Hypertension Flashcards
Coarctation of the aortas
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
CV comps of HTN
Weakens vessel wall
Accelerated atherosclerosis
Inc afterload of ther heart - systolic and diastolic (due to LVH) dysfunction….also inc myocardial oxygen demand
Comps of HTN
LVH
LVH with chamber dilatation
HF with reduced or preserved EF
LA abnormalities
Myocardial ischemia
Atrial and ventricular arrhythias
Sudden death
LVH
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
Chronic HT hypertrophy pathology
Myocyte length increases
Fibrosis
Maybe diastolic dysfunction
Can progress to cardiac dilation
Axis deviation in LVH
Get leftward deviation of the heart
HFpEF
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
Ischemia
Inc CAD
LVH subendocardial blood flow may be reduced
Leading to ischemia, infarction, fibrosis
Arrhtyhmia
Dilated LA —- PACs and Afib
Fibrosis predisposes to ventricular ectopy and potentiallly lethal arrhythmias that may lead to sudden death
Regression of LVH
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
MAP
CO
SV
COTPR
CO=SVHR
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
Dihydropyridines vs. non
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
SE and toxoicty of CCBs
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
Mech of CCB edema
Amlodipine dilatedo nly arterioles
Inc capillary pressue and permeability
CCB plus RAS inhibitor
Arteriolar dilation AND venous dilation so edema is reduced
Use with ARBs and ACEI
Hydralazine and minoxidil
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
1st line drugs
Non-black - thiazide, CCB, ACEI, ARB
Black - thiazide, CCN
Elderly - CCB, thiazide
Thiazide plus K sparing
Provides diuresis with lower risk of hypokalemia
ACE plus diuretic
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
ACE/ARB and CCBs
CCB associated natriuresis complements ACEI
AT2 independet additional vasodilation
ACEI dilates efferent and CCB dilates affarent
BB and CCB
BB can attnuate the tachycardia and SNS stimulation
CCB can inhibit adrenergic vasoconstriction associated with beta-blockade
Combos to avoid
ACE/ARB with K+ sparing - risk ofr hyperkalemia
Verapamil and BB - risk of HB
JNC8
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
1st and later line txs
Thiazides, CCBs, ACEIs, and ARBS
