Removal of infected pacemaker leads with deep hypothermic circulatory arrest and open surgical exploration of the superior vena cava and innominate veins.

Despite the use of transvenous methods for extraction of infected leads, failed attempts may result in retained lead fragments. Retained lead fragments may be a focus of continued infection leading to sepsis. We present two patients in which conversion from cardiopulmonary bypass to hypothermic circulatory arrest allowed direct visualization, using venotomies in the superior vena cava and innominate vein to achieve complete removal of retained pacemaker lead fragments. Use of venotomies in the extracardiac venous system is a technical addition to prior descriptions of lead extraction using deep hypothermia and circulatory arrest.

Effect of early versus delayed hypoxic environment on neonatal rabbits.

We developed a low-cost, nonsurgical small animal model simulating the condition of cyanotic heart disease. Six groups of New Zealand white rabbits were studied: Group (1-C), 1-week-old control rabbits (n = 9) reared in room air; Group (1-H), 1-week-old rabbits placed in a hypoxic environment (10% O2) at birth (n = 5); Group (1-H-3), 1-week-old rabbits (n = 11) reared in room air for 3 days and then placed under hypoxic conditions identical to those for Group (1-C); Group (4-C), 4-week-old control rabbits (n = 12); Group (4-H), 4-week-old rabbits placed in hypoxia since birth (n = 11); Group (4-H-3), 4-week-old rabbits kept in room air after birth for 3 days (n = 7) before being exposed to hypoxia. Animals were anesthetized, heparinized, and instrumented for measurement of hemodynamic parameters. Right ventricular (RV) hypertrophy and hematocrit were assessed. Lung tissue was analyzed using quantitative morphometric techniques to assess arterial size, number, and muscularity. Group (1-H) and Group (4-H) developed RV hypertrophy, pulmonary hypertension, and erythrocytosis. The RV hypertrophy developed rapidly, as early as 1 week of age and became so pronounced by 4 weeks as to result in high mortality rate (35%). None of the animals in Groups (1-H-3) or (4-H-3) died while chronic changes of hypoxemia still developed. Placing rabbits after birth in room air for 3 days before exposing them to hypoxia appeared to play a protective role, moderating the development of pulmonary hypertension and severe RV hypertrophy. The effects of hypoxia appear to be at least partially dependent on the time of exposure. Utilizing our low-cost model will allow future work, including study of the effects of chronic hypoxemia on systemic ventricle exposed to an ischemic insult.

Exosurf treatment following wood smoke inhalation.

Pulmonary surfactant deactivation is an important factor in the pathophysiology caused by wood smoke inhalation. Surfactant replacement is beneficial in treatment of surfactant-deficient neonates and possibly the adult respiratory distress syndrome (ARDS). In this study, the effect of exogenous Exosurf treatment for acute wood smoke injury was examined in four groups of rabbits. All groups were anaesthetized, placed on a ventilator, and surgically prepared for haemodynamic, peak airway pressure (P(aw)), and blood gas measurements. Rabbits were monitored for 2 h following smoke or sham smoke inhalation. At the conclusion of the experiment pulmonary oedema and surfactant function were measured. A Control group (n = 5) was followed without intervention. A Smoke group (n = 4) was ventilated with wood smoke for 3 min. A third group (Smoke+Exo, n = 4) was subjected to smoke followed by pulmonary instillation of Exosurf (5 ml/kg). Saline (5 ml/kg) was instilled into the lungs of the fourth group (n = 3) as a control for Exosurf instillation. Saline, Smoke and Smoke+Exo all significantly lowered PO2 and elevated P(aw) compared to baseline and the Control group. Exosurf treatment did not reduce the pulmonary oedema or restore surfactant function caused by smoke exposure. This study indicates that wood smoke inhalation acutely damages the lung and that administration of Exosurf by instillation is not an effective treatment.

Recovery of hypoxic neonatal hearts after cardioplegic arrest.

OBJECTIVES: Surgery for repair of congenital heart defects in the infant may be affected by hypoxia associated with the defect. The effects of chronic hypoxia on systemic ventricular function are not well characterised and few studies have considered myocardial preservation in the hypoxic neonatal heart. The aim was to determine how chronic hypoxia would affect left ventricular function in neonatal rabbit hearts subjected to global ischaemia. METHODS: Hearts from rabbits one, four, and six weeks of age and raised at 9% O2 were compared with hearts from rabbits raised in ambient air. Haemodynamic variables were measured with an isolated heart preparation before and after cardioplegic arrest. Creatine kinase was measured during reperfusion and myocardial oxygen consumption (MVO2) during ischaemia. RESULTS: At all ages, hypoxic hearts had significantly lower peak dP/dt and contractility index (dP/dt/left ventricular pressure (LVP)) than normoxic controls. After ischaemia and reperfusion, one week hypoxic hearts did not differ significantly in recovery from controls. Four week hypoxic hearts had significantly higher stroke volume and aortic flow, and six week hearts had significantly higher coronary flow than age matched controls. Contractility index did not show significant differences between hypoxic and control animals at any age. Hypoxic hearts released less creatine kinase in the coronary effluent during reperfusion than did control hearts of similar age. Six week hypoxic hearts had significantly higher MVO2 measured during the second administration of cardioplegia compared with six week control hearts but MVO2 did not differ significantly at one and four weeks of age. CONCLUSIONS: Despite reduced baseline function, chronically hypoxic immature rabbit hearts can recover from an ischaemic insult as well as age matched controls, with less evidence of myocardial necrosis. This parallels clinical findings in cyanotic infants.