HTN II Flashcards
- What BP is HTN for home monitoring?
2. 24-hr BP Dx of HTN
- > 135/85 mmHg (office measure is 140/90)
2. >130/80 mmHg
BP Follow-Up Timeline:
- Normal
- Pre-HTN
- Stage 1
- Stage 2
- Recheck in 2 years
- Recheck in 1 year
- Confirm w/in 1 month
- Evaluate or refer w/in 2 weeks
If BP is =/> 180/110, evaluate and treat immediately or within 1 week
Initial Dx of HTN: 3 key steps
- Identify possible secondary causes of high blood pressure
- Identify other cardiovascular disease
risk factors - Assess for target organ damage
Physical Exam for Dx HTN
Physical Examination • Check the BP in both arms • Obtain orthostatic blood pressures (especially elderly) • Cardiac: palpation and auscultation • Vascular: pulses, carotid, abdominal, and femoral bruits • Abdomen: masses and aortic pulsation • Lower extremities: edema • Palpate thyroid • Examine optic fundi
Initial Lab Tests
Initial Laboratory Tests • Urinalysis • Blood glucose • Hematocrit • Serum potassium • Serum calcium • Serum creatinin, GFR • 12-lead ECG • TSH • Fasting lipid panel: HDL-c, LDL-c, TGs
Major classes of anti-HTN drugs:
• Angiotensin -converting enzyme inhibitors • Angiotensin receptor blockers • Calcium channel blockers • Diuretics
Other anti-HTN drugs
• β-Blockers • α-Blockers • Direct vasodilators • Aldosterone antagonists • Direct renin inhibitors • Central α2 agonists
What drugs must you not use for HTN in pregnant women?
ACE-inhibitors, angiotensin receptor blockers, renin inhibitors
ACE-inhibitors:
- Name/example:
- Mechanism
- Effects
- Side Effects
- Misc.
- “…pril”–captopril
- Bind to angiotensin converting enzyme
- Effects:
a) ++ Ang I
b) – Ang II
c) ++ Renin
d) – aldosterone
e) –peripheral arterial resistance
f) –intravascular volume - CATCHH
- Protects the kidneys: dilates vessels, lowers intraglomerular pressure
ACE-I Side Effects
CATCHH
a) Cough
++ BK in lungs
5-20%
dose-dependent
b) angioedema
*potentiation of BK
>90% can take an ARB
-usually in 1st month
-Swelling of tongue and laryngeal mucosa
•Greater risk among African
Americans
c) teratogen
- Need Ang II for fetal kidney
d) creatine bump (up to 30%)
- can cause worsening renal fxn in those with CKD, renal artery stenosis, cardiomyopathy, DM
e) hyperkalemia
- typical of all RAAS inhibitors
- Na+/K+ pump: we dump Na+ therefore we keep K+
f) hypotension-blocking RAAS
Angiotensin Receptor Blockers (ARBs)
- Name/example:
- Mechanism
- Effects
- Side Effects
- Misc.
- “…sartan”
- Selectively block AT1 receptor; thus Ang II can’t bind
- Effects:
a) ++ Renin
b) – aldosterone
c) –peripheral arterial resistance
f) –intravascular volume
g) inhibits sympa activation, vasoconstriction, cell growth, Na+ fluid retention - Similar S/E to ACE-i but better S/E profile
- hyperkalemia
- ++creatinine - No effect on BK (thus less incidence of cough and angioedema)
AT1 Receptor
Blocked by ARBs from binding Angiotensin II
Normally: vasoconstriction, sympathetic activation, cell growth, Na+ fluid retention
Diuretics:
- Mechanism
- Effects
- Side Effects
- Loop
- Thiazide
- Misc.
- Increase urinary excretion of sodium
at various sites in the kidney - Venodilation, decreases intravascular
volume, lowering blood pressure
3. Side Effects: Volume depletion • Hypotension, orthostasis • Electrolyte changes: −Hypokalemia −Hypomagnesemia −Hyponatremia (thiazide) −Hypercalcemia (thiazide) •Hyperkalemia (potassium sparing) diuretics) -stable after 1st 3-7 days • Ototoxicity (Loop) • Metabolic side effects: −Hyperglycemia −Hypercholesterolemia −Hyperuricemia (loop)-->gouty arthritis • Erectile dysfunction • Sulfa-allergy
- Loop: more potent
- ex) furosemide
- great in decompensated heart failure
- potent venodilators, natriuretic agent
- S/E: ototoxicity, ++Ca2+ excretion–>worsens osteoporosis - Thiazide
ex) hydrochlorothiazide (chlorthalidone)
- cheap and useful
- Decreases ECF and dilates peripheral arterioles
a) short term effects (1-2 weeks): decreases ECF volume, small bump in peripheral resistance, decreased BP
b) long-term effects: Steady lower levels of BP, peripheral resistance, and fluid volume
- as CO returns to baseline, SVR decreases - Not good for diabetics
Ca2+ Channel Blockers
- Mechanism
- Effects:
- Dihydropyridine
- Non-dihydropyridine
- Side Effects
- L-type Ca2+
channels: Ca2+ influx and smooth muscle contraction
•
CCBs bind
to receptors:
-vasodilate arteriolar smooth muscle
-decrease peripheral
vascular resistance - Effects:
* ++ RBF–> ++nariuresis
* dilating afferent arterioles
* ++glomerular filtration pressure - Dihydropyridine (amlodipine)
-Decrease Ca2+ influx into vascular SMCs
-chronic use-little effect on resting HR
-Can cause reflex tachycardia
S/E (due to arteriolar dilation): edema, headache, flushing, dizziness,
palpitations - Non-dihydropyridine
-verapamil, diltiazem
-also decrease Ca2+ influx into myocardium (decreases HR)
-S/E: bradycardia, AV
block, CONSTIPATION - General S/E:
-Gingival hyperplasia
-Aggravate
gastroesophageal
reflux due to
inhibition of LES
contraction
-inhibits CYP34A: increasing blood levels of other meds
-hypotension
-headache
-ankle edema
-nausea
Direct Renin Inhibitors
- Mechanism
- Warnings
- Side Effects
- Example
- Advantages?
- Blocks the “rate
limiting step” of
RAAS
2. Do not use with ACE-I or ARB: Increased incidence of nonfatal stroke, worsening kidney function especially with diabetes
3.Side effects overlap
with ACE-Is and ARBs
- Aliskiren
- ACE-Is and ARBs cause compensatory increase in renin (decreases their efficacy), whereas renin inhibitors do not
Aldosterone Antagonists
- Mechanism
- Effects
- Benefits
- Risks
- Spironolactone
- Eplenerone
- Aldosterone interacts with mineralcorticoid
receptors; Antagonist BLOCK receptors - Effects:
* –NaCl reabsorption
* blocks vasoconstriction
* blocks endothelial dysfunction
* blocks hypertrophy of vascular SMCs - Beneficial in resistant hypertension and
when combined with other diuretics - Increased risk of hyperkalemia when
combined with
ACE-I or ARB
5. Spironolactone (non-selective): −Men: erectile dysfunction, gynecomastia (10%) −Women: menstrual abnormalities -also helps in heart failure
- Eplerenone
(selective) -better S/E profile
β-Adrenoceptor Blockers (β-Blockers) 1. Effects: 2. B1 vs. B2 3. Intrinsic sympathomimetic activity 4.Vasodilatory Properties 5. Misc.
“…lol”
- Effects: Generally inhibits effects of catecholamines (Epi and NE), decreasing SNS activity
•Decreased CO, inhibit renin secretion, inhibit NE release •Reductions in HR due to decreased automaticity in sinus node (negative chronotropic effect) •Reduces ventricular hypertrophy, stroke, heart failure, coronary events, and mortality
- •β1 (selective): myocardium, less effect
on airways
•β2 (non-selective): myocardium, vascular, bronchial cells - weak β-adrenergic activation
- (ex: carvedilol):
antagonize α-adrenergic receptor and increase NO release - Not 1st line HTN tx
- used for heart failure - Side Effects:
•Bradycardia, heart block, dizziness
•Bronchospasm, cold extremities (β2 effect)
•CNS effects: fatigue, depression, mental
slowness, vivid dreams, dry mouth
•Erectile
dysfunction,
hyperglycemia
•Lipid abnormalities (triglyceride elevation,
HDL reduction)
Direct Vasodilators:
General
•Usually given
with a diuretic and
β-blocker to prevent
“pseudotolerance”
−compensatory increased SNS activity and increased RAAS: Tachycardia and edema
•4th or 5th line due to side effects and dosing frequency
Direct Vasodilators: Hydralazine
•Directly relaxes vascular smooth muscle •Decreases peripheral resistance •Metabolism is genetically determined −N-acetyltransferase -Takes places in liver -Slow acetylators: greater S/E's •high doses increase risk for lupus-like syndrome rxn •parenterally for HTN Emergency
Direct Vasodilators:
Minoxidil
•more potent
•Opens K+channels in vascular SMC
•Similar hemodynamics as hydralazine
•Most useful in patients with severe hypertension
•Use limited by S/E: pericardial effusion (3%),
tachycardia, facial hirsutism, elevated pulmonary artery pressure
-ST segment depression
-T-wave changes due to increased myocardial demand
•rapidly absorbed via GI
α-Adrenergic Receptor Blockers
•Selective α1-antagonists -Blocks site for norepinephrine, inhibiting SMC contraction •Decrease arteriolar resistance •Beneficial in patients with prostate symptoms (ex:doxazosin) to decrease urinary symptoms •Side effects: −Postural hypotension −Dizziness, syncope −Reflex tachycardia −Nasal congestion −Volume expansion
- *not a monotherapy
- **Non-selective a-adrenergic receptor blockers are NOT effective for HTN
Central
Sympatholytics
•α2 agonists (clonidine, methyldopa)
•Directly reduce sympathetic outflow to the heart and blood vessels by acting on BS
-stimulation inhibits SNS–>vasodilation
•Side-effects: sedation, DRY MOUTH, erectile dysfunction, depression
•Clonidine: rapid onset
-REBOUND hypertension, skin hypersensitivity (20%)
•Methyldopa: pregant HTN
-Coombs’positive hemolytic anemia, elevated lever function tests
Compelling
Indications for
Specific Blood Pressure Medication Classes:
- Heart Failure
ARB (or ACE-I) + β-blocker + diuretic + spironolactone;
Add dihydropyridinefor
improved BP control if needed
Compelling Indications for Specific Blood Pressure Medication Classes: Post-myocardial infarction/Coronary Artery Disease
1st: ACE-I (or ARB) + β-blocker*
2nd: CCB or thiazide diuretic
* some patients will need a β-blocker based on LV ejection fraction
Compelling
Indications for
Specific Blood Pressure Medication Classes: DM or CKD
1st: ACE-I (or ARB)
2nd: CCB or diuretic
Goal for DM:
Compelling
Indications for
Specific Blood Pressure Medication Classes:Recurrent Stroke Prevention
1st: ACE-I (or ARB)
2nd: Thiazide or CCB
Hypertensive Urgency/Emergency
*Medications for either
•Urgency: high blood pressure but without acute target organ damage −Receive immediate treatment with oral (+/− IV)antihypertensive therapy
•Emergency: Severe hypertension and
acute target organ damage
−Requires hospitalization and immediate parenteral medication therapy
-pulmonary edema, MI, stroke, retinal bleeding
-Tx Goal: reduce MAP by no more than 25% w/in 2 hours or decrease to approx. 160/100
- Meds generally for emergency:
1. Vasodilators: - nitroprusside
- nitroglycerine
- hydralazine
- enalapril
- Adrenergic Inhibitors
- Labetalol (a, B-blocker)
- esmolo (B1-selective blocker)
**Can use the above for urgency, but usually oral clonidine
Resistant Hypertension
- Definition
- Dx
- Risk Factors/Characteristics of Pts
Resistant Hypertension
1. •BP ≥140/90 mmHg while on 3 different
BP medication classes (incl. diuretic)
−or on 4 antihypertensive drug
classes regardless of
blood pressure
-significant factor: excess Na+ retention–>excess volume
-obesity –> impaired Na+ excretion, increased SNS, sleep apnea
- •Exclude pseudo-resistance (make sure they’re taking their meds)
•Identify and reverse contributing
factors
•Discontinue/minimize interfering substances: alcohol, OTCs, drugs, other meds
•Screen for secondary causes - Factors:
- Older
- obese
- LVH
- Na+/volume retention
- female
- African American
- DM
- CKD
Factors Affecting Patient Adherence
Misunderstanding of condition or need for treatment • Absence of symptoms • Adverse effects of medications • Cost and simplicity of medication regimen • Cost of follow-up visits • Perceived lack of involvement in care plan
HTN Treatment Goals
Less than 140/90 for most people and diabetics
But if 80 or older, the goal is less than 150/90
