Postoperative Care

Cardiac Index

Cardiac index (cardiac output expressed as L · min ⁻¹ · m ⁻² ) is one measure of adequacy of the cardiovascular subsystem, as evidenced by the oft-demonstrated relation between cardiac index and survival (described by Dietzman and colleagues in 1969 ). In adults, a cardiac index of at least 2.0 L · min ⁻¹ · m ⁻² during the first few hours in the ICU and one of at least 2.4 on the morning after operation are required for normal convalescence ( Fig. 5-1 ). This is at the lower end of the range of normal, which is 2.2 to 4.4. Infants and small children appear, in general, to require a somewhat higher cardiac index for normal convalescence ( Fig. 5-2 ). Also, in young patients, cardiac index tends to be lower about 4 hours after operation than it was soon after discontinuing CPB, and then begins to rise after 9 to 12 hours.

Cardiac indices below these values are usually inadequate for maintaining a normal convalescence; this can be formalized in the inverse relation between cardiac index early postoperatively and the probability of hospital death. This relation can be refined by considering not only cardiac output but also mixed venous oxygen levels, with lower levels worsening prognosis at any given value of cardiac output. ²

Arterial Blood Pressure

2 Although dye dilution or thermodilution is the standard for measuring cardiac output, caution is required in interpreting measurement values. In small individuals, confidence intervals around the measurement may be large; low core temperature may diminish accuracy; and tricuspid regurgitation, absence of an adequate mixing chamber, lack of steady state, and intracardiac shunts (as originally articulated by Stewart and Hamilton ) invalidate the measurement.

Arterial blood pressure is an insensitive method of estimating adequacy of cardiac output early postoperatively, primarily because systemic vascular resistance (Rs) is usually elevated. This may be related to increased levels of circulating catecholamines, plasma renin, angiotensin II, or other mechanisms. This high resistance may result in a normal or high arterial blood pressure even when cardiac output is low.

Some patients tend early postoperatively to have low Rs and arterial blood pressure, even when cardiac performance is good. This may occur more frequently in children with cyanotic heart disease, adults with diabetes, and patients with sepsis or drug interactions (especially preoperative use of angiotensin-converting enzyme [ACE] inhibitors). Arterial hypotension is an indication for thoughtful evaluation. Children cannot be considered to be convalescing normally when mean arterial blood pressure is lower than about 10% below normal for the patient's age ( Table 5-1 ). For adults, particularly the elderly, arterial blood pressure may mandate maintenance at or above commonly accepted normal values to ensure adequate perfusion of various organs like the brain, viscera, and kidneys.

Pedal Pulses

Simple observation of pedal pulses is a commonly used, useful, but not infallible method of estimating adequacy of cardiac output in children and young adults. Normal (grade 4) pedal pulses early postoperatively are highly but not perfectly correlated with adequate cardiac output and a high probability of survival. In older adults, estimation of the adequacy of perfusion by amplitude of pedal pulses is often confounded by the presence of peripheral arterial occlusive disease.

Skin Temperature

Skin temperature in the foot is another indirect but reasonably reliable estimator of adequacy of cardiac output. A study of cardiac surgery in infants younger than 3 months of age indicated that pedal pulses and skin temperature predicted probability of hospital death from cardiac causes and thus were reasonably good estimators of adequacy of cardiac output. As with assessment of pedal pulse amplitude, in older adults skin temperature offers guidance but not solid evidence for adequacy of perfusion.

Whole Body Oxygen Consumption

Whole body is infrequently calculated, but knowledge of it is useful; in some circumstances, it is a better basis for prognostic and therapeutic inferences than cardiac output or mixed venous oxygen levels. Whole body can be calculated by a rearranged Fick equation, ³ which states:

3 The Fick equation states:

where is cardiac output in L · min ⁻¹ , is oxygen consumption in mL · min ⁻¹ , Ca o ₂ is arterial O ₂ content in mL · L ⁻¹ , and is mixed venous O ₂ content in mL · L ⁻¹ . The oxygen content of blood consists of combined plus dissolved oxygen:

where Hb is hemoglobin concentration in g · L ⁻¹ , S o ₂ is O ₂ saturation as a percentage of capacity, P o ₂ is O ₂ tension in mmHg, 1.38 is effective O ₂ capacity of 1 g of hemoglobin in mL · g ⁻¹ , and 0.03 is solubility of O ₂ in blood at 37°C in mL · L ⁻¹ · mmHg ⁻¹ . Rearranging equation 5-2 and substituting for Ca o ₂ from equation 5-3,

where Sa o ₂ is arterial O ₂ saturation as a percentage of capacity, and Pa o ₂ is arterial O ₂ tension in mmHg. For a given , equation 5-4 indicates that to increase , there must be an increase in Sa o ₂ , Pa o ₂ , Hb, or . varies directly with , and varies directly with cellular P o ₂ , unless there is shunting in the peripheral circulation. Thus, to maximize tissue oxygen supply, there must be an increase of one or more of the following: Pa o ₂ (and thus Sa o ₂ ), Hb, or .

The normal value for
at 37°C is 155 mL · min ⁻¹ · m ⁻² . The value for whole body
in the patient recovering from cardiac surgery must be interpreted in light of his or her body temperature; residual hypothermia is the most common explanation for the somewhat low
usually present within the first few hours after open heart surgery. This reduced
is in part due to reduced capillary density (reduced area of capillary flow) and increased heterogeneity of capillary flow through the muscle mass and other tissues of the body in the early hours after CPB. Normally convalescing patients operated on with hypothermic CPB generally require 4 to 8 hours for this to disappear and their peripheral perfusion to return to normal.

When is appreciably reduced below the normal level for the existing body temperature, a hazardous condition exists; indeed, one useful definition of shock is “a condition characterized by an acute reduction in .” Abnormally low may result from reduction or extreme heterogeneity of capillary flow (of which “no reflow” is an extreme example) in one or more organs of the body (sometimes termed a reduction in capillary density ), lengthening of the diffusion path between capillaries and cells, or intracellular metabolic derangement. One or all of these may exist in patients early after cardiac surgery. When important reduction in , considering the temperature, persists for more than a few hours, probability of death increases.

Mixed Venous Oxygen Level

Mixed venous oxygen level, generally expressed as oxygen tension ( ) or saturation ( ), is a useful index of circulatory adequacy, because it reflects to some extent mean tissue oxygen levels. When is less than 30 mmHg, cardiac output is likely to be inadequate; when it is below about 23 mmHg, the inadequacy is apt to be severe ( Fig. 5-3 ). However, normal or near-normal venous oxygen levels are not reassuring as to the adequacy of cardiac output, unless it is known that is approximately normal for the existing body temperature.

In a nonsurgical but critically ill ICU population, Jain and colleagues found a weak relationship between and cardiac index. There was considerable variability among all patients in various conditions, but when normalized for and hemoglobin concentration, the correlation coefficient improved ( Fig. 5-4 ). Using indwelling fiberoptic reflectance oximetry, other investigators have found no or only a very weak relationship between or and measured cardiac index. Following CPB, changes in may be useful in detecting low cardiac output, one of many causes of decreased oxygen delivery. Identifying decreases may be of particular value in patients coming to surgery with a high severity of illness index. Online continuous oximetry is useful in critically ill patients because it reflects unanticipated events or occasionally the usefulness (or nonusefulness) of therapeutic maneuvers. These aspects of postoperative care illustrate the need for uniformity in monitoring techniques and highlight the conflict between overreliance on devices and the ability to form accurate estimates (in this case, of cardiac performance) based on previous correlations. However, many surgeons rely on continuous monitoring to detect deviations from normal convalescence early postoperatively. Catheters that allow measurement of both and cardiac output are optimal.

Urine Flow and Serum Potassium

Urine flow and serum potassium levels are useful indirect guides to the adequacy of cardiac output. Early postoperative oliguria suggests inadequate cardiac output and thus is often an indication for treatment of the cardiovascular subsystem. Hyperkalemia rising over a 4-hour period (with sampling every 2 hours) to a level of about 5 mEq · L ⁻¹ is a sensitive indicator of a low or falling cardiac output in neonates and infants, and hence an indication for intensifying treatment. Hyperkalemia is usually accompanied by a fall in pedal skin temperature and a rise in esophageal temperature, but it often precedes the appearance of a base deficit or of arterial hypotension.

Metabolic Acidosis

A frequently used but somewhat nonspecific and insensitive indicator of the adequacy of cardiac output is the acid-base status of blood. Metabolic acidosis during and after cardiac surgery is almost always a result of lactic acidemia. Lactate production is a byproduct of anaerobic metabolism, which most often occurs under conditions in which cardiac output and oxygen consumption are suboptimal. Occasionally, excess lactate may occur with high measured cardiac output under conditions of high metabolic rate, diabetes, sepsis, or intestinal ischemia.

Concentration of lactic acid in blood may be measured directly. Normally, little or none is present, normal values in plasma being 0.7 to 2.1 mEq · L ⁻¹ . A concentration of about 5 mEq · L ⁻¹ correlates in general with moderate metabolic acidosis, and one of 10 mEq · L ⁻¹ with severe metabolic acidosis and usually markedly reduced cardiac output. Moderate elevation of lactic acid concentration is a common finding early after cardiac surgery, but in the normally convalescing patient, lactic acid gradually declines to normal values within 12 to 24 hours.

When arterial pH is less than about 7.4, acidosis is present but may be the result of retention of carbon dioxide; this is reflected in an arterial Pa co ₂ greater than 40 mmHg. Alternatively, acidosis may be “metabolic” and due primarily to accumulation of lactic acid. Quantification of metabolic acidosis is expressed by a derived value obtained from an equation after measuring arterial pH and Pa co ₂ . Either the buffer base deficit or the standard bicarbonate is calculated. Most commercially available equipment calculates the buffer base deficit or excess (which takes account of the buffering capacity of blood as well as that of bicarbonate) after measuring Pa o ₂ , Pa co ₂ , and pH of whole blood. The normal buffer base is about 48 mEq · L ⁻¹ , and the normal base excess or deficit is 0.

Ventricular Preload

Ventricular preload, which is correlated directly with the force of contraction, is equated with sarcomere length at end-diastole, and thus with change in ventricular volume between end-systole and end-diastole. This volume change is determined by transmural pressure during diastole, compliance and thickness of the ventricular wall, and curvature of the wall (La Place effect). Transmural geometric arrangement of fibers also plays a role but changes little during the postoperative period.

Transmural pressure is determined by intraventricular pressure and intrapericardial pressure. Intraventricular pressure at end-diastole (which is a determinant of the force of contraction) is related to phasic changes in atrial pressure, and these are affected by blood volume and systemic venous capacitance. The latter is decreased early after CPB. Because transmural pressure is affected by intrapericardial pressure, it is affected by closure of the pericardium and sternum, both of which increase intrapericardial pressure and decrease transmural pressure. Daughters and colleagues have demonstrated that pericardial closure in the setting of cardiac surgery, both itself and independent of sternal closure, increases intrapericardial pressure, decreases transmural pressure, and unfavorably affects cardiac performance. Changes in myocardial compliance during and after cardiac operations are due primarily to changes in myocardial water content.

After cardiac surgery in patients with normal atrioventricular (AV) valves, most acute changes in preload are equated with acute changes in mean left (in the case of the LV) or right (in the case of the RV) atrial pressure. This is because in this setting, and when the atria are functioning normally as reservoirs, ventricular end-diastolic pressure is similar to the mean pressure in the corresponding atrium. Therefore, mean atrial pressure is measured in cardiac surgical patients to deduce ventricular end-diastolic pressure. Right atrial pressure is usually measured using a fine polyvinyl catheter introduced through the right atrial appendage or internal jugular vein. Left atrial pressure is measured through a fine catheter introduced through the right superior pulmonary vein (or the left atrial appendage in neonates and young infants). In the absence of pulmonary vascular disease and important pulmonary congestion or edema, pulmonary artery diastolic pressure is a reasonable approximation of left atrial pressure. In most adult patients following CPB, pulmonary capillary wedge pressure exceeds left atrial pressure, and this discrepancy increases through the twelfth postoperative hour. It is thought this difference is due to accumulation of interstitial lung water ( Fig. 5-6 ).

Ventricular Afterload

In the intact ventricle, afterload is defined as systolic wall stress. This is the analog of the load that resists shortening in the isolated papillary muscle. Other things being equal, increased afterload results in decreased stroke volume. In the intact ventricle, afterload is related to (1) ventricular transmural pressure during systole, (2) ventricular wall curvature as determined by ventricular volume (La Place effect), (3) ventricular wall thickness, and (4) shape of the ventricle.

Ventricular wall determinants of afterload change little during and early after operations. Instead, acute changes in afterloads of the LV and RV are usually produced by changes in intraventricular pressures during systole. These changes are equated with changes in proximal aortic and pulmonary arterial systolic pressures. During and early after operation, proximal pulmonary arterial pressures may be monitored directly, but proximal aortic pressures are not. They must be inferred from measured radial (or femoral) artery pressures. Because of the many determinants of the magnitude of systolic amplification, systolic blood pressure at the radial artery is usually higher than in the ascending aorta, except in the situation of peripheral vasoconstriction secondary to low cardiac output or high-dose α-adrenergic agents. In most instances, systolic pressure variability between the aorta and peripheral arteries is not clinically important, but an awareness of it is advantageous in some situations. Mean pressures are similar in the two areas.

A tendency toward arterial hypertension is present in many adult patients early postoperatively, related to increased systemic arteriolar resistance. This complication (1) increases ventricular afterload and thereby decreases stroke volume, (2) increases aortic wall tension and thereby increases the likelihood of tearing the aortic purse-string sutures and suture lines, and (3) increases LV metabolic demands that exacerbate any latent myocardial ischemia. An appropriate criterion for treatment to lower arterial blood pressure in this setting is a mean arterial blood pressure 10% above the normal value. Mean arterial blood pressure, not systolic pressure, is monitored for this purpose because of the interrelations between peripheral and central arterial pressures discussed earlier. However, the patient's preoperative blood pressure must be taken into account, and to avoid cerebral complications, markedly hypertensive patients must not be rendered hypotensive. In the ICU, sodium nitroprusside is generally used for this purpose (see Appendix 5A ), but nitroglycerin may be preferred when myocardial ischemia is present, because it decreases coronary resistance. Negative intrathoracic pressure also increases LV load resisting shortening by increasing LV transmural pressure. Positive-pressure ventilation negates this effect, but labored spontaneous ventilation may augment afterload, and this may decrease cardiac output.

Myocardial Contractility

When a change in stroke volume cannot be explained by a change in end-diastolic fiber length (preload) or load resisting shortening (afterload), it is considered to result from a change in the contractile state. Contractility in a given ventricle can be acutely depressed or increased. When an attempt is made to compare ventricular contractility from patient to patient, and from time to time in the same patient, problems arise. A papillary muscle that is twice as thick as others might appear to have twice the contractility when studied in the usual way. In the ventricle, and at least theoretically in papillary muscle, data interpreted in terms of contractility must be normalized according to muscle thickness and length.

In vivo assessment of myocardial contractility and the resultant quantification of ventricular pump function are desirable goals postoperatively. The simplest representation of the capacity of the heart as a pump is a determination of any of several modifications of the Frank-Starling mechanism. For instance, the measured change in cardiac output (or stroke volume) with aliquot infusions of blood or blood substitute serves as a surrogate for assessment of contractile function. Clearly this is not reflective of intrinsic contractile properties of the myocardium, because the pressure-volume relationship is affected not only by preload but also by load resisting shortening, myocardial compliance, and intact vagal and sympathetic reflex activity. Changes in the instantaneous ventricular pressure (or aortic pressure) over time, dp/dt, may reflect myocardial contractility, but this quantity is exquisitely sensitive to afterload and preload and cannot be assumed to be an index of contractility that can be transferred from one patient to another or within the same patient over a period of time.

The relationship between ventricular pressure and volume (pressure-volume loop) is currently the nearest approximation to an in vivo assessment of contractility. Additionally, the area within the loop represents stroke work. The end-systolic pressure and the pressure at end-diastole of several different loops allow an expression of contractility and stiffness, respectively. The loops are composed of four segments: isovolumic contraction, ejection, isovolumic relaxation, and filling ( Fig. 5-7 ). When ventricular volume or resistance is altered, a group of points at end-systole fall along a line, the slope of which Suga and colleagues called Emax . Emax is an index of contractility ( Fig. 5-8 ). Changes of the slope in a steeper direction reflect increased inotropy. A shift in the rightward direction represents negative inotropy. With the use of catheters to measure LV pressure and transesophageal echocardiography (TEE) for instantaneous border detection, pressure-volume loops and Emax (contractility at zero volume) can be interpreted online in the ICU. It is paradoxical that the least clearly and directly defined determinant of the force of cardiac contraction is the one most discussed and treated. Its specific treatment is by the administration of inotropic drugs, usually catecholamines (see “ Treatment of Low Cardiac Output ” later in this section).

Relative Performance of Left and Right Ventricles

During and early after cardiac operations, one of the two ventricles is usually the factor limiting cardiac performance, not both. It is usually advantageous to consider and treat patients with this concept clearly in mind. The clue of greatest importance in this regard, when the AV valves are normal, is the relation between the left and right atrial pressures, because they represent the closest approximation available to ventricular end-diastolic pressure and, by implication, sarcomere length. When the cardiac valves are normal, the ventricle with the highest corresponding atrial pressure is the one limiting cardiac performance. Echocardiography can often provide supportive information.

Inadequate Operation

The surgeon's responsibility for obtaining an adequate operation demands that he or she continue to search for evidence of this postoperatively, particularly when the patient has low cardiac output. Using the methods described in this and other chapters, a search is made for residual intra- or extracardiac shunting, pathway obstructions, valvar regurgitation, graft or conduit dysfunction, or cardiac compression. If the operation is found to be inadequate in any of these regards, prompt reoperation is usually indicated.

Myocardial Dysfunction

Myocardial dysfunction was once thought to explain low cardiac output after cardiac surgery when atrial pressures were elevated above the usual postoperative values in the absence of any other explanation. The availability of two-dimensional echocardiography in the OR and ICU, particularly TEE, makes possible both direct demonstration of ventricular wall motion and assessment of end-diastolic and end-systolic volumes. These studies can lead more directly to the inference that low cardiac output is due to myocardial necrosis or stunning or to impaired cardiac reserve in the face of increased stress. This inference can be supported by the finding of increased creatine kinase (CK)-MB isoenzyme or troponin in the serum.

Reduced Preload

Increased Ventricular Afterload

Increased RV afterload may appear quickly as a result of a sudden rise in pulmonary artery pressure and vascular resistance. Consequently, during an episode of paroxysmal pulmonary hypertension (often provoked by intratracheal suctioning), cardiac output may fall rapidly and apparently “sudden” death may occur, particularly in neonates and infants. These outcomes are probably not purely the result of increased RV afterload, because they reflect impaired RV reserve as well.

Increased LV afterload may result from a sudden elevation of systemic arterial pressure, such as may occur during suctioning, restlessness, or hypoxia. These result in a sudden increase in LV afterload that, combined with impaired LV reserves, can result in low cardiac output early postoperatively. Sustained increase in systemic vascular resistance and LV afterload is present early after cardiac operations in at least half the adult patients operated on for acquired heart disease.

Often, disturbances of afterload (afterload mismatch) and preload (preload reserve) are neither independent nor isolated events. Increased RV afterload leads to decreased LV preload. Similarly, but not as important, increased LV afterload leads to decreased RV preload. A common situation in which a corrective operation leads to increased LV afterload is restoration of mitral valve competence or closure of a ventricular septal defect (VSD). In a physics analogy, mitral regurgitation or left-to-right flow through a VSD represents a pair of resistors in a parallel circuit in which R _T = 1/r ₁ + 1/r ₂ , where r ₁ and r ₂ represent resistances in the two outflow streams and R _T is total resistance. Closure of one outflow (r) increases downstream resistance to ventricular shortening; by inference, wall tension and myocardial oxygen consumption ( ) increase.

Patient-Specific

Chronic impairment of ventricular preload, afterload, and/or contractility by any mechanism (ventricular hypertrophy, stiffness, chronic heart failure) increases the risk of low cardiac output after the cardiac surgical procedure. These are for the most part immutable risk factors for low cardiac output, because they do not change quickly after the operation. However, when a patient who had been alive and ambulatory preoperatively has inadequate cardiac output postoperatively, the assumption must be that intraoperative damage has been superimposed on the chronic state. On the other hand, certain surgical procedures, such as ablation of the regurgitant volume of aortic regurgitation or closure of a defect with a large left-to-right shunt, have an immediately favorable impact on cardiac output. Thus, the cardiac surgical procedure itself often increases cardiac output; it is myocardial damage during the procedure that decreases it.

Acute reduction in ventricular contractility preoperatively can sometimes be ameliorated by intraoperative maneuvers. For the most part, these maneuvers are directed toward increasing an acutely reduced energy charge (see “Cold Cardioplegia, Controlled Aortic Root Reperfusion, and [When Needed] Warm Cardioplegic Induction” under Methods of Myocardial Management during Cardiac Surgery in Chapter 3 ).

Procedural

The most important intraoperative risk factor for low cardiac output early postoperatively, other than an incomplete operation, is a discrepancy between the duration of any global myocardial ischemia and the efficacy of the measures used for myocardial management (see complete discussion in Chapter 3 ). This is often reflected in the finding of long global myocardial ischemic time as a risk factor for low cardiac output and for death after operation. Coronary air embolization during CPB is said to adversely affect cardiac performance after the operation, but most air entering the coronary arteries while the heart is not supporting the circulation passes quickly into the coronary sinus and may have little deleterious effect.

The extensiveness of the “whole body inflammatory response” to CPB affects the heart as well and relates to the probability of low cardiac output after operation. This is one aspect of the association of duration of CPB with death after operation; another is that long CPB duration is sometimes the result, rather than the cause, of poor cardiac performance.

Low cardiac output can be the result of (1) an incomplete or inadequate operation; (2) acute myocardial ischemia, with or without necrosis, from impaired coronary blood flow resulting from failure of some part of a coronary artery bypass operation (CABG); (3) incomplete relief of ventricular inflow or outflow obstruction; (4) important residual or created AV valve or semilunar valve regurgitation that may increase the stroke volume requirements of the ventricle; and (5) residual VSD and large left-to-right shunt that may similarly increase LV stroke volume requirements.

One of the reasons for placing temporary fine polyvinyl catheters in the left atrium, right atrium, occasionally the pulmonary trunk via the RV and uncommonly the LV, and for placing temporary epicardial atrial and ventricular wires, is that they can be helpful in intraoperative and early postoperative efforts to identify an inadequate or incomplete operation as the cause of low cardiac output. TEE with color flow Doppler imaging is also important in identifying an incomplete or inadequate operation. The possibility of residual left-to-right shunting contributing to low cardiac output must always be considered after repair of congenital heart disease. With the materials now used as patches for repair of VSDs, an appreciable left-to-right shunt ( > 1.5) early postoperatively must be assumed to represent an incomplete repair or an overlooked defect. The shunt can be quantified by double indicator dilution, a method rarely used in the current era. Alternatively, the left-to-right shunt may be estimated in terms of the pulmonary ( ) to systemic ( ) flow ratio by simultaneously removing samples from the radial artery, right atrium, and pulmonary artery and solving the simplified shunt equation:

where Sa o ₂ is the percent oxygen saturation of arterial blood, S rao ₂ that of blood withdrawn from the right atrium, and S pao ₂ that of blood withdrawn from the pulmonary artery.

TEE with color flow Doppler imaging now can sometimes settle the issue simply, but without the desirable quantification. Intraoperative TEE has become standard of care for intracardiac repairs of congenital heart disease for patients 3 kg or larger. In one study, intraoperative TEE during post-repair evaluation led to surgical revision in 4% of cases.

Noninvasive Methods

When cardiac output is low, preload is manipulated by increasing blood volume with an appropriate fluid until the higher of the two atrial pressures is about 15 mmHg. If the wall thickness of the LV is unusually great or its contractility or compliance is decreased, it may be helpful to raise mean left atrial pressure to 20 mmHg. However, the tendency to pulmonary edema is increased when left atrial pressure is elevated to this level. When the RV is the limiting factor in cardiac performance, right atrial pressure usually can be raised advantageously only to about 18 mmHg. Above this, a descending limb on the Starling curve usually becomes apparent, and cardiac output falls. Also, the tendency to whole body fluid retention, pleural effusion, and ascites is increased by high right atrial pressure.

When LV performance is the limiting factor and systemic arterial blood pressure is more than 10% above normal (see Table 5-1 ), vasodilating agents should be used to reduce LV afterload to between normal and 10% above normal. Nitroprusside is generally the drug of choice because it is a potent arterial, and to a lesser extent venous, dilator with a short half-life (see Appendix 5A ). The drug appears to be as safe in very young patients as it is in adults. Calcium channel antagonists (e.g., nifedipine, diltiazem) lead to similar arteriolar vasodilatation and may improve coronary perfusion in this setting. However, their longer half-life and depressive effect on ventricular contractility make nitroprusside the preferred drug.

Rarely in patients with severe long-standing mitral valve disease or congenital heart disease with pulmonary vascular obstructive changes, RV dysfunction associated with elevated pulmonary artery pressure may limit cardiac performance. Reduction of RV afterload with vasodilating agents is occasionally dramatic in its increase of RV, and thus cardiac, stroke volume. Nitroprusside (0.5 to 3 µg · kg ⁻¹ · min ⁻¹ ), nitroglycerin (0.5 to 3 µg · kg ⁻¹ · min ⁻¹ ), or phentolamine (1.5 to 2 µg · kg ⁻¹ · min ⁻¹ ) may be effective in this setting. In infants, maintaining near-anesthesia for 24 to 48 hours with fentanyl or another intravenously administered agent may minimize paroxysms of pulmonary artery hypertension and the consequent increased RV afterload (see “ Pulmonary Hypertensive Crises ” later in this section).

Alternatively, management of neonates and infants may be based on use of the long-acting α-receptor blocking agent phenoxybenzamine (see Appendix 5A ). It is administered first at the commencement of CPB (see “Other Additives” under Perfusate in Section II of Chapter 2 ). An additional dose is usually given about 12 hours after returning to the ICU.

Heart rate is adjusted to optimal levels when necessary by atrial pacing, by ventricular pacing when atrial fibrillation is present, or by AV sequential pacing when AV dyssynchrony or dissociation is present. When tachyarrhythmias are present, pharmacologic means of control may be used (see text that follows).

If these relatively simple measures do not quickly bring cardiac performance to an adequate level, inotropic agents are begun (see Appendix 5B for details), although their disadvantages are recognized. There is no ideal inotropic agent, nor are there specific indications for specific agents. In their review, Doyle and colleagues classified inotropic drugs based on their effect on intracellular cyclic adenosine monophosphate (cAMP): cAMP-independent drugs include calcium, digoxin, and α-adrenergic agonists; cAMP-dependent agents include epinephrine (and levarterenol), dobutamine, and isoproterenol. These are β-adrenergic agonists that, coupled with dopaminergic drugs (dopamine), have variable effects on peripheral resistance. Phosphodiesterase inhibitors (amrinone, milrinone, enoximone) may enhance contractility while producing myocardial relaxation (lusitropism) and relaxation of vascular smooth muscle. They are not susceptible to receptor down-regulation.

Initially, dopamine may be infused at 2.5 µg · kg ⁻¹ · min ⁻¹ . This dose can be increased to 15 or 20 µg · kg ⁻¹ · min ⁻¹ if needed, but if a favorable response is not obtained at 10 µg · kg ⁻¹ · min ⁻¹ , it is not likely to be obtained at higher doses. Dopamine has the advantage of augmenting renal blood flow in addition to increasing cardiac contractility. Dopamine increases ventricular automaticity (hence the probability of ventricular arrhythmias), but to a lesser extent than isoproterenol. At low doses (2 to 4 µg · kg ⁻¹ · min ⁻¹ ), systemic peripheral vascular resistance is decreased or unchanged by dopamine, whereas higher doses (>6 µg · kg ⁻¹ · min ⁻¹ ) increase peripheral resistance. Tachycardia may limit the rate at which dopamine can be administered. When dopamine is ineffective, dobutamine is gradually added in similar doses. Dobutamine, although more expensive than dopamine, appears to augment myocardial blood flow more ; in general, its effectiveness is similar to dopamine. Isoproterenol may be preferred initially and is probably superior in the presence of predominantly RV dysfunction and decreased or normal heart rate because of its favorable effect on pulmonary vascular resistance.

Occasionally, hypotension exists in the presence of normal and adequate cardiac output. Under that special circumstance, norepinephrine administered through a central venous catheter is rational treatment; a very low dose (0.01 µg · kg ⁻¹ · min ⁻¹ ) is often sufficient under these circumstances. Under more dire circumstances, larger doses can be used.

Epinephrine is the catecholamine of choice of some, but its powerful vasoconstricting effects make it less desirable than dopamine or dobutamine. When an insufficient response is obtained from other drugs, or excessive tachycardia develops, epinephrine is added or substituted. The drug is initially infused at a dose of 0.01 to 0.05 µg · kg ⁻¹ · min ⁻¹ , which may be increased as needed.

Milrinone also is useful in patients with low cardiac output after cardiac surgery, because it combines a peripheral vasodilatory action with its inotropic effect. This drug is different in structure and mode of action from catecholamines in that it is a phosphodiesterase enzyme inhibitor in cardiac and vascular tissue, not a β-adrenergic receptor agonist. Administration is usually initiated with a loading dose of 5 µg · kg ⁻¹ over 10 minutes, followed by a maintenance dose of 0.3 to 0.75 µg · kg ⁻¹ · min ⁻¹ . The drug is effective in neonates and infants as well as adults, but in small patients, particular care is necessary to maintain an adequate blood volume because of the vasodilatory effect of the drug. The indications for this drug vs. catecholamines remain arguable. However, it appears to cause less tachycardia and fewer atrial arrhythmias than catecholamines.

Additionally, 10% calcium chloride is administered in a dose of 0.1 mmol · kg ⁻¹ , with supplemental doses if the ionized serum calcium level is below 1.2 mmol · L ⁻¹ .

Once the acute problems have subsided, some patients in sinus rhythm appear to require chronic augmentation of ventricular contractile function. Use of digitalis in this setting has long been argued, but there is evidence that it does increase contractility. Digitalization appears to be useful, particularly in children (see “ Atrial Arrhythmias ” under Cardiac Arrhythmias later in this section), but it is not recommended in neonates because it may impair diastolic function.

Intraaortic Balloon Pump

The concept of intraaortic balloon pumping (IABP) to produce diastolic augmentation of coronary and systemic blood flow was elucidated by Moulopoulos, Topaz, and Kolff in 1962. The procedure was first performed clinically by Kantrowitz and colleagues in 1968. IABP uses the principle of diastolic counterpulsation, which augments diastolic coronary perfusion pressure, reduces systolic afterload, favorably affects the myocardial oxygen supply/demand ratio, and augments cardiac output.

IABP is used in adult patients with inadequate cardiac performance not responsive to optimized preload, afterload, and heart rate or to moderate doses (up to 10 µg · kg ⁻¹ · min ⁻¹ ) of dopamine or equivalent doses of dobutamine or epinephrine (see Appendix 5B ). Whenever possible, the decision to insert an IABP is made in the OR rather than postoperatively. It is used in preference to catecholamines postoperatively for patients with severe LV dysfunction, with or without evidence of myocardial necrosis, and for patients with evidence of myocardial necrosis and inadequate cardiac output or severe ventricular arrhythmias. This technique has led to survival of some patients who would otherwise have died. Survival is less than 50% if renal failure develops from low cardiac output postoperatively. IABP has been effective in patients with ischemic heart disease and valvar and congenital heart disease.

Preoperative prophylactic insertion of the IABP is sometimes advisable. In addition to its use in myocardial infarction with low cardiac output or shock, preoperative insertion is often helpful in unstable angina, left main disease with ongoing ischemia, and ischemia leading to ventricular arrhythmias. In the era of more complex arterial revascularization for ischemic heart disease (see Chapter 7 ), IABP support is helpful intraoperatively for pre-bypass support of patients with low ejection fraction. For patients with acute mitral regurgitation or ventricular septal rupture, insertion upon diagnosis is often lifesaving. Perhaps the most frequent indication for preoperative IABP insertion is poor perfusion from either low cardiac output or peripheral arterial disease. It follows that the best survival following IABP occurs when the device is in place preoperatively.

Insertion by arterial puncture is generally used, despite its somewhat higher prevalence of vascular complications, because of the technical ease of balloon insertion and removal. When the patient is still on CPB, or the femoral pulse cannot be palpated because of hypotension, an incision only in the skin is made over the femoral artery. Through this incision, the femoral artery can nearly always be palpated and the arterial puncture technique used.

Important aortoiliac occlusive disease and abdominal aortic aneurysm greatly increase the risk of vascular complications or failure of insertion when the femoral route is used. In their presence, the balloon can be inserted into the ascending aorta through a purse-string suture. This is usually performed before discontinuing CPB. A pledgeted mattress suture of 2-0 or 3-0 polypropylene is placed in the midportion of the ascending aorta. A tie is placed on the shaft of the intraaortic balloon to indicate the point that should be level with the aortic wall when the balloon is in proper position within the descending aorta. An aortic stab wound is made and controlled digitally, and the balloon is introduced through the wound and passed into the descending aorta. Proper position is verified by appearance of the characteristic aortic pressure pulse when pumping is begun. The balloon shaft is usually brought out through the lower end of the sternotomy incision. When pumping is no longer needed, the patient is returned to the OR, the median sternotomy reopened, and another pledgeted mattress suture placed outside the original one. As the balloon is removed, the stab wound is controlled digitally, and the pledgeted mattress suture is made snug and tied. In severe atheromatous aortic wall disease, use of other assist devices is probably indicated (see “ Temporary Ventricular Assistance ” in text that follows).

IABP is begun in a 1 : 1 ratio with ventricular diastole, as judged by electrocardiographic (ECG) and arterial pressure pulse signals. Often the patient's hemodynamic state improves promptly; consideration is then given to weaning the patient from IABP as early as 6 to 12 hours after insertion. If catecholamines have also been required, they are reduced as rapidly as possible to 5 µg · kg ⁻¹ · min ⁻¹ of dopamine or less, or the equivalent doses of dobutamine or epinephrine (see Appendix 5B ). Once the hemodynamic state is improved, the IABP ratio is progressively reduced to 1 : 8 (or 1 : 3 with some systems). In most postoperative patients, the final reduction can be reached within 12 to 48 hours. The balloon can then be removed using a closed method. Although objections have been raised to use of this method, most of the problems have occurred when the balloon inadvertently was inserted through the superficial rather than the common femoral artery. After removing the balloon percutaneously, firm pressure is applied to the groin and held for half an hour. If circulation to the leg becomes impaired or a hematoma becomes apparent, prompt exploration in the OR is indicated.

Circulation in the leg distal to the site of balloon insertion is observed systematically. If signs of ischemia appear, generally the balloon is removed. Complications that importantly impede convalescence occur in about 3% of patients.

Temporary Ventricular Assistance

Ventricular assist devices (VADs), probably first used in a planned fashion by Cooley and colleagues in 1969, are now used (1) for support after cardiac operations, (2) as a bridge to transplantation, and (3) as a bridge to recovery. Without VADs, nearly all patients assisted would likely have died; however, uncertainty about this makes interpreting outcomes and indications for them difficult. It also hampers efforts to determine their direct risks. The following discussion relates to use of various temporary VADs for cardiopulmonary failure after cardiac operations. (A discussion of use of these devices for other indications can be found in Chapter 22 .)

Cardiopulmonary Support and Extracorporeal Membrane Oxygenation

Right and left heart bypass (biventricular assist) works only if pulmonary function is adequate to support gas exchange. In situations of severe compromise of the respiratory system, support of that system is also required. Portable CPB systems (cardiopulmonary support [CPS]) include both a centrifugal blood pump and a membrane oxygenator, with heparin-coated tubing. These systems are usually referred to as extracorporeal membrane oxygenation (ECMO). Successful use has been reported, particularly in infants and children, and there is little doubt that in some patients, it is an effective means of biventricular support. (It may be used occasionally in venovenous configuration to support respiration in the face of severe postoperative arterial desaturation from impaired pulmonary function. ) This methodology has also been used in patients undergoing myocardial infarction or sustaining a catastrophic event in the cardiac catheterization laboratory, and as a support technique during angioplasty.

Only two cannulae have to be inserted, one in the right atrium and the other in a systemic artery. These cannulae are present during surgery and may simply be attached to the system. Oxygenation is achieved in a closed system without an air-to-blood interface. Alternatively, separate venous and arterial cannulae may be inserted through the femoral artery and femoral or jugular vein by percutaneous technique (see “Cardiopulmonary Bypass Established by Peripheral Cannulation” under Special Situations and Controversies in Section III of Chapter 2 ). This places the cannulae in a position for ready control of hemorrhage. Centrally placed cannulae are removed so that the wound may be closed. Percutaneous placement of cannulae and use of the CPS system can be used for emergency support of the failing circulation at the bedside. The CPS system does not ordinarily provide decompression of the LV. LV unloading depends on total diversion of blood from the right atrium to the extracorporeal circuit and the ability of the LV to empty pulmonary venous return to the aorta. A beating heart and absence of aortic valve regurgitation are necessary.

Ventricular Electrical Instability

Ventricular electrical instability includes PVCs, ventricular tachycardia, and ventricular fibrillation. Controversy exists concerning the proportion of postoperative patients with frequent PVCs and some types of ventricular tachycardia who are at risk of developing ventricular fibrillation. Despite this, it is prudent to assume that such arrhythmias early postoperatively place the patient at an increased risk of sudden death. Therefore, to detect such arrhythmias, the ECG is monitored continuously for at least the first 48 hours after operation.

Unifocal isolated PVCs occurring outside the T waves fewer than six times per minute are not known to increase the risk of cardiac death and are compatible with normal convalescence. Other arrhythmias indicate an abnormal convalescence and may require special management. Rarely, atrial fibrillation or isolated premature ventricular beats occurring early (within 2-4 hours) after operation in the presence of hypothermia or low potassium level lead to profound ventricular instability, including ventricular fibrillation.

Management of ventricular electrical instability occurring in cardiac surgery patients after postoperative day 1 or 2 has been importantly affected by the results of the Cardiac Arrhythmia Suppression Trial (CAST). This trial demonstrated that drugs used to suppress ventricular electrical instability can themselves be lethal and are often ineffective. Application of these findings to the postoperative patient and implications for treatment are not well understood. For example, CAST patients for the most part had persisting ischemia; most postoperative patients (coronary disease or not) are probably well revascularized. In the postoperative period, however, many antiarrhythmic agents are proarrhythmic; therefore, treating ventricular arrhythmias other than ventricular tachycardia is probably not necessary.

In patients with an ejection fraction under 40% with postoperative ventricular tachycardia, early electrophysiologic study is indicated. Paradoxically, patients in whom such studies demonstrate acute suppression of PVCs or ventricular tachycardia with the administration of drugs have a good prognosis without drug treatment; such patients probably should be discharged from the hospital on no drug therapy. By contrast, patients whose ventricular arrhythmias cannot be suppressed with drugs have a relatively poor prognosis, and consideration should be given to implanting an implantable cardioverter-defibrillator (ICD; see “Ventricular Tachycardia and Ventricular Fibrillation in Ischemic Heart Disease” in Section V of Chapter 16 ).

When during the first day or two of convalescence, ventricular electrical instability develops in the form of PVCs occurring more than six times per minute or ventricular tachycardia persisting more than 20 to 30 seconds, treatment is prudent even if cardiac performance is good ( Appendix 5C ). Often, PVCs or bursts of ventricular tachycardia can be suppressed by atrial or ventricular pacing using temporary electrodes, without need for drug therapy. When the hemodynamic state is impaired by ventricular tachycardia, immediate direct current cardioversion (100 J initially in adults and, if ineffective, 200 J) is indicated. When these measures are ineffective, advice of an experienced electrophysiologically oriented cardiologist is indicated.

Atrial Arrhythmias

During Intubation

Adequacy of pulmonary function early postoperatively while the patient is still intubated and receiving controlled ventilation is judged by the response of Pa o ₂ and arterial carbon dioxide pressure (Pa co ₂ ) to the minute volume of ventilation and ventilating gas mixture being used. The response of the arterial oxygen levels can be expressed as the alveolar-arterial oxygen difference, P(A − a)O ₂ , which in intact humans is normally only a few mmHg. Nearly all patients early after cardiac operations have abnormally large alveolar-arterial oxygen differences due to intrapulmonary right-to-left shunting of 3% to 15%. This assumes that no right-to-left intracardiac shunting is present. Response of the carbon dioxide levels can be expressed as the minute volume of ventilation required to maintain Pa co ₂ at 30 to 45 mmHg. Usually this is about 15 to 20 mL · kg ⁻¹ in both adults and children.

When anesthesia and heavy sedation are no longer present and the ventilator is in a mode of intermittent mandatory ventilation (IMV), the patient's ventilatory rate is a useful guide to the ease with which the respiratory center's needs are met, and thus to the adequacy of pulmonary function. In an adult, a patient-triggered respiratory rate of 8 to 12 breaths · min ⁻¹ , with the usual tidal volume, inspiratory gases, and end-expiratory pressure, indicates adequacy of lung function.

Positive end-expiratory pressure (PEEP) may be used as a routine or on indication, with a setting of 5 to 8 cm H ₂ O for adults and children older than 12, and 4 cm H ₂ O for younger patients. Unless the hemodynamic state is suboptimal, PEEP does not alter it, even in infants. PEEP is used because of studies that suggest it is associated with larger lung volumes, fewer perfused but nonventilated alveoli during ventilation, and smaller P(A − a)O ₂ after extubation. PEEP is generally not advisable in patients with chronic obstructive lung disease (to avoid air trapping and rupturing a bulla, with consequent pneumothorax) and in infants and children who have undergone a Fontan operation or cavopulmonary anastomosis (to avoid still further elevation of jugular venous pressure; see Chapter 41 ).

Continuous positive airway pressure (CPAP) may be used in infants once their cardiovascular state is stable, obviating the need for intermittent positive-pressure breathing (IPPB) and IMV. Should IPPB be required initially, the infant is transferred to IMV and sometimes to CPAP for several hours before extubation.

Extubation

Traditionally, continued intubation after cardiac operations has been recommended to maintain more precise control of cardiopulmonary physiology. However, early extubation may shorten ICU and hospital stay. Therefore, a protocol beginning with anesthesia induction may be designed to expedite awakening and spontaneous breathing.

Once the patient has been extubated, Pa co ₂ and Pa o ₂ levels, as well as the visually estimated work of breathing, are useful indices of pulmonary function. Pa co ₂ of less than 45 mmHg in adults, less than 50 mmHg in young children, and less than 55 mmHg in small infants indicates an adequate minute volume of ventilation. Higher values indicate inadequate alveolar ventilation. Pa o ₂ is often mildly depressed at this time and usually remains so for the first few days after cardiac surgery performed with CPB ( Fig. 5-9 ). This results from the somewhat widened alveolar-arterial oxygen difference. These measurements are valuable, but when a patient is comfortable, breathing easily and slowly, and the chest radiograph is essentially normal, it is highly probable pulmonary function is adequate and convalescence will be satisfactory.

Patient-Specific

Patient-specific risk factors for pulmonary dysfunction after cardiac surgery have long been recognized, but formal identification and quantification are rare. In a formal observational study, young age at operation was identified as a risk factor, particularly when the patient was younger than about 2 years old ( Fig. 5-10 ). Similar observations were made by Lell and colleagues. Increased risk with young age is associated with the increased tendency of the very young to develop whole body edema after CPB. In the experience of most institutions, and in a study by Gallagher and colleagues, older age , particularly older than 60 years, has also been associated with increased prevalence of pulmonary dysfunction after cardiac surgery. Chronic obstructive lung disease is an important risk factor for pulmonary dysfunction postoperatively and increases the overall risk of operation because it predisposes patients to increased work of breathing and air trapping. Preoperative pulmonary arterial hypertension , even when associated with low pulmonary arteriolar resistance, predisposes infants to pulmonary dysfunction and also to paroxysms of pulmonary arteriolar constriction and pulmonary hypertension early postoperatively (see “ Pulmonary Hypertensive Crises ” later in this section). Congenital morphometric pulmonary abnormalities like the alveolar hypoplasia frequently present in patients with congenital heart disease and Down syndrome increase the prevalence of postoperative pulmonary dysfunction. Some drugs given during the period before operation increase the prevalence of pulmonary complications postoperatively; amiodarone , used to control cardiac arrhythmias, has been linked to severe pulmonary dysfunction after cardiac surgery.

Procedural

The type of oxygenator used is probably related to the amount of pulmonary dysfunction generated by the operation, with oxygenators other than membrane-type being risk factors for pulmonary damage. Proper filters in the arterial tubing may reduce pulmonary dysfunction postoperatively. Longer duration of CPB is a risk factor. This is probably related in part to the direct correlation between duration of CPB and increase in the patient's extracellular water ( Fig. 5-11 ). The amount of C3a generated by complement activation during CPB is a risk factor for pulmonary dysfunction; this may relate to a greater amount of neutrophil activation with higher levels of C3a. Use of external cardiac cooling , particularly by ice slush rather than cold saline, increases the prevalence of left phrenic nerve paralysis, hence the tendency to postoperative pulmonary dysfunction.

Postoperative

Postoperative events can increase the probability of pulmonary dysfunction. Elevated left atrial pressure , with consequent elevation of pulmonary capillary and venular pressures, aggravates the tendency toward increased lung water and pulmonary dysfunction. The longer the patient is on a ventilator, the greater the chances of continuing pulmonary dysfunction. Paralysis of the phrenic nerve and the consequent elevation of the left hemidiaphragm predispose patients to continuing pulmonary dysfunction, particularly small patients.

General Measures

Patients who are convalescing normally are extubated either in the OR or during the early hours after operation. In most ICUs, it is advisable to extubate patients in the daytime rather than at night; this consideration is a reasonable cause of delay of extubation for a few hours. Otherwise, when pulmonary function is good, extubation should be delayed only under special circumstances, including the presence of cardiac assist devices and the possibility of early reoperation. In general, criteria for extubation include stable and satisfactory cardiac performance, lack of important cardiac arrhythmia, and appropriate awakening with satisfactory neurologic status. There should be no anticipation of return to the OR (e.g., for bleeding) and satisfactory mechanics and ventilatory lung function, as assessed by arterial blood gas analysis and a clinical estimate of inspiratory force and volume. Increasing emphasis has been placed on the advisability of routine extubation of the normally convalescing patient within 6 hours of arrival in the ICU.

A major cause of postoperative pulmonary dysfunction is atelectasis and the associated loss of functional alveolar units. Standard prophylactic measures include chest physiotherapy and use of devices to encourage deep inspirations to recruit atelectatic areas. Zarbock and colleagues demonstrated a beneficial effect of prophylactic nasal positive airway pressure at 10 cm H ₂ O for at least 6 hours.

Treatment of patients with pulmonary dysfunction who are still intubated during the early hours after operation is in large part an intensification of the usual management, as effective specific therapy is not available. Fractional inspired oxygen (F io ₂ ) is appropriately adjusted upward if P(A − a)O ₂ is large. Minute volume of respiration (not only measured, but judged visually by excursion of the chest wall) and respiratory rate are adjusted to maintain Pa co ₂ at about 30 to 35 mmHg. The airway is kept clear by appropriate tracheal suctioning (see “ Pulmonary Hypertensive Crises ” later in this section for special precautions in neonates and infants). When hemoconcentration develops from leakage of plasma from the intravascular space into the interstitial space of the lungs, and at times into all other organs and the pleural and peritoneal spaces, administration of concentrated serum albumin is helpful in counteracting this trend. Diuretics are useful because they reduce extracellular fluid volume and, in turn, extravascular lung water. During all this, efforts continue to reduce ventilatory support and work toward extubation of the patient (see Appendix 5F ). Spontaneous breathing trials and decreasing levels of pressure support appear equally effective in patients who are difficult to wean.

Prolonged Intubation

A prolonged period of endotracheal intubation is necessary when:

• ▪

  Criteria for extubation are not met.

• ▪

  Neurologic complications are present.

• ▪

  Severe dysfunction of the cardiac subsystem is present.

• ▪

  Persistent chest drainage or a residual cardiac defect make early return to the OR likely.

During periods of prolonged ventilation, active decisions are required regarding use of continuous vs. intermittent sedation and neuromuscular blockade, depending on hemodynamic stability, effectiveness of ventilation, and timing of ventilator weaning. Commonly used sedation and paralytic agents are described in Tables 5-4 and 5-5 .

When patients are agitated after cardiac surgery, particularly during ventilator weaning, the first priority is evaluating cardiac and pulmonary subsystems to ensure that agitation is not an indicator of important cardiac or pulmonary dysfunction. If these subsystems have satisfactory function, the next level of intervention targets communication with the patient by nursing or physician staff, or both, to allay patient anxiety. When these interventions are insufficient, pharmacologic agents commonly used to alleviate agitation and anxiety in the ICU include benzodiazepines (e.g., diazepam, lorazepam, midazolam), opioid analgesics (e.g., fentanyl, hydromorphone, morphine, remifentanil), propofol, dexmedetomidine, and neuroleptics (e.g., haloperidol).

Prolonged intubation (≥48 hours) entails problems necessitating fastidious care of the patient. A pneumothorax occasionally develops from positive-pressure breathing, usually requiring urgent aspiration and underwater drainage. Bronchospasm may become a particular problem, probably as a reflex response to proteinaceous tracheobronchial fluid often present under these circumstances. Administration of nebulized isoetharine every hour can be helpful. In extreme cases, aminophylline is given as a continuous intravenous infusion in 10% dextrose in a dose of 0.15 mg · kg ⁻¹ · min ⁻¹ . An initial loading dose of about 4 mg · kg ⁻¹ is given over 20 minutes. Neonates, infants, and young children who require intubation and ventilation for more than about 14 days often have phrenic nerve paralysis; in these patients, plication of the hemidiaphragm often permits prompt extubation. Plication usually does not interfere with recovery of phrenic nerve and diaphragmatic function.

In those unusual circumstances when intubation in older children and adults is necessary for more than about 10 days, consideration is given to tracheostomy. Both patient comfort and effectiveness of ventilation are thereby usually increased. This procedure has disadvantages but is sometimes helpful in weaning the patient from the ventilator. Tracheostomy is rarely performed in neonates, infants, and young children, because it is difficult to manage in this age group.

Reintubation

When the patient meets all criteria for extubation, reintubation is usually unnecessary. However, reintubation is indicated when:

• ▪

  Pa co ₂ rises above 50 mmHg over 4 hours in the absence of appropriate respiratory compensation for metabolic alkalosis.

• ▪

  Signs of decreasing cardiac output are noted.

• ▪

  Signs of exhaustion from breathing spontaneously are observed.

• ▪

  Excessive pulmonary secretions with ineffective coughing are evidenced.

When the situation is borderline, proper management requires careful observation by senior members of the team. Reintubation should be performed by a competent professional.

Pulmonary Hypertensive Crises

Prevention

Because pulmonary hypertensive crisis may be fatal despite intense therapy, its prevention is critical. An important preventive measure in neonates and infants is maintenance of paralysis and sedation (with pancuronium [or a similar agent] and fentanyl) for at least the first 20 to 24 postoperative hours, and for at least another 24 hours or longer if the patient remains intubated (see Section IV, “ General Care of Neonates and Infants ,” later in this chapter). Fentanyl has been shown to be a safe agent in neonates and adults, with little adverse effect on cardiac function or systemic and pulmonary circulations. A paralytic agent (see Table 5-4 ) is given along with fentanyl to prevent rigidity. Fentanyl (in a dose of 25 µg · kg ⁻¹ ), along with pancuronium, should be given before suctioning the endotracheal tube in any neonate or infant who is not already well paralyzed and sedated, because it appears to minimize the possibility of a pulmonary hypertensive crisis. In addition to sedation, aggressive treatment of acidosis, including hyperventilation to P co ₂ = 30 to 34 mmHg, decreases prevalence and severity of pulmonary hypertensive crises. When the monitored pulmonary artery pressure becomes paroxysmally elevated early postoperatively, efforts are made to control and reduce it. A high F io ₂ is maintained because this is as useful an agent as exists for reducing pulmonary vascular resistance. Direct infusion of nitroprusside into the pulmonary artery has also been useful. Many agents have been advanced as being optimal on the grounds that they selectively reduce pulmonary vascular resistance, but few do so, and no clearly superior one has been identified.

There are encouraging results from use of inhaled nitric oxide to reduce pulmonary artery pressure in cardiac transplant recipients, patients on LV assist devices, and generally in infants and children prone to pulmonary hypertensive crises. Journis and colleagues found that 15 of 17 children having critical pulmonary hypertension following operation for congenital heart disease responded to inhaled nitric oxide (20 ppm) after failure of conventional medical treatment ( Table 5-6 ). Pulmonary arterial pressure decreased without a change in systemic arterial pressure but with concomitant increase of Sa o ₂ and . Other investigators have also shown an increase in cardiac index and improvement of indices of RV function after nitric oxide treatment. Intrapulmonary shunt fraction may decrease as well. The response in postoperative patients with valvar heart disease may be less satisfactory.

Table 5-6

Effects of Inhaled Nitric Oxide on Hemodynamics after Operations for Congenital Heart Defects ^a

	T 0 (before NO)	T 1 (20 min after NO)	P
HR (beats · min −1 )	153 ± 22	145 ± 21	.008
Systolic P pa (mmHg)	60 ± 14	40 + 11	.0003
Mean P pa (mmHg)	42 ± 14	27 ± 8	.0008
Diastolic P pa (mmHg)	31 ± 14	18 ± 10	.0003
Systolic P ao (mmHg)	68 +12	69 ± 7	.18
Mean P ao (mmHg)	55 ± 11	56 ± 6	.4
Diastolic P ao (mmHg)	44 ± 10	46 ± 6	.12
P la (mmHg)	7.2 ± 1.9	6.8 ± 1.5	.3
P cv (mmHg)	6.6 ± 2.5	5.2 ± 1.8	.04
(%)	50 ± 13	67 ± 12	.003
Sa o 2 (%)	87 ± 8	96 ± 3	.0007

Key: HR, Heart rate; NO, nitric oxide; P ao , systemic arterial pressure; P cv , central venous pressure; P la , left atrial pressure; P pa , pulmonary arterial pressure; Sa o ₂ , arterial oxygen saturation;
, mixed venous blood oxygen saturation.

a Nitric oxide inhaled at 20 ppm reduces pulmonary artery pressure and improves while having no effect on systemic artery pressure when given to a group of patients following operations for defects associated with pulmonary hypertension.