Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
A cough is a common adverse event associated with ACE inhibitor therapy, occurring in 5% to 20% of patients. It is thought to be due to increased production of bradykinins or substance P, both of which lower the cough reflex.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
Hypotension may occur with any of the ACE inhibitors and is usually observed after the first dose. It is more common in patients who are sodium or volume depleted, such as those treated with diuretics or dialysis and in patients with heart failure.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
Angioedema associated with throat or laryngeal edema may be fatal because of airway blockage, which causes suffocation. Patients should be advised about this possible adverse effect and told to go to an emergency department immediately.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
The most common adverse reactions of ACE inhibitors are dizziness, headache, fatigue, cough, and hypotension. Angioedema of the face, extremities, lips, tongue, glottis, or larynx also has been reported in patients treated with ACE inhibitors.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
When taken by pregnant women during the second and third trimesters, ACE inhibitors can cause injury or death to the fetus. When pregnancy is detected, the ACE inhibitor should be discontinued due to the teratogenic effects.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
Patients should not receive an ACE inhibitor if they have experienced life-threatening adverse effects (angioedema or anuric renal failure) during previous exposure or if they are pregnant.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
The hemodynamic effects of ACE inhibitors in heart failure include decreased preload, afterload and mean arterial pressure, as well as increased cardiac output. Ejection fraction is also improved.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
Because angiotensin II stimulates aldosterone secretion by the adrenal cortex and provides negative feedback for plasma renin, inhibition of angiotensin II may lead to decreased aldosterone and increased renin activity.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
Angiotensin II interacts with at least two known membrane receptors, type 1 and type 2 (AT1 and AT2). By blocking the formation of angiotensin II, ACE inhibitors produce vasodilation and a decrease in systemic vascular resistance (LV afterload).

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
Activation of the RAAS is an important compensatory mechanism in heart failure. ACE catalyzes the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor and stimulant of aldosterone secretion.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
The New York Heart Association (NYHA) classifies the functional incapacity of patients with cardiac disease into four levels depending on the degree of effort needed to elicit symptoms.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
Depressed ventricular function can be confirmed by echocardiography, ventriculography or cardiac catheterization. Abnormalities in the ECG are common and include arrhythmias, conduction delays, hypertrophy and ST changes.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
When the left ventricle malfunctions, congestion initially occurs in the lungs. When the right ventricle functions inadequately, congestion in the supplying systemic venous circulation results in peripheral edema and liver congestion.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
When the heart fails as a pump and cardiac output (the volume of blood pumped out of the ventricle per unit of time) decreases, a complex scheme of compensatory mechanisms to raise and maintain cardiac output occurs.

Nursing Tip of the Day! - Fundamentals

Category: Fundamentals 
Heart failure is a pathophysiologic state in which abnormal myocardial function inhibits the ventricles from delivering adequate quantities of blood to metabolizing tissues at rest or during activity.