Effectiveness of Congesting Cuffs("Rotating Tourniquets")

in Patients with Left Heart FailureBy PHILIP A. HABAK, M. D., ALLYN L. MARK, M. D., J. MICHAEL KioSCHOS, M.D.,

DONALD R. MCRAVEN, M.D., AND FRANCOIS M. ABBOUD, M.D.

SUMMARYCongesting cuffs or "rotating tourniquets' are often used to treat patients with acute pulmonary edema

secondary to left heart failure. The purpose of this study was to evaluate the effectiveness of congesting cuffsin pooling blood in the extremities and decreasing pulmonary congesting pressures in patients with leftheart failure and to define optimal congesting cuff pressures. Congesting cuffs on three extremities were in-flated to 20, 40, 60 and 80 mm Hg in 16 patients with left heart failure and in 7 normal subjects. The ex-tremities were elevated to collapse the veins before inflating the cuffs. The amount of venous pooling was

measured with mercury-in-silastic strain gauge plethysmographs. Inflation of the cuffs producedsignificantly less venous pooling in patients with heart failure than in normal subjects. Decreases in rightatrial pressure during inflation of the cuffs were also significantly less in the patients with heart failure thanin the normal subjects. In patients with heart failure, pulmonary congesting pressure (left ventriculardiastolic pressure or mean pulmonary arterial wedge pressure) averaged 24.2 + 1.5 (SE) mm Hg in thecontrol period and 24.6 2.2, 22.9 ± 1.9, 23.2 ± 2.1 and 20.3 ± 1.6 mm Hg during inflation of the cuffs at20, 40, 60 and 80 mm Hg, respectively. The decreases in pulmonary congesting pressure (PCP) were notsignificant (P> 0.05) at cuff pressures of 20, 40 and 60 mm Hg. Decreases in PCP were statistically signifi-cant at a cuff pressure of 80 mm Hg, but only 6 of 16 patients had decreases greater than 4 mm Hg. Theresults suggest that in patients with heart failure the effectiveness of congesting cuffs is limited by decreasesin venous distensibility which are characteristic of heart failure.

Additional Indexing Words:PlethysmographyPulmonary arterial wedge pressureCapillary filtration coefficient

Venous distensibility Right atrial pressureLeft ventricular end diastolic pressure

CONGESTING CUFFS are frequently used inthe treatment of patients with pulmonary edema

resulting from left heart failure in order to pool bloodin the veins and decrease venous return andpulmonary congestion. Despite the fact that this formof treatment has been used for many years" 2 there hasbeen no systematic study either of its effectiveness indecreasing pulmonary congesting pressures inpatients with heart failure or of the optimal con-

From the Cardiovascular Division, Department of InternalMedicine, University of Iowa College of Medicine and the VeteransAdministration Hospital, Iowa City, Iowa.

Supported by a Clinical Investigatorship from the Veterans Ad-ministration and by Program Project Grant HL-14388, TrainingGrant HL-5729, and Research Grants IIL-2644 and HL-16149 fromthe National Heart and Lung Institute.

Dr. McRaven's current address is St. Francis Hospital, Peoria,Illinlois.

Address for reprints: Allyn L. Mark, M.D., Cardiovascular Divi-siorn, Department of Internal Medicine, University of Iowa Collegeof Medicine, Iowa Citv, Iowa 32242.

Received Februarv 1, 1974; revision accepted for publicationApril 19, 1974.

366

gesting pressures. Ebert and Stead3 demonstrated that580-980 ml of blood may be impounded in three ex-tremities when congesting cuffs are inflated todiastolic pressure in normal subjects, but these in-vestigators did not study patients with heart failure orevaluate effectiveness of lower congesting pressures.

There are several reasons why patients with heartfailure might respond differently from normal subjectsto congesting cuffs. Wood4 has demonstrated that thesystemic veins of patients with congestive heart failureare less distensible than normal. This suggests thatcongesting cuffs might be less effective in poolingblood in the veins and decreasing venous return andpulmonary congestion in these patients. On the otherhand, pulmonary vascular pressure-volume curves arethought to be steep in patients with heart failure, sothat small changes in pulmonary blood volume resultin large changes in pulmonary congesting pressure.5This suggests that even small amounts of pooling anddecreases in venous return might be associated withlarge decreases in pulmonary congesting pressures.The systemic veins are more distensible at low dis-

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CONGESTING CUFFS IN LEFT HEART FAILURE

tending pressures than at high pressures.6 Conse-quently, lower congesting pressures might pool almostas much blood as higher pressures without some of theundesirable effects which might result from the latter.For example, hypotension has been reported duringapplication of high congesting pressures.7 High con-

gesting pressures also may produce excessive capillaryfiltration8 and, thereby, increase blood viscosity andvascular resistance. These considerations suggest thatlower congesting pressures, if effective in decreasingpulmonary congesting pressure, might be more

desirable than high pressures in the treatment ofpatients with pulmonary edema.The purpose of the study was, therefore, to evaluate

the effectiveness of congesting cuffs in patients withleft heart failure and to define optimal congesting cuffpressures. We compared responses to lower con-

gesting cuff pressures (20 and 40 mm Hg) withresponses to higher pressures (60 and 80 mm Hg) innormal subjects and in patients with left heart failure.

MethodsFourteen patients were studied during diagnostic cardiac

catheterization. Two other patients were studied in the cor-

onary care unit. The diagnoses and some of thehemodynamic data on these patients are shown in table 1.All sixteen patients had evidence of left ventricular failurebased on a recent history of orthopnea and paroxysmal noc-

turnal dyspnea and elevated left ventricular end diastolic or

mean pulmonary arterial wedge pressure (> 15 mm Hg). Allbut one had large left ventricular end diastolic volumes(> 110 ml/m2 BSA), and all but two had ejection fractionsless than 50%. In four of the patients studied in thecatheterization laboratory and one of the patients (KM)studied in the coronary care unit, the onset of cardiacdecompensation was recent. None of the patients had pit-ting edema. The majority of the patients were takingdigitalis and diuretics, and no change in therapy was madefor the study.The patients were studied in the supine position with

both legs and the left forearm elevated 15 cm above thelevel of the right atrium to collapse the veins. The ambienttemperature was 24°C. Sphygmomanometer cuffs, 13 cm

wide for the arm and 20 cm wide for the thighs, were used as

congesting cuffs. The cuffs were fitted around the left arm

and both thighs close to the trunk and taped to facilitatetransmission of pressure in the cuff to the extremity. A cuffpressure of 5-7 mm Hg was necessary to initiate venous con-

gestion and increases in limb volunme. This pressure, whichhas previously been referred to as ---cuff zero,"6 was taken as

the zero level for subsequent inflation to 20, 40, 60 and 80mm Hg. The increase in volume of the forearm (15 patients)

able 1

Diagnosis and Hemodynamic Data on Patients with Heart Failure

MRAP PCP LVEDV LVSEFPatient Diagnosis (mm Hg) (mm Hg) (mi/M2) (%)

SM Cardiomyopathy 6 15 161 26CA Aortic stenosis 7 24 15.5 12WS Cardiomyopathy 2 21 141 9DC Mitral regurgitationt 9 25 144 48FH Cardiomyopathy a 20* 131 16JK Cardiomyopathy 13 33 180 36GSm Cardiomyopathy 11 22 204 10GS Aortic stenosis a 25* 133 34HH Aortic regurgitationt

Aortic stenosis ) 16* 221 54WD Coronary artery disease

Left ventricular aneurvsm 14 31 133 27GT Aortic stenosist 12 35* 105 43RlP Cardiomyopathy 13 24 1 58 16DD Mitral regurgitation a 25 189 19RH Ruptured chordae tendineae 7 16 129 76

Mitral regurgitationtKM Acute myocardial infarctiont 29tRA Coronary artery disease

Left ventricular aneurysm 26tX 8.1 24.2 1.56.0 30.4SE 1.0 1.5 8.6 5.2N 14 16 14 14

Abbreviations: MRAP = mean right atrial pressure; PCP - pulmonary congesting pressure. Entries forPCP represent left ventricular end diastolic pressure except for entries indicated by * which represent leftventricular diastolic pressure before a large atrial wave and entries indicated by t which represent mean pul-monary arterial wedge pressure; LVEDV = left ventricular end diastolic volume: normal = 30-110 ml/m2BSA; LVSEF = left ventricular systolic ejection fraction: normal = > .50%.

tPatients with recent onset decompensation.Circulationi. Xolure 59. Atugtust 1974

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and calf (6 patients) during congestion was measured withmercury-in-silastic strain gauge plethysmographs and ex-pressed in ml/100 ml limb volume. Capillary filtration dur-ing congestion was estimated from the increase in limbvolume above control volume after the cuffs were deflatedand was expressed in ml/100 ml of limb volume.

Right atrial, systemic arterial and pulmonary congestingpressures were measured with conventional pressuretransducers and were recorded on a physiologic recorder.The reference point for these pressures was the mid-chest.Values for pulmonary congesting pressure consist ofmeasurements of mean pulmonary arterial wedge pressurein the two patients studied in the coronary care unit, leftventricular end diastolic pressure in 10 patients, and leftventricular diastolic pressure just before a large atrial wavein 4 patients. In these 4 patients it was found that because ofthe large atrial wave, measurements of left ventriculardiastolic pressure just before the atrial wave provided bettercorrelation with mean pulmonary arterial wedge pressurethan did end diastolic pressure. None of the patients hadmitral stenosis. In four patients in whom end diastolic andpulmonary wedge pressure were measured simultaneouslyduring congestion, the changes in mean pulmonary wedgepressure paralleled changes in end diastolic pressure.Consequently, left ventricular end diastolic pressure,diastolic pressure before the atrial wave, or mean pulmonaryarterial wedge pressure are referred to as pulmonary con-

gesting pressure.After obtaining control measurements, the cuffs were in-

flated consecutively to 20, 40, 60 and 80 mm Hg for threeminutes each without releasing congestion between eachlevel and the subsequent one. Measurements of limbvolume and pressures were taken at the end of each periodof congestion. Similar studies were performed on seven nor-

mal subjects, except that left ventricular and pulmonaryarterial wedge pressures were not measured.

In two normal subjects, we measured the total volume ofthe extremities (2 lower and 1 upper) distal to the cuffs bymeasuring the amount of water displaced and found that itwas approximately 12 liters (5 liters for each lower and 2liters for the upper). These values for total limb volumewere then used to calculate the estimated total amount offluid pooled at each level in the rest of the subjects. Thetotal amount of fluid pooled at each level was calculated bymultiplying the amount pooled in ml/100 ml by the volumeof the extremities expressed in 100 ml units. For example,increases in calf volume of 4.3 ml/100 ml represent an es-timated pooling of 430 ml (4.3 X 100) and increases in

forearm volume of 4.4 ml/100 ml represent estimated pool-ing of 88 ml (4.4 X 20) for a total estimated pooling in thethree extremities of 518 ml. It might be noted here that thiscalculation is not a critical part of the study and was per-formed only to provide an estimate of the total amount ofpooling; it almost certainly overestimates the total amountof pooling for the following reasons. The poolingpresumably occurs in skin and skeletal muscle and not inbone, but the calculation is expressed in ml/100 ml of totallimb volume (skin, muscle and bone). Since the actualmeasurements were made at the level of the extremity (mid-calf or upper forearm) where the ratio of skin and musclevolume to total limb volume is higher than at any other levelof the limb distal to the cuffs, the calculation of total amountof pooling derived from the measurement at this levelprobably overestimates the total amount of pooling.

Analysis of variance and Dunnett's test for multiple com-

parisons were used for statistical analysis.9 Values ofP < 0.05 were taken as statistically significant.

Results

Limb Volumes

Increases in forearm and calf volume duringinflation of the congesting cuffs were significantly lessin patients with heart failure than in normal subjects(table 2). The increases in forearm volume expressedin ml/100 ml limb volume did not differ significantlyfrom the increases in calf volume in either group

(table 2).The average of the estimated total amount pooled

in the three extremities at a congesting pressure of 40mm Hg was 518 ml in the normal subjects and 366 mlin the patients with heart failure. Correspondingvalues at a congesting pressure of 80 mm Hg were 736ml in normal subjects and 596 ml in patients withheart failure.The amount of pooling in the forearm of the

patients with recent cardiac decompensation did notdiffer significantly from that in patients with a historyof chronic heart failure. Increases in the former group

averaged 1.7 ± 0.3, 2.5 0.2, 3.8 + 0.4 and5.1 ± 0.4 (SE) ml/100 ml limb volume compared withincreases in the latter group of 1.8 ± 0.2, 2.9 ± 0.3,

Table 2

Increases in Limb Volumes During Inflation of Congesting Cuffs

Forearm volume Calf volume(ml/100 ml) (ml/100 ml)

Congesting cuff pressures (mm Hg): 20 40 60 80 R* 20 40 60 80 R*

Normal subjects X 3.0 4.4 5.8 6.8 0.9 2.6 4.3 5.3 6.0 0.6sE 0.3 0.3 0.6 0.6 0.1 0.3 0.6 0.7 0.8 0.1N 7 7 7 7 7 7 7 7 7 7

Patients with left heart failure X 1.8 2.8 4.0 5.3 0.3 1.9 3.1 4.1 4.9 0.1SE 0.2 0.2 0.2 0.3 0.1 0.4 0.5 0.6 0.6 0.1N 14 14 14 14 14 6 6 6 6 6

*R represents the difference in limb volume in the recovery period after deflation of the cuffs minus limb voluIme in the controlperiod. This value represents loss of intravascular fluid by capillary filtration.

Increases in forearm and calf volumes at each level of congesting pressure were statistically significant (P <0.03) in both groups.

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4.0 ± 0.3, 5.3 ± 0.4 ml/100 ml at 20, 40, 60 and 80mm Hg, respectively.

Capillary filtration at the end of congestionaveraged 0.9 ± 0.1 and 0.6 + 0.1 ml/100 ml inforearm and calf, respectively, in the normal subjectsand 0.3 ± 0.1 and 0.1 0.1 ml/100 ml in the forearmand calf, respectively, in the patients with heartfailure. Thus, the patients with heart failure not onlypooled less blood, but also had less estimated capillaryfiltration during congestion.

Right Atrial Pressure

Control values for right atrial pressure did not differsignificantly in the two groups (table 3), but decreasesin right atrial pressure with inflation of the cuffs were

significantly less in patients with heart failure than innormal subjects (table 3).

Pulmonary Congesting Pressure

This variable was not measured in normal subjects.In patients with heart failure, pulmonary congestingpressure did not decrease significantly at cuffpressures of 20, 40 and 60 mm Hg, but did decreasesignificantly at a cuff pressure of 80 mm Hg (table 3).At 40 mm Hg, 3 of 16 patients had a decrease inpulmonary congesting pressure greater than 4 mmHg. At 60 mm Hg, 3 of 11 patients had decreasesgreater than 4 mm Hg. At 80 mm Hg, 6 of 16 patientshad decreases greater than 4 mm Hg.

Arterial Pressure

In patients with heart failure, mean arterialpressure averaged 82 ± 4.1 mm Hg before congestionand 84 3.7 and 86 ± 3.9 mm Hg at congestingpressures of 40 and 80 mm Hg, respectively. In nor-

mal subjects, arterial pressure averaged 82 ± 3.3 mmHg before congestion and 86 ± 2.2 and 91 ± 3.1 mmHg at 40 and 80 mm Hg, respectively. Changes in

arterial pressure were not significant at 40 mm Hg,but were significantly greater than control (P < 0.05)at 80 mm Hg in both groups.

Discussion

Previous studies have demonstrated that venous

distensibility is decreased in patients with heartfailure.4 Consequently, it was not surprising that con-

gesting cuffs produced less venous pooling in patientswith heart failure than in normal subjects (table 2).But because of reports that pulmonary vascularpressure-volume curves are steep in heart failure,5 weanticipated that even small amounts of venous pool-ing might cause large decreases in pulmonary con-

gesting pressure and cardiac filling pressures. In con-

trast, the results demonstrated that decreases in rightatrial pressure were less in patients with heart failurethan in normals during inflation of congesting cuffs(table 2). Although limb volumes increased and rightatrial pressure decreased with increasing cuff pressure

from 20 to 80 mm Hg, these changes were notreflected in significant decreases in pulmonary con-

gesting pressure except at the highest level of conges-

tion. Thus, in patients with heart failure congestingcuffs produced statistically significant decreases inpulmonary congesting pressure only when the cuffswere inflated to 80 mm Hg, and even at this high cuffpressure, only 6 of 16 patients had decreases inpulmonary congesting pressure of greater than 4 mmHg. At congesting cuff pressures of 40 and 60 mm Hg,3 patients had decreases greater than 4 mm Hg.The smaller amounts of venous pooling in the

patients with heart failure were not the result of pre-

existing venous distension from elevated venous

pressure. Only five of the patients had mean rightatrial pressure higher than 10 mm Hg and there was

no significant difference between right atrial pressure

Table 3

Cardiac Filling Pressures at Various Congesting Cuff Pressures

Right atrial pressure Pulmonary congesting pressture(mm Hg) (mm Hg)

C 20 40 60 80 R C 20 40 60 80 R

Normal subhjects X 7.0 3.3 3.7 2.9 2.4 7.3SE 0.6 0.6 0.6 0.6 0.7 0.3P <0.03 <0.05 <0.03 <0.03

Patients with leftheart failure X 7. 8.4 6.3 6.0 4.6 6.6 24.2 24.6 22.9 23.2 20.3 24.0

SF; 1.0 1.3 1.0 1.0 0.7 0.6 1.3 2.2 1.9 2.1 1.6 1.N 11 7 11 6 11 10 16 11 16 11 16 13P <0.03 <0.03 <0.03 < 0.03

Abbreviationis: C = control values before inflation of the cuiffs; R pressure recorded in the recovery period three miniutesafter release of the congestinig cuffs, P < 0.03 = valties which were significantly different from control valuies: N = ntumberof patients studied.

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in the normal subjects and the patients with left heartfailure. Furthermore, before the cuffs were inflated,the extremities were elevated to collapse the veins.The mechanism of decreased resting venous disten-sibility in patients with heart failure is not clear, but itis not dependent on elevations in peripheral venouspressure.4 Parenthetically, we might note here thatthe baseline values for mean right atrial pressure inthe normal subjects are slightly higher than previouslyreported values. Although this may have resultedfrom elevation of the lower extremities, we would notethat the values in this study are similar to valuesobserved in healthy young normal subjects withoutelevation of the legs in a previous study in our

laboratory.10 The important point is that the lower ex-

tremities were elevated to collapse the veins in bothgroups in the present study and baseline right atrialpressures before congestion were similar in the twogroups so that lesser venous pooling in the patientswith heart failure cannot be explained by pre-existingvenous distension.We cannot explain why some patients had ap-

preciable decreases (> 4 mm Hg) in pulmonary con-

gesting pressure and others did not. We compared one

group which had decreases in pulmonary congestingpressure ranging from -5 to -14 mm Hg (average-8; N = 6) and another group which had changesranging from -1 to +4 mm Hg (average +1; N = 6).There were no significant differences between the twogroups in resting pulmonary congesting pressure,arterial pressure and right atrial pressure. There were

also no significant differences between the two groupsin the amount of venous pooling or the changes inright atrial and arterial pressures. Since the amount ofpooling was not different, we might suggest that thedecreases in pulmonary blood volume in "responders"and "nonresponders" were not different, and that,therefore, the patients who had appreciable decreasesin congesting pressures had steeper pulmonaryvascular pressure-volume curves. This explanation isspeculative, however, since pulmonary blood volumewas not measured in these patients.

Increases in systemic arterial pressure occurredduring congestion in both normal subjects andpatients. The mechanism is not clear but might in-volve vasoconstriction produced by decreases in car-

diac filling pressures and activation of reflexesoriginating in low pressure cardiopulmonarybaroreceptors.10 In addition, at high levels of con-

gesting pressure the cuffs may have produced a

mechanical increase in vascular resistance or a sym-

pathetic discharge related to discomfort. We con-

sidered the possibility that increases in arterialpressure and afterload may have prevented decreasesin pulmonary pressure during decreases in preload,

but the magnitude of the increase in arterial pressuredid not correlate with the decrease in pulmonarypressure.Limb volumes tended to plateau during the three

minutes of congestion at 20 mm Hg and 40 mm Hg.This is consistent with previous studies1' which in-dicate that venous volume and distending pressurereach a plateau during this period. Therefore, longerperiods of congestion would not produce significantlygreater venous pooling at 40 mm Hg. However, at 60and 80 mm Hg limb volume did not plateau after theinitial increment, but instead continued to increaseslowly. This slow increase represented capillary filtra-tion since the volume of the extremities remainedabove control values after the cuffs were deflated. Theestimated value for capillary filtration coefficient inthe normal subjects (0.0033 ml/min X mm Hg X 100ml) was similar to that reported by Landis,8 butcapillary filtration coefficient in patients with heartfailure was 0.0011 ml/min X mm Hg X 100 ml, or

about 33% of the normal value.*These data suggest that the rate of capillary filtra-

tion may be reduced in patients with heart failure,perhaps because of increased tone of precapillaryvessels and decreased capillary surface area or perhapsbecause of occult edema and increased tissue pressure.Despite decreased capillary filtration, prolonged infla-tion of congesting cuffs at 80 mm Hg as is usually per-formed in the clinical setting of left heart failuremight produce additional sequestration of fluid in theextremities. It should be noted, however, that the rateof capillary filtration decreases rapidly with prolongedcongestion,8 presumably because of increases in in-terstitial fluid and pressure which oppose filtration.The patients in this study had chronic or subacute

left heart failure, but when studied did not have frankpulmonary edema. We should, therefore, consider thelimitations of applying these results to use of con-

gesting cuffs in patients with acute pulmonary edema.Many patients who develop acute pulmonary edemahave subacute or chronic heart failure, but some

*In calculating capillary filtration coefficient (CFC), capillaryfilitra-tion in ml/100 was the increase in limb volume above control afterdeflation of the cuffs. The increment in postcapillarv pressure wascalculated assuming that resting postcapillary pressure ap-proximated 30 mm Hg and that increases in congesting pressurebelow 30 mm Hg were not transmitted to the capillaries. Therefore,the calculated increment in capillary pressure during congestion at20, 40, 60 and 80 mm Hg was zero, 10, 30 and 50 mm Hg, respec-tivelv. Using this approach the increment in capillary pressure dur-ing the 9 minutes of inflation (congesting period at 20 mm Hg ex-cluded) averaged 30 mm Hg. The validity of this approach is sup-ported by two observations: first, the value of CFC in forearm ofnormal subjects is similar to that reported by Landis, and second,limb volumes plateaued during congestion at 20 and 40 mm Hg in-dicating little or no capillary filtration at these pressures.

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patients develop heart failure and pulmonary edemaabruptly. It is possible that decreases in venous disten-sibility, particularly those decreases which result fromlocal factors, may not have developed in patients withabrupt onset of heart failure. If this is true, thenpatients with abrupt onset of heart failure andpulmonary edema might pool more blood and havegreater decreases in pulmonary congesting pressuresthan the patients in our study. In contrast, there areseveral factors which might contribute to less venouspooling in patients with acute pulmonary edema.First, in many patients with pulmonary edema thereare potent reflex vasoconstrictor stimuli such ashyperventilation,12 apprehension or pain which tendto decrease the amount of pooling. A second factor isthe amount of blood in the veins before inflation ofthe cuffs. In our studies, the extremities were elevatedin order to collapse the veins before congestion, but intreating patients with acute pulmonary edema it is un-usual and inadvisable to elevate the extremities andcollapse the veins before inflating the cuffs. With theextremities at or below the level of the right atrium, asis usual in the clinical setting, the veins are partiallydistended before the cuffs are inflated. Consequently,the increment in venous pooling might be less in theclinical setting than in our study. On the other hand,it is possible that pulmonary vascular pressure-volumerelationship may be steeper in patients with acutepulmonary edema than in our patients with chronicleft heart failure so that small decreases in pulmonaryblood volume might produce greater benefit inpatients with acute pulmonary edema than in patientswith chronic left heart failure. The results of this studyshould, therefore, be applied cautiously to considera-tion of congesting cuffs in the treatment of patientswith acute pulmonary edema. The study indicates,

however, that the decreases in venous distensibilitywhich are characteristic of heart failure limit theamount of venous pooling produced by congestingcuffs.

AcknowledgmentWe wish to thank Ms. Julianne Garvey for secretarial assistance.

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MCRAVEN and FRANCOIS M. ABBOUDPHILIP A. HABAK, ALLYN L. MARK, J. MICHAEL KIOSCHOS, DONALD R.

FailureEffectiveness of Congesting Cuffs ("Rotating Tourniquets") in Patients with Left Heart

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1974 American Heart Association, Inc. All rights reserved.

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