HTN Flashcards
What percentage of HTN is PRIMARY
90-95%
What percentage of HTN is SECONDARY?
5-10%
Think secondary HTN if
▪ If sudden onset, esp. if age of onset < 20 or > 50 years
▪ BP > 180/100
▪ Resistance to therapy
▪ Pt with well-controlled HTN has sudden increase in BP
▪ There are symptoms that could cause secondary HTN: headache, daytime
somnolence, fatigue, tachycardia, claudication, cold feet, sweating, thinning of
skin, flank pain, muscle weakness, tremor
HTN Diagnosis
Average of readings taken at 2 or more visits
• Must have 2 separate elevated readings
Describe steps in Renin Angiotensin System (RAS)
Drop in BP to renal arteries stimulates secretion of renin
• Renin activates renin-angiotensin system, yields angiotensin I
• Angiotensin converting enzyme (ACE) converts angiotensin I converted to angiotensin II
• Angiotensin II constricts blood cells, increases secretion of antidiuretic hormone (ADH) and
aldosterone, causes reabsorption of Na+ in kidneys –> water retention, increased blood volume,
increased BP.
Factors that affect BP
Peripheral vascular resistance
• Body position
• Activity
• Blood volume
• Obesity – leads to increased intravascular volume and increased cardiac output
• Lifestyle
• Environmental factors
• Alcohol – increases BP by increasing plasma catecholamines
• Cigarettes – raises BP by increasing plasma norepinephinre
• NSAIDs – cause fluid retention, which can lead to HTN
• Excessive intake of Na+ or low levels of K+ - can contribute to HTN by increasing blood volume
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HTN is a major risk factor for…
Cardiovascular dz o Ischemic heart dz o Heart attack o Heart failure • Stroke • Kidney dz, renal failure • Peripheral vascular dz
Each increase of 20 mm Hg in SBP or 10 mm Hg in DBP
DOUBLES risk of cardiovascular dz
Initial drug therapy for Prehypertension 120-139 or 80-89
none
Initial drug therapy for Stage 1 HTN 140-159 or 90-99
Thiazide diuretic
-may consider ACE,
ARB, BB, CCB, or
combo
Initial drug therapy for Stage 2 HTN ≥160 or ≥100
Two-drug combo
(usually thiazide + ACE,
ARB, BB, or CCB)
Centrally acting α-2 agonists (antiadrenergics) MOA
Stimulate central inhibitory α-adrenergic receptors
• Stimulate sympathetic cardioaccelerator and vasoconstrictor areas
• Results in decreased sympathetic outflow from CNS that causes reduced peripheral resistance,
renal vascular resistance, decreased HR, decreased BP
Clonidine:
• Onset of action: 30-60 min
• Duration of action: 6-10 hr
• Metabolism: extensive hepatic
• Excretion: kidney 65%, feces 22%
• Drug interactions:
▪ Tricyclic antidepressants decease effects of clonidine
▪ Clonidine may enhance CNS effects of alcohol or sedatives
▪ Use cautiously with β-blockers. Clonidine can cause bradycardia. Discontinue gradually.
• Side effects:
▪ Dry mouth, drowsiness, dizziness, sedation, orthostatic hypotension
Methyldopa
Onset of action: 3-6 hr • Duration of action: 12-24 hr • Metabolism: complex liver • Excretion: kidney 70% drug and conjugates • Drug interactions: ▪ Lithium ▪ MAOIs ▪ Iron salts ▪ COMT inhibitors • Pregnancy: preferred HTN drug in pregnancy • Side effects: ▪ Headache, asthenia, dizziness, gynecomastia, GI distress
what are the characteristics of systolic dysfunction?
reduced left ventricular , low ejection fraction
EF usually less than 40%
what are the characteristics of diastolic dysfunction?
Characterized by “stiffening” of the left ventricle
EF is typically preserved,
i.e. normal
What is preload?
Stretch of the ventricle prior to contraction. Preload is
created by blood filling the ventricle in preparation for
contraction
What is afterload?
Resistance the left ventricle has to overcome to empty its
contents into peripheral circulation
What is peripheral vascular resistance?
Pressure (within the periphery) that the left ventricle
must overcome with each contraction
What is the New York Heart Association (NYHA)
HF Classification I-IV?
I –asymptomatic or only symptomatic with activities that
would limit anyone
II– symptomatic with usual exertion
III– symptomatic with minimal exertion
IV—symptomatic at rest
What are Non-Pharmacologic Management of HF?
Sodium restriction
Smoking cessation when applicable
Limited alcohol intake (one drink per day in women or 2 drinks per day in men)
Daily aerobic exercise
Lipid control
Glucose control in diabetics
Tight BP control
Avoid NSAIDS due to potential of increased fluid
retention
Treatment of thyroid conditions when applicable
How do Loop diuretics treat HF?
Work in the ascending loop of Henle to inhibit sodium
and potassium reabsorption
Causes decreased renal blood flow resulting in less fluid
being absorbed back into the bloodstream
How do ACE Inhibitors work to control HF?
Produce vasodilation by inhibiting the conversion of
angiotensin I to angiotensin II
Inhibit the breakdown of bradykinin which is a
powerful vasodilator
Reduce CV preload
Reduce CV afterload
How do ARBs work to treat HF?
Blocks angiotensin II (a powerful vasoconstrictor) on the
surface of target cells
Angiotensin receptors noted as AT1 or AT2
Does not interfere with bradykinin
How do Beta blockers work to treat HF?
Blockade of beta adrenergic receptors resulting in: Decreased heart rate Decreased BP Decreased oxygen demand Promote peripheral vasodilation
How does Spironolactone work to treat HF?
Works in the distal renal tubule
Aldosterone antagonist
Sodium and water are excreted
Potassium is retained
How does Digoxin work to treat HF?
Inhibits NA+/K+ pump+
Increases myocardial contractility
Decreases heart rate
Very long half-life: 36 hours
5-6 days to reach steady state
Requires loading dose
Narrow therapeutic window
What is some Patient Teaching for HF ?
Medication compliance
Patient participation in treatment plan
Daily weights
Healthy diet
Fluid restriction when applicable
Name the drug classes for HTN - ABCD
ACE Inhibitors (angiotensin-converting enzyme inhibitors)
ARBs (Angiotensin II Receptor Blockers)
Alpha blockers
Beta Blockers
Calcium Channel Blockers
Diuretics
which class of HTN meds end in ‘pril’
ACE inhibitors
which class or HTN meds end in ‘sartan’
ARBs
which class or HTN meds end in ‘osin’ or ‘zosin’?
alpha blockers
which class or HTN meds end in ‘lol’ ?
Beta Blockers
which class or HTN meds end in ‘dipine’?
calcium channel blockers
which class or HTN meds end in ‘ide’?
diuretics
What is the indication for Beta Blockers?
systolic and diastolic failure, but esp. If diastolic HF is caused by increased diastolic filling time
What is the MOA for Beta Blockers?
Blockade of beta adrenergic receptors resulting in:
- Decreased HR
- Decreased BP
- Decreased O2 demand
- Increase diastolic filling time
- Peripheral vasodilation
- Regression of L-ventricular hypertrophy
What are the precautions for Beta blockers and labs to monitor?
Pt has to be dry and in stable HF (minimal fluid retention)
Don’t start or change dose if pt has exacerbation of HF or fluid overload
• Monitoring: CBC, CMP
Why should beta blockers NOT be used as first line for HTN?
high risk of developing DM
Beta Blockers are contraindicated in…
African American pt asthma/COPD severe peripheral vascular dx Raynaud’s depression bradycardia 2nd/3rd defer heart block hypoglycemic prone diabetic patient
Patient education for Beta Blockers
- Reports SOB, nocturnal cough, lower extremity edema
- Don’t stop abruptly
- Monitor pulse, notify MD < 50
- w/ diabetic pts: can mask signs of hypoglycemia
- use caution when performing hazardous task bc of CNS side effects
- exercised induced fatigue may develop
Mechanism of Action for Beta blockers
MOA → competitive blockade of the B adrenergic receptor
• Results in decrease HR, myocardial contractility, BP and myocardial oxygen
demand
• Suppresses renin release
• Relieve the symptoms of angina by competitively inhibiting sympathetic
stimulation of the heart (so reduced HR and contractility)
• Promote peripheral vasodilation
β1 receptor →
mainly in the heart and stimulation from catecholamines causes an
increase in HR, BP, myocardial contractility and AV conduction
β2 receptors →
also in heart but mainly in lungs/ peripheral vascular smooth muscles
Pharmacokinetics of Beta Blockers?
• Either excreted by liver or kidney
Propranolol and metoprolol → lipid soluble; almost completely absorbed by the
small intestine and largely metabolized by the liver(These drugs readily enter CNS; SE: lethargy, confusion, sleep disturbances and depression
• Needs to enter the CNS bc it is used to treat migraines
• Have adverse metabolic effects → limits their usefulness in pts w/
hypercholesterolemia and DM (may blunt s/s of hypoglycemia)
β-Blockers must be used w/ caution in pts w/ certain heart conditions, such as …
heart block,
sinus brady
cardiogenic shock or HF
Βeta blockers can be used to treat:
Angina, arrhythmia, compensated HF, post MI, tremors, glaucoma and vascular
HA
the treatment of choice for CHRONIC STABLE and UNSTABLE angina
Most pts will be on nitrates, but β blockers are used when the pt needs to be nitrate
free
Briefly explain the Renin Angiotensin System (RAS)?
drop in blood flow to the renal arteries results in the release of Renin which subsequently activates RAS
Angiotensin is produced in the liver, separated by renin and then converted to Angiotensin I
Angiotensin Converting Enzyme (ACE) converts angiotensin I to Angiotensin II
Angiotensin II is a powerful vasoCONSTRICTOR.
It also stimulates the release of aldosterone, antidiuretic hormone and causes sodium reabsorption of Na+
This leads to Increased fluid retention, higher blood volume, & higher BP
What is the MOA of alpha 1 receptor blockers?
blocks post synaptic alpha 1 adrenergic receptors resulting in vasodilation and decreased peripheral vascular resistance
tends to affect DIASTOLIC BP more than systolic
also results in relaxation of bladder neck and prostate so often used for the Tx of bladder outlet obstruction such as BPH
examples: doxazosin, prazosin
Describe MOA of centrally acting alpha 2 antagonists
stimulate central inhibitory alpha adrenergic receptors
stimulate sympathetic cardioaccelerator and vasoconstrictor areas
results in decreasedsympathetic outflow from the CNS
-reduced peripheral vascular resistance, reduced pressure in the renal system and decreased heart rate
EXAMPLES: clonidine, methyldopa
nonpharmalogical treatment for HTN?
lifestyle modification is number 1 recommendation dietary modification (low sodium) exercise stress management avoid ETOH smoking cessation
MOA of direct vasodilators?
relaxation of vessel smooth muscle and decreases peripheral vascular resistance
stimulates carotid sinus baroreceptors that can increase HR, renin release and Na+ + H20 retention
EXAMPLE: hydralazine, Minoxidil
MOA of Renin inhibitors
blocks the action of Renin as the RAS cascade begins
EXAMPLE: Tekturna
patient monitoring for Methyldopa?
- CBC at baseline
- LFT’s within 12 weeks of initiating therapy
- periodic LFT’s
- Renal function at baseline and periodically
Patient monitoring for direct vasodilators?
consider EKG at baseline
renal function at baseline and periodically
monitor for blood dyscrasias
watch for weight gain and other signs of edema
ANA (check for autoimmune disease)before initiation of Hyrdalazine
what type of hypertension is more common in the elderly?
systolic
What are the dangers with alpha 1 in the lederly?
can cause tachycardia and syncope which can be more exaggerated in the elderly
which type of HTN med should be used for pts with renal insufficiency?
central acting alpha 2 adrenergics
What is the risk with clonidine use for the elderly?
can cause sedation which can increase risk for falls
what OTC meds should be avoided by pts w/ HTN?
cold/cough meds –can raise BP
What is preload?
stretch of the ventricles prior to contraction
preload is created by blood filling the ventricle in preparation for contraction
What is afterload?
resistance the left ventricle has to overcome to empty its contents into peripheral circulation
What is peripheral vascular resistance?
pressure (within the periphery) that the left ventricle must overcome w/ each contraction
Secondary Risk Factors for high cholesterol
- Diabetes mellitus
- Cardiovascular disease
- Thyroid disease
- Chronic renal disease
- Chronic obstructive liver disease
- Certain medications
- Beta blockers
- Oral contraceptives
- Corticosteroids
- Thiazide diuretics
Screening Recommendations for hyperlipidemia
Patients age 20 and older every 5 years
• The USPSTF recommends using fasting total cholesterol
and HDL alone in males age 35 and older and females
age 45 and above
• ACC/AHA recommends screening via a non-fasting
triglyceride level. If the level is below 200mg/dl then no
further testing is warranted. If the level is above 200mg/dl,
a fasting lipid panel is warranted
Components of a Lipid Panel
Total cholesterol (<200mg/dl) • Triglycerides (<150mg/dl) • HDL (>60mg/dl) • LDL (<190mg/dl in non-diabetics and patients without CVD)
Non-Pharmacologic Therapy for hyperlipidemia
In some individuals therapeutic lifestyle changes (TLC)
can result in a 5-15% decrease in LDL
• No more than 200mg of cholesterol per day
• 20-30g of fiber per day
• Total fat intake less than 30% of total calorie intake
• BP control
• 30 minutes of aerobic exercise 5 times per week
• Smoking cessation when applicable
• Healthy weight management
what are the Current guidelines target 4 high risk groups that
necessitate statin therapy:
Group 1: Patients with known ASCVD
Group 2: Patients with an LDL > 190mg/dl
Group 3: Diabetics aged 40-75 with an LDL of
79-189mg/dl
Group 4: 10 year risk for ASCVD > 7.5% and an
LDL 70-189mg/dl
HMG-CoA Reductase Inhibitors (Statins)
• Mechanism of action (MOA)
Reversible competitive inhibitors of HMG CoA reductase which is a
rate limiting enzyme used for cholesterol synthesis
• Cholesterol synthesis is reduced thereby reducing intracellular
cholesterol
***Statins may cause a moderate increase in HDL and a mild
decrease in triglycerides
• Statin medications are categorized into 3 categories
based upon “strength” or effect at lowering LDL-C
Low intensity(lowers LDL by approx. 30%)
- Simvastatin 10mg
- Pravastatin 10-20mg
- Lovastatin 10mg
- Fluvastatin 20-40mg
- Pitavastatin 1mg
• Statin medications are categorized into 3 categories based upon “strength” or effect at lowering LDL-C Moderate intensity (lowers LDL approx. 30-49%)
- Atorvastatin 10-20mg
- Rosuvastatin 5-10mg
- Simvastatin 20-40mg
- Pravastatin 40-80mg
- Lovastatin 40mg
- Fluvastatin XL 80mg
- Fluvastatin 40mg BID
- Pitavastatin 2-4mg
Statin medications are categorized into 3 categories
based upon “strength” or effect at lowering LDL-C
High intensity (lowers LDL approx. > 50%)
- Atorvastatin 40-80mg
* Rosuvastatin 20-40mg
Monitoring parameters for statins
Liver function tests (LFTs) at baseline and as clinically
indicated thereafter
• Repeat lipid profile 1-3 months after statin therapy is
initiated
• CK only if clinically indicated i.e. patient reports significant
myalgia
Statin Adverse Effects
- Myalgias
- Increased LFTs
- Fatigue
- Headache
- Insomnia
- Erectile dysfunction
Patient Teaching for Patients
on Statin Therapy
• Importance of follow up lab checks
• Importance of immediately reporting myalgias, weakness,
fever
• Importance of taking medication daily
• Importance of therapeutic lifestyle changes in addition to
medication therapy
Other Statin Considerations
Cholesterol and triglyceride levels increase during
pregnancy
• Statin use is contraindicated during pregnancy and
lactation
• May need dose reduction when prescribed to elderly
Other Lipid Lowering Medications
Statin therapy is primary treatment for hyperlipidemia
according to ATP IV guidelines
• Fibric acid derivatives
Primarily focused on lowering triglycerides
May increase HDL
• Bile acid sequestrants
Safe treatment because there is no systemic absorption
Exchange anions for bile acids preventing bile acid absorption from
the GI tract
Nicotinic acid
• Increases lipase activity resulting in increased greater triglyceride
removal from plasma
• Selective cholesterol absorption inhibitors
• Inhibits absorption of cholesterol from food intake and internal
sources
JNC 7 recs for HTN
120-140 (pre HTN)
140-160 (HTN stage 1)
160 + (HTN stage 2)
NEW GUIDELINES for HTN
120-130 (elevated BP)
130-140 (stage 1)
140 + (stage 2)
Main classes of HTN meds
A- ACE/ARB (don’t use these together) these increase K+
B – beta BLCOKERS (NOT FIRST LINE)
C -Calcium Channel Blocker (better for AfrAme)
D -Diuretics (better for AF AMER) –LASIX good for low EF
Heart Failure is..
Heart muscles inability to properly function and move blood into the peripheral circulation
Leads to pulmonary congestion and peripheral volume expansion, subsequently the renin-angiotensin -adolsterone system in activated
s/s SOB, dyspnea on exertion, peripheral edema, fatigue, malaise
LOOP DIURETICS are
Foundational Tx
START HF pts w/ lood diuretic as soon as Dx
Low dose at first (20-40mg)
Ascending loop of henle to inhibit sodium and potassium reabsorption
Less fluid absorbed back into blood stream= less overall circulating blood volume
EX- Lasix
ACE INHIBITORS
Produce VASODILATION through the inhibition of the conversion of angiotensin I to angiotensin II
Also inhibit the breakdown of bradykinin which is a powerful vasodilator-more frefloating bradykinin in the syatem
Reduce preload and afterload
ACE inhibitors can cause a dry hacking cough in some pts – result of build-up of bradykinin (best to stop the drug)
ARBS (angiotensin receptor blockers)
Blocks angiotensisn II receptor s (powerful vasoconstrictor) on surface of target cells
ARBs do not interfere with bradykinin
(s no cough)
BETA BLOCKERS
Block beta adrenergic receptors Decreased HR, BP, O2 demand. Promotes peripheral vasodilation Pt needs to be stable in HF and ‘dry’ (no fluid overload) for use. Esp at initiation or dose changes Otherwise might worsen pt’s condition EX-carvedilol, metoprolol
SPIRONOLACTONE
Add on therapy for HF (usually for pts already on a diuretic) – short term use
Works in the distal renal tubule
Potassium sparing – MUST monitor electrolytes
DIGOXIN
Inhibits sodium/potassium pump Increases myocardial contractility LOG half-life 36 hours Requires loading dose NARROW therapeutic window Frequent lab monitoring required Pt ed re : digoxin toxicity
Pt teaching for HF
Understand dosing regimens Take meds as prescribed Diet restrictions Daily weights (3-5 lbs + /week needs to be reported - fluid gain) Fluid restriction when applicable
ACE INHIBITORS AND ANGIOTENSIN RECEPTOR BLOCKERS
• (ACEIs) and (ARBs) : similar in their therapeutic uses,, mechanisms of action and adverse effects
• ACEIs and ARBs : commonly used in the treatment of HTN
• They slow the rate of progression of chronic renal failure and diabetic nephropathy
• Mechanism of Action
o 2 types of angiotensin receptors: AT1 and AT 2
o ACEIs inhibit the breakdown of bradykinin (a potent vasodilator) by blocking the enzyme
kininase II (this is thought to cause the classic cough associated w/ taking this)
o ARBs block the effects of angiotensin II by blocking the binding of angiotensin II to its
receptors
ARBS differ from ACEIs in 4 ways:
▪ (1) ARBs are more active against AT1 receptors that are ACEIs
▪ (2) ACE inhibition is not associated with increased levels of angiotensin II as are
ARBs
▪ (3) ACEIs may increase angiotensin I levels
▪ (4) ACEIs increase levels of bradykinin in contrast to ARBs
Treatment Principles for ACE Inhibitors
ACEIs generally considered safe and effective in pts with mild to moderate renal
impairment (if renal clearance diminished needs dosage reduction)
o Dehydration and renal insufficiency increase risk of elevated K when ACEI is started
o Advantage of ACEIs/ ARBs: relative lack of serious adverse reactions
o Most common side effect of ACEIs : cough (persistent, dry and hacking)
o ARBs: most serious and potentially life threatening adverse reaction is ANGIOEDEMA
o Pt presents to EC with angioedema – must rule out use of ACEIs
o Other serious adverse effects:
▪ Hyperkalemia, hypotension, acute renal failure
▪ Abrupt withdrawal has NOT resulted in rebound HTN
HTN meds for Prevention of Renal Failure in Diabetes
o ACEIs and ARBs have been proven to slow the progression of diabetic nephropathy
How to Monitor ACE Inhibitors
Baseline chemistry, BUN, Cr and UA
o Once dose stable, recheck Cr and K after 2-4 weeks
o Periodic monitor of WBCs for leukopenia
o Monitor supine BP weekly while titrating dose
o ACEIs may cause angioedema… most cases develop within 1 week of starting med ; > 65
yrs, hx of drug rash, seasonal allergies and AA all at high risk of developing angioedema
Patient Education for ACe inhibitors
ake missed dose ASAP; never take 2 doses together o Common side effects: ▪ Nonproductive cough ▪ Dizziness ▪ Light headedness o Serious adverse effects (notify MD) ▪ Swelling (face, mouth, hands, tongue, feet) ▪ Severe itching ▪ fainting ▪ Cloudy urine ▪ Sore throat ▪ Fever ▪ Sudden onset of abdominal pain ▪ Diarrhea/vomiting
Signs of excessive K in body:
▪ Irregular heartbeat ▪ Leg weakness ▪ Numbness or tingling of hands/ feet ▪ Extreme nervousness ▪ * avoid the use of K containing meds or salt substitutes while receiving this drug
fosinopril
Food affects rate but not extent of absorption
captopril and moexipril
Take captopril and moexipril 1 hour before meals
Ramipril capsules
can be opened and mixed w/ food
quinapril
Don’t take quinapril w/ high fat meal, reduces absorption by 25%
Lisinopril, captopril, enalapril, ramipril
decrease dose in renal insufficiency
• Lisinopril
Neutropenia and agranulocytosis can occur
o Typically takes 2 weeks for BP reduction to occur and 4 weeks for full effects to be seen
ACE and ARBS w/ Pregnancy and Lactation
Associated w. significant fetal risk
▪ Major congenital malformations – esp CV and CNS noted w/ use of ACEIS during
1st trimester
▪ captopril and enalapril classified by AAP as usually compatible w/ BF and may be
alternatives in certain clinical situations
Geriatrics and ACE and ARBs
Lower dose for pts w/ renal or hepatic insufficiency
▪ Monitor for volume depletion
HTN meds for pts w/ left ventricular
EF < 40% and in those w. HTN, DM or CKD
ACE inhibitors should be started and continued indefinitely
Don’t give ACE inhibitors to pts w/:
ACEI allergy , renal failure, hypotension, shock, hx of bilateral renal artery
stenosis
Guidelines o the management of STEMI recommends
ACEIs should be initiated
within 24 hours of presentation in pts who are stable
How ACEs work Post MI/ High Risk of CV events
ACEIs prevent ventricular remodeling and improve endothelial fxn after MI
o Decrease action of fibrin, thereby reducing clotting
Calcium Channel Blockers (CCB)
Mechanism of Action
- Cardiac muscle
• CCBs decrease the force of myocardial contraction
• Decreasing the amount of calcium ions causes fewer actin and myosin cross-bridges to be
formed
→ decreases the force of contraction
→ results in negative inotropic effect
→ decreases cardiac output - Cardiac conduction system
• CCBs decrease automaticity in the SA node and decrease conduction in the AV node
• Automaticity: depolarized cell initiates an action potential without an external stimulus
• Normal characteristic of SA node
• Depolarization: inward calcium ion current generates an action potential
• Agents blocking inward calcium ions across SA nodal tissue decrease depolarization and
suppress automaticity.
• Agents decreasing calcium ion influx across AV nodal tissue slow AV nodal conduction and AV
refractory time.
• When AV conduction is prolonged, rate iv ventricular conduction slows - Vascular smooth muscle
• CCBs dilate the main coronary arteries and arterioles in normal and ischemic regions
• Helpful in treatment of angina pectoris
• CCBs reduce arterial pressure by dilating peripheral arterioles, resulting in reduced BP
• CCBs effective in treating vasospastic angina
How to monitor CCB?
Weekly titration
• Monitor periodically (3-6 months) once patient stable.
• Monitor digoxin levels if also taking CCBs
• Kidney and liver function tests
Geriatrics and CCBs
lower doses to avoid orthostatic hypotension; CCBs often drug of choice for elderly
Pregnancy/lactation and CCBs
Category C, excreted in breast milk (Nifedipine, verapamil, and diltiazem)
Race and CCBs
More effective in African-Americans
Nifedepine
• Indication:
vasospastic angina, stable angina, Raynaud’s disease, hypertension
o No effect on cardiac conduction => do not cause/treat arrythmias
Nifedepine Mode of action:
dilator of vascular smooth muscle, mild negative inotropic effect (less than
verapamil)
Nifedepine
Onset of action: 20 min
• Half-life: 2-5 hours
• Duration: 4-8 hours
• Excretion: renal (80%)
• Precautions: acute hepatic injury (elevated LFTs), peripheral edema
• Side effects: Pedal edema, cough, dyspnea, nausea, headache, flushing, dizziness
- Verapamil
• Indication: stable angina, vasospastic angina, hypertension.
• Mode of action: dilator of smooth muscle – less potent than nifedipine significant negative
inotropic effect, relieves coronary spasms
• Onset of action:
• Half-life:
• Duration:
• Excretion: renal and feces
• Precaution: hypotension, may cause first degree block, elevated liver enzymes, antiplatelet
effect
• Side effects: constipation, muscle cramps, Stevens-Johnson syndrome
- Diltiazem
Indication: stable angina, vasospastic angina, hypertension, Raynaud’s disease.
• Mode of action: more effect on cardiac muscle than vascular smooth muscle
• Onset of action: 30 min
• Half-life: 3-7 hours
• Duration:
• Excretion: renal and bile
• Precaution: aortic stenosis, bradycardia, breastfeeding, hepatic disease, ventricular dysfunction.
• Side effects: pedal edema, headache, Stevens-Johnson syndrome
pt education for CCBs
• May experience hypotensive effects during titration
• Report swelling of feet or shortness of breath, irregular heartbeats, nausea, dizziness,
constipation
• Extended-release tablets may appear as inert shells in feces
• Avoid grapefruit juice
• Abrupt withdrawal of CCBs may cause increased chest pain => gradually taper dose
Angina classification
Stable or chronic - no change in past 2 months in terms of frequency, duration (<15 min), or
causes. Symptom pattern is reproducible.
• Unstable – change in pattern of pain (frequency, severity, duration), less precipitating factors.
Pts should be admitted to coronary care unit.
• Variant (Prinzmetal’s angina) - coronary artery spasm. Very rare. Pain occurs at rest and
develops b/c of spasm and not result of increased myocardial O2 demand
• Silent ischemia – asymptomatic episodes of myocardial ischemia that can be detected with ECG
Stable or chronic angina
no change in past 2 months in terms of frequency, duration (<15 min), or
causes. Symptom pattern is reproducible.
unstable angina
change in pattern of pain (frequency, severity, duration), less precipitating factors.
Pts should be admitted to coronary care unit.
Variant (Prinzmetal’s angina)
coronary artery spasm. Very rare. Pain occurs at rest and
develops b/c of spasm and not result of increased myocardial O2 demand
Silent ischemia
asymptomatic episodes of myocardial ischemia that can be detected with ECG
treatment of Stable angina (long-term mgmt):
antiplatelets, β-blockers, CCBs, long-acting nitrates, potassium channel openers (ranolazine), ACEI, aspirin, statin, possible revascularization
treatment of Unstable angina
aspirin, clopidogrel/ticlopidine
treatment of Acute attack of angina
nitrates
Acute Attack of angina
Remember MONA (minus the morphine and not in that order)
• Give NTG sublingually at 3-5 min intervals for 3 doses. If angina is worse or unimproved 5 min
after 1st dose, call EMS.
• Give O2, at 2L/min, via nasal cannula.
• Chew regular aspirin (325 mg) while waiting for EMS.
• Thrombolytic therapy
Nitrates
• Mode of action:
Relax vascular smooth muscle via stimulation of intracellular cyclic guanosine
monophosphate production
o Reduce myocardial O2 demand, by decreasing preload and (to a lesser extent) afterload
o Major dilation of venous bed
o Increase use of coronary collaterals so perfusion to myocardium is improved
Drug interactions: for nitrates
Alcohol. (NTG + ETOH can lower BP)
Precautions w/ nitrates
Older pts at risk for syncope with NTG
o Tolerance to nitrates is an issue. To prevent tolerance, interrupt therapy for 8-12
hours/day (take off patch or stop oral medication in PM and restart in AM)
Side effects w/ nitrates
flushing of face, brief throbbing headache, increased HR, dizziness, light-headed
when change position rapidly
teaching for nitrates
Have pts keep record of PRN medication use, bring to appts
o Keep record of anginal attacks, frequency, NTG side effects
o Have pt sit or lie down before take NTG
o Obtain new Rx every 3 months and discard old NTG. (NTG loses its strength 3 months
after opening the bottle.)
o Store NTG in original dark glass container w/o cotton wadding and out of sunlight.
o Rest for 10-15 min after pain is relieved
o Notify provider if you have blurring of vision, persistent headache, or dry mouth
o Use NTG in prevention of possible anginal attacks (exercise, sex)
o Don’t stop taking NTG abruptly
Cardinal Points of Treatment for HTN meds
Loop diuretics for fluid retention
• ACE inhibitor (ACEI) unless contraindicated / or ARB if ACEI not tolerated
• Β-blocker – esp. For diastolic HF (start only when pt is stable on ACEI)
• Digoxin for systolic HF and a-fib
• Spironolactone if above are not effective
• Nitrates and hydralazine in African-Americans only, if cannot tolerate above
• CCB only if needed for angina or HTN, and if EF is preserved
• Na+ restriction
Digoxin
Digoxin uses
• Indication: Used for systolic HF b/c of its inotropic properties, a-fib, diuretic failure
• Mode of action:
o Inhibits Na+/K+ pump
o Increases myocardial contractility
o Decreases HR
• Onset of action: Requires loading dose, 5-6 days to reach steady state
• Duration: Very long half-life: 36 hours
• Excretion: excreted unchanged, so levels can quickly reach toxic proportions. Excreted over 6
days d/t long half-life
HMG – CoA Reductase Inhibitors (Statins)
MOA
decreases cholesterol synthesis causing a decrease in LDL. Also increases HDL.
HMG – CoA Reductase Inhibitors (Statins)
monitoring
Ask pt about myalgias; check CPK if present
• Eye exam for cataract risk
• LFTs at baseline and as clinically indicated thereafter
• Lipid panel at baseline and 1-3 months after therapy initiation
• Protease inhibitors and statins taken together may raise the blood levels of statins and
increase the risk of muscle injury
Atorvastatin (Liptor) Contraindications
- Contraindications:
- Active liver disease
- Pregnancy/lactation
- Precautions:
- Liver dysfucnction
- Rhabdo with acute renal failure
- Peak Concentration– 1-2 hr
- Half Life– 14hr
