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Cardio Drugs 4

Advanced Pharm for Nursing Practice 4

QuestionAnswer
*REMEMBER THAT A DECR IN blood flow and Na+ content causes the release of Renin *REMEMBER THAT A DECR IN blood flow and Na+ content causes the release of Renin
What is the prototype for Renin Inhibitors? Aliskiren (Tekturna) is the prototype for Renin Inhibitors
What the method of action of renin inhibitors? these drugs inhibit renin itself; blocking renin blocks the whole renin-angiotensin-aldosterone mechanism
What is the indication for using Aliskiren (Tekturna)? the renin inhibitors like Aliskiren Tekturna are used PO x1/day for HTN (HBP)
What are the pharmacokinetics of aliskiren (Tekturna)? they’re best absorbed on empty stomach, they have a ½-life of 24hrs, and once in the bld, it’s not metabolized and is excreted unchanged in the feces
What are the SE/ADR of renin inhibitors like aliskiren (Tekturna)? the side effects of renin inhibitors is 1% rash, 2% diarrhea
*O2 supply: cardiac O2 supply determined by myocardial bld flow. Under resting conditions, the heart extracts nearly all O2 delivered to it by the coronary vessels. *O2 supply: cardiac O2 supply determined by myocardial bld flow. Under resting conditions, t/ heart extracts nearly all O2 delivered to it by the coronary vessels.
What are the 3 different types of angina? stable occlusive: pt is stable w/o exertion; unstable angina: pt is unstable even w/o exertion; vasospastic angina (Prinzmetal’s): variant angina that happens mostly to women under stress (their coronary arteries were NOT occluded)
*THE ONLY WAY TO ACCOMMODATE AND INCR IN DEMAND IS TO INCR BLOOD FLOW *THE ONLY WAY TO ACCOMMODATE AND INCR IN DEMAND IS TO INCR BLOOD FLOW
What are the main drugs used to treat HTN? Nitrates (Nitroglycerin) are the main drugs used to treat HTN
What’s the method of action of nitrates? Nitrates act directly on the smooth muscle cell to release myosin (in t/ actin-myosin contraction) to allow the smooth muscle cell to relax
What’s the action of nitrates? /c nitrates, relaxation of smooth muscle cell results in vasodilation. /c preload, you decr t/ amt of bld coming in heart (which was stretching the muscle). You decr wk on damaged part of heart and dilate other bld vessels not involved in angina
What’s the indication for nitrates? nitrates are used for t/ tx/prevention of angia pectoris; they can also be used in acute MIs (usually as result of not responding to other drugs). IV nitro is available for acute MI
What are the pharmacokinetics of nitroglycerin? the main action/prob of nitrates is LARGE 1ST PASS EFFECT; nitrates have short ½-life; if nitrates given sublingually, you bypass 1st pass effect
What are the 2 diff thoughts for Nitro admin & angina attacks? 1-Traditional) place nitro tablet sublingual max x3/ q 5min, /p 2nd placemt, call EMS or 911. 2-Amer Col of Cardiology) take max 2 nitro tabs sublingual q5 min, if no improvmt /p 1st one, call EMS/911
Why call an EMS or 911 if having an angina attack instead of self transport? b/c EMS usually generate bttr assistance than self transport
What are the SE/ADR of nitrates? since nitrates cause vasodilation, may hv postural hypotension, might get palpitations, tachycardia, dizziness, headache
What are warnings about nitrates? nitrate tolerance builds up fast, so have NITRATE FREE PERIODS EVERYDAY of 10-12hrs (unless pt only taking nitrates for acute attacks); nitrates are volatile & should be kept in glass bottle /c screw cap –anything else will make it ineffective
What are the ways to administer nitroglycerin? emergency (usually acute MI): IV, acute attack: sublingual tablet/oral spray; capsule tablets for prevention maintenance /c nitrate free period & CCB used @ night; patch: place on hairless torso /c daily site change and nitrate free period
What is a drug very similar to nitrates? isosorbide mononitrate (ISMO) are drugs very similar to nitrates; it doesn’t have large 1st pass effect, and can be prescribed for 1 or 2x/day to prevent angina attacks
What’s the method of action of beta adrenergic antagonists? beta-blockers slow the heart rate and decr contractility (inotrope-how strong) which releases workload on heart; beta-blockers do not cause vasodilation
What are SE/ADR of beta-blockers? bradycardia; at first it was contraindicated in thos with diminished cardiac output, until they realized that actualy slowing the heart gave it enough time to refill with O2 rich blood during diastole
What’s a serious Beta-blcoker warning? DON’T STOP BETA-BLOCKERS ABRUPTLY (remember up regulation)
What’s the indication for Ca++ Channel blockers? CCBs are useful in vasospastic (Prenzmetal’s) angina b/c they cause VASODILATION
What are the 2 groups of CCBs and what are their actions? NON-DIHYDROPYRIDINE group (Verapamil), acts on heart to DECR CONTRACTILITY & HEART RATE, Verapamil also has a vasodilating effect; DIHYDROPYRIDINE group (Norvasc) Amlodipine or (Procardia) hv mainly a VASODILATING effect, and no effect on heart
*All Ca++ channel blockers decr preload and postload *All Ca++ channel blockers decr preload and postload
What is Ranolozine (Ranexa), and what is its indication? Ranexa is an anti-anginal med for the tx of chronic angina in pts who don’t respond to other agents; it’s used in combo with amlodipine, Beta-blockers, or nitrates and given 2x/day
What’s the method of action of ranolozine (Ranexa)? the MOA is unknown, though it seems to wrk like a metabolic modulator and seems to improve exercise duration
What are SE/ADR of ranolozine (Ranexa)? dizziness, HA, constipation; main worry is RANEXA PROLONGS Q-T INTERVAL, so it’s contraindicated /c other Q-T interval drugs
What’s the plan of action with acute myocardial infarctions/ acute coronary syndrome? you want EARLY PERFUSION of coronary vessels, so: O2, heparin, sublingual nitro while prepping IV, and Beta-blocker for tachycardia; tx depends on whether there’s an ST-segment elevation or not
What is heart failure? heart failure is a serious progressive disorder characterized by: ventricular dysfunction, decr cardiac output, insufficient bld flow to tissues, ultimately leading to fluid retention (not enough bld to kidneys)
What happens when there is decr bld flow to tissues? Compensatory Responses /c Sympathetic NS causing: vasoconstriction mostly in skin & splanchnic area, incr hrt rate & strength of contraction (if poss); this sets of renin-angiotensin-aldosterone sys (which could be vry dangerous to damaged hrt)
In heart failure, the aim of tx is what? the aim of tx in chronic heart failure is to decr sympathetic activity and decr t/ renin-angiotensin-aldosterone systems
What’s the drug of choice in chronic heart failure? ACETs are the drug of choice in chronic heart failure (beta-blockers are also liked bc it slows down hrt enough for it to refill /c O2 rich bld)
*ONLY ACEIs & beta-blockers are known to improve morbidity and mortality in pts /c heart failure *ONLY ACEIs & beta-blockers are known to improve morbidity and mortality in pts /c heart failure
Most pts with CHF hv edema and need which kind of diuretic? Why? pts /c CHF hv edema bc of poor cardiac output to kidneys, therefore only loop diuretics (which work with malfunctioning heart) will work in reducing edema; loop diruretics DO NOT IMPROVE MORBIDITY OR MORTALITY
How does digoxin work on the heart? Digoxin slows the heart and incr contractility (inotrope), making the heart a better pump (IT DOES NOT improve mortality)
Is heart failure a slow of fast developing process? heart dz is a very SLOW developing process
Reminders of spironolactone (a K+-sparing diuretic) /c the renin-angiotensin-aldosterone sys release, aldosterone tends to cause remodeling of the heart; spironolactone is a relatively poor diuretic, but it DOES BLOCK ALDOSTERONE and blocks heart remodeling, so some list it as step 1 drug
What is digitalis glycoside, and what are the trade names? Digoxin (Lanoxin, Digitek)
What’s the clinical use of digoxin? primary: tx of heart failure if symptoms continue /p use of 1st line drugs; used in atrial fib or flutter bc it blocks AV conduction (allowing heart to not beat sooo fast)
Explain how the DIRECT THERAPEUTIC levels of Digoxin work on the heart therapeutic levels of 0.5-0.8nanograms/mL will act on the Na+/K+ -ATPase pump. (/c lower serum K+, there’s less K+ to pump into cell so hv decr pump action. Digoxin works by blocking Na+/K+ pump, there’s risk of dysrrhthmias
Digoxin in a DIRECT way blocks the NA+/K+ ATPase pump which then acts on the Na+/Ca++ pump, incr Ca++ and releasing actin and myosin to contract==INCR CONTRACTILITY Digoxin in a DIRECT way blocks t/ NA+/K+ ATPase pump which then acts on t/ Na+/Ca++ pump, incr Ca++ and releasing actin and myosin to contract==INCR CONTRACTILITY
AT THERAPEUTIC DOSES, THE MAIN DIRECT EFFECT OF DIGOXIN IS TO INCR CONTRACTILITY AT THERAPEUTIC DOSES, T/ MAIN DIRECT EFFECT OF DIGOXIN IS TO INCR CONTRACTILITY
Explain how toxic Digoxin levels directly affect the heart: they reduce the resting potential esp in ventricular cells; after a while, ventricles get “itchy” to contract and you’ll see PVCs (premature ventricular contractions), this leads to 2 PVCs in a row (bigeminy), and then 3 PVCs (trigeminy), & then ventricular fib. If treating sinus fib, need to use larger doses of digoxin
Explain how INDIRECT EFFECTS OF Digoxin on the heart Digoxin stimulates the vagus nerve which slows the heart at therapeutic doses bc there’s a reflex induced decr sympathetic tone associated /c improvement in circulation (vagus thinks bld pressure too high)
If you slow the heart and pump out more bld to tissues, then that reduces the 911/sympathetic activity If you slow the heart and pump out more bld to tissues, then that reduces the 911/sympathetic activity
What are the pharmacokinetics of Digoxin? bioavailability of 70%; there are some who metabolize drugs in their gut, they get a larger dose; in elderly, give smaller dose of digoxin
What are SE/ADR of Digoxin? digoxin-caused cardiac arrhythmias due to pt also on diuretic --> hypokalemia –OR- pt has decr renal function & digoxin dose too big & causing cardiac dysrhythmias (from toxicity)
What are early signs of digoxin toxicity? pt is hungry, nauseated, seeing halos around lights
If on Digoxin & pts hrt rate goes below 60bpm, what should you do? call physician and make sure if should continue dose
XS digoxin = pt death from ventricular fibrillation XS digoxin = pt death from ventricular fibrillation
What are different Digoxin interactions? quinidine, verapamil, & amiodarone are enzyme & p-glycoprotein inhibitors, so could raise digoxin toxicity
*hypokalemia sensitizes the heart to digitalis w/o changing the bld level *hypokalemia sensitizes the heart to digitalis w/o changing the bld level
Why are ACEIs the drug of choice for the heart? ACEI decr pre and afterload, so it tends to improve cardiac function; they also stop the remodeling of the heart (*start low and incr as needed; drug may take a couple weeks to show max effect)
Aldosterone causes what of the heart? What blocks that? aldosterone causes remodeling of the heart; aldactone blocks that
*Carvedilol (Coreg) ws 1st Beta-blocker approved for tx of mild/moderate HF of ischemic or cardiomyopathic origin in /c digitalis, diuretics, & ACEIs to reduce dz progression *Carvedilol (Coreg) ws 1st Beta-blocker approved for tx of mild/moderate HF of ischemic or cardiomyopathic origin in /c digitalis, diuretics, & ACEIs to reduce dz progression
Created by: Fukanwa