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USMLE Step 1 > Cardio > Flashcards

Flashcards in Cardio Deck (30):
1

Essential HTN

(Antihypertensive therapy)

Drugs: diuretics, ACE inhibs, ARBs, CCBs

See Renal for more info about diuretics, ACE inhibs & ARBs

2

CHF

(Antihypertensive therapy)

Drugs: diuretics, ACE inhibs, ARBs, Beta blockers (compensated CHF), K+ sparing diuretics

Notes: Beta blockers must be used cautiously in decompensated CHF, and are contraindicated in cardiogenic shock

3

Diabetes mellitus

(Antihypertensive therapy)

Drugs: ACE inhibs, ARBs, CCBs, diuretics, Beta blockers, alpha blockers

Notes: ACE inhibs are protective against diabetic nephropathy. See pharm chapter for more details about alpha- blockers

4

Calcium Channel Blockers

Drugs: nifedipine, verapamil, diltiazem, amlodipine

MoA: block voltage-dependent L-type calcium channels of cardiac and smooth mm-> reduced mm contractility

Use: HTN, angina, arrhythmias (NOT nifedipine), Prinzmetal's angina, Raynaud's

Toxicity: cardiac depression, AV block, peripheral edema, flushing, dizziness, & constipation

5

Hydralazine

MoA: increases cGMP-> smooth mm relaxation. Vasodilates arterioles more than veins; after load reduction.

Use: severe HTN, CHF. 1st line therapy for HTN in pregnancy, w/ methyldopa. Frequently coadministered w/ a Beta-blocker to prevent reflex tachycardia.

Toxicity: compensatory tachycardia (contraindicated in angina/ CAD), fluid retention, nausea, headache, angina. SLE-like syndrome

6

Malignant HTN Tx

Commonly used drugs include nitroprusside, nicardipine, clevidipine, labetalol, and fenoldopam

Nitroprusside: short acting; increases cGMP via direct release of NO. Can cause cyanide toxicity (releases cyanide).

Fenoldopam: Dopamine D1 receptor agonist- coronary, peripheral, renal, and splanchnic vasodiln. Decreases blood pressure and increases natiriuresis.

7

Nitroglycerin, isosorbide dinitrate

MoA: vasodilator by releasing nitric oxide in smooth mm, causing increased cGMP and smooth mm relaxation. Dilates veins>>> arteries. Decreases preload

Use: angina, pulmonary edema

Toxicity: reflex tachycardia, hypotension, flushing, headache, "Monday disease" in industrial exposure: development of tolerance for vasodilating axn during work week and loss of tolerance over weekend results in tachycardia, dizziness, and headache upon reexposure.

8

Antianginal therapy

Goal: reduction of myocardial O2 consumpn (MVO2) by decreasing 1 or more of the determinants of MVO2: end-diastolic volume, blood pressure, heart rate, contractility, ejection time

Notes:
- CCBs: Nifedipine is similar to Nitrates in effect; verapamil is similar to Beta blockers in effect
- Pindolol & acebutolol: partial Beta- agonists contraindicated in angina

9

Nitrates

(antianginal therapy affecting preload)

EDV: decreased
BP: decreased
Contractility: Increased (reflex response)
HR: increased (reflex response)
Ejection time: decreased
MVO2: decreased

10

Beta blockers

(antianginal therapy affecting after load)

EDV: increased
BP: decreased
Contractility: decreased
HR: decreased
Ejection time: increased
MVO2: decreased

11

Nitrates + Beta blockers

(antianginal therapy)

EDV: no effect or decreased
BP: decreased
Contractility: little/ no effect
HR: decreased
Ejection time: little/ no effect
MVO2: greatly decreased

12

HMG- CoA reductase inhibitors

(lipid-lowering agents)

Drugs: lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin)

LDL: greatly decreases
HDL: mildly increases
TGs: mildly decreases

MoA: inhibit conversion of HMG-CoA to mevalonate (cholesterol precursor)

Side effects: hepatotoxicity (increased LFTs), rhabdomyolysis

13

Niacin (vit B3)

(lipid-lowering agent)

LDL: moderately decreases
HDL: moderately increases
TGs: mildly decreases

MoA: inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation

Side effects:
- red, flushed face (decreased by aspirin or long-term use)
- hyperglycemia (acanthosis nigricans)
- hyperuricemia (exacerbates gout)

14

Bile acid resins

(lipid-lowering agent)

Drugs: cholestyramine, colestipol, colesevelam

LDL: moderately decreases
HDL: slightly increases
TGs: slightly increases

MoA: prevent intestinal reabsorpn of bile acids; liver must use cholest to make more

Side effects:
- pts hate it- tastes bad & causes GI discomfort
- decreased absorpn of ADEK
- Cholest gallstones

15

Cholesterol absorpn blockers

(lipid-lowering agents)

Drugs: ezetimibe

LDL: moderately decreases
HDL: none
TGs: none

MoA: prevent cholest reabsorpn at SI brush border

Side effects: rare increased LFTs, diarrhea

16

Fibrates

(lipid-lowering agents)

Drugs: gemfibrozil, clofibrate, bezafibrate, fenofibrate

LDL: Mildly decreases
HDL: mildly increases
TGs: greatly decreases

MoA: upregulate LPL-> TG clearance

Side effects: myositis hepatotoxicity (increased LFTs), cholest gallstones

17

Cardiac glycosides

Drugs: digoxin (75% bioavailability, 20-40% bound, half life= 40 hrs, urinary excretion)

MoA: direct inhibn of Na+/ K+ ATPase leads to indirect inhibn of Na+/ Ca+2 exchanger/ antiport. Increases intracellular Ca+2-> positive isotropy. Stimulates vagus nerve-> decreased HR

Use: CHF (increases contractility); A fib (decreases conduction at AV node and depression of SA node).
Toxicity:
continued on next card

18

Cardiac glycosides (cont.)

Toxicity:
- cholinergic: nausea, vomiting, diarrhea, blurry yellow vision (think Van Gogh)
- ECG: increased PR, decreased QT, ST scooping, T wave inversion, arrhythmia, AV block
- Can lead to hyperkalemia (poor prognostic indicator)
- Factors predisposing to toxicity- renal failure (decreased excretion), hypokalemia (permissive for digoxin binding at K+ binding site on Na+/ K+ ATPase), quinidine (decreased digoxin clearance; displaces digoxin from tissue-binding sites).

Antidote: slowly normalize K+, lidocaine, cardiac pacer, anti-digoxin Fab fragments, Mg+2

19

Antiarryhmthmics
Na+ channel blockers (class I)
(good diagram pg 283 FA)

- Local anesthetics. Slow or block conduction (esp in depolarized cells). Decreases slope of phase 0 depolarization and increases threshold for firing in abnormal pacemaker cells. Are state dependent (selectively depress tissue that is frequently depolarized (e.g. tachycardia))
- Hyperkalemia causes increased toxicity for ALL class I drugs

20

Class IA antiarryhthmics

Drugs: Quinidine, procainamide, disopyramide
Mnemonic: Queen Proclaims Diso's Pyramid

MoA: increases AP duration, increases effective refractory pd (ERP), increases QT interval. Affect both atrial and vent arrhythmias, esp reentrant and ectopic supra ventricular and ventricular tachycardia

Toxicity: quinidine (cinchonism- headache, tinnitus); procainamide (reversible SLE-like syndrome); disopyramide (heart failure); thrombocytopenia; torsades de points due to increased QT interval

21

Class IB antiarrhythmics

Drugs: Lidocaine, Mexiletine, Tocainide

MoA: decreases AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue. Useful in acute ventricular arrythmias (esp post-MI) and in digitalis- induced arrhythmias.

Toxicity: local anesthetic. CNS stimulation/ depression, cardio depression

22

Class IC antiarrhythmics

Drugs: flecainide, propafenone

- No effect on AP duration. Useful in vent tachycardias that progress to VF and in intractable SVT. Usually used only as last resort in refractory tachyarrythmias. For pts w out structural abnormalities
- Toxicity: proarrhythmic, esp post-MI (contraindicated). Significantly prolongs refractory pd in AV node

23

Class II antiarryhtmics (Beta blockers)

Mechanism

Drugs: metoprolol, propranolol, esmolol, atenolol, timolol

MoA: decreases SA & AV nodal activity by decreasing cAMP, decreases Ca currents. Suppress abnormal pacemakers by decreasing slope of phase 4. AV node= particularly sensitive; increases PR interval

- Esmolol= very short acting

24

Class II antiarryhtmics (Beta blockers)

Use & Toxicity

Use: vent tachycardia, SVT, slowing ben rate during A fib and A flutter

Toxicity: impotence, exacerbation of asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). May mask signs of hypoglycemia. Metoprolol can cause dyslipidemia. Tx overdose w glucagon. Propranolol can exacerbate vasospasm in Prinzmetal's angina

25

Antiarrhytmics- K+ channel blockers (class III)

(drugs & mechanism)

Drugs: Amiodarone, Ibutilide, Dofetilide, Sotalol
Mnemonic : AIDS

MoA: increases AP duration, increases ERP. Used when other antiarrhythmics fail. Increases QT interval

25

Antiarrhytmics- K+ channel blockers (class III)

(drugs & mechanism)

Drugs: Amiodarone, Ibutilide, Dofetilide, Sotalol
Mnemonic : AIDS

MoA: increases AP duration, increases ERP. Used when other antiarrhythmics fail. Increases QT interval

26

Antiarrhytmics- K+ channel blockers (class III)

(Toxicity)

- Sotalol: torsades de pointes, excessive Beta block
- Ibutilide: torsades
- amiodarone: pulm fibrosis, hypo/ hyperthyroidism (amiodarone is 40% iodine by weight), corneal deposits, skin deposits (blue/ gray) resulting in photo dermatitis, neuro effects, constipation, cardio effects (bradycardia, heart block, CHF)
**amiodarone has class I, II, III, and IV effects b/c it alters lipid membrane
**Remember to check PFTs, LFTs, and TFTs, when

26

Antiarrhytmics- K+ channel blockers (class III)

(Toxicity)

- Sotalol: torsades de pointes, excessive Beta block
- Ibutilide: torsades
- amiodarone: pulm fibrosis, hypo/ hyperthyroidism (amiodarone is 40% iodine by weight), corneal deposits, skin deposits (blue/ gray) resulting in photo dermatitis, neuro effects, constipation, cardio effects (bradycardia, heart block, CHF)
**amiodarone has class I, II, III, and IV effects b/c it alters lipid membrane
**Remember to check PFTs, LFTs, and TFTs, when using amiodarone

27

Class IV antiarrhythmics (CCBs)

Drugs: verapamil, diltiazem

MoA: decreases conduction velocity, increases ERP, increases PR interval. Used in prevention of nodal arrhythmias (e.g. SVT)

Toxicity: constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)

28

Other antiarrhythmics

Adenosine: increases K+ out of cells-> hyper polarizing the cell and decreases intracellular Ca. Drug of choice in Dx/ abolishing supraventricular tachycardia. Very short acting (~ 15 sec). Toxicity includes flushing, hypotension, chest pain. Effects blocked by theophylline and caffeine.

Mg+2: effective in torsades de pointes & digoxin toxicity