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ACE Inhibitors
 ACE Inhibitors are medications that belong in the
class of medications known as antihypertensive
medications.
 ACE Inhibitors work on the Renin-Angiotensin-
Aldosterone System
Renin-Angiotensin-Aldosterone System
 A system which works to increase blood pressure
when the pressure within the kidneys drops.
 As a result of low blood pressure and/or oxygenation
in the nephron, renin is released from the
juxtaglomerular cells.
 Renin travels to the liver via the cardiovascular system
and combines with angiotensinogen to form
angiotensin I.
 Angiotensin I travels through the cardiovascular
system and arrives at the lungs where it is changed
into Angiotensin II.
 The alveoli use Angiotensin Converting Enzyme also
known as kinase II to cause this conversion.
Renin-Angiotensin-Aldosterone System cont.
 Angiotensin II is a powerful vasoconstrictor which
causes a rise in peripheral resistance and
increases pressure.
 Angiotensin II works to increase the release of
aldosterone from the adrenal glands.
 Aldosterone causes renal retention of sodium and
water, which further increases blood pressure by
increasing volume.
Mechanism of Action for ACE Inhibitors
 ACE Inhibitors work in the lungs to inhibit
Angiotensin Converting Enzyme from turning
Angiotensin I into Angiotensin II.
 These medications cause an increase of bradykinin,
which inhibits kinase II, another name for
Angiotensin Converting Enzyme.
 Blood Pressure is decreased due to a decrease in blood
volume, peripheral resistance, and cardiac load.
 ACE Inhibitors, inhibit vasoconstriction and release
of aldosterone which inhibits the retention of sodium
and water.
Indications For Use
 Hypertension-used especially for malignant
hypertension and hypertension secondary to renal
arterial stenosis.
 Benefits of Using an ACE Inhibitor as they:
 Do not interfere with cardiovascular reflexes
 Do not interfere with patients who have asthma, like
beta-blockers do.
 Do not decrease potassium levels.
 Do not cause lethargy, weakness and sexual
dysfunction.
 “ACE inhibitors reduce the risk of cardiovascular
mortality caused by hypertension.”
Indications For Use cont.
 Heart Failure
 By decreasing arteriolar tone region blood flow to the
heart improves.
 By decreasing afterload, cardiac output increases.
 Venous dilation increases causing a decrease in
pulmonary congestion and peripheral edema.
 Dilates the vessels of the kidneys increasing renal flow
and helps to excrete sodium and water. This helps to
decrease edema and blood volume.
 Prevents pathologic changes in the heart that result from
reducing the angiotensin II levels in the heart.
Indications For Use cont.
 Myocardial Infarction (MI)
 Decreases the chance of heart failure after an MI.
 Should be given for 6 weeks post MI. If heart failure
occurs it should be considered for permanent use.
 Nephropathy
 Slows renal disease of diabetic or nondiabetic origins
 Decreases glomerular filtration pressure.
Indications For Use cont.
 Type 2 Diabetes
 Decreases morbidity in high risk patients.
 Increased levels of angiotensin II have a correlation to
type 2 diabetes.
 ACE inhibitors increase kinin levels, which increase
production of prostaglandins and nitric oxide.
 Prostaglandins and nitric oxide improve muscular
sensitivity to insulin.
 May preserve pancreatic function and prevent onset of
diabetes especially with people who have hypertension.
Common Trade Names
Generic Name Trade Name
 benazepril
 captopril
 enalapril
 enalaprilat
 fosinopril
 lisinopril
 moexipril
 perinodopril
 quinapril
 ramipril
 Lotensin
 Capoten
 Vasotec
 Vasotec IV
 Monopril
 Prinivil, Zestril
 Univasc
 Aceon
 Accupril
 Altace
 Benazepril: 10 mg once daily in patients initial dose (not on a
diuretic). Usual dose: 20-40 mg in a single or 2 divided doses.
 Captopril: HFrEF (Heart failure with reduced ejection fraction)/
HTN/Left ventricular dysfunction after myocardial infarction (LVD
after MI): 6.25-12.5 mg three times a day (with diuretic) with goal
of 50 mg three times a day for HFrEF. Diabetic nephropathy: 25 mg
three times a day.
 Enalapril: HFrEF/HTN: 2.5-5 mg once or twice daily, increased up
to 40 mg/day every 1-2 weeks in 2.5 mg intervals. IV : 1.25 mg/dose
every 6 hours
 Fosinopril: HFrEF/HTN: 10 mg daily initially, then titrate to effect
(max dose 40 mg daily). Usual dose: 20-40 mg daily.
 Moexipril: Hypertension: 7.5 mg once daily (not on a diuretic) or
3.75 mg once daily (when combined with a diuretic). Administer 1
hr prior to meal. Maintenance: 7.5-30 mg daily in 1-2 divided
doses
 Perindopril: HTN: Initial: 4 mg daily; titrate to desired effect
every 1-2 weeks to a max dose of 16 mg/day. Usual dose 4-8
mg/day in 2 divided doses. Stable coronary artery disease (CAD):
Initial: 4 mg once daily for 2 weeks then increase to 8 mg once
daily as tolerated.
 Quinapril: HTN: 10-20 mg daily initially. Initial dose may be
reduced to 5 mg daily (if patient on a diuretic). Range: 10-40 mg
once daily. HFrEF: 5 mg once or twice daily; titrate to desired
effect every week to a dose of 20-40 mg daily in 2 divided doses.
 Lisinopril: HTN: Initial 10 mg daily (no diuretic) or 5 mg daily
(if on diuretic). Dose range: 10-40 mg daily. HFrEF: Initial: 2.5-5
mg once daily; titrate by 10 mg increments every 2 weeks to
target of 20-40 mg/day. Acute MI: 5mg immediately, uptitrated
to 10mg daily
 Ramipril: HTN: 2.5-5 mg once daily (max dose of 20 mg/day).
Left ventricular dysfunction (LVD) post-MI: 2.5 mg twice-daily;
titrate to 5 mg twice daily as tolerated. Reduced risk of stoke, MI
and death Initial: 2.5 mg once daily for first week, then 5 mg
once daily for weeks 2-4, then titrate to 10 mg once daily as
tolerated.
 Trandolapril: CHF/LVD Initial: 1 mg/day, titrate to 4 mg/day as
tolerated. HTN: 1 mg/day initially (may use 2 mg/day in black
patients) max dose=8mg/day; titrate to desired effect in 1 week
intervals.
Side effects:
 Altered sense of taste (Metallic taste)
 Allergic skin rashes
 Fatigue
 Dizziness
 Dry cough
 Headaches
Adverse Effects
 First-Dose Hypotension
 Usually occurs with initial dose.
 Worse in patients with severe hypertension, or are on
diuretics, or are sodium or volume depleted.
 Cough
 “Persistent, dry, irritating, nonproductive cough can
develop with all ACE inhibitors.”
 Due to rise in bradykinin which occurs due to inhibition
of kinase II.
 Occurs in 5-10% of patients and is more common in
women and the elderly.
Adverse Effects cont.
 Hyperkalemia
 Potassium levels rise due to the inhibition of aldosterone,
which causes potassium to be retained by the kidneys.
 Renal Failure
 Can cause renal insufficiency in people who have bilateral
renal artery stenosis, because dropping the pressure in the
renal arteries in these patients can cause glomerular
filtration to fail.
 Fetal Injury (Teratogenicity)
 In the second and third trimesters a fetus can experience
hypotension, hyperkalemia, skull hypoplasia, renal failure,
and death. Recent evidence also implies 1st trimester
exposure has increased teratogenic risk.
Drug Interactions
 Antihypertensive agents
 Can cause an increased effect of medications especially with
diuretics.
 Potassium increasing medications
 Cause an increased risk of hyperkalemia due to the
suppression of aldosterone. (ACEIs, NSAIDs, ARBs &
Potassium-sparing diuretics )
 Lithium
 Increases to risk of lithium toxicity.
 Allopurinol
 Increases hypersensitivity to medication
 NSAIDS (Ibuprofen, Naproxen)
 Reduce antihypertensive effects of medication.
Considerations
 Encourage lifestyle changes
 Weight loss
 Quit smoking
 Decrease alcohol intake
 Encourage exercise to help lower blood pressure
 Monitor Renal Function
 BUN, Creatinine, and Potassium levels
 Monitor for decreased fluid volume which can bottom our
blood pressure
 Excessive sweating
 Diarrhea
 Vomiting
 Dehydration
Considerations cont.
 Monitor for 1st-dose hypotension
 May have to stop other antihypertensive medications at
initiation of ACE inhibitors.
 May have to give these medications in lower doses going
forward.
 Discontinue diuretics for 2-3 days prior to starting an ACE
inhibitor.
 Monitor BP for several hours and if patient becomes
hypotensive lay patient supine and consider discussing IV
bolus of saline with the MD.
 Educate Patient
 Educate the patient about the medication including name
adverse effects, drug interactions.
 Educate the patient about the signs of hypotension,
hyperkalemia, and renal failure. If patient is taking lithium
discuss the signs of lithium toxicity.
References
 Karch, A. (2011). Focus on nursing pharmacology (5th
ed.). Philadephia, PA: Wolters Kluwer | Lippincott
Williams & Wilkins.
 Lehne, R. (2007). Pharmacology for nursing care (6th ed.).
St. Louis, MO: Saunders|Elsevier.
 Solski, L. V. & Longyhore. (2008). Prevention of type 2
diabetes mellitus with angiotensin-converting-
enzyme inhibitors. American Journal of Health-
System Pharmacy, 65(10): 935-40.
 Waterfield, J. (2008). ACE inhibitors: use, action, and
prescribing rationale. Nurse Prescribing, 6(3): 110-4.
THANK YOU

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Aceinhibitors

  • 2. ACE Inhibitors  ACE Inhibitors are medications that belong in the class of medications known as antihypertensive medications.  ACE Inhibitors work on the Renin-Angiotensin- Aldosterone System
  • 3. Renin-Angiotensin-Aldosterone System  A system which works to increase blood pressure when the pressure within the kidneys drops.  As a result of low blood pressure and/or oxygenation in the nephron, renin is released from the juxtaglomerular cells.  Renin travels to the liver via the cardiovascular system and combines with angiotensinogen to form angiotensin I.  Angiotensin I travels through the cardiovascular system and arrives at the lungs where it is changed into Angiotensin II.  The alveoli use Angiotensin Converting Enzyme also known as kinase II to cause this conversion.
  • 4. Renin-Angiotensin-Aldosterone System cont.  Angiotensin II is a powerful vasoconstrictor which causes a rise in peripheral resistance and increases pressure.  Angiotensin II works to increase the release of aldosterone from the adrenal glands.  Aldosterone causes renal retention of sodium and water, which further increases blood pressure by increasing volume.
  • 5.
  • 6.
  • 7. Mechanism of Action for ACE Inhibitors  ACE Inhibitors work in the lungs to inhibit Angiotensin Converting Enzyme from turning Angiotensin I into Angiotensin II.  These medications cause an increase of bradykinin, which inhibits kinase II, another name for Angiotensin Converting Enzyme.  Blood Pressure is decreased due to a decrease in blood volume, peripheral resistance, and cardiac load.  ACE Inhibitors, inhibit vasoconstriction and release of aldosterone which inhibits the retention of sodium and water.
  • 8. Indications For Use  Hypertension-used especially for malignant hypertension and hypertension secondary to renal arterial stenosis.  Benefits of Using an ACE Inhibitor as they:  Do not interfere with cardiovascular reflexes  Do not interfere with patients who have asthma, like beta-blockers do.  Do not decrease potassium levels.  Do not cause lethargy, weakness and sexual dysfunction.  “ACE inhibitors reduce the risk of cardiovascular mortality caused by hypertension.”
  • 9. Indications For Use cont.  Heart Failure  By decreasing arteriolar tone region blood flow to the heart improves.  By decreasing afterload, cardiac output increases.  Venous dilation increases causing a decrease in pulmonary congestion and peripheral edema.  Dilates the vessels of the kidneys increasing renal flow and helps to excrete sodium and water. This helps to decrease edema and blood volume.  Prevents pathologic changes in the heart that result from reducing the angiotensin II levels in the heart.
  • 10. Indications For Use cont.  Myocardial Infarction (MI)  Decreases the chance of heart failure after an MI.  Should be given for 6 weeks post MI. If heart failure occurs it should be considered for permanent use.  Nephropathy  Slows renal disease of diabetic or nondiabetic origins  Decreases glomerular filtration pressure.
  • 11. Indications For Use cont.  Type 2 Diabetes  Decreases morbidity in high risk patients.  Increased levels of angiotensin II have a correlation to type 2 diabetes.  ACE inhibitors increase kinin levels, which increase production of prostaglandins and nitric oxide.  Prostaglandins and nitric oxide improve muscular sensitivity to insulin.  May preserve pancreatic function and prevent onset of diabetes especially with people who have hypertension.
  • 12. Common Trade Names Generic Name Trade Name  benazepril  captopril  enalapril  enalaprilat  fosinopril  lisinopril  moexipril  perinodopril  quinapril  ramipril  Lotensin  Capoten  Vasotec  Vasotec IV  Monopril  Prinivil, Zestril  Univasc  Aceon  Accupril  Altace
  • 13.  Benazepril: 10 mg once daily in patients initial dose (not on a diuretic). Usual dose: 20-40 mg in a single or 2 divided doses.  Captopril: HFrEF (Heart failure with reduced ejection fraction)/ HTN/Left ventricular dysfunction after myocardial infarction (LVD after MI): 6.25-12.5 mg three times a day (with diuretic) with goal of 50 mg three times a day for HFrEF. Diabetic nephropathy: 25 mg three times a day.  Enalapril: HFrEF/HTN: 2.5-5 mg once or twice daily, increased up to 40 mg/day every 1-2 weeks in 2.5 mg intervals. IV : 1.25 mg/dose every 6 hours  Fosinopril: HFrEF/HTN: 10 mg daily initially, then titrate to effect (max dose 40 mg daily). Usual dose: 20-40 mg daily.
  • 14.  Moexipril: Hypertension: 7.5 mg once daily (not on a diuretic) or 3.75 mg once daily (when combined with a diuretic). Administer 1 hr prior to meal. Maintenance: 7.5-30 mg daily in 1-2 divided doses  Perindopril: HTN: Initial: 4 mg daily; titrate to desired effect every 1-2 weeks to a max dose of 16 mg/day. Usual dose 4-8 mg/day in 2 divided doses. Stable coronary artery disease (CAD): Initial: 4 mg once daily for 2 weeks then increase to 8 mg once daily as tolerated.  Quinapril: HTN: 10-20 mg daily initially. Initial dose may be reduced to 5 mg daily (if patient on a diuretic). Range: 10-40 mg once daily. HFrEF: 5 mg once or twice daily; titrate to desired effect every week to a dose of 20-40 mg daily in 2 divided doses.
  • 15.  Lisinopril: HTN: Initial 10 mg daily (no diuretic) or 5 mg daily (if on diuretic). Dose range: 10-40 mg daily. HFrEF: Initial: 2.5-5 mg once daily; titrate by 10 mg increments every 2 weeks to target of 20-40 mg/day. Acute MI: 5mg immediately, uptitrated to 10mg daily  Ramipril: HTN: 2.5-5 mg once daily (max dose of 20 mg/day). Left ventricular dysfunction (LVD) post-MI: 2.5 mg twice-daily; titrate to 5 mg twice daily as tolerated. Reduced risk of stoke, MI and death Initial: 2.5 mg once daily for first week, then 5 mg once daily for weeks 2-4, then titrate to 10 mg once daily as tolerated.  Trandolapril: CHF/LVD Initial: 1 mg/day, titrate to 4 mg/day as tolerated. HTN: 1 mg/day initially (may use 2 mg/day in black patients) max dose=8mg/day; titrate to desired effect in 1 week intervals.
  • 16. Side effects:  Altered sense of taste (Metallic taste)  Allergic skin rashes  Fatigue  Dizziness  Dry cough  Headaches
  • 17. Adverse Effects  First-Dose Hypotension  Usually occurs with initial dose.  Worse in patients with severe hypertension, or are on diuretics, or are sodium or volume depleted.  Cough  “Persistent, dry, irritating, nonproductive cough can develop with all ACE inhibitors.”  Due to rise in bradykinin which occurs due to inhibition of kinase II.  Occurs in 5-10% of patients and is more common in women and the elderly.
  • 18. Adverse Effects cont.  Hyperkalemia  Potassium levels rise due to the inhibition of aldosterone, which causes potassium to be retained by the kidneys.  Renal Failure  Can cause renal insufficiency in people who have bilateral renal artery stenosis, because dropping the pressure in the renal arteries in these patients can cause glomerular filtration to fail.  Fetal Injury (Teratogenicity)  In the second and third trimesters a fetus can experience hypotension, hyperkalemia, skull hypoplasia, renal failure, and death. Recent evidence also implies 1st trimester exposure has increased teratogenic risk.
  • 19. Drug Interactions  Antihypertensive agents  Can cause an increased effect of medications especially with diuretics.  Potassium increasing medications  Cause an increased risk of hyperkalemia due to the suppression of aldosterone. (ACEIs, NSAIDs, ARBs & Potassium-sparing diuretics )  Lithium  Increases to risk of lithium toxicity.  Allopurinol  Increases hypersensitivity to medication  NSAIDS (Ibuprofen, Naproxen)  Reduce antihypertensive effects of medication.
  • 20. Considerations  Encourage lifestyle changes  Weight loss  Quit smoking  Decrease alcohol intake  Encourage exercise to help lower blood pressure  Monitor Renal Function  BUN, Creatinine, and Potassium levels  Monitor for decreased fluid volume which can bottom our blood pressure  Excessive sweating  Diarrhea  Vomiting  Dehydration
  • 21. Considerations cont.  Monitor for 1st-dose hypotension  May have to stop other antihypertensive medications at initiation of ACE inhibitors.  May have to give these medications in lower doses going forward.  Discontinue diuretics for 2-3 days prior to starting an ACE inhibitor.  Monitor BP for several hours and if patient becomes hypotensive lay patient supine and consider discussing IV bolus of saline with the MD.  Educate Patient  Educate the patient about the medication including name adverse effects, drug interactions.  Educate the patient about the signs of hypotension, hyperkalemia, and renal failure. If patient is taking lithium discuss the signs of lithium toxicity.
  • 22. References  Karch, A. (2011). Focus on nursing pharmacology (5th ed.). Philadephia, PA: Wolters Kluwer | Lippincott Williams & Wilkins.  Lehne, R. (2007). Pharmacology for nursing care (6th ed.). St. Louis, MO: Saunders|Elsevier.  Solski, L. V. & Longyhore. (2008). Prevention of type 2 diabetes mellitus with angiotensin-converting- enzyme inhibitors. American Journal of Health- System Pharmacy, 65(10): 935-40.  Waterfield, J. (2008). ACE inhibitors: use, action, and prescribing rationale. Nurse Prescribing, 6(3): 110-4.