Acute Heart Failure Syndromes

KELOMPOK C

DEFINITION

AHFS can be defined as new onset or gradual or rapidly worsening HF signs

and symptoms requiring urgent therapy. Irrespective of the underlying cause

(e.g., ischemic event) or precipitant (e.g., severe hypertension), pulmonary and

systemic congestion due to elevated ventricular filling pressures with or without

a decrease in cardiac output is a nearly universal finding in AHFS (5).

Coronary artery disease(CAD), hypertension, valvular heart disease, and/or

atrial fibrillation, as well as noncardiac conditions such as renal dysfunction,

diabetes, anemia, and medications (i.e., nonsteroidal anti-inflammatory drugs,

glitazones), may also contribute to these abnormalities (5,9–11). The majority of

AHFS patients have worsening chronic HF; after initial management resulting

in stabilization, they should no longer be consideredacute but chronic HF.

EPIDEMIOLOGYIncidence and prevalence:

One hundred to 400 new cases of heart failure are diagnosed per 100,000 persons per year

One thousand or more new cases are diagnosed per 100,000 persons over age 65 per year

There are approximately 1,000 to 2,000 cases of heart failure per 100,000 persons

Five thousand or more cases are diagnosed per 100,000 persons over age 65; heart failure is the most common inpatient diagnosis in the U.S. in patients over age 65

Heart failure occurs at some stage in patients with most forms of severe heart disease, regardless of the underlying cause

Heart failure leads to a total of 12 to 15 million office visits per year

Demographics:

Incidence increases with age

Heart failure is more common in men than in women between 40 and 75 years of age, but among persons over age 70, both sexes are affected equally

The prevalence of heart failure is estimated to be 25% greater in black persons than in white persons

Dilated and hypertrophic forms of cardiomyopathy may run in families, and specific genetic defects are known. Susceptibility to myocardial infarction, which is a frequent cause of heart failure, may have a genetic component. Hypertension is frequently familial. Hemochromatosis can lead to both cardiomyopathy and accelerated coronary artery disease

RISK FACTORS

Obesity

Obstructive sleep apnea

Cigarette smoking

Pregnancy

Infection, especially pulmonary infection

Diabetes

Physical inactivity

Renal insufficiency

CLINICAL CLASIFICATION

PATHOPHYSIOLOGYAHFS are characterized by severe hemodynamic and neurohormonal abnormalities that may cause myocardial injury and/or renal dysfunction or may be a result of it These abnormalities may be caused or precipitated by ischemia, hypertension, atrial fibrillation, other noncardiac conditions (e.g., renal insufficiency), or untoward drug effects

Congestion

Myocardial injury

Renal impairment

Untoward drug effects

Congestion

High LV diastolic pressure resulting in pulmonary and systemic congestion with or without

low cardiac output is the main reason for presentation in the majority of patients . Systemic

congestion manifests clinically by jugular venous distention with or without peripheral

edema and gradual increases in BW are often seen ..

High LV diastolic pressure, by itself, may contribute to the progression of HF by further

causing activation of neurohormones, subendocardial ischemia, and/or changes in LV size

and shape (remodeling) that often results in mitral insufficiency.

Body weight is often used as a marker of congestion in both inpatient and outpatient

settings. However, recent data suggest a more complex relationship among BW, congestion,

and outcomes. Although an increase in BW predicts hospitalization, a reduction in BW in

response to different therapies may not necessarily result in decreased hospitalization or

mortality.

Myocardial injury

Troponin release often occurs in AHFS, particularly in patients

with CAD. This likely reflects myocardial injury, which may

be related to hemodynamic and/or neurohormonal

abnormalities or the result of an ischemic event (MI).

Injury may also be the consequence of a high LV diastolic

pressure, further activation of neurohormones, and/or inotropic

stimulation, resulting in a supply and demand mismatch

(increased myocardial oxygen demand and decreased coronary

perfusion. These conditions may precipitate injury, particularly

in patients with CAD, who often have hibernating and/or

ischemic myocardium. This is supported by experimental data

in dogs where stimulation of hibernating myocardium with

low-dose dobutamine resulted in myocardial necrosis

Renal impairment

In AHFS, renal abnormalities promote sodium and water retention.

Renal dysfunction resulting from neurohormonal or hemodynamic abnormalities (vasomotor nephropathy) may be preventable or reversible and it is often referred as the cardio-renal syndrome.

In a given patient, distinguishing between vasomotor nephropathy from abnormalities related to intrinsic kidney disease is often difficult and remains an important area for research.

Both intrinsic/pre-existing structural kidney disease and potential contributors to renal injury from acute heart failure (HF) syndromes characterize the cardio-renal syndrome. Figure illustration by Rob Flewell.

Untoward drug effects

Non–potassium-sparing intravenous (IV) loop diuretics are first-line agents to alleviate congestive symptoms. High-dose administration of IV loop diuretics has been associated with worse outcomes in HF patients.

Dobutamine, milrinone, and levosimendan improve hemodynamics; however, these effects may be associated with increased myocardial oxygen consumption (tachycardia and increased contractility) and hypotension due to their vasodilatory effects.

Decreasing coronary perfusion due to hypotension in the presence of increased myocardial oxygen demand may result in myocardial injury, particularly in patients with CAD who often have ischemic or hibernating myocardium.

Hypotension associated with the use of vasodilators may also result in myocardial and renal hypoperfusion and possibly injury.

MANAGEMENT OF ACUTE HEART FAILURE SYNDROME

Pharmalogical Treatment

Acute Management Oxygen Oxygen may be given to treat

hypoxaemia (SpO2 ,90%), which is associated with an increased risk of short-term mortality.

Oxygen should not be used routinely in non-hypoxaemic patients as it causes vasoconstriction and a reduction in cardiac output.

Diuretics

Most patients with dyspnoea caused by pulmonary oedema obtain rapid symptomatic relief from administration of an i.v. diuretic, as a result of both an immediate venodilator action and subsequent removal of fluid. The optimum dose and route of administration (bolus or continuous infusion) are uncertain. A recent, small, prospective RCT compared 12-hourly bolus injection with continuous infusion and low-dose (equal to pre-existing oral dose) with highdose (×2.5 times previous oral dose) using a 2 × 2 factorial design.

Opiates

Opiates such as morphine may be useful in some patients with acute pulmonary oedema as they reduce anxiety and relieve distress associated with dyspnoea. Opiates are also thought to be venodilators, reducing preload, and may also reduce sympathetic drive. Conversely, opiates induce nausea (necessitating the concomitant administration of an antiemetic, one of which, cyclizine, has vasoconstrictor activity) and depress respiratory drive, potentially increasing the need for invasive ventilation.

Vasodilators

Although vasodilators such as nitroglycerine (Table 20) reduce preload and afterload and increase stroke volume, there is no robust evidence that they relieve dyspnoea or improve other clinical outcomes. Vasodilators are probably most useful in patients with hypertension and should be avoided in patients with a systolic blood pressure ,110 mmHg. Excessive falls in blood pressure should also be avoided because hypotension is associated with higher mortality in patients with AHF. Vasodilators should be used with caution in patients with significant mitral or aortic stenosis.

Nesiritide

Nesiritide—a human BNP that acts mainly as a vasodilator—was recently shown to reduce dyspnoea by a small but statistically significant amount when added to conventional treatment (mainly diuretic)

Inotropes

Use of an inotrope such as dobutamine should usually be reserved for patients with such severe reduction in cardiac output that vital organ perfusion is compromised. Such patients are almost always hypotensive (‘shocked’). Inotropes cause sinus tachycardia and may induce myocardial ischaemia and arrhythmias.

Vasopressors

Drugs with prominent peripheral arterial vasoconstrictor action such as norepinephrine are sometimes given to severely ill patients with marked hypotension. These agents are given to raise blood pressure and redistribute cardiac output from the extremities to the vital organs.

Dopamine

In large doses (.5 mg/kg/min) dopamine has inotropic and vasoconstrictor activity. At lower doses (,3 mg/kg/min) dopamine may have a selective renal arterial vasodilator activity and promote natriuresis, although this is uncertain. Dopamine may cause hypoxaemia.

After stabilization

Angiotensin-converting enzyme inhibitor /angiotensin receptor blocker

In patients with reduced EF not already receiving an ACE inhibitor (or ARB), this treatment should be started as soon as possible, blood pressure and renal function permitting.

Beta-blocker

In patients with reduced EF not already receiving a beta-blocker, this treatment should be started as soon as possible after stabilization, blood pressure and heart rate permitting

Mineralocorticoid (aldosterone) receptor antagonist

In patients with reduced EF not already receiving an MRA, this treatment should be started as soon as possible, renal function and potassium permitting

Digoxin

In patients with reduced EF, digoxin may be used to control the ventricular rate in AF, especially if it has not been possible to up-titrate the dose of beta-blocker. Digoxin may also provide symptom benefit and reduce the risk of HF hospitalization in patients with severe systolic HF

Non-pharmacological/non-device therapy

Ventilation Non-invasive ventilation Continuous positive airway pressure

(CPAP) and non-invasive positive pressure ventilation (NIPPV) relieve dyspnoea and improve certain physiological measures (e.g. oxygen saturation) in patients with acute pulmonary oedema.

Endotracheal intubation and invasive ventilation

The primary indication for endotracheal intubation and invasive ventilation is respiratory failure leading to hypoxaemia, hypercapnia, and acidosis. Physical exhaustion, diminished consciousness, and inability to maintain or protect the airway are other reasons to consider intubation and ventilation.

Mechanical circulatory support Intra-aortic balloon pump

The conventional indications for an intra-aortic balloon pump (IABP) are to support the circulation before surgical correction of specific acute mechanical problems (e.g. interventricular septal rupture and acute mitral regurgitation), during severe acute myocarditis and in selected patients with acute myocardial ischaemia or infarction before, during, and after percutaneous or surgical revascularization.

Ventricular assist devices Ventricular assist devices and other

forms of mechanical circulatory support (MCS) may be used as a ‘bridge to decision’ orvlonger term in selected patients

Ultrafiltration Venovenous isolated ultrafiltration is

sometimes used to remove fluid in patients with HF, although is usually reserved for those unresponsive or resistant to diuretics.

REFERENCES