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Simultaneous left ventricular and aortic pressure measurements in the evaluation of aortic valve surgery
SIM~lLT~~NEOUS LEFT VENTRICIJLAR AND AORTI(: PRESSI~RE MEASUREMENTS IN THE EVALUATION OF AORTIC VALVE SURGERY-
s
TENOTIC lesions of the aortic valve are now amenable to surgical correction. The present report deals with a practical method for the determination of the hemodynamic effectiveness of corrective aortic dilatation in patients with aoi-tic stenosis. By comparing the pressures simultaneously obtained from within the left ventricle and the aorta at the operating table before and after surger>., two objectives may be achieved. It is possible (1) to appraise the physiologk significance of an aortic murmur, and (2) to assess the degree of relief affordetl to the left ventricle by surgery. PROCEDVRE AXD METHOD
AQl patients are intubated endotracheally and maintained under positive pressure respiration. They are anesthetized with intravenous pentothal an{1 succinyl choline in conjunction with nitrous-oxygen supplement. The patients are placed in the left lateral position with the pericardium opened longitudinak~. Pressures are now obtained with the left chest open, the atria1 needle being iiiserted into either the auricular appendage or the atria1 wall. The aortic needle is inserted into the arch of the aorta at approximately the origin of the left subclavian artery and is directed proximally. The ventricular needle is inserted into the left ventricle through its lateral wall. The pressures are transmitted through the twentlr-gauge, short-bevelled needles attached to specially-made, thick-walled Saran tubing, approximately 24 inches long, with an outside diameter of % inch, ancl an inside diameter of !,i inch. TheJ. are connected to three Statham P23D pressure transducers, which are mounted in tandem at identical levels. The zero point is at approximately the mid-atria1 level as determined b!. the operating surgeon. AA five-channel single-beam cathode-ray photographic recording sJ.stem is emplol.ed, embodying three pressure channels, one channel for the zero base line, and one for the electrocardiogram. The paper speed may be fixed at 25 or 75 mm. per second. The recording machine permits the direct superimposition of the three pressure tracings, simultaneously and synchronously, using a manometric system adjusted to equal sen.sitivit>r and identical base lines. The delay which is noted between the left ventricular and aortic pressure curves during ejection ;jnd From the Division oP Thcmcic Surgery, and the I-do M. Rehmch Card&Pulmonary The Jewish Hospital of Brooklyn, Brooklyn, N. Y. Received for publication April 4, 1956.X 193
Laboratory,
protodiastole may be due to the preseirce of aortic stenosis. On the ot-her hand, it may also be explained by the fact that the aortic needle is introduced at some distance from the aortic valve. Insertion of the needle into the wall of the left ventricle is routinely followed by several ventricular premature coIltractions which do not recur while the needle is in situ, and never necessitate the interruption of the procedure. There is no significant bleeding from the puncture sites at either the aorta, atrium, or ventricle. A minor jet of blood from the aortic puncture site is easily controlled by moderate pressure with a gauze sponge for a few minutes. REXTLTS
Simultaneous needle have been performed in with normal hearts, during with mitral stenosis; and nosis.
punctures of the aorta, left ventricle, and left atrium twelve patients falling into three groups: (1) those surgical procedures within the left chest; (2) patients (3) in patients with combined mitral and aortic ste-
1. Tracing of .the Normal Cardiac Cycle.-The normal cardiac cycle of the left side of the heart as described by Wiggersr6 will be adhered to in these comments. l’entricular contraction begins with virtual simultaneous closure of the mitral valve, which marks the onset of isometric contraction. This consists of an initial slow phase followed by a rapid phase of pressure rise. In the normal heart, the rapidity of pressure rise increases progressively to the peak of ventricular systole (Fig. 4,A). The period of isometric contraction ends when the aortic valve opens. This is demonstrated graphically by the point at which the ventricular systolic pressure curve crosses that of the aorta. Aortic systole There is no gradient between the ventricular ends at the point of the incisura. and the aortic systolic pressures (Fig. 4,A and B) although there may be a slight lag between their peaks of systole. Isometric relaxation follows, and ventricular filling begins after the mitral valve reopens. This is indicated by the crossing of the ventricular and atria1 pressure curves. 2. Tracing of the Cardiac Cycle in Mz&al Stenosis.-In diastole, after the mitral valve opens, there is a pressure gradient between the left atrium and ventricle. This is somewhat higher during end diastole and is a measure of the physiologic significance of the stenotic mitral lesion. The period of left ventricular isometric contraction in mitral stenosis may, therefore, be subdivided into two phases, an initial one of left ventricular contraction with the mitral valve open, and a second of rapid increase in left ventricular pressure following closure of the mitral valve (Figs. 1,/l and g and 4,A and B). Gordon and associates,1 Moscovitz and associateq2 and Braunwald and associate9 suggest the interesting paradox of filling of the left ventricle during its initial phase of contraction, because of the positive pressure gradient between the left atrium and ventricle (Fig. l,B, point X). the end-diastolic pressure gradient Following mitral commissurotomy, between the left atrium and ventricle is abolished (Figs. 2,A and B, and 5,A and B).
Fig. l.-The cardiac cyrIe of the left side of the heart in a patient with combined miwal and :wrti~~ steno& prior to surgery. A, Simultaneous pressure tracings with paper speed of 25 mm per swond. 0, Sam! as above at paper speed of 75 mm. per second. Ventricular syst,ole hegins at, 1 and mitrzzl valv~t ~~losuw is represented at X. The auricular C wave begins at, this time. Isometric contxa(!tiot~ ends al 2, whw~ t,he aortic valve opens. The period of maximum ejecLion lasts from .2 to J, the peak ,~f the J wpr+.ventricular pulse. This precedes 4, the peak of the aortic pressure pulse, which is delayed. writs the point of slowing of the rate of ventricular systolr, and coincides wit,h Z, t hfx anacrotic 11o1vh on thv ascending limb of the aortic pulse pressure tracing. Sots (1) The gradient between the end-dia&olic left, atria1 anti ventricular pre~~urw, .JJ rhv pwssurv ditWxwt~ial between ventricular and aort~ir systolic, prvaqure. and (3) the delay in tht-it p~+~li~ of pwssnr*~.
3, Tracings of the Cardiac Cycle ,in Combined Mitral and Aortic Stenosis.In the patients with combined mitral and aortic stenosis, the atrioventricular pressure gradient is similar to that described in pure mitral stenosis. The delay
Fig.
Z.-Cardiac cycle oP patient (Fig. 1) titer mitral commissurotomy and aortic dilatation. ES, Paper speed at 75 mm. per second. speed at 25 mm. per second, Note that (1) the gradient between the The aortic and atria1 pressures are somewhat damped. end-diastolic left atria1 and ventricular pressures has been abolished, (2) the pressure differential between ventricular and aortic systolic pressure has been diminished, and (3) point Y of ventricular slowing is no longer manifest. A, Paper
between the onset of ventricular systole and closure of the mitral valve measures 0.02 second (Fig. 1,A and B). The pressure curves obtained simultaneously from the left ventricle and aorta vary from the normal in two respects. First,
there is a significant gradient between their systolic pressures, and second, there is a delay between their peaks of systole (Table I j. 0f interest is the anacrotic notch in the aortic pulse pressure tracing, which has been described by Goldberg and associates.15 This notch on the ascending limb of the aortic pressure tracing coincides with a change on the ascending limb of the ventricular pressure tracing. Close inspection of the ascending limb of the ventricular pressure tracing 03%. lJ3) reveals the following: Initially there is a slow phase of pressure rise, imlicated by the line beginning at point 1 of ventricular contraction aud enditlg where the tracing crosses that of the left atrium at point X. Here, the ascending limb of the ventricular pressure curve becomes a dotted line. tiecause 01 the characteristics of the recording machine, in which a single beam os&~te* between all five channels, the rapidity of pressure change is indicated 115, the spacing of the dots. The dots become spaced farther and farther apart to thy, point of crossover of the ventricular pressure curve with that of the aortzi. .I11 proximately 0.02 second after the end of isometric contraction at point J-, these dots coalesce for O,O2 second, after which the triicing becomes dotted i\~i~i~~ The coalescence of these dots is indicative of a 0.02 second period during which the rise in ventricular pressure becomes less rapid. It. Would appear though the left ventricle paused to take a “second breath” immediateI>. aft~l the opening of the aortic valve. This period of “ second breath” during ~PIJtricular q.stole probably produces the anacrotic notch (point Z) on the aortit. pressure tracing. The period of ventricular slowing precedes the :~t~act-(~t~c notch on the aortic limb by approximately 0.02 second. This time lag ma>. 1~ due to the distance at which the needle is pliiced into the aorta from the 1~~~~1 of the valve, and provides a base-line measurement for the lag between lhe pressure recordings of the ventricle and the aorta. Xext, there is a significant lag (measuring 0.1 second) between the ps;ti;s of systole of the ventricular and aortic curves. The peak of aortic q-stole ctoikltides with the period of reduced ventricular ejection (Fig. lJ3). Korrnall~~~ immediately after the aortic valve opens, there is a sharp rise in aortic l)ressure. In the patient with aortic stenosis, however, the rise in aortic pressure is gradu:tl, and the aortic valve closes almost immedi;jtely after the peak of pressure is obtained (Fig. 1 ,/I and B). i~lKlOSt
it5
4. Tracings of the Cardiac Cycle After Corm& Aortic Dilatutiopz. &After instrumental dilatation of the aortic valve, there is a marked decrease in the ventricular-aortic pressure gradient. In Case 1, before surgery, a ventricular systolic pressure of 148 mm. Hg produced an aortic systolic pressure of 94 mm. Hg. After opening the aortic valve, ventricular s>.stolic pressure fell to 125 mm. Hg and was accompanied by a rise in concomitant aortic qstolic pressure to 98 mm. Hg. (The aortic pressure tracing is damped and undoubtedly rqesents an even higher pressure.) In Case 2, prior to aortic dilatatioii, :L left ventricular systolic pressure of 120 mm. Hg produced an aortic systolic l)rtzssurc of 8.5 mm. Hg. After the aortic valve was opened, ventricular q.stolit. prcssurc fell to 92 mm. Hg and was accompanied 1~1.a11 aorti(- q.stolic pressure oi 81 mm. Hg. In both cases, there is a conspicuous fall in t-he ~~lltri(.~ll~tr-~~~lrti(. gradient,
198
Fig. 3.-The cardiac cycle of the left side of the heart in a patient with combined mitral and aortic Note the marked stenosis. A, Before surgery. B, After mitral commissurotomy and aortic dilatation, diminution in the systoIic pressure differential between the left ventricle and aorta after aortic dilatation.
Preop. Postop.
I‘. s.
~ 1
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i
14 0
13
25
LEFT ATRIAL PRESSURE
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I
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TRICULAR FILLWG GRADIENT
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LEFTVENTRICULAR PRESSURE ~~ -
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AORTIC PRESSURE
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LEFTVENTRICULAR AORTK! SYSTOLIC PRESSURE GRADIENT
DELAY IN LEFTVEN; TRKULAR 1AORTICPEAK OFSYSTOLE (SEC.) ,-.--~~. BEFORE hi. v. CLOSURE
I-
,-
.08 .06
.4FTER M. V. CLOSURE
ISOMF,TRIC CONTRACTION
.I6 .16
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PERIOD OF MAXIMUM EJECTION
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, ,I2 .08
.14 .12
PERIOD OF REDUCED FJECTION
.08 06
.c16
.06
TOTAL TIMEOF SOMEmlIC ZONTRACTION
i
~
.36 30
.32 .30
TOTAL TIME OF SYSTOLE
200
lL\KST,
COHEN,
AND
LOEWE
Moreover, after aortic dilatation, there is a change in the systolic cardiac cycle. Prior to the correction of the mitral and isometric contraction lasted for 0.06 second and the time from the aortic valve to the peak of ventricular systole measured 0.12
Am. Heart J. February, 1957
timing of the aortic stenosis, the opening of second. Ven-
Fig. 4.-The cardiac cycle of the left side of the heart in a patient with mitral stenosis, and suspected, but nonexistent aortic stenosis, before surgery. *4, Paper speed at 25 mm. per second. I3, Paper speed at 75 mm. per second. Note (1) The gradient between the end-diastolic pressures of the left atrium and the left ventricle, and (2) the absence of a pressure gradient between the left ventricle and aorta. This finding rules out the presence of a physiologically significant aortic stenosis.
tricular systole lasted for 0.32 second before, and 0.30 second after aortic dilatation. This difference is due solely to the shortened time between the peak of ventricular systole and the closure of the aortic valve.
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202
ILIKST,
COHEN,
AND
LOEWE
Am. Heart .l. l~elmary, 19s7
There was a rough systolic murmur in the second right intercostal space, not associated with a thrill. The aortic second sound was present but was diminished in intensity. On the operating table, a faint systolic thrill was palpated over the ascending aorta. The pressure tracings (Fig. 4+4 and B) taken at the time of surgery, revealed a significant pressure gradient between the left atrium and ventricle, which corroborated the diagnosis of mitral stenosis. However, there was no pressure gradient between the left ventricle and the aorta. The aortic systolic murmur was probably caused by eddies of flow across a pathologically involved aortic valve, without the presence of a hemodynamically significant stenosis. Therefore, after the mitral valve was opened (Fig. 5+4 and B), aortic dilatation was not performed. This, of course, significantly reduced the operative risk and other complications which attend the performance of a transventricular aortic dilatation. This case demonstrates the extreme importance of measuring the ventricularaortic pressure gradient on the operating table before aortic valvular surgery is performed. It illustrates the error which may be made in attempting to diagnose the physiologic significance of a systolic murmur at the aortic area. DISCUSSION
At the present time, the clinical response of the patient and the postoperative brachial arterial pulse pressure tracings constitute the two major means of evaluating the adequacy of aortic valvular surgery. Both methods are inadequate to scientifically evaluate the degree to which the mechanical obstruction to the aortic valve has been relieved. Moreover, the psychologic effect of cardiac surgery has been demonstrated to be a significant and frequently misleading factor. Goldberg and associatest5 have demonstrated that the anacrotic notch present in the brachial arterial tracing of patients with proved aortic stenosis may disappear after aortic dilatation. However, they were unable to quantitate the degree and significance of the stenosis. Moreover, the finding was inconstant. The only practical method by which a stenotic lesion of the aortic valve can be evaluated is to determine the pressure gradient between the left ventricle and the aorta. Rheumatic cardiac patients may have deformities of the aortic valve, consisting of mild thickening and rolling of the cusps without significant of the aortic valve per se is not synonymous with an obstenosis. Deformity structive lesion at that site, as it is possible to have an aortic murmur with little Only in those patients demonif any change in the ventricular-aortic gradient. strating a significant gradient between the systolic pressure of the left ventricle and the aorta is there a physiologically significant aortic stenosis. Ideally, these results should be complemented by another variable, namely, determination of blood flow. This phase of the study was not projected for technical reasons, the objective being to establish a procedure which could be carried out readily and simply under operative conditions. Left heart pressures have been measured sporadically. Wynn and coworkers,4 Connolly and his associates,5 and Bedell and co-workers6 have meas-
tired left atria1 pressures at the operating table. ~~llisoti7 has measured lx-essures within the left atrium transbronchially, and Bj6rk and FisherS-i’ h;tve measured pressures within this chamber by needling it through the right postcriot thoracic wall. In a refinement of this technique, Fishet-*~~ has utilizell this needle for the insertion of fine polyethylene catheters into the left vetttriclc :1n(1 aorta. Hansen and co-workers,lz and Pederson and his associates’3 have m(s:tsured ventricular pressures at the operating table. Gordon and associates? have devised an ingenious method b>, \vhich left six-ial, left ventx%xtlar, and aortic pressures are obtained by needte pttnctttt-c itt the open chest-, and are inscribed simultaneously and s~xchrortousl~. ttsi~tg :I manometric s>-stem adjusted to equal sensitivit>,, and with identical base littes. -4 record of the changes in pressure, as well as an accurate timing of the l)h;tsey of the cardiac cycle may be obtained. In patients with mitt-al stenosis, a preysure gradient between the left atrium and ventricle is noted. It is hightast &tl end diastole. This finding has been substxntiated b\T the present ittvestigatiott (Fig. 4,A and B). Moreover, the end-diastolic pressure gradient m;t\- lhc itho ishecl 1~1,an adequate mitral commissurotom!~ (Fig, .5,*4 and B 1. The method of simultaneousl>. recording pressures it-m the txrdiac c.tt:ttn. hers has been utilized in the current investigaCon of combined mitral att~i :Lortic stenosis. .q lleiilod~,tl~~n~ic~~ll~signilicant stenosis of the aortic v;tlve must proclttcc :I slxtotic pressure gradient between the left ventricle at~d aorta. The ti~~~tsui-v~~ ment of this left ventricular-aortic pressure gradient at thy operating t :tt)l(. provides precise means of evaluating the severit?, of this lesiott. %loreovcbt-, the effectiveness of the correcCon of the lesion can be ~alttat~~d b\. the abolit iot: oi the ventricular-aortic pressure gradient. Conversely, in the absence of a significant left vetttricul:tr-aortic i)t-ex+tttx gradient (Fig. 4+4 and B), the diagnosis of a significant stenotic lesiott 01 1ht. aortic valve should be abandoned.
1. The urgent need for a pracCca1 method of evaluating the :tdequ;tt~>. oi corrective surgery for stenotic lesions of the aot-tic valve is emphasized, 2. The necessity for an accurate means of differentiating a physiologicall~~ significant from a physiologically insignificant aortic stenosis, on the operating table, is stressed. 3. LA method for recording the pressure gradient between the left :\urich~, left vetttricle, and the aorta by inscribing s>xchronous a~td simultaneott? prossure pulses of the left heart is presented. 4. The presence of a left auricular-vett~ricular pressure gradient iti j)atiettts with mitral stenosis is noted, and the abolition of this gradient by. an ;t~tcqtt:t~~ mitral commissurotomy is demonstrated. 5. The left ventAcular-aort?c pressure gradiettt presettt in lxttiettts \vith significant aortic stenosis is stressed, and its reduction 1)~ effective ol)ct-:tt ii.<& dilatation of the aortic valve is described.
2Q4
BAKST,
COHEN,
AND
LOEWE
Am. Heart J. February, 1957
REFERENCES
;:
9.
2
12. 13. 14. 1.5. 16.
Gordon, A. J., Braunwald, E., and Ravitch, M. M.: Circulation Research 2:432, 19.54. Moscovitz, H. L., Gordon, A. J., Braunwald, E., Atnram, S. S., Sapin, S O., Lasser, R. P., Himmelstein, A., and Ravitch, M, M.: Am. J. Med. 18:406, 195.5. Braunwald, E., Moscovitz, H. L., Amram, S. S., Lasser, R. P., Sapin, S. O., Himmelstein, A., Ravitch, M. M., and Gordon, A. J.: Circulation 12:69, 1955. Wynn, A., Matthews, M. B., McMillan, I. K. R., and DaIey, R.: Lancet 2:216, 1952. Connolly, D. C., Tompkins, R. G., Lev, R., Kirkhn, J. W., and Wood, E. H.: Proc. Staff Meet. Mayo Clin. 27:72, 1953. BedelI, G. N., Wilde, J. D., Ehrenhaft, J. L., and Culbertson, J. W.: J. Lab. & Clin. Med. 42:781, 1953. Allison, P. R., and Linden, R. J.: Circulation 7:669, 1953. Fisher! D. L., Childs, T. B., Ford, W. B., and Kent, E. D.: Left Atrium Pressure Pulses m Mitral Valve Disease, Abstracts of Scientific Meetings of American Heart Association, April, 19.54. Fisher, D. L.: J. Thoracic Surg. 30:379, 19.55. Bjork, V, O., Malmstrom, G., and LJggla, L. G.: Ann. Surg. 138:718, 1953. Bjork, V. O., BIakemore, W. S., and MaImstrom, G.: AM. HEART J. 48:197, 1954. Hansen, A. T., Eskildsen, P., and Gotzsche, M.: Circulation 3:81, 1951. Pederson, A., and Hansen, A. T.: Acta chir. scandinav. 106:241, 1953. Venner, A., and Helling, H. E.: Brit. Heart J. 15:20.5, 19.53. Goldberg, H., Bakst, A. A., and Bailey, C. P.: AM. HEART J. 47527, 19.54. in Health and Disease, Philadelphia, 1949, Lea & Febiger, Wiggers, C. J.: Physiology pp. 646-654.
s
TENOTIC lesions of the aortic valve are now amenable to surgical correction. The present report deals with a practical method for the determination of the hemodynamic effectiveness of corrective aortic dilatation in patients with aoi-tic stenosis. By comparing the pressures simultaneously obtained from within the left ventricle and the aorta at the operating table before and after surger>., two objectives may be achieved. It is possible (1) to appraise the physiologk significance of an aortic murmur, and (2) to assess the degree of relief affordetl to the left ventricle by surgery. PROCEDVRE AXD METHOD
AQl patients are intubated endotracheally and maintained under positive pressure respiration. They are anesthetized with intravenous pentothal an{1 succinyl choline in conjunction with nitrous-oxygen supplement. The patients are placed in the left lateral position with the pericardium opened longitudinak~. Pressures are now obtained with the left chest open, the atria1 needle being iiiserted into either the auricular appendage or the atria1 wall. The aortic needle is inserted into the arch of the aorta at approximately the origin of the left subclavian artery and is directed proximally. The ventricular needle is inserted into the left ventricle through its lateral wall. The pressures are transmitted through the twentlr-gauge, short-bevelled needles attached to specially-made, thick-walled Saran tubing, approximately 24 inches long, with an outside diameter of % inch, ancl an inside diameter of !,i inch. TheJ. are connected to three Statham P23D pressure transducers, which are mounted in tandem at identical levels. The zero point is at approximately the mid-atria1 level as determined b!. the operating surgeon. AA five-channel single-beam cathode-ray photographic recording sJ.stem is emplol.ed, embodying three pressure channels, one channel for the zero base line, and one for the electrocardiogram. The paper speed may be fixed at 25 or 75 mm. per second. The recording machine permits the direct superimposition of the three pressure tracings, simultaneously and synchronously, using a manometric system adjusted to equal sen.sitivit>r and identical base lines. The delay which is noted between the left ventricular and aortic pressure curves during ejection ;jnd From the Division oP Thcmcic Surgery, and the I-do M. Rehmch Card&Pulmonary The Jewish Hospital of Brooklyn, Brooklyn, N. Y. Received for publication April 4, 1956.X 193
Laboratory,
protodiastole may be due to the preseirce of aortic stenosis. On the ot-her hand, it may also be explained by the fact that the aortic needle is introduced at some distance from the aortic valve. Insertion of the needle into the wall of the left ventricle is routinely followed by several ventricular premature coIltractions which do not recur while the needle is in situ, and never necessitate the interruption of the procedure. There is no significant bleeding from the puncture sites at either the aorta, atrium, or ventricle. A minor jet of blood from the aortic puncture site is easily controlled by moderate pressure with a gauze sponge for a few minutes. REXTLTS
Simultaneous needle have been performed in with normal hearts, during with mitral stenosis; and nosis.
punctures of the aorta, left ventricle, and left atrium twelve patients falling into three groups: (1) those surgical procedures within the left chest; (2) patients (3) in patients with combined mitral and aortic ste-
1. Tracing of .the Normal Cardiac Cycle.-The normal cardiac cycle of the left side of the heart as described by Wiggersr6 will be adhered to in these comments. l’entricular contraction begins with virtual simultaneous closure of the mitral valve, which marks the onset of isometric contraction. This consists of an initial slow phase followed by a rapid phase of pressure rise. In the normal heart, the rapidity of pressure rise increases progressively to the peak of ventricular systole (Fig. 4,A). The period of isometric contraction ends when the aortic valve opens. This is demonstrated graphically by the point at which the ventricular systolic pressure curve crosses that of the aorta. Aortic systole There is no gradient between the ventricular ends at the point of the incisura. and the aortic systolic pressures (Fig. 4,A and B) although there may be a slight lag between their peaks of systole. Isometric relaxation follows, and ventricular filling begins after the mitral valve reopens. This is indicated by the crossing of the ventricular and atria1 pressure curves. 2. Tracing of the Cardiac Cycle in Mz&al Stenosis.-In diastole, after the mitral valve opens, there is a pressure gradient between the left atrium and ventricle. This is somewhat higher during end diastole and is a measure of the physiologic significance of the stenotic mitral lesion. The period of left ventricular isometric contraction in mitral stenosis may, therefore, be subdivided into two phases, an initial one of left ventricular contraction with the mitral valve open, and a second of rapid increase in left ventricular pressure following closure of the mitral valve (Figs. 1,/l and g and 4,A and B). Gordon and associates,1 Moscovitz and associateq2 and Braunwald and associate9 suggest the interesting paradox of filling of the left ventricle during its initial phase of contraction, because of the positive pressure gradient between the left atrium and ventricle (Fig. l,B, point X). the end-diastolic pressure gradient Following mitral commissurotomy, between the left atrium and ventricle is abolished (Figs. 2,A and B, and 5,A and B).
Fig. l.-The cardiac cyrIe of the left side of the heart in a patient with combined miwal and :wrti~~ steno& prior to surgery. A, Simultaneous pressure tracings with paper speed of 25 mm per swond. 0, Sam! as above at paper speed of 75 mm. per second. Ventricular syst,ole hegins at, 1 and mitrzzl valv~t ~~losuw is represented at X. The auricular C wave begins at, this time. Isometric contxa(!tiot~ ends al 2, whw~ t,he aortic valve opens. The period of maximum ejecLion lasts from .2 to J, the peak ,~f the J wpr+.ventricular pulse. This precedes 4, the peak of the aortic pressure pulse, which is delayed. writs the point of slowing of the rate of ventricular systolr, and coincides wit,h Z, t hfx anacrotic 11o1vh on thv ascending limb of the aortic pulse pressure tracing. Sots (1) The gradient between the end-dia&olic left, atria1 anti ventricular pre~~urw, .JJ rhv pwssurv ditWxwt~ial between ventricular and aort~ir systolic, prvaqure. and (3) the delay in tht-it p~+~li~ of pwssnr*~.
3, Tracings of the Cardiac Cycle ,in Combined Mitral and Aortic Stenosis.In the patients with combined mitral and aortic stenosis, the atrioventricular pressure gradient is similar to that described in pure mitral stenosis. The delay
Fig.
Z.-Cardiac cycle oP patient (Fig. 1) titer mitral commissurotomy and aortic dilatation. ES, Paper speed at 75 mm. per second. speed at 25 mm. per second, Note that (1) the gradient between the The aortic and atria1 pressures are somewhat damped. end-diastolic left atria1 and ventricular pressures has been abolished, (2) the pressure differential between ventricular and aortic systolic pressure has been diminished, and (3) point Y of ventricular slowing is no longer manifest. A, Paper
between the onset of ventricular systole and closure of the mitral valve measures 0.02 second (Fig. 1,A and B). The pressure curves obtained simultaneously from the left ventricle and aorta vary from the normal in two respects. First,
there is a significant gradient between their systolic pressures, and second, there is a delay between their peaks of systole (Table I j. 0f interest is the anacrotic notch in the aortic pulse pressure tracing, which has been described by Goldberg and associates.15 This notch on the ascending limb of the aortic pressure tracing coincides with a change on the ascending limb of the ventricular pressure tracing. Close inspection of the ascending limb of the ventricular pressure tracing 03%. lJ3) reveals the following: Initially there is a slow phase of pressure rise, imlicated by the line beginning at point 1 of ventricular contraction aud enditlg where the tracing crosses that of the left atrium at point X. Here, the ascending limb of the ventricular pressure curve becomes a dotted line. tiecause 01 the characteristics of the recording machine, in which a single beam os&~te* between all five channels, the rapidity of pressure change is indicated 115, the spacing of the dots. The dots become spaced farther and farther apart to thy, point of crossover of the ventricular pressure curve with that of the aortzi. .I11 proximately 0.02 second after the end of isometric contraction at point J-, these dots coalesce for O,O2 second, after which the triicing becomes dotted i\~i~i~~ The coalescence of these dots is indicative of a 0.02 second period during which the rise in ventricular pressure becomes less rapid. It. Would appear though the left ventricle paused to take a “second breath” immediateI>. aft~l the opening of the aortic valve. This period of “ second breath” during ~PIJtricular q.stole probably produces the anacrotic notch (point Z) on the aortit. pressure tracing. The period of ventricular slowing precedes the :~t~act-(~t~c notch on the aortic limb by approximately 0.02 second. This time lag ma>. 1~ due to the distance at which the needle is pliiced into the aorta from the 1~~~~1 of the valve, and provides a base-line measurement for the lag between lhe pressure recordings of the ventricle and the aorta. Xext, there is a significant lag (measuring 0.1 second) between the ps;ti;s of systole of the ventricular and aortic curves. The peak of aortic q-stole ctoikltides with the period of reduced ventricular ejection (Fig. lJ3). Korrnall~~~ immediately after the aortic valve opens, there is a sharp rise in aortic l)ressure. In the patient with aortic stenosis, however, the rise in aortic pressure is gradu:tl, and the aortic valve closes almost immedi;jtely after the peak of pressure is obtained (Fig. 1 ,/I and B). i~lKlOSt
it5
4. Tracings of the Cardiac Cycle After Corm& Aortic Dilatutiopz. &After instrumental dilatation of the aortic valve, there is a marked decrease in the ventricular-aortic pressure gradient. In Case 1, before surgery, a ventricular systolic pressure of 148 mm. Hg produced an aortic systolic pressure of 94 mm. Hg. After opening the aortic valve, ventricular s>.stolic pressure fell to 125 mm. Hg and was accompanied by a rise in concomitant aortic qstolic pressure to 98 mm. Hg. (The aortic pressure tracing is damped and undoubtedly rqesents an even higher pressure.) In Case 2, prior to aortic dilatatioii, :L left ventricular systolic pressure of 120 mm. Hg produced an aortic systolic l)rtzssurc of 8.5 mm. Hg. After the aortic valve was opened, ventricular q.stolit. prcssurc fell to 92 mm. Hg and was accompanied 1~1.a11 aorti(- q.stolic pressure oi 81 mm. Hg. In both cases, there is a conspicuous fall in t-he ~~lltri(.~ll~tr-~~~lrti(. gradient,
198
Fig. 3.-The cardiac cycle of the left side of the heart in a patient with combined mitral and aortic Note the marked stenosis. A, Before surgery. B, After mitral commissurotomy and aortic dilatation, diminution in the systoIic pressure differential between the left ventricle and aorta after aortic dilatation.
Preop. Postop.
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LEFT ATRIAL PRESSURE
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LEFTVENTRICULAR AORTK! SYSTOLIC PRESSURE GRADIENT
DELAY IN LEFTVEN; TRKULAR 1AORTICPEAK OFSYSTOLE (SEC.) ,-.--~~. BEFORE hi. v. CLOSURE
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,-
.08 .06
.4FTER M. V. CLOSURE
ISOMF,TRIC CONTRACTION
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, ,I2 .08
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i
~
.36 30
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TOTAL TIME OF SYSTOLE
200
lL\KST,
COHEN,
AND
LOEWE
Moreover, after aortic dilatation, there is a change in the systolic cardiac cycle. Prior to the correction of the mitral and isometric contraction lasted for 0.06 second and the time from the aortic valve to the peak of ventricular systole measured 0.12
Am. Heart J. February, 1957
timing of the aortic stenosis, the opening of second. Ven-
Fig. 4.-The cardiac cycle of the left side of the heart in a patient with mitral stenosis, and suspected, but nonexistent aortic stenosis, before surgery. *4, Paper speed at 25 mm. per second. I3, Paper speed at 75 mm. per second. Note (1) The gradient between the end-diastolic pressures of the left atrium and the left ventricle, and (2) the absence of a pressure gradient between the left ventricle and aorta. This finding rules out the presence of a physiologically significant aortic stenosis.
tricular systole lasted for 0.32 second before, and 0.30 second after aortic dilatation. This difference is due solely to the shortened time between the peak of ventricular systole and the closure of the aortic valve.
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202
ILIKST,
COHEN,
AND
LOEWE
Am. Heart .l. l~elmary, 19s7
There was a rough systolic murmur in the second right intercostal space, not associated with a thrill. The aortic second sound was present but was diminished in intensity. On the operating table, a faint systolic thrill was palpated over the ascending aorta. The pressure tracings (Fig. 4+4 and B) taken at the time of surgery, revealed a significant pressure gradient between the left atrium and ventricle, which corroborated the diagnosis of mitral stenosis. However, there was no pressure gradient between the left ventricle and the aorta. The aortic systolic murmur was probably caused by eddies of flow across a pathologically involved aortic valve, without the presence of a hemodynamically significant stenosis. Therefore, after the mitral valve was opened (Fig. 5+4 and B), aortic dilatation was not performed. This, of course, significantly reduced the operative risk and other complications which attend the performance of a transventricular aortic dilatation. This case demonstrates the extreme importance of measuring the ventricularaortic pressure gradient on the operating table before aortic valvular surgery is performed. It illustrates the error which may be made in attempting to diagnose the physiologic significance of a systolic murmur at the aortic area. DISCUSSION
At the present time, the clinical response of the patient and the postoperative brachial arterial pulse pressure tracings constitute the two major means of evaluating the adequacy of aortic valvular surgery. Both methods are inadequate to scientifically evaluate the degree to which the mechanical obstruction to the aortic valve has been relieved. Moreover, the psychologic effect of cardiac surgery has been demonstrated to be a significant and frequently misleading factor. Goldberg and associatest5 have demonstrated that the anacrotic notch present in the brachial arterial tracing of patients with proved aortic stenosis may disappear after aortic dilatation. However, they were unable to quantitate the degree and significance of the stenosis. Moreover, the finding was inconstant. The only practical method by which a stenotic lesion of the aortic valve can be evaluated is to determine the pressure gradient between the left ventricle and the aorta. Rheumatic cardiac patients may have deformities of the aortic valve, consisting of mild thickening and rolling of the cusps without significant of the aortic valve per se is not synonymous with an obstenosis. Deformity structive lesion at that site, as it is possible to have an aortic murmur with little Only in those patients demonif any change in the ventricular-aortic gradient. strating a significant gradient between the systolic pressure of the left ventricle and the aorta is there a physiologically significant aortic stenosis. Ideally, these results should be complemented by another variable, namely, determination of blood flow. This phase of the study was not projected for technical reasons, the objective being to establish a procedure which could be carried out readily and simply under operative conditions. Left heart pressures have been measured sporadically. Wynn and coworkers,4 Connolly and his associates,5 and Bedell and co-workers6 have meas-
tired left atria1 pressures at the operating table. ~~llisoti7 has measured lx-essures within the left atrium transbronchially, and Bj6rk and FisherS-i’ h;tve measured pressures within this chamber by needling it through the right postcriot thoracic wall. In a refinement of this technique, Fishet-*~~ has utilizell this needle for the insertion of fine polyethylene catheters into the left vetttriclc :1n(1 aorta. Hansen and co-workers,lz and Pederson and his associates’3 have m(s:tsured ventricular pressures at the operating table. Gordon and associates? have devised an ingenious method b>, \vhich left six-ial, left ventx%xtlar, and aortic pressures are obtained by needte pttnctttt-c itt the open chest-, and are inscribed simultaneously and s~xchrortousl~. ttsi~tg :I manometric s>-stem adjusted to equal sensitivit>,, and with identical base littes. -4 record of the changes in pressure, as well as an accurate timing of the l)h;tsey of the cardiac cycle may be obtained. In patients with mitt-al stenosis, a preysure gradient between the left atrium and ventricle is noted. It is hightast &tl end diastole. This finding has been substxntiated b\T the present ittvestigatiott (Fig. 4,A and B). Moreover, the end-diastolic pressure gradient m;t\- lhc itho ishecl 1~1,an adequate mitral commissurotom!~ (Fig, .5,*4 and B 1. The method of simultaneousl>. recording pressures it-m the txrdiac c.tt:ttn. hers has been utilized in the current investigaCon of combined mitral att~i :Lortic stenosis. .q lleiilod~,tl~~n~ic~~ll~signilicant stenosis of the aortic v;tlve must proclttcc :I slxtotic pressure gradient between the left ventricle at~d aorta. The ti~~~tsui-v~~ ment of this left ventricular-aortic pressure gradient at thy operating t :tt)l(. provides precise means of evaluating the severit?, of this lesiott. %loreovcbt-, the effectiveness of the correcCon of the lesion can be ~alttat~~d b\. the abolit iot: oi the ventricular-aortic pressure gradient. Conversely, in the absence of a significant left vetttricul:tr-aortic i)t-ex+tttx gradient (Fig. 4+4 and B), the diagnosis of a significant stenotic lesiott 01 1ht. aortic valve should be abandoned.
1. The urgent need for a pracCca1 method of evaluating the :tdequ;tt~>. oi corrective surgery for stenotic lesions of the aot-tic valve is emphasized, 2. The necessity for an accurate means of differentiating a physiologicall~~ significant from a physiologically insignificant aortic stenosis, on the operating table, is stressed. 3. LA method for recording the pressure gradient between the left :\urich~, left vetttricle, and the aorta by inscribing s>xchronous a~td simultaneott? prossure pulses of the left heart is presented. 4. The presence of a left auricular-vett~ricular pressure gradient iti j)atiettts with mitral stenosis is noted, and the abolition of this gradient by. an ;t~tcqtt:t~~ mitral commissurotomy is demonstrated. 5. The left ventAcular-aort?c pressure gradiettt presettt in lxttiettts \vith significant aortic stenosis is stressed, and its reduction 1)~ effective ol)ct-:tt ii.<& dilatation of the aortic valve is described.
2Q4
BAKST,
COHEN,
AND
LOEWE
Am. Heart J. February, 1957
REFERENCES
;:
9.
2
12. 13. 14. 1.5. 16.
Gordon, A. J., Braunwald, E., and Ravitch, M. M.: Circulation Research 2:432, 19.54. Moscovitz, H. L., Gordon, A. J., Braunwald, E., Atnram, S. S., Sapin, S O., Lasser, R. P., Himmelstein, A., and Ravitch, M, M.: Am. J. Med. 18:406, 195.5. Braunwald, E., Moscovitz, H. L., Amram, S. S., Lasser, R. P., Sapin, S. O., Himmelstein, A., Ravitch, M. M., and Gordon, A. J.: Circulation 12:69, 1955. Wynn, A., Matthews, M. B., McMillan, I. K. R., and DaIey, R.: Lancet 2:216, 1952. Connolly, D. C., Tompkins, R. G., Lev, R., Kirkhn, J. W., and Wood, E. H.: Proc. Staff Meet. Mayo Clin. 27:72, 1953. BedelI, G. N., Wilde, J. D., Ehrenhaft, J. L., and Culbertson, J. W.: J. Lab. & Clin. Med. 42:781, 1953. Allison, P. R., and Linden, R. J.: Circulation 7:669, 1953. Fisher! D. L., Childs, T. B., Ford, W. B., and Kent, E. D.: Left Atrium Pressure Pulses m Mitral Valve Disease, Abstracts of Scientific Meetings of American Heart Association, April, 19.54. Fisher, D. L.: J. Thoracic Surg. 30:379, 19.55. Bjork, V, O., Malmstrom, G., and LJggla, L. G.: Ann. Surg. 138:718, 1953. Bjork, V. O., BIakemore, W. S., and MaImstrom, G.: AM. HEART J. 48:197, 1954. Hansen, A. T., Eskildsen, P., and Gotzsche, M.: Circulation 3:81, 1951. Pederson, A., and Hansen, A. T.: Acta chir. scandinav. 106:241, 1953. Venner, A., and Helling, H. E.: Brit. Heart J. 15:20.5, 19.53. Goldberg, H., Bakst, A. A., and Bailey, C. P.: AM. HEART J. 47527, 19.54. in Health and Disease, Philadelphia, 1949, Lea & Febiger, Wiggers, C. J.: Physiology pp. 646-654.