Handbook of Clinical Anesthesia

Chapter 41

Anesthesia for Cardiac Surgery

Management of anesthesia for cardiac surgery requires a thorough understanding of normal and altered cardiac physiology; knowledge of the pharmacology of anesthetic, vasoactive, and cardioactive drugs; and familiarity with the physiologic derangements associated with cardiopulmonary bypass (CPB) and specific surgical procedures (Skubas N, Lichtman AD, Sharma A, Thomas SJ: Anesthesia for cardiac surgery. In Clinical Anesthesia. Edited by Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC. Philadelphia: Lippincott Williams & Wilkins, 2009, pp 1073–1107).

  1. Coronary Artery Disease (CAD)

Prevention or treatment of myocardial ischemia during coronary artery bypass graft (CABG) surgery decreases the incidence of perioperative myocardial infarction. Optimizing oxygen delivery to the myocardium is equally important for hemodynamic management.

  1. Myocardial Oxygen Demand.The principal determinants of myocardial oxygen demand are wall tension and contractility. Interventions that prevent or promptly treat ventricular distention and decrease myocardial oxygen consumption decrease myocardial oxygen demand.
  2. Myocardial Oxygen Supply.Increases in myocardial oxygen requirements can only be met by increasing coronary blood flow.
  3. Coronary Blood Flow(Table 41-1)
  4. The left ventricular subendocardium is most vulnerable to ischemia because myocardial oxygen requirements are high and predictable perfusion can occur only during diastole. The time available for diastole decreases with an increasing heart rate.
  5. A low ventricular filling pressure is desirable for improving perfusion (higher pressure gradient)


and decreasing myocardial oxygen requirements (decreased ventricular volume and wall tension).

Table 41-1 Determinants of Coronary Blood Flow

Perfusion pressure
Vascular tone
Time available for perfusion (heart rate)
Severity of intraluminal obstructions
Presence of collateral circulation

  1. It is common during anesthesia for patients to exhibit signs of myocardial ischemia without any change in blood pressure, heart rate, or ventricular filling pressure.
  2. Hemodynamic Goals
  3. Although the precise relationship between intraoperative myocardial ischemia and postoperative myocardial infarction remains controversial, there is consensus that a primary goal of a successful anesthetic is the prevention of myocardial ischemia.
  4. Combinations of anesthetics, sedatives, muscle relaxants, and vasoactive drugs are selected to decrease myocardial oxygen requirements and thus prevent or decrease the likelihood of myocardial ischemia.
  5. Pharmacologic agents that may benefit patients with CAD include statins and angiotensin-converting enzyme (ACE) inhibitors (stabilize atherosclerotic plaques) and volatile anesthetics (anesthetic preconditioning).
  6. Monitoring for Ischemia.The ideal monitoring technique for detecting myocardial ischemia is not yet available (Table 41-2).
  7. Selection of Anesthesia.There is no one ideal anesthetic for patients with CAD. The choice of anesthetic depends primarily on the extent of pre-existing myocardial dysfunction and the pharmacologic properties of the specific drugs. Myocardial depression and associated decreases in myocardial oxygen requirements are only harmful in a patient whose heart cannot be further depressed without precipitating congestive heart failure.
  8. Early tracheal extubation is popular for both on- and off-pump cardiac procedures. Volatile anesthetics in


combination with low-dose opioids or total intravenous (IV) anesthesia with short-acting drugs (midazolam, alfentanil, propofol) has been used to facilitate the likelihood of early tracheal extubation. Neuraxial opioids placed before induction of anesthesia decrease postoperative pain and facilitate early tracheal extubation.

Table 41-2 Monitoring for Myocardial Ischemia

Electrocardiogram (ST segment analysis of leads V5 and II)
Heart rate and blood pressure (rate-pressure product is not a sensitive predictor of myocardial ischemia)
Pulmonary artery catheter (V waves reflect ischemia-induced papillary muscle dysfunction but are probably not a sensitive indicator of myocardial ischemia)
TEE (regional wall motion abnormalities are the most sensitive indicator of myocardial ischemia)

TEE = transesophageal echocardiography.

  1. Opioidslack myocardial depressant effects and are useful in patients with severe myocardial dysfunction. In critically ill patients, opioids such as fentanyl (50–100 µg/kg IV) can be administered as the sole anesthetic. In patients with good left ventricular function, opioids may be inadequate to depress sympathetic nervous system activity, requiring the addition of a volatile anesthetic or vasoactive drug.
  2. Inhalation anestheticshave the advantages of dose dependency; easily reversible, titratable myocardial depression; amnesia; and reliable suppression of sympathetic nervous system responses to surgical stress and CPB. Disadvantages include myocardial depression, systemic hypotension, and lack of postoperative analgesia.
  3. Combinations of opioids and volatile anesthetics may produce the advantages of each with minimal undesirable side effects. It is likely that any volatile anesthetic could be used as a balanced technique.
  4. Isofluraneis a coronary vasodilator (more so than other volatile anesthetics), but this effect is clinically insignificant in doses below 1 MAC.


There is no evidence of an increased incidence of myocardial ischemia or worsened outcome.

  1. Desfluraneand sevoflurane possess hemodynamic profiles similar to isoflurane but have the advantage of faster recovery. A sudden increase in the inspired concentration of desflurane may result in increased heart rate, systemic blood pressure, and plasma epinephrine concentration.
  2. Intravenous Sedative Hypnotics.An alternative adjuvant anesthetic to the low-dose opioid technique is a titratable infusion of a short-acting sedative (propofol, midazolam, dexmedetomidine) that can be continued after surgery and after discontinuation affords a predictable and fairly rapid awakening.
  3. Treatment of Ischemia.Anesthetics or vasoactive drugs that enable the heart to return to a slower rate, smaller size, and well-perfused state are frequently essential during anesthesia (Table 41-3).
  4. Nitrates.Nitroglycerin is the drug of choice for the treatment of coronary vasospasm. As a venodilator, this drug decreases venous return and decreases ventricular filling pressures and thus wall tension.

Table 41-3 Treatment of Intraoperative Myocardial Ischemia

Event Associated with Ischemia


Increased blood pressure and pulmonary wedge pressure

Increase anesthetic depth
Nitroglycerin (0.5–3.0 mg/kg/min IV)
Sodium nitroprusside (0.5–3.0 µg/kg/min IV)

Increased heart rate

Calcium channel blockers

Decreased blood pressure

Decrease anesthetic depth

Decreased blood pressure and increased pulmonary capillary wedge pressure


Normal hemodynamics

Calcium channel blocker

*The goal is to return the heart to a slow, small, perfused state.
IV = intravenous.

  1. P.654
  2. Vasoconstrictors.Phenylephrine increases myocardial oxygen requirements, but this increase is offset by improvements in oxygen delivery produced by the increased coronary perfusion pressure.
  3. Beta-Blockers.β-blockade improves myocardial oxygen balance by preventing or treating tachycardia and by decreasing contractility. Atenolol improves long-term survival in patients with heart disease undergoing noncardiac surgery.
  4. Calcium Channel Blockers
  5. Verapamilis useful in the treatment of supraventricular tachycardia and slowing the ventricular response in atrial fibrillation and flutter. Myocardial depressant effects may limit its usefulness in some patients.
  6. Nifedipineand diltiazem are coronary vasodilators that are used as antianginal drugs and in the prevention of coronary vasospasm.
  7. Valvular Heart Disease

Valvular Heart Disease is characterized by pressure or volume overload of the atria or ventricles. Transesophageal echocardiography (TEE) has become a commonly used monitor in the perioperative management of patients undergoing cardiac surgery.

  1. Aortic Stenosis
  2. The normal aortic valve is composed of three semilunar cusps attached to the wall of the aorta. The normal annular diameter is 1.9 to 2.3 cm with an aortic valve area of 2 to 4 cm2. The normal diameter of the left ventricular outflow tract is 2.2 cm.
  3. Pathophysiology(Fig. 41-1). Chronic obstruction to left ventricular ejection results in concentric ventricular hypertrophy, which makes the heart susceptible to myocardial ischemia even in the absence of CAD. Because the ventricle is stiff, atrial contraction is critical for ventricular filling and stroke volume.
  4. Anesthetic Considerations.Maintenance of adequate ventricular volume and sinus rhythm is crucial. If hypotension develops, it must be treated early to prevent the catastrophic cycle of hypotension-induced ischemia, subsequent ventricular dysfunction, and worsening hypotension. Bradycardia is a common cause of hypotension in patients with aortic stenosis.


  1. Hypertrophic cardiomyopathyis a genetically determined disease characterized by development of a hypertrophic intraventricular septum, resulting in left ventricular outflow obstruction (resembling aortic stenosis). Outflow obstruction is increased by increases in myocardial contractility or heart rate or decreases in preload or afterload. Anesthetic management is based on maintenance of left ventricular filling and controlled myocardial depression.

Figure 41-1. The pathophysiology of aortic stenosis. LV = left ventricle.

  1. Aortic Insufficiency
  2. Pathophysiology(Fig. 41-2). Chronic volume overload of the left ventricle evokes eccentric hypertrophy but only minimal changes in filling pressures.
  3. Anesthetic Considerations.Maintenance of adequate ventricular volume in the presence of mild vasodilation and increases in heart rate is most likely to optimize forward left ventricular stroke volume. An incompetent aortic valve may prevent the delivery of cardioplegia to the coronary system to produce diastolic arrest of the heart. (The alternative is injecting


cardioplegia directly into the coronary ostia or into the coronary sinus.)


Figure 41-2. The pathophysiology of aortic insufficiency. ART = arterial; LV = left ventricle; LVEDP = left ventricular end-diastolic pressure.

  1. Mitral Stenosis
  2. Pathophysiology(Fig. 41-3). Increased left atrial pressure and volume overload are inevitable consequences of the narrowed mitral orifice. Persistent increases in left atrial pressure are reflected back through the pulmonary circulation, leading to right ventricular hypertrophy and perivascular edema in the lungs.
  3. Anesthetic Considerations.Avoiding tachycardia is crucial for preventing inadequate left ventricular filling with concomitant hypotension. Continued preoperative administration of digitalis and β-antagonists, selection of anesthetics with minimal propensity to increase heart rate, and achievement of an anesthetic depth sufficient to suppress sympathetic nervous system responses are recommended.
  4. Mitral Regurgitation
  5. Pathophysiology(Fig. 41-4). Chronic volume overload of the left atrium is the cardinal feature of mitral regurgitation.



Figure 41-3. The pathophysiology of mitral stenosis. AFib = atrial fibrillation; LA = left atrium; LV = left ventricle; PA = pulmonary artery; RV = right ventricle.


Figure 41-4. The pathophysiology of mitral regurgitation. LA = left atrium; LV = left ventricle.

  1. P.658
  2. Anesthetic Considerations.Selection of anesthetics that promote vasodilation and increase the heart rate is useful.

III. Aortic Diseases

  1. Aortic dissectionis characterized by rapid development of an intimal flap separating the true and false lumens. Severe chest pain (dissection of the ascending aorta) or back pain (descending aorta dissections) is the most common presenting symptom. A variety of diagnostic techniques (contrast-enhanced computed tomography, TEE, magnetic resonance imaging) are accurate in the diagnosis of acute aortic dissection. Surgery is the definitive treatment for ascending aortic dissections.
  2. Anesthetic Considerations.Acute aortic dissection is a surgical and anesthetic emergency necessitating IV access and invasive monitoring, including TEE.
  3. Aortic Aneurysm.Thoracic aneurysms may involve one or more aortic segment (aortic root, ascending aorta, arch, descending aorta). The surgical replacement of an aortic arch aneurysm requires circulatory arrest and introduces the risk of global cerebral ischemia. Surgical replacement of the descending aorta is associated with postoperative paraplegia secondary to interruption of spinal cord blood supply.
  4. Anesthetic Considerations.The anesthetic technique is focused on preservation of cardiac function (descending thoracic aortic aneurysm) and neurologic integrity (aortic arch or descending thoracic aneurysms). Drainage of cerebral spinal fluid improves spinal cord perfusion pressure. Left heart bypass (left atrium to femoral artery) provides nonpulsatile retrograde aortic perfusion.
  5. Cardiopulmonary Bypass

CPB incorporates a circuit to oxygenate venous blood and return it to the patient's arterial circulation (Table 41-4 and Fig. 41-5).

  1. Blood Conservation in Cardiac Surgery
  2. Intraoperative autologous hemodilution involves the removal of whole blood before bypass (spared damaging effects [coagulopathy] of the bypass circuit) for reinfusion after bypass. Red blood cells may also



be salvaged from the surgical field and bypass tubing, washed, and retransfused (Cellsaver). Cellsaver blood may worsen coagulopathy because factors causing coagulopathy are not removed by the filtering process.

Table 41-4 Components of Cardiopulmonary Bypass

Circuit (blood is drained from the right atrium and returned to the ascending aorta)
   Bubble (time-dependent trauma to the blood)
   Membrane (less damage to the blood)
Pump (generate pressure required to return perfusate to the patient)
   Roller (nonpulsatile)
   Pulsatile (controversy exists whether this is better than standard flow)
Heat exchanger (allows production of systemic hypothermia)
Prime (decreased hematocrit offset changes in blood viscosity caused by hypothermia)
Anticoagulants (activated coagulation time >480 seconds; resistance to heparin occurs in patients with antithrombin III deficiency and is treated with fresh-frozen plasma or antithrombin III concentrate)
Myocardial protection (hypothermia to 10°C to 15°C and potassium to ensure diastolic arrest)
Aortic root (not feasible in patients with aortic insufficiency; the coronary ostia must be cannulated)
Retrograde via coronary sinus
Newly created bypass grafts


Figure 41-5. Diagram of a cardiopulmonary bypass circuit. IVC = inferior vena cava; LV = left ventricle; RA = right atrium; SVC = superior vena cava.

  1. Pharmacologic measures include antifibrinolytics (epsilon-aminocaproic acid).
  2. Myocardial Protection.The most common method of myocardial protection is use of intermittent hyperkalemic cold cardioplegia (diastolic electrical arrest) and moderate systemic hypothermia.
  3. During CPB, the onset of left ventricular distention and lack of rapid electrical arrest may be evidence of poor myocardial protection and the possibility of difficulty in separation from bypass.
  4. TEE is helpful in diagnosing ventricular distention that is relieved by venting or manual decompression.
  5. Preoperative and Intraoperative Management

Data from the history, physical examination, and laboratory investigation are used to delineate the degree of left ventricular or right ventricular dysfunction (Table 41-5).

  1. Current drug therapy,including β-adrenergic antagonists, calcium channel blockers, ACE inhibitors, and digitalis preparations (heart rate or rhythm control), is usually continued until the time of surgery.
  2. Premedicationfor cardiac surgery often combines an opioid (0.1–0.2 mg/kg intramuscularly [IM] of morphine) with scopolamine (0.006 mg/kg IM) with or


without a benzodiazepine (0.05–0.1 mg/kg of diazepam or 0.05–0.07 mg/kg of lorazepam orally). Patients with valvular heart disease may be more susceptible to the ventilatory depressant effects of premedication than those with CAD who are scheduled for CABG operations.

Table 41-5 Data from Preoperative Evaluation

History of myocardial infarction
Signs of congestive heart failure
Evidence of myocardial ischemia or infarction on electrocardiography
Chest radiography
Left ventricular end-diastolic pressure >18 mm Hg
Ejection fraction <0.4
Cardiac index <2 L/min/m2
TEE (wall motion abnormalities)

TEE = transesophageal echocardiography.

  1. Monitoringshould emphasize the areas particularly relevant to cardiac surgery (Table 41-6). Use of specialized equipment or procedures (hypothermia, tight glucose control) have unproven benefit on neurologic outcomes.
  2. Selection of Anesthetic Drugs.There is no single best drug, and the most critical factor governing anesthetic selection is the degree of left ventricular dysfunction. The anticipated time to tracheal extubation may influence the choice of anesthetic (“fast track”). It is useful to be able to alter the anesthetic depth to accommodate the varying intensity of the surgical stimulus (intense with tracheal intubation, sternotomy,


and manipulation of the aorta and minimal during hypothermic CPB).

Table 41-6 Monitors for Cardiac Surgery Requiring Cardiopulmonary Bypass

Pulse oximeter (placed as the first monitor to detect unsuspected episodes of hypoxemia during catheter placement)
Temperature (gradients during cooling and rewarming should be observed)
Intra-arterial blood pressure (radial artery blood pressure may be lower than central aortic pressure early after CPB)
Central venous pressure catheter (infusion of cardioselective drugs; assumed to reflect left-sided filling pressures in the absence of left ventricular dysfunction)
Pulmonary artery catheter (awake vs asleep placement; distal migration occurs during CPB, so some recommend withdrawing the catheter a few centimeters before initiation of CPB)
TEE (provides information about cardiac structure and function that exceeds any other monitor [valve function, ventricular filling, myocardial contractility, myocardial ischemia, presence of intracardiac air, assessment of the aorta for plaques, congenital heart lesion repairs])
Central nervous system function (electroencephalography, SSEPs)

CPB = cardiopulmonary bypass; SEEP = somatosensory evoked potential; TEE = transesophageal echocardiography.

  1. Volatile anesthetics are useful as the primary anesthetic and as adjuvants to treat or prevent hypertension associated with high-dose opioid techniques. Volatile anesthetics may be administered during CPB through a vaporizer incorporated into the CPB circuit.
  2. Opioidslack negative inotropic effects, and in high doses (50–100 µg/kg IV of fentanyl or 10–20 µg/kg IV of sufentanil) they may be used as the sole anesthetic.
  3. In patients with good left ventricular function, it is often necessary to include adjuvant drugs to provide amnesia (benzodiazepines) and control hypertension (volatile anesthetics, vasodilators).
  4. Excessive bradycardia may accompany the use of opioids, especially if nondepolarizing muscle relaxants are administered without heart rate effects.
  5. Nitrous oxidehas limited usefulness because of its myocardial depressant effects in the presence of opioids and its ability to enhance the size of air emboli, which may be present in coronary arteries after CABG operations.
  6. Neuromuscular Blocking Drugs.The selection of muscle relaxants is influenced by the hemodynamic and pharmacokinetic properties associated with each drug, the patient's myocardial function, and the anesthetic technique used.
  7. Intraoperative Management(Table 41-7)
  8. Preinduction Period.Supplemental oxygen is administered via nasal cannula after the patient is transferred to the operating table. Angina is promptly treated with oxygen and nitroglycerin (sublingual or IV). Placing a functioning pulse oximeter with the volume audible should precede line placement.
  9. Induction and Intubation.The dose, speed of administration, and specific drugs selected depend primarily on the patient's cardiovascular reserve and desired cardiovascular profile. A brief duration of laryngoscopy is desirable, although intubation of the trachea may be associated with myocardial ischemia, even in the absence of blood pressure or heart rate changes.


Table 41-7 Checklist for Management of Patients Undergoing Cardiopulmonary Bypass

Before Cardiopulmonary Bypass
Laboratory Values
   Adequate heparinization (activated coagulation time or other method)
   Adequate depth using amnestics or opioids
   Nitrous oxide off
   Muscle relaxants supplemented
   Arterial pressure (initial hypotension and then return)
   Central venous pressure (indicates adequate venous drainage)
   Pulmonary capillary wedge pressure (elevated with left ventricular distention reflecting inadequate drainage, aortic insufficiency; the catheter should be pulled back 1 to 2 cm)
Patient and Field
   Cannulas in place (no clamps or air locks)
   Face (suffusion reflects inadequate superior vena cava drainage; unilateral blanching reflects innominate artery cannulation)
   Heart (signs of distention reflect ischemia or aortic insufficiency)
   Usually not necessary
During Cardiopulmonary Bypass
Laboratory Values
   Adequate heparinization
   ABG analysis (evidence of acidosis)
   Hematocrit, electrolytes, ionized calcium, glucose
   Discontinue ventilation
   Arterial hypotension (inadequate venous return, low pump flow, aortic dissection, decreased vascular tone, dampened waveform)
   Arterial hypertension (high pump flow, vasoconstriction)
   Venous pressure (transducer higher than atrial level, obstruction to chamber drainage)
   Adequate body perfusion (acidosis, mixed venous oxygen saturation)
   Urine output
Patient and Field
   Conduct of operation (heart distention, fibrillation)
   Venous engorgement
   Signs of light anesthesia (movement, breathing)
   Assist adequacy of pump flow (anesthetics or vasodilators for hypertension or constrictors for hypotension)
Before Separation from Cardiopulmonary Bypass
Laboratory Values
   Hematocrit and ABG analysis
   Potassium (may be elevated from cardioplegia)
   Ionized calcium
Anesthetic and Machine
   Initiate ventilation (evaluate lung compliance)
   Vaporizers off
   Alarms on
   Normothermia (37°C nasopharyngeal; 35.5°C bladder)
   Electrocardiogram (rate, rhythm, ST wave)
   Transducers zeroed and calibrated
   Arterial and filling pressures
   Activate recorder
Patient and Field
   Look at heart (contractility, rhythm, size)
   De-aired (TEE)
   Vascular resistance
Support as necessary (inotrope, vasodilator)

ABG = arterial blood gas; EEG = electroencephalography;
TEE = transesophageal echocardiography.

  1. P.664
  2. The preincision periodbetween tracheal intubation and skin incision should be one of minimal stimulation. (Blood pressure may need to be supported.)
  3. The period from incision to bypassis characterized by periods of intense surgical stimulation that often require alteration in the depth of anesthesia or administration of a vasodilator to blunt responses (hypertension, tachycardia) that may predispose the patient to myocardial ischemia. Any evidence of new myocardial ischemia (ST segment changes on the electrocardiogram) should be treated appropriately and the surgeon notified.
  4. Cardiopulmonary bypassis initiated after confirmation of adequate anticoagulation with heparin. There is no consensus about the optimal


mean arterial pressure during CPB, although pump flows of 50 to 60 mL/kg usually produce perfusion pressures of 50 to 60 mm Hg.

  1. The effect of decreased viscosity (acute hemodilution) and loss of pulsatile flow may initially cause the perfusion pressure to decrease below 40 mm Hg.
  2. Phenylephrine may be administered to increase perfusion pressure if it is deemed necessary for maintenance of organ blood flow.
  3. After full CPB is established, there is no need to continue ventilation of the patient's lungs. There is no consensus about management of the lungs (positive end-expiratory pressure vs zero airway pressure, oxygen vs room air) during CPB.
  4. Anesthetic requirements are decreased during hypothermic CPB, an effect that may offset the dilutional effect of CPB on plasma concentrations of injected drugs.
  5. Continued skeletal muscle paralysis is desirable to prevent increases in oxygen requirements owing to skeletal muscle activity.
  6. Monitoring and Management During Bypass
  7. It is important to continuously observe the surgical field and cannulae to permit early detection of mechanical causes of hypotension or hypertension during CPB.
  8. Maintenance of adequate depths of anesthesia is important during CPB, although clinical signs are few.
  9. Maintenance of urine output with diuretics is a common practice during CPB. Nevertheless, postoperative renal failure is most likely caused by aggravation of pre-existing renal dysfunction or persistent low cardiac output after CPB.
  10. Rewarmingis begun when the surgical repair is nearly complete; the anesthesiologist should remember that patients may regain awareness as the anesthetic effects of hypothermia dissipate. (Administration of a volatile anesthetic should be considered if a smooth postbypass course is anticipated and early weaning from mechanical ventilation and extubation are planned.)
  11. Discontinuation of CPBis considered when rewarming is adequate. A low cardiac output must


prompt a search for explanations (kinked grafts, air in coronary grafts, coronary artery spasm, global ischemia from inadequate myocardial protection) and consideration of pharmacologic support (inotropes, vasodilators) (Tables 41-8 and 41-9).

Table 41-8 Causes of Right or Left Ventricular Dysfunction After Cardiopulmonary Bypass

Inadequate myocardial protection
Intraoperative infarction
Reperfusion injury
Coronary spasm
Coronary embolism (air, thrombus)
Technical difficulties (kinked or clotted grafts)
Uncorrected Structural Defects
Nongraftable vessels
Diffuse coronary artery disease
Residual or new valve pathology
Pre-existing cardiac dysfunction
Cardiopulmonary Bypass–Related Factors
Excessive cardioplegia
Unrecognized cardiac distention

  1. Intra-aortic Balloon Pump(Table 41-10). The balloon pump functions as a mechanical assist device in the thoracic aorta (25-cm balloon on a 90-cm vascular catheter) using the principle of synchronized counterpulsation to enhance left ventricular stroke volume.
  2. The balloon deflates immediately before systole to decrease afterload and myocardial oxygen requirements. Subsequently, the balloon inflates during diastole to provide diastolic augmentation that increases coronary blood flow.
  3. It is crucial to control the heart rate and to suppress cardiac dysrhythmias to ensure proper balloon timing.
  4. As cardiac function improves, the assist ratio is gradually weaned from every beat to every other beat and then removed.
  5. Ventricular Assist Device.When the heart is unable to meet systemic metabolic demands



despite maximal pharmacologic therapy and insertion of the intra-aortic balloon pump, a device that pumps blood and bypasses the left or right ventricle may be useful.

Table 41-9 Diagnosis and Therapy of Cardiovascular Dysfunction After Cardiopulmonary Bypass

Blood Pressure

Filling Pressures

Cardiac Output







Remove volume







Poor contractility











Give volume









Poor contractility

Mechanical assist










Give volume

Table 41-10 Indications and Contraindications for Intra-aortic Balloon Pumps

Complications of Myocardial Ischemia
   Hemodynamic (cardiogenic shock)
   Mechanical (mitral regurgitation, ventricular septal defect)
   Intractable dysrhythmias
   Extension of infarct
   Acute cardiac instability
   Unstable angina
   Failed PTCA
   Cardiac contusion
   Possibly septic shock
   Open heart surgery
   Separation from cardiopulmonary bypass
   Ventricular failure
   Increasing inotropic requirements
   Progressive hemodynamic deterioration
   Refractory ischemia
Severe aortic insufficiency
Technical difficulties with insertion
Irreversible cardiac disease
Irreversible brain damage

PTCA = percutaneous transluminal coronary angioplasty.

Table 41-11 Side Effects of Protamine

Hypotension (less likely when administered over 5 minutes)
Allergic reaction (more likely in patients receiving protamine-containing insulin preparations [NPH, PZI])
Pulmonary hypertension (mediated by release of thromboxane and C5a anaphylatoxin)

NPH = neutral protamine Hagedorn; PZI = protamine zinc insulin.

  1. Postcardiopulmonary Bypass
  2. Reversal of Anticoagulation.Heparin is partially reversed with protamine administered intravenously while the arterial cannula remains in place for continued transfusion of pump contents. Adequate reversal of anticoagulation with protamine is verified by measurement of the activated coagulation time. Protamine administration may be accompanied by side effects (Table 41-11). Whether protamine should be administered through the right atrium, left atrium, aorta, or a peripheral vein remains controversial.
  3. Postbypass Bleeding.Persistent oozing after heparin reversal is common and usually reflects inadequate surgical hemostasis or platelet dysfunction.
  4. Closure of the chest is occasionally associated with transient decreases in blood pressure. If hypotension persists despite volume replacement, the chest must be reopened to rule out cardiac tamponade or kinking of a venous graft.
  5. Minimally Invasive Cardiac Surgery

The desire to avoid the complications of CPB (stroke, neurocognitive defects, renal failure, pulmonary insufficiency, coagulopathy, activation of systemic inflammatory response)


as well as the complications of sternotomy led to the development of techniques not requiring CPB (minimally invasive direct coronary artery bypass [MIDCAB], off-pump coronary bypass [OPCAB], robotic surgery).

Table 41-12 Reasons for Postoperative Re-exploration

Persistent bleeding
Excessive blood loss
Cardiac tamponade
Unexplained low cardiac output

VII. Postoperative Considerations

  1. Bring-backsof the patient for postoperative re-exploration are necessary in 4% to 10% of cases, usually in the first 24 hours (Table 41-12).
  2. Tamponademust always be included in the differential diagnosis of unexplained low cardiac output (Table 41-13). The diagnosis of tamponade is confirmed by TEE. Ketamine is useful for induction and maintenance of anesthesia in patients with cardiac tamponade because the goal is to avoid vasodilation and cardiac depression.
  3. Pain Management.Intrathecal opioids provide analgesia that facilitates early extubation. Use of nonsteroidal anti-inflammatory drugs may play an increasing role in management of postoperative pain after cardiac surgery.

Table 41-13 Manifestations of Cardiac Tamponade

Equalization of diastolic filling pressures (when the pericardium is no longer intact, loculated areas of clot may compress only one chamber, causing isolated increases in filling pressures)
Fixed stroke volume (cardiac output and blood pressure become dependent on heart rate)
Peripheral vasoconstriction
Potential for concurrent myocardial ischemia


VIII. Anesthesia for Children with Congenital Heart Disease

Congenital heart defects cause either too much blood flow to a cardiac chamber or obstruction of flow to a chamber (Table 41-14). Because “anatomy dictates physiology,” the anesthetic management of children with congenital heart disease requires knowledge of anatomical defects and planned surgical procedures and comprehensive understanding of the altered physiology.

  1. Preoperative Evaluation(Tables 41-15 and 41-16)
  2. Premedicationis intended to render the child calm but without oversedation.
  3. Monitoringbeyond the standard monitors may include peripheral and central temperature monitoring, central venous pressure monitoring (right atrial or left atrial), and TEE.
  4. Anesthetic and Intraoperative Management
  5. Inhalation agents are useful for induction and may be continued for maintenance.

Table 41-14 Classification of Congenital Heart Defects

Volume Overload of the Ventricle or Atrium Resulting in Increased Pulmonary Blood Flow
Atrial septal defect (high flow, low pressure)
Ventricular septal defect (high flow, high pressure)
Patent ductus arteriosus (high flow, high pressure)
Endocardial cushion defect (high flow, high pressure)
Cyanosis Resulting from Obstruction to Pulmonary Blood Flow
Tetralogy of Fallot
Tricuspid atresia
Pulmonary atresia
Pressure Overload on the Ventricle
Aortic stenosis
Coarctation of the aorta
Pulmonary stenosis
Cyanosis Caused By a Common Mixing Chamber
Total anomalous venous return
Truncus arteriosus
Double outlet right ventricle
Single ventricle
Cyanosis Caused By Separation of the Systemic and Pulmonary Circulations
Transposition of the great vessels

  1. P.671

Table 41-15 Preoperative Evaluation of Children with Congenital Heart Disease

Symptoms (poor weight gain, respiratory distress, easily exhausted, cyanosis, upper respiratory infections)
Medications (potential interactions with anesthetics)
Previous surgical procedures
Physical Examination
Evidence of cardiac failure (irritability, diaphoresis, rales, jugular venous distention, hepatomegaly)
Failure to thrive (pulmonary hypertension, poor peripheral oxygenation)
Blood pressure in the arms and legs
Auscultation of the heart (murmur reflects lesion; see Table 41-17)
Airway evaluation
Laboratory Evaluations
Hemoglobin (anemia vs polycythemia)
Coagulation profile (platelet count, prothrombin time, partial thromboplastin time)
Potassium (diuretic therapy), glucose, calcium
ABG analysis
Cardiac Evaluations
Echocardiography (delineates cardiac anatomy and permits noninvasive measurement of ventricular size, function, and cardiac output
Chest radiography (cardiac size, abnormal vessels, pneumonia)
Electrocardiography (rate and rhythm)

ABG = arterial blood gas.

Table 41-16 Classification of Cardiac Murmurs

Atrial septal defect
Ventricular septal defect
Coarctation of the aorta
Regurgitant semilunar valves
Stenotic atrioventricular valves
Mitral flow rumble
Tricuspid flow rumble
Patent ductus arteriosus
Arteriovenous fistula
Excessive bronchial collaterals
Aortopulmonary window
Surgical shunt
Severe pulmonic stenosis

  1. P.672

Table 41-17 Choice of Drugs During Maintenance of Anesthesia for Correction of Congenital Cardiac Defects

Intravenous Agents (fentanyl 50–100 µg/kg or remifentanil 1 µg/kg/min; bradycardia is a risk)
Inhalational Agents
Isoflurane (myocardial contractility may be better preserved than with halothane; there is a propensity for laryngospasm if it is used for induction of anesthesia)
Sevoflurane (may be used for inhalation induction and lacks significant myocardial depression because decreases in systemic blood pressure are principally caused by decreases in systemic vascular resistance)
Neuromuscular Blocking Drugs
Succinylcholine (bradycardia limits its usefulness)
Nondepolarizing relaxants (facilitate tracheal intubation and provide paralysis during surgery; pancuronium is useful when increased heart rate is desirable)

  1. The choice of anesthetic drugs after induction of anesthesia is influenced by ventricular function, the use of CPB, and anticipation of controlled mechanical ventilation or tracheal extubation at the end of the operation (Table 41-17).

Table 41-18 Medications Administered by Continuous Intravenous Infusion


Usual Initial Dose (µg/kg/min)

Usual Dose Range (µg/kg/min)































Prostaglandin E1




1µg (4 U)


*Requires initial bolus of 750 µg/kg over 3 minutes before start of infusion.
†For chronotropic effect after cardiac transplantation, dosages of 0.005 to 0.01 µg/kg/min are used.

  1. P.673

Table 41-19 Criteria for Tracheal Extubation After Complex Procedures

Ability to maintain oxygenation during spontaneous respiration
Coordination of thoracic and abdominal components of respiration
Acceptable chest radiographs (absence of significant atelectasis, effusions, and infiltrates)
Short period of time without caloric support
Stable inotropic support

  1. CPB produces marked hemostatic derangements (dilution of clotting factors, activation of clotting cascade and consumption of clotting factors and platelets, and activation of the fibrinolytic pathway).
  2. Separation from CPB may require pharmacologic intervention (Table 41-18).
  3. Tracheal Extubation and Postoperative Ventilation(Table 41-19)
  4. Children undergoing correction of congenital cardiac defects that do not require ventricular incisions (atrial septal defect, ventricular septal defect repaired across the tricuspid valve) can often have their tracheas extubated at the conclusion of surgery.
  5. Those with risk factors (complex surgery, circulatory arrest, Down syndrome, pulmonary hypertension, postoperative cardiovascular and pulmonary complications) for ventilatory failure must fulfill tracheal extubation criteria.

Editors: Barash, Paul G.; Cullen, Bruce F.; Stoelting, Robert K.; Cahalan, Michael K.; Stock, M. Christine

Title: Handbook of Clinical Anesthesia, 6th Edition

Copyright ©2009 Lippincott Williams & Wilkins

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