Class: Statin (PCKS9 Inhibitors) o High Intensity: Atorvastatin (Lipitor), Rosuvastatin (Crestor)

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PHARMACOLOGY FOR CARDIO CAT:

General Guidance:

- For each medication CLASS, know: mechanism of action, indications for use, contraindications
for use, MOST COMMON side effects.
- Names of examples of medications under this class are listed. You DO NOT need to know details
(such as dosing) of these medications, but you DO need to be able to recognize them as
belonging to a certain class. Choose to commit the GENERIC drug names to memory rather than
brand names.
- Think about which clinical situations you might use each drug class/medication. Most
pharmacology questions are clinical case-based.

_____________________________________________________________________________________

- Class: Statin (PCKS9 inhibitors)


o High intensity: Atorvastatin (Lipitor), Rosuvastatin (Crestor)
 MOA: decrease cholesterol production, increase the LDL receptor
 Indications: based off ASCVD, past HD, peripheral vascular disease, primary
elevations of LDL >190, diabetics, 45-75 10-year risk score of 7.5% = best drug to
decrease LDL
 Atorvastatin (40-80mg)
 Rosuvastatin (10-40 mg) (~63% reduction, most potent)
 Strong>Least RAP SLP F
 Goal is 50% reduction, not actual number level
 Contraindication: CYP-34A metabolizers, Gemfibrozil, fibrates
 Common Side Effects: myopathies, algias (muscle soreness & rhabdo)
o Moderate and low intensity statins: will be a prefix + “statin”

- Class: Niacin
o Vitamin B-3
 MOA: has antihyperlipidemic effects, can decrease the release of free-fatty acids
from adipose tissue, can increase HDL, can reduce triglycerides, total cholesterol
and LDL
 Indications: best drug to increase HDL, give aspirin, or NSAID prior may
decrease flushing
 Contraindications: take @ bedtime w/ food, not to be used w/ acute gout or
unexplained abdominal pain or GI symptoms
 Common Side Effects: flushing, nausea, vomiting, increased blood glucose
(hyperglycemia)

- Class: Bile Acid Sequestrants


o “Questrans”, Colestipol, Colesevelam
 MOA: binds to bile salts in intestine preventing reabsorption and producing an
insoluble complex which is excreted in the feces, leads to an increase of LDL
receptors collecting LDL from blood stream
 Indication: hyperlipidemia, heterozygous familiar hypercholesterolemia, DM
type 2
 Contraindication: caution if baseline fasting triglyceride levels >300 mg/dL,
discontinue if triglyceride >400, history of bowel obstruction, history of
hypertriglyceridemia-induced pancreatitis
 Common Side Effects: constipation, abd pain, nausea

- Class: Fibrates
o Gemfibrozil, fenofibrate, clofibrate
 MOA: activates peroxisome proliferator-activated-receptor-alpha and decreases
VLDL levels. Total plasma triglycerides reduced by 30-60%, may increase HDL
10-15%
 Indications: hyperlipidemia, best drug to decrease triglycerides
 Contraindications: don’t give w/ anticoagulant & stains (may potentiate effect
of them), must monitor INR closely, severe renal disease
 Common Side Effects: GI upset, rash, dizzy, enhanced formation of gallstones,
myositis syndrome of myalgia, weakness, malaise, and possibly elevated CK
levels

- Class: Thiazide diuretics


o Hydrochlorothiazide (multiple brand names, not important)
o Chlorthalidone (Thalitone)
 MOA: usually well tolerated and affects BP by inhibiting Na+/Cl- reabsorption @
distal tubule
 Indication: treatment of choice as initial therapy in uncomplicated HTN,
cardioprotective, CHF, edema, African-Americans
 Contraindications: Gout patients & diabetic patients, SULFA ALLERGIES
 Common Side Effects: hypokalemia, metabolic alkalosis, hyperuricemia,
hyponatremia, hyperglycemia, weakness/fatigue

- Class: ACE-inhibitors
o All drug names in this class will end in “-pril”
 MOA: impairment and decreased synthesis of angiotensin-converting enzyme
(ACE)  generating angiotensin II. Will decrease preload/afterload. Also
promotes the degradation of natural vasodilator bradykinin (thus results in an
accumulation of bradykinin)
 Indication: HTN, lowering BP w/ little change in CO or HR (HTN especially if
history of diabetes, nephropathy, CHF, or post MI) (renoprotective!)
 Contraindications: don’t give in pregnancy!
 Common Side Effects: cough, hypotension, hyperkalemia
- Class: Angiotensin Receptor Blockers (ARB)
o All drug names in this class will end in “-sartan”
 MOA: AIIT1 receptor antagonists interferes w/ the renin-angiotensin system.
(AT1 is responsible for vasoconstriction, aldosterone release, renal Na+
reabsorption and sympathetic NS stimulation) ARBs inhibit all these. Don’t raise
bradykinin levels!
 Indications: HTN, CHF, those who cannot tolerate BB or ACEi. Use w/ thiazide for
enhanced BP lowering effects
 Contraindications: don’t give in pregnancy!
 Common Side Effects: hypotension, hyperkalemia

- Class: Beta blockers


o All drugs in this class end in -lol
o Cardio-selective (B1 antagonists) (AMEN BB)
 Metoprolol, Esmolol, Atenolol, Bisoprolol
 MOA: decrease CO, HR & Contractility by binding to specific B-1
adrenergic receptors, decreases post MI remodeling, decreases renin
secretion, decrease myocardial oxygen demand
 Indications: rate control for atrial flutter/atrial fibrillation, PSVT, v-tach,
post MI prophylaxis, +/- PVCs, HTN, tachyarrhythmias, CHF, acute MI,
migraine prophylaxis, aortic dissection
 Contraindications: try and avoid use w/ CCBs, caution in diabetic
patients (masks signs of hypoglycemia), sinus bradycardia, 2/3 rd degree
heart blocks, shock, decompensated CHF
 Common Side Effects: bradycardia, fatigue, depression, AV blocks, CNS
dysfunction
o Non-selective beta antagonists
 Carvedilol, labetalol + all other beta blockers
 Similar as above, however non-specific so may have more widespread
side-effects, less cardio specific (ex: bronchospasms)

- Calcium Channel Blockers


o CCB that affect cardiac conduction (HR) [non-dihydropyridines]
 Verapamil
 Diltiazem
 MOA: impede influx of Ca2+ through membrane channels in cardiac and
smooth muscle cells therefore affect cardiac contractility & conduction
(negative intropes), vasodilation
 Indications: African-American, HTN, Cocaine-induced myocardial
infarction (variant angina/ prinzmetal) Raynaud’s, angina, atrial
arrhythmias (a-flutter/a-fib) PSVT
 Contraindications: caution w/ use w/ beta-blockers, CHF, 2/3 rd degree
heart blocks
 Common Side Effects: Verapamil = constipation, hypotension, dizzy, h/a

o CCB without cardiac conduction effect


 Nifedipine
 Amlodipine
 MOA: potent vasodilators w/ little or no effect on cardiac contractility or
conduction
 Rest is similar as above^, less worried about cardiac side effects w/
these

- Class: Loop diuretics


o Furosemide (Lasix)
 MOA: inhibit water transport across the loop of Henle  increase excretion of
water, NA+, Cl+, K+
 Indications: STRONGEST CLASS OF DIURETICS, HTN, CHF, hypercalcemia, severe
edema, mild renal disease
 Contraindications: Sulfa-allergies!
 Common Side Effects: volume depletion, hypokalemia/natremia/calcemia,
hyperglycemia, ototoxicity

- Class: Potassium-sparing diuretics


o Spironolactone
o Triamterene
 MOA: aldosterone antagonist, potassium sparing
 Indications: ADDED to other therapy in severe CHF, associated w/ decreased
mortality
 Contraindications: not given <30 CrCl (or renal failure), hyponatremia
 Common Side Effects: hyperkalemia, gynecomastia

- Class: Direct vasodilators


o Hydralazine
o Sodium nitroprusside
 MOA: arterial (hydralazine) & venous dilation (SNP) via activation of cGMP
(sodium NP)
 Indications: HTN emergencies, CHF
 Contraindication/Side Effects: (hydralazine = Drug Induced Lupus) (sodium
nitroprusside = Cyanide toxicity)
- Class: Nitrates
o Nitroglycerin
o Isosorbide dinitrite or mononitrite
 MOA: nitrates activate guanylyl cyclase  increase cyclic guanosine
monophosphate and subsequent decreases in cytosolic free calcium. Leads to a
decrease in preload by venodilation and afterload via arterial dilation. Increases
myocardial blood supply
 Indications: angina, ACS, pulmonary edema, HF, HTN emergencies, vasospastic
disorders
 Contraindications: phosphodiesterase-5 inhibitors (tadalafil, sildenafil), systolic
BP <90
 Common Side Effects: h/a, flushing, reflex tachycardia, hypotension

- Central alpha agonists


o Clonidine
 MOA: stimulates alpha-2 receptors, decrease sympathetic NS activity
 Indications: HTN, ADHD
 Contraindications/Side Effects: sedation, dry mouth, fatigue

- Class: Alpha blockers


o Drug names in this class end in -zosin
 MOA: stimulates alpha-1 blockade  vasodilation, relax prostate and bladder
neck
 Indications: HTN, BPH
 Common Side Effects: vasodilation on 1st dose w/ syncope, reflex tachycardia

- Class: DOACs (direct oral anti-coagulants)


o Know specific clinical circumstances about the three below:
 Rivaroxaban (no UFH lead-in)
 Dabigatran (Pradaxa) [not approved for VTE prevention]
 Edoxaban
 MOA: small molecule that binds to active enzymatic site of thrombin
(Dabigatran)
 Indication: treat and prevent DVT, PE, reduce risk of stroke and systemic
embolism in patient w/ nonvalvular a-fib, post-op thromboprophylacxis
 Contraindications: active bleeds, patients w/ mechanical heart valves
 Common Side Effects/Black Box: Spinal/Epidural hematomas, dyspepsia,
hemorrhage
 Other: Factor ‘Xa’ inhibiors Xa ban, MONITOR RENAL FXN prior to
initiation, gingival hemorrhage, anemia, bruise hematoma
- Class: Anticoagulants
o Know Mechanism of action/clinical indications for the drugs below:
 Heparin
 MOA: potentiates antithrombin III (inhibits conversion of fibrinogen 
fibrin)
 Indications: thrombosis, PE, DVT, PE/DVT prophylaxis, ACS, SAFE IN
PREGNANCY (does not cross placenta)
 Monitor: aPTT, intrinsic pathway, half-life= 30-60 minutes
 Contraindications: prior HIT, hemophilia, severe HTN, safer than LMWH
in kidney disease
 Common Side Effects: hemorrhage, hyperkalemia, osteoporosis
 Enoxaparin
 MOA: LMWH, inactivation of factor Xa, more-anti-Xa than UFH
 Indications: longer half-life = 12 hours, no need to monitor aPTT,
thrombosis, PE, coagulopathies, DVT, ACS, more predictable, less side
effects, and longer half-life than UHF
 Contraindications: RENAL FAILURE/Cleared, use caution, elderly, not as
easily reversible as UFH
 Common Side Effects: hemorrhage, anemia, thrombocytopenia,
osteoporosis, HIT LESS LIKELY!
 Argatroban
 MOA: binds and inhibits thrombin directly
 Indications: DVT/PE/a-fib, DRUG OF CHOICE for heparin-induced
thrombocytopenia (HIT)
 Contraindications: acute bleeds, renal dosing
 Common Side Effects: increased LFTs, abdominal pain
 Warfarin (Coumadin)
 MOA: inhibit vitamin-k dependent clotting factors II, VII, IX, X (2, 7, 9,
10)
 Monitor/Indications: PT/INR, extrinsic pathway, a-fib, mechanical valves
 Contraindications: don’t give in Pregnancy!, must be bridged w/ heparin
(see chart below), interacts w/ CYP450, inducers of CYP450 may
decrease warfarin levels

- Class: Inotrope
o Dobutamine
 MOA: synthetic analogue of dopamine, stimulates B-1, B-2 and alpha receptors
POSITIVE INOTROPE, increases renin-release, stimulates heart and kidney,
peripheral vasodilation
 Indications: CHF not associated w/ hypotension (Systolic CHF), stress testing,
great in emergency situations, short-term
- Class: Anti-arrhythmic – know mechanism of action of the different sub-classes of anti-
arrhythmic drugs
o Be more familiar with the following medications:
 Lidocaine
 MOA: decrease conduction velocity/shorten repolarization and shorten
AP
 Indications: Stable V-Tach
 Contraindications: narrow complex SVT
 S/E: NEUROTOXICITY, CNS
 Adenosine
 MOA: temporarily decrease SA nodal automaticity, SHORT HALF LIFE
 Indications: drug of choice for SVT, & narrow regular complex
tachycardia
 Contraindications: not used in atrial flutter, a-fib, or tachycardia not
caused by AV nodal reentry
 S/E: transient flushing, chest pressure
 Amiodarone
 MOA: Class III, K+ channel blocker, prolongs AP, QT prolongation
 Indications: Atrial/Ventricular Arrhythmias
 S/E: hepatotoxicity, pulmonary fibrosis
 Digoxin
 No benefit if there is GOOD/NORMAL ejection fraction
 MOA: Negative chronotrope, Positive inotrope
 Indications: heart failure w/ left ventricular systolic dysfunction, a-fib in
some patients (CHF w/ reduced contractility/CHF w/ A-fib)
 Contraindications: AMIODARONE!
 Common Side Effects: Hypokalemia exacerbates toxicity, N/V

1st line treatments for certain conditions

Stable Narrow Complex SVT

- Adenosine = 1st line, vagal maneuvers first


- AV nodal blockers 2nd line (BB, CCBs)

Stable Wide Complex V-Tach

- Amiodarone
- Procainamide if WPW suspected
Prevention ACS

- Aspirin/Clopidogrel

ACS

- MONAB

Multifocal Atrial Tachycardia

- CCB, Verapamil

Wolff-Parkinson White

- Stable: Procainamide
- Unstable: Cadiovert

Angina

- Nitroglycerin (except on sildenafil, or sys BP <90)


- B-Blockers (1st line for chronic mgmt)
- CCBs (Prinzmetal Angina)
- Aspirin (Prevents progression  ACS)

UA/NSTEMI

- Aspirin
- Clopidogrel
- GPIIb/IIIa inhibitors
- UFH
- LMWH
- Fondaparinux

Adjunctive

- BB
- Nitrates
- Morphine
- CCBs

Refractory Angina

- PCI/Stenting
- CABG (if LCA)
STEMI

- Reperfusion therapy (PCI/Thrombolytics! Most Important!)


- Antithrombotics
- Adjunctive Therapy
- Door  PCI ~90min
- Door  Lytics ~30min

Other

- ASA
- Anticoagulant
- BB
- Nitrate Therapy (can be drip in ER)

Heart Failure

- ACEi
- BBs (Both decrease mortality)
- Spironolactone (decreased mortality)

Consider

- ARBs (if no ACEi)


- Hydralazine + Nitrates (for African-Americans)
- Diuretics
- Positive Inotropes
o Digoxin
o Dobutamine
o Dopamine
- LMNOP
o Lasix
o Morphine
o Nitrates
o Oxygen
o Position

Acute Pericarditis

- NSAIDs
- Colchicine
- +/- Steroids
Pericardial Effusion

- Tx underlying cause
- +/- pericardiocentesis if tamponade or large effusion

Tamponade

- Pericardiocentesis ASAP

Constrictive Pericarditis

- Pericardiectomy = definitive

Dilated Cardiomyopathy

- Standard Heart failure = ACEi, diuretics, BB, Digoxin, ICD (EF<35%)

Restrictive Cardiomyopathy

- Treat underlying disorder

Hypertrophic Cardiomyopathy

- Surgical ICD placement!


- Beta Blockers 1st line!
- CCB
- Disopyramide
- (^ all increase Ventricular filling time)

If fails

Surgical Myomectomy

Rheumatic Fever

- Aspirin +/- steroids


- PCN-G/Erythromycin

Aortic Stenosis

- Surgical valve replacement (PAV) (AVR)

Aortic Regurgitation

Afterload reducers:

- ACEi
- ARBs
- Nifedipine
- Hydralazine

Definitive

- Surgical

Mitral Stenosis

- Surgical (Percutaneous balloon valvuloplasty)


- Repair/Replace (symptomatic)
- Loop diuretics/BB/Digoxin (A-fib)

Mitral Regurgitation

- Repair>replace
- Chronic Tx like CHF (ACEi/ARB/BB/Diuretics)

Hypertension

- Uncomplicated (no comorbidities)


o 1st Thiazide Diuretics
o ACEi
o ARBs
o CCBs
- Complicated
- A-fib = BB/CCBs
- Angina = BB/CCBs
- Post-MI = BB/CCBs
- Systolic Heart Failure = ACEi/ARB/BB/Diuretics
- Diabetes II/CKD = ACEi, ARB
- Osteoporosis = Thiazides
- African American = Thiazide/CCBs
- Young/White/Males = Thiazides/ACEi/ARB/BB
- Gout = CCBs

Hyperlipidemia

- Lowering LDL
o Statins, bile acid sequestrants
- Lowering Triglycerides
o Fibrates, Niacin
- Increasing HDL
o Niacin, Fibrates
- Type II Diabetes
o Fibrates, Statins
- Pregnancy
o Bile Acid Sequestrants
- Intestinal (Brush Boarder Cholesterol)
o Ezetimibe

Infective Endocarditis

- Acute
o Nafcillin/Gentamicin x 4 weeks
o Vanco if suspect MRSA
- Subacute
o PCN/Ampicillin + Gentamicin
- Prosthetic Valve
o Vanco + Genta + Rifampin
- Fungal
o Amph-B 6-8 weeks

Peripheral Arterial Disease

- Cilostazol (claudication)
- Asprin/Clopidogrel

Abdominal Aortic Aneurysm

- SURGURY
- Beta-Blockers (reduce shearing force)

Aortic Dissection

- Nitroprusside/BB pre-surgery (bring BP down fast SYS 100-120)


o Esmolol
o Labetalol
- Surgery (TYPE A)

DVT

- Heparin (UFH/LMWH)
- Warfarin
- What is the definition of hypertension?
o Normal = <120/80
o Elevated = 120-129/80
o Stage 1 = 130-139/80-89
o Stage 2 = >140 and/or >90

- Nuclear Imaging

o TC99= SPECT
 Lipophilic analogue
 Viewed moment of injection
 So there are no trends in viewing for viability purposes
o Tl201=potassium analogue
 During a stress test to see which areas after exercise showed uptake
abnormalities or ischemia. Myocytes should have equal concentrations 3-4
hours after. The ‘cold spots’ if any are fixed defects or infarcts
 Better perfusion into tissues
 Cold spots in infarcts

Blood Supply of the Conduction Systems of the Heart

- SA node
o RCA
- AV node
o RCA
- Bundle of His
o LAD (septal branches)
- Right Bundle Branch
o Proximal portion = LAD
o Distal portion = RCA
- Left Bundle Branch
o Left anterior fascicle = LAD
o Left posterior fascicle = LAD / PDA

Murmurs:

ASD

o Systolic ejection crescendo-decrescendo flow murmur @ pulmonic area (upper left


sternal border)
o Widely split S2
 Non-synchronous closure of A2 / P2 that does not vary with respirations
VSD

o MCC HARSH Holosystolic Murmur @ Lower Left Sternal Border


o Systolic thrill can be palpated over murmur

PDA

o MOST COMMON = Continuous Machine-Like Murmur


o Loudest @ pulmonic area

Congenital AS

o A2 to close after P2 “REVERSED SPLITTING”

Coarctation of Aorta

o Murmur that radiates to the back/scapula/chest

Tetralogy of Fallot

o Harsh holosytolic murmur @ left upper sternal border


o Right ventricular heave

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