CHAPTER 16: ANTIHYPERTENSIVES- Treatments Flashcards
Beta Blockers, ACE Inhibitors, Calcium Channel Blockers, Vasodilators
what types of drugs can be used to control blood pressure?
ACE inhibitors, angiotensin II receptor blockers, calcium channel blockers, vasodilators, diuretics, alpha/beta blockers, renin inhibitors
what is the first step before implementing drugs in the treatment of hypertensive patients?
lifestyle modifications!!!
BETA BLOCKERS: main actions and side effects
we want to reduce CO, dec BP as a result
ACTION: REDUCE CO
- dec HR, force of contraction, and AV conduction
SIDE EFFECTS:
- bradycardia
- lethargy
- GI disturbances
- CHF
- dec BP
- depression
B-adrenoceptor blocking agents
- therapeutic actions
- reduce BP by dec CO
- dec sympathetic outflow from CNS
- inhibit renin release–> dec angiotensin II and aldosterone
B-adrenoceptor blocking agents: list drugs and the receptors they target
propanolol: non-selective, prototype
metoprolol and atenolol: common B1 blocker
nebivolol: B1 blocker, inc production of nitric oxide in arteries—> VASODILATION
B-adrenoceptor blocking agents: therapeutic uses/indications
hypertensive PTs w/heart disease
- contraindication with reversible bronchospastic disease–> asthma, heart block, PVD, COPD
-if non-selective may go on B2 in lungs
-peripheral vascular disease: may worsen with the inc of peripheral resistance
B-adrenoceptor blocking agents: adverse effects
COMMON
-hypotension, bradycardia, fatigue, insomnia, sexual dysfunction
METABOLIC
-disrupt lipid metabolism (B2 is sugar metab, B1 inc lipolysis when activated, dec when disrupted)
abrupt withdrawal: severe rebound hypertension, angina, MI, MUST TAPER DRUG
ACE Inhibitors
- ACE stands for what?
- used for what type of patients?
- Angiotensin-converting enzymes
- end in -pril
first line of treatment for hypertension in patients with OTHER conditions
ACE INHIBITORS: overview
-action, MOA, and effects
ACTION: dec peripheral vascular resistance
MOA: block enzyme ACE, cleaves angiotensin I to form vasoconstrictor angiotensin II
EFFECTS
- dizziness
-orthostatic hypotension
-GI distress
-nonproductive cough/ dry cough
- headache
ACE Inhibitors: therapeutic effects
-dec BP by reducing peripheral vasc resistance WITHOUT reflex inc CO/HR/Contractility
-dec aldosterone secretion–>dec sodium and water retention
-reduce cardiac preload and afterload–> dec workload on heart
PRELOAD and AFTERLOAD
Pre: BV in ventricles at end of diastole
After: resistance left ventricle must overcome to circulate blood
INC AFTER LOAD=INC CARDIAC WORKLOAD
ACE Inhibitors: therapeutic uses/indications
-hypertension
-hypertensive PT w/diabetic nephropathy
-myocardial infarction & systolic dysfunction
-L ventricular hypertrophy, prevention of ventricular remodeling after MI
-HF, hypertensive PT w/chronic kidney disease, those w/inc risk of CAD
what is diabetic nephropathy?
kidney damage from diabetes
what is ventricular hypertrophy?
the thickening of ventricle walls
what is ventricular remodeling and why might we want to prevent it?
remodeling/thickening the walls of the ventricles after an MI could be bad for patients who just experienced heart problems, we want to prevent this by giving less work to the ventricles
ACE Inhibitors: pharmacokinetics
- oral drugs
- only enalaprilat is IV (not a pro-drug)
ACE inhibitors:
- captopril and lisinopril
-fosinopril
- only drugs that don’t undergo hepatic conversion to active metabolites
- good for PTs with hepatic impairment
fosinopril: not eliminated primarily by kidneys, no dose adjustment in patients w/ renal impairment
pro-drug
is it the inactive form of the drug
- so enalapril is the inactive form and enalaprilat is the active form
-metabolism in the liver and drug w/specific enzymes make the drug active
ACE Inhibitors: adverse effects
-MOST COMMON: dry cough
-angioedema
-hyperkalemia, monitor K+, use supplements and potassium sparing diuretics with caution
-serum creatinine monitored in renal-diseased PTs
- fetal malformations (teratogenic)
Calcium Channel Blockers: overview
- actions, side effects
ACTIONS
-BLOCK calcium access to cells
-causes DEC contractility and conductivity, DEC demand for O2
EFFECTS
-DEC BP, bradycardia, AV block, headache, abdominal discomfort (constipation/nausea), peripheral edema
Calcium Channel Blockers: when is it used
- avoid high doses why?
- 1st treatment for African American PTs
- hypertensive PTs w/diabetes or stable ischemic heart disease
-AVOID high doses of short-acting Ca blockers, can cause excessive vasodilation and reflex cardiac stimulation (INC risk of MI)
Calcium Channel Blockers: MOA and therapeutic effect
MOA: block inward movement of calcium, binding to L-type calcium channels in the heart and smooth muscle of coronary and peripheral arteries
effect: relax vasc smooth muscle, dilate arteriole
DO NOT DILATE VEINS
Calcium Channel Blockers: therapeutic uses/indications
-manage hypertension
-treat hypertensive PTs with asthma, diabetes, PVD
-angina
-atrial fibrillation
which two calcium channel blockers are used for atrial fibrillation?
diltiazem and verapamil
- they have a positive profile–> least adverse effects
Calcium Channel Blockers: VERAPAMIL
-cardiac and vasc smooth muscle effects
-use for supraventricular tachyarrhythmias
-prevent migraine and cluster headaches
CROSSES THE BBB
Calcium Channel Blockers: DILTIAZEM
-cardiac and vasc smooth muscle effects
-LESS neg inotropic effect on heart compared to verapamil
-favorable side effect profile
Calcium Channel Blockers: NIFEDIPINE
-prototype
-amlodipine, felodipine, isradipine, nicardipine, nisoldipine: great affinity for vasc than heart calcium channels—> helpful to treat hypertension
-little interaction w other CV drugs like digoxin or warfarin
Calcium Channel Blockers: compare dilation of coronary vessels, AV conduction, and frequency of adverse effects
Dilation of coronary vessels: nifedipine and diltiazem best
AV conduction: verapamil most, nifedipine least
Freq of Adv Effects: nifedipine most, diltiazem least
Calcium Channel Blockers: adverse effects
verapamil: dose-dependent atrioventricular block and constipation
verapamil and diltiazem: avoid in PT with HF or AV block due to NEG INOTROPIC and DROMOTOPIC effects
nifedipine/-dipines: dizziness, headaches, fatigue due to dec BP, peripheral edema, gingival hyperplasia (swollen gums)
what to consider for calcium channel blockers?
- ER
if EXTENDED RELEASE, cannot be crushed or cut
-too much of drug will be released at one time and induce toxic levels of the drug
VASODILATORS: which drugs and uses?
hydralazine, minoxidil, nitroprusside
-used when previous drugs are not effective
-reserved for SEVERE hypertension/hypertensive emergencies
-act on potassium channels of vasc smooth muscles
vasodilators: methods of administration for each drug
hydralazine: PO, IV, IM
minoxidil- PO
nitroprusside- IV
VASODILATORS: therapeutic effects
direct-acting on smooth muscles
- produce vasc muscle relaxation and vasoDILATION
-DEC peripheral resistance, DEC BP
hypertensive urgency vs emergency
URGENCY: severe elevated BP, no current evidence of end-organ damage ( may occur if left untreated)
-DEC BP soon
EMERGENCY: severe elevated BP w/evidence of end-organ damage
-DEC BP IMMEDIATELY
VASODILATORS: adverse effects
CV: reflex stimulate heart–> INC CO, HR, O2 consumption, angina, MI, or cardiac failure
-use B blocker to balance reflex tachycardia
GU: inc plasma renin conc–> sodium and water retention
-use diuretics to dec sodium retention
VASODILATORS: hydralazine, minoxidil, nitroprusside—->specific adverse effects
hydralazine: headache, tachycardia, nausea, sweating, arrhythmia, precipitation of angina
-lupus like syndrome w HIGH doses
minoxidil: hypertrichosis (excessive hair growth)
nitroprusside: metabolized into cyanide–>cyanide toxicity, dyspnea, ataxia, loss of conscious, distant heart sounds, dilated pupil
what is dyspnea?
difficult/labored breathing
what is ataxia?
impaired coordination/loss of balance due to damage to brain, nerves, or muscles
