Morris Stampfer

Role of the Capacitance and Resistance Vessels in Vasovagal Syncope

Withdrawal of sympathetic tone to the veins resulting in peripheral pooling of blood has been suggested as an important factor contributing to the decrease in cardiac output and hence arterial pressure that occurs during vasovagal syncope. However, no measurements of venous tone during syncope have been reported. In the course of other studies on the circulatory effects of negative pressure below the iliac crests, and 80° head-up tilt, vasovagal reactions occurred in 10 subjects. Heart rate, central venous pressure, arterial pressure, forearm blood flow, forearm vascular resistance, and forearm or hand venous tone were measured. The typical vasovagal reaction could be divided into two phases. A gradual fall in arterial pressure signified the onset of phase I, during which forearm vascular resistance did not change significantly. The duration of phase I was highly variable. The onset of phase II was denoted by an abrupt fall in arterial pressure and heart rate and a decrease of 62% in forearm vascular resistance, from 36 to 14 mm Hg/ml/100 g/min. However, venoconstriction rather than venodilatation occurred in the forearm or hand veins. Since central venous pressure did not change prior to or during the onset of the reaction, it is unlikely that venodilatation occurred in other vascular beds. It is concluded that two of the major mechanisms responsible for the hypotension of vasovagal syncope initiated by orthostasis or lower body negative pressure are bradycardia and dilatation of the resistance vessels. In contrast, it appears that the venous bed, by constricting, tends to maintain filling pressure and thereby cardiac output, and thus works in an opposite direction.

Characterization of the Circulatory Response to Maximal Upright Exercise in Normal Subjects and Patients with Heart Disease

The circulatory responses to mild and maximal upright exercise were studied in six normal subjects and 21 patients with various types of cardiac disease. It was found that the usual hemodynamic indices employed to evaluate cardiac performance during exertion were unreliable in separating patients from normal persons. In contrast, the cardiac index achieved at a pulmonary arterial (PA) O2 saturation of 30% was found to be highly reliable and sensitive for distinguishing the normal from the abnormal response to exercise. At a level of exercise that lowers PA O2 saturation to 30%, all normal subjects achieved a cardiac index greater than 7.0 L/minm2 while no patient exceeded 4.8 L/min/m.2 In addition, the maximal capacity to extract O2 was greater in patients than in normal subjects; thus, during maximal exercise it was not unusual for patients to achieve PA O2 saturations of 15% or less, while the lowest value achieved in normal subjects was 23%.

Impairment of cardiac function in patients with pectus excavatum, with improvement after operative correction.

Abstract Although pectus excavatum is thought to impair cardiac performance, no consistent hemodynamic abnormalities have been identified. We hypothesized that cardiac function might be impaired during upright exercise when the heart descends into the pectus deformity. Catheterization of the right side of the heart in six patients with pectus excavatum gave normal results, and the hemodynamic response to supine exercise was normal. In contrast, cardiac output (CO) during intense upright exercise was low in two patients, at the lower limits of normal in one, and low normal in two. The CO and stroke-volume responses to mild upright exercise also differed from normal. After operative repair in three patients, CO during intense upright exercise increased an average of 38 per cent, and hemodynamic responses to mild upright exercise also changed toward normal. No alterations occurred in the response to supine exercise. Thus, pectus excavatum can reduce the pumping capacity of the heart during upright exercise, ...

Effects of a Reduction in Environmental Temperature on the Circulatory Response to Exercise in Man: Implications Concerning Angina Pectoris

Abstract The physiologic basis for the frequent complaint of worsening of symptoms in a cold environment was investigated in six patients with and five without coronary-artery disease, at rest and during identical levels of mild upright exercise at 25 and 15°C, with similar results. Significantly higher at the lower temperature were mean systemic arterial pressure (105 vs 92 mm of mercury at rest and 110 vs 92 during exercise; p less than 0.001), total peripheral resistance (1821 vs 1609 dynes-sec-cm-5 at rest, 1213 vs 993 during exercise; p less than 0.02) and left ventricular minute work (6.5 vs 5.7 kg-m at rest, 10.9 vs 9.0 during exercise; p less than 0.001). Exposure to cold did not change heart rate, cardiac output or stroke volume at rest or during exercise. These results indicate that a cold environment increases peripheral resistance at rest and during exercise. The consequent rise in arterial pressure, by augmenting myocardial oxygen requirements, would thus more readily provoke an attack of angina.

Circulatory Effects of Electrical Stimulation of the Carotid Sinus Nerves in Man

The effects of carotid sinus nerve (CSN) stimulation were studied at rest and during a mild level of supine bicycle exercise in seven patients in whom CSN stimulators had been implanted for the treatment of angina pectoris. At rest, CSN stimulation produced a fall in mean arterial pressure (MAP) averaging 23% and an 8% decrease in cardiac output (CO). Total peripheral resistance (TPR) fell by 14% and forearm vascular resistance (FVR) by 16%. During exercise, MAP fell 16%, but no significant change occurred in CO. Thus, the fall in MAP could be attributed to a reflexly induced decrease in peripheral vascular resistance. Only small decreases occurred in heart rate. No changes in venous tone, central venous pressure, or the maximum transverse end-diastolic diameter of the heart were produced by stimulation either at rest or during exercise. Thus, at rest, CSN stimulation reduces MAP by reflexly decreasing both vascular resistance and CO; during exercise, the diminution in CO no longer occurs. Finally, the venous system does not appear to participate in reflexes activated by CSN stimulation.

Hemodynamic Effects of Diuresis at Rest and During Intense Upright Exercise in Patients with Impaired Cardiac Function

Although diuretic therapy appears to improve the exercise capacity of patients with moderately impaired cardiac function, the hemodynamic basis for this improvement is not clear. It is also unknown to what extent the moderate diuresis that often occurs during the first few days of hospitalization contributes to the normal or nearly normal hemodynamic measurements obtained in certain patients with cardiac impairment who are thought clinically to have signs and symptoms of pulmonary congestion. Accordingly, the circulatory response to moderate diuresis resulting in a loss of weight averaging 3.4 kg was investigated in 15 patients with heart disease. At rest in the supine position mean pulmonary arterial wedge pressure fell after diuresis from an average of 24 to 13 mm Hg. Reductions also occurred in mean pulmonary arterial pressure (42 to 26 mm Hg), mean right atrial pressure (9 to 4 mm Hg), and right ventricular end-diastolic pressure (11 to 6 mm Hg). Cardiac output decreased by an average of 20%, mean systemic arterial pressure by 12%, right ventricular stroke work by 44%, and left ventricular stroke work by 25%. Diuresis also caused similar reductions in these values in the sitting position at rest and during mild and intense levels of treadmill exercise. Despite the reductions in cardiac output, all but one of the patients studied achieved substantial clinical improvement from the diuresis. Such improvement probably resulted from the fact that the beneficial effects of lower pulmonary vascular pressures outweighed the deleterious effect of a reduction in cardiac output. Thus, moderate changes in body weight brought about by either fluid retention or fluid loss may result in substantial alterations in circulatory dynamics. These changes, if unrecognized, can lead to considerable confusion when attempts are made to correlate the hemodynamic findings with the degree of cardiac decompensation as judged clinically.

Role of the venous system in baroreceptor-mediated reflexes in man

Although baroreceptor stimulation produced by marked alterations in arterial pressure has been shown to produce reflex changes in venous tone in animals, the effects on venous tone in man of altering arterial pressure within the physiologic range have not been clear. In six subjects, venous tone did not change when mean arterial pressure was raised by 25-40 mm Hg, although heart rate fell reflexly by 40%. Venous tone remained constant in 10 subjects when arterial pressure was lowered. This contrasted to the sustained rise in forearm vascular resistance and the persistent tachycardia that occurred. However, 12 subjects continued to respond to these interventions by transient venoconstriction. To eliminate possible emotional influences on venous tone due to the experimental intervention, venous responses were studied before and during general anesthesia in five of these subjects. In contrast to the response before anesthesia, an equivalent fall in arterial pressure during anesthesia no longer evoked a venoconstrictor response. Venous reactivity and the baroreceptor reflex arc remained intact during anesthesia, since venous tone always rose after a deep inspiration, and tachycardia always accompanied the fall in arterial pressure. It is concluded that changes in arterial pressure in the physiologic range in man do not induce measurable reflex alterations in venous tone, and that the increases sometimes seen with decreases in arterial pressure appear to be due to extraneous psychic factors.

Comparison of the Peak Inotropic Effects of a Catecholamine and a Digitalis Glycoside in the Intact Canine Heart

The relative peak effects of isoproterenol and ouabain on myocardial contractility and cardiac output were compared by infusing increasing amounts of these two drugs into seven open-chest anesthetized dogs until toxicity developed. Just prior to the development of toxicity isoproterenol increased contractile force an average of 149% and the peak rate of force development (df/dt) an average of 278% of control values, compared to an increase of only 49% and 35%, respectively, with the administration of ouabain. Cardiac output and stroke volume were also significantly greater with the catecholamine than the glycoside. The combination of isoproterenol and ouabain produced essentially the same contractile force and stroke volume achieved by isoproterenol alone. Suppression of ouabain-induced arrhythmias by ventricular pacing allowed additional glycoside to be infused until ventricular fibrillation terminated the study. With pacing and ouabain, contractile force increased 131% above control, a level similar to that achieved by isoproterenol; peak df/dt increased to 200% above control, a value significantly lower than that obtained with isoproterenol. However, stroke volume decreased despite a substantial increase in left ventricular end-diastolic pressure. It is concluded that maximal doses of isoproterenol produce significantly greater increases in myocardial contractility and cardiac output compared to ouabain, even when the toxicity produced by the latter is suppressed by electrical stimulation.