Exam 3 Flashcards
Antidysrhythmics, beta blockers, calcium channel blockers, itraconazole
negative inotropes and may worsen HF
cyclophosphamide (Cytoxin), daunorubicin (cerubidine), doxorubicin (adriamycin)
cardiotoxic and may worsen HF
androgens, estrogens, glucocorticoids, NSAIDS, rosiglitazone (Avandia), pioglitazone (Actos)
drugs that cause increased blood volume and may worsen HF
6 mechanisms of action against HF
adrenergic blockers cardiac glycosides phophodiesterase inhibitors vasodilators ACEI and ARBs Diuretics
adrenergic blockers
treat HF by decreasing cardiac workload by slowing HR (B1) and decreasing BP (A1)
Carvedilol
Cardiac Glycosides
treat HF by increasing cardiac output by increasing the force of myocardial contraction
Digoxin
Phophodiesterase inhibitors
treat HF by increasing CO by increasing force of myocardial contraction
Milrinone
Carvedilol
adrenergic blocker-treats HF
Digoxin
cardiac glycoside treats HF
milrinone
phophodiesterase inhibitor treats HF
vasodilators
treat HF by decreasing cardiac workload by dilating vessels and reducing preload
isosorbide dinitrate with hydralazine
ACEI and ARBs
treat HF by increasing CO by lowering BP and decreasing blood volume
lisinopril
Diurectics
treat HF by increasing CO by reducing fluid volume and decreasing blood pressure
furosemide
isosorbide dinitrate with hydralazine
vasodilator to treat HF by decreasing cardiac workload by dilating vessels and reducing preload
lisinopril
ACEI or ARB that treats HF by increasing CO by lowering BP and decreasing blood volume
furosemide
diuretic that treats HF by decreasing fluid volume and BP to increase CO
nitrates aspirin clot-preventing drugs beta blockers statins Calcium channel blockers
drugs to manage angina pectoris
Nitroglycerin
dilates veins and arteries
decrease myocardial workload
decrease preload (pooling of blood in periphery)
decrease myocardial ischemia to prevent vasospasm and dilates coronary arteries to increase perfusion
can be used for prevention of treatment
action of nitroglycerin
inactivate myosin and permissive vasodilation or relaxation of vessel tone occurs
Nitrates side effects/teaching
orthostatic hypotension
headaches, dizziness, vertigo, flushing, sweating
with the onset of angina, sit down and place on NTG tab under the tonge and wait 3-5 mins. If the angina has not subsided, take another tablet sublingually and wait 3-5 mins. If the angina has not subsided, take a third tablet and call 911 for help. Notify physician immediately.
Metoprolol, labetalol, propanolol
beta blockers for treatment of stable angina prevention
IV or PO
decrease HR, BP, contractility
cardioprotective
afterload of heart is reduced due to vasodilation
perfusion is improved through the coronaries bc of vasodilation and prolonged diastole
the heart can experience a greater Ejection Fraction due to prolonged diastolic filling time
Calcium Channel Blockers
diltiazem (Cardizem)
verapamil (Calan, Isoptin)
nifedipine (procardia, Adalat)
PO
Action of CCBs
decrease SA node automaticity and AV conduction to decrease HR and myocardial contractility
Decrease HR, BP, cause vasodilation, decrease preload and afterload, decrease myocardial oxygen needs
side effects of CCbs
Cardiovascular-hypotension, palpitations, and tachycardia
GI-constipation and nausea
Other-rash, flushing, and peripheral edema
Ranolazine (Ranexa)
can be used alone or with other angina meds, such as CCBs, beta blockers, or nitroglycerin
Unlike some other angine meds, Ranexa can be used with oral erectile dysfunction meds
Ranexa changes the metabolism of myocardium from fatty acid use for fuel to glucose, thereby decreasing metabolic needs
Treatment of Stable Angina
NTG, Beta Blockers, CCBs, ACEIs
treatment of unstable angina
NTG, heparin, clopidogrel, morphine, ASA
treatment of Prinzmetals angina
NTG and CCbs
Goals for treatment of MI (5)
reperfusion of blood supply to damage myocardium
reduce myocardial oxygen demand
control and prevent future myocardium dysrythmias
reduce post MI mortality
manage pain
10 drug classes to manage MI
thrombolytic agents aspirin ADP receptor blockers Glycoprotein IIb/IIIa Inhibitors anticoagulants nitrates beta blockers ACEIs and ARBs Pain management (morphine or demerol) statins-post MI
OANM
oxygen aspirin nitroglycerin morphine treatment of MI
Thrombolytics
directly break up clots; give within 30 mins-12 hours following MI enhance activation of plasminogen streptokinase (Streptase) alteplase (tPA, Activase) anistrplase (Eminase) reteplase (Retevase) tenecteplase (TNKase)
thrombolytics contraindications
active bleeding or known bleeding d/o Hx of hemorrhagic stroke or intracranial vessel malformation recent major surgery or trauma uncontrolled HTN Pregnancy
enoxaparin (Lovenox)
LMWH
fibrinolysis should be started within 12 hrs to treat MI
Post MI care
ACEI/ARB
ASA or Antiplatelet agent
beta blocker or CCB
Statin
Captopril (Capoten)
Enalapril (Vasotec)
Benazepril (Lotensin)
Fosinpril (Monopril)
ACEI
Aspirin
Clopidogrel (Plavix)
Ticlopidine (Ticlid)-rarely used, neutropenia
antiplatelet agents
Prevent cardiac remodeling
beta blockers Metoprolol (Lopressor) Atenolol (Tenormin) Propranolol Esmolol Labetalol
Amlodipine (Norvasc)
Diltiazem (Cardizem, Adalat)
CCBs
Statins action
lower cholesterol lovastatin (Mevacor) pravastatin (Pravachol) simvastatin (Zocor) atorvastatin (Lipitor)
Dihydropyridine
treats MI?
nifdeipine (Adalat, Procardia XL)
blocks Calcium channels in the vascular smooth muscle decreasing the amount of intracellular calcium available for muscle contraction this results in the fall of BP
decrease myocardial oxygen demand due to the reduced afterload
Nondihydropyridines
verapamil (Calan, Isoptin)
Block l type calcium channels in vascular smooth muscle causing vasodilation
verapamil and diltiazem block calcium channels in the myocardium decreasing the rate of conduction reducing the HR reducing the contractility of the myocardium
benefit of Ranolazine (Ranexa)
effect on HR is minimal as the drug acts on myocardial metabolism
Nitrates adverse effects
secondary to vasodilation: headache, flushing, orthostatic hypotension
potential cardiovascular collapse if mixed with alcohol
nitrates disadvantage
tolerance builds quickly
What happens if you D/C a long acting nitroglycerin (Isosorbide dinitrate) abruptly?
vasospasm
nitrates contraindications
preexisting hypotension, head trauma (vasodilation would make these worse)
pericardial tamponade and constrictive pericarditis (vasodilation would make heart unable to maintain CO to maintain BP)
no sustained release tabs on pts with glaucoma (nitroglycerin may increase introcular pressure)
caution severe kidney/liver disease (toxic levels)
dehydration and hypovolemia should be corrected before nitroglycerin is administered (severe hypotension may occur)
Nitrate drug interactions
viagra none within 24 hrs before or after-cardiovascular collapse–>hypotension
ethanol, CCBs, antidepressants, phenothiazines, and anti HTN may cause additive Hypotension
sympathomimetics (EPI) antagonize vasodilation
Do you take beta blockers for Prinzmetals angina
no, they make it worse
Beta Blockers action in treating Angina
prevention
decrease HR, BP, contractility, workload
cardioprotective
Why beta blockers over nitrates for prevention of angina?
tolerance not an issue
possess antidysrythmic properties
ideal for common disorder combo of HTN and CAD
cardioprotective
when to DC beta blockers
gradually unless fatigue, lethargy, and depression occur
With long term care, the heart becomes more sensitive to catecholamines, which are blocked by beta blockers. when w/d abruptly, adrenergic receptors are activated and rebound excitation occurs. In pts with CAD, this can exacerbate angina, precipitate tachycardia, or cause an MI
beta blockers adverse effects at high doses?
SOB and respiratory distress secondary to bronchoconstriction therefore use caution with asthma and COPD pts
Beta blockers and diabetes?
beta blockers may mask the symptoms of hypoglycemia so diabetics should monitor blood glucose more closely
beta blockers contraindications
bradycardia (may lead to primary heart block)
cardiogenic shock
overt cardiac failure
Atenolol (Tenormin)
beta blocker (beta one selective)
anti anginal agent
treats HF, HTN, stable angina, and acute MI
PO 1/day
excreted 50% renal, 50% feces not metabolized!
anticholinergic may decrease GI absorption
beta blockers drug interactions
digoxin (and other antidysrythmics that depress myocardial conduction may lead to AV block)
adverse effects of beta blockers
bradycardia and hypotension
dyspnea on exertion, fatigue, pulmonary cogestion, peripheral edema
classic symptoms of HF
Why are ACEIs (or ARBs) a preferred drug in the treatment of HF?
ACEIs block the detrimental effects of angiontensin II and aldosterone on cardiac remodeling
Nesiritide (Natrecor)
has a limited role in HF treatment; ANP and BNP (Natrecor is BNP) cause diuresis, vasodilation, and decrease aldosterone secretion. Basically, Natriuretic peptides counteract the RAAS and SNS
give to patients with acutely decompensated heart failure
Patients at high risk for HF
make lifestyle changes
treat and control HTN, dyslipidemia, and diabetes
if htn, start ACEI
Patients with structural evidence of heart diseaes (MI or valvular disease) but no symptoms of HF
lifestyle, control of modifiable factors (HTN, lipids, diabetes)
ACEIs (ARBs)
Beta blockers if prior HF symptoms
Diurectics and salt restriction if fluid retention
Patients with structural evidence of heart disease with symptoms of HF such as fatigue, fluid retention, dyspnea
ACEI (ARB) and Beta Blocker
Add Digoxin and Spironolactone if needed to control sympotoms
If symptoms do not improve, add a loop or thiazide diuretic and a combo nitrate with hydralazine
3 goals of Pharmacotherapy of HF
reduce preload reduce afterload (reduce vascular resistance-BP) Inhibit RAAS and SNS (which are vasoconstrictors)
adrenergic blockers for HF
Carvedilol
decrease cardiac worload by slowing the HR (B1) and decreasing BP (alpha 1)
Vasodilators for HF
isosorbide dinitrate with hydralazine
decrease cardiac workload by dilating blood vessels and reducing preload
ACEI and ARBs for HF
lisinopril, captopril
increase cardiac output by lowering BP and decreasing blood volume
Phosphodiesterase Inhibitors for HF
Milrinone
increase cardiac output by increasing the force of myocardial contraction
Cardiac glycosides for HF
Digoxin
increase CO by increasing the force of myocardial contraction
Main ACEI adverse effects
hypotension (worse at beginning of treatment and when dose is changed) caution with Beta blockers and diuretics
renal insufficiency resultant of decreased blood flow or hyponatremia from diurectics
angioedema, cough, hyperkalemia
What is a risk associated with ACEI + spironlcatone?
hyperkalemia
Losartan (Cozaar)
ARB used for HF when ACEI is not tolerated
Diurectics Action
reduce peripheral edema reduce pulmonary congestion reduce blood volume reduce BP reduce cardiac workload INCREASE CO **only use diuretics in HF pts if fluid retention is present
Can you give loop diuretics to pts with renal insufficiency?
yes
examples of loop diurectics
furosemide (Lasix)
bumetanide (Bumex)
torsemide (demadex)
What diuretic is prescribed for mild-moderate HF and can be combined with loop diuretics?
Thiazide diuretics: chlorotiazide (Diuril), hydrochlorothiazide (HCTZ, HydroDIURIL)
Spironolactone (Aldactone)
potassium sparing and aldosterone antagonist diuretic
limited efficacy in HF pts bc low performing diuretic
blocks cardiac remodeling of aldosterone
when is it best to give ACEI for HF
within 36 hrs of onset
Diuretic cautions
dehydration and electrolyte imbalances
weigh self frequently
electrolyte tests (hypokalemia loop or thiazide especially when combined with digoxin)
If beta blockers, being negative inotropes, make HF worse, then why do we prescribe them to HF patients?
Beta Blockers stop the SNS compensatory response that makes HF worse and is a vicious cycle by blocking NE and other catecholamines that cause cardiac remodeling and disease progression. The result of beta blocker therapy is reduced HR and BP which leads to decreased cardiac workload.
After several mos of therapy, heart shape, size, and function can actually return to normal-> reverse remodeling
Which medication can cause reverse remodeling in HF patients?
beta blockers, carvedilol (Coreg) and metoprolol (Toprol), propranolol (nonselective)
How must beta blockers be administered to HF patients?
To prevent making HF worse, beta blockers must be given very specifically:
Initial doses must be 1/0-1/20 target dose and then doubled every two weeks until target dose is reached.
Beta Blockers are contraindicated for
COPD
bradycardia
heart block
beta blockers are used with caution on pts with
PVD, diabetes, or hepatic impairment
What lab tests do you monitor for pts on beta blockers?
liver function studies for signs of toxicity
How do vasodilator reduce symptoms of HF?
Vasodilators reduce preload or afterload
Hydralazine with isosorbide dinitrate
vasodilators: relax blood vessels and lower bp creating less workload for the heart;
use is limited due to risk of orthostatic hypotension and reflex tachycardia
Hydralazine
antiHTN acts on arterioles to decrease peripheral resistance, reduce afterload, and increase CO; not a first choice drug bc of hypotension and reflex tachycardia risks
Isosorbide Dinitrate
a long acting organic nitrate that reduces preload by directly dilating veins. not effective as monotherapy and tolerance develops quickly
what triggers the release of BNP in the body?
increased ventricular stretch releases BNP which then enhances diuresis and renal excretion of sodium (counteracts RAAS and aldosterone)
Patients with acutely decompensated heart failure are prescribed which vasodilator?
Nesiritde (BNP) and monitor this patient continuously bc hypotension may occur
What drug do you give to patients with supraventricular tachyarrythmias (afib)?
Digoxin-now a drug reserved for late stage HF
digoxin has antidysrythmic properties
Why are cardiac glycosides used in late stage HF only?
they have a narrow therapeutic window and severe side effects
When do you hold digoxin?
when HR is <60bpm
Two Primary classes of positive inotropic agents administered to pts with acute decompensated HF:
Beta AGONISTS
Phosphodiesterase Inhibitors
Beta Agonists
isoproterenol (Isuprel)
EPI, NE, Dopamine
Dobutamine (Dobutrex)** ability to rapidly increase myocardial contractility with min changes to HR and BP
two common adverse effects of beta agonists
tachycardia and dysrythmias
When do you give dopamine in HF?
when the pt has both HF and hypotension bc dopamine can increase myocardial contractility and activates alpha receptors to increase BP
How do phosphodiesterase III inhibitors work?
they block the enzyme which leads to increases in the amount of calcium available for myocardial contraction. Two benefits:
positive inotropic and vasodilation, thus CO is increaseed due to increased contractility and decreased in left ventricular afterload. There is little effect on HR
Prototype drug for phosphodiesterase III inhibitor
milrinone (Primacor)
ACEI action r/t HF
Lower peripheral resistance through inhibition of angiotensin II formation
reduce blood volume through inhibition of aldosterone
yields reduced arterial BP (afterload), increased CO, and dilated veins (preload)
digoxin action (4)
decreases SNS activity and increases PNS activity-can suppress SA node and slow conduction through AV node;
inhibits NaKATP Pump
increases intracellular calcium via sodium/calcium exchange pump
positive inotrope; by increasing mycardial contractility, digoxin increase CO and that improves exercise tolerance and urine production to restore fluid balance and decrease pulmonary congestion.
special considerations when administering digoxin
must give over a min of 5 mins, can dilute in 4-5mL
can give PO but NEVER IM or SC
Is digoxin highly protein bound?
Yes, so be aware of hypoalbumuria-toxic dig
Adverse effects of digoxin
ventricular dysrhythmias including sudden cardiac death. most common cause is hypokalemia from combined diuretic therapy; hypomagnesemia and hypo calcemia and impaired renal function are add’l risk factors. AV Block, atrial dysrhythmias, sinus bradycardia
Normal serum digoxin levels
0.5-1.5ng/dL drawn 6-12 hrs after last dose
toxicity often presents with flu like symptoms/ earliest sign is anorexia
H2antagonist
antagonist agent against histamine that decreases gastrin secretion
cathartic
agent with purgative action
Rapid, intense fluid evacuation of bowel.
surfactant
a surface active agent also known as a wetting agent, tension depressant, detergent and emulsifier
Methoscopalamine
blocks effect of Ach and relaxes smooth muscles
GI Stimulant
adjunct therapy for treating peptic ulcer disease
Dexpanthenol
minimizes risk of paralytic ileus when used post op
metoclopramide PO meal consideration and what does it treat?
take 30 mins before meals and at bedtime
dopaminergic blocker
treats v/n, and expedites gastric emptying
metoclopramide IV considerations
give 30 mins prior to chemo for antiemetic effect
GI stimulants
decrease reflux by increasing sphincter tone and enhancing acid clearance and decreasing gastric emptying.
Used for delayed gastric emptying caused by diabetic gastroparesis, GERD, or post op N/V
Stimulates gastric mobility w/o stimulating gastric, biliary, or pancreatic secretion
GI Stimulants contraindications
Hx seizure d/o, pheochromocytoma, PD (metoclopramide)
GI hemorrhage, obstruction or perforation
allergy to dextran, CHF, renal failure (dexpanthenol)
depression, HTN
nursing considerations for GI stimulants
monitor for possible hypernatremia and hypokalemia paricularly if pt has CHF or liver cirrhosis
monitor BP closely with metoclopramide IV
Client edu for GI stimulants
report signs of acute dystonia immediately
do not drive a few hours after taking metoclopramide
avoid humid environments with methoscopolamine
Anticholinergic and Antispasmodics
medications for decrease GI tone and motility
pylorospasm, ileitis, and IBS
give 30-60 mins before meals and at bedtime
Anticholinergic and Antispasmodics Contraindications
narrow angle glaucoma, obstructive GI disease, paralytic ileus, obstructive uropathy, adhesions between iris and lens, myocardial ischemia, and toxic megacolon.
Caution if renal dysfunction
Atropine may increase the effect of
phenothiazines
increased effects of atenolol with
anticholinergic drugs
what decreases absorption of anticholinergics
antacids
Cytotec (Misoprostol) contraindications
contraindicated if allergic to prostaglandins, pregnant, or lactating. May cause spontaneous abortion.
Prostaglandin Analog