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PubMed1986

Differential effects of lower body negative pressure on forearm and calf blood flow.

Modest degrees of lower body negative pressure (less than 20 mmHg) cause a reflex constriction of forearm resistance vessels attributable to a decrease in activity of cardiopulmonary mechanoreceptors. In the present study, we sought to determine whether the calf vessels respond similarly. Left forearm and right calf blood flows were measured simultaneously by strain-gauge plethysmography in 10 healthy volunteers. Forearm flows decreased significantly from control during negative pressures of 10, 15, or 20 mmHg, whereas calf flows did not decrease significantly until 20 mmHg; at 10, 15, and 20 mmHg, decreases in forearm flow were significantly greater than those of the calf. Similar results were obtained in a second series of experiments in which venous pooling in the right leg during lower body negative pressure was prevented by enclosing it in a boot. At 40 mmHg, or after a Valsalva maneuver, both forearm and calf vessels constricted markedly and to the same degree. It appears that the reflex reduction in blood flow to the skeletal muscles of the limbs resulting from deactivation of the low-pressure intrathoracic mechanoreceptors is directed primarily to the arm.

Adult↗

PubMed1987

Fluid shifts and endocrine responses during lower body negative pressure and dynamic arm exercise.

The use of lower body negative pressure (LBNP) is proposed as a means of reducing the effect of spaceflight on body water loss by stimulation of renin angiotensin aldosterone system (RAAS) activity. Seven subjects were successively submitted to LBNP exposure, arm cranking physical exercise, and to a combination of both procedures (LBNP + arm cranking) in order to check whether this combination enhances RAAS activity. The results showed that exposure to 40 min of LBNP to a level of -40 mm Hg was a more potent stimulus for renin secretion than submaximal and maximal arm cranking. The combination of LBNP with exercise does not further enhance the RAAS activity induced by LBNP alone. These data suggest that the fluid shift toward the lower body induced by LBNP counteracts triggering of renin secretion due to physical exercise.

Adult↗

PubMed1995

Quantification of tolerance to lower body negative pressure in a healthy population.

Subtolerance and presyncopal lower body negative pressure (LBNP) has been used extensively to investigate the effect of various forms of exercise training on central hypovolemic tolerance. However, there are no population data concerning LBNP tolerance, and the validity of common LBNP tolerance indices has not been investigated. LBNP tolerance data from 86 males and 33 females were analyzed. All LBNP exposures were terminated with the onset of presyncopal signs and/or symptoms. LBNP tolerance was quantified using duration of exposure (DNP), maximal negative pressure tolerated (MNP, cumulative stress index (CSI), and the LBNP tolerance index (LTI). Average (+/- SD) LBNP tolerance was 22.12 +/- 5.01 min (DNP), -77 +/- 16 mm Hg (MNP), 975 +/- 402 mm Hg.min-1 (CSI), or 222 +/- 50 mm Hg.min-1 (LTI). All cardiovascular parameters exhibited the same responses as have been documented in the literature. While DNP, MNP, and LTI were normally distributed, CSI in this population was not normally distributed. Age, weight, height, gender, and VO2peak were not associated with LBNP tolerance. Compared to this population, it appears that the subjects that have participated in previous LBNP tolerance studies have had abnormally high LBNP tolerances and that the LTI is the most valid index of LBNP tolerance. Furthermore, in this population LBNP tolerance could not be predicted from physical characteristics.

Adult↗

PubMed1992

Carotid arterial haemodynamics after mild degrees of lower-body negative pressure in man.

1. Pulsatile changes in the diameter of the common carotid artery were studied transcutaneously using an echo-tracking technique in 15 normal subjects: eight subjects before and during application of graded lower-body negative pressure from -5 to -15 mmHg, and seven subjects before and during weight-bearing head-up tilt at 30 and 60 degrees. 2. In concomitant studies of changes in forearm vascular resistance, it was seen that mild lower-body negative pressure produced deactivation of cardiopulmonary receptors without changes in systemic blood pressure or heart rate. 3. After lower-body negative pressure, a significant decrease in carotid arterial diastolic diameter [from 0.662 +/- 0.028 to 0.624 +/- 0.033 cm (lower-body negative pressure -10 mmHg) and 0.640 +/- 0.030 cm lower-body negative pressure -15 mmHg), P < 0.001 and < 0.05] was observed. 4. After head-up tilt, carotid arterial diameter was also significantly decreased at 30 and 60 degrees, whereas a significant increase in heart rate occurred only at 60 degrees and mean blood pressure did not change. 5. The study provides evidence that the geometry of the arterial wall is substantially modified by non-invasive manoeuvres such as head-up tilting and lower-body negative pressure. The latter is assumed to selectively deactivate human cardiopulmonary receptors, but the present data suggest that local changes may also influence carotid baroreceptors.

Adult↗

PubMed2004

Lower body negative pressure as a model to study progression to acute hemorrhagic shock in humans.

Hemorrhage is a leading cause of death in both civilian and battlefield trauma. Survival rates increase when victims requiring immediate intervention are correctly identified in a mass-casualty situation, but methods of prioritizing casualties based on current triage algorithms are severely limited. Development of effective procedures to predict the magnitude of hemorrhage and the likelihood for progression to hemorrhagic shock must necessarily be based on carefully controlled human experimentation, but controlled study of severe hemorrhage in humans is not possible. It may be possible to simulate hemorrhage, as many of the physiological compensations to acute hemorrhage can be mimicked in the laboratory by applying negative pressure to the lower extremities. Lower body negative pressure (LBNP) sequesters blood from the thorax into dependent regions of the pelvis and legs, effectively decreasing central blood volume in a similar fashion as acute hemorrhage. In this review, we compare physiological responses to hemorrhage and LBNP with particular emphasis on cardiovascular compensations that both share in common. Through evaluation of animal and human data, we present evidence that supports the hypothesis that LBNP, and resulting volume sequestration, is an effective technique to study physiological responses and mechanisms associated with acute hemorrhage in humans. Such experiments could lead to clinical algorithms that identify bleeding victims who will likely progress to hemorrhagic shock and require lifesaving intervention(s).

Acute Disease↗

PubMed1985

Effects of diltiazem on hormonal and hemodynamic responses to lower body negative pressure and tilt in patients with mild to moderate systemic hypertension.

Mean arterial blood pressure, forearm vascular resistance, plasma norepinephrine, plasma renin activity and aldosterone responses to graded lower body negative pressure and tilt at 80 degrees were examined in 10 men with mild to moderate essential hypertension before and after 12 weeks of diltiazem (240 to 360 mg/day) therapy. Diltiazem therapy lowered basal supine systolic and diastolic blood pressures without affecting basal heart rate. Mean arterial blood pressure and forearm vascular resistance were decreased from 114 +/- 1.5 to 105 +/- 1 mm Hg, p less than 0.01 and from 29.3 +/- 3.5 to 18.9 +/- 2.1 units, p less than 0.01, respectively. Diltiazem therapy had no effect on basal supine levels of norepinephrine, plasma renin activity or aldosterone, nor on the responses of these hormones to lower body negative pressure. Diltiazem did decrease the forearm vascular resistance responses to lower body negative pressure and tilt. Diltiazem abolished an orthostatic increase (10 +/- 0.3 mm Hg) in mean arterial blood pressure and this was associated with a greater plasma norepinephrine response to tilt. These results suggest that diltiazem decreases vascular resistance through a reduction in the postjunctional effects of norepinephrine on vascular smooth muscle.

Adult↗

PubMed1997

[Preliminary study on method for predicting lower body negative pressure tolerance].

To find out a method to predict lower body negative pressure (LBNP) tolerance with noninvasive physiological measurements, 11 healthy young subjects were tested in an LBNP chamber in sitting position. Incremental negative pressure was used for evaluating LBNP tolerance time. End points of the test were onset of presyncopal symptoms or completion of 15 min test. According to their reactions, the 11 subjects were divided into good tolerance group (group A, n = 5) and poor tolerance group (group B, n = 6); At the 11th minute of LBNP, mean arterial pressure (MAP), magnitude of decrease of regional cerebral oxygen saturation (delta SrO2) and cardiac output (delta CO) showed significant difference between group A and B(P <0.05); Mean error was 0.54 +/- 0.42 min when LBNP tolerance was predicted using MAP and delta SrO2 at this moment by regression analysis.

Aerospace Medicine↗

PubMed1990

Atrial natriuretic factor attenuates sympathetic reflexes during lower body negative pressure in normal men.

To assess further the effects of atrial natriuretic factor on autonomic nervous system reflexes in normal humans, the hemodynamic and neurohormonal responses to lower body negative pressure were measured at control and during infusions of atrial natriuretic factor and nitroglycerin in nine normal male subjects. The control -20 mm Hg lower body negative pressure was characterized by significant reductions in right atrial and pulmonary wedge pressures, as well as stroke volume and cardiac output. This was associated with a reflex increase in forearm vascular resistance and plasma norepinephrine. During the infusion of atrial natriuretic factor, the same -20 mm Hg lower body negative pressure produced a larger decrease in mean arterial pressure of 7.9 +/- 3.9 mm Hg (p less than 0.05), as well as a larger decrease in stroke volume (41.3 +/- 4.2 ml/beat) and cardiac output (2.0 +/- 0.3 L/min). Atrial natriuretic factor infusion did not affect the increase in forearm vascular resistance during lower body negative pressure, but did attenuate the increase in plasma norepinephrine. To control for nonspecific vasodilator actions, lower body negative pressure was also repeated during nitroglycerin infusion. Nitroglycerin infusion did not significantly change the responses of blood pressure, cardiac output, stroke volume, forearm vascular resistance, or plasma norepinephrine during lower body negative pressure. Thus, these data demonstrate that atrial natriuretic factor infusion can attenuate sympathetic nervous system reflexes evoked during lower body negative pressure. These inhibitory effects on the sympathetic nervous system may contribute to many of the observed hemodynamic actions of atrial natriuretic factor.

Aged↗

PubMed1994

Exercise against lower body negative pressure as a countermeasure for cardiovascular and musculoskeletal deconditioning.

Exposure to lower body negative pressure (LBNP) with oral salt and water ingestion has been tested by astronauts as a countermeasure to prevent postflight orthostatic intolerance. Exercise is another countermeasure that astronauts commonly use during spaceflight to maintain musculoskeletal strength. We hypothesize that a novel combination of exercise and simultaneous exposure to lower body negative pressure during spaceflight will produce Earth-like musculoskeletal loads as well as cardiovascular stimuli to maintain adaptation to Earth's gravity. Results from recent studies indicate that leg exercise within a LBNP chamber against the suction force of 100 mmHg LBNP in horizontal-supine posture produces an equivalent, if not greater exercise stress compared to similar leg exercise in upright posture (without LBNP) against Earth's gravity. Therefore, the concept of LBNP combined with exercise may prove to be a low cost and low mass technique to stress the cardiovascular and the musculoskeletal systems simultaneously.

Adult↗

PubMed1993

Effects of lower-body negative pressure on blood flow with applications to the human cardiovascular system.

The paper reports a theoretical investigation into the effects of lower-body negative pressure on blood flow through the human cardiovascular system. The human cardiovascular system is modelled as a closed network of arteries, arterioles, capillaries, venules and veins of different lengths and cross-sections. The pumping action is provided by the contraction of the ventricles. The model has been analysed using the finite-element method. The pertinent equations incorporating the effects of lower-body negative pressure for the pressures and flow velocities have been derived, and the quantitative results have been computed. Percentage changes in flow velocities, pressure drops and conductances under the application of lower-body negative pressure in the various segments and organs of the entire cardiovascular system are obtained. The lower-body negative pressure has no effect on the flow rates in carotid, ulnar and coronary arteries, nor on the supply of blood to the upper extremities, kidneys, spleen and liver. The major effects are found in the lower extremities.

Blood Vessels↗

PubMed2001

Doppler measurement of cerebral and lower limb flow during a lower body negative pressure test for predicting orthostatic intolerance.

OBJECTIVE: To quantify the cardiovascular response to an orthostatic test for predicting orthostatic intolerance. METHODS: Cerebral and lower limb arterial flow and resistance were assessed by Doppler ultrasonography during lower body negative pressure (7 minutes each at -25 and -45 mm Hg). Cardiovascular deconditioning was induced by 42 days in head-down tilt at -6 degress (7 subjects) and 6-month spaceflights (10 cosmonauts). RESULTS: Orthostatic intolerance during a stand test was observed in 57% of the head-down-tilt subjects and 83% of the cosmonauts. At the lower body negative pressure after head-down tilt and during or after flight, the average cerebral flow velocity and vascular resistance did not change significantly from before head-down tilt and before flight. Conversely, there was a lack of lower limb arterial vasoconstriction (-24% from before head-down tilt and -43% from before flight; P < .01), and the cerebral-femoral flow ratio increased less (-27% from before head-down tilt and -52% from before flight; P < .01). The lack of vasoconstriction was more pronounced in intolerant subjects (-25% from before head-down tilt and -48% from before flight) compared with tolerant subjects (-22% from before head-down tilt and -14% from before flight; P > .01). Also, the lack of a cerebral-femoral flow ratio increase was more pronounced in intolerant subjects (-49% from before head-down tilt and -55% from before flight; P < .01) than in tolerant subjects (-1% from before head-down tilt and -33% from before flight; P < .01). The cerebral flow deficit at the lower body negative pressure before head-down tilt was greater than 8% in 3 of the 4 intolerant head-down-tilt subjects and less than 8% in the 3 tolerant subjects. The 3 cosmonauts who were intolerant after flight had a preflight cerebral flow deficit greater than 8%, whereas the tolerant cosmonaut had a cerebral flow deficit less than 8%. CONCLUSION: Lack of lower limb vasoconstriction and a lower cerebral-femoral flow ratio during lower body negative pressure in disadapted subjects were associated with orthostatic intolerance. A cerebral flow deficit during lower body negative pressure before disadaptation allowed measurement of the predisposition of the subjects to become intolerant.

Blood Pressure↗

PubMed1980

Circulation and respiration response to arm exercise and lower body negative pressure.

The effects of supine arm exercise and lower body negative pressure (LBNP) were studied in six subjects with 10 min of LBNP at -40 mmHg (L), arm cranking for 8 min at a work load of 225 kpm/min (E) and both combined (L + E) preceded by 2 min of LBNP. Initial responses of ventilation (VI) and VO2 were curtailed and heart rate was significantly higher after the first min of L + E than E, reflecting the less accessible venous reservoir and reduced stroke volume due to L. Leg volume was significantly reduced after 30 s of E and continued to decline and remained below baseline during 6 min of recovery. With L + E, leg volume remained constant after E began, indicating both a shift of blood from legs to arms and reduced extra-vasation with LBNP. End-tidal PO2, VI and VI/VO2 were higher and PCO2 lower during the latter stages of L + E than during E, indicating less effective lung perfusion and greater alveolar deadspace caused by LBNP. The release of pooled blood from the lower body after L + E caused a greater VI, VO2 and lower RE than after E and produced marked transients in PCO2 and PO2, thereby slowing the recovery of gas exchange.

Adult↗

PubMed2003

Design of a chamber for lower body negative pressure with controlled onset rate.

We have designed a lower body negative pressure (LBNP) chamber and control system that makes it possible to apply LBNP either very rapidly (< 300 ms), or more gradually, according to predefined protocols. The capability of the new, high-performance agile aircraft to reach a high-G onset rate makes it highly desirable to be able to study immediate, rapid, and transient cardiovascular responses to simulated gravitational stress. Our new LBNP chamber has been used to study the main cardiovascular variables during onset and release of mild LBNP (-20 mmHg). We have revealed large transient physiological responses during the onset and release of mild LBNP. This new finding was largely made possible by precise control of the onset and release of LBNP during the experiments. The purpose of this paper is therefore to describe some of the technical solutions which made rapid and controlled changes in LBNP possible, focusing on the importance of precise control of the LBNP chamber.

Atmosphere Exposure Chambers↗

PubMed1992

Subcutaneous and skeletal muscle vascular responses in human limbs to lower body negative pressure.

Cardiopulmonary baroreceptor unloading in humans comparably increases sympathetic discharge to skeletal muscle in the forearm and calf, but blood flow studies have disclosed differential rather than uniform vasomotor responses in the extremities. The aim of the present study was to address the issue of differential effects of orthostatic stress on forearm and calf vascular adjustment and to extend previous studies by determining changes in vascular responses separately in various vascular beds of the limbs. The local [133Xenon] washout method was used for recording blood flow rates in subcutaneous tissue and skeletal muscle. Simultaneous recordings from the forearm and calf were performed in 11 healthy young males during lower body negative pressure at -10 mmHg. Heart rate, arterial mean and pulse pressures did not change during lower body negative pressure. In the forearm blood flow rates decreased significantly, in subcutaneous tissue by 16 +/- 2% (mean +/- SEM) and in skeletal muscle by 16 +/- 1%. In the calf lower body negative pressure induced a significant decrease in blood flow rates of 17 +/- 3% in subcutaneous tissue and of 30 +/- 2% in skeletal muscle. This vasoconstriction in calf skeletal muscle was consistently disclosed in both legs and was about the same magnitude in each calf when studied with the one leg exposed to lower body negative pressure and the other outside the lower body negative pressure chamber. These findings suggest that during unloading of cardiopulmonary afferents, reflex sympathetic activation as an important autonomic adjustment to orthostatic stress is accompanied by uniform vasoconstriction in subcutaneous and skeletal muscle vascular beds of human limbs.

Adult↗

PubMed2003

Regulation of arterial blood pressure in humans during isometric muscle contraction and lower body negative pressure.

Previous studies have shown that the blood pressure response to isometric handgrip remains unchanged during reductions in preload induced by lower body negative pressure (LBNP). The purpose of the present study was to assess the beat-by-beat haemodynamic mechanisms allowing for precise control of mean arterial pressure (MAP). We have followed the cardiovascular variables involved in the regulation of MAP during isometric handgrip with and without additional application of LBNP during defined periods of the ongoing contraction. Sixteen subjects participated. Mean arterial blood pressure (MAP), heart rate (HR), stroke volume (SV), cardiac output (CO), blood flow velocity in the brachial artery, acral skin blood flow, as well as total (TPR) and local (LPR) peripheral resistance were continuously recorded/calculated before, during and after 2 min of handgrip both with and without concomitant LBNP. The main finding was that MAP increased at the same rate and to the same absolute level whether or not LBNP was applied. A uniform increase in MAP was observed even though the cardiovascular variables evolved differently in the periods with and without LBNP. At the onset of LBNP at -20 mmHg, there was a transient drop in MAP and a transient increase in HR, but within seconds, MAP was regulated back to the slope caused by the isometric handgrip proper. CO and SV, which were declining gradually, showed an additional marked but gradual reduction upon LBNP application. At the same time, both LPR and TPR increased markedly and continuously. In summary, the increase in MAP during isometric handgrip remained essentially unchanged by LBNP-induced alterations in preload. The increase in MAP was caused by a marked increase in peripheral resistance. This supports the concept of a central set point, continuously regulated upwards as long as the isometric handgrip persists. Furthermore, it reveals a considerable flexibility in the cardiovascular control mechanisms used to achieve the desired arterial pressure.

Adaptation, Physiological↗

PubMed1993

Arterial pulse pressure and vasopressin release in humans during lower body negative pressure.

The hypothesis was tested that narrowing of arterial pulse pressure (PP) is a determinant of arginine vasopressin (AVP) release in humans. Six normal males completed a two-step lower body negative pressure (LBNP) protocol of -20 and -50 mmHg, respectively, for 10 min each. None of these subjects experienced presyncopal symptoms. Arterial plasma AVP and plasma renin activity (PRA) (at 2-min intervals) only increased subsequent to a decrease in PP (invasive brachial arterial measurements) and stroke volume (ultrasound Doppler technique, n = 4). Simultaneously, mean arterial pressure did not change. A selective decrease in central venous pressure and left atrial diameter (echocardiography, n = 4) at LBNP of -20 mmHg did not affect AVP or PRA, whereas arterial plasma norepinephrine increased (n = 4). During LBNP, significant (P < 0.05) intraindividual linear correlations were observed between log(AVP) and PP in four of the subjects with r values from -0.75 to -0.99 and between log(PRA) and PP in all six subjects with r values from -0.89 to -0.98. In conclusion, these results are in compliance with the hypothesis that narrowing of PP in humans during central hypovolemia is a determinant of AVP and renin release.

Adult↗

PubMed2006

Renal stone risk in a simulated microgravity environment: impact of treadmill exercise with lower body negative pressure.

PURPOSE: Prolonged exposure to microgravity during spaceflight causes metabolic changes that increase the risk of renal stone formation. Studies during the Gemini, Apollo, Skylab and Shuttle missions demonstrated alterations in renal function, fluid homeostasis and bone resorption that result in increased urinary supersaturation of calcium oxalate, brushite, sodium urate and uric acid. Developing countermeasures to increased urinary supersaturation is an important priority as the duration of space missions increases. MATERIALS AND METHODS: A total of 11 sets of identical twins remained on 6-degree head down, tilt bed rest for 30 days to simulate prolonged microgravity. One twin per pair was randomly selected to exercise while supine in a lower body negative pressure chamber 6 days weekly for 40 minutes, followed by 5 minutes of resting lower body negative pressure at 50 mm Hg. The other twin served as a nonexercise control. Pressure in the exercise lower body negative pressure chamber (52 to 63 mm Hg) was adjusted to produce footward forces equivalent to those for upright running on Earth at 1.0 to 1.2 x body weight. Pre-bed rest urinary stone risk profiles were done elsewhere after 5 days of a standardized diet, consisting of 170 mEq sodium, 1,000 mg calcium, 0.8 gm/kg animal protein and 2,500 kcal, and then throughout the bed rest and recovery phases of the protocol. RESULTS: A significant increase in urinary calcium after just 1 week of bed rest was noted in the nonexercise control group (p = 0.001). However, no such increase was noted in the exercise group. Brushite supersaturation increased significantly from bed rest in each group, although the increase was significantly higher in the nonexercise control group than in the exercise group (p = 0.006). Calcium oxalate supersaturation increased during bed rest in the exercise group (p = 0.004). It trended toward a higher level in the nonexercise control group, although this did not achieve significance (p = 0.055) Mean urine volume +/- SD was significantly higher in the nonexercise control group than in the exercise group at bed rest week 2 and at week 3 (2.01 +/- 0.21 vs 1.63 0.18 l and 2.03 +/- 0.22 vs 1.81 +/- 0.20, respectively). Urinary pH was significantly higher in the nonexercise control group than in the exercise group at week 1 and week 3 (6.62 +/- 0.7 vs 6.49 +/- 0.5 and 6.58 +/- 0.6 vs 6.49 +/- 0.8, respectively, p = 0.01). CONCLUSIONS: Bed rest significantly alters the urinary environment to favor calculous formation. Lower body negative pressure chamber treadmill exercise offers some protection against increases in stone risk during simulated microgravity, particularly with regard to the risks of hypercalciuria and brushite stone formation. The use of lower body negative pressure to augment aerobic exercise in space may decrease the risk of stone formation in astronauts. Adjunct measures, including aggressive hydration and alkalinization therapy, should be considered.

Adult↗

PubMed2000

Gender differences in tolerance to lower body negative pressure.

BACKGROUND: Previous studies suggest that women have lower tolerance than men do to lower body negative pressure (LBNP). The mechanism(s) responsible has not been determined. HYPOTHESES: Women would be less tolerant to presyncopal LBNP than men as determined by several indices of LBNP tolerance. Additionally, men and women, regardless of LBNP tolerance, would have similar cardiovascular responses to LBNP as presyncope was reached. METHODS: The subjects were 18 men and 18 women (average age 25) of similar fitness levels who volunteered for the study. A step-wise LBNP protocol to presyncope was employed. HR, stroke volume (SV), cardiac output (Q), BP, and systemic vascular resistance (SVR) were measured before and throughout the LBNP stress. Data from women were compared with those from all men, and to men with similar and higher LBNP tolerance. RESULTS: Women had significantly less LBNP tolerance than men regardless of index used: 30% less by duration of LBNP, 21% less by maximal LBNP tolerated, 44% less by a cumulative stress index, and 27% less by a linear tolerance index. Cardiovascular responses to LBNP were similar for women and men as presyncope was approached, whether the men were low-tolerant (LT) or high-tolerant (HT). In the 2 min pre-presyncope, HR increased by 80 +/- 6% in women, 72 +/- 7% in LT men and 96 +/- 14% in HT men; Q decreased by 47 +/- 3% in women, 52 +/- 6% in LT men and 55 +/- 2% in HT men. Similar comparisons occurred for the decline in BP and the rise in SVR. CONCLUSION: Women have lower LBNP tolerance than do men, although there is considerable gender overlap in tolerances. The cardiovascular response to LBNP is similar regardless of gender or tolerance level as presyncope is approached. Understanding the gender differences in LBNP tolerance may lie in determining how the LBNP stress is translated into a "trigger" for cardiovascular decompensation.

Adult↗