Airway and Ventilation

All patients will be sedated and mechanically ventilated via an endotracheal tube until they are ready for extubation. Many sedative drugs cause vasodilatation and drive use of potentially deleterious vasopressors. Mechanical ventilation must be used with care. Excessive tidal volume and positive end-expiratory pressure (PEEP) should be avoided. Both increase right atrial pressure, worsen tricuspid regurgitation and increase right ventricular work by increasing pulmonary vascular resistance. Hypoxia should not be permitted because it will cause pulmonary vasoconstriction, increase pulmonary vascular resistance and increase right ventricular work. Inhaled therapies such as nitric oxide and iloprost may be used to reduce pulmonary vascular resistance in selected patients.

Cardiovascular

Sinus node dysfunction and atrioventricular (AV) block are common after heart transplantation. All patients should leave the operating room with temporary epicardial pacing wires. It is important to ensure that these are attached to a temporary pulse generator and that the pacing system is working correctly. Sinus tachycardia should be expected in the denervated heart. However, this is not always present in the immediate post transplant period. Demand pacing in a dual chamber mode (DDD) with a lower rate limit of 90–100 beats per minute is routine. A relatively high heart rate may improve cardiac output in a transplanted heart when the ability to augment stroke volume is limited. Pacing threshold, sensing and underlying rhythm should be assessed on a daily basis. Sinus rhythm and AV conduction typically return within 1 to 3 weeks of transplantation but around 10% of patients will require a permanent pacemaker.

All patients require continuous invasive monitoring of cardiovascular performance in the immediate postoperative period. This is most commonly achieved with a pulmonary artery catheter. It is helpful to establish desirable haemodynamic ranges; an example is provided in Table 40.4. Measurements outside the desirable range should prompt review and exclusion of a surgical problem such as haemopericardium or haemothorax. In the absence of a surgical problem, abnormal haemodynamics may represent a target for treatment. Abnormalities such as hypovolaemia may be easy to identify and treat. It is important to recognise that right ventricular dysfunction is common after heart transplantation and a leading cause of primary graft failure. Risk factors for right ventricular dysfunction include older donor age, longer ischaemic time, low donor height/weight relative to recipient and high pulmonary vascular resistance in recipient. Right ventricular dysfunction is normally identified by a low cardiac index and rising right atrial pressure. Treatment of right ventricular dysfunction is complex and the principles are outlined in Figure 40.1. It is vital that high right atrial pressure is not permitted because this will lead to right ventricular distension and a downward spiral of right heart failure.

Figure 40.1 Treatment of right ventricular dysfunction. CVVH continuous venovenous haemofiltration.

Use of inotropic or vasoactive medications in isolation or combination after heart transplantation is common but there is no good evidence base to support the superiority of any particular regime. Agents should be selected according to individual patient physiology and the desired effect. The expected effects in a typical patient are outlined in Table 40.5. In general, the dose of inotropic or vasoactive medications should be minimised and the medications should be progressively weaned as recovery of allograft and end-organ function is seen. Intra-aortic balloon pump (IABP) counterpulsation will increase coronary blood flow and reduce left atrial pressure, both of which may be helpful in right ventricular dysfunction.

Mechanical circulatory support may be required when inotropic, vasopressor/vasodilator and intra-aortic balloon pump support is insufficient to achieve desired haemodynamic parameters. Percutaneous devices to mechanically support the right ventricle are now available but have not been widely used after heart transplantation. VA ECMO is thought to be the best treatment for severe primary graft failure. Central cannulation may be preferable to peripheral cannulation to allow longer support duration, permit left ventricular venting and reduce the risk of peripheral vascular complications. Primary graft dysfunction may improve sufficiently for VA ECMO to be weaned in up to 90% of patients within 1 week. In the most severe cases, central VA ECMO may be used as a bridge to acute re-transplantation.