Cardiovascular Flashcards
Diuretics, ACE inhibitors (cause for COUGH), angiotensin II receptor blockers (ARBs), calcium channel blockers
Essential Hypertension
Diuretics, ACE inhibitors, angiotensin II receptor blockers, beta-blockers, K+-sparring agents
CHF
ACE inhibitors, angiotensin II receptor blockers, diuretics, calcium channel blockers, beta-blockers, alpha-blockers
Diabetes mellitus
Use them cautiously in decompensated CHF
Contraindicated in cardiogenic shock
Beta-blockers
They are protective against diabetic neuropathy
ACE inhibitors
Block voltage-dependent L-type calcium channels
cardiac and smooth muscle
HTN, angina, arrhythmias, Prinzmetal’s angina, Raynaud’s
Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation
Calcium channel blockers
Nifedipine, verapamil, diltiazem, amlodipine
Tissue where:
amlodipine = nifedipine > diltiazem > verapamil
Vascular smooth muscle
Tissue where:
verapamil > diltiazem > amlodipine = nifedipine
Heart muscle
Causes smooth muscle relaxation due to increased cGMP
Arterioles > veins
(afterload reduction)
Severe HTN, CHF
1st line: HTN in pregnancy
Compensatory tachycardia, fluid retention, nausea, headache, angina, lupus-like syndrome
Hydralazine
Add methyldopa for HTN in pregnancy
Add beta-blocker to prevent reflex tachycardia
Direct release of NO increases cGMP
Malignant HTN
S.E. Cyanide toxicity at large doses
Nitroprusside
D1 receptor agonist
coronary, peripheral, renal, splanchnic vasodilation
Decreases BP (vasodilation) so used for Malignant HTN via
Increases Na+ loss
Fenoldopam
Nitroprusside, nicardipine, clevidipine, labetalol, fenoldopam
Malignant HTN
Release NO in smooth muscle
Increases cGMP
Veins >> arteries
(decreased preload)
Angina, pulmonary edema
Reflex tachycardia, hypotension, flushing, headache, Monday disease
Nitroglycerin,
Isosorbide dinitrate
Dizziness, tachycardia (reflec to NO dilation effects), headache
Loss of tolerance over weekend
Develop tolerance during work week
Monday disease
Due to nitroglycerin reexposure at beginning of work week.
These are determinants of what?
End-diastolic volume, blood pressure, heart rate, contractility, ejection time
Myocardial O2 consumption
Contraindicated in angina
(2)
Partial beta-agonists
Pindolol, acebutolol
Which Calcium Channel Blocker (CCB) is similar to:
Nitrates
and
beta-blockers
Nifedipine - nitrates
and
Verapamil - beta-blockers
Effects of nitrates:
EDV
BP
Contractility
HR
Ejection time
MVO2
EDV - decrease
BP - decrease
Contractility - increase (reflex)
HR - increase (reflex)
Ejection time - decrease
MVO2 - decrease
Effects of beta-blockers:
EDV
BP
Contractility
HR
Ejection time
MVO2
EDV - increase
BP - decrease
Contractility - decrease
HR - decrease
Ejection time - increase
MVO2 - decrease
Combined nitrates and beta-blockers reduce what?
(3)
BP, HR, MVO2 (greatly)
Inhibit conversion of HMG-CoA to mevalonate
Greatly reduces LDL
Slightly increases HDL
Hepatotoxicity, rhabdomyolysis (muscle breakdown)
HMG-CoA reductase inhibitors
Lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin
Reduces hepatic VLDL secretion
Inhibits lipolysis in adipose tissue
Greatly increases HDL
Decrases LDL
Red, flushed face, hyperglycemia, hyperuricemia
Niacin
(Vit B3)
Flushing reduced by aspirin
Hyperglycemia may cause acanthosis nigricans
Prevent intestinal reabsorption of bile acids
(Liver uses cholesterol to make more bile)
Decreases LDL
Bad taste, GI discomfort, malabsorption of fat-soluble vitamins, cholesterol gallstones
Bile acid resins
Cholestyramine, colestipol, colesevelam
Prevents cholesterol reabsorption
at small intestine brush border
Decreases LDL
Rare hepatotoxicity, diarrhea
Cholesterol absorption blockers
Ezetimibe
Upregulates lipoprotein lipase (LPL)
(Increases triglyceride clearance)
Greatly reduces triglycerides
Myositis, hepatotoxicity, cholesterol gallstones
Fibrates
Gemfibrozil, clofibrate, bezafibrate, fenofibrate
Inhibits Na+/K+ ATPase
indirectly inhibits Na+/Ca2+ antiport
increases Ca2+ in cells (positive inotropy)
Stimulates vagus nerve to decrease HR
CHF, atrial fibrillation
Cardiac glycosides
Digoxin
CHF - increases contractility
A fib - decreases conduction at AV, depresses SA
Drug causes
Increased PR interval, decreased QT, ST scooping, T-wave inversion, arrhythmia, AV block
Can lead to hyperkalemia
Exceted in urine
Renal failure, hypokalemia (allows binding), quinidine (displaces from tissue binding sites):
Increase toxicity
Digoxin
Nausea, vomiting, diarrhea, blurry yellow vision
(Cholinergic effects)
Treatment for OD?
Digoxin
Normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments, MG2+
Local anesthetics
Slow or block conduction
Decrease slope of phase 0
Increase threshold for firing in abnormal pacemaker cells
Hyperkalemia increases toxicity
Class I antiarrhythmics
Na+ channel blockers
Increases:
AP duration, effective refractory period, QT interval
For both atrial and ventricular arrhythmias
esp reentrant and ectopic SVT, VT
Thrombocytopenia, torsades de pointes
Class IA : “PRO QUIN DI”
Quinidine, procainamide, disopyramide
Quin - cinchonism, headaches, tinnitus
Pro - reversible SLE syndrome
Diso - heart failure
Decreases:
AP duration
Preferentially affects ischemic/depolarized Purkinje and ventricular tissue
Acute ventricular arrhythmias (post-MI), digitalis induced arrhythmias
CNS stimulation/depression, cardiovascular depression
_Class IB: _“I‘d Buy Liddy’s funny (Pheny) Mexican Tacos”
Lidocaine, Mexiletine, Tocainide
No effect on AP duration
V-tach that progresses to V-fib, intractible SVT
Prolongs refractory period in AV node
Contraindicated with structural abnormalities, MI
Proarrhythmic
Class IC: “For Pushing Extasy”
Flecainide, propafenone
Class 1 A, IB and IC (Na+ blockers)
Mneumonic:
“Police Department Questions (Class 1A-AP increases)- The Little Man (Class 1B-AP decreases) - For Pushing Extasy (Class 1C-No change in AP)”
Decreases cAMP, Ca2+ current in SA, AV nodes
Decreased nodal activity, esp AV node (inc. PR)
Decreases phase 4 in abnormal pacemakers
V-tach, SVT
Slows ventricular rate in A-fib and A-flutter
Impotence, bradycardia, AV block, CHF, CNS depression
Class II: Beta-blockers
Metoprolol, propranolol, esmolol, atenolol, timolol
Metoprolol- dyslipidemia (Tx: glucagon)
Propranolol- vasospasm in Prinzmetal’s angina
Esmolol- very short acting
Which class II antiarrhythmic can exarcerbate
vasospasm in Prinzmetal’s angina?
Propranolol
Increases AP duration, QT interval
Increases effective refractory period
Used when other antiarrhythmics fail
Class III: K+ channel blockers
Amiodarone, ibutilide, dofetilide, sotalol
(AIDS)
Toxicity of:
Sotalol, Ibutilide
Sotalol - torsades de pointes, excessive beta-block
Ibutilide - torsades de pointes
Toxicity of:
Amiodarone
Which function tests?
Why does it have class I, II, III and IV effects?
Pulmonary fibrosis, hepatotoxicity, hypo/hyperthyroidism
Corneal, skin deposits, photodermatitis
neurologic effects, constipation
bradycardia, heart block, CHF
Check PFTs, LFTs, TFTs
40% iodine by weight
Amiodarone alters the lipid membrane
Decreases conduction velocity
Increases effective refractory period, PR interval
Prevents nodal arrhythmias (SVT)
Constipation, flushing, edema, CHF, AV block, sinus node depression
Class IV: Ca2+ channel blockers
Verapamil, diltiazem
Increases K+ outflow
Hyperpolarizes cell, decreases Ca2+ in
(Na+/Ca2+ antiport)
Abolishes SVT (first line)
Very short acting (15 seconds)
Flushing, hypotension, chest pain
What blocks all effects? (2)
Adenosine
Effects blocked by theophylline and caffeine
For torsades de pointes, digoxin toxicity
Mg2+