Internafional Elsevier
Journal
of Cardiology, 20 (1988) 365-372
365
IJC 00729
Changes in the impedance cardiogram occurring with change in posture in patients with heart disease N.T. Richards ’ and D.J. McBrien 2 ’ St. Thomas’ Hospital, London, U.K.; ’ Worthing Hospital, Worthing, West Sussex, U.K. (Received 26 September 1987; revision accepted 22 February 1988)
Richards NT, McBrien DJ. Changes in the impedance cardiogram occurring with change in posture in patients with heart disease. Int J Cardiol 1988;20:365-372. The response of the heart to changes in posture from supine through sitting to standing was recorded by impedance cardiography. Tbe study comprised 22 normal subjects and 74 patients with a variety of heart diseases. Tbe results demonstrate that in normal subjects acceleration of blood in systole decreased on sitting and standing. In subjects with impaired cardiac function this acceleration increased on sitting and standing from the supine position. This clear-cut difference in response provides a subtle method of detecting impaired function and in addition, provides a method of monitoring the effects of vasodilator or other treatment. Key words: Impedance sistance
cardiography;
Heather index; Contractility;
Peripheral
re-
Introduction Impedance cardiography is routinely used in our hospital for the initial assessment and follow-up of patients with cardiac disease. In our department we have recently described the applications of impedance cardiography in the assessment of patients with heart failure [l]. We have now expanded this work to involve the changes seen in the impedance cardiogram with changes in posture from supine, through sitting to standing in both normal subjects and patients with heart disease. An excellent up-to-date account of the scientific basis of impedance cardiography has been produced by Lamberts [12].
Correspondence to: Dr. N.T. Richards, The Renal Laboratory. St. Thomas’ Hospital, Lambeth Palace Road, London SEl, U.K.
0167-5273/88/$03.50
0 1988 Elsevier Science Publishers B.V. (Biomedical Division)
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Patients and Methods Impedance cardiograms were recorded from 74 patients (mean age 62.3 years, range 21-84 years, 58 males) and from 22 normal volunteers, (mean age 50 years, range 33-64 years, 11 males). The diagnoses in the patient group were: ischaemic heart disease (42), mitral regurgitation (8), mitral stenosis (5), aortic stenosis (7) aortic regurgitation (3), complete heart block (3) cardiomyopathy (4) pericardial disease (1) and congenital heart disease (2). The normal group had no history or signs suggestive of cardiac disease. The recordings were obtained using a Minnesota Impedance Cardiograph Model 304 simultaneously with an electrocardiograph. Four aluminium coated strip electrodes (3M) with an adhesive tape backing were used. Electrode 1 was placed on the forehead between the hair lines, electrode 2 around the neck and electrodes 3 and 4 around the thorax, at least 3 cm apart at the level of the xiphistemum. A constant sinusoidal current of 4 mA with a frequency of 100 kHz was applied between the two outer electrodes (1 and 4). The electrical impedance between electrodes 2 and 3 was continually recorded. The transthoracic impedance, its first derivative and the electrocardiogram were all recorded simultaneously using a Bell and Howell ultraviolet recorder, at a paper speed of 400 cm/mm. After a calibration signal of 1 ohm/set, an initial record of at least six consecutive heart beats was made with the subject supine; recordings were then made with the subject sitting upright with his legs over the side of the bed and finally standing upright. A typical trace is shown (Fig. 1). The Heather Index (ohm/set’) was obtained using the formula (dZ/dt)max/RZ [ll], where the (dZ/dt)max is the maximum peak of the first derivative of the transthoracic impedance (ohm/set) and RZ is the interval in seconds between the
Sllllng
Slandlng
dZ/dl
ECG
Fig. 1. A simultaneous recording of the thoracic impedance (AZ), the first derivative of the impedance change (dZ/dt) and the electrocardiogram. The typical changes in dZ/dt with changes in posture in a patient with heart disease are shown. The (dZ/dt)max and RZ are used in the calculation of the Heather index.
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peak of the R wave of the electrocardiogram and the peak of the dZ/dt waveform (Fig. 1). The index is a measure of cardiac contractility. There is good correlation between the index and the two standard indices of contractility, namely right ventricular wall tension and the maximum rate of pressure rise in the left ventricle [3]. The index shows some individual variation but is low in states of reduced contractility and rises with improvement in myocardial performance. A mean index (ohm/sec2) was calculated for at least three cardiac cycles in the supine, sitting and standing positions.
Results All values are expressed as mean * standard error of the mean unless otherwise stated. Changes in Heather index
Normal subjects. When supine the index was 16.6 + 0.92 ohm/see’; this fell to 16.4 k 0.87 ohm/sec2 on sitting (NS) and to 15.8 f 0.91 ohm/sec2 on standing (NS) (Fig. 2). The absolute changes noted when posture changed from supine to sitting and supine to standing (obtained by subtracting the supine value from the value sitting and the value standing) were - 0.35 f 0.62 and - 0.72 + 0.53 ohm/sec2, respectively (Fig. 3).
?
18P
5
17-
PATIENTS
0
B G
16-
:
15
NORMALS
z z
14 _
13 -
t SUPh
Fig. 2. Change
in Heather
index with change
I sitting
in position
I Standing
from supine through
sitting to standing.
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Patients. When supine the index for the patient group as a whole was lower than the normal group at 13.4 & 0.84 ohm/set’ (P -c 0.05), this increased on sitting and standing to 16.9 f 1.1 ohm/set’ (P < 0.05) (Fig. 2). The changes from supine to sitting and supine to standing were 3.7 k 0.47 and 3.7 + 0.58 ohm/set’, which are significantly greater than those seen in normal subjects (P < 0.00005 and P < 0.0001, respectively) (Fig. 3). The patient group was subdivided for further analysis by diagnosis (Fig. 4) treatment (Fig. 5) and ventricular function as assessed by the index (normal severely index > 15 ohm/sec2, moderately impaired index > 7.5 < 15 ohm/set’, impaired index < 7.5 ohm/sec2) (Fig. 6). In all groups the index increased with change in posture from supine through sitting to standing. When supine the index for patients with ischaemic heart disease was lower than that for patients with valvar disease (P < 0.05) and normal subjects (P < 0.001). On sitting and standing, the index increased but failed to reach the values seen in normal subjects, or those seen in patients with valvar disease, which exceeded the normal values (P < 0.02). The greatest changes were seen in patients with mitral stenosis, aortic regurgitation and mitral regurgitation. When supine the index for patients taking vasodilators was 11.5 + 0.82 ohm/set’ compared to 16.6 f 0.92 ohm/set ’ for normal subjects (P > 0.001). Values for patients taking diuretics or on no medication were not significantly different from normal. The change in the index from supine to sitting and supine to standing for patients taking no medication was 3.5 + 0.72 and 4.5 _t 1.4 ohm/sec2 (P > 0.0001);
Standing
Fig. 3. Absolute
change
in Heather
index over supine value with change sitting to standing.
in position
from supine
through
369 12
-
11
-
10
-
9
-
Mitral
Stenosis
Aortic
Regurgitation
Mitral
Regurgitation
Aortic
Stenosis
lschaemic Disease 2
-
1
-
Heart
0
-1
-
NORMALS
Fig. 4. Absolute change in Heather index with change in position for patient group divided by diagnosis.
for patients taking diuretics 5.4 k 1.2 and 4.3 f 1.1 ohm/sec2 (P > 0.001) and for patients taking vasodilators 1.86 k 0.64 and 2.5 + 0.73 ohm/sec2 (P > 0.02). Analysing the patient group by degree of ventricular dysfunction showed that the abnormal response held true irrespective of the degree of dysfunction. The greatest response was seen in the group with a supine index S- 15 ohm/set’ index was significantly greater than normal in all groups.
(Fig.
6). The
Changes in R-R interval Normal subjects. The supine R-R interval was 0.91 + 0.02 set, falling to 0.87 f 0.02 and
0.82 + 0.02
set
on
sitting
and
standing,
respectively.
The
absolute
change
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’
No
Treatment
Vasodilators
Fig. 5. Absolute
change
in Heather
index with change
in position
for patient
group divided
Supine HI + 15
SITTING
Fig. 6. Absolute
change
in Heather
by treatment.
-2 ohm
STANDING
index with change in position Heather index.
for patient
group
divided
by supine
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(AR-R) from supine to sitting - 0.08 + 0.014 set, respectively.
and
supine
to standing
being
-0.04
+ 0.013 and
Patients. The R-R intervals were significantly shorter than in the normal group supine, sitting and standing, being 0.77 + 0.02, 0.73 + 0.02 and 0.69 f 0.02 set, respectively (P < 0.001). The AR-R intervals for the patients were not significantly and different from the normal group being - 0.04 -+_0.007 set (supine-sitting) -0.07 k 0.008 set (supine-standing). This held true for all subgroups.
Discussion In practical terms, the impedance cardiograph is a simple investigative tool which carries no risk or discomfort to the patient. Recordings can be made in only a few minutes. The Heather index was used as the definitive measure rather than cardiac output as derived from Kubicek’s formula [2] in order to obviate the need to measure the distance between the inner two electrodes, thereby increasing accuracy [l]. The dZ/dt waveform represents the rate of change in thoracic impedance with respect to time. During the cardiac cycle variations in thoracic impedance are due to changes in the volume of blood in the thorax and to the orientation of the red cells [12]. Therefore the systolic dZ/dt waveform represents the acceleration of blood into the thorax, which in its turn is a balance between ventricular ejection and peripheral resistance. Blood within the ventricles is electrically isolated by the myocardium. A greater force of contraction will produce a greater acceleration and a greater (dZ/dt)max [12]. The time taken for this to occur, the RZ interval, includes isovolumetric contraction which is known to vary inversely with the state of contractility. Both these measures are incorporated in the calculation of the Heather index. The patients with heart disease clearly behaved differently from the normal subjects. The abnormal response was independent of the heart rate and was present irrespective of the degree of heart disease. Those patients who had an index similar to that seen in the normal subjects, showed a greater response than patients with a reduced index rather than approximating to the normal group which might have been expected. The greatest changes in the index were seen in patients whose primary problem was volume overload of a relatively normal ventricle, i.e. mitral and aortic regurgitation. The abnormal response occurred in 70 out of 75 patients and was present in the absence of an abnormal 0 wave, which has been demonstrated in patients with severe heart failure [l]. Thus this response is a more sensitive indicator of disease. The mechanism behind the increased rate of ejection of blood from the ventricles on change of posture from supine to erect in the diseased heart, but not in the normal, is hard to explain, although the fact that it occurs is apparent clinically by the symptomatic improvement of patients with heart failure when they stand up. In normal subjects the upright posture is associated with significant peripheral pooling of blood, a fall in right-sided filling pressures and a fall in right ventricular end-diastolic volume [4-71. Orthostatic hypotension does not occur because reflex
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increase of heart rate and systemic vascular resistance compensate for peripheral pooling. The reflex change in patients with heart failure is atypical in that there is no significant peripheral pooling, no fall in right ventricular end-diastolic volume and although right-sided filling pressures fall they remain above normal values [8,9]. The normal compensatory mechanisms that protect blood pressure from the gravitational stress of peripheral pooling do not occur [lo]. The atypical response returns toward normal with institution of vasodilator therapy [lo] and has been attributed to intense volume expansion and vasoconstriction [8,9]. The interactions of controlling mechanisms are not known. In conclusion, the changes in the Heather index occurring with change in posture as described above provide a subtle tool which is sensitive and non-invasive for use in the assessment of patients with heart disease. An increase in the Heather index on standing correlated with the presence of heart disease, not only in patients with overt signs and symptoms, but also in that group of patients with non-specific symptoms and no signs, but with poor myocardial function as assessed by other means.
References 1 Hubbard WN, Fish DR. McBrien DJ. The use of impedance cardiography in heart failure. Int J Cardiol 1986;12:71-79. 2 Kubicek WG, Kamegis JN, Patterson RP, Witsoe DA, Matterson RH. Development and evaluation of an impedance cardiac output system. Aerospace Med 1966;37:1208-1212. 3 Thompson FD. Joekes AM. Thoracic impedance. Cardiodynamic assessment: validation and clinical use. St. Peters Hospital. London: Geigy Pharmaceuticals. 1981. 4 Tuckman J, Shillingford J. Effect of different degrees of tilt on cardiac output, heart rate and blood pressure in normal man. Br Heart J 1965;28:32-39. 5 Eckberg DL, Abboud FM, Mark AL. Modulation of carotid baroreflex responsiveness in man: effects of posture and propranolol. J Appl Physiol 1976;41:383-387. 6 Frohlich ED. Tarazi RC. Ulrych M. Dunstan HP, Page IH. Tilt test for investigating a neural component in hypertension. Circulation 1967;36:387-393. 7 Tarazi RC, Melsher HJ, Dunstan HP, Frohlich ED. Plasma volume changes with upright tilt: studies in hypertension and syncope. J Appl Physiol 1970;28:121-126. 8 Ableman WH. Fareeduddin K. Increased tolerance of orthostatic stress in patients with heart disease. Am J Cardiol 1969;23:354-363. 9 Ableman WH. Alterations in orthostatic tolerance after myocardial infarction and in congestive heart failure. Cardiology 1976:61(suppl 1):236-240. 10 Cody RJ. Franklin KW. Kluger J. Laragh JH. Mechanisms govermng the postural response and baroreceptor abnormalities in chronic congestive heart failure: effect of acute and long term converting enzyme inhibition. Circulation 1982;66:1355142. 11 Mohapatra SN. Non-invasive cardiovascular monitoring by electrical impedance technique. London: Pitman Medical, 1981. 12 Lamberts R, Visser KR. Zijlstra WG. Impedance cardiography. Assen. The Netherlands: Van Gorcum, 1984.