Class Drug MOA Indication Pharmacokinetics Route of Adverse effects Notes

administration

Class I (Na channel Quinidine and Slows Broad spectrum Cinchonism (tinnitis, -​ Use
blockers) procainamide depolarization and headaches) for quinidine dependence
Rhythm control Class 1a conduction velocity Significant toxicity -​ Low effect on
Decrease slope of Can cause prolonged QT conduction
phase 0 velocity
Widens QRS -​ Mid binding
complex
Lidocaine Membrane Post MI acute Never given orally IV or IM -​ CNS effects can -​ 0 effect on
Class 1b stabilizing agents ischemic ventricular because of high first cause convulsions conduction
Binds to open or arrhythmias pass effect and the -​ CVS depression velocity
inactivated Na Emergency metabolites are -​ allergies -​ Fast on-off
channels conditions CARDIOTOXIC speed
-​ Use
dependence
-​ More use when
used in
ventricular
tachyarrythmias
-​ Low binding

Felcainide Both ventricular and High risk of proarrythmia -​ Strong binding

Class 1c supraventricular do not use in patients with to Na channels
arrhythmia structural heart diseases -​ Huge effect on
conduction
velocity slows it
down

Class II (Beta blockers) Metoprolol Heart rate Tachyarrythmias Can cause AV block due to its Negative inotropy
Rate control controlling (mainly effects on it (contractility)
Acts to block the supraventricular) Negative dromotropy
sympathetic post-MI prophylaxis (conductivity)
activation of the SA Negative chronotropy
and AV nodes not (automaticity)
muscles
Reduces adenylate
cyclase which
reduces cAMP,
which closes
calcium channels
Class Drug MOA Indication Pharmacokinetics Route of Adverse effects Notes
administration

Prolongs PR
mainly bc it affects
AV more

Class III (potassium Amiodarone Prolongs phase 2 Shares actions of Very long half life Oral or IV Hypo or hyperthyroidism Get baseline CXR, PFT,
channel blockers) and 3 class I,II, III, IV Lipophilic, hates Pulmonary fibrosis LFT. TFT
Rhythm control Slows Broad spectrum of staying in the blood Neuropathy
repolarization action Needs a loading Liver toxicity Patient must be
Increases EFP Iodine containing dose Nausea hospitalized for a week at
(because it’s thyroxine analogue 6 weeks without least
essentially most of loading dose to see
the repolarization) effect
Increases QT
Ibutilide NORMAL QRS Acute conversion to IV
It affects phases and chronic
Dofetilide 2-3 aka maintenance of Oral
repolarization it will sinus rhythm in afib
slow down the
potassium
channels

Class IV (calcium Verapamil RATE CONTROL Converting AV

channel blockers) Delay AV node nodal reentry to
non-dihydropiridines Diltiazem conduction normal sinus
Rate control Decrease rhythm
contractility of the Rate control in
heart CHRONIC atrial
Prolong PR fibrillation (like class
III)
Prevention of PSVT

Class V Adenosine Transient block in Acute Very short half life IV injection Hypotension
AV nodal supraventricular 15 seconds saline flush Flushing
conduction tachycardia Angina-like chest pain
Significant
systemic
vasodilation
 Antihypertensives
Class Drug MOA Indication pharmacokinetics Adverse effects Notes

Diuretics Hydrochlorothiazide DCT First line agents of primary Hyperuricemia They will also stimulate
True thiazide Blocking NaCl HTN Hypokalemia due to prostaglandin synthesis locally
transporters, keeping Na Normal renal function increased absorption of to vasodilate the systemic
Chlorthalidone and Cl in the filtrate Longer half life hypokalemia in the CD blood vessels and decrease
Natriuresis but only 5% Less safety Hypotension the PVR
But they will fail at one point so
Loop diuretics Thick AL Fluid retention states such as you have to combine with
Furosemide Block the NaClK heart failure pulmonary edema another drug like a RAAS
transporter keeping all of renal failure inhibitor
these in the filtrate NO NSAIDS
25%

Spironolactone Aldosterone receptor Resistant hypertension

antagonists Aldosteronism (aldosterone
Eplerenone 1-2% increases Na absorption so it No hypokalemia in K+
causes hypertension) sparing
Amiloride ENaC blockers
1-2% Add on only to another diuretic
Triamterene Particularly if patient has
hypokalemia

RAAS ACE inhibitors Inhibition of conversion of First line in HTN Enalapril is a prodrug Hyperkalemia (due to Contraindicated in pregnancy
inhibitors Captopril and enalapril angiotensin I to inhibition of aldosterone
angiotensin II by ACE Especially in patients with HF bc no angiotensin) C/I In bilateral renal artery
and post MI (its an anti-heart stenosis ( it will dilate the
failure drug) Hypotension efferent arteriole where the
ACE breaks down flow is already very low, it will
bradykinin (a vasodilator), Use in diabetic patients and Dry cough due to low make it worse)
but when we inhibit ACE, CKD but not ESRD bradykinin (switch to
bradykinin will build up and ARBs) C/I End stage renal disease
cause edema It dilates the efferent arteriole, (GFR is already low, this will
which takes some of the load Angioedema decrease it even more)
off of the kidney, making it
nephroprotective

Candesartan Angiotensin receptor Hyperkalemia

inhibitor
Valsartan But no dry cough or
angioedema
Class Drug MOA Indication pharmacokinetics Adverse effects Notes

Ca channel Nifepidine (old school) Block L-type calcium For black patients this is a Headache
blockers Amlopidine (better) channels in SMOOTH first-line, may have natriuretic Edema
muscle, no effect on heart effect but we use a diuretic Constipation
anyway Hypotension

A-adrenergic Prazosin Blocks a1 receptors in the Mild-moderate HTN First dose Can cause orthostatic
blockers vascular smooth muscle, phenomenon hypotension, since we
blocking sympathetic HTN + BPH (relaxes detrusor are decreasing the BP
innervation leading to muscle treating the symptom Start with a smaller by vasodilating, all the
relaxation,vasodilation , only) dose and at bedtime blood will pool in the
decrease in PVR, and peripheral tissues
decrease in overall blood NOT MONOTHERAPY!! which can cause
pressure Combine with beta blocker dizziness and it is a fall
risk
However the decrease in
BP will cause a reflex Reflex tachycardia
tachycardia so use it with a combine with
B2 blocker betablocker

B1 adrenergic Atenolol Negative inotropy, -​ Firstline only in Dont use in asthma Rebound HTN
blockers (cardioselective) dromotropy, and patients with and COPD Angina in CAD patients
chronotropy → decrease comorbidities following sudden
Carvedilol (non CO and BP specifically heart stopping
selective b1/b2 blocker) diseases like HF
JG cells are innervated by -​ Selectivity is lost with Bradycardia
B1, so it causes inhibition high doses for Sexual dysfunction
of rennin atenolol, so it might Insomnia
cause the asthma and Hypotension
Decrease in PVR inhibits all those side effects
RAAS -​ Abrupt discontinuation
leads to rebound HTN
and angina in CAD
patients

Sympatholytic Clonidine A2 agonist, which is a -​ Resistant HTN -​ Rebound HTN

s presynaptic receptor that
inhibits sympathetic effects
Methyldopa Pregnancy
Preferred for hypertension in
pregnancy
 Class Drug MOA Indication pharmacokinetics Adverse effects Notes

Direct Hydralazine Promotes K+ efflux by Acute emergency HTN Short half life Reflex tachycardia
vasodilators activating more K+ Use betablocker
channels to cause a
hyperpolarization and Lupus-like syndrome
prevent opening of L type
calcium channels
In the vascular smooth
muscle cell
More effect on arterioles
than veins bc we have
more muscles there
In HTN emergency: use nitroprusside its an NO donor, infuse continuously, immediate onset of action but 1-2 min duration
Labetalol is an a/B receptor blocker give IV injection or infusion it has a slower onset of action but longer duration

Anti-anginal drugs

Class Drug MOA Indication Pharmacokinetics Adverse effects Notes

Nitrates Nitroglycerin Induce vasodilation Acutely for symptomatic Nitroglycerin has a fast Postural hypotension and All nitrates are absolutely
predominantly in systemic veins relief of stable IHD angina onset of action fainting is common contraindicated with
sublingually, but only PDE5 inhibitors such as
Increases VD in all coronary Transdermal during the works for 25 mins, use Throbbing headache is common, sildanefil (viagra).
vessels (no coronary steal) nighttime multiple times in ACS be careful with patients with
Very high first pass migraines (mainly in They both work on
Stenotic, healthy, epicardial, and Prinzmetal or variant metabolism so we take it nitroglycerin) iincreasing cGMP, so we
intracoronary collaterals angina sublingually will have excess cGMP
Flushing and excess vasodilation
Nitrates provide NO, which Oral and transdermal PDE5 inhibitors inhibit
activates guanylyl cyclase, forms have longer It can have a small effect on phosphodiesterase 5,
which will convert GTP to cGMP durations of action, arterial vasodilation, so we can which will break down
cGMP will activate protein transdermal is get reflex tachycardia (use a cGMP and reduce
kinase G, which will activate specifically for patients beta blocker) smooth muscle relaxation
phosphatase which will remove with nighttime symptoms
the phosphate from the myosin
Isosorbide light chains and relaxes the Chronic maintenance of Highest duration of Blood vessels can
mononitrate muscle symptoms action needs to be taken become desentisized to
only once a day vasodilation by nitrates,
(dinitrate needs to be so we need to provide a
Class Drug MOA Indication Pharmacokinetics Adverse effects Notes

taken 3 times a day) nitrate-free interval of

Long bioavailability and about 10-12 hours it can
long duration of action be at night, or late in the
due to stability against afternoon for patients
hepatic breakdown with variant angina

We can reevaluate the

regiment and maybe add
beta blockers or CCB

Beta blockers Atenolol b1 Reduce myocardial oxygen Use with nitrates to selective and non
selective consumption by decreasing HR mitigate compensatory selective;
(negative chronotropy) and tachycardia C/I in
decreasing myocardial Vasospastic angina
contractility (inotropy) and Severe bradycardia
afterload
propanolol b1/b2 C/I in Severe asthma and
selective Reduce frequency and severety COPD (acts on B2
of anginal attacks and improve receptors and cause
exercise duration and tolerance bronchospasm)

PVD

CCB Non Induce coronary vasodilation to Variant angina Can cause coronary steal
dihidropyridine and increase coronary blood flow
dihydropyridine Avoid in patients with heart
Reduce myocardial oxygen failure and condiction blocks
consumption by decreasing (decreases Ca influx, which
contractility and afterload prolongs PR and also delays AV
node conduction because it
slows down phase 0)

Sodium channel Ranolazine Explained below Add on therapy to We use a sustained Can cause constipation and QT
blocker Selective inhibition of late traditional antianginal release preparation prolongation but we dont worry
sodium current agents about this unless the patient alr
Improves myocardial function has QT syndrome or is taking
and perfusion, no effect on HR, another drug that can prolong
or BP QT
Newer generation, not available everywhere.
Late vs early Na+ current: during phase 0 we have opening of the Na+ channels and we start getting influx of Na+ and it is a very rapid one, but once it gets to that
positivity it starts slowing down, and giving us those inactivated forms of the Na+ channel because we want to stop the Na+ entry at this point.
So there is the very rapid and big Na+ current, and then later on, we start having the slow Na+ current. Under normal circumstances, this late Na+ current is not
big (< 5% of Na+ influx).
The problem with IHD is that there is some sort of abnormality on the Na+ channels that they start expanding the late Na+ current, so you continue to have more
Na+.
So the Na+/Ca2+ exchanger starts working --> Na+ out, Ca2+ in.
There is something called Ca2+ stunning, where you get so much overload of that Ca2+ onto the heart, and then we get more contractility, but is that needed in
IHD? No, because we need to rest the heart.
Ranolazine is a drug that was discovered to inhibit this late Na+ current, by doing so, it has no effect on heart rate/blood pressure, it has no effect other than
rejecting this increased Ca2+ entry and thus, reducing the workload on the heart
 Anti lipids
Class Drug MOA Indication Pharmacokinetics Adverse effects Notes

HMG CoA Atorvastatin Inhibit hepatic cholesterol 1st line in patients Excellent absorption Hepatotoxicity, get a baseline LFT Patients with pre-existing
reductase Rosuvastatin synthesis by inhibiting the rate with elevated LDL with oral administration because we will inevitably get an hepatic impairment are not
inhibitors (hydrophilic) limiting enzyme HMG CoA increase in ALT and AST contraindicated to use
(statins) High to moderate reductase C/I in pregnancy and First pass hepatic statins, but we have to
intensity breastfeeding and metabolism This drug is elimated via liver, so manage intensity as they
Long half life Which decreases VLDL due to low children if we screw up the liver, the drug are more susceptible to
intrahepatic cholesterol, Simvastatin and will accumulate in it and we will adverse effects
decreasing the mobility of Can be used in renal lovastatin are prodrugs, have more liver damage then
cholesterol insufficiency but may meaning they need the more accumulation and it’s a Using another drug that
need to adjust the liver to be functional to vicious cycle causes hepatic impairment
Simvastatin Liver will compensate by trying to dosage be activated, but they is bad
(lipophilic) and upregulate LDL receptors and are hepatotoxic which Myopathy will occur in some
lovastatin have increase internalization of them, can cause them to patients, they will experience Doing a LFT every month is
moderate to low therefore it removes LDL from accumulate muscle pain and cramping but it not indicated bc it isnt cost
intensity blood, decreasing its is generally tolerated effective, just do it if the
Both pro drugs concentration Dysfunctional liver can patient starts showing S&S
cause accumulation of However dont let it get to of hepatic impairment like
Low LDL = low total cholesterol the drug rhabdomyolysis which is muscle jaundice
and TG disintegration. Test CK if you are
excretion = bile and suspecting rhabdo (dark tea
Fluvastatin It can also decrease TG but not as feces but also through coloured urine) Discontinue in patients with
(extended release much as LDL urinary. Don’t worry too intolerable symptoms of
formulation) much about renal More common in patients with myalgia, if resolved,
Can decrease HDL but not too disease patients unless advanced age, renal insufficiency, resume at a lower dose
much it’s end stage hypothyroidism, or D-D with a different statin
interactions Hydrophilic statins
Can have anti-atherosclerotic and (rosuvastatin) are better
anti-inflammatory effects tolerated than lipophilic
statins (simvastatin)
Exclude other causes of
muscle pain such as
hypothyroidism and vit D
deficiency before
rechallenging statins
Try alternative dosing
strategies like dosing every
other day or using statins
with longer half lives like
atorvastatin and
rosuvastatin
Class Drug MOA Indication Pharmacokinetics Adverse effects Notes

Consider non-statin therapy

in case of multiple failures

Niacin Reduced TG, VLDL, and LDL by Combination therapy Intense cutaneous flushing and
10-20% of pruritis
hypercholesterolemia -​ Pretreat with aspirin or
Inhibits lipolysis in adipose tissue, , NSAIDs to reduce
which decreases FFA in the blood hypertriglyceridemia, intensity (it’s PG
→ less cholesterol taken up by and low HDL mediated so NSAIDs will
liver → lower VLDL decrease it)
-​ Tolerance develops
Mostly increases HDL, most within a few days
effective agent for that.
Hepatotoxicity, especially with
It also increases secretion of tPa, extended release formulations
which decreases plasma
fibrinogen, and reverses some Inhibits tubular secretion of uric
endothelial cell dysfunction and acid, thus, predisposes to
atherosclerosis hyperuricemia and gout

Fibrates Gemfibrozil Induce the expression of capillary Hypertriacylglycerole Completely absorbed Myopathy Do not use with statins due
endothelial cell associated LPL, mias after oral dose to overlapping side effect of
thus clears TG-rich lipoproteins GI disturbances (gallstones) myopathy
like VLDL and chylomicrons C/I in pregnant and Extensive hepatic
nursing metabolism
Increases HDL by increasing
expression of apo AI and apo AII

Little or no effect on LDL

Bile acid binding Cholestyramine Resin that binds to bile acids in Familial Extensive hepatic Constipation (ur pooping bile Safe drug, can use in
resins the intestine, preventing its hyperlipidemias metabolism acids) pregnancy
reabsorption
Nausea Statins must be given 1
This will lead the liver to convert hour before or 4 hours after
more cholesterol into bile acids Flatulence resins, why? Because
statins decrease the
Low cholesterol will lead to formation of cholesterol,
upregulation of LDL receptors in which is needed to produce
Class Drug MOA Indication Pharmacokinetics Adverse effects Notes

the liver to take up LDL from the the bile acids that the resin
blood will bind to

Causing a modest reduction in

LDL and total plasma cholesterol
13-20%

Ezetimibe Prevents absorption of dietary and

biliary cholesterol, reducing
hepatic cholesterol pool

Results in compensatory increase

in LDL receptors, increase in
removal of LDL from the blood

Can reduce LDL by about 20% as

monotherapy

PCSK9 mAbs against PCSK9 enzyme, Used with maximally

modulating increase LDL-R recycling to the tolerated statins in
therapies cell surface, which increases high risk patients
removal of LDL form the blood unable to reach
desired LDL levels
Reduce LDL as much as 60% with a statin alone
when added to therapy with
background of statins