Virtually all patients undergoing open‐heart surgery will have some element of postoperative pulmonary dysfunction.1 However, in the vast majority of patients, it is well tolerated with minimal impairment in oxygenation and ventilation. Thus, it is possible and desirable in most patients to achieve early endotracheal extubation within the first 4–6 hours after surgery. This reduces pulmonary complications, encourages earlier mobilization, and reduces costs and the hospital length of stay.2,3 Some centers recommend extubation in the operating room (OR) in lower‐risk patients and have documented improved outcomes and lower costs.4–7
The use of general anesthesia and a median sternotomy incision for most open‐heart operations and the use of the internal thoracic artery (ITA) for virtually all coronary bypass operations have significant adverse effects on pulmonary function and chest wall mechanics.8–10 Although the use of cardiopulmonary bypass (CPB) is associated with a systemic inflammatory response that has been incriminated as the major cause of postoperative pulmonary dysfunction, studies comparing postoperative pulmonary function in patients undergoing on‐ and off‐pump surgery have not demonstrated a significant difference, except perhaps in patients with advanced pulmonary disease.11–14 Thus, anesthetic management and intensive care unit (ICU) protocols to achieve early extubation should be the goal after both types of operations.
Minimally invasive incisions preserve a more stable chest wall and have less impact on chest wall mechanics. Ministernotomies for aortic valve replacement, for example, are associated with less atelectasis than a full sternotomy incision.15 Both sternotomy and thoracotomy incisions produce moderate pain with splinting, which can be minimized using epidural or intercostal analgesia or a continuous infusion pump (On‐Q, Avanos Medical Inc).16–18 Generally, pulmonary function is better preserved with limited incisions. However, the potential adverse influence of CPB on gas exchange will still be noted following minimally invasive valve operations that require CPB.
Postoperative respiratory impairment and the likelihood of “delayed extubation” or the need for prolonged ventilatory support can be predicted fairly reliably based on clinical variables.19–26 Careful preoperative evaluation for obstructive or restrictive pulmonary disease with review of baseline arterial blood gases (ABGs) should identify patients at high risk for pulmonary complications after surgery. However, most patients without severe preoperative respiratory compromise have adequate pulmonary reserve to tolerate the insults imposed by cardiac surgery. Standard protocols for ventilatory management and early extubation can be applied to all but the very highest‐risk patients, with excellent results. In approximately 5–10% of patients, mechanical ventilatory support beyond 48 hours is necessary because of marked hemodynamic compromise, poor oxygenation, or inadequate ventilation.
An understanding of the postoperative changes in pulmonary function, basic concepts in oxygenation and ventilation, routine pulmonary management, and contributing factors to respiratory dysfunction allows for the early identification and treatment of problems to optimize the recovery of pulmonary function.
II. Postoperative Changes in Pulmonary Function
During the early postoperative period, the principal mechanisms underlying poor gas exchange with borderline oxygenation are ventilation/perfusion (V/Q) mismatch and intrapulmonary shunting.27 Comparison of pre‐ and postoperative pulmonary function tests has shown a reduction of about 30–50% in many parameters, including the peak expiratory flow rate (PEFR), forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), functional residual capacity (FRC), forced expiratory flow at 50% of vital capacity (FEF50), maximum voluntary ventilation, and expiratory reserve volume after surgery.10 These abnormalities persist in the postoperative period and may only partially recover out to 3.5 months.8 Contributing factors include the following issues:
General anesthetics, neuromuscular relaxants, and narcotics decrease the central respiratory drive and contribute to decreased respiratory muscle function.
The median sternotomy incision produces chest wall splinting that reduces alveolar ventilation and most pulmonary function testing variables.
The presence of chest tubes for mediastinal or pleural drainage impairs respiratory function, although less so with subxiphoid than intercostal insertion sites for pleural tubes.28
Harvesting of the ITA is associated with a decrease in chest wall compliance and deterioration of pulmonary function to a greater degree than when no ITA is harvested.29 Furthermore, pleural entry for ITA harvesting is associated with even more deterioration in pulmonary function in both on‐ and off‐pump surgery,30–32 and is associated with a higher incidence of bleeding, pleural effusions, and atelectasis.32 Interestingly, a few studies have shown that the incidence of respiratory complications and the degree of respiratory impairment is no greater if bilateral, rather than just unilateral, ITA harvesting was performed in patients without preexisting lung disease.33,34
Diaphragmatic dysfunction from phrenic nerve injury may result from direct injury or devascularization during harvesting of the IMA, the latter arguably being more frequent in diabetic patients.35–38 The use of ice slush without an insulation pad may also contribute to phrenic nerve injury, with an eightfold increase noted in one study.36
CPB produces numerous problems that can contribute to postoperative respiratory dysfunction.1,39 It is curious that most studies demonstrate comparable deterioration in pulmonary function after on‐ and off‐pump surgery when all of these factors are taken into consideration.
Cardiogenic pulmonary edema may result from hemodilution, fluid overload, and reduction in oncotic pressure. Postcardiotomy left ventricular (LV) dysfunction with elevated pulmonary artery (PA) pressures may contribute to pulmonary edema and lead to impairment of right ventricular (RV) function.
Noncardiogenic interstitial pulmonary edema is a manifestation of the “systemic inflammatory response”, which produces an increase in endothelial permeability and accumulation of extravascular lung water; this also decreases lung surfactant, contributing to atelectasis. Contributory factors to this syndrome include:
Complement activation
Release of cytokines and other inflammatory mediators
Pulmonary sequestration of neutrophils activated by blood contact with the extracorporeal circuit, resulting in release of proteolytic enzymes, such as neutrophil elastase, that may damage tissue and increase alveolar‐endothelial permeability.
Hyperoxia may increase oxygen free‐radical damage.
Pulmonary ischemia‐reperfusion injury or failure to ventilate the lungs during CPB may impair pulmonary function.40 The efficacy of gas exchange post‐pump may be improved if the lungs remain inflated with CPAP during CPB.41
Blood transfusions introduce microemboli and proinflammatory mediators that may elevate pulmonary vascular resistance and PA pressures, increase inspiratory pressures, impair oxygenation, and reduce RV function. Transfusions are associated with an increased risk of pulmonary morbidity that may be also associated with the development of transfusion‐related acute lung injury (TRALI), which is considered an immune‐mediated phenomenon, and transfusion‐associated circulatory overload (TACO), caused by rapid transfusion of blood to a patient with preexisting fluid overload (see page 482).42,43
Preexisting conditions may impair postoperative pulmonary function, such as chronic obstructive pulmonary disease (COPD) with any active bronchitic component, and obesity, which produces V/Q imbalance and impairs oxygenation.44,45
III. Routine Ventilator, Sedation, and Analgesia Management
For open‐heart surgery, patients generally receive a balanced anesthetic regimen consisting of a narcotic (fentanyl, sufentanil, or remifentanil), an inhalational anesthetic, a neuromuscular blocker, and a sedative, such as propofol. Surgical outcomes appear comparable with a balanced technique using “volatile anesthesia” and total intravenous anesthesia.46 In addition to taking the patient’s underlying cardiac disease and comorbidities into consideration, the use and dosing of medications should be modified based upon plans for postoperative extubation. Generally, remifentanil is used only in patients for whom very early extubation is planned because of its rapid offset of action. This allows for very early awakening, and is associated with less respiratory depression and less atelectasis after extubation.
If not extubated in the OR, the patient should be placed on a volume‐cycled respirator for full ventilator support upon arrival in the ICU, using either the synchronized intermittent mandatory ventilation (SIMV) or assist/control (A/C) mode (Table 10.1). The patient remains anesthetized from the residual effects of narcotics, anxiolytic medications, and muscle relaxants given during surgery. Before the patient can initiate and achieve adequate spontaneous ventilation, controlled ventilation will provide efficient gas exchange and decrease oxygen consumption by reducing the work of breathing. This may be very important during the first few postoperative hours when hypothermia, acid–base and electrolyte disturbances, and hemodynamic instability are most pronounced.
The tidal volume and respiratory rate are selected to achieve a minute ventilation of approximately 100 mL/kg/min. Low tidal volumes may be preferable to higher ones, which have been associated with the development of adult respiratory distress syndrome (ARDS) after surgery.39 In contrast, patients with COPD often benefit from lower respiratory rates and higher tidal volumes with increased inspiratory flow rates. The latter allows more time for the expiratory phase and can reduce the potential for developing high levels of “auto‐PEEP” and air‐trapping that may adversely affect hemodynamics. Lower tidal volumes with higher respiratory rates are often beneficial for patients with restrictive lung disease.
A low level (5 cm H2O) of PEEP is routinely added to the respiratory circuit to prevent atelectasis. Despite this common practice, studies suggest that this level of PEEP does not reopen atelectatic lung and produces no significant improvement in oxygenation over zero PEEP.47 A PEEP level of 10 cm H2O or higher is usually necessary to improve lung recruitment, but it must be used judiciously because it may reduce venous return and impair RV and LV function. Caution is required when the patient is hypovolemic from peripheral vasodilation or when RV function is impaired.
Continuous pulse oximetry is used during mechanical ventilation with display of the arterial oxygen saturation (SaO2) on the bedside monitor. This can bring attention to abrupt changes in oxygenation and should obviate the need to obtain ABGs on a frequent basis in the stable patient. Concern should be raised when the SaO2 is <95%.
Although not commonly used in the ICU, capnography (end‐tidal CO2) can be used to provide a relative assessment of the level of PCO2, although it is inaccurate when V/Q mismatch is present. For example, the end‐tidal CO2 will be much lower than the PCO2 when there is an increase in physiologic dead space (increased V/Q). It is also affected by the degree of CO2 production, the minute ventilation, and the cardiac output. Nonetheless, an abrupt change in the contour of the capnogram signifies an acute problem with the patient’s ventilatory status, hemodynamics, or metabolic state.
A chest x‐ray should be checked after arrival in the ICU. The position of the endotracheal tube, Swan‐Ganz catheter or any central line, and intra‐aortic balloon pump (IABP) should be identified. The lung fields should be evaluated for lung expansion/atelectasis, pneumothorax, undrained pleural effusion, pulmonary edema, or infiltrates. Attention should be paid to the width of the mediastinum, primarily for later comparison in the event of postoperative hemorrhage.
An initial ABG should be checked about 15–20 minutes after arrival in the ICU. The FiO2 is initially set at 1.0 as a safety margin until the patient’s oxygenation is assessed. Then it should be reduced to 0.40 and the tidal volume and respiratory rate adjusted to maintain the ABGs within a normal range. The extent of hypothermia should be taken into consideration when making these adjustments, anticipating that the PCO2 will rise as the patient warms. The metabolic demand and CO2 production are decreased 10% for every degree less than 37 °C. Acceptable ABGs include:
PaO2 >80 torr (SaO2 >95%)
PCO2 32–48 torr
pH 7.32–7.48
Adequate sedation and analgesia must be provided in the early postoperative period to minimize anxiety, pain, and hemodynamic stress, which may contribute to myocardial ischemia and hypertension. This often seems difficult when the goal is to have a stable and comfortable patient who is awakening from anesthesia with an indwelling endotracheal tube.
For patients extubated in the OR, adequate analgesia must be provided while minimizing sedation. Thoracic epidural analgesia, a parasternal injection of bupivacaine (0.5% 2 mg/kg in 50 mL injected prior to sternal closure), or a continuous subcutaneous bupivacaine infusion of 4 mL/h × 48 hours using the On‐Q Pain Relief System are beneficial in reducing pain.16–18,48–51 Patient‐controlled IV and thoracic epidural analgesia can also be used with comparable pain relief.52,53 Nonsteroidal anti‐inflammatory drugs or IV acetaminophen are useful nonsedating analgesics that may supplement the use of low‐dose narcotics.
Most patients will arrive in the ICU sedated from narcotics and short‐acting medications, such as propofol (usually at a dose of 25 μg/kg/min), started at the conclusion of surgery. Once standard criteria for weaning are met, the propofol infusion is weaned off over a short period of time. Most patients will awaken within 20 minutes of termination of a propofol infusion, although it may take several more hours before they can be extubated. The offset of propofol is related to its dose, the duration of use, and the patient’s body habitus. For example, with light sedation for up to 24 hours, emergence occurs in only 13 minutes, but in heavily sedated patients, it may take up to 25 hours!54
Dexmedetomidine is an α‐2 adrenergic agonist that may be used as an alternative to propofol when very early extubation is planned or when weaning of propofol is poorly tolerated. It may be started in the OR or later with a loading dose of 1 μg/kg over 10 minutes followed by a continuous infusion of 0.2–1.5 μg/kg/h. It provides analgesia, anxiolysis, and sympatholysis, but only mild sedation and no amnesia. It allows for use of lower doses of other medications and can be continued after extubation. In comparison with propofol and midazolam, dexmedetomidine is generally associated with earlier extubation, a lower risk of delirium, and also a lower risk of acute kidney injury.55–61 However, it is associated with more hypotension and bradycardia and more pain. It remains a useful alternative for patients requiring mechanical ventilation for over 24 hours.62–65
If delayed extubation is anticipated, propofol remains an excellent choice for several days and may be converted to fentanyl for longer‐term sedation. Although use of dexmedetomidine has only been recommended for 24 hours, several studies have found it to be comparable to or better than propofol or midazolam for long‐term sedation.62–65
Numerous options can be used to optimize perioperative analgesia.
Most commonly, initial analgesia consists of IV narcotics, which are then transitioned to oral medications. With plans for early extubation, lower doses of narcotics should be selected to minimize respiratory depression. Small doses of IV narcotics or a continuous infusion of narcotics (such as morphine sulfate 0.02 mg/kg/h for patients under age 65 and 0.01 mg/kg/h for patients over age 65) may be given to provide analgesia and blunt the sympathetic response while minimizing respiratory depression associated with the peaks and valleys of bolus doses of narcotics. Use of low‐dose narcotics may often be given safely after the patient is extubated, but elderly patients are more prone to persistent respiratory depression and delirium with narcotics.
An alternative approach is to give ketorolac (Toradol) 30 mg IV just before propofol is discontinued to decrease narcotic requirements. Its use should be limited to 72 hours, and it should be avoided in patients with renal dysfunction or concerns about mediastinal bleeding. Other nonsteroidal anti‐inflammatory medications, such as indomethacin 50 mg PR or ibuprofen given with a proton‐pump inhibitor, may be administered safely as well.66
Intravenous acetaminophen may be effective in providing analgesia after cardiac surgery, but a significant benefit of reducing the requirement for opioids for pain control has not been demonstrated.67 One study did demonstrate that IV acetaminophen given with propofol or dexmedetomidine significantly and equivalently reduced the incidence of delirium.68
Epidural narcotics are beneficial in providing analgesia, but there may be reluctance to place these catheters because of concerns about heparinization and the risk of producing an epidural hematoma.
Patient‐controlled analgesia (PCA) using narcotics (morphine, fentanyl, or remifentanil) provides adequate analgesia with few side effects in patients with a low pain threshold.48,69,70
Arterial blood gases should be checked if there is a significant change in the patient’s clinical picture or if noninvasive monitoring (pulse oximetry or end‐tidal CO2) suggests a problem. A cautious approach is to check the ABGs after 4–6 hours, before initiating weaning, and just before extubation. Once criteria for weaning have been met, the patient may be given a spontaneous breathing trial (SBT) on continuous positive airway pressure (CPAP) with 5 cm of PEEP. If satisfactory mechanics and ABGs are present, the patient is extubated.
Respiratory rate (usually in the IMV mode): 10–12/min
FiO2: 1.0
PEEP: 5 cm H2O
Display pulse oximetry on bedside monitor
Chest x‐ray after arrival in ICU (or in OR)
Check ABGs 15–30 minutes after arrival
Reduce FiO2 to 0.4 as long as the O2 sat is >95%
Adjust ventilator settings to maintain PCO2 >30 torr with pH 7.30–7.50
Propofol 25–75 μg/kg/min; gradually decrease dose once standard weaning criteria are present and then initiate weaning when patient is mentally alert with reversal of neuromuscular blockade
Utilize dexmedetomidine if propofol weaning is not tolerated
IV. Basic Concepts of Oxygenation
The first of the two primary goals of mechanical ventilation is the achievement of satisfactory arterial oxygenation. Although this is usually assessed by the arterial PO2 (PaO2), it should be remembered that the PaO2 is a measurement of the partial pressure of oxygen dissolved in the bloodstream – it indirectly reflects oxygen saturation of hemoglobin (Hb) in the blood and does not measure the oxygen content of the blood.
Blood oxygen content is determined primarily by the Hb level and the amount of oxygen bound to Hb (the SaO2), and to a lesser extent by that dissolved in solution (the PaO2). Each gram of Hb can transport 1.39 mL of oxygen per 100 mL of blood (vol %), whereas each 100 torr of PaO2 transports 0.031 vol %. Thus, correction of anemia does significantly more to improve blood oxygen content than does raising the level of dissolved oxygen (PaO2) by increasing the FiO2.
The oxygen–hemoglobin dissociation curve demonstrates the relationship between PaO2 and O2 saturation (Figure 10.1). The amount of oxygen delivered to tissues depends on a number of factors that can affect this relationship. A shift to the left, as noted with hypothermia and alkalosis, indicates more avid binding of oxygen and less release to the tissues, whereas a shift to the right, noted with acidosis, improves tissue oxygen delivery. Blood transfusions have very low levels of 2,3‐DPG, which will also result in a leftward shift of the curve, resulting in less tissue oxygen delivery.
Note that a PaO2 of 65 torr corresponds to an O2 saturation of 90%, but this lies at the shoulder of the sigmoid curve. Below this level, a small decrease in PaO2 causes a precipitous fall in O2 saturation. Therefore, although a PaO2 of 60–70 torr is certainly acceptable, there is little margin of safety in the event of a sudden change in hematocrit (HCT), cardiac output, or ventilator function.
The correlation of PaO2 and oxygen saturation dissociates when methemoglobinemia is present. This occurs when more than 1% of available Hb is in an oxidized form (methemoglobin) and unable to bind oxygen. It has been noted in patients receiving high‐dose intravenous nitroglycerin (IV NTG) (over 10 μg/kg/min for several days), especially when hepatic or renal dysfunction is present.71 When methemoglobinemia is present, the PaO2 may be high, but the O2 saturation measured by oximetry is lower than expected because the O2 saturation of metHb is only 85%. Because some of the hemoglobin is not carrying oxygen, ischemia may be exacerbated by a reduced oxygen‐carrying capacity despite the high PaO2. It should be remembered that the O2 saturation reported back from the blood gas laboratory is usually calculated from a nomogram based on the PaO2, pH, and temperature – it is not measured directly.
Pulse oximetry is beneficial in measuring O2 saturations continuously when the PaO2 is low, but, because it measures several forms of hemoglobin, it will overestimate the oxyhemoglobin content when methemoglobinemia is present.
The amount of oxygen available to tissues depends not only on the SaO2, pH, and the blood Hb content, but also on the cardiac output. An attempt to improve oxygen saturation at the expense of a decrease in cardiac output is counterproductive. This may be noted when increasing levels of PEEP are applied in the hypovolemic patient.
The PaO2 is generally used to assess the adequacy of oxygenation, but its relationship to the FiO2 should be examined. The PaO2/FiO2 ratio is a reliable predictor of pulmonary dysfunction and can also be used to assess whether weaning is feasible. The calculation of the alveolar–arterial oxygen difference (D(A–a)O2) also takes the FiO2 into consideration and is a very sensitive index of the efficiency of gas exchange. This is calculated according to the following equation:
In patients with normal pulmonary function, the PaO2 should usually be greater than 350 torr on 100% oxygen immediately after surgery. The FiO2 should then be decreased to 0.40 as tolerated to prevent adsorption atelectasis and oxygen toxicity. However, it should not be lowered any further, even if the PaO2 seems high, in order to maintain a safety margin for oxygenation in the event that hypotension, dysrhythmias, bleeding, or a pneumothorax should suddenly develop.
The definitions of ARDS and TRALI include poor oxygenation with a PaO2/FiO2 ratio less than 200 and 300, respectively.39 However, such ratios are not that uncommon following open‐heart surgery, especially in patients with significant COPD or in hypertensive smokers with low preoperative PaO2 levels.72 Impaired oxygenation may be both cardiogenic and noncardiogenic in etiology, caused by fluid overload and/or a transient capillary leak from CPB. Acute pulmonary dysfunction is of concern when the PaO2/FiO2 ratio is <150. This would correspond, for example, to a PaO2 of 150 torr on an FiO2 of 1.0 or 75 torr on an FiO2 of 0.5. This is more likely to occur in patients with advanced age, obesity, pulmonary hypertension, low cardiac output syndromes, surgery requiring very long pump runs, and postoperative renal dysfunction.72,73
Some patients with chronic pulmonary disease have a relatively “fixed shunt” with a PaO2 of 60–70 torr despite a high FiO2 and moderate levels of PEEP. It is best to avoid an FiO2 greater than 0.5 for more than a few days, if possible, to avoid complications associated with oxygen toxicity. Keep in mind that a PaO2 of 65 torr corresponds to an O2 saturation of 90% and is acceptable in these patients.
Figure 10.1Oxygen–hemoglobin dissociation curve. The sigmoid curve delineates the saturation of hemoglobin at increasing levels of PO2. Note that a PO2 of 65 mm Hg (torr) corresponds to a saturation of 90%. Higher levels of O2 produce only small increments in blood oxygen content, but a PO2 below this level results in a precipitous fall in O2 saturation. A shift of the curve to the left, as is noted with alkalosis and hypothermia, increases the affinity of hemoglobin for oxygen and decreases tissue oxygen delivery. A shift to the right occurs with acidosis and improves tissue oxygen delivery.
V. Basic Concepts of Alveolar Ventilation
The second goal of mechanical ventilation is that of alveolar ventilation, which regulates the level of PCO2. This is controlled by setting the tidal volume and the respiratory rate on the ventilator and should provide a minute ventilation of approximately 8 L/min. The level of PCO2 is determined most reliably from ABGs. Noninvasive monitoring with end‐tidal CO2 gives a reasonably accurate assessment of PCO2, although the correlation depends on the amount of physiologic dead space.
Hypocarbia
Mild hypocarbia (PCO2 of 30–35 torr) is quite acceptable in the immediate postoperative period, especially when the patient is hypothermic. It produces a mild respiratory alkalosis that:
Decreases the patient’s respiratory drive
Allows for increased CO2 production to occur from the increased metabolic rate associated with warming and shivering without producing respiratory acidosis. Remember that the metabolic rate is decreased 10% for every degree below 37 °C, and most patients return to the ICU from the OR with a core temperature of around 35–36 °C.
Compensates for the mild metabolic acidosis that frequently develops from hypoperfusion and peripheral vasoconstriction when the patient is still hypothermic.
A more profound respiratory alkalosis has potential detrimental effects and must be avoided.
It leads to hypokalemia and may predispose to ventricular arrhythmias.
It shifts the oxygen–hemoglobin dissociation curve to the left, decreasing oxygen release to the tissues.
It induces cerebral vasoconstriction, reducing cerebral blood flow.
Note: hypocarbia with a normal or somewhat acidotic pH, sometimes resulting from tachypnea of unclear etiology, may be masking a metabolic acidosis that may need to be evaluated and addressed.
Management of hypocarbia is best accomplished by lowering the IMV rate. The amount of dead space in the tubing can also be increased. Adding 10% of the tidal volume in mL/kg to the tubing will raise the PCO2 approximately 5 torr.
Although the addition of PEEP to the ventilator circuit usually prevents alveolar collapse by maintaining volume in the lungs above the critical closing volume, alveolar hypoventilation and atelectasis are best prevented by maintaining an adequate tidal volume, which at the minimum should be 6 mL/kg. The tidal volume should usually not be lowered any further unless the peak inspiratory pressures are excessively high (over 35–40 cm H2O).
Occasionally, hypocarbia may develop in a patient who is “fighting the ventilator” with repeated triggering. These patients seem to be unable to breathe in synchrony with delivered breaths, such that the phases of respiration vary between the patient and the ventilator. This may be noted in patients with hypoxia, mental confusion, delirium, anxiety, or inadequate sedation. Some patients also become very agitated when spontaneous breaths are initiated against high levels of PEEP. Patient–ventilator dyssynchrony usually occurs in the assist mode when the patient’s breath does not trigger the demand valve due to too insensitive a trigger. It may also occur when the tidal volume is set too high with a low inspiratory flow rate, resulting in an increase in the inspiratory time. Thus the patient becomes short of breath and has an increased work of breathing.
It is important to assess the adequacy of ventilation and oxygenation first and ensure that there are no major pleuropulmonary issues (mucus plugs, bronchospasm, tension pneumothorax) or mechanical issues with the ventilator.
The ventilator settings can be readjusted to increase the inspiratory flow rate or increase the time between the end of inspiration and the beginning of expiration with an end‐inspiratory pause.
If no specific issues can be identified, additional sedation or selection of a different medication (propofol, fentanyl, or dexmedetomidine) and/or paralysis may be necessary to minimize the patient’s respiratory drive.
Full ventilation is then resumed in the controlled mandatory ventilation (CMV) mode. PEEP levels should be decreased to 5 cm H2O or less if PaO2 permits.
Pressure support ventilation (PSV) (see page 496) increases the comfort of the spontaneously breathing patient and may reduce the work of breathing.
Hypercarbia
Hypercarbia indicates that the minute ventilation provided by the ventilator is inadequate to meet ventilatory demands. Adjustment of ventilator settings must accommodate the progressive increase in PCO2 that occurs during the early postoperative period as the metabolic rate increases from warming and postanesthetic shivering. During the weaning process, a slightly elevated PCO2 in the range of 48–50 torr is usually acceptable, since the patient is still somewhat sedated. Higher levels of PCO2 usually mean that the patient is not awake enough to maintain adequate ventilation.
A lower tidal volume may be requested by the surgeon to minimize tension on a short ITA pedicle. In these patients, it is preferable to increase the IMV rate rather than the tidal volume to compensate for an elevated PCO2.
During weaning from mechanical ventilation, hypercarbia may represent compensatory hypoventilation in response to a metabolic alkalosis. This frequently results from aggressive diuresis in the early postoperative period. Use of acetazolamide (Diamox) 250–500 mg IV q8–12h in conjunction with other diuretics is beneficial in correcting a primary metabolic alkalosis. However, the metabolic component should only be partially corrected in patients with chronic CO2 retention.
Manifestations of significant hypercarbia and respiratory acidosis include tachycardia, increasing PA pressures, hypertension, and arrhythmias.
Treatment
Moderate hypercarbia in the fully ventilated patient is corrected by increasing either the respiratory rate or the tidal volume, as long as the peak inspiratory pressure is less than 30 cm H2O.
Significant hypercarbia usually indicates a mechanical problem, such as ventilator malfunction, endotracheal tube malposition, or a pneumothorax. The latter may still be present even when bilateral breath sounds seem to be heard above all the other extraneous noises of the ICU setting. Temporary hand‐bag ventilation, adjustment of ventilator settings, repositioning of the endotracheal tube, or insertion of a chest tube will usually resolve the problem.
Sedation can be obtained with short‐acting narcotics or other sedatives. These include:
Propofol 25–75 μg/kg/min
Morphine sulfate 2.5–5 mg IV q1–2 h
Dexmedetomidine 1 μg/kg over 10 minutes followed by a continuous infusion of 0.2–1.5 μg/kg/h. The loading dose provides sedation within 10–15 minutes after the infusion is started. The mix is 2 mL/50 mL normal saline, which gives a final concentration of 4 μg/mL.
Fentanyl drip can be used when a more prolonged period of sedation is indicated. The usual dose is a 50–100 μg IV bolus over five minutes with subsequent doses every two hours prn or an infusion of 50–200 μg/h of a 2.5 mg/250 mL mix.
Midazolam 2–4 mg IV q1h or 2–10 mg/h as a continuous infusion is often given along with fentanyl. This can reduce the total narcotic requirement but will delay extubation.
Shivering is best controlled using meperidine 25–50 mg IV or dexmedetomidine.74 More persistent and refractory shivering that is deleterious to hemodynamics may need to be controlled with pharmacologic paralysis. It is important never to paralyze an awake patient without also administering sedation. Paralytic agents, including vecuronium or atracurium, can be used if these medications fail to control shivering (see Appendix 12 for doses).
If the patient becomes hypercarbic because of “fighting the ventilator” and is receiving inadequate tidal volumes, the steps noted in section B.3.b (change in ventilator settings, sedation, and conversion to PSV) will allow for improved ventilation.
The persistence of hypercarbia during the weaning process requires further investigation. In the absence of preexisting pulmonary dysfunction, concerns such as a neurologic event or phrenic nerve injury should be entertained. Issues related to the management of acute and chronic respiratory insufficiency are presented later in this chapter.
VI. Considerations to Achieve Early Extubation
Some centers have standard protocols to extubate patients in the OR and have shown this to be safe with a low incidence of reintubation and a reduction in ICU and postoperative length of stay and costs.4–7,75,76 Anesthetic protocols often use lower doses of fentanyl or remifentanil combined with propofol and thoracic epidural analgesia for pain control. Identification of favorable factors for early extubation is useful in deciding which patient will benefit from this approach. A predictive risk score was devised which combined factors which independently were found to be associated with successful extubation in the OR. These included younger age, lower BMI, higher albumin, absence of COPD or diabetes, a less invasive approach, isolated CABG (especially OPCAB), elective surgery, and use of lower doses of fentanyl.6 Predictive factors in other studies included good LV function, shorter pump times, and OPCABs.76
A more common approach is to transfer the patient to the ICU sedated with propofol or dexmedetomidine with some residual narcotic effect. This provides a brief period for monitoring and observation while the patient warms to normothermia, achieves hemodynamic stability, and has the degree of mediastinal bleeding assessed. Then, either “ultrafast extubation” within 1–3 hours or “early extubation” within 4–6 hours can be achieved. Compared to maintaining a patient on the ventilator for longer periods of time, these approaches decrease pulmonary complications, require less medication, and allow for more rapid mobilization and a faster recovery. Virtually all studies have demonstrated the safety and efficacy of “early extubation” with documentation of decreased length of stay and hospital costs, with probably little difference between the two protocols. Having a multidisciplinary, protocol‐driven approach in the ICU is effective in expediting extubation.2,3
The important concept is that extubation, no matter when it is accomplished, requires that standard criteria be met. It should never represent “premature” extubation, when discontinuation of mechanical ventilation may prove deleterious to the patient’s recovery. Following appropriate protocols, overnight extubation appears to be safe with a very low risk of reintubation.77,78
The potential disadvantages of very early extubation must always be taken into consideration. These include:
Increased sympathetic tone causing tachycardia and hypertension that can adversely affect myocardial recovery and can contribute to myocardial ischemia during the first 4–6 hours in the ICU.
Failure to differentiate between comfortable breathing and persistent residual narcotic/sedative effect that may be worsened by additional use of narcotics.
Increased risk of bleeding if hypertension develops.
More chest pain and splinting if inadequate analgesia is given. This may result in hypoventilation and atelectasis, potentially contributing to oxygen desaturation and the need for reintubation. Ineffective lung expansion is less capable of tamponading chest wall bleeding than positive‐pressure ventilation (PPV). Thus, provision of adequate analgesia without respiratory depression is a critical aspect of an early extubation protocol.
Compromise of ventilatory status if there is significant fluid overload.
The selection of patients for early extubation should not be overly restrictive, yet it does depend on an understanding of potential risk factors for pulmonary dysfunction and delayed extubation. Some of these factors can be modified or influenced by therapeutic measures, whereas others cannot. The Society of Thoracic Surgeons (STS) risk model for operative mortality also provides a risk calculator for numerous complications, including prolonged ventilation beyond 48 hours. This can be accessed at the STS website (www.sts.org). One study, in fact, showed that the STS mortality risk had the highest correlation with the need for prolonged ventilation.23 In addition, several studies have identified risk factors for acute pulmonary dysfunction upon arrival in the ICU and for increased respiratory morbidity and prolonged ventilation (Figure 10.2).19–26,79–81 All of these factors must be taken into consideration when deciding whether early extubation is feasible or whether more prolonged support will be in the patient’s best interest. Generally, about 5–10% of patients require ventilation for over 48 hours.24,25 Evaluating these risk factors, one can define some exclusion criteria for early extubation (Table 10.2). Factors that delay extubation include:
Preoperative factors: older patient age, females, low and high body surface areas, preexisting impairment of cardiac (NYHA class IV/HF, poor LV function, shock), respiratory (smoking, severe COPD, preoperative intubation and ventilation), and renal (elevated creatinine) subsystems, diabetes,82 urgent or emergent surgery with hemodynamic instability, and active endocarditis.
Intraoperative factors: reoperations, long duration of CPB (often for combined valve‐CABGs or double valve operations), requirement for multiple blood products, significant fluid administration, elevated blood glucose on CPB, poor hemodynamic performance requiring inotropes or IABP support, and perioperative MI.
Postoperative factors: hypothermia upon arrival in the ICU,83 excessive mediastinal bleeding, re‐exploration for bleeding or use of multiple blood products, low cardiac output syndromes, sepsis, pneumonia, renal dysfunction, stroke, or depressed level of consciousness, and GI bleeding.
The pharmacologic protocol for postoperative sedation should be similar for most patients, since propofol or dexmedetomidine can be used for several days if prolonged support is necessary. However, use of a longer‐acting medication (such as fentanyl) can be considered. Lorazepam has been used successfully as well, but it is associated with a higher incidence of delirium and is not recommended.84 Use of standard protocols and criteria for weaning should allow for extubation when clinically indicated, even if it takes a little longer than desired. The duration of intubation should not be based on risk factors alone or dictated by a rigid time schedule. Of interest, although smoking is a significant risk factor for postoperative morbidity, one study showed that it is advantageous to extubate smokers earlier rather than later to reduce the risk of respiratory complications.85
Figure 10.2Logistic model to predict risk of postoperative respiratory failure following cardiac surgery. A score >18 had a greater than 80% risk of requiring prolonged ventilation >48 hours.
(Reproduced with permission from Reddy et al. Ann Thorac Surg 2007;84:528–36.)25
Table 10.2 Relative Exclusion Criteria for Early Extubation
Preoperative Criteria
Intraoperative Criteria
Postoperative Criteria
Pulmonary edema
Deep hypothermic circulatory arrest
Mediastinal bleeding
Intubated
Coagulopathy
Hemodynamic instability or need for an IABP
Cardiogenic shock
Severe myocardial dysfunction
Respiratory failure or hypoxia
Sepsis
Long pump run >4–6 hours
Stroke
VII. Therapeutic Interventions to Optimize Postoperative Respiratory Performance and Early Extubation
Recognition of risk factors for pulmonary dysfunction can direct attention to potential therapeutic steps that can be taken to optimize postoperative respiratory performance. The treatment of modifiable factors, performance of a proficient operation, and aggressive postoperative management of all subsystems are essential to achieve early extubation and minimize the risk of postoperative respiratory failure.
Preoperative considerations
Pulmonary function testing (PFTs) with room air ABGs should be considered in patients with respiratory symptoms that cannot be attributed to their cardiac disease. Although the patient’s clinical limitations (climbing stairs, walking short distances) often supersede abnormal PFTs in determining operability, markedly abnormal PFTs can provide an indication of the patient’s risk for pulmonary complications and mortality. Patients with a PO2 <60 torr or PCO2 >50 torr on room air, and those who are oxygen‐dependent or on chronic steroids for advanced lung disease, should be considered at very high risk for respiratory complications. Alternative procedures, such as coronary stenting or transcatheter approaches for valve pathology, should be considered.
Attempt to convince the patient to stop cigarette smoking at least one month prior to surgery. Recommend use of nicotine patches or start the patient on varenicline (Chantix) or bupropion HCL (Wellbutrin, Zyban).
Treat all active cardiopulmonary disease processes, such as pneumonia, bronchospasm, or CHF, to optimize oxygenation and ventilatory status.
Consider intensive inspiratory muscle training in patients at high risk for pulmonary complications.86
Transfuse profoundly anemic patients to a HCT of at least 28% prior to surgery to minimize the degree of hemodilution during surgery and the requirement for blood and blood components.
Optimize hemodynamic performance and renal function as best as possible prior to surgery.
Intraoperative considerations
Modify the CPB circuit to minimize the inflammatory response, hemodilution, and bleeding: use membrane oxygenators, centrifugal pumps, biocompatible circuits, or miniaturized circuits, if available; avoid cardiotomy suction; consider retrograde autologous priming and perhaps use of leukocyte‐depleting filters. Use of steroids to potentially minimize the inflammatory response has not been shown to improve outcomes and cannot be recommended.39,87,88
Process shed mediastinal blood at the conclusion of CPB through a cell‐saving device to eliminate fat, particulate matter, and vasoactive mediators. This has been shown to improve cardiopulmonary hemodynamics and may reduce ventilatory requirements after surgery.89
Minimize fluid administration during CPB or off‐pump surgery.
Perform an expeditious, technically proficient operation with excellent myocardial protection to achieve complete revascularization or satisfactory valve function.
Use inotropic and/or vasopressor support or an IABP as necessary to achieve satisfactory hemodynamic performance (cardiac index >2 L/min/m2) and avoid excessively high filling pressures. Avoidance of hypotension and low cardiac output syndromes may also reduce the risk of acute kidney injury, allowing for more effective diuresis after surgery. Pharmacologic intervention shown to reduce this risk is limited, with only fenoldopam showing some promise.90
Use antifibrinolytic therapy to minimize perioperative bleeding.
Maintain blood glucose <180 mg/dL on CPB with IV insulin.
Consider ventilating the lungs during bypass (shown to improve post‐pump oxygenation).40
Consider hemofiltration to remove fluid in patients with preoperative CHF or renal dysfunction and to remove inflammatory mediators92
Use short‐acting narcotics, inhalational anesthetics, and propofol or dexmedetomidine for sedation to allow for early extubation.
Postoperative considerations
Select medications to provide short‐acting anxiolysis and sedation that either allow the patient to awaken and be extubated within hours of its discontinuation (propofol) or while still being given (dexmedetomidine).
Provide adequate analgesia without producing respiratory depression (continuous low‐dose IV morphine, ketorolac, IV acetaminophen, epidural analgesia, ON‐Q bupivacaine).
Use antihypertensive medications (clevidipine, nitroprusside), rather than sedatives, to control hypertension.
Administer volume judiciously to optimize hemodynamics, and then use diuresis once hemodynamics have stabilized to eliminate extravascular lung water.
Have a restrictive threshold for blood transfusions (HCT in the low 20s) except for patients with hemodynamic compromise (hypotension, tachycardia), oxygenation issues, or end‐organ dysfunction (usually renal) in whom a higher HCT may be beneficial. Although it may seem logical to transfuse profoundly anemic patients in these situations, blood transfusions are initially not that effective in improving oxygen‐carrying capacity and carry multiple potential risks which can worsen pulmonary function.91
Initiate aggressive management of postoperative bleeding, yet have a low threshold for re‐exploration to minimize use of blood products, which can increase pulmonary morbidity, including the risk of TRALI.42,43,93,94 Avoid transfusing blood products to correct abnormal coagulation parameters when bleeding is insignificant.
VIII. Ventilatory Weaning and Extubation in the Immediate Postoperative Period
Criteria for weaning. Weaning a patient from the ventilator depends on the ability and desire of the nursing and medical staffs to identify when the patient is ready to be weaned, and their willingness to initiate weaning when indicated, no matter what time of the day or night, not when it is convenient to do so. The criteria for weaning are noted in Table 10.3.
Method of weaning after short‐term ventilation
Minimize sedation or use dexmedetomidine.
Maintain the FiO2 at 0.5 or below with PEEP of no more than 5–7.5 cm H2O. If the patient still requires a higher level of PEEP, weaning is usually not indicated. If oxygenation is satisfactory, lower the PEEP in 2.5–5 cm H2O increments to 5 cm H2O and initiate weaning.
If the patient is alert with good respiratory efforts and meets the criteria listed in Table 10.3, they may be immediately placed on CPAP of 5 cm H2O for a SBT. Gradual reduction in the IMV rate to “wean” the patient off the ventilator is usually not necessary in the early postoperative period. If the ABGs are acceptable after a 30–60 minute SBT on either T‐piece or CPAP of 5 cm H2O (see extubation criteria below), the endotracheal tube is removed. Obtaining respiratory mechanics may be helpful, but usually is not necessary in the “routine” patient.
Weaning should be stopped and ventilation resumed at a higher rate when there are clinical signs that it is not being tolerated. These signs are noted in Table 10.4.
Note: a rise in PA pressures is often the first hemodynamic abnormality noted in the patient who is not tolerating weaning very well. Tachypnea is the first clinical sign of ineffective weaning.
Extubation criteria include the weaning criteria listed in Table 10.3 as well as the additional considerations noted in Table 10.5.
Extubation may be accomplished from CPAP or T‐piece. Although oxygenation may be slightly better during a CPAP than a T‐piece trial, postextubation oxygenation is frequently better in patients weaned with T‐piece, because the PaO2 declines less than in patients who were extubated from CPAP.95
Additional considerations
Some patients get very agitated when sedatives are weaned. Even though adequate ABGs may be maintained, agitated patients are frequently given more sedation throughout the night with another attempt at weaning in the morning. Steps noted on page 468 may be taken if the patient is breathing dyssynchronously with the ventilator. Gradual weaning of sedation, substituting dexmedetomidine for propofol, assurance from the nurses that “you’re doing well”, and then a very rapid wean to CPAP and extubation is often the best course for these patients.
If the patient was very difficult to intubate in the OR, it is essential to ensure that the ABGs and respiratory mechanics are satisfactory before extubation. Extubation in the middle of the night should be performed cautiously in these patients. An individual experienced in difficult intubations should be present. A flexible laryngoscope, video laryngoscope (GlideScope [Verathon]), or bronchoscope should also be available.
Elderly patients and those with more advanced cardiac disease or hepatic dysfunction often take longer to awaken from anesthesia, even if sedatives are not administered. This may reflect slow metabolism of medications administered intraoperatively or may occasionally represent transient obtundation from borderline cerebral hypoperfusion during surgery or other causes. It is important to resist the temptation to reverse narcotic effect with naloxone. This medication can precipitate severe pain, anxiety, hypertension, dysrhythmias, and bleeding, and may result in recurrent respiratory depression when its effects have worn off. Similarly, flumazenil to reverse benzodiazepines should be avoided early in the postoperative period. Keep in mind that the offset of propofol is significantly greater when doses producing deep sedation are used.54
However, if a patient fails to awaken after 24–36 hours and the question arises as to whether this represents a stroke, encephalopathy, or simply residual sedation, one might consider the cautious use of a reversal agent to sort out the nature of the problem. Naloxone (Narcan) may be given by administering 1–2 mL/min of a mix of a 1 mL vial containing 0.4 mg/mL in 9 mL of NS (0.04–0.08 mg/min) to a total dose of 0.4 mg. Flumazenil is given in a dose of 0.2 mg IV over 30 seconds, followed by additional doses of 0.2 mg to a maximum of 1 mg. To address resedation, additional doses may be given up to a maximum of 3 mg in one hour.
Many patients, especially those who have received supplemental narcotics, will demonstrate excellent respiratory mechanics when stimulated, but then drift off to sleep and become apneic. Constricted pupils may be noted in patients with persistent narcotic effect. These patients are not yet ready for weaning and extubation. Do not confuse comfortable breathing with a persistent narcotic or sedative effect. These tend to be the patients who require reintubation.
Table 10.3 Weaning Criteria from Mechanical Ventilation
Place on facemask or nasal cannula to achieve SaO2 >90%
Consider high‐flow nasal cannula (Oxymizer®) or a BPAP mask for patients with borderline hypoxemia or hypercarbia
Administer adequate analgesia while minimizing sedation (ketorolac, low‐dose narcotics, IV acetaminophen)
Chest x‐ray after pleural tubes are removed
Incentive spirometer/deep breaths q1–2h; use cough pillow
Mobilize as soon as possible; frequent repositioning in bed
Compression stockings (T.E.D.) for VTE prophylaxis; consider Venodyne boots or SC heparin if high‐risk
Aggressive diuresis once hemodynamically stable
Bronchodilators for bronchospasm (consider steroids if severe COPD)
Antibiotics for a positive sputum culture
After extubation, the patient’s breathing pattern, SaO2, and hemodynamics must be observed carefully. Occasionally, especially in the patient who was difficult to intubate, laryngeal stridor may be prominent and may require use of racemic epinephrine, steroids, or even reintubation. Failure to demonstrate a “cuff leak” during PPV when the cuff is deflated usually indicates laryngotracheal edema, which may cause upper airway obstruction after extubation. This phenomenon is uncommon after short‐term intubation, but it may be noted after several days of mechanical ventilation, especially if the patient is fluid overloaded (see page 498).
Because the median sternotomy incision is associated with moderate discomfort and decreased chest wall compliance, patients tend to splint, take shallow breaths, and cough poorly. Oxygenation may be compromised by fluid overload and atelectasis from poor inspiratory effort. It is advisable to supply 40–70% humidified oxygen by facemask for a few days.
If the patient has borderline oxygenation, higher levels of oxygen or some form of noninvasive ventilation (NIV) may be utilized to improve oxygenation and avoid reintubation.96,97
Use of a high‐flow oxygen system is preferable in the patient with moderate hypoxemia or hypercarbia.98,99 It produces more comfortable breathing, reduces the respiratory rate, and improves gas exchange. The oxygen is heated and humidified and supplied at up to 60 L/min and the FiO2 is kept at a constant level. The system decreases anatomic dead space, improves alveolar ventilation, decreases the work of breathing, minimizes atelectasis, improves mucociliary clearance, and reduces airway resistance. Because there is some resistance to expiratory flow, there is an increase in airway pressure, producing some degree of PEEP with an increase in end‐expiratory lung volume.
A nonrebreather mask covers the patient’s nose and mouth and is attached to a reservoir bag, which is continuously filled with oxygen at a rate of 8–15 L/min. The patient inhales oxygen from the reservoir bag and then exhales through a one‐way valve to the atmosphere, thus ensuring that little exhaled gas or room air is inspired during the next breath. Partial rebreather masks lack the one‐way valve, but ensure a higher FiO2 than a simple facemask because of a tighter fit and the oxygen reservoir bag.
Bilevel positive airway pressure (BPAP) is a form of NIV during which the patient breathes spontaneously and each breath is supported by positive pressure. BPAP provides preset inspiratory and expiratory positive airway pressure at two different levels, with the inspiratory pressure usually set at 8–12 cm H2O and expiratory pressure set at 3–5 cm H2O. The pressure difference determines the tidal volume delivered. It is superior to incentive spirometry in improving oxygenation in the first few postoperative days.100 It has also been shown to prevent the increase in extravascular lung water associated with the weaning process that is noted in patients placed on nasal cannula after extubation.101 Although often abbreviated as BiPAP, that is actually the name of a ventilator manufactured by Respironics. Inc.
Continuous positive airway pressure (CPAP) provides a continuous level of positive airway pressure without any ventilatory support. Nasal CPAP masks are helpful in patients with cardiogenic pulmonary edema by preventing alveolar collapse, redistributing intra‐alveolar fluid, improving pulmonary compliance, and reducing the pressure of breathing.102 A study of prophylactic nasal CPAP of 10 cm H2O for at least six hours showed that it improved oxygenation better than CPAP for 10 minutes every four hours, with a lower incidence of pneumonia and reintubation.103 However, another study found noninvasive pressure support ventilation (NIPSV) superior to CPAP in preventing atelectasis after surgery.104
Another useful mode of NIV is airway pressure release ventilation, which cycles between high and low CPAPs. This may decrease peak airway pressures, improve alveolar recruitment and oxygenation, and increase the ventilation of dependent lung zones. Demonstration of the clinical benefits of this modality are not uniform.105
Upon transfer to the floor, most patients benefit from the use of supplemental oxygen via nasal cannula for a few days. Monitoring of SaO2 by pulse oximetry is helpful in patients with borderline oxygenation, especially during ambulation. The patient should be mobilized and encouraged to cough and take deep breaths. A cooperative patient who can actively participate in these maneuvers can generally prevent atelectasis and pulmonary complications, but additional support is commonly necessary in elderly patients and those with significant chest wall discomfort. A “cough pillow” should be used to brace the chest during deep breathing and coughing to minimize discomfort and splinting.
An incentive spirometer is very beneficial in maintaining the FRC and preventing atelectasis, although its effectiveness in preventing postoperative pulmonary complications is unclear.106 A literature review showed that CPAP, BPAP, or intermittent positive‐pressure breathing (IPPB) produced better pulmonary function and oxygenation than incentive spirometry, although the incidence of complications was comparable. However, none of these was more effective than preoperative patient education.107 One study showed that the same benefit could be derived from taking 30 deep breaths without mechanical assistance as from use of a blow bottle device or inspiratory resistance positive expiratory pressure mask.108
Chest physical therapy may be helpful in patients with significant underlying lung disease, borderline pulmonary function, or copious secretions, but otherwise is of little additional benefit.109 Albuterol administered via nebulizer is frequently beneficial in patients with bronchospasm.
Although dysphagia with difficulty swallowing foods is unusual in patients intubated for less than 24 hours, it is not uncommon following a longer duration of intubation. Careful attention must be paid to the patient’s initial oral intake to observe for potential aspiration. Patients who require longer periods of intubation usually require a full swallowing evaluation before initiating oral intake (see pages 804–805). The risk of dysphagia is greater in patients intubated >24 hours, with a twofold increase for every 12 hours of intubation, and it is also related to the duration of sedative use, prolonged nasogastric tube drainage, use of TEE during surgery, and a history of a remote stroke or perioperative stroke.110,111
Once the patient is hemodynamically stable and no longer requires volume administration to maintain intravascular volume, aggressive diuresis with IV furosemide, either with intermittent bolus doses or a continuous infusion, should be initiated to eliminate excess extravascular lung water. Diuretics are continued until the patient has approached their preoperative weight and can be weaned from nasal cannula with an acceptable SaO2 (>90% on room air).
Satisfactory analgesia is very helpful in improving the patient’s respiratory effort. A few doses of ketorolac are given initially after extubation, and most patients are then given oral narcotics such as oxycodone or hydrocodone with acetaminophen. Patients with significant pain issues may benefit from PCA pumps that provide morphine, fentanyl, or remifentanil.69,70 Alternatively, a fentanyl patch (Duragesic) can be used in patients with persistent pain despite opioid use. A common dose is 25 μg/h, which is the dose delivered by a 10 cm2 patch. Note that the fentanyl plasma concentration is increased by amiodarone. There is a delicate balance between achieving adequate analgesia and minimizing opiate use.
Venous thromboembolism (VTE) is rarely detected, but not that uncommon, following cardiac surgery. A literature review found the incidence of symptomatic deep venous thrombosis (DVT), pulmonary embolism (PE), and fatal PE to be 3.2, 0.6, and 0.3%, respectively.112 In the early postoperative period, patients may be prothrombotic, with contributory factors including elevated fibrinogen levels, thrombin generation, tissue factor activation, reduced fibrinolysis, return of normal platelet aggregation, and aspirin resistance.113,114 Thus, it is recommended that elastic graduated compression (anti‐embolism) stockings (GCS) should be used routinely for patients after surgery to reduce the risk of VTE. Mobilization is probably more important in reducing this risk, so once the patient is stable, getting them out of bed and ambulating is very important. For patients remaining in the ICU who may be sedated on mechanical ventilation and poorly mobilized, sequential or intermittent pneumatic compression (IPC) devices, such as the Venodyne system, should be used. Most patients are started on aspirin 81 mg daily after surgery, although higher doses might be necessary to reduce the risk of VTE because of early aspirin resistance. However, the ICU patient may also benefit from pharmacologic prophylaxis (see also pages 750–752).112
The literature remains contentious on whether early initiation of pharmacologic prophylaxis with either SQ heparin (5000 units SC q12h) or low‐molecular‐weight heparin (40 mg SC daily) should be considered in selected patients and when it should be started. If so chosen, it may be considered once mediastinal bleeding has tapered off, but the risk of developing a hemopericardium and delayed tamponade must always be taken into consideration.
A systematic literature review published in 2015 noted an increased risk for VTE associated with older age, obesity, heart failure, a history of VTE, prolonged bed rest, and mechanical ventilation.112 The 2018 European guidelines also identified age >70, transfusion of more than four units of RBC concentrate/fresh frozen plasma/cryoprecipitate/fibrinogen concentrate, mechanical ventilation >24 hours, or a postoperative complication (e.g. acute kidney injury, infection/sepsis, neurological complication), as placing a patient at higher risk for VTE.115 For these patients, early initiation of pharmacologic prophylaxis was “highly” recommended, even as soon as the first postoperative day, once bleeding becomes insignificant. However, the earlier 2012 American College of Chest Physicians guidelines concluded that the risk of bleeding exceeded that of VTE in cardiac surgery patients and therefore only recommended pharmacologic therapy for patients with prolonged hospitalization postsurgery.116
X. Acute Respiratory Insufficiency/Short‐term Ventilatory Support
Prolonged mechanical ventilation beyond 48 hours is necessary in about 5–10% of patients undergoing open‐heart surgery on CPB.24,25 The STS database defines “prolonged ventilation” as the requirement for ventilation for over 24 hours from the time of exit from the OR. This usually results from a significant perioperative cardiopulmonary insult (such as a long duration of CPB or postcardiotomy low cardiac output syndrome) that is superimposed on preexisting lung disease. Mechanical ventilation may be required until hemodynamic issues, significant mediastinal bleeding, or transient pleuropulmonary insults, such as pulmonary edema, have resolved. It may also be indicated for patients without intrinsic pulmonary problems who are sedated, obtunded, or sustain neurologic insults. These patients may have adequate gas exchange but need an endotracheal tube for airway protection.
Acute respiratory insufficiency is usually characterized by inadequate oxygenation (PaO2 <60 torr with an FiO2 of 0.5 or PaO2/FiO2 ≤120) or ventilation (PCO2 >50 torr). Predisposing factors to acute pulmonary dysfunction are fairly comparable to those that are predictive of the need for prolonged ventilatory support (see pages 471–472). One study found that the STS mortality risk score was the best predictor of the need for prolonged ventilation.23
Preoperative risk factors include a critical preoperative state (HF), advanced age, significant COPD or renal dysfunction, endocarditis, active smoking history, reoperative surgery, obesity (BMI >30 kg/m2), diabetes, a mean PA pressure ≥20 mm Hg, depressed LV function (stroke volume index ≤30 mL/m2), low serum albumin, and a history of cerebrovascular disease.19–26,79–81,117
Intraoperative factors include emergency surgery and CPB time ≥140 minutes. The latter is often associated with a significant inflammatory response, with patients usually receiving a significant amount of volume during and after surgery.
The development of acute respiratory insufficiency is associated with more renal dysfunction, gastrointestinal and neurologic complications, and an increased risk of nosocomial infections. The development of multisystem organ problems explains the high mortality rate of postoperative respiratory failure, which averages 20–25%.
Several logistic models have been created which are predictive of prolonged ventilatory failure (>72 hours).24–26 A sophisticated bedside model is noted in Figure 10.2.25
“Acute lung injury” defined by poor oxygenation is a clinical spectrum that ranges from a transient phenomenon with low risk to that of ARDS, which carries a very high mortality rate. In most patients with a PaO2/FiO2 ratio <200–300 immediately after surgery, a short period of ventilatory support while the patient is stabilized hemodynamically and diuresed usually results in improvement in oxygenation and the need for very short‐term ventilation. However, acute lung injury may progress to a chronic phase of ventilatory dependence in about 5% of patients. This is more likely to occur in older patients with preexisting pulmonary, cardiac, or renal problems that compromise postoperative recovery or when postoperative care is complicated by stroke, bleeding, and multiple blood transfusions.24,25 Chronic respiratory insufficiency/ventilator dependence is discussed in section XI (pages 488–494).
Etiology. During the first 48 hours, oxygenation problems predominate and can produce tissue hypoxia. Inadequate ventilation (hypercapnia) at this time is usually the result of a mechanical problem.
Inadequate O2 delivery and ventilation (mechanical problems)
Endotracheal tube problems: cuff leak, incorrect endotracheal tube placement (larynx, mainstem bronchus, esophagus), kinking or occlusion of the tube
Low cardiac output states leading to mixed venous desaturation, venous admixture, and hypoxemia
Pulmonary problems
Atelectasis or lobar collapse, possibly associated with diaphragmatic paralysis from phrenic nerve injury
Pulmonary edema
Cardiogenic from fluid overload and/or LV dysfunction, hemodilution on pump with reduced colloid oncotic pressure
Noncardiogenic from pulmonary endothelial injury with increased micro‐vascular permeability. This may be related to activation of complement, neutrophils, and macrophages with release of inflammatory mediators associated with extracorporeal circulation. This problem is more prominent as the duration of CPB lengthens and is more common in patients receiving multiple blood transfusions.
Pneumonia
Intrinsic pulmonary disease (COPD), bronchospasm, or air trapping
Blood transfusions: microembolization, transfusion of proinflammatory mediators, TRALI, TACO
Intrapleural problems
Pneumothorax
Hemothorax or pleural effusion
Metabolic problems: shivering leading to increased peripheral oxygen extraction
Transfusion‐related acute lung injury (TRALI) is a problem of acute respiratory distress with hypoxemia (PaO2/FiO2 <300) and pulmonary infiltrates on chest x‐ray that occurs within six hours of a blood or blood product transfusion when other risk factors for acute lung injury, such as sepsis or aspiration, are not present. It is most likely an immune‐mediated phenomenon with interaction between donor plasma antibodies and recipient leukocyte antigens that causes release of cytotoxic substances that damage lung tissue and causes noncardiogenic pulmonary edema from increased microvascular permeability. It is more common in older patients and those with longer durations of CPB. This is an acute phenomenon that rarely progresses to an ARDS picture and has a more favorable prognosis, although the mortality rate is still quite high at around 15–30%. Although transfusions per se are associated with increased pulmonary morbidity and increased mortality, TRALI appears to be a distinct entity.42,43,94,119,120
TRALI is to be differentiated from TACO (transfusion‐associated circulatory overload), which is another cause of acute respiratory distress that occurs within 12 hours of a blood transfusion. This is not immune‐mediated, but rather a phenomenon that occurs when a patient with preexisting fluid overload, often with LV dysfunction, HF, or chronic kidney disease, receives too large a volume of blood products or is transfused too rapidly. The patient may become hypertensive, tachycardic, and hypoxemic when the circulatory system is “overwhelmed” by the transfusion volume. It therefore represents a picture of cardiogenic pulmonary edema that should be preventable by administering diuretics at the time of blood transfusion or treatable with short‐term ventilatory support and diuresis.120
The acute development of shortness of breath after extubation or an abrupt change in ABGs during or after extubation should raise suspicion of the following problems:
Pneumothorax, possibly tension
Atelectasis or lobar collapse from poor inspiratory effort or mucus plugging
Aspiration pneumonia
Acute pulmonary edema (from myocardial ischemia, LV dysfunction, new ventricular septal defect, worsening mitral regurgitation, or undetected renal insufficiency)
Delayed tamponade causing a low cardiac output syndrome
Compensation for an evolving metabolic acidosis
Pulmonary embolism
Manifestations
Tachypnea (rate >30 breaths/min) with shallow breaths
Paradoxical inward movement of the abdomen during inspiration (“abdominal paradox”)
Agitation, diaphoresis, obtundation, or mental status changes
Tachycardia or bradycardia
Arrhythmias
Hypertension or hypotension
Assessment and management of acute respiratory insufficiency during mechanical ventilation (Table 10.7)
Examine the patient: auscultate for bilateral breath sounds and listen over the stomach to make sure the tube has not slipped into the larynx or been placed in the esophagus.
Increase the FiO2to 1.0 until the causative factors have been identified. Manually ventilate with a resuscitation bag (Ambu) if ventilator malfunction is suspected. This not only provides ventilation but also permits an assessment of pulmonary compliance. Note: make sure the gas line on the bag is attached to the oxygen (green) and not the room air (yellow) connector and the gas has been turned on.
Ensure adequate alveolar ventilation
Check ventilator function and settings and optimize the following:
Tidal volume
Ventilator trigger sensitivity
Inspiratory flow rate. Patients with COPD may have significant air trapping which produces an auto‐PEEP effect. This is noted when inspiration commences before expiratory airflow is completed, resulting in positive airway pressure at the end of expiration. It can exacerbate the adverse hemodynamic effects of PPV, cause barotrauma, and impair patient triggering of assisted ventilation. Steps that can be taken to eliminate this problem are discussed on page 497.
Consider using PSV to minimize the risk of high airways pressures.
Obtain a chest x‐ray to look for any of the potential etiologic factors listed above; specifically note any mechanical problems that can be corrected by simple repositioning of the endotracheal tube or chest tube insertion.
Repeat the ABGs
Note: an acute increase in peak inspiratory pressure may signify the development of a pneumothorax, although it can also result from severe bronchospasm, flash pulmonary edema, mainstem intubation, or an obstructed airway (copious secretions, the patient biting the endotracheal tube).
Assess and optimize hemodynamic status. A Swan‐Ganz PA catheter is useful in assessing the patient’s fluid status and cardiac output. The latter can also be assessed less invasively using other noninvasive monitoring systems, including the FloTrac device, which uses pulse wave analysis from the arterial line to calculate continuous cardiac outputs, although it is not helpful when the patient is in atrial fibrillation. A low cardiac output reduces oxygen delivery, lowers the mixed venous oxygen saturation, and increases venous admixture, further decreasing the PaO2. Inotropic support or diuresis may be indicated to improve oxygenation. An echocardiogram may be helpful in identifying a contributory problem, such as significant LV or RV dysfunction, cardiac tamponade, mitral regurgitation, or a new or recurrent ventricular septal defect.
Alveolar recruitment maneuvers that increase the mean airway pressure can open previously closed alveoli to increase the surface area for oxygen exchange and prevent early airway closure. This will decrease intrapulmonary shunting by improving ventilation to perfused areas. It will also redistribute lung water from the alveoli to the perivascular interstitial space, although it does not decrease extravascular lung water content.
A baseline level of 5 cm H2O of PEEP is usually added to the circuit for all patients admitted to the ICU. This substitutes for the loss of the “physiologic PEEP” of normal breathing caused by the endotracheal tube. This level of PEEP is well tolerated by the heart, but probably does little to improve oxygenation.
PEEP is added in increments of 2.5–5 cm H2O up to 10 cm H2O or greater to improve oxygenation and allow for weaning of the FiO2 to less than 0.5. With low mean airway pressures, intrapulmonary shunting may result from inadequate ventilation of perfused alveoli, and increasing the FiO2 alone will often be ineffective in improving oxygenation if the shunt exceeds 20%. This problem can be overcome by increasing the tidal volume and the level of PEEP. Furthermore, using an FiO2 >0.5 for several days can produce alveolar‐capillary damage, alveolar collapse, and stiff, noncompliant lungs (so‐called oxygen toxicity).
Caution must be exercised when using high levels of PEEP because it will accentuate the adverse effects of PPV on hemodynamics by creating high positive airway and intrathoracic pressures. Increasing levels of PEEP reduce venous return, increase pulmonary vascular resistance which can depress RV performance, and will lead to decreased LV filling and a reduced cardiac output in the hypovolemic patient. Thus, adding PEEP could be counterproductive because it may actually reduce oxygen transport and tissue oxygenation, lower the mixed venous oxygen saturation, and increase admixture, further decreasing the PaO2. Volume infusion is necessary to counteract these effects before increasing the level of PEEP. The optimal level of PEEP can be determined by observation of the arterial waveform and serial assessments of cardiac function while adjustments are being made.
Adding high levels of PEEP to patients with severe COPD results in increased transmission of airway pressure to the lungs, resulting in overdistention of alveoli that are highly compliant and poorly perfused. This may result in increased V/Q shunting, possibly producing endothelial damage, and progressive hypoxia.
In patients with intrinsic pulmonary disease, and especially ARDS, the pulmonary vascular resistance may be elevated and the lungs less compliant. Increasing levels of PEEP may produce RV failure and dilatation, shifting the interventricular septum and compromising filling and compliance of the LV. In these patients, volume infusion must be given cautiously.
High levels of PEEP can result in “barotrauma” (pneumothorax, subcutaneous emphysema, or pneumomediastinum), which can compromise ventilation and produce acute hemodynamic embarrassment. Barotrauma is caused by alveolar overdistention, and is attributable more directly to the severity of the underlying lung disease than to the peak airway pressure. Nonetheless, modes of ventilation that provide lower tidal volumes have been used in patients with ARDS to improve oxygenation and are now recommended routinely during early ventilatory support.39,121
Note: care must be exercised when suctioning a patient on high levels of PEEP. Oxygenation can become very marginal when PEEP has been temporarily discontinued. A PEEP valve should be used during manual ventilation if the patient’s oxygenation is dependent on PEEP.
The interpretation of pressure tracings from a Swan‐Ganz PA catheter is influenced by PEEP. The measured CVP, PA, and left atrial pressures are elevated, but transmural filling pressures, which determine the gradient for venous return, are decreased, because pressure is transmitted through the lungs to the pleural space. A general rule is that the true pulmonary capillary wedge pressure (PCWP) is equal to the measured pressure minus one‐half of the PEEP level at end‐expiration (minus one‐quarter if lung compliance is decreased). Another way of assessing the PCWP is the “index of transmission”:
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