Biomedical subjects
Publications and source records attributed to M Guazzi.
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Arteriovenous O2 content (a-vCO2) differences increase during exercise in normal subjects through several mechanisms including PO2, O2 pressure at which hemoglobin (Hb) is half saturated with O2 (P50), and Hb concentration changes. The present study was undertaken to evaluate how much these biochemical changes are relevant to a-vCO2 difference through exercise in patients with heart failure. Twenty-seven patients with congestive heart failure [10 patients in functional class A (peak exercise O2 uptake >20 ml x kg-1 x min-1), 9 in class B (20-15 ml x kg-1 x min-1), and 8 in class C (15-10 ml x kg-1 x min-1)] underwent a cardiopulmonary exercise test with once-per-minute simultaneous blood sampling from the pulmonary and systemic arteries for determination of Hb, PO2, PCO2, pH, O2 content (CO2), Hb saturation and lactic acid (pulmonary artery only), and calculation of P50. Analysis of data was done at six exercise stages: the first at rest, the last at peak exercise, and the second to the fifth at one-, two-, three-, and four-fifths of O2 consumption increase. a-vCO2 difference at peak exercise was 14.3 +/- 2.1, 16.9 +/- 2.4, and 14.7 +/- 2.1 (SD) ml/dl in class A, B, and C patients, respectively. The contribution of Hb, P50, and PO2 changes to the increments of a-vCO2 difference during exercise was 21, 17, and 63%, respectively; the only interclass difference observed was for P50, which plays a greater role in a-vCO2 difference in class A. Hb changes act mainly at the arterial site, whereas P50 and PO2 act at the venous site. Hb increase was constant through the test, venous P50 increase was greater above anaerobic threshold, and venous PO2 reduction was most remarkable at the onset of exercise; in class C patients, no venous PO2 change was recorded in the second half of exercise. Thus a-vCO2 difference increase during exercise is notable in patients with heart failure but unrelated to the severity of the syndrome. Hb, P50, and, to the greatest degree, PO2 changes participate in the increment of a-vCO2 difference. In class C patients, the lack of PO2 reduction in the second half of exercise suggests the achievement of a "whole body critical venous PO2."
Our hypothesis is that regulation of the lung vessel tone and microvascular permeability may be disrupted in chronic heart failure (CHF) and angiotensin converting enzyme (ACE) inhibition may contribute to their readjustment. This hypothesis is based on the fact that KII-ACE, the same enzyme that converts angiotensin I and inactivates bradykinin, is highly concentrated in the luminal surface of the lung vessels and its blockade in CHF may reduce their exposure to an excess of angiotensin II and augment the action of prostaglandins and nitric oxide (NO) deriving from local kinin hyperconcentration. We probed whether ACE-inhibitors influence the pulmonary function; this is peculiar of CHF; they act as KII- or ACE-blockers. Aspirin was utilized as a prostaglandin synthesis inhibitor. We investigated 16 CHF patients and 16 age- and sex-matched normal volunteers or mild untreated hypertensives. All were non-smokers, not taking ACE-inhibitors, aspirin or other cyclooxygenase inhibitors. Pulmonary function tests, exercise testing with respiratory gases and echocardiography were performed in the run-in and repeated at the end of placebo, enalapril (10 mg t.i.d.), enalapril plus aspirin (325 mg/day) and aspirin given in random order and double-blind fashion for 15 days each. Enalapril, as compared to placebo, caused an increase in mean voluntary ventilation (MVV) and alveolar-capillary diffusing capacity for carbon monoxide (DLCO) in CHF, that were counteracted by the addition of aspirin. Aspirin alone was not effective. Enalapril and aspirin were ineffective on the pulmonary function of controls. As to the functional capacity, enalapril increased exercise tolerance time, oxygen consumption (VO2p), minute ventilation (VEp) tidal volume (VTp) and reduced the ratio of volume of dead space gas (VDp) to VTp (VD/VTp), at peak exercise in CHF patients. These effects all were inhibited by the combination of aspirin and were not observed in controls. In CHF VO2p changes from placebo correlated with those in DLCO (r = 0.80, p < 0.0001) and not with those in ejection fraction. This correlation was abolished by aspirin and was not seen in controls. Variations in VD/VTp in CHF patients while on enalapril were related to those in DLCO (r = -0.69, p = 0.003). In CHF the ventilatory equivalent for carbon dioxide production per minute at 1 liter was diminished with enalapril and not in combination with aspirin. Derangements related to CHF are the substrate for benefits of ACE-inhibition on pulmonary function and exercise capacity. Pulmonary diffusion limitation is an important mediator of exercise impairment and its improvement with enalapril goes in parallel with VD/VT, MVV, VT, VE to VCO2 relationship and not with ejection fraction. These patterns reflect changes occurring within the lung that are not related to left ventricular function. The counteracting influence of aspirin on these affects bespeaks a substantial participation of prostaglandins that might readjust capillary permeability and lung interstitial fluid content or alveolar capillary membrane diffusing capacity.
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We investigated exercise capacity after fluid depletion in patients with moderate congestive heart failure (CHF). Twenty-one patients underwent ultrafiltration (mean volume +/- SEM: 1,770 +/- 135 ml). Echocardiography, tests of pulmonary function, and a cardiopulmonary exercise test with hemodynamic and esophageal pressure monitoring were performed before ultrafiltration and 3 months later. Tests without invasive measurements were repeated 4 and 30 days after ultrafiltration. Twenty-one control patients followed the same protocol but did not have ultrafiltration. Patients who underwent ultrafiltration and increased their oxygen consumption at peak exercise (peak VO2) by > 10% at the 3-month evaluation (group A1, n = 9) were separated from those who did not (group A2, n = 8); 3 patients did not complete the follow-up. Four days after the procedure, peak VO2 had risen from 17.3 +/- 0.8 to 19.3 +/- 0.9 ml/min/kg in group A1, and from 11.9 +/- 0.7 to 14.1 +/- 0.7 ml/min/kg in group A2 (p < 0.01). Plasma norepinephrine and pulmonary function were consistent with a greater severity of the syndrome in group A2. At 3 months in group A1, the relations of filling pressure to cardiac index of the right and left ventricles were shifted upward; the esophageal pressure swing (differences between end-expiratory and end-inspiratory pressure) for a given tidal volume was lower; the peak exercise dynamic lung compliance had increased from 0.10 +/- 0.05 to 0.14 +/- 0.03 L/mm Hg (p < 0.01). None of these changes were detected in group A2 and control patients.(ABSTRACT TRUNCATED AT 250 WORDS)
Adenosine is a possible mediator of cardiac pain during myocardial ischemia; however, little is known about the influence of adenosine on cardiac sympathetic afferent activity and thereby on its algogenic mechanism. In 20 anaesthetized, decerebrated, curarized and artificially ventilated cats, we studied the impulse activity of 20 single afferent sympathetic fibers with a left ventricular receptive field in relation to epicardial applications of adenosine, coronary artery occlusions and arterial pressure rises. All fibers increased their impulse activity (from 1.2 +/- 0.2 to 2.6 +/- 0.5 imp/s; P < 0.001) during slight (20 +/- 8%) rises in aortic pressure, thus exhibiting low-threshold receptor characteristics. In 10 cats, epicardial applications of three different doses of adenosine (0.1, 1 and 10 mg/ml) caused a brief increase in neural activity with dose-related responses. This response was abolished by aminophylline, a P1 purinergic inhibitor. In the other group of 10 cats, four subsequent 30-s occlusions of the coronary arterial vessel supplying the receptive fields of the fibers were performed, in control conditions and 30 s, 3 and 7 min, respectively, after the end of excitation induced by adenosine (1 mg/ml) application. During the control coronary occlusion the impulse activity increased from 1.1 +/- 0.1 to 5.5 +/- 0.7 imp/s (P < 0.0001). A similar activation was present during the second occlusion initiated 30 s after the end of adenosine-induced activation. In contrast, a significant potentiation of the response was observed (8.8 +/- 1.2 vs. 5.3 +/- 0.9 imp/s; P < 0.001) during the occlusion initiated 3 min after the end of excitation by adenosine. This effect was no longer present during the last occlusion performed after 7 min. When the protocol was repeated substituting adenosine with saline (n = 5) or after i.v. administration of aminophylline (n = 5), no potentiation was observed, even though the excitatory response to coronary occlusion was preserved. These data show that adenosine can activate cardiac sympathetic afferent fibers in a dose-related manner, and potentiate their responses to coronary occlusion, while leaving unaffected the responsiveness to a hemodynamic stimulus. The excitatory effects are likely to involve the P1 purinergic receptors. The potentiation phenomenon might play a role in the genesis of an algogenic code.
OBJECTIVES: The study sought to probe whether the adaptation of the right ventricle to reduced preload may influence that of the left ventricle (interdependence) and whether and how this mechanism contributes to maintain an adequate pump function. BACKGROUND: A study like this requires that subjects be normal, restraint of venous return be gradual, systolic function and diastolic filling and dimensions of either ventricle be monitored. METHODS: Of 30 healthy men (mean [+/- SD] age 35 +/- 7 years) studied with Doppler echocardiography, 20 were studied in the supine position and after 20 degrees, 40 degrees and 60 degrees tilting for 10 min; the remaining 10 subjects were also studied at the same levels of tilting for 45 min. RESULTS: At 20 degrees, heart rate, blood pressure and stroke volume were steady; the diastolic right ventricular area was reduced (p < 0.001); and the end-diastolic dimension of the left ventricle did not vary. Tilting at 40 degrees and 60 degrees increased heart rate and diastolic pressure, decreased systolic pressure and stroke volume and reduced the diastolic dimensions of both ventricles. At any tilting level, right and left peak early inflow velocities (E) were decreased, peak late velocities (A) were unchanged, and E/A ratios were reduced, suggesting that the atrial-ventricular pressure difference was diminished bilaterally and that the atrial contribution to ventricular filling was maintained. Tachycardia at 40 degrees and 60 degrees tilting was not associated with enhancement of left ventricular fiber fractional shortening or mean velocity of shortening for any corresponding end-systolic wall stress; changes in heart rate also did not correlate with those in fiber fractional shortening and velocity of shortening. The adaptive responses to the same degrees of tilting for a duration of 45 min were comparable to those at 10 min. CONCLUSIONS: With moderate restraint of venous return, the left ventricle maintains filling and output in response to a reduction in right ventricular diastolic volume, which increases left ventricular compliance (interdependence), and to the pulmonary blood reservoir, which compensates for an immediate decrease in right ventricular stroke volume. The decreased lung blood volume would facilitate right ventricular ejection, resulting in a normal stroke output despite the reduced preload. Thus, mechanical adjustments fully compensate for moderate reduction of venous return. A more severe reduction requires chronotropic support for the maintenance of cardiac output. With prolongation of tilting time to 45 min, adaptive mechanisms do not become exhausted in normal persons.
OBJECTIVE: Ultrafiltration (UF) can improve the exercise performance of patients with moderate congestive heart failure (CHF). Our aim was to define the starting levels of performance below which UF is beneficial. PATIENTS AND METHOD: We studied 26 patients in 2 to 3 NYHA class, whose clinical condition was stable, left ventricle ejection fraction (echocardiography) was < 35% and peak exercise oxygen uptake (VO2) was > or = 14 mL/min/kg. They underwent a single extracorporeal UF (about 600 mL of ultrafiltrate per hour). Before that, we evaluated pulmonary function (PFT), functional capacity (cardiopulmonary exercise test [CPX]), cardiac index, left ventricle ejection fraction, ventricular filling pressures, and plasma norepinephrine at rest. The PFTs and CPXs were repeated 3 months after UF. RESULTS: Sixteen patients had a rise of peak exercise VO2 > 1 mL/min/kg at the 3-month evaluation (group A, ultrafiltrate = 2,040 +/- 241 mL) and 10 did not (group B, ultrafiltrate = 1,870 +/- 169 mL). Forced expiratory volume (1 s), maximal voluntary ventilation, and vital capacity were lower in group A than in group B and improved after UF only in group A. Before UF, VO2 at peak exercise and at anaerobic threshold (15.5 +/- 0.4 mL/min/kg and 11.0 +/- 0.5, respectively) was also lower in group A than in group B (21.2 +/- 0.7 mL/min/kg and 14.8 +/- 0.9, p < 0.01). Patients whose pre-UF peak exercise VO2 was > 18.5 mL/min/kg (group B) had no increase in this variable. No significant group differences were detected regarding norepinephrine, left ventricular ejection fraction, and hemodyanmic parameters at rest. CONCLUSION: In patients with moderate CHF undergoing UF, exercise capacity improvement is inversely related to the pre-UF level of physical performance and pulmonary function; VO2 at peak exercise seems useful for identification of patients not benefiting from the procedure.
Dead space (VD)/tidal volume (VT) ratio is an indirect index of ventilation/perfusion matching. Therefore, it is currently evaluated in patients with congestive heart failure to detect the organ system limiting the exercise tolerance. The VD/VT calculation requires measurement of arterial CO2 partial pressure (PaCO2). For practical reasons, the software of most metabolic carts substitutes the PaCO2 with the end-expiratory CO2 (PETCO2) or the PJCO2 (calculated as PJCO2 = 5.5 +/- 0.9 PETCO2-2.1 VT). Nonetheless, the applicability of these methods in congestive heart failure is unknown. We compared in 63 patients with congestive heart failure 326 measurements of PaCO2 versus PETCO2 and PJCO2 and VD/VT measured with PaCO2 versus VD/VT estimated with PETCO2 (estimation 1) or PJCO2 (estimation 2). Comparisons were made at rest (Phase 1), during submaximal exercise (Phase 2), and at peak exercise (Phase 3). We found a strong correlation, but not an identity, between PaCo2 and PETCO2 (PaCO2 = 7.25 +/- 0.80 PETCO2, r = 0.84; p < 0.0001); similarly for PaCO2 and PETCO2. Several observations were out of 95% confidence interval, and some measurements exceeded mean +/- 2 SD when the differences between PaCo2 and PETCO2 or PJCO2 were plotted against the averages from the two (Bland and Altman method). Measured VD/VTs also strongly correlated with the estimated ones (VD/VT measured = -0.03 +/- 1.11 VD/VT estimated 1 r = 0.90; p < 0.0001 e VD/VT measured = 0.03 +/- 0.92 VD/VT estimated 2 r = 0.90; p < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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Hypovolemia stimulates the sympathoadrenal and renin systems and water retention. In congestive heart failure (CHF) reduced cardiac output and blood pressure have been suggested to be perceived as a volume deficit, which, if persistent, would perpetuate humoral activation and fluid retention. In the aim of probing this hypothesis, we monitored in patients with CHF the neurohumoral response to reduction of the body fluid obtained by ultrafiltration. In 22 patients with advanced CHF and fluid retention, ultrafiltration was performed with a diafilter, which was part of an external venous circuit, whose flow was regulated to produce 500 ml/hour of ultrafiltrate (average total amount 3,122 +/- 1,199 ml) until right atrial pressure was reduced to 50% of baseline. Hemodynamics, plasma renin activity, norepinephrine and aldosterone were measured before and in the 48 hours after ultrafiltration. Soon after the procedure, associated with a 20% reduction of plasma volume and a moderate decrease of cardiac output and blood pressure (consistent with a diminished degree of filling of the arterial compartment), there was an obvious fall of norepinephrine, plasma renin activity and aldosterone. In the next 48 hours we recorded an increasing neurohumoral axis depression, in spite of recovery of plasma volume, cardiac output and blood pressure and a striking enhancement in urinary output. Changes in norepinephrine, plasma renin activity or aldosterone were not related to the combination of changes in plasma volume, cardiac output and blood pressure (variations in the state of arterial filling) and significantly correlated with the increase in urinary output and sodium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)
We report a case of right main pulmonary artery compression due to a type II dissecting aortic aneurysm simulating massive pulmonary artery embolism. Aortic tear and intimal splitting developed around an aortocoronary bypass graft performed 11 months earlier. Ultrasound detected the aortic aneurysm and pulmonary hypertension, and excluded emboli in the pulmonary artery. Pulmonary angiography explained the lung involvement, showing compression of the right main pulmonary artery. Coronary and aortic angiograms demonstrated that the aortic aneurysm developed around the right venous bypass graft. Surgery confirmed the angiographic findings and the pathogenesis of the syndrome.
OBJECTIVE: To evaluate the incidence, characteristics, and haemodynamic consequences of pericardial effusion after cardiac surgery. DESIGN: Clinical, echocardiographic, and Doppler evaluations before and 8 days after cardiac surgery; with echocardiographic and Doppler follow up of patients with moderate or large pericardial effusion after operation. SETTING: Patients undergoing cardiac surgery at a tertiary centre. PATIENTS: 803 consecutive patients who had coronary artery bypass grafting (430), valve replacement (330), and other types of surgery (43). 23 were excluded because of early reoperation. MAIN OUTCOME MEASURES: Size and site of pericardial effusion evaluated by cross sectional echocardiography and signs of cardiac tamponade detected by ultrasound (right atrial and ventricular diastolic collapse, left ventricular diastolic collapse, distension of the inferior vena cava), and Doppler echocardiography (inspiratory decrease of aortic and mitral flow velocities). RESULTS: Pericardial effusion was detected in 498 (64%) of 780 patients and was more often associated with coronary artery bypass grafting than with valve replacement or other types of surgery; it was small in 68.4%, moderate in 29.8%, and large in 1.6%. Loculated effusions (57.8%) were more frequent than diffuse ones (42.2%). The size and site of effusion were related to the type of surgery. None of the small pericardial effusions increased in size; the amount of fluid decreased within a month in most patients with moderate effusion and in a few (7 patients) developed into a large effusion and cardiac tamponade. 15 individuals (1.9%) had cardiac tamponade; this event was significantly more common after valve replacement (12 patients) than after coronary artery bypass grafting (2 patients) or other types of surgery (1 patient after pulmonary embolectomy). In patients with cardiac tamponade aortic and mitral flow velocities invariably decreased during inspiration; the echocardiographic signs were less reliable. CONCLUSIONS: Pericardial effusion after cardiac surgery is common and its size and site are related to the type of surgery. Cardiac tamponade is rare and is more common in patients receiving oral anticoagulants. Echo-Doppler imaging is useful for the evaluation of pericardial fluid accumulations after cardiac surgery. It can identify effusions that herald cardiac tamponade.
BACKGROUND: Hypovolaemia stimulates the sympathoadrenal and renin systems and water retention. It has been proposed that in congestive heart failure reduction of cardiac output and any associated decrease in blood pressure cause underfilling of the arterial compartment, which promotes and perpetuates neurohumoral activation and the retention of fluid. This study examined whether an intravascular volume deficit accounts for patterns that largely exceed the limits of a homoeostatic response, which are sometimes seen in advanced congestive heart failure. METHODS AND RESULTS: In 22 patients with congestive heart failure and water retention the body fluid mass was reduced by ultrafiltration and the neurohumoral reaction was monitored. A Diafilter, which was part of an external venous circuit was regulated to produce 500 ml/hour of ultrafiltrate (mean (SD) 3122 (1199) ml) until right atrial pressure was reduced to 50% of baseline. Haemodynamic variables, plasma renin activity, noradrenaline, and aldosterone were measured before and within 48 hours of ultrafiltration. After ultrafiltration, which produced a 20% reduction of plasma volume and a moderate decrease in cardiac output and blood pressure (consistent with a diminished degree of filling of the arterial compartment), there was an obvious decrease in noradrenaline, plasma renin activity, and aldosterone. In the next 48 hours plasma volume, cardiac output, and blood pressure recovered; the neurohumoral axis was depressed; and there was a striking enhancement of water and sodium excretion with resolution of the peripheral oedema and organ congestion. The neurohumoral changes and haemodynamic changes were not related. There were significant correlations between the neurohumoral changes and increase in urinary output and sodium excretion. CONCLUSIONS: In advanced congestive heart failure arterial underfilling was not the main mechanism for activating the neurohumoral axis and retaining fluid. Because a decrease in circulating hormones was associated with reabsorption of extravascular fluid it is likely that hypoperfusion and/or congestion of organs, such as the kidney and lung, reduce the clearance of circulating noradrenaline and help to keep plasma concentrations of renin and aldosterone raised. A positive feedback loop between fluid retention and plasma hormone concentrations may be responsible for progression of congestive heart failure.
In moderate congestive heart failure pulmonary overhydration may be detected at chest X-ray even if therapy is optimized to keep the urinary output normal and to prevent weight gain and dependent edema formation. Removal of overhydration of the lung may help to define its significance. This study was aimed at investigating whether a subclinical accumulation of fluid in the lung interstitium in moderate congestive heart failure interferes with the patient's functional capacity, and whether furosemide is able to promote reabsorption of the excessive fluid. Patients whose digoxin, oral furosemide and ACE-inhibitor therapeutic regimen was kept constant, were randomly allocated to ultrafiltration (8 cases) or iv bolus (mean dose = 248 mg) of supplemental furosemide (8 cases). The amount of body fluid removed with each method approximated 1.600 ml. Functional performance was assessed with cardiopulmonary exercise tests. Soon after fluid withdrawal with either procedure the filling pressures of the two ventricles and body weight were reduced and plasma renin activity, norepinephrine and aldosterone were augmented. After furosemide hormones remained elevated in the subsequent 4 days, and, during this period, patients had positive water metabolism, recovery of the elevated ventricular filling pressures, recurrence of lung congestion without any improvement in functional capacity. In ultrafiltrated patients, renin, norepinephrine and aldosterone fell below control values within the first 48 hours and water metabolism was equilibrated at a new set point (less fluid intake and diuresis without weight gain). Functional capacity in these patients was improved through favorable circulatory and ventilatory adjustments consequent on reabsorption of lung water. This may also have restored the ability of the lung to clear norepinephrine, thus restraining its facilitation of renin release. Improvement persisted at 3 months after the procedure. In congestive heart failure the set point of fluid balance is altered despite oral furosemide; supplemental iv furosemide does not shift the set point, at least in the presence of ACE-inhibition; excessive, although silent, lung water limits the functional capacity of the patient.
Multiplane transesophageal echocardiography (TEE) allows visualization of the heart and great vessels through an infinite number of imaging planes and improves the diagnostic capabilities of mono and biplane TEE. This study was undertaken to test whether MTEE is a useful intraoperative monitoring method during cardiac surgery. Intraoperative multiplane TEE was performed in 200 patients (mean age 56 +/- 19 years) as a part of the routine clinical care. We systematically acquired cardiac images from the gastric fundus (short and long axes of the ventricles), lower esophagus (four-chamber, two-chamber, and long axis), upper esophagus (13 views concerning the aorta, pulmonary artery, left and right atrium, systemic and pulmonary veins, coronary arteries, right ventricular outflow tract), and searched for complete views of the thoracic descending aorta. All views analyzed in the preoperative (immediately before cardiopulmonary bypass), intraoperative and postoperative phases evaluating: the angle between current and 0 degree at which each view was obtained; the success rate of each view; the usefulness of the different views in providing essential additional clinical information compared to 0 degrees and 90 degrees of the traditional biplane TEE. Most views of the heart and great vessels were visualized in oblique planes, and other views were significantly improved thanks to slight angle corrections. Multiplane TEE was particularly useful in the preoperative and postoperative phases of aortic dissection (11 cases), mitral valve repair (13 cases), left ventricular aneurysmectomy (9 cases), right atrial thrombosis (1 case), positioning of left ventricular hemopump (2 cases), mitral-aortic endocarditis (3 cases), bleeding from proximal suture of an aortic heterograft (1 case).(ABSTRACT TRUNCATED AT 250 WORDS)
PURPOSE: We investigated the mechanisms involved in the regulation of salt and water metabolism in patients with congestive heart failure (CHF). Extracorporeal ultrafiltration was utilized as a nonpharmacologic method for withdrawal of body fluid. PATIENTS, METHODS, AND RESULTS: In 32 consecutive patients with CHF (New York Heart Association functional class II to IV) and different degrees of water retention, 24-hour diuresis and natriuresis were inversely best correlated with the combination of circulating renin, aldosterone, norepinephrine, and renal perfusion pressure (RPP, mean aortic pressure minus mean right atrial pressure). Fluid withdrawal (600 to 5,000 mL) at a rate of 500 mL/h, until right atrial pressure decreased to 50% of baseline, caused variable humoral, circulatory, and diuretic effects that were mainly related to the extent of fluid retention. In fact, in 10 patients (Group 1) with overhydration refractory to drug therapy and with urinary output less than 1,000 mL/24 h (mean, 370 mL), soon after the procedure, plasma renin (-39%), aldosterone (-50%), and norepinephrine (-47%) were reduced and RPP was increased (+16%), and in the subsequent 24 hours, diuresis was increased by 493%; in 9 patients (Group 2) whose baseline urinary output exceeded 1,000 mL/24 h (mean, 1,785 mL), renin increased by 40%, norepinephrine, aldosterone, and RPP each decreased by 12%, and diuresis remained unchanged; in 13 patients (Group 3) with a daily urinary excretion as in Group 2 and without overhydration, RPP decreased (-7%), renin (+196%), aldosterone (+170%), and norepinephrine (+52%) increased, and diuresis decreased by 45%. There was an overall correlation (p < 0.0001) between the combination of changes in these circulatory and hormonal variables and changes in diuresis and natriuresis with ultrafiltration. CONCLUSIONS: It appears that in CHF, (1) retention of sodium and water results from an interaction of hormonal and hemodynamic (primarily RPP) alterations that may exert a reciprocal positive feedback; (2) depending on the presence and severity of fluid retention, the response to withdrawal of body fluid may vary from neurohumoral activation and restriction of diuresis to neurohumoral depression and extreme potentiation of salt and water excretion; (3) refractory CHF requires the interruption of the humoral-hemodynamic vicious circle, and ultrafiltration is able to accomplish that.
We investigated the mechanisms involved in the regulation of salt and water metabolism in patients with congestive heart failure (CHF). Extracorporeal ultrafiltration was utilized as a nonpharmacologic method for withdrawal of body fluids. In 32 consecutive patients with CHF (NYHA class II to IV) and different degrees of water retention, 24-hour diuresis and natriuresis were inversely best correlated with the combination of circulating renin, aldosterone, norepinephrine, and renal perfusion pressure (RPP). Fluid removal (600 to 5,000 ml) at a rate of 500 ml/h, until right atrial pressure decreased to 50% of baseline, caused variable humoral, circulatory, and diuretic effects that were mainly related to the extent of fluid retention. In fact, in 10 patients (Group 1) with overhydration refractory to drug therapy and with urinary output less than 1,000 ml/24 h (mean 370 ml), soon after the procedure, plasma renin (-39%), aldosterone (-50%), and norepinephrine (-47%) were reduced and RPP was increased (+ 16%), and in the subsequent 24 hours, diuresis was increased by 493%; in 9 patients (Group 2) whose baseline urinary output exceeded 1,000 ml/24 h (mean 1,785 ml), renin increased by 40%, norepinephrine, aldosterone and RPP each decreased by 12%, and diuresis remained unchanged; in 13 patients (Group 3) with a daily urinary excretion as in Group 2 and without overhydration, RPP decreased (-7%), renin (+ 196%), aldosterone (+ 170%), and norepinephrine (+ 52%) increased, and diuresis decreased by 45%. There was an overall correlation (p < 0.0001) between the combination of changes in these circulatory and hormonal variables and changes in diuresis and natriuresis with ultrafiltration.(ABSTRACT TRUNCATED AT 250 WORDS)