An episode ofhypotension is common during cemented joint replacement, and has been associated with circulatory collapse and sudden death. We studied the mechanism of hypotension in two groups of six dogs after simulated bilateral cemented arthroplasty. In one group, with no lavage, the insertion of cement and prosthesis was followed by severe hypotension, elevated pulmonary artery pressure, decreased systemic vascular resistance and a 21% reduction in cardiac output. In the other group, pulsatile intramedullary lavage was performed before the simulated arthroplasties. Hypotension was less, and although systemic vascular resistance decreased, the cardiac output did not change. The severity ofthe hypotension, the decrease in cardiac output and an increase in prostaglandin metabolites were related to the magnitude of pulmonary fat embolism. Pulsatile lavage prevents much of this fat embolism, and hence the decrease in cardiac output. The relatively mild hypotension after lavage was secondary to transient vasodilatation, which may accentuate the hypotension caused by the decreased cardiac output due to a large embolic fat load. We make recommendations for the prevention and management of hypotension during cemented arthroplasty.

Lung areas with a low V/Q ratio cause hypuxaemia. The low alveolar oxygen concentration may cause local hypoxic pulmonary vasoconstriction (HPV) which reduces peffusion, raises the V/Q ratio, and hence reduces the tendency to a low Paul. By changing Pco2, the HPV response can be altered. We examined this relationship in anaesthetized dogs by using a tracheal divider to separate hypoxic (nitrogen ventilated) from oxygenated (100 per cent oxygen ventilated) lung. Relative perfusion was assessed from total 1~3Xe exhaled from each lung area after intravenous infusions. When Paco~ was changed by changing ventilation, we found that an increasing Paco, increased HPV and also Paul. At a Paco~ of 3.3 kPa, HPV was abolished and Pao, fell. We also changed Paco2 by altering Plco, to one or both lung areas while ventilation remained constant throughout the experiment. Again as Paco, increased, HPV and Pao2 increased. When Pacoz fell and end tidal carbon dioxide in the hypoxic lung (PETco~) remained eleyated (by maintaining Ptco, in the hypoxic lung and removing COz from the oxygenated lung) HPV was maintained. Thus it is the alveolar concentration of COz in the hypoxic lung which is important in modifying HPV.We conclude that in this model a low PETco, (3.3 kPa) in hypoxic lung will reduce HPV, and will result in more severe hypoxaemia. This may have relevance in both anaesthetized and intensive care unit patients when a higher Pao, may be obtained by increasing hypoxic lung PETco v The effect of PETco 2 on Pao, will be influenced by other variables, but when hypoventilated or hypoxic lung areas exist, increasing PETco ~ may reinforce hypoxic pulmonary vasoconstriction and thus may increase Paul.KEY WOADS: LUNG, hypoxic vasoconstriction, carbon dioxide.RESPIRATORY GAS EXCHANGE depends on the ratio of ventilation to perfusion. A low VIQ ratio and hypoxaemia will result from poorly ventilated lung unless perfusion is also reduced in the same region. Alveolar oxygen concentration helps to match regional perfusion to ventilation through a mechanism of hypoxic pulmonary vasoconstriction (HPV).I-3The mechanism of HPV is still not understood, but several events which occur under anaesthesia are reported to reduce HPV (and therefore to create hypoxaemia). Sykes, et al.,[4][5][6][7] Benumof and Wahrenbrock, s and Bjertnaes 9"1~ have found that inhaled anaesthetics reduce HPV. Benumof, et al. I1 have found that increased pulmonary vascular pressure can reduce HPV. Pc02 is also known to affect HPV.II-~3 Pc02 during anaesthesia may be increased, decreased, or normal. If HPV were present and a low Pc02 reduced HPV, the low Pc02 could create hypoxaemia by increasing perfusion to hypoxic lung. Pc02 may also alter Paoz through its effect in the alveolar gas equation or by changing the position of the oxyhaemoglobin dissociation curve, cardiac output, or R values. In order to document which effect was dominant we assessed HPV in dogs and observed the effect of altering ventilation and therefore Paco2 on both HPV and Pao~ when one t...

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Inhaled nitric oxide does not alter pulmonary or cardiac effects of fat embolism in dogs after cemented arthroplasty Purpose: We examined the effect of inhaled nitric oxide (NO) on the acute pulmonary hypertension and right ventricular (RV) dilation after fat embolism. Methods: A bilateral cemented arthroplasty (BCA), created fat embolism in 20 dogs. In Part A, 12 dogs were randomized to an NO group (n = 6, inhaled NO 40 ppm before BCA and throughout the study) or a control group (n =6). In Part B, a third group of dogs (n=8) were given NO 20-40 ppm 2-3 min after BCA when pulmonary artery pressure (PAP) increased. Transesophageal echocardiography (TEE) and invasive hemodynamic monitoring evaluated the hemodynamic response to BCA. Postmortem, quantitative morphometry was used to estimate the number of fat emboli and diameter of lung vessel occluded by fat. Results: Part A: The increase in PAP in the NO group (I 6 -+ I to 34 _+ 9 mmHg) within three minutes of BCA was not different from that in the control group ( 14 _+ 4 to 35 +-9 mmHg). W~hin three minutes of BCA, TEE demonstrated RV dilation in all groups (P ~ 0.05) but there was no difference in the change in RV area in the NO and control groups. When NO was given after BCA, no difference in PAP or RV dilation was noted from that in the control group. There were no differences, at post mortem, between the groups in the diameter of lung vessel occluded by fat Conclusion: Whether given before the embolic insult or two to three minutes after the onset of pulmonary hypertension, inhaled NO did not attenuate the acute pulmonary hypertension or RV dilation after cemented arthroplasty.