383CHAPTER 36 Critical Care After Surgery for Congenital Cardiac Disease (Box 36 2) The details of the specific considerations for selected lesions are presented in their respective sections The initi[.]
Trang 1(Box 36.2) The details of the specific considerations for selected
lesions are presented in their respective sections
The initial assessment following cardiac surgery begins with a
review of the operative findings This includes details of the
op-erative repair and CPB, particularly total CPB time, myocardial
ischemia (aortic cross-clamp), and circulatory arrest or antegrade
perfusion times; concerns about myocardial protection; recovery
of myocardial contractility; typical postoperative systemic arterial
and central venous pressures; findings from intraoperative
trans-esophageal or epicardial echocardiography, if performed;
vasoac-tive medication requirements; and hemostatic management This
information guides subsequent examination, which should focus
on the quality of the repair or palliation plus a clinical assessment
of cardiac output (Box 38.3) In addition to a complete
cardio-vascular examination immediately upon arrival to the PICU, a
routine set of laboratory tests should be obtained, including a
chest radiograph, 12- or 15-lead electrocardiography (ECG),
blood gas analysis, serum electrolytes and glucose, ionized
calcium and lactate measurements, complete blood count, and
coagulation profile
This information, together with an understanding of the
preoperative and postoperative loading conditions of the heart, are
essential for clinical management in the immediate postoperative period Optimizing preload involves more than just giving volume
to a hypotensive patient There are numerous considerations to fluid balance involving types of isotonic fluid, ultrafiltration in the operating room, optimal hematocrit, and the use of diuretics or vasopressors Fluid itself can be detrimental if excess extravascular water results in interstitial edema and end-organ dysfunction of vital organs such as the heart, lungs, and brain Occasionally, per-mitting a right-to-left shunt at the atrial level can optimize preload
to the left ventricle in some conditions (discussed later) Maintain-ing aortic perfusion after CPB and improvMaintain-ing the contractile state
of the heart with higher doses of catecholamines are reasonable goals, but they may have particularly deleterious consequences in the newborn myocardium after hypothermic CPB The benefits of afterload reduction are well known but, if excessive, may result in hypotension, coronary insufficiency, and cardiovascular collapse Pacing the heart can stabilize the rhythm and hemodynamics, but
it also may contribute to dyssynchronous, inefficient cardiac con-traction or may induce other arrhythmias Although lifesaving in many instances, mechanical support of the failing myocardium in the form of extracorporeal life support (ECLS) or ventricular assist devices has its own set of limitations and morbidities Almost every treatment approach has its own set of adverse effects Supporting cardiac output in the postoperative patient is a balance between the promise and poison of therapy
Monitoring
The goal of postoperative monitoring following cardiac surgery primarily focuses on assessing the adequacy of circulatory status and oxygen delivery The level of vigilance in the immediate post-operative period can be optimized by the combination of labora-tory values and physical examination findings with data obtained via noninvasive devices and invasive monitoring to assess intracar-diac pressures and oxygen saturations
Near-infrared spectroscopy (NIRS) provides a noninvasive, continuous estimate of regional oxygen supply and demand that serves as a surrogate for hemodynamics and cerebral and somatic oxygenation It is based on the differential absorption of varying wavelengths of light by hemoglobin as it associates with oxygen to measure oxygen content in a localized tissue bed.22 While data demonstrating a definitive impact on overall outcome are lacking, there are reports that correlate decreased cerebral and/or somatic NIRS with increased mortality, prolonged length of stay (LOS), and worsening neurologic outcomes.23 , 24
Invasive monitoring of central venous pressure is routine for most patients following cardiac surgery Intracardiac or transtho-racic left atrial (LA) catheters are often used to monitor patients after complex reparative procedures Pulmonary arterial (PA) catheters now are seldom used but may be particularly useful if one anticipates postoperative pulmonary hypertension, allowing rapid detection of pressure changes and assessment of the response to interventions
LA catheters are especially helpful in the management of pa-tients with ventricular dysfunction, coronary artery perfusion abnormalities, or mitral valve disease The mean LA pressure typically is 1 to 2 mm Hg greater than mean right atrial (RA) pressure, which generally varies between 1- and 6-mm Hg in nonpostoperative pediatric patients undergoing cardiac catheter-ization In postoperative patients, mean LA and RA pressures are often greater than 6 to 8 mm Hg However, they generally should
be less than 15 mm Hg The compliance of the right atrium is
• BOX 36.2 Ten Intensive Care Strategies to Diagnose
and Support Low–Cardiac Output States
1 Know in detail the cardiac anatomy and its physiologic consequences.
2 Understand the specialized considerations of the newborn and
implica-tions of reparative rather than palliative surgery.
3 Diversify personnel to include experts in neonatal and adult congenital
heart disease.
4 Monitor, measure, and image the heart to rule out residual disease as a
cause of postoperative hemodynamic instability or low cardiac output.
5 Maintain aortic perfusion and improve the contractile state.
6 Optimize preload (including atrial shunting).
7 Reduce afterload.
8 Control heart rate, rhythm, and synchrony.
9 Optimize heart-lung interactions.
10 Provide mechanical support when needed.
• BOX 36.3 Signs of Heart Failure or Low–Cardiac
Output States
Signs
Cool extremities/poor perfusion
Oliguria and other end-organ failure
Tachycardia
Hypotension
Acidosis
Cardiomegaly
Pleural effusions
Monitor and Assess
Heart rate, blood pressure, intracardiac pressure
Extremity temperature, central temperature
Urine output
Mixed venous oxygen saturation
Arterial blood gas pH and lactate
Laboratory measures of end-organ function
Echocardiography
Trang 2greater than that of the left atrium except in the newborn; thus,
pressure elevations in the right atrium of older patients with two
ventricles typically are less pronounced Possible causes of
abnor-mally elevated LA pressure are listed in Box 38.4
In addition to pressure data, intracardiac catheters in the right
atrium (or a percutaneously placed central venous catheter), left
atrium, and pulmonary artery can be used to monitor the oxygen
saturation of systemic or pulmonary venous blood and indicate
the presence or absence of atrioventricular synchrony Following
reparative surgery, patients with no intracardiac shunts and
ade-quate cardiac output may have a mild reduction in RA oxygen
saturation to approximately 60% Lower RA oxygen saturation
does not necessarily indicate low cardiac output If a patient has
arterial desaturation (complete mixing lessons, lung diseases, and
so on), the arteriovenous oxygen saturation difference is normally
,30% Hence, even a low RA saturation may be in keeping with
appropriate oxygen delivery and extraction Elevated RA oxygen
saturation often is the result of left-to-right shunting at the atrial
level (e.g., from the left atrium, anomalous pulmonary vein, or
left ventricular [LV]-to-RA shunt) Blood in the LA normally is
fully saturated with oxygen (i.e., approximately 100%) The two
chief causes of reduced LA oxygen saturation are an atrial-level
right-to-left shunt and pulmonary venous desaturation from
ab-normal gas exchange
In the absence of left-to-right shunts, PA oxygen saturation is
the best representation of the “true” mixed venous oxygen
satura-tion because all sources of systemic venous blood should be
thor-oughly mixed as they are ejected from the RV When elevated, this
saturation is useful in identifying residual significant left-to-right
shunts following repair of a VSD The absolute value of the PA
oxygen saturation is a predictor of significant postoperative
re-sidual shunt In patients following TOF or VSD repair, PA
oxy-gen saturation greater than 80% within 48 hours of surgery with
a fractional inspired oxygen concentration (Fio2) less than 0.5 is a
sensitive indicator of significant left-to-right shunt (Qp/Qs 1.5)
1 year after surgery.25
Low Cardiac Output Syndrome
Although low cardiac output after CPB is often attributable to
residual or undiagnosed structural lesions, progressive low–cardiac
output states do occur A number of factors have been implicated
in the development of myocardial dysfunction following CPB,
including (1) the inflammatory response associated with CPB,
(2) myocardial ischemia from aortic cross-clamping, (3)
hypother-mia, (4) reperfusion injury, (5) inadequate myocardial protection,
and (6) ventriculotomy (when performed) The typical decrease in
cardiac index has been well characterized in newborns following an
arterial switch operation (ASO).26 In a group of 122 newborns, the
median maximal decrease in cardiac index that typically occurred
6 to 12 hours after separation from CPB was 32%, and 1 in 4 of these newborns reached a nadir of the cardiac index lower than
2 L/min per square meter.26 Anticipation of this low cardiac out-put syndrome (LCOS) and appropriate intervention can do much
to avert morbidity or the need for mechanical support Mixed ve-nous oxygen saturation, whole-blood pH, and lactate are labora-tory measures commonly used to evaluate the adequacy of tissue perfusion and, hence, cardiac output
Volume Adjustments
After CPB, the factors that influence cardiac output—such as preload, afterload, myocardial contractility, heart rate, and rhythm—must be continuously assessed and manipulated as needed Volume expansion (increased preload) is commonly nec-essary, followed by appropriate use of vasoactive agents Atrial pressure and the ventricular response to changes in atrial pressure must be evaluated Ventricular response is judged by observing systemic arterial pressure and waveform, heart rate, skin color, peripheral extremity temperature, peripheral pulse magnitude, urine output, core body temperature, and acid-base balance
Preserving and Creating Right-to-Left Shunts
Selected children with low cardiac output may benefit from strat-egies that allow right-to-left shunting at the atrial level in the face
of expected postoperative RV dysfunction A typical example is early repair of TOF, when the hypertrophied and poorly compli-ant right ventricle may be further compromised by increased volume load from pulmonary regurgitation secondary to a trans-annular patch on the RV outflow tract These children will benefit from leaving the foramen ovale patent to permit right-to-left shunting of blood, thus preserving cardiac output and oxygen delivery despite the attendant transient cyanosis When the fora-men ovale is not patent or is surgically closed, RV dysfunction can lead to reduced LV filling, low cardiac output, and, ultimately, LV dysfunction In infants and neonates with repaired truncus arte-riosus, the same concerns apply and may even be exaggerated if
RV afterload is elevated because of pulmonary hypertension
Other Strategies
Additional strategies to support low cardiac output associated with cardiac surgery in children include the use of atrioventricular pacing for patients with complete heart block or prolonged inter-ventricular conduction delays and asynchronous contraction.27
Appreciation of the hemodynamic effects of positive and negative pressure ventilation may be used to assist cardiac output Avoid-ance of elevated body temperatures and even inducing hypother-mia along with appropriate sedation and even paralysis may provide end-organ protection during periods of low cardiac out-put and aid in the management of postoperative arrhythmias, such as junctional ectopic tachycardia
Mechanical Cardiac Support
Perioperative mechanical circulatory support (MCS) can be life-saving for critically ill children and young adults with CHDs.28 , 29
The most common form of pediatric MCS is extracorporeal membrane oxygenation (ECMO) ECMO can be used as rescue during extracorporeal cardiopulmonary resuscitation (ECPR), in failure to wean from CPB, or in patients who develop low–cardiac output states postoperatively despite high levels of pharmacologic support.30 , 31 it is presently less commonly used as a bridge to heart
• BOX 36.4 Common Causes of Elevated Left Atrial
Pressure After Cardiopulmonary Bypass
Decreased ventricular systolic or diastolic function
Left atrioventricular valve disease
Large left-to-right intracardiac shunt
Chamber hypoplasia
Intravascular or ventricular volume overload
Cardiac tamponade
Arrhythmia
Trang 3transplantation—it is more often used as a prelude to long-term
mechanical assist devices or simply to allow time for
decision-making.29 , 32 An analysis of 96,596 operations from 80 centers
reporting to the Society of Thoracic Surgeons Congenital Heart
Surgery Database showed that MCS was used in 2.4% of cases.33
Children who underwent Norwood procedures (17%) or
com-plex biventricular repairs (14%) were more likely to receive MCS
Substantial variation exists in MCS rates across both high- and
low-volume centers Overall, 53% of those children who received
MCS did not survive to hospital discharge, with mortality greater
than 70% for certain operative lesions (truncus arteriosus repair,
Ross-Konno operation).33 Despite this high mortality, it is
impor-tant to recognize that survival would have been virtually zero for
those children without MCS
In a recent report from the Pediatric Cardiac Critical Care
Consortium Registry,34 of the 14,526 eligible medical as well as
surgical cardiac ICU hospitalizations, 449 (3.1%) had at least one
ECMO run Of these, 329 (3.5%) were surgical and 120 (2.4%)
were medical hospitalizations Of the surgical group, 33 (10%)
included preoperative ECMO only and 296 (90%) included
post-operative ECMO Overall, in-hospital mortality was 48.9% in
the surgical group and 63.3% in the medical group; mortality
rates for hospitalizations including ECPR were 82.7% (surgical)
and 50% (medical).34
Due to improved technology, reliability, and mechanical
dura-bility of devices, higher rates of patient survival, reduced adverse
events, and limited availability of organs for transplantation,
intra-corporeal MCS has become an accepted long-term inpatient and
outpatient therapy for those with advanced heart failure awaiting
heart transplantation.35 Ventricular assist devices (VADs) can
sup-port function of the left ventricle (left ventricular assist device
[LVAD]), right ventricle (right ventricular assist device [RVAD]),
or both (biventricular assist device [BiVAD]) A total artificial
heart (TAH) replaces the heart itself VADs have two different
mechanisms of blood flow: pulsatile or continuous Continuous
flow devices contain an impeller that rotates at high speed to
pro-pel blood These include axial flow impro-pellers (e.g., HeartMate II
[Thoratec Corp.]), or centrifugal pumps (e.g., HeartWare HVAD
[HeartWare Corp.]) Paracorporeal pulsatile devices (e.g., Thoratec
PVAD-BiVAD [Thoratec Corp.], Berlin Heart EXCOR BiVAD
[Berlin Heart Corp.]) are also used in selected cases Guidelines
exist with regard to CPR in children with MCS.35 A more detailed
discussion of MCS can be found in Chapter 28
Right Ventriculotomy and Restrictive Physiology
Right ventricular restrictive physiology has been demonstrated by
echocardiography as persistent anterograde diastolic blood flow
into the pulmonary circulation following reconstruction of the
RV outflow in infants and children This occurs in the setting of
elevated RV end-diastolic pressure and RV hypertrophy when the
right ventricle demonstrates diastolic dysfunction with an
inabil-ity to properly relax and fill during diastole The poorly compliant
RV usually is not dilated in this circumstance, and pulmonary
valve regurgitation is limited because of the elevated RV diastolic
pressure.36 , 37
The term restrictive RV physiology is also commonly used in the
immediate postoperative period in patients who have a stiff,
poorly compliant, and sometimes hypertrophied RV The elevated
ventricular end-diastolic pressure restricts filling during diastole,
causing an increase in RA filling pressure and, ultimately, systemic
venous hypertension Because of the phenomenon of ventricular
interdependence, changes in RV diastolic function and septal position in turn affect LV compliance and function Factors con-tributing to diastolic dysfunction include lung and myocardial edema following CPB, inadequate myocardial protection of the hypertrophied ventricle during aortic cross-clamp, coronary ar-tery injury, residual outflow tract obstruction, volume load on the ventricle from a residual VSD or pulmonary regurgitation, and dysrhythmias In many centers, a residual atrial communication is left to mitigate the perioperative sequelae associated with restric-tive RV physiology, namely, a low–cardiac output state In such a scenario, patients may be desaturated following surgery (typically
in the 75% to 85% range) because of this right-to-left shunting, but they maintain systemic cardiac output while avoiding significant systemic venous hypertension As RV compliance and function improve (usually within 2 to 3 postoperative days), the amount of shunt decreases and both anterograde pulmonary blood flow and Sao2 increase
If significant restrictive RV physiology develops in the absence
of an unrestrictive atrial communication, a low–cardiac output state with increased right-sided filling pressure (usually 12 mm Hg) ensues Such patients often have cool extremities, oliguria, and metabolic acidosis As a result of the elevated RA pressure, hepatic congestion, ascites, increased chest tube output, and pleu-ral effusions may be evident These patients may be tachycardic and hypotensive, with a narrow pulse pressure Preload must be maintained despite an already elevated RA pressure Significant inotropic support often is required (typically, epinephrine 0.05–0.1 µg/kg per minute) A phosphodiesterase inhibitor, such
as milrinone, can be beneficial because of its lusitropic properties; however, one must be cautious in the use of these agents with renal impairment.38 Sedation and paralysis often are necessary for the first 24 to 48 hours to minimize energy expenditure and as-sociated myocardial work Factors that further impair ventricular diastolic filling—such as loss of AV synchrony, accumulation of pleural fluid or ascites, and high tidal volume ventilation with air trapping—should be mitigated early in the postoperative course Mechanical ventilation, either hypoinflation or hyperinflation
of the lung, hypothermia, and acidosis can contribute to increased afterload on the right ventricle and pulmonary regurgitation Synchronized intermittent positive-pressure ventilation with the lowest possible mean airway pressure should be the aim, as dis-cussed previously
Diastolic Dysfunction
Occasionally, there is an alteration of ventricular relaxation, an active energy-dependent process, which reduces ventricular com-pliance This is particularly problematic in patients with a hyper-trophied ventricle undergoing surgical repair, such as TOF or Fontan surgery, and following CPB in some neonates when myo-cardial edema may significantly restrict diastolic function.37 , 38 The poorly compliant ventricle with impaired diastolic relaxation has
a reduced end-diastolic volume and stroke volume b-Adrenergic antagonists and calcium channel blockers add little to the treat-ment of this condition In fact, hypotension or myocardial de-pression produced by these agents often outweighs any gain from slowing the heart rate Calcium channel blockers are relatively contraindicated in neonates and small infants because of their dependence on transsarcolemmal flux of calcium to both initiate and sustain contraction
A gradual increase in intravascular volume to augment ven-tricular capacity, in addition to the use of low doses of inotropic
Trang 4agents, is of modest benefit in patients with diastolic dysfunction
Tachycardia must be avoided and AV synchrony maintained to
optimize diastolic filling time and decrease myocardial oxygen
demands If low cardiac output persists despite treatment,
vasodi-lators can be carefully attempted to alter systolic wall tension
(afterload) and thus decrease the impediment to ventricular
ejec-tion Because the capacity of the vascular bed increases after
vaso-dilation, simultaneous volume replacement is often necessary A
noncatecholamine inodilator with vasodilating and lusitropic
(improved diastolic state) properties, such as milrinone, is useful
under these circumstances in contrast with other inotropic
agents.39
Pharmacologic Support
General principles of pharmacologic support in the neonatal and
pediatric patient center on the recognition of the developmental
limitations of the neonatal myocardium and the well-described
reductions in cardiac output 6 to 12 hours after separation from
CPB.26 Despite ongoing development and maturity of adrenergic
receptors and L-type calcium channels, catecholamine-based
ino-tropic agents and vasodilators are efficacious in this population
Other nonvasoactive agents serve as adjuncts to optimizing
post-operative hemodynamics and fluid balance The combination of a
low-dose inotrope and an afterload reducing agent—or, more
commonly, a phosphodiesterase inhibitor—has been shown to
decrease the occurrence of postoperative LCOS following CPB.39
It should be understood that the need for vasoactive and
ino-tropic support varies greatly among patients recovering from
car-diac surgery and even over time for an individual patient
progress-ing through the postoperative care continuum The intensity of
pharmacologic support employed must be constantly evaluated
One must not embrace a false sense of security when caring for a
patient with adequate cardiac output when this requires
dispro-portionate pharmacologic support The current approach is to
employ the lowest level of inotropic and vasoactive support
neces-sary for the achievement of hemodynamic goals Due to advances
in preoperative stabilization, anesthetic strategies, surgical
tech-nique, myocardial protection, and CPB, it is not uncommon for
a patient to return to the PICU requiring only low doses of
milrinone or epinephrine or no pharmacologic support at all A
detailed discussion of cardiovascular pharmacology is beyond the
scope of this chapter but can be found in Chapter 31
Managing Acute Pulmonary Hypertension
in the Intensive Care Unit
Children with many forms of CHD are prone to perioperative
elevations in pulmonary vascular resistance (PVR).40 This
situa-tion complicates the postoperative course when transient
myocar-dial dysfunction is further challenged by increased RV afterload.41
Although postoperative patients with pulmonary hypertension
often are presumed to have active and reversible pulmonary
vaso-constriction as the source of their pathophysiology, the intensivist
is obligated to explore anatomic causes of mechanical obstruction
that impose a barrier to pulmonary blood flow Elevated LA
pres-sure, pulmonary venous obstruction, branch pulmonary artery
stenosis, or surgically induced loss of the vascular tree all raise RV
pressure and impose an unnecessary burden on the right heart
Similarly, a residual or undiagnosed left-to-right shunt raises
pul-monary artery pressure postoperatively and must be addressed
surgically In these cases, the use of pulmonary vasodilator strate-gies augments only residual or undiagnosed shunts and increases the volume load on the heart
Several factors peculiar to CPB may raise PVR: pulmonary vascular endothelial dysfunction, microemboli, pulmonary leu-kostasis, excess thromboxane production, atelectasis, hypoxic pulmonary vasoconstriction, and adrenergic events all have been suggested to play a role in postoperative pulmonary hypertension Postoperative pulmonary vascular reactivity has been related not only to the presence of preoperative pulmonary hypertension and left-to-right shunts but also to the duration of total CPB The threat of postoperative pulmonary hypertensive crises can be partially addressed by providing surgery at earlier ages, pharmaco-logic interventions, and other postoperative management strate-gies (Table 36.1)
Pulmonary Vasodilators
Nitric oxide (NO) is the mainstay of therapy in patients with pulmonary hypertension requiring critical care NO is a vasodila-tor formed by the endothelium from l-arginine and molecular oxygen in a reaction catalyzed by NO synthase NO then diffuses
to the adjacent vascular smooth muscle cells, where it induces vasodilation through a cyclic guanosine monophosphate-depen-dent pathway.42 , 43 Because NO exists as a gas, it can be delivered
by inhalation to the alveoli and, hence, to the adjacent blood sels Once it diffuses across the wall of the pulmonary blood ves-sels, NO enters the vascular lumen There, it is rapidly inactivated
by hemoglobin, resulting in selective pulmonary vasodilation Inhaled NO (iNO) has advantages over intravenously adminis-tered vasodilators that may cause systemic hypotension and in-crease intrapulmonary shunting Inhaled NO lowers pulmonary artery pressure in a number of diseases without the unwanted ef-fect of systemic hypotension This efef-fect is especially dramatic in children with cardiovascular disorders and postoperative patients with pulmonary hypertensive crises.41 , 44 , 45
Therapeutic uses of iNO in children with CHD abound in the ICU Newborns with total anomalous pulmonary venous connec-tion (TAPVC) frequently have obstrucconnec-tion of the pulmonary venous pathway where it connects anomalously to the systemic
TABLE 36.1 Critical Care Strategies for Postoperative Treatment of Pulmonary Hypertension
Anatomic investigation Residual anatomic disease Opportunities for right-to-left
shunt as pop-off Intact atrial septum in right heart failure Sedation/anesthesia Agitation/pain
Moderate hyperventilation Respiratory acidosis Moderate alkalosis Metabolic acidosis Adequate inspired oxygen Alveolar hypoxia Normal lung volumes Atelectasis or overdistension Optimal hematocrit Excessive hematocrit Inotropic support Low output and coronary perfusion Vasodilators Vasoconstrictors/increased afterload
Trang 5venous circulation When pulmonary venous return is obstructed
preoperatively, pulmonary hypertension is severe and requires
urgent surgical relief Use of iNO in this or other settings of
sus-pected pulmonary venous obstruction is contraindicated On the
other hand, increased neonatal pulmonary vasoreactivity,
endo-thelial injury induced by CPB, and remodeling of the pulmonary
vascular bed in this disease contribute to postoperative pulmonary
hypertension Postoperatively in the patient with TAPVC after
adequate surgical relief of obstruction, iNO dramatically reduces
pulmonary hypertension without adverse changes in heart rate,
systemic blood pressure, or vascular resistance
Postoperative patients with TAPVC, congenital mitral stenosis,
and other pulmonary venous hypertensive disorders associated
with low cardiac output are among the most responsive to iNO
These infants are born with significantly increased amounts
of smooth muscle in their pulmonary arterioles and venules
Histologic evidence of muscularized pulmonary veins and
pulmo-nary arteries suggests the presence of vascular tone and capacity
for change in resistance at both the arterial and venous sites The
increased responsiveness to iNO seen in younger patients with
pulmonary venous hypertension may result from pulmonary
va-sorelaxation at a combination of precapillary and postcapillary
vessels Resolving the primary venous obstruction is of utmost
importance before using iNO in these lesions
Several groups have reported successful use of iNO in a variety
of other congenital heart defects following cardiac surgery
Inhaled NO is especially helpful when administered during a
pulmonary hypertensive crisis.46 Successful iNO use has been
described after the Fontan procedure, following late VSD repair,
and with a variety of other anatomic lesions for which patients are
at risk of developing postoperative pulmonary hypertensive
cri-ses.45–47 Oxygen saturation in response to iNO generally does not
improve in very young infants who are excessively cyanotic after a
bidirectional Glenn anastomosis.48 In these cases, increasing
car-diac output and cerebral blood flow will have a much greater
impact on arterial oxygenation because elevated pulmonary
vascu-lar tone is seldom the limiting factor in the hypoxemic patient
after the bidirectional Glenn operation.49
Inhaled NO can be used diagnostically in neonates with RV
hypertension after cardiac surgery to discern those with
revers-ible vasoconstriction In patients with Ebstein anomaly, a
clini-cal response to iNO can accurately differentiate between
func-tional and anatomic pulmonary atresia.50 In addition, the use of
iNO in such patients can facilitate anterograde pulmonary
blood flow and hemodynamic stabilization Failure of the
post-operative newborn to respond to iNO should be regarded as
strong evidence of anatomic and possibly surgically remediable
obstruction.50
If iNO must be discontinued before the pathologic process has
been resolved, hemodynamic instability can be expected The
withdrawal response to iNO can be attenuated by pretreatment
with the type V phosphodiesterase inhibitor sildenafil.51 Sildenafil
inhibits the inactivation of cyclic guanosine monophosphate
within the vascular smooth muscle cell and has the potential to
augment the effects of either endogenous or exogenously
admin-istered NO to affect vascular smooth muscle relaxation Sildenafil
can be administered in an oral or intravenous (IV) form and has
a somewhat selective pulmonary vasodilating capacity while
low-ering LA pressure and providing a modest degree of systemic
af-terload reduction in some postoperative children Chronic oral
administration of sildenafil to adults with primary pulmonary
hypertension improves exercise capacity This phenomenon has
also been demonstrated in pediatric patients with a Fontan circu-lation, perhaps suggesting a broad therapeutic application on older patients after operation for CHD
Many other vasodilators have been used with variable suc-cess in patients with pulmonary hypertensive disorders requir-ing critical care IV vasodilators—such as tolazoline, phenoxy-benzamine, nitroprusside, and isoproterenol—have little biological basis for selectivity or enhanced activity in the pul-monary vascular bed.52 However, if myocardial contractility is depressed and the afterload reducing effect on the left ventricle
is beneficial to myocardial function and cardiac output, then these drugs may be of some value In addition to drug-specific side effects, intravenous vasodilators all have the potential to produce profound systemic hypotension, critically lowering coronary perfusion pressure while simultaneously increasing intrapulmonary shunt, thus limiting their usefulness in the management of acute postoperative pulmonary hypertension
In fact, in patients with idiopathic pulmonary hypertension who have adequate LV contractility, the use of a vasopressor may help the RV coronary perfusion pressure, LV preload and systolic interventricular dependence, thus preventing a pulmo-nary hypertensive crisis
Management of Postoperative Bleeding
Infants and children undergoing cardiac surgery are at high risk for hemorrhage and need for transfusion CPB is a major throm-bogenic stimulus that causes a multifactorial coagulopathy due to dilution and consumption of clotting factors and inactivation of platelets This is further exacerbated by an immature coagulation system and the presence of hypoxia and hypothermia While upward of 79% of children undergoing cardiac surgery will re-quire transfusion,53 the need for transfusion is associated with increased morbidity.54 , 55 Transfusion criteria for packed red blood cells is determined by balancing the inherent risks associ-ated with transfusion and the need to optimize oxygen delivery
in the face of hemodynamic instability However, there are in-creasing data suggesting that the use of more restrictive transfu-sion parameters results in less transfutransfu-sion with no difference in clinical outcome.56 To minimize the need for excessive blood products, careful attention to ongoing bleeding and coagulopa-thy is necessary Baseline complete blood count and coagulation profile should be measured on return from the operating room Chest tube outputs of 10 mL/kg in the first hour or 5 mL/kg per hour for subsequent hours should prompt aggressive repletion of abnormal clotting factors, initially with platelets and fresh-frozen plasma (FFP), assessment of adequate reversal of anticoagulants, and a discussion with the surgeon When bleeding is resistant to therapy, transfusion of factor concentrates should be considered These include fibrinogen concentrate, prothrombin complex concentrates, or even activated factor VII in selected patients Significant repletion of red blood cells also necessitates the con-current transfusion of platelets and FFP to avoid further dilution
of clotting components Ongoing chest tube output that does not abate despite normalization of factors suggests the possibility
of surgical bleeding that could necessitate reexploration Further, while control of postoperative bleeding is the goal, the abrupt cessation of chest tube output—particularly when accompanied
by increasing CVP, tachycardia, and hypotension—suggests evolving tamponade Ensuring chest tube patency may be suffi-cient to reverse the process If not, reexploration of the mediasti-num may be necessary