventricular beta-adrenergic receptors compared with healthy control subjects (30.3 +/- 2.9 vs. 97.4 +/- 8.7 fmol/mg protein, p less than 0.001), but long-term treatment with metoprolol caused a moderate up-regulation (from 30.3 +/- 2.9 to 49.0 +/- 7.1 fmol/mg protein, p less than 0.05), which may facilitate a more normal response to sympathetic stimulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Hemodynamic tolerance of hemodialysis in septic patients with acute renal failure: comparison between recirculating and single-pass bicarbonate hemodialysis

Septic patients with acute renal failure (ARF) are especially intolerant to acetate hemodialysis (HD). Hemodynamic tolerance in septic patients is improved by using bicarbonate dialysis and high Na concentration dialysate. The potential improvement of hemodynamic tolerance with recirculating v single-pass bicarbonate HD (BiHD) has not been evaluated in such patients. We then compared the hemodynamic tolerance in a randomized cross-over study, using a pulmonary artery catheter and biologic changes during the two types of HD in eight severe septic patients with ARF. Patients were dialysed for four hours with a 1 m 21 cuprophan dialyzer, alternatively using single-pass and recirculating system. No absorbent cartridge was used in recirculating BiHD. Intravascular volume expansion (IVE) was used as needed to maintain a systolic arterial pressure of at least 80 mm Hg. Similar doses of catecholamines (dopamine essentially) and equal ultrafiltration rate (mean, 1.55 ± 0.61 for four hours) were used during the two types of dialysis in each patient. No hemodynamic parameter was significantly different between the two procedures, but IVE was lower (370 ± 550 mL v 740 ± 590 mL; P < .05) and weight loss higher (1.06 ± 0.88 kg v 0.68 ± 0.99 kg; P < .05) in recirculating BiHD than in single-pass BiHD. No biologic differences were found between recirculating and single-pass BiHD except for a lower decrease of blood urea (Δ, 10.5 ± 3.4 μmol/L v 12.8 ± 4.9 mmol/L; P <.05) and creatinine (Δ, 107 ± 40 μmol/L v 153 ± 69 μmol/L; P < .05) in recirculating BiHD. Recirculating BiHD was better tolerated than single-pass BiHD, requiring less IVE. This lesser IVE during recirculating BiHD with similar decrease in pulmonary wedge pressure suggests a venoconstrictor effect. This venoconstrictor effect is likely due to a lower loss of catecholamines (dopamine) in the dialysate. Recirculating BiHD is better tolerated than single pass, providing higher weight loss. This procedure is particularly interesting in patients with cardiovascular instability, especially after septic shock.

Hemodynamic effects of felodipine in congestive heart failure.

The hemodynamic effects of increasing dosages of felodipine, a new calcium antagonist with selective vasodilator properties, were studied in 13 patients with chronic cardiac failure. A Swan-Ganz thermodilution catheter was positioned in the pulmonary artery and hemodynamic parameters were monitored from 9 am to 6 pm for five days. On the first and the fifth day patients received placebo (P) and on the second, third, and fourth day patients received felodipine 5, 10, and 20 mg, respectively. Symptom-limited exercise tests with a bicycle ergometer were performed on both days of P and on the fourth day. A marked reduction of systemic vascular resistance (SVR) and a significant increase of cardiac index without increments of heart rate (HR) were observed after felodipine at rest. A dose response effect could be demonstrated. During exercise a significant increment of cardiac index and decrease of pulmonary wedge pressure was observed after felodipine. Felodipine showed a potent vasodilator action on systemic circulation with significant changes on both stroke volume and filling pressures at rest and during exercise without side effects.

Use of invasive ergometric exercise to assess the hemodynamic response to nicardipine

The calcium antagonists are potent vasodilators. This physiologic property suggests that these agents have a potential role in the treatment of patients with hypertension and congestive heart failure. Although the clinical response to calcium antagonism in hypertension is promising, the response in patients with congestive heart failure is less than hoped for; this is due to the fact that this class of agents may induce a hemodynamically important degree of negative inotropic effect. To test the hemodynamic response to nicardipine, a second-generation dihydropyridine, the hemodynamic response to maximal ergometric exercise was evaluated in a group of patients with moderate to severe chronic congestive heart failure. One week of nicardipine therapy was associated with a significant reversal of vasoconstriction at rest and during peak exercise with a secondary increase of cardiac index, and a decrease in pulmonary wedge pressure. The reversal of vasoconstriction was associated with a decrease in mean arterial pressure, with no change in the heart rate. There was no change in oxygen consumption or carbon dioxide production; however, there was a decrease in arteriovenous oxygen difference, consistent with a reduction of oxygen extraction. This short-term study identified the potent vasodilator properties of nicardipine in patients with chronic congestive heart failure; a hemodynamically significant negative inotropic effect could not be identified. Although the use of calcium antagonists for the treatment of congestive heart failure may have a limited role, this study nonetheless suggests that nicardipine may have a favorable vasodilator effect without an overt negative inotropic effect. This would be of considerable advantage in the treatment of hypertension, when compared with β-adrenergic blocking agents.

Hemodynamic effects of a new inotropic agent, piroximone (MDL 19205), in patients with chronic heart failure

The hemodynamic and neurohumoral effects of cummulative intravenous doses of piroximone (MDL 19205), a noncatecholamine, nonglycoside, imidazole derivative with positive inotropic and vasodilating properties, were studied in eight patients with severe congestive heart failure. A dose of 1.25 mg/kg in seven patients and 1.75 mg/kg in one patient increased cardiac index by 75% from 1.96 to 3.41 liters/min per m2 and decreased systemic vascular resistance (-41%), right atrial (-66%) and pulmonary wedge pressure (-35%) (all p less than 0.005). Mean arterial pressure was slightly reduced from 78 to 71 mm Hg (p less than 0.05) and forearm blood flow increased by 42%. Plasma norepinephrine decreased from 830 to 542 pg/ml (p less than 0.05) and plasma renin activity tended to increase. In four patients, dobutamine (15 micrograms/kg per min) produced a comparable increase in cardiac index (+100%), but less decrease in pulmonary wedge pressure (-21 versus -41%, p less than 0.05 versus piroximone) and, unlike piroximone, significantly increased heart rate (+22%, p less than 0.05 versus piroximone) and heart rate-blood pressure product (+30%, p less than 0.01 versus piroximone). In four other patients, a single intravenous dose of piroximone (1 mg/kg) resulted in a 35% increase in the first derivative of left ventricular pressure (dP/dt) from 796 to 1,068 mm Hg/s (p less than 0.01). Thus, piroximone is a potent inotropic agent with an acute hemodynamic profile that may be more favorable than that of dobutamine. Because the drug is orally absorbed, clinical trials of chronic efficacy are indicated.

Amrinone in the treatment of chronic cardiac failure

The efficacy and safety of oral amrinone were examined in 17 patients with moderately severe to severe heart failure that was refractory to standard medical therapy and vasodilators. The short-term and 28 week response to open amrinone therapy was assessed first, followed by a placebo-controlled, double-blind withdrawal study of two 13 week stages in nine patients. Rest and exercise ventricular function were determined before and after 32 hours of amrinone; aerobic capacity was serially assessed. After 2 hours, 1.64 mg/kg amrinone produced a 40% (p less than 0.001) increase in cardiac output and a 32% (p less than 0.02) decrease in pulmonary wedge pressure without altering heart rate or blood pressure. The exercise cardiac index-wedge pressure curve obtained 32 hours after the first oral dose was significantly shifted (p less than 0.05) above control values. A sustained improvement in maximal oxygen uptake was noted during long-term open amrinone therapy. Subsequently, seven of the patients randomized to placebo therapy had a significant deterioration of symptoms or exercise tolerance, or both. After 4 weeks of readministration of amrinone, clinical stability was once again established and exercise tolerance was improved by Weeks 8 to 16. Adverse effects of thrombocytopenia (one patient) and hepatic dysfunction (one patient) attributable to amrinone were observed. It is concluded that amrinone is effective in the long-term treatment of chronic cardiac failure.

Hemodynamic effects of dobutamine in patients below and over 65 years, with left heart failure secondary to an acute myocardial infarction.

The cardiac response to sympathomimetic agents has been reported to be reduced in the elderly. We studied the hemodynamic effects of dobutamine in two groups of patients with acute myocardial infarction (AMI) and left heart failure: group A included 10 patients aged 65 years or less and group B 10 others older than 65. After a 1-hour infusion the increase in cardiac index was highly significant in both groups (27%, p less than 0.001 and 25%, p less than 0.001), and the decrease in pulmonary wedge pressure was greater in group A (42%, p less than 0.001 and 17%, p less than 0.02). The increase in double product was similar in both groups (14%, p less than 0.001 and 18%, p less than 0.005); nevertheless the 4 patients developing angina pectoris during dobutamine infusion were over 65 years. We conclude that dobutamine remains effective in the elderly with AMI and left heart failure but is less well tolerated.

Hemodynamic And Clinical Response To Three-Day Infusion Of Sulmazol (Ar-L 115 Bs) In Severe Congestive Heart Failure

Sulmazol (AR-L 115 BS) is a new positively inotropic drug with arterial and venous vasodilating properties. We studied the effects of sulmazol (three-day infusion) on clinical tolerance, hemodynamics, and blood gas levels in ten patients with severe chronic heart failure. The hemodynamic monitoring included a Swan-Ganz catheter in the pulmonary artery and a radial catheter. Blood gas levels were determined on samples of arterial and mixed venous blood. After 24 hours of infusion, there was a significant increase in cardiac index (2 to 2.5 L/min/sq m; p less than 0.005) and a significant decrease in pulmonary wedge pressure (28 to 19 mm Hg; p less than 0.001) and in right atrial pressure (7 to 4 mm Hg; p less than 0.001) without significant changes in heart rate and systolic blood pressure. These beneficial effects lasted during the three days of infusion. Oxygen delivery was significantly increased (350 to 443 ml/min/sq m; p less than 0.005) without significant change in arterial oxygen tension. The side effects included nausea, vomiting, anorexia, and mild thrombocytopenia. We conclude that sulmazol is a potent drug which may improve severely deteriorated left and right ventricular function in patients with chronic refractory heart failure without affecting the heart rate and the systolic blood pressure.

The effective plasma concentrations of sulmazol (AR-L 115 BS) on haemodynamics in chronic heart failure.

Sulmazol (AR-L 115 BS) is a new inotropic drug which has arterial and venous vasodilating properties. We used it in seven patients with severe refractory heart failure to determine the effective plasma concentration levels and the most effective bolus dose on haemodynamics. The haemodynamic monitoring included a Swan-Ganz catheter in the pulmonary artery and a radial catheter. Haemodynamic measurements and plasma concentration determinations were performed before sulmazol injection and at 5, 10 and 30 min after a bolus 0.25, 0.50, 0.75 mg/kg. We observed a gradual increase in cardiac index and decrease in pulmonary wedge pressure when plasma concentration levels rose but the beneficial effects were mainly observed for sulmazol plasma concentrations above 1 microgram/ml. A bolus injection of 0.75 mg/kg was effective in all cases: a significant increase of cardiac index (1.9 to 2.5 1 min-1 m-2; P less than 0.001) and a significant decrease in pulmonary wedge pressure (30 to 25 mm Hg; P less than 0.005) and right atrial pressure (13 to 10 mm Hg, P less than 0.01) were observed. In these patients sulmazol improved the severely deteriorated left ventricular function without affecting heart rate and blood pressure.

Effects of negative pleural pressure on left ventricular hemodynamics

Negative pleural pressure alters left ventricular (LV) function. LV volume changes have been studied in human subjects, but little is known of the hemodynamic effects. The effect of changes of pleural pressure on LV hemodynamics during a Mueller maneuver (inspiration against an obstruction) was studied in 11 subjects and during quiet, unobstructed inspiration in 3. During the Mueller maneuver, there was an initial decrease in pulmonary wedge pressure and aortic systolic pressure, almost as great as the decrease in pleural pressure. Thereafter, these pressures increased despite a sustained reduction in pleural pressure. Toward the end of the Mueller maneuver, pulmonary wedge transmural pressure averaged 31 ± 12 mm Hg and in 6 patients large v waves developed. The increase in aortic transmural pressure averaged 30 ± 16 mm Hg. Aortic pulse pressure decreased on the first beat from control levels of 59 ± 21 to 47 ± 21 (p < 0.001) and then returned to control levels. During normal breathing in 3 subjects, studied with intraesophageal balloons, there was a similar increase in both transmural aortic and transmural pulmonary wedge pressures with a decrease in pleural pressure 6 mm Hg during inspiration. Thus, increased negative pleural pressure was associated with a marked increase in pulmonary wedge transmural pressure; the increase was approximately proportionate to the decrease in pleural pressure. It is suggested that this increase was due to increased impedance to LV ejection and to right ventricular expansion interfering with LV diastolic filling.

Hemodynamic responses to combined therapy with captopril and hydralazine in patients with severe heart failure

The hemodynamic benefits and safety of combined therapy with captopril and hydralazine were studied during invasive hemodynamic monitoring in 14 patients with severe heart failure. In eight patients, the individual effects of both drugs were evaluated before the administration of combined therapy, whereas hydralazine was added to maintenance captopril therapy in the other six patients. In the first group, captopril alone produced a marked decrease in pulmonary wedge pressure (28 +/- 4 to 18 +/- 5 mm Hg) and mean arterial pressure (85 +/- 20 to 69 +/- 13 mm Hg) (both p less than 0.001) without a significant increase in cardiac index. Hydralazine alone produced a marked increase in cardiac index (1.6 +/- 0.4 to 2.7 +/- 0.5 liters/min per m2) (p less than 0.001), but with a minimal decrease in pulmonary wedge pressure (28 +/- 4 to 23 +/- 4 mm Hg) (p less than 0.05) and without a significant change in mean arterial pressure. The combination of captopril and hydralazine produced an increase in cardiac index similar to that of hydralazine alone and decreases in pulmonary wedge pressure and mean arterial pressure similar to those with captopril alone. Most important, when hydralazine was added to captopril in the entire group of 14 patients, cardiac index increased markedly with little additional decrease in mean arterial pressure and no significant increase in heart rate. The one patient who experienced symptomatic hypotension with combination therapy also had dizziness with captopril alone. Seven of the nine patients maintained on long-term treatment experienced symptomatic improvement. Thus, in patients with severe chronic heart failure, the combined use of captopril and hydralazine is feasible and produces acute hemodynamic improvement superior to that from either drug alone.