Effects of the Valsalva maneuver on the cardiac systolic intervals: Beat-to-beat versus timed analysis

Effects systolic

of the Valsalva intervals:

Bea

Athanassdos P. Plessas, AUr.D.* Sudarshan Kumar, M.B.” David H. Spodick, M.D.“” Boston, Mass.

he Valsaiva maneuver (VM) is designed to raise intrathoracic pressure sufficiently to significantly reduce right heart inflow during a prescribed time interval. The consequences of this challenge are a test of cardiocirculatory integrity with numerous experimental and clinical applications. r-l2 Fundamental parameters affected by the VM include heart rate, blood pressures and flows, chamber volumes, and autonomic nervous function. The development of noninvasive techniques has made it possible to study changes in the intervals of the cardiac cycle by atraumatic methods which are suited to clinical application as well as physiologic study of the VM. These methods are particularly appropriate for beat-tobeat evaluation. The wide range of normal resting heart rates and the rate dependency of many aspects of cardiac function suggested that beat-to-beat analysis would be more sig-

nificant than rime-based measurements in a situation characterized by beat-to-beat changes in cycle length. This report is a comparison of the beat-to-beat effects of the VM on the principal systolic cardiac intervals with the corresponding timebased measurements. Materiab

and

methods

Subjects. We studied 11 active, though not athletically trained, male volunteers (ages 22 to 32) who had no clinical or graphic evidence of cardiac or other disease and who were not taking medication of any kind. ‘“Hospital normals” were excluded. Equipment. Simultaneous recordings of electrocardiogram (Lead I I), apical phonocardiogram, apexcardiogram (AGG), and right external carotid arteriogram were made on a Sanborn .568-IOOA eight-channel optical recorder at a paper speed of 75 mm. per second with time lines at 40 msec.

From

the Cardiology Division, Lemuel Shattuck Hospital. and the Department SE Medicine. Tuits University School of Medicine, Boston, Mass. This investigation was supported by Grant NGR 22-012-066 from the National Aeronautics and Space Administration through the NASA Electronics Research Center, Cambridge, Mass. Received for publication Dec. 31, 1969. Reprint requests to: David H. Spodick, M.D., Lemuel Shattuck Hospital, 170 Morton St., Boston, Mass. 02130. *Fellow in Cardiology, Cardiology Division, Lemuel Shattuck Hospital. Assistant in Medicine, Tufts University School of Medicine. **Chief, Cardiology Division, Medical Services, Lemuel Shattuck Hospital. Associate Professor of Medicine, Tufts University School of Medicine. Lecturer in Medicine, Boston University School of Medicine.

522

American Heart Journal

October,1970 Vol. 80, No. 4, pp. 522-531

Volume

80

Number

4

Procedure and technical details of sensors and microphones are described elsewhere.13 The VM was performed via a Tycos aneroid manometer attached to a replaceable cardboard mouthpiece by a 25 cm. semirigid plastic tube. Test procedure. The manometer dial was positioned in clear view of the recumbent subjects who were coached on and had practiced the procedure. On command, following a normal inspiration, the needle was rapidly blown to a pressure of 40 mm.

Table I. Heart-rate

changes during Heart-rate

Phases

Hg which was sustained for 12 seconds and then abruptly released. Recordings were taken continuously from just before (control) to 20 seconds after release. Measurements and calculations. Heart rate (HR) was expressed per beat as 60 divided by the preceding R-R interval. Left ventricular ejection time (LVET) was measured from the rapid upstroke to the incisura of the carotid tracing.‘* Predicted ejection time for rate was calculated from the regression elquation relating LVET to

Valsalva maneuvw

changes

Timing

vs. beat-to-beat

Mean heart rate

S.D.

Control

71.8

13.24

3.99

0.0

-

-

Strain Initial rise Lowest End strain rise

76.4 67.0 88.5

11.19 11.25 15.00

3.54 3.39 4.52

2.2 4.8 -

0.92 1.17

41.8 24.2 -

Post release Rise Fall Rebound

99.0 63.2 68.2

12.51 8.76 10.58

3.77 2.64 3.35

4.5 8.8 10.7

0.82 1.40 1.42

18.4 15.9 13.2

Coq$cient

Table II. Left vent&x&w

SE.

Mean beat

ejection time (LVET)

L VET

S.D.

of variation (Yo)

Mean time (msec.)

Coeficient S.D.

of oariation (%)

0.0

changes

Timing

-

-

1273.5 3240.9 12,000.0

757.6 1156.0 -

59.5 35.7 -

2426.4 5573.6 7364.0

494.2 1481.7 1747.2

20.4 26.6 23.7

vs. beat-to-beat

Mean LVET

S.D.

S.E.

Meaz beat

S.D.

Cofzjicient of variation (%)

Control

296

23

7

0.0

-

-

Strain Initial fall Lowest End strain

281 226 229

22 27 27

7 8 8

5.0 14.0 -

2.20 I. 79

44.7 12.8 -

220 284 306

20 14 15

8 4 5

1.4 6.2 12.7

0.79 1.74 2.24

55.0 27.7 17.6

rise

analysis

changesduring Valsalva maneuver

Phases

Post release Fall Initial rise Maximum

523

Effects of the VM on th.e cardiac systolic intervals

analysis

Mean

Co&cient

time (msec.)

SD.

of variation (%I

-

-

3715.0 10,489.O 12,000.0

2234.0 1691.0 -

60.1 16.1 -

561.4 3394.5 8970.9

208.7 892.5 2421.7

37.2 26.3 27.0

0.0

HR previously reported from this iaboratory for comparable subjects,‘* viz.: 376 1.2 HR rrt 12 msec. (1 SD.).* Pre-ejection period (PEP) was measured as interval from qI1 to the onset of ejection. Onset of ejection was determined as the time of the rapid carotid upstroke (CARu) minus pulse transmission time (PTT) ; PTTr7 is the interval between the aortic component of the second heart sound (11~) and the carotid incisura (CARIn). Two components of the PEP were also measured, qI1 to the first rapid vibration of the first heart sound (I,) and In to onset of ejection. This

regression equation is almost identical with those of Willems and Kesteloot’~ (3i7 - 1.2 HR) and of Penati and SimeonP (378 - 1.2 HR).

We had hoped to use the apexcardiogram to measure external isovolumic contraction time,r3 electromechanical 1ag,18 and other intervals, lgm but ACC curves proved unrejiable in most subjects owing to gross distortion during strain. Graphic handling of results. Curves for each parameter were plotted for each subject and grouped (Figs. 2 to 4) to visualize the points of change for each trend. These points were analyzed quantitatively and expressed as means & 1 standard error for the LVET and HR changes (Fig. 5). A timing versus beat-to-beat analysis i 1 standard deviation was made and the coefficient of variation calculated for each point of change on these curves (Tables f and II).

CONTROL

HEART RATE SYS. AORTIC PRESSURE

Q/AS.

SYMPATHETIC ACTIVITY CARDIAC OUTPUT STROKE VOLUME LV VOLUME PEP LVET

to maneuver, I+.&. 1. Schema of reported cardiocirculatory responses . the Valsalva heart rate, pre-ejection period (PEP) and left ventricular ejection time (LVET). numerals) separated by verticai lines.

including, Traditional

from this report, phases (Koma~l

525

Efeects of the VM on the cardiac systolic intervals

Results

the beginnings of phases 1 and 3 of the traditional partition of the VM (Fig. 1). PEP curves (Fig. 2) showed no definite trends; this was equally true of the PEP components, qII-I M and I If-ejection. The LVET and HR curves showed dis-

The results are presented in Tables I and II and Figs. 2 to 4. It was considered that two basic physiologic challenges were imposed on the subjects: strain and release corresponding to msec

150

50 -

-STRAIN+

+I

2

3

4

5

6

7

8

9

IO BEATS

II

12

I3

I4

I5

16

17

I8

I9

20

21

msec

+I

2

3

4

5

6

i

8

9

IO

II

I2

13

14

15

I6

I7

18

19

BEATS Fig. ZA. Valsalva trends. (See text.),

significanttren&.

maneuver. Pre-ejection B. Valsalva maneuver. (See text.)

period during strain. Beat-to-beat Pre-ejection period after release.

analysis Beat-to-beat

revealed no significant analysis revealed no

33Q 320 310 300 290 280 270 260 250 240 230 220 210 200

CONTROL

i90 -STRAIN--+

\

x

I

I

I

II

13

14

15

16

I80 I

+I

I

III1

2

3

Fig. 3d. Valsaiva maneuver. suknarized in Fig. 5.

4

5

Left

6

ventricuiar

I

I

I

7

8

9

I

10 BEAYS

ejection

kinct trends (Figs. 3 and 4), with points of change occurring within a very narrow range of beats after either strain or release (Tables I and 11). The beat-to-beat courses of change in LVET and HR are expressed (A 1 S.E.) in Fig. 5. Fig. 5 shows broken lines following the fourteenth strain beat because this was the mean beat (Table II) at which LVET plateaued (while HR continued to rise steadily to the 12 second release point). Open circles in Fig. 5 represent the predicted LVET’s per beat. These were within 1 S.D. (12 msec.) of the measured LVET’s only at the beginning of strain and as recovery was approached at the end of the postrelease period. In the midportions of the curves, LVET’s deviated widely from those expected from HR measurement. The successive changes in LVET and HR permitted division into six phases each (three each following strain and release) ;

period

II

Ii

12

changes

during

strain.

There

11

17

18

19

is a progressive

[

,

20

21

drop,

several of these were approximately synchronous (Fig. 5). These phases are described as increments and decrements in Tables I and iI along with the corresponding mean beat and mean time A 1 S.D. following strain or release. There was a consistently lower coefficient of variation for beat-to-beat analysis, with two minor exceptions: (1) the postrelease rise in LVET, in which the coefficients were approximateiy equal, and (2) the brief postrelease fall in LVET in which timing appears less variable. Fig. 5, however, shows the latter to be insignificant, since it is small, with a relatively large standard error which overlaps the SE. of the preceding phaseiscwssiorp

To establish the frame of reference of our results, Fig. 1 summarizes the pressure, flow, ventricular volume, stroke volume,

Ejects

524

of the YM on the cardiac systolic inten&

msec 320

7

310 300

-

290

-

260

-

270 260 -3 250

-

240 -

I +I

I 2

I 3

I 4

I 5

I 6

I 7

I 8

I1 9

IO

I It

I 12

I 13

after

release.

r----f-I 14 15

16

17

I8

19

20

BEATS Fig. sB. Valsalva maneuver. rapid reascent, summarized

Left ventricular in Fig. 5.

ejection

and sympathetic activity changes during the Valsalva maneuver reported by different investigators’-5,‘-12,z1,zz plus the heartrate and ejection-time changes in this report. Heart rate (Figs. 4 and 5 and Table I). Heart-rate response during the Valsalva maneuver has been extensively studied and is a reliable index of the dynamic changes which occur.*~B~~,g The rate response of our subjects agrees closely with those previously reported. Lower coefficients of variation and smaller standard deviations for beat-to-beat analysis indicate that particular beats characterize better than a given time the points of change of NR along the course of the VM. Pre-ejection $eriod (Fig. 2). Because of the technical failure of apexcardiogram recordings during strain, external isovolumic contraction time13 could not be measured; the PEPz3 which parallels the isovolumic contraction period was meas-

period

A small

initial

drop

is succeeded

by

ured from the electrocardiogram, phonocardiogram, and carotid trace. The PEP did not demonstrate any significant trends nor did its components, the q to first heart-sound interval and first sound to onset of ejection. Stability of the PEP and its components implies that the isovolumic period remained stable during the Valsalva maneuver. The isovolumic period changes directly with aortic diastolic pressure and inversely with ventricular end-diastolic and stroke volumes, each of which have the same directional tendencies during most of the VM and could, therefore, mutually cance1.23-26 Yforeover, recent studies27 have shown that the PEP tends to be stable during interventions which change HR and stroke volume in opposite directions-conditions characteristic of the VM. Left ventricuh ejection time (I’+&. 3 a?zd 5 and Table II). Changes of LVET during the Valsalva maneuver were similar in all

+CONTROL -STRAIN--J I +I

A I

I

I

I

I

I

I

I

I

I

I

I

I

I

I

I

I

I

2

3

4

5

6

7

8

9

IO

I!

12

13

14

15

16

17

18

19

I1

20

21

BEATS Fig. fd. Valsalva rise, summarized

maneuver. in Fig. 5.

Kate

changes

during

strain.

subjects: LVET begins to shorten after the third (average) beat, reaches its lowest point late in straining (fourteenth beat), stays stable thereafter up to release, falls slightly but insignificantly for about one to two beats, starts increasing quickly after the third postrelease beat, reaches almost control levels at the fifth postrelease beat, and exceeds slightly the control levels for one to two beats at about the thirteenth beat. LVET varies inversely with heart rate and directly with stroke volume. An inverse relation with aortic diastolic pressure has been reported for dogs,Z4 but studies in humans report a direct relationz5 To demonstrate the degree of dependence of LVET changes upon heart-rate changes, we calculated the predicted LVET for heart rate beat by beat (open circles in Fig. 5), using the rate-LVET regression equation previously reportedi4-lG and compared these two curves (Fig. 5)- If HR

Slight

net rise and fall

is followed

by a progressive

were the only determinant of LVET, observed and predicted LVET’s would have coincided. As expected, the Valsalva maneuver imposed a marked divergence during most of the period of observations. After beginning of strain (beats 3 to 8), the rate remains either at or below control levels, while EVICT has begun to decrease sharply thereafter, remaining low until after release. Following the third postrelease beat, LVET quickly increases and by the fifth beat it has almost returned to control values, while the rate achieves its !lighest level. The behavior of LVET thus far would be paradoxic if rate alone were the controlling factor. Following this the curves diverge and LVET again behaves as predicted for rate. If we compare our LVET results with reported stroke volume (SV) changes occurring during the VA4 (Fig. I), we see a very close parallel relationship. A study of stroke volume during the VM2 shows

60

I +I

I 2

I 3

I 4

I 5

I 6

I 7

I 8

I 9

I IO

I II

I I2

I I3

I I4

I I5

I I6

I 17

I I8

I 19

I 20

i 21

BEATS

Fig. JB. Vaisalva precipitous

fall

maneuver. and thereafter

Rate changes after r&ease. Colltinued rise is followed, a slight rebound, summarized in Fig. 5.

that SV falls after the third strain beat and continues falling up to release. At about the third postrelease beat, SV starts increasing and reaches control values between the sixth and ninth beat and its highest value at the fifteenth beat. These reported data for SV are in striking agreement with our LVET changes, not only in direction, but also for the particular beats where changes take place. The fact that both SV and LVET tend to change after the third beat of straining and the third postrelease beat is in accord with the delay of the left ventricle in following stroke volume changes of the right ventricle, which averages three beats.1’~28~2s The curve of changes in LVET in Fig. 3 also bears a striking resemblance to the curve of changes in aortic flow reported during the VlU,r which also reflects the dependence of LVET on stroke volume during the VM and early postrelease period. Thus, the close dependence of LVET upon

after

beats

4 to 5, by a

SV and not upon FIR during strain and the early postrelease period implies not only that HR and SV can be independent determinants of LVET,12s24*3nbut also that during the VM, SV is the main determinant. It is thus apparent that LVET changes during the VIM sensitively reflect SV rather than HR changes. Beat-to-bed nnalysis (Tables I and II). It is noteworthy that the significant changes in the LVET and HR curves for each subject tended to occur within narrow (1 to 3 beat) ranges. Comparison of coefficients of variation in Tables I and II indicate that beat-to-beat analysis of HR and LVET responses during the VM defined more precisely the points of change following strain and release than did timings of these points. Because of normal variability in basal heart rates and autonomic “tone” among subjects, this result is not unexpected. It implies that it would

Q =

Predicted

LVET

Fig. 5. Beat-to-beat analysis of responses of left ventricuiar ejection time and of hear-t rate to the VaMva maneuver. Dots: mean * S.E. of results in 11 subjects (plotted in Fig. 3 and 1;) at mean beat for trend changes (S.D. for beats given in Tables I and II). Circles: predicted ejection time for corresponding heart rate from regression equation. Three discernible trend changes following control and release in both LVET and HR (listed in Tables I and II). Overlap of standard errors of LVET values at lowest prerelease, end of strain, and (less so) immediately after release suggest a plateauin, g tendency before the rapid reascent. be more physiologic to evaluate the VA4 on a beat-to-beat rather than a time basis.

less variability. among subjects than do time-based measurements.

Conclusions 1. TFhe heart maneuver in classic pattern. 2. Changes time occurred

rate response our subjects

to the Valsalva followed the

in left ventricular ejection as expected for the known

changes in stroke volume and aortic flow during strain and immediately after release, and were largely independent of heart rate. 3. Stability of the pre-ejection period was consistent with effects known to change its determinants in opposite directions during the Valsalva maneuver. 4. Beat-to-beat analysis of changes during strain and following release results in

Beat-to-beat and timed measurements of Valsalva-induced changes in pre-ejection Teriod (PEP), left ventricular ejection time (LVET), and heart rate (HR) were made in I1 normal volunteers. External isovolumic contraction time and other intervals could not be measured because the apexcardiogram was distorted during straining. HR followed the classic pattern. PEP and its components tended to be stable, reflecting mutual cancellation of opposite effects of -‘IR and stroke volume. Following strain, LVET fell and remained low until just after release and departed widely from

Volume Number

80 4

Effects oj the VM on the cardiac systolic intervais

predicted values for the corresponding heart rates, reflecting its primary dependence on stroke volume rather than HR. Beat-to-beat analysis of changes in LVET and HR showed less variability among subjects than did time-based determinations of the same points. REFERENCES

1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

Fox, I. J., Crowley, W. P., Jr., Grace, J. B., and Wood, E. H.: Effects of the Valsalva maneuver on blood flow in the thoracic aorta in man, J. Appl. Physiol. 21:1553, 1966. Greenfield, J. C., Cox, R. L., HernLndez, R. R., Thomas, C., and Schommaker, F. V.: Pressureflow studies in man during the Valsalva maneuver with observations on the mechanical properties of the ascending aorta, Circulation 35:653, 1967. Sarnoff, S. J., Hardenbergh, E., and Whittenberger, J. L.: Mechanism of the arterial pressure response to the Valsalva test: The basis for its use as an indicator of the intactness of the sympathetic outflow, Amer. J. Physiol. 154:316, 1948. Gorlin, R., Knowles, J. H., and Storey, C. F.: The Valsalva maneuver as a test of cardiac function, Amer. J. Med. 22:197, 1957. Elisberg, E., Singian, E., Miller, G., and Katz, L. N.: Effect of the Valsalva maneuver on the circulation; influence of heart disease on the expected poststraining overshoot, Circulation 7:880, 19.53. Levin, A. B.: A simple test of cardiac function based upon the heart rate changes induced by the Valsalva maneuver, Amer. J. Cardiol. 18:90, 1966. Elisberg, E. I., Miller, G., Weinberg, S. L., and Katz, L. N.: The effect of the Valsalva maneuver on the circulation. II. The role of the autonomic nervous system in the production of the overshoot, AMER. HEARTJ. 45:227, 1953. 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, 19.52. Elisberg, E. I.: Heart rate response to the Valsalva maneuver as a test of circulatory integrity, J. A. M. A. 186:200, 1963. Booth, R. W.: The hemodynamics of the Valsalva maneuver in normal subjects, Clin. Res. 8:178. 1960. Harrison, D. C., Goldblatt, A., and Braunwald, E.: Studies on cardiac dimensions in intact. unanesthetized man, Circ. Res. 13:448, 1963: Braunwald, E., Sarnoff, S. J., and Stainsby, W. D.: Determinants of duration and mean rate of ventricular ejection, Circ. Res. 6:319, 1958. Spodick, D. H., and Kumar, S.: Isovolumetric contraction period of the left ventricle, AMER.

HEART J. 76:498, 1968.

14.

Spodick,

D. H., and Kumar,

S.: Left

ventricular

531

ejection period, AMER. HEART J. 76:70, 1968. Willems, J., and Kesteloot, H.: The left ventricular ejection. Its relation to heart rate, mechanical systole and some anthropometric data, Acta Cardiol. 22:401, 1967. 16. Penati, F., and Simeoni, 0.: 11 tempo di tensione e di espulsione della sistole cardiaca in fuzione della frequenza nell’ vomo ad apparata cardiovascolare normale, Arch. Sci. Med. 77:121, 1944. T. J., Hefner, L. L., Jones, W. B., 17. Reeves, Coghlan. C.. Pneto. G.. and Carroll. 1.: The hemodynamic determinants of the’ Gate of change in pressure in the left ventricle during isometric contraction, AMER. HEART J. 60:745, 1960. D. H., and Kumar, S.: Electromechan18. Spodick, ical lag of the left ventricle. Cardiovasc. Res. 2:338,-1968. D. H., and Kumar, S.: Atraumatic 19. Spodick, measurement of the isometric relaxation period of the left ventricle, Aerospace Med. 39:968, 1968. 20. Spodick, D. H., and Kumar, S.: Rapid filling period of the left ventricle: Measurement by apexcardiography, Aerospace Med. 39:135 1, 1968. 21. Whitley, J. E., and Martin, J. F.: The Valsalva maneuver in roentgenologic diagnosis, Amer. J. Roentgen. 91:297, 1964. 22. Rushmer, R. F.: Circulatory effects of three modifications of the Valsalva experiment,

15.

AMER. HEART J. 34:399, 1947. 23.

Weissler, A. M., Harris, W. S., and Schoenfeld, C. D.: Systolic time intervals in heart failure in man, Circulation 37:149, 1968. 24. Wallace, A. G., Mitchell, J. H., Skinner, N. S., and Sarnoff, S. J.: Duration of the phases of left ventricular systole, Circ. Res. 12:611, 1968. 25. Shaver, J. A., Kroetz, F. W., Leonard, J. J., and Puley, H. W.: The effects of steady-state increases in systemic arterial pressure on the duration of left ventricular ejection time, J. Clin. Invest. 47:217, 1968. 26. Harris, W. S., Schoenfeld, C. D., and Weissler, A. M.: Effects of adrenergic receptor activation and blockade on the systolic preejection period, heart rate and arterial pressure in man, J. Clin. Invest. 46:1704, 1967. 27. Harley, A., Stavner, C. F., and Greenfield, J. C., Jr.: Pressure-flow studies in man. An evaluation of the duration of the phases of systole, J. Clin. Invest. 48:895, 1969. 28. Franklin, D. L., Van Citters, R. L., and Rushmer, R. F.: Balance between right and left ventricular output, Circ. Res. 10:17, 1962. 29. Hoffman, J. I. E., Guz, A., Charlier, A. A., and Wilcken, D. E. L.: Stroke volume in conscious dogs; effect of respiration, posture, and vascular occlusion, J. Appl. Physiol. 20:865, 1965. 30. Weissler, A. M., Peeler, R. G., and Roehll, W. H., Jr.: Relationships between left ventricular ejection time, stroke volume, and heart rate in normal individuals and patients with cardiovascular disease, AMER. HEART J. 62:367,

1961.