Overinflation of pneumatic antishock garments in the elderly

The hemodynamic effects of pneumatic antishock garment application in high-risk elderly patients were examined in 10 preoperative patients (mean age 66.5 +/- 6.4 years) with the pneumatic antishock garments uninflated, after 15 minutes of inflation to 50 mm Hg, and after 15 minutes of inflation to 75 mm Hg. After inflation, significant increases in right atrial pressure (89 percent), pulmonary capillary wedge pressure (34 percent), and mean pulmonary artery pressure (21 percent) were noted. Mean peripheral arterial pressure increased 11.2 percent. Depression of the cardiac index (18 percent), left ventricular stroke work (20 percent), and right ventricular stroke work (16.4 percent) with associated increases in total peripheral resistance (26 percent) and pulmonary vascular resistance (18 percent) occurred in 5 of 10 patients. Left ventricular function curves revealed a progressive decrease in ventricular function at 50 mm Hg and 75 mm Hg. We have concluded that the effect of the pneumatic antishock garment on myocardial function is variable and unpredictably dangerous in the elderly patient with diminished myocardial reserve. As no significant benefit was derived from inflation pressures greater than 50 mm Hg in these patients, the lowest combination of pressures producing the most efficacious results should be used.     

Elevated coronary sinus pressure does not alter myocardial blood flow or left ventricular contractile function in mature sheep. Implications after the Fontan operation

The hypothesis that elevation of coronary sinus pressure affects coronary blood flow and ventricular function was tested in this study of seven adult ewes placed under pentobarbital anesthesia. Coronary sinus pressure was elevated by partial balloon occlusion. Right atrial, left atrial, and aortic mean pressures and rate of rise of left ventricular pressure were measured. Coronary blood flow was determined with radioactive microspheres. Studies were performed at control and at moderate (15 to 20 mm Hg) and marked (30 to 35 mm Hg) elevation of coronary sinus mean pressures. Despite increase of coronary sinus pressure from a control value of 2 mm Hg +/- 1 to levels of 19 mm Hg +/- 1 and 34 mm Hg +/- 1, no significant changes were observed in right atrial, left atrial, or aortic mean pressure or rate of rise of left ventricular pressure. Both endocardial and epicardial blood flows were unaffected. The endocardial/epicardial flow ratio at moderate coronary sinus pressure elevation was significantly increased, which suggested local subendocardial vasodilation in the absence of changes in transmural perfusion. The findings suggest that isolated increase in coronary sinus pressure is not a major determinant of myocardial blood flow or ventricular performance in the normal ewe.     

Reversibility of pulmonary artery hypertension in aortic stenosis after aortic valve replacement

Fifty-two surgical patients with isolated aortic valve stenosis were studied preoperatively and postoperatively to determine the incidence of pulmonary hypertension and its response to surgical intervention. Pulmonary artery systolic hypertension was classified as absent (group 1, less than 30 mm Hg), mild (group 2, 30 to 39 mm Hg), moderate (group 3, 40 to 59 mm Hg), and severe (group 4, greater than 60 mm Hg). Thirty-seven of our patients (71%) had preoperative pulmonary hypertension. There was a positive correlation between left ventricular end-diastolic pressure and both systolic and diastolic pulmonary artery pressures preoperatively (p less than 0.001). After operation we found a decrease in mean systolic pulmonary pressure in group 4, from 85.8 +/- 23 mm Hg to 41.2 +/- 10.4 mm Hg (a 52% decrease, p less than 0.001), and in group 3, from 48.9 +/- 5.9 mm Hg to 32.1 +/- 7.1 mm Hg (a 34% decrease, p less than 0.001). A significant decrease in the mean diastolic pressure was found only in group 4, in which the pressure decreased from 33.7 +/- 8.7 mm Hg to 26.0 +/- 7.6 mm Hg (p less than 0.05). The operative mortality was 1.9%. Our data indicate that pulmonary artery hypertension in aortic stenosis is common, is related to end-diastolic pressure, and can be expected to improve in the early postoperative period.     

Left ventricular pressure and volume unloading during pulsatile versus nonpulsatile left ventricular assist device support

BACKGROUND: Nonpulsatile axial or centrifugal pumps are the latest generation of left ventricular assist devices (LVAD). Whether left ventricular (LV) unloading and outcome in these devices is similar to pulsatile LVADs during long-term support has not been investigated. We compared LV unloading and mortality between different types of LVAD support (pulsatile versus nonpulsatile). METHODS: In 31 patients undergoing long-term LVAD implantation (nonpulsatile = 10, pulsatile = 21) preoperative and postoperative echocardiographic and hemodynamic assessment with right heart catheterization had been obtained. RESULTS: All patients had similar echocardiographic, hemodynamic, and clinical heart failure characteristics at baseline. The degree of LV pressure unloading was the same in both device types, caused by similar reduction of mean pulmonary pressure (18.6 +/- 5.1 versus 18.3 +/- 7.5 mm Hg) and pulmonary capillary wedge pressure (8.9 +/- 4.4 versus 8.0 +/- 7.0 mm Hg). Left ventricular volume unloading was pronounced with a pulsatile device owing to a statistically significant higher pump output (5.1 +/- 1.0 L/min) in comparison with nonpulsatile LVADs (3.6 +/- 0.9 L/min, p < 0.001). Echocardiographic-determined end-systolic indicators confirm this augmentation in pulsatile LVADs. Etiology or the time interval of hemodynamic reassessment had no impact in left ventricular pressure unloading, but LV volume unloading decreased between day 60 and 120 in patients with nonpulsatile LVADs. The preoperative and postoperative transplant mortality was comparable in both groups. CONCLUSIONS: Left ventricular pressure unloading is similar in patients with nonpulsatile as compared with pulsatile implantable long-term assist devices. Left ventricular volume unloading is pronounced in pulsatile LVADs.     

Effects of dynamic cardiomyoplasty on indices of left ventricular systolic and diastolic function in a canine model of chronic heart failure.

The effects of cardiomyoplasty were evaluated with multiple-gated equilibrium radionuclide angiocardiography and catheterization in a canine model of chronic heart failure. Doxorubicin was administered to 12 dogs at a dose of 1 mg/kg/wk intravenously for 10 weeks. Left ventricular ejection fraction was reduced from a mean of 53.6% +/- 3.4% to 33.5% +/- 2.3% preoperatively. Two dogs died of presumed arrhythmia during this period. Cardiomyoplasty with the left latissimus dorsi muscle was performed on 10 dogs. The muscle was wrapped around both the left and right ventricles. Five dogs died of infection or arrhythmia after the operation. Postoperatively the muscle remained unstimulated for 2 weeks to allow adhesion to the heart. After this period, the latissimus dorsi muscle was conditioned by a progressive stimulation protocol. After the muscle was conditioned, multiple-gated equilibrium radionuclide angiocardiography studies showed that left ventricular global ejection fraction was 18.4% +/- 7.2% at 0 volts (nonstimulation), 26.2% +/- 3.7% at 5-volt stimulation (p less than 0.05), and 31.0% +/- 5.4% at 10-volt stimulation (p less than 0.05). Regional ejection fractions in low lateral, apical, and low septal regions at 5 volts and 10 volts were higher than those at 0 volts (p less than 0.05). Regional wall motion (percent radial shortening) of the low lateral region was higher than that during nonstimulation (p less than 0.05). Peak emptying rate was 2.07 +/- 0.95 end-diastolic counts per second at 0-volt, 3.10 +/- 0.67 at 5-volt, and 3.34 +/- 0.89 at 10-volt stimulation (p less than 0.05). Peak filling rate was 1.81 +/- 0.52 end-diastolic counts per second at 0-volt, 2.67 +/- 1.18 at 5-volt, and 3.11 +/- 0.65 at 10-volt stimulation (p less than 0.05). Cardiac catheterization data showed a nonsignificant increase in left ventricular rate of pressure rise with increasing voltage (1302 +/- 355 mm Hg/sec at 0 volts, 1450 +/- 413 mm Hg/sec at 5 volts, and 1568 +/- 455 mm Hg/sec at 10 volts). Left ventricular systolic pressures were unchanged. End-diastolic pressures decreased (11.2 +/- 1.48 mm Hg at 0 volts, 10.4 +/- 2.30 mm Hg at 5 volts, and 9.6 +/- 1.52 at 10 volts; p less than 0.05). These data show that cardiomyoplasty can improve indices of systolic and diastolic function in a canine model of chronic heart failure.     

Regression of hypertrophy after Carpentier-Edwards pericardial aortic valve replacement

BACKGROUND: The purpose of this study was to determine whether significant regression of left ventricular hypertrophy is seen after implantation of small sizes (19 to 23 mm) of the Carpentier-Edwards (CE) pericardial valve, a stented pericardial valve. METHODS: Echocardiograms and electrocardiograms (ECGs) were performed at least 1 year after surgery (mean 18 months) in patients with 19-, 21-, and 23-mm CE pericardial aortic valves and compared with preoperative echocardiograms and ECGs. RESULTS: A total of 41 patients, mean age 79 +/- 9 years (range 46 to 93 years), were studied, including 7 19-mm, 22 21-mm, and 12 23-mm patients. The mean postoperative gradient was 22 +/- 7 mm Hg for 19-mm valves, 18 +/- 5 mm Hg for 21-mm valves, and 16 +/- 4 mm Hg for 23-mm valves. The postoperative valve areas were 1.1 +/- 0.3 cm2 for the 19-mm, 1.3 +/- 0.3 cm2 for the 21-mm, and 1.5 +/- 0.4 cm2 for the 23-mm valves. Left ventricular end diastolic diameter, end systolic diameter, septal thickness, and posterior wall thickness all decreased significantly (p <0.05) postoperatively. The proportion of patients with significant left ventricular hypertrophy on ECG decreased from 63% to 47% (p = 0.001). Left ventricular mass decreased significantly by echocardiography from 265 g preoperatively to 208 g postoperatively (p = 0.004). Left ventricular mass decreased for each valve size, and the greatest absolute reduction in mass occurred in the 19-mm valve recipients. CONCLUSIONS: Implantation of the 19-, 21-, and 23-mm CE pericardial valves results in significant reductions in left ventricular mass. These findings suggest that stented pericardial valves can be used in the small aortic root without the need for aortic root enlargement procedures.     

Therapeutic use of right atrial pressures early after the Fontan operation

In 334 patients undergoing the Fontan operation, the right atrial pressure was 16 +/- 36 mm Hg (mean value +/- SD) 3 h postoperatively, and was on average higher in those who died or had a takedown of the operation than in those who did not (P = 0.0001). Twenty-four hours after operation, the right atrial pressure was 18 +/- 5.5 mm Hg, was higher in those who died or had a takedown than in those who did not (P less than 0.0001); and in those who died or had takedown it was 23.5 +/- 1.66 mm Hg and higher than at 3 h postoperatively (18.7 +/- 0.52). The left atrial pressure 3 h postoperatively was 9 +/- 3.6 mm Hg, and on average was higher in the patients who died or had a Fontan takedown than in those who did not. The continuous relation between right atrial pressure and the probability of death or takedown during the first 24 postoperative hours was such as to recommend consideration of takedown whenever the right atrial pressure reaches 22 mm Hg, and when higher, the recommendation is made with greater urgency.     

Inhaled epoprostenol (prostacyclin) and pulmonary hypertension before cardiac surgery

OBJECTIVE: Pulmonary hypertension is commonly found in patients undergoing valvular surgery and can be worsened by cardiopulmonary bypass. Inhaled epoprostenol (prostacyclin) has been used for the treatment of pulmonary hypertension, but its effects compared with those of placebo on hemodynamics, oxygenation, echocardiographic examination, and platelet function have not been studied during cardiac surgery. METHODS: Twenty patients with pulmonary hypertension undergoing cardiac surgery were randomized in a double-blind study to receive inhaled epoprostenol (60 microg) or placebo. The inhalation occurred after induction of anesthesia and before surgical incision. The effects on left and right systolic and diastolic cardiac functions evaluated by means of pulmonary artery catheterization and transesophageal echocardiography, as well as oxygenation and platelet aggregation, were studied. RESULTS: Inhalation of epoprostenol significantly reduced indexed right ventricular stroke work from 10.7 +/- 4.57 g. m. m(-2) to 7.8 +/- 3.94 g. m. m(-2) (P =.003) and systolic pulmonary artery pressure from 48.4 +/- 18 mm Hg to 38.9 +/- 11.9 mm Hg (P =.002). The effect was correlated with the severity of pulmonary hypertension (r = 0.76, P =.01) and was no longer apparent after 25 minutes. There was no significant effect on systemic arterial pressures, left ventricular function, arterial oxygenation, platelet aggregation, and surgical blood loss. CONCLUSION: Inhaled epoprostenol reduces pulmonary pressure and improves right ventricular stroke work in patients with pulmonary hypertension undergoing cardiac surgery. A dose of 60 microg is hemodynamically safe, and its effect is completely reversed after 25 minutes. We did not observe any evidence of platelet dysfunction or an increase in surgical bleeding after administration of inhaled epoprostenol.     

The effects of positive end-expiratory pressure during active compression decompression cardiopulmonary resuscitation with the inspiratory threshold valve

The use of an inspiratory impedance threshold valve (ITV) during active compression-decompression (ACD) cardiopulmonary resuscitation (CPR) improves perfusion pressures, and vital organ blood flow. We evaluated the effects of positive end-expiratory pressure (PEEP) on gas exchange, and coronary perfusion pressure gradients during ACD + ITV CPR in a porcine cardiac arrest model. All animals received pure oxygen intermittent positive pressure ventilation (IPPV) at a 5:1 compression-ventilation ratio during ACD + ITV CPR. After 8 min, pigs were randomized to further IPPV alone (n = 8), or IPPV with increasing levels of PEEP (n = 8) of 2.5, 5.0, 7.5, and 10 cm H(2)O for 4 consecutive min each, respectively. Mean +/- SEM arterial oxygen partial pressure decreased in the IPPV group from 150 +/- 30 at baseline after 8 min of CPR to 110 +/- 25 torr at 24 min, but increased in the PEEP group from 115 +/- 15 to 170 +/- 25 torr with increasing levels of PEEP (P <0.02 for comparisons within groups). Mean +/- SEM diastolic aortic minus diastolic left ventricular pressure gradient was significantly (P < 0.001) higher after the administration of PEEP (24 +/- 0 vs 17 +/- 1 mm Hg with 5 cm H(2)O of PEEP, and 26 +/- 0 vs 17 +/- 1 mm Hg with 10 cm H(2)O of PEEP), whereas the diastolic aortic minus right atrial pressure gradient (coronary perfusion pressure) was comparable between groups. Furthermore, systolic aortic pressures were significantly (P < 0.05) higher with 10 cm H(2)O of PEEP when compared with IPPV alone (68 +/- 0 vs 59 +/- 2 mm Hg). In conclusion, when CPR was performed with devices designed to improve venous return to the chest, increasing PEEP levels improved oxygenation. Moreover, PEEP significantly increased the diastolic aortic minus left ventricular gradient and did not affect the decompression phase aortic minus right atrial pressure gradient. These data suggest that PEEP reduces alveolar collapse during ACD + ITV CPR, thus leading to an increase in indirect myocardial compression. IMPLICATIONS: Inspiratory impedance during active compression-decompression cardiopulmonary resuscitation improves perfusion pressures, and vital organ blood flow during cardiac arrest. Increasing levels of positive end-expiratory pressure during performance of active compression-decompression cardiopulmonary resuscitation with an inspiratory impedance valve improves oxygenation, and increases the diastolic aortic-left ventricular pressure gradient and systolic arterial blood pressure.     

The results of operation in patients with hypertrophic cardiomyopathy and pulmonary hypertension

The clinical course and hemodynamic results in patients undergoing operation for obstructive hypertrophic cardiomyopathy with preoperative pulmonary arterial hypertension were unknown. The hypothesis tested in this retrospective study was that operative relief of left ventricular outflow tract obstruction resulted in a substantial reduction in pulmonary artery pressures and mitral regurgitation without necessitating mitral valve replacement. Patients were included if their preoperative pulmonary systolic pressure was greater than 35 mm Hg and if they were without concomitant cardiac disease, with the exception of mitral regurgitation. Since 1962, 49 patients who fit our criteria underwent left ventricular myotomy and myectomy with 98% follow-up. Mean follow-up was 7.9 +/- 0.7 (mean +/- standard error of the mean) years with a range of 0.8 to 18.4 years. Early hospital mortality rate was 12% (n = 6); two deaths from low cardiac output and four from arrhythmia. There were 43 (88%) hospital survivors and 18 late deaths. Actuarial survival rate after operation was 87% +/- 5% (n = 31) at 5 years and 55% +/- 8% (n = 9) at 10 years. Thirty-nine of 43 survivors (91%) returned 9 +/- 1 months postoperatively for follow-up evaluation including cardiac catheterization. The majority (83%) were in New York Heart Association functional class I or II postoperatively. Cardiac catheterizations indicated a fall in pulmonary arterial systolic pressure from 62 +/- 3 (range = 36 to 105) to 38 +/- 2 (range = 21 to 65) mm Hg (p = 0.0001) with no difference in right atrial pressure or cardiac output. Pulmonary arterial wedge mean pressure decreased from 24 +/- 1 to 16 +/- 5 mm Hg (p = 0.0002) and preoperative mitral regurgitation improved or was abolished in 85% of patients studied (n = 13). Rest and maximal provocable left ventricular outflow tract gradients decreased from 81 +/- 7 and 103 +/- 5 to 14 +/- 3 and 45 +/- 8 mm Hg, respectively (p = 0.0001). Comparison of the above-mentioned patients, operated on since 1982, with a preoperatively matched group who underwent mitral valve replacement in the same interval showed no statistically significant difference in mortality, morbidity, hemodynamic outcome, or functional outcome with a mean follow-up of 2 years. We conclude that a consistent, significant reduction (mean = 40%) in preoperative pulmonary arterial systolic pressure, clinical symptoms, and mitral regurgitation occurs with relief of outflow tract obstruction by left ventricular myotomy and myectomy and that pulmonary hypertension and mitral regurgitation are not indications for mitral valve replacement in these patients.     

Acute descending aortomyoplasty induces coronary blood flow augmentation

BACKGROUND: Aortomyoplasty is a procedure aimed to improve cardiac output in patients suffering from heart failure. Stimulation of the latissimus dorsi muscle around the aorta produces hemodynamic effects similar to those of the intraaortic balloon pump. These may be maintained without the accompanying complications or the need for anticoagulation. The objective of this study was to test the acute effects of aortomyoplasty on coronary artery blood flow. METHODS: Eight mongrel dogs (18 to 30 kg) underwent acute descending aortomyoplasty. Several stimulation protocols were applied after wrapping of the latissimus dorsi muscle around the aorta in different surgical configurations. The left anterior descending coronary blood flow was measured using a transonic Doppler flow probe. Left ventricular and aortic pressures, proximal and distal to the aortomyoplasty site, were monitored continuously. RESULTS: Significant aortic diastolic pressure augmentation was expressed both as an increase in peak values, from 110 +/- 24 mm Hg to 120 +/- 24 mm Hg (p < 0.001) and as an increase in the diastolic integral, from 64 +/- 23 mm Hg x s to 84 +/- 37 mm Hg x s (p < 0.001). Concomitantly, peak left anterior descending coronary blood flow increased from 26 +/- 10 mL/min to 32 +/- 12 mL/min (p < 0.001). This was associated with an increase in the diastolic flow integral from 11 +/- 4 mL to 14 +/- 6 mL (p < 0.001). CONCLUSIONS: Descending aortomyoplasty induces significant augmentation of coronary blood flow. Optimal timing of muscle stimulation is important in achieving the best assist. This procedure may prove beneficial for end-stage ischemic patients.     

Effect of l-norepinephrine on left ventricular diastolic pressures in man

Left ventricular systolic pressure, left ventricular diastolic pressure, left ventricular end-diastolic pressure, left ventricular cardiac output, systemic vascular resistance, and central blood volume were specifically measured in seven patients with normal cardiovascular systems before and during the tenth minute of an infusion of l-norepinephrine and the emergence of a `square wave' pattern in the peripheral arterial blood pressure during Valsalva's manœuvre. At that time point the mean left ventricular systolic pressure exceeded the resting level. The mean left ventricular diastolic pressure rose by 6 mm. Hg, and the mean left ventricular end-diastolic pressure rose by 5·5 mm. Hg. The left ventricular output remained unchanged. A reduction in the heart rate of 13 beats/minute was found, and the calculated mean systemic vascular resistance, mean left ventricular stroke volume, and left ventricular stroke work continued to be above resting levels. No change was apparent in the central blood volume. The results indicate that the left ventricular diastolic pressure and left ventricular end-diastolic pressure rise significantly in the course of a prolonged infusion of l-norepinephrine coinciding with left ventricular after-loading. The magnitude of this elevation affects all diastolic pressures passively throughout the lesser circulation, including the central venous pressure. l-Norepinephrine is markedly inotropic when released within the myocardium. In the usual clinical dose and during a period of 10 minutes' infusion its efferent vagal, peripheral, arteriolar constrictor, and left ventricle after-load effects reduce the initial inotropy.     

In Vitro Development of Automatic Control for the Actively Filled Electrohydraulic Heart

The in vitro development of automatic control of the actively filled, alternately pumped, volumetrically coupled, electrohydraulic total artificial heart was the goal of this investigation. Control features under study were (a) cardiac output (CO) response to preload; (b) CO relationship to mean aortic pressure (AoP); and (c) control of balanced ventricular outputs. A modified pulmonic valve to increase backflow was used as a balancing mechanism. Hydraulic fluid pressure transducers monitored diastolic pressures, and microprocessor control of motor speed maintained in a mild suction to yield filling rate dependent on atrial pressure. Results indicated a rise in CO from 5 to 9 L/min, with a change in mean right atrial pressure (RAP) from 0 to 7 mm Hg. No significant difference in CO was found as AoP was varied from 80 to 120 mm Hg with a maximum variation of +/- 0.5 L/min on CO and +/- 1 mm Hg on RAP. Balance was maintained for bronchial flows up to 50% with mean left atrial pressure never exceeding 15 mm Hg. An alternately pumped electrohydraulic heart was automatically controlled to respond sensitively to preload changes. Afterload changes did not alter the CO response curve. Automatically controlled, balanced ventricular outputs were maintained.     

The perioperative fate of residual gradients after repair of discrete subaortic stenosis and time-related blood levels of catecholamines

The fate of the residual peak systolic left ventricular-aortic gradient was studied perioperatively in 14 patients with membranous discrete subaortic stenosis. In nine (group A) the initial postrepair left ventricular-aortic gradient was greater than 35 mm Hg (mean 56.8 +/- 13.4), and in five (group B) there was no significant postoperative gradient (mean 15.3 +/- 3.2 mm Hg). The operation included membranectomy and myectomy. Peak left ventricular-aortic pressure gradient, endogenous levels of norepinephrine, peak rate of rise of left ventricular pressure, cardiac index, systemic vascular resistance, heart rate, and central venous pressure were recorded at the end of cardiopulmonary bypass and in 3-hour intervals for the next 9 hours. In group A during that period there was a 67% reduction in peak systolic left ventricular-aortic gradient (from 56.8 +/- 13.4 to 18 +/- 14 mm Hg, p less than 0.001). Concomitant reduction in the initial endogenous norepinephrine level was observed (from 982.1 +/- 181 to 422.6 +/- 109 pg/ml, p less than 0.001). A consistent linear relationship between norepinephrine levels and peak systolic left ventricular-aortic gradient was found (r = 0.78). Systolic left ventricular pressure decreased from 174.2 +/- 24.8 to 113.8 +/- 14.7 mm Hg (p less than 0.001). Marked reduction in peak rate of rise of left ventricular pressure (from 3455 +/- 636 to 2161 +/- 680 mm Hg/sec, p less than 0.001) was observed. Cardiac index increased and systemic vascular resistance decreased during the study period (from 2.11 +/- 0.2 to 3.07 +/- 0.26 L/min, p less than 0.001, and from 2172 +/- 331 to 1233 +/- 202 dynes/sec/cm-5, p less than 0.001, respectively). There were no significant changes in heart rate (p = not significant) and central venous pressure p = not significant). Conclusion: Some of the residual perioperative left ventricular-aortic gradients in patients with discrete subaortic stenosis undergoing repairs are dynamic and transient, and are probably related to increased postoperative sympathetic activity.     

Acute volume reduction with aortic valve replacement immediately improves ventricular mechanics in patients with aortic regurgitation

OBJECTIVES: Few data have been available regarding the immediate response in ventricular mechanics to acute volume reduction caused by aortic valve replacement for aortic regurgitation. METHODS: We studied 9 patients in the operating room immediately before and after the institution of cardiopulmonary bypass. Left ventricular pressure and cross-sectional area (a surrogate of left ventricular volume) were measured with a catheter-tip manometer and a transesophageal echocardiographic system equipped with automated border-detection technology. Left ventricular pressure-area loops were constructed, and the caval occlusion method was used to obtain the slope of the end-systolic pressure-area relationship and the end-systolic area associated with 100 mm Hg. From the steady-state beats, stroke area was obtained by subtracting the minimum area from the maximum area. Effective arterial elastance, a measure of ventricular afterload, was calculated from end-systolic pressure, and stroke area as follows: effective arterial elastance equals end-systolic pressure divided by stroke area. RESULTS: Reductions in maximum area (21.0 +/- 8.5 to 16.0 +/- 6.8 cm(2) [SD])and minimum area (15.3 +/- 8.4 to 12.0 +/- 6.1 m(2)) shifted the baseline pressure-area loops to the left. The slope of the end-systolic pressure-area relationship (11.6 +/- 4.8 to 16.0 +/- 7.5 mm Hg/cm(2)) and afterload (effective arterial elastance, 17.9 +/- 11.6 to 26.3 +/- 16.4 mm Hg/cm(2)) were increased, and the end-systolic area associated with 100 mm Hg was reduced (18.3 +/- 10.0 to 13.7 +/- 5.8 cm(2)). CONCLUSION: Correction of volume overload reduced preload (minimum area), shifted the end-systolic pressure-area relationship to the left (decreased end-systolic area), and improved ventricular contractility (increased slope of the end-systolic pressure-area relationship). The result indicated that acute volume reduction favorably influenced ventricular mechanical parameters immediately after the operation.     

Dynamic cardiomyoplasty acutely impairs left ventricular diastolic function.

In patients with congestive heart failure, medical treatment has a high rate of mortality and morbidity, and transplantation is limited by the availability of donor hearts. Dynamic cardiomyoplasty is being investigated as surgical therapy to improve left ventricular function in these patients. To evaluate the early postoperative effects of this procedure on left ventricular diastolic function, we studied seven dogs through the use of sonomicrometry and micromanometry in a canine model of dynamic cardiomyoplasty. Left ventricular diastolic parameters were determined before wrapping the latissimus dorsi muscle (baseline), after latissimus dorsi muscle wrap but without stimulation, and with synchronous left ventricular contraction-latissimus dorsi muscle stimulation. End-diastolic pressure was increased in both conditions after latissimus dorsi muscle wrap (without stimulation, 5 +/- 1; with stimulation, 6 +/- 2 mm Hg; p < 0.05) compared with baseline (3 +/- 2 mm Hg). The peak rate of diastolic pressure decay was greater at baseline (1560 +/- 370 mm Hg/sec) than after latissimus dorsi muscle wrap, both without (1260 +/- 330 mm Hg/sec, p < 0.01) and with (1120 +/- 420 mm Hg/sec, p < 0.01) stimulation. The constant of pressure decay was prolonged both without (53 +/- 10 seconds, p < 0.05) and with (62 +/- 11 seconds, p < 0.01) latissimus dorsi muscle stimulation compared with the baseline (38 +/- 5 seconds). Compared with baseline (0.2 +/- 0.2 cm-2), the constant of passive chamber stiffness increased after the latissimus dorsi muscle was wrapped around the heart (1.6 +/- 0.7 cm-2, p < 0.05) and with stimulation (2.1 +/- 1.0 cm-2, p < 0.01). The maximal diastolic filling rate (baseline, 18.1 +/- 6.7; without stimulation, 16.6 +/- 8.9; with stimulation, 16.6 +/- 4.1 cm2/sec, not significant) and end-diastolic short-axis area (baseline, 7.3 +/- 2.3; without stimulation, 7.4 +/- 2.1; with stimulation, 7.5 +/- 2.3 cm2, not significant) were similar among the three conditions. The latissimus dorsi muscle wrap prolonged relaxation and increased left ventricular passive stiffness. Synchronous latissimus dorsi muscle stimulation with left ventricular contraction did not improve diastolic function in this model. The results suggest that in the early postoperative period, dynamic cardiomyoplasty impairs diastolic function.     

Right ventricular assistance for experimental right ventricular dysfunction

Right ventricular dysfunction frequently occurs in patients undergoing correction of congenital cardiac defects, as well as in other clinical settings. The purpose of the present study was to surgically induce right ventricular dysfunction and then provide circulatory support with a right ventricular assist device. Right ventricular hypertrophy was created in 13 neonatal lambs by pulmonary artery banding. Right ventricular dysfunction was produced in all animals by performing a right ventriculotomy with the animal supported by cardiopulmonary bypass. In four unassisted animals the circulation failed after separation from bypass. Seven experimental animals underwent the insertion of a pneumatically activated ventricular assist device between the proximal pulmonary artery and the right ventricular apex. Periods with the right ventricular assist device on and off in each animal were compared. The right ventricular assist device increased cardiac output from 0.72 +/- 0.15 to 2.24 +/- 0.23 L/min (p less than 0.0002), increased left atrial pressure from 7 +/- 1 to 11 +/- 1 mm Hg (p less than 0.0005), and increased aortic systolic pressure from 53 +/- 9 to 85 +/- 9 mm Hg (p less than 0.0001). Right ventricular assistance significantly reduced the right ventricular end-diastolic pressure from 19 +/- 3 to 12 +/- 1 mm Hg (p less than 0.0001). Pulmonary artery peak pressure distal to the band increased from 27 +/- 3 to 52 +/- 5 mm Hg (p less than 0.0001). The results indicate that right ventricular dysfunction can be produced by a vertical cardiotomy in a hypertrophied right ventricle with persistent outflow tract obstruction. Right ventricular dysfunction can be effectively reversed by a right ventricular assist device, which may prove clinically useful in managing patients with refractory right ventricular failure.     

A comparison of the Vasotrac with invasive arterial blood pressure monitoring in children after pediatric cardiac surgery

The Vasotrac is a device that provides near-continuous and noninvasive arterial blood pressure monitoring and may be an alternative to direct intraarterial measurement. It has been evaluated in adult patients, but minimal information is available for pediatric patients. We evaluated agreement between measurements of arterial blood pressure and heart rate obtained from the Vasotrac versus an arterial catheter in a pediatric population. Children undergoing corrective cardiac surgery were enrolled. Simultaneous arterial blood pressure measurements were obtained postoperatively from the Vasotrac unit and an arterial catheter. Bland-Altman plots were constructed to assess agreement. Paired correlation analysis, bias, and precision calculations were performed. Sixteen patients, mean age 10.1 +/- 2.3 yr and weight 34.6 +/- 11.9 kg, were enrolled. Four-thousand-one- hundred- two paired measurements were obtained. Arterial blood pressures measured noninvasively correlated with catheter measurements with Pearson r values of 0.90, 0.80, and 0.91 for systolic, diastolic, and mean arterial blood pressures, respectively (all P < 0.001). There was excellent agreement between arterial blood pressure measurement methods. Absolute mean differences based on mixed-model regression with 95% confidence intervals were 4.0 mm Hg (3.0-5.0 mm Hg), 4.3 mm Hg (3.1-5.5 mm Hg), and 3.5 mm Hg (2.5-4.0 mm Hg) for systolic blood pressure, diastolic blood pressure, and mean blood pressure, respectively. Arterial blood pressure measurements obtained from the Vasotrac agreed well with invasive arterial monitoring in pediatric patients.     

Experimental model of left ventricular failure

A model of chronic cardiac failure has undergone extensive hemodynamic investigation. Under anesthesia the homonymous and second diagonal coronary arteries of sheep have been ligated. The resulting myocardial infarction caused significant acute hemodynamic impairment (paired two-tailed t tests), mean pulmonary artery pressure increasing from 7.31 +/- 0.94 to 13.80 +/- 1.19 mm Hg (p less than 0.001), pulmonary artery diastolic pressure increasing from 4.94 +/- 1.03 to 11.13 +/- 1.27 mm Hg (p less than 0.001), and directly measured left ventricular end-diastolic pressure increasing from 9.31 +/- 1.52 to 17.42 +/- 1.82 mm Hg (p less than 0.001) after infarction documented with invasive monitoring. There was a hemodynamically significant left ventricular aneurysm (paired two-tailed t tests) in animals studied 3 months later, with increased mean pulmonary artery pressure from 7.20 +/- 1.15 to 13.80 +/- 2.00 mm Hg (p = 0.009), an increase in pulmonary artery diastolic pressure from 4.60 +/- 1.30 to 12.10 +/- 2.06 mm Hg (p = 0.006), and an increase in left ventricular end-diastolic pressure from 11.00 +/- 1.94 mm Hg before infarction to 17.00 +/- 2.69 mm Hg (p = 0.038). We conclude that this is a useful model of chronic left ventricular failure that is reproducible and applicable to investigations of therapeutic options in chronic heart failure.     

Increased coronary artery blood flow with aortomyoplasty in chronic heart failure

BACKGROUND: We hypothesized that diastolic counter-pulsation using aortomyoplasty will increase coronary blood flow. METHODS: In dogs (n = 6, 20 to 25 kg), the left latissimus dorsi muscle was isolated, wrapped around the descending thoracic aorta, and conditioned by chronic electrical stimulation. Heart failure was induced by rapid ventricular pacing. In a terminal study, left ventricular and aortic pressures, and blood flow in the left anterior descending coronary artery and descending aorta were measured. The endocardial-viability ratio was calculated. RESULTS: Aortomyoplasty increased mean diastolic aortic pressure (70 +/- 5 to 75 +/- 5 mm Hg, p < 0.05) and reduced peak left ventricular pressure (86 +/- 4 to 84 +/- 4 mm Hg, p < 0.05), leading to a 16% increase in endocardial-viability ratio (1.29 +/- 0.05 to 1.49 +/- 0.05, p < 0.05). Coronary blood flow was increased by 15% (8.2 +/- 1.5 to 9.4 +/- 1.6 mL/min, p < 0.05). During muscle contraction, 2.7 +/- 0.5 mL was ejected from the wrapped aortic segment. CONCLUSIONS: These data demonstrate that aortomyoplasty provides successful diastolic counterpulsation after muscle conditioning and heart failure.