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Impedance plethysmography of thoracic region: impedance cardiography.
Correspondence Address:
Impedance plethysmograms were recorded from thoracic region in 254 normal subjects, 183 patients with coronary artery disease, 391 patients with valvular heart disease and 107 patients with congenital septal disorder. The data in 18 normal subjects and 55 patients showed that basal impedance decreases markedly during exercise in patients with ischaemic heart disease. Estimation of cardiac index by this technique in a group of 99 normal subjects has been observed to be more consistent than that of the stroke volume. Estimation of systolic time index from impedance plethysmograms in 34 normal subjects has been shown to be as reliable as that from electrocardiogram, phonocardiogram and carotid pulse tracing. Changes in the shape of plethysmographic waveform produced by valvular and congenital heart diseases are briefly described and the role of this technique in screening cardiac patients has been highlighted.
Impedance plethysmography of the thoracic region, commonly known as impedance cardiography (ICG), has been extensively used for the estimation of stroke volume during the past several decades[6],[8].[9]. The stroke volume estimates from WG have been found to be inaccurate in patients with valvular regurgitation and intra-cardiac shunts. Modifications over Kubicek's formula incorporating correction for haematocrit percentage[9] have not yielded any significant improvement in stroke volume estimation. Yet ICG remains a method of choice for relative measurement of stroke volume during patient monitoring. Impedance cardiography has also been used for the assessment of systolic time index (STI), myocardial contractility (Heather's index), aortic regurgitation fraction (ARF) and mitral regurgitation fraction (MRF) with reasonable precision[9],[10],[11],[14]. In addition, it has been used for monitoring changes in transthoracic fluid volumes at high altitudes and during submaximal treadmill exercise[1],[2]. In the last decade impedance technique has made its way in tomographic imaging of heart and other body segments[3],[5]. We have used this techniques for variety of applications such as estimation of cardiac index, STI and left ventricular election fraction (LVEF), detection of ischaemic heart disease (IHD) using stress ICG and diagnosis of various cardiac diseases from ICG waveform, which are described in this paper.
Two hundred fifty four normal subjects and 681 patients suspected of cardiac disorders were subjected to this study. Out of these 18 normal subjects (Group I-A) and 55 patients (Group I-B) for stress-ICG and 99 normal subjects (Group II-A) and 13 patients with myocardial infarction (Group II-B) for ICG were investigated at Isotope Unit, JJ Hospital; 34 normal subjects (Group III-A) and 115 patients with myocardial infarction (Group III-B) were studied at BARC Hospital; and 103 normal subjects (Group IV-A), 391 patients with valvular diseases of the heart (Group IV-B) and 107 patients with congenital septal disorders (Group IV-Q were examined at Non-invasive Vascular Laboratory, King Edward Memorial Hospital. Impedance cardiography was carried out, in the manner described by Bhuta et al+[4] in all the subjects using BARC made impedance plethysmograph system. However, in Group I-A and I-B subjects electro-cardiogram (ECG) and basal impedance (ZO) were monitored in standing position during rest, hyper-ventilation and treadmill exercise. The exercise was terminated either at the appearance of significant S-T changes in ECG or on attaining the target heart rate. [Figure - 1] shows a typical ICG waveform recorded from a normal subject simultaneously with ECG. Amplitudes of various waves and time intervals are measured as shown in the figure. Various ICG parameters were calculated from this data as follows: 1. Cardiac Index = 150 x L2 (cM) x c(ohms/sec) x LVET (Sec) x P.R Zo2 (ohms) x surface area. where L is distance between sensing electrodes and surface area is obtained from standard tables as per body height and weight of the subject. 2. Systolic time index = PEPILVET, or alternatively STI = (RB + 0.04) 1 (RX - RB), where RB and RX are measured as described by Bhuta et al[4]. 3. Left ventricular ejection fraction = 1.125 - 1.25 STI. 4. AB/C ratio = ab/c. 5. O/C ratio = o(desc)/c.
Variation in Zo during stress: Average (AV) and standard deviation (SD) values of Zo before stress, during hyperventilation and during exercise were 28.5 ? 5.5, 29.8 ? 6.5 and 27.9 ? 6.8 ohms in normal subjects (Group PA) and 27.6 ? 6.5, 28.5 ? 6.5 and 21.3 ? 7.1 ohms in patients suspected of IHD (Group I-B) respectively. The decreases in the value of Zo during stress in group I-B was found to be significant as indicated by high value of student's ‘t’ (3.61). Comparison of stress -ICG data with angiography in 15 of these patients revealed 82% correlation. Similar decrease in Zo has been reported by Balsubramanian and Hoon[1],[2] and has been attributed to increase in thoracic blood volume and pulmonary extra-vascular water due to transient left ventricular dysfunction in IHD. Therefore, a hand held battery operated Zo-meter can be of great use in early detection of IHD. Estimation of cardiac index and LVEF: AV ? SD values of cardiac index in group II-A subjects were found to be 2.96 ? 0.67 litres/min-m[2] in males (56) and 3.09 ? 0.65 litres/min-m[2] in females (43). These values were statistically not different unlike those of stroke volume obtained by Kubick's formula (79.5 ? 13.6 cc in males and 56.5 ? 14.3 cc in females). Similarly no statistical difference due to sex was observed in the value of STI (0.338 ? 0.038 for males and 0.323 ? 0.040 for females) and value of LVEF (0.701 ? 0.046 for males and 0.719 ? 0.049 for females). Estimated values of LVEF in 13 patients (Group II-B) with history of myocardial infarction were found to be significantly different from those obtained by Gamma-ray scintigraphy, but regression analysis exhibited 85% correlation between these two methods. Estimation of STI: AV ? SID values of ST1 obtained from ECG and ICG and those obtained from ICG alone in Group III-A control subjects were found to be 0.335 ? 0.039 and 0.325 ± 0.058 respectively, which are statistically the same as indicated by low value of student's ‘t’ (0.834). Similar values obtained from ECG, phonocardiogram and carotid pulse tracing have been reported to be 0.34 ? 0.04 by Stack et al[1],[2] and suggest that estimation of STI from ICG alone is equally reliable. The AV ? SD values of ST1 in 115 patients with coronary artery disease (Group III-B) were observed to be 0.59 ? 0.08 and 0.485 ? 0.09 during the acute phase and the recovery period respectively. These observations suggested the use of STI as a sensitive index for evaluation of left ventricular performance in such patients. Shape of ICG waveform: ICG waveforms recorded from normal subjects (Group IV-A) exhibited significant variation. Sixty-seven subjects recorded type - A ICG waveform (See [Figure - 2] below), 14 recorded type-B waveform, 9 recorded type-C waveform and 13 recorded type-D waveform. Generally type-B waveform was recorded by subjects aging more than 40 years and type-D waveform was recorded by smokers, hypertensives or diabetics. There fore type-A waveform was considered representative control waveform. It is interesting to mention that 4 subjects recording type-D waveform suffered myocardial infarction 3-5 years later. In type-B waveform the A-wave is more negative and B-point is almost in the mid of upstroke of C-wave. The estimation of SV and S-n in this type of waveform becomes unreliable due to ambiguity in marking the opening The shape of ICG waveform was observed to be markedly different in patients with mitral regurgitation (MR) and tricuspid regurgitation (TR), moderately different in patients with aortic regurgitation (AR) and congenital septal defect (CSD) and significantly different in patients with mitral stenosis (MS), aortic stenosis (AS) and pulmonary stenosis (PS) as described below. Fifty-five patients with mild to moderate uncomplicated mitral stenosis recorded M-shaped 0-wave of decreased amplitude and 33 patients with tight mitral stenosis produced flat and broad 0- wave with further decrease in amplitude. The O/C ratio in these two groups of patients were 0.35 ? 0.14 and 0.29 ? 0.10 respectively which were significantly different from that of control subjects (0.43 ? 0. 09). These changes in the O-wave were also observed in 63 out of 69 patients having MS mixes with AR. Similarly in 61 patients having MS with MR, large M-shaped O-wave was recorded exhibiting the characteristic features of both the lesions. However, in 25 patients having MS with TR the characteristic changes of MS were suppressed by those of TR, with the result large O-wave and diminished C-wave were recorded. The values of AB/C and O/C ratios in these cases were found to be 0.68 0.18 (control value 0.15 ? 0.038) and 1.03 0.21 respectively. Thirty-seven out of 45 patients with isolated MR, large 0-wave and diminished C-wave were recorded. In remaining 8 patients with grade-I MR mild to moderate increase in the amplitude of O-wave was observed. The values of O/C ratio were 0.59 ? 0.12, 0.81 ? 0.15, 1.25 ? 0.23 and 2.41 ? 0.34 in patients with grade-I MR, grade-II MR, grade-III MR and grade-IV MR (graded on the basis of cardiac cathetarisation) respectively. Thus large O-wave was a characteristic feature of MR, which was also observed by Schieken et al[11] and Karnegis et al[7]. Large O-wave was also observed in patients with mixed valvular lesions (See [Figure:3] alongside) as described above. In 15 patients having MR with TR, increase in amplitude of O-wave and decrease in amplitude of C-wave were further enhanced. The values of AB/C and O/C ratios in these cases were found to be 0.75 ? 0.20 and 2.59 ? 0.60 respectively. Fourteen patients with aortic stenosis recorded C-wave of decreased amplitude and increased duration. These changes of AS were, however, suppressed when as was associated with AR and therefore it was not possible to diagnose AS in the presence of AR. Forty, out of 48 patients with AR recorded C-wave of increased amplitude with a slur (See Fig. 3) in its down stroke. Deeper X- point, as reported by Schieken et al [10], was recorded in 29 patients in this group. Thus 21 patients recorded both the characteristic features i.e. slur in the down stroke of C-wave and deeper X-point. Size of the slur or depth of X-point was observed to be proportionate with the severity of the lesion. These features of AR were retained in patients with mixed valvular lesions (MS with AR) as described above. However, in 16 patients having AR with MR, either the features of MR were present (10 cases) or those of AR were present (6 cases) depending upon haemodynamic dominance of the lesion. Prominent Y-wave was recorded in eight out of 10 patients with pulmonary stenosis. However, this feature was also recorded in patients having pulmonary hypertension or atrial septal defect. Increase in amplitude of C-wave and prominent Y-wave were the characteristic features of congenital septal defect and were recorded in 98 out of 107 patients in Group IV-C. Remaining nine patients recorded normal C-wave with a very prominent Y-wave. Cardiac catheterisation in these 9 patients revealed pulmonary stenosis associated with CSD. It is evident from above that unique changes are observed in ICG waveform in patients with isolated valvular or septal disorder, which are sufficiently diagnostic. In patients with mixed lesions, however, the features of hemodynamically dominant lesion suppress the features of the associated lesion. Thus impedance cardiography provides an effective and inexpensive screening procedure to 2D-echo, cardiac-catheterisation and angiography.
The authors are thankful to Dr SK Ganeriwal, Dean, Grant Medical College and JJ Hospital, Bombay, Dr SM Sharma, Assoc. Director, Medical Group, BARC Bombay and Dr Usha Desai, Head, Medical Division, BARC Bombay for giving continuous support and encouragement for this study. The authors are also thankful to Dr JP Goyal, Ex. Head, Medical Unit, BARC Hospital, Dr JB Dharani, Lecturer, Dept. of Physiology, Seth GS Medical College and King Edward Memorial Hospital and Shri SP Agrawal, Scientific Officer, DRP, BARC, for their valuable help and suggestions.
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