Peripheral Venous Pooling Research Articles

Effects Of Artificial Gravity On Human Haemodynamics And Cardiovascular Function

PURPOSE: Short radius centrifuge (SRC) devices have been amongst the most important facilities for astronauts for several decades, requiring a high relative velocity in order to generate adequate g-loads for experiments and training. SRCs caught the attention of space agencies due to ongoing plans for interplanetary missions to Mars and the Moon. This study aimed to assess changes in haemodynamics induced by artificial gravity (AG) during centrifugation on a SRC. METHODS: Eleven healthy subjects (29.57 ± 6.61 years, 183.21 ± 5.11 cm, 82.14 ± 7.24 kg) participated, none of them showing any history of vasovagal syncope. Two different AG-protocols were conducted with at least a 48h time lag in between. The continuous AG-protocol included an acceleration phase of 1g, 2g and 3g for 120 s each, followed by a continuous acceleration of 2g for 30 min and a final acceleration phase of 1g, 2g and 3g for 120 s each. In contrast, the intermittent protocol included a phase of intermittent g-load of 2g for 180 s interrupted by a pause of 180 s (baseline rotation of 5RPM). This sequence of acceleration was repeated four times. Changes in oxygenated blood (O2Hb) and deoxygenated blood (HHb) in the underlying tissue were recorded using a 4-channel Near Infrared Spectroscopy (NIRS) system on the prefrontal cortex (PFC), musculus biceps brachii (MBB) and musculus gastrocnemius (MG). RESULTS: Concentration in O2Hb decreased (F(13, 130) = 26,356, p < .05) and in HHb increased (F(13, 130) = 11.119, p < .05) during acceleration phases 1 and 2 in the PFC in both AG profiles. Similarly, concentration in O2Hb decreased (F(13, 130) = 16,478, p < .05) and in HHb increased (F(13, 130) = 11,178, p < .05) during same phases in the MBB. Peripheral venous pooling was indicated by increased concentration in both, O2Hb (F(13, 117) = 11,830, p < .05) and HHb (F(13, 117) = 5,3686, p < .05) during acceleration phases in the MG. Continuous acceleration induced peripheral accumulation of both O2Hb and HHb, whereas intermittent acceleration kept concentration in both parameters stable. CONCLUSION: NIRS is an appropriate method for assessing cranial blood oxygenation and venous pooling in the peripheral extremities during application of AG. Haemodynamics and the regulation of the cardiovascular system appear to be affected by the g-load applied by an SRC.

Vasovagal syncope during spirometric exercise.

Sir, A 48-year-old male patient operated for aortic valve replacement was extubated uneventfully. Patient was off inotropic and vasoconstrictor support. During the recovery period, patient was advised to do spirometric breathing exercises. While doing spirometric breathing, patient suddenly had a sudden loss of consciousness with bradycardia and hypotension. Immediately the patient was intubated, and atrial pacing was started with epicardial pacing. As patient recovered consciousness and hemodynamic stability, he was extubated. The reflex syncopes are because of a sudden failure of the autonomic nervous system to maintain adequate vascular tone during orthostatic stress, resulting in hypotension with bradycardia resulting in cerebral hypoperfusion and loss of consciousness.[1] Reflex syncope is (1) neurocardiogenic (vasovagal) syncope and (2) carotid sinus syndrome. It is commonly seen in younger patients and presents with a prodromal phase (nausea, lightheadedness, visual changes or diaphoresis) followed by a sudden loss of consciousness. Recovery is generally rapid and uneventful. The reasons for neurocardiogenic syncope are unclear. Predisposing factors can be pain, emotional distress, or prolonged standing. Pathophysiology of vasovagal syncope is often related to orthostatic stress.[2] Increased amount of peripheral venous pooling decreases venous return to the heart so precipitously that a significant rise in ventricular inotropy occurs. This hypercontractile state stimulates mechanoreceptors that would normally discharge impulses only during stretch.[3] The sudden increase in neural signal to the medulla causes “paradoxic” decline in sympathetic activity that results in bradycardia, hypotension and syncope.[4,5] Spirometric breathing exercises are routine practices after cardiac surgery to improve pulmonary function. In the present case, forceful and repeated blowing while performing spirometry breathing exercises might have caused sudden decrease in venous return to the heart and precipitated vasovagal syncope. Slow and steady breathing exercise can be helpful in preventing such a complication.

Autonomic Modulation

A variety of experimental and clinical reports have engendered a different approach to cardiac arrhythmias as well as other cardiovascular conditions. The focus of a new paradigm is the autonomic nervous system and its important role in various pathological states. From an overall standpoint, this new paradigm can be encompassed by the term “autonomic modulation,” which would include autonomic nerve stimulation or autonomic denervation to modulate the autonomic activity in physiological or pathophysiological functions of the heart as well as other visceral organ systems. Article see p 279 Vaso-vagal syncope is the most common form of neurally mediated syncope.1 The pathophysiology of vaso-vagal syncope is still controversial, but it is thought to be related to prolonged orthostatic stress, which causes increased peripheral venous pooling with a subsequent fall in venous return to the heart. This in turn causes a hypercontractile state, which leads to activation of ventricular mechanoreceptors and a sudden increase in the afferent neural traffic to the brain. The result is sympathetic withdrawal and parasympathetic enhancement that manifests as hypotension (vasodepressor type), bradycardia (cardioinhibitory type), and syncope.1 In other words, vaso-vagal syncope is a disorder caused by an abnormally amplified autonomic reflex involving both sympathetic and parasympathetic components. Over the past 2 decades, β-blockers, α-agonists, mineralocorticoids, selective serotonin reuptake inhibitors, and dual-chamber pacemaker implantation all produced initial promising but later disappointing results.1–3 Vaso-vagal syncope continues to be a vexing clinical arrhythmia. In this issue of Circulation Arrhythmia and Electrophysiology , Yao et al4 reported 10 patients who had drug-refractory, frequent, and highly symptomatic vaso-vagal syncope. Based on the hypothesis that …

Direct and reflex effects of nitroglycerin on the blood volume distribution, evaluated by regional weighing in the cat.

The effects of nitroglycerin on the blood volume distribution were studied with a method of regional weighing in the anaesthetized cat. An i.v. bolus injection of nitroglycerin produced a dose-dependent decrease in arterial pressure accompanying a decrease in the thoracic blood volume. The latter change was associated with blood volume increases principally in the abdomen, and slightly in the hindquarters. Elimination of the cardiovascular reflex effects by carotid sinus denervation and cervical vagotomy signficantly enhanced and prolonged the following changes: the hypotension, the decrease in thoracic blood volume and the volume pooling in the abdomen. The magnitude of increase in hindquarters blood volume was not significantly affected by the denervation procedures, but the duration was much prolonged. The results indicate that the major site of nitroglycerin-induced venous pooling is in the splanchnic circulation. The peripheral venous pooling is produced at the expense of a decrease in the central or pulmonary blood volume. The secondary reflex adjustments tend to minimize the direct effects of nitroglycerin on the blood pressure and blood volume distribution.

Postural Tachycardia Syndrome

When a person stands up, he or she assumes that the body will automatically make any changes necessary to compensate for the increased gravitational stress this change of position brings. Indeed, standing causes gravity to try to pull nearly one quarter of the body’s blood downward toward the lower arms, legs, and abdomen, reducing the amount of blood available to keep the brain supplied with oxygen. To maintain a constant oxygen supply to the brain and upper body, standing is normally accompanied by an automatic increase in heart rate and the force with which the heart contracts and, most important, a tightening of the blood vessels in the lower part of the body. The combination of these 3 actions pushes blood upward against the force of gravity, thereby maintaining an uninterrupted flow of blood to the brain. The aspect of the nervous system that governs these …

Neurocardiogenic Syncope and Related Disorders of Orthostatic Intolerance

Received September 14, 2004; revision received January 31, 2005; accepted March 9, 2005. “We shall not cease from exploration and the end of all our exploring will be to arrive where we started and know the place for the first time” — —T.S. Eliot, Four Quartets Syncope, defined as transient loss of consciousness and postural tone with spontaneous recovery, has both challenged and perplexed physicians since the dawn of recorded time. The earliest written accounts come from Hippocrates, and the word syncope itself is derived from an old Greek term meaning “to cut short” or “interrupt.” Recurrent episodes of syncope may result from a large number of different disorders, all of which cause a transitory reduction in cerebral blood flow sufficient to disturb the normal functions of the brain. Over the last 2 decades, considerable attention has been given to types of syncope that occur due to a centrally mediated (or “reflex”) fall in systemic blood pressure, a condition that has been referred to as vasovagal (and later neurocardiogenic) syncope. However, research into the nature of this disorder revealed that it is but one aspect of a broad and varied group of disturbances in the normal functioning of the autonomic nervous system (ANS), each of which may result in orthostatic intolerance, hypotension, and ultimately syncope. Continued investigations into the nature of these similar yet different disorders has led to the development of a system of classification that attempts to more accurately reflect our understanding of these conditions and their interrelationships.1 The present system of classification has proven both functional and clinically relevant and includes a group of disorders that most investigators have thought to be principally autonomic in nature. Because both the cardiologist and the cardiac electrophysiologist frequently are expected to both diagnose and treat these conditions, the following …

839 Thermoregulatory responses in heart failure

Purpose: During environmental heat exposure in humans blood is dis- tributed to the compliant skin vasculature to facilitate heat loss. This causes peripheral venous pooling, decreases venous return and may com- promise cardiac output. Competition for limited maximal cardiac output therefore exists between the skin, to subserve thermoregulatory demands, and central blood pressure regulation. No previous studies have examined the impact of heating on skin blood flow (SkBF) responses in patients with heart failure (HF).

Haemodynamic response to peripheral venous congestion in patients with unexplained recurrent syncope.

In patients with recurrent unexplained syncope, exaggerated peripheral venous pooling and impaired circulatory adjustment is thought to contribute to the outcome of a head-up tilt (HUT) test. The present study investigated the role of leg volume changes during venous congestion in the haemodynamic response of patients with recurrent unexplained syncope and the ability to predict the outcome of a HUT test. Changes in calf volume (strain gauge plethysmography), heart rate and arterial blood pressure were recorded in 60 patients with history of unexplained syncope (without postural tachycardia symptom) during venous congestion provoked by pneumatic thigh cuffs while supine at rest and during the initial 10 min of a 45 min 70 degrees HUT test. Twenty-seven patients [age (mean+/-S.D.), 39+/-16 years] exhibited symptoms [HUT(+)] and 33 patients (45+/-14 years) were asymptomatic [HUT(-)]. During venous congestion, mean+/-S.E.M. calf volume increased in both groups [HUT(-), 4.5+/-0.2; HUT(+), 4.8+/-0.4 ml x 100 ml(-1), not significant), but significantly less during head-upright tilt [HUT(-), 3.3+/-0.2, P <0.01; HUT(+), 2.6+/-0.3 ml x 100 ml(-1), P <0.001] without differences between the groups. During venous congestion, arterial pressure increased significantly in asymptomatic HUT(-) patients, but not in the HUT(+) patients. Calf volume changes did not correlate with a symptomatic outcome to a 70 degrees HUT. The lack of exaggerated venous pooling during venous congestion and the inability of calf volume changes to predict a positive HUT suggest that excessive venous pooling does not contribute to the outcome of HUT. Attenuated changes in arterial pressure during venous congestion while supine suggest impaired adjustment of peripheral resistance to leg venous occlusion.

RESPONSIVENESS OF THE ABIOCOR™ ARTIFICIAL HEART TO CHANGES IN PATIENT POSTURE

The AbioCor™ completely implantable artificial heart system provides total circulatory support while operating by manual or automatic control. While the AbioCor™ operated in the automatic motor speed and fixed heat rate control modes, the hemodynamic response during changes In posture in the first two patients was measured on 27 occasions during the first three weeks of implantation. Arterial and central venous pressure (AP, CVP) were continuously measured with clinical, fluid-filled catheters left atrial pressure (LAP) was measured with a gravity-insensitive catheter (Millar Instruments). Cardiac output (CO), left and right systolic motor speed (LMS, RMS), and other control parameters were measured simultaneously. The patients had acceptable circulating volume status as indicated by the CVP preceding the change in posture. Patient transition from supine (SUP) to upright-seated (UPS) posture resulted in no reduction in AP (SUP=84±9, UPS = 87±12 mm Hg) and CO (SUP=7.0±0.5, UPS = 7.1±0.4 l/min) while the LAP always dropped (SUP=17±4, UPS=12±4 mm Hg). The motor speed response was variable (LMS:SUP= 6911±273, UPS = 6995±323 RMS: SUP=6925±418, UPS=7071±469). The decrease in LAP is likely due to peripheral venous pooling. CO was maintained at the lower filling pressures due to the active filling properties of the device. These data provide evidence of the adequacy of AbioCor™ pumping and control performance in normovolemic patients with changes in posture. Additional testing during hypovolemic, exercise, and other conditions is needed to confirm the adequacy of the controller.

Factitious anisocoria and orthostatic hypotension

A 30-year-old woman employed by a veterinarian had many episodes of syncope. At presentation, she had anisocoria and premature ventricular beats. Hemodynamic workup revealed only moderate peripheral venous pooling. The circumstances of the fainting spells and eye examination led to the identification of medications which, if taken surreptitiously, will induce the perplexing clinical picture which the patient presented.

Acute hemodynamic effects of molsidomine in patients with ischemic cardiomyopathy

Molsidomine (N-ethoxycarbony l-3-morpholinosy dnonimine) is an antianginal agent that belongs to the class of sydononimines. Experimental [1] and human studies [2,3] suggest that molsidomine reduces preload by its direct action on the venous system, resulting in peripheral venous pooling, and thus in a decreased venous return. This effect leads to increased myocardial perfusion by reducing ventricular wall tension [4]. We studied 20 patients, 18 men and 2 women (age range 32-75, mean 50 years • 8), with symptoms and signs of congestive heart failure. All patients were in New York Heart Association functional classification III-IV, with severe coronary artery disease by coronary angiography (>75% luminal diameter narrowing in at least two major coronary branches). The onset of the heart failure ranged from 9 months to 11 years. Severe left ventricular dysfunction was present in all, with an angiographic ejection fraction of 0.18 mean (range 0.16-0.28). Eight patients had mitral insufficiency, which was angiographically mild to moderate. Informed consent to administer molsidomine and to carry out hemodynamic measurements was obtained from all

Deep venous contribution to hydrostatic blood volume change in the human leg

The causes of orthostatic intolerance following prolonged bed rest, head-down tilt or exposure to zero gravity are not completely understood. One possible contributing mechanism is increased venous compliance and peripheral venous pooling. The present study attempted to determine what proportion of the increased calf volume during progressive venous occlusion is due to deep venous filling. Deep veins in the leg have little sympathetic innervation and scant vascular smooth muscle, so their compliance may be determined primarily by the surrounding skeletal muscle. If deep veins make a large contribution to total leg venous compliance, then disuse-related changes in skeletal muscle mass and tone could increase leg compliance and lead to decreased orthostatic tolerance. The increase in deep venous volume during progressive venous occlusion at the knee was measured in 6 normal subjects using calf cross-sectional images obtained with magnetic resonance imaging. Conventional plethysmography was used simultaneously to give an independent second measurement of leg volume and monitor the time course of the volume changes. Most of the volume change at all occlusion levels (20, 40, 60, 80 and 100 mm Hg) could be attributed to deep venous filling (90.2% at 40 mm Hg and 50.6% at 100 mm Hg). It is concluded that a large fraction of the calf volume change during venous occlusion is attributable to filling of the deep venous spaces. This finding supports theories postulating an important role for physiological mechanisms controlling skeletal muscle tone during orthostatic stress.

Circulatory autoregulation in chronic congestive heart failure: Responses to head-up tilt in 41 patients

To evaluate mechanisms that regulate the response to postural change in patients with chronic congestive heart failure (CHF), the hemodynamic and vasoactive hormonal responses to head-up tilt were examined in 41 patients. Peripheral venous pooling was present in only 18 patients and was inversely correlated with baseline pulmonary wedge pressure. Baseline supine hemodynamic indexes of these 18 patients indicated less severe CHF compared with those of the 23 patients who did not demonstrate venous pooling. The 18 patients with intact afferent pooling also had lower levels of plasma renin activity and demonstrated increases in both plasma renin activity and norepinephrine on tilt; these reflex increases in vasoactive hormones were not seen in the 23 patients with severe CHF. Overall, 3 patterns could be identified. Of the 18 patients with venous pooling, 12 maintained many of the elements of normal postural response, with increases in systemic vascular resistance and circulating norepinephrine that maintain blood pressure constant. Six patients did not increase resistance in response to peripheral venous pooling and had major decreases in blood pressure analogous to idiopathic orthostatic hypotension. The larger group of 23 patients with more severe CHF did not have peripheral venous pooling and, hence, no afferent stimulus for reflex changes. Thus, the hemodynamic and neurohormonal responses to head-up tilt in CHF are heterogeneous and may be influenced by the severity of disease. The abnormalities of response may reflect the progression of vascular adaptation with loss of myocardial pump function and are important in terms of the pathophysiology and treatment of chronic heart failure.

Vasodilators: minoxidil and drugs used in peripheral vascular and cerebral disorders.

Vasodilator drugs relax vascular smooth muscle, either directly or indirectly through adrenergic neurones. Different vasodilators may act principally on arteries, principally on veins, or on both arteries and veins. Dilatation of arterioles reduces peripheral vascular resistance and hence lowers arterial blood pressure. Dilatation of veins increases peripheral venous pooling of blood, reducing venous return to the heart and tending to lower cardiac output and arterial blood pressure. Reflex sympathetic tachy? cardia tends to restore cardiac output and blood pressure. There is sound rationale and proof of efficacy for using vasodilators in three disorders?hypertension, angina, and heart failure. In hypertension blood pressure is lowered by reducing peripheral vascular resistance. In angina the reductions in venous return (reducing preload) and arterial blood pressure (reducing afterload) reduce the workload of the left ventricular myo? cardium and hence reduce its requirement for oxygen. In heart failure reduction of the workload of the ventricles improves their performance. Of the newer vasodilators, prazosin, calcium antagonists, and captopril are covered in separate articles in this series. Minoxidil, reviewed here, is a recently introduced arterial vasodilator for treating severe hypertension. Although the effi? cacy of vasodilators in peripheral and cerebral vascular disease has not been proved, new drugs continue to be marketed and these are considered later in this article.

Action of Nitroglycerin and Amyl Nitrite in Labile and Essential Hypertension

Seventeen patients with labile hypertension received nitroglycerin and 18 received amyl nitrite. Twelve patients with established essential hypertension received nitroglycerin and 12 received amyl nitrite. Nitroglycerin reduced the systolic and mean arterial pressures and cardiac output in both groups, but had no effect on diastolic pressure and total peripheral resistance. Amyl nitrite decreased systolic, diastolic, and mean arterial pressures and peripheral vascular resistance and increased heart rate and cardiac output in labile hypertensives. In established hypertensive patients, amyl nitrite decreased systolic, diastolic, and mean arterial pressures and cardiac output, and had little effect on peripheral vascular resistance. Nitroglycerin reduced arterial pressure in labile and established hypertensives through venodilation and peripheral venous pooling. Amyl nitrite and effects similar to nitroglycerin in established hypertensives; in labile hypertensives it reduced arterial pressure through arterial dilation and a decrease in peripheral vascular resistance.

Comparison of chronic and acute effects of morphine sulfate on cardiovascular function

Circulatory effects of morphine sulfate on supine anesthetized dogs were investigated to define acute and chronic effects of this drug upon cardiovascular function. Right atrial injection of morphine produced a sustained fall of systemic pressure, cardiac output and heart rate without a significant change in systemic resistance. The mechanism of its efficacy in treatment of acute pulmonary edema may be due to two major factors: (1) peripheral venous pooling of blood resulting in pulmonary decongestion which appears to be a short-lasting effect, and (2) a sustained decrease in left ventricular minute work with no apparent change in myocardial contractility, as demonstrated in this study.N-allylnormorphine abolished the morphineinduced bradycardia but not the reduced cardiac output and systemic pressure.

Orthostatic hypotension. Observations on the effect of levarterenol and hypertensin II.

Bradbury and Eggleston 1 first recognized hypotension as a clinical entity in 1925. However, it continues to be relatively uncommon, since only about 100 cases have been published to date. The term orthostatic (or postural) hypotension has been used in the broadest sense for any excessive fall in blood pressure on assuming the erect position. This syndrome falls into 2 major groups based on clinical and pathogenetic characteristics. The first group comprises those cases in which there is an excessive fall of the systolic pressure and a rise, or no significant fall, of the diastolic pressure. The pulse rate generally rises. On maintaining the erect posture, syncope usually occurs with a sudden fall of both systolic and diastolic pressure, preceded by pallor and vagotonic effects such as sweating, nausea, and a sudden bradycardia. The defect in this group is inadequate cardiac venous return secondary to excessive peripheral venous pooling.

Peripheral venous pooling and left atrial pressure pulse in mitral disease.

Peripheral venous pooling and left atrial pressure pulse in mitral disease.

Pulmonary blood volume determined by a radioactive tracer technique

A semiquantitative technique for assaying shifts in intrapulmonary blood volume is described. The method consists of the external monitoring of radioactivity over the anterior thorax after the intravenous administration of radioactive iodinated albumin utilizing a sensitive scintillation counter with a focusing collimator attachment. While this method does not yield the quantitative data of the indicator dilution and body plethysmographic techniques, it offers the advantage of confining observations to the intrapulmonary rather than the intrathoracic blood volume. Employing this technique, the effects of the upright posture, peripheral venous pooling and the Valsalva maneuver have been studied. A fall in estimated pulmonary blood volume was noted with each procedure, averaging 28%, 9% and 11%, respectively, below control levels. Submitted on January 16, 1959