**4. Management of complications**

#### **Atrial fibrillation**

Atrial fibrillation following cardiac surgery is common and occurs in up to 35 % of patients. While the cause of AF is not completely understood, it is associated with an increase in mortality, stroke, and prolonged hospital stay. AF has been discussed in Section I of this chapter.

#### **Low cardiac output syndrome**

A low cardiac output state may result from decreased left ventricular preload (hypovolemia, cardiac tamponade, vasoplegia), decreased contractility (myocardial stunning, ischemia or infarction related to poor intraoperative myocardial protection, incomplete myocardial revascularization, anastomotic stenosis, or coronary artery spasm), arrhythmias, increased afterload or diastolic dysfunction.

Transoesophageal echocardiography can help define whether a low cardiac output state is related to left ventricular systolic or diastolic dysfunction, right ventricular dysfunction or cardiac tamponade. The management of low cardiac output has been discussed in Section I of this chapter.

*Right ventricular dysfunction* produces inadequate filling of the left heart resulting in a low cardiac output state. It may be attributable to poor myocardial protection, prolonged ischemic times, coronary embolism, hypotension, RV pressure overload (pulmonary disease, ARDS, pulmonary embolism) or acute pulmonary hypertension due to vasoactive substances, LV dysfunction, protamine or hypoxia and acidosis.

complete arch repair with the ascending aortic graft serving as proximal landing zone. Type III repairs have inadequate proximal and distal landing zones: after total arch replacement with a distal elephant trunk, the descending thoracic aortic repair is completed by

Concerning aortic *dissection*, the Penn classification of a type A dissection integrates type of clinical presentation with dissection extent to stratify perioperative outcome and facilitate

The American Heart Association recently published a position paper on the integrated management of decending thoracic aortic disease that complements the recent guidelines from the Society of Thoracic surgeons. (72) These guidelines together summarize the paradigm shift in the management of descending thoracic aortic pathologies due to endovascular therapies. In Stanford type B aortic dissection, the conservative management of refractory pain and hypertension is associated with significant short-term mortality. Therefore, although a survival advantage has not been demonstrated yet, endovascular

Depending on the type of organ protection applied during aortic surgery (deep hypothermic circulatory arrest, selective perfusion of brain and kidneys) coagulopathies and neurologic deficit may occur. Brain damage may be due to ischemia or embolisation and paraplegia may result from crossclamping of the descending aorta. Careful neurologic evaluation

Also, the hypotensive regimen used in the early postoperative period must reduce systolic blood pressure and the force of cardiac contraction. The most common regimens include the

Atrial fibrillation following cardiac surgery is common and occurs in up to 35 % of patients. While the cause of AF is not completely understood, it is associated with an increase in mortality, stroke, and prolonged hospital stay. AF has been discussed in Section I of this

A low cardiac output state may result from decreased left ventricular preload (hypovolemia, cardiac tamponade, vasoplegia), decreased contractility (myocardial stunning, ischemia or infarction related to poor intraoperative myocardial protection, incomplete myocardial revascularization, anastomotic stenosis, or coronary artery spasm),

Transoesophageal echocardiography can help define whether a low cardiac output state is related to left ventricular systolic or diastolic dysfunction, right ventricular dysfunction or cardiac tamponade. The management of low cardiac output has been discussed in Section I

*Right ventricular dysfunction* produces inadequate filling of the left heart resulting in a low cardiac output state. It may be attributable to poor myocardial protection, prolonged ischemic times, coronary embolism, hypotension, RV pressure overload (pulmonary disease, ARDS, pulmonary embolism) or acute pulmonary hypertension due to vasoactive

endovascular stentingwith the elephant trunk serving as the proximal landing zone.

decision-making about the type of surgical repair. (71)

before and after surgery are important.

**4. Management of complications** 

**Low cardiac output syndrome** 

arrhythmias, increased afterload or diastolic dysfunction.

substances, LV dysfunction, protamine or hypoxia and acidosis.

use of beta-blockers.

**Atrial fibrillation** 

chapter.

of this chapter.

intervention of these type B dissections is now more often applied.

Right coronary artery disease, right ventricular infarction and pulmonary hypertension associated with mitral/aortic disease predispose to RV failure after cardiac surgery.

PAC's and TEE are very helpful in assessing the status of the RV function. In the absence of LV dysfunction, a high RA/PCWP pressure ratio is suggestive for RV dysfunction. The goals of treatment are to optimize RV preload, maintain systemic perfusion pressure, improve RV contractility, and reduce RV afterload by reducing pulmonary vascular resistance. (27)

*Diastolic dysfunction* , defined as increased resistance to filling of one or both cardiac chambers, is a common finding after cardiac surgery, especially after cardioplegic arrest. Echocardiography has greatly improved the knowledge of diastole by showing the real-time activities in the heart, as related to filling pressures, shape and relaxation. Failure of the RV can contribute to left-sided diastolic dysfunction by increasing cardiac pressures, which causes decreased relaxation of the myocardium yielding decreased myocardial distensibility. Factors responsible for increased chamber stiffness include fibrosis, cellular disarray, and hypertrophy. Factors responsible for decreased relaxation include asynchrony, abnormal loading, ischemia, abnormal calcium ion flux and hypertrophy. Note that ventricular hypertrophy affects both stiffness and relaxation, increasing the risk of diastolic dysfunction. (73)

#### **Cardiac tamponade**

Cardiac tamponade is primarily the result of impaired filling of one or more of the cardiac chambers and leads to low cardiac output. Adrenergic and endocrine mechanisms are activated resulting in tachycardia and vasoconstriction.

The diagnosis of cardiac tamponade depends on a high degree of suspicion. Tamponade after cardiac surgery is different from a medical tamponade due to compressing fluid within an intact pericardium. In the setting of cardiac surgery, the pericardial space is often left open and in open communication with one or both the pleural spaces, and the compressing blood is at least in part clotted and able to cause localized compression of the heart. Serious suspicion for tamponade should rise in patients with deteriorating haemodynamics or gradually increasing requirements for inotropic drugs. The classic signs of elevated CVP or equalization of CVP and PAOP are often absent. Cardiac tamponade is difficult to distinguish from biventricular failure. A useful clue may be the pronounced respiratory variation of blood pressure in association with high filling pressures and low cardiac output. TEE may be helpful in diagnosing cardiac tamponade. Echolucent crescents between the RV wall and the pericardium or the posterior LV wall are discernible. A classic sign is diastolic collapse of the right atrium or RV.

A rule of thumb in the acute management of cardiac tamponade is to keep the patient *Full*, *Fast* and *Thight*. Full, the delivery of volume expansion in order to achieve an adequate preload. Fast, using pacing or medication to increase the heart rate to maintain cardiac output since the strokevolume is compromised. Tight, applying vasopressor therapy to increase preload, maintain bloodpressure and coronary perfusion pressure.

The definitive treatment of tamponade is surgical exploration with evacuation of hematoma.

#### **Renal insufficiency**

No clear definition exists as to what constitutes renal impairment or failure following CPB. Renal failure requiring dialysis is infrequent following CPB, although reductions in creatinine clearance are more frequent. There are several risk factors for postoperative renal failure, including postoperative low cardiac output, repeat cardiac surgery, valve surgery, age greater than 65, and diabetes.

The primary cause may be prerenal (low pressure, low output, ACE, NSAID's), renal (Acute Kidney Injury) from ischaemic insult or interstitial drug-related nephritis or postrenal.

Management of these patients consists of supportive treatment ensuring adequate cardiac ouput, perfusion pressure and volume status and of determining the primary cause, and then directing specific treatment as necessary such as discontinuing the offending drug.

If patients do require dialysis, continuous dialysis may be better than intermittent dialysis. (6,74,75,76)

#### **Impediments to weaning and extubation**

The most important factors limiting weaning and extubation in the early postoperative period after cardiac surgery include:


The diagnosis of diaphragmatic paralysis should be considered whenever a patient fails to wean from mechanical ventilation and can be documented by observing paradoxical movement of the diaphragm during inspiration.

2. unstable haemodynamics

Postoperative cardiac surgical patients with unstable haemodynamics and/or low cardiac output syndromes may not well tolerate the extra work of breathing associated with weaning. Weaning is difficult and may further deteriorate the already compromised myocardium.

Weaning affects cardiac output due to changes in pulmonary vascular resistance. Increased pulmonary vascular resistance (PVR) leads to septal shifts and reduced efficiency of biventricular function. It is therefore better to keep the patient sedated on full ventilator support until the cardiac problem is resolved. (77)

3. fluid overload

Cardiac surgery and CPB result in a systemic inflammatory response syndrome which produces a capillary leak. The duration and severity of this syndrome include factors related to the patient characteristics, severity of the surgical trauma, administration of blood products and CPB management. The use of heparin-coated tubings, membrane oxygenator, centrifugal pumps, steroids and leukocyte filters may reduce the SIRS. The capillary leak syndrome is usually most predominant the first 6 to 8 hours after the termination of CPB.

failure, including postoperative low cardiac output, repeat cardiac surgery, valve surgery,

The primary cause may be prerenal (low pressure, low output, ACE, NSAID's), renal (Acute Kidney Injury) from ischaemic insult or interstitial drug-related nephritis or postrenal. Management of these patients consists of supportive treatment ensuring adequate cardiac ouput, perfusion pressure and volume status and of determining the primary cause, and then directing specific treatment as necessary such as discontinuing the offending drug. If patients do require dialysis, continuous dialysis may be better than intermittent dialysis.

The most important factors limiting weaning and extubation in the early postoperative



The diagnosis of diaphragmatic paralysis should be considered whenever a patient fails to wean from mechanical ventilation and can be documented by observing paradoxical

Postoperative cardiac surgical patients with unstable haemodynamics and/or low cardiac output syndromes may not well tolerate the extra work of breathing associated with weaning. Weaning is difficult and may further deteriorate the already

Weaning affects cardiac output due to changes in pulmonary vascular resistance. Increased pulmonary vascular resistance (PVR) leads to septal shifts and reduced efficiency of biventricular function. It is therefore better to keep the patient sedated on

Cardiac surgery and CPB result in a systemic inflammatory response syndrome which produces a capillary leak. The duration and severity of this syndrome include factors related to the patient characteristics, severity of the surgical trauma, administration of blood products and CPB management. The use of heparin-coated tubings, membrane oxygenator, centrifugal pumps, steroids and leukocyte filters may reduce the SIRS. The capillary leak syndrome is usually most predominant the first 6 to 8 hours after the

age greater than 65, and diabetes.

**Impediments to weaning and extubation** 

period after cardiac surgery include:

1. neurologic dysfunction

oriented and tranquil.

the phrenic nerve. (6)

2. unstable haemodynamics

3. fluid overload

termination of CPB.

compromised myocardium.

movement of the diaphragm during inspiration.

full ventilator support until the cardiac problem is resolved. (77)

(6,74,75,76)

During this period, fluid resuscitation is necessary to offset the capillary leak syndrome and the vasodilation secondary to medications and rewarming. Crystalloid and colloid infusions are used to maintain intravascular volume, although this usually occurs at the expense of expansion of the interstitial space. After the capillary leak has ceased and haemodynamics are stable, diuretics contribute to a faster recovery from surgery.

Succesfull early extubation is compromised by fluid overload. Optimal monitoring and adequate measures should therefore be taken in the operation room and in the intensive care to minimize the positive fluid balance while maintaining adequate tissue perfusion. (78)

#### **Central nervous system dysfunction**

Neurologic complications are dreaded sequelae of cardiac surgery. Notwithstanding a progressive decrease in cardiac surgical mortality over the past decades, the incidence of postoperative neurological complications remains relatively unchanged.

#### *Focal neurologic complications*

Focal neurologic events complicate approximately 2 % of cardiac procedures requiring CPB, but may increase as more patients with advanced age and diffuse vascular disease undergo cardiac surgery. Focal deficits may include hemiparesis or hemiplegia, aphasia, dysarthria, hand incoordination and visual field deficits.

Preoperative risk factors include increasing age (risk of up to 10 % in patients older than age 75), pre-existing cerebrovascular disease, hypertension, peripheral vascular disease, and poor LV function. Intraoperative and postoperative risk factors include: ascending aortic atherosclerosis and calcification, LV mural thrombus, complex surgery and prolonged bypass and haemodynamic instabilities.

The mechanisms for neurologic injury include some combination of cerebral embolism, hypoperfusion, and inflammation; associated vascular disease and cerebral autoregulatory dysfunction make the brain more susceptible to injury. Particulate embolism due to atherosclerotic plaque, blood thrombus embolus, and air and platelet-fibrin debris is the most common cause of stroke. Cerebral hypoperfusion may be the result of systemic hypotension or impaired regional cerebral blood flow. Although cerebral autoregulation should protect the brain during CPB, hypothermia, blood gas regulation, diabetes and preexisting hypertension may affect the adequacy of cerebral autoregulation. (6,79,80,81)

In the prevention of focal neurologic complications, preoperative evaluation for extracranial carotid disease should be considered in any patient with neurologic symptoms. Symptomatic carotid disease warrants carotid endarterectomy(CE) prior or at the time of cardiac surgery. Asymptomatic carotid disease in the presence of a carotid bruit should be evaluated by non-invasive testing. There is a trend toward performance of combined CABG-CE in these patient groups. (82)

Intraoperative echocardiograhic scanning of the ascending aorta to identify atherosclerosis might alter cannulation sites and clamping - and manipulation techniques of this diseased aorta. Techniques to avoid embolic load include the use of membrane oxygenators, arterial filters in the CPB circuit, meticulous débridement and irrigation of valves, removal of LV thrombi and of air after intracardiac procedures.

In general, in patients with hypertension or intracranial vascular disease, blood pressure during CPB should be maintained at a higher level.

In the treatment of embolic stroke, heparin is recommended when there is no evidence of intracranial hemorrhage on the CT scan. Heparin prevents propagation of intracardiac thrombus and improves cerebral microcirculation, but is of unclear benefit in preventing further atheroembolism from dislodged plaque.

#### *Encephalopathy*

Encephalopathy is fairly common after cardiac surgery and is usually manifested by disorientation and confusion, lethargy or agiation, and paranoia and hallucinations.

The ethiology of this syndrome is multifactorial. It may be related to brain inflammation, cerebral hypoperfusion or microemboli from the CPB circuit. Other factors include patient characteristics, hypoxia, metabolic disturbaces, perioperative psychotropic drugs used for anaesthesia, pain relief and sedation, and drug or alcohol withdrawal.

Initial management consists of reassurance and orientation of the patient and control of pain with opioids. Resedation for a period or the use of haloperidol may be usefull until the patient is oriented and tranquil. The encephalopathy has a fluctuating course but is usually transient. (79,81)

#### **5. References**


thrombus and improves cerebral microcirculation, but is of unclear benefit in preventing

Encephalopathy is fairly common after cardiac surgery and is usually manifested by

The ethiology of this syndrome is multifactorial. It may be related to brain inflammation, cerebral hypoperfusion or microemboli from the CPB circuit. Other factors include patient characteristics, hypoxia, metabolic disturbaces, perioperative psychotropic drugs used for

Initial management consists of reassurance and orientation of the patient and control of pain with opioids. Resedation for a period or the use of haloperidol may be usefull until the patient is oriented and tranquil. The encephalopathy has a fluctuating course but is usually

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