Anesthesia for Cardiac Surgery - Induction


Induction is a critical time in the anesthetic management of the patient. A surgeon should be available, and the CPB pump should be ready in the event of severe hemodynamic instability during induction. A systematic and gradual induction involves minimizing the degree of cardiovascular depression while maintaining an adequate anesthetic depth.

  1. Agents useful in the induction and maintenance of anesthesia in the cardiac surgical patient include the following:
    1. IV opioids produce various degrees of vasodilation and bradycardia without significant myocardial depression. Fentanyl (50 to 100 μg/kg) or sufentanil (10 to 20 μg/kg) can be used as both the induction and primary maintenance agents. Alternatively, a smaller induction bolus (fentanyl 25 to 50 μg/kg) may be supplemented with a continuous opioid infusion. Alternatively, even lower doses (fentanyl 10 to 25 μg/kg, or sufentanil 1 to 5 μg/kg) may be used in conjunction with other central nervous system depressants as part of a balanced technique.
    2. Sedative hypnotics and amnestics, including benzodiazepines, propofol, and etomidate, may be useful as coinduction agents in particular situations. Of these drugs, etomidate causes the least myocardial depression.
    3. Volatile inhalation anesthetics are useful supplementary agents, especially in the treatment of hypertension.
    4. Muscle relaxants with minimal cardiovascular effects are commonly chosen (e.g., vecuronium, cisatracurium, and rocuronium). Pretreatment with a “priming dose” and early relaxant administration help to counteract chest wall rigidity often encountered during opioid-based inductions. Succinylcholine is used for rapid sequence inductions for patients with reflux or a full stomach. The parasympatholytic actions of pancuronium can counteract the bradycardic effects of opioids.
  2. Specific considerations for valvular heart disease (see also Chapter 2).
    1. Aortic stenosis (AS). Physiologic goals include the maintenance of adequate intravascular volume, sinus rhythm, contractility and systemic vascular resistance (SVR) and the avoidance of tachycardia. Patients with AS typically have a hypertrophied and noncompliant ventricle and require higher filling pressures (LVEDP of 20 to 30 mm Hg). Anesthetic agents that reduce vascular tone or myocardial contractility should be avoided. An infusion of phenylephrine can be started 1 to 2 minutes before induction to decrease the risk of developing significant hypotension associated with induction. Dysrhythmias must be treated aggressively.
    2. Aortic insufficiency (AI). Physiologic goals include the maintenance of adequate intravascular volume and adequate contractility. Bradycardia and increases in SVR must be avoided. Patients with AI are often highly dependent on endogenous sympathetic tone. Patients with coexisting CAD may decompensate with significant bradycardia due to very low diastolic perfusion pressure. A means for rapid pacing should be available.
    3. Mitral stenosis (MS). Hemodynamic goals mandate the maintenance of a slow rhythm, preferably sinus, and adequate intravascular volume, contractility, and SVR. Patients with severe MS and elevated pulmonary vascular resistance (PVR) are challenging to induce. Elevated PVR, often secondary to hypoventilation or positive end-expiratory pressure (PEEP), must be avoided. Atrial fibrillation with rapid ventricular response must be treated aggressively, such as with immediate cardioversion.
    4. Mitral regurgitation (MR). Physiologic goals include the maintenance of adequate intravascular volume, myocardial contractility, a normal or elevated heart rate, and a reduction of systemic vascular tone. Increased SVR should be avoided. Anesthesia-induced decreases in SVR are usually well tolerated.
    5. In patients with mixed valvular lesions, the most hemodynamically significant lesion will dominate the management goals. The addition of CAD to mixed valvular lesions makes planning even more complex (e.g., AS with AI and CAD). In all situations, determine the three most likely problems that could occur during induction and plan the management for each.
  3. Specific considerations for emergent inductions
    1. Pulmonary embolus. Induction of general anesthesia and the institution of positive-pressure ventilation can precipitate cardiovascular collapse. It is prudent to prepare and drape the unstable patient prior to induction. In patients with compromised RV function, cannulation of the femoral vessels under local anesthesia should be performed prior to induction to allow for the emergent institution of CPB if needed.
    2. Pericardial tamponade. Similar concerns are present for patients with pericardial tamponade. Adequate volume administration is essential. Starting an inotropic agent and a vasopressor before induction may be helpful. A rapid sternotomy may be required if hemodynamic collapse occurs with anesthesia induction. If possible, the pericardial effusion should be drained under local anesthesia prior to induction.
    3. Aortic dissection. Hypertension can precipitate aortic rupture. Packed red blood cells must be available in the OR before induction. Proximal extension of the dissection into the coronary arteries can occur leading to myocardial ischemia or tamponade.
    4. Ventricular septal defect (VSD) and papillary muscle rupture after myocardial infarction. Patients may present with extreme hypotension. Rapid initiation of CPB is essential. Preinduction initiation of intra-aortic balloon counterpulsation therapy is indicated in many of these patients.

The prebypass period

The prebypass period is characterized by variable levels of stimulation during the preparation for CPB initiation. Stimulating periods include sternotomy and sternal retraction, pericardiotomy, and aortic cannulation.

  1. Baseline PaO2, PaCO2, pH, hematocrit (Hct), and activated clotting time (ACT) should be obtained.
  2. Consider autologous blood procurement in otherwise healthy patients with a starting Hct of 40% or greater. 1 to 2 units of whole blood may be drained passively into sterile blood bags and later transfused into the patient following conclusion of CPB and heparin reversal.
  3. The lungs are deflated during sternotomy. Physical alterations of the chest wall can produce ECG changes (especially T-wave changes), which should be noted to avoid confusion with ischemia.
  4. Left internal mammary artery dissection may cause ispilateral hemothorax and negatively affect pulmonary mechanics in patients with reduced pulmonary reserve.
  5. Anticoagulation for cannulation and bypass
    1. Prior to the induction of anesthesia, heparin at a dose of 350 units/kg should be drawn up and kept readily available in case the emergent initiation of CPB is necessary. The dose may be increased to 500 units/kg if the patient has been receiving heparin infusion or is being treated with IABP counterpulsation. The heparin should be administered through a centrally placed catheter.
    2. Vasodilation often follows the heparin bolus and should be anticipated.
    3. The ACT is used to monitor the degree of anticoagulation. It should be measured approximately 5 minutes after heparin administration. Baseline values are 80 to 150 seconds. Heparin treatment sufficient to prevent microthrombus formation during CPB correlates with an ACT of more than 400 seconds (at higher than 35°C). An ACT value of greater than 450 seconds is preferred, given the variability that exists in this point-of-care test. Patients on continuous IV heparin preoperatively may become relatively “heparin resistant.” If an ACT longer than 400 seconds is not achieved with the standard heparin dose, an additional 200 to 300 units/kg is administered. If this fails, antithrombin concentrate (500 to 1,000 units) or 2 to 4 units of FFP may be necessary to correct a probable antithrombin III deficiency.
    4. Patients with a diagnosis of HIT type 2 (also known as HIT with thrombotic syndrome [HITTS]) require alternative anticoagulation management during CPB. The classification of HIT is determined by immune involvement. HIT type 1 is a nonimmunologic reaction of heparin with platelets that causes a mild thrombocytopenia. HIT type 2 is an immune-mediated phenomenon that activates platelets, resulting in platelet aggregation. Biochemical mediators from activated platelets can induce the generation of thrombin, leading to diffuse arterial and venous clotting. The diagnosis requires serologic and clinical evidence. Patients with a positive functional assay (serotonin release assay or platelet aggregation study), greater than 50% reduction in platelets (irrespective of starting platelet count), drop in platelet count less than 150k, or history of a thrombotic event associated with heparin use are more likely to have an adverse outcome when re-expose to heparin. Patients with a positive ELISA test in the absence of a positive functional assay or clinical symptoms have a lower likelihood of having an adverse reaction to heparin.
    5. For patients with HIT type 2 or HITTS, alternatives to standard heparin treatment exist (Table 24.4); each has significant limitations that should be discussed with the surgeon and a hematologist before use.
      1. All forms of heparin are removed preoperatively. Saline is used to flush pressure transducers, and citrated saline is used to wash salvaged blood during the centrifugation process.
      2. A heparin-free PA catheter is used.
      3. Alternative anticoagulant regimens may be used. These include bivalirudin, or unfractionated heparin in combination with an antiplatelet agent (see Table 24.4).
      4. If unfractionated heparin is used, then a bypass dose of porcine heparin is administered before aortic cannulation (to minimize the likelihood of a repeat dose of heparin).
      5. Aspirin is administered early in the postoperative period, and initiation of systemic anticoagulation with a direct thrombin inhibitor and warfarin may be indicated to prevent both early and late postoperative thromboembolic complications.
  6. Antifibrinolytic drugs such as ε-aminocaproic acid (Amicar) are usually given as a bolus 10 g followed by an infusion 2 g/h during all on-pump procedures, with the intention of inhibiting excessive fibrinolysis (i.e., plasmin activity and d-dimer formation) and possibly preserving platelet function.
  7. Aortic cannulation is conducted in the ascending aorta just proximal to the innominate artery. Epiaortic scanning is used to sonographically direct the cannulation site in patients with known atherosclerotic disease. Maintaining a systolic blood pressure near 100 mm Hg during aortic cannulation decreases the risk of dissection.
  8. Some surgeons will perform the proximal saphenous vein graft anastomoses before initiating CPB. An improperly placed side-biting clamp may occlude more than 50% of the aortic lumen and markedly increase afterload, causing myocardial decompensation. The early signs are hypotension, elevation of PA pressures and ST-segment changes.
  9. One or two venous return cannulas are inserted via the right atrium. A single cavoatrial catheter is placed in the right atrial appendage, with the tip in the IVC and fenestrations in the mid-atrium. For open-heart procedures (i.e., mitral and tricuspid valve surgeries), bicaval cannulation, consisting of separate superior vena cava (SVC) and IVC cannulas is conducted.
  10. Retrograde autologous priming (RAP) can be used to reduce the hemodilution from the crystalloid priming solutions (typically 1,600 mL) of the bypass circuit. During RAP, the patient's blood pushes the crystalloid prime out of the circuit, often necessitating use of α-agonist agents to maintain vascular tone and prevent hypotension. RAP is most beneficial in patients with small blood volumes and low hemoglobin concentrations.

Cardiopulmonary Bypass

Cardiopulmonary Bypass

  1. Initiation of CPB. After an ACT greater than or equal to 450 seconds is obtained, the clamp on the venous line is released and CPB is initiated. After the perfusionist is convinced that the venous return is adequate, he or she will turn on the pump and progressively increase the rate to a flow of 2.0 to 2.4 L/min/m2 or roughly 50 mL/kg/min for adults. Depending on the vascular resistance, intravascular volume, and blood viscosity, a mean arterial pressure (MAP) of 40 to 120 mm Hg may be achieved by such flow. Observe the bright red blood entering the aorta during this initiation to confirm that the membrane oxygenator is working properly. Once adequate flows and venous drainage are established, volatile anesthetics from the anesthesia machine, IV fluids, and pulmonary ventilation are discontinued. Muscle relaxants are readministered to prevent shivering. Anesthesia is maintained using IV agents or inhalational agents administered through a vaporizer in the fresh gas line of the circuit. It is advisable to withdraw the PA catheter 1 to 5 cm to prevent the catheter tip from migrating into a wedge position during CPB. If two venous return lines are used and tourniquets are applied to achieve complete CPB, the CVP measured above the tourniquet is the SVC pressure. High CVP may indicate obstruction of SVC cannula. After fibrillation or arrest, mean PA pressures are displayed. A vent cannula may be inserted into the left ventricle to prevent LV distention.
  2. Maintenance of CPB
    1. Myocardial protection during the cross-clamp period is achieved primarily by reducing myocardial oxygen consumption through hypothermia, hyperkalemic arrest, or both.
      1. Intermittent cold cardioplegia is a commonly used technique. Cold (4°C to 6°C) hyperkalemic solution with or without blood is delivered to the coronary circulation approximately every 20 minutes (or sooner if cardiac electrical activity returns). Systemic cooling of the patient and topical cooling of the heart augment myocardial protection.
      2. The warm cardioplegia technique delivers a warm (32°C to 37°C) hyperkalemic solution mixed with blood at approximately a 1:5 ratio. The solution is delivered continuously during the cross-clamp period with a few interruptions to allow visualization of the anastomotic sites. Mild systemic cooling to 32°C to 34°C is frequently performed. Serum glucose levels will increase dramatically and are treated with IV insulin.
    2. Hypothermia (20°C to 34°C) is commonly used during CPB. Oxygen consumption and blood flow requirements are reduced while blood viscosity is increased, thus counteracting prime-induced hypoviscosity. Adverse effects of hypothermia include impaired autoregulatory, enzymatic, and cellular membrane function; decreased oxygen delivery (leftward shift of the hemoglobin oxygen dissociation curve); and potentiation of coagulopathy. Metabolic requirements decrease about 7% for every degree Celsius reduction in body temperature below 37°C.
    3. Hemodynamic monitoring during CPB is the shared responsibility of the perfusionist, anesthesiologist, and surgeon.
      1. Hypotension during the initiation of CPB is usually due to hemodilution and hypoviscosity. Other important causes include inadequate pump flow, vasodilation, acute aortic dissection, and incorrect placement of the aortic cannula (e.g., directing flow toward the innominate artery not supplying the cannulated radial artery). The PA pressure and LV vent flow rate should be inspected to ensure that aortic incompetence has not compromised forward pump flow. A phenylephrine infusion may be required to treat transient hypotension. During the course of CPB, a pressure gradient (as high as 40 mm Hg) may develop between the radial artery and the aorta. The lower radial artery pressure could lead to unnecessary administration of vasopressors if the discrepancy is not recognized. In the presence of carotid stenosis, MAP should be maintained at a higher level than usual (e.g., 80 to 90 mm Hg), and hypocarbia should be avoided.
      2. Hypertension (MAP > 90 mm Hg) may be due to excessive flow rates or increased vascular resistance, which may be treated with vasodilators or anesthetics.
      3. Elevated PA pressures indicate left heart distention, which may be due to inadequate venting, AI, or inadequate isolation of venous return. Severe distention may result in myocardial injury.
    4. Acid–base Management. In the setting of hypothermia, gas solubility increases and the dissociation constant for water decreases, resulting in a lower [H+] and [OH] and a higher pH. While total CO2 content remains constant, the partial pressure of CO2 decreases.
      1. pH-stat corrects the patient's blood gas for temperature and strives to maintain a neutral pH of 7.4 and CO2 near 40 mmHg by adding CO2 to the CPB circuit. This strategy results in cerebral vasodilatation and more uniform cerebral cooling, however at an increased risk of cerebral microembolism.
      2. Alpha-stat involves the use of uncorrected gas tensions during hypothermia. No CO2 is added to the oxygenator. The basis of the approach is that the total CO2 content of blood and the intracellular electroneutrality (as primarily governed by the imidazole rings of histidine residues) are unchanged during hypothermia. Cerebral blood flow is autoregulated and coupled to cerebral oxygen demand.
      3. Most studies fail to reveal any significant difference in patient outcomes between the two methods. Generally, α-stat is used in adults and pH-stat in children when circulatory arrest is used.
    5. Metabolic acidosis and oliguria suggest inadequate systemic perfusion. Additional volume (blood or crystalloid depending on Hct) may be required to achieve increased flow. Brisk urine output should be established within the first 10 minutes of CPB.
      1. Oliguria (<1 mL/kg/h) should be treated with a trial of increased perfusion pressure and/or flow, mannitol (0.25 to 0.5 g/kg), or dopamine (1 to 5 μg/kg/min). Patients on chronic furosemide therapy may require their usual dose during CPB to sustain diuresis. Fenoldopam, a selective dopamine agonist, will promote natriuresis and may provide renoprotective effects during CPB.
      2. Hemolysis during CPB is usually due to mechanical trauma to red blood cells from the bypass machine and the pump suction. Released pigments may cause acute renal failure postoperatively. For hemoglobinuria, diuresis is maintained using IV fluids with mannitol or furosemide. In severe cases, the urine is alkalinized by administering sodium bicarbonate at 0.5 to 1.0 mEq/kg.
    6. Additional heparin bolus and/or infusion may be needed for prolonged CPB. The duration of heparin anticoagulation may be shorter in patients on chronic heparin therapy or during cases in which systemic hypothermia is not used. The ACT does not correlate well with plasma heparin levels when the patient is on CPB, but many centers routinely monitor the ACT during hypothermic (25°C to 34°C) CPB.
    7. Blood glucose should be controlled between 80 and 200 mg/dL during bypass. Hyperglycemia may be associated with an increased risk of neurologic injury. Diabetic patients following a warm cardioplegia technique will typically require an insulin infusion.
    8. Table 24.5 lists some of the problems that can be encountered during CPB. Anesthesiologists should be alerted to these issues as they may significantly affect subsequent separation from CPB.

Discontinuing CPB

Discontinuing CPB implies transferring cardiopulmonary function from the bypass system back to the patient. In preparation for this transition, the anesthesiologist must examine and optimize the patient's metabolic, anesthetic, and cardiorespiratory conditions.

  1. Preparation for discontinuing CPB begins during rewarming. The arterial blood is warmed. The core (nasopharyngeal) temperature should reach but not exceed 38°C before discontinuation from CPB.
    1. Laboratory data to be acquired during rewarming include PaO2, PaCO2, pH, potassium, calcium, glucose, Hgb, and ACT. Clinical decisions concerning pH are usually made according to the values measured at 37°C (alpha-stat management).
    2. Adequate anticoagulation during rewarming and separation from CPB is ensured with additional heparin if necessary.
    3. Metabolic acidosis should be treated with sodium bicarbonate, and the perfusionist may elect to increase the sweep rate to remove CO2. Hyperkalemia, commonly seen following the use of cardioplegia, frequently corrects spontaneously by redistribution and diuresis. If not, the administration of IV insulin/glucose or sodium bicarbonate will lower serum potassium.
    4. Usually, a Hct of over 20% should be achieved before separation, either by transfusion or by hemoconcentration, as indicated by the CPB reservoir volume.
    5. FFP should be thawed before separation from bypass (requiring 30 to 45 minutes) if the patient is at risk for postoperative bleeding. Platelets should also be readily available for these patients.
  2. Anesthetic considerations during rewarming include maintenance of adequate neuromuscular blockade, analgesia, and amnesia. Supplementary relaxants, opioids, and benzodiazepines may be given. If MAP is elevated, nitroglycerin or sodium nitroprusside may be used for blood pressure control as well as to facilitate rewarming.
  3. Separation from CPB
    1. After procedures in which the heart has been opened (e.g., valve replacements), de-airing maneuvers under TEE guidance are used to prevent air embolism to the cerebral or coronary circulations. Positive-pressure ventilation accompanied by clamping of the venous return lines will move air forward from the pulmonary veins. Air in the ventricular trabeculae can be liberated by shifting the OR table from side to side and lifting the apex of the heart; it can then be evacuated by needle aspiration of the apex. Direct aspiration of air bubbles visible within coronary artery vein grafts may help prevent myocardial ischemia.
    2. Aortic cross-clamp removal reestablishes coronary perfusion. A nitroglycerin infusion may be started in CABG patients to reduce coronary vasospasm and reperfusion injury.
    3. Defibrillation may be spontaneous; ventricular fibrillation is treated with internal paddles delivering 5 to 10 J of energy with a biphasic waveform defibrillator. Failure may indicate inadequate warming, graft problems, a metabolic disturbance, or inadequate myocardial protection. Additional lidocaine, magnesium (1 g IV slowly), or amiodarone (150-mg IV bolus followed by infusion at 1 mg/min for 6 hours, then 0.5 mg/min) may be required.
    4. Rhythm is assessed. With bradycardia, atrial pacing is established through epicardial wires. Ventricular pacing is added if there are atrioventricular conduction abnormalities. Hypothermia as well as hypocalcemia, hyperkalemia, and hypermagnesemia caused by cardioplegia solutions may contribute to a high incidence of reversible heart block immediately after CPB. Atrial tachycardia may also indicate inadequate anesthesia and may be treated with fentanyl. Other atrial dysrhythmias may be treated with overdrive pacing, cardioversion, and antiarrhythmics (e.g., esmolol, propranolol, amiodarone, verapamil, or rarely digoxin).
    5. The ECG should be inspected for evidence of ischemia possibly related to intracoronary air or inadequate revascularization.
    6. During separation from CPB, volume administration may be guided by monitoring LV filling using TEE, mean PA pressure, PA occlusion pressure, or a surgically placed LA line. RV filling is indicated by the CVP or direct RV visualization. The determination of target postbypass filling pressures should consider the patient's preoperative pressures, the degree of left ventricular hypertrophy (LVH), the adequacy of the myocardial revascularization, and the anticipated physiologic effects of corrective valvular surgery. A normotensive patient without LVH will most likely need an LA pressure of 10 mm Hg or a mean PA pressure of 20 mm Hg. A patient with severe LVH and inadequate revascularization may need an LA pressure of 20 mm Hg or a mean PA pressure of 30 mm Hg. TEE is particularly helpful in assessing LV filling.
    7. Comparison is made between central (aortic) and peripheral (radial) arterial pressures to ensure that no significant pressure gradient exists. If a significant gradient exists, a femoral arterial line can be placed.
    8. Compliance and resistance of the lungs are tested with a few trial breaths. Ventilation should be reestablished when LV ejection begins even if the patient is still on CPB. To facilitate reexpansion of the lungs, the stomach is suctioned, and, if previously opened, the pleural cavities are drained. If the lungs are difficult to ventilate, tracheobronchial suctioning and the administration of bronchodilators may be indicated.
    9. Visual inspection of the heart confirms atrioventricular synchrony. Contractility is assessed both by gross appearance and by systolic performance, as estimated by peak systolic and pulse pressure (taking into account pump flow and LA and PA pressures). If poor myocardial performance is demonstrated or anticipated (e.g., impaired preoperative function or intraoperative ischemia), initiation of inotropic support before separation from CPB may be indicated. Pump flow rate is checked and compared with the patient's preoperative cardiac output. Significantly higher flows indicate the need to increase vascular tone (using agents such as norepinephrine and phenylephrine).
    10. Ionized Ca2+ may be corrected slowly 15 minutes after cross-clamp removal. Rapid Ca2+ administration, especially in the presence of myocardial ischemia, is associated with Ca2+-induced myocardial injury. Calcium will increase both contractility and SVR.

At the time of actual separation from CPB

At the time of actual separation from CPB, venous lines to the pump are slowly clamped, allowing the heart to gradually fill and eject with each contraction. Prolonged partial venous line occlusion allows for “partial bypass,” during which time cardiopulmonary function is shared and hemodynamics are assessed. After complete venous line occlusion, once adequate filling pressures are achieved, perfusion through the aortic cannula is stopped, and the heart alone provides systemic perfusion.

  1. Pressure maintenance. Transfusion from the CPB reservoir maintains the LA pressure or mean PA pressure at an optimal level. Care is taken not to overdistend the heart. Should overdistention occur, the surgeon may “empty” the heart by transiently unclamping a venous line. Alternatively, the patient may be temporarily placed in reverse Trendelenburg position to decrease venous return to the overdistended heart.
  2. At termination of bypass, it is important to assess the ECG, systemic blood pressure, left-sided filling pressure, right-sided filling pressure, and the cardiac output. These values are compared with target values for the patient. If the patient is unstable, correct any pacing problems, have the surgeon assess the patency of the grafts, and use TEE to assess the valve replacement or repair. Assuming there is no surgical cause for hemodynamic instability, the unstable patient will usually fall into one of the categories listed in Table 24.6. If a return to CPB is necessary, adequate anticoagulation must be ensured. A full dose of heparin is indicated if protamine has been administered.

Postbypass Period

Postbypass Period

  1. Hemodynamic stability is the primary goal. CPB gives rise to myocardial functional impairment and a systemic inflammatory response. Maintain adequate volume status, perfusion pressure, and appropriate rate and rhythm. Continuously monitor and reassess the surgical field.
  2. Hemostasis. Once cardiovascular stability has been achieved and the surgeon is confident that the bleeding is controlled, protamine administration begins. Initially, 25 to 50 mg is given over 2 to 3 minutes, and the hemodynamic response is observed. Protamine often causes systemic vasodilation (type I reaction) that can be avoided by slow administration over 10 to 15 minutes and reversed with α-agonist support. Rarely, an anaphylactic or anaphylactoid reaction (type II reaction) resulting in hypotension, bronchospasm and pulmonary edema is encountered. Type II reactions are more likely observed in diabetic patients taking subcutaneous injections of protamine-containing insulin preparations (i.e., NPH) and men who have had a vasectomy. Finally, catastrophic pulmonary hypertension (type III reaction) can occur, manifested by elevated PA pressures, right ventricular dilatation, systemic hypotension, and myocardial depression. Upon severe reaction, protamine is immediately discontinued, appropriate resuscitative measures are used, and, if necessary, the patient is retreated with heparin (with a full loading dose), and CPB is reinitiated. If forward flow is compromised, ask the surgeon to inject the heparin into the right atrium.
    1. It is advisable to monitor PA pressures while administering protamine (even if LA pressure is available).
    2. In general, 1 to 1.3 mg of protamine is administered for each 100 units of heparin administered throughout the procedure. Alternatively, the protamine dose can be calculated based on the patient's whole blood heparin level. Automated heparin-protamine titration assays are available to calculate the protamine dose for complete heparin neutralization; this method is associated with reduced protamine requirement.
    3. Four to five minutes following protamine administration, the ACT is compared with baseline. Additional protamine is given to return the ACT toward control. The aPTT also serves as a sensitive indicator of residual circulating heparin. Thromboelastography may be used to provide information about coagulation factor activity, platelet function, and degree of fibrinolysis during and after CPB.
    4. During transfusion of blood obtained from the hemoconcentrator, additional protamine (25 to 50 mg) is given to reverse the heparin. Blood obtained from red blood cell salvage devices is devoid of heparin.
    5. Antifibrinolytic agents, such as aminocaproic acid and tranexamic acid, are used to decrease postoperative bleeding and transfusion requirements.
    6. Achievement of normothermia reduces the severity of post-CPB coagulopathy.
  3. Pulmonary dysfunction may follow CPB. Aggressive treatment of bronchospasm before sternal closure is imperative.
  4. Pulmonary hypertension may arise during the post-CPB period. See Table 24.6 for approaches to management.
  5. Sternal closure may precipitate acute cardiovascular decompensation. Cardiac tamponade may develop from compression of the heart and great vessels in the mediastinum.
    1. Volatile anesthetics and other negative inotropes are reduced in anticipation of sternal closure. Intravascular volume should be optimized.
    2. Immediately after sternal closure, the filling pressures and cardiac output are compared with preclosure values, and appropriate adjustments in volume or drug infusions are made.
    3. Mediastinal and pleural tubes are placed on suction to prevent tamponade and quantify blood loss.
    4. The LA waveform and the ability of pacemakers to capture are rechecked to verify that displacement has not occurred.
    5. If the patient is hemodynamically unstable or ventilation is inadequate, the sternum should be reopened. The patient may require transfer to the intensive care unit (ICU) with the sternum open.

Transfer to the ICU

Transfer to the ICU

  1. Patients should always be hemodynamically stable before transport. Transport involves standard transport monitoring, defibrillator, and a transport ventilator if the patient remains intubated.
  2. Upon arrival to the ICU, mediastinal and pleural drainage tubes are attached to suction. An anteroposterior chest radiograph and a 12-lead ECG are obtained, and blood samples are sent for ABG, electrolytes, Hct, platelet count, PT, and aPTT. Before leaving the ICU, the anesthesiologist should review the ECG and ABG and check the chest radiograph for the presence of abnormal findings (e.g., atelectasis, pneumothorax, malpositioned tubes and catheters, widened mediastinum, or pleural effusion).


Alternative CPB Anticoagulation in Patients with HIT (Table 24.4)

DrugMechanismHalf-lifeLab MonitorReversible?
Bivalirudin (Angiomax)Direct thrombin inhibitor25 min (normal renal function)ACTNo
ArgatrobanDirect thrombin inhibitor40–50 min (prolonged in hepatic insufficiency)ACTNo
Tirofiban (Aggrastat) + unfractionated heparinaGlycoprotein IIb/IIIa receptor inhibitor prevents platelet aggregation in HIT1.5–3 hACT (platelets and d-dimer if heparin-induced thrombosis is suspected)No

a Additional training is required to safely use this anticoagulation technique for patients requiring CPB.

Potential Problems during CPB (Table 24.5)

ProblemPossible Cause
Inadequate systemic pressuresVasoplegia, inadequate flow, hemodilution
Poor gas exchangeOxygenator failure, hypoxic gas mixture, inadequate coagulation, poor perfusion
High arterial line pressureMechanical obstruction, malpositioned aortic cannula, aortic dissection, inadequate anticoagulation, or cold agglutination
Distension of heartPoor venous drainage, inadequate venting, increased regurgitation, or shunting
High coronary sinus pressure (during retrograde cardioplegia)Small coronary sinus, malpositioning of catheter

Hemodynamic Changes and Management After CPB (Table 24.6)

Clinical ScenariosSBPCOPAPCVPManagement Options
HypovolemiaVolume administration
LV failureInotropes, IABP, CPB, and LVAD
RV failureInotropes, increase MAP, decrease PVR, CPB, and RVAD
Biventricular failureTreatment for LV and RV failure
Low SVRNormalNormalVasopressors; decrease anesthetic
High SVRNormalNormalVasodilators; deepen anesthetic
pHTNInotropes with pulmonary dilating properties (e.g., milrinone), nitrous oxide; reinstitute CPB

MAP, mean arterial pressure; CO, cardiac output; PA, pulmonary artery pressure; CVP, central venous pressure; LV, left ventricle; RV, right ventricle; IABP, intra-aortic balloon pump; CPB, cardiopulmonary bypass; LVAD, left ventricular assist device; RVAD, right ventricular assist device; PVR, pulmonary vascular resistance; pHTN, pulmonary hypertension.


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