Right and left ventricular pressure-volume response to respiratory maneuvers

With respiration, right ventricular end-diastolic volume fluctuates. We examined the importance of these right ventricular volume changes on left ventricular function. In six mongrel dogs, right and left ventricular volumes and pressures and esophageal pressure were simultaneously measured during normal respiration, Valsalva maneuver, and Mueller maneuver. The right and left ventricular volumes were calculated from cineradiographic positions of endocardial radiopaque markers. Increases in right ventricular volume were associated with changes in the left ventricular (LV) pressure-volume relationship. With normal respiration, right ventricular end-diastolic volume increased 2.3 +/- 0.7 ml during inspiration, LV transmural diastolic pressure was unchanged, and LV diastolic volume decreased slightly. This effect was accentuated by the Mueller maneuver; right ventricular end-diastolic volume increased 10.4 +/- 2.3 ml (P less than 0.05), while left ventricular end-diastolic pressure increased 3.6 mmHg (P less than 0.05) without a significant change in left ventricular end-diastolic volume. Conversely, with a Valsalva maneuver, right ventricular volume decreased 6.5 +/- 1.2 ml (P less than 0.05), and left ventricular end-diastolic pressure decreased 2.2 +/- 0.5 mmHg (P less than 0.05) despite an unchanged left ventricular end-diastolic volume. These changes in the left ventricular pressure-volume relationship, secondary to changes in right ventricular volumes, are probably due to ventricular interdependence. Ventricular interdependence may also be an additional factor for the decrease in left ventricular stroke volume during inspiration.     

Impaired left ventricular filling due to right-to-left ventricular interaction in patients with pulmonary arterial hypertension

The aim of this study was to investigate the contribution of direct right-to-left ventricular interaction to left ventricular filling and stroke volume in 46 patients with pulmonary arterial hypertension (PAH) and 18 control subjects. Stroke volume, right and left ventricular volumes, left ventricular filling rate, and interventricular septum curvature were measured by magnetic resonance imaging and left atrial filling by transesophageal echocardiography. Stroke volume, left ventricular end-diastolic volume, and left ventricular peak filling rate were decreased in PAH patients compared with control subjects: 28 +/- 13 vs. 41 +/- 10 ml/m(2) (P < 0.001), 46 +/- 14 vs. 61 +/- 14 ml/m(2) (P < 0.001), and 216 +/- 90 vs. 541 +/- 248 ml/s (P < 0.001), respectively. Among PAH patients, stroke volume did not correlate to right ventricular end-diastolic volume or mean pulmonary arterial pressure but did correlate to left ventricular end-diastolic volume (r = 0.62, P < 0.001). Leftward interventricular septum curvature was correlated to left ventricular filling rate (r = 0.64, P < 0.001) and left ventricular end-diastolic volume (r = 0.65, P < 0.001). In contrast, left atrial filling was normal and not correlated to left ventricular end-diastolic volume. In PAH patients, ventricular interaction mediated by the interventricular septum impairs left ventricular filling, contributing to decreased stroke volume.     

Effects of enhanced ventricular filling on cardiac pump performance in exercising dogs

The extent to which the normal increase in stroke volume during exercise can be augmented by increasing preload by dextran infusion was studied in seven dogs. Each dog ran 3 min on a level treadmill at mild (3-4 mph), moderate (6-8 mph), and severe (9-13 mph) loads during the control study and immediately after 10% dextran 14 ml/kg iv. During severe exercise dextran-augmented stroke volume (+5.4 ml or 19% vs. exercise without dextran, P less than 0.01) and left ventricular end-diastolic diameter and pressure did not change heart rate, aortic pressure, or maximum derivative of left ventricular pressure but decreased systemic vascular resistance by 16%. Similar increases in stroke volume and preload after dextran occurred during mild and moderate exercise when arterial pressure and heart rate were unchanged or increased and systemic vascular resistance was decreased. Thus altering preload above those levels normally encountered during exercise is a potential mechanism to increase stroke volume and cardiac output.     

An anatomic basis for fetal right ventricular dominance and arterial pressure sensitivity

Fetal right ventricular dominance of flow and arterial pressure sensitivity were recently recognized but controversial findings. We investigated ventricular volumes, weights and dimensions in order to understand if there were anatomic differences between the ventricles which might explain these differential functional findings in the fetal sheep. Forty-four near term lambs and their hearts were weighed. Right and left ventricular free wall weights were not different. Volumes were measured by generating in vitro pressure-volume relations and by casting the two ventricles after fixation at equal, physiologic pressures. Right ventricular volume was greater than left ventricular volume by both techniques. Ventricular interaction and a restraining effect of the pericardium were present. Measurements of the fixed ventricles and their casts revealed the following: left ventricular wall thickness was slightly greater than right ventricular wall thickness; lateral ventricular diameters were not different but anteroposterior ventricular diameters were much greater in the right than left ventricle. Because of these findings, the right ventricular circumferential radii of curvature were greater than for the left ventricle as was the radius to wall thickness ratio. Greater right ventricular volume and radius to wall thickness ratio may be important factors in right ventricular flow dominance and greater sensitivity to arterial pressure.     

THEORETICAL DESIGN CONSIDERATIONS AND PHYSIOLOGIC PERFORMANCE CRITERIA FOR AN IMPROVED INTRACORPOREAL (ABDOMINAL) ELECTRICALLY ACTUATED LONG-TERM LEFT VENTRICULAR ASSIST DEVICE ("E-TYPE" ALVAD) OR PARTIAL ARTIFICIAL HEART

Our laboratories are engaged in the design of a clinically-oriented electrically actuated long-term intracorporeal (abdominal) left ventricular assist device ("E-type" ALVAD) or partial artificial heart. This infradiaphragmatic blood pump is designed to be powered by implantable electrical to mechanical energy converter systems. THE FOLLOWING ANALYSES WERE UNDERTAKEN TO: [List: see text] The proposed "E-type" ALVAD should be capable of pumping 4-7 liters per minute at heart rates of 75-100 beats per minute during rest, and 10 liters per minute at rates of 120 beats per minute during moderate exercise. These performance levels should be exceeded with a maximum device stroke volume of 85-90 ml and a mean pump inflow (filling) impedance of 相似文献   

Modeling the relation between cardiac pump function and myofiber mechanics

Complexity of the geometry and structure of the heart hampers easy modeling of cardiac mechanics. The modeling can however be simplified considerably when using the hypothesis that in the normal heart myofiber structure and geometry adapt, until load is evenly distributed. A simple and realistic relationship is found between the hemodynamic variables cavity pressure and volume, and myofiber load parameters stress and strain. The most important geometric parameter in the latter relation is the ratio of cavity volume to wall volume, while actual geometry appears practically irrelevant. Applying the found relationship, a realistic maximum is set to left ventricular pressure after chronic pressure load. Pressures exceeding this level are likely to cause decompensation and heart failure. Furthermore, model is presented to simulate left and right ventricular pump function with left-right interaction.     

Determinants of cardiac augmentation by elevations in intrathoracic pressure

We studied the cardiovascular effects of phasic increases in intrathoracic pressure (ITP) by high-frequency jet ventilation in an acute pentobarbital-anesthetized intact canine model both before and after the induction of acute ventricular failure by large doses of propranolol. Chest and abdominal pneumatic binders were used to further increase ITP. Respiratory frequency, percent inspiratory time, mean ITP, and swings in ITP throughout the respiratory cycle were independently varied at a constant-circulating blood volume. We found that pertubations in mean ITP induced by ventilator adjustments accounted for all observable steady-state hemodynamic changes independent of respiratory frequency, inspiratory time, or phasic respiratory swings in ITP. Changes in ITP were associated with reciprocal changes in both intrathoracic vascular pressures (P less than 0.01) and blood volume (P less than 0.01). When cardiac function was normal, left ventricular (LV) stroke volume decreased, whereas in acute ventricular failure, LV stroke volume increased in response to increasing ITP when apneic LV filling pressure was high (greater than or equal to 17 Torr) and did not change if apneic LV filling pressure was low (less than or equal to 12 Torr). However, in all animals in acute ventricular failure, LV stroke work increased with increasing ITP. Our study demonstrates that the improved cardiac function seen with increasing ITP in acute ventricular failure is dependent upon adequate LV filling and decreased LV afterload in a manner analogous to that seen with arterial vasodilator therapy in heart failure.     

Ventricular performance in diabetic rabbits with norepinephrine cardiomyopathy

The purpose of this investigation was to examine the effects of norepinephrine cardiomyopathy (NE-CM) on left ventricular (LV) performance in diabetic rabbits. Diabetes mellitus was produced in 11 rabbits by giving them alloxan monohydrate, 120 mg/kg. Cardiomyopathy was produced in five animals by a 90-min infusion of norepinephrine (2 micrograms/min/kg). Left ventricular contractility and pump function (VF) were examined 2 days later. The effects of hypercapnia and inotropic responsiveness to NE were also determined. VF was assessed by means of left ventricular function curves obtained with constant mean aortic pressure and heart rate and quantified by determining stroke volume (SV) at a left ventricular pressure of 10 cm H2O (SV10). Mean SV10 was 1.22 +/- 0.08 ml in control diabetics but averaged only 0.95 +/- 0.08 ml in diabetics with NE-CM (P less than 0.05). NE-CM markedly reduced LV dP/dt max responses to NE infusion but the increments in SV10 did not differ. Hypercapnia caused significantly greater ventricular depression in NE-CM than in control diabetic rabbits (P less than 0.001). The depressive effect of hypercapnia can be countered in part by the administration of NE in both groups, but differential depression in VF to hypercapnia was persistent between the two groups.     

21毫米人造心脏瓣膜泵的设计及研制

为了研究能够长期置入主动脉瓣环的左心室辅助装置,研制出直径21毫米重27克可植入的主动脉瓣膜泵.装置包括一个转子和一个定子.转子由驱动磁钢和叶轮组成;定子装有带铁心的电机线圈和出口导叶.装置被置於主动脉瓣位置,所以不占用额外的解剖空间.血泵能像自然心脏一样直接将血液由心室输送到主动脉,不需要连接管道和旁路,因此对自然生理循环的干扰可以减到最低.血泵流量由最大到零周期变化.血液动力学测试表明,当血泵转速为17500转/分钟时,可以产生流量5升/分钟、压力增益50毫米汞柱的血流;同一转速下,当流量为零时,血泵能保持主动脉舒张压为80毫米汞柱.     

Cardiac resynchronization therapy modulation of exercise left ventricular function and pulmonary O₂ uptake in heart failure

To better understand the mechanisms contributing to improved exercise capacity with cardiac resynchronization therapy (CRT), we studied the effects of 6 mo of CRT on pulmonary O(2) uptake (Vo(2)) kinetics, exercise left ventricular (LV) function, and peak Vo(2) in 12 subjects (age: 56 ± 15 yr, peak Vo(2): 12.9 ± 3.2 ml·kg(-1)·min(-1), ejection fraction: 18 ± 3%) with heart failure. We hypothesized that CRT would speed Vo(2) kinetics due to an increase in stroke volume secondary to a reduction in LV end-systolic volume (ESV) and that the increase in peak Vo(2) would be related to an increase in cardiac output reserve. We found that Vo(2) kinetics were faster during the transition to moderate-intensity exercise after CRT (pre-CRT: 69 ± 21 s vs. post-CRT: 54 ± 17 s, P < 0.05). During moderate-intensity exercise, LV ESV reserve (exercise - resting) increased 9 ± 7 ml (vs. a 3 ± 9-ml decrease pre-CRT, P < 0.05), and steady-state stroke volume increased (pre-CRT: 42 ± 8 ml vs. post-CRT: 61 ± 12 ml, P < 0.05). LV end-diastolic volume did not change from rest to steady-state exercise post-CRT (P > 0.05). CRT improved heart rate, measured as a lower resting and steady-state exercise heart rate and as faster heart rate kinetics after CRT (pre-CRT: 89 ± 12 s vs. post-CRT: 69 ± 21 s, P < 0.05). For peak exercise, cardiac output reserve increased significantly post-CRT and was 22% higher at peak exercise post-CRT (both P < 0.05). The increase in cardiac output was due to both a significant increase in peak and reserve stroke volume and to a nonsignificant increase in heart rate reserve. Similar patterns in LV volumes as moderate-intensity exercise were observed at peak exercise. Cardiac output reserve was related to peak Vo(2) (r = 0.48, P < 0.05). These findings demonstrate the chronic CRT-mediated cardiac factors that contribute, in part, to the speeding in Vo(2) kinetics and increase in peak Vo(2) in clinically stable heart failure patients.     

Pericardium modulates left and right ventricular stroke volumes to compensate for sudden changes in atrial volume

The pericardium may modulate acute compensatory changes in stroke volumes seen with sudden changes in cardiac volume, but such a mechanism has never been clearly demonstrated. In eight open-chest dogs, we measured left and right ventricular pressures, diameters, stroke volumes, and pericardial pressures during rapid (approximately 300 ms) systolic infusions or withdrawals of approximately 25 ml blood into and out of the left atrium and right atrium. Control beats, the infusion/withdrawal beat, and 4-10 subsequent beats were studied. With infusions, ipsilateral ventricular end-diastolic transmural pressure, diameter, and stroke volume increased. With the pericardium closed, there was a compensatory decrease in contralateral transmural pressure, diameter, and stroke volume, mediated by opposite changes in transmural end-diastolic pressures. The sum of the ipsilateral increase and contralateral decrease in stroke volume approximated the infused volume. Corresponding changes were seen with blood withdrawals. This direct ventricular interaction was diminished when pericardial pressure was <5 mmHg and absent when the pericardium was opened. Pericardial constraint appears essential for immediate biventricular compensatory responses to acute atrial volume changes.     

Theoretical and empirical derivation of cardiovascular allometric relationships in children.

Basic fluid dynamic principles were used to derive a theoretical model of optimum cardiovascular allometry, the relationship between somatic and cardiovascular growth. The validity of the predicted models was then tested against the size of 22 cardiovascular structures measured echocardiographically in 496 normal children aged 1 day to 20 yr, including valves, pulmonary arteries, aorta and aortic branches, pulmonary veins, and left ventricular volume. Body surface area (BSA) was found to be a more important determinant of the size of each of the cardiovascular structures than age, height, or weight alone. The observed vascular and valvar dimensions were in agreement with values predicted from the theoretical models. Vascular and valve diameters related linearly to the square root of BSA, whereas valve and vascular areas related to BSA. The relationship between left ventricular volume and body size fit a complex model predicted by the nonlinear decrease of heart rate with growth. Overall, the relationship between cardiac output and body size is the fundamental driving factor in cardiovascular allometry.     

Volumetric responses of right and left ventricles during upright exercise in normal subjects

We evaluated the volumetric responses of the right and left ventricles to upright exercise using two noninvasive methods, first-pass radionuclide angiocardiography and the CO2 rebreathing technique, in nine normal subjects. Right (RV) and left (LV) ventricular ejection fractions, heart rate, and cardiac index were determined at rest and during steady-state exercise on the bicycle ergometer at 50% of maximal O2 consumption. From these data, stroke volume index (SVI), end-diastolic volume index (EDVI), and end-systolic volume index (ESVI) were derived. SVI increased from 40 +/- 7 ml/m2 at rest to 59 +/- 13 ml/m2 with exercise (P less than 0.001). RVEDVI increased significantly from 82 +/- 16 ml/m2 at rest to 95 +/- 21 ml/m2 during exercise (P = 0.008), while there was no significant change in RVESVI with exercise. Changes in LVEDVI and LVESVI during upright exercise were similar to the right ventricle. The increase in systolic blood pressure during exercise, along with no change in LVESVI, indicated enhanced ventricular contractility. The normal augmentation in SVI during submaximal exercise was due to both the Frank-Starling mechanism and an increased contractile state. Application of these or similar techniques may be useful in evaluating ventricular performance in patients with cardiorespiratory dysfunction.     

Effects of positive end-expiratory pressure on the right ventricle

Transmural cardiac pressures, stroke volume, right ventricular volume, and lung water content were measured in normal dogs and in dogs with oleic acid-induced pulmonary edema (PE) maintained on positive-pressure ventilation. Measurements were performed prior to and following application of 20 cmH2O positive end-expiratory pressure (PEEP). Colloid fluid was given during PEEP for ventricular volume expansion before and after the oleic acid administration. PEEP significantly increased pleural pressure and pulmonary vascular resistance but decreased right ventricular volume, stroke volume, and mean arterial pressure in both normal and PE dogs. Although the fluid infusion during PEEP raised right ventricular diastolic volumes to the pre-PEEP level, the stroke volumes did not significantly increase in either normal dogs or the PE dogs. The fluid infusion, however, significantly increased the lung water content in the PE dogs. Following discontinuation of PEEP, mean arterial pressure, cardiac output, and stroke volume significantly increased, and heart rate did not change. The failure of the stroke volume to increase despite significant right ventricular volume augmentation during PEEP indicates that positive-pressure ventilation with 20 cmH2O PEEP decreases right ventricular function.     

RV filling modulates LV function by direct ventricular interaction during mechanical ventilation

During mechanical ventilation, phasic changes in systemic venous return modulate right ventricular output but may also affect left ventricular function by direct ventricular interaction. In 13 anesthetized, closed-chest, normal dogs, we measured inferior vena cava flow and left and right ventricular dimensions and output during mechanical ventilation, during an inspiratory hold, and (during apnea) vena caval constriction and abdominal compression. During a single ventilation cycle preceded by apnea, positive pressure inspiration decreased caval flow and right ventricular dimension; the transseptal pressure gradient increased, the septum shifted rightward, reflecting an increased left ventricular volume (the anteroposterior diameter did not change); and stroke volume increased. The opposite occurred during expiration. Similarly, the maneuvers that decreased venous return shifted the septum rightward, and left ventricular volume and stroke volume increased. Increased venous return had opposite effects. Changes in left ventricular function caused by changes in venous return alone were similar to those during mechanical ventilation except for minor quantitative differences. We conclude that phasic changes in systemic venous return during mechanical ventilation modulate left ventricular function by direct ventricular interaction.     

Implications of QRS duration in dogs with pacing-induced heart failure

The objective of this study was to find out the implication of QRS duration in dogs with rapid pacing-induced heart failure. Sixteen Beagle dogs were implanted with transvenous cardiac pacemakers and underwent rapid right ventricular pacing for 3 weeks at 260 bpm to induce heart failure. Dogs were divided into two groups according to the QRS duration: 9 with normal QRS duration (<100 ms) and 7 with prolonged QRS duration (≥100 ms). Cardiac systolic function and size was analyzed by real time 3-dimensional echocardiography and left ventricular dyssynchrony was assessed by speckle tracking strain imaging. Congestive heart failure developed 3 weeks after rapid right ventricular pacing. Dogs with prolonged QRS duration showed more extensive radial strain and circumferential strain dyssynchrony than dogs with normal QRS duration. At the end of 4-week recovery, greater improvement of left ventricular ejection fraction and left ventricular end-systolic volume was detected in dogs with normal QRS duration. The findings suggested that left ventricular dyssynchrony, indicated by a prolonged QRS duration, predicted an unsatisfying recovery in dogs with rapid pacing-induced heart failure. QRS duration had the potential to be a prognostic indicator for dogs with heart failure.     

Progression of heart failure after myocardial infarction in the rat

This study examined the early neurohumoral events in the progression of congestive heart failure (CHF) after myocardial infarction (MI) in rats. Immediately after MI was induced by coronary artery ligation, rats had severely depressed left ventricular systolic function and increased left ventricular end-diastolic volume (LVEDV). Both left ventricular function and the neurohumoral indicators of CHF underwent dynamic changes over the next 6 wk. LVEDV increased continuously over the study interval, whereas left ventricular stroke volume increased but reached a plateau at 4 wk. Plasma renin activity (PRA), arginine vasopressin, and atrial natriuretic factor all increased, but with differing time courses. PRA declined to a lower steady-state level by 4 wk. Six to 8 wk after MI, CHF rats had enhanced renal sympathetic nerve activity and blunted baroreflex regulation. These findings demonstrate that the early course of heart failure is characterized not by a simple "switching on" of neurohumoral drive, but rather by dynamic fluctuations in neurohumoral regulation that are linked to the process of left ventricular remodeling.     

Volume expansion potentiates cardiac sympathetic afferent reflex in dogs

Our previous study (27) showed that the cardiac sympathetic afferent reflex (CSAR) was enhanced in dogs with congestive heart failure. The aim of this study was to test whether blood volume expansion, which is one characteristic of congestive heart failure, potentiates the CSAR in normal dogs. Ten dogs were studied with sino-aortic denervation and bilateral cervical vagotomy. Arterial pressure, left ventricular pressure, left ventricular epicardial diameter, heart rate, and renal sympathetic nerve activity were measured. Coronary blood flow was also measured and, depending on the experimental procedure, controlled. Blood volume expansion was carried out by infusion of isosmotic dextran into a femoral vein at 40 ml/kg at a rate of 50 ml/min. CSAR was elicited by application of bradykinin (5 and 50 microg) and capsaicin (10 and 100 microg) to the epicardial surface of the left ventricle. Volume expansion increased arterial pressure, left ventricular pressure, left ventricular diameter, and coronary blood flow. Volume expansion without controlled coronary blood flow only enhanced the RSNA response to the high dose (50 microg) of epicardial bradykinin (17. 3 +/- 1.9 vs. 10.6 +/- 4.8%, P < 0.05). However, volume expansion significantly enhanced the RSNA responses to all doses of bradykinin and capsaicin when coronary blood flow was held at the prevolume expansion level. The RSNA responses to bradykinin (16. 9 +/- 4.1 vs. 5.0 +/- 1.3% for 5 microg, P < 0.05, and 28.9 +/- 3.7 vs. 10.6 +/- 4.8% for 50 microg, P < 0.05) and capsaicin (29.8 +/- 6.0 vs. 9.3 +/- 3.1% for 10 microg, P < 0.05, and 34.2 +/- 2.7 vs. 15.1 +/- 2.7% for 100 microg, P < 0.05) were significantly augmented. These results indicate that acute volume expansion potentiated the CSAR. These data suggest that enhancement of the CSAR in congestive heart failure may be mediated by the concomitant cardiac dilation, which accompanies this disease state.     

Haemodynamic effects of respiratory alkalosis independent of changes in airway pressure in anaesthetized newborn dogs

We have recently reported a decrease in cardiac output in newborn dogs during respiratory alkalosis which is independent of changes in airway pressure. The present study was designed to characterize the mechanism responsible for this reduction in cardiac output. Twelve newborn coonhounds were anaesthetized with pentobarbital, paralyzed with pancuronium and hyperventilated to an arterial carbon dioxide tension (PaCO2) of 20 torr. Subsequent changes in PaCO2 were achieved by altering the FiCO2. Measurements were made after 30 min at either 40 or 20 torr PaCO2. The sequence of PaCO2 levels was randomized. Compared to normocarbia, respiratory alkalosis resulted in significantly decreased cardiac output (279 +/- 16 to 222 +/- 10 ml/min per kg, mean +/- SEM, P less than 0.001), stroke volume (1.60 +/- 0.10 to 1.24 +/- 0.06 ml/kg; P less than 0.001), maximum left ventricular dP/dt (1629 +/- 108 to 1406 +/- 79 mmHg/s, P less than 0.01) and left ventricular end diastolic pressure (3.9 +/- 0.4 to 2.9 +/- 0.3 mmHg; P less than 0.001). The decrease in cardiac output during respiratory alkalosis is manifest through a decrease in stroke volume, which is due, at least in part, to the decrease in left ventricular end diastolic pressure. The decrease in maximum left ventricular dP/dt is likely a reflection of the decrease in preload, however, a change in myocardial contractility cannot be excluded. We speculate the decrease in filling pressure may be due to an increase in venous capacitance.     

Atrial natriuretic peptide and vasopressin in human plasma

Using a specific radioimmunoassay for atrial natriuretic peptide (ANP), plasma immunoreactive ANP was measured in 17 normal subjects and 83 patients with various diseases. Plasma ANP concentration in normal subjects was 14.1 +/- 1.7 pg/ml (mean +/- S.E.). Relatively high plasma ANP concentrations were detected in patients with diabetes mellitus, hyperthyroidism, atrial fibrillation and liver cirrhosis. Plasma ANP concentrations in the patients correlated positively with mean arterial blood pressure and plasma AVP concentrations. Plasma ANP concentrations in the patients also had positive correlations with left atrial dimension and left ventricular diastolic dimension determined by echocardiography. Another positive correlation was observed in the patients between plasma AVP concentrations and mean arterial blood pressure. These results suggest that ANP is a volume regulatory hormone but also that ANP may be involved in the blood pressure regulating system.