Changes In Intracardiac Pressures Research Articles

Quantitative Blood Volume Analysis and Hemodynamic Measures of Vascular Compliance in Patients With Worsening Heart Failure

The role of blood volume (BV) expansion vs a change in vascular compliance in worsening heart failure (HF) remains under debate. We aimed to assess the relationship between BV and resting and stress hemodynamics in worsening HF and to further elucidate the significance of BV in cardiac decompensation. Patients with worsening HF underwent radiolabeled indicator-dilution BV analysis and cardiac catheterization. Intravascular volumes and resting/stress hemodynamics were recorded. Provocative stress maneuvers included change in systolic blood pressure (ΔSBP) from lying to standing and Valsalva and intracardiac pressure changes with leg raise. Correlation between BV and invasive hemodynamics were assessed by linear regression. Of 27 patients with worsening HF, patients' characteristics included mean age 61 ± 12 years, 70% male, 19% Black, and mean ejection fraction 29% ± 15%. Of the patients, 13 (48%) had hypervolemia as measured by total BV, which weakly correlated with ΔSBP by position (R2 = 0.009) and Valsalva (R2 = 0.003) and with right atrial (R2 = 0.049) and pulmonary capillary wedge (R2 = 0.047) pressure changes during leg raise. In patients with worsening HF, BV mildly correlated with intracardiac pressures at rest. Provocative maneuvers intended to test vascular compliance did not correlate with BV, indicating that compliance may serve as a stand-alone metric in HF.

Small-Group Activity to Reinforce the Impact of Valvular Defects and Heart Failure on Cardiac Pressure-Volume Relationships.

An important topic in cardiac physiology is the relationship between changes in intracardiac pressures and volumes during the cardiac cycle. This topic lends itself well to utilizing active learning principles to facilitate student understanding of pressure and volume changes in normal cardiac physiology and in the pathophysiology of valve disease and heart failure. We describe an active learning exercise regarding this topic that engages and facilitates student learning in a small-group setting. Following an overview lecture on the normal cardiac physiology, small groups of students under the guidance of a facilitator were provided with a worksheet consisting of questions related to background knowledge of cardiac physiology. Additional questions related to five valve disease and heart failure cases were also provided to promote the application of basic physiology principles to clinically relevant problems. The facilitator was provided with a guide to help facilitate the student interactions. Following the group worksheet activity, an animated slide presentation was shown to further engage student learning through active discussion of their worksheet answers. Students were assessed by written examination, and were found to have a higher performance on the subset of questions related to this learning activity compared to the overall exam. Of the 175 students completing the exercise, 23 voluntarily provided feedback via a survey. Student surveys provided overwhelmingly positive feedback on the benefits of this active learning exercise. Small group, active learning exercises benefited student learning by providing a framework for analysis, synthesis, and application of clinically relevant cardiac physiology concepts.

Ambulatory Heart Failure Monitoring: A Systemic Review.

Heart failure (HF) is one of the leading causes of morbidity and mortality and has a large effect on the country’s economy. Although there have been major advances in HF monitoring, including more advanced pharmacological management and device-based therapy, HF-related mortality remains high. It is important to monitor HF so that HF-related hospitalization and mortality can be prevented. Due to the lower sensitivity of clinical features and biochemical markers, as well as the failure of telemonitoring in early detection of HF, more advanced techniques have been sought to more accurately predict impending HF, in order to address timely pharmacological management and prevent heart failure hospitalization (HFH). Device-based therapy has passed through various stages and culminated in the recently introduced CardioMEMSTM (St. Jude Medical, Inc., Saint Paul, Minnesota). CardioMEMSTM is a wireless pulmonary artery pressure (PAP) monitoring device, which continuously monitors PAP and transmits data to a healthcare provider. It rapidly identifies changes in intracardiac pressure and allows timely pharmacological management. CardioMEMSTM showed a higher reduction of HFH compared to any other devices.

Symptom burden, Metabolic profile, Ultrasound findings, Rhythm, neurohormonal activation, haemodynamics and health-related quality of life in patients with atrial Fibrillation (SMURF): a protocol for an observational study with a randomised interventional component

IntroductionAtrial fibrillation (AF) is the most common cardiac arrhythmia, with an estimated prevalence of 1.5–2%. It is an independent risk factor for ischaemic stroke and is estimated to cause about...

The decrease of cardiac chamber volumes and output during positive-pressure ventilation

Positive-pressure ventilation (PPV) is widely used for treatment of acute cardiorespiratory failure, occasionally at the expense of compromised cardiac function and arterial blood pressure. The explanation why has largely rested on interpretation of intracardiac pressure changes. We evaluated the effect of PPV on the central circulation by studying cardiac chamber volumes with cardiac magnetic resonance imaging (CMR). We hypothesized that PPV lowers cardiac output (CO) mainly via the Frank-Starling relationship. In 18 healthy volunteers, cardiac chamber volumes and flow in aorta and the pulmonary artery were measured by CMR during PPV levels of 0, 10, and 20 cmH2O applied via a respirator and a face mask. All cardiac chamber volumes decreased in proportion to the level of PPV. Following 20-cmH2O PPV, the total diastolic and systolic cardiac volumes (±SE) decreased from 605 (±29) ml to 446 (±29) ml (P < 0.001) and from 265 (±17) ml to 212 (±16) ml (P < 0.001). Left ventricular stroke volume decreased by 27 (±4) ml/beat; heart rate increased by 7 (±2) beats/min; and CO decreased by 1.0 (±0.4) l/min (P < 0.001). From 0 to 20 cmH2O, right and left ventricular peak filling rates decreased by -146 (±32) and -187 (±64) ml/s (P < 0.05) but maximal emptying rates were unchanged. Cardiac filling and output decrease with increasing PPV in healthy volunteers. The decrease is seen even at low levels of PPV and should be taken into account when submitting patients to mechanical ventilation with positive pressures. The decrease in CO is fully explained by the Frank-Starling mechanism.

Changes in cardiac performance during hypoxic exposure in the grass shrimpPalaemonetes pugio

In hearts of higher invertebrates as well as vertebrates, the work performed by the ventricle is a function of both rate and contractility. Decapod crustaceans experience a hypoxia-induced bradycardia that is thought to result in an overall reduction in cardiac work; however, this hypothesis has not yet been tested and is the primary purpose of this study. In the grass shrimp Palaemonetes pugio, cardiac pressure and area data were obtained simultaneously, and in vivo, under normoxic (20.2 kPa O(2)) and hypoxic (6.8 or 2.2 kPa O(2)) conditions and integrated to generate pressure-area (P-A) loops. The area enclosed by the P-A loop provides a measure of stroke work and, when multiplied by the heart rate, provides an estimate of both cardiac work and myocardial O(2) consumption. Changes in intra-cardiac pressure (dp/dt) are correlated to the isovolemic contraction phase and provide an indication of stroke work. At both levels of hypoxic exposure, intra-cardiac pressure, dp/dt, stroke work and cardiac work fell significantly. The significant decrease in intra-cardiac pressure provides the primary mechanism for the decrease in stroke work, and, when coupled with the hypoxia-induced bradycardia, it contributes to an overall fall in cardiac work. Compared with normoxic P-A loops, hypoxic P-A loops (at both levels of hypoxia) become curvilinear, indicating a fall in peripheral resistance (which might account for the reduction in intra-cardiac pressure), which would reduce both stroke work and cardiac work and ultimately would serve to reduce myocardial O(2) consumption. This is the most direct evidence to date indicating that the hypoxia-induced bradycardia observed in many decapod crustaceans reduces cardiac work and is therefore energetically favorable during acute exposure to conditions of low oxygen.

A Randomized Invasive Cardiac Electrophysiology Study of the Combined Ion Channel Blocker AZD1305 in Patients After Catheter Ablation of Atrial Flutter

This study assessed the cardiac electrophysiological and hemodynamic effects of an intravenous infusion of the combined ion channel blocker AZD1305. After successful ablation of atrial flutter, patients were randomized to receive placebo (n = 12) or AZD1305 (n = 38) in 4 ascending dose groups. Electrophysiological and hemodynamic measurements were performed before and commencing 20 minutes after start of infusion. Left atrial effective refractory period increased dose and the primary outcome measure increased dose and plasma concentration dependently, with a mean increase of 55 milliseconds in dose group 3. There was a corresponding increase in right atrial effective refractory period of 84 milliseconds. The right ventricular effective refractory period and the paced QT interval also increased dose and concentration dependently, by 59 and 70 milliseconds, respectively, in dose group 3. There were indications of moderate increases of atrial, atrioventricular nodal, and ventricular conduction times. No consistent changes in intracardiac pressures were observed, but there was a small transient decrease in systolic blood pressure. Adverse events were consistent with the study population and procedure, and there were no signs of proarrhythmia despite marked delay in ventricular repolarization in some individuals. AZD1305 shows electrophysiological characteristics indicative of potential antiarrhythmic efficacy in atrial fibrillation.

Use of Dynamic Computed Tomography to Evaluate Pre- and Postoperative Aortic Changes in AAA Patients Undergoing Endovascular Aneurysm Repair

To utilize dynamic computed tomographic angiography (CTA) on pre- and postoperative endovascular aneurysm repair (EVAR) patients to characterize cardiac-induced aortic motion within the aneurysm neck, an essential EVAR sealing zone. Electrocardiographically-gated CTA datasets were acquired utilizing a 64-slice Philips Brilliance CT scanner on 15 consecutive pre- and postoperative AAA patients. Axial pulsatility measurements were taken at 2 clinically relevant levels within the aneurysm neck: 2 cm above the highest renal artery and 1 cm below the lowest renal artery. Changes in aortic area and diameter were determined. Significant aortic pulsatility exists within the aneurysm neck during the cardiac cycle. Preoperative aortic area increased significantly, with a maximum increase of up to 12.5%. The presence of an endograft did not affect aortic pulsatility (p=NS). Postoperative area also changed significantly during a heart cycle, with a maximum increase of up to 14.5%. Diameter measurements demonstrated an identical pattern, with significant pre- and postoperative intracardiac pulsatility within and above the aneurysm neck (p<0.05). An increase in maximum diameter change up to 15% was evident. Patients undergoing EVAR experience aortic diameter changes within and above the aneurysm neck. The presence of an endograft does not abrogate this response to intracardiac pressure changes. Static CT imaging may not adequately identify patients with large aortic pulsatility, potentially resulting in endograft undersizing, stent-graft migration, intermittent type I endoleaks, and poor patient outcomes. The current standard regime of 10% to 15% oversizing based on static CT may be inadequate for some patients.

How do Changes in Daily Weight Compare to Changes in Intracardiac Pressures Using an Implantable Hemodynamic Monitor?

How do Changes in Daily Weight Compare to Changes in Intracardiac Pressures Using an Implantable Hemodynamic Monitor?

Atrial natriuretic factor and catecholamine levels during exercise in patients with and without coronary artery disease

To investigate the effects of exercise-induced ischemia on the release of atrial natriuretic factor (ANF), we measured peripheral plasma ANF, epinephrine and norepinephrine in 18 male patients with and without coronary artery disease. The patients underwent tomographic thallium treadmill stress tests. After exercise, patients with coronary artery disease showed higher increments of plasma ANF than patients without coronary disease, but the increase of ANF was not related to exercise-induced ischemia, nor to changes in catecholamines, heart rate, or blood pressure. This suggests that ANF release is not associated with myocardial ischemia per se, but to other factors which are more pronounced in the presence of coronary disease, such as changes in intracardiac pressures associated with exercise. Further studies are needed to clarify the role of myocardial ischemia on ANF release.

Assessment of vasodilator therapy in patients with severe congestive heart failure: Limitations of measurements of left ventricular ejection fraction and volumes

Although noninvasive techniques are often used to assess the effect of vasodilator therapy in patients with congestive heart failure, it is unknown whether changes in noninvasively determined left ventricular ejection fraction, volume, or dimension reliably reflect alterations in intracardiac pressure and flow. Accordingly, we compared the acute effect of sodium nitroprusside on left ventricular volume and ejection fraction (determined scintigraphically) with its effect on intracardiac pressure and forward cardiac index (determined by thermodilution) in 12 patients with severe, chronic congestive heart failure and a markedly dilated left ventricle. Nitroprusside (infused at 1.3 ± 1.1 [mean ± standard deviation] μg/kg/min) caused a decrease in mean systemic arterial, mean pulmonary arterial and mean pulmonary capillary wedge pressure as well as a concomitant increase in forward cardiac index. Simultaneously, left ventricular end-diastolic and end-systolic volume indexes decreased, but the scintigraphically determined cardiac index did not change significantly. Left ventricular ejection fraction averaged 0.19 ± 0.05 before nitroprusside administration and increased by less than 0.05 units in response to nitroprusside in 11 of 12 patients. The only significant correlation between scintigraphically and invasively determined variables was that between the percent change in end-diastolic volume index and the percent change in pulmonary capillary wedge pressure (r = 0.68, p = 0.01). Although nitroprusside produced changes in scintigraphically determined left ventricular ejection fraction end-systolic volume index and cardiac index, these alterations bore no predictable relation to changes in intracardiac pressure, forward cardiac index, or vascular resistance. Furthermore, nitroprusside produced a considerably greater percent change in the invasively measured variables than in the scintigraphically determined ones.

INTRACARDIAC PRESSURE CHANGES WITH OVERTRANSFUSION OF NORMAL DOGS.

INTRACARDIAC PRESSURE CHANGES WITH OVERTRANSFUSION OF NORMAL DOGS.

88. Changes in intracardiac pressures produced by selective cineangiography

88. Changes in intracardiac pressures produced by selective cineangiography

Hemodynamic effects of amyl nitrite and phenylephrine on the normal human circulation and their relation to changes in cardiac murmurs

The effects of amyl nitrite and phenylephrine on the intracardiac pressures and cardiac output have been studied in a group of patients having either no hemodynamic abnormality or trivial pulmonary stenosis. Amyl nitrite has been clearly demonstrated to decrease systemic pressures while pressures in the right side of the heart show no significant change, except in the presence of mild pulmonary stenosis. Cardiac output is increased and there is indirect evidence of an increased venous return to the heart. Phenylephrine causes a marked rise in systemic pressure and a lesser rise in pressures of the right side of the heart, while cardiac output is always decreased. The softening of left-sided regurgitant murmurs after amyl nitrite and their intensification following phenylephrine are explained on the basis of the changes in intracardiac pressures. Similarly, the intensification of ejection murmurs after amyl nitrite and the variable changes after administration of phenylephrine are discussed in relation to changes in cardiac output.

Intracardiac pressure changes with rapid fluid injection into the right heart.

Intracardiac pressure changes with rapid fluid injection into the right heart.

Intracardiac Pressure Changes with Rapid Fluid Injection into the Right Heart

Intracardiac Pressure Changes with Rapid Fluid Injection into the Right Heart