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CHAPTER 38: Acute Right Heart Syndromes 315

decision making. If no benefit can be detected, further fluids should
TABLE 38-7 Therapeutic Objectives for the Management of Acute Right
Heart Syndromes not be given, and attention should shift to vasoactive drugs.
1. Establish effective circulating but not excessive volumes to optimize RV filling and ■ MAXIMIZE RV MYOCARDIAL FUNCTION; OPTIMIZE
maintain effective systemic perfusion for vital organ perfusion.
2. Maximize RV myocardial function. CORONARY SINUS PERFUSION
3. Reduce right ventricle afterload and RV ischemia. Vasoactive Drug Therapy: A wide variety of vasoactive drugs have
4. Maintain optimal coronary sinus pressure to stabilize right coronary arterial perfusion. been evaluated with variable success in patients or animal models for
Causes of Acute Right Ventricular Failure (Creagh Brown) the treatment of acute RHS due to pulmonary embolism, ARDS, or
right ventricular infarction. These include nonspecific vasodilators
Acute rise in pulmonary vascular resistance, such as due to acute pulmonary embolism or (hydralazine and nitroprusside 90,95,96 ), vasoconstrictors (norepi-
94
rapidly progressive pulmonary parenchymal/vascular disease nephrine, 14,89,97 epinephrine, phenylephrine, 99,100 dopamine, and
98
101
Acute right ventricular ischemia, often due to diminished right coronary perfusion conse- vasopressin 102,103 ), inotropes (dobutamine, 90,91,104-106 amrinone, mil-
107
108
quent upon inadequate systolic and diastolic pressures in shocked states rinone, isoproterenol, epinephrine, and levosimendan 109,110 ),
98
14
Acute high left atrial pressures, perhaps due to acute left ventricular failure of any cause and pulmonary vasodilators (prostaglandin E , 1 111,112 prostaglandin
I , and nitric oxide 96,102,113-120 ). Predicting the response to any of
113
Decompensation of chronic pulmonary arterial hypertension 2
these drugs a priori is complicated by their tendency toward oppos-
Decompensation of congenital heart defects with pulmonary arterial hypertension or left- ing effects. Conflicting data from studies of an agent in different
to-right intracardiac shunts animal models suggest that the interspecies variation and prevailing
After surgery necessitating cardiopulmonary bypass per se pulmonary vascular tone are important in determining if a particular
agent has a predominantly pulmonary vasodilatory or vasoconstrict-
Hypoxemia causing hypoxic pulmonary vasoconstriction
ing effect. 105,106 Thus the choice of vasoactive drugs cannot be based
solely on the presumed pathophysiology, but also must be based on the
results of human and animal studies summarized below. We contend
of pulmonary embolism, as well as from studies of patients with right that a vasoactive drug is effective in RHS when it significantly raises
ventricular infarction, demonstrate that fluid therapy may be unhelpful cardiac output without significantly worsening systemic hypotension,
or even detrimental. , or RV ischemia. Dobutamine is our preferred positive ino-
In a canine autologous clot model of pulmonary embolism, the effects Sa O 2
trope. Inhaled aerosolized prostacyclin (and inhaled NO, although
of fluid loading were studied before embolism, then following embo- the commercially available delivery system is exorbitantly expen-
lism. Before embolism, fluid loading significantly raised the right atrial sive) has salutary short-term pulmonary vasodilatory effects and can
88
pressure, the transmural left ventricular end-diastolic pressure (LVEDP), be combined with the oral phosphodiesterase inhibitor, sildenafil.
and the left ventricular end-diastolic area index (a measure of left ven- Norepinephrine may provide added benefit as a systemic vasoconstric-
tricular volume using sonomicrometry). Following multiple emboli, fluid tor and positive inotrope by raising coronary perfusion pressure to an
loading raised right atrial pressure, but transmural LVEDP fell signifi- ischemic RV.
cantly as did the left ventricular end-diastolic area index. These findings
indicate that fluid loading following embolism causes further leftward Catecholamines: In massive pulmonary embolism, dobutamine, and
displacement of the interventricular septum, further compounding LV norepinephrine appear superior to other vasoactive drugs. 14,104,121
diastolic dysfunction. In a canine glass bead embolization model, fluid In human acute right heart syndromes, (including PE and
104
loading was found to precipitate right ventricular failure, even when decompensated cor pulmonale ), dobutamine has been most inten-
122
relatively small volumes were infused. 89 sively studied. Dobutamine improves cardiac output by improving right
Similar results have been shown in human right ventricular infarction. 90,91 ventricular function and/or reducing pulmonary vascular resistance.
Despite raising the right atrial and wedge pressures, fluid loading failed Although fewer data are available regarding norepinephrine in human
to increase the cardiac index, blood pressure, or left and right ventricular embolism, animal studies and limited human data support its use. 14,97,104
stroke work. In a canine model of pulmonary embolism, dobutamine and dopamine
101
Dynamic assessments of volume responsiveness such as variations in had essentially identical hemodynamic effects. Data from a separate
stroke volume (SVV) or pulse pressure (PPV) in response to cyclic posi- canine study suggest that at doses less than 10 µg/kg per minute, dobu-
tive pressure breaths or passive leg raising maneuvers are useful in many tamine-induced pulmonary circulatory changes are exclusively flow
shock states (see Chap. 34). However, this assessment may be insensitive dependent. At higher doses, changes in pulmonary vascular resistance
106
in patients with acutely impaired RH function. 92,93 Amongst 35 critically are variable and may depend on the prevailing pulmonary vascular
ill and mechanically ventilated adults with circulatory failure preload tone. These drugs should be titrated according to clinical measures of
volume responsiveness was assessed by PPV in response to positive the adequacy of perfusion, such as renal function, mentation, thermo-
pressure breaths. In a third of patients with preinfusion PPV >12% dilution cardiac output, or central venous oxyhemoglobin saturation,
suggesting preload volume responsiveness, a 500-mL colloid bolus was rather than to blood pressure alone. We begin dobutamine at 5 µg/kg
ineffective in improving hemodynamics. RV dysfunction was identified per minute, raising the dose in increments of 5 µg/kg per minute every
by TTE as the source of this false positive response. 92 10 minutes. If the patient fails to respond to dobutamine (or the response
These findings should serve as a caution regarding fluid administra- is incomplete), we substitute (or add) norepinephrine infused at 0.4 to
tion to patients with shock due to acute RHS. Since some patients may 4 µg/kg per minute, which, in addition to inotropic effects can increase
be volume depleted at presentation, a fluid challenge is reasonable, both SVR and PVR. These effects are dose dependent but are poten-
especially if the neck veins are flat or right heart filling pressures are tially salutary in terms of improving pulmonary ventriculo-vascular
low. Nevertheless, fluid should be given with a healthy degree of skepti- coupling and coronary perfusion. 100,123 In patients with hypoperfu-
cism and careful attention to the consequences. We recommend that a sion due to right ventricular infarction, dobutamine is superior to
discrete crystalloid fluid bolus of no more than 250 mL be administered nitroprusside (and to fluid infusion 90,91 ) significantly improving
90
while assessing relevant indicators of perfusion such as blood pressure, right ventricular ejection fraction and cardiac output. Therefore
heart rate, pulsus paradoxus, cardiac output, central venous oxyhemo- dobutamine is the drug of first choice in all cases of RHS. We avoid
globin saturation, or urine output. We find that intracavitary pressure the use of dopamine because of its highly variable pharmacokinetics
5,85
measurements including CVP can vary widely and are unhelpful in and concern for disproportionate splanchnic vasoconstriction, even in
guiding assessments of volume responsiveness and may confound relatively low doses.

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