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Hypertension > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Pre-Hypertension

Classification and management

A
  • systolic bp 120-139 mm Hg
  • diastolic bp 80-89 mm Hg
  • without compelling indication - no drug therapy indicated
  • with compelling indication - drugs for compelling indication
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2
Q

Stage 1 HTN

Classification and management

A
  • SBP - 140 - 159 mm Hg
  • DBP - 90 - 99 mm Hg
  • without compelling indication - thiazide-type diuretic, ACEI, ARB, DHP-CCB
  • with compelling indication - drugs for compelling indications. other antihypertensives as needed
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3
Q

Stage 2 HTN

Classification and management

A
  • SBP of 160 mm Hg or greater
  • DBP of 100 mm HG or greater
  • Without compelling indication: two drug combination for most (usually thiazide-like diuretic and ACEI, ARB or DHP-CCB)
  • with compelling indication - drugs for compelling indications. Other antihypertensives as needed
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4
Q

Identifiable causes of HTN

A
  • sleep apnea
  • drug induced or related causes
  • CKD
  • primary aldosteronism
  • renovascular disease
  • chronic steroid therapy or Cushings syndrome
  • pheochromocytoma
  • coarctation of the aorta
  • thyroid or parathyroid disease
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5
Q

Risks of HTN

A
  • pts 40 -70 years each increment of 20mmHg SBP or 10mmHg DBP doubles the risk of CVD across the range of 115/75 - 185/115 mmHg
  • Target organ damage:
    • heart
      • left ventricular hypertophy
      • angina or MI
      • coronary revascularization
      • heart failure (HF)
        • reduced left ventricular ejection fraction
        • preserved left ventricular EF
    • brain - stroke or TIA
    • CKD
    • PAD
    • Retinopathy
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6
Q

Benefits of Lowering BP

A
  • Associated with the relative risk reduction in the incidence of:
    • Stroke - 35-40%
    • MI - 20-25%
    • HF - greater than 50%
  • in patients with stage 1 HTN and additional cardiac risk factors, achieving a sustained 12mm Hg over 10 years will prevent one death for ever 11 patients treated
  • In the presence of CVD or other target organ damage, only nine patients would require such a BP reduction to prevent a death.
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7
Q

Accurate BP measurement

A
  • seated quietly for 5 minutes with feet on floor, back supported, and arm supported at heart level
  • appropriate sized cuff
  • at least two measurements should be made
  • clinicians should provide to patients, both verbally and in writing, their specific BP readings and goals
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8
Q

Self-Measurement of BP

A
  • helpful in evaluating white-coat HTN and long-term BP monitoring
  • home measurement devices should be checked regularly for accuracy
  • Automatically inflating arm devices are preferred over wrist monitors or manual inflation devices for accuracy
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9
Q

Lifestyle modification and HTN

A

1) weight reduction
- can reduce SBP by 5-20 mm HG for every 10kg
2) diet
- DASH diet can reduce SBP by 8-14 mm Hg
- Na restriction can reduce SBP by 2-8 mm Hg
3) exercise
- 30 minutes of aerobic activity on most days of the week can reduce SBP by 4-9 mm HG
4) moderation of alcohol consumption
- limiting to no more than two drinks a day for men or one drink a day for women can reduce SBP by 2-4 mm Hg

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10
Q

ACEIs

Mechanism of action

A
  • prevents conversion of angiotensin I to angiotensin II (potent vasoconstrictor) by competitive inhibition of ACE
  • results in lower BP secondary to lower levels of angiotensin II, increased levels of plasma renin activity, and a reduction in aldosterone secretion
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11
Q

ACEIs

Evidence

A
  • HOPE (Heart Outcomes Prevention Evaluation Study)
    - effects of ramipril on CV events in high risk patients
  • EUROPA
    - efficacy of perindopril in reduction of cardiovascular events among patients with stable coronary artery disease
  • PEACE
    - ACEI in stable coronary artery disease
  • PROGRESS
    - randomized trial of a perindopril-based BP lowering regimen among 6,105 patients with previous stroke or TIA
  • SAVE (Survival and Ventricular Enlargement trial)
    - effect of captopril on maortality and morbidity in patients with left ventricular dysfunction after MI
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12
Q

ACEIs

Clinical use

A
  • Compelling indications to use ACEIs 1st line
    • DM - reduces the progression of nephropathy and alunminuria
    • CKD - reduces the progression of diabetic and non diabetic renal disease
    • HF or left ventricular dysfunction with LVEF <40%
    • Post MI
    • High CAD risk
    • recurrent stoke prevention - reduces recurrence when used in combination with thiazide diuretic
  • Recommended add-on therapy to thiazide diuretic
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13
Q

ACEIs

contraindications

A
  • bilateral renal artery stenosis
  • pregnancy
  • angioedema
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14
Q

ACEIs

Important adverse drug reactions

A
  • increasing Cr - limited rise as much as 30% above baseline is acceptable. This becomes the patients new baseline
  • hyperkalemia
  • angioedema - occurs two to four times more frequently in African Americans
  • cough (dry)
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15
Q

ACEIs

Dosing and monitoring

A
  • consider avoiding in women during childbearing years
  • consider starting at lower-than-average dose if patient id elderly, in on concommitant diuretic therapy or has renal impairment
  • Monitor Cr and K 7-10days after initiation or titration
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16
Q

ARBs

Mechanism of action

A
  • selective, competitive antiotensin II receptor type 1 receptor antagonist, reducing end-organ response to angiotensin II
  • results in decreased total peripheral resistance (afterload) and cardiac venous return (preload)
  • reduction in BP occurs independently of the status of the renin-antiotensin system
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17
Q

ARBs

Evidence

A
  • LIFE - Losartan Intervention for Endpoint reduction in hypertension study
    • randomized trial against atenolol
  • VALIANT
    • valsartan, captopril, or both in MI complicated by HF, left ventricular dysfunction, or both
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18
Q

ARBs

Clinical use

A
  • recommended as first line, but generally reserved for patients who have ACEI intolerance
  • Compelling indications (typically after ACEI fail)
    • HF or left ventricular systolic dysfunction with LVEF of 40% or less
    • DM - reduces the progression of nephropathy and albuminuria
    • CKD - reduces the progression of diabetic and non diabetic renal disease
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19
Q

ARBs

Contraindications

A
  • bilateral renal artery stenosis
  • pregnancy
  • angioedema (ARB-induced or idiopathic)
    • although ARBs may be considered alternative therapy for patients who have developed angioedema while taking an ACEI, patients have also developed angioedema with ARBs.
      - extreme caution is advised when substituting an ARB in a patient who has had angioedema associated with ACEI use
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20
Q

ARBs

Important adverse drug reactions

A
  • Increasing SCr - limited rise of as much as 30% above baseline is acceptable. This becomes the patients new baseline
  • hyperkalemia
  • angioedema - less than with ACEIs
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21
Q

ARBs

Dosing and monitoring

A
  • consider avoiding in women during childbearing years

- monitor Scr and K 7-10 days after initiation and titration

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22
Q 
Renin inhibitor (aliskiren)
Mechanism of action
A
  • direct renin inhibition

- decreasing plasma renin activity and inhibiting the conversion of angiotensinogen to angiotensin I

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23
Q 
Renin inhibitor (aliskiren)
Evidence
A
  • no outcomes data available for aliskiren mono therapy
  • ALTITUDE - Aliskiren Trial in Type 2 Diabete Using Cardiovascular and Renal Disease Endpoints
    • trial terminated early
    • aliskiren added to ACEI or ARB therapy in patients with type 2 DM and renal impairment compared with placebo
    • an increase in adverse events (nonfatal stroke, renal complications, hyperkalemia and hypotension)
    • no apparent benefit to patients randomized to aliskiren
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24
Q 
Renin inhibitor (aliskiren)
Contraindicaitons
A
  • pregnancy

- do not use with ARBs or ACEIs in patients with diabetes

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25
Q 
Renin inhibitor (aliskiren)
Important adverse drug reaction
A
  • angioedema

- hyperkalemia if used concomitantly with ACEI

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26
Q 
Renin inhibitor (aliskiren)
Dosing and monitoring
A
  • consider avoiding in women during childbearing years
  • high-fat meals decrease absorption substantially
  • patients with renal insufficiency were excluded from trials
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27
Q

Beta blockers

Mechanism of action

A
  • selective (beta-1) or nonselective (beta1 and 2) receptor blocker results in negative inotropic and chronotropic actions
  • some (pindolol and acebutolol) exhibit intrinsic sympathomimetic activity meaning they are cpable of exerting low-level agonist activity at the beta receptor while simultaneously acting as an antagonist
  • cardioselective agents without intrinisic sympathomimetic activity are usually used for HTN
  • Carvedilol and labetalol also have alpha1 blocking activity
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28
Q

Beta blockers

Evidence

A

ACCF/AHA guidelines since the 1980s

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29
Q

Beta blockers

clinical use

A

1) Compelling indications
- HF or left ventricular systolic dysfunction wiht LVEF <40% or less - 1st line with ACEI
- Post-MI (within first 3 yearr) = First line
- High CAD risk
- DM

2) Controversy regarding the appropriateness of using as first line agent in patients without a compelling indication.

Beta-blockers with alpha1-blocking activity are likely more effective antihypertensive agents than beta-blockers without this mechanism

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30
Q

Beta-blockers

Contraindications

A
  • SA or AV node dysfunction
  • decompensated HF
  • severe bronchospastic disease
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31
Q

Beta-blockers

Important adverse drug reactions

A
  • bradycardia
  • heart block
  • bronchospastic disease
  • exercise intolerance, sexual dysfunction, fatique
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32
Q

Beta-blockers

Dosing and monitoring

A
  • relative contraindications include significant sinus or AV note dysfunction, hypotension, decompensated HF, and severe bronchospastic lunch disease
  • Monitor HR regularily
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33
Q

Thiazides

A
  • hydrochlorothiazide
  • chlorthalidone
  • metolazone
  • indapamide
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34
Q

Thiazides

Mechanism of action

A
  • Acts on kidneys to reduce Na reabsorption in the distal convoluted tubule.
  • by impairing Na transport in the distal convoluted tubule, natriauresis and concomitant water loss in induced
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35
Q

Thiazides

Evidence

A
  • ALLJAT
  • Preventnion of stroke by antihypertensive drug treatment in older people with isolated systolic HTN: Final results of the Systolic Hypertension in the Elderly Program (SHEP)
  • Medical Research Council (MRC) trial of treatment of mild hypertension: Principal results
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36
Q

Thiazides

Clinical use

A
  • prevents CVD complications
  • option as first-line therapy for most patients wiht HTN, either alone or in combination with other classes (ACEI, ARBs, beta-blockers, CCBs)
  • enhances the effect of multi-drug regimens
  • affordable but often underused
37
Q

Thiazides

Contraindications

38
Q

Thiazides

Important adverse drug reactions

A
  • electrolyte abnormalities (hypokalemia, hyponatremia)

- hyperuricemia

39
Q

Thiazides

dosing and monitoring

A
  • ineffective for patients with GFR less than 30 mL/minute

- monitor SCr, Na and K 7-10 days after initiation or titration

40
Q

Loop diuretics

A

furosemide
bumetanide
torsemide
ethacrynic acid

41
Q

Loop diuretics

Mechanism of action

A
  • acts by reversibly binding to the Na, K, chloride cotransport mechanism on the luminal side of the ascending loof of Henle, thereby inhibiting the active reabsorption of these ions
42
Q

Loop dirutetics

Clinical use

A
  • HTN management for patients with HF and CKD using scheduled twice-daily dosing
43
Q

Loop diuretics

Contraindications

44
Q

Loop diuretics

Important adverse drug reactions

A
  • electrolyte abnormalities (hypokalemia, hyponatremia, hypomagnesemia)
  • dehydration
45
Q

Loop diuretics

Dosing and monitoring

A
  • avoid in patient with a CrCl less than 10ml/min

- monitor SCr and K 7-10 days after initiation or titration

46
Q

DHP-CCBs

A

amlodipine
felodipine
nefidipine
nicardipine

47
Q

DHP-CCBs

Mechanism of action

A
  • act by relaxing the smooth muscle in the arterial wall, decreasing total peripheral resistance, and hence reducing BP
  • in angina they increase blood flow to the heart muscle
48
Q

DHP-CCBs

Evidenc

A
  • ACCOPLISH
  • Prevention ov CV efentwi the anti hypertensive regimen of amlodipine, adding perindopril as required vs atenolol, adding bedroflumethazine as required, in the Anglo-Scandinavian Cardiac Outcomes Trial-Blood Pressure Lowring Arm; a multicentre randomised controlled trial (ASCOT_BPLA)
  • Outcoms in hpertensive patients at high CV risk treated with regimes based on amlodipine or amlodipine (VALUE)
  • Effects of intensive BP lowering and low-dose aspirin in patients with HTN: Principal results of the Hypertension Optimal Treatment (HOT) randomized trial
49
Q

DHP-CCBs

Clinical Use

A
  • Option as first-line therapy for most patients with HTN
  • Potent BP lowering
  • improves anginal symptoms
50
Q

DHP-CCBs

Important adverse drug reactions

A
  • Peripheral edema
51
Q

DHP-CCBs

Dosing and monitoring

A
  • start at a low dose for elderly patients
52
Q

nonDHP-CCBs

A

verapamil

diltiazem

53
Q

nonDHP-CCBs

Mechanism of action

A
  • acts as a potent vasodilator of coronary vessels, increasing blood flow and decreasing the HR by strong depression of AV node conduction
  • also acts as a potent vasodilator of peripheral vessels, reducing peripheral resistance and afterload.
  • has negative inoptropic effects
54
Q

nonDHP-CCBs

Evidence

A
  • Principal results of the Controlled Onset Verapamil Investigation of Cardiovascular End Points trial (CONVINCE)
  • a calcium antagonist versus a non-calcium antagonist treatment strategy for patients with CAD: The International Verapamil-Trandopril Study: A randomized controlled trial (INVEST)
  • randomized trial of effects of calcium antagonists compared with diuretics and beta-blockers on CV morbidity and mortality in HTN: The Nordic Diltiazem study (NORDIL)
55
Q

nonDHP-CCBs

Clinical use

A
  • used for HTN in patients iwht concomitant conditions (e.g. atrial fibrillation or stable angina) who would benefit from these medications
56
Q

nonDHP-CCBs

Contraindications

A
  • heart block

- Sick sinus syndrome

57
Q

nonDHP-CCBs

Important drug reaction

A
  • bradycardia
  • heart block
  • constipation
58
Q

nonDHP-CCP

Dosing and monitoring

A
  • potent CYP inhibitors; potentially serious drug-drug interactions
  • do not use with concomitant systolic dysfunction HF (ejection fraction less than 40%)
  • use with caution in patient on concomitant beta-blocker therapy
59
Q

alpha-blockers

A

terazosin
doxaosin
prazosin

60
Q

alpha-blockers

mechanism of action

A
  • selective alpha-antagonsit that works by blocking the actions of adrenaline on smooth muscle of the blood vessel wall
61
Q

alpha-blockers

Evidence

A

ALLHAT showed a 25% higher rate of combine CVD and a 2-fold higher rate of HF compared with the diuretic arm

62
Q

alpha-blockers

Clinical use

A
  • in general, reserved for hypertensive patient with concomitant BPH
  • usually viewed as fourth- or fifth-line agent for HTN
63
Q

alpha-blockers

Important adverse drug reactions

A
  • dizziness

- orthostatic hypotension

64
Q

alpha-blockers

Dosing and monitoring

A
  • start with a very low dose
  • patient should consider taking the first dose at night while in bed
  • titrate slowly over time as needed
65
Q

Aldosterone receptor blockers

A
  • spironolactone

- eplerenone

66
Q

Aldosterone receptor blockers

Mechanism of action

A
  • inhibit the effect of aldosterone by competing for intracellular aldosterone receptors in the cortical collecting duct.
  • this decreases the reabsorption of Ns and water while decreasing the secretion of K
67
Q

Aldosterone receptor blockers

Evidence

A
  • efficacy of low-dose spironolactone in subjects with resistant HTN
  • the role of spironolactone in the treatment of patients with refractory HTN
68
Q

Aldosterone receptor blockers

Clincial use

A
  • resistant HTN

- patients with HTN and HF

69
Q

Aldosterone receptor blockers

Contraindications

A
  • Anuria
  • Acute renal insufficiency
  • Hyperkalemia
70
Q

Aldosterone receptor blockers

Important adverse drug reactions

A
  • hyperkalemia

- gynecomastia with spironolactone

71
Q

Aldosterone receptor blockers

Dosing and monitoring

A
  • monitor Cr and K -10 days after initiation or titration
72
Q

Central alpha2-agonists

A
  • clonidine
  • methyldopa
  • guanfacine
73
Q

Central alpha2-agonists

Mechanism of action

A
  • stimulates alpha2-receptors in the brain, which decreases sympathetic outflow cardiac output and peripheral vascular resistance, lowering BP and HR
74
Q

Central alpha2-agonists

Clinical use

A
  • may be useful for resistant HTN

- beneficial for hypertensive urgency

75
Q

Central alpha2-agonists

Important adverse drug reactions

A
  • dizziness and orthostatic hypotension
  • drowsiness
  • dry mouth
76
Q

Central alpha2-agonists

Dosing and monitoring

A
  • rebound HTN possible if withdrawn too quickly, especially if on concomitant beta-blocker (except carvedilol and loabetolol, because of unopposed alpha stimulation)
  • avoid in patients with HF
77
Q

Vasodilators

A
  • hydralazine

- minoxidil

78
Q

Vasodilators

Mechanism of actions

A
  • direct-acting smooth muscle relaxant that acts as a vasodilator primarily in arteries and arterioles
79
Q

Vasodilators

Clinical use

A
  • may be useful for resistant HTN

- may be beneficial for patients with HTN and HF (hydrazine)

80
Q

Vasodilators

Important adverse drug reactions

A 
Hydralazine
  - tachycardia (use with beta-blocker)
  - drug-induced lupus-like syndrome
Minoxidil
  - fluid retention (use with diuretic)
  - paricardial effusion
  - hirsutism
81
Q

Vasodilators

Dosing and monitoring

A
  • can dose two to four times daily
82
Q

Achieving BP control

A
  • most patients who are hypertensive will require two or more antihypertensive medications to achieve their BP goals
  • adding a second drug from a different class should be initiated when use of a single drug in adequate doses fails to achieve the BP goal
  • When BP is more than 20/10 mmHG above goal, consider initiating therapy with two drugs. Use caution in patients at risk of orthostatic hypotension
  • Patients should return for follow-up and adjustment of medications at monthly intervals until goal is achieved. Appropriate laboratory tests (based on medications used) should be obtained and may be mecessary at closer intervals after initiation of therapy.
  • More frequent visits may be necessary for patients with stage 2 HTN or with complicating conditions
  • once BP is at goal and stable, follow-up visits can occur at less-frequent intervals
83
Q

Compelling indications for HTN treatment

Ischemic Heart disease

A

Stable angina
- beta blocker, alternatively a long acting CCB can be used

Acute Coronary Syndrome
- initial treatment should be beta-blocker and ACEI

Post MI - ACEI, beta-blocker (for at least 3 years), aldosterone antagonist

84
Q

Compelling indications for HTN treatment

Heart failure

A

Asymptomatic with demonstrable ventricular function
- ACEI and beta-blockers

Symptomatic ventricular dysfunction or end-stage heart disease:
- ACEI, beta-blocker, ARB, aldosterone antagonist (with loop diruretics

85
Q

Compelling indications for HTN treatment

Diabetic

A
  • Two or more often needed to achieve <140/80
  • Combination should include ACEI or ARB but not both
  • ACEIs and ARBs based treatments favourably affect the progression of diabetic nephropathy and reduce aluminuria
86
Q

Compelling indications for HTN treatment

CKD

A
  • GFR < 60 and presence of albuminuria
  • goal of <130/80 (often require 3 or more drugs)
  • ACEIs and ARBs have favorable effects on the progression of diabetic and nondiabetic renal disease. Limited rise in SCr as much as 30% above baseline is acceptable
87
Q

Compelling indications for HTN treatment

Cerebrovascular disease

A

-recurrent stroke rates are lowered by the combination of an ACEI and a thiazide diuretic

88
Q

Other potential effects of antihypertensive drug choices

Favorable

A

Thiazides
- slow demineralization in osteoporosis

Beta-blocker
- treat atrial fibrillation and tachyarrythmias, angina, migraine prophylaxis, and essential tremor

CCB
- treat Raynaud syndrome and certain arrythmias, migraine prophylaxis

Alpha-blockers
- used in prostatism

ACEIs
- may show favourable effect on blood glucose

89
Q

Other potential effects of antihypertensive drug choices

Unfavorable

A

Thiazides

  • use with caution in gout or hyponatremia
  • may negatively affect blood glucose

Beta-blocker

  • use caution with asthma or heart block
  • may negatively affect blood glucose (except carvedilol

ACEI or ARB
- avoid in women who are, or are likely to become, pregnant

Aldosterone antagonists and K sparing diuretics
- avoid in patients with K values greater than 5.0 mEq/L or CrCl < 30ml/min

Hypertension (1 decks)

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