Angiotensin converting enzyme inhibitors (ACEi) are one type of medication that disrupts the RAAS pathway. To really understand how these drugs work, it’s important to review RAAS, which is one of the main ways the body controls blood pressure and fluid balance:

  • Renin is secreted by the kidneys in response to lower blood pressure or when Na levels are decreased.
  • Renin is an enzyme that acts upon angiotensinogen to convert it into angiotensin I.
  • Angiotensin converting enzyme (ACE) cleaves amino acids from angiotensin I, converting it into angiotensin II.
  • Angiotensin II exerts its influence in may ways: 
    • It increases SVR and MAP through vasoconstriction
    • It stimulates the reabsorption of sodium in the renal tubule to promote fluid retention
    • It stimulates the pituitary to release ADH, which increases fluid retention
    • It triggers the thirst center in the brain to promote fluid intake
    • It facilitates the release of norepinephrine, which is a potent vasoconstrictor
    • It stimulates cardiac hypertrophy
    • And, it tells the adrenal cortex to release aldosterone
  • Aldosterone tells the kidneys to increase Na and fluid retention.

So if the RAAS pathway results in higher blood pressure, a disrupted RAAS pathway is used to lower blood pressure. And ACE inhibitors definitely disrupt this pathway by inhibiting that conversion from angiotensin I to angiotensin II. Make sense? 

What drugs are ACE inhibitors?

ACE inhibitors end in “-pril” and some common ones are lisinopril, enalapril and captopril. 

What conditions are ACE inhibitors used to treat? 

ACE inhibitors are used to treat heart failure, hypertension and are often given after myocardial infarction. 

  • Hypertension:  When we disrupt the RAAS pathway, we get arterial dilation (the opposite of vasoconstriction) and decreased blood volume (the opposite of fluid retention) which leads to decreased blood pressure. 
  • Heart failure: The benefit of ACE inhibitors in heart failure are relative to its effect on fluid volume. Recall that patients with heart failure often have fluid volume excess, which can affect pulmonary function. ACE inhibitors decrease fluid volume, reduce afterload, improve cardiac output, decreases preload and reduces edema in the periphery. Working together, the effects of ACE inhibitors reduce workload on the heart and enable it to work more efficiently.
  • Post myocardial infarction: Captopril and lisinopril have been shown to reduce mortality after MI and are most effective when started within 1 to 2 days.

What are some adverse effects of ACE inhibitors? 

  • Hyperkalemia, especially when used with potassium-sparing diuretics (avoid this combo!)
  • Cough (many patients will stop therapy because the cough is so bothersome)
  • Hypotension and orthostatic hypotension
  • Disruptions in taste
  • Can increase lithium levels and put the patient at risk for lithium toxicity
  • Angioedema of the lips, tongue and face. Any time there is swelling of the face, think AIRWAY! Angioedema can be life threatening!

 

Get this on audio in episode 145 of the Straight A Nursing podcast.

References:

Deglin, Judith Hopfer, and April Hazard Vallerand. Davis’s Drug Guide for Nurses, with Resource Kit CD-ROM (Davis’s Drug Guide for Nurses). Philadelphia: F A Davis Co, 2009. Print.

Holland, N., & Adams, M. P. (2007). Core Concepts in Pharmacology (2nd ed.). Pearson Prentice Hall.

 

ACE Inhibitors Nursing Student Pharmacology