Abstract
A comprehensive review of the complications of cardiac surgery would fill an entire volume. This chapter covers the more common and life-threatening complications. The reader is directed to the publications list under further reading.
A comprehensive review of the complications of cardiac surgery would fill an entire volume. This chapter covers the more common and life-threatening complications. The reader is directed to the publications list under further reading.
Cardiovascular Complications
Haemodynamic instability following CPB is common. The goal of cardiovascular management in the ICU is to maintain adequate oxygen transport to end organs until complete recovery of cardiac function.
Cardiac Arrest
Resuscitation of cardiac arrest after cardiac surgery differs from conventional advanced life support (see Figure 8.1):
In shockable rhythms, up to three shocks should be administered in rapid succession before chest compressions
In asystole, epicardial pacing should be attempted before chest compressions
In pulseless electrical activity (PEA), pacing-induced VF should be excluded
Epinephrine administration may be deferred and doses reduced to reduce the risk of hypertension after return of spontaneous circulation
Figure 8.1 Algorithm for resuscitation after adult cardiac surgery. Six suggested modifications to the standard ALS algorithm are highlighted in the bright yellow boxes to the sides and below. Therapeutic hypothermia may be considered after successful resuscitation.
Initial Optimization
The response to increasing preload can be thought of in three distinct phases (Box 8.1).
In health, preload optimization typically occurs with a PAWP of 10–15 mmHg. Many cardiac surgical patients have reduced LV compliance, which becomes further reduced by the effects of CPB and catecholamines. In these patients, a higher PAWP (i.e. >15 mmHg) is often required to maintain adequate SV.
Heart rate, rhythm and myocardial contractility are the major determinants of myocardial VO2. Because of its 30% augmentation of end-diastolic volume (EDV), NSR is desirable whenever possible. Atrial or atrioventricular (A-V) pacing at 80–100 bpm can improve endocardial perfusion by shortening the diastolic filling time and reducing the EDV.
VF, and unstable ventricular and supraventricular tachydysrhythmias should be immediately converted by either electrical or chemical cardioversion. Maintenance of normal or supranormal [K+] (i.e. 4.5–5.5 mmol l–1) and [Mg2+] reduces ventricular irritability.
Cardiodepressant antidysrhythmics should be used with caution in patients with impaired myocardial function.
Afterload can be viewed as the sum of external forces opposing ventricular ejection, of which the SVR is one component (Box 8.2). Laplace’s law states that the LV wall tension or stress is directly proportional to the intracavity pressure and cavity radius, and is inversely proportional to the LV wall thickness.
History of preoperative essential or secondary hypertension
Increased endogenous catecholamines released during CPB
Hypothermia
Emergence from anaesthesia
Response to pain can lead to arteriolar vasoconstriction
Administration of exogenous vasoconstrictors
Considering the CO, MAP and PAWP in the patient with optimal preload simplifies haemodynamic management (Box 8.3).
LV Dysfunction
Ventricular function is commonly depressed for 8–24 hours following CPB. The ideal measure of LV performance, the slope of the end-systolic pressure–volume relationship (ESPVR), cannot easily be derived at the bedside. For this reason, surrogate measures of contractility (i.e. RA pressure, PAWP, MAP, PAP and CO) are used. Although echocardiography can be used to assess ventricular function, the findings are generally load-dependent (Figure 8.2).
Figure 8.2 LV pressure–volume loops illustrating (A) the normal ventricle, and (B) the decrease in slope of the ESPVR line with decreased contractility. This decrease in contractility can also be accompanied by a decrease in the SV, and an increase in the LVEDP.
Decreased contractility can be secondary to metabolic abnormalities, cardiodepressant agents, reperfusion injury and myocardial ischaemia (coronary vasospasm, thrombosis or occlusion). The incidence of perioperative MI (often clinically silent) is thought to be ~5%. The diagnosis of MI in the post-CABG patient may be challenging (Box 8.4).
Before initiating inotropic therapy, all remediable factors (i.e. rate, rhythm, preload and afterload) should be addressed. Indications for use of the IABP and mechanical cardiac support are discussed in Chapters 6 and 16).
RV Dysfunction
RV failure can be difficult to manage because of the dependence of the LV filling on right-sided function. If the RV output falls, the LV filling and therefore the LV output are reduced. The RV is extremely sensitive to increases in afterload (i.e. PVR). Although more effective in LV failure, the IABP may reduce the RV afterload and improve coronary perfusion. Short-term use of an RV assist device may allow time for RV recovery.
Reducing the RV afterload can improve the RV systolic performance and the right heart CO. Drug therapy includes inhaled milrinone, NO (5–10 ppm) and epoprostenol (PGI2); IV PGI2 (2–5 ng kg–1 min–1); and oral agents, such as sildenafil and bosentan.
Pericardial Tamponade
Pericardial tamponade is characterized by hypotension, tachycardia and an elevated CVP. Although it typically occurs acutely within 24 hours of cardiac surgery, it can develop chronically over several days. In tamponade, the decrease in the LV filling during inspiration is accentuated. The fall in the SV produces a reflex increase in HR and myocardial contractility. Diagnostic clues include those described in Box 8.5.
Oliguria
Reduced or absent chest tube drainage
Pulsus paradoxus
Equalization of the RA pressure, PA diastolic pressure and PAWP
Loss of the y-descent in RA pressure and PAWP
Low voltage ECG/electrical alternans pattern
In addition to detecting an obvious extracardiac collection, the most common TOE manifestation is the collapse of the right-sided chambers when their intracavity pressures are at their lowest – i.e. the RV in early diastole and the RA in early systole. Management consists of resuscitation (Box 8.6) and prompt surgical drainage.
- Preload
Elevated – avoid high PEEP
- HR
High – because of reduced SV
- Rhythm
Sinus preferable but limited atrial kick
- SVR
High
- Contractility
Normal or elevated
Postoperative AF
AF and atrial flutter are the most common postoperative supraventricular tachydysrhythmias following cardiac surgery. New-onset AF occurs within 24–72 hours of surgery in up to 30% patients. Independent predictors of AF include age >65 years, hypertension, male sex, a previous history of AF and valve surgery.
In the absence of contraindications, all patients who develop AF should be anticoagulated within 24–48 hours. If AF has persisted for >48 hours and therapeutic anticoagulation has not been maintained, TOE should be performed to exclude the presence of LA thrombus.
Electrical or chemical cardioversion to NSR is preferred, especially when patients are haemodynamically unstable, symptomatic or unable to receive anticoagulation. Pharmacological ventricular rate control may be acceptable in some cases.
Respiratory Complications
Some degree of impairment of respiratory function occurs in all patients undergoing cardiac surgery. As many as 10% of cardiac surgical patients will have postoperative impairment of gas exchange that is sufficient to cause concern, prolong mechanical ventilation and delay discharge from the ICU. This ranges from transient atelectasis and retained secretions, to overwhelming acute lung injury (ALI) and ARDS. The causes of respiratory complications following cardiac surgery are summarized in Box 8.7. It should be borne in mind that the major determinant of pulmonary outcome following cardiac surgery is cardiac function.
Respiratory Failure
Acute respiratory failure is the inability to perform adequate intrapulmonary gas exchange causing hypoxia with or without hypercarbia. The accepted quantitative criteria for the diagnosis are PaO2 <8.0 kPa (60 mmHg) on air and PaCO2 >6.5 kPa (49 mmHg) in the absence of primary metabolic alkalosis.
Atelectasis affects dependent areas of lung – particularly the left lower lobe following internal mammary artery harvest. The combined effects of anaesthesia, mechanical ventilation and sternotomy reduce functional residual capacity, vital capacity and tidal volume (Vt). These effects may be compounded by diaphragmatic dysfunction caused by direct or thermal (cold) injury to the phrenic nerve. Recruitment manoeuvres, such as PEEP and full lung expansion prior to chest closure, may reverse some of the atelectasis that inevitably occurs during surgery. Postoperative atelectasis is best managed by adequate analgesia, physiotherapy, recruitment manoeuvres, incentive spirometry and forced coughing.
ALI and ARDS
Hypoxia with bilateral pulmonary infiltrates and low LA pressure following cardiac surgery used to be known as ‘pump lung’. The clinical features, which resemble those of sepsis with severe hypoxaemia, include increased PVR, increased vascular permeability and an elevated alveolar–arterial O2 gradient. This ALI usually resolves within 48 hours or progresses to ARDS (Table 8.1).
ALI | PaO2/FiO2 <40 kPa (300 mmHg) | |
ARDS | Bilateral pulmonary infiltrates on CXR PAWP <18 mmHg | |
Mild PaO2/FiO2 26–40 kPa (201–300 mmHg) PEEP/CPAP ≥5 | ||
Moderate PaO2/FiO2 <26 kPa (≤200 mmHg) PEEP/CPAP ≥5 | ||
Severe PaO2/FiO2 13 kPa (<100 mmHg) PEEP/CPAP ≥ 5 |
The incidence of ARDS following CPB is reported to be as high as 2.5% in some series. Predisposing factors include redo cardiac surgery, hypotension, sepsis and massive transfusion. The aetiology and subsequent complications, rather than respiratory failure itself, dictate mortality from ARDS. Death is usually due to multiple organ dysfunction. The avoidance of CPB does not eliminate the risk of ALI or ARDS. The management of ARDS following cardiac surgery is summarized in Box 8.8.
Gastrointestinal Complications
The reported incidence of GI complications after cardiac surgery is low (<3%). The morbidity and mortality associated with GI complications, however, are disproportionately high. The pathogenesis of GI complications after cardiac surgery is multifactorial. Apart from the stress of major surgery, anaesthesia, anticoagulation and hypothermia, cardiac surgery is associated with a reduction and redistribution in systemic blood flow. GI complications are summarized in Box 8.9.
Bleeding and mesenteric ischaemia are the most common GI complications. A number of risk factors have been identified (Box 8.10). Despite improvements in perioperative care, anaesthesia and operating techniques, the incidence of GI complications has not changed in recent years due to the older surgical population with more numerous co-morbidities.
Demographic
Age >65 years
Poor nutritional status
History of peptic ulcer disease
Preoperative drugs
NSAIDs
Aspirin/clopidogrel/prasugrel
Corticosteroids
Warfarin
Type of surgery
Emergency operations (e.g. aortic dissection)
Redo operations
Valve operations
Combined procedures (e.g. valve and CABG)
Preoperative factors
Peripheral vascular disease
Renal insufficiency
Hepatic impairment
Preoperative LV ejection fraction < 40%
Significant arrhythmia (e.g. AF)
Cardiogenic shock
Intraoperative and postoperative
Profound hypotension/hypoperfusion
Prolonged duration of CPB (>120 minutes)
Significant arrhythmia (e.g. AF)
Inotrope and vasoconstrictor therapy
IABP or TOE use
Haemorrhage and transfusion
Surgical re-exploration within 24 hours
Respiratory failure – requiring prolonged ventilatory support
Renal failure
Sternal/mediastinal infection
The symptoms and signs of GI complications may be subtle; their onset insidious and masked by sedatives and analgesics. Transient, mild GI dysfunction after cardiac surgery needs to be distinguished from more serious conditions requiring medical or surgical intervention. The lack of early signs and delayed diagnosis contributes to the high morbidity and mortality.
Renal Failure
The overall incidence of postoperative ARF requiring renal replacement therapy (RRT) in the adult cardiac surgical population is around 5%. This ranges from <1%, in patients with normal preoperative creatinine concentration, to >40% in patients with preoperative creatinine concentration >200 μmol l–1 (2.3 mg dl–1). ARF after cardiac surgery increases the length of ICU and hospital stay. The additional costs associated with ARF are considerable, particularly as a small proportion of patients remain dependent on RRT after hospital discharge. Although rarely a primary cause of death, ARF is an independent risk factor of mortality after cardiac surgery and is associated with 50% mortality.
Definitions
Nowadays, the term ARF has been replaced by the term acute kidney injury (AKI). The RIFLE classification (Risk of renal dysfunction, Injury to the kidney, Failure of kidney function, Loss of kidney function and End-stage kidney disease) defines AKI according to changes in serum creatinine concentration and urine output (Figure 8.3).