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PubMed1980

Effects of ventricular pacing on regional left ventricular performance in the dog.

Changes in regional left ventricular (LV) performance induced by ventricular pacing were studied in two groups of open-chest anesthetized dogs. In the first group of five dogs, local function at the LV anterior base, anterior apex, and posterior apex was assessed by ultrasonic crystal pairs with atrial, right ventricular, LV apical, and LV base pacing. Ventricular pacing produced asynchrony of contraction and marked changes in the shortening pattern at each site, as well as an average 27% reduction in peak systolic pressure and peak dP/dt compared to atrial pacing. Moreover, the extent of shortening during LV ejection was reduced or unchanged at all sites measured during ventricular pacing. In the second group of five dogs, function of the septum and opposing LV lateral wall was studied with atrial and LV lateral wall pacing. Lateral function was assessed with a crystal pair and septal function by cineradiography of a lead bead implanted in the septum. Ventricular pacing produced reciprocal interaction between the two walls, with early lateral shortening inducing septal bulging and late septal shortening inducing lateral wall systolic lengthening. We conclude that ventricular pacing produces significant changes in regional myocardial function, likely induced by reciprocal interaction of opposing myocardial regions. Furthermore, such interaction appears deleterious to global ventricular function, presumably because volume is sequestered and pressure is dissipated into relatively inactive segments that are out of phase with the bulk of contracting myocardium.

Animals↗
PubMed1983

Response of the right ventricle to exercise in patients with chronic heart disease.

The response of the right ventricle to exercise was examined in 19 patients with heart disease by constructing right ventricular function curves and determining the relationship between right ventricular afterload and preload. Simultaneous cardiac output and right heart pressures were measured at rest, during exercise, and 10 minutes after exercise. The patients were divided into two groups: those in whom the mean right atrial pressure did not rise above 7 mm Hg during exercise (group I, nine patients) and those in whom this variable did rise above 7 mm Hg (group II, 10 patients). A normal range for right ventricular function curves was derived from data reported in the literature. All of the patients in group I remained within this normal range during exercise. Half the patients in group II, however, fell outside the normal range during exercise. For all 19 patients, a linear relationship existed between right ventricular preload and afterload during exercise with a correlation between right atrial mean pressure and pulmonary arterial systolic pressure of r = 0.86.

Blood Pressure↗
PubMed1993

Changes in left and right atrial size after cardioversion of atrial fibrillation: role of mitral valve disease.

OBJECTIVES: The aim of this study was to examine the effect of cardioversion on left and right atrial volume in patients with chronic atrial fibrillation and to determine the influence of mitral valve disease on atrial size. BACKGROUND: Atrial enlargement is a common finding in atrial fibrillation and has been associated with an increased risk for embolic stroke. In addition, atrial enlargement may hamper long-term maintenance of sinus rhythm after cardioversion. METHODS: Forty-one patients with chronic atrial fibrillation (mean duration +/- SD, 45 +/- 62 months) underwent two-dimensional echocardiography before and 6 months after cardioversion to determine left and right atrial dimensions. Underlying heart disease was present in 26 patients: mitral valve disease in 12 (stenosis in 5, regurgitation in 5 and a combination in 2 patients) and other heart diseases in 14. Fifteen patients had lone atrial fibrillation. Patients with sustained sinus rhythm were compared with those who had a relapse of the arrhythmia 6 months after cardioversion. RESULTS: Six months after cardioversion, 28 patients still had sinus rhythm, whereas 13 patients had a relapse of the arrhythmia. In the 28 patients who had sinus rhythm after 6 months, left and right atrial volume decreased from a mean (+/- SD) 72.6 +/- 15.1 to 58.5 +/- 13.8 cm3 (-20%, p < 0.05) and from 68.7 +/- 14.6 to 58.6 +/- 11.6 cm3 (-14%, p < 0.05), respectively. Atrial dimensions also decreased significantly in the subgroup of patients with mitral valve disease. In contrast, no change in atrial size occurred in the 13 patients who had a relapse of atrial fibrillation. Left ventricular function did not change between the two echocardiographic studies, although New York Heart Association class improved in patients who had sinus rhythm after 6 months. CONCLUSIONS: Restoration of sinus rhythm reverts the process of left and right atrial enlargement in patients with chronic atrial fibrillation and mitral valve disease. Therefore, cardioversion may reduce the incidence of thromboembolic complications and prevent the arrhythmia from becoming refractory to medical therapy.

Aged↗
PubMed1982

Long-term follow-up study after closure of secundum atrial septal defect in children: an echocardiographic study.

Serial echocardiography was performed in 51 children with isolated secundum atrial septal defect before and after surgery to measure the effects of chronic right ventricular overload on ventricular function. Right ventricular dilation increased dramatically with growth and with size of the left to right shunt only in the youngest children (body surface area less than 0.5 m2). A lesser effect of growth and no significant effect of shunt size were noted in older children. Although an initial decrease in right ventricular size occurred in the first 3 months after operation, persistent right ventricular dilation remained up to 5 years after closure of the interatrial defect in more than 80 percent of patients. Preoperatively, the ratio of the right ventricular preejection period to ejection time was significantly less than that of normal children. This ratio increased dramatically after operation, exceeding normal values early in the postoperative period in 18 of 48 children and persisting in 6 of 22 after 3 months. Left ventricular dimensions were normal early and late after operation. Left ventricular function was apparently normal, although an exceptionally high shortening fraction was noted in 22 (44 percent) of 51 children after operation. Aortic systolic time interval ratios decreased after operation from high normal to low normal values. It is hypothesized that the persistent enlargement of the right ventricle after operation may be due to the chronic preoperative dilation secondary to chronic interatrial shunting. The abnormally high shortening fraction after operation may result from an abnormal left ventricular geometric configuration or abnormality of filling. It is suggested that surgical closure of the atrial defect in the first 3 years of life may prevent these abnormalities.

Adolescent↗
PubMed1975

Pulmonary stenosis and impaired myocardial function.

Two young Black female patients with pulmonary valve stenosis and intact ventricular septa are presented in protracted congestive cardiac failure with severe tricuspid insufficiency and, in one, atrial fibrillation. Right ventricular systolic dysfunction was manifested by peak systolic pressures below systemic level, raised end-diastolic pressures and low cardiac output, but without right-to-left shunt. These findings are in strong contrast to those found in most patients with pulmonary stenosis of long standing, where persistent impairment of right ventricular function is diastolic with a high end-diastolic pressure and reversal of an interatrial shunt which result from poor right ventricular compliance. Evidence of left ventricular dysfunction was also present in both cases. Protracted heart failure in these patients is believed to have been the result of coincidental cardiomyopathy in a racial group highly predisposed to this disorder. A diagnostic appreciation of this phenomenon is important in the evaluation of heart disease in the Black, since cardiomyopathy may modify or even mask the features of the underlying disorder.

Adolescent↗
PubMedDate not supplied

Pharmacology of furosemide in the horse: a review.

Furosemide, a diuretic, is frequently administered to horses for the prophylaxis of exercise-induced pulmonary hemorrhage and the treatment of a number of clinical conditions, including acute renal failure and congestive heart failure. Furosemide increases the rate of urinary sodium, chloride, and hydrogen ion excretion. Plasma potassium concentration decreases after furosemide administration but urinary potassium excretion in horses is minimally affected. Renal blood flow increases after furosemide administration. Systemically, furosemide increases venous compliance and decreases right atrial pressure, pulmonary artery pressure, pulmonary artery wedge pressure, and pulmonary blood volume. The systemic hemodynamic effects of furosemide are only manifest in the presence of a functional kidney, but can occur in the absence of diuresis, emphasizing the importance of the renal-dependent extra-renal effects of furosemide. The renal and systemic hemodynamic effects of furosemide are modified by prior administration of nonsteroidal anti-inflammatory drugs. Furosemide administration attenuates exercise-induced increases in right atrial, aortic, and pulmonary artery pressures in ponies. Furosemide prevents exercise and allergen-induced bronchoconstriction in humans and decreases total pulmonary resistance in ponies with recurrent obstructive airway disease. These pharmacologic effects are frequently used to rationalize its questionable efficacy in the prevention of exercise-induced pulmonary hemorrhage. Neither the effect of furosemide on athletic performance nor its efficacy in the prevention of exercise-induced pulmonary hemorrhage has been convincingly demonstrated.

Animals↗
PubMed1990

Effects of chronic pindolol treatment on human myocardial beta 1- and beta 2-adrenoceptor function.

To evaluate the effects of chronic pindolol treatment on human myocardial beta-adrenoceptor, membrane preparations from right atrial auricles from patients on chronic pindolol treatment and from patients not treated with beta-blocker were compared with respect to specific binding of [125I]-iodocyanopindolol [( 125I]-ICYP) and adenylate cyclase (AC) activity. Pindolol treatment was associated with a 25% increase in total beta-adrenoceptor density (72.3 vs. 58.3 fmol/mg protein). This increase was due a 40% increase of the beta 1-adrenoceptor subtype (62.2 vs. 44.3 fmol/mg protein), while beta 2-adrenoceptor density was decreased by about 25% (10.0 vs. 14.0 fmol/mg). Isoprenaline 5 mumol/l (9.7 vs. 14.2 pmol/min/mg) and terbutaline 50 mumol/l (4.9 vs. 8.3 pmol/min/mg protein) stimulated adenylate cyclase activity was reduced, whereas fluoride (10 mmol/l) stimulated cAMP production to the same extent in both groups (9.4 vs 9.4 pmol/min/mg protein). Thus, chronic treatment with pindolol was associated with upregulation of the beta 1-adrenoceptors and a down-regulation of the beta 2-adrenoceptors. The total level of beta-adrenoceptors was slightly increased. In spite of this, adenylate cyclase activity and response was reduced.

Adenylyl Cyclases↗
PubMed2004

Right and left ventricular cardiac function in a developed world population with human immunodeficiency virus studied with radionuclide ventriculography.

BACKGROUND: Cardiac dysfunction has been reported in a substantial part of patients infected with the human immunodeficiency virus (HIV). However, most studies are from a time before the introduction of highly active antiretroviral treatment (HAART), which has significantly reduced HIV-associated morbidity and mortality rates. Accordingly, the prevalence of HIV-associated cardiac dysfunction may also have changed. The aim of the study was to establish the prevalence of right- and left-sided cardiac dysfunction in a Danish HIV population, most of whom were undergoing HAART, with radionuclide ventriculography. METHODS: Ninety-five consecutive patients with HIV infection were included. Mean HIV duration was 104 months, and 84% of the patients received HAART. All patients underwent radionuclide ventriculography, and plasma levels of atrial natriuetic peptide (ANP), brain natriuetic peptide (BNP), and endothelin-1 (ET-1) were measured. Thirty age- and sex-matched healthy volunteer subjects were included to establish reference values of radionuclide measurements of left and right ventricular ejection fraction and of left ventricular volume. RESULTS: Of 95 patients with HIV, 1 (1%) had a reduced left ventricular ejection fraction and 6 (7%) had a reduced right ventricle ejection fraction (0.35-0.42) compared with reference values from the age- and sex-matched reference population. Patients with HIV and reduced cardiac function did not differ in the duration of HIV, CD4 count, CD4 nadir, or HIV RNA load. No correlations were found between reduced cardiac function and levels of the 3 peptides measured. CONCLUSIONS: No major dysfunction of the left ventricle is present in a developed world HIV population. However, a small but significant part of this population has modestly reduced right-sided systolic function.

Adult↗
PubMed1992

Preload-dependent hemodynamic effects of milrinone in moderate heart failure.

Milrinone, a bipyridine derivative with positive inotropic and balanced type vasodilating properties, acutely improves cardiac pump function in patients with severe and moderate to severe heart failure. Whether it has similar effects in patients with mild to moderate heart failure is unknown. A hemodynamic evaluation of oral milrinone in dosage of 2.5, 5 and 10 mg was carried out on 3 consecutive days in 18 patients with NYHA class 2.7 heart failure. Patients continued with diuretics and digitalis, administered 15 h before each hemodynamic study. Peak milrinone plasma levels ranged from 77 to 252 micrograms/ml and were attained at 60-90 min following administration. Concomitantly, milrinone significantly reduced pulmonary wedge and right atrial pressures with 24, 47 and 44, and 25, 42 and 38% with the 2.5-, 5- and 10-mg doses, respectively. Milrinone had no effect on cardiac or stroke indices with either dose. Moreover, systemic vascular resistance only decreased by 12% with the highest dose, together with a 7% fall in mean arterial pressure and a 13% rise in heart rate (all p less than 0.05 vs. baseline). Patients were subsequently grouped depending on baseline pulmonary wedge pressure greater than or equal to 18 mm Hg (Gr I, n = 9) or less than 18 mm Hg (Gr II, n = 9). Changes in pulmonary wedge, pulmonary artery and right atrial pressure were similar in both groups following each dose. In contrast, the effect on cardiac pump function clearly differed in patients with high versus normal baseline wedge pressure. In Gr I, cardiac index increased significantly by 16% (5 and 10 mg). In Gr II, cardiac index decreased with 13% following the 10-mg dose (p less than 0.05 vs. baseline). When maximal individual changes in cardiac index were compared, 10 mg milrinone resulted in an improvement of cardiac index in all patients with baseline wedge pressures greater than 15 mm Hg, but in a decrease in cardiac index in patients with lower wedge pressures. It is concluded that milrinone induces contrasting effects on cardiac pump function in patients with mild to moderate heart failure, which may negatively affect its early and, possibly, also late efficacy in this patient group.

Administration, Oral↗
PubMed1989

Cardiac refractoriness. Age-dependence in normal subjects.

The effects of age on cardiac electrophysiologic measurements were assessed in 30 subjects between the ages of 18 and 73 years and free of structural heart disease. Occult heart disease was excluded by a normal treadmill exercise tolerance test, a rest and exercise radionuclide angiogram, and/or a cardiac catheterization. Effective and functional refractory periods of right atrium, right ventricle, and atrioventricular node were assessed. The relationship between these measurements and age was examined using linear regression. There were significant correlations between age and atrial effective and functional refractory periods, atrioventricular effective refractory period, and ventricular effective and functional refractory periods. Other electrophysiologic measures showed no such relationship with age.

Adult↗
PubMed2005

Coenzyme Q10 therapy before cardiac surgery improves mitochondrial function and in vitro contractility of myocardial tissue.

OBJECTIVES: Previous clinical trials suggest that coenzyme Q(10) might afford myocardial protection during cardiac surgery. We sought to measure the effect of coenzyme Q(10) therapy on coenzyme Q(10) levels in serum, atrial trabeculae, and mitochondria; to assess the effect of coenzyme Q(10) on mitochondrial function; to test the effect of coenzyme Q(10) in protecting cardiac myocardium against a standard hypoxia-reoxygentation stress in vitro; and to determine whether coenzyme Q(10) therapy improves recovery of the heart after cardiac surgery. METHODS: Patients undergoing elective cardiac surgery were randomized to receive oral coenzyme Q(10) (300 mg/d) or placebo for 2 weeks preoperatively. Pectinate trabeculae from right atrial appendages were excised, and mitochondria were isolated and studied. Trabeculae were subjected to 30 minutes of hypoxia, and contractile recovery was measured. Postoperative cardiac function and troponin I release were assessed. RESULTS: Patients receiving coenzyme Q(10) (n = 62) had increased coenzyme Q(10) levels in serum (P = .001), atrial trabeculae (P = .0001), and isolated mitochondria (P = .0002) compared with levels seen in patients receiving placebo (n = 59). Mitochondrial respiration (adenosine diphosphate/oxygen ratio) was more efficient (P = .012), and mitochondrial malondialdehyde content was lower (P = .002) with coenzyme Q(10) than with placebo. After 30 minutes of hypoxia in vitro, pectinate trabeculae isolated from patients receiving coenzyme Q(10) exhibited a greater recovery of developed force compared with those in patients receiving placebo (46.3% +/- 4.3% vs 64.0% +/- 2.9%, P = .001). There was no between-treatment difference in preoperative or postoperative hemodynamics or in release of troponin I. CONCLUSIONS: Preoperative oral coenzyme Q(10) therapy in patients undergoing cardiac surgery increases myocardial and cardiac mitochondrial coenzyme Q(10) levels, improves mitochondrial efficiency, and increases myocardial tolerance to in vitro hypoxia-reoxygenation stress.

Administration, Oral↗
PubMed1982

Influence of the right ventricle on canine left ventricular function with PEEP.

In anesthetized dogs we evaluated the influence of increased right ventricular (RV) pressures on left ventricular (LV) function by comparing the hemodynamic effects of increases in RV afterload (pulmonary arterial pressure) produced by positive end-expiratory pressure (PEEP) with those due to pulmonary arterial occlusion (PAO). Left atrial (Pla) and right atrial (Pra) pressures increased with PEEP and PAO [for Pla: 3.1 +/- 0.7 Torr (PEEP), 2.4 +/- 0.9 Torr (PAO); for Pra: 2.9 +/- 0.4 Torr (PEEP), 3.1 +/- 1.2 Torr (PAO)]. RV septal-free wall dimension (RVD) increased, and LV septal-posterolateral dimension (L2) decreased with both conditions [increases in RVD: 1.9 +/- 0.3 mm (PEEP), 2.2 +/- 0.5 mm (PAO); decrease in L2: 1.1 +/- 0.4 mm (PEEP), 0.9 +/- 0.3 mm (PAO)]. Extracorporeal bypass of the great veins did not alter these findings. LV function curves showed less stroke work at any Pla during PEEP, this being unaffected by vagotomy. When the RV was bypassed, there were no PEEP or PAO related changes in Pla or LV function. Thus diminished LV function with PEEP is probably due to the influence on the LV of a stressed RV in this situation.

Animals↗
PubMed2004

Diazoxide provides protection to human myocardium in vitro that is concentration dependent.

BACKGROUND: Diazoxide has been shown to confer significant myocardial protection in many experiments. This study was designed to assess its influence on the structural injury and functional recovery of human myocardium subjected to hypoxia/reoxygenation in vitro. METHODS: The isolated electrically driven human right atrial trabeculae, obtained during cardiac surgery, were studied. The tissue bath was oxygenated with 95% oxygen and 5% carbon dioxide, hypoxia being obtained by replacing oxygen with argon. The influence of diazoxide on atrial contractility was studied first. Next, the two trabeculae from one atrial appendage were studied simultaneously, adding diazoxide to the tissue bath 10 minutes before hypoxia in one, with another serving as a control. We tested 10(-4.5) mol/L and 10(-4) mol/L diazoxide in three sets of experiments testing 30, 60, and 90 minutes of hypoxia. We continued reoxygenation for 120 minutes (in 60-minute and 90-minute hypoxia experiments) and subsequently tested reaction to 10(-4) mol/L norepinephrine. Apart from continuous recording of the contraction force, we measured the troponin I release into the tissue bath after ischemia and reoxygenation. RESULTS: Diazoxide exerted a negative inotropic effect in human atrial muscle (pD(2)=3.96 +/- 0.18). Both concentrations of diazoxide studied resulted in better functional recovery of atrial trabeculae subjected to 30 minutes of hypoxia. With longer hypoxia, only the higher diazoxide concentration provided significant protection as assessed by contractility. After 120 minutes of reoxygenation, only diazoxide-treated muscle was viable enough to respond to norepinephrine. Only 10(-4) mol/L diazoxide resulted in lower troponin I release during hypoxia and reoxygenation. CONCLUSIONS: This study shows that diazoxide provides significant concentration-dependent protection against hypoxia/reoxygenation injury to human myocardium in vitro.

Cell Hypoxia↗
PubMed1990

Endothelin-induced vasoconstriction and release of atrial natriuretic peptides in the rat.

Endothelin-1 (ET-1) was given to male Sprague-Dawley rats in i.v. bolus injections to evaluate its effects on blood pressure and the release of atrial natriuretic peptides (ANP). In awake rats ET-1 (0.3, 1 and 3 nmol kg-1 body wt) transiently reduced mean arterial pressure (MAP) and increased heart rate (HR), followed by a prolonged increase in MAP. The magnitude of these changes and the duration of the increase in MAP were dose-related. The increase in MAP was completely blocked by verapamil, reversed by sodium nitroprusside, slightly reduced by rat atrial natriuretic factor (103-126) and unaffected by saralasin. The initial fall in MAP was also unaltered by these agents. In all groups HR changes were mirror-images of MAP. In anaesthetized rats ET-1 (1 nmol kg-1 body wt) induced a sustained release of ANP. Right atrial pressure increased transiently and then fell below baseline. When the increase in MAP was blocked with sodium nitroprusside, ET-1 still produced an increase in ANP. In conclusion we find that repeated i.v. administration of ET-1 induces immediate vasodilatation, without signs of tachyphylaxis, followed by long-lasting severe vasoconstriction. Baroreceptor function seems to be unchanged. ET-1 appears to induce ANP release by a direct action on atrial myocytes, independent of right atrial and systemic arterial pressure. We hypothesize that endothelin may be a mediator of stretch-induced release of ANP.

Animals↗
PubMed1975

Cardiorenal effects of lidocaine and procaine amide in the conscious dog.

Simultaneous measurements of hemodynamics, arterioventricular (AV) conduction, and renal functioner were obtained in conscious dogs. Catheters were implanted for the long-term measurement of central aortic, right ventricular, and pulmonary artery pressure. AV conduction was assessed following surgical implantation of multipolar electrode plaques in the area of the bundle of His, as well as on the epicardium of the right and left atria and ventricles. Renal function was assessed utilizing standard techniques. Following control measurements, lidocaine, 1 mg/kg, or procaine amide, 10 mg/kg, was administered intravenously. Subsequently, serial measurements were obtained for a 90-min period. No significant changes in hemodynamics were observed following either drug. Procaine amide produced a significant increase in heart rate and a minimal increase in QRS duration associated with a decrease in low right atrial to His bundle conduction time. However, no significant changes in cardiac conduction were observed after lidocaine administration. Renal function was unaffected by lidocaine but significantly depressed by procaine amide, as demonstrated by a decrease in GFR and effective renal flow. In summary, acute administration of procaine amide significantly alters renal function in the conscious dog with minimal effects on AV conduction and hemodynamics.

Aminohippuric Acids↗
PubMed1982

Normal left ventricular systolic function in adults with atrial septal defect and left heart failure.

Systolic left ventricular contractile function has not been extensively evaluated in patients with atrial septal defect who have symptoms of left-sided congestive heart failure. This study examined left ventricular systolic function hemodynamically and angiographically in 6 such adult patients (Group A), 12 adult patients with atrial septal defect without heart failure (Group B) and 20 normal subjects. The mean ( +/- standard error of the mean) left ventricular end-diastolic pressure was higher in patients in Group A (17 +/- 0.8 mm Hg) than in patients in group B (6.9 +/- 0.6 mm Hg) (p less than 0.001). Both right atrial pressure ( 11 +/- 1.3 versus 4.9 +/- 0.5 mm Hg) (p less than 0.001) and mean pulmonary arterial pressure (30 +/- 1.8 versus 15 +/- 1 mm Hg) were also higher in Group A than in Group B. Left ventricular cardiac index and stroke work index did not differ in the two groups. Variables of left ventricular systolic function were similar in both groups of patients and in normal subjects: Ejection fraction was 0.71 +/- 0.05 in Group A, 0.74 +/- 0.02 in Group B and 0.74 +/- 0.01 in normal subjects. Velocity of circumferential shortening was 1.38 +/- 0.14 circumferences/s in Group A, 1.38 +/- 0.07 circumferences/s in Group B and 1.27 +/-0.04 circumferences/s in normal subjects. There was no difference in left ventricular contractile function as indicated by the ratio of end-systolic wall stress to end-systolic volume index among the three groups: normal subjects, average 5.6 +/- 0.19 versus 6.1 +/- 0.5 in Group B and 6.0 +/- 0.6 dynes X 10(3)/cm(2)/(ml/m(2) in Group A. This study of patients with atrial septal defect and left heart failure indicates that abnormal left ventricular systolic contractile function is probably not the cause of the symptoms and elevated left heart filling pressures observed in this group. An abnormality in left ventricular diastolic filling, perhaps related to the volume loaded right ventricle, may explain these changes.

Adolescent↗
PubMed1998

Effect of oxygen on pulmonary hemodynamics and incidence of atrial fibrillation after noncardiac thoracotomy.

OBJECTIVE: The mechanism of postthoracotomy atrial fibrillation (AF) could be related to right ventricular (RV) strain. The effect of oxygen on the occurrence of postoperative AF and on RV function was studied. DESIGN: A prospective, randomized study. SETTING: A university hospital. PARTICIPANTS: Twenty-four noncardiac thoracotomy patients. INTERVENTIONS: At the end of the postoperative anesthesia care unit period, the patients were randomly allocated to receive 35% oxygen until either the third (P = prolonged group) or the first postoperative morning (S = short group). MEASUREMENTS AND MAIN RESULTS: Measurement of hemodynamic variables using a thermodilution pulmonary artery catheter, oxygenation, concentration of plasma atrial natriuretic peptide (ANP) and Holter monitoring were started preoperatively and continued for the 3 postoperative days (PODs). Systolic RV pressure (systolic RVP) and pulmonary vascular resistance (PVR) increased postoperatively only in group S. Major changes in RV performance were not seen with echocardiography or the thermodilution method in any patient. Silent episodes of AF occurred in three patients (25%) in group P and in one patient (8%) in group S (not significant [NS]) without deviations in plasma ANP concentration. On each of the 3 PODs, all patients were exposed to 60% oxygen for 15 minutes. Systolic RVP decreased significantly during the exposure to 60% oxygen only in group S, but not in patients developing AF. Predictive factors for AF were a high preoperative PVR, intraoperative bleeding necessitating volume loading, and elevated systolic RVP immediately after thoracotomy. CONCLUSION: Short episodes of AF occurred irrespective of the length of oxygen therapy. Occurrence of AF could not be explained by changes in RV function.

Atrial Fibrillation↗
PubMed1993

Right ventricular function during orthotopic liver transplantation.

Right ventricular (RV) function was assessed in 20 patients undergoing orthotopic liver transplantation to determine its role in the hemodynamic instability frequently seen during this procedure. A modified pulmonary artery catheter equipped with a fast response thermistor was used to determine RV ejection fraction (EFrv), allowing for calculation of RV end-diastolic volume index (EDVIrv, as the ratio of stroke index [SI] to EFrv) and RV end-systolic volume index (ESVIrv, as the difference between EDVIrv and SI). The above hemodynamic measures were taken during dissection for hepatectomy (stage I), during the anhepatic stage (stage II), and after reperfusion of the grafted liver, the neohepatic stage (stage III). No patient had pulmonary hypertension during the study interval. No correlation was observed between right atrial pressure (Pra) and EDVIrv, indicating that Pra is a less reliable clinical indicator of RV preload. RV function appeared to be well preserved throughout the procedure, as indicated by a relatively constant and supranormal EFrv, although a small and probably clinically unimportant decrease in EFrv was observed during the anhepatic stage (0.52, 0.50, and 0.55 during stages I, II, and III, respectively). There was a strong correlation between SI and EDVIrv for pooled data over a wide range of EDVIrv (60-185 mL.m-2). Although unstable central blood temperature precluded the determination of EFrv within the first 5 min after reperfusion, RV function was unaltered otherwise during uncomplicated orthotopic liver transplantation using venovenous bypass, indicating that orthotopic liver transplantation per se is not associated with significant RV dysfunction.

Adult↗