Cardio Flashcards
Essential HTN
Antihypertensive therapy
Drugs: diuretics, ACE inhibs, ARBs, CCBs
See Renal for more info about diuretics, ACE inhibs & ARBs
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
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
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
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
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.
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.
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
Nitrates
antianginal therapy affecting preload
EDV: decreased BP: decreased Contractility: Increased (reflex response) HR: increased (reflex response) Ejection time: decreased MVO2: decreased
Beta blockers
antianginal therapy affecting after load
EDV: increased BP: decreased Contractility: decreased HR: decreased Ejection time: increased MVO2: decreased
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
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
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)
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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)
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
