ACE Inhibitors: List, Description and Nursing interventions

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ACE Inhibitors
ACE Inhibitors

ACE Inhibitors or Angiotensin converting enzymes inhibitors are also called vasoactive peptides because of their direct effect on blood vessels. ACE inhibitors are widely used medicine and first line of treatment in hypertension and congestive heart failure. ACE inhibitors decrease systemic vascular resistance without increasing heart rate and also promotes natriuresis.

List of Common ACE Inhibitors:

ACE Inhibitors list contains many important drugs extensively used nowadays, which are as follows:

GENERIC NAME BRAND NAME
Benazepril Lotensin
Captopril Capoten, Acepril, Capozide
Fosinopril Fositen, Monopril, Staril
Lisinopril Lopril, Zestrin, Prinivil, Novatec
Enalapril Vasotec, Epaned, Enap, Ranitec

 

RENIN-ANGIOTENSIN ALDOSTERONE SYSTEM (RAS):

The RAS (The renin–angiotensin system) significantly participates in pathophysiology of hypertension, congestive heart failure, myocardial infarction, diabetic nephropathy. The renin-angiotensin aldosterone system leads to produce Angiotensin II which is the most active angiotensin. Angiotensin II produce by the series of proteolytic steps. A pre enzyme Angiotensinogen produced from the liver. Angiotensinogen is acted upon by renin and converted into Angiotensin I. Renin is an enzyme released from the juxtaglomerular cells of kidney in response to low fluid moves through nephrons. Angiotensin I is further converted into Angiotensin II by the Angiotensin converted enzymes (ACE). The resulting compound Angiotensin II is responsible to increase blood pressure and retention of sodium and water from kidneys.

THREE MAJOR EFFECTS OF ANGIOTENSIN II:

The production of Angiotensin II resulted in three major effects which leads to cause different cardiopathies, increase blood pressure and nephropathy.

1. Altered Peripheral resistance

Angiotensin II increase peripheral resistance by the following mechanism:

  • direct vasoconstriction
  • Increase Nor-epinephrine release and decreased Nor-epinephrine reuptake
  • released catecholamine
  • increase CNS discharged

All these above changes cause Rapid Pressor response, blood pressure increases.

2. Altered Renal function
  • Direct effect to increase Na+ reabsorption from PCT
  • release of aldosterone from adrenal cortex (increase Na+ reabsorption and increase K+ excretion from DCT)
  • direct renal vasoconstriction
3. Altered Cardiovascular structure

Long term Angio II release results in cardiac remodeling as follows.

  • increase after load (Cardiac)
  • Increase wall tension (vascular)
  • Increase production of growth factors
  • Increase expression of pro-oncogenes
  • Increase synthesis of extracellular protein matrix.

MECHANISM OF ACTION:

ACE is an ectoenzyme and glycoprotein which is the main component of RAS. It coverts Angio I to Angio II which controls blood pressure by controlling the volume of body fluids in the body.

ACE inhibitors controls blood pressure by the following two steps

Firstly, ACE inhibitors inhibits the Angiotensin converting enzyme and thus inhibits the production of Angiotensin II. As a result of inhibition of Angio II, all the functions performed by Angio II stopped as a result of which ACE inhibitors decrease systemic vascular resistance without increasing heart rate.

Secondly, ACE inhibitors inhibits the degradation of Bradykinin, Substance P, enkephalin. Bradykinin is a vasoactive peptide that causes dilation of blood vessels and decrease blood pressure. ACE degrades bradykinin and increase vasoconstriction results in increase blood pressure. ACE I inhibits the degradation of bradykinin which decreases the peripheral vascular resistance thus, control the blood pressure.

PHARMACOKINETICS

All ACE inhibitors are different in their structure and pharmacokinetics, but in clinical use, they are interchangeable. Currently available ACEI are all active when given orally. ACE inhibitors are highly polar and eliminated in urine except fosinopril and moexipril. Doses should be reduced in renal insufficiency. A number of ACEI are and active (e.g. Lisinopril, captopril) while some are prodrugs (e.g. enalapril). ACE inhibitors do not penetrate the central nervous system. Many ACE inhibitors are given once daily because of longer half-life except Captopril. Lisinopril and Enalapril have half-life of 12 hours.

INDICATIONS

  • Hypertension
  • Congestive heart failure
  • Decrease morbidity and mortality in heart failure
  • Myocardial Infarction
  • Diabetic nephropathy
  • Left ventricle systolic dysfunction

CONTRAINDICATIONS

  • Hypersensitivity
  • During second and third trimester of pregnancy
  • Previous angioedema

SIDE EFFECTS & ADVERSE EFFECTS

ACE inhibitors are generally well tolerated but some side effects may be shown which are as follows:

  • First dose hypotension
  • Dry cough (due to bradykinin, more frequent and sometime troublesome)
  • Functional renal failure (in renal arterial stenosis patient)
  • Hyperkalemia
  • Headache
  • Dizziness
  • Fetal injury
  • Urticaria
  • Angio oedema
  • Proteinuria, neutropenia, rashes and taste disturbance (patient taking captopril)

DRUG INTERACTION

  • Potassium supplements and potassium-sparing diuretics results in hyperkalemia when given with ACE inhibitors.
  • NSAIDs may impair the hypotensive effects of ACE inhibitors and increase blood pressure.
  • Antacids may reduce the bioavailability of ACE inhibitors
  • Capsaicin may worsen the cough induced by ACE inhibitors.
  • ACE inhibitors may increase plasma levels of Digoxin and lithium
  • Hypersensitivity reaction of Allopurinol may increase with when given with ACE inhibitors.
  • ACE inhibitors may increase the effects of RAAS blockers, NSAIDS, anticoagulants, DPP4 inhibitors and cyclosporine.
  • Alcohol may increase the antihypertensive effect of ACE inhibitors.

NURSING INTERVENTIONS

  • Take complete health history of patient.
  • Monitor blood pressure and pulse frequently to avoid initial dose hypotension.
  • Daily check the weight and fluid overload.
  • Check the s/s of angioedema (swelling of face and extremities)
  • Monitor BUN, serum potassium, creatinine, AST, ALT, serum bilirubin level
  • ACE inhibitors may cause false urine acetone level
  • Monitor kidney function.

PATIENT EDUCATION

  • Counsel the patient right dose and time of medicine
  • Low blood pressure may be experienced, discontinue medicine when severe hypotension occur and report health practitioner.
  • Drink plenty of water.
  • Increase in urination.
  • Do not take alcohol it will further decrease blood pressure.
  • Don not breast feed.
  • Avoid strict exercise routine while taking the medicine
  • Avoid use of potassium supplements and potassium rich diet.
  • Ask HP prior taking multivitamins or fortified supplements
  • Report immediate if having persistent cough specially at night.

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