Pulmonary Artery Wedge Research Articles

Hemodynamic time course of acute and chronic isosorbide dinitrate treatment at rest and during exercise in patients with stable ischemic heart disease

The study was undertaken to establish differences between venous and arterial isosorbide dinitrate (ISDN) effects during acute and chronic treatment, hemodynamics at rest, and during supine exercise. These effects were assessed invasively in 16 patients with stable ischemic heart disease before and at hourly intervals for 4 h after administration of peroral 30 mg ISDN. Eight patients were previously untreated (acute group), and eight were treated with 30 mg ISDN asymmetrically b.i.d. for two weeks (chronic group). Prior to ISDN administration, right atrial, mean pulmonary artery, pulmonary artery wedge, and mean arterial pressure (RAP, MPAP, PAWP, and MAP) rose from normal resting to pathologic values during exercise. One h after ISDN administration, all exercise pressures were normalized (p < 0.001). During the following 3 h, exercise RAP rose similarly in both groups (p < 0.01), while MPAP rose particularly in the chronic group (p < 0.001). Exercise PAWP and MAP, however, remained low in the acute group, but increased markedly in the chronic group (p < 0.01), particularly from the third to the fourth hour after ISDN. The daily, asymmetric administration of 30 mg ISDN b.i.d. maintained beneficial, anti-ischemic effects for 2 to 3 h after a morning dose of the drug, but thereafter attenuation of the effects occurred in the arteries but not in the veins.

Impact of Medical Therapy on Pulmonary Hypertension in Patients With Congestive Heart Failure Awaiting Cardiac Transplantation

Pulmonary artery (PA) hypertension in transplant recipients increases mortality from right heart failure following heart transplantation. We examined the impact of long-term medical therapy on the severity of PA hypertension in patients with end-stage congestive heart failure on a transplant waiting list. The initial and final, quarterly right heart catheterization data on 60 patients (50 men, aged 50 ± 9 years, New York Heart Association class III to IV) awaiting heart transplantation were analyzed and the patients divided into 2 groups: group A, those with persistent elevated systolic PA pressures throughout the 10-month follow-up (n = 31 of 60), and group B, those who had any decrease in systolic PA pressure during that period (n = 29 of 60). Group A had no change in hemodynamics. Group B had a significant decrease (± SD) in right atrial (11 ± 7 to 5 ± 4 mm Hg), PA (57 ± 11 to 37 ± 11 mm Hg), and PA wedge (25 ± 9 to 14 ± 7 mm Hg) pressures, with increases in cardiac output (3.8 ± 0.9 to 4.7 ± 1.1 L/min) and ejection fraction (18 ± 6% to 27 ± 11%) (p <0.05). The combined end point of transplant or death occurred in 28 of 31 patients (90%) in group A versus 14 of 29 (50%) in group B (p = 0.0004). Ischemic etiology was present in 71% of patients in group A versus 68% with idiopathic dilated cardiomyopathy in group B (p = 0.003). The reversibility of PA hypertension rather than its initial severity is predictive of patient clinical outcome. Idiopathic, as opposed to ischemic, cardiomyopathy responds better to medical therapy. (Am J Cardiol 1996;78:440–443)

Hemodynamic responses to Pasteurella haemolytica inoculation in calves given type 2 serotonergic antagonist

The effects of saline (control, group C) and metrenperone (treated, group M) on systemic and pulmonary hemodynamics were determined in conscious 7- to 15-day-old calves after they were intratracheally inoculated with Pasteurella haemolytica. Metrenperone, a specific serotonin (5-hydroxytryptamine) receptor antagonist, was injected intramuscularly (100 micrograms.kg-1) 2 h after the calves were inoculated. Central venous, pulmonary arterial and capillary wedge, and systemic arterial pressures were measured, using fluid-filled catheters. Cardiac output was measured by the thermodilution technique. Heart rate, stroke volume, and pulmonary and systemic vascular resistances were calculated. The parameters were measured hourly from the 1st to the 10th h after inoculation. In group C, cardiovascular response to P. haemolytica inoculation was marked and typically consisted of two systemic hypotensive phases and two pulmonary hypertensive phases. The first phase occurred by the 2nd h post inoculation and was induced by a transient bradycardia and a systemic vasodilation, leading to profound hypotension and reduced venous return. Cardiac performance then transiently recovered, but systemic hypotension persisted. The second hypotensive hypodynamic phase occurred by the 7th h after inoculation, and was associated with a decline in stroke volume, an increase in heart rate, and pulmonary hypertension and vasoconstriction. In group M, the early response to P. haemolytica exposure was similar to that in controls, indicating that, as in sheep, 5-hydroxytryptamine does not contribute to the early hypodynamic response to endotoxemia. In contrast, metrenperone completely abolished late increases in pulmonary arterial pressure and pulmonary vascular resistance, suggesting that 5-hydroxytryptamine contributes to the late pulmonary vasoconstriction. Metrenperone treatment also allowed better restoration of heart rate, and hence, cardiac output was maintained. In conclusion, 5-hydroxytryptamine might have a role in mediating pasteurellic endotoxin induced changes in pulmonary hemodynamics through its type-2 receptors.

Systemic and pulmonary hypertension after abrupt cessation of prostacyclin: role of thromboxane A2.

Chronic administration of prostacyclin (PGI2) improves hemodynamics in patients with primary pulmonary hypertension, but abrupt cessation of infusion can cause severe dyspnea of unknown etiology. We hypothesized that the discontinuation of PGI2 results in platelet activation, thromboxane A2 production, and increased pulmonary vascular tone. To test this, six sheep with indwelling catheters were monitored during infusion of PGI2 and after its cessation. Infusion of PGI2 caused a reduction in mean systemic arterial pressure (MAP) and systemic (SVR) and pulmonary vascular resistances (PVR), a rise in cardiac output (CO), and no change in pulmonary arterial or pulmonary capillary wedge pressure (PCWP). After discontinuation of PGI2, MAP and SVR rebounded to 30 and 67% above baseline, respectively, and PVR rose 26%. CO was depressed 23% within 10 min, and PCWP nearly doubled after stoppage of the drug. Concurrent treatment with a cyclooxygenase inhibitor did not attenuate these responses. 11-Dehydro-thromboxane B2 levels were not elevated during infusion or after cessation of PGI2. We conclude that the abrupt cessation of PGI2 infusion leads to systemic and pulmonary hypertension and transient cardiac dysfunction not mediated by cyclooxygenase metabolites of arachidonic acid.

Select dietary fatty acids attenuate cardiopulmonary dysfunction during acute lung injury in pigs.

We examined the effect of substituting linoleic acid (LA) with eicosapentaenoic acid (EPA) and gamma-linolenic acid (gamma-LA), precursors of trienoic and monoenoic eicosanoids, respectively, on acute lung injury (ALI). Three groups (n = 8/group) of pigs were fed enteral diets containing LA (diet A), EPA (diet B), or EPA+gamma-LA (diet C) for 8 days. ALI was then induced with a 0.1 mg/kg bolus of Escherichia coli endotoxin followed by a continuous infusion for 4 h (0.075 mg.kg-1.h-1). Pulmonary arterial and capillary wedge pressures, cardiac index (CI), arterial blood gases, arterial O2 content, and plasma thromboxane B2 (TxB2) were measured. Arterial PO2 decreased at 20 min in animals fed diet A. This change was attenuated with diets B and C. The EPA- and EPA + gamma-LA-enriched diets attenuated the fall in O2 delivery at 20 min, an improvement that was sustained throughout the 4-h study period with the EPA+gamma-LA-enriched diet only. This improvement in O2 delivery was due not only to the improved arterial PO2, but also to the maintenance of CI at 20 min in animals fed diets B and C and throughout the 4-h study period in animals fed diet C. At 4 h, TxB2 increased 10-fold over baseline in animals fed diet A, whereas in animals fed diets B and C the increase was only 3-fold. These decreased TxB2 levels in animals fed diets B and C correlate with an attenuation in the increase in pulmonary vascular resistance that was observed at 20 min after endotoxin infusion in animals fed diet A. These data suggest that specialized enteral diets enriched in EPA+gamma-LA improve gas exchange and O2 delivery, presumably in part through a modification of TxB2 production with a decrease in pulmonary vascular resistance and an increase in CI, during ALI.

Hemodynamic Effects of Anesthetic Induction with Eltanolone-Fentanyl Versus Thiopental-Fentanyl in Coronary Artery Bypass Patients

We evaluated the hemodynamic profile of eltanolone and fentanyl versus thiopental and fentanyl anesthetic induction in patients with documented coronary artery disease. Fifty patients scheduled for coronary artery bypass grafting were randomly assigned to two treatment groups (25 patients each). Anesthesia was induced by eltanolone (0.5 mg/kg) or by thiopental (3 mg/kg). Each patient also received 3 micrograms/kg fentanyl and 0.1 mg/kg vecuronium. Heart rate, arterial, pulmonary arterial, central venous, and pulmonary capillary wedge pressures, and cardiac output were determined in the awake state, 2 min after induction of anesthesia, and at 1 and 5 min after intubation, which was performed 3 min after induction. Between-group statistics showed significantly (P < 0.05) lower mean arterial pressure and systemic vascular resistance for eltanolone-treated patients at all measuring points. Pulmonary capillary wedge pressure was lower at 1 min after intubation; left ventricular stroke work index was lower at 1 and 5 min after intubation in the eltanolone group. We conclude that the lower mean arterial pressure with eltanolone as compared to thiopental is a result of greater peripheral vasodilation.

Comparison of three methods of measurement of pulmonary artery catheter readings in critically ill patients

Pulmonary artery catheter readings are critical for clinical decision making and therapeutic intervention in critically ill patients. Research data of digital display versus graphic strip chart recording of hemodynamic pressures during spontaneous breathing and mechanical ventilation are inconclusive. To compare three methods of measurement of hemodynamic pressure readings from the pulmonary artery catheter in critically ill patients during mechanical ventilation and spontaneous breathing. A nonrandomized, repeated-measures design was used to compare hemodynamic pressures (right atrial, systolic, diastolic, and wedge pressures) from the pulmonary artery catheter in cardiovascular patients during mechanical ventilation (n = 25) and again during spontaneous breathing (n = 19). Using repeated measures analysis of variance, statistically significant differences were noted in the pulmonary artery diastolic, wedge, and right atrial pressure during mechanical ventilation. During spontaneous breathing, significant differences occurred in pulmonary artery systolic and wedge pressures only. No statistically significant difference occurred in the systolic pressure during mechanical ventilation, or the pulmonary artery diastolic and right atrial pressures during spontaneous breathing. The results of this study indicate that graphic recording is the most reliable means of measuring hemodynamic pressure at end-expiration. Further research is needed to validate these findings with other models of monitoring equipment and other patient populations.

Unsteadiness of pulmonary vascular pressures in rapid acceleration supramaximal exercise

SummaryIn competitive racing, horses rapidly accelerate to their top speed and probably perform supramaximal work. Therefore, the primary objective of this study was to examine changes in pulmonary vascular pressures of Thoroughbreds with rapid acceleration to supramaximal exercise which could not be sustained for more than 90 s. Right atrial and pulmonary vascular pressures were studied at rest and during supramaximal exercise in 10 healthy, sound, exercise trained Thoroughbred horses. Exercise was performed on separate days without (control) and with frusemide administration 250 mg i.v., 4 h before exercise. The protocol consisted of a warm‐up at treadmill speeds of 2 to 6 m/s (trot) for 60 s each followed by 8 m/s (canter) for 60 s. Thereafter, the treadmill was raised to 10% uphill incline and speed accelerated from 8 to 15 m/s in 8 s. None of the horses could sustain exercise at 15 m/s + 10% incline for more than 90 s. Mean right atrial, pulmonary arterial, pulmonary artery wedge and pulmonary capillary pressures increased sharply as horses accelerated rapidly attaining their zenith as speed reached 15 m/s. Peak values of various pressures were maintained only for the first 45 s of exercise at 15 m/s +10% uphill incline. Thereafter, a declining trend emerged and all pressures decreased significantly as exercise duration increased. Although frusemide significantly lowered the magnitude of pulmonary vascular pressures both at rest and during exercise, it did not affect the rapid escalation in pulmonary vascular pressures upon rapid acceleration of horses or their unsteadiness in the latter 45 s of supramaximal exercise. It is suggested that rapid rate of rise of pulmonary capillary blood pressure during a sudden burst of supramaximal exercise may be a crucial factor in precipitating stress failure of pulmonary capillaries and onset of exercise induced pulmonary haemorrhage.

1024-78 Long Term (6 year) Outcome After Catheter Balloon Valvuloplasty in Patients with Mitral Stenosis

Catheter balloon valvuloplasty (CBV) for mitral stenosis was performed in 132 patients (pts) from 1986 to ‘94. There were 104 women (79%) and 28 men, aged 44 ± 14 years. Pre-CBV, 12 pts were NYHA Functional Class (FC) IV, 87 in FC III, 28 FC II and 2 were FC I. CBV increased mitral valve area (MVA) from 0.98 ± 0.26 to 1.94 ± 0.57 cm 2 , p &lt; 0.001. There were 6 early deaths up to 1 month (“procedure-related”); all 4 late deaths occurred after elective valve replacement (VR) was performed 18.2 ± 25 months later. Actuarial 6 yr survival was 83 ± 6% when mortality after VR is included, excluding these 6 yr survival was 95 ± 1%. Actuarial 1, 3 and 6 yr event-free survival (survival without VR or repeat CBV) were 80 ± 4%, 76 ± 4% and 63 ± 7%. Pre-CBV variables were not significant predictors of outcome. On multivariate analysis, post-CBV independent predictors of 6 yr event-free survival were 1) MVA ≥ 1.5 vs &lt; 1.5 cm 2 , 73 ± 8% vs 32 ± 12%; 2) Pulmonary artery (PA) wedge ≤ 18 vs &gt; 18 mmHg, 84 ± 6% vs 38 ± 12%, P &lt; 0.001 for both. Pts. with MVA ≥ 1.5 cm 2 (n = 96) could be further divided into high and low-risk subgroups for 6 yr event-free survival by 3 post-CBV variables: 1) PA wedge ≤ 18 vs &gt; 18, 90 ± 6% vs 46 ± 15% (p = 0.002); 2) Mean PA &lt;30 vs ≥ 30, 89 ± 6% vs 54 ± 14% (p = 0.06); 3) Cardiac Index (CI) ≥ 2.5 vs &lt;2.5.82 ± 8% vs 53 ± 17% (p = 0.002). Pts with post-CBV MVA &lt;1.5 (n = 24) had no additional predictors of event-free survival. Of those pts who did not undergo VR or repeat CBV 94% were FCI or FCII. CBV for mitral stenosis has good long term results up to 6 yrs. Late deaths were related to elective surgery. 6 yr event-free survival was very good in pts with post-CBV MVA ≥ 1.5 cm 2 especially if PA wedge was ≤ 18 or CI was ≥ 2.5.

1024-79 Late Cardiac Catheterization Results of Catheter Balloon Commissurotomy for Mitral Stenosis at Rest and Exercise

Cardiac catheterization (cath) was performed on 132 patients (pts) both pre and immediately post catheter balloon commissurotomy (CBC). Sixty eight pt's had cath performed at 3–6 months post-CBC and twenty had a late follow-up cath (mean 3.2 yrs, range 1–7 yrs). At late follow-up cath 16 of the 20 pts were NYHA functional class (FC) I or II; 13 females and 3 males age 40 ± 11 yrs, We have reviewed the sequential hemodynamic findings in these 16 pt's to see if hemodynamic improvement achieved by CBC is sustained. The following parameters were measured: mitral valve gradient (MVG). mean pulmonary artery wedge (PAW), mean pulmonary artery pressure (PA), Fick cardiac index (CI), mitral valve area (MVA), left ventricular (LV) end-diastolic volume index (EDVI) and LV ejection fraction (EF), Exercise treadmill times (En) were also recorded. Variable Baseline mean ± SD Immed. Post mean ± SD 3-6 Month mean ± SD 3.2 yrs mean ± SD CI (FICK)-REST 2.8 ± 6 3.3 ± 0.8 3.2 ± 0.7 33 ± 10 CI (FICK)-EXER 3.7 ± 0.8 5.0 ± 0.6 4.8 ± 1.1 MVG-REST 16.2 ± 5.6 5.0 ± 1.9 * 6.9 ± 3.2 * 8.3 ± 4.7 MVG-EXER 27.1 ± 5.6 18.2 ± 5.7 15.5 ± 76 PAW-REST 28 ± 6.9 15.8 ± 3.8 * 18.2 ± 6.8 * 21.4 ± 5.8 PAW-EXER 45.5 ± 9.6 29.0 ± 8.1 29.6 ± 8.9 MVA-REST 1.1 ± 0.3 2.3 ± 0.6 2.0 ± 0.7 2.0 ± 0.7 MVA-EXER 1.1 ± 0.3 2.4 ± 0.7 2.3 ± 0.9 mPA-REST 43.3 ± 13.4 33.1 ± 9.8 28.3 ± 102 313 ± 10.2 mPA-EXER 64.8 ± 21.4 43.1 ± 11.6 41.9 ± 15.7 LVEDVI 73.3 ± 18.2 79.6 ± 17.2 82.7 ± 21.3 79.3 ± 13.8 LVEF 0.58 ± 0.06 0.60 ± 0.06 * 0.59 ± 0.10 * 0.68 ± 0.06 ETT TIMES (SEC) 442 ± 180 596 ± 114 520 ± 158 * p-value ≤ 0.05 For 3-6 month and Late follow-up vs. Immediate post CBC (ANOVA With repeated measures) Patients who are clinically stable (FC I or II) show sustained improvement in hemodynamics and En immediately post-CBC to an average of 3.2 yrs later; LV size and function remains normal.

Atrial and ventricular myocardial blood flows in horses at rest and during exercise

Summary Right atrial, pulmonary artery, pulmonary capillary, pulmonary artery wedge, and systemic blood pressures of strenuously exercising horses increase markedly. As a consequence, myocardial metabolic O2 demand in exercising horses must be high. Experiments were, therefore, carried out on 9 healthy, exercise-conditioned horses (2.5 to 8 years old; 481 ± 16 kg) to ascertain the regional distribution of myocardial blood supply in the atria and ventricles at rest and during exercise. Blood flow was measured, using 15-μm-diameter radionuclide-labeled microspheres that were injected into the left ventricle while reference blood samples were being withdrawn at a constant rate from the thoracic aorta. Myocardial blood flow was determined at rest and during 2 exercise bouts performed on a high-speed treadmill at 8 and 13 m/s (0% grade). The sequence of exercise bouts was randomized among horses, and a 60-minute rest period was permitted between exercise bouts. There was considerable heterogeneity in the distribution of myocardial perfusion in the atria and the ventricles at rest; the right atrial myocardium received significantly (P &lt; 0.05) less perfusion than did the left atrium, and these values were significantly (P &lt; 0.05) less than those for the respective ventricular myocardium. The right ventricular myocardial blood flow also was significantly less than that in the left ventricle. With exercise, myocardial blood flow in all regions increased progressively with increasing work intensity and marked coronary vasodilation was observed in all cardiac regions. During exercise at 8 or 13 m/s, right and left atrial myocardial blood flows (per unit weight basis) were not different from each other. Although at treadmill speed of 8 m/s, left ventricular myocardial blood flow exceeded that in the right ventricle, this was not the case at 13 m/s, when perfusion values (per unit weight basis) became similar. These data suggested that, in exercising horses, myocardial metabolic O2 requirements increase markedly in all regions. However, the right atrial and right ventricular myocardial blood flows increased out of proportion to those in the left atrium and left ventricle, respectively.

Tracheal mucosal edema in hydrostatic pulmonary edema

Airway edema has been described in heart failure, and, in animal experiments, airway narrowing was observed with elevated left atrial pressure (Pla). On the basis of double-indicator-dilution principles using helium and dimethylether, we were able to measure a water compartment of the tracheal mucosa (VH2O) in dogs. Hypervolemia with an attendant increase in Pla caused by infusion of 2 liters of dextran increased VH2O from 368 +/- 71 (SE) to 794 +/- 177 microliters (P < 0.01). Pulmonary arterial wedge and central venous pressures (Pcv) rose concomitantly. Increases in pulmonary arterial wedge and Pcv by a left atrial balloon catheter produced similar increases in VH2O, whereas increases in Pcv alone by a right atrial balloon did not increase VH2O. Increasing VH2O by dextran infusion was associated with an increase in pulmonary resistance from 1.16 +/- 0.19 to 2.15 +/- 0.24 cmH2O.l-1.s (P < 0.01). These observations show that fluid accumulation in the lung during pulmonary congestion also involves extraparenchymal airways and is related to Pla rather than right atrial pressure. This indicates that sufficient collateral drainage exists during right-sided but not left-sided pressure elevations.

Interluminal Communication in a Pulmonary Artery Catheter Causing Artifactual Pressure Measurement

Although pulmonary artery (PA) catheterization is recognized as an important diagnostic and monitoring technique for critically ill patients, serious adverse effects have been associated with this procedure (1,2). Complications caused by PA catheter monitoring are usually divided into three categories: those associated with gaining central venous access, those caused by the flotation/catheterization procedure itself, and those occurring during catheter residence in the pulmonary artery (1,3). Considered within this last category, unrecognized or misinter-preted artifacts recorded in PA or PA wedge pressure traces may result in erroneous diagnosis and inappropriate therapy (4–6). Artifacts of this type may be caused by structural defects in the PA catheter itself, but these have been reported only rarely (7,8) and are not emphasized as causes of misinformation (1,4,5). Pulmonary artery catheter structural defects are probably uncommon because of modern industrial quality testing, and defects may be under-reported because some defects are obvious to the clinician checking the catheter prior to insertion (9). This report describes an unusual and subtle structural defect detected in a PA catheter, which, if unrecognized, would result in misinformation and the potential for improper patient treatment. Two simple, inexpensive methods for confirming the nature of this problem are presented, and the importance of attention to waveform morphology is emphasized.

Comparative effects of the flavonoids luteolin, apiin and rhoifolin on experimental pulmonary hypertension in the dog

AbstractThe acute effects were compared of selected flavonoids on the pulmonary vascular circuit in two experimental models of pulmonary hypertension, produced by hypoxia and by prostaglandin F2α (PGF2α) in anaesthetized dogs. In all dogs, haemodynamic variables (pulmonary artery pressure, pulmonary artery wedge and aortic pressure, pulmonary vascular resistance, cardiac output) were recorded in the control state, during hypoxia or PGF2α‐induced pulmonary vasoconstriction, and after equimolar doses (5 mM/kg/i.v.) of luteolin, apiin and rhoifolin. The effects observed after flavonoid administration were compared with those of equimolar doses of nifedipine. The results obtained have shown that luteolin and apiin caused a decrease of hypoxic pulmonary vascular resistance to normoxic values and of the pulmonary arterial pressure while cardiac output remained unchanged. Rhoifolin produced no change in hypoxic pulmonary vasoconstriction, but decreased cardiac output and aortic pressure. The response of the pulmonary hypertension induced by PGF2α to flavonoids and nifedipine was nearly identical to that of hypoxia‐induced pulmonary hypertension. The mechanism of action of these flavonoids is discussed.

Estimation of pulmonary artery pressure from pulmonary vein wedge pressure

Correlations between pulmonary artery and pulmonary vein wedge pressures were investigated in 13 patients with atrial septal defect and 1 patient with Tetralogy of Fallot. Pulmonary vein wedge pressure wave form resembled that of pulmonary artery pressure, and the former lagged behind the latter by 70 to 110 msec (mean 88 +/- 14) as observed by the fluid-filled catheter system. Diastolic pulmonary artery and diastolic pulmonary vein wedge pressures were nearly identical. Although systolic and mean pulmonary artery pressures correlated well with respective pulmonary vein wedge pressures, there were discrepancies when systolic and mean pulmonary artery pressure exceeded 35 and 20 mm Hg, respectively. However, systolic and mean pulmonary artery pressures could be estimated by adding the difference between the diastolic pulmonary vein wedge pressure and the mean left atrial pressure to corresponding systolic or mean pulmonary artery pressure. In conclusion, pulmonary artery pressures can be estimated by measuring pulmonary vein wedge pressures and the mean left atrial pressure.

Hemodynamic effects of argon pneumoperitoneum.

The hemodynamic effects of argon pneumoperitoneum were studied to define its possible role as an alternative gas for intraperitoneal insufflation during minimally invasive surgery. Adult pigs were anesthetized and placed on mechanical ventilation. Parameters measured or determined included mean arterial (MAP), pulmonary arterial (PAP), pulmonary arterial wedge (PAWP), right atrial (CVP), and inferior vena cava venous (IVC) pressures, total excretion of CO2 (VCO2), oxygen consumption (VO2), minute ventilation, and arterial blood gases. Also determined were cardiac output, stroke volume, and systemic vascular resistance all indexed to weight (CI, SVI, SVRI). Data were recorded during a 1-h baseline, 2 h of insufflation with argon gas at a constant pressure of 15 mmHg, and 1 h recovery after desufflation. There was no significant change from baseline in VCO2, VO2, MAP, PAP, PAWP, CVP, PaCO2, or arterial pH. Argon pneumoperitoneum significantly increased systemic vascular resistance index and exerted a depressant effect on stroke volume index and cardiac index by 25% and 30% from baseline values, respectively (P < 0.05). Inferior vena cava pressure increased as a reflection of the intraabdominal pressure. Argon insufflation had no effect on respiratory function. Argon gas may not be physiologically inert, and in patients with cardiovascular disease its effects may be clinically important.

Predictive value of prominent pulmonary arterial wedge V waves in assessing the presence and severity of mitral regurgitation

Indwelling pulmonary arterial catheters are often used to monitor and to guide therapy in critically ill patients. The magnitude of the V wave recorded from the pulmonary arterial wedge (PAW) position is sometimes used to assess the presence and severity of mitral regurgitation (MR). The present study was performed to assess the relation (or lack thereof) between a “prominent” PAW V wave and qualitative and quantitative estimates of MR. In 903 subjects (445 men and 458 women, aged 49 ± 13 [mean ± SD] years) referred for cardiac catheterization, an oximetrically confirmed PAW pressure was recorded with a large-lumen stiff catheter, and a left ventriculogram was recorded. In 646 of these subjects (328 men and 318 women, aged 50 ± 13 years), forward cardiac output was measured by the Fick principle, and a regurgitant fraction was calculated. Prominent PAW V waves-as defined in several ways—were insensitive and had poor positive predictive value in identifying moderate or severe MR. At the same time, the absence of prominent PAW V waves was relatively specific for the absence of moderate or severe MR, and the negative predictive value of small V waves was very good. Thus, the prominence of a PAW Vwave cannot be used to assess the presence or severity of MR.

A comparative study of the influences of pulmonary arterial pressure and pulmonary capillary wedge pressure on impedance rheopneumogram in patients with three different diseases

In the present study right heart catheterization and impedance rheopneumogram examinations were performed simultaneously on 21 patients suffering from congenital cardiovascular diseases with atrial or ventricular septal defect accompanied by the left to right shunt (CCD) and 17 patients suffering from rheumatic valvular disease with mitral stenosis (MS) in order to investigate the differences in the impedance rheopneumogram parameters between CCD patients and patients with chronic obstructive pulmonary disease (COPD) as well as between MS and COPD patients. The results showed that when patients with different diseases had the same level of pulmonary arterial pressure, CCD patients had significantly higher Hs than COPD patients, while MS patients had significantly higher Hd/Hs ratio than COPD patients and CCD patients. The linear regressional equation between Hd/Hs ratio and pulmonary capillary wedge pressure (PCWP) was as follows: PCWP (kPa) = 0.17 + 0.98 x Hd/Hs (kappa = 155, gamma = 0.422, p < 0.001). These results suggest that: (1) impedance rheopneumographic regressional equations with Hs as one of the major variables suitable for predicting secondary pulmonary hypertension in COPD patients are not suitable for use on CCD patients; (2) Hd/Hs ratio is useful in clinical work as an index for differential diagnosis between MS and Cor Pulmonale; and (3) PCWP can be roughly and noninvasively measured based on the measurement of impedance rheopneumogram parameter Hd/Hs.

Right ventricular-vascular interaction in congestive heart failure. Importance of low-frequency impedance.

Vasodilator agents are widely used in congestive heart failure. These agents may have important effects on the pulsatile aspects of right ventricular hydraulic load. Fifteen patients with severe congestive heart failure were studied during cardiac catheterization by use of high-fidelity pressure transducers and a catheter-mounted flow velocity probe. Three graded doses of nitroprusside were infused as pulmonary artery (PA) pressure and flow were continuously recorded. From Fourier transforms of signal-averaged waves, PA impedance, hydraulic power, and wave reflection indices were derived. At the highest dose of nitroprusside (66 +/- 41 micrograms/min), cardiac output was significantly improved, whereas PA mean and wedge pressure, resistance, impedance at the first harmonic, characteristic impedance, and wave reflection amplitude were all reduced. At the dose (32 +/- 20 micrograms/min) at which cardiac output first showed improvement, only PA mean pressure and first-harmonic impedance were significantly reduced. Hydraulic power cost per unit of forward flow was also lowered at this dose, despite lack of significant change in pulmonary vascular resistance. At the lowest dose of nitroprusside (11 +/- 4 micrograms/min), six patients experienced a decrease in stroke volume, whereas the other nine were either unchanged (n = 1) or showed an increase (n = 8). Multiple regression revealed that only the change in first-harmonic impedance correlated with this effect, increasing when stroke volume decreased and decreasing when stroke volume increased (P = .02). The change in first-harmonic impedance at this dose appeared to be caused by alterations in the amplitude of PA wave reflections. At higher doses, changes in mean PA pressure (but not in pulmonary vascular resistance) correlated with changes in stroke volume. Nitroprusside vasodilation at low doses alters PA hemodynamics in congestive heart failure primarily through changes in low-frequency impedance. In some patients, this effect is associated with decreased stroke output. At higher doses, favorable alterations in resistance, low- and high-frequency impedance, and wave reflections all contribute to increased forward flow and decreased power requirement per unit forward flow. These findings show that ventricular-vascular interaction is importantly affected by pulmonary vasodilation and that appreciation of pulsatile properties is required to understand the effects of pulmonary vasodilation on cardiac output.

Cardiac Depressant Effects of Oxygen Free Radicals

In many clinical situations, including cardiac ischemia/reperfusion, elective cardiac arrest, and renal dialysis, the chances of increased production of oxygen free radicals (OFR) exist. OFR have been implicated as a causative factor of cell damage in several pathologic conditions. The effects of exogenous OFR, generated by xanthine plus xanthine oxidase, in the absence and in the presence of OFR scavenger (superoxide dismutase [SOD]) on the contractility of isolated perfused heart of rabbit were studied. OFR produced concentration-dependent decreases in the contractility of perfused heart. SOD prevented the OFR-induced decreases in the left ventricular contractility. Xanthine produced an increase in the contractility of isolated perfused rabbit's heart. Xanthine oxidase produced a marked decrease in the left ventricular contractility. Repeated administration of xanthine oxidase produced accelerated and greater decreases in the contractility of perfused heart when compared with that of the initial administration of the drug. Effects of xanthine or xanthine oxidase on the cardiac function and contractility were also studied in anesthetized dogs. Xanthine alone had no significant effect on the cardiac function and indices of myocardial contractility. However, xanthine oxidase produced a marked decrease in the mean aortic pressure, left ventricular work index, heart rate, cardiac index, left ventricular systolic pressure, left ventricular end-diastolic pressure, (+) and (-) dp/dt of left ventricular pressure, and other indices of myocardial contractility [(dp/dt)/PAW (pulmonary arterial wedge pressure)]; and an increase in the total systemic and pulmonary vascular resistance. Repeated administration of xanthine oxidase in anesthetized dogs had lesser effects on the cardiovascular system when compared with those from the initial dose of the drug. These results suggest that OFR are cardiac depressant. Clinical situations wherein there is an increased production of OFR or increased formation of xanthine and xanthine oxidase may be associated with decreased cardiac function and contractility. Scavengers of OFR may protect the heart from the deleterious effects of OFR in such clinical conditions.