Chapter 24 Heart Failure Flashcards
Heart failure is a clinical syndrome caused by numerous
cardiac disorders. It is a pathologic state in which the heart is unable to?
pump blood in sufficient amounts from the ventricles to meet the body’s metabolic needs, or can do so only at elevated filling pressures. The signs and symptoms typically associated with this insufficiency make up the syndrome of heart failure.
Heart failure occurs due to a?
reduced ratio of ejection fraction to left ventricular end-diastolic volume.
The physical defects causing heart failure are of two types:
(1) a myocardial defect such as myocardial infarction or
valve insufficiency, which leads to inadequate cardiac contractility and ventricular filling
(2) a defect outside the myocardium (e.g., coronary artery disease, pulmonary hypertension, or diabetes), which results in an overload on an otherwise normal heart.
The best way to prevent heart failure is to control risk factors associated with heart failure including?
hypertension, coronary artery disease, obesity, and diabetes.
(An inotrope is an agent that alters the force or energy of muscular contractions)
- Inotropic drugs affect the force of myocardial contraction
1) positive inotropics
2) negative inotropics
- positive inotropics (e.g., digoxin) increase the force of contractions,
- negative inotropics (e.g., beta blockers, calcium channel blockers) decrease myocardial contractility.
Chronotropics affect heart rate per minute, with positive
chronotropics and negative chronotropics
- positive chronotropics increasing heart rate
- negative chronotropics decreasing the heart rate
Dromotropic drugs affect the conduction of electrical
impulses through the heart;
- positive dromotropic drugs
-negative dromotropic drugs
- positive dromotropic drugs increase the speed of electrical impulses through the heart
- negative dromotropic drugs have the opposite effect.
Be aware of the important physiologic concepts such as ejection fraction. A patient’s ejection fraction reflects the?
contractility of the heart and is about 65% (0.65) in a normal heart. This value decreases as heart failure progresses; therefore, patients with heart failure have low ejection fractions because their hearts are failing to pump effectively.
American Heart Association and American College of Cardiology Guidelines for the Diagnosis and Management of Heart Failure in Adults (2005, updated in 2013) approach to the treatment of chronic heart failure revolves around?
reducing the effects of the renin-angiotensin-aldosterone system and the sympathetic nervous system (SNS).
Drugs of choice at the start of therapy are?
1) angiotensin converting enzyme (ACE) inhibitors (lisinopril, enalapril, captopril, and others)
2) angiotensin receptor blocker (ARBs; valsartan, candesartan, losartan, and others)
3) certain beta blockers (metoprolol, a cardioselective beta blocker; carvedilol, a nonspecific beta blocker).
Loop diuretics (furosemide) are used to?
reduce the symptoms of heart failure secondary to fluid overload, and the aldosterone inhibitors (spironolactone, eplerenone) are added as the heart failure progresses.
The newest class of medications for heart failure, the B- type natriuretic peptides, currently includes only one drug
nesiritide.
Nesiritide is a synthetic B-type natriuretic hormone that has what effects?
vasodilating effects on both arteries and veins. This vasodilation takes place in the heart itself and throughout the body.
The effects of nesiritide have been shown to include diuresis, natriuresis (urinary sodium loss), and vasodilation. These properties lead to an indirect increase in cardiac output and suppression of neurohormonal systems such as the renin-angiotensin system.
Nesiritide is a synthetic version of human B-type natriuretic peptide. B-type natriuretic peptide (BNP) is a stubstance secreted from the ventricles of the heart in response to changes in pressure that occur when heart failure develops. The level of BNP in the blood increases when heart failure symptoms worsen. Nesiritide is a synthetic b-type natriuretic hormone that is used in the?
intensive care setting as a final effort to treat severe, life-threatening heart failure, often in combination with several other cardiostimulatory medications. Its use is no longer recommended as a first-line drug for heart failure due to worsened renal function and mortality reported
Nesiritide-human B-type natriuretic peptide contraindication
known drug allergy, not recommended for use in pt’s with low cardiac filling pressures
Nesiritide-B-type natriuretic peptide AEs
hypotension, cardiac dysrhythmias, insomnia, HA, abdominal pain
Nesiritide-B-type natriuretic peptide Interactions
additive hypotensive effects w/coadministration w/ACE inhibitors & diuretics
Phosphodiesterase inhibitors (PDIs) are a group of inotropic drugs that work by?
inhibiting the action of an enzyme called phosphodiesterase
Phosphodiesterase inhibitors (PDIs) drug
Presently milrinone (Primacor) is the only drug in this category available in the United States.
Phosphodiesterase inhibitors (PDIs) mechanism of action
Differs from other inotropic drugs such as digoxin and the catecholamines.
-Inhibit action of phosphodiesterase, resulting in an increase in intracellular cyclic adenosine monophosphate (cAMP). However milrinone is more specific for phosphodiesterase type III, which is common in the heart and vascular smooth muscles
Milrinone causes an intracellular increase in cyclic adenosine monophosphate (cAMP), which results in two beneficial effects in a patient with heart failure
(1) a positive inotropic response
2) vasodilation. For this reason, this class of drugs may also be referred to as inodilators (inotropics and dilators
Milrinone has a 10-100 times greater affinity for?
Smooth muscle fibers surrounding pulmonary and systemic blood vessels than they do for cardiac muscle. This suggests that the primary beneficial effects of inodilators come from their vasodilating effects, causing a reduction in the force against which the heart must pump to eject its volume of blood
Inhibition of phosphodiesterase results in the?
Availability of more Ca+ for myocardial muscle contraction>increase in force of contraction (positive inotropic effect)
- increased Ca+ present in heart muscle is taken back up into its storage sties at faster rate than normal. As a result, the heart muscle relaxes more than normal and is also more compliant
- PDIs have positive inotropic and vasodilatory effects. May also increase HR in some instances & therefore may also have positive chronotropic effects as well
Phosphodiesterase Inhibitors (PDIs) are primarily used in?
the intensive care setting for the short-term management of acute heart failure
-Not recommended for long-term infusion