Changes In Pulmonary Wedge Pressure Research Articles

Effects of acute changes in pulmonary wedge pressure on periodic breathing at rest in heart failure patients

Patients with heart failure (HF) display a number of breathing abnormalities including periodic breathing (PB) at rest. Although the mechanism(s) contributing to PB remain unclear, we examined whether changes in pulmonary wedge pressure (PWP) and pulmonary vascular resistance (PVR) alter PB in patients with established HF. We studied 12 male patients with HF (age, 50 +/- 11 years; ejection fraction, 18.3 +/- 3.8 %; New York Heart Association class, 3.2 +/- 0.4), with PB at rest, who are undergoing right heart catheterization with infusion of nitroprusside. At baseline, patients with HF displayed minute ventilation (V(E)) oscillations with amplitude of 5.5 +/- 2.7 L/min (57 +/- 34% of the average V(E)) and cycle length of 61 +/- 18 seconds. Cardiac index (CI), PVR, and mean PWP averaged 2.0 +/- 0.4 L min(-1) m(-2), 281.9 +/- 214.9 dyne/s per cm(-5), and 28.3 +/- 5.4 mm Hg, respectively. During nitroprusside infusion, CI increased to 3.1 +/- 0.6 L min(-1) m(-2), PVR decreased to 163.9 +/- 85.2 dyne/s per cm(-5), and PWP fell to 10.0 +/- 4.2 mm Hg. Nitroprusside reduced the amplitude (2.6 +/- 2.4 L/min, 23 +/- 21% of average V(E); P < .01) and cycle length (41.4 +/- 28.8 seconds; P < .01) of V(E) oscillations while abolishing oscillations in 3 patients. Although average V(E) and PaCO2 remained unchanged, there was a significant increase in the ratio of tidal volume to inspiratory time (V(T)/T(I); P < .01), suggesting an increase in ventilatory drive. The change in the amplitude of V(E) oscillations was positively correlated with the change in PWP (r = 0.75; P < .01), negatively correlated with the change in PVR (r = 0.63; P < .05), and not correlated with the change in CI. These data suggest that PWP (left atrial pressure) may play a direct role in the PB observed in HF at rest.

Acute hemodynamic effects of endogenous adenosine in patients with chronic heart failure

Objective The objective of this study was to assess the acute hemodynamic effects of endogenous adenosine accumulation in patients with chronic heart failure. Exogenously administered adenosine has been shown to reduce pulmonary vascular resistance and to increase cardiac index in normal subjects and in patients with pulmonary hypertension or end-stage biventricular heart failure. Endogenous adenosine accumulation can be provoked by dipyridamole. Methods and Results Ultra-low-dose dipyridamole (0.07 mg/kg/min for 4 minutes) was administered in 20 patients with either symptomatic idiopathic ( n = 12) or ischemic ( n = 8) dilated cardiomyopathy and reduced left ventricular ejection fraction (mean 25% ± 5%). Hemodynamic variables were measured before and within 1 minute from the end of dipyridamole infusion. After dipyridamole administration, a mild but significant increase in heart rate (4.5%; p = 0.03) and reduction in mean blood pressure (6.8%; p < 0.001) without changes in right atrial pressure ( p = NS) were detected. Dipyridamole increased cardiac output by 26.6% ( p < 0.001), cardiac index by 24% ( p < 0.001), and stroke volume by 19.8% ( p < 0.001), with concomitant 24.6% reduction of systemic vascular resistance ( p < 0.001). Moreover, dipyridamole reduced mean pulmonary artery pressure by 8.3% ( p < 0.01) and pulmonary vascular resistance by 33.3% ( p = 0.001), without changes in pulmonary wedge pressure ( p = NS). A significant correlation between percent decrease from baseline in pulmonary and systemic vascular resistance ( r = 0.66; p = 0.002) was found after administration of dipyridamole. Conclusions Endogenous adenosine accumulation induced by ultra-low-dose dipyridamole infusion acutely improves the hemodynamic profile, decreasing pulmonary and, to a lower extent, systemic vascular resistance and increasing cardiac index in patients with severe chronic heart failure. (Am Heart J 1998;136:37-42.)

Mitral flow velocity changes after 6 months of optimized therapy provide important hemodynamic and prognostic information in patients with chronic heart failure

Transmitral flow velocity patterns evaluated by Doppler echocardiography provide important hemodynamic and prognostic information in various cardiac conditions. However, these patterns may change over time, and so far the hemodynamic and prognostic significance of these changes has not been established. Accordingly, we performed this study to determine the hemodynamic and prognostic value of changes in transmitral flow velocity patterns after 6 months of optimized medical treatment in patients with chronic heart failure due to ischemic or nonischemic dilated cardiomyopathy. Ninety-eight consecutive patients with chronic heart failure underwent a clinical examination, a cardiopulmonary exercise test, and simultaneous Doppler echocardiographic and hemodynamic studies at baseline and after 6 months of optimized medical therapy. After the examination at 6 months, patients were followed up for 12 ± 7 months. Cardiac death and heart transplantation while patients were in critical condition were considered events. A restrictive pattern was defined by an early-to-late peak diastolic velocity ratio >1 and an early diastolic deceleration time ≤ 130 msec. Patients were grouped according to their mitral flow pattern at baseline and its changes after chronic optimized therapy. No significant changes in clinical, ergometric, and hemodynamic variables were found after 6 months in the 49 patients who had a persistent restrictive transmitral flow pattern or the 24 patients who had a persistent nonrestrictive transmitral flow pattern. In the 19 patients who had a restrictive pattern at baseline that reverted into a nonrestrictive pattern, this change was accompanied by a highly significant reduction in pulmonary wedge pressure (from 25 ± 7 mm Hg to 11 ± 3 mm Hg) and by an increase in exercise capacity, whereas in the 6 patients who had a nonrestrictive pattern that became restrictive, hemodynamic features markedly deteriorated. Seventeen of the 21 events occurred in the 49 patients (event rate 35%) with a persistent restrictive pattern, whereas the event rate was much lower in the 19 patients with a reversible restrictive pattern (5%) and in the 24 patients with a persistent nonrestrictive pattern (4%). Two (33%) of the 6 patients in whom a restrictive pattern developed had events. Cox analysis revealed that a restrictive transmitral flow pattern ( p = 0.0068) and peak rate of oxygen consumption ( p = 0.0056) detected at the late examination were significantly related to cardiac events. These results show that in patients with chronic heart failure, changes in transmitral flow patterns after chronic optimized therapy are correlated with changes in pulmonary wedge pressure, are accompanied by changes in functional capacity, and provide relevant independent prognostic information.

Immunosuppression switch in pediatric heart transplant recipients: Cyclosporine to FK 506

We studied rejection, allograft function and side effects, such as hypertension, renal dysfunction and hypercholesterolemia, in seven patients switched from cyclosporine-based triple-drug immunosuppression to FK 506. A subset of pediatric heart transplant recipients treated with triple-drug immunosuppression consisting of cyclosporine, azathioprine and prednisone experience either persistent rejection when attempts are made to taper corticosteroids or morbidity from cyclosporine and corticosteroids. Experience with the new immunosuppressive agent FK 506 has demonstrated its effectiveness as a single agent in heart transplant recipients, and anecdotal evidence has shown that side effects such as hypertension and hypercholesterolemia may be lower. Seven patients whom we deemed corticosteroid dependent were switched to FK 506-based therapy. Allograft function, episodes of rejection, need for corticosteroids and incidence of side effects from FK 506 were monitored. The switch to FK 506 was performed using an established protocol. Follow-up time has ranged from 15 to 41 months. Serial right heart catheterizations and endomyocardial biopsies were performed after each reduction of corticosteroid dosing. Catheterization data showed no significant change in pulmonary wedge pressure, mean right atrial pressure or cardiac index, indicating no decline in allograft function. Serial echocardiographic variables of allograft function were also stable. At present, all seven patients are free of the corticosteroid portion of their immune suppression. There have been only two episodes of significant acute rejection requiring treatment with intravenous corticosteroids. Antihypertensive medications have been discontinued in five of six patients previously treated with these drugs. Plasma cholesterol, low density lipoprotein and triglyceride levels were decreased, and renal function was stable. Preliminary studies suggest that FK 506 may be an alternative immunosuppressive agent for pediatric and adolescent patients experiencing ongoing rejection or significant morbidity from cyclosporine and corticosteroids and in those patients dependent on corticosteroids for immune suppression.

Increased Incidence of Silent Ischemia After Acute Myocardial Infarction

To determine the incidence of angina pectoris during induced myocardial ischemia in patients who have had thrombolytic therapy for acute myocardial infarction in comparison with patients with angina pectoris. During percutaneous transluminal coronary angioplasty, both study groups had coronary artery occlusion by the balloon dilatation catheter for 5 minutes. A tertiary, cardiology referral center. Twenty-five patients with angina pectoris who were undergoing angioplasty were compared with 30 patients having angioplasty 2 days after thrombolytic therapy for acute myocardial infarction. Development of angina pectoris during balloon occlusion of the coronary artery was the primary end point; the ischemic response and muscle viability were assessed using both surface and intracoronary electrocardiograms and pulmonary artery wedge pressure. During balloon occlusion 16 (64%) of 25 patients in the angina pectoris group developed angina. In contrast, nine (30%) of 30 patients in the thrombolysis group had angina pectoris during balloon occlusion of the infarct artery (P less than .01). The electrocardiographic response to ischemia and changes in pulmonary wedge pressure were similar in the two study groups. After thrombolytic therapy for myocardial infarction, silent ischemia may be the rule rather than the exception.

Exercise-induced secretion of atrial natriuretic factor and its relation to hemodynamic and sympathetic stimulation in untreated essential hypertension

This study evaluates the release of atrial natriuretic factor (ANF) during maximal exercise in 7 patients with untreated moderate to severe hypertension with invasive monitoring of hemodynamic characteristics in relation to sympathetic activity. Peripheral venous ANF (fmol/ml) was determined at rest and maximal exercise producing a respiratory exchange ratio of 1.14 ± 0.10. In 5 of 7 patients, simultaneous right ventricular and peripheral venous ANF samples could be obtained to assess exercise myocardial secretion of ANF. With exercise, mean blood pressure increased from 150 ± 26 to 192 ± 29 mm Hg (p < 0.001), pulmonary wedge pressure increased from 7 ± 3 to 18 ± 10 mm Hg (p < 0.05) and ANF increased from 11.7 ± 8.2 to 25.7 ± 15.9 (p < 0.02). This ANF response correlated weakly with pulmonary wedge pressure (r = 0.497, p = not significant), since patients without an increase in pulmonary wedge pressure had no increase in ANF. However, changes in pulmonary wedge pressure and plasma norepinephrine during exercise were inversely correlated (r = −0.811, p < 0.02), with the greatest increase in norepinephrine occurring with a minimal increase in pulmonary wedge pressure. Similarly, ANF and plasma norepinephrine were inversely correlated during exercise (r = −0.869, p < 0.05). A significant increase in right ventricular ANF indicated myocardial secretion. Plasma ANF therefore increased because of active myocardial production during exercise in patients with moderate to severe hypertension. These findings further suggest a directionally opposing relation between ANF release resulting from increased atrial tension and sympathetic nervous system influence on cardiac performance during exercise.

Clinical Experience with Intravenous Fenoldopam

Fenoldopam (Corlopam), a new dopaminergic agent in clinical development by SmithKline Beecham Pharmaceuticals, is a dopamine-1 (DA1) agonist at post-synaptic dopamine receptors. Preclinical and clinical studies have demonstrated that it is a potent renal vasodilator as well as a peripheral vasodilator. In both normal volunteers and hypertensive patients intravenous fenoldopam causes dose-related decreases in blood pressure and important increases in renal hemodynamics and function including increased renal blood flow, diuresis and natriuresis. Fenoldopam does not alter glomerular filtration. Intravenous fenoldopam has been demonstrated to be efficacious in severe hypertensive patients in several multicenter, multinational trials. In severe hypertension efficacy trials fenoldopam was judged to be as effective as sodium nitroprusside and to produce less serious side effects. In patients with moderate to severe heart failure, fenoldopam has been demonstrated to produce dose-related acute increases in cardiac output, stroke volume and work index, decreased systemic vascular resistance but no important changes in pulmonary wedge pressure or right atrial pressure. In CHF patients fenoldopam has been demonstrated to be as efficacious as sodium nitroprusside. Fenoldopam, as a specific (DA1) agonist resulting in decreased peripheral and renal vascular resistance, diuresis, natriuresis and increases in cardiac hemodynamics on intravenous administration, appears to be an efficacious agent which offers a reasonable alternative in the treatment of severe hypertension and acute congestive heart failure.

Pharmacology, pharmacodynamics and pharmacokinetics of sotalol

Sotalol is a nonselective, water-soluble β-adrenoceptor antagonist with no membrane-stablizing activity or intrinsic sympathomimetic activity. Sotalol is, essentially, completely absorbed and is not metabolized. Consequently, bioavailability is close to 100%. Age and food have slight but unimportant effects on bioavailability. C max of sotalol is 2 to 3 hours with a t 1 2 between 7 and 15 hours. Excretion of sotalol is primarily through the kidneys, with no metabolism by liver and no first-pass effect. Therefore, sotalol plasma levels and half-life are directly related to creatinme clearance and glomerular filtration rate. Appropriate dose adjustments must be made for patients with impaired renal function or increased renal blood flow, as in pregnancy. The β-adrenoceptor antagonistic effects of sotalol are directly related to plasma levels, which, in turn, are directly related to dose. However, the β-adrenoceptor antagonism t 1 2 is longer than the sotalol plasma t 1 2 . As a consequence of its ability to prolong the action potential duration, sotalol also increases cardiac contractility in isolated ventricular, but not atrial, preparations by 20 to 40%. This positive inotropic effect is not blocked by β or α blockade or reserpine pretreatment and seems to be related to sotalol's effects on cardiac ionic currents. Like the effects of sotalol on action potential duration, the positive inotropic effects are inversely proportional to rate. The hemodynamics of sotalol indicate a relative lack of direct cardiac depressant activity in both animals and humans. The typical hemodynamic effects of sotalol in normotensive humans, even with depressed myocardial function, are a reduction in heart rate with little or no change in blood pressure, a reduction in cardiac output with no change in stroke volume, and little or no change in pulmonary wedge pressure and left ventricular end-diastotic pressure or volume, and little or no change in ejection fraction either at rest or during exercise.

Feasibility of physical training in post-infarct patients with left ventricular aneurysm: a haemodynamic study.

To investigate the haemodynamic changes after physical training in patients with left ventricular aneurysm, 60 uncomplicated patients, mean age 51 +/- 10 years, underwent a maximal ergometric test in the supine position with haemodynamic monitoring (Swan-Ganz catheter) 37 +/- 10 days from acute myocardial infarction and after a 4-week period of supervised physical training. The size of aneurysmatic dilatation (aneurysm area-total end-diastolic area ratio %) and resting left ventricular ejection fraction (Dodge's method) were obtained from a two-dimensional echocardiogram (apical approach) performed on the same day of the pre-training ergometric test. On average, left ventricular ejection fraction was reduced (39 +/- 11%), with values below 35% in 25 patients. Resting pulmonary wedge pressure was greater than 12 mm Hg in 42 patients and greater than 20 mm Hg at peak exercise in 48 subjects. The entity of aneurysmatic dilatation was significantly related to left ventricular ejection fraction (r = 0.60, less than 0.001), but not to the values of pulmonary wedge pressure at rest (r = 0.22) or at peak exercise (r = 0.11). No complication during the physical training period was observed. After training, maximal work capacity increased (77 +/- 29 vs 94 +/- 35 W, P less than 0.001) as well as cardiac output and stroke volume with a slight change in pulmonary wedge pressure (24 +/- 7 vs 28 +/- 7 mm Hg, P less than 0.05). At matched submaximal exercise, heart rate decreased (P less than 0.05), stroke volume and arterio-venous oxygen difference increased (P less than 0.05) without significant changes in cardiac output and left ventricular filling pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic Assessment by Handgrip Exercise of Patients With Recent Myocardial Infarction

Hemodynamic responses to isometric handgrip exercise at 30% maximal voluntary contraction and to maximal symptom-limited cycle exercise were analyzed in 90 patients, who had New York Heart Association functional classes I and II 21 to 65 days after acute myocardial infarction. Neither angina, electrocardiographic changes, nor symptoms or signs of heart failure occurred during handgrip exercise, whereas each did, in some cases, during cycle exercise. Both handgrip and dynamic exercise produced significant cardiovascular activation; in particular, stroke volume decreased and total systemic resistance increased during handgrip, whereas they behaved in an opposite manner during cycle exercise. Left ventricular stroke work index was not increased during handgrip even in persons with a normal response to this test (change in pulmonary wedge pressure [PWP] >m 4 mm Hg). Resting PWP was normal (ltm12 mm Hg) in 79% of the patients. It increased normally during both dynamic (<m20 mm Hg) and handgrip exercise in 35% and responded abnormally to both types of work in 30%, whereas it was normal only during handgrip exercise in 18% and only during dynamic exercise in 17%. A PWP greater than 16 mm Hg during handgrip exercise was predictive (96%) of abnormal response to dynamic exercise. Correlations were not found between invasive (PWP and cardiac index) and noninvasive (rate-pressure product) recordings during handgrip exercise. In patients with myocardial infarction, the hemodynamic responses to handgrip and to dynamic exercise are qualitatively and quantitatively different; a normal PWP during handgrip work does not indicate normal left ventricular function; handgrip exercise is not a useful detector of myocardial ischemia or arrhythmias in patients with uncomplicated infarction.

Poor correlation between pulmonary arterial wedge pressure and left ventricular end-diastolic volume after coronary artery bypass graft surgery.

The authors studied 12 surgical patients in the intensive care unit post coronary artery bypass graft surgery and ten nonsurgical patients in the coronary care unit with chronic heart failure to determine the usefulness of the pulmonary arterial wedge pressure as an indicator of left ventricular preload. Left ventricular end diastolic volume was derived from concomitant determination of ejection fraction (gated blood pool scintigraphy) and stroke volume (determined from thermodilution cardiac output). In the nonsurgical patients, there was a significant correlation between changes in pulmonary arterial wedge pressure and left ventricular end-diastolic volume (P less than 0.05, r = 0.57). In the 12 patients studied during the first few hours after surgery, there was a poor correlation between changes in pulmonary wedge pressure (range = 4-32 mmHg) and left ventricular end-diastolic volume (range = 25-119 ml/m2), and a poor correlation between pulmonary arterial wedge pressures and stroke work index. In contrast, there was a good correlation between left ventricular end-diastolic volume and stroke work index. The poor correlation between the pulmonary arterial wedge pressure and left ventricular end-diastolic volume was not explained by changes in systemic or pulmonary vascular resistance. The altered ventricular pressure-volume relationship may reflect acute changes in ventricular compliance in the first few hours following coronary artery bypass graft surgery. While measurement of pulmonary arterial wedge pressure remains valuable in clinical management to avoid pulmonary edema, it cannot reliably be used as an index of left ventricular preload while attempting to optimize stroke volume in patients immediately following coronary artery bypass graft surgery.

Hemodynamic effects of vasodilators and long-term response in heart failure

Hemodynamic responses to vasodilators are commonly assessed when starting long-term vasodilator treatment in patients with chronic left ventricular failure, although the relation between short- and long-term responses is not established. Thus, short- and long-term hemodynamic responses to placebo and vasodilators (isosorbide dinitrate, minoxidil and enalapril or captopril) were measured and long-term clinical efficacy was assessed by changes in exercise capacity after 1 to 5 months of vasodilator administration (plus digitalis and diuretic agents) in 46 patients with New York Heart Association functional class II to IV heart failure caused by cardiomyopathy. There were no significant changes in hemodynamics or exercise capacity during placebo treatment. After initial doses and during long-term administration of vasodilator drugs, hemodynamics were significantly improved. After long-term vasodilator treatment, maximal oxygen uptake during exercise increased by 2.9 +/- 5.7 ml/min per kg from a control value of 14.1 +/- 5.6 ml/min per kg (p less than 0.01), and exercise duration also increased by 1.8 +/- 3.5 minutes (p less than 0.01). Changes in maximal oxygen uptake, however, did not correlate with short-term changes in pulmonary wedge pressure (correlation coefficient [r] = -0.14), cardiac index (r = -0.01) or systemic vascular resistance (r = -0.20). Long-term hemodynamic changes also failed to correlate with changes in exercise capacity. Baseline hemodynamics, cardiac dimensions and left ventricular ejection fraction before vasodilator administration all failed to correlate with baseline exercise capacity or with long-term changes in exercise capacity. Thus, hemodynamic measurements at initiation or during follow-up of vasodilator therapy do not relate to long-term clinical efficacy assessed by exercise capacity in patients with chronic left ventricular failure. Therefore, the rationale for making invasive hemodynamic measurements before initiating long-term vasodilator therapy for heart failure is questioned.

Haemodynamic study of patients with severe sepsis during haemodialysis.

A study was performed in order to observe haemodynamic changes induced by haemodialysis in 14 patients with acute renal failure and severe sepsis. Left ventricular function, as assessed by changes in pulmonary wedge pressure and left ventricular stroke work index through plasma volume expansion, did not change during haemodialysis. Ultrafiltration-induced decreases in cardiac index provoked in 8 patients, with nearly normal initial systemic arteriolar resistance, had adequate and constant increase in their resistance (p less than 0.001), whereas 6 patients with low initial systemic arteriolar resistance did not increase their resistance and had a frequent (9/13 measurements) and significant (p less than 0.001) fall in mean aortic pressure. This abnormality of vascular tone is probably due to severe sepsis and explains why hypotension is a frequent occurrence during haemodialysis in such patients.

Evaluation of haemodynamic effects of intravenous propranolol at low dosage (1 and 2 mg) in acute myocardial infarction.

The haemodynamic effects of intravenous propranolol at low dosage (1 and 2 mg) have been evaluated on 14 patients in the acute stage of myocardial infarction. The first 1 mg propranolol was not followed by any significant variation in the variables measured. After the second 1 mg propranolol, the heart rate, cardiac index, and stroke index decreased significantly but moderately. Changes in pulmonary wedge pressure were not significant. It is concluded that intravenous propranolol in the small dosage of 1 or 2 mg, at which antiarrhythmic effect is still produced, has only a negligible depressant myocardial effect.