Valvular Disease

The incidence and types of valvular disease have changed over the past 50 years.¹ Valvular disorders, such as mitral stenosis and aortic regurgitation, often arise from infectious diseases like rheumatic fever and syphilis, which are much less common today. Conversely, there has been a rise in the rate of aortic stenosis, which is due to degenerative disease common in ageing. In contrast to these trends, the prevalence of rheumatic fever and rheumatic heart disease among Indigenous Australians is one of the highest in the world.² Also, Pacific Islanders living in New Zealand have much higher rates of rheumatic fever than the general population.³ As a result, valvular disorders are much more common in these groups. Rheumatic fever is discussed under infective endocarditis in Chapter 10.

Stenotic valves have a tightened, restricted orifice, so that blood must be forced through at higher pressure (Figure 12.1). In regurgitation, also called valvular incompetence or insufficiency, incomplete closure of the valve leaflets results in backflow of blood. Valvular conditions can result from congenital deformities, but also from the degenerative changes associated with ageing, from infection and rheumatic diseases. When a valve is stenosed, higher pressure is required to push blood through the narrow opening and the heart compensates by hypertrophy and dilation. When a valve is incompetent the heart does not empty sufficiently, so again the heart compensates by hypertrophy and dilation. In both these conditions heart failure may result; however, in regurgitation, pressure in the ventricles and atrium grows and this pressure is reflected back into the pulmonary or venous system. Although the heart contains four valves, the majority of disorders affect the mitral and aortic valves in the left side of the heart.

FIGURE 12.1 Valvular stenosis and regurgitation: (A) normal position of valve leaflets (cusps) when the valve is open and closed; (B) open position of a stenosed valve (left) and closed position of a regurgitant valve (right); (C) haemodynamic effect of mitral stenosis shows the mitral valve is unable to open completely during left atrial systole, limiting left ventricular filling; (D) haemodynamic effect of mitral regurgitation shows the mitral valve does not close completely during left ventricular systole, allowing blood to re-enter the left atrium.⁴³

Ischaemic Heart Disease

The pathophysiology and implications of ischaemic heart disease are explained in detail in Chapter 10. Single lesions can be treated by angioplasty and stent; however, multiple, longer lesions may need coronary artery bypass surgery.⁵

Coronary Artery Bypass Graft Surgery

CABG uses a section of vein or artery to bypass a blockage in the patient’s coronary artery. The vessels used for grafting arise from the internal mammary artery, or are taken from the saphenous vein or radial artery. Saphenous veins are removed from the legs, and the radial artery from the forearm and used as a free graft with anastomoses at the ascending aorta and distally to one or more coronary arteries. When saphenous veins are used as grafts (SVG), they often develop diffuse intimal hyperplasia, which ultimately contributes to restenosis. Patency rates are lowest in saphenous vein grafts attached to small coronary arteries or coronary arteries supplying myocardial scars. Consequently, arterial grafts are used more often, as they are more resistant to intimal hyperplasia. Internal mammary arteries (IMAs) and radial artery grafts may be used.⁶ The IMA remains attached to the subclavian artery and is mobilised from the chest wall and anastomosed to the coronary artery distal to the occlusion (Figure 12.2). If the radial artery is being harvested for grafting, the collateral circulation in the forearm is assessed. Echo colour Doppler provides best accuracy of forearm circulation, although the clinical Allen test is quite commonly used. The disadvantage of the Allen test is that it has around 5% false patency result.⁷ A selection of IMA, SVG and radial artery grafts may be necessary over time as repeat procedures are needed or in patients with extensive disease requiring multiple grafts.

FIGURE 12.2 Internal mammary artery graft⁵.

Over recent years a new approach to CABG – minimally invasive direct coronary artery bypass grafting (MIDCABG) – has been used. This procedure uses intercostal incisions and a thorascope instead of a sternotomy to access the heart and coronary arteries. MIDCABG is also often performed without cardiopulmonary bypass (off pump coronary artery bypass, OPCAB); instead, the heart is slowed with beta-blockers to allow the surgery to be performed on a beating heart.⁸ OPCAB procedures may also be performed using full or partial sternotomy to provide access for multiple vessels grafting. Both procedures have been successful responses to the drive to reduce recovery times, patient stays in hospital and costs.⁸ MIDCABG is currently only used in single-vessel disease, particularly the left anterior descending (LAD) artery. More recently, robotically-assisted cardiac surgery has been performed in America and Europe and has been introduced at a small number of Australian hospitals for CABG and mitral valve surgery. This technique has further reduced the invasiveness of cardiac surgery, as little more than stab wounds are required in the right chest for thoroscopy and the robotic instruments. Avoiding true thoracotomy or sternotomy improves postoperative pain experiences and shortens length of stay.⁹

Although CABG is the most common cardiac surgical procedure undertaken in Australia, the incidence has declined since 2005/06 to be 61 procedures/100,000 population in 2007–08.¹⁰ The decline in surgery rates is due to changes in the treatment of CHD, including the advent of percutaneous coronary intervention (PCI). More procedures are now being performed in older patients, with 73% of current patients aged over 60 years.¹ CABG is used to relieve the symptoms of angina by increasing coronary blood flow distal to occlusive coronary lesions. It is a palliative, not curative, treatment as the underlying disease process continues.¹¹ CABG is more effective than PTCA in patients with extensive, multi-vessel disease.^9,11 CABG is also used in left main vessel lesions due to the high risk of extensive infarction associated with PTCA in this area. Women do not appear to have the same access to CABG surgery, as men are three times more likely to have surgery, although only twice as likely as women to have CHD.¹² CABG surgery is commonplace, and many cardiothoracic centres have highly efficient, effective systems in place with mortality rates as low as 2%.

Valve Repair and Replacement

Valve surgery is usually undertaken to repair the patient’s valve or, more often, to replace the valve with either a mechanical or tissue prosthesis. The clinical decision for valve surgery is primarily based on the clinical state of the patient using the New York Heart Association (NYHA) classification system and echocardiographic findings.⁵ The type of surgery used will depend on the valves involved, the valvular pathology, the severity of the condition and the patient’s clinical condition. Often valve surgery is not a single procedure, and it may involve multiple valves, CABG and implantable cardioverter defribillator (ICD). Valve surgery is palliative, not curative, and patients will require lifelong health care.

Valve repair may involve resecting and/or suturing prolapsed or torn leaflets (valvuloplasty) and repairing the ring of collagen the valve sits in (annuloplasty), and is commonly used for mitral and tricuspid regurgitation. Commissurotomy (incising valve leaflets and debriding calcification) is the treatment of choice for mitral stenosis. Both repair processes have demonstrated lower operative mortality than replacement, although complete valve competence may not be able to be achieved. Open procedures are preferred because thrombi and calcification can thereby be removed.

Valve replacement may be necessary, but could be associated with higher risks due to long-term disease process and poor underlying left ventricular function. The most common indication for valve replacement is aortic stenosis, and accounts for 60–70% of valve surgery.¹³ Prosthetic valves may be mechanical or biological. Mechanical valves are made of metal alloys, pyrolite carbon and Dacron (Figure 12.3). Biological valves are constructed from porcine, bovine or human cardiac tissue. Mechanical valves are more durable but have an increased risk of thromboembolism, so lifelong anticoagulation is required. Biological valves suffer from the same problems as the patient’s valve (i.e. calcification and degeneration). The choice of valve depends on the age of the patient and potential difficulties with taking anticoagulants.

FIGURE 12.3 Prosthetic valves: (A) the Bjork-Shiley valve, with a pyrolyte-carbon disc that opens to 60 degrees; (B) the Starr-Edwards caged-ball valve model 6320, with satellite ball; (C) the St Jude Medical mechanical heart valve, with a mechano-central flow disc; (D) the Hancock II porcine aortic valve, with stent and sewing ring covered in Dacron cloth.⁵

Mortality for valvular surgery is higher than for CABG, reflecting the underlying loss of ventricular function and additional procedures that are common. Risk stratification models have been developed to help determine the patients that are most likely to have poor recovery and outcomes.¹⁴ The major factors that contribute to poor outcomes are worse left ventricular function and age over 70 years old.

Cardiopulmonary Bypass

CPB was developed to enable surgery to be performed on a still, relatively-bloodless heart, while preserving the patient’s circulation. CPB temporarily performs the functions of the heart in circulating blood and of the lungs by enabling gas exchange with the blood. Silicone cannulae are inserted into the venae cavae and venous blood circulated through a circuit outside the body. In this circuit the blood is oxygenated, carbon dioxide removed and blood temperature controlled. Drugs and anaesthetics may be added. A roller pump is generally used to provide the pressure to create blood flow in the circuit and back to the patient’s aorta.

Adverse effects of CPB are diverse, and include the following:¹⁵

These effects are well documented, and routine CPB management and postoperative care are designed to minimise and treat the complications. Heparin is added at the commencement of CPB and is reversed with protamine (1 mg of protamine for every 100 units of heparin) when CPB ceases; activated clotting times are monitored throughout and after CPB. Blood returning to circulation is filtered, and surgical procedures proceed carefully to reduce microemboli. Monitoring and maintenance of adequate arterial flow rates are used to prevent low perfusion. Temperature gradients and a rewarming process are instituted slowly so that cardiac output can meet metabolic demands.

Myocardial Preservation

One of the processes involved in CPB is that the aorta is clamped where a cannula is inserted to return blood to the circulation. This clamp prevents blood flow into the coronary arteries; therefore, the myocardium must be protected from ischaemia. This protection is achieved through several mechanisms directed towards reducing oxygen demand: first, oxygen demand is reduced by mild to moderate hypothermia (28–32°C); second, by reducing myocardial temperature (0–4°C), through infusing cold fluids directly into the coronary arteries; and third, by preventing normal conduction by arresting the heart during diastole, through infusing a concentrated potassium solution into the coronary arteries. Return to normal rhythm is usually achieved by circulation of warm blood, though defibrillation may be necessary.

The Immediate Postoperative Period

Patients should be transported to intensive care accompanied by at least an anaesthetist, an appropriately qualified nurse and transport personnel under continuous cardiac monitoring and assisted ventilation. It is prudent to include capnography during patient transport to detect ventilator disconnection, dysfunction, or endotracheal tube migration. Intensive care or theatre nursing staff may be a component of the transport team. The admission to intensive care requires a team approach, with the participation of intensive care nursing and medical staff and/or technician input. The immediate postoperative decision making on patient management is influenced by handover from anaesthetists, settling in procedures and collegial assistance.¹⁶ Admission activities are commonly divided between nurses, with one nurse taking responsibility for establishing monitoring and haemodynamic assessment and management, and a second nurse managing ventilation and endotracheal tube security, as well as managing chest drains, gastric tube and urinary catheter. If staffing permits, additional nurses may take responsibility for documentation, performing arterial blood gases, 12-lead ECG and providing assistance as required.

The objectives of immediate post operative management of cardiac surgical patients may include:

Haemodynamic Monitoring and Support

Typical haemodynamic monitoring includes an intra-arterial catheter for continuous blood pressure monitoring and arterial blood sampling. Cardiac output and preload measurement are achieved most commonly with either a pulmonary artery or central venous catheter configured for pulse contour cardiac output (PiCCO) monitoring (see Chapter 9).

Preload measures provided by the pulmonary artery catheter include right atrial pressure (RAP) to approximate right ventricular filling, and pulmonary artery pressure (PAP) to approximate right ventricular systole and provide insight into pulmonary vascular resistance and left heart function. The pulmonary capillary wedge pressure (PCWP) is available to approximate left ventricular filling and left heart function. Alternatively, the PiCCO monitoring system represents preload by intrathoracic blood volume index (ITBVI) and global end-diastolic volume index (GEDVI). In addition, the extravascular lung water index (EVLWI) can demonstrate the accumulation of interstitial lung water.¹⁷

Cardiac output is measured by either intermittent or continuous thermodilution via pulmonary artery catheters, or measured intermittently and then approxi-mated continuously on a beat-to-beat interpretation of pulse contour by the PiCCO monitoring system. Cardiac output measurement can be combined with other pressure variables to calculate systemic and pulmonary vascular resistance, stroke volume and measures of ventricular work.

Certain common haemodynamic patterns are seen in the early postoperative phase. These must be detected through thorough monitoring and interpretation of variables, and managed according to specific needs. During the initial two hours of recovery period, 95% of patients will experience haemodynamic instability.¹⁸

Ventilatory Support

Ventilation should be approached according to the general principles described in Chapter 15. As anaesthesia is not typically reversed at the end of the operation, patients are generally admitted apnoeic, and within 1–3 hours return to wakefulness and spontaneous breathing.

Ensuring a secure airway is an initial priority; the following should be undertaken:

There has been a general trend to more rapid ventilatory weaning in recent years, and in some centres ‘fast-track’ cardiac surgical recovery includes extubation at the end of the operation before transfer to a recovery unit for suitable patients. Indices of respiration show no improvement when intubation is maintained for longer compared with early extubation,³⁰ and pooled results from randomised early extubation trials show earlier ICU discharge and shorter lengths of stay (by 1 day) when early extubation is undertaken.³¹

Apart from these fast-track approaches, ventilation is commonly employed for 2–6 hours in the uncomplicated patient. Reasons for continuing ventilation beyond this time frame may include:

For many patients, ventilation is provided purely for initial airway and apnoea protection rather than for treatment of pulmonary deficits. In the absence of pulmonary disease, many centres provide fairly uniform approaches to parameter settings that aim at sustaining ventilation and oxygenation, while limiting traumatic risk to the lungs (see Table 12.1). However, approaches to ventilation will need to be tailored in the presence of operative complications or coexisting lung disease.

TABLE 12.1 Postoperative ventilation settings

Ventilation challenges specific to the postcardiac surgical setting include:

Assessment and Management of Postoperative Bleeding

The harvest sites for radial arteries or saphenous veins are uncommon sources of significant blood loss and are generally easily managed with dressings or compression. Intrathoracic bleeding, however, may be torrential and threaten life. Occasionally surgical bleeding from the aorta, arterial grafts or myomectomy sites may exceed replacement capabilities, and at times patients succumb to overwhelming haemorrhage. Maintenance of drain patency and strict recording of losses and total fluid balance are paramount, and fluid balance assessments over shorter intervals, even every 5–10 minutes, become necessary during active bleeding. Because of the potential rates of bleeding, the cardiac surgical unit must be equipped to institute rapid volume replacement, and have access to adequate blood and blood product stores, blood warmers, and all necessary procoagulant therapies. In addition, dedicated equipment should be available to facilitate emergency resternotomy to control haemorrhage.

One or more chest drains are inserted to remove and monitor blood loss, but the positioning of drains is variable, depending in part on the procedure performed, the surgical route taken, and surgeon preference. Regardless of these considerations there will always be a retrosternal/anterior mediastinal drain, as the sternum is generally the major source of bleeding in the absence of complications. Additional drains may be inserted in the pericardial or pleural spaces. Pericardial drains are more likely to be inserted following aortic valve surgery, while pleural drains become necessary following mammary artery harvesting or when the pleura is opened for any other reason. Pleural drains may be anterior, posterior, or ‘wrap-around’ configurations in which they project over the anterior lung, following the pleural space first from midline, to lateral and then finally the posterior pleural space.

Reportable postoperative blood losses vary, but greater than 100 mL/h, or greater than 400 mL in the first 4 hours, would generally be regarded as excessive and worthy of surgeon notification. Importantly, excessive bleeding does not always represent a surgical defect that reoperation might correct, as there are many contributors to impaired haemostatic capability in the cardiac surgical patient (see below).

Chest drainage should be monitored closely, and while bleeding is active, volumes should be assessed every 5 minutes and patency of drains ensured to avert tamponade. Sudden cessation of drainage should always raise the possibility of the loss of tube patency and risk of tamponade, but tamponade may also occur while drainage continues, as collections and compression may occur at sites isolated from drains, or losses may simply be occurring faster than that able to be removed by patent drains.

Chest drains should also be observed for bubbling, to assess for air leaks originating from either system faults or patient leaks. When bubbling can be attributed to the patient, the patency of tubes becomes additionally important to avert tension pneumothorax, which may accumulate rapidly, even over the course of a few breaths in the ventilated patient.

Blood transfusions are not aimed at restoring haemoglobin to normal levels, and, despite variations in acceptable levels, relative anaemia is almost universally tolerated. Haemoglobin levels are thus not routinely treated unless below 80 g/L, except in the elderly or when there are significant comorbidities.^19,32 From these levels patients return to normal haemoglobin status within 1 month postoperatively.³²

Assessment and Management of Pericardial Tamponade

Postoperative pericardial tamponade results from the accumulation of blood or effusion fluid within the pericardium. An increasing volume within the pericardial space eventually compresses cardiac chambers, impeding venous return and therefore causing low cardiac output and hypotension. Pericardial tamponade is an emergency, and varies in severity from shock to pulseless electrical activity.

Described as one of the extra-cardiac obstructive shocks, pericardial tamponade often resembles cardiogenic shock. The low cardiac output and hypotension result in oliguria, altered mentation, peripheral hypoperfusion and development of lactic acidosis. Compensation includes tachycardia and marked vasoconstriction, elevating the systemic vascular resistance. As in cardiogenic shock, there is usually elevation of the filling pressures (right atrial, pulmonary artery and pulmonary capillary wedge pressures), sometimes with a particularly suggestive merging of the pulmonary artery diastolic, right atrial and pulmonary artery wedge pressures.²³ Additional features that may be present include muffled heart sounds, decreased QRS voltage, electrical alternans, narrowing pulse pressure and pulsus paradoxus, along with features of increasing anxiety and/or dyspnoea in the awake patient.

Echocardiography is the definitive assessment tool to reveal the presence of pericardial collections as well as identifying the impact on relaxation, filling and contraction of each cardiac chamber. The chest X-ray is of limited use and may show little, even with significant pericardial collections.

Importantly, the ‘classic’ or typical haemodynamic profile described above is not uniformly seen in tamponade, and tamponade should never be excluded because the haemodynamic status does not match this profile. This may be because classic tamponade implies uniform compression of the entire heart, which may not be the case with haemorrhagic tamponade. A clot may develop over just one chamber rather than occupying the entire pericardium, and so there may be compromise to only a single chamber rather than the whole heart.^21,23

Assessment and Management of Postoperative Pain

As much an art as a science, pain control in the cardiac surgical patient remains a major challenge and continues to provide uncertainty and opportunities for nursing clinicians and researchers. Principles are similar to those outlined in Chapter 7. Surgical pain, often complicated by pericardial inflammation, results in differing pain types, requiring different approaches.³⁴ These different approaches to pain management must be balanced against the promotion of spontaneous breathing, chest physiotherapy, mobilisation, and participation in education and lifestyle modification programs.

Analgesic options include intravenous, oral or rectal analgesics, antiinflammatories and, less commonly, epidural therapies and nerve blocks. Intravenous opiates and codeine/paracetamol preparations provide the mainstay of postoperative analgesia. When insufficient, or when clinical and electrocardiographic features suggest pericarditis, antiinflammatory agents such as rectal indomethacin are appropriate. The place of IV COX-2 inhibitors such as parecoxib appear uncertain, as analgesic efficacy now must be weighed against emerging data suggesting increased thrombotic complications.³⁵

Fluid and Electrolyte Management

Fluid therapy in the postoperative period is aimed at maintaining blood volume, replacing recorded and insensible losses, and providing adequate preload to sustain haemodynamic status. Isotonic dextrose solutions (5%) or dextrose 4% + saline 0.18% are commonly used at approximately 1.5 L/day as maintenance fluids.¹⁴

Potassium replenishment is generally necessary according to measured serum potassium. Polyuria is usually evident in the early postoperative period due to deliberate haemodilution while on cardiopulmonary bypass. With polyuria comes potassium losses, which must be treated to avert atrial or ventricular ectopy and tachyarrhythmias. Because of these predictable potassium losses, protocols for potassium replacement may be instituted, with standing orders for potassium replacement (e.g. 10 mmol over 1 hour if the serum potassium is <4.5 mmol/L, or 20 mmol over 2 hours if <4.0 mmol/L). Main line hydration infusions may also have added potassium to avoid hypokalaemia. Hypomagnesaemia may also develop due to polyuria, and is likewise proarrhythmic. Supplementation (magnesium chloride) is often used for arrhythmia management postoperatively, but its effectiveness has been questioned in many trials.³⁶

Hyperkalaemia occurs less often but is seen particularly when there is impaired renal function. Additional contributors to a rising potassium level include acidosis, administration of stored blood, haemolysis, inotrope use, and any postoperative use of depolarising muscle relaxants such as suxamethonium.

Emotional Responses and Family Support

The experience of being diagnosed with a cardiac disorder, waiting for surgery, the surgical experience and recovery is an emotional journey for patients and their families. Regardless of low mortality rates, the possibility of death and painful wounds can concern patients. Consequently, patients undergoing cardiac surgery often experience anxiety and depression, which can be distressing for patient and family.^37–39 Women appear to be more vulnerable to these emotions in relation to cardiac surgery than men.⁴⁰ Although it is normal and potentially protective to experience anxiety, higher levels of these emotions can be destructive. Anxiety and depression are predictive of worse postoperative outcomes, including poorer psychosocial adjustment and quality of life, more cardiac symptoms and readmissions.⁴¹ Therefore, it is essential to consider and address anxiety and depression when providing care for cardiac surgical patients.

Preoperative preparation provided by nurses usually incorporates information and support, so that patients and their families are familiar with procedures and can cooperate during recovery.⁴² However, seeing a patient who is successfully recovering from surgery may instil more confidence. Patients who have had their surgery postponed or who have been operated on in an emergency setting may need additional support. For many patients, fast-track procedures, including admission on day of surgery, early extubation and early discharge processes, decrease the discomfort associated with being away from home and surgical costs. For other patients there is too little time to be informed and understand postoperative and post-discharge care. Also, critical pathways for cardiac surgery do not include assessing the patient’s psychological state, so nurses must take care to consider this aspect. Consequently, family members assume an important role in supporting patients and helping them understand recovery requirements. It is vital that family members understand and anticipate a certain amount of anxiety and depression, particularly in the first week post-discharge. Family members may also be distressed by seeing their loved one ill and the unfamiliar ICU environment and equipment, so the additional requirement for them to assess and support the patient may be onerous. Printed information regarding the surgery, recovery and emotions will be useful for the patient and family.

Balloon Inflation

At the onset of diastole, the balloon is rapidly inflated with (most commonly) 40 mL helium. This inflation causes a sudden rise in pressure in the aortic root during diastole, raising mean arterial pressure and, importantly, coronary perfusion pressure. The blood displaced by the balloon expansion improves blood flow into the coronary circulation (which fills largely during diastole), as well as to the brain and systemic circulation. Thus there is improved myocardial oxygen supply, increased mean arterial pressure, as well as improved systemic perfusion.⁴⁶ The balloon remains inflated for the duration of diastole. The arterial pressure wave should reveal a sharp rise in pressure at the dicrotic notch, with a second pressure peak now appearing on the waveform, described as the ‘augmented diastolic’ or ‘balloon-assisted peak diastolic’ pressure. This peak is usually at least 10 mmHg higher than the systolic pressure (Figure 12.6).

FIGURE 12.6 IABP during 1 : 1 assist (counterpulsation on every beat). Balloon inflation at the start of Diastole and deflation just before next systole. IABP during 1 : 2 assist (counterpulsation on every second beat). Inflation of the balloon rapidly at the inflation point (IP) raises diastolic pressure, producing a peak diastolic pressure (PDP) that exceeds the systolic pressure (PSP). The balloon remains inflated during diastole. With balloon deflation just prior to the next systole there is a rapid decline in pressure to the balloon-assisted end-diastolic pressure (BAEDP), which is lower than normal, reducing afterload. The ensuing systole is achieved with a reduced systolic pressure (the assisted peak systolic pressure, APSP).

Balloon Deflation

As the inflated balloon largely obstructs the aorta, it must be deflated to permit systolic emptying of the left ventricle. Two separate approaches to the timing of balloon deflation have emerged: ‘conventional timing’, and ‘real timing’.

Maintenance of Limb Perfusion

The use of smaller-gauge catheters has reduced the potential for obstruction of arterial flow past the catheter to the lower limbs, as has the trend to sheathless insertion. Nevertheless, the threat of limb ischaemia remains an important issue in patient care, as IABP is most commonly undertaken in patients with atherosclerosis, potentially involving the lower limbs, even in the absence of overt peripheral vascular deficits. Identification of patients at risk (known claudication, chronically cold feet and peripheral vascular diseases) may be useful to ensure appropriate vigilance and prompt intervention where necessary. Peripheral perfusion may also be compromised by arterial embolisation should thrombi develop on the catheter. Although catheter materials are non-thrombogenic, the risk of thrombi formation remains and is heightened if periods of catheter stasis (interrupted pumping) are encountered. Systemic heparinisation is usually undertaken if indicated and according to specific hospital protocol (no literature available to support systemic heparinisation).

Hourly assessments of peripheral perfusion (colour, warmth, movement, sensation) should be performed to identify potential deficits. Dorsalis pedis and posterior tibialis pulses should be palpated and may sometimes require examination with a Doppler probe. Deficits should be promptly reported and consideration given to catheter removal or reinsertion on the contralateral limb. When pulses cannot be demonstrated, the limb should be assessed for the development of compartment syndrome. At times the viability of a limb must be weighed against the potential survival benefit of IABP to the patient.

Prevention and Treatment of Bleeding

Significant bleeding is uncommon,⁵¹ but blood loss may occur from the femoral arterial access site. In addition to physical factors at the insertion site, contributors to bleeding include heparinisation, thrombocytopenia from the physical effect of the pump on platelets, and/or other anticoagulants or antiplatelet agents used for the primary disease. Regular observation should be made of the insertion site for bruising or external bleeding, as well as other possible sites of bleeding due to heparinisation. Treatment includes pressure at the insertion site (including the use of sandbags), reinforcement of dressings, and/or topical procoagulant agents. Monitoring of coagulation status and haemoglobin should be undertaken and blood or blood products may (uncommonly) be required.

Prevention of Immobility-related Complications

The need for immobilisation of the patient, and in particular the leg, is often overemphasised, and may heighten the risk of atelectasis, pressure area development and venous stasis and thrombosis. Sensible limitation of leg movement is advised, but patients can generally still move in bed, and should still be turned 2-hourly for pressure relief as long as the insertion site is adequately protected and supported. The femoral access limits flexion at the hip beyond 30 degrees, which may also hamper effective chest physiotherapy and increase the risk of atelectasis and pneumonia.

Migration of the balloon catheter towards the aortic arch or towards the abdominal aorta may cause compromised perfusion to left arm (occlusion of left subclavian artery), kidneys (renal arteries) or abdominal viscera (superior mesenteric artery). Therefore, neurovascular observation of upper limbs, urine output and bowel sounds are part of nursing management of patient with IABP in situ.

Weaning of IABP

Weaning of intra-aortic balloon pumping therapy is generally undertaken once the patient has stabilised, is free of ischaemic signs and symptoms and is on minimum or no inotropic support. Algorithms have been offered for approaches to weaning therapy,⁵² but their impact on weaning duration or success has not been studied. Weaning is carried out by either gradual reductions in balloon inflation volume (volume weaning) or gradual reductions in assist frequency from 1 : 1 through 1 : 2 and 1 : 4 (ratio weaning). Hybrids of the two approaches are sometimes used. Support is reduced at intervals while the patient is observed for haemodynamic deterioration, pulmonary congestion, or the return of ischaemic signs and symptoms.

Assessment of Timing and Timing Errors

Accurate timing of inflation and deflation in relation to the cardiac cycle is required to maximise IABP benefit. Errors in timing may lessen the potential benefit, or in some cases may worsen cardiac performance and increase demands on the myocardium. Nurses are required to continually assess the haemodynamic impact of balloon pumping, the accuracy of timing via inspection of the arterial pressure waveform, and to adjust timing to optimise the impact of balloon pumping.

Early inflation

Early inflation will at times be difficult to differentiate from correct inflation timing but is recognised by the onset of inflation soon after the peak systolic pressure, before the pressure has declined to the level of the dicrotic notch (Figure 12.7). Early inflation may limit the stroke volume and cardiac output, as terminal systole is impeded and may result in increased myocardial oxygen demands. The inflation point should be adjusted (to later) until the inflation upstroke emerges smoothly out of the dicrotic notch.

FIGURE 12.7 IABP during 1 : 2 assist. Early inflation. The inflation point (IP) can be seen high in the downstroke of systole, in this case well before the dicrotic notch (DN).

Late inflation

The arterial pressure waveform reveals the onset of diastole (the dicrotic notch) before balloon inflation commences (Figure 12.8). This generally results in a lower augmented diastolic pressure than could otherwise be achieved. As the duration of balloon inflation is lessened, the desired rise in mean arterial pressure and coronary perfusion will not be achieved. The inflation marker should be set to ‘earlier’ until the inflation upstroke emerges smoothly out of the dicrotic notch.

FIGURE 12.8 IABP during 1 : 2 assist. Late inflation. Note that the inflation point (IP) occurs well after the dicrotic notch (DN). Late inflation is also obvious in 1 : 1 assist with balloon inflation well after the dicrotic notch.

Early deflation

Deflating the balloon earlier than necessary shortens the duration for which the balloon remains inflated and therefore limits the benefit of IABP. When deflation is very early, it may cause harm. Deflation sees the aortic pressure drop markedly but there is now time for blood to fill the space left by the balloon before systole commences. Aortic end-diastolic pressure increases and may even exceed the normal end-diastolic pressure, increasing the duration of isovolumetric phase, worsening left ventricular afterload and increasing myocardial oxygen demand (Figure 12.9). Correction is achieved by setting deflation to later until the pressure drop of deflation occurs just in advance of the succeeding systole.

FIGURE 12.9 IABP during 1 : 2 assist. Early deflation. The balloon has been deflated well in advance of the subsequent systole. The aortic pressure does drop off (not much from non assisted diastole) but then begins to rise again before the next systole gets underway, and may even exceed the normal end-diastolic pressure. Early deflation is also obvious in 1 : 1 assist.

Late deflation

When deflation begins too late, systole commences before complete emptying of the intra-aortic balloon. The typical reduction of aortic end-diastolic pressure is not seen. When significantly late, the end-diastolic pressure may even be increased prolonging the duration of the isovolumetric contraction phase, and worsening afterload. As systole occurs against an incompletely deflated balloon, the stroke volume and cardiac output suffer and ventricular work and oxygen demand increases (Figure 12.10). Deflation should be set to earlier until the systolic upstroke emerges out of the reduced end-diastolic pressure dip.

FIGURE 12.10 IABP during 1 : 2 assist. Late deflation. The late deflation is seen here as the sharp drop-off before systole and a balloon assisted end diastole that does not fall to below the normal patient end-diastolic pressure.

Gas loss alarms

Most devices will determine the severity of gas losses and classify them as slow, rapid or disconnect. In all gas loss states it is imperative that assessments be made to exclude balloon rupture and helium leak into the arterial circulation. Small gas losses of helium may or may not be of clinical significance, but the delivery of sizeable helium volumes may behave as gas emboli, and if delivered into the coronary circulation may result in lethal arrhythmias or result in neurological complications if delivered into the cerebral circulation. In all gas loss alarm states, the helium drive line should be inspected for the presence of blood to indicate loss of integrity of the balloon. If blood is present in the drive line (Figure 12.11), pumping should be suspended and no attempts at recommencing balloon pumping should be made. Prompt removal and/or replacement, along with thorough patient assessment, is essential.

FIGURE 12.11 Intra-aortic balloon rupture and presence of blood in helium drive line.

Hyperacute Rejection

Hyperacute rejection is now a rare form of humoral rejection that occurs minutes to hours after transplantation and results from ABO blood group incompatibility or the recipient having preformed, donor-specific antibodies.⁹² ABO blood group and panel reactive screening of anti-human lymphocyte antigen (anti-HLA) antibodies preoperatively minimises the possibility of hyperacute rejection, particularly in health care systems where blood that has been prospectively cross-matched is routinely used. If it occurs, hyperacute rejection leads to organ failure and rapid activation of the complement cascade, producing severe damage to endothelial cells, platelet activation, initiation of the clotting cascade, and extensive microvascular thrombosis.⁷⁸ There is no effective treatment for hyperacute rejection apart from mechanical circulatory support or interim retransplantation.

Acute Rejection

Acute rejection can be classified as either cellular or humoral.⁹³ Cellular rejection involves T-cell infiltration of the allograft. Cellular rejection occurs much more commonly than humoral rejection, but both may occur simultaneously.⁹⁴ Humoral or microvascular rejection is thought to be primarily mediated by antibodies. Humoral rejection may occur due to the presence of a positive donor-specific cross-match, or in a sensitised recipient with preformed anti-HLA antibodies.⁹⁵

Percutaneous transvenous endomyocardial biopsy is considered the gold standard for detecting cardiac rejection.⁹⁶ Grading of cardiac rejection is noted in Table 12.4.⁹⁷ In humoral rejection, endomyocardial biopsy reveals increased vascular permeability, microvascular thrombosis, interstitial oedema and haemorrhage, and endothelial cell swelling and necrosis.⁷⁸ An echocardiogram is also performed to evaluate systolic cardiac function.

TABLE 12.4 Standardised cardiac biopsy grading⁹⁸

Therapeutic interventions for rejection vary between centres and are based on the grade of rejection, degree of haemodynamic compromise, clinical findings and time elapsed since transplantation. Asymptomatic mild rejection (grade 1) is rarely treated, and only 20–40% of mild cases progress to moderate rejection (grade 3A), usually requiring treatment.^95,98 Grades 3B and 4 rejection are always treated, as they represent myocyte necrosis. Cellular rejection is usually treated with higher doses of corticosteroids, such as ‘pulse’ doses of methylprednisolone (1–3 g IV over 3 days), and antilymphocyte antibody agents (ATG, ATGAM or OKT3). Humoral rejection is treated with plasmapheresis, high-dose corticosteroids, cyclosphosphamide therapy and antilymphocyte antibody therapy.^99,100 It may be judicious to review the patient’s medications during periods of rejection to ensure that drugs capable of reducing cyclosporin or tacrolimus serum levels such as certain anticonvulsants and antibiotics have not been taken. In addition to augmentation of immunosuppression therapy, fluid, pharmacological and mechanical therapeutic interventions are instituted to support cardiac function, depending on the degree of ventricular dysfunction.

Immunosuppression Therapy

In this section, a brief discussion of immunosuppression therapies and associated nursing implications is provided. To prevent rejection of the transplanted organ, recipients receive a triple-therapy regimen of immunosuppression agents for the remainder of their life. Triple-therapy usually consists of corticosteroids (prednisolone or prednisone), a calcineurin antagonist (cyclosporine or tacrolimus [FK506]) and an antiproliferative cytotoxic agent (mycophenolate mofetil, azathioprine or sirolimus/rapamycin).^101,102 For heart patients, sirolimus or rapamycin may become the cytotoxic drug of choice following findings of a recent study that demonstrated a lower incidence of cardiac allograft vasculopathy at 6 and 24 months, and lower rejection rates with sirolimus compared with azathioprine.¹⁰³

Immunosuppression therapy is commenced preoperatively or in operating theatre. Maintenance immunosuppression regimen is usually instituted within hours of admission to ICU, with each patient’s immunosuppressive needs individually assessed. For instance, the administration time for introduction of the selected immunosuppressive agent(s) may be delayed in patients with preexisting renal dysfunction. When the administration of the usual regimen of immunosuppression is delayed, induction therapy with anti-lymphocyte agents (anti-thymocyte globulin (ATG), ATGAM or OKT3) or interleukin-2 receptor antagonists (basiliximab, daclizumab) may be used in the immediate postoperative period.^104,105 Induction therapy may be used in circumstances of primary allograft failure perioperatively, e.g. HLA mismatch (rare), or early humoral rejection, or to allow for a delay in initiating cyclosporine in patients at risk of renal failure.^106,107 The common drugs used to suppress the immune system and the nursing implications are illustrated in Table 12.5. As highlighted in the table, some immunosuppressive agents are cytotoxic (e.g. mycophenolate mofetil), requiring safety measures during preparation, delivery and disposal. Likewise, some immunosuppressive agents will be given IV (e.g. azathioprine) until patients can eat and drink as they cannot be crushed for naso-gastric administration. In addition, as blood levels of some immunosuppression agents (e.g. cyclosporine, sirolimus) are taken regularly to assess efficacy, nurses need to be aware of timing blood sampling to dosage times in order to obtain accurate data to inform doses.

Infection

Infection is a major risk factor for transplant recipients due to their immunosuppressed state. The periods of greatest risk for patients are the first 3 months after transplantation, and after episodes of acute rejection when immunosuppression agents are increased.^108,109 In addition to the nosocomial bacterial infections that all surgical patients are exposed to in critical care (see Chapter 6), immunosuppressed transplant recipients are at risk of acquiring opportunistic bacterial, viral or fungal infections; latent infections acquired from the donor organ such as cytomegalovirus (CMV); or reactivation of their own latent infections (e.g. CMV or Pneumocystis carinii). To combat Pneumocystis carinii, patients receive trimethoprim with sulfamethoxazole twice weekly.¹¹⁰ Despite preoperative screening for CMV, the shortage of donor organs often necessitates CMV mismatching. Effective prophylaxis for CMV infection is provided by administering CMV hyperimmune globulin to CMV-positive and CMV-negative recipients who receive a heart from a seropositive donor.¹¹¹ This commences within 24–48 hours of surgery.¹⁰⁵ For CMV-negative recipients of organs from seropositive donors, ganciclovir for 1–2 weeks followed by oral therapy for 3 months is required in addition to CMV hyperimmune globulin.^111–113

Haemorrhage/Cardiac Tamponade

The risk of haemorrhage or cardiac tamponade is greater for heart transplant recipients than for patients undergoing coronary artery bypass graft or valvular surgery. Preoperative anticoagulation for end-stage heart failure or atrial fibrillation, impairment of hepatic function secondary to right heart failure, redo surgery, surgical suture lines connecting major vessels and atria, and a larger than usual pericardium are all contributing factors. Good surgical technique is mandatory in preventing postoperative bleeding. As the promotion of haemostasis is a major therapeutic goal postoperatively, blood products, procoagulants and antifibrinolytics are commonly administered according to laboratory and clinical data. Postoperative mortality from bleeding has been reported to occur in up to 6.7% of cases.¹¹⁸

Acute Renal Failure

Acute renal failure or varying degrees of renal dysfunction can occur in the initial postoperative period due to preexisting renal dysfunction, cyclosporin, nephrotoxic antibiotics, or sustained periods of hypotension secondary to cardiopulmonary bypass or allograft dysfunction. Diuretic therapy is invariably needed in the initial postoperative period due to these factors, as well as the fluid retention effects of corticosteroids and raised filling pressures secondary to a transient loss of right and/or left ventricular compliance.¹¹⁹ High doses or continuous infusions of diuretics may be required in patients who were on diuretic therapy preoperatively. Close monitoring of serum electrolyte levels will indicate the need for any supplements.

Early Allograft Dysfunction and Failure

Primary allograft failure is the leading cause of death in the first month and year after surgery.^120,121 In the immediate postoperative period, myocardial performance is depressed due to the clinical sequelae of cardiopulmonary bypass and ischaemic injury associated with surgical retrieval, hypothermic storage, prolonged ischaemic times, and reperfusion. Despite a preferred time period between organ retrieval and reimplantation of 2–6 hours, the vast distances between capital cities (up to 3000 km) over which donor hearts may be transported, and a decision to accept marginal, suboptimal organs, led Australian researchers and transplant teams to pioneer prolonged ischaemic times of up to 8 hours (New Zealand, 7 hours).¹²²

Heart transplants have been, and are likely to continue to be, performed in Australia and New Zealand and other countries that encompass long distances with ischaemic periods beyond 6 hours, as excellent short-term (30-day mortality) and long-term (ejection fraction at 1 year) outcomes have been reported.¹²² These outcomes were achieved by using innovative preservation techniques and postoperative mechanical assistance in the form of intra-aortic balloon counterpulsation and/or a right ventricular assist device.^122,123 Adrenaline is invariably commenced intraoperatively, irrespective of ischaemic time, to provide inotropic support to the transplanted heart.

Early allograft dysfunction can present as left, right or biventricular dysfunction. Management of cardiac dysfunction is dependent on clinical signs and underlying aetiologies that include pulmonary hypertension, acute rejection, and ischaemic injury. Right ventricular dysfunction is usually secondary to pulmonary hypertension, whereas left ventricular or biventricular dysfunction results from acute rejection and ischaemic injury.

To prevent right ventricular dysfunction and failure secondary to raised pulmonary pressures, prospective heart transplant recipients are screened preoperatively for the degree and reversibility of pulmonary hypertension. Reversible pulmonary hypertension is a transpulmonary gradient less than 15 mmHg that responds to pulmonary vasodilator therapies, such as prostaglandin E1, prostacyclin or inhaled nitric oxide (NO).¹²⁴ Right ventricular dysfunction or failure can also occur in the postoperative context due to ischaemic injury, an undersized heart (greater than 20% difference in body surface area between donor and recipient), or hypoxic pulmonary vasoconstriction.⁷⁹ Isoprenaline or milronine, dobutamine and adrenaline are administered in this situation.¹¹²

Left ventricular dysfunction cannot be anticipated preoperatively, so when signs first emerge peri- or post-operatively, fluid management strategies (filling or diuresis as deemed appropriate) and inotropic agents are commenced immediately.¹¹² In patients with prolonged ischaemic times, mechanical assistance in the form of an IABP is invariably instituted perioperatively.

In the initial postoperative period, cardiac dysfunction can also occur as a result of a low systemic vascular resistance (SVR) syndrome, characterised by a calculated SVR of less than 750 dynes/sec/cm⁻⁵ in the presence of an unsustainable high cardiac output.^125,126 The cause of low SVR syndrome is not fully understood, although it has been linked with systemic inflammatory response syndrome (SIRS) associated with cardiopulmonary bypass (see Chapter 20), the chronic use of angiotensin-converting enzyme inhibitors for end-stage heart failure (see Chapter 10), and a deficiency of vasopressin.^125,127 Noradrenaline is titrated to achieve a calculated SVR within normal parameters and to lower the unsustainably high cardiac index. In severe cases, vasopressin may be infused at doses of 0.04–0.1 units/min concurrently with noradrenaline.¹²⁸ Experience suggests that the dose of adrenaline should be minimised in the presenceof metabolic acidosis, and the noradrenaline infusion increased to achieve normotension, a calculated SVR higher than 900 dynes/sec/cm^-5 and a sustainable cardiac index.

Denervation

Donor heart implantation severs both afferent and efferent nervous system connections to the heart. Hence, the transplanted heart has no direct autonomic nervous system innervation but is responsive to circulating catecholamines. Denervation impairs circulatory system homeostasis, as evidenced by: a volume-expanded state; a tendency to hypertension; no sensation of angina pectoris; a high resting heart rate; a slow or absent baroreceptor reflex (to increase heart rate/cardiac output in response to hypotension); and no rises in heart rate and contractility due to hypovolaemia or vasodilation.⁷⁹ As the cardiac allograft is dependent on an adequate preload, the effects of postural changes in recipients are important. (A detailed discussion of physiology of the transplanted heart is provided elsewhere.⁷⁹)