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Cardiopulmonary/Endo/ENT #1 > Pharm Exam 2 > Flashcards

Pharm Exam 2 Flashcards

1
Q

Nitroglycerin (NTG)

A

Organic nitrate (prototype)
Prodrug: metabolized to NO in VSM by mitochondrial ALDH2 (aldehyde dehydrogenase)
Efficacy: prevent and termination of acute angina attacks, improves exercise tolerance, abolishes ST segment depression
No survival benefit/prevention of MI
Adverse: HA (severe), facial flushing, orthostatic hypotension, reflex tachycardia (increases O2 demand negating therapy; suppressed with beta blockers or Ca-ch blockers)
Tolerance
Interactions: ED vasodilator drugs (sildenafil; can precipitate severe refractory hypotension and possible MI within 24h of PDE-5 inhibitors); alcohol (inhibits ALDH2; accentuates orthostatic hypotension)

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2
Q

Isosorbide dinitrate

A

Organic nitrate
Oral and sublingual tablets
Prodrug: metabolized to isosorbide mononitrate
Longer duration (q4-6h) added if angina not controlled by NTG and B-blockers/CCBs
Efficacy: prevent and termination of acute angina attacks, improves exercise tolerance, abolishes ST segment depression
No survival benefit/prevention of MI

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3
Q

Organic Nitrates

A

Prodrug: metabolized to NO in VSM by mitochondrial ALDH2 (aldehyde dehydrogenase) (also used in EtOH metabolism)
MOA: venous > arterial dilation at therapeutic doses, reduces preload (decreased venous return; reduced O2 demand)
Efficacy: prevent and termination of acute angina attacks, improves exercise tolerance, abolishes ST segment depression
No survival benefit/prevention of MI **
CBF: vasodilator action on epicardial (lg) arteries (blood to endothelium); dilation on spastic coronary arteries
CV: usual doses (no inotropic or chronotropic effects nor changes in BP); higher doses (reflex tacky if MAP reduced–baroreceptor reflex); arterioles in face/neck and meningeal arteries sensitive to vasodilation (HA)
Pharmacogenetics: ALDH2 polymorphism (ALDH22 is low activity, high prevalence in Asians, possibly lower efficacy)
PK: sublingual (circumvents 1st pass metabolism, therapeutic levels in 1-2m, rapid relief, duration is <1h); tablets unstable to heat/light/moisture; tingling sensation under tongue (indicates tablet is effective); oral or cutaneous (slower onset 30-60m, longer duration 4-24h)
Contact EMS if angina not gone within 5m
TOLERANCE: nitrate-mediated inactivation of ALDH2; most common with oral and transdermal meds; minimized with eccentric dosing (nitrate-free interval of 10-12h)
Adverse: HA (severe), facial flushing, orthostatic hypotension, reflex tachycardia (increases O2 demand negating therapy; suppressed with beta blockers or Ca-ch blockers)
Interactions: ED vasodilator drugs (sildenafil; can precipitate severe refractory hypotension and possible MI within 24h of PDE-5 inhibitors); alcohol (inhibits ALDH2; accentuates orthostatic hypotension)

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4
Q

Calcium channel blockers

A

Vasodilator. Effect on after load.
MOA: block inward flow of Ca++ through voltage-gated L-type Ca channel (bind channel alpha-1 subunit). Marked decrease in TRANSMEMBRANE Ca current (decreased Ca intracellularly) in VSM, cardiac myosotes, and nodal tissue. Vasodilators in peripheral and coronary arteries (decreased after load –> reduced O2 demand).
Efficacy: prophylaxis against angina attacks (reduce consumption of NTG). Long-acting preps or 2nd gen preferred (immediate release –> reflex tachycardia). As effective as beta-blockers in controlling angina. No survival benefit.
Adverse: Bradyarrhythmia (ver,dil), reflex tachycardia (nifed), cardiac depression (ver,dil), flushing, peripheral edema (nifed), constipation (ver–geriatrics)

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5
Q

Nifedipine

A

CCB (dihydropyridine) (prototype)
Immediate release (causes reflex tachycardia)
Greater inhibitory action on VSM than myocardium.
Less depression of myocardial contractility and minimal effects on SA automaticity and AV conduction velocity (compared to non-DHP)
CYP3A4 metabolism (grapefruit juice)
Adverse: reflex tachycardia, flushing, peripheral edema

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6
Q

Verapamil

A

CCB (HR lowering) (non-dihydropyridine)
Act on SA and AV nodal issue (decrease HR and contractility; less potent vasodilators than DHPs)
C/i in SICK SINUS SYNDROME and AV nodal block
Adverse: bradyarrhythmia, cardiac depression, constipation (inhibits peristalsis in GI SM by CCB effect, geriatrics)

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7
Q

Diltiazem

A

CCB (HR lowering) (non-dihydorpyridine)
Act on SA and AV nodal issue (decrease HR and contractility; less potent vasodilators than DHPs)
**Less cardiac depression than verapamil; better tolerated
C/i in SICK SINUS SYNDROME and AV nodal block
Adverse: bradyarrhythmia, cardiac depression

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8
Q

Propranolol

A

Beta-blocker (non-selective–blocks B1 and B2)
MOA: decrease HR, contractile force, and BP which decrease myocardial oxygen demand. Increases perfusion during diastole (negative chronotropism). Decreases resting HR; effect on exercise-induced tachy is more pronounced.
Use: maintain resting HR at ~55bpm and limit peak HR during exertion to ~110 (titrate dose to this). Reduce severity and frequency of stable anginal attacks. Reduces mortality** and decrease incidence of sudden cardiac death. Not useful for vasospastic angina (may worsen condition dt unopposed alpha-adrenergic receptor activity)
Adverse: effects on ventricular function (acute, B1); increase airway resistance (B2); precipitate acute MI on sudden withdrawl; c/i in agents with intrinsic B1-receptor agonist activity (pindolol); fatigue, depression, sexual dysfunction

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9
Q

Ranolazine

A

Antianginal effects without changes in HR or BP
MOA: Inhibits “late phase” of inward sodium current, thereby blocking calcium overload–>reduced O2 demand. (increased Na+ influx in ischemic myocytes leads to Ca++ overload (Na-Ca exchanger)–> increases O2 demand, impaired relaxation, and decreased perfusion.)
Use: prophylaxis against angina attacks, anti arrhythmic properties. In combo in pts with uncontrolled angina.
Adverse: prolonged QT-interval. C/i with other drugs that promote this effect. CYP3A4 metabolism.

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10
Q

Sildenafil

A 
PDE5 inhibitor (prolongs activity of NO/cGMP)
PDE (break-down cGMP. cGMP causes vasodilation) 
MOA: relax corpora cavernosa SM. No effect in the absence of sexual stimulation (NANC--parasympathetic nonadrenergic noncholinergic--innervation must be intact) 
PK: take 1h before sexual activity. Onset is ~60m. Duration is 2-4h. Onset delayed by a high fat meal. CYP3A4 metabolism. Related agents have longer duration of action. 
Effective in 50-90% of cases.
Adverse: HA and flushing (PDE1), nasal congestion, dyspepsia, abnormal vision (blue color tinge, blurring, light sensitivity (retinal PDE6)), risk of sudden hearing loss, priapism (rare--treat with vasoconstrictors) 
Interactions: potentiate the effects of organic nitrates and alpha blockers.
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11
Q

Alprostadil

A

Prostaglandin eicosanoid (PGE1)
MOA: agonist for EP2 receptor in VSM. Direct vasodilation upon LOCAL administration. Bypasses need for intact NANC innervation. Auto-erection within minutes.
Intercavernous injection or urethral suppository. Short duration of action (<1h)
Alternative to PDE5 inhibitors.
Adverse: pain at injection site and hypotension; priapism and penile fibrosis (rare)

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12
Q

JNC 8 guidelines

A
  1. First line: thiazide diuretics, ACE-I, ARB, CCB (DHP)
  2. Second-line: higher doses of first-line agents
  3. Third-line: beta blockers, loop diuretics, aliskiren, alpha-1 blockers, vasodilators, central alpha-2 agonists, reserpine, aldosterone antagonists
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13
Q

Chlorthalidone

A

Thiazide diuretic
Antihypertensive, not hypotensive
Longer DOA than hydrochlorthiazide
Initial increase in TPR dt RAAS (baroreceptor reflex)
Thought: decreased sodium from vasculature
Hemodynamics: no change in HR or CO
Use: low dose for stage 1 (lower BP 10-15 in 4-6w); reduces mortality; Shallow ANTIHYPERTENSIVE dose-dependence (doses >25mg only increase side effects); in combo with others for mod to severe HTN (synergistic effect); reduce Na+ retention cured by vasodilators and some sympathetics; effective in volume-dependent HTN
Adverse: hypokalemia, hyperuricemia, hyperglycemia, hyperlipidemia, erectile dysfunction

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14
Q

Furosemide

A

Loop diuretic
Modest effect on BP despite brisk diuresis
Shorter DOA than thiazides
Use: malignant HTN, volume-dependent patients with GFR <30mL/min
Adverse: similiar to thiazides (hypokalemia, hyperuricemia, hyperglycemia, hyperlipidemia, erectile dysfunction), OTOTOXICITY, INCREAED EXCRETION OF CALCIUM

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15
Q

Captopril

A

ACE-I
Inhibits ACE, decreases TPR
Use: antihypertensive (even if patient has normal Plasma Renin Activity); no interference with CV reflexes (baroreceptor; no effect on exercise tolerance); safe in pts with bronchial asthma; no effects on lethargy, weakness, or sexual dysfxn
Reduces risk of HTN-related mortality
1st dose phenomenon (function of PRA; start with low doses) (high PRA due to salt restriction possible)
Adverse: hypERkalemia, cough (bradykinin), angioedema, teratogen (category X)

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16
Q

Losartan

A

ARB
MOA: AT1 receptor antagonist; decreases TPR
Use: alternative to ACE-I
Adverse: similar to ACE-I (hypERkalemia, teragogen) but cough/angioedema less prevalent

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17
Q

Eplerenone

A

Aldosterone antagonist
MOA: selective aldosterone antagonist (1. little/no effect on other hormone receptors, 2. promotes excretion of Na+ and water by blocking aldo receptors in kidney; 3. prevents/reverses CV remodeling)
Use: additional decrease in BP in pots taking ACE-I or ARB
Adverse: hypERkalemia, reduced side effects assc with spironolactone

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18
Q

Aliskiren

A

Direct renin inhibitor (DRI)
MOA: blocks conversion of angiotensinogen –> AngI
Use: alone or in combo with other anti-HTN agents
Adverse: hypERkalemia, c/i in pregnancy

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19
Q

Nifedpine (anti-HTN)

A

CCB
MOA: block voltage-gated L-type Ca++ ch in VSM
Decreases TPR, distinguished in regard to cardiac effects
Use: first-line for mild to mod HTN; administered at max doses in “vasoreactive” patients
Adverse: reflex tachy, bradycardia

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20
Q

Verapamil (anti-HTN)

A

CCB
MOA: block voltage-gated L-type Ca++ ch in VSM
Decreases TPR, distinguished in regard to cardiac effects
Use: first-line for mild to mod HTN
Adverse: reflex tachy, bradycardia

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21
Q

Nitroprusside

A

Vasodilator
Compound contains NO and Cyanide (released on decomposition)
MOA: non-enzymatically decomposes to release NO (arterial and venous dilation, mech. similar to NTG but no tolerance develops)
PK: constant infusion (IV); immediate effect; BP can be adjusted by changing infusion rate (monitor this); short DOA; BP returns to pre-treatment levels in 3-5m; unstable and light sensitive in solution
Met: non-enzymatic conversion; CN- metabolized by liver by rhodanase to SCN-; avoid CN- accumulation by admin of thiosulfate (antidote for CN- poisoning)
Use: HTN emergencies (diastolic >120; it never fails!); hypotensive surgery; give furosemide simultaneously to reduce fluid retention
Adverse: excessive vasodilation/hypotension; cyanide toxicity (rare); hypothyroidism (thiocyanate accumulation–goitregernic)

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22
Q

Hydralazine

A

Vasodilator
MOA: arteriolar dilation; NO donor and may decrease Ca++ release
Met: low oral bioavailability (high 1st pass); acetylated by NAT2 (inactivates drug); reduce the dose in slow-acetylators
Use: severe HTN in combo with other agents, HTN crisis, in combo with isosorbide denitrate (BiDil) for CHF/HTN in African Americans
Adverse: Reflex tachy and HA; lupus-like syndrome in slow-acetylators

23
Q

Minoxidil

A

Vasodilator (dangerous; rarely used)
MOA: arterial dilation by opening K+ ch on VSM (K+ efflux causes hyper polarization, reducing contraction; reflex increase in HR and contractility)
Prodrug: met in liver to minoxidil sulfate
Use: seldom; add-on for severe HTN; topical to promote hair growth (Rogaine)
Adverse: edema (salt/water retention; may need a loop); pericardial effusion (boxed warning; tamponade); reflex tachy (use with Beta blocker); Hypertrichosis (hair growth on face, back, arms, and legs)

24
Q

Epoprostanol

A

Prostacyclin (PGI2)
MOA: mimics effect of PGI2 on VSM; binds to receptor and stimulates cAMP synthesis; promotes vascular relaxation, suppress growth of VSM; inhibits platelet aggregation
Use: Pulmonary arterial hypertension (PAH) (improves short-term survival)
Infusion pump, kept cold (difficult to use)
Adverse: flushing, HA, nausea, risk of bleeding

25
Q

Bosentan

A

Endothelin-1 antagonist (endothelial-derived vasoconstrictor peptide; mirror image of NO)
ET-1 induces infl, fibrosis, and proliferation of VSM
MOA: competitive antagonist of ET-a and ET-b receptors
Use: PAH; toxicity restricts use
Adverse: teratogenic, hepatotoxic

26
Q

Clonidine

A

Sympatholytics
Centrally-acting alpha-2 adrenergic agonist
Decreases sympathetic outflow by stimulating alpha-2 receptors in NTS
Also binds imidazoline receptor
Compensatory Na+/water retention
Use: for patients not responding to other drugs; no evidence for reducing risk of adverse CV events
Adverse: dry mouth, sedation, sexual dysfxn, postural hypotension; c/i in depressed pts
Abrupt withdrawal syndrome: rebound HTN, HA, tachy

27
Q

Methyldopa

A

Sympatholytic
Alpha-2 adrenergic agonist
Metabolized to methylNE; effects similar to clonidine
Adverse: dry mouth, sedation, sexual dysfxn, postural hypotension; c/i in depressed pts; (similar to clonidine but without rebound effect); positive Coomb’s test
Safely used during pregnancy

28
Q

Propranolol (HTN)

A

Beta-blocker (non-selective)
B1 blockade: reduces CO, reduces TPR long-term despite B2 blockade (inhibits renin release), reduces sympathetic outflow (CNS)
Use: no longer recommended unless specific indication (MI, CHF, SIHD); less effective in African-Americans and geriatric patients; prevent reflex tachy in severe HTN treated with vasodilators
Used most widely: metoprolol and atenolol (cardioselective)
Adverse: bradycardia (reduced contractility and AV conduction); bronchoconstriction; reduced exercise capacity; sexual dysfxn

29
Q

Terazosine

A 
Alpha-1 blocker 
MOA: block a-1 on VSM
Salt and water retention 
Use: anti-hypertensive
Adverse: first-dose effect (postural hypotension); reflex tachy; nasal congestion; inhibits ejaculation
30
Q

HTN Treatment Algorithm (JNC8)

A
  1. Lifestyle Changes (first)
  2. Drugs when sustained BP ≥140/90 despite lifestyle changes
  3. Goal: maintained BP 20/10
  4. Comorbid conditions req more aggressive tx
  5. Multi-drug tx: enhanced efficacy, dose reduction, offset compensatory responses
31
Q

Atorvastatin calcium

A

HMG-CoA reductase inhibitor (rate-limiting step in chol biosynthesis)
3-hydroxy-3-methylglutarate –HMg-CoA reducatse–> mevalonate
Long half-life, 3A4 and 2C9
Increase synth of hepatic LDL-R and increase removal of LDL particles form circulation. Enhance clearance of LDL precursors (VLDL and IDL).
Lower LDL by 20-55%. Decrease TG by 20%. Increase HDL by 5-10%.
Use: first line tx for hypercholesterolemia (elevated LDL)
Cardioprotective (lower CRP, anti-infl., enhance NO synthesis, stabilize plaques, reduce lipoprotein oxidation, reduce platelet aggregation)
PK: oral, in evening, first-pass metabolism in liver, statins are excreted by liver into bile
Interactions: CYP3A4 and 2C9 (fibrates, digoxin, warfarin, macrolides); pravastatin avoids P450 interactions
Adverse: GI irritation, HA, rash, hepatotoxicity, myopathy (creatining phosphokinase levels >10x ULN; enhanced by fibrates and niacin)
C/i: Category X, liver disease

32
Q

Colesevelam (WEL-CHOL)

A

Bile acid-binding resin
Less GI irritation, more pleasant to take
MOA: prevent bile acid reabsorption, increased breakdown of hepatic cholesterol (decreases feedback inhibition of enzyme converting cool to bile acid), increased catabolism of chol –> increased LDL-R (similar to statins, except slight increase in HMG CoA reductase activity)
Lower LDL (10-20%), small rise in HDL (5%), no effect on VLDL
Use: familial or primary hypercholesterolemia or very high LDL, in conjunction with HMG CoA reductase inhibitors
PK: not absorbed by GI tract
Interactions: Bild acids bind many drugs and interfere with absorption (take other meds 1h before or 3-4 days after)
Adverse: bloating, dyspepsia, constipation, mild steatorrhea (decreased compliance)
C/i: pregnancy (category B)

33
Q

Ezetimibe

A

Cholesterol absorption inhibitor
Inhibits cholesterol transport protein (NPC1L1) (inhibits reabsorption of chol excreted in the bile)
Reduces [LDL] (25%)
Use: combination prep no more beneficial than a statin alone, so primarily used in pts who are statin-intolerant
PK: well absorbed, excreted in feces unchanged (78%), rest is conjugated by liver (glucuronidation), t1/2 18-30h.
Interactions: other anti-lipidemic drugs, fibrates increase risk of cholelithiasis, levels increased by niacin (increased risk of myopathy), increase prothrombin time with warfarin
Adverse: diarrhea, low incidence or reversible impaired hepatic fxn
C/i: category C

34
Q

Fenofibrate

A

Fibric acid derivatives (PPAR-alpha activators)
Peroxisome proliferator activated receptor-alpha
MOA: increase FA oxidation, increase activity of lipoprotein lipase (catabolizes VLDL),
Lower [VLDL]–> lower TG (40-55%)
[HDL] increases (10-25%)
Variable effects on LDL
Use: type III hyperlipoproteinemia, severe hyper-TG (>1000) at risk for pancreatitis, hyper-TG with low HDL
PK: rapid/efficient absorption (90%), t1/2 from 1-20h, MORE INFORMATION IN SLIDES
Interactions: oral anticoagulant tx may be enhanced, in combo with statins (myositis-flu-like illness, myopathy)
Adverse: GI disturbance (frequent), skin rash, urticaria, hair loss, myalgia, fatigue, HA (infrequent)
C/i: pregnancy and lactation (category C), children, renal failure, hepatic dysfunction

35
Q

Niacin

A

Nicotinic acid (water-soluble B vitamin–B3)
MOA: in adipose tissue** it inhibits lipolysis of TGs by hormone-senstiive lipase (reduces transport of FFA to liver)
In liver**, reduces TG synthesis (inhibits synth and esterification of FA’s)
Red. TG synth red. hepatic VLDL prod
Raises HDL by decreasing fractional clearance of HDL-apoA-I rather than enhancing HDL synth
Lower TG by lowering VLDL (35-50%)
Lowers LDL more slowly (25%)
Increases HDL (15-30%)
Use: hypertriglyceridemia and elevated LDL, esp if HDL is low
PK: absorbed from intestines, t1/2= 60m, liver metabolism, excreted unchanged
Interactions: myopathy with statins
Adverse: cutaneous flush and pruritis, GI disturbance, hepatic toxicity, activation on peptic ulcer, hyperglycemia, decreased glucose tolerance, hyperuricemia
C/i: pregnancy (category C), hepatic disease, peptic ulcer, gouty arthritis

36
Q

ACE Inhibitors

A

Decrease production of AngII –> lower aldo and SNS.
AngII levels return to baseline with sustained use (“angII escape”) but efficacy remains (bradykinin-related effects–vasodilation, decrease remodeling)
High dose: reduce mortality

37
Q

Aldosterone Antagonists

A

K+ sparing
Inhibit remodeling
Reduce mortality
Hyperkalemia possible

38
Q

Angiotensin (AT1) Receptor Blockers

A 
Block AT1 (GPCR) but not AT2 receptors. 
Maintains beneficial AT2-mediated effects. 
Avoids AngII escape
Use when intolerant to ACE-Is
reduces mortality
39
Q

Beta blockers

A

Improvement in CHF and decreased mortality
(weird: beta-blockers reduce contractile force)
Mechanism: Unclear
Prevent ischemia and tachyarrhythmias
Inhibit cardiac remodeling; reduces renin secretion
Reduce EF in short term but increase EF in long-term
Cardioselective: metoprolol, bisoprolo, carvedilol
Initiate tx at very low doses (<1/10 of final dose) and titrate

40
Q

Diuretics

A

Reduce Congestive symptoms (decrease water and Na+ retention)
Reduced Preload without reduction in CO
Dietary salt restriction
Efficacy determined by daily body weight
No reduction in mortality
Loop diuretics: work when GFR is low. K+ depletion. Less effective in later CHF stages.
Thiazides: ineffective with low GFR. K+ depletion.
Aldosterone antagonists: K+ sparing. Hyperkalemia (esp. with ACE-I/ARB)

41
Q

Vasodilators

A

Nitrovasodilators: reduce preload; tolerance
Hydralazine: reduces pulmonary and systemic vascular resistance (reduces afterload); positive inotropic effect
Isosorbide dinitrate-hydralazine (BiDil): reduces mortality; AA patients

42
Q

Digoxin

A

Cardiac glycoside
Digitalis glycoside (foxglove: Digitalis lanata)
Increase strength of myocardial contraction (pos. inotropy)
Increased contractile force –> Increased CO
No decrease in mortality
Inhibits Na/K/ATPase (alpha subunit: reduces Na extrusion and increases cytosolic [Na])
Reduced activity of Na/Ca exchanger (NCX)
Cytosolic Ca increaes
Hyperkalemia: reduces digoxin binding
Hypokalemia: increases efficacy (and toxicity), promotes Ca overload
WATCH K+ LEVELS
Enhances PNS (vagal) tone, reduces SNS outflow
AV node: decreases conduction velocity
Toxic levels: enhances SNS tone –> reentry arrhythmias
Toxic: calcium overload –> DADs
PK: long half life, excreted unchanged by kidneys, skeletal muscle distribution (dose on lean body mass), Eubacterium lentum (in gut) metabolizes digoxin in 10%
Use: LV systolic dysfunction plus A fib
Toxicity: T.I. = 2 (monitor dig (<1ng/mL) and K+ levels); arrhythmias (DAD); SA/AV nodal block
Mgmt: anti arrhythmic drugs (lidocaine, atropine), FAB
Warning signs of toxicity: GI (nausea/vomiting, anorexia), CNS (fatigue, visual disturbances)
Interactions: diuretics (hypokalemia), ACE-I/ARB (hyperkalemia), antiarrhythmics (quinidine and verapamil can increase [dig] plasma)

43
Q

Digoxin immune FAB

A

Prevents digoxin from binding to ATPase

44
Q

Quinidine

A

Class 1a: Na ch blocker
Moderately slow dissociation (1sec < t < 10 sec)
Moderate reduction in phase 0 and conduction velocity
Prolong AP duration (K+ ch effect)
Widened QRS, prolonged QT
Low [K+] –> enhanced proarrhthmagenicity (longer AP)
1. Blocks Na ch
2. Blocks K ch (prolonged refractory pd)
3. alpha-adrenergic blockade
4. anticholinergic (atropine-like)
Use: A flutter and fib; suppress SVT and VT
Effects: prolonged QT (risk TdP)
Interaction with dig (increased [ ])
Cinchonism (HA, tinnitus) at high dose

45
Q

Procainamide

A

Class 1a: Na ch blocker
Moderately slow dissociation (1sec < t < 10 sec)
Moderate reduction in phase 0 and conduction velocity
Prolong AP duration (K+ ch effect)
Widened QRS, prolonged QT
Low [K+] –> enhanced proarrhthmagenicity (longer AP)
1. avoid long-term use
2. Metabolism: N-acetyl procainamide (NAPA) blocks Na+ ch and is pro-arrhythmic (long QT0
3. Lupus-like syndrome (ANA ab) esp in slow acetylators

46
Q

Lidocaine

A 
Class 1b: Na ch blocker
Fast dissociation (t < 1 sec) 
Reduces rate of phase 0 depolarization/excitability in depolarized cells 
Minimal effects on EKG
1. Blocks Na ch (ventricle selective) 
Use: IV tx for ventricular arrhythmias
Concern about increased mortality 
Not useful for atrial arrhythmias 
Effects: CNS (seizures with rapid admin, paresthesias, tremor, drowsiness); cardiac depression 
Local anesthetic
47
Q

Flecainide

A

Class 1c: Na ch blocker
Very long dissociation (t > 10sec) (marked effect on phase 0 depolarization)
Wide QRS, prolonged PR, prolonged QT
1. blocks Na ch (high rate)
2. Blocks K ch (prolonged RP)
Use: SVT, ventricular arrhythmias (life-threatening)
Increased mortality in pts recovering from MI
Effects: blurred vision, pro-arrhythmic (severe heart disease), blocks Ca ch (suppresses LV fxn, worsens CHF)

48
Q

Propafenone

A

Class 1c: Na ch blocker
Very long dissociation (t > 10sec) (marked effect on phase 0 depolarization)
Wide QRS, prolonged PR, prolonged QT
Beta-adrenergic blockade (bradycardia, bronchospasm)
CYP2D6 (increased blood levels in slow 2D6 metabolizers)

49
Q

Metoprolol

A

Class 2: beta blocker
Blocks B1-R regulated activity of Ca++ and K+ ch in myocardium
Blocks sympathetic infl on automaticity
Blocks sympathetic-induced EAD and DADs
Increases RP of AV node (incr PR)
Use: decrease mortality, suppress tachyarrhythmias (A fib/flutter, exercise/emotional induced), PSVT (AV nodal reentry or WPW)
Effects: SA and AV nodal block, sudden withdrawal syndrome, decrease ventricular fxn (negative inotropic)

50
Q

amiodarone

A

Class 3: prolong refractory period
1. blocks K+ ch (prolongs RP in fast response tissue)
2. Blocks Na+ ch (decreases excitability, increased RP)
3. Blocks Ca++ ch (increased RP)
4. non-competitive adrenergic R blocker
5. Prolonged PR (Ca), QRS (Na), and QT (K)
Use: V tachy or fib. To maintain sinus rhythm in A fib.
Effects: pulmonary fibrosis (long term use at 400 mg/day dose), thyroid dysfxn (analog of TH)
PK: highly lipophylic, long half-life, inhibition of CYP 3A4/2C9 and P-glycoproteins

51
Q

Sotalol

A

Class 3: prolong refractory period
Non-selective B-blocker that also blocks K+ ch
Ventricular tachy or severe atrial flutter or fib
Adverse: TdP in overdose, B-blocker assc.-toxicities, NOT approved as a anti-HTN or antianginal

52
Q

Dofetilide

A

Class 3: prolong refractory period
“pure” K+ (delayed rectifier) ch blocker
No extra cardiac effects
Maintain sinus rhythm in pts with A fib (with MI/HF)
TdP (only used under super close monitoring)

53
Q

Verapamil

A

Class 4: Ca ch blocker
1. blocks Ca ch (L-type); decreases SLOW tissue automaticity and excitability
2. Effects similar to B-blockers
3. Depresses AV nodal conduction
Use: control ventricular rate in atrial flutter/fib, SVD (dt AV nodal reentry)
Effects: depressed cardiac force (c/i in CHF), constipation
Interactions: drugs that inhibit SA and AV nodes, B blockers, dig (bradycardia and AV block)

54
Q

Adenosine

A
  1. Stimulates adenosine A1 GPCR (Gi): decrease cAMP
  2. Activates K ch in sa and AV! nodes (hyperpolarization, decreased automaticity, (inward rectifier))
  3. Reduces AV node Ca++ (Go)
  4. Increased PR
    Use: termination of AVNR, WPW (c/i if A fib present)
    Effects: safe dt short action (5 sec asystole); flushing, metallic taste
    Rapid IV bolus (10-20sec), inactivated by adenosine deaminase, interaction with caffeine (blocks A1 receptors)

Cardiopulmonary/Endo/ENT #1 (2 decks)

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