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176 Cardio Diabetes Medicine 2017

vasopressor (eg, phenylephrine or norepinephrine), • Milrinone: – Milrinone is a phosphodiesterase inhib-
and gentle hydration if pulmonary edema is not itor that increases myocardial inotropy by inhibiting
present. Ultrafiltration is an option for patients with degradation of cyclic adenosine monophosphate.
HFrEF or HFpEF with refractory volume overload not Other direct effects of milrinone include reducing
responding to diuretic strategies. systemic and pulmonary vascular resistance (via
inhibition of peripheral phosphodiesterase) and
Vasodilator therapy — Intravenous vasodilator therapy improving left ventricular diastolic compliance .
is suggested in patients with refractory HF who re- These changes lead to an increase in cardiac index
quire reduction in preload, afterload, or both. Nitrates and decrease in left ventricular afterload and filling
reduce LV filling pressure primarily via venodilation pressures. Patients should receive a loading dose
and at higher doses, lower SVR and LV afterload. of 50 mcg/kg over 10 minutes, followed by a main-
Nitroprusside and nesiritide both provide balanced tenance dose of 0.375 to a maximum of 0.750
arterial and venous dilation. The use of these agents mcg/kg per min. Dose adjustment is required in
should be reserved for patients in whom improved the presence of renal insufficiency, hypotension,
hemodynamic function is likely to lead to clinically or arrhythmias.
useful improvements in oxygenation and/or organ
perfusion, but monitored with utmost caution in in- Since milrinone does not act via beta receptors, its
tensive care setting. effects are not as diminished as those of dobutamine
or dopamine by concomitant beta blocker therapy.
Inotropic agents
• Dobutamine: Dobutamine acts primarily on beta-1
Indications — Intravenous inotropic agents such as adrenergic receptors, with minimal effects on beta-
dobutamine and/or milrinone may be required as 2 and alpha-1 receptors. The hemodynamic effects
a temporizing measure in patients with severe left of dobutamine include increases in stroke volume
ventricular systolic dysfunction and low output syn- and cardiac output, and modest decreases in sys-
drome until definitive therapy (eg, coronary revascu- temic vascular resistance and pulmonary capillary
larization, mechanical circulatory support, or heart wedge pressure . It should be started at 2.5 mcg/
transplantation) is instituted or resolution of the kg per min and, if tolerated and needed, can be
acute precipitating problem has occurred. Continu- gradually increased to 20 mcg/kg per min.
ous intravenous inotropic support has been felt to be
reasonable as “bridge therapy” in patients with stage • Dopamine : Although it has been proposed that
D HF refractory to guideline-directed medical therapy dopamine might improve renal function in patients
and device therapy who are eligible for and awaiting with severe HF by increasing renal blood flow and
mechanical circulatory support or cardiac transplan- possibly by reducing renal venous pressure, data
tation. In addition, the 2013 ACC/ AHA guidelines supporting such a potential benefit are limited.
note that inotropic therapy “may be reasonable” (a Inotropic agents may adversely impact outcomes
very weak recommendation) in the following settings: by increasing heart rate and myocardial oxygen
short-term, continuous intravenous inotropic support consumption and thus mask underlying ischemia
in hospitalized patients presenting with document- and even lead to atrial and ventricular arrhythmias.
ed severe systolic dysfunction who present with low Routine use of inotropes in patients hospitalized
blood pressure and significantly depressed cardiac for HF was found to be harmful in the OPTIME-CHF
output to maintain systemic perfusion and preserve trial,where milrinone therapy was associated with
end-organ performance; and long-term continuous significant increases in hypotension requiring in-
intravenous inotropic support as palliative therapy tervention and atrial arrhythmias, and with nonsig-
for symptom control in select patients with stage D nificant increases in mortality in-hospital
HF despite optimal guideline-directed medical ther- • Vasopressor therapy- In patients with ADHF and
apy and device therapy who are not eligible for ei- marked hypotension, vasopressor therapy can be
ther mechanical circulatory support or cardiac trans- used as a temporizing measure to preserve sys-
plantation. If symptomatic hypotension or worsening temic blood pressure and end-organ perfusion, al-
tachyarrhythmias develop during inotrope adminis- though at the cost of increasing afterload and de-
tration, dose reduction or discontinuation is suggest- creasing cardiac output. Vasopressor use should
ed.Similar recommendations are echoed in the 2010 be limited to patients with persistent hypotension
Heart Failure Society of America and 2012 European with symptoms or evidence of consequent end-or-
Society of Guidelines .Inotropes are not indicated for gan hypoperfusion despite optimization of filling
treatment of ADHF in the setting of preserved sys- pressures and use of inotropic agents. With inva-
tolic function.

GCDC 2017