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Biomedical subjects

G R Cutfield

Publications and source records attributed to G R Cutfield.

7 recordsLinked to original sources
PubMed1992

Alveolar oxygenation and mouth-to-mask ventilation: effects of oxygen insufflation.

The effect on alveolar oxygen fraction (FAO2) of insufflating oxygen under a mask (or through an inflow nipple provided in the mask) during simulated mouth-to-mask ventilation was investigated using a lung model. A variety of commercially produced masks were evaluated. Two patterns of artificial ventilation were applied: 1. 500 ml tidal volume at 20 breaths per minute, and 2. 900 ml tidal volume at 12 breaths per minute. The ventilating gas mixture was oxygen 16% in nitrous oxide, and oxygen was insufflated at flow rates of 2, 4, 6, 8, 10, 12 or 14 litres per minute. The rate of rise of FAO2 and the equilibrium FAO2 attained were greatest at high oxygen inflow rates. The relationship between oxygen flow and FAO2 was not linear however, and an oxygen flow rate of 10 l/min was adequate to generate FAO2's around 50% with either ventilatory pattern. The equilibrium FAO2 achieved was greater with smaller tidal volumes and with larger mask deadspace. We also found that several breaths were required for equilibration of FAO2 during each trial, supporting recommendations that several breaths should be given on commencement of artificial ventilation during cardiopulmonary resuscitation.

Equipment Design↗
PubMed1988

Endocardial viability ratio and ischaemic dysfunction of the left ventricle during halothane anaesthesia.

In normal hearts, the critical value of the endocardial viability ratio (EVR) is thought to be less than 0.5. As myocardial regional dysfunction is a sensitive index of subendocardial ischaemia, the relationship between EVR and regional function has been studied in an experimental model of coronary artery constriction. In 13 dogs anaesthetized with halothane (0.5-2.0% inspired concentration), diastolic and systolic pressure time indices were obtained by planimetry, and their ratio (EVR) correlated with regional function. Halothane alone caused a significant reduction in EVR from 1.38 +/- 0.08 to 1.15 +/- 0.04 (mean +/- SEM). In the presence of coronary artery constriction a similar decrease in EVR was observed and was accompanied by post-systolic shortening (PSS), an indicator of regional dysfunction. At high concentrations of halothane, there was an inverse correlation between reduction in EVR and increase in PSS. Mean EVR of approximately 0.9 (mean = 0.92 +/- 0.02) was associated with significant worsening of regional function.

Anesthesia, Inhalation↗
PubMed1988

Isoflurane and large coronary artery haemodynamics. A study in dogs.

In the dog, stepped increases in isoflurane concentration (up to 1.5 MAC) caused peripheral and coronary vasodilatation. In the presence of significant decreases in arterial pressure (-35%), contractility (-46%), cardiac output (-17%) and coronary perfusion pressure (-40%), coronary blood flow remained unchanged, while the effective coronary vascular resistance was halved. The coronary reserve, estimated by the hyperaemic response to short periods (10 s) of coronary occlusion was reduced by the stepped increases in isoflurane concentration. Linear relationships were observed between peak hyperaemic flow, volume repayment, repayment: deficit ratio and coronary perfusion pressure. The vasodilation induced by isoflurane was of such magnitude that, at 1.5 MAC, the repayment: deficit ratio was close to unity, indicating that the vasodilatory reserve was almost exhausted.

Anesthesia, Inhalation↗
PubMed1987

Beta-blockade reverses regional dysfunction in ischemic myocardium.

To determine the protective effect of oxprenolol-induced beta-blockade on the compromised myocardium (critical constriction of the left anterior descending coronary artery) against the adverse effect of high concentrations of halothane, halothane dose-response curves were obtained in six dogs in each of three phases: preconstriction (control), critical constriction, and critical constriction with the addition of 0.3 mg/kg intravenous oxprenolol. The extent of depression of ventricular function was essentially the same in the three phases. However, at high halothane concentrations (2.0% inspired), the depression of systolic shortening in the compromised segment was significantly minimized after oxprenolol so that shortening was 10.2% +/- 1.8 instead of 6.5% +/- 1.4 (P less than 0.05); moreover the large increase in postsystolic shortening observed during critical constriction was abolished after oxprenolol. This suggests a protective effect of oxprenolol on regional myocardial function in the presence of critical constriction, possibly by an effect on myocardial metabolism or endocardial blood flow.

Adrenergic beta-Antagonists↗
PubMed1986

Halothane-verapamil causes regional myocardial dysfunction in the dog.

Regional myocardial function was studied using sonomicrometry in six mongrel dogs, anaesthetized with halothane (1% inspired), as increasing doses of verapamil were given i.v. In addition to a gradual increase in end-diastolic length and a reduction in systolic shortening, an abnormal (paradoxical) contraction pattern appeared in the apical region. This occurred in the absence of coronary artery damage and at coronary perfusion pressures unlikely to result in ischaemia. Administration of verapamil in the presence of halothane results in regional dysfunction similar to that caused by the intracoronary administration of nifedipine.

Animals↗