Session V - Geriatrics


Saturday, October 23, 1999 Session V, Paper #37, 9:23 a.m.

Cardiac Output during Hip Hemiarthroplasty: A Prospective, Controlled Trial of Cemented and Uncemented Designs

Christopher G. Moran, MD, FRCS; David I. Clark, FRCS; Aemer B. Ahmed, FRCA; Bryn R. Baxendale, FRCA, University Hospital, Nottingham, England

Alterations in cardiovascular physiology during cemented hip hemiarthroplasty are well recognised, occasionally resulting in fatal cardiovascular collapse around the time of cement fixation. The etiology of these cardiovascular changes is unknown but may include fat and marrow embolism, peripheral vasodilatation and activation, within the lungs, of the clotting cascade. Precise evaluation of cardiac function during surgery requires the measurement of cardiac output. Until recently, this has required the insertion of a pulmonary artery catheter, a procedure which is associated with significant risks. Trans esophageal echo allows a qualitative evaluation of pulmonary embolisation but the probe is relatively large and esophageal rupture is a recognised complication. The trans-esophageal Doppler is a new instrument that allows measurement of cardiac output using a small (6mm) probe in the oesophagus.

Objective: The aim of this study was to use the trans-esophageal Doppler to measure the effect of methylmethacrylate cement on cardiac output during hip hemiarthroplasty.

Design: A prospective, matched-case controlled trial

Subjects: 20 matched elderly patients (mean age: 69 years) with displaced subcapital fractures treated with either a cemented or an uncemented hip hemiarthroplasty.

Measurements: Cardiac output measured using trans-esophageal Doppler during 1) baseline prior to incision, 2) surgical approach, 3) femoral canal reaming, 4) femoral canal lavage, 5) introduction of cement, 6) insertion of prosthesis, 7) reduction of joint and closure.

Results: The two groups were matched for age, height, weight and pre-operative left ventricular function. There was no difference in mean stroke volume (mean: 56 ± 6.6 mls) or cardiac output (mean: 4.8 ± 0.5 lmin-1) between the cemented and uncemented groups prior to insertion of cement (p>0.5). The introduction of cement produced a significant 33% reduction in cardiac output (p<0.01) and 44% reduction in stroke volume (p<0.02). These changed were transient and there was no significant difference in cardiac function when the prostheses were inserted. The cardiovascular changes were not detected by routine anaesthetic monitoring and there was no difference between the cemented and uncemented groups at cement insertion in heart rate, mean arterial pressure or end-tidal CO2.

Conclusion: This study has demonstrated a significant reduction in cardiac output during femoral canal cementation. This fall in stroke volume and cardiac output may be due to embolism during cement insertion but it was not seen at other times when the femoral canal was instrumented (e.g., reaming and prosthesis insertion). The changes were not detected by standard, non-invasive haemodynamic monitoring. It may explain some of the sudden, catastrophic deaths that are seen during cemented hemiarthroplasty.