What is HTN?

systemic/arterial HTN
o increase hydrostatic pressure in systemic arterial systems
pressures should be similar everywhere
o mostly measure in the brachial artery
Systolic Blood Pressure (SBP)
o Pressure during cardiac contraction when aortic valve open
Diastolic Blood Pressure (DBP)
o Pressure when heart not beating and is relaxing
Former classification of BPs:
Category Systolic Pressure Diastolic Pressure
Optimal <12 !nd <"
Normal <1# !nd <"$
High%normal 1#%1#& Or "$%"&
HTN 'stage 1( 1)%1$& Or &%&&
HTN 'stage 2( 1*%1+& Or 1%1&
HTN 'stage #( ,- 1" Or ,- 11
New JNCVII Classification:
Category Systolic Pressure Diastolic Pressure
Normal <12 !nd <"
re!"N #$%&#'( )* +%&+(
HTN 'stage 1( 1)%1$& or &%&&
HTN 'stage 2( ,- 1* or ,- 12
o Pre&!"N:
.P in this ultimately become HTN
/mphasi0es that range o1 .P used to be normal and now are signi1icant ris2s 1or
end%organ disease
NOT optimal3 sa1e .P range
4o not get drug therapy pushed to change li1estyle
What is Essential HTN?
"ye , of !"N Pts Clinical Clues
/sssential &$5 %!ge o1 onset6 2%$
%7Hx o1 HTN
%normal serum 89:;3 urinalysis
<hronic renal disease 2%)5 %increased 8creatinine;3 abnormal urinalysis
=enovascular 15 %abdominal bruit
%sudden onset 'especially i1 age ,$ or <2(
%decreased serum 89:;
Pheochromocytoma >25 %Paroxysms o1 palpitaions3 diaphoresis and anxiety
%episodic HTN in 1/# o1 pts
<oarctation o1 aorta >15 %.P in arms , legs3 or right arm , le1t arm
%midsystolic murmur between scapulae
%<?=6 aortic indentation3 rib%notching due to collaterals
Primary aldosteronism >15 %decreased serum 89:;
<ushing@s syndrome >15 %A<ushingoidB appearance 'e>g>3 central obesity3 hirsutism(
-!:
o &$5 o1 all HTN cases
o use cues !N4 dx o1 exclusion i1 no secondary cause 1ound
o typically 1ound in )s with positive 7Hx
$ndary !"N:
o i1 cause 1ound3 then Tx geared towards cause
o other causes 'other than listed above( include slee anea and regnancy
Define incidence, prevalence, associated mortality of HTN by age, race, gender and secular trends
age:
o more men than women until $$
o more women than men a1ter $$
o SBP rises linearly wit. age
4.P pea2s at $%$& then drops
SB is better predictor of HTN, especially in elderly, and used for T! choices
race:
o blac2 males/1emales , white males , Hispanic males/1emales , white 1emales
re/alence
HTN '7in2( % 1
o increases with age with shi1t in gender a1ter $$
o higher probability above + despite having Hx o1 normal .P
$ million have HTN
a/erage BP in 0S droing since #(1%s due to:
o better awareness
o more 2nown treatments
o better 2nown controls 'putting pts in optimal .P range3 yet still only 1 in #(
associated complications6
o chronic renal disease
o <H7
o Cinear increasing relationship with .P and relative ris2 1or end%organ complication such
as stro2e and coronary .eart disease
=is2 extends down all the way to preHTN stage 'although ris2 is smaller(
B effect on "HD ris# independent of other ris# factors
.P can be additive to other ris2 1actors
Nevertheless3 in the absence o1 ris2 1actor3 there is still an increased ris2 1or <H4 b/c o1 high D.P
!1ter 11$/+$3 CVD ris2 dou3les wit. eac. $%4#% rise
People who are normotensi/e at 55 still .a/e (%, lifetime ris2 for getting !"N
$ssessment of target organ damage due to HTN
Cardiac <linical3 /<E3 <?= evidence o1
<!43 CFH by /<E3 CF
dys1unction
Cere3ro/ascular Transient ischemic attac2 or stro2e
Peri.eral /ascular !bsence o1 peripheral pulseG
aneurysm
*enal Hncreased serum creatinine3
proteinuria3 microalbuminuria
*etinal Hemorrhage3 exudates3 possibly
papilledema
dri/ing forces for organ damage
o magnitude o1 HTN
o how long .P has been elevated
cardiac changes tend to come on earlier than others3 but most o1ten the others are present when
one o1 them is present
Benefits of HTN therapy
decrease in prevalence o1 stro2e and <H4 as well as hospitali0ation o1 <H7
o with 1alling o1 .P with better detection and Tx
o stro2e reduction6 #$%)5
o IH reduction6 2%2$5
o H7 reduction6 $5
e6cet wit. renal disease and c.ronic renal failure
o worsened by HTN and still worsened despite Tx b/c o1 obesity and Type 2 4I
%dentify genetic ris# factors for HTN
correlation with 1amily members due to bac2ground3 shared environment3 li1estyle habits
$5 concordance with mono0ygotic tiwns
HTN can be inherited with single gene mutation 'very rare(
o HTN most o1ten a olygenic disorder with gene interaction to each other J environment
%dentify environmental and behavioral ris# factors for HTN
Smo2ing .P increases while smo2ingG smo2ing N)" at increased ris2 1or HTN3 yet still strong ris2
1actor 1or <F disease tend to have lower .Ps because smo2ers are thinner
)3esity S"*)N7-S" *IS8 F9C")* especially truncal obesity
9lco.ol Highly correlated 2 beers or 1 wine per day may lower HTN
Sodium /lderly3 !! and obese who are salt%sensitive
Potassium High 9: inta2e decreases .P and lowers <F diseases
Calcium Dmall anti%HTN 1x
:agnesium Dmall anti%HTN 1x
Dietary fats; car3s; roteins NO 1x 'unless it a11ects weight and obesity(
HTN '7in2( % 2
Caffeine NO 1x
Stress <!N elevate .P acutely rela6ation4stress management N)" effecti/e means to "6
!"N
What causes HTN?
too muc. fluid
narrowing of arteries
o ma2ing the tubes less stretchable
reduce diameter and less distentibility o1 the arteries
at.erosclerosis /s< !"N:
o the 1ormer does NOT cause HTN except in the renal arteries where 1low occluded
because atherosclerosis mainly a11ects larger .Fs
their distentibility does not determine blood pressure
o .P determined by smaller vessels
What are the contributions of heart, B&s, $NS, #idneys, and hormones to development of HTN?
B=))D P*-SS0*- determined 3y:
o <ardiac Output '<O( and Total Peripheral =esistance
BP > C) ? "P*
Note' in most, increase in T( )ill cause B rather than caused by "*
<O determined by6
o Dtro2e Folume 'DF( and Heart =ate H=(
<O - DF K H=
o DF determined by6
9idneys
!ND
o H= determined by6
!ND
TP= determined by6
o Fascular smooth muscle tone
!ND
Hormones
Diameter of BVs
o Fascular smooth muscle structure
!ND
Hormones
Is small vessel occluded, then increase resistance and pressure
8idney:
o <ontrol volume o1 1luid in circulation
9NS:
o !11ect smooth muscle tone and structure
!ormones:
o !11ect heart and .Fs
Blood Vessels:
o Iost common hemodynamic cause o1 HTN is increased "P*
Iost .Fs that abnormal in HTN are the arterioles and re&caillaries because
o1 their small lumen si0e
These changes are best seen using a 1undiscope and retinal vessels
Carge arteries are o1ten normal
V9S)DI=9"I)N 'rapid( /s< V9S)C)NS"*IC"I)N 'rapid(
&Nitric Oxide %N/
%PEH2 %!ngiotensin
%.rady2inin %/ndothelin
%/PH %DND activity
%lowers HTN -raises HTN
-larger lumen -narrowing of lumen to increase
resistance to flow
HTN '7in2( % #
constrictors are rapid continuous exposure will lead to /ascular remodeling so t.at lumen are
smaller and muscle walls muc. t.ic2er
o one 2nown cause o1 HTN is too much constrictors O= too little dilators
the mediators o1 constriction are the targets 1or HTN Tx
3loc2age of constrictors will lower BP rig.t away and *-V-*S-
*-:)D-=IN7 )V-* "I:-
9C-&I are 2nown to increase dilating mediators 1or Tx
/PH6
o at low levels3 they activate receptors to relax s2eletal muscle and dilate
-ndot.elial cells of BVs
o Produce chemicals that cause vasodilation or vasoconstriction
Nitric o6ide production I:P9I*-D in HTN
at normal levels3 will dilate and lower remodeling
-ndot.elin production !I7!-* IN B=9C8 in HTN
!t normal levels3 will constrict and INC*-9S- remodeling
9NS:
o There is an increased num3er of acti/ation and acti/ity in HTN pts than normal3
especially in truncal obese pts
Ceads to constriction of BV and increased !* both increase H=
o <auses o1 increased SNS acti/ity
Obesity
Dtress
Hormones
=e1lexes
8idneys:
o !11ects .P through three mechanisms6
Body fluid /olume regulation (slow 3ut owerful)
Na/H2O retention blood volume cardiac 1illing <O
.P
*&9&S system (/olume and /asoconstriction)
!ng HH6
o Na: retention
o !ldosterone release
o Fasoconstriction
o DND activation
o Can be controlled b !C"-I and !#Bs
+nderstand ho) patient characteristics in addition to B can affect choice of anti,HTN therapy
decision to Tx determined by6
o le/el of BP
more emphasi0ed by LN<FHH
o resence4a3sence of target organ damage4ot.er ris2 factors
li1estyle modi1ications a11ecting .P6
o weight loss and exercise
probably best way to lower .P
o salt/alcohol restriction
1actors in1luencing choice o1 drug6
o socio%economic 1actors 'costs3 availability(
o evidence 1or e11icacy at <F ris2 reduction
o drug bioavailability and pharmaco2inetics
o pt%to%pt variability in responsiveness to a drug class
o possible drug interactions
o presence o1 co%existing potentially a11ected by drug
anti&!"N drugs
o 4iuretics
o .eta%bloc2ers
o <a:2 channel bloc2ers
HTN '7in2( % )
4ihydropyridine
Non%dihydropyridine
o !</%H/!=.s
These top four are most commonl used and better tolerated
o !lpha%bloc2ers
o <entra symphatholytics
o Hydrala0ine/minoxidil
4rug bioavailability and pharmaco2inetics
o Optimal 1ormulations should provide $@ .our efficacy wit. once&daily dose
!t least $5 o1 pea2 e11ect remaining at end o1 2) hours
Hmprove adherence
Cowers cost
Provide persistent .P control
Prevent morning .P increments
Dex No 2nown di11erences
!ge /lderly respond better to diuretics3 <a:2 channel bloc2ers
=ace !! respond better to diuretics3 <a:2 channel bloc2ers
Strong indications (in a3sence of contraindications)
4I with proteinuria !</%H
H7 !</H
4iuretics
.eta bloc2ers
Hsolated systolic HTN 4iuretics
<a:2 channel bloc2ers 'long(M
IH .eta%bloc2ers
!</%H
Possi3le C):BIN-D -FF-C" on co&e6isting disorder
!ngina .eta%bloc2er
.PH !lpha bloc2er
4I type 2 with proteinuria !</%H
4yslipidemia !lpha bloc2er
Hyperthyroidism .eta%bloc2er
Iigraine .eta%bloc2er
IH 4iltia0em
Ferapamil
Osteoporosis Thia0ides
=enal insu11iciencty !</%H
Tachyarrhythmias .eta%bloc2er
<a:2 channel bloc2er
Possi3le 0NF9V)*9B=- -FF-C" on co&e6isting disorder
.ronchospasm .eta%bloc2ers
4epression .eta%bloc2ers
=eserpine
4I .eta%bloc2er
4iuretics
4yslipidemia .eta%bloc2er
4iuretics
Eout 4iuretics
Heart .loc2 .eta%bloc2er
<a:2 channel bloc2er 'non%4HP(
H7 .eta%bloc2er
Civer disease Cabetalol
Iethyldopa
Peripheral vascular disease .eta%bloc2ers
Pregnancy !</%H
!ng HH antagonists
=enal insu11iciency 9: sparing diuretics
-no) ma.or side effects associated )ith class of anti,HTN drug
Thia0ide diuretics Hncreased cholesterol and glucose
4ecreased 93 Na3 Ig
Hncreased uric acid and <a
Coop diuretics 1luid/electrolyte changes
ototoxicity
HTN '7in2( % $
.eta%bloc2ers .ronchospasm
.radycardia
Ias2 insulin%induced hypoglycemia
Hnsomnia
7atigue
/xercise intolerance
!</%H <ough
!ngioedema
Hyper2alemia
=ash3 loss o1 taste
<a:2 channel bloc2ers '4HP( !n2le edema3 1lushing3 headache3 gingival hypertrophy
<a:2 channel bloc2ers 'non%4HP( <onduction de1ects3 worsening <HE3 gingival hyperplasia
HTN '7in2( % *
harmacogenomics of anti,HTN therapy
allow precise tailor therapy to meet the individual@s personal needs
"onsider rational drug combos in anti,HTN therapy
about 2/# o1 patients will reNuire 2 or more drugs to reach optimal .P
note6 always use lowest possible dose when treating to minimi0e side 1x
principles o1 combination6
o use drugs 1rom different classes to achieve additi/e .yotensi/e f6
o minimi0e comensatory pro%hypertensive drug actions
o lower doses results in 1ewer side e11ects 1or a given reduction in .P
t.iaAides s.ould 3e initial drug t.eray for most
o either alone or combine with other classes
certain high%ris2 conditions are compelling indicatiosn 1or other drug classes
if BP B $%4#% mm!g a3o/e goal; initiate t.eray wit. $ agents; one usually s.ould 3e a
t.iaAide&tye diuretics
common combinations6
o diuretics : beta%bloc2ers
o diuretics : !</%H
o !</%H : <a:2 channel bloc2ers
o !=.s and diuretics
o <entrally acting drug and diuretic
o 4iuretic and diuretic
HTN '7in2( % +