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Essential Hypertension Management

This document provides guidelines for the management of essential hypertension. The goals are to reduce cardiovascular and renal risks by maintaining BP below 130/80 mmHg for patients with diabetes or kidney disease, and below 140/90 mmHg for others. Non-pharmacological treatments include sodium and potassium intake modification, weight control, exercise, and stress reduction. First-line drug classes discussed are thiazide diuretics, beta-blockers, ACE inhibitors, ARBs, calcium channel blockers, alpha-blockers, and centrally acting drugs. Specific drugs and dosages are provided within each class. Hypertensive emergencies requiring rapid BP reduction within 1 hour are distinguished from urgencies requiring reduction within hours.

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0% found this document useful (0 votes)
122 views5 pages

Essential Hypertension Management

This document provides guidelines for the management of essential hypertension. The goals are to reduce cardiovascular and renal risks by maintaining BP below 130/80 mmHg for patients with diabetes or kidney disease, and below 140/90 mmHg for others. Non-pharmacological treatments include sodium and potassium intake modification, weight control, exercise, and stress reduction. First-line drug classes discussed are thiazide diuretics, beta-blockers, ACE inhibitors, ARBs, calcium channel blockers, alpha-blockers, and centrally acting drugs. Specific drugs and dosages are provided within each class. Hypertensive emergencies requiring rapid BP reduction within 1 hour are distinguished from urgencies requiring reduction within hours.

Uploaded by

spicychips7
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
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ESSENTIAL HYPERTENSION-MANAGEMENT Goals Reduce cardiovascular and renal morbidity and mortality.

BP < 130/80 mmHg for patients it! diabetes or "idney disease BP < 1#0/$0 mmHg for all ot!ers Non-pharmacological treatment Sodium restriction %odest salt restriction may !elp lo er t!e BP& ' moderate diet( i.e.( ) g sodium per day is not only a useful t!erapeutic measure but is also feasible. *!is target can be accomplis!ed by eliminating table salt( by reducing t!e salt in coo"ing( and by consuming more natural food and less processed food. Potassium enrichment +n certain patient groups ,t!e elderly-( potassium supplementation may yield measurable t!erapeutic benefits. !ypertensive patients s!ould be encouraged to consume a diet ric! in potassium ,vegetables( fruits-. Calcium supplementation *!e effects of calcium supplementation in !ypertension are !ig!ly variable and unpredictable. *!e best advice is to ensure proper inta"e of calcium in t!e diet. Reducing alcohol intake ./cessive consumption of alco!ol could elevate BP levels. *!erefore alco!ol use s!ould be curtailed ,or pro!ibited- for patients it! !ypertension. Physical exercise, relaxation, and stress reduction ' purely static p!ysical e/ercise increases t!e systolic BP and t!erefore s!ould be avoided. Regular dynamic e/ercise may lo er t!e BP and protect against coronary events. Bio0feedbac"( stress reduction( rela/ation( and yoga training ,particularly shavasana- yield benefits in t!e s!ort0term and !enever possible s!ould be encouraged. Weight control 1or obese patients it! !ypertension( eig!t loss s!ould be vigorously pursued. 2eig!t control also decreases salt sensitivity and increases t!e effectiveness of anti0!ypertensive drug t!erapy. Dr g therap! General principles *!e starting dose s!ould be lo and t!e increments s!ould be made in a gradual fas!ion on t!e basis of clinical evaluation utili3e drugs it! a long duration of action !ic! permits once0a0day administration and ensures continuous control of !ypertension including protection from t!e morning surges Thia"i#e an# other #i retics$ Mechanism o% action 0promoting sodium e/cretion and by s!rin"ing t!e plasma volume.

Dr gs an# #oses-t!ia3ide diuretic0 bendroflumet!ia3ide ).4 mg or cyclopent!ia3ide 0.4 mg$loop diuretics0 furosemide #0 mg daily or bumetanide 1 mg daily. Si#e e%%ects 0 !ypo"alaemia( !yperglycaemia( dyslipidaemia( !ypomagnesaemia. Potassium0sparing drugs can potentially cause !yper"alaemia

&eta-a#renoceptor antagonists '(-)loc*ers+$ Mechanism o% action0 t!e cardiac output is reduced but in t!e long0term( t!e perip!eral vascular resistance falls. anti0renin and 567 mec!anisms may contribute to t!e anti0!ypertensive actions Dr gs an# #oses-%etoprolol ,1000)00 mg daily-( atenolol ,400100 mg dailyand bisoprolol ,4010 mg daily- are cardioselective ,ontrain#ications Bronc!ospasm 05ardioselective 80bloc"ing agents ,so0called 81 bloc"ers( e.g.( metoprolol( atenolol- may be superior to nonselective 8 bloc"ers in patients it! bronc!ospasm. 9ecompensated congestive !eart failure 'trioventricular bloc" and bradycardia Si#e e%%ects Bronc!ospasm( depression( fatigue %etabolic c!anges: increase 7erum triglycerides Alpha an# )eta receptor antagonist Mechanism o% action lo ers perip!eral vascular resistance Dr gs an# #oses ;abetalol ,)00 mg0).# g daily in divided doses- and carvedilol ,<.)40)4 mg 1)0!ourly- are combined 80 and =0adrenoceptor antagonists !ic! are sometimes more effective t!an pure 80bloc"ers. ;abetalol can be used as an infusion in malignant p!ase !ypertension. Si#e e%%ects:postural !ypotension Angiotensin-con.erting en"!me 'A,E+ inhi)itors$ Mechanism o% action +n!ibit t!e en3yme converting angiotensin + into angiotensin ++( a potent vasoconstrictor Retard t!e degradation of a potent vasodilator ,brady"inin Reduce t!e activity of t!e adrenergic nervous system Dr gs an# #oses Ramipril: ).4>)0 mg/d(.nalapril: 4>#0 mg once or t ice daily(;isinopril: 10>#0 mg/d(Perindopril: #>8 mg/d A#.erse e%%ects > 6onproductive coug! (Hyper"alemia( especially in patients it! renal insufficiency ('ngioedema( an idiosyncratic reaction (Renal failure(first0 dose !ypotension

Angiotensin receptor )loc*ers$ Mechanism o% action 5ompetitively in!ibit t!e binding of angiotensin ++ receptor Dr gs an# #oses0 +rbesartan: 140>300 mg/d(;osartan: )40100 mg once or t ice daily(?alsartan: 80> 3)0 mg/d Si#e e%%ects0 same as '5. in!ibitors e/cept coug! or angioedema ,alci m antagonists$ Mechanism o% action %odify calcium entry into cells by interacting it! specific binding sites on t!e =1 subunit of t!e ;0type voltage0dependent calcium c!annel 5ause vasodilation Bot! diltia3em and verapamil can slo atrioventricular conduction. Dr gs an# #oses 9i!ydropyridines0'mlodipine: ).4>10 mg/d1elodipine: ).4>10 mg/d(6ifedipine( long acting: 30>$0 mg/d 6ondi!ydropyridines 09iltia3em( e/tended release: 180>300 mg/d(?erapamil( long acting: 1)0>#80 mg once or t ice daily(?erapamil: 30>1)0 mg # times daily Si#e e%%ects'n"le oedema(5onstipation(all !ave negative inotropic effects and s!ould be used cautiously in patients it! congestive !eart failure /0-a#renoceptor antagonists '/-)loc*ers+ Mechanism o% action 0 bloc" t!e post0synaptic a1receptors located on t!e vascular surface and t!ereby prevent vasoconstriction and promote vasodilation Dr gs0 pra3osin ,0.40)0 mg daily in divided doses-( do/a3osin ,101< mg daily1aso#ilators Mechanism o% action 5ause direct rela/ation of vascular smoot! muscle Dr gs an# #oses !ydrala3ine ,)40100 mg 1)0!ourly- and mino/idil ,10040 mg daily-. Si#e-e%%ects first0dose and postural !ypotension( !eadac!e( tac!ycardia and fluid retention. %ino/idil also causes increased facial !air ,entrall! acting #r gs Mechanism o% action

7timulate =) receptors in t!e vasomotor centers of t!e brain( reducing sympat!etic outflo and arterial pressure 9ecrease in cardiac output and !eart rate usually occurs. Dr gs 2 clonidine and met!yldopa. Si#e e%%ects Postural !ypotension( dro siness( rebound !ypotension Dr g choices %or special in#ications 9iabetes melitus ,type +- it! proteinuria Heart failure +solated systolic !ypertension ,older persons%yocardial infarction Benign prostatic !ypertrop!y @ '5. in!ibitors @ '5. in!ibitors @ 9iuretics @ 9iuretics preferred @ ;ong0acting di!ydropyridine calcium0c!annel antagonists @ A0bloc"ers ,non0+7'@ '5. in!ibitors , it! systolic function/-)loc*ers

H!pertensi.e 3rgencies 4 Emergencies A+ H!pertensi.e rgencies Hypertensive urgencies are situations in !ic! blood pressure must be reduced it!in a fe !ours. Parenteral drug t!erapy is not usually reBuired( and partial reduction of blood pressure it! relief of symptoms is t!e goal. &+H!pertensi.e emergencies Hypertensive emergencies reBuire substantial reduction of blood pressure it!in 1 !our to avoid t!e ris" of serious morbidity or deat!. .mergencies include !ypertensive encep!alopat!y( !ypertensive nep!ropat!y( intracranial !emorr!age( aortic dissection( preeclampsia0eclampsia. Malignant h!pertension- c!aracteri3ed by encep!alopat!y or nep!ropat!y it! accompanying papilledema. *!e t!erapeutic approac! is identical to t!at used it! ot!er anti!ypertensive emergencies. Pat!ologically( t!e syndrome is associated it! diffuse necroti3ing vasculitis( arteriolar t!rombi( and fibrin deposition in arteriolar alls. 1ibrinoid necrosis !as been observed in arterioles of "idney( brain( retina( and ot!er organs Parenteral t!erapy is indicated in !ypertensive emergencies.

*!e initial goal in !ypertensive emergencies is to reduce t!e pressure by no more t!an )4C , it!in minutes to 1 or ) !ours- and t!en to ard a level of 1<0/100 mm Hg it!in )>< !ours. Parenteral 'gents0 7odium nitroprusside is t!e agent of c!oice for t!e most serious emergencies because of its rapid and easily controllable action. +n t!e presence of myocardial isc!emia( intravenous nitroglycerin or an intravenous beta0bloc"er( suc! as labetalol or esmolol( is preferable. Dt!er drugs t!at can be used are .nalaprilat( Hydrala3ine RE5RA,TORY HYPERTENSION 1ailure to reac! blood pressure control in patients !o are ad!erent to full doses of an appropriate t!ree0drug regimen ,including a diuretic-. 5auses Patients consuming e/cess of salt do not respond as ell to anti0!ypertensive drugs. ?olume retention from "idney disease +nappropriate combinations 7ympat!omimetics ,decongestants( anorectics 6onsteroidal anti0inflammatory drugs& cycloo/ygenase0) in!ibitors

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