Journal of Postgraduate Medicine
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Year : 2002  |  Volume : 48  |  Issue : 4  |  Page : 329-30  

Cardiac output monitoring based on thoracic electrical bioimpedance.

VK Mohan, Chanderlekha, L Kashyap 
 

Correspondence Address:
V K Mohan





How to cite this article:
Mohan V K, Chanderlekha, Kashyap L. Cardiac output monitoring based on thoracic electrical bioimpedance. J Postgrad Med 2002;48:329-30


How to cite this URL:
Mohan V K, Chanderlekha, Kashyap L. Cardiac output monitoring based on thoracic electrical bioimpedance. J Postgrad Med [serial online] 2002 [cited 2023 Sep 25 ];48:329-30
Available from: https://www.jpgmonline.com/text.asp?2002/48/4/329/62


Full Text

Sir,

Hypertrophic obstructive cardiomyopathy (HOCM) is characterised by hypertrophied interventricular septum and anterolateral septal wall causing interference in systolic emptying. There is little involvement of the posterior left ventricular wall.[1] Pneumoperitoneum may affect preload and afterload and that depends on intraabdominal pressure, posture, ventilatory settings and intravascular volume status.[2] These changes during pneumoperitoneum in HOCM may be deleterious. Therefore intensive cardiac monitoring in these patients is recommended.[3]

A 33-year-old, 82 kg female was scheduled for laparoscopic cholecystectomy. On examination her pulse rate was 92/min and her blood pressure was 184/106 mm Hg. On auscultation the lungs were clear and a grade III/IV systolic murmur, maximal at fifth intercostal space was present radiating to the base and the axilla. Her ECG showed left ventricular hypertrophy with non-specific ST changes. Chest x-ray showed clear lung fields with cardiomegaly. Echocardiogram showed interventricular septum(ed) 29.6 mm/m2 and left ventricular posterior wall LVPW(ed) 12.3mm/m2 that was suggestive of HOCM. In view of HOCM, non-invasive cardiac output monitoring was planned. CIC-1000TM Monitor (SORBA Medical Systems INC, Brookfield) based on thoracic electrical bioimpedance principle was used. After administration of general anaesthesia, pneumoperitoneum was created by insufflation of carbon dioxide at the rate of 2 l/min and intra-abdominal pressure was maintained at 12 mmHg. After pneumoperitoneum cardiac output decreased from 2.6 l/min. to 1.9 l/min. Heart rate and blood pressure decreased from 68/min and 110/78 mmHg to 51/min and 98/56 mmHg respectively. The fall in cardiac output was treated with rapid infusion of ringer lactate solution (600 ml), change in position from head up tilt to supine. At this time the surgeon was asked to decrease and maintain intra-abdominal pressure at 10 mmHg. Cardiac output recovered following these measures and haemodynamic parameters remained stable during the rest of the intraoperative period.

Patients with HOCM for non-cardiac surgery have increased risk of adverse cardiac events like congestive heart failure, myocardial infarction, dysrhythmias and hypotension.[4]

Cardiac output monitoring based on thoracic bioimpedance has been found to be as accurate and reliable as other invasive techniques.[5] Thorax is assumed to be a cylinder having electrical length between neck and xiphoid and has a basic impedance. A constant small current is passed between two outer electrodes, voltage change is sensed by two inner electrodes and impedance is derived according to the equations described by Sramek and Bernstein.[5] Stroke volume and cardiac output can be measured continuously and at fixed intervals.

Anaesthetic management of patients with HOCM requires avoidance of such measures that decrease preload and afterload.[6] Any decrease in venous return and cardiac output can be managed by increasing the circulatory volume and by head down tilt before insufflation of gas and a low intraperitoneal pressure.[7] In this case intraoperative decrease in cardiac output was managed with change in patientís position, intravenous fluids and by decreasing the intra-abdominal pressure. Thoracic electrical bioimpedance technique may be useful for monitoring adverse cardiac events and to guide fluid therapy and inotropic support during the intraoperative period. [7]


  ::   AcknowledgmentTop


We are indebted to Dr. Perminder Singh for the preparation of the manuscript.

References

1Maron BJ, Gottdiener JS, Epstein SE. Patterns and significance of distribution of left ventricular hypertrophy in hypertrophic cardiomyopathy. A wide angle, two-dimensional echocaridiographic study of 125 patients. Am J Cardiol 1981;48:418-28.
2Wahba RWM, Beique F, Kleiman SJ.Cardiopulmonary function and laparoscopic cholecystectomy. Can J Anaesth 1995;42:51-63.
3Tessler MJ, Hudson R, Naugler-Colville MA, Biehl DR. Pulmonary edema in two parturients with hypertrophic obstructive cardiomyopathy (HOCM). Can J Anaesth 1990;37:469-73.
4Haering JM, Comunale ME, Parker RA, Lowenstein E, Douglas PS, Krumholz HM et al. Cardiac risk of non-cardiac surgery in patients with asymmetric septal hypertrophy. Anesthesiology 1996;85:254-9.
5Castor G, Klocke RK, Stoll M, Helms J, Niedermark I. Simultaneous measurement of cardiac output by themodilution, thoracic electrical bioimpedance and Doppler ultrasound. Br J Anaesth 1994;72:133-8.
6Loubser P, Suh K, Cohen S.Adverse effects of Spinal Anesthesia in a patient with Idiopathic Hypertrophic Subaortic Stenonsis.Anesthesiology 1984;60:228-30.
7Joris JL.Anesthesia for Laparoscopic Surgery. In: Miller RD, editor. Anesthesia, 5th edn. Philadelphia: Churchill Livingstone; 2000. pp. 2003-23.

 
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