Hypertension Flashcards

1
Q

Coarctation of the aortas

A

Elevated SBP in upper extremeities and diminished in lower

Late systolic heard bt scapula

LVH, rib-notching on CXR**

Visuallization of coartation sys

Tx - surgery or endovascular repair

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2
Q

CV comps of HTN

A

Weakens vessel wall

Accelerated atherosclerosis

Inc afterload of ther heart - systolic and diastolic (due to LVH) dysfunction….also inc myocardial oxygen demand

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3
Q

Comps of HTN

A

LVH
LVH with chamber dilatation

HF with reduced or preserved EF

LA abnormalities

Myocardial ischemia

Atrial and ventricular arrhythias

Sudden death

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4
Q

LVH

A

Increased afterload —-pressure overload of LV

LV wall thickness increases (concentric hypertrophy) - intially

When LV can no longer compensate for inc afterload, LV begins to dilate (eccentric hypertrophy) and LV performance drops

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5
Q

Chronic HT hypertrophy pathology

A

Myocyte length increases

Fibrosis

Maybe diastolic dysfunction

Can progress to cardiac dilation

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6
Q

Axis deviation in LVH

A

Get leftward deviation of the heart

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7
Q

HFpEF

A

LVH—dec elasticity of LV

This is diasotlic dysfunction

Diastolic filling becomes more difficult

Depends on LA systole

LV end diastolic and LA pressure increased

LA enlargment

Pulm venous congestion and pulmonary congestion

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8
Q

Ischemia

A

Inc CAD

LVH subendocardial blood flow may be reduced

Leading to ischemia, infarction, fibrosis

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9
Q

Arrhtyhmia

A

Dilated LA —- PACs and Afib

Fibrosis predisposes to ventricular ectopy and potentiallly lethal arrhythmias that may lead to sudden death

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10
Q

Regression of LVH

A

Impoved systolic performance and enhanced SV

No increase is risk of decompensation if BP rises

Whether these changes diminish risk of sudden death is unknown

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11
Q

MAP
CO
SV

A

COTPR
CO=SV
HR
SV=EF*LVEDV

LVEDV determined by preload

Preload determined by venous resistance and volume…interventiron - dec HR, dec TPR (afterload), dec preload, dec vascular volume

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12
Q

Dihydropyridines vs. non

A

Amlodipine and nifedipine …greater ratio of vascular msooth muscle effects relative ot cardiac effects….differ in potency in different vascular bets…CYP3A4 substrates

Non - verapamil and diltiazime…more used for cardiac effects….angina and cardiac cysrhythmias…reduce cardiac conctraction in dos-dep fashion..dec HR and CO

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13
Q

SE and toxoicty of CCBs

A

EDEMA is big one

Liver dysfunction and gum hypertrophy

Sx may worsen bc reduced ability for heart to pump blood…excessive inhibition of Ca channel blockage may induce cardiac depression such as cardaic arrest…bradycardia, AV block, HF

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14
Q

Mech of CCB edema

A

Amlodipine dilatedo nly arterioles

Inc capillary pressue and permeability

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15
Q

CCB plus RAS inhibitor

A

Arteriolar dilation AND venous dilation so edema is reduced

Use with ARBs and ACEI

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16
Q

Hydralazine and minoxidil

A

SMooth muscle relaxers of the arterioels

Baroreceptors sense dropped BP…will inc sympathetic output which will increase CO

HR will increase and cardiac contractility will increase

Can tx with diuretics

17
Q

1st line drugs

A

Non-black - thiazide, CCB, ACEI, ARB

Black - thiazide, CCN

Elderly - CCB, thiazide

18
Q

Thiazide plus K sparing

A

Provides diuresis with lower risk of hypokalemia

19
Q

ACE plus diuretic

A

Can enhance efficacy of ACE if low-renin HTN

ACEI can enhance efficacy of normal to hgih renin HTN

ACE inhibitor can ameliorate many of adverse effect of diuetics including hypokalemia

20
Q

ACE/ARB and CCBs

A

CCB associated natriuresis complements ACEI

AT2 independet additional vasodilation

ACEI dilates efferent and CCB dilates affarent

21
Q

BB and CCB

A

BB can attnuate the tachycardia and SNS stimulation

CCB can inhibit adrenergic vasoconstriction associated with beta-blockade

22
Q

Combos to avoid

A

ACE/ARB with K+ sparing - risk ofr hyperkalemia

Verapamil and BB - risk of HB

23
Q

JNC8

A

If goal not met after 1 mo…inc dose or add second drug

If goal not met with 2 meds…add and titirate 3rd med…do NOT use ACE and ARB together

Can use other classes if goal not met with 3 meds or contraindication to thiazide, ACE/ARB, or CCB

24
Q

1st and later line txs

A

Thiazides, CCBs, ACEIs, and ARBS

25
Q

2nd and 3rd lines

A

Combinations

26
Q

4th line

A

Any beta blockers or alpha blockers

Direct vasodilators

Loop diuretic

Aldosterone antags

27
Q

Preferred thiazide

A

Chlorthalidone - more potent, longer 1/2 life

HCTZ - less expensive

28
Q

Beta-blockers not rcommened as 1st line BC

A

higher rate of primary composite outcome of CV death, MI, or stroke compared to use of ARB

29
Q

Alpha blocker not 1st line bc

A

Worse cerebrovascular, HF< and combined CV outcomes than initial tx with a diuretic

30
Q

Aliskerin

A

Should NOT be used in combo with ACE or ARBs in diabetic pts

31
Q

Sprinolactone

A

Only use in refractory HTN

32
Q

Exceptions for B-blocker in HTN

A

Use if arrhythmia