Introduction

Cardiac surgery has significant and well studied effects on pulmonary physiology. A major impact of surgery is to decrease pulmonary compliance (Cp) (1,2,3). Causes for the decreased Cp include increased pulmonary capillary volume and extravascular lung water as a consequence of the crystalloid solution patients receive in the course of cardiopulmonary bypass (CPB), as well as microatelectasis which is multifactorial in etiology (1). Atelectasis is caused, in part, by anesthetic and neuromuscular blockade (paralysis), which typically cause cephalad shift of the diaphragm in supine patients. This decreases functional residual capacity (FRC) below the lungs' closing volume (4). The lungs are also typically deflated to some degree during cardiac surgery to allow clear access to the to the heart, even if the procedure is done off CPB and through new "minimal access" techniques. This, as well, contributes to atelectasis. Chest wall compliance, by view of recent studies (5), is also decreased after sternotomy, though minimally and for only a brief (<4 hours) period. Airway resistance (AR) is generally increased after cardiac surgery (2) for unclear reasons, but possibly because of bronchial edema.

The clinical effects of these physiologic changes are primarily two. Ventilation/perfusion (V/Q) relationships are altered creating physiologic shunting through poorly ventilated lung units resulting in an increased alveolar-arterial oxygen difference (A-a O2D). Though this effect can be very different between patients, it is on average about 70 mm Hg. To prevent hypoxemia, therefore, post cardiac surgery patients require, typically, increased fraction of inspired O2 (FiO2). It is noteworthy that this effect is seen in patients whose surgery is performed off CPB, through minimal access approaches, in addition to patients receiving traditional treatment (6). This effect can last only hours or for a few days, depending upon the patient. The other effect of physiologic changes post surgery is that patients experience increased work of breathing (WOB) consequent to the increased AR, and decreased Cp. For the vast majority of heart surgery patients this is inconsequential to their clinical course. However, in patients with significant underlying neuromuscular disease or pulmonary pathology, especially those with chronic obstructive lung disease (COPD), these changes may prove troublesome and result in prolonged mechanical ventilation (MV).

Incidence of pulmonary complications

There are many potential pulmonary complications of cardiac surgery. They will be individually discussed in detail through the other sections of this chapter. However, it is helpful to know the general incidence of the more common and morbid problems.

Prolonged MV (>48 hours), is required in from 10 - 23% of post cardiac surgery patients (7,8). o Atelectasis of a great enough extent to be present on chest X - ray (CXR), is common post cardiac surgery. One recent study reported an incidence of left lung atelectasis at 88%, and right lung Atelectasis at 61% (9).

Pulmonary edema, to greater or lesser degrees, typically is present in patients post CPB (10).

Diaphragm dysfunction, not necessarily effecting clinical outcome, but when looked for aggressively with sophisticated techniques, is present in 25% to 50% of post cardiac surgery patients (11).

Pleural effusions are common after cardiac surgery, occurring in 40% to 90% of patients depending upon the series (12,13). Most effusions are small in size, however, and do not require treatment. Large effusions (>25% of the hemithorax) occur in slightly less than 1% of cardiac surgery patients (14).

The Adult Respiratory Distress Syndrome (ARDS) occurs in 1% to 2% of post cardiac surgery cases but is associated with significant mortality (15). o Pneumonia occurs in 4 - 6% of cardiac surgery patients (16,17).

Pulmonary embolism (PE) is thought to be rare after cardiac surgery, but in a recent large series it complicated 3% of the cases (18). When PE occurs post cardiac surgery, it is associated with a mortality of 18% to 34% (18,19).

Pulmonary arterial hypertension is common after cardiac surgery, but is only unusually associated with notable clinical problems. However, patients with severe biventricular failure and those undergoing congenital heart surgery, mitral valve replacement, orthotopic heart transplant, and left ventricular assist device placement are at particular risk for the development of severe pulmonary hypertension which can lead to right ventricular decompensation and, rarely, mortality (20).

Mechanical ventilator supoort

Following cardiac surgery patients are taken off CPB and sent back to the RR on a mechanical ventilator. Uncomplicated patients will require mechanical ventilatory support typically for some hours until they are ready to "wean" from the ventilator and have their ETT tube removed. During this time the patient recovers from hypothermia, anesthesia, neuromuscular blockade, and typically regains hemodynamic stability. The ventilator for this period is set in a "support mode", that is a mode, which essentially does all of the WOB for the patient. The two commonly used support modes are assist control (AC) and synchronized intermittent mandatory ventilation (SIMV) with pressure support (PS). These are "volume cycled ventilator modes". In each of these modes a respiratory rate and tidal volume is set for the ventilator. For example, a typical respiratory rate (RR) would be 10 and tidal volume (Vt) 800 mL. In both of these modes the patient will, at least 10 times a minute, get a Vt of 800 mL. In either mode, patients can initiate breaths between the preset Vts. In both modes the ventilator will augment those breaths, but in different ways. In AC, when the ventilator senses that the patient is initiating a breath, it will give the patient the preset Vt. For example, if our patient on AC set at a RR of 10 with a Vt of 800 mL initiates 5 extra breaths a minute, each of those breaths will be 800 mL. The patient's total minute ventilation (Ve) will be 15 breaths x 0.8 L = 12 L. In the SIMV mode with PS, a PS level is selected in addition to a RR and Vt. When the patient initiates a breath between the preset Vts, the ventilator will generate air flow through it's inspiratory loop. The amount of airflow will be enough to maintain a positive airway pressure, at the selected PS level, while the patient is actively inspiring. The purpose of PS is to aid the patient in breathing through the ventilator tubing and circuitry. The size of the Vt that the patient actually receives depends upon how strongly he or she inspires, the level of pressure support, and the length of time that he or she inspires. For example, if our patient is placed on SIMV at a RR of 8 with a Vt of 800 mL and PS of 15 cm H2O, Ve will be at least 8 x 0.8 L = 0.64 L. If, however, he initiates 5 extra breathes per minute which are pressure supported to a Vt of, on average, 0.5 L, his Ve will be 5 x 0.5 L = 0.25L added to the 0.64 L for a total Ve of 0.89 L.

There are no studies to show which of these two volume-cycled-ventilator modes are superior in supporting patients post CS or supporting patients with respiratory failure in general. It is very important, however, that when the SIMV mode is used that it be used in conjunction with pressure support. Pressure support compensates for the work of breathing through ventilator circuitry. Without PS, the work of breathing through the ventilator can be fatiguing for patients' respiratory muscles, and actually prolong the need for MV (31). Typical settings for using the either the AC or SIMV ventilator modes are: o RR: 8 - 12 breaths per minute o Vt: 10 - l5 mL per kg o PS: 5 - 15 cm H2O (our institution routinely uses 10 in our post cardiac surgery patients) These settings were developed from anesthesia experience to prevent both over distention of the lung resulting in "barotrauma" and under distention of the lungs resulting in atelectasis. These settings, additionally, will generally result in eucapnia, but it's appropriate and routine practice to check arterial blood gasses approximately 20 minutes after arriving in the recovery room. When patients arrive in the RR the FiO2 delivered by the ventilator is typically 0.60 or 60%, as long as the oxygen carrying capacity of the blood is not compromised by an O2 saturation of less than 90%. FiO2 above 0.60 is generally considered to be toxic to the lungs through generation of oxygen radicals.

Ventilators in common use typically offer several options for the inspiratory flow pattern and allow peak inspiratory flow rate to be set. The "decelerating ramp" flow pattern is generally considered to deliver gas in the most physiologic way and is usually preferred. Peak inspiratory flow rates are generally initially set at 60 L/min but may be varied up and down substantially depending upon the needs of the patient. The latest generation of ventilators, utilizing sophisticated computer programs, will calculate the AR and Cp of the patient's lung, on a breath-to-breath basis, and deliver Vts through a flow rate and pattern that is most physiologically appropriate. Positive end expiratory pressure (PEEP) use, as a standard post cardiac surgery, varies from institution to institution. Argument for using a low level of PEEP routinely in post cardiac patients is that it helps prevent microatelectasis. "Physiologic PEEP" is usually set at about 5 cm H2O. Argument against its routine use is that it can negatively impact hemodynamics by increasing intrathoracic pressure, thereby decreasing venous return to the right heart as well as increasing right ventricular afterload. Again, no data exists as to whether routine use of PEEP in post CS patients is beneficial or not. At our institution, because of concern for hemodynamics we do not routinely use PEEP.

Ventilator trouble shooting

The ventilator is adjusted in the early postoperative period based on arterial blood gas (ABG) sampling and "peak inspiratory pressure" (PIP). In general, the partial pressure of arterial CO2 (paCO2) is targeted to be 35 - 45 mm Hg, which, unless there is a concurrent metabolic acid base disturbance, should result in an acceptable pH of 7.35 - 7.45. paCO2 is directly proportional to the alveolar ventilation (Va) which is equal to the Ve minus the dead space ventilation (Vd) (that portion of the lung which ventilated but not perfused such as the airways). Ve is equal to the RR x the Vt. In normal lungs about 150 mL. of each Vt is Vd. Va is, therefore, equal to the RR x (Vt - 0.15).

So to treat respiratory acidosis or alkalosis that has developed on the ventilator the Va is adjusted up or down in proportion to the amount of change in the CO2 required to achieve eucapnea. This can be done by adjusting the Vt or the RR, which is usually preferred. Suppose for example, if we have a patient with a paCO2 of 50 and a pH of 7.32 immediately post operatively on MV settings of AC, RR 8, and Vt of 800 mL who is not initiating any breaths. The Va is equal to 8 x (0.8 - 0.15) = 5.2 L. To bring the pCO2 down 20% to 40 mm Hg, the Va needs to be increased 20% to about 6.24 L. By increasing the RR to 10 the Va will increase to 6.5 L, approximately the Va needed. Partial pressure of arterial oxygen (PaO2) is targeted to be greater than 60 mm Hg (correlating to an arterial oxygen saturation greater than 90%) hopefully using a FiO2 of 60% or less.

Ventilator strategies to improve oxygenation are discussed in the section on hyperemia. It is important to pay attention to PIPs. Ventilators measure pressures in the ventilator circuitry as a way to estimate the patients' airway pressures. PIP is the peak positive pressure detected while the patient is receiving a breath from the ventilator. Elevated PIP (>35 cm H2O) signifies pulmonary pathology or patient-ventilator malinteraction. High PIPs are caused by either an increase in AR, a decrease in Cp, or extra pulmonary parenchymal pathologies causing increased pleural pressure which is then transmitted to the airways. When the PIP is elevated the first question is if it is due to increased AR. Some ventilators will calculate and display AR on a breath by breath basis. Values above 4 cm/L/second are elevated. Otherwise, a quick maneuver to assess AR is to have the ventilator hold the Vt in the patient for 1 - 2 seconds. This is usually done through the "inspiratory pause" function of the ventilator. At the end of the pause the ventilator will read out a "plateau pressure" (PP). This pressure should roughly reflect the alveolar pressure, as there is no airflow between the ventilator pressure transducer and the alveoli during an inspiratory pause. If the PP is low, and the PIP is high, the problem is one of AR. If the PP is high, as well as the PIP, the problem is one of poor Cp or increased pleural pressure. Causes of increased AR include:

• Malposition of the ETT.
• Bronchospasm and/or airway edema
• Biting of the ETT

The ETT can be too high with the tip being in the larynx. The ETT tube can be too low, either up against the carina or in one of the main stem bronchi. Occasionally the ETT can be up against the tracheal wall in patients with airway, abnormalities from, for example, kyphoscoliosis, or a prior extensive lung injury resulting in a torturous trachea. Mucus or mucopurulent plugging of the ETT tube or airway.

Assessment for these possibilities should include physical examination with inspection of the ETT tube where it exits the mouth. Look for biting of the tube and tube position. In general the ETT should be approximately 21 cm at the teeth for an average size woman and 23 cm for an average size man. Ausculation should be performed for rhonchi suggesting airway secretions and wheezing suggesting bronchospasm. Focally decreased breath sounds can signify bronchial obstruction by mucous plugging, as well as pneumothorax and pleural effusion. CXR examination after cardiac surgery is routine and should be checked for the position of the ETT (3 cm. +/- 1 cm from the carina). If, after inspection, auscultation, and review of the CXR the cause of AR is not obvious, a suction catheter should be introduced through the ETT to feel for resistance and to suction possible mucous plugs. If resistance is met, the ETT should be repositioned if poor positioning appears to be the problem. If ETT positioning is not the problem, and the patient has relatively stable gas exchange, then a bronchoscope should be performed through the ETT to inspect the etiology of the airway obstruction. The bronchoscope can sometimes more efficiently clear secretions and guide the position adjustment of the ETT. There are occasions when the airway is obstructed and gas exchange rapidly deteriorates into a dangerous range. In these circumstances it is most appropriate to emergently extubate and reintubate the patient. This should be done by an anesthesiologist or a pulmonologist experienced in difficult airway management.

If PIP elevation is not caused by AR then the problem is pathology causing poor Cp or increased pleural pressure. PP is elevated in both of these circumstances and Cp (static) is decreased. Many modern ventilators will calculate the static Cp, but you can calculate it yourself through the following formula: Cp = Vt / PP - PEEP. Cp less than 50 mL./cm H2O indicates a problem. Lung parenchymal problems causing significantly decreased Cp include any air space filling or interstitial infiltrative processes.

In the post cardiac surgery population the most common cause is pulmonary edema from congestive heart failure and/or volume over load. Nonhydrostatic pulmonary edema (adult respiratory distress syndrome) and diffuse, severe pneumonia can markedly decrease lung compliance as well. Increased pleural pressure can be created by chest wall edema, abdominal distention, pneumothorax, pleural effusions, patient ventilator malinteraction, or "intrinsic PEEP". Intrinsic peep (Pi) is a pathophysiology that can occur in patients with obstructive lung disease which can create markedly elevated PPs (32). In this disorder, because of expiratory flow limitation, air is trapped in the lung, creating large increases in pleural pressure. Evaluation for these possibilities should begin with inspection to look for signs of patient ventilator malinteraction such as patient inspiratory or expiratory efforts out of synchrony with the ventilator cycle. The chest wall and abdomen should be inspected as well. Auscultation for crackles, signifying interstitial or air space filling processes and for decreased focal breath sounds consistent with pneumothorax or pleural fluid should be performed. Again, the postoperative CXR will be an important diagnostic tool to look for these pathologies. To diagnose Pi the ventilator's expiratory port is occluded at the end of expiration, if positive pressure is detected Pi is present. Many recent vintage ventilators have automated programs to do this. Treatment of specific entities causing elevated PP and depressed Cp will be discussed below. However, while specific underlying pathologies are being treated it is very important to adjust the ventilator to decrease the PIP (ideally to less than 35 cm H2O) and especially the PP (to less than 30 cm H2O).

Remember the PP reflects the pressure seen by the alveoli. High pressures in the alveoli can cause them to rupture creating a pneumothorax or pneumomediastinum, and are also associated with overdistension of these lung units and consequent injury (sometimes called "volutrauma") (33). The first therapeutic maneuver is to decrease the Vt. If the pressures are still elevated, then, depending upon the ventilator, the peak inspiratory flow rate should be decreased or the inspiratory time increased. Maneuvers thereafter are dependent upon the specific causative problem