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314 PART 3: Cardiovascular Disorders

Cardiac Surgery and Cardiopulmonary Bypass: Acute right heart fail- TABLE 38-5 Goals of Therapy in the Right Heart Syndromes
ure following cardiac surgery, especially in patients operated on for
severe mitral valve disease, some congenital cardiac defects, acute Correct hypoxemia
pulmonary embolism, or following heart transplantation or institu- Find optimal volume
tion of left ventricular mechanical assistance, continues to vex cardiac Exclude or treat concomitant left ventricular dysfunction
surgeons and surgical intensivists. The mechanisms underlying this are
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multifactorial and include cardiopulmonary bypass–induced activa- Minimize volume of oxygen utilization
tion of pulmonary inflammatory pathways, increased circulating Reduce intrinsic positive end-expiratory pressure and other causes of elevated alveolar pressure
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levels of endothelin-1 and impairment of nitric oxide production by Dobutamine, begin at 5 µg/kg per minute
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pulmonary endothelial cells. A favorable response to inhaled NO has
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been demonstrated when used postoperatively 73,74 or perioperatively. Norepinephrine, begin at 0.4 µg/kg per minute
Similar effects were reported with the PDE-4 inhibitor, sildenafil. Nitric oxide, begin at 18 ppm
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Inhaled prostacyclin has also been demonstrated to improve Pa
hypertension and RV dysfunction post CPB. In 46 patients with
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established PH undergoing CPB who were at increased risk of acute expert opinion, hinges on two primary treatment aims: to reduce sys-
RV dysfunction when weaned from CPB, inhaled prostacyclin (20 µg) temic oxygen demand while improving oxygen delivery (Table 38-5).
was more effective at reducing PVR and mean PAP while increasing Oxygen demand can be lowered by treating fever, sedating the
cardiac output, when compared with a fixed dose of inhaled NO patient, instituting mechanical ventilation, and in severe cases, using
(20 parts per million—ppm). 78 therapeutic muscle relaxation. Oxygen delivery can be enhanced by
■ ACUTE-ON-CHRONIC PULMONARY HYPERTENSION hypoxia, infusing vasoactive drugs, and avoiding detrimental ventila-
correcting hypovolemia, transfusing red blood cells, relieving alveolar
Many patients with acute RHS have preexisting pulmonary vascular dis- tor settings. The goals of oxygen therapy in RHS are to enhance arte-
) and to block alveolar hypoxic vasoconstriction
ease, at times with clinically recognized pulmonary hypertension, but often rial saturation (Sa O 2 is
without (see Tables 38-2 and 38-4). In such patients, intercurrent critical (AHV). Using a sufficient oxygen concentration to achieve 88% Sa O 2
advocated in ARDS and other alveolar flooding diseases (see Chap. 52),
illness may unmask pulmonary vascular disease when a higher-than-
normal cardiac output is needed. Both graded exercise and graded acute but in RHS not associated with intrapulmonary shunt, we target Sa O 2
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to >96% to ensure alveolar oxygen values sufficient to block AHV
80
hypoxia provoke acute-on-chronic elevations in pulmonary arterial, right >55 mm Hg). It may be useful to correct anemia with red blood
atrial and right ventricular pressures. Additionally RV end-diastolic and (Pa O 2
cell transfusion, raising the arterial oxygen content, and reducing the
end-systolic volume indexes increase significantly. Consistently, however, necessary cardiac output. The resulting increased blood viscosity (and
LV stroke volume indexes and ejection fraction change significantly. 79,80 its tendency to raise pulmonary vascular resistance) probably does
The obesity epidemic in post-industrial societies has led to a burgeon- not outweigh the reduced demand for forward flow.
ing in the incidence of sleep-disorder associated chronic PH (particularly Some patients with acute RHS may benefit from specific therapies,
amongst patients with obstructive sleep-apnea syndromes, OSA). As such as thrombolysis for acute pulmonary embolism (see Chap. 39) and
many as three-quarters of OSA patients may have moderate-to-severe coronary reperfusion for acute myocardial infarction (see Chap. 37).
PH. These data demonstrate convincingly that an OSA diagnosis is In most patients, however, the fluid therapy, ventilator management, and
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strongly associated with development of chronic PH, independent of vasoactive drug infusion are discussed below and have been the subject
systemic hypertension and LV dysfunction. It is our recent experience of recent reviews. 84,86
that these patients who are frequently undiagnosed and undertreated, Contemporary approaches to the critical care management of
are at particular risk for both systemic hypertension and acute-on- right heart syndromes emphasize four major treatment of objectives
chronic exacerbations of PH with cor pulmonale as a consequence of (Table 38-6). 85,87 Specific therapeutic and pharmacologic options to
intercurrent critical illness. achieve these goals, are reviewed below (Table 38-7).
When pulmonary hypertension is diagnosed during the course of
critical illness, the potential for underlying chronic pulmonary vascu- ■ ESTABLISH EFFECTIVE CIRCULATING VOLUMES
lar disease should be considered, especially when the history suggests
chronic disease, the mean Pa pressure is higher than 40 mm Hg, or echo- Fluid Therapy: In most patients with shock it is appropriate to admin-
cardiography shows evidence of RV hypertrophy. Acute decompensation ister fluid, often to restore left ventricular diastolic filling and boost
of chronic PH is associated with a poor prognosis. Amongst 119 patients cardiac output. Despite the recognition that the right heart becomes
with PH hospitalized for acute right heart failure (207 episodes), death extremely preload dependent during ischemia and infarction, exces-
49
or urgent transplantation was the outcome in 34 patients (28.6%) by sive fluid administration is likely to worsen hemodynamic stability. In
90 days from admission. Tachypnea, hyponatremia, severe renal dysfunc- many of these patients the right-sided pressures are already well above
tion and severe tricuspid regurgitation on admission were independently normal, signaled by neck vein distention. Data from animal models
associated with death or need for urgent transplantation. 83
Treatment of Acute Right Heart Syndromes: Current recommenda- TABLE 38-6 Management Principles for Treatment of Acute Right Heart Syndromes
tions for the management of acute RHS are limited by generally low
quality of available clinical evidence. 84,85 Our approach, informed by A. Establish effective circulating volumes avoid volume loading or over-diuresis if RV
volume-overloaded
B. Maximize RV myocardial function; optimize coronary sinus perfusion
TABLE 38-4 Features of Right Heart Syndromes C. Reduce right ventricle afterload, PVR and RV ischemia
Diagnosis not readily apparent: a high index of suspicion aids recognition a. Pulmonary vasodilators
b. Treat reversible factors that may increase PVR Metabolic state: anemia, acidosis,
Routine therapy for congestive heart failure may be detrimental
hypoxemia high P CO 2 ,
Fluid loading may lower cardiac output c. Reduce sympathetic overstimulation
Vasodilators may cause abrupt deterioration D. Maintain adequate systemic vascular resistance (SVR)
Vasoconstrictors may have a role in some patients Modified with permission from Price LC, Wort SJ, Finney SJ, et al. Pulmonary vascular and right ven-
tricular dysfunction in adult critical care: current and emerging options for management: a systematic
Echocardiography is extremely valuable
literature review. Crit Care. 2010;14(5):R169.

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