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Clinical Presentation and Management 173
of Acute Heart Failure

maintained and that the diuresis can be continued if creased rates of hypotension, and did not alter rates
the patient is still edematous. of death, rehospitalisation at 30 days, or worsening
renal function .
Management of worsening renal function- General
principles for management of patients with ADHF Nitroglycerin: Nitrates,probably the most commonly
with elevated or rising BUN and/or serum creatinine used vasodilators in ADHF, cause greater venous
include the following : than arterial vasodilation,thus reducing LV filling
pressure. At higher doses, nitrates variably lower sys-
• Other potential causes of kidney injury (eg, use temic vascular resistance and LV afterload, and may
of nephrotoxic medications, urinary obstruction) thereby increase stroke volume and cardiac output.
should be evaluated and addressed.
In patients with ADHF receiving nitrate therapy, an
• Patients with severe symptoms or signs of con- intravenous route is used for greater speed and reli-
gestion, particularly pulmonary edema, require ability of delivery and ease of titration. An initial dose
continued fluid removal independent of changes of 5 to 10 mcg/min of intravenous nitroglycerin is
in GFR. In the presence of elevated central venous recommended with the dose increased in increments
pressure, renal function may improve with diuresis. of 5 to 10 mcg/min every three to five minutes as re-
quired and tolerated (dose range 10 to 200 mcg/min).
• If the BUN rises and the serum creatinine is sta-
ble or increases minimally, and the patient is still The longer half-life of isosorbide dinitrate compared
fluid overloaded, the diuresis can be continued to to intravenous nitroglycerin (four hours versus three
achieve the goal of eliminating clinical evidence to five minutes) is a major disadvantage in setting of
of fluid retention with careful monitoring of renal hypotension with these agents.
function. Tachyphylaxis, hypotension and headache are major
limiting side effects of this class of drugs and it is
• If increases in serum creatinine appear to reflect
intravascular volume depletion, then reduction in avoided in right ventricular infarction or aortic steno-
or temporary discontinuation of diuretic and/or sis and concomitant sildenafil therapy.
ACE inhibitor/ARB therapy should be considered. Nitroprusside: In contrast to nitroglycerin, nitroprus-
Adjunctive inotropic therapy may be required side causes balanced arterial and venous dilation
thus lowering left ventricular filling pressures and sys-
• If substantial congestion still persists,then ultrafil-
tration or( renal replacement therapy)dialysis may temic vascular resistance, thereby increasing stroke
be considered. volume without lowering blood pressure; whereas
if systemic vascular resistance is not elevated, ni-
Vasodilator therapy :Vasodilators are required to cor- troprusside may cause hypotension. These proper-
rect elevated filling pressures and/or left ventricular ties are of value in patients with depressed stroke
afterload in patients with ADHF. volume due to elevated LV afterload such as acute
aortic regurgitation, acute mitral regurgitation, acute
Indications for vasodilator therapy in the setting of
ADHF include the following: early vasodilator therapy ventricular septal rupture, or hypertensive emergen-
(eg, nitroprusside) being recommended for patients cy. Because of its very potent hemodynamic effects,
with urgent need for afterload reduction (eg, severe the use of nitroprusside requires close hemodynam-
hypertension); vasodilator therapy (eg, nitroglycerin) ic monitoring, typically with an intra-arterial catheter.
is suggested as an adjunct to diuretic therapy for pa- The initial dose of 5 to 10 mcg/min is titrated up every
tients without adequate response to diuretics; and five minutes as tolerated to a dose range of 5 to 400
vasodilator therapy is a component of therapy for mcg/min.
patients with refractory HF and low cardiac output. It The major limitations to the use of nitroprusside is
is suggested that early vasodilator therapy (typically, thiocyanate, toxicity, which may be fatal esp with
nitroprusside) in patients with severe hypertension, doses above 400 mcg/min and rebound vasocon-
acute mitral regurgitation, or acute aortic regurgita- striction upon discontinuation. Thus, the use of nitro-
tion be initiated. Reliable blood pressure monitoring prusside is limited to selected patients for durations
is required, with careful patient monitoring( prefera- of less than 24 to 48 hours.
bly with intra arterial line) for drug tolerance .
Nesiritide: Nesiritide, like nitroprusside, is a balanced
Routine use of vasodilators does not improve out- arterial and venous dilator. In carefully selected pa-
comes, and should be avoided, as exemplified in tients with appropriate hemodynamics (absence of
ASCEND-HF, where nesiritide showed a borderline hypotension or cardiogenic shock) who remain symp-
significant trend toward reducing dyspnea, but in- tomatic despite routine therapy, a trial of nesiritide

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