Percentage Change In Heart Rate Research Articles

Relationships between heart rate variability, functional capacity, and left ventricular function following myocardial infarction: an evaluation after one week and six months.

Relationships between heart rate (HR) variability and different prognostic markers such as ejection fraction, functional capacity, and patency of the infarct-related artery, as well as the comparison of their time courses are not fully elucidated. The aim of study was to assess prospectively the early postinfarction changes in HR variability and its evolution over a period of 6 months: the relationships between HR variability and functional capacity in exercise testing; left ventricular function in cardiac catheterization: status of the infarct-related artery; and the comparison of their time courses. In 42 patients with anterior myocardial infarction, a study was made of the early changes in HR variability analyzed by the complex demodulation method, its evolution over a period of 6 months. and the relationships between HR variability and (1) functional capacity in exercise testing, (2) left ventricular function in cardiac catheterization, and (3) status of the infarct-related artery. At 1 week HR variability parameters correlated directly with functional capacity indicators such as METS, percent change in HR from rest to peak exercise (%deltaHR), difference between initial and peak HR (HR range), percent peak theoretical HR (% peak HR), left ventricular ejection fraction (EF), and, inversely, with end-systolic volume (ESV). Stepwise multiple regression analysis to establish HR variability parameters (recorded at 1 week) as related to functional capacity and left ventricular function at 1 week and 6 months postinfarction established the following variables: (1) At 1 week: standard deviation (SD) of the RR cycles in relation to %deltaHR (r = 0.60, p <0.0001), HR range (r = 0.43, p < 0.01), and EF (r = 0.79, p < 0.0001). (2) At 6 months, the sole accepted HR variability parameter was the SD in relation to %deltaHR (r = 0.38, p < 0.05) and HR range (r = 0.45, p < 0.01). No variability parameter was accepted in relation to METS, % peak HR, or ESV. Relationship between EF or ESV and HR variability parameters was not significant when both were evaluated at 6 months. At that time, there was a significant increase in all HR variability parameters among all surviving patients (n = 39), with the exception of the LF/HF ratio and mean RR cycle. The percent increase in HR variability between the first week and 6 months was greater among those patients with the lowest basal EF. No relation was established between HR variability and patency of the infarct-related artery. The decrease in HR variability observed following myocardial infarction is associated with a diminished functional capacity and an increased alteration of the EF. This does not affect the recovery of HR variability, which was observed in all surviving patients.

Comparison of Oral Glucose and Sucrose Solutions on Pain Response in Neonates

Abstract: In this study, we aimed to compare the analgesic effect of 30% sucrose and 10% and 30% glucose in a group of healthy term newborns. A total of 113 infants whose heels were pricked for the guthrie test were included in the study. The babies were randomized into 4 groups, receiving 2 ml of 30% sucrose, 10% glucose, 30% glucose, or distilled water. Response to pain was assessed by mean crying time, recovery time, maximum heart rate, and percent change in heart rate at 1, 2, and 3 minutes. Mean crying times were 60, 102, 95, and 105 seconds in the sucrose, 10% glucose, 30% glucose, and placebo groups, respectively (P = .02). Although mean recovery time was shorter in the sucrose group (102 seconds), there was neither a significant difference between the groups (10% glucose, 121 seconds; 30% glucose, 109 seconds; control group, 132 seconds [P = .09]), Nor was there a difference in maximum heart rate and percent change in heart rate at 1, 2, and 3 minutes after heel prick (P = .14, P = .05, P = .53 For the first, second, and third minutes, respectively ). However, a statistically borderline difference existed at the end of 2 minutes favoring sucrose (P = .05). We conclude that 30% sucrose is superior to 10% and 30% glucose solutions in relieving pain, showing its primary effect in crying time. As glucose solutions are readily available in neonatal intensive care units and easier to use in routine practice, further trials are needed to evaluate the antinociceptive effect of glucose when combined with other nonpharmacologic methods.

Effects of pretreatment with magnesium on muscle relaxation and cardiovascular responses in tracheal intubation using the priming principle for vecuronium.

In addition to its direct effects on blood vessels, the myocardium, and neuromuscular junctions, magnesium can act as an adrenergic antagonist and can inhibit the release of catecholamines both from adrenergic nerve terminals and from the adrenal medulla. This study was undertaken to evaluate these effects of magnesium on muscle relaxation and cardiovascular response during tracheal intubation. Forty ASA I or II patients undergoing elective surgery were allocated to a magnesium or a control group. Three minutes after priming with vecuronium 0.015 mg·kg-1, the magnesium group received vecuronium 0.085 mg·kg-1 and magnesium sulfate 40 mg·kg-1, while the control group received an equivalent volume of vecuronium and saline. The percent change from baseline in mean arterial pressure after tracheal intubation was significantly smaller (P<0.01) in the magnesium group than in the control group, but the percent change in heart rate was similar. There were no significant changes in plasma catecholamine concentrations after tracheal intubation in either group. The onset time of vecuronium was significantly shorter in the magnesium group than in the control group. The duration of action of vecuronium was significantly longer in the magnesium group than in the control group. Serum magnesium concentrations at 90 min after its administration were significantly higher than baseline. We concluded that vecuronium priming with magnesium pretreatment inhibits the hypertension associated with tracheal intubation and shortens the onset time of vecuronium, but prolongs it duration of action.

Heart rate and cardiac output after atropine in anaesthetised infants and children.

Heart rate is considered to be a major determinant of cardiac output in infants and small children but the relationships between age, heart rate and cardiac output in humans have never been clearly established. This study was designed to determine the change in cardiac output following atropine iv to anaesthetised infants and small children. Following Institutional Ethics Committee approval and written-informed consent, 20 ASA I or II unpremedicated patients aged from 1 to 36 mo were studied. Anaesthesia was induced with 5 mg.kg-1 thiopentone, 2 micrograms.kg-1 fentanyl and maintained with halothane 0.5% in nitrous oxide 66% in oxygen. Vecuronium 0.1 mg.kg-1 was used to provide muscular relaxation. Cardiac output was measured by non-invasive transthoracic blind continuous-wave Doppler echocardiography before and after the administration of 0.02 mg.kg-1 atropine iv. Atropine increased both heart rate and cardiac index by 31.1 +/- 12.8% and 29.4 +/- 17.3% respectively (P < 0.05). The cardiac index before atropine was 5.1 +/- 1.2 L.min-1.m-2 and the increase after atropine varied widely from 1.4 to 52.1%. Although atropine did not alter the overall stroke index the recorded changes ranged from -20.8 to +18.0%. There was no association between age and either cardiac index or % change in cardiac index after atropine. However, there was a positive but weak correlation between percentage change in heart rate and cardiac output (r2 = 0.46). Atropine causes a variable increase in cardiac output in infants and children aged between 1 and 36 mo. The change in cardiac output, considering the limits of the transthoracic echocardiography methodology, suggests that this is related to the increase in heart rate but is not dependent of age.

The effects of atropine and glycopyrrolate on heart rates in conscious mature goats.

The effects of intravenously administered atropine (0.2 mg/kg) and glycopyrrolate (0.01 mg/kg) on heart rate were studied in 10 conscious mature goats. In a drug cross-over fashion, either atropine, glycopyrrolate, or 0.9% saline solution was administered using the same volume (0.05 mL/kg). Atropine and glycopyrrolate caused a significant increase in heart rate (P < .05), whereas saline solution (0.09%) did not. The mean percent changes in heart rate from baseline were similar for atropine and glycopyrrolate up to 14 minutes after administration. Thereafter, glycopyrrolate had a significantly greater mean change in heart rate than atropine, ie, up to 29 minutes (P < .05). Within the atropine group, the mean percentage changes in heart rate became significantly lower compared with the initial increase (1 minute) starting at 11 minutes. For the glycopyrrolate group, the mean percent changes became significantly lower starting at 27 minutes. Glycopyrrolate and atropine had a mean percentage change in heart rate of greater than 1.0%, up to 31 and 22 minutes, respectively. At the doses used, glycopyrrolate had longer duration of action than atropine but the magnitude of increase was similar.

901-78 Early Noninvasive Detection of Hypovolemia Secondary to Acute Blood Loss Using Pulse Volume Analysis

Hypovolemic shock is difficult to recognize in its early stages because clinically significant changes in heart rate (HR), blood pressure (BP), and urine output occur late in its course. This study was conducted to determine if changes in peripheral pulse volume (PV) occur early in acute blood loss, prior to clinically significant changes in HR or BP. PV is defined as the maximum change in volume of a limb segment (e.g. calf) occuring during the cardiac cycle and is measured noninvasively with a digitally enhanced admittance plethysmograph. HR, systolic BP (SBP), diastolic BP (DBP), and calf PV (in microliters, μL) were measured in 35 male blood donors (age = 38.7 ± 11.1 [sd] yrs, weight = 87.7 ± 15.3 [sd] kg) before and after donating a unit of whole blood (the average blood loss was 5.3 ± 0.9 [sd] ml/kg). Pre and post donation measurements were compared using paired Student's t-test. The results (mean ± se) are tabulated below and illustrated above: Pre-Donation Post-Donation Change Significance HR (/min) 68.5 ± 1.5 69.8 ± 1.5 1.4 ± 0.6 p &lt; 0.02 SBP (mmHg) 143.1 ± 2.5 1458 ± 3.1 2.9 ± 2.3 n.s DBP (mmHg) 732 ± 2.0 75.7 ± 1.7 1.9 ± 1.5 n.s. PVIJ (μL) 1151 ± 64 954 ± 39 -197 ± 53 p &lt; 0.0001 There were no significant changes in either SBP or DBR. The HR increased significantly, but by only 2.0% (p &lt; 0.02). The PV decreased by 17.1% (p &lt; 0.0001), which is 8.6 times greater than the percent change in heart rate (p &lt; 0.01). The PV decrease correlated with the blood loss per kg (r = 0.46, p &lt; 0.01). We conclude that a significant change in PV occurs with relatively minor blood loss. Pulse volume analysis may therefore provide an early indication of hypovolemia due to acute blood loss.

Mixtures of Sodium Nitroprusside and Trimethaphan for Induction of Hypotension

A mixture of sodium nitroprusside (SNP) and trimethaphan, empirical 1:10 weight ratio, has been advocated to decrease untoward side effects of SNP when used to induce hypotension during anesthesia and operation. The purpose of this study was to investigate the effects of various ratios of mixtures of SNP and trimethaphan on heart rate (HR), renal sympathetic nerve activity (RSNA), and renal artery blood flow to find the best ratio of SNP and trimethaphan for producing induced hypotension. Five mixtures with different ratios of SNP and trimethaphan, as well as each drug alone, were given intravenously to mongrel dogs in amounts adequate to achieve a stable mean arterial blood pressure of 75 +/- 5 mm Hg. Sodium nitroprusside alone significantly increased HR (163% +/- 14.5%) and RSNA (222% +/- 24%). Trimethaphan alone significantly decreased RSNA (11.6% +/- 4.5%). There were significant positive correlations between SNP-to-trimethaphan ratios and percent changes in HR (r2 = 0.301, P less than 0.01) and in RSNA (r2 = 0.648, P less than 0.01). Renal artery blood flow was well maintained with all ratios. Sodium nitroprusside and trimethaphan interacted synergistically to produce hypotension. However, they antagonize each other in their effects on arterial baroreflex-mediated changes in HR and RSNA. According to linear regression lines, HR changed least with a SNP-to-trimethaphan ratio of 1:5, and RSNA changed least with SNP-to-trimethaphan ratios of 1:2.5 and 1:5. Our results indicate that mixtures of SNP and trimethaphan in ratios of approximately 1:2.5 to 1:5 may produce induced hypotension with stable reflex sympathetic nerve activity.

Evaluation of the pharmacokinetics and electrocardiographic effects of intravenous verapamil with intravenous calcium chloride pretreatment in normal subjects

To evaluate the effects of calcium pretreatment on the disposition and etectrocardiographic effects of verapamil, 8 healthy male volunteers received treatment in each of 3 phases in a randomized, double-blind, crossover manner. Phase I denoted 10 ml of 0.9% intravenous sodium chloride followed by 10 mg of intravenous verapamil; phase II denoted 10 ml of 10% intravenous calcium chloride followed by 4 ml of 0.9% intravenous sodium chloride; and phase III denoted 10 ml of 10% intravenous calcium chloride followed by 10 mg of intravenous verapamil. Blood samples for the determination of verapamil concentrations were drawn at 5, 10, 15, 20, 30, 45, 60 and 90 minutes, and at 2, 4, 6, 10 and 24 hours. Blood pressure, heart rate and PR intervals were also measured at these times. Pretreatment of verapamil with intravenous calcium did not alter the disposition of intravenous verapamil. Blood pressure was not significantly altered in any treatment phase, although calcium tended to increase mean arterial pressure and verapamil abolished this effect. Cakium had no significant affect on verapamil-induced PR prolongation (maximum percent change in PR interval: phase I = 19 ± 11%, phase III = 18 ± 7%; time to maximal prolongation: phase I = 0.38 ± 0.21 hours, phase III = 0.37 ± 0.26 hours; and area under the percent change in PR vs time curve: phase I = 15.5 ± 10, phase III = 21 ± 9). Verapamil caused a reflex increase in heart rate of similar magnitude in both phases I and III (24 ± 10% and 21 ± 7%, respectively). However, calcium in phase III caused an initial decrease in heart rate, such that the net change in heart rate over time was significantly different (p < 0.05) than with verapamil alone (area under the percent change in heart rate vs time curve: phase I = 5 ± 28, phase III = −23 ± 12). In doses frequently used in a clinical setting, calcium and verapamil produce opposing effects on the sinus rate and arterial blood pressure, but not on atrioventricular conduction. These findings show that the atrioventricular nodal and thus antiarrhythmic effects of verapamil are preserved despite pretreatment with calcium.

Simulation technique for difficult intubation: Teaching tool or new hazard?

This investigation evaluated the risks of a simulation drill designed to improve the skill of anesthesia personnel in dealing with an unexpected difficult intubation. In a controlled prospective study, 40 patients with normal airways scheduled to undergo noncardiothoracic surgery were randomized into two groups of 20 patients. In the control group, intubation was performed by standard techniques. In the simulation group, intubation of a difficult airway was simulated and performed with the aid of an endotracheal tube introducer. Heart rate (HR); systolic, mean, and diastolic blood pressures (BPs); and arterial oxygen saturation were measured noninvasively during the preinduction period and 1 minute postintubation. A record was kept of all adverse events, including electrocardiogram (EKG) evidence of myocardial ischemia or cardiac arrhythmias, esophageal intubation, pulmonary aspiration, or tracheal injury. There were no significant differences in percent changes in HR, BP, or oxygen saturation between the two groups. There were five uncomplicated esophageal intubations in the simulation group compared with none in the control group ( p = 0.001). No other adverse events were recorded. The potential hazards of esophageal intubation should be considered before this simulation drill is performed.

Effect of Coenzyme Q10 on Hemodynamic Response to Ocular Timolol

Coenzyme Q10 (CoQ10) is an essential component of the mitochondrial membrane and plays an important role in the maintenance of normal cardiac function. To evaluate the effects of ocular timolol on the cardiovascular system and determine the protective effect of CoQ10, 16 patients with glaucoma were studied using impedance cardiography. Following instillation of 1 mg timolol maleate in each eye, heart rate (HR) and stroke index (SI) decreased, and total peripheral resistance index (TPRI) increased significantly. Reexamination was performed after 6 weeks of 90 mg oral CoQ10. Despite decreases in HR, percent changes in HR were significantly less after CoQ10 at 120 min. Stroke index showed an initial increase which was not observed without CoQ10. These data suggest that CoQ10 delayed the appearance of inotropic blockade of timolol and hastened the disappearance of chronotropic blockade. Additional study of six normal volunteers with 6 weeks of oral CoQ10 showed a similar decrease of intraocular pressure after timolol instillation as compared to those without CoQ10. Thus, administration of oral CoQ10 in patients receiving ocular timolol may be useful in mitigating cardiovascular side effects without affecting intraocular pressure in the treatment of glaucoma.

Hypoxia reinforces laryngeal reflex bradycardia in infants.

The laryngeal chemoreflex involves bradycardia, apnea, swallowing and peripheral vasoconstriction. This reflex was studied in twelve infants, aged 5 days-28 weeks, who had sustained an apparent life-threatening event or were siblings of infants who had died of the sudden infant death syndrome. The bradycardic and apneic components of the reflex were found to be significantly, and sometimes powerfully, reinforced when elicited by pharyngeal water instillation during acute, mild hypoxia (transcutaneous PO2 4.6-8.3 kPa). Apnea duration during normoxia was 0.7-15 sec, and during hypoxia 2-30 sec. Heart rate change ranged from +26% to -21% during normoxia, as compared with -4% to -63% during hypoxia. The percentage change in heart rate was found to inversely correlate with the transcutaneous PO2-level prevailing when the reflex was elicited. The conclusion is that there is a significant reinforcement of the cardiorespiratory adjustments when the laryngeal reflex is activated during simultaneous excitation of the peripheral arterial chemoreceptors. One infant, showing a particularly strong increase of the cardiorespiratory response to laryngeal receptor stimulation during hypoxia, later died of sudden infant death syndrome.

Mechanisms for attenuated pressor responses to α-agonists in ovine pregnancy

Attenuated pressor responses to angiotensin II and α-agonists normally occur during ovine pregnancy; however, for α-agonists it is not known to what extent this reflects alterations in cardiac output. We therefore compared peripheral and cardiac responses to α-agonists in pregnant (n = 6) and nonpregnant (n = 6) sheep, measuring mean arterial pressure, heart rate, and cardiac output before and during steady-state dose responses to norepinephrine (0.458 to 45.84 μg/min) and phenylephrine (1.29 to 129 μg/min). Both α-agonists caused dose-dependent increases in mean arterial pressure and systemic vascular resistance, more so in nonpregnant than pregnant sheep (p < 0.01), and decreases in cardiac output and heart rate (p < 0.01). In both nonpregnant and pregnant sheep the percent change in systemic vascular resistance generally exceeded the percent change in mean arterial pressure, reflecting decreases in cardiac output; however, at equivalent increases in percent change in mean arterial pressure and percent change in systemic vascular resistance, the fall in the percent change in cardiac output was greatest in pregnant sheep (p < 0.05). Also, at similar increases in mean arterial pressure the percent change in heart rate was greatest in pregnant sheep (p < 0.01). In contrast to angiotensin II, the attenuated pressor responses to α-agonists observed during ovine pregnancy are partly a result of reflex decreases in cardiac output mediated mainly through falls in heart rate.

The Reptilian Baroreceptor and Its Role in Cardiovascular Control

Anatomical evidence for the existence of a depressor nerve in reptiles was first reported 100 years ago. Electrical stimulation of the central end of the cut nerve, however, did not produce an unequivocal fall in heart rate and blood pressure, so it was thought not to function as a depressor nerve. This remained the state of knowledge for fifty years when Marco Fedele performed a superb anatomical and physiological study of the depressor nerves of turtles and lizards. He demonstrated that there were two depressor nerves from each vagus; the superior nerve originated from the jugular ganglion or superior laryngeal nerve in turtles and from the superior laryngeal nerve or vagus in lizards; the inferior nerve originated from the nodose ganglion or slightly caudad of this ganglion. The nerves were shown to terminate in the proximal truncus arteriosus. Unlike the earlier workers, Fedele obtained a clear depressor effect on stimulating the depressor nerves. In more recent times baroreflexes have been demonstrated in response to hemorrhage and body tilting in reptiles, with snakes receiving particular attention. The evidence indicates that aquatic snakes are less effective at maintaining blood pressure than terrestrial and arboreal forms. The sensitivity (gain) of the baroreceptor-heart rate reflex, when it is expressed as a percentage change in heart rate per unit pressure change, is approximately the same in reptiles, amphibians, and mammals. In addition, the ultrastructural appearance of the baroreceptors of lizards is similar to that of mammals. A quantitative assessment of the ability of reptiles to correct disturbances in blood pressure has not yet been made, but techniques for obtaining this information are now available.

Attenuation of the ventilatory and heart rate responses to hypoxia and hypercapnia with aging in normal men.

The response of ventilation and of heart rate to hypoxia and hypercapnia was determined in eight young normal men age 22-30 yr and eight elderly men age 64-73. The elderly men were selected and carefully screened to eliminate the possibility of cardiopulmonary disease. All the subjects were born at low altitude and had no significant prior exposure to hypoxia. The ventilatory response to hypoxia was measured as the exponential slope constant. k, of regression lines relating the logarithm of incremental ventilation to PAo(2) during isocapnic progressive hypoxia. The heart rate response to hypoxia was measured as the percentage change in heart rate between PAo(2) = 100 and PAo(2) = 40 mm Hg. The ventilatory response to hypercapnia was measured as the slope of regression lines relating ventilation to PAco(2) during rebreathing with PAo(2) > 200 mm Hg. The heart rate response to hypercapnia was measured as the percentage change in heart rate between control values at the start of the rebreathing test and PACO(2) = 55 mm Hg. The ventilatory and heart rate responses to both hypoxia and hypercapnia were significantly decreased in the elderly men as compared to the young men. Hypoxic ventilatory drive was decreased by 51+/-6% (mean +/-SEM: P < 0.001) and hypercapnic drive by 41+/-7% (P < 0.025). The percentage change in heart rate produced by hypoxia was 34+/-5% (mean +/-SEM) in the young normals and 12+/-2% in the old normals (P < 0.005). Similar figures for heart rate in response to hypercapnia were 15+/-3% and -1+/-1% for the young and old normal groups (P < 0.001). We conclude that ventilatory and heart rate responses to hypoxia and hypercapnia diminish with age. These alterations in both ventilatory and circulatory controls could make older individuals more vulnerable to hypoxic disease states.

Coronary artery occlusion in the conscious dog. Effects of alterations in heart rate and arterial pressure on the degree of myocardial ischemia.

Bradycardia, with or without hypotension, frequently occurs in the early phases of acute myocardial infarction. To determine the relative effects of alterations in heart rate and blood pressure on the degree of ischemic injury, the left anterior descending coronary artery was occluded for 15-min periods in closed-chest conscious dogs by inflating a balloon cuff previously implanted around the artery. The degree of myocardial ischemia was estimated by summating the S-T elevation recorded from 12 myocardial electrodes. Heart rate was increased by atropine or pacing and decreased by electrical stimulation of the vagus nerve. Hypotension was produced by venesection (average decrease in mean BP, 56 mm Hg). At normal arterial pressures there was a positive correlation between percent change in heart rate (range 30-215 beats/min) and percent change in S-T elevation (y = 0.75 X + 30.2, r = 0.93, P &lt; 0.01). When myocardial ischemia was induced during hypotension and bradycardia, S-T elevation totaled 68 mv at 15 min of ischemia. When heart rate was increased to control levels in the presence of hypotension S-T elevation during myocardial ischemia was greater (mean difference 29 mv, P &lt; 0.05). In contrast, when blood pressure was increased to control in the presence of bradycardia, S-T elevation in seven of 10 dogs was less than during hypotension and bradycardia. Thus, during experimental acute myocardial ischemia, hypotension induced by hemorrhage increases ischemic injury, and bradycardia reduces it. It is concluded that in acute myocardial ischemia increases in heart rate, even from slow baseline rates; may be deleterious to the myocardium. It remains to be determined whether alterations in the degree of myocardial ischemia induced by hemorrhagic-hypotension are analogous to those caused by the type of hypotension that often accompanies bradycardia occurring during acute myocardial infarction in man.

The role of gross locomotor restriction in the acquisition of motor and cardiac conditional discrimination in the dog

The effects of gross locomotor restriction and lack of restriction, respectively, on the acquisition of a motor and cardiac discrimination task was investigated. Litter-mate dogs were used in a counterbalanced design involving two treatment conditions (free and restrained) and two discrimination learning problems. Each learning problem included eight daily training sessions with 10 CS+ tones and ten CS—tones presented randomly. The US was a shock to the left foreleg. Degree of foot flexion and percentage change in heart rate in response to CS tones were recorded. Dogs subjected initially to the free condition manifested a superior and more rapid motor and cardiac discrimination than Ss initially restrained. The free condition was not as facilitatory when presented to Ss which first had been exposed to the restraint condition. The results are discussed in terms of activation and negative transfer.

DEPRESSION OF VENTRICULAR CONTRACTILITY BY STIMULATION OF THE VAGUS NERVES.

In three different types of canine heart preparations, it was demonstrated that efferent vagal stimulation exerts a potent, negative inotropic influence upon the ventricular myocardium. In the paced, isovolumetric, left ventricle preparation, vagal stimulation evoked a reduction of left ventricular systolic pressure which, within limits, varied directly with the magnitude of the stimulus. Supramaximal stimulation elicited a mean reduction of 23% in the peak pressure generated by the left ventricle. No differences could be detected between the effects of the right and left vagi upon ventricular contractility. The percentage changes induced by vagal stimulation upon ventricular contractility in the paced heart were less than the percentage changes in heart rate induced in the spontaneously beating heart. In a pumping heart preparation in which a constant rate of venous return was delivered to the left atrium, vagal stimulation consistently elicited an appreciable elevation of left ventricular end diastolic pressure. Another pumping heart preparation was employed in which changes in atrial transport function and mitral valve closure were excluded by the expedient of introducing a balloon into the left ventricle through an apical incision. This balloon was connected to an artificial external circuit with fixed venous reservoir height and peripheral resistance. Vagal stimulation consistently diminished stroke volume, "arterial" pressure, and stroke work in such a circuit.