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SECTION 4 Pre-, intra-, and postoperative management ofthe coronary artery bypass graft patient168

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has shown modest outcome benet in preliminary studies of postCABG patients.

Serial measurements of serum lactate levels are surrogate markers of adequacy of perfusion such that mildly elevated lactate levels (>2mmol/ L) represent occult hypoperfusion while increasing and markedly elevated levels (>4mmol/ L) are predictive of major complications and overall mortality in cardiac surgical patients and are

However, the value of PACs has been seriously questioned in studies in which no survival or outcome benets were found in PACmonitored critically ill patients, resulting in reduced utilization of PACs in post- CABG patients. PACs are, however, found to be most valuable in certain patient subgroups having right heart failure, pulmonary hypertension, or patients undergoing o- pump CABG with poor underlying cardiac function.

thus of key importance in early postoperative surveillance.

The haemodynamically unstablepatient

It is important to maintain a high index of suspicion for lifethreatening but readily amenable complications such as coronary gra occlusion or spasm, pericardial tamponade, and tension pneumothorax. Asystematic approach assessing preload, aerload, contractility, and heart rate can greatly facilitate identication of causes of instability and thus guide the management of haemodynamically unstable patients (Fig. 20.1).

Heart rate and rhythm are the most readily assessable parameters and are readily amenable to optimization. Hypovolaemia, whether assessed via central venous pressure or pulse contour analysis must be corrected prior to administration of inotropes or vasopressors (Table 20.1). Cardiac output and contractility, and distinguishing between le and right heart failure, are not easily assessed from the routine bedside monitoring and may require use of echocardiography and/ or a PAC.

Management

Optimize cardiacrhythm

Heart rate is one of the most important determinants of cardiac output and coronary perfusion. Ahigh normal heart rate (80– 90 beats per minute) is the usual target in post- cardiopulmonary bypass (CPB) patients. Atrial contraction contributes around 15– 25% of ventricular lling and is especially important in post- CPB patients who have a high prevalence of diastolic dysfunction. Transient sinus node or atrioventricular node dysfunction is not uncommon in CABG surgery, resulting in sinus asystole, sinus or junctional bradycardia, or atrioventricular block. If temporary pacing is required, atrial pacing is preferred over atrioventricular sequential pacing, followed by ventricular pacing.

Postoperative atrial brillation and supraventricular tachycardia should be aggressively treated as they have been associated with higher stroke risk and prolonged hospital length of stay. Increased age, sleep apnoea, pre- existing arrhythmia, congestive heart failure, bicaval cannulation, and prolonged CPB are all risk factors for atrial

Echocardiography

Echocardiography, either transthoracic or transoesophageal, is a valuable tool for managing unstable post- CABG patients. e key roles of echocardiography are to ascertain volume status and biventricular function, rule out mechanical complications such as tamponade and pneumothorax, and to monitor treatment eects. Incompatible echocardiographic pictures can alert physicians to seek other causes for shock. Currently, the use of echocardiography for evaluating ventricular function and its determinants in acute and persistent haemodynamic instability is listed as a classIindication in the American College of Cardiologists/ American Heart Association (ACC/ AHA) guidelines. Goal- directed echocardiography is now widely regarded as core knowledge in critical care residency in many countries. e role of echocardiography in diagnosing complications in post- CABG patients is summarized in Box 20.1.

Pulmonary arterycatheter

dysrhythmia. Hypothermia and electrolyte imbalance further exacerbate these risks.

Fluidresuscitation

Fluid status should be optimized before initiation of inotropes and vasopressors. Intravascular volume depletion in post- CABG patients is usually caused by postoperative blood loss, vasodilation due to rewarming, and third- space loss due to systematic inammatory response from CPB or cell salvage devices. Fluid requirement is higher in patients with diastolic dysfunction because high lling pressure is required for ventricular lling. Crystalloids, either normal saline or buered salt solution (e.g. lactated Ringer’s), are preferred over the synthetic colloids largely based on studies in critically ill patients demonstrating an association with coagulopathy and renal failure. Albumin was found to be non- inferior to crystalloid in a large- scale study in critically ill non- cardiac patients; however, its relative cost is a signicant concern.

Inotropicsupport

A degree of le ventricular dysfunction is common post CPB and may result in acute decompensated heart failure in 20% and post-

e thermodilution technique using a PAC remains the gold standard for cardiac output monitoring. APAC allows continuous monitoring of pulmonary artery pressures and intermittent measurements of pulmonary capillary wedge pressure, cardiac output, pulmonary and systemic vascular resistance, and mixed venous oxygen saturation (reecting the adequacy of global perfusion), parameters all useful in guiding uid and inotropic management especially when echocardiography is unavailable.

cardiotomy cardiogenic shock in 2– 6% of all cardiac surgery patients. e term post- cardiotomy syndrome is used to describe patients developing signicant le ventricular or biventricular systolic dysfunction in the rst few postoperative hours aer separation from CPB. is tends to gradually return to preoperative state aer 8– 24 hours. Long aortic cross- clamp and total CPB time, residual cardioplegic eects, poor myocardial preservation, reperfusion injury, and residual hypothermia are potential causes.

Post-Operative Low Cardiac Output or Shock

1: Assess Cardiac Rhythm

Shock Persists

Management

Adequate CO

Management

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16920 Postoperative management after coronary artery bypass graftsurgery

(Bradycardia, heart block, or inadequate rate)

Normal or Hypertensive

3: Assess Cardiac Output

Continue

Too Slow

Pace if able

(A>AVS>V)

Low CO

Reduce Afterload

(if tolerated)

Adequate CO

Appropriate Too Fast

2: Assess Blood Pressure

Adequate or High Low

5: Assess Cardiac Output

Inotropic

Support

(SVT)

Cardioversion

Hypotensive

4: Assess Preload

Volume

Resuscitation

Adequate COLow CO

Ongoing Volume

Requirement

Bleeding?

Low CO

Inhaled

Vasodilators

Consider

IABP

Consider

IABP

Angiography or Graft Revision if

Ischemia Persists

Mechanical Support

(VAD, ECMO) if

Consider

IABP

CXR, Echo

ECG, PAC

Surgical

Exploration

PTX, HTXTamponadeIschemiaLV FailureRV Failure

Tube

Thoracostomy

Surgical Exploration if

Ongoing Bleeding

Support

NoVasopressor

Correct Coagulopathy

Return to 2:

Continue Management

Ongoing Bleeding

Surgical

Exploration

Yes

Transfuse PRBC

Bleeding

Stopped

Return to 2:

Continue

Fig.20.1 Algorithm for management of low cardiac output and refractory shock after cardiac surgery. A, atrial; AVS, atrial– ventricular sequential; CO,

cardiac output; CXR, chest X- ray; ECG, electrocardiogram; Echo, echocardiogram; ECMO, extracorporeal membrane oxygenation; HTX, haemothorax; IABP, intra- aortic balloon pump; LV, left ventricle; PAC, pulmonary artery catheter; PRBC, packed red blood cells; PTX, pneumothorax; RV, right ventricle; SVT, supraventricular tachycardia; V, ventricular; VAD, ventricular assist device.

Reproduced from Stephens RS, Whitman GJ. Postoperative Critical Care of the Adult Cardiac Surgical Patient:Part II:Procedure- Speciﬁc Considerations, Management of Complications, and Quality Improvement. Crit Care Med. 2015;43:1995– 2014 with permission from Wolters Kluwer.

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Table20.1 Pharmacological properties ofcommonly used inotropes and vasopressors

Drug Dosage range Receptors Blood

Epinephrine 0.01– 0.2 mcg/ kg/ min

Dobutamine 3– 15 mcg/ kg/ min

Dopamine <5 mcg/ kg/ min D

5– 10 mcg/ kg/ min

>10 mcg/ kg/ min

Norepinephrine 0.01– 0.3 mcg/ kg/ min

Isoprenaline 0.01– 0.2 mcg/ kg/ min D1, D

Dopexamine 0.5– 4 mcg/ kg/ min

Milrinone Bolus:50 mcg/ kg

Infusion:0.25– 1 mcg/ kg/ min

PVR, pulmonary vascular resistance; SVR, systemic vascular resistance.

β1, β2, α

β1, β

α, β

β2, D1, D

PDE ⇄ ↑↑ ↑ ↓↓ ↓ ↑ ↓

pressure

↑↑ +++ ↑↑ ↑ ↑ ↑ ↑↑

⇄/ ↓ ↑↑↑ ↑ ↓ ↓ ↑↑ ↑

⇄ ↑ ↑ ⇄ ⇄ ↑ ↑

↑ ↑↑ ↑↑ ↓ ↓ ↑ ↑↑

↑↑ ↑↑ ↑↑ ↑ ⇄/ ↑ ↑↑ ↑↑

↑↑ ⇄ ⇄/ ↑ ↑↑ ↑↑ ⇄ ↑

⇄/ ↑ ↑ ↑ ⇄ ⇄ ↑↑↑ ↑↑

⇄ ↑ ↑ ⇄ ⇄ ↑ ↑

Other causes of impaired myocardial contractility such as kinked or occluded coronary gras or coronary vasospasm must be ruled out. In these settings, high- dose inotropes could paradoxically worsen myocardial ischaemia. Coronary angiogram or re- exploration is required in suspected cases. Nitroglycerine, milrinone, and calcium channel blocker infusions have been successfully used to reverse coronary vasospasm.

e optimal choice of inotropes and vasopressors has not been systematically evaluated in post- cardiac surgical patients, resulting in signicant variations in practice between centres. Inotropes are

Cardiac output

Contractility SVR PVR Heart

rate

Myocardial O2 consumption

commonly classied into calcium sensitizers (e.g. levosimendan, thyroxine), adrenergic receptor agonists (e.g. epinephrine, dobutamine), and phosphodiesterase (PDE) III inhibitors (e.g. milrinone).

Adrenergicagonists

All beta- adrenergic receptor agonists are catecholamine derivatives and possess variable degrees of alpha- and beta- adrenergic receptor specicity (Table 20.1). Epinephrine, norepinephrine, dopamine, and dobutamine are the most common rst- line inotropes in postcardiotomy patients. Dopamine has gradually fallen out of favour

Box 20.1 The role ofechocardiography inpost- CABGpatients

• Assess volume status and monitor the response of ﬂuid resuscitation.

• Assess the global and regional ventricular function (e.g. ejection frac-

tion). In the presence of inotropic agents or mechanical circulatory support devices, echocardiographic examination of ventricular function may be misleading.

• Identify diastolic dysfunction. High- pressure preload measurements

often fail to reﬂect the true preload status in patients with diastolic dysfunction.

• Distinguish between left, right, and biventricular failure and identify

pulmonary hypertension.

• Identify postoperative mechanical complications in the postoperative

period:

— Identify any undiagnosed structural heart lesions (e.g. crit-

ical aortic stenosis, hypertrophic obstructive cardiomyopathy, vegetations, intracardiac shunt, and undiagnosed adult congenital heart disease) or mechanical obstruction whether inﬂow (e.g. left atrial myxoma, mitral stenosis) or outﬂow (e.g. hypertrophic obstructive cardiomyopathy, dynamic left ventricular outﬂow tract obstruction).

— Identify pericardial effusions/ tamponade and determine whether

ventricular ﬁlling is impaired or surgical drainage is indicated. Notably, tamponade is a clinical diagnosis based on the full haemodynamic picture and the rate of pericardial ﬂuid accumulation rather than the presence or size of the effusion per se. Practically, drainage may be appropriate in many situations despite absence of the classic echocardiographic criteria of tamponade.

— Identify acute mitral regurgitation caused by papillary muscle

rupture.

— Identify ventricular septal ruptures and pseudo- aneurysm from re-

cent or previous myocardial infarction.

— Identify intracardiac thrombus or clot.

in critically ill and post- CABG patients because of unpredictable inotropic and vasopressor eects, and as it has not proven renal protective. In a recent randomized, controlled study, dopamine was associated with increased mortality in a cardiogenic shock subgroup. Epinephrine is oen blamed for causing tachycardia; however, several studies have shown it to be associated with less tachycardia than dopamine or dobutamine if equivalent cardiac output is achieved. Increased lactic acidosis has been observed secondary to epinephrine- induced stimulation of aerobic glycolysis.

Phosphodiesteraseinhibitors

Milrinone is the most commonly used of the PDE inhibitors which are all inodilators bypassing the beta- adrenergic pathway to increase cyclic adenosine monophosphate and which have pronounced lusitropic eects, enhancing both myocardial contraction during systole and relaxation during diastole. is can increase right ventricular (RV) cardiac output and reduce pulmonary vascular resistance in right heart failure patients. ey are commonly used as second- line inotropes. All PDE inhibitors (enoximone, milrinone, amrinone, olprinone, piroximone) have very similar pharmacodynamic properties with dierences mainly in their pharmacokinetic proles (i.e. onset time and half- time) aecting the dosing regimen. e use of PDE inhibitors may be associated with hypotension during bolus administration, particularly in the absence of concomitant beta- adrenergic therapy. While some studies had reported lesser hypotension associated with inhaled administration of milrinone, a recent network meta- analysis of 30 studies involving inhaled milrinone and intravenous milrinone found lower pulmonary and systemic vascular resistance and higher cardiac index

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with intravenous milrinone but no dierence in any outcome between inhaled milrinone and placebo, thus failing to demonstrate ecacy of inhaled milrinone.

Calciumsensitizer

Levosimendan has emerged as a novel agent in post- CABG cardiogenic shock. In patients following CPB, it has been shown to decrease inotropic requirement without provoking arrhythmias and to reverse stunning with only a moderate increase in myocardial oxygen consumption. However, the peak eect time of levosimendan via bolus is about 30 minutes versus 2– 3 hours without bolus, making it more appropriate for prophylactic administration versus acute therapy. Meta- analysis of 14 randomized trials has shown levosimendan was associated with shortened ICU length of stay and extubation times, and reduced incidences of postoperative atrial brillation and myocardial infarction (MI). However, there have also been reports of increased postoperative bleeding.

Vasopressor and vasoplegicsyndrome

Vasoplegic syndrome occurs in 5– 25% of patients aer CPB and is signicantly associated with higher morbidity and mortality. Exaggerated systematic inammatory response, prolonged CPB, preoperative LV dysfunction, and blood transfusion are all thought to contribute. It is oen diagnosed by unexplained requirements for high- dose vasopressors (e.g. norepinephrine >0.1 micrograms/ kg/ min). In many cases, the addition of vasopressin (up to 0.01 to 0.6 IU/ min) may be required; however, such high- dose vasopressors may induce digit and mesenteric ischaemia. In refractory vasoplegia, methylene blue (2 mg/ kg bolus, infusion 0.5mg/ kg/ hour) has been used with variable success.

Right ventricularfailure

RV failure signicantly increases perioperative morbidity and mortality and is oen more dicult to manage than le heart failure. Diagnosis and management of RV failure can be challenging in the

absence of echocardiography or PAC insertion and either or both of these measures should be strongly considered.

Certain aspects of RV pathophysiology are important to highlight. As the RV free wall is perfused during both systole and diastole, adequate mean arterial pressure is important for perfusion. RV is extremely load sensitive and even modest increases in outow impedance (e.g. elevated pulmonary vascular resistance secondary to respiratory acidosis, pleural eusion) can cause RV dilation and dysfunction. When the RV is dilated and non- compliant, atrial contraction is fundamentally important, and RV dilatation can cause a leward shi of the interventricular septum interfering with lling of the le ventricle and further decreasing cardiac output and RV perfusion.

Administration of pulmonary vasodilators with concomitant inotropic support is the mainstay of therapy. Intravenous pulmonary vasodilators may reduce systemic arterial pressure mandating the simultaneous administration of vasoconstrictors or use of inhaled pulmonary vasodilators which may have lesser systemic eects (Table 20.2).

Inhaled nitric oxide stimulates pulmonary vasodilation via increasing cyclic guanosine monophosphate with only limited systemic vasodilation due to its rapid inactivation by haemoglobin. Recommended inhaled nitric oxide dose is 20 ppm and since it combines with haemoglobin monitoring of methaemoglobin levels is required. Inhaled prostacyclin and inhaled milrinone, either alone or in combination, have been used in many centres because of the reduced costs, rapid onset of action, minimal systemic eects, and simplicity of administration. Notably, use of intra- aortic balloon counterpulsation has also been shown to reduce pulmonary artery pressure and pulmonary vascular resistance and to improve mixed venous saturation even in patients in whom RV failure was mainly responsible for circulatory decompensation. ese benecial eects are likely mediated via increased RV coronary perfusion.

In post- CABG patients with refractory RV failure, keeping the sternum open to reduce ventricular compression and usage of a RV assist device should be considered.

Table20.2 Commonly used pulmonary vasodilators inpost- cardiotomy patients withright heart failure

Nitric oxide Inhaled prostacyclin Phosphodiesterase inhibitors

Mechanism Activates cytosolic guanylate cyclase and

Example Inhaled nitric oxide Epoprostenol Iloprost Inhaled Milrinone Sildenaﬁl

Route Inhaled; require specialized delivery

Dosage 5– 20 ppm 10- 20 mcg/

Side effects

cAMP, cyclic adenosine monophosphate; cGMP; cyclic guanosine monophosphate; PG, prostaglandin.

increases intracellular levels of cGMP, resulting in relaxation of the smooth muscles in the pulmonary arteries

system

• Toxicity from nitrogen dioxide and

methaemoglobin.

• Rebound pulmonary hypertension

from abrupt discontinuation

• Pulmonary vascular congestion

because of increased pulmonary blood ﬂow in patients with poor LV function

Binds to PG receptors and activates adenylate cyclase and protein kinase Ato cause a decrease in cytosolic free calcium Stimulates endothelial release of nitric oxide

Nebulized Nebulized Nebulized Oral/ sublingual

mL; continuous nebulization with 2– 3 L/ min of oxygen ﬂow

• Vagus- mediated bradycardia

• Rebound pulmonary hypertension for abrupt

withdrawal

• Pulmonary vascular congestion in patients

with poor LV function

2.5– 5 mcg every 3– 4 hours

Inhibition of PGE- 5, PGE- 3 isoenzymes lead to increased levels of cAMP and cGMP, resulting in pulmonary vasodilation

60– 90 mcg/ kg bolus followed by 0.08– 0.11 mg/ kg/ min infusion

• Systemic hypotension

0.25– 0.75 mg/ kg every 4– 6 hours

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Continuance ofmedication afterCABG

Antiplateletmedication

ACC/ AHA guidelines recommended aspirin should be resumed or initiated within 6 hours aer surgery once haemostasis has been achieved and continued indenitely. Early initiation of aspirin (<24 hours) signicantly improves saphenous vein gra patency and reduces adverse cardiovascular events versus delayed administration (>48 hours).

Clopidogrel and ticlopidine are thienopyridine prodrugs having an antiplatelet eect via irreversible P2Y adenosine diphosphate receptor inhibition. Ticagrelor is a newer directly acting and reversibly bound P2Y inhibitor. In a subgroup analysis of the Clopidogrel in Unstable Angina to Prevent Recurrent Ischemic Events (CURE) study, perioperative clopidogrel signicantly reduced the incidence of cardiovascular death, MI, and stroke compared with placebo. In a recent study of 500 patients 1year post CABG who were randomized (1:1:1) to aspirin, ticagrelor, or aspirin plus ticagrelor, saphenous vein gra patency was signicantly increased in patients receiving aspirin plus ticagrelor versus aspirin alone (88.7% vs

76.5%; P <0.001).

Statins

ere is evidence of a benecial eect of preoperative statins as several retrospective studies reported an association between statin therapy and lowered risks of postoperative non- fatal MI, death, atrial brillation, neurological dysfunction, renal dysfunction, and infection. Asmall randomized study showed statins commenced a week before CABG reduced the postoperative levels of cardiac biomarkers. ACochrane systematic review in 2015 demonstrated signicantly reduced atrial brillation (1765 patients from 12 studies) and shortened length of stay; however, perioperative mortality, stroke, MI, and renal failure were not impacted.

the primary aim of reducing postoperative atrial brillation, and possibly reducing in- hospital mortality and perioperative MI. e timing of re- initiation and duration of postoperative beta- blocker therapy remains unclear. Several studies have reported no survival benet up to 2years postoperatively, while others have reported a reduction in mortality with continuance of beta blockers.

Interestingly, the bioavailability of oral beta- blocker therapy is signicantly altered in the postoperative period because of changes in gastrointestinal perfusion. Arandomized study found continuation of intravenous rather than oral metoprolol signicantly reduced the incidence of postoperative atrial brillation.

Angiotensin- converting enzyme inhibitors/ angiotensin receptorblockers

e cardiovascular and ventricular remodelling benets of chronic angiotensin- converting enzyme inhibitor and angiotensin receptor blocker therapy are well established in patients with LV systolic dysfunction, hypertension, diabetes mellitus, or chronic renal insuciency. However, there are signicant concerns about continuing angiotensin- converting enzyme inhibitors/ angiotensin receptor blockers perioperatively because of signicant intraoperative hypotension due to blunted pressor and inotrope responses and postulated associations with vasoplegic syndrome and renal dysfunction.

Initiation or resumption of angiotensin- converting enzyme inhibitors/ angiotensin receptor blockers in the postoperative period has also been reported to increase the risk of systolic hypotension while a reduction in postoperative atrial brillation has not been consistently demonstrated. As a result, angiotensin- converting enzyme inhibitors/ angiotensin receptor blocker therapy should be withheld in the perioperative period and while the best timing is unknown, the general view is to delay restarting therapy until either ICU discharge or even hospital discharge and then to continue indenitely.

ACC/ AHA guidelines recommended patients should receive statin therapy to achieve a therapeutic target low- density lipoprotein concentration less than 100mg/ dL or reduction of 30% from baseline, unless contraindicated. Statin therapy should be resumed once oral medication is tolerated and should be continued indenitely. Acute cessation of statin therapy in post- CABG patients has been associated with increased mortality in a cohort study.

Betablockers

Beta- blocker therapy initiated preoperatively has been consistently shown to reduce postoperative supraventricular and ventricular arrhythmias in CABG patients whereas evidence on their ecacy to reduce mortality and MI are inconsistent. In small randomized controlled trials and observational studies, an association with reduced in- hospital mortality and perioperative MI has been shown. Acohort analysis of the Society of oracic Surgeons National Database involving 629,877 patients found a small but consistent survival rate associated with preoperative beta- blocker therapy in patients with an ejection fraction greater than 30%. However, a more recent Cochrane review reported no association between beta- blocker therapy and perioperative mortality or stroke in CABG patients while conrming a salutary eect on postoperative arrhythmias.

e ACC/ AHA guidelines recommended all patients with LV ejection fraction greater than 30% undergoing CABG should receive beta- blocker therapy preoperatively and postoperatively with

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Fast- track cardiac anaesthesia and earlyextubation

Janet Martin and Davy Cheng

Background:rationale forfast- track cardiaccare

‘Fast- track’ cardiac anaesthesia and recovery is the term given to a multicomponent intervention during cardiac surgery and postoperatively, with the ultimate goal of early extubation (within 1– 6 hours) in order to reduce duration of mechanical ventilation, length of stay in the intensive care unit (ICU), and overall resource utilization. Key components of fast- track cardiac care include balanced anaesthesia (low- dose opioids together with inhaled or intravenous anaesthetics) and a time- directed extubation protocol.

While it is oen assumed that ‘fast- tracking’ cardiac surgical patients would be primarily dependent on anaesthetic technique, in reality, a focus on anaesthesia is not enough. Fast- track cardiac recovery also requires a coordinated multicomponent approach across the full spectrum of intraoperative and postoperative care pathways in order to successfully achieve reduced time to extubation and ICU length of stay without increasing the risk of adverse events such as haemodynamic instability, respiratory distress, reintubation, and readmission.

In 1970s and 1980s, cardiac surgery was conducted on patients under deep hypothermia who were anesthetized with high- dose opioids. However, high- dose opioids required prolonged intubation times, oen exceeding 24 hours. roughout the 1990s, in response to the economic pressures of increased demand for cardiac surgery that outpaced available operating room and ICU capacity, cardiac anaesthesia shied away from high- dose opioid- based anaesthesia to a more balanced approach using low- dose opioids together with volatile or intravenous anaesthetics, and shorter- acting neuromuscular blocking agents.

ese eorts were further stimulated by observational studies conducted by Westaby and colleagues showing that the use of a dedicated cardiac recovery area outside of the ICU setting provided improved eciency of care with faster times to extubation, excellent clinical outcomes, low rates of reintubation or unplanned ICU admission, and improved overall resource utilization., is paradigm shi was consolidated when randomized trials demonstrated favourable clinical and resource- related outcomes with low- dose

opioid balanced anaesthesia instead of high- dose opioid- based anaesthesia.

Evidence supporting fast- track cardiaccare

In a pivotal randomized controlled trial (RCT) of fast- track cardiac recovery, Cheng etal. showed that a strategy of balanced anaesthesia with low- dose opioids and inhaled anaesthesia together with an early weaning protocol (extubation within 8 hours) signicantly reduced time to extubation (4.1 vs 18.9 hours; P <0.02) and hospital length of stay (7.6 vs 10.0days; P <0.02) when compared to usual care with high- dose opioids and no weaning protocol., Furthermore, there were no increases in adverse clinical events including death, stroke, myocardial infarction, reoperation for bleeding, low cardiac output syndrome, and reintubation compared with high- dose opioid- based anaesthesia., In addition, ICU costs were reduced by 53%, and cost of hospital stay was decreased by 17%., In a subsequent 1- year follow- up of this study, there was no increased risk of readmission in the fast- track group, and total cost of care was lower in the fast- track group compared with conventional high- dose anaesthesia.

roughout the late 1990s and 2000s, further randomized trials of fast- track anaesthesia were conducted, which eventually paved the evidence base for universal acceptance of the fast- track recovery model as standard of care. A2003 meta- analysis of ten randomized trials showed that fast- track anaesthesia using balanced anaesthesia with low- dose opioids and weaning protocols signicantly reduced time to extubation (−8.1 hours, 95% condence interval (CI) 3.7–

12.5 hours) and length of ICU stay (−5.4 hours, 95% CI −0.3 to −10.5 hours), without increases in mortality or complications. A2006 meta- analysis of 27 RCTs showed that while low- dose opioids and normothermia were important, the use of an early extubation protocol was the most important predictor of time to extubation and ICU length of stay.

Recently updated meta- analyses of 28– 30 RCTs, involving approximately 4000 patients, have conrmed that fast- track cardiac recovery models are safe, and reduce time to extubation and ICU length of stay, but have variable net impact on hospital stay and

SECTION 4 Pre- , intra- , and postoperative management ofthe coronary artery bypass graft patient176

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Table21.1 Meta- analysis ofreduced- dose opioid anaesthesia

Outcome Number of studies OR or RR (95% CI) I2 (heterogeneity)

Clinical outcomes

Death, in hospital 7 OR=0.58 (0.24– 1.39) 0%

Death, at end of study 8 OR=0.53 (0.25– 1.12) 0%

Myocardial infarction 8 RR=0.98 (0.48– 1.99) 6%

Stroke 5 RR=1.17 (0.36– 3.78) 0%

Renal failure, acute 4 RR=1.19 (0.33– 4.33) 0%

Bleeding, major 4 RR=0.48 (0.16– 1.44) 27%

Reintubation 5 RR=1.77 (0.38– 8.27) 0%

Resource- related outcomes Mean difference (95% CI)

Time to extubation 14 −7.4 hours (−10.5 to −4.3 hours)

ICU length of stay 12 −3.7 hours (−7.0 to −0.4 hours)

Hospital length of stay 8 −0.3days (−1.0 to +0.4days) 85%

P <0.05. CI, conﬁdence interval; OR, odds ratio; RR, relative risk.

Reproduced from Wong WT, Lai VK, Chee YE, Lee A.(2016) ‘Fast- track cardiac care for adult cardiac surgical patients’, Cochrane Database Syst Rev, 9, pp. CD003587 with permission from John Wiley and Sons.

99%

98%

resource utilization., Earlier concerns about inducing risk of myocardial infarction, need for reintubation, and increasing the risk of intraoperative awareness (due to low- dose opioids) have been allayed due to the assurance of safety provided across the more than 30 RCTs considered in aggregate. e lack of consistent impact on hospital stay across RCTs, however, re- emphasizes the fact that reductions in opioid dose and extubation time do not alone guarantee improvements in downstream eciencies such as ICU and hospital length of stay, unless concerted eort is applied to ensure patients are moved out of the ICU and hospital once discharge criteria have been met. e latter requires changes to discharge policies, and interdisciplinary alignment towards achieving eciency of patient ow. Sometimes these additional logistical issues can negate the purported benets, if they too are not addressed as a routine component of fast- track cardiac recovery.

Table21.2 Meta- analysis oftime- based weaning protocol

Outcome Number of studies OR or RR (95% CI) I2 (heterogeneity)

Clinical outcomes

Death, in hospital 5 OR=0.23 (0.05– 1.04) 0%

Death, at end of study 10 OR=0.80 (0.45– 1.45) 37%

Myocardial infarction 8 RR=0.59 (0.27– 1.31) 39%

Stroke 11 RR=0.85 (0.33– 2.16) 0%

Renal failure, acute 9 RR=1.11 (0.42– 2.91) 0%

Bleeding, major 10 RR=0.92 (0.53– 1.61) 0%

Reintubation 12 RR=1.34 (0.74– 2.41) 0%

Resource- related outcomes Mean difference (95% CI)

Time to extubation 16 −7.4 hours (−10.5 to −4.3 hours)

ICU length of stay 13 −3.7 hours (−7.0 to −0.4 hours)

Hospital length of stay 8 −0.3days (−1.0 to +0.4days) 77%

P <0.05. CI, conﬁdence interval; OR, odds ratio; RR, relative risk.

Table 21.1 and Table 21.2 summarize the expected benets for

a fast- track recovery approach to care in cardiac patients. As the evidence base has grown and matured, concerns about inducing complications of myocardial ischaemia, haemodynamic instability, respiratory distress, reintubation, and intraoperative awareness have been allayed. Syntheses of all available evidence to date have shown no dierences in clinical outcomes, even aer combination through meta- analysis. Contemporary ‘real- world’ evidence from observational studies have conrmed faster times to extubation, reduced ICU length of stay, and improvements in cost- eectiveness.

Since the accumulation of supporting evidence from randomized trials in the 1990s and 2000s, fast- track cardiac anaesthesia and surgical management has become the new standard of care. As expected, once a new standard has been ushered in, research eorts have moved away from evaluating fast- track versus non- fast- track

99%

94%

21 Fast-track cardiac anaesthesia and earlyextubation 177

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approaches to cardiac surgery, and has rather focused on how to further improve fast- track management. As a result, more recent studies have compared dierent versions of ‘fast track’ including renements of dierent drugs, technologies, and techniques to assess which combination of modalities can incrementally improve clinical and resource- related outcomes, such as longer- term survival and morbidities while further improving recovery parameters and costs.

Practicalconsiderations

In the current paradigm of universal acceptance of fast- track recovery, balanced anaesthesia has become the norm, and it is expected that most cardiac surgical patients will be extubated within 1– 6 hours from arrival in the postoperative ICU. It is also expected that fast- track recovery will be attempted on all patients as routine practice, even in very elderly patients, unless there are good reasons to do otherwise. Very rarely, comorbidities or preoperative conditions may preclude a fast- track weaning protocol from the outset.

Given that fast- track cardiac care is now the standard of care,

Table21.3 Fast- track cardiac anaesthesia regimens

Induction (opioid + hypnotic + muscle relaxant)

Maintenance (opioid + hypnotic)

Transfer to cardiac recovery area (opioid + hypnotic)

Opioid:

• Fentanyl 5– 10 mcg/ kg

• Sufentanil 1– 2 mcg/ kg

• Remifentanil infusion 0.5– 1.0 mcg/ kg/ min

Hypnotic:

• Propofol 0.5– 1.5 mg/ kg

• Midazolam 0.05– 0.1 mg/ kg

Muscle relaxant:

• Rocuronium 0.5– 1 mg/ kg

• Vecuronium 1– 1.5 mg/ kg

Opioids:

• Fentanyl 1– 5 mcg/ kg

• Sufentanil 1– 1.5 mcg/ kg

• Remifentanil infusion 0.2– 0.5 mcg/ kg/ min

Hypnotic:

• Inhaled anaesthetic 0.5– 1.0 MAC

• Propofol infusion 50– 100 mcg/ kg/ min

Opioid:

• Morphine 2–20 mg

Hypnotic:

• Propofol infusion 25–50 mcg/ kg/ min

more recent research has focused on which components of anaesthesia and perioperative care contribute tangibly to reductions in time to extubation, postoperative complications, and length of stay. In general, most studies have suggested that the additional components of care to further optimize extubation time and facilitate discharge are through improved intraoperative anaesthesia (inhaled versus intravenous anaesthetics), fluid management (colloids versus crystalloids), perioperative monitoring, and perioperative pain management (regional blocks, intrathecal morphine, and other multimodal management including nonopioid analgesics such as son- steroidal anti- inflammatories, acetaminophen, gabapentin, and pregabalin).

General anaesthesia forfast- track cardiacrecovery

Most anaesthetics in current use have been available for several years, and yet the optimal anaesthetic regimen for cardiac surgery continues to be a subject of ongoing research. Few trials have specically addressed optimal doses of each individual component of balanced anaesthesia, though general guidelines for practice have

MAC, minimum alveolar concentration. Derived from the following: Cheng DC, Newman MF, Duke P, etal. The efﬁcacy and resource utilization of

remifentanil and fentanyl in fast- track coronary artery bypass graft surgery:a prospective randomized, double- blinded controlled, multi- center trial. Anesth Analg 2001;92:1094.

Engoren M, Luther G, Fenn- Buderer N.Acomparison of fentanyl, sufentanil, and remifntanil for fast- track cardiac anesthesia. Anesth Analg 2001;93:859.

Mollhoff T, Heregods L, Moerman A , etal. Comparative efﬁcacy and safety of remifentanil and fentanyl in ‘fast track’ coronary artery bypass graft surgery:a randomized, double- blind study. Br J Anaesth 2001;87:718.

Wong WT, Lai VK, Chee YE, Lee A .Fast- track cardiac care for adult cardiac surgical patients. Cochrane Database Syst Rev. 2016 Sep 12;9:CD003587.

Source data from Bainbridge D, Cheng D.(2011) ‘Postoperative cardiac recovery and outcomes’, in Kaplan JA, Reich DL, Savio JS (eds.) Kaplan’s cardiac anesthesia:The echo era. Philadelphia, PA:Saunders, p1010– 1024.

meta- analyses providing additional detail regarding balanced anaesthetic subcomponents are highlighted in the following two subsections.

Short- acting versus long- actingopioids

Meta- analysis of head- to- head comparisons of fentanyl, sufentanil, and remifentanil as a component of balanced anaesthesia in cardiac

been derived from the convergence of balanced regimens used across clinical trials, which have subsequently been rened during evolving practical experience in the contemporary setting of fasttrack cardiac care.

Table 21.3 outlines commonly used components of a balanced

anaesthesia regimen, derived from existing randomized trials. Welldesigned RCTs have generally failed to convincingly demonstrate that selection of dierent components within each category across those represented in Table 21.4 makes a meaningful dierence in terms of clinical outcomes and recovery time. As a result, the choice between these agents has largely been based on local availability, familiarity, and cost.

As evidence from randomized trials has cumulated in recent years, combination through meta- analysis has suggested some potential differences between agents, though it is clear that any such dierences are likely to pale compared to the importance of a protocolized approach with a universal intent towards early extubation and ecient movement out of recovery and intensive care areas., Recent

Table21.4 Extubation criteria forfast- track cardiac recovery

Initial ventilation parameters

Maintain ABGs pH 7.35– 7.45

Extubation criteria Awake and alert

A/ C, assisted control; ABGs, arterial blood gases; ECG, electrocardiogram; PEEP, positive end- expiratory pressure

A/ C ventilation with pressure support of 10– 12cmH2O Tidal volume 8– 10 mL/ kg PEEP 5cmH2O

PaCO2 35– 45mmHg PaO2 >90mmHg O2 sats >95%

ABGs as above Haemodynamically stable No signiﬁcant ECG abnormalities No active bleeding Temperature >36°C Muscle strength (>5 seconds of head lift and strong hand grip)

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