Cardiology Meds

• Diuretics
• Sympatholytics
• ACE Inhibitors
• Angiotensin
• II Receptor Blockers (ARB)
• Calcium Channel Blockers (CCB)
• Additional Drugs

• Beta-Blocker (Non-selective)
• blocks beta-1 receptors of heart-->decreases HR/contractility--> decreases BP.  (May also blocks beta-2 receptors of lungs)

• Main uses:hypertension, angina, cardiac arrhythmias, post
• myocardial infarction, hyperthyroidism

• ADR’s:Cardiac effects: bradycardia, heart failure, Bronchoconstriction(problem for asmatics)  CNS:depression, insomnia, nightmares Inhibit glycogenolysis of liver and muscle, hypoglycemia(tell diabetes pt to look for other signs of hypoglycemia), Tired or fatigue(transient)
• (CNS ones and sexual dysfunction will go away w/time) 

• Interactions with calcium channel blockers (also suppress cardiac function)
• Precautions:Diabetes-blocks early warning signal of hypoglycemia(tachycardia) and promotes hypoglycemia, Cardiac disease, Asthma/COPD

Monitor HR & BP

Beta-Blocker (Non-selective)blocks beta-1 receptors of heart-->decreases HR/contractility--> decreases BP.  (May also blocks beta-2 receptors of lungs)

Main uses:hypertension, angina, cardiac arrhythmias, postmyocardial infarction, hyperthyroidism

• ADR’s:
• Cardiac effects: bradycardia, heart failure, Bronchoconstriction(problem for asmatics)  CNS:depression, insomnia, nightmares Inhibit glycogenolysis of liver and muscle, hypoglycemia(tell diabetes pt to look for other signs of hypoglycemia), Tired or fatigue(transient)(CNS ones and sexual dysfunction will go away w/time) 

Interactions with calcium channel blockers (also suppress cardiac function)

Precautions:Diabetes-blocks early warning signal of hypoglycemia(tachycardia) and promotes hypoglycemia, Cardiac disease, Asthma/COPD

Monitor HR & BP

Beta-blockers (Selective)

Mechanism of action: blocks only beta-1 receptors of heart --> decrease BP (decreases HR)

No bronchoconstriction at lower doses (so okay for asthmatics to a degree; may lose selectivity at higher doses)

Does not inhibit glycogen breakdown (so okay for diabetics)

• Beta-blockers (Selective)
• Mechanism of action: blocks only beta-1 receptors of heart --> decrease BP (decreases HR)

No bronchoconstriction at lower doses (so okay for asthmatics to a degree; may lose selectivity at higher doses)

Does not inhibit glycogen breakdown (so okay for diabetics)

Alpha/Beta blockers

Mechanism of action: blocks alpha-1 receptors of vessels and beta receptors (beta 1&2) of heart-->decrease BP

Main use: hypertension

Main ADR: orthostatic hypotension(b/c alpha 1-->vasodilation); slow HR

 Do not use for asthmatics (b/c beta 2)

First dose response- Give at bedtime

Alpha/Beta blockers

Mechanism of action: blocks alpha-1 receptors of vessels and beta receptors (beta 1&2) of heart-->decrease BP

Main use: hypertensionMain

ADR: orthostatic hypotension(b/c alpha 1-->vasodilation); slow HR 

Do not use for asthmatics (b/c beta 2)

First dose response-Give at bedtime

Alpha-1 Blockers

Main use: Hypertension and BP

ADR’s: Hypotension, Nasal congestion(use alpha agonist which is vasoconstrictor), Sexual dysfunction (retrograde ejaculation)

First dose response-take at bedtime

• Alpha-1 Blockers
• Main use: Hypertension and BP

ADR’s: Hypotension, Nasal congestion(use alpha agonist which is a vasoconstrictor), Sexual dysfunction (retrograde ejaculation)

First dose response-take at bedtime

Alpha-2 agonist (centrally acting)

Mechanism of action: stimulates alpha-2 receptors in CNS-->suppress SNS-->decrease BP (b/c norepinephrine)

Main use: hypertension

ADR’s: Rebound hypertension (avoid by discontinuing slowly), Drowsiness, Fatigue(dont operate heavy mech), dry mouth(hard candy), constipation, impotence

Can be very sedating (take at bedtime)

change patch every 7 days

HTN crisis- give orally

0.1-0.2 mg

ACE inhibitors

Mechanism of action: block ACE -->decrease production of angiotensin II -->decrease BP

Main uses: Hypertension, Heart failure,To decrease mortality after MI, Diabetic and non-diabetic renal disease, Prevent MI/stroke/death in those at high risk

• ADR’s:Dry hacking cough (~ 5%, most common reason to d/c and start ARBS instead), First-dose hypotension, Hyperkalemia(can cause arrhythmias), Renal failure (okay to use if one kidney), Angioedema-rare but potentially fatal
• **swelling of tongue and face medical emergency- stop meds, give Benedryl, steroid, or epinephrine, and never give ACE inhibitor or ARBS again.

Drug interactions: Drugs that lower BP, Drugs that increase potassium, Lithium

Contraindications: Dont use in pregnancy 

Monitor K

stay hydrated- dehyrdation can cause renal failure

dont take salt substitute b/c na=K-->hyperkalemia

For microalbuminemia in diabetes

ACE inhibitorsMechanism of action: block ACE -->decrease production of angiotensin II -->decrease BP

Main uses: Hypertension, Heart failure,To decrease mortality after MI, Diabetic and non-diabetic renal disease, Prevent MI/stroke/death in those at high risk

ADR’s:Dry hacking cough (~ 5%, most common reason to d/c and start ARBS instead), First-dose hypotension, Hyperkalemia(can cause arrhythmias), Renal failure (okay to use if one kidney), Angioedema-rare but potentially fatal

**swelling of tongue and face medical emergency- stop meds, give Benedryl, steroid, or epinephrine, and never give ACE inhibitor or ARBS again.

Drug interactions: Drugs that lower BP, Drugs that increase potassium, Lithium

Contraindications: Dont use in pregnancy 

Monitor K

stay hydrated- dehyrdation can cause renal failure

dont take salt substitute b/c na=K-->hyperkalemia

For microalbuminemia in diabetes

ACE inhibitors

Mechanism of action: block ACE -->decrease production of angiotensin II -->decrease BP

Main uses: Hypertension, Heart failure,To decrease mortality after MI, Diabetic and non-diabetic renal disease, Prevent MI/stroke/death in those at high risk

ADR’s:Dry hacking cough (~ 5%, most common reason to d/c and start ARBS instead), First-dose hypotension, Hyperkalemia(can cause arrhythmias), Renal failure (okay to use if one kidney), Angioedema-rare but potentially fatal

**swelling of tongue and face medical emergency- stop meds, give Benedryl, steroid, or epinephrine, and never give ACE inhibitor or ARBS again.

Drug interactions: Drugs that lower BP, Drugs that increase potassium, Lithium

Contraindications: Dont use in pregnancy

 Monitor K

stay hydrated- dehyrdation can cause renal failure

dont take salt substitute b/c na=K-->hyperkalemia

For microalbuminemia in diabetes

Angiotensin II Receptor Blockers (ARBS)

blocks the actions of angiotensin II 

Main use: hypertension and heart failure

• ADR’s: Hyperkalemia (less than ACEI), Angioedema, Renal
• failure(can give if have one kidney)

Dont use in pregnancy

Monitor K and SrC, urinalysis, albumin, bilirubin

Given when cough is seen in ACE inhibitors

Angiotensin II Receptor Blockers (ARBS)

blocks the actions of angiotensin II 

Main use: hypertension and heart failure

ADR’s: Hyperkalemia (less than ACEI), Angioedema, Renalfailure(can give if have one kidney)

Dont use in pregnancy

Monitor K and SrC, urinalysis, albumin, bilirubin

Given when cough is seen in ACE inhibitors

CCA act on peripheral vascular smooth muscle (VSM) and heart (slows HR and decreases BP) (acts like beta blockers)

Block calcium channels of VSM --->vasodilation -->decrease in BP

Block calcium channels of heart that regulate heart muscle, pacemaker of SA node, and conduction through AV node-->decrease in heart rate and conduction-->decrease in BP

• Main uses: Hypertension, Angina, Cardiac
• dysrhythmias

ADR’s: Constipation, Hypotension, Bradycardia (if HR slows too much put on another agent)

Drug interactions: Digoxin(also has cardiac effects), Verapamil(may increase digoxin levels), Beta-blockers(also decrease HR and conduction)

Dont give to HF pts b/c can worsen HF

CCA act on peripheral vascular smooth muscle (VSM) and heart (slows HR and decreases BP) (acts like beta blockers)

Block calcium channels of VSM --->vasodilation -->decrease in BP

Block calcium channels of heart that regulate heart muscle, pacemaker of SA node, and conduction through AV node-->decrease in heart rate and conduction-->decrease in BP

Main uses: Hypertension, Angina, Cardiacdysrhythmias

ADR’s: Hypotension, Bradycardia (if HR slows too much put on another agent)

Drug interactions: Digoxin(also has cardiac effects), Verapamil(may increase digoxin levels), Beta-blockers(also decrease HR and conduction)

Dont give to HF pts b/c can worsen HF

Mechanism of action: blocks calcium channels of VSM-->vasodilation-->decreases BP (doesn't slow HR)

Main uses: Hypertension, Angina

ADR’s: Reflex tachycardia- combined with a beta- blocker to counteract (r/t barocepter), Hypotension, Edema(duiretics sometimes used), 



Monitor weight (b/c edema)

Mechanism of action: blocks calcium channels of VSM-->vasodilation-->decreases BP (doesn't slow HR)

Main uses: Hypertension, Angina

ADR’s: Reflex tachycardia- combined with a beta- blocker to counteract (r/t barocepter), Hypotension, Edema(duiretics sometimes used),

Dilates arterioles only

Main use: hypertensive crisis

3rd or 4th line 

ADR’s: Lupus-like syndrome(joint pain, fever, monitor CBC), Reflex tachycardia- combine with a beta-blocker

MOnitor CBCS (infection)

Lupus like syndrome goes away after drug is stopped

Dilates arterioles only

• Use: severe hypertension refractory to safer drugs, topical
• minoxidil (Rogaine®) is used to promote hair growth

ADR’s: Hypertrichosis(hair growth), Significant water/retention (combine with diuretic), Reflex tachycardia (combine with a beta-blocker)

dilates arterioles and veins 

Main use: hypertensive crisis

similar to nitroglycerin

• ADR’s: Rarely, cyanide poisoning can occur(usualy if used for sign. amount of time).  More common
• in liver disease.  Infuse slowly and coadminister
• thiosulfate.

Fasting acting hypertensive available

can decrease BP quickly

Can only be on for 24 hours

Antedote= Sodium Thiocyanate

ACEI’s, ARB’s, CCB’s, low dose diuretics

ACEI’s, ARB’s

beta-blockers, ACEI’s, potassium-sparing diuretic

thiazide diuretics

Beta-blockers, ACE inhibitors less effective

beta-blockers or thiazide diuretics

Treats Angina Pectoris

Primary mech. of action: directly dilates veins--> decreases venous return to heart and ventricular filling (preload)-->decreases oxygen demand of heart (lowers BP and vasodilates) 

Effective; fast-acting; inexpensive

ADR’s: (all due to vasodilation) Headache(take tylenol), Orthostatic hypotension,Tachycardia

Important drug interactions: Antihypertensives, Viagra®

• for long-term prophylaxis:
• Sustained-release
• oral tablets/capsules
• Transmucosal tablets
• Topical ointments
• Transdermal
• IV administration (when nothing else works)

Do slow to avoid vasospasm

intermittent schedule that allows at least 8 hours of drug-free hours each day

Should use lowest effective dose 

for acute attacks and prophylaxis prior to exertion:

• Sublingual tablets
• Translingual spray
• Transmucosal tablets

Drugs that inhibit RAAS:ACE Inhibitors, ARBS, Aldosterone, antagonists (spironolactone)

Beta-blockers(selective)

Diuretics

Inotropic agents: Digoxin

Used for Heart Failure

Inotropic agent

• Mechanism of action: increases force of ventricular
• contractions-->increases CO-->decreases signs and symptoms of CHF.

A cardiac glycoside

• Main uses: Second-line drug for heart failure(Used with
• ACEI’s, beta-blockers, diuretics if inadequate response),Dysrhythmias(A-fib)

Most significant ADR: cardiac dysrhythmias (Most commonly due to hypokalemia from diuretic use)

Theraputic level= <1 but up to 2 (low TI so monitor)

mortality associated with women

used to treat arrhythmia but can also cause

• Non-cardiac ADR’s (which usually precede cardiac
• dysrhythmias):
• GI:anorexia, nausea, vomiting
• CNS: fatigue, visual disturbances (blurred vision, yellow-tinged vision, halos around objects)

drug interactions:Thiazide and loop diuretics (cause hypokalemia which may increase digoxin level)

Extreme overdose: give Digibind

Used for HR

Inotropic Drugs

Mechanism: a catecholamine that activates receptors of sympathetic nervous system

• oBeta-1 receptors in heart- increases CO
• oDopamine receptors in kidney, 
• oAlpha-1 of vessels at high doses

Main use: rescue drug for severe heart failure

Administered: only IV, constant monitoring

Inotropic Drug

Mechanism: a synthetic catecholamine that activates only beta-1 receptors

Main use: rescue drug for severe heart failure

• oHMG-CoA Reductase Inhibitors (“Statins”)
• oBile-Acid Sequestrants
• oNicotinic Acid
• oFibrates
• oOthers: Ezetimibe (Zetia®)

Used for hypercholesterolemia (to reduce cholestrol)

Mechanism of action: inhibit HMG- CoA reductase in liver to decrease cholesterol synthesis à liver cells make more enzyme and more LDL receptors -->more LDL removed from blood

Reduces LDL, VLDV and increases HDL

ADR:Hepatotoxicity, Myositis, Rhabdomyolysis

DO NOT use in pregnancy (cat X)

monitor LFT, AST, ALT (b/c hepatotoxicity), monitor CK or CPK(b/c rhabdomyolysis)

Keep hydrated

Used for hypercholesterolemia (to reduce cholestrol)

Mechanism of action: inhibit HMG- CoA reductase in liver to decrease cholesterol synthesis à liver cells make more enzyme and more LDL receptors -->more LDL removed from blood

Reduces LDL, VLDV and increases HDL

ADR:Hepatotoxicity, Myositis, Rhabdomyolysis

DO NOT use in pregnancy (cat X)

monitor LFT, AST, ALT (b/c hepatotoxicity), monitor CK or CPK(b/c rhabdomyolysis)

Keep hydrated

Bile-acid sequestrant

• Mechanism of action: bind to bile acids in gut and prevent
• reabsorption-->liver makes more bile acids out of LDL-->liver increases LDL receptors--> increases LDL uptake -->decreases LDL

Main use: decrease LDL (want LDL <100)

• ADR’s: Limited to GI tract: constipation, gas, cramping
• No systemic effects because not absorbed 
• **Interfere with absorption of fat-soluble vitamins(A,E,K)

Dont work as well as statins-use if not too high choles. or cant take statin

*Give at separate time than other meds b/c binds to other meds

Bile-acid sequestrant

Mechanism of action: bind to bile acids in gut and preventreabsorption-->liver makes more bile acids out of LDL-->liver increases LDL receptors--> increases LDL uptake -->decreases LDL

Main use: decrease LDL (want LDL <100)

• ADR’s: Limited to GI tract: constipation, gas, cramping
• No systemic effects because not absorbed
•  **Interfere with absorption of fat-soluble vitamins(A,E,K)

Dont work as well as statins-use if not too high choles. or cant take statin

*Give at separate time than other meds b/c binds to other meds

Bile-acid sequestrant (newer)

Mechanism of action: bind to bile acids in gut and preventreabsorption-->liver makes more bile acids out of LDL-->liver increases LDL receptors--> increases LDL uptake -->decreases LDL

Main use: decrease LDL (want LDL <100)

• ADR’s: Limited to GI tract: constipation(causes less than older BS), gas, cramping
• No systemic effects because not absorbed

Dont work as well as statins-use if not too high choles. or cant take statin

*Give at separate time than other meds b/c binds to other meds

Has fewer drug interactions than older BS

• Mechansim of action: decreases production of VLDL by
• decreasing fat breakdown in adipose tissue-->decreases LDL

Uses:Decreases LDL and VLDL; increases HDL

CommonADR’s: Flushing/itching of skin( pre-treat with aspirin), Nausea/vomiting,diarrhea *Hepatotoxic,*Hyperglycemia

Monitor AST, ALT (b/c hepatatoxicity), Blood Sugar(hyperglycemia)*careful in diabetic pts

Cheap!

Can increase Uric acid *monitor gout pts

Fibrate

Mechanism of action: activate PPARs of liver and adipose which leads to increased clearance of VLDLs (triglycerides) and increased formation of HDL

Uses:Most effective drugs for lowering triglycerides (dont use to decrease LDL)

Common ADR: rash, nausea diarrhea

Significant but less common ADR’s: Gallstones, Myopathy--> rhabdomyolysis and hepatotoxicity

Drug interactions: Statins (also associated with myopathy)

Fibrate

Mechanism of action: activate PPARs of liver and adipose which leads to increased clearance of VLDLs (triglycerides) and increased formation of HDL

Uses:Most effective drugs for lowering triglycerides (dont use to decrease LDL)

Common ADR: rash, nausea diarrhea

Significant but less common ADR’s: Gallstones, Myopathy--> rhabdomyolysis and hepatotoxicity

Drug interactions: Statins (also associated with myopathy)

Fibrate

Mechanism of action: activate PPARs of liver and adipose which leads to increased clearance of VLDLs (triglycerides) and increased formation of HDL

Uses:Most effective drugs for lowering triglycerides (dont use to decrease LDL)

Common ADR: rash, nausea diarrhea

Significant but less common ADR’s: Gallstones, Myopathy--> rhabdomyolysis and hepatotoxicity

Drug interactions: Statins (also associated with myopathy)

New class of drug for high cholesterol

• Mechanism of action: inhibits cholesterol absorption in small
• intestine

Uses:Decreases LDL, Decreases triglycerides, Increases HDL

ADR’s: Well-tolerated

diploplia, tachycardia, HA, hungry, sweating, tingling or numbness, weakness, trouble sleeping, aggitation

below ~70 is considred low