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Aortic flow and other hemodynamic responses to the Valsalva maneuver in the dog
Aortic flow and to the Valsalva
other hemodynamic responses maneuver in the dog
Howard Cohen, M.D.* Chicago, Ill.
S
ince the work of Weber in 1851,’ the Valsalva maneuver (VM) has been recognized as a means by which the hemodynamic condition in man or the laboratory animal can be readily altered. The changes are quickly reversible with cessation of the VM. Exhaling forcibly against the closed glottis produces hemodynamic changes by raising intrathoracic pressure, and thus diminishes the intrathoracic blood content and impedes venous return to the right side of the heart. That blood is actually kept out of the thorax during the VM has been conclusively shown2 by means of Ps2 and Diodrast injected into the deep abdominal veins. The changes in blood pressure which occur when blood flow is temporarily impeded in this way have allowed the gleaning of much information concerning basic physiologic circulatory mechanisms and the effects of drugs and disease states on these mechanisms.3-30 Discussion in this presentation will be limited to the pressure overshoot (PO) of the VM. This pressure overshoot in the systemic arterial system occurs just after cessation of the VM. According to various investigator, the PO is abolished by tetraethylammonium chloride,4,5,7 norepinephrine,6Je previously existing high venous From
pressure,6 bretylium tosylate, hexamethonium,* orthostatic hypotension,i2J3J3 significant heart failure,i6J7J8 significant mitral stenosis,5J6J7*22v23 aortic stenosis,16 constrictive pericarditis,5n20 severe pulmonary vascular disease,16J*,20*27 and occlusion of the common carotid artery.26 Thus, the VM has been used as a test to evaluate these drugs and disease states in the laboratory and even at the bedside. Various mechanism have been postulated separately or in combination to account for the loss of the Phase IV response of the VM: (1) a venous pressure too high to be effectively impeded by the VM, so that no pool of blood will have stagnated and be ready to go through to the left side when the VM is released6; (2) a weakened myocardium which will not respond with forceful contractions to the onrush of the released bloodi6Js; (3) a blunting of the normal reflex peripheral vasoconstriction so that, even when the blood pool is passed rapidly through the left side of the heart, peripheral resistance is too low to elicit a rise above control blood pressure5~*J0*23~26; (4) a mechanical obstruction, such as a stenotic valvular lesion or severe pulmonary vascular disease, preventing the pooled blood from advancing through the left side with enough velocity to effect an overshoot16J8; (5) maximal vasoconstric-
the Cardiovascular Institute, and the Division of Cardiovascular Disease, Department of Medicine, Michael Reese Hospital and Medical Center, Chicago, Ill. Supported in part by Grant HE-5252 from the National Heart Institute. United States Public Health Service. Received for publication Feb. 10, 1966. *Address: Michael Reese Hospital and Medical Center, 29th St., and Ellis Ave., Chicago, Ill., 60616.
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Hemodynamic
tion at the onset of the VM, as with norepinephrine, allowing no further vasoconstriction after release of the VM, and thus no overshoot.2” No one has demonstrated, with certainty, the actual mechanism of the normal overshoot. One reason for this is that there has not been, until recently, a good method of measuring instantaneous aortic flow in the intact animal. Without such measurements of flow, it cannot be determined whether the rise in pressure during the pressure overshoot is due to an increase in blood flow or an increase in peripheral resistance (vasoconstriction), or to a combination of the two. Although ganglionic blocking agents abolish the PO, this, in the absence of concomitant measurements of flow, does not prove that the normal overshoot must be based on vasoconstriction. It only means that the normal overshoot might not be seen when marked vasodilatation pre-exists. Flows have been measured with indicator-dilution methods,9 and have suggested that flow is actually decreased during the pressure overshoot, implying that the PO is due solely to peripheral vasoconstriction. This method, however, does not give instantaneous flows, and flow values averaged over a period of time cannot be compared with instantaneous pressures in these circumstances. Thus, changes in resistance, or peripheral vasoconstriction, cannot be determined at any given moment in time. Such information can be obtained, at least in the laboratory animal, by using the electromagnetic flowmeter. The purpose of this study was to determine the simultaneous conditions of blood pressure, blood flow, and peripheral resistance in the systemic arterial system during the PO (Phase IV) of the VM in anesthetized dogs. It will be shown that, almost always, a flow overshoot accompanies the pressure overshoot, and that peripheral resistance may be increased or decreased during the PO of the VM.
785
responses to Valsalva maneuver
rubber cannula with a balloon cuff was secured in place, and an ordinary blood pressure cuff was placed around the thorax. An aneroid sphygmomanometer was connected by plastic tubing into a single pressure system with the compressed air source, the 2-liter glass reservoir, and the endotracheal tube and blood pressure cuff. The reservoir could be filled and then suddenly opened into the entire system so that the resultant pressure was 25 mm. Hg. Intrapulmonary pressure, therefore, also reached 25 mm.Hg. The pressure could be released simply by disengaging the tubing from the endotracheal cannula (see Fig. 1). This system for simulating the VM is similar to one previously described.26 Arterial pressures obtained through polyethylene catheters inserted via the femoral or carotid artery were recorded on a Sanborn multichannel direct writer. Aortic flows were obtained by placing a Medicon Model M4001 electromagnetic flowmeter probe on the arch of the aorta through an incision in the lower left thorax, and the flow was recorded on the Sanborn writer (Fig. 2). Positive-pressure artificial respiration was used during surgery. With the flowmeter probe in place, the chest was closed airtight, the pneumothorax was reduced through a 20-gauge needle, and the animal was allowed to resume spontaneous respiration. Pressure during the VM was
Q
ANEROID SPHYGMOMANOMETER
/
-TO
AIR
Methods and materials
One hundred sixteen VMs were induced in 13 mongrel dogs (male and female) weighing from 12 to 18 kilograms, anesthetized with sodium pentobarbital in a dose of 25 mg. per kilogram. An endotracheal
Fig. 1. Diagrammatic representation of the method of inducing the Valsaiva maneuver in the closedchest dog. The reservoir air bottle was connected to a compressed-air tap.
786
Cohen
maintained until arterial pressure began to rise (second part of Phase II of the VM). Results
Fig. 3 shows a typical trial with the Valsalva maneuver. Of the 116 trials in which systemic arterial flows and pressures were obtained, there were 80 in which the typical pressure overshoot was present, and 36 in which it was absent. A flow overshoot was detected in 80 trials and was absent in 36 (Tables I and II). (Flow refers to flow per beat.*) Of the 80 trials with a pressure overshoot, there were 72, or 90 per cent, which had concomitant flow overshoots. Thus, in only 10 per cent was the typical pressure overshoots of the VM not associated with an increase in flow. Of 68 trials with a concomitant peak instantaneous flow rate overshoot (as distinguished from flow per beat), 30, or 44 per cent, had a greater increase in flow than in pressure, when expressed as per cent of their respective control values (see Fig. 2. Diagrammatic of measuring systemic flow.
representation of the method arterial pressure and aortic
*Flow per beat was used to indicate changes in flow during the overshoot. Peak instantaneous flow rate (flow rate) was compared with the corresponding pressure to determine the peripheral resistance at a given point in-time.
Fig. 3. Typical response to Valsalva maneuver. Top curue: Systemic arterial pressure. Botlom curye: Aortic flow rate, 10 mm. = 3,250 C.C. per minute. Middle curve: Aortic flow from area of flow rate curve, 3.5 mm. = 12 CL. of flow. C: Control. IR: Initial rise. F: Fall during sustained compression. .SR: Secondary rise. D: Drop with release of Valsalva. POP: Pressure overshoot period. RN: Return to normal. FOP: Flow overshoot period. U: Valsalva begins. VE: Valsalva ends. Intrapulmonary pressure was 25 mm. Hg. Time (bottonz line) in seconds.
Hemodynamic
Table I. Summary overshoot
of
trials
showing
pressure
Induced Valsalva maneuver in the dog 80 Trials showing pressure overshoot in Phase IV Trials with concomitant flow overshoot-72 (90%)
Trials without concomitant flow overshoot-8 (10%)
Table IV. Summary sure overshoot
of trials without
Per cent refers to ratio ber of triala in immediately flow per beat.
of stated number of trials to numpreceding box. All flows refer to
Table II. Summary of trials without pressure overshoot
pres
Induced Vaisalva maneuver in the dog 36 Trials showing no pressure overshoot in Phase IV Trials with flow rate overshoot-17 (47%)
Trials without overshoot-19
flow rate (53c5’0) --A
---
Peripheral N&c:
787
responses to Valsalva maneuver
Trkls 17 (100%)
Nofc:
resistance
Fall
Peripheral Trials
resistance
16 (84%) Fall 1 ( SO/,) Rise 2 ( llo/O) No change
Per cent refers to ratio of stated number of trials to number of trials in immediately preceding box. All flows refer to peak instantaneous flow rate.
Induced Valsalva maneuver in the dog 36 Trials showing no pressure overshoot in Phase IV Trials with flow overshoot-18 (50%) Nofc:
Trials without flow overshoot-18 (50%)
Per cent refers to ratio of stated number of trials to number of trials in immediately preceding box. All flows refer to flow per beat.
Table III. Summary of trials showing pressure overshoot Induced Valsalva maneuver in the dog 80 Trials showing pressu-e overshoot in Phase IV Trials with concomitant flow rate overshoot-68 (85 70)
Trials without concomitant flow rate overshoot-12 (1501,)
Peripheral T&k 30 (44%) 34 (SO’%)
4 ( 6%) Nate:
rate. Thus, these pressure overshoots were due to an increase in both flow rate and peripheral vasoconstriction. In 4 trials (6 per cent of those with both a pressure and flow rate overshoot) the ffow rate and pressure overshoots were equal, and denoted no change in peripheral vasoconstriction.” Of the 36 trials with no pressure overshoot, 47 per cent showed a flow rate overshoot indicating a peripheral vasodilatation. In the remaining 19 trials, both pressure and ffow rate fell, but to different degrees: 16 showed a decreased, and 1 showed an increased, peripheral resistance, and 2 showed no change. Thus, in 116 trials, peripheral resistance decreased in 63, or approximately 54 per cent, increased in 47, or 41 per cent, and remained the same in 6, or about 5 per cent.
Pe7ipheral
resistance
TYiUlS
Fall Rise No change
12(100%)
Discussion
msistance
Rise
Per cent refen to ratio of stated number of trials to rmmber of trials in immediately preceding box. All flows refer to peak instantaneous flow rate.
Tables III and IV). This indicates that in these cases there was a decreasein peripheral resistance, a vasodilatation. In 34 (SO per cent of those with both flow rate and pressure overshoots) the pressure increased percentagewise more than the flow
Classically, the changes in arterial pressure associated with the Valsalva maneuver are divided into four phases. Phase I is a *With
reference to the calculation of peripheral resistance, two facts need be mentioned: (1) Pressures were measured from the transverse thoracic aorta or the abdominal aorta, whereas flow was measured at the begirming of the deacending thoracic aorta. Because of this, and because of the differences in response time of the measuring devices, the curves for flow rate and pressure were not ayncbronous. Correction for this was attempted by using the Peak values of each of the curves. These peaks varied no more than 0.05 aecoud. (2) It is recognized that peripheral dilatation during Phase IV may be due to active va%diIatatfoa, loss of active vaaocoustriction, or passive vascular dilation because of a charrge in blood volume aasodated with the flow overshoot in this phaee of the Valaalva maueuver.
short initial rise in pressure immediately after straining has begun. Phase II is the subsequent marked drop in pressure, followed by a slow rise. Phase III is the sudden short drop in pressure when the straining is released. Phase IV is the overshoot, which is followed by a return to normal. Phase I is associated with a bradycardia initiated by the initial rise in pressure. Early in Phase II the bradycardia may become more marked, possibly because of vagal stimulation by the expanded lungs. Later during Phase II, there is a tachycardia initiated by low blood pressure and hypoxia. With Phase IV, a bradycardia occurs which is associated with an overshoot in pressure and a decrease in hypoxia. These changes in heart rate indicate the presence of intact sympathetic and parasympathetic pathways. In the present study, almost every pressure overshoot was associated with a bradycardia, and was preceded by a tachycardia, indicating that these autonomic pathways were intact. In those trials in which no pressure overshoot was seen, 47 per cent had a flow rate overshoot, signifying that the pressure overshoot had been lost solely because of peripheral vasodilatation, probably secondary to the anesthesia. In the other 53 per cent there was no flow rate overshoot. Surgical trauma to the heart, great vessels, and lungs may have prevented the rapid inflow of blood in Phase IV and explain the loss of the flow and pressure overshoots. The main points brought out in this study concern the 80 trials which demonstrated the classic pressure overshoot. In 90 per cent, a flow overshoot was present. This is in agreement with the classic concepts of these events but contrary to evidence cited when indicator-dilution curves were used. Forty-four per cent of the trials showing a concomitant flow rate overshoot showed a decrease in peripheral resistance. The data presented here have demonstrated that, in the dog, under the conditions of these experiments, a flow rate overshoot alone can effect the typical pressure overshoot of the Valsalva maneuver. This is also suggested by recent work in human beings.30
Summary 1. One hundred sixteen Valsalva maneuvers were performed on 13 anesthetized closed-chested dogs, and recordings were made of aortic flow with an electromagnetic flowmeter, and of aortic pressure with catheters threaded into the femoral or carotid arteries. 2. Of 36 trials which showed no pressure overshoot during Phase IV, half showed a flow overshoot. In 47 per cent, loss of pressure overshoot was ascribed to peripheral vasodilatation. The other 53 per cent showed that a drop in flow rate (or flow rate and peripheral resistance) was the etiology of the loss of pressure overshoot. 3. In 80 trials demonstrating a pressure overshoot during Phase IV of the Valsalva maneuver, 72 (90 per cent) showed a concomitant flow overshoot. Of the 80 pressure overshoots, 30 showed a decreasein peripheral resistance during the overshoot. 4. This study supports the classic concept that there is a flow overshoot associated with the pressure overshoot of the Valsalva maneuver. It also indicates that the pressure overshoot can occur in the face of decreased peripheral resistance in dogs under the conditions of this experiment. I should like to acknowledge the assistance of Dr. L. J. Hirsch, Dr. A. B. Shaffer, and Dr. L. N. Katz in the planning of these experiments and in the preparing of the manuscript. I am indebted to Messers A. Ellis, A. Rone, and N. Jones for their technical assistance. REFERENCES
1. Derbes,
V. J., and Kerr, A., Jr.: Valsalva maneuver and Weber’s experiment, New England J. Med. 253:822, 1955. 2. Stucki, P., Hatcher, J. D., Judson, W. E., and Wilkins, R. W.: Studies of circulation time during the Valsalva Tests in normal subjects and in patients with congestive heart failure, Circulation 11:900, 1955. 3. Dawson, P. M., and Hodges, P. C.: Cardiovascular reaction in the Valsalva experiment and in lifting, with a note on parturition, Am. J. Physiol. 50:481, 1920. 4. Lee, G. deJ., Mathews, M. B., and SharpeySchafer, E. P.: The effect of the ValsaIva maneuver on the systemic and pulmonary arterial pressure in man, Brit. Heart J. 16:311, 1954. E. I., Miller, G., Weinberg, S. L., and 5. Elisberg, Katz, L. N.: The effect of the Valsalva maneuver on the circulation. II. The roie of the autonomic nervous system in the production of the overshoot, AM. HEART J. 45:227, 1953.
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Price, H. L., and Conner, E. H.: Certain aspects of the hemodynamic response to the Valsalva maneuver, J. Appl. Physiol. 5:449, 1952-1953. Bunnell, I. L., Greene, D. G., and Kurz, W. W.: Influence of tetraethylammonium chloride on the circulatory responses to the Valsalva maneuver, J. Appl. Physiol. 4:345, 1951-52. Finnerty, F. A., Jr., and Freis, E. D.: Experimental and clinical evaluation in man of hexamethonium (C6). A new ganglionic blocking agent, Circulation 2:828. 1950. F&n,. W. O., Otis, A. B:, Rahn, H., Chadwick, L. E., and Hegnauer, A. H.: Displacement of blood from the lungs by pressure breathing, Am. J. Physiol. 151:258, 1947. Bondurant, S., and Wallace, I. M.: Reaction of an occluded artery during normal and abnormal Valsalva responses, Circulation 14:913, 1956. Klein, L. J., Saltzman, H. A., Heyman, A., and Sieker, H. 0.: Syncope induced by the Valsalva maneuver. A study of the effects of blood gas tensions, glucose concentration and blood pressure, Am. J. Med. 37:263, 1964. Maclean, A. R., Allen, E. V., and Magath, T. B.: Orthostatic tachycardia and orthostatic hypotension: Defects in the return of venous blood to the heart, AM. HEART J. 27:145, 1944. Page, E. B., Hickam, E. B., Sieker, H. D., McIntosh, H. D., and Pryor, W. W.: Reflex venomotor activity in normal persons and in patients with postural hypotension, Circulation 11:262, 1955. Flack, M.: Some simple tests of physical efficiency, Lancet 1:210, 1919. Flack, M.: Respiratory efficiency in relation to health and disease, Lancet 2:637, 1921. Gorlin, R., Knowles, J. H., and Storey, C. F.: The Valsalva maneuver as a test of cardiac function. Pathologic physiology and clinical significance, Am. J. Med. 22:197, 1957. Elisberg, E. I., Singian, E., and Miller, G.: Influence of heart disease on expected overshoot in blood pressure following a Valsalva maneuver, Fed. Proc. 11:42, 1952. Cosbv, R. S.. Herman. L.. and Freibrun. L.: Abnormal behavior of pulmonary and brachial artery pressures during the Valsalva maneuver in patients with emphysema, Circulation
18:708, 1958. 19.
Burroughs, R. W., and cance of abnormal Phase
20.
21.
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23.
24.
25.
26.
27.
28.
29.
30. Bruce, R. A.: SignifiI I response to Valsalva
responses to Valsalva maneuver
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maneuver in cardiac patients, Circulation 14:72, 1956. Elisberg, E., Singian, E., Miller, G., and Katz, L. N.: The effect of the Valsalva maneuver on the circulation. III. The influence of heart disease on the expected poststraining overshoot, Circulation 7:880, 1953. Judson, W. E., Hatcher, J. D., and Wilkins, R. W.: Blood nressure resnonse to the Valsalva maneuver in cardiac patients with and without congestive failure, Circulation 11:889, 19.55. Goldberg, H., Elisberg, E. I., and Katz, L. N.: The effects of the Valsalva-like maneuver upon the circulation in normal individuals and patients with mitral stenosis, Circulation 5:38, 1952. McIntosh, H. D., Burnum, J. F., Hickman, J. B., and Warren, J. V.: Circulatory changes produced by the Valsalva maneuver in normal subjects, patients with mitral stenosis, and autonomic nervous system alterations, Circulation 9:511, 19.54. Bjork, V. O., MaImstrom, G., and Uggla, L. G.: Left atrial and pulmonary “capillary” pressure curves during Valsalva’s experiment, AM. HEART J. 47:635, 1954. Zinsser, H., Jr., and Kay, L. F.: The straining procedure as an aid in the anatomic localization of cardiovascular murmurs and sounds, Circulation 1523, 1950. Sarnoff, S. J., Haldenbergh, E., and Whittenberger, J. L.: Mechanism of the arterial response to the Valsalva test. The basis for its use as an indicator of the intactness of the sympathetic outflow, Am. J. Physiol. 154:316, 1948. Mills, H., and Kattus, A. A.: The emphysema response to forced straining (Valsalva’s maneuver), Circulation 17:65, 19.58. Marcus. F. I.. Westura. E. E.. and Summa, 1.: The hemodynamic effect of the Valsalva ‘maneuver in muscular stenosis, AM. HEART J. 67:325, 1964. Carter, S. A., Birkhead, N. C., and Wood, E. H.: Effect of the Valsalva maneuver on oxygen saturation of arterial and central venous blood in patients with intracardiac shunts, Circulation 20:574, 1959. Stone, D. J., Lyon, A. F., and Teirstein, A. S.: A reappraisal of the circulatory effects of the Valsalva maneuver, Am. J. Med. 39:923, 1965.
other hemodynamic responses maneuver in the dog
Howard Cohen, M.D.* Chicago, Ill.
S
ince the work of Weber in 1851,’ the Valsalva maneuver (VM) has been recognized as a means by which the hemodynamic condition in man or the laboratory animal can be readily altered. The changes are quickly reversible with cessation of the VM. Exhaling forcibly against the closed glottis produces hemodynamic changes by raising intrathoracic pressure, and thus diminishes the intrathoracic blood content and impedes venous return to the right side of the heart. That blood is actually kept out of the thorax during the VM has been conclusively shown2 by means of Ps2 and Diodrast injected into the deep abdominal veins. The changes in blood pressure which occur when blood flow is temporarily impeded in this way have allowed the gleaning of much information concerning basic physiologic circulatory mechanisms and the effects of drugs and disease states on these mechanisms.3-30 Discussion in this presentation will be limited to the pressure overshoot (PO) of the VM. This pressure overshoot in the systemic arterial system occurs just after cessation of the VM. According to various investigator, the PO is abolished by tetraethylammonium chloride,4,5,7 norepinephrine,6Je previously existing high venous From
pressure,6 bretylium tosylate, hexamethonium,* orthostatic hypotension,i2J3J3 significant heart failure,i6J7J8 significant mitral stenosis,5J6J7*22v23 aortic stenosis,16 constrictive pericarditis,5n20 severe pulmonary vascular disease,16J*,20*27 and occlusion of the common carotid artery.26 Thus, the VM has been used as a test to evaluate these drugs and disease states in the laboratory and even at the bedside. Various mechanism have been postulated separately or in combination to account for the loss of the Phase IV response of the VM: (1) a venous pressure too high to be effectively impeded by the VM, so that no pool of blood will have stagnated and be ready to go through to the left side when the VM is released6; (2) a weakened myocardium which will not respond with forceful contractions to the onrush of the released bloodi6Js; (3) a blunting of the normal reflex peripheral vasoconstriction so that, even when the blood pool is passed rapidly through the left side of the heart, peripheral resistance is too low to elicit a rise above control blood pressure5~*J0*23~26; (4) a mechanical obstruction, such as a stenotic valvular lesion or severe pulmonary vascular disease, preventing the pooled blood from advancing through the left side with enough velocity to effect an overshoot16J8; (5) maximal vasoconstric-
the Cardiovascular Institute, and the Division of Cardiovascular Disease, Department of Medicine, Michael Reese Hospital and Medical Center, Chicago, Ill. Supported in part by Grant HE-5252 from the National Heart Institute. United States Public Health Service. Received for publication Feb. 10, 1966. *Address: Michael Reese Hospital and Medical Center, 29th St., and Ellis Ave., Chicago, Ill., 60616.
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Hemodynamic
tion at the onset of the VM, as with norepinephrine, allowing no further vasoconstriction after release of the VM, and thus no overshoot.2” No one has demonstrated, with certainty, the actual mechanism of the normal overshoot. One reason for this is that there has not been, until recently, a good method of measuring instantaneous aortic flow in the intact animal. Without such measurements of flow, it cannot be determined whether the rise in pressure during the pressure overshoot is due to an increase in blood flow or an increase in peripheral resistance (vasoconstriction), or to a combination of the two. Although ganglionic blocking agents abolish the PO, this, in the absence of concomitant measurements of flow, does not prove that the normal overshoot must be based on vasoconstriction. It only means that the normal overshoot might not be seen when marked vasodilatation pre-exists. Flows have been measured with indicator-dilution methods,9 and have suggested that flow is actually decreased during the pressure overshoot, implying that the PO is due solely to peripheral vasoconstriction. This method, however, does not give instantaneous flows, and flow values averaged over a period of time cannot be compared with instantaneous pressures in these circumstances. Thus, changes in resistance, or peripheral vasoconstriction, cannot be determined at any given moment in time. Such information can be obtained, at least in the laboratory animal, by using the electromagnetic flowmeter. The purpose of this study was to determine the simultaneous conditions of blood pressure, blood flow, and peripheral resistance in the systemic arterial system during the PO (Phase IV) of the VM in anesthetized dogs. It will be shown that, almost always, a flow overshoot accompanies the pressure overshoot, and that peripheral resistance may be increased or decreased during the PO of the VM.
785
responses to Valsalva maneuver
rubber cannula with a balloon cuff was secured in place, and an ordinary blood pressure cuff was placed around the thorax. An aneroid sphygmomanometer was connected by plastic tubing into a single pressure system with the compressed air source, the 2-liter glass reservoir, and the endotracheal tube and blood pressure cuff. The reservoir could be filled and then suddenly opened into the entire system so that the resultant pressure was 25 mm. Hg. Intrapulmonary pressure, therefore, also reached 25 mm.Hg. The pressure could be released simply by disengaging the tubing from the endotracheal cannula (see Fig. 1). This system for simulating the VM is similar to one previously described.26 Arterial pressures obtained through polyethylene catheters inserted via the femoral or carotid artery were recorded on a Sanborn multichannel direct writer. Aortic flows were obtained by placing a Medicon Model M4001 electromagnetic flowmeter probe on the arch of the aorta through an incision in the lower left thorax, and the flow was recorded on the Sanborn writer (Fig. 2). Positive-pressure artificial respiration was used during surgery. With the flowmeter probe in place, the chest was closed airtight, the pneumothorax was reduced through a 20-gauge needle, and the animal was allowed to resume spontaneous respiration. Pressure during the VM was
Q
ANEROID SPHYGMOMANOMETER
/
-TO
AIR
Methods and materials
One hundred sixteen VMs were induced in 13 mongrel dogs (male and female) weighing from 12 to 18 kilograms, anesthetized with sodium pentobarbital in a dose of 25 mg. per kilogram. An endotracheal
Fig. 1. Diagrammatic representation of the method of inducing the Valsaiva maneuver in the closedchest dog. The reservoir air bottle was connected to a compressed-air tap.
786
Cohen
maintained until arterial pressure began to rise (second part of Phase II of the VM). Results
Fig. 3 shows a typical trial with the Valsalva maneuver. Of the 116 trials in which systemic arterial flows and pressures were obtained, there were 80 in which the typical pressure overshoot was present, and 36 in which it was absent. A flow overshoot was detected in 80 trials and was absent in 36 (Tables I and II). (Flow refers to flow per beat.*) Of the 80 trials with a pressure overshoot, there were 72, or 90 per cent, which had concomitant flow overshoots. Thus, in only 10 per cent was the typical pressure overshoots of the VM not associated with an increase in flow. Of 68 trials with a concomitant peak instantaneous flow rate overshoot (as distinguished from flow per beat), 30, or 44 per cent, had a greater increase in flow than in pressure, when expressed as per cent of their respective control values (see Fig. 2. Diagrammatic of measuring systemic flow.
representation of the method arterial pressure and aortic
*Flow per beat was used to indicate changes in flow during the overshoot. Peak instantaneous flow rate (flow rate) was compared with the corresponding pressure to determine the peripheral resistance at a given point in-time.
Fig. 3. Typical response to Valsalva maneuver. Top curue: Systemic arterial pressure. Botlom curye: Aortic flow rate, 10 mm. = 3,250 C.C. per minute. Middle curve: Aortic flow from area of flow rate curve, 3.5 mm. = 12 CL. of flow. C: Control. IR: Initial rise. F: Fall during sustained compression. .SR: Secondary rise. D: Drop with release of Valsalva. POP: Pressure overshoot period. RN: Return to normal. FOP: Flow overshoot period. U: Valsalva begins. VE: Valsalva ends. Intrapulmonary pressure was 25 mm. Hg. Time (bottonz line) in seconds.
Hemodynamic
Table I. Summary overshoot
of
trials
showing
pressure
Induced Valsalva maneuver in the dog 80 Trials showing pressure overshoot in Phase IV Trials with concomitant flow overshoot-72 (90%)
Trials without concomitant flow overshoot-8 (10%)
Table IV. Summary sure overshoot
of trials without
Per cent refers to ratio ber of triala in immediately flow per beat.
of stated number of trials to numpreceding box. All flows refer to
Table II. Summary of trials without pressure overshoot
pres
Induced Vaisalva maneuver in the dog 36 Trials showing no pressure overshoot in Phase IV Trials with flow rate overshoot-17 (47%)
Trials without overshoot-19
flow rate (53c5’0) --A
---
Peripheral N&c:
787
responses to Valsalva maneuver
Trkls 17 (100%)
Nofc:
resistance
Fall
Peripheral Trials
resistance
16 (84%) Fall 1 ( SO/,) Rise 2 ( llo/O) No change
Per cent refers to ratio of stated number of trials to number of trials in immediately preceding box. All flows refer to peak instantaneous flow rate.
Induced Valsalva maneuver in the dog 36 Trials showing no pressure overshoot in Phase IV Trials with flow overshoot-18 (50%) Nofc:
Trials without flow overshoot-18 (50%)
Per cent refers to ratio of stated number of trials to number of trials in immediately preceding box. All flows refer to flow per beat.
Table III. Summary of trials showing pressure overshoot Induced Valsalva maneuver in the dog 80 Trials showing pressu-e overshoot in Phase IV Trials with concomitant flow rate overshoot-68 (85 70)
Trials without concomitant flow rate overshoot-12 (1501,)
Peripheral T&k 30 (44%) 34 (SO’%)
4 ( 6%) Nate:
rate. Thus, these pressure overshoots were due to an increase in both flow rate and peripheral vasoconstriction. In 4 trials (6 per cent of those with both a pressure and flow rate overshoot) the ffow rate and pressure overshoots were equal, and denoted no change in peripheral vasoconstriction.” Of the 36 trials with no pressure overshoot, 47 per cent showed a flow rate overshoot indicating a peripheral vasodilatation. In the remaining 19 trials, both pressure and ffow rate fell, but to different degrees: 16 showed a decreased, and 1 showed an increased, peripheral resistance, and 2 showed no change. Thus, in 116 trials, peripheral resistance decreased in 63, or approximately 54 per cent, increased in 47, or 41 per cent, and remained the same in 6, or about 5 per cent.
Pe7ipheral
resistance
TYiUlS
Fall Rise No change
12(100%)
Discussion
msistance
Rise
Per cent refen to ratio of stated number of trials to rmmber of trials in immediately preceding box. All flows refer to peak instantaneous flow rate.
Tables III and IV). This indicates that in these cases there was a decreasein peripheral resistance, a vasodilatation. In 34 (SO per cent of those with both flow rate and pressure overshoots) the pressure increased percentagewise more than the flow
Classically, the changes in arterial pressure associated with the Valsalva maneuver are divided into four phases. Phase I is a *With
reference to the calculation of peripheral resistance, two facts need be mentioned: (1) Pressures were measured from the transverse thoracic aorta or the abdominal aorta, whereas flow was measured at the begirming of the deacending thoracic aorta. Because of this, and because of the differences in response time of the measuring devices, the curves for flow rate and pressure were not ayncbronous. Correction for this was attempted by using the Peak values of each of the curves. These peaks varied no more than 0.05 aecoud. (2) It is recognized that peripheral dilatation during Phase IV may be due to active va%diIatatfoa, loss of active vaaocoustriction, or passive vascular dilation because of a charrge in blood volume aasodated with the flow overshoot in this phaee of the Valaalva maueuver.
short initial rise in pressure immediately after straining has begun. Phase II is the subsequent marked drop in pressure, followed by a slow rise. Phase III is the sudden short drop in pressure when the straining is released. Phase IV is the overshoot, which is followed by a return to normal. Phase I is associated with a bradycardia initiated by the initial rise in pressure. Early in Phase II the bradycardia may become more marked, possibly because of vagal stimulation by the expanded lungs. Later during Phase II, there is a tachycardia initiated by low blood pressure and hypoxia. With Phase IV, a bradycardia occurs which is associated with an overshoot in pressure and a decrease in hypoxia. These changes in heart rate indicate the presence of intact sympathetic and parasympathetic pathways. In the present study, almost every pressure overshoot was associated with a bradycardia, and was preceded by a tachycardia, indicating that these autonomic pathways were intact. In those trials in which no pressure overshoot was seen, 47 per cent had a flow rate overshoot, signifying that the pressure overshoot had been lost solely because of peripheral vasodilatation, probably secondary to the anesthesia. In the other 53 per cent there was no flow rate overshoot. Surgical trauma to the heart, great vessels, and lungs may have prevented the rapid inflow of blood in Phase IV and explain the loss of the flow and pressure overshoots. The main points brought out in this study concern the 80 trials which demonstrated the classic pressure overshoot. In 90 per cent, a flow overshoot was present. This is in agreement with the classic concepts of these events but contrary to evidence cited when indicator-dilution curves were used. Forty-four per cent of the trials showing a concomitant flow rate overshoot showed a decrease in peripheral resistance. The data presented here have demonstrated that, in the dog, under the conditions of these experiments, a flow rate overshoot alone can effect the typical pressure overshoot of the Valsalva maneuver. This is also suggested by recent work in human beings.30
Summary 1. One hundred sixteen Valsalva maneuvers were performed on 13 anesthetized closed-chested dogs, and recordings were made of aortic flow with an electromagnetic flowmeter, and of aortic pressure with catheters threaded into the femoral or carotid arteries. 2. Of 36 trials which showed no pressure overshoot during Phase IV, half showed a flow overshoot. In 47 per cent, loss of pressure overshoot was ascribed to peripheral vasodilatation. The other 53 per cent showed that a drop in flow rate (or flow rate and peripheral resistance) was the etiology of the loss of pressure overshoot. 3. In 80 trials demonstrating a pressure overshoot during Phase IV of the Valsalva maneuver, 72 (90 per cent) showed a concomitant flow overshoot. Of the 80 pressure overshoots, 30 showed a decreasein peripheral resistance during the overshoot. 4. This study supports the classic concept that there is a flow overshoot associated with the pressure overshoot of the Valsalva maneuver. It also indicates that the pressure overshoot can occur in the face of decreased peripheral resistance in dogs under the conditions of this experiment. I should like to acknowledge the assistance of Dr. L. J. Hirsch, Dr. A. B. Shaffer, and Dr. L. N. Katz in the planning of these experiments and in the preparing of the manuscript. I am indebted to Messers A. Ellis, A. Rone, and N. Jones for their technical assistance. REFERENCES
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6
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