HTN Flashcards

1
Q

Special considerations

A

Renal disease- Initial increase in creatinine normal….. Contraindicated in bilateral renal artery stenosis ACE might temporarily increase creatinine but should level off if not they might have bilat renal artery stenosis- we are blocking BF to renal arteries

CAD- BB’s may be added to ACE-I

Diabetes Mellitus- Usually need multiple agents Avoid adverse glucose metabolism Lower BP goal ACE-I or ARB 1st line

Reproductive women- Estrogen stimulation of hepatic angiotensinogen

Elderly : > 75y/o Modest doses reduce stroke

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2
Q

Stages of hypertension

A

•Stage 1

Modify lifestyle

May add monotherapy anti-hypertensives w/ co-morbidities

CAD/stroke risk or DM/CRI (renal disease)

•Stage 2

Will use combo therapy (systolic 140 or higher/ diastolic 90 or higher) diuretic and beta blocker or something

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3
Q

Which number is more related to cardiovascular risk? Systolic or diastolic?

A
  • Systolic- Max pressure to eject blood out of heart; higher max pressure on a constant basis= more ling term weakening to BV’s
  • Diastolic- Lowest pressure arteries go thru; lowest pressure is still pressure; also not enough can cause poor coronary artery perfusion
  • Also pulse pressure matters= the wider it gets the less coronary artery filling you have
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4
Q

Why does BP control matter???

A
  • 7/10 people having their 1st MI= uncontrolled BP
  • 8/10 people having 1st stroke= uncontrolled BP
  • 7/10 people with CHF= uncontrolled BP
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5
Q

Types of Hypertension

A

Essential/ Primary/ Idiopathic: an identifiable cause cannot be found: Interrelated renal, hormonal, vascular

Secondary: an identifiable cause is present (pheocromcytoma

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6
Q

Essential: Commonalities

A
  • Familial incidence
  • Deficiencies of endogenous prostaglandins and NO
  • Renin or adrenergic dysfunction
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7
Q

RAAS

A
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8
Q

Low renin hypertension- subset of essential HTN

A
  • Salt-sensitivity
  • Diuretic responsiveness
  • Expanded extracellular fluid volume
  • African descent, diabetics, elderly- thiazides
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9
Q

High renin hypertension

A
  • Plasma renin levels above normal
  • Poorly responsive to competitive antagonists of angiotensin II- 50%
  • Increased adrenergic activity- give beta-blocker
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10
Q

Modulation defect

A
  • Salt-sensitivity: kidney doesn’t excrete Na+ properly
  • More insulin-resistant: getting type II DM at the same time
  • Susceptible to ACE-I
  • Males, postmenopausal
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11
Q

Diagnosis of HTN

A

•Persistently high resting blood pressure

Per month x 3

Seated, back supported, feet on floor

Not talking, arm on flat surface, level with heart

Correct sized cuff

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12
Q

Diagnosis Lab

A
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13
Q

Treatment of Stage I w/out co-morbidities

A

•Lifestyle modifications

***Diet/weight loss

Moderate alcohol intake

Increase physical activity

Cessation of smoking

Sodium restriction

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14
Q

Initial Pharmacotherapy- HTN

A

•Stage I – risk for CAD or stroke/ already have DM

Monotherapy: Diuretics, CCB, ACE/ARB

BP goal < 130/80

Sequential addition if needed- 2nd drug of different class

•Stage II

2 agents, different classes= usually ACE/ARB or CCB and diuretic

Separate or combo (can have both drugs in one pill)

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15
Q

Diuretics

A

thiazide most used for HTN, loop more short-term, can swap to K+ sparing if loop causing prob

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16
Q

Diuretic therapy considerations

A
  • Sodium diuresis/volume depletion
  • May decrease PVR: max pressure to artery
  • Effective within 3-4 days
  • Out of favor (d/t hypokalemic side effects but….. < 25 mg/day HCTZ we don’t have bad hypokalemia
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17
Q

ACE INhibitors

18
Q

ACE-I therapy

A
  • Inhibit generation of potent vasoconstrictor
  • Retards degradation of bradykinin- 2 armed approach w/ vasoconstriction
  • Especially useful in diabetic patients- prevent negative side effects of excessive carbohydrates
  • Cough 5-10%, hyperkalemia, angioedema- w/ ARBS don’t have
19
Q

ARB’s

20
Q

ARB therapy

A
  • Most selective blockers of R/A system
  • Fewer side effects than ACE-I
  • Blocks Ang II from attaching to receptor- we do not currently know if there is a long term effect of blocking but still circulating Ang II
21
Q

CCB’s

22
Q

CCB therapy

A
  • Modify calcium entry thru α-1 L-type voltage channels but more than 1 type (at least 3)
  • Specificity to unique binding sites…
  • All: vasodilation
  • Only Diltiazem and Verapamil: slow AV conduction
23
Q

Secondary Hypertension

A
  • 5% of cases
  • Renal artery stenosis most common cause
  • Other examples

Pheochromocytoma

PIH

Cushings’s syndrome

Coarctation of the aorta

24
Q

Systemic Hypertension: AHA

25
NY classifications of CHF
26
CXR of failure
27
CXR of failure: Kerley B
28
Echocardiogram
29
•LVH- Diagnostic criteria: look at V1 (tall S wave) and V5 (tall R waves \>35) •Strain pattern: ST changes
30
Management strategies
31
Management of failure
32
Neurologic effects of HTN
33
Altered Cerebral Autoregulation
34
Autoregulation theory
35
Anesthesia Considerations for hypertensive patients
36
Physical assessment changes fm HTN
37
Where do we delay/cancel?
38
Lab Parameters
39
Special considerations- 5 subgroups in HTN
40
what do wil we be considering?
A. Left ventricular hypertrophy * Concentric hypertrophy * Increased wall thickness B. Heart Failure * Typically diastolic failure * Age dependent * \<15% pts \<45y/o * 35% pts 50-70y/o * \>50% pts \>70y/o C. Neurologic effects of HTN * Retinal changes * CNS dysfunction * Occipital HA * Dizziness * Vertigo * Syncope * Cerebral infarction vs cerebral hemorrhage D. Altered Cerebral Autoregulation