Hypertension

Guidelines

JNC8-BP Goals ACC/AHA-BP Goals

Uncomplicated: <140/90 <65 years old: <130/80
Age >60: <150/90 >65 years old: SBP<130-no good evidence for diastolic in elderly
Diabetes Mellitus: <140/90 Diabetes/CKD: <130/80
Chronic Kidney Disease: <140/90 Other comorbidities: <130/80

Drug MOA Dose Adverse Effects Clinical Pearls

Hydrochlorothiazide Inhibits sodium 25-50mg/day Electrolyte imbalance Doses above 25mg/day
(HCTZ) reabsorption in the ↓K, Mg, Na offer no therapeutic
distal tubule 1st line in ↑Ca, uric acid benefit but increased
uncomplicated HTN can increase blood AE
alone or in combo glucose
C/I in anuria, severe Avoid if eGFR
electrolyte imbalance <30mL/min (decreases
Monitor: BP, electrolytes, efficacy since it works
renal function in the kidneys)
Chlorthalidone Inhibits sodium 12.5-25mg/day Electrolyte imbalance Doses above 25mg/day
reabsorption in the ↓K, Mg, Na offer no therapeutic
distal tubule Preferred thiazide due ↑Ca, uric acid benefit but increased
to prolonged t ½ can increase blood AE
Patients with low K and glucose
increased glucose C/I in anuria, severe ALLHAT trial
intolerance shows electrolyte imbalance recommends this
increased incidence of Monitor: BP, electrolytes, should be DOC for HTN
DM renal function

JC 1
 Lisinopril (Prinivil, Inhibits ACE to block 10-40mg/day Hypotension Not recommended to
Zestril) production of AT II Hyperkalemia use in AA due to higher
Inhibits breakdown of 1st line in Angioedema→AA pts risk of angioedema
bradykinin→ promote uncomplicated HTN ↑SCr
vasodilation alone or in combo in Dry cough-bradykinin Watch for cough
Dilates the efferent non-AA patients
arterioles C/I in renal artery
stenosis, pregnancy,
history of angioedema

Monitor: BP, SCr and K q

2-4 weeks
Enalapril (Vasotec) Inhibits ACE to block 5-40mg/day Hypotension Not recommended to
production of AT II Hyperkalemia use in AA due to higher
Inhibits breakdown of 1st line in Angioedema→AA pts risk of angioedema
bradykinin→ promote uncomplicated HTN ↑SCr
vasodilation alone or in combo in Dry cough-bradykinin Watch for cough
Dilates the efferent non-AA patients
arterioles C/I in renal artery
stenosis, pregnancy,
history of angioedema

Monitor: BP, SCr and K q

2-4 weeks

Losartan (Cozaar) Prevents angiotensin II 50-100mg/day Similar to ACE inhibitors Do not use in combo
from binding to AT I MAX 100mg for HTN with ACE inhibitors or
and AT II receptors direct renin inhibitors

AT I > AT II affinity

JC 2
 Valsartan (Diovan) Prevents angiotensin II 80-320mg/day Similar to ACE inhibitors
from binding to AT I
and AT II receptors

AT I > AT II affinity
Amlodipine (Norvasc) Inhibits calcium from 2.5-10mg/day Peripheral edema- dose- Superior to Lisinopril in
entering voltage MAX dose is 10mg for related AA patients for BP
sensitive areas of HTN Hypotension control and stroke
vascular smooth muscle Reflex tachycardia reduction
during depolarization 1st line alone or in
to relax smooth muscle combination no monitoring! *limit dose of
leading to vasodilation simvastatin when used
and reduced BP anti-angina effects concurrently with
amlodipine 10mg
Diltiazem (Cardizem) Blocks calcium channels Look it up for dosing it Bradycardia Avoid in patients with
in the heart, which comes in so many Hypotension heart failure with
Verapamil (Calan) slows action potential formulations Worsening HF reduced ejection
(Verelan) in cardiac tissue to slow Constipation (verapamil) fraction
heart rate and reduce 1st line alone or in
CO → reduce BP combo Substrates and
inhibitors of CYP3A4→
may increase
concentrations of other
substrates: simvastatin,
lovastatin,
carbamazepine,
cyclosporine,
tacrolimus
Atenolol (Tenormin) Inhibits stimulation of 25-100mg/day Bradycardia C/I: bradycardia, mild
SA node and inhibits Not 1st line Heart block to moderate asthma or
stimulation of Exercise intolerance

JC 3
 myocardium to Fatigue!!! COPD, hypotension
decrease both HR and May mask symptoms of (SBP <100)
contractility hypoglycemia
Abrupt discontinuation→
rebound HTN
Monitor: BP and HR no
labs

Metoprolol tartrate Inhibits stimulation of 100-200mg/day BID Bradycardia C/I: bradycardia, mild
(Lopressor) SA node and inhibits Heart block to moderate asthma or
stimulation of Exercise intolerance COPD, hypotension
myocardium to Fatigue!!! (SBP <100)
decrease both HR and May mask symptoms of
contractility hypoglycemia
Abrupt discontinuation→
rebound HTN

Monitor: BP and HR no
labs
Metoprolol succinate Inhibits stimulation of 50-200mg/day Bradycardia C/I: bradycardia, mild
(Toprol XL) SA node and inhibits Heart block to moderate asthma or
stimulation of Exercise intolerance COPD, hypotension
myocardium to Fatigue!!! (SBP <100)
decrease both HR and May mask symptoms of
contractility hypoglycemia
Abrupt discontinuation→
rebound HTN

Monitor: BP and HR no
labs

JC 4
 Propranolol (Inderal) Inhibits pulmonary Not used for HTN May exacerbate asthma C/I: bradycardia, mild
smooth muscle or COPD to moderate asthma or
relaxation COPD, hypotension
Monitor: BP and HR no (SBP <100)
labs
Carvedilol (Coreg) Prevents compensatory 12.5-50mg/day BID Bradycardia C/I: bradycardia, mild
vasoconstriction of Heart block to moderate asthma or
systemic vasculature→ Exercise intolerance COPD, hypotension
decreased BP Fatigue!!! (SBP <100)
May mask symptoms of
hypoglycemia
Abrupt discontinuation→
rebound HTN

Monitor: BP and HR no
labs
Labetalol (Trandate) Prevents compensatory 200-800mg/day BID Bradycardia C/I: bradycardia, mild
vasoconstriction of Heart block to moderate asthma or
systemic vasculature→ Exercise intolerance COPD, hypotension
decreased BP Fatigue!!! (SBP <100)
May mask symptoms of
hypoglycemia
Abrupt discontinuation→
rebound HTN

Monitor: BP and HR no
labs
Spironolactone Prevents reabsorption N/A Hyperkalemia If patients get
(Aldactone) of sodium in collecting Gynecomastia/impotence gynecomastia from
duct to work as Common add on Dizziness spironolactone- try
therapy and pts with HF eplerenone

JC 5
 diuretic—> water gets 5th line Monitor: BP, renal
excreted function, potassium
Prevents secretion of
K+
Aliskiren Direct renin inhibitor Not first line Hyperkalemia Do NOT use in combo
Renal dysfunction with ACE inhibitors or
Angioedema ARB
Hypotension
C/I in pregnancy and
bilateral renal artery
stenosis
Clonidine, methyldopa Alpha-2 agonists Last line due to CNS AE Dry mouth Methyldopa may be
Dizziness used in pregnancy!
Orthostatic hypotension
Drowsinesss
Rebound HTN if abruptly
d/c
Methyldopa- hepatitis,
hemolytic anemia (Rare)
Doxazosin, Prazosin, Alpha-1 blockers Fourth of fifth line First dose hypotension- Consider as 2nd line
Terazosin agent dose at bedtime with BPH patients
orthostatic hypotension Patients with PTSD
nightmares
Hydralazine, Minoxidil Direct arterial Reserved for resistant Sodium and water
vasodilator hypertension retention
Reflex tachycardia
Hirsutism (minoxidil)
Drug-induced lupus-like
syndrome (hydralazine)-
dose dependent

JC 6
 Dyslipidemia
Guidelines-ACC/AHA 2018
LDL-c lowering (dominant form of atherogenic cholesterol) Clinical ASCVD
-In clinical practice, absolute responses to statin therapy -In patients who are ≤75 years of age with clinical ASCVD, high-
depends on baseline LDL-c concentrations intensity statin therapy should be initiated or continued with
-A more reliable indicator of statin efficacy is percentage the aim of achieving ≥50% LDL reduction
reduction - In patients with clinical ASCVD in whom high-intensity statin is
-As a rough guide, a lowering of LDL-c level of 1% gives an contraindicated or who experience statin-associated side
approximate 1% reduction in ASCVD risk effects, moderate-intensity statin therapy
a. Healthy diet: 5-10% -In patients with clinical ASCVD on max tolerated statin and
b. Weight loss: 3-5% judged to be at very high risk with LDL-c ≥70 mg/dL, it is
c. Supplements: 4-10% reasonable to add ezetimibe therapy
Lifestyle modifications can reduce LDL-c by 12-25%!! - In patients with clinical ASCVD who are judged to be at very
high risk and considered for PCSK9 inhibitor, max tolerated LDL-
4 major Statin Benefit Groups lowering therapy should include max tolerated statin and
1. Clinical ASCVD (secondary) ezetimibe
2. LDL >190mg/dL - In patients with clinical ASCVD judged to be very high risk on
3. Diabetes (age 40-75) (LDL 70-189) max tolerated LDL-lowering therapy with LDL ≥70 mg/dL, it is
4. Age 40-75, LDL 70-189 mg/dL based on 10 year ASCVD reasonable to add PCSK9 inhibitor following a clinical-patient
risk discussion about the net benefit, safety, and cost.
*2-4 are all primary prevention - In patients with clinical ASCVD who are receiving max
tolerated statin therapy and LDL ≥70 mg/dL, it may be
Severe Hypercholesterolemia reasonable to add ezetimibe
-In patients 20 to 75 years old with LDL-c 190mg/dL or higher, - In patients >75 years with clinical ASCVD, it is reasonable to
maximally tolerated statin therapy is recommended initiate moderate- or high- intensity statin therapy after
evaluation of potential for ASCVD risk reduction, adverse
Diabetes Mellitus effects, and drug-drug interactions, as well as patient facility
-In adults 40 to 75 years old with DM regardless of 10-year and patient preferences
ASCVD risk, moderate intensity statin is indicated - In patients >75 years who are tolerating high-intensity statin,
it is reasonable to continue

JC 7
 -In adults with DM with multiple ASCVD risk factors, it is Based on ASCVD Risk
reasonable to prescribe high-intensity statin therapy with the -Low risk <5% → emphasize lifestyle modifications
aim to reduce LDL-c by >50% -Borderline risk <7.5% → if risk enhancer is present discuss
moderate intensity statin
Elderly Patients -Intermediate risk <20% → initiate moderate intensity statin
-In adults over 75 with LDL 70-189mg/dL, initiating a moderate- -High risk >20% → initiate statin to reduce LDL-c by 50% (high-
intensity statin may be reasonable intensity)
-In adults over 75 it may be reasonable to stop statin therapy
when functional decline, multimorbidity, fraility, or reduced
life-expectancy limits the potential benefits of statin therapy

Drug MOA Dose Adverse Effects Clinical Pearls

Atorvastatin (Lipitor) HMG-CoA reductase 1stline Muscle symptoms: Cornerstone of therapy
inhibitor → preventing myalgia, myopathy, in addition to healthy
body from producing High intensity: 40, 80mg rhabdomyolysis (rare) lifestyle interventions
more cholesterol Hepatotoxicity (rare)
Mod-intensity: 10,20mg Show reduced CV
C/I: pregnancy, active events and mortality
Long acting- does not liver disease
matter what time you Substrate of CYP3A4 –
take it ALS
Monitor: baseline labs-
lipid panel, liver Avoid gemfibrozil→
transaminase increased risk of
Follow up- lipid panel q myopathy
3 months

JC 8
 Simvastatin (Zocor) HMG-CoA reductase Mod-intensity: 20-40mg myalgia, myopathy, Cornerstone of therapy
inhibitor → preventing rhabdomyolysis (rare) in addition to healthy
body from producing Low intensity: 10mg Hepatotoxicity (rare) lifestyle interventions
more cholesterol
C/I: pregnancy, active Show reduced CV
In the evening- liver disease events and mortality
cholesterol is made at
night! Avoid gemfibrozil→ Cannot start anyone per
increased risk of FDA on simvastatin
myopathy 80mg → increased risks
of muscle damage
Monitor: baseline labs-
lipid panel, liver Max dose of 20mg with
transaminase concurrent amlodipine
Follow up- lipid panel q use of 10mg →major
3 months DDI

Substrate of CYP3A4

Rosuvastatin (Crestor) HMG-CoA reductase 1st line myalgia, myopathy, Cornerstone of therapy
inhibitor → preventing rhabdomyolysis (rare) in addition to healthy
body from producing High intensity: 20,40mg Hepatotoxicity (rare) lifestyle interventions
more cholesterol
Mod intensity: 5, 10mg C/I: pregnancy, active Show reduced CV
liver disease events and mortality

Avoid gemfibrozil→
Monitor: baseline labs- increased risk of
lipid panel, liver myopathy
transaminase Follow up- lipid panel q
3 months

JC 9
 Fluvastatin (Lescol) HMG-CoA reductase 1st line myalgia, myopathy, Cornerstone of therapy
inhibitor → preventing rhabdomyolysis (rare) in addition to healthy
body from producing Mod intensity: 40mg Hepatotoxicity (rare) lifestyle interventions
more cholesterol BID
XL-80mg C/I: pregnancy, active Show reduced CV
liver disease events and mortality
Low intensity: 20,40mg
Avoid gemfibrozil→
increased risk of
In the evening- myopathy
cholesterol is made at
night! Monitor: baseline labs-
lipid panel, liver
transaminase
Follow up- lipid panel q
3 months

Pravastatin (Pravachol) HMG-CoA reductase 1st line myalgia, myopathy, Cornerstone of therapy
inhibitor → preventing rhabdomyolysis (rare) in addition to healthy
body from producing Mod intensity: 40,80mg Hepatotoxicity (rare) lifestyle interventions
more cholesterol
Low intensity: 10,20mg C/I: pregnancy, active Show reduced CV
liver disease events and mortality
In the evening-
cholesterol is made at Avoid gemfibrozil→ Follow up- lipid panel q
night! increased risk of 3 months
myopathy

Monitor: baseline labs-

lipid panel, liver
transaminase

JC 10
 Pitavastatin (Livalo) HMG-CoA reductase 1st line myalgia, myopathy, Cornerstone of therapy
inhibitor → preventing rhabdomyolysis (rare) in addition to healthy
body from producing Mod intensity: 1-4mg Hepatotoxicity (rare) lifestyle interventions
more cholesterol *1mg is most well
tolerated for statin- C/I: pregnancy, active Show reduced CV
associated-muscle liver disease events and mortality
symptoms
Avoid gemfibrozil→ Only really used when
In the evening- increased risk of patient has failed every
cholesterol is made at myopathy other statin
night!
Monitor: baseline labs- Expensive but works
Follow up- lipid panel q lipid panel, liver well
3 months transaminase

Lovastatin (Mevacor) HMG-CoA reductase 1st line myalgia, myopathy, Cornerstone of therapy
inhibitor → preventing rhabdomyolysis (rare) in addition to healthy
body from producing Mod intensity: 40mg Hepatotoxicity (rare) lifestyle interventions
more cholesterol
Low intensity: 20mg C/I: pregnancy, active Show reduced CV
In the evening- liver disease events and mortality
cholesterol is made at
night! Avoid gemfibrozil→ Substrate of CYP3A4
increased risk of
myopathy

Monitor: baseline labs-

lipid panel, liver
transaminase
Follow up- lipid panel q
3 months

JC 11
 Ezetimibe (Zetia) Inhibits absorption of 10mg Very well tolerated Add on to further lower
cholesterol in the small LDL-c
intestine LDL lowering ~20% Low frequency of
diarrhea and abdominal
2nd line due to only pain
lowering by 20%
compared to statins *no reports of
>30% additional myalgia
when added to statin
Evolocumab (Repatha) PSCK9 inhibitor- inhibits 140mg SC q 2 weeks Very well tolerated Add on to statin
PCSK9 from binding to therapy for further LDL-
LDL-R → increased LDL- 420mg SC once/month Common cold, flu-like c reduction in
R for LDL uptake symptoms secondary prevention
one time use injection/ Injection site rxns Indications:
1x/month 1. Established CVD
2. Hyperlipidemia
LDL lowering ~ 3. Homozygous FH
additional 50%
Alirocumab (Praluent) PSCK9 inhibitor- inhibits Initial: 75mg SC q 2 Indications:
PCSK9 from binding to weeks 1. Established CVD
LDL-R → increased LDL- 2. Heterozygous
R for LDL uptake Max: 150mg SC q 2 FH
weeks

Single use pens/ pre-

filled syringes

JC 12
 Colestipol (Colestid) Binds to bile acids in the 2-16g/day Constipation DDI
intestine to prevent 1-2 times/day GI upset -directly bind to other
their absorption into ↑TG agents and decrease
the blood → liver uses absorption
blood cholesterol to -separate
produce more bile → administration with
reduces LDL other drugs

C/I in GI obstruction,
history of dysphagia, TG
value >500mg/dL→
AVOID use: can worsen
the level even more
-
Cholestyramine Binds to bile acids in the 8-16g/day Constipation DDI
(Questran) intestine to prevent 1-2 times/day GI upset -directly bind to other
their absorption into ↑TG agents and decrease
the blood → liver uses absorption
blood cholesterol to -separate
produce more bile → administration with
reduces LDL other drugs

C/I in GI obstruction,
history of dysphagia, TG
value >500mg/dL→
AVOID use: can worsen
the level even more

JC 13
 Colesevelam (WelChol) Binds to bile acids in the 3.75g/day Constipation DDI
intestine to prevent 1-2 times/day GI upset -directly bind to other
their absorption into ↑TG agents and decrease
the blood → liver uses absorption
blood cholesterol to -separate
produce more bile → administration with
reduces LDL other drugs

C/I in GI obstruction,
history of dysphagia, TG
value >500mg/dL→
AVOID use: can worsen
the level even more

Less binding
interactions

Niacin Inhibits TG synthesis→ 2nd line for elevated Hepatotoxicity (rare)- IR has most amount of
decreased secretion of LDL-c or higher with SR flushing
VLDL and LDL hypertriglyceridemia GI upset, flushing, C/I: active liver disease,
itching (IR) active pud, active gout
*start at low dose, take Decreased glucose ER is most common due
with food, avoid intolerance to limited risk of
anything that will make Flushing hepatotoxicity and
you warm, and take -secondary to release flushing
with NSAIDs or ASA of prostaglandin D2;
-frequency diminishes
over weeks or months
with repeated dosing

JC 14
 Gemfibrozil Activate specific 600mg/dose BID Hepatotoxicity (very Avoid statin use with
transcription factors rare) this → increased
termed peroxisome 1st line for severe Rhabdomyolysis (less myopathy
proliferator-activated hypertriglyceridemia than statins)
receptors (PPAR) → Gall stones C/I: active liver disease,
reduces TG add on to statin therapy (uncommon) gallbladder disease,
for mixed lipid severe CKD
modifying effects (eGFR<30mL/min)

DDI
-warfarin-increased
bleeding risk!
Fenofibrate Activate specific 48-145mg QD Hepatotoxicity (very Avoid statin use with
transcription factors rare) this → increased
termed peroxisome 1st line for severe Rhabdomyolysis (less myopathy
proliferator-activated hypertriglyceridemia than statins)
receptors (PPAR) → Gall stones C/I: active liver disease,
reduces TG add on to statin therapy (uncommon) gallbladder disease,
for mixed lipid severe CKD
modifying effects Avoid if CrCl <30, dose (eGFR<30mL/min)
adjust if CrCl <60
DDI
-warfarin-increased
bleeding risk!
Omega 3 Fatty Acids Lowers TG- FDA 1g capsule~0.9g O3FA Fishy breath/taste Docosahexanoic acid
(Lovaza) approved for TG 500 or 4g/day (DHA)
more Use what has the
Icosapent Ethyl May affect platelet 1g of EPA highest omega 3 Eicosapentaenoic acid
(Vascepa) aggregation and or 4g BID content for fish oil (EPA)
vitamin-K dependent supplements
coagulation factors

JC 15
 Ischemic Heart Disease-(CSA, ACS)
Guidelines
Angina Pectoris-chest pain caused most often by myocardial anoxia Chronic Stable Angina
as a result of occlusion of the coronary arteries from either CSA- predictable and reproducible left anterior chest
atherosclerosis or spasm discomfort after physical activity, emotional stress, or
IHD- lack of oxygen and decreased or no blood flow to the both
myocardium resulting from coronary artery narrowing or obstruction -typically worse symptoms in cold weather or after meals,
→ occurs as result of imbalance between oxygen supply(pressure, relieved by rest or sublingual nitroglycerin
blood flow, vasospasm) and oxygen demand (heart rate, contractility, Grade:
wall thickness, BP) 1. Ordinary physical activity does not cause angina,
such as walking and climbing stairs. Angina with
IHD- EKG changes strenuous or rapid or prolonged exertion at work
Cardiac markers: troponin (best biomarker for cell injury) or recreation.
CK-MB, myoglobin 2. Slight limitation of ordinary activity. Walking or
climbing stairs rapidly, walking uphill, walking or
ACS Pain occurs with ECG changes stair climbing after meals, or in cold or in wind, or
(UA/STEMI/NSTEMI) or without Troponin T or I, under emotional stress, or only during the few
physical exertion, ↑ myoglobin or hours after awakening.
and rest CK-MB 3. Marked limitation of ordinary physical activity.
(medicine may Walking one or two blocks on the level and
not relieve the climbing one flight of stairs in normal conditions
pain) and at normal pace.
4. Inability to carry on any physical activity without
Stable angina Pain occurs when Normal cardiac discomfort, angina symptoms may be present at
the heart is enzymes rest.
working harder
than usual. Stable IHD
angina has a Treatment Goals
“regular pattern” 1. Reduce frequency and severity of symptoms
2. Prevent progression of disease

JC 16
 Silent ischemia Patients may ST segment 3. Reduce risk of CV events
have no angina elevation or 4. Avoid or minimize AE
Risk reduction symptoms at any depression Non-Pharm
B-blockers 1st line time or have both Lifestyle
symptomatic and -reduce intake of saturated fats, trans fatty acids,
asymptomatic cholesterol
episodes -30-60mins of mod-intensity aerobic activity, 5-7 days per
week
Vasospastic angina Pain usually ST segment weight loss, smoking cessation
(Prinzmetal’s occurs at rest and elevation
angina) in the early Don’t forget modifiable risk factors such as
morning hypertension, dyslipidemia, obesity, sedentary lifestyle,
CCBs are 1st line psychosocial factors such as stress and type A behavior
patterns, and the use of certain drugs that may be
detrimental including progestins, corticosteroids, and
CCBs calcineurin inhibitors. These factors are preventable!!!
Class I Angina
CCBs or long-acting nitrates should be prescribed for relief of NTG for Acute Symptoms
symptoms when beta blockers are contraindicated or cause -Class I: sublingual NTG or NTG spray for immediate relief
unacceptable side effects in patients with SIHD of angina
CCB or long-acting nitrates, in combination with beta blockers, should -1st line as needed for immediate relief
be prescribed for relief of symptoms when initial treatment with beta
blockers is unsuccessful in patients with SIHD Chronic Management
-1stline is beta blockers for CSA
Class IIa Class I
Treatment with a long-acting nondihydropyridine CCB (verapamil or Beta-blockers should be prescribed as initial therapy for
diltiazem) instead of a beta blocker as initial therapy for relief of relief of symptoms in patients with SIHD in the absence of
symptoms is reasonable in patients with SIHD contraindications.
Beta-blocker therapy should be started and continued for
3 years in all patients with normal LV function after MI or
ACS

JC 17
 LA NTG Beta-blocker therapy should be used in all patients with
Class I LV systolic dysfunction (EF<40%) with heart failure or
Sublingual NTG or NTG spray for the immediate relief of angina prior MI, unless contraindicated. (Use should be limited to
CCBs or long-acting nitrates should be prescribed for relief of carvedilol, metoprolol succinate, or bisoprolol, which
symptoms when beta blockers are contraindicated or cause have been shown to reduce risk of death.)
unacceptable side effects in patients with SIHD Class IIb
CCB or long-acting nitrates, in combination with beta blockers, Beta-blockers may be considered as chronic therapy for
should be prescribed for relief of symptoms when initial treatment all other patients with coronary or other vascular disease.
with beta blockers is unsuccessful in patients with SIHD
• BB and nitrates
Ranolazine • Nitrates can cause reflex tachycardia which
Class IIa is blocked by BB
Ranolazine can be useful when prescribed as a substitute for beta- • BB can cause an increase in LV volume
blockers for relief of symptoms in patients with SIHD if initial which is reduced by nitrates
treatment with beta-blockers leads to unacceptable side effects or is • BB and CCB
ineffective or if initial treatment with beta-blockers is contraindicated • Combination with non-dihydropyridines
Ranolazine in combination with beta-blockers can be useful when can worsen LV function and cause
prescribed for relief of symptoms when initial treatment with beta- bradycardia or AV block
blockers is not successful in patients with SIHD • Dihydropyridines can cause reflex
tachycardia which is blocked by BB
Care Card for CSA • A long-acting dihydropyridine and a BB is
A = Aspirin and Antianginal therapy usually efficacious and well tolerated
B = Beta-blocker and Blood pressure ACEI and ARBs
C = Cigarette smoking and Cholesterol ACE inhibitors should be prescribed in all patients with
D = Diet and Diabetes SIHD who also have hypertension, diabetes mellitus, LVEF
E = Education and Exercise 40% or less, or CKD, unless contraindicated
ARBs are recommended for patients with SIHD who have
hypertension, diabetes mellitus, LV systolic dysfunction,
or CKD and have indications for, but are intolerant of, ACE
inhibitors

JC 18
 Aspirin Treatment with an ACE inhibitor is reasonable in patients
-Aspirin 75 to 162 mg daily should be continued indefinitely in the with both
absence of contraindications in patients with SIHD SIHD and other vascular disease
-Treatment with clopidogrel is reasonable when aspirin is It is reasonable to use ARBs in other patients who are ACE
contraindicated in patients with SIHD inhibitor intolerant
-Treatment with aspirin 75 to 162 mg daily and clopidogrel 75 mg
daily might be reasonable in certain high-risk patients with SIHD
-Dipyridamole is not recommended as antiplatelet therapy for
patients
with SIHD

Drug MOA Dose Adverse Effects Clinical Pearls

Nitroglycerin Vasodilate arteries and 1 tablet SL Q5mins Hypotension Cannot have child
(NitroQuick) arterioles (do not exceed 3 Burning of the tongue safety lock → need
(NitroStat) ↓ Artery wall stress/tension doses in 15 mins) with SL, buccal or spray to be able to remove
↑ Oxygen supply Headache cap right away for
↓ Oxygen demand should relieve pain Reflex tachycardia emergencies
in 3 mins
When emergency services Avoid use with -amber vial
should be notified: sildenafil, tadafanil,
-within 5 mins after 1st dose → vardenafil→ SEVERE SL NTG will relieve
take 2nd dose while you call 911 hypotension pain in 75% of
-if they do not improved after patients within 3
2nd dose minutes with
-if dose not go away completely another 15%
after 3rd dose becoming pain free
in 5-15 minutes.

JC 19
 B-blockers All are equally efficacious in CSA Do not need to know Hypotension Avoid abrupt
for CSA Decompensated HF withdrawal (taper
Metoprolol tartrate Avoid pindolol and acebutolol in Bradycardia over 1-2 weeks)
CSA → intrinsic 1st line in chronic Heart block,
Nadolol sympathomimetic activity management in bronchospasm, altered
STABLE angina glucose metabolism
Bisoprolol ↓HR
↓BP Start low and titrate C/I in vasospastic
Atenolol ↓myocardial contractility slow to resting HR angina
between 55-60bpm
Labetalol Not been shown to be
Low doses are better cardio protective
Carvedilol than none!
CCBs Coronary vasodilation Do not need to know Use with caution b/c it Significant FPM →
↓HR (NDP) ↓BP, ↓myocardial doses reduces HR and use with caution in
Verapamil contractility contractility hepatic impairment
(verapamil>diltiazem>nifedipine) Alternate therapy to
Diltiazem b-blockers in 1st line Hypotension NDP: avoid in pts
Flushing with EF <35%
Nifedipine 1st line for HA In combo with B-
vasospastic angina Peripheral edema(DHP) blocker ↓ HR
Amlodipine Heart block (NDP)
Constipation DHP: avoid IR
Felodipine nifedipine in CSA

Nicardipine Verapamil- IV use C/I

with IV b-blockers
NitroBid or NitroDur- Dilate systemic and coronary 2nd to 3rd line for LA nitrates are No mortality
ointment arteries → venous pooling of chronic maintenance associated with benefits
blood therapy for stable tolerance/tachyphylaxis
angina after prolonged dosing

JC 20
 Nitro-Dur- ↓cardiac work and chamber size -added to b-blocker C/I with PDE5 inhibitors Long-term nitrate
transdermal may increase exercise tolerance or CCB in patients monotherapy is not
who do not have Rebound ischemia may an appropriate
Isosorbide dinitrate adequate occur upon choice due to the
(IsoDitrate) symptomatic control discontinuation of long need for a nitrate-
acting nitrates free interval
Isosorbide All patients on
mononitrate (Imdur) chronic nitrate
therapy need a
“nitrate free
interval” of at least
8 hours (12 hours
preferred)

Do not need to know

doses for IHD
Ranolazine (Ranexa) ↓calcium overload in ischemic Indicated for chronic QTc prolongation Reserved for pts
myocytes by selectively angina who do not respond
inhibiting late sodium channels Constipation to other agents →
500mg SR BID HA QTc prolongation
no effect on BP, HR or max 1000mg BID Tinnitus
contractility Vertigo Met by CYP3A4!
Dry mouth DDIs

Monitor: ECG, BP in
patients with severe
renal function, K+
ACE inhibitors Inhibits conversion of AT I to AT Initiate at low dose Monitor K, SCr and BP Associated with CV
II titrate slowly C/I: Angioedema protecting effects!
Unstented bilateral C/I-pregnancy
renal artery stenosis

JC 21
 Aspirin Inhibit both PG synthesis and Loading: 325mg PO GI bleed Bleeding is major
platelet aggregation qd GI upset risk factor
(irreversible) via acetylation of Maintenance: 81mg Heartburn
COX PO qd Rash Should be continued
Hives indefinitely if there
are no C/I
DDI: increase risk for
bleeding when
administered with
anticoagulant
Clopidogrel (Plavix) Inhibits platelet aggregation by Maintenance: 75mg SJS Should be
selectively and irreversibly PO daily GI bleed discontinued 5 days
binding to adenosine Poor CYP2C19 met Pancytopenia before elective
diphosphate P2Y12 receptors may need higher Thrombotic surgery or CABG
doses! thrombocytopenic
Prodrug→ needs to purpura (TTP) DDI: met by
be metabolized Hepatitis CYP2C19, CYP3A4,
and CYP1A2
C/I: active bleeding -avoid use with
strong or moderate
CYP2C19 →
increases risk for
bleeding

Reasonable if aspirin
is C/I in patients

Combination of both
are for high risk
patients

JC 22
 Peripheral Vascular/Arterial Disease
Guidelines
Clinical Presentation PAD
1. Intermittent claudication ( >50% stenosis) -Patients with PAD should receive a comprehensive program of
reproducible fatigue, discomfort, cramping, pain, or GDMT including structured exercise and lifestyle modification
numbness during exercise and resolves at rest -Customized to individual risk factors
2. Pain at rest in lower extremities ( >80% stenosis) -Previous studies have demonstrated that patients with PAD are
Typically occurs later in disease when blood supply is less likely to receive GDMT than patients with other form of CV
not adequate to perfuse extremity (critical limb ischemia) disease

ABI <0.9 → risk of having or getting PAD Smoking Cessation

- Patients with PAD who smoke cigarettes or use other forms of
Supervised Exercise Therapy (SET) tobacco should be advised at every visit to quit
- In patients with claudication, a supervised exercise program is - Patients with PAD who smoke cigarettes should be assisted in
recommended to improve functional status and QoL and to developing a plan for quitting that includes pharmacotherapy
reduce leg symptoms. (ie, varenicline, bupropion, and/or nicotine replacement
- A supervised exercise program should be discussed as a therapy) and/or referral to a smoking cessation program.
treatment option for claudication before possible - Patients with PAD should avoid exposure to environmental
revascularization. tobacco smoke at work, at home, and in public places.

Walking Exercise Programs Hypertension

-ACC/AHA recommends a minimum of 30-45 minutes at least - Antihypertensive therapy should be administered to patients
three times per week for a minimum of 12 weeks with hypertension and PAD to reduce the risk of MI, stroke,
Glycemic Control heart failure, and cardiovascular death
- Management of diabetes mellitus in the patient with PAD - The use of angiotensin-converting enzyme inhibitors or
should be coordinated between members of the healthcare angiotensin-receptor blockers can be effective to reduce the
team. risk of cardiovascular ischemic events in patients with PAD.
- Glycemic control can be beneficial for patients with CLI to
reduce limb-related outcomes Beta Blockers

JC 23
 Lipid Management -Beta blockers should be used with caution in patients with
-Clinical ASCVD includes: acute coronary syndromes, history of critical leg ischemia
MI, stable or unstable angina, coronary or other arterial -ischemic pain (burning sensation) in lower extremities at
revascularization, stroke, TIA or peripheral arterial disease rest of ABI <0.4 → worsen claudication symptoms
presumed to be of atherosclerotic origin
-Increased risk for recurrent ASCVD and ASCVD death Antiplatelets
Age<75- high intensity statin - Antiplatelet therapy with aspirin alone (range 75–325 mg per
Age>75: moderate intensity statin day) or clopidogrel alone (75 mg per day) is recommended to
reduce MI, stroke, and vascular death in patients with
Intermittent Claudication symptomatic PAD.
-Cilostazol is an effective therapy to improve symptoms and
increase walking distance in patients with claudication Dual Antiplatelet
-The effectiveness of dual-antiplatelet therapy (aspirin and
clopidogrel) to reduce the risk of CV ischemic events in patients
with symptomatic PAD is not well established.
-Dual-antiplatelet therapy (aspirin and clopidogrel) may be
reasonable to reduce the risk of limb-related events in patients
with symptomatic PAD after lower extremity revascularization.

Drug MOA Dose Adverse Effects Clinical Pearls

Aspirin Irreversibly inhibits 81mg daily Bleeding Has the most
COX-1 and COX-2 in compelling evidence for
platelets, preventing treatment in PAD
formation of TXA2
Aspirin and Unknown, may act by Should not be used in Increase bleeding risk Reduce further CV
dipyridamole ER inhibiting platelet patients used in events compared to
(Aggrenox) aggregation patients with aspirin but no
CAD→coronary steel statistically significant

JC 24
 Clopidogrel (Plavix) Inhibits binding of ADP N/A Alternative to ASA if
analogues to its platelet patient has an
receptor causing intolerance to it
irreversible platelet
inhibition Can use this and ASA if
the pt is very high risk
Ticlopidine (Ticlid) Inhibits binding of ADP N/A BBW: neutropenia and Efficacy is
analogues to its platelet agranulocytosis, overshadowed by
receptor causing thrombocytopenia, and severe hematologic
irreversible platelet aplastic anemia effects
inhibition
Cilostazol (Pletal) Phosphodiesterase 100mg BID on empty BBW: avoid use in Increases maximum
inhibitor, irreversibly stomach patients with PAD and walking distance
inhibits platelet OR coexisting HF of any Increases pain free
aggregation, thrombin, ½ hr before or 2 hrs severity→ reduced walking
and ADP after breakfast/dinner ejection fraction % = Superior to
Torasdes! pentoxifylline
For intermittent
Does not improve claudication! Headache Only recommends in
mortality or quality of Palpitation patient with PAD who
life CYP3A4 inhibitors- Diarrhea are not candidates for
verapamil and diltiazem surgical interventions to
CYP2C19-omeprazole improve severe IC
Reduce dose to 50mg refractory to exercise
BID therapy and therapeutic
life changes

JC 25
 Anticoagulation/VTE
Guidelines
VTE VTE Prophylaxis
DVT-fibrin blood clot occurring in a major vein usually in the Acute or critically ill patients and cancer
lower extremities -LMWH for 6 months started to prior injury
-diagnostic; D-dimer (-), Doppler or deuplex ultrasonography -oral anticoagulants indefinitely
PE- blood clot usually originating from a DVT that travels to the
lungs→ major cause of mortality Major orthopedic surgery (hip and knee replacement)
-diagnostic; Spiral CT -Proplyaxis for a minimum of 35 days
-LMWH should be started 12 hrs pre or postoperatively
Risk Factors -should be given in combination with IPC
-age, (>50). history of VTE, venous stasis, vascular injury,
hypercoaguable states, drug therapy Provoked or transient: at least 3 months
Unprovoked: at least 3 months then evaluate risk vs benefit of
Atrial Fibrillation long-term
-In patietns with CHA2DS2-VASc ≥2 (male) or ≥3(female):
recommend stroke prevention CHEST Guidelines
DOAC>Warfarin- if patient is eligible for DOAC (2019AHA/ACC) DOAC>VKA (Grade2B) >LMWH (Grade2C)
-In patients with CHA2DS2-VASc ≥1 (male) or ≥2 (female):
recommend stroke prevention Cancer duration
DOAC>warfarin (CHEST) LMWH>VKA>DOAC

Valvular Heart Disease TAVR

Bioprosthetic: ASA 81 mg → lifelong (Class IIa/B) ASA 81 mg → lifelong (Class IIb/C)
Warfarin x 3-6 months Low bleed risk:
Target INR: 2-3 (Class IIa/B-NR) • Clopidogrel 75 mg x 6 months
• Warfarin x 3 months
Mechanical: Aortic: No risk factors for TE*: • Target INR: 2-3 (Class IIa/B-NR)
• Warfarin → lifelong High bleed risk:
• Target INR: 2-3 (Class IB) • Clopidogrel 75 mg x 6 months
• Risk factors for TE*:

JC 26
 • Warfarin → lifelong On-X-Aortic Valve
• Target INR: 2.5-3.5 (Class IB) ASA 81 mg → lifelong (Class IIb/B-R)
Mitral: ASA 81 mg → lifelong (Class IA) Initial 3 months Post-Op:
• Warfarin → lifelong • Warfarin
• INR 2.5-3.5 (Class IB) • Target INR: 2-3
DOACs: Class III: Harm After initial 3 months:
DOACs not recommended in mechanical prostheses • Warfarin → lifelong
No comment on bioprosthetic • Target INR: 1.5-2 (Class IIb/B-R)

HIT
-rare immunologic reaction characterized by thrombocytopenia HIT: 4T Score
requiring immediate intervention 6-8: High
-usually by IgG antibodies that bind PF4-heparin complexes 4-5: Intermediate
UFH > LMWH risk of HIT 0-3: Low
1. HIT Type I- non-immune <4 days Diagnosis: consider clinical and lab assessment (ELISA and SRA)
2. HIT Type II- immune mediated 5-10 days → sometimes they do not come back fast enough!
3. HITTs- immune mediated and thrombosis

Drug MOA Dose Adverse Effects Clinical Pearls

Warfarin (Coumadin) Antagonist of vitamin K Adjusted to target INR Bleeding → avoid C/I: pregnancy
which in turns prevents Highly individualized NSAIDs (category X), active
the formation of bleeding, hemorrhagic
vitamin K dependent Usual starting dose: Food interactions disorders, previous
clotting factors II, VII, IX 5mg daily warfarin induced skin
and X VERY High in Vit K necrosis, recent or
Monitor: q 3-7 days Kale contemplated surgery
Also prevents the until INR is therapeutic Spinach (frozen, and anesthesia, history
formation of vitamin K -once therapeutic, may cooked) of falls or seizures,
dependent proteins extend to weekly and Collards unsupervised patients
such as protein C and S eventually to 8 weeks Turnip greens

JC 27
 Therapeutic doses with potential high
reduce vitamin K typically adjust dose by High in Vit K levels of non-adherence
dependent production 10-20% Beet greens
by up to 50% Dandelion Greens S is more potent than R
**weight requires Mustard greens S-met by CYP2C9
Indications: more warfarin to reach Increase warfarin
1. Prophylaxis and INR goals** Medium in Vit K effect: amiodarone,
treatment in Spinach (raw) fluconazole,
thromboembolic elevated INR: Brussel sprouts metronidazole, SMX-
complications black stool, blood in Broccoli TMP
associated with atrial stool/urine, excessive Onion
fibrillation and/or menstrual bleeding, Lettuce CYP2C9 Variation
cardiac valve bruising, excessive Cabbage -Genetic variation (*2
replacement nosebleeds or bleeding Asparagus or *3 alleles) may lead
2. Treatment and gums, persistent oozing to lower daily
prevention of VTE from superficial injuries, STAY CONSISTENT in maintenance dose
3.Anticoagulation in bleeding from tumor, diet
Coronary Artery Disease ulcer, other lesions
Do NOT double up on
Follow up: verify missed doses VKORC1 Variation
current dose patient is -Genetic variation
taking, double check Avoid contact sports (haplotypes) may lead
color and strength of to lower or higher daily
tablet (AVOID using 2 maintenance doses
strengths), assess
changes in med/OTC, Counseling:
adherence, changes in
diet/EtOH, access for Initial: basic info;
bleeding, assess lifestyle diet, thorough
exacerbation of med history
thromboembolytic dis.

JC 28
 Dabigatran (Pradaxa) Direct thrombin NVAF-150mg BID GERD No intensive monitoring
inhibitor → inhibits CrCl <30-75mg BID Indigestion
activated factor II Myocardial infarction Not recommended in
NOT recommended in pts with renal
Reversal Agent: CrCl <15 impairment → renal
Praxbind C/I in mechanical heart elimination is 80%
VTE treatment and valves
secondary prevention- Should be stored and
When converting from Initial 5-10 days of Geriatrics: risk of dispensed in the
dabigatran to warfarin, parental bleeding with age original container to
adjust the starting time anticoagulation is prevent loss of potency
of warfarin based on required before -bottle should not be
creatinine clearance as initiating Can use activated left open for extended
follows: -150mg BID charcoal to reverse periods of time
-For CrCl ≥50 mL/min, -CrCl <30→ not toxicity! -only good for 4 months
start warfarin 3 days recommended -removal of unabsorbed once opened
before discontinuing dabigatran pro-drug
PRADAXA. When converting from GI tract within 2 absorption may be
-For CrCl 30-50 mL/min, patients form warfarin hrs of last dose decreased if not in
start warfarin 2 days to dabigatran, acidic environment→
before discontinuing discontinue warfarin Hemodialysis to not recommended for
PRADAXA. and start when INR is reverse→ ONLY patients on PPIs or
-For CrCl 15-30 mL/min, below 2.0 dialyzable DOAC H2RAs
start warfarin 1 day
before discontinuing cannot crush
PRADAXA.
-For CrCl <15 mL/min,
no recommendations
can be made.

JC 29
 Apixaban (Eliquis) Factor Xa inhibitor NVAF-5mg BID Thrombocytopenia No intensive monitoring
If 2 of following: age
Reversal Agent: >80, weight <60kg, Cr Pregnancy B
Andexxa >1.5: 2.5mg BID

VTE: 10mg PID 7 days,

then 5mg PO BID
Rivaroxaban (Xarelto) Factor Xa inhibitor NVHA CrCl >50: 20mg Short t ½ but once daily No intensive monitoring
PO qd with evening drug
Reversal Agent: meal 3A4 metabolism
Andexxa CrCl 15-50- 15mg PO qd Agranulocytosis
with evening meal Hepatitis 2.5mg BID to reduce
risk of MACE in patients
VTE-CrCl >30: 15mg PO GI-abdominal pain, with CAD/PAD
BID for 21 days, then nausea(better tolerated Conversion from
20mg PO daily than dabigatran) warfarin to
CrCl <30 not -can affect liver rivaroxaban:
recommended enzyme! -Discontinue warfarin
-ALT >3x ULN and initiate rivaroxaban
Converting to as soon as INR falls to
Parenteral DDIs <3.0
Anticoagulants CYP3A4 and Pgp Conversion to warfarin:
-15 or 20 mg: start =When apixaban is co- Initiate warfarin and a
when next rivaroxaban administered with parenteral
dose was due drugs that are strong anticoagulant 24 hours
-10 mg: start dual inhibitors of after discontinuation of
irrespective of time cytochrome P450 3A4 rivaroxaban (VTE >
Converting from UFH (CYP3A4) and P- NVAF)
continuous infusion glycoprotein (P-gp) -Rivaroxaban affects
-Start rivaroxaban when (e.g., ketoconazole, INR; therefore, initial
infusion is stopped itraconazole, ritonavir, INR measurements

JC 30
 Converting from LMWH clarithromycin) → the after initiating warfarin
or fondaparinux recommended dose is may be unreliable
-Initiate rivaroxaban 2.5 mg twice daily Conversion to other
within 2 hours prior to -In patients already DOACs
the time of the next taking 2.5 mg twice -15 or 20 mg: start
scheduled dose daily, co-administration when next rivaroxaban
of apixaban with strong dose was due
dual inhibitors of -10 mg doses: start
CYP3A4 and P-gp should irrespective of time
be avoided
Edoxaban (Savaysa) Factor Xa inhibitor • NVAF: CrCl > 95 Do not use in CrCl <15 No intensive monitoring
mL/min: NOT or >95→ cleared too
recommended quickly if renal function Premature
• CrCl 51-95 is good discontinuation
mL/min: 60 mg increases risk of
PO once daily Abnormal LFTs ischemic events
• CrCl 15-50 Rash
mL/min: 30 mg
PO once daily
• CrCl < 15
mL/min: not
recommended
VTE: Begin after 5-10
days of initial therapy
with a parenteral
anticoagulant
• CrCl > 50
mL/min: 60 mg
PO once daily
• CrCl 15-50
mL/min or

JC 31
 weight ≤60 kg or
on P-gp
inhibitor: 30 mg
PO once daily

Betrixaban (Bevyxxa) Factor Xa inhibitor Prophylaxis of VTE n CrCl 15-30, dose No intensive monitoring
adults hospitalized for reduced by 50%
an acute medical illness
who are at risk forVTE
Day 1: 160mg QD
Therefore after 80mg
QD
Idarucizumab Dabigatran binding 5g provided as 2 For emergency and life-
(Praxbind) affinity is 350x higher separate vials threatening bleeding
for idarucizumab IV when on dabigatran
compared to
thrombin→ binds to 2.5g x2 no more than
this and reverses effects 15 mins apart

JC 32
 Andexanet alfa Reversal agents for life IV bolus with target The only FDA approved
(Andexxa) threatening bleeding on range of 30mg/min reversal agent
rivaroxaban or apixaban followed by continuous
infusion for up to 120 Very expensive: full
mins course can be 24k-50k

Low: 400mg of
30mg/min then
4mg/min for up to 120
mins

High: 800mg at
30mg/min then
8mg/min for up to 120
mins
Unfractionated heparin Indirect thrombin DVT: IV 80 units/kg Bleeding, heparin Hepatically metabolized
inhibitor → helps push followed by induced- -no renal adjustment
antithrombin deactivate continuous infusion of thrombocytopenia (HIT) -t ½ is dose dependent
clotting factors 18 units/kg/hr Monitor: aPTT, affected by obesity,
-Inhibits factor Ixa, Xa, Prophylaxis: 5,000 SC platelets, Hgb, Hctk renal function,
XIIa, and IIa activity units every 8-12 hours signs for bleeding malignancy, presence of
*each institution will pulmonary embolism,
-UFH-antithrombin have their own and infections
complex is more potent therapeutic range for
as an anticoagulant aPTT→ do not measure inexpensive, better for
compared to when given for VTE renally dysfunction pts,
antithrombin alone prophylaxis fast on/off, reversible,
(100-1,000x) monitor aPTT q6h until may be used in
within therapeutic pregnancy
range on 2 consecutive
draws

JC 33
 Enoxaparin (Lovenox) Indirect thrombin DVT Prophylaxis Bleeding, HIT Check patients renal
LMWH inhibitor → helps Hip: 40mg SC q 24h or function
antithrombin deactivate 30mg SC q 12h Monitor: anti-Xa levels
Dalteparin (Fragmin) clotting factors in special populations Dose adjustment
Knee: 30mg SC q 12h (not routine), platelets, needed in pts eCrCl <40
Inhibits Xa Hgb, Hct, signs for
preferentially Abdomen: 40mg SC q bleeding, renal function Fragmin is only
24h (start 2 hrs after indicated for VTE
surgery) treatment in patients
with active malignancy
Acute medical illness:
40mg SC q 24h Renal <30
Lovenox→1mg/kg daily
VTE 30mg SC QD
Lovenox: 1mg/kg ABW
SC BID Fragmin→ check anti Xa
Or 1.5mg/kg ABW SC levels
QD
Fragmin: 200 units/kg Good F
SC daily for 30 days Predictable PK/PD
then 150 units/kg after profile, less monitoring,
*max daily dose is preferred for pregnant,
18,000U/day cancer and trauma
patients, outpatient
utility, lower incidence
of HIT

JC 34
 Fondaparinux (Arixtra) Indirect thrombin VTE prophylaxis: 2.5mg Bruising at injection site Renally eliminated
inhibitor → helps SC QD Rash Long t ½ (17-21h)
antithrombin deactivate Fever
clotting factors Acute DVT/PE: given SC Bleeding C/I in severe renal
<50mg→ 5mg QD Anemia impairment CrCl<30,
Causes an antithrombin 50-100kg→ 7.5mg QD VTE prophylaxis in pts
III-mediated selective, >100kg→10mg QD Monitor: anti-factor Xa, <50kg, and
inhibition of factor Xa signs of bleeding, Hgb. thrombocytopenia
only HIT: 5-10mg SC daily Hct, platelets, renal
function CrCl 30-50: 50%
reduction in dose
Significantly more
effective than Reserved for patients
enoxaparin in with history of HIT
preventing DVTs in high
risk orthopedic Start either 6-8 h after
procedures however is surgery or the next day
associated with more to prevent post-
bleeding operative bleeding

Has NO reveral agent!

Protamine Cationic protein that UFH- 1mg per 100 units Flushing Use of protamine not
binds to heparin of UFH slow IV infusion N/V recommended in
Dyspnea LMWH administered
LMWH- 1mg for 1mg Bradyarrythmia more than 12 hrs earlier
enoxaparin in previous Hypotension
8 hrs
-second dose of Caution in shellfish
0.5mg/1mg enoxaparin allergy
can be given if bleeding
continues

JC 35
 Vitamin K Reverses warfarin IV- begin to see some
effect within 4-6 hrs
Never use SC PO and IV will reach
erratic and peak efficacy at 24h
unpredictable
absorption Smallest PO tab: 2.5mg
IV→ PO
4F-PCC (Kcentra) Works on Factors II, VII, Dosing based on units when calculating, it is
IX, X, and Protein C and of Factor IX and pre- important to check
S dose INR and body each vial for Factor IX
weight units, since each lot can
vary in potency!
INR 2-4: 25 units/kg
4-6: 35 units/kg
>6: 50 units/kg
Argatroban Direct thrombin Treatment of HIT: Give false elevation of
inhibitor 2mcg/kg/min INR→ not indicative of
a bleed in patients

Needs hepatic dose

adjustment
Bivalirudin Direct thrombin PCI/Cardiac surgery for Give false elevation of
inhibitor pts with history of HIT: INR→ not indicative of
0.2mg/kg/hr a bleed in patients

JC 36
 Chronic Heart Failure
Guidelines for HF
Diuretics Beta-blockers
*symptomatic management no mortality benefit! Stage B HFrEF
Recommend diuretic use (along with salt restriction) in patients -In patients with MI and reduced EF, evidence-based beta-
with HFrEF who have evidence of fluid retention blockers should be used to prevent HF
Diuretics should be used for relief of symptoms due to volume -Beta-blockers should be used in all patients with a reduced EF
overload to prevent HF
Should not be used alone in HFrEF Stage C
Stage C HFrEF
Thiazides -Use of 1 of the 3 beta blockers proven to reduce mortality is
ACCF/AHA recommends the following for sequential nephron recommended for all stable patients
blockade: Metolazone, HCTZ, Chlorothiazide (IV) 1. Carvedilol
2. Bisoprolol
3. Metoprolol Succinate
ARBs
Stage B HFrEF ACE inhibitors
- In patients with history of MI and reduced EF, ACE inhibitors Stage B HFrEF
and ARBs should be used to prevent HF -In patients with history of MI and reduced EF, ACE inhibitors
and ARBs should be used to prevent HF
Stage C HFrEF -ACE inhibitors should be used in all patients with a reduced EF
-ARBs are recommended in patients with HFrEF who are ACE- to prevent HF
inhibitor intolerant
-ARBs are reasonable as alternatives to ACE inhibitors as first Stage C HFrEF
line therapy in HFrEF -ACE inhibitors should be used in all patients with a reduced EF
-Addition of an ARB may be considered in persistently to prevent HF
symptomatic patients with HFrEF on GDMT
-Routine combined use of ACE inhibitor and ARB and
aldosterone antagonist is potentially harmful

JC 37
 Aldosterone Antagonists ARNI
-Aldosterone antagonists are recommended in patients with -In patients with chronic symptomatic HFrEF NYHA class II or III
NYHA class II-IV HF who have LVEF <35% who tolerate an ACE inhibitor or ARB, replacement by an ARNI
-Innapropriate use of aldosterone antagonists may be harmful is recommended to further reduce morbidity and mortality
because of life-threatening hyperkalemia when: in conjunction with evidence-based beta blockers, and
a. SCr >2.5mg/d in men or >2.0 mg/dL in women aldosterone antagonists in selected patients, is recommended
b. eGFR <30mL/min for patients with chronic HFrEF to reduce morbidity and
c. K>5.0mEq/L mortality
OR <40% if history of acute
Hydralazine/ISDN
Ivabradine -The combination of hydralazine/ISDN is recommended for
-Ivabradine can be beneficial to reduce HF hospitalization for African Americans with NYHA class III-IV HFrEF on GDMT
patients with: -A combination of hydralazine and isosorbide dinitrate can be
a. HFrEF (EF <35%) useful in patients with HFrEF who cannot be given ACE
b. NYHA class II-III inhibitors or ARBs
c. On GDMT, including max tolerated doses of a beta blocker
d. In sinus rhythm with resting HR > 70bpm Digoxin
Stage C:
-Digoxin can be beneficial in patients with HFrEF, unless
CCBs contraindicated to decrease hospitalizations for HF
-Non-DHP should be AVOIDED in patients with HFrEF
-associated with increased risk for hospitalization, fluid
retention, disease progression and mortality
-DHP CCB may be safe but has no mortality benefits→ not
recommended

JC 38
 Drug MOA Dose Adverse Effects Clinical Pearls

Furosemide (Lasix) Blocks sodium- 40mg Resistance- no longer *may use ethacrynic
potassium-chloride MAX: 120mg BID producing the same acid in severe sulfa
cotransporter→ ↑Na effect from the original allergy!
excretion, ↑K Best given early AM dose
excretion, ↑Cl And around noon if BID Titrate to effect and
excretion dosing Electrolyte reduce PRN
Goal weight loss; 1-2 abnormalities (Na, K)
lbs/day until IBW Renal dysfunction
achieved Hypotension

Monitor: SCr, K, BP,

weight
Torsemide (Demadex) Blocks sodium- 10mg Resistance- no longer Has more reliable and
potassium-chloride MAX: 60mg BID producing the same rapid oral absorption
cotransporter→ ↑Na effect from the original than furosemide
excretion, ↑K Best given early AM dose Longest t ½ (3.5h)
excretion, ↑Cl And around noon if BID Associated with
excretion dosing Electrolyte significant
Goal weight loss; 1-2 abnormalities (Na, K) improvement in NYHA
lbs/day until IBW Renal dysfunction classs and reduced HF-
achieved Hypotension readmissions

Monitor: SCr, K, BP,

weight

JC 39
 Bumetanide (Bumex) Blocks sodium- 1mg Resistance- no longer Has more reliable and
potassium-chloride MAX: 2mg BID producing the same rapid oral absorption than
cotransporter→ ↑Na effect from the original furosemide
excretion, ↑K Best given early AM dose
excretion, ↑Cl And around noon if BID
excretion dosing Electrolyte
Goal weight loss; 1-2 abnormalities (Na, K)
lbs/day until IBW Renal dysfunction
achieved Hypotension

Monitor: SCr, K, BP,

weight\
Metolazone Blocks sodium-chloride 2.5-10mg QD Electrolyte Most commonly
transporter → ↑NaCl want to give 30-60 abnormalities (Na, K) prescribed for combo
excretion mins prior to Renal dysfunction therapy in US
furosemide Hypotension Retains efficacy in
advanced renal failure
want to take loop and Monitor: SCr, K, BP,
thiazide at the same weight
time!
Bisoprolol (Zebeta) Selective b1 Initial: 1.25mg QD Fatigue, weakness, Titrate!
Target: 10mg QD lassitude Start at low dose and
Fluid retention increase q 2-4 weeks
Bradycardia toward target dose

Monitor: BP, HR, No lab checks!

weight, HF symptoms

C/I similar to carvedilol

JC 40
 Carvedilol (Coreg) Mixed alpha and beta Initial: 3.125mg BID More hypotension and Take with food to slow
Target: 25mg BID dizziness (rapid down the absorption to
absorption and alpha limit AE
*50mg BID if patient is blockade)
>85kg
Fatigue, weakness, Titrate!
lassitude Start at low dose and
Fluid retention increase q 2-4 weeks
Bradycardia toward target dose

Monitor: BP, HR, No lab checks!

weight, HF symptoms

C/I in cardiogenic
shock, symptomatic
bradycardia, 2nd or 3rd
degree block without
pacemaker, use with
considerable caution in
patients with marked
bradycardia <55bpm or
marked hypotension
<80mHg

Metoprolol succinate Selective b1 Initial: 12.5-25mg QD Similar to Carvedilol Titrate!

(Toprol XL) Loses selectivity at Target: 200mg QD but no hypotension Start at low dose and
higher doses risk increase q 2-4 weeks
*use metoprolol if toward target dose
patient is hypotensive
No lab checks!

JC 41
 Lisinopril (Prinivil, Inhibits ACE to block Initial: 2.5-5mg daily Hypotension Drug interactions
Zestiril) production of AT II Angioedema Lithium
Inhibits breakdown of Target: 20-40mg daily Renal effects: ↑Scr NSAIDs
bradykinin→ promote Hyperkalemia Salt substitutes
vasodilation Teratogenic Loop
Dilates the efferent Cough K+ sparing
arterioles Rash and taste
disturbance (captopril)

Monitor within 2wks;

BP (qd), BMP( SCr, K)
Expect 20-30% ↑ in
SCr after initiation
A rise of >0.5 needs
evaluation

C/I in pregnancy,
bilateral renal artery
stenosis, history of
angioedema
Enalapril (Vasotec) Inhibits ACE to block Initial: 2.5mg BID Hypotension Drug interactions
production of AT II Angioedema Lithium
Inhibits breakdown of Target: 10-20mg BID Renal effects: ↑Scr NSAIDs
bradykinin→ promote Hyperkalemia Salt substitutes
vasodilation Expect 20-30% ↑ in Teratogenic Loop
Dilates the efferent SCr after initiation Cough K+ sparing
arterioles A rise of >0.5 needs Rash and taste
evaluation disturbance (captopril) C/I in pregnancy, bilateral
renal artery stenosis,
Monitor within 2wks; history of angioedema
BP (qd), BMP( SCr, K)

JC 42
 Losartan (Cozaar) Prevents angiotensin II Initial: 25-50 mg daily Hypotension Lower doses than HTN, on
from binding to AT I Target: 150mg daily Angioedema multiple meds so we start
and AT II receptors Renal effects: ↑Scr lower
*not FDA approved for Hyperkalemia
AT I > AT II affinity HF Teratogenic Drug interactions
Cough Lithium
Expect 20-30% ↑ in Rash and taste NSAIDs
SCr after initiation disturbance (captopril) Salt substitutes
A rise of >0.5 needs Loop
evaluation Monitor within 2wks; K+ sparing
BP (qd), BMP( SCr, K)

Expect 20-30% ↑ in
SCr after initiation
A rise of >0.5 needs
evaluation

C/I in pregnancy,
bilateral renal artery
stenosis
Valsartan (Diovan) Prevents angiotensin II Initial: 40mg BID Hypotension Drug interactions
from binding to AT I Target: 160mg BID Angioedema Lithium
and AT II receptors Renal effects: ↑SCr NSAIDs
Expect 20-30% ↑ in Hyperkalemia Salt substitutes
AT I > AT II affinity SCr after initiation Teratogenic Loop
A rise of >0.5 needs Cough K+ sparing
evaluation Rash and taste
disturbance (captopril) C/I in pregnancy, bilateral
Lower doses than HTN, renal artery stenosis
on multiple meds so Monitor within 2wks;
we start lower BP(qd), BMP( SCr, K)

JC 43
 Sacubitril/Valsartan Inhibits neprilysin Initial: 24/26 mg BID Angioedema Do not use in combination
(Entresto) (which degrades ANP, or 49/51mg BID Hypotension with ACE or ARB or with
BNP, C-type natriuretic Target: 97/103 mg BID Hyperkalemia patients with history of
peptide) and inhibits Renal effects: ↑SCr angioedema
degradation of AT II Titrate by doubling
dose q 2-4 weeks to Monitor similar to ACE
We give with ARB so target dose as and ARBs
the degradation of AT II tolerated by patient
does not happen!
Spironolactone Initial: 12.5-25mg daily Significant risk of Patients with underlying
(Aldactone) Target: 25mg daily hyperkalemia hypokalemia may consider
10% risk gynecomastia addition of aldosterone
Dizziness, worsening antagonist in patients
renal function already on standard
therapy
Monitor: BMP 3-7 days
after starting then
once monthly for 3
months, then
periodically PRN
K+, SCr
Eplerenone (Inspra) Initial: 25mg daily Significant risk of Patients with underlying
Target: 50mg daily hyperkalemia hypokalemia may consider
Dizziness, worsening addition of aldosterone
Titrate q 4-8 weeks renal function antagonist in patients
towards target dose already on standard
Monitor: BMP 3-7 days therapy
after starting then
once monthly for 3
months, then
periodically PRN (K,SCr)

JC 44
 Hydralazine Antioxidant- inhibits Initial: 25-50mg TID or Hypotension
destruction of NO→ QID Headache
arteriole dilator Tachycardia
Lupus like symptoms
with positive ANA

Isosorbide dinitrate Nitric oxide donor, Initial: 20-30mg TID or Hypotension

large and small artery QID Headache
dilator→ venous Flushing
dilator Tolerance*

Ivabridine (Corlanor) Novel MOA Do not need to know Bradycardia Reserved for patients who
Hypertension are on max dose of b-
Selective If current Titrate doses ~ Atrial fibrillation blockers that still have a
(funny current) HR (50-60bpm) Phosphine HR >70bpm
blockade prolongs
diastolic time resulting Max is 7.5mg BID Monitor: HR, BP, No mortality benefits
in pure reduction in cardiac rhythm-a-fib,
heart rate with no visual changes
other direct CV effects

Shown to have
antianginal effects in
CSA

JC 45
 Digoxin Unclear Loading dose: only if CNS: HA, dizziness, Historically a cornerstone
Likely due to need rapid response changes in of HF treatment
neurohormonal 0.5-1mg IV/PO over 24 yellow/green color,
inhibiton NOT positive hr visual halos
inotropic effect May be used if concurrent
→ decrease Maintenance: 0.125- GI: anorexia, N/V, atrial fibrillation
sympathetic outflow 0.25mg/day diarrhea, constipation
and improves Target Cp: 0.5-0.9ng/mL
baroreceptor function *low doses should be Cardiac: bradycardia
and ↑ vagal tone used initially if patient (AV block), HR there is no survival benefit
is >70 yrs, has impaired <50bpm, ↑PR interval,
renal function, or has a PVCs, other Risk Factors: renal
low lean body mass arrhythmias insufficiency,
hypo/hyperkalemia
start low and titrate Monitor: serum
based on symptom concentrations when DDIs
relief steady state is reached ↑serum conc:
→ 7-10 days after -
initiation or dose Amiodarone,Erythromycin,
adjustment + trough Itraconazole, Omeprazole
level, and HR
↓serum conc:
-antacids, colestipol,
laxative

JC 46