Along with diuretics, vasodilators are a mainstay in the management of acute heart failure (HF), particularly when accompanied by elevated blood pressure (BP). The primary intent of vasodilator therapy is to reduce systemic vascular resistance in an effort to offset impedance to forward cardiac flow.
What are the treatment options for acute decompensated heart failure?
Management of acute decompensated heart failure 1 Loop diuretics. Volume overload is central to the pathophysiology of most episodes... 2 Ultrafiltration. Peripheral ultrafiltration may be the most promising new treatment option... 3 Vasodilators. Preload reduction with venodilators is thought to be helpful in acute decompensated...
What is the role of vasodilators in the treatment of heart failure?
Introduction Along with diuretics, vasodilators are a mainstay in the management of acute heart failure (HF), particularly when accompanied by elevated blood pressure (BP). The primary intent of vasodilator therapy is to reduce systemic vascular resistance in an effort to offset impedance to forward cardiac flow.
Does decompensated heart failure require intravenous vasoactive drugs?
In-hospital mortality in patients with acute decompensated heart failure requiring intravenous vasoactive medications: an analysis from the Acute Decompensated Heart Failure National Registry (ADHERE). J Am Coll Cardiol 2005; 46:57.
What is the role of afterload reduction in the treatment of heart failure?
Afterload reduction is also thought to be helpful in some patients with acute decompensated heart failure by decreasing myocardial oxygen demand and improving forward flow. The majority of patients with acute decompensated heart failure have systemic hypertension at presentation.
How do vasodilators treat heart failure?
Medicines that make your blood vessels get wider are called vasodilators. They're used to treat heart failure and control high blood pressure because they cause your blood vessels to relax so that all-important fluid can flow more easily through your body.
What is the treatment for decompensated heart failure?
Early intravenous vasodilator therapy with an agent that lowers arterial tone (eg, nitroprusside) is suggested in selected patients with ADHF who require a rapid decrease in systemic vascular resistance and LV afterload (eg, those with severe hypertension, acute mitral regurgitation, or acute aortic regurgitation).
What is the role of vasodilator?
Vasodilators are medications that open (dilate) blood vessels. They affect the muscles in the walls of the arteries and veins, preventing the muscles from tightening and the walls from narrowing. As a result, blood flows more easily through the vessels. The heart doesn't have to pump as hard, reducing blood pressure.
How does vasodilator therapy improve myocardial function?
Venodilators, such as nitrates, decrease ventricular filling pressures by redistributing blood so that more is pooled in peripheral veins. Vasodilators that produce both effects (nitro-prusside, prazosin, captopril, for example) are usually helpful in short-term improvement of hemodynamics.
What happens in acute decompensated heart failure?
Acute decompensated heart failure (ADHF) is a sudden worsening of the signs and symptoms of heart failure, which typically includes difficulty breathing (dyspnea), leg or feet swelling, and fatigue. ADHF is a common and potentially serious cause of acute respiratory distress.
What is acutely decompensated heart failure?
Definition. Acute decompensated heart failure can be defined as the sudden or gradual onset of the signs or symptoms of heart failure requiring unplanned office visits, emergency room visits, or hospitalization.
What is the mechanism of action of vasodilators?
Mechanism of Action In general, Vasodilators dilate or prevent constriction of the blood vessels, which allow greater blood flow to various organs in the body. [3] Many vasodilators bind to receptors on endothelial cells of the blood vessel, which stimulate calcium release.
How does vasodilation affect cardiac output?
Thus, vasodilators increase lowered cardiac output by diminishing peripheral vascular resistance and/or decreasing increased left ventricular end-diastolic pressure (ventricular preload) by reducing venous tone.
Why does vasodilation decrease blood pressure?
Vasodilation and hypotension The process of vasodilation naturally leads to a drop in blood pressure. This is due to the widening of the blood vessels, which leads to a greater blood flow and therefore less pressure on the walls of the blood vessels.
Do vasodilators increase cardiac output?
Vasodilators can lead to renal retention of sodium and water, which increases blood volume and cardiac output and thereby compensates for the reduced systemic vascular resistance.
Do vasodilators increase afterload?
The impaired vasodilator response to β-adrenergic stimulation with age is most important during exercise and contributes to the increased afterload associated with aging. Increased afterload causes an increase in blood pressure. With aging, there is an increase in systolic blood pressure and a widened pulse pressure.
Does vasodilation increase or decrease venous return?
As shown in Fig. 13.15, a decrease in SVR caused by vasodilation will increase the slope of the venous return curve, whereas an increase in SVR caused by vasoconstriction will decrease the slop of the venous return curve.
What is vasodilator therapy?
A vasodilator that decreases arterial tone (eg, nitroprusside) is recommended for patients with urgent need for afterload reduction (eg, severe hypertension). A vasodilator therapy that primarily decreases venous tone (eg, nitroglycerin) may be used as an adjunct to diuretic therapy for patients without an adequate response to diuretics. Vasodilator therapy is a component of therapy for patients with refractory HF and low cardiac output , as discussed below and separately. (See "Management of refractory heart failure with reduced ejection fraction", section on 'Approaches to specific refractory heart failure presentations' .)
What is the target oxygen saturation for COPD?
However, patients who also have chronic obstructive pulmonary disease (COPD) may not require aggressive oxygen therapy, since the target O 2 saturation in such patients is 88 to 92 percent. In patients with both acute heart failure and COPD, we aim for the upper end of that range.
How long can you take Nitroprusside?
Thus, the use of nitroprusside is limited to selected patients, usually for durations of less than 24 to 48 hours. Use of nitroprusside in patients with ADHF is based largely upon expert opinion since available published evidence is very limited [ 14 ].
Can inotropes increase atrial arrhythmias?
In addition, inotropic agents can increase atrial [ 32] and ventricular [ 34] arrhythmias. Given these concerns, careful patient selection is required for inotrope use. (See "Use of vasopressors and inotropes" and "Inotropic agents in heart failure with reduced ejection fraction", section on 'Intravenous therapy' .)
Is sodium restriction recommended for HF?
Sodium restriction — Sodium restriction has been commonly recommended in patients with acute or chronic HF, although there are insufficient data to support any specific level of sodium intake in patients with symptomatic HF, as noted in the 2013 ACC/AHA and 2012 European Society of Cardiology (ESC) guidelines [ 5,19 ]. Given the available evidence, we suggest sodium restriction (eg, <2 g/d) in patients with symptomatic HF. The 2013 ACC/AHA guidelines suggest some degree (eg, <3 g/d) of sodium restriction in patients with symptomatic HF [ 19 ], while the 2012 ESC guidelines note that the safety and efficacy of salt restriction require further study [ 19 ]. (See "Patient education: Low-sodium diet (Beyond the Basics)" .)
Is morphine sulfate used in ADHF?
Morphine therapy is not mentioned in the 2010 Heart Failure Society of America guidelines on management of ADHF or in the 2013 ACC/AHA guidelines. The role of morphine sulfate in patients with ADHF who have an acute myocardial infarction is discussed separately.