85 terms

BN pharm cardio II


Terms in this set (...)

goal of dysrhythmia treatment-
to treat the symptoms
-remember, however, that dysrhythmia drugs can also cause dysrhythmias, and are therefore NOT first line
-find the underlying cause and treat that
considerations/balancing risks and benefits for treating dysrhythmias
-sustained v. nonsustained
-asymptomatic v. symptomatic
-supraventricular v. ventricular(ventricular impairs pumping of heart)
prolonging ventricular DEpolarization widens....
prolonging ventricular REpolariztion widens...
depolarization: widens QRS
repolarization: widens QT
causes of dysrhythmias (2 main ones)
1. disturbance of automaticity (tachycardia, bradycardia...)
2. disturbance of conduction (heart block)
classes of antidysrhythmic drugs (5)
1. Class 1: sodium channel blockers
2. Class 2: beta blockers
3. Class 3: potassium channel blockers
4. Class 4: calcium channel blockers
5. Others (verapamil, diltiazem)
supraventricular dysrhythmias
-aka atrial dysrhythmias
1. A fib
2. A flutter
3. sustained supraventricular tachycardia
-if rate is controlled, they are usually put on a Calcium channel blocker, a beta blocker, and/or an anticoagulant (usually coumadin/warfarin)
-uncontrolled rate: defibrillation
ventricular dysrhythmias
1. sustained ventricular tachycardia (pt. may or may not have a pulse)
2. V fib (pulseless)
3. PVCs
4. digoxin-induced dysrhythmias
5. torsades de points
-much worse than atrial dysrhythmias- first line is defibrillation and CPR, second line are meds
Quindine MOA and uses
MOA: Na channel blocker that slows impulse conduction, delays depolarization, and blocks vagal input into the heart
Uses: supra ventricular and ventricular dysrhythmias
Quindine adverse effects (3) and interactions (1)
1. diarrhea (most common)
2. cardiotoxicity (AV block, asystole)
3. arterial embolism
-interacts with digoxin, increasing levels
Propanolol MOA and uses
MOA: non selective beta blocker (1&2), decreases automaticity in SA node, decreases conduction through SA node, and decreases contractility, essential decreasing HR
uses: tachy dysrhythmias
Propanolol adverse effects (6)
1. heart block
2. heart failure
3. AV block
4. hypotension
5. bronchospasm (in asthma pts- NOT used)
6. blocks tachy in diabetics
Amiodarone MOA and uses(3)
MOA: K channel blocker that delays depolarization and is highly effective, reducing automaticity in SA node, reducing contractility, and reducing conduction velocity
1. only approved for life-threatening ventricular dysrhythmias (used in ACLS algorithm)
2. unapproved use for Afib
3. used if nothing else works
Amiodarone adverse effects (5)
-last a long time b/c of the long half life (20-120 days
1. pulmonary toxicity (biggest concern! fibrosis, dyspnea- look at lung fnxn)
2. cardiotoxicity (bradycardia, HF)
3. toxic in pregs
4. corneal micro deposits that can cause blurriness, photophobia
5. blindness from optic neuropathy
verapamil and diltiazem MOA and uses
MOA: Calcium channel blocker that reduces SA automaticity, delays AV node conduction, reduces contractility (same as B blocker)
1. slow ventricular rate (A fib)
2. terminate SVT
-pt. must be put on an anticoagulant, too
verapamil and diltiazem adverse effects (6)
1. bradycardia
2. AV block
3. HF
4. hypotension
5. edema (blocking Ca channels leads to vasodilation)
6. can elevate digoxin levels
-increased risk of these effects when combined w/ a beta blocker
adenosine/adenocard MOA and uses
MOA: decreases automaticity in SA node, slows conduction through AV node, prolongs PR interval
-termination of paroxysmal SVT- HR>150 where we can't see what is going on- this slows the heart down so we can see it
-quick half life of 3s, so given IV in a quick push- given max 3x
Adenosine/Adenocard adverse effects (5)
1. sinus bradycardia
2. dyspnea (from bronchoconstriciton)
3. hypotension and facial flushing (from vasodilation)
4. chest discomfort (from heart actually stopping)
-keep resuscitation equipment handy
- teach vagal maneuver (bear down and cough) to try and get them out of the rhythm
digoxin as an antidysrhythmic- MOA, uses, adverse effects
MOA: suppresses dysrhythmias by decreasing conduction through AV node and automaticity in SA node-
Uses: primary indication is HF, but can be used to treat atrial dysrhythmias especially for rate control (NOT first line)
Adverse effects: 1. cardiotoxicity (risk increased by hypokalemia)
-apical pulse for 60 seconds and hold for <60
general cholesterol med info
-cholesterol is made in the liver
-cholesterol meds take ~ 2 weeks to work
types of cholesterol
1. LDL: BAD cholesterol- fatty streaks develop, then plaques
2. HDL: good cholesterol!
3. VLDL: very low density lipoproteins (transport triglycerides and break down to release LDL)
cholesterol screening recommendations and levels
screening: Q5 years over age of 20
LDL: < 100
HDL > 40
triglycerides <150 (also high in binge drinkers)
CHD risk equivalents (2)
1. DM
2. Atherosclerotic disease other than CHD
lifestyle modifications for cholesterol
-first line! We don't want to give meds unless we have to
-modifiable risk factors: exercise, smoking cessation
types of cholesterol meds (4)
1. statins
2. bile-acid sequestrates
3. nicotinic acid (niacin)
4. fibrates (for triglycerides only)
Statins (HMG CoA reductase inhibitors) general info and MOA
MOA: increases metabolism of LDL and removes it from blood
-most effective drug for lowering LDL
-may elevate HDL
-reduces triglycerides
-promotes plaque stability and reduces the risk for cardiovascular events
-is now generic- yay!
statin therapeutic uses (4) and dosing
1. hyperlipidemia
2. prevention of cardiovascular events
3. post-MI therapy
4. DM (ALL DM pts should be on a statin!)
-take at night because cholesterol synthesis takes place at night
statin adverse effects
1. headache, rash, GI issues (common)
2. myopathy (muscle breakdown- look at CK enzymes) can progress to rhabdomyolysis (BAD breakdown)
3. hepatotoxicity (evaluate liver before taking med)
Nicotinic Acid/Niacin MOA and uses
MOA: reduce VLDL, therefore reducing LDL and triglycerides
-INCREASES HDL more than any other med
-not often used
Nicotinic Acid/Niacin adverse effects
1. flushing/itching of skin that can be somewhat pretreated with aspirin
2. GI issues
3. hepatotoxicity (look at liver enzymes)
(skin/GI issues are main reasons for noncompliance)
bile-acid sequestrates/Wellchol
- used to be first line, now used as adjunct to statins
MOA: reduces LDL, may increase VDL in some
-used adjunct with statins
-also lowers blood sugar, so used in DM as adjunct treatment
-adverse effects: constipation (b/c it works in GI)
Ezetimibe/Zetia MOA and uses
MOA: inhibits cholesterol absorption in SI
-can be used or alone or with statin
-reduces total cholesteral, LDL
Ezetimibe/Zetia adverse effects (4)
1. myopathy
2. hepatotoxicity (esp. with statin)
3. pancreatitis (intractable vomiting, pain, jaundice, diarrhea)
4. thrombocytopenia (<150,000)
Fibrates (Gemfibrozil/Lopid) MOA and uses
-most effective at lowering triglycerides
-used for patients who haven't responded to diet modifications or in pts who have high triglycerides from heavy drinking
fibrates Gemfibrozil/Lopid adverse effects (5)
-usually when combined with a statin
1. GI issues
3. myopathy/rhabdomyolysis
4. liver injury
5. can increase risk of bleeding when combined with coumadin/warfarin
-prescription omega 3
-lowers triglycerides
-can cause increased risk of bleeding
-used to be used as an adjunct treatment for hyperlipidemia, NOT anymore b/c of side effects (cardiovascular events)
2 goals of angina drug therapy
1. prevent myocardial infarction and death
2. prevent myocardial ischemia and anginal pain
drugs used for angina
1. nitro
2. beta blockers (propanolol)
3. calcium channel blockers (verapamil)
treatment strategies for unstable angina (2) and therapies (3)
1. maintain oxygen supply
2. decrease oxygen demand
1. anti-ischemic therapy
2. antiplatelet therapy
3. anticoagulant therapy
anti-ischemmic therapy (5)
1. Nitro (dilates veins and ventricle, decreasing preload)
2. beta blocker (decreases workload)
3. supplemental O2
4. IV morphine (decreases pain and workload)
5. ACE inhibitor (decreases afterload, workload, remodeling)
antiplatelet therapy (3)
1. aspirin
2. plavix
3. integrilin (eptifibatide)
Nitro MOA, uses, adverse effects
MOA: vasodilator that dilates veins and ventricle to decrease preload, cardiac workload
-tries to maintain balance of 02 supply and demand
-angina (acute and sustained)
-uncontrolled blood pressure (IV)
-treatment of HF with MI
adverse effects:
-headache, orthostatic hypotension, flushing, reflex tachycardia
Nitro interactions (4)
1. hypotensive drugs
2. viagra, cialis
3. beta blockers
4. verapamil, diltiazem
nitro tolerance
-can develop rapidly
-cross-tolerance to all other nitrates
-take off for 8 hours at night
-if taking long acting, d/c slowly
beta blockers and angina (propanolol, metoprolol) MOA and adverse effects
MOA: decrease cardiac oxygen demand
Adverse effects:
-asthmatic effects
-heart block
-heart failure
calcium channel blockers (verapamil, diltiazem) and angina
uses and adverse effects (7)
uses: stable and variant angina
adverse effects:
1. dilation of peripheral arterioles
2. hypotension
3. bradycardia
4. HF
5. AV block
6. edema
7. constipation w/ diltiazem
types of revascularization therapy for MI (3)
1. CABG (for multi-vessel involvement- more invasive)
2. PTCA (coronary angioplasty)
3. PCI (stint)
drugs to prevent MI (4)
1. anti platelet drugs (baby aspirin)
2. cholesterol-lowering drugs
3. ACE inhibitors
4. antianginal agents PRN
variant angina management (vasospastic angina)
-start with calcium channel blocker and/or long-acting nitrate
-beta blockers don't work
-use CABG if they don't work
1. Formation of platelet plug through platelet aggregation
2. coagulation (extrinsic or intrinsic)
intrinsic pathway v. extrinsic pathway
intrinsic: everything you have is there
extrinsic: you need TF to keep the clotting process going
Virchow's triad
1. Hypercoagulability (increased risk of clotting)
2. venous stasis (pooling of blood in the vasculature)
3. injury of a vessel or phlebitis
heparin (unfractionated) MOA and administration
-works on the intrinsic pathway, enhancing antithrombin
-rapid acting
-doesn't get rid of existing clots- just prevents them from growing
-IV or subQ in abdomen, 2 inches from belly betting (no PO b/c of first pass)
-rapid acting, so 3x dosing a day
heparin (unfractionated) uses (6)
1. Pregnancy (doesn't cross BBB)
2. PE
3. stroke (ischemic only...duh)
4. DVT
5. hemodialysis for fistulas
6. DIC (microclots r/t sepsis)
heparin (unfractionated) adverse effects
1. Hemorrhage
2. HIT (heparin induced thrombocytopenia- <100,000)
3. hypersensitivity rxns (comes from animals)
heparin (unfractionated) contraindications
1. Thrombocytopenia
2. uncontrolled bleeding
3. during and immediately after eye, brain, spinal cord surgery
antidote for heparin OD
protamine sulfate (also for lovenox)
-short half life, so may need to be given more than once
activated partial thromboplastin time
-how many seconds it takes for clotting to happen
-ideal range for heparin is 60-80s (normal is 40s)
-anything over 80s is too long
low-molecular-weight heparins (lovenox) MOA, uses, administration
-made up of shorter molecules than heparin
1. DVT prophylaxis
2. prevention of ischemic complications (unstable angina, non-Q-wave MI, STEMI)
-dosed in units calculated by body weight
differences between unfractionated heparin and lovenox (5)
1. Lovenox has a longer half-life, so given once or twice a day
2. Lovenox can be given at home b/c no need to check PPT like with unfrac. heparin
3. lovenox is more expensive b/c not generic
4. heparin is based in units, lovenox is weight based
5. higher bioavailability
adverse effects of lovenox (3)
1. Bleeding
2. immune-mediated thrombocytopenia
3. severe neurologic injury for pts undergoing spinal puncture or epidural anesthesia
warfarin (Coumadin) info, MOA, uses
-MOA: blocks vit. K clotting factors and prothrombin
-uses: oral anticoagulant for long-term prophylaxis of thrombosis (PE, venous thrombosis, Afib pts)
-NOT useful in emergencies b/c it takes ~1 week to take effect
Monitoring for warfarin
-INR (how long blood takes to clot- more specific to warfarin- standardized whereas PT can vary)
-goal of clotting is 2-3 of normal (if lower, increase dose, vice versa)
warfarin adverse effects (3)
1. Hemorrhage
2. NO pregs or use during lactation (unlike heparin)
3. GI bleeds
warfarin antidote
-vitamin K- they antagonize each other
warfarin/Coumadin drug interactions(6)
1. Drugs that increase or decrease anticoagulant effects
2. vit. K foods (leafy vegetables, bananas....keep consistent)
3. drugs that promote bleeding (aspirin, heparin, acetaminophen) -but you can bridge over from heparin to warfarin in pts going home
warfarin compared to heparin
-both anticoagulants
-warfarin is oral, heparin is injection
-heparin activates thrombin and factor XA, warfarin inhibits synthesis of clotting factors
-heparin is quick onset and fades quickly, warfarin is slow but persists
-PTT for monitoring heparin, PT and INR for warfarin
-overdose of heparin=protamine, overdose of warfarin = vit. K
antiplatelet drugs (2)
1. Aspirin
2. clopidogrel/Plavix
aspirin MOA and uses(5)
MOA: irreversible COX blocker
1. ischemic stroke
2. TIA
3. angina
4. stents
5. MI and MI prevention (baby aspirin if at risk, full aspirin if Hx of MI)
aspirin adverse effects(3)
1. Bleeding
2. GI bleed (enteric coated may not help)
3. hemorrhagic stroke
MOA: blocks ADP receptors on platelets, preventing clotting
1. prevents blockage of coronary artery stents
2. reduces thrombotic events in people with ACS
-adverse effects: same as ASA
-no antidote
-no need for drug monitoring
-now generic- YAY!
Glycoprotein IIb/IIIa receptor antagonists (integrilin)
-"super aspirins"
-most effective antiplatelet drugs
-reversible blockade of GP IIb/IIIa receptor
-IV only
-emergency situation (ex: pre PCI)
Alteplase (tPa) MOA and uses
MOA: thrombolytic that dissolves existing clots by converting plasminogen to plasmin
-give 4.5 hours w/in stroke onset, 4-6 hours for MI onset
-uses: MI, stroke, massive PE
alteplase (tPa) concerns and cautions
-major adverse effect from oozing to hemorrhage
-may need to consider blood products
-cautions: recent surgeries, active bleeding, invasive procedure sites
-anticoagulants increase risk
STEMI and management
-acute MI caused by complete interruption of regional myocardial blood flow
-management includes catheterization, pt. contact to cath w/in 90 min, MONA (OANM)
non-STEMI management
-cath lab, not emergent (w/in a day or 2)
-usually managed inpatient, medically with anticoagulants, ACE inhibitors, beta blockers
-can't see this on an EKG
thrombolytic therapy
-most effective when given early (again, first 4-6 hours)
-goals is to improve ventricular function, limit size of infarct, reduce mortality
-best for pts younger than 75
adjunct treatment to reperfusion (3)
1. unfractionated heparin or lovenox given post MI
2. antiplatelet drugs (Plavix, GP inhibitors)
3. low dose aspirin (may be concurrent with Plavix), take indefinitely
teaching for PCI pts on low dose aspirin and Plavix indefinitely
-DON'T MISS a dose of Plavix. Death.
-GI issues r/t aspirin
-easy bruising
ACE and ARBS r/t STEMI management
-decrease short-term mortality in all pts
-start treatment w/in 24 hours
Calcium channel blockers and STEMI management
-antianginal, vasodilation, and antiHTN actions
-not all pts will be on theses post STEMI
STEMI complications (4)
1. Ventricular dysrhythmias (but vtach is good at first!)
2. cardiogenic shock (poor pump, low BP, low CO)
3. HF
4. cardiac rupture (FATAL)
secondary prevention of STEMI
-lifestyle changes
-all post MI pts should be on a beta blocker, ACE inhibitor, antiplatelet drug or anticoagulant
lidocaine (xylocaine)
MOA: Na channel blocker, slowing conduction from atria to ventricles (PR interval widens) and reducing automaticity in ventricles, and accelerating repolarization (QT shorter)
-given IV
Adverse effects:
1. CNS effects (drowsiness, confusion, paresthesias)
2. seizures
3. respiratory effects
-have resuscitation equipment handy at all times
decreases efficacy of plavix- switch them to another drug in the same class