Hypertension Drug List Flashcards
What factors determine arterial pressure? What determines those factors?
Arterial Pressure = CO x peripheral resistance
CO = HR x SV
HR: ~50-100 bpm
SV: ~70 mLs/beat
CO determined by HR, contractility, blood volume, venous return
Peripheral resistance (PR) is determined by arterial constriction (afterload)
In other words, for anti-HTN drugs to lower BP they must do one (or all) of the following: decrease HR, SV, or PR.
What are the prototype / first-line medications for hypertension?
Hydrochlorothiazide Metoprolol Lisinopril Valsartan Nifedipine Hydralazine
What are the nursing implications of anti-hypertensive drugs?
BLOOD PRESSURE GOALS:
< 140 / < 90
< 130 / < 80 (DM, CKD, gout)
Withhold if BP < 90 / < 60, HR < 50
PATIENT SAFETY:
Orthostatic HTN
Rebound HTN
NONCOMPLIANCE:
Availability / cost
Patient teaching
Often asymptomatic
LIFE-TIME THERAPY
What side effects are associated with hydrochlorothiazide as an anti-hypertensive? What group of patients is it most useful for?
Hydrochlorothiazide (thiazide diuretic)
Associated with hyperglycemia, hypercholesterolemia, triglyceridemia, hyperuricemia (especially with patients of DM, gout, hyperlipidemia)
Especially useful for African American patients (salt sensitivity)
How does Metoprolol modify HTN? What side effects are associated with metoprolol as an anti-hypertensive?
Metoprolol (sympatholytic)
Blocks beta receptors and suppresses renin-angiotensin-aldosterone system.
May cause bradycardia and hypotension.
What are the RAA drugs for HTN?
Angiotensin converting enzyme (ACE) Inhibitors (Lisinopril) and Angiotensin II Receptor Blocker (ARBs) (Valsartan)
How do ACE inhibitors work?
ACE inhibitors block enzyme needed to convert angiotensin I to angiotensin II resulting in decreased angiotensin II (vasodilation and increased renal blood flow) and decreased aldosterone (increased renal excretion of sodium and water).
What is the MOA of Lisinopril?
Lisinopril: ACEI
Blocks ACE, prevents conversion of Angiotensin I –> II causing
- reduced angiotensin II
- reduced aldosterone
- increased bradykinin
What is Lisinopril used for?
Valsartan (and Lisinopril) are used for Hypertension as well as ALL other indications: heart failure, post MI, coronary disease risk, diabetes, chronic kidney disease, recurrent stroke
What are the PK of Lisinopril? Some nursing implications?
Lisinopril:
Excreted via kidney - careful with ppl w/ kidney problems
reduces risk of CV mortality r/t HTN
Doesn’t interfere w/ Cardiovascular reflexes: no exercise impairment, orthostatic HTN minimal
Can cause severe renal insufficiency w/ bilateral renal artery stenosis
Don’t use with pregnant women in 2nd or 3rd trimester
Can be used in combination w/ thiazide
What is Valsartan used for?
Valsartan (and Lisinopril) are used for Hypertension as well as ALL other indications: heart failure, post MI, coronary disease risk, diabetes, chronic kidney disease, recurrent stroke
What is the MOA of Valsartan?
Valsartan: ARB
Blocks angiotensin II receptors, causing:
- reduced angiotensin II
- reduced aldosterone
- increased bradykinin
What are the effects of Valsartan and Lisinopril?
Effects:
- peripheral vasodilation
- renal vasodilation
- aldosterone suppressed (Na/H20 is excreted / K+ retention increased)
Side / adverse effects:
- Hypotension
- Hyperkalemia: blocks aldosterone
- Fetal injury
- Angioedema - caused by bradykinin, life threatening, contraindication for continued treatment
- Cough r/t increased bradykinin
- NO COUGH WITH VALSARTAN
Doesn’t interfere w/ Cardiovascular reflexes: no exercise impairment, orthostatic HTN minimal
- renal vasodilation
- suppression of aldosterone - causes Na/H20- excreted and K+ increased
What is the MOA of metoprolol?
blocks beta receptors suppressess RAAS system reducing oxygen demand on the heart - decreases blood pressure - decreases contractility - decreases heart rate
What is the MOA of Nifedipine?
MOA of Nifepidine:
dihydropyridine type:
blocks calcium channels in vascular smooth muscle including peripheral arterioles and coronary arteries
blood vessels have actin/myocin which interdigitate under influence of Ca, increasing BP. Blocking Ca decreases interdigitation and lowers arterial pressure (not venous).
