Increase In Atrial Pressure Research Articles

Modulation of alveolar fluid clearance by reactive oxygen-nitrogen intermediates

in this issue of AJP-Lung , Kaestle et al. ([28][1]) report that an increase in left atrial pressure in isolated perfused lungs induces a Ca2+-dependent increase of endothelial nitric oxide (NO) production, which decreases reabsorption of fluid across the alveolar epithelium, resulting in pulmonary

Interpreting the lung microvascular filtration coefficient

since its introduction in the classic paper by Gaar et al. ([2][1]), determination of the microvascular filtration coefficient, K f, has become a popular approach for quantifying the lung microvascular barrier. The method entails establishing a sustained step increase of the left atrial pressure to

Ventricular fibrillation induced by transoesophageal cardiac pacing: A new model of cardiac arrest in rats

To investigate whether transoesophageal cardiac pacing can induce ventricular fibrillation (VF) and how long the cardiac pacing has to be sustained to prevent the reversion of the VF induced. A pacing electrode was inserted orally into the oesophagus and high-frequency ventricular pacing was performed so as to elicit VF in 25 Sprague-Dawley rats. Incidences of VF and time of cardiac pacing were observed and recorded. Four minutes after onset of VF cardiopulmonary resuscitation (CPR) was initiated. A short interval of high-frequency ventricular pacing caused an immediate drop of blood pressure, loss of pulse and increase of right atrial pressure in the same time frame. When the cardiac pacing was terminated, VF was elicited at least once or more than once in all of the 25 rats. However, the VF elicited by the burst stimulation could be defibrillated spontaneously. With the prolongation (120-180 s) of cardiac pacing, the incidence of defibrillation of VF decreased from 100 to 0%. VF persisted in 19 of 25 animals, developed into asystole in 5 of 25 animals and converted into pulseless electrical activity in 1 of 25 animals prior to CPR. Following CPR 22 of 25 animals were resuscitated. Transoesophageal cardiac pacing can induce VF in rats. However, the cardiac pacing is required for at least 120-180 s to ensure that VF does not spontaneously convert. We can use the technique to establish a new and simpler rat cardiac arrest (CA) model, which may facilitate experimental investigation on CPR.

Initial orthostatic hypotension: review of a forgotten condition

Several studies have shown that standing up is a frequent (3-10%) trigger of loss of consciousness both in young and old subjects. An exaggerated transient BP (blood pressure) fall upon standing is the underlying cause. IOH (initial orthostatic hypotension) is defined as a transient BP decrease within 15 s after standing, >40 mmHg SBP (systolic BP) and/or >20 mmHg DBP (diastolic BP) with symptoms of cerebral hypoperfusion. It differs distinctly from typical orthostatic hypotension (i.e. BP decrease >20 mmHg SBP and/or >10 mmHg DBP after 3 min of standing) as the BP decrease is transient. Only continuous beat-to-beat BP measurement during an active standing-up manoeuvre can document this condition. As IOH is only associated with active rising, passive tilting is of no diagnostic value. The pathophysiology of IOH is thought to be a temporal mismatch between cardiac output and vascular resistance. The marked decrease of vascular resistance during rising is similar to that observed at the onset of leg exercise and is absent during head-up tilting. It is attributed to vasodilatation in the working muscle through local mechanisms. Standing up causes an initial increase in venous return through the effects of contraction of leg and abdominal muscles. The consequent sudden increase in right atrial pressure may contribute to the fall in systemic vascular resistance through a reflex effect. This review alerts clinicians and clinician scientists to a common, yet often neglected, condition that occurs only upon an active change of posture and discusses its epidemiology, pathophysiology and management.

Percutaneous Technique for Creation of Tricuspid Regurgitation in an Ovine Model

Experimental models of tricuspid regurgitation (TR) are needed to study the percutaneous placement of prosthetic atrioventricular valves. The purpose of this study was to develop an appropriate simple and reproducible percutaneous experimental model for creation of tricuspid regurgitation. Tricuspid regurgitation was successfully created through papillary muscle avulsion using a guide-wire loop in seven sheep with regurgitation documented on right ventricular angiograms and a significant increase in heart rate and right atrial pressures. Acute onset of tricuspid regurgitation was poorly tolerated in one animal that died. Autopsy examinations showed avulsion of one papillary muscle in four animals and two papillary muscles in three animals.

Impact of a somatostatin analog on vascular capacity in conscious dogs

Octreotide is a somatostatin analog which is thought to selectively induce splanchnic constriction and octreotide has recently been shown to markedly increase orthostatic tolerance in humans. Our goal was to test the hypothesis that octreotide-induced reductions in vascular capacity constitute a mechanism by which this agent improves orthostatic tolerance. Studies were carried out in acepromazine sedated, hexamethonium treated conscious dogs with atrioventricular block. Dogs were lightly restrained in right lateral recumbency while beat-by-beat cardiac output was held constant at 4.10 l min−1 by computer controlled ventricular pacing as changes in cardiac output are known to alter right atrial pressure. Under control conditions, right atrial pressure and mean arterial pressure averaged 1.9 ± 0.4 mmHg and 64.8 ± 2.3 mmHg, respectively. Following administration of octreotide (1.5 ug kg−1 i.v.), right atrial pressure averaged 2.5 ± 0.4 mmHg (p<0.05 vs. control) and mean arterial pressure averaged 72.5 ± 2.3 mmHg (p<0.05 vs. control). These data demonstrate that octreotide induces a modest but significant increase in right atrial pressure which corresponds to a decrease in vascular capacity of approximately 2.0 ml kg−1. We conclude that a reduction in vascular capacity constitutes a mechanism by which octreotide improves orthostatic tolerance. Supported by NIH HL46314

The “A-dip” of diastolic mitral regurgitation: An unusual Doppler flow pattern in a patient with severe aortic insufficiency and complete heart block

This is an unusual case of diastolic mitral regurgitation (MR) with a high diastolic velocity jet and prolonged jet duration related to a combination of acute severe aortic insufficiency and high-degree atrioventricular block. This case illustrates an interesting hemodynamic phenomenon with multiple transient decreases in the pressure gradient between the left ventricle and left atrium during diastole related to a temporary increase in left atrial pressure associated with atrial contraction.

Effects of ramipril on renal function during progressive overpacing-induced heart failure in dogs

To investigate the effects of preventive angiotensin converting enzyme inhibitor treatment with ramipril in dogs with progressively severe experimentally induced heart failure. 20 dogs. Dogs were randomly allocated to receive no treatment (control) or ramipril (0.125 mg/kg, PO, daily) for 7 weeks. Physical examination, repetitive catheterization of the right side of the heart, and echocardiography were performed before the study (day 0) and weekly for 7 weeks. Renal plasma flow (RPF) as determined by para-aminohippuric acid clearance and glomerular filtration rate (GFR) as determined by creatinine and iohexol clearances were measured on day 0 and at weeks 4 and 7. Overpacing induced a progressive increase in right atrial pressure (RAP) and pulmonary artery pressure, occluded (PAPO), with a decrease in systemic arterial pressure. There were progressive alterations of echocardiographic indices of diastolic and systolic ventricular function. The RPF and GFR decreased before cardiac output decreased, and filtration fraction increased. The logarithm of the urinary sodium-to-potassium concentration ratio (log(10)[Na(+)/K(+)]) decreased. Significant effects of ramipril included a delay in clinical signs of heart failure, a late decrease in RAP and PAPO, and increases in the sodium excretion fraction and log(10)(Na(+)/K(+)). There was a satisfactory agreement between the creatinine and iohexol clearance measurements. Results suggest that, in this rapid-evolving, dilated cardiomyopathy, activation of the renin-angiotensin system contributes to the pathophysiology of heart failure late in the disease and essentially by an activation of renal salt and water retention.

Tricuspid Valve Malfunction and Ventricular Pacemaker Lead: Case Report and Review of the Literature

Pacemaker implantation can be associated with several complications, including myocardial perforation with or without pericardial effusion, venous thrombosis, vegetations of the tricuspid valve (TV) or pacing lead, and tricuspid regurgitation (TR). The TR is thought to be derived from deformity or perforation of the TV by the pacing lead or secondary to atrioventricular discordance with asynchronous ventricular pacing. Severe TR can be deleterious to the patient because it raises the central venous pressure by increasing the right sided preload. Chronically, the increase in right sided blood volume can result in an increase in the right atrial pressure leading to a decrease in venous return and low cardiac output. Severe TR from leaflet adhesion to the pacemaker lead has not been reported before. With the aging of the population and the expanding use of pacemakers and implantable cardioverter defibrillators (ICD) in clinical practice, this complication may be seen more frequently. We present a patient diagnosed with severe TR, years after his pacemaker implantation. His TR was thought to be caused by adhesion of the tricuspid valve to his pacemaker lead.

Passive pericardial constraint protects against stretch-induced vulnerability to atrial fibrillation in rabbits

Atrial fibrillation is more common in conditions with elevated atrial pressure and can be induced experimentally with acute increases in atrial pressure. We examined the effect of increased atrial pressure with and without pericardial constraint to better separate the effects of increased pressure and atrial stretch. In Langendorff-perfused rabbit hearts with intact pericardium, after ligating the pulmonary and caval veins, intra-atrial pressures were increased in a stepwise manner by adjusting the pulmonary outflow cannula. Rapid burst pacing was applied to induce atrial fibrillation at increasing intra-atrial pressures from 0 to 24 cmH(2)O. The atrial refractory period was recorded at each pressure using a single extra stimulus. The protocol was repeated after the pericardium was removed. When the pericardium was intact, atrial stretch was limited by passive constraint, and sustained atrial fibrillation could not be induced despite atrial pressures in excess of 20 cmH(2)O. In contrast, when the pericardium was removed, atrial fibrillation could be reliably induced when atrial pressure exceeded 15 cmH(2)O. This suggests that the electrophysiological effects of acute atrial volume loading rely on atrial stretch rather than increased atrial pressure alone.

Metalloproteinase‐9 in circulating monocytes in pulmonary hypertension

The role of matrix metalloproteinases (MMPs) in pulmonary hypertension (PH) is complex as MMPs are involved in both the vascular and cardiac remodelling associated with PH. To gain insight into this problem, monocytes were isolated from pulmonary arterial blood in patients suffering from PH, related to chronic obstructive pulmonary disease (n = 6), chronic pulmonary thromboembolism (n = 3) or pulmonary arterial hypertension (n = 8). The severity of PH was associated with decreases in cardiac index (CI) and mixed venous blood oxygen saturation (SO(2)), and an increase in right atrial pressure (). Monocyte pro-MMP-9 content (zymography) was positively correlated with SO(2) (r = 0.73, P < 0.05) and CI (r = 0.66, P < 0.05), and negatively with (r = 0.54, P < 0.05); there was no significant correlation with pulmonary vascular resistance. In conclusion, the pro-MMP-9 content of circulating monocytes was lower in the more severe forms of PH which showed heart failure suggesting that such MMP enzymatic activity reflects heart failure following pulmonary vascular and myocardial remodelling in PH.

Increased propensity for apnea in response to acute elevations in left atrial pressure during sleep in the dog

Periodic breathing is commonly observed in chronic heart failure (CHF) when pulmonary capillary wedge pressure is abnormally high and there is usually concomitant tachypneic hyperventilation. We hypothesized that acute pulmonary hypertension at pressures encountered in CHF and involving all of the lungs and pulmonary vessels would predispose to apnea/unstable breathing during sleep. We tested this in a chronically instrumented, unanesthetized dog model during non-rapid eye movement (NREM) sleep. Pulmonary hypertension was created by partial occlusion of the left atrium by means of an implanted balloon catheter in the atrial lumen. Raising mean left atrial pressure by 5.7 +/- 1.1 Torr resulted immediately in tachypneic hyperventilation [breathing frequency increased significantly from 13.8 to 19.9 breaths/min; end-tidal P(CO2) (P(ET(CO2))) fell significantly from 38.5 to 35.9 Torr]. This tachypneic hyperventilation was present during wakefulness, NREM sleep, and rapid eye movement sleep. In NREM sleep, this increase in left atrial pressure increased the gain of the ventilatory response to CO2 below eupnea (1.3 to 2.2 l.min(-1).Torr(-1)) and thereby narrowed the CO2 reserve [P(ET(CO2)) (apneic threshold) - P(ET(CO2)) (eupnea)], despite the decreased plant gain resulting from the hyperventilation. We conclude that acute pulmonary hypertension during sleep results in a narrowed CO2 reserve and thus predisposes toward apnea/unstable breathing and may, therefore, contribute to the breathing instability observed in CHF.

Beta1‐Adrenoceptor activation decreases atrial myocytic ANP release via cAMP‐protein kinase signaling

Although beta-adrenergic receptor (AR) blockade-induced increase in plasma atrial natriuretic peptide (ANP) levels is implicated in the therapeutic significance of beta-AR blockade, the role of beta-AR in the regulation of atrial ANP release is not clearly defined. The purpose of the present study was to define the role of beta-AR subtypes in the regulation of atrial ANP release. Experiments were performed in perfused beating rabbit atria allowing measurements of atrial contractile response, cAMP efflux and atrial myocytic ANP release. beta-AR activation with (-) isoproterenol (ISO) decreased atrial myocytic ANP release concomitantly with increases in cAMP efflux concentration and atrial pulse pressure in a concentration-dependent manner. The ANP response was inversely related to the change in cAMP efflux concentration. ISO-induced decrease in ANP release was blocked by beta 1-AR blockade with CGP20712A but not by beta 2-AR with ICI118551. ISO-induced change in ANP release was attenuated by staurosporine, an inhibitor of nonselective protein kinase. These findings suggest that beta 1-AR activation decreases atrial myocytic ANP release via adenylyl cyclase-cAMP-protein kinase signaling pathway. Supported by KOSEF (R01-2003-000-10507-0).

The role of pacing mode in the development of atrial fibrillation

Asynchronous ventricular pacing has been shown to increase the risk of development of atrial fibrillation (AF) because of various mechanisms: retrograde atrioventricular (AV) conduction with increase in atrial pressure causing acute atrial stretch and reverse flow in the pulmonary veins, mitral regurgitation, reduced coronary blood flow, adverse neuroendocrine reactions, etc. Dual-chamber pacing preserves atrioventricular synchrony. However, in randomized multicentre trials comparing VVI(R) with DDD(R) pacing, AF is only slightly less frequent in the dual-chamber mode. This is most likely due to unnecessary ventricular pacing, which is frequent in dual-chamber pacing. At nominal values, dual-chamber devices usually do not permit intrinsic AV conduction but promote delivery of the ventricular stimulus at an inappropriate time in an inappropriate place. Programming of long AV delays facilitates spontaneous AV conduction but usually cannot completely avoid unnecessary ventricular pacing and causes other problems in the dual-chamber mode. Atrial septal lead placement can improve left-sided AV synchrony and promote spontaneous AV conduction. Programming of the AAI(R) mode is superior to the dual-chamber mode but cannot be used if AV conduction is impaired intermittently or permanently. Therefore, dedicated algorithms enhancing spontaneous AV conduction in the dual-chamber mode are desirable for a large proportion of pacemaker patients.

Point: The muscle metaboreflex does restore blood flow to contracting muscles

Imposed reductions in oxygen delivery to active skeletal muscle during dynamic exercise in conscious dogs evoke a powerful pressor response, termed the muscle metaboreflex. During submaximal work rates, the major mechanism used by this reflex is to increase cardiac output (CO), which generates a

Physiologic Effect of Stent Therapy for Inferior Vena Cava Obstruction Due to Malignant Liver Tumor

To understand systemic the influence of stent therapy for inferior vena cava (IVC) obstruction due to advanced liver tumor. Seven patients with symptomatic IVC obstruction due to advanced primary (n = 4) or secondary (n = 3) liver tumor were subjected to stent therapy. Enrollment criteria included high IVC pressure over 15 mmHg and the presence of edema and ascites. Z-stents were deployed using coaxial sheath technique via femoral venous puncture. Physiologic and hematobiochemical parameters were analyzed. All procedures were successful, and the stents remained patent until patient death. Promptly after stent placement, the IVC flow recovered, and the venous blood pressure in the IVC below the obstruction level showed a significant decrease from 20.8 +/- 1.2 mmHg (mean +/- SE) to 10.7 +/- 0.7 mmHg (p < 0.01). Transient mild increase of right atrial pressure was observed in 1 patient. During the following week prominent diuresis was observed in all patients. Mean urine output volume in the 3 days before the stent therapy was 0.81 +/- 0.09 l/day compared with 2.1 +/- 0.2 l/day (p < 0.01) in the 3 days after. The edema and ascites decreased in all patients. The caval pressure change correlated well (r > 0.6) with the urine volume increase, and with the decreased volume of edema and ascites. The urine volume increase correlated well with the decrement of edema, but not with that of ascites. Improvements for various durations in the levels of blood urea nitrogen, serum creatinine, lactate dehydrogenase, fibrinogen, and platelet count were found (p < 0.05). These hematobiochemical changes were well correlated with each other and with the decrement of ascites. Two patients showed a low blood sodium level of 128.5 mEq/l after intensive natriuresis, and one of them died on day 21 with hepatic failure, which was interpreted as maladaptation aggravation. The mean survival time was 94.1 +/- 34.1 days (mean +/- SD), ranging from 21 to 140 days after stent treatment. The stent therapy for IVC obstruction due to malignant liver tumors was followed by a series of physiologic and hematobiochemical consequences, most of them favorable but some possibly unfavorable. Rational interpretations and predictions of sequelae based on physiologic science including cardiology, hepatology, and nephrology would facilitate the best management of stent therapy for malignant IVC obstruction.

Diastolic Dysfunction Beyond Distensibility

In order for the left ventricle (LV) to function as an effective pump, it must not only be able to empty but also to fill without requiring an elevated left atrial pressure. Furthermore, the stroke volume must be able to increase in response to stress, such as exercise, without much increase in left atrial pressure. Thus, LV diastolic function is an important determinant of cardiac performance. Article p 2921 Diastolic function has conventionally been assessed on the basis of the LV end-diastolic pressure-volume relation (Figure 1). A shift of this curve upward and to the left (curve A, Figure 1) has been considered to be the hallmark of diastolic dysfunction. In this situation, each LV end-diastolic volume is associated with a higher end-diastolic pressure, and therefore, the ventricle is less distensible. Figure 1. LV end-diastolic pressure-volume relations. Stiffnesses at typical operating points are shown as the change in pressure (ΔP) divided by the change in volume (ΔV). See text for discussion. In contrast, in dilated cardiomyopathy, the LV end-diastolic pressure-volume relation is shifted substantially to the right (curve B, Figure 1). In this situation, each volume is associated with a lower pressure; thus, the ventricle is more distensible. This has been interpreted as indicating there is enhanced diastolic function. However, patients with dilated cardiomyopathy have abnormal LV filling dynamics, elevated left atrial pressure, and an inability to increase stroke volume without further elevation of left atrial pressure. The severity of heart failure and prognosis are related to the severity of the filling abnormalities regardless of ejection fraction.1 Why are measures of LV diastolic function so abnormal in a dilated ventricle with enhanced distensibility? Is this merely a manifestation of overfilling of the LV that has displaced the operating point to a portion of the pressure-volume relation at which the …

Cardiovascular Issues in Respiratory Care

The hemodynamic effects of ventilation are complex but can be grouped under four clinically relevant concepts. First, spontaneous ventilation is exercise, and critically ill patients may not withstand the increased work of breathing. Initiation of mechanical ventilatory support will improve oxygen delivery to the remainder of the body by decreasing oxygen consumption. To the extent that mixed venous oxygen also increases, Pao(2) will increase without any improvement in gas exchange. Similarly, weaning from mechanical ventilatory support is a cardiovascular stress test. Patients who fail to wean also manifest cardiovascular insufficiency during the failed weaning attempts. Improving cardiovascular reserve or supplementing support with inotropic therapy may allow patients to wean from mechanical ventilation. Second, changes in lung volume alter autonomic tone and pulmonary vascular resistance (PVR), and at high lung volumes compress the heart in the cardiac fossa. Hyperinflation increases PVR and pulmonary artery pressure, impeding right ventricular ejection. Decreases in lung volume induce alveolar collapse and hypoxia, stimulating an increased pulmonary vasomotor tone by the process of hypoxic pulmonary vasoconstriction. Recruitment maneuvers, positive end-expiratory pressure, and continuous positive airway pressure may reverse hypoxic pulmonary vasoconstriction and reduce pulmonary artery pressure. Third, spontaneous inspiration and spontaneous inspiratory efforts decrease intrathoracic pressure (ITP). Since diaphragmatic descent increases intra-abdominal pressure, these combined effects cause right atrial pressure inside the thorax to decrease but venous pressure in the abdomen to increase, markedly increasing the pressure gradient for systemic venous return. Furthermore, the greater the decrease in ITP, the greater the increase in left ventricular (LV) afterload for a constant arterial pressure. Mechanical ventilation, by abolishing the negative swings in ITP, will selectively decrease LV afterload, as long as the increases in lung volume and ITP are small. Finally, positive-pressure ventilation increases ITP. Since diaphragmatic descent increases intra-abdominal pressure, the decrease in the pressure gradient for venous return is less than would otherwise occur if the only change were an increase in right atrial pressure. However, in hypovolemic states, positive-pressure ventilation can induce profound decreases in venous return. Increases in ITP decrease LV afterload and will augment LV ejection. In patients with hypervolemic heart failure, this afterload reducing effect can result in improved LV ejection, increased cardiac output, and reduced myocardial oxygen demand.

The Effect of Gravitational Acceleration on Cardiac Diastolic Function: A Biofluid Mechanical Perspective with Initial Results

Echocardiographic measurements of astronaut cardiac function have documented an initial increase, followed by a progressive reduction in both left ventricular end-diastolic volume index and stroke volume with entry into microgravity (micro-G). The investigators hypothesize that the observed reduction in cardiac filling may, in part, be due to the absence of a gravitational acceleration dependent, intraventricular hydrostatic pressure difference in micro-G that exists in the ventricle in normal gravity (1-G) due to its size and anatomic orientation. This acceleration-dependent pressure difference, DeltaP(LV), between the base and the apex of the heart for the upright posture can be estimated to be 6660 dynes/cm(2) ( approximately 5 mm Hg) on Earth. DeltaP(LV) promotes cardiac diastolic filling on Earth, but is absent in micro-G. If the proposed hypothesis is correct, cardiac pumping performance would be diminished in micro-G. To test this hypothesis, ventricular function experiments were conducted in the 1-G environment using an artificial ventricle pumping on a mock circulation system with the longitudinal axis anatomically oriented for the upright posture at 45 degrees to the horizon. Additional measurements were made with the ventricle horizontally oriented to null DeltaP(LV)along the apex-base axis of the heart as would be the case for the supine posture, but resulting in a lesser hydrostatic pressure difference along the minor (anterior-posterior) axis. Comparative experiments were also conducted in the micro-G environment of orbital space flight on board the Space Shuttle. This paper reviews the use of an automated cardiovascular simulator flown on STS-85 and STS-95 as a Get Away Special payload to test this hypothesis. The simulator consisted of a pneumatically actuated, artificial ventricle connected to a closed-loop, fluid circuit with adjustable compliance and resistance elements to create physiologic pressure and flow conditions. Ventricular instrumentation included pressure transducers in the apex and base as well as immediately upstream of the inflow valve and downstream of the outflow valve, and a flow probe downstream of the outflow valve. By varying the circulating fluid volume, ventricular function could be determined for varying preload pressures at a regulated, mean afterload pressure of 95 mm Hg. This variation in preload condition permitted the construction of a ventricular function curve for the micro-G environment for comparison to the same curve for the 1-G environment. Data were collected from both missions at the upper end of the ventricular function curve. Experiment operation in the 1-G, supine orientation or in the micro-G environment eliminated the DeltaP(LV) observed in the 1-G, upright orientation. Consistent with the hypothesis, additional atrial pressure was required in micro-G to obtain stroke volumes and flow rates similar to those measured in 1-G for the upright posture. The necessary increase in atrial pressure was approximately 5 mm Hg in these experiments. In the same range of flow rates and stroke volumes, similar flows were observed in the 1-G supine posture for atrial pressures intermediate to the 1-G upright and micro-G values, also consistent with the hypothesis. Additional experiments on board the Space Shuttle are in preparation to gather data across the rest of the normal physiologic range of the ventricular function curve.

Giant Flow Reversal in Pulmonary Venous Flow as a Possible Mechanism for Asynchronous Pacing-induced Heart Failure

Mechanistic roles of the immediate increase in left atrial (LA) pressure in pacing-induced congestive heart failure have not been clearly understood. We evaluated the impact of asynchronous rapid ventricular pacing on LA hemodynamics in this model. Transthoracic and transesophageal echocardiography and hemodynamic assessment were performed in 23 healthy mongrel dogs. Data were acquired before and 5 minutes after initiation of rapid right ventricular pacing (200/min). At 5 minutes after initiation of the pacing, giant pulmonary venous (PV) flow reversal (-76 cm/s) was observed in association with 1:1 ventriculoatrial conduction or complete atrioventricular dissociation. This giant PV flow reversal corresponded to an inappropriately timed atrial contraction, especially during systole. Cardiac output (3.21 vs 2.00 L/min, P < .001) was decreased corresponding to the decrease in the forward blood volumes as described by decrease in the Doppler left ventricular (LV) outflow (8.99 vs 4.73 cm, P < .0001), mitral inflow (6.89 vs 3.19 cm, P < .0001), and PV flow (14.15 vs 7.22 cm, P < .0001) velocity integrals. As a result, there was a marked elevation of the mean pulmonary capillary wedge (9.1 vs 17.1 mm Hg, P < .001) and LV end-diastolic (8.2 vs 17.4 mm Hg, P < .01) pressures leading to congestive heart failure. The giant PV flow reversal seen during asynchronous rapid right ventricular pacing corresponds to an inappropriate atrial contraction, immediately elevates LA pressure, and may initially promote congestive heart failure. The increase in LV end-diastolic pressure associated with decreased LV ejection fraction caused decrease in the LV filling volume leading to further increase in the LA pressure. This sustained marked elevation in the LA pressure and LV end-diastolic pressure could contribute to the heart failure process.