Effect of pulmonary circulation on vector impedance cardiogram.
SA Pedhnekar, GD Jindal, SN Nerurkar, JB Dharani, AK Deshpande, GB Parulkar
Department of Cardiovasular and Thoraeic Surgery, K.E.M. Hospital, Bombay, India., India
S A Pedhnekar
Department of Cardiovasular and Thoraeic Surgery, K.E.M. Hospital, Bombay, India.
Vector impedance cardiograms in horizontal lead configuration [VICG(H)] were recorded in 34 normal subjects, 18 patients with mitral stenosis, 9 patients with mitral regurgitation, 14 patients with aortic regurgitation and 13 patients with non- cyanotic septal disorders. Data in normal subjects revealed that most of the phase reversal points in VICG(H) waveform did not coincide with those of conventional impedance cardiogram. The shape of VICG(H) waveform and values of VICG indices were observed to be markedly affected in patients having significant alteration in the pulmonary circulation and the changes observed were specific of the type of the disorder. The results of the study suggested that right side of the heart had dominant contribution in generation of VICG(H) waveform.
|How to cite this article:|
Pedhnekar S A, Jindal G D, Nerurkar S N, Dharani J B, Deshpande A K, Parulkar G B. Effect of pulmonary circulation on vector impedance cardiogram. J Postgrad Med 1990;36:213-8
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Pedhnekar S A, Jindal G D, Nerurkar S N, Dharani J B, Deshpande A K, Parulkar G B. Effect of pulmonary circulation on vector impedance cardiogram. J Postgrad Med [serial online] 1990 [cited 2022 Oct 2 ];36:213-8
Available from: https://www.jpgmonline.com/text.asp?1990/36/4/213/826
Impedance plethysmogram recorded from thorax in Kubicek's neck- abdomen configuration, commonly known as impedance cardiogram (ICG), is a precisely defined waveform in the time domain. For instance points B, X, Y, and O of the ICG waveform are synchronous with the aortic valve opening, the aortic valve closure, the pulmonary valve closure and the mitral valve opening respectively. Precise definition of ICG in time domain has led to its use in the assessment of left ventricular function, mitral regurgitating fraction and aortic regurgitating fraction as described elsewhere. However, events of the right heart such as tricuspid valve opening, pulmonary valve opening etc. did not produce any discernible points in the ICG waveform and therefore ICG had little role in the study of pulmonary circulation. Jindal et al recorded first time derivative of the impedance (dz/dt) in directions perpendicular to that of the aorta. They passed carrier current in horizontal and anterio-posterior directions and the electrical impedance was measured along the current path. The waveforms thus obtained were named as Vector Impedance Cardiogram Horizontal Lead (VICG (H) and Vector Impedance Cardiogram Anterio-posterior lead (VICG (AP). Vector Impedance cardiogram Anterio-posterior Lead (VICG (AP)). Kubicek's neck-abdomen configuration was also included as the vertical lead and was referred to as Vector Impedance Cardiogram Vertical (VICG (V) for the sake of completeness. The results of the preliminary study showed VICG (H)) waveform to be significantly different from VICG (V) waveform in time domain. In this paper we present the temporal co-relation between VICG (V) and VICG (H) waveforms and changes in the shape of the later in the presence of cardiac disorders.
Thirty four normal subjects of age between 6 and 45 years (Group I), 18 patients with isolated mitral stenosis Group II), 9 patients with mitral regurgitation (Group III), 11 patients with aortic regurgitation (Group IV) and 13 patients with non-cyanotic septal disorder (Group V) were subjected to this study at Non- invasive Vascular laboratory, King Edward Memorial Hospital. The results of routine investigations (X-ray chest, ECG), special investigations (echo cardiography, cardiac catheterisation) and operation table findings were obtained for confirmation of diagnosis in all the patients. With the subject in supine VICG (V) was recorded in Kubicek's configuration using BARC made microprocessor based impedance plethysmograph system. For recording VICG (H) waveform the current electrodes (11, 12) were applied around upper extremities at brachial level and the voltage electrodes (V1, V2), spot electrodes of size 6 x 4 cm (2), were applied on the lateral walls of the chest just below the axillae as shown in [Figure:1]. Average VICG waveforms of 50 cardiac cycles were recorded on the strip chart recorder. 10 mm deflection on Yaxis represented 1 ohm/sec of dZ/dt. Elapsed time from R-wave of ECG to various phase reversal points in VICG(V) and VICG(H) waveforms were measured as shown in [Figure:2]. Various VICG indices namely B, Bc, Bx, Yy, Yo, vo and vz were calculated from these intervals as follows:
? = Pb?/PB?,
?c = RCh/RCv,
?x = RXh/RXv,
?y = RXh/Ryv,
?o = RXH/Rov,
?o = Roh/Rov and
?z = Roh/RZv
[Table:1] gives the average and standard deviation (SD) values of various time intervals of VICG (V) and VICG (H) waveforms in 34 normal subjects. Time intervals of VICG (V) waveform are compared with corresponding time intervals of VICG (H) waveform by using student's ‘t’ test. Time interval RYh is not measured as the point Yh was not discernible in majority of VICG (H) waveforms. As can be seen from the table there is a significant difference between RCv and RCh, RXv and RXh, ROv and ROh, and RZv and RZh (p). It therefore appears that points Ch, Xh, Oh and Zh of VICG (H) waveform represent different events of the cardiac cycle than those represented by Cv, Xv, Ov and Zv of VICG(V) respectively. It is, interesting to observe that RXh is closer to RYv as indicated by low value of student's ‘t’ (1.354). This suggests that Xh of VICG (H) and Yv of VICG (V) may be originated from the same event of the cardiac cycle, namely the pulmonary valve closure.
[Table:2] gives the average and SD values of VICG indices in Group I to Group V subjects. The values of student's ‘t’ for each VICG index in patient groups in comparison to that of normal subjects are also given in the table. The important observations in this table are:
1. The value of ? is significantly increased in patients with mitral stenosis or noncyanotic septal disorder.
2. The value of ?c is significantly decreased in patients with mitral stenosis and significantly increased in patients with mitral regurgitation.
3. The values of ?x, ?y and ?o are significantly decreased in patients with mitral stenosis or aortic regurgitation and significantly increased in patients with non-cyanotic septal disorders.
4. The value of ?o is significantly decreased in patients with mitral stenosis.
5. The value of ?z is significantly decreased in patients with mitral stenosis, mitral regurgitation or aortic regurgitation.
Thus increase in the value of ?x, ?y and ?o is specific for non- cyanotic septal disorder, increase in the value of pc is specific for mitral regurgitation and decrease in the value of ?c is specific for mitral stenosis. Other conditions are specified by a combination of these indices.
The shape of VICG (H) waveform recorded in some of the cardiac lesions has also been observed to be significantly different from that of normal subjects. For instance:
1. The amplitude of O-wave of VICG (H waveform is markedly increased in patients with tricuspid regurgitation associated with mitral regurgitation (see [Figure:3]).
2. The amplitude of C-wave of VICG (H) waveform is markedly reduced in patients with mitral stenosis associated with severe pulmonary hypertension (see [Figure:4]).
3. The amplitude of C-wave of VICG (H) waveform is significantly increased in patients with non-cyanotic septal disorders.
Data in control subjects show that VICG (H) is synchronous with Yv of VICG (V) and is likely to represent pulmonary valve closure. Bv and Bh appear to be synchronous in normal subjects, however, increase in b in patients with mitral stenosis and those with non-cyanotic septal disorders has demonstrated that Bv and Bh are not originated from the same event of cardiac cycle. Furthermore the increase in value of ? has been observed to be in correlation with the degree of pulmonary hypertension in patients with valvular disorders. Therefore it will be interesting to have simultaneous recording of M-mode echo-cardiogram and VICG (H) to demonstrate that Bh and Xh are synchronous with pulmonary valve opening and pulmonary valve closure respectively.
Decrease in the amplitude of C-wave of VICG (H) in patients with severe pulmonary hypertension associated with mitral stenosis (see [Figure:4]) and cyanotic septal disorders (not reported here), and increase in the amplitude of same in patients with noncyanotic septal disorders further corroborate the origin of C-wave of VICG (H) from right side of the heart. Similarly marked increase in the amplitude of O-wave of VICG (H) in patients with tricuspid regurgitation associated with mitral regurgitation suggests dominant contribution of right side of the heart in VICG (H) waveform.
As described elsewhere by us, 3 majority of investigators agree that conventional impedance cardiogram is originated from aorta, vena-cava and chambers of the heart. The contribution from aorta dominates because of its anatomical alignment with the axis of the measurement of impedance. Though venacava is also anatomically aligned with the axis of impedance measurement, the pressure gradients and peak flow rate are considerably smaller in vena-cava to those of the aorta, and therefore the contribution from vena-cava is expected to be smaller than that of aorta. Similarly pulmonary arteries being oblique to the axis of measurement though have significant projections along vertical axis, their contribution in conventional ICG is masked by the aortic contribution.
As VICG (H) waveform is recorded along horizontal axis, contribution from aorta and vena-cava are likely to be minimal as they are anatomically perpendicular to the axis of measurement. The pulmonary arteries, therefore, are expected to make significant contribution to VICG (H) waveform. This explains the dominant contribution from the right side of the heart to VICG (H) waveform as observed in this study. Thus vector impedance cardiography offers a simple, inexpensive and non-invasive modality for the study of pulmonary circulation.
The authors gratefully acknowledge Dr (Mrs.) Pragna Pai, Dean, Seth GS Medical College and King Edward Memorial Hospital, Dr MD Kelkar, Ex. Prof. and Head, Dept. of Radiology, King Edward Memorial Hospital, Dr (Miss) RA Maghotra, Head, Cardio-vascular and Thoracic Surgery Dept., King Edward Memorial Hospital, Mr Hari Singh, Scientific Officer, NUMAC, BARC and Mr SP Agarwal, Scientific Officer, DRP, BARC for giving valuable suggestions in the analysis of the data.
Bhuta AC, Babu JP, Jindal GD, Parulkar GB. Technical aspects of impedance plethysmography. J Postgrad Med 1990; 36:64-70.|
|2||Deshpande AK, Jindal GD, Jagasia PM, Murali KVS, Bharadwaj PA, Tahlilkar KI, Parulkar GB, et al. Impedance plethysmography of thoracic region: impedance cardiography. J Postgrad Med 1990, pp 36.|
|3||Dharani JB, Jindal GD, Tahlikar KI, Deshpande AK, Parulkar GB. Physiological correlates of impedance plethysmograpbic waveform. J Postgrad Med 1990; 36:71-79.|
|4||Jindal GD, Dharani JB, Parulkar GB. Vector impedance cardiography. Ind Heart J 1982; 34:232-235.|
|5||Jindal GD, Suraokar SB, Babu JP, Dharani JB, Kelkar MD, Parulkar GB, et al. Assessment of pulmonary hypertension in patients with mitral stenosis using vector impedance cardiography, “Progress in Angiology”, Minerva Medica; 186, pp. 83-86.|
|6||Mohapatra, SN. Non-invasive cardio-vascular monitoring by electrical impedance technique. London: Pitman Medicals; 1981.