Hypertensive drugs that are safe in pregnancy
Hydralazine, labetalol, methyldopa, nifedipine
Hypertensive drugs that at protective against diabetic nephropathy
ACE inhibitors and ARBs
Hypertensive drugs used with diabetes mellitus
ACE inhibitors/ARBs, CCBs, thiazide diuretics, B-blockers
Hypertensive drugs used in HF
Diuretics (spironolactone)
ACE inhibitors/ARBs
B-blockers (compensated HF)
Aldosterone antagonist
Hypertensive drug contraindicated in decompensated HF and cardiogenic shock
B-blockers
Primary hypertensive drugs
Thiazide diuretics
ACE inhibitors/ARBs
Dihydropyridine CCBs
Hypertensive drug that should be avoided in renal artery stenosis
Thiazide diuretics
CCBs that act on the heart
Non-dihydropyridines: dilitiazem and verapamil
CCBs that act on vascular smooth muscle
CANNN: Clevidipine Amlodipine Nifedipine Nimodipine Nicardipine
Dihydropyridine CCB not indicated for HTN
Nimodipine
Indicated for HTN, angina, and Raynaud phenomenon
Dihydropyridine CCBs (except nimodipine)
CCBs best for vascular smooth muscle
Amlodipine = nifedipine > dilitiazem > verapamil
CCBs best for heart
Verapamil > dilitiazem > amlodipine = nifedipine
CCBs MOA
Block voltage gated L-type Ca channels of cardiac and smooth muscle cells decreasing muscle contractility
CCB indicated for subarachnoid hemorrhage
Nimodipine - prevents cerebral vasospasms
CCB indicated for hypertensive urgency or emergency
Nicardipine and clevidipine
CCB indicated for HTN, angina, and atrial fibrillation/flutter
Non-dihydropyridines verapamil and diltiazem
CCBs that cause cardiac depression, AV block, hyperprolactinemia, constipation
Non-dihydropyridines
CCBs that cause peripheral edema, flushing, dizziness, gingival hyperplasia
Dihydropyridines
Hypertensive used for severe HTN, HF with organic nitrate and safe to used during pregnancy
Hydralazine
Frequently co-administered with hydralazine to prevent reflex tachycardia
B-blocker
When is hydralazine contraindicated
Angina and CAD
Hypertensive that causes compensatory tachycardia, fluid retention, headache, angina, Lupus-like syndrome
Hydralazine
D1 receptor agonist used for hypertensive emergency
Fenoldopam
B-blocker used for hypertensive emergency
Labetolol
CCB blocker used for hypertensive emergency
Clevidipine and Nicardipine
Nitrite used for hypertensive emergency
Nitroprusside
D1 receptor agonist used in hypertensive emergency that causes coronary, peripheral, renal, and splanchnic vasodilation
Fenoldopam
Antihypertensive used postoperatively that can cause hypotension and tachycardia as side effects
Fenoldopam
Short-acting antihypertensive that increases cGMP via direct release of NO
Nitroprusside
Can cause cyanide toxicity
Nitroprusside
Cause vasodilation by increasing NO in vascular smooth muscle leading to increased cGMP and smooth muscle relaxation
Nitrates
Effect of nitrates on vessels at low doses
Veins»_space; arteries leads to decreased preload
Effect of nitrates on vessels at higher doses
Arteries > veins leads to decreased afterload
Indications for nitrates
Angina, ACS, pulmonary edema
When are nitrates contraindicated
Right ventricular infarction
Biochemical precursor of nitric oxide
Arginine
Nitrate side effects
Reflex tachycardia, HoTN, flushing, headache and “Monday disease” in industrial exposure
Hydralazine MOA
Increase cGMP causing smooth muscle relaxation
Effect of hydralazine on vessels
Vasodilates arterioles > veins decreasing afterload
Exposure to nitrates at work causes tolerance to vasodilatory effects during work week and loss of tolerance over the weekend leading to tachycardia, dizziness, and headache upon re-exposure
Monday disease
Goal of antianginal therapy
Reduce myocardial O2 consumption by decreasing >1 of HR, BP, EDV and contractility
Drug given with nitrates to prevent reflex tachycardia
B-blockers
Effect of nitrates on cardiac function
EDV - decreased BP - decreased Contractility - no effect HR - increased (reflex tachycardia) Ejection time - decreased MVO2 - decreased
Effect of B-blockers on cardiac function
EDV - no effect or increased BP - decreased Contractility - decreased HR - decreased Ejection time - increased MVO2 - decreased
Effect of nitrates + B-blockers on cardiac function
EDV - no effect or decreased BP - decreased Contractility - little to no effect HR - no effect or decreased Ejection time - little to no effect MVO2 - greatly decreased
B-blockers that should be used with caution in angina
Pinodolol and acebutolol (partial B-agonists)
CCB that is similar to B-blockers in effect
Verapamil
Partial B-blockers
Pinodolol and acebutolol
What are the nitrates
Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate
Antianginal that inhibits the late phase of sodium current causing reduction in diastolic wall tension and O2 consumption without affecting contractility
Ranolazine
Indications for ranolazine
Refractory angina
Antianginal that causes constipation, dizziness, headache, nausea, and QT prolongation
Ranolazine
Selective PDE-3 inhibitor indicated for short-term use in acute decompensated HF
Milrinone
Milrinone side effects
Arrhythmias and hypotension
Milrinone MOA on cardiomyocytes
Increases cAMP causing Ca influx leading to increased inotropy and chronotropy
Milrinone MOA on vascular smooth muscle
Increases cAMP inhibiting MLCK and causing general vasodilation
Lipid lowering agents that causes myopathy when used with fibrates or niacin
Statins
Mechanism of statins
HMG-CoA reductase inhibitors
Cholesterol precursor that is inhibited by use of statins
Mevalonate
Effect of statins on CAD patients
Decreases mortality
Lipid lowering agent that causes hepatotoxicity
Statins
Lipid lowering agents that inhibit HMG-CoA reductase
Statins
Lipid lowering agent that causes decreased absorption of other drugs and fat soluble vitamins
Bile acid resins
Bile acid resin drugs
Cholestyramine
Colestipol
Colesevelam
Lipid lowering agent that prevents intestinal reabsorption of bile acids causing liver to use cholesterol to make more
Bile acid resins
Lipid lowering agent that slightly increases HDL and triglyceride levels with moderate decrease in LDL levels
Bile acid resins
Side effect of Bile acid resins
GI upset
Decrease absorption of drugs and fat soluble vitamins
Lipid lowering agent that causes rare increases in LFTs and diarrhea
Ezetimibe
Lipid lowering agent that prevents absorption at intestinal brush border
Ezetimibe
Lipid lowering agent with moderate decrease in LDL, minimal to no increase in HDL, and minimal to no decrease in triglyceride levels
Ezetimibe
Lipid lowering agent that can cause myopathies and cholesterol gallstones
Fibrates
Myopathy risk with fibrates is increased when used in combination with what other lipid lowering agents
HMG CoA reductase inhibitors (statins)
Side effect of Ezetimibe
Rare LFTs and diarrhea
Fibrate drugs
Gemrfibrozil
Bezafibrate
Fenofibrate
Lipid lowering agents with minimal decrease in LDL, minimal increase in HDL and marked decrease in triglyceride levels
Fibrates
Lipid lowering agents that activates PPAR-a to induce HDL synthesis
Fibrates
Lipid lowering agents upregulate LDL to increase triglyceride clearance
Fibrates
Side effect of fibrates
Myopathy (increased with statins) and cholesterol gallstones
Side effect of niacin
Flushing
Hyperglycemia
Hyperuricemia
Lipid lowering agent that increases risk of gout, diabetes, and can cause acanthosis nigricans
Niacin
Lipid lowering agents with moderate decrease in LDL, moderate increase in HDL, and minimal decrease in triglyceride levels
Niacin
Lipid lowering agents that inhibit lipolysis in adipose tissue and reduce hepatic VLDL synthesis
Niacin
Enzyme that is inhibited by niacin in order to inhibit lipolysis
Hormone-sensitive lipase
Drug taken to reduce flushing caused by niacin
NSAIDs
Best lipid lowering agent to take to decrease LDL and increase HDL
Niacin
Best lipid lowering agent to take to decrease LDL
Statins and PCSK9 inhibitors
Best lipid lowering agent to take to decrease triglycerides
Fibrates
Lipid lowering agents that cause myalgias, delirium, dementia, and other neurocognitive effects
PCSK9 inhibitors
Lipid lowering agents which inactivate LDL receptor degradation increasing removal of LDL from blood
PCSK9 inhibitors
Lipid lowering agents with marked decreases in LDL, minimal increases in HDL, minimal decreases in triglycerides
PCKSK9 inhibitors and HMG CoA reductase inhibitors
Cardiac glycoside that directly inhibits Na/K/ATPase
Digoxin
Digoxin MOA to increase intracellular Ca levels
Direct inhibition of Na/K/ATPase causing indirect inhibition of Na/Ca exchanger increasing intracellular Ca levels leading to positive inotropy
What are the two mechanisms of Digoxin
Direct inhibition of Na/K/ATPase leading to positive inotropy
Stimulates vagus causing decreased HR
Indications for digoxin
HF - increases contractility
A-fib - AV node conduction decreased and SA node depressed
Changes seen on ECG with digoxin
Increased PR, decreased QT interval and T-wave inversions
Digoxin side effects
Cholinergic effects, arrhythmias, AV block, hyperkalemia
Drugs that displace digoxin from tissue-binding sites and decrease its clearance
Verapamil, amiodarone, quinidine
Treatment for digoxin toxicity
- slowly normalize K
- cardiac pacemaker
- anti-digoxin Fab fragments
- give magnesium
Side effect of digoxin toxicity that indicates poor prognosis
Hyperkalemia
Predisposing factor for digoxin toxicity that decreases its clearance
renal failure
Predisposing factor for digoxin toxicity that is permissive for digoxin binding to K site on Na/K/ATPase
Hypokalemia
Class IA antiarrhythmic that causes headache and tinnitus
Quinidine
Class IA antiarrhythmic that causes reversible SLE-like syndrome
Procainamide
Class IA antiarrhythmic that cause HF
Disopyramide
Indicated for atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT
Class IA antiarrhythmics
Antiarrhythmic that can cause torsades de pointes
Class IA antiarrhythmics
Antiarrhythmics that increase AP, ERP, QT
Class IA antiarrhythmics
Antiarrhythmics that decrease AP, ERP, QT
Class IB antiarrhythmics
Class I antiarrhythmics with some potassium channel blocking
Class IA antiarrhythmics
Class I antiarrhythmic with minimal decrease on slope of phase 0
Class IB antiarrhythmics
Class I antiarrhythmic with marked decrease on slope of phase 0
Class IC antiarrhythmics
Antiarrhythmics with significant increase in ERP in AV node and accessory bypass tracts, no effect on ERP in Purkinje and ventricular tissue and normal AP duration
Class IC antiarrhythmics
Class I antiarrhythmics have the most effect on which phase of action potential
Phase 0
Which phase of myocyte action potential is not modulated by any antiarrhythmic
Phase 1 and Phase 4
Phase II (plateau phase) of myocyte action potential is blocked by which class of antiarrhythmics
Class IV (CCBs)
Antiarrhythmics indicated post-MI for acute ventricular arrhythmias and digitalis-induced arrhythmias
Class IB
Sodium channels are blocked by which class of antiarrhythmics
Class I antiarrhythmics
Antiarrhythmics that preferentially affect ischemic or depolarized Purkinje and ventricular tissue
Class IB antiarrhythmics
Anti-epileptic drug indicated for post-MI acute ventricular arrhythmias or digitalis-induced arrhythmias
Phenytoin
Anti-epileptic drug that can fall under Class IB antiarrhythmics
Phenytoin
Class I antiarrhythmics that can cause CNS stimulation or depression and cardiovascular depression
Class IB antiarrhythmics
Class IB antiarrhythmics
Lidocaine and Mexiletine
Class IC antiarrhythmics
Flecainide and Propafenone
Class I antiarrhythmic indicated for SVTs, including a-fib
Class IC antiarrhythmics
Class I antiarrhythmic used only as a last resort in refractory VT
Class IC antiarrhythmics
Antiarrhythmic contraindicated post-MI because of its pro-arrhythmic properties
Class IC antiarrhythmics
Mechanism of Class II antiarrhythmics
B-blockers
Effect of Class II antiarrhythmics on conductivity of the heart
Decrease SA and AV nodal activity by decreasing cAMP and calcium currents
Which phase of the pacemaker action potential is affected by Class II antiarrhythmics
Slope of phase 4 is depressed
Very short acting beta blocker
Esmolol
Which node is more sensitive to Class II antiarrhythmics
AV node causing increased PR interval
Antiarrhytmics indicated for SVT and ventricular control for a-fib and atrial flutter
Class II antiarrhythmics
Antiarrhythmics that cause exacerbation of COPD and asthma
Class II antiarrhythmics
Antiarrhythmics that cause impotence, sedation, and sleep alterations
Class II antiarrhythmics
Class II antiarrhythmic that can cause dyslipidemia
Metoprolol
Class II antiarrhythmics that can exacerbate Prinzmetal angina
Propranolol
Beta blockers that are safe to give alone for cocaine toxicity or pheochromocytoma
Carvedilol and Labetalol
Antiarrhythmics contraindicated in cocaine toxicity or pheochromocytoma because of unopposed a-agonism
Beta blockers (except carvedilol and labetalol)
Beta blockers that are non-selective alpha and beta antagonists
Carvedilol and Labetalol
Treatment for beta blocker toxicity
Glucagon, Atropine, Saline (GAS)
Drugs contraindicated with beta blockers due to worsening of HoTN and conduction abnormalities
TCAs
Class III antiarrhythmics
Amiodarone, Ibutilide, Dofetilide, Sotalol (AIDS)
Class III antiarrhythmics mechanism of action
Increase AP, ERP, an QT
Antiarrhythmics which increase AP, ERP, an QT by affecting phase 3
Class III antiarrhythmics
Antiarrhythmics with markedly prolonged repolarization
Class III antiarrhythmics
Class III antiarrhythmic indicated for ventricular tachycardia
Amiodarone and Sotalol
Indication for Class III antiarrhythmics
Atrial flutter and a-fib Ventricular tachycardia (Amiodarone and Sotalol only)
Class III antiarrhythmics that causes torsades de pointes and excessive beta blockade
Sotalol
Antiarrhytmics that can cause torsades de pointes
Sotalol, Ibutilide and Class IA antiarrhythmics
Antiarrhythmic with Class I, II, III, and IV effects
Amiodarone
What labs need to be drawn when using Amiodarone
PFTs, LFTs, and TFTs
Pulmonary side effect of Amiodarone
Pulmonary fibrosis
Endocrine side effect of Amiodarone
Hypo or hyperthyroidism
GI effect of Amiodarone
Hepatotoxicity
Skin effects of Amiodarone
Blue/gray skin deposits resulting in photodermatitis
Eye effects of Amiodarone
Corneal deposits
Cardiovascular effects of Amiodarone
Bradycardia, heart block, HF
Channels blocked by Class III antiarrhythmics
Potassium channels
Class IV antiarrhythmics
Diltiazem and Verapamil
Effect of Class IV antiarrhythmics on pacemaker action potential
Decrease conduction velocity, increased ERP, and PR interval
Antiarrhythmics that decrease conduction velocity, increased ERP, and PR interval of pacemaker action potential
Class IV antiarrhythmics
Antiarrhythmics indicated for prevention of nodal arrhythmias and rate control in a-fib
Class IV antiarrhythmics
Antiarrhythmics that cause constipation, flushing, edema, HF, AV block, and sinus node depression
Class IV antiarrhythmics
Class IV antiarrhythmics block which channels
Calcium channels
Drug of choice in diagnosing and terminating certain forms of SVT
Adenosine
Antiarrhythmic that decreases AV node conduction by increasing K out of cell causing hyperpolarization and decreased intracellular calcium
Adenosine
Duration of action of Adenosine
About 15 seconds
Adenosine receptor antagonist that blunt the affects of adenosine
Caffeine and theophylline
Antiarrhythmic that causes flushing, HoTN, CP, sense of impending doom and bronchospasms
Adenosine
Given for treatment of torsades de pointes and digoxin toxicity
Magnesium
Antiarrhythmic indicated for chronic stable angina in patients who cannot take B-blockers
Ivabradine
Antiarrhythmic indicated for reduced ejection fraction and chronic HF
Ivabradine
Antiarrhythmic that selectively inhibits I-funny channels, prolonging slow depolarization phase (phase 4)
Ivabradine
Antiarrhythmic that causes luminous phenomena or visual brightness, HTN and bradycardia
Ivabradine