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3
PreventiveCardiology
LaurenEast,DominiqueS.Williams,AnneC.Goldberg
Hypertension
GENERALPRINCIPLES
Hypertensionisdefinedasthepresenceofbloodpressure(BP)elevationtoalevelthatplacespatients
atincreasedriskfortargetorgandamageinseveralvascularbedsincludingtheretina,brain,heart,
kidneys,andlargeconduitarteries(Table3-1andTable3-2).
TABLE3-1
MANIFESTATIONSOFTARGETORGANDISEASE
OrganSystem Manifestation
Largevessel Aneurysmaldilation
Acceleratedatherosclerosis
Aorticdissection
Cardiac Acute:Pulmonaryedema,myocardialinfarction
Chronic:ClinicalorECGevidenceofCAD;LVHbyECGorechocardiogram
Cerebrovascular Acute:Intracerebralbleeding,coma,seizures,mentalstatuschanges,TIA,
stroke
Chronic:TIA,stroke
Renal Acute:Hematuria,azotemia
Chronic:Serumcreatinine>1.5mg/dL,proteinuria>1+ondipstick
Retinopathy Acute:Papilledema,hemorrhages
Chronic:Hemorrhages,exudates,arterialnicking
CAD,coronaryarterydisease;LVH,leftventricularhypertrophy;TIA,transientischemicattack.
TABLE3-2
CLASSIFICATIONOFBLOODPRESSUREFORADULTSAGE18YEARSANDOLDER
A
Category SystolicPressure(mmHg) DiastolicPressure(mmHg)
Normal <120 <80
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Elevatedbloodpressure 120–129 <80
Hypertension,stage1 130–139 80–89
Hypertension,stage2 ≥140 ≥90
a
Nottakingantihypertensivedrugsandnotacutelyill.Whensystolicanddiastolicpressuresfallintodifferentcategories,the
highercategoryshouldbeselectedtoclassifytheindividual’sbloodpressurestatus.
DatafromWheltonPK,CareyRM,AronowWS,etal.2017ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA
guidelinefortheprevention,detection,evaluation,andmanagementofhighbloodpressureinadults:areportoftheAmerican
CollegeofCardiology/AmericanHeartAssociationtaskforceonclinicalpracticeguidelines.JAmCollCardiol.2018;71:e127-
e248.
Classification
The following definitions and recommendations are based on the 2017 American College of
Cardiology (ACC)/American Heart Association (AHA) guidelines. The 2018 European Society of
CardiologyandEuropean SocietyofHypertension(ESC/ESH)guidelinesand2019 NationalInstitute
for Health and Care Excellence (NICE) guidelines do differ, particularly in terms of treatment
thresholds.
1,3
Normal BP is defined as systolic blood pressure (SBP) <120 mm Hg and diastolic blood pressure
(DBP)<80mmHg;pharmacologicinterventionisnotindicated.
Elevated blood pressure is defined as SBP of 120–129 mm Hg and DBP of >80 mm Hg. These
patients should engage incomprehensive lifestyle modificationsto delayprogressionor preventthe
developmentofhypertension.Bloodpressureshouldbereassessedin3–6months.
In stage 1 hypertension (SBP 130–139 mm Hg or DBP 80–89 mm Hg), low-risk adults (no
atherosclerotic cardiovascular disease [ASCVD] and10-year cardiovascular disease [CVD] risk of
<10%)shouldstartwithnonpharmacologictherapyandcomprehensivelifestylemodifications.Blood
pressure should be reassessed in 3–6 months. If not at goal, pharmacological therapy should be
considered.InthosewithASCVDora10-yearCVDriskof≥10%,pharmacologictherapyshouldbe
initiatedinadditiontolifestyle modification.Bloodpressureshouldbereassessedin1monthwitha
targetof<130/80mmHg.Ifatgoal,reassessevery3–6months.Ifnotatgoal,assessforadherenceand
considerintensificationoftherapy.
1,4
Instage 2hypertension(SBP≥140mmHg orDBP≥90mmHg),pharmacologictherapyshouldbe
initiatedinadditiontolifestylemodificationtolowerBPto<130/80mmHg.PatientswithBPlevels
>20/10 mm Hgabove their treatment targetwill often require more than one medication to achieve
adequatecontrol,andatwo-drugregimenmaybeinitiatedasinitialtherapy.Bloodpressureshouldbe
reassessed in1month.If atgoal,reassessevery3–6months.If notatgoal,assessforadherenceand
considerintensificationoftherapy.
Ifthereisadisparityincategorybetweensystolicanddiastolicbloodpressures,individualsshouldbe
designatedtothehigherBPcategory.
1,5
Hypertensiveemergencyistheassociationofsubstantiallyelevatedbloodpressurewithevidenceof
acute end-organ damage (retina,brain,heart,largearteries, kidneys). Itusuallydevelops inpatients
with a previous history of elevated BP but may arise in those who were previously normotensive.
Appropriate treatment of hypertensive emergency lowers blood pressure to prevent continued endorgan damage butdoes soslowlyandgraduallytoprevent ischemicdamage.Meanarterial pressure
should be reduced by 10%–20% in the first hour and a further 5%–15% over the next 23 hours.
Exceptionstogradualbloodpressureloweringincludeacuteischemicstroke,acuteaorticdissection,
andintracerebralhemorrhage.
6-8
Malignanthypertensionisseverebloodpressureelevation(largelyBP>200/120)withassociated
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advancedbilateralretinopathy.
Hypertensive encephalopathy is severe blood pressure elevation associated with lethargy,
seizures,corticalblindness,andcomaintheabsenceofotherpossibleetiologies.
Other examples of clinical presentations of hypertensive emergencies include hypertensive
thrombotic microangiopathy, acute coronary syndrome, acute stroke, cerebral hemorrhage, flash
pulmonaryedema,andaorticaneurysm/dissection.
Patientswithsevere asymptomatichypertensionwholackacutehypertension-mediatedorgan damage
are not considered to have hypertensive emergency. Treatmentwith oral antihypertensive therapyin
thesepatientsisoftenappropriateasthereisnoprovenbenefitfromrapidreductionofbloodpressure
inpatientswithsevereasymptomatichypertension.
6,9,11
Isolatedsystolichypertension,definedasanSBP≥140mmHgandDBP<90,occursfrequentlyinthe
elderly(beginningafterthefifthdecadeandincreasingwithage).Nonpharmacologictherapyshouldbe
initiatedwithmedicationsaddedasneededandtoleratedtolowerSBP.
Resistant hypertension is defined as BP ≥130/80 in hypertensive patients on ≥3 antihypertensive
agents,oneofwhichisadiuretic,orcontrolledBPon≥4antihypertensiveagents.Allagentsshouldbe
prescribed at maximally recommended (or maximally tolerated) doses. Causes of pseudoresistance
should be ruled out prior to diagnosis with resistant hypertension (inaccuracy in BP measurement,
white coat hypertension, poor adherence, or poor regimen).
12,13
Potential causes of resistant
hypertension include ingestion of exogenous substances (e.g., decongestants, oral contraceptives,
appetite suppressants, sympathomimetics, venlafaxine, tricyclic antidepressants, monoamine oxidase
inhibitors [MAOIs], chlorpromazine, some herbal supplements [e.g.: ma huang], steroids, NSAIDs,
cyclosporine,caffeine,thyroidhormones,cocaine,alcohol use,erythropoietin) andsecondarycauses
ofhypertension.
1
Whitecoathypertensionisdefinedasbloodpressurethatisconsistentlyelevatedbyofficereadings
butdoesnotmeetdiagnosticcriteriaforhypertensionbasedonout-of-officereadings.
Masked hypertension is defined as blood pressure that is consistently elevated by out-of-office
measurementsbutdoesnotmeetthecriteriaforhypertensionbasedonofficereadings.
Epidemiology
The public health burden of hypertension is enormous. According to recent estimates from the
NationalHealthandNutritionExaminationSurvey(NHANES)throughtheCentersforDiseaseControl
andPrevention(CDC), hypertension affects an estimated 116 millionAmericanadults,up from 103
millionper ACC/AHA guidelinesin2017.
14,15
Ofthepopulation withhypertension,73.9%ofpeople
withhypertensionintheUnitedStateshaveuncontrolledhypertension.Fornonhypertensiveindividuals
aged55–65years,thelifetimeriskofdevelopinghypertensionis90%.
16
Data derived from the Framingham Study have shown that hypertensive patients have a fourfold
increase incerebrovascular accidentsanda sixfoldincrease incongestive heartfailure(CHF)when
comparedwithnormotensivecontrolsubjects.
16
Disease-associated morbidity and mortality, including ASCVD, stroke,heartfailure(HF), andrenal
insufficiency, increase with higher levels of SBP andDBP. Elevated blood pressureis the strongest
modifiableriskfactorforCVDworldwide.
17
Overthelast3decades,aggressivetreatmentofhypertensionhasresultedinasubstantialdecreasein
death ratesfrom strokeandcoronaryheartdisease(CHD).Althoughtheincidenceofend-stage renal
disease(ESRD)hasstabilizedandhospitalizationsforCHFhaveoveralldecreased,18BPcontrolrates
remainpoor,with53%oftreatedhypertensivepatientshavingBPabovetargetgoal.
15
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Etiology
BP rises with age. Other contributing factors includeobesity, decreased physical activity, increased
dietarysodiumintake,increased alcoholconsumption,andlowerdietaryintakeoffruits,vegetables,
andpotassium.
Of all hypertensive patients, more than90% have primary or essential hypertension.The remainder
have secondary hypertension due to renal parenchymal disease, renovascular disease,
pheochromocytoma, Cushing syndrome, primary hyperaldosteronism, coarctation of the aorta,
obstructive sleep apnea, and uncommon autosomal dominant or autosomal recessive diseases of the
adrenal–renalaxis,whichresultinsaltretention.
DIAGNOSIS
ClinicalPresentation
BPelevationisusuallydiscoveredinasymptomaticindividualsduringroutinehealthvisits.However,
appropriately measured out-of-office BP measurements should be used in complement with office
readingsfor purposes of confirmingthediagnosis ofhypertension,titatringBP-loweringmedication,
andexcludingwhitecoatandmaskedhypertension.
1,2,19
OptimaldetectionandevaluationofhypertensionrequireaccuratenoninvasiveBPmeasurement,which
shouldbeobtainedinaseatedpatientwiththearmrestingatheartlevel.Thepatientshouldberelaxed
andsittinginthechairwiththeirfeetonthefloorandbacksupportedformorethan5minutespriorto
obtainingthebloodpressurereading.Theyshouldavoidcaffeine,exercise,andsmokingforatleast30
minutesbeforemeasurementandshouldhaveanemptybladder.Acalibrated,appropriatelyfittingBP
cuff (inflatable bladder encircling at least 80% of the arm) should be used because falsely high
readingscanbeobtainedifthecuffistoosmall.Neitherthepatientnortheobservershouldtalkduring
measurement.
Tworeadingsshouldbetaken,separatedby2minutesontwoseparateoccasions.SBPshouldbenoted
withthe appearanceofKorotkoffsounds(phaseI)andDBP withthedisappearanceofsounds(phase
V).
Incertainpatients,theKorotkoffsoundsdonotdisappearbutarepresentat0mmHg.Inthiscase,the
initialmufflingofKorotkoffsounds (phaseIV)should betakenastheDBP.Oneshouldbecarefulto
avoid reporting spuriously low BP readings because of anauscultatory gap,whichis causedby the
disappearanceandreappearanceofKorotkoffsoundsinhypertensivepatientsandmayaccountforup
toa25-mmHggapbetweentrueandmeasuredSBP.
Hypertensionshouldbeconfirmedinbotharms,andthehigherreadingshouldbeused.
HISTORY
Historyshouldseektodiscoversecondarycausesofhypertensionandnotethepresenceofmedications
andsupplementsthatcanaffectBP(seeexamplesofsubstancesaboveunder“Resistanthypertension”
definition).
Adiagnosisofsecondaryhypertensionshouldbeconsideredinthefollowingsituations:
Ageatonsetyoungerthan30years
Onsetofdiastolichypertensioninpersonsolderthan65years
Hypertensionthatisdifficulttocontrolaftertherapyhasbeeninitiated
Stablehypertensionthatbecomesdifficulttocontrol
Resistanthypertension
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Clinicaloccurrenceofahypertensiveemergency
Thepresenceofsignsorsymptomsofasecondarycausesuchashypokalemiaormetabolicalkalosis
thatisnotexplainedbydiuretictherapy
Inpatientswhopresentwithsignificanthypertensionatayoungage,acarefulfamilyhistorymaygive
cluestoformsofhypertensionthatfollowsimpleMendelianinheritance.
The 2011 ACC/AHA and 2017 ACC/AHA guidelines for peripheral vascular disease recommend
diagnostictestingforrenalarterystenosisinindividualswithonsetofhypertensionat<30yearsofage,
or new-onsetdiastolic hypertension aftertheageof55, unexplaineddeteriorationofkidney function
during antihypertensive therapy, severe hypertension in patients with diffuse atherosclerosis, and/or
systolic-diastolicbruitthatlateralizestooneside(lowsensitivity,highspecificity).
1,20
A newer body of evidencesuggeststhat primaryaldosteronism is partofa spectrum ofaldosterone
excessstatesandfoundthat aldosteroneexcess is much morecommon eveninprimaryhypertension
thanpreviouslythought (plasma aldosterone/reninratios hadpoorsensitivityandnegative predictive
value),suggestingthatfurtherinvestigationofaldosteroneexcessinthosewithuncontrolledorresistant
hypertensionmaybewarranted.
21,22
PHYSICALEXAMINATION
Physicalexaminationshouldincludemeasurementofbloodpressureinbothextremities,andinvestigation
fortargetorgandamageorasecondarycauseofhypertensionbynotingthepresenceofcarotidbruits,an
S3orS4,cardiacmurmurs,neurologicdeficits,elevatedjugularvenouspressure,rales,retinopathy,
unequalpulses,enlargedorsmallkidneys,cushingoidfeatures,andabdominalbruits.
DifferentialDiagnosis
Hypertension may be partly due to withdrawal from drugs, including alcohol, cocaine, and opioid
analgesics.ReboundincreasesinBPmaybeseeninpatientswhoabruptlydiscontinueantihypertensive
therapy,particularlyβ-adrenergicantagonistsandcentralα2-agonists(see“Complications”).
Cocaine and other sympathomimetic drugs (e.g., amphetamines, phencyclidine hydrochloride) can
producehypertensioninthesettingofacuteintoxicationandwhentheagentsarediscontinuedabruptly
afterchronicuse.Hypertensioninthesecasesisoftencomplicatedbyotherend-organinsults,suchas
ischemicheartdisease,stroke,andseizures.Phentolamine(anonselectiveα-adrenergicantagonist)is
effectiveinacutemanagement,andsodiumnitroprussideornitroglycerincanbeusedasanalternative.
β-Adrenergic antagonists should be avoided because of the riskofunopposed α-adrenergic activity,
whichcanexacerbatehypertension.
DiagnosticTesting
Testsareneededtohelpidentifypatientswithpossibletargetorgandamage,toassesscardiovascular
risk,andtoprovideabaselineformonitoringtheadverseeffectsoftherapy.
Basic laboratorydatashouldincludeurinalysis, hematocrit, plasma glucose,serumpotassium, serum
creatinine,calcium,uricacid,hemoglobinA1c,andfastinglipidlevels.
Other testing includes ECG and chest radiography. Echocardiography may be of value for certain
patientstoassesscardiacfunctionordetectionofleftventricularhypertrophy(LVH)orotherstructural
abnormalitiessuchasvalvulardiseases.
Ambulatory blood pressure monitoring can also be particularly useful in evaluating those with
suspected white coat hypertension or possible drug resistance after initiation of pharmacologic
therapy.
1
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TREATMENT
The goal oftreatmentis to prevent long-term sequelae (i.e., target organdamage) while controlling
othermodifiable cardiovascularriskfactors. BPshould bereducedtoagoalof<130/80mmHg for
most patients. Discretion is warranted in prescribing medication to lower BP that may affect
cardiovascularriskadverselyinotherways(e.g.,glucosecontrol,lipidmetabolism,uricacidlevels).
Lifestyle modificationsshould be encouraged inall hypertensive patientsregardless ofwhetherthey
requiremedication(Table3-3).Thesechangesmayhavebeneficialeffectsonothercardiovascularrisk
factors.
TABLE3-3
LIFESTYLEMODIFICATIONSANDEFFECTS
Modification ApproximateSBPReduction(mm
Hg)
Weightreduction(forevery10-kgweightloss) 5–20
AdoptionofDASHeatingplan 8–14
Dietarysodiumreduction(intake<2g/d) 2–8
Physicalactivity(150min/wk) 4–9
Moderationofalcoholconsumption(intake
<2drinks/d)
2–4
DASH,DietaryApproachestoStopHypertension;SBP,systolicbloodpressure.
Barringanovertneedforimmediatepharmacologictherapy,ordiagnosisofstage2hypertension,most
patientsshould be giventheopportunitytoachieve a reductioninBPover aninterval ofamonth by
applyingnonpharmacologicmodificationspriortoinitiationofpharmacologictherapies.
Monitoring/Follow-Up
BP measurements should be performed onmultiple occasionsundernonstressfulcircumstances (e.g.,
rest, sitting with legs uncrossed, empty bladder, comfortable temperature) to obtain an accurate
assessmentofBPinagivenpatient.
Hypertensionshouldnotbediagnosedbasedononemeasurementalone,unlessitis>180/120mmHg
or accompanied by target organ damage (i.e., hypertension urgency or emergency). Two or more
abnormal readings should be obtained,preferablyover a period of several weeks,beforetherapyis
considered.
Careshouldalso beusedtoexcludepseudohypertension,whichusuallyoccursinelderlyindividuals
with stiff, noncompressible vessels. A palpable artery that persists after cuff inflation (Osler sign)
shouldalertthephysiciantothispossibility.
Home and ambulatory BP monitoring can be used to assess a patient’s true average BP, which
correlatesbetterwithtargetorgandamage.
23-25
Medications
Initialdrugtherapy.
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Druginteractions,cost,andcoexistentfactorssuchasage,race,angina,HF,renalinsufficiency,LVH,
obesity, hyperlipidemia, gout, and bronchospasm should be considered in initial drug choice. The
amountofbloodpressurereductionisthemajordeterminantofreductionincardiovascularrisk,notthe
choiceofantihypertensivedrug.TheBPresponseisusuallyconsistentwithinagivenclassofagents;
therefore,ifadrugfailstocontrolBP,anotheragentfromthesameclassisunlikelytobeeffective.At
times, however, a change within drug class may be useful in reducing adverse effects. The lowest
possibleeffectivedosageshouldbeusedtocontrolBP,adjustedevery1–2monthsasneeded(Table3-
4).
TABLE3-4
COMMONLYUSEDANTIHYPERTENSIVEAGENTSBYFUNCTIONALCLASS
DrugsbyClass Properties InitialDose Dosage
Range(mg)
β-AdrenergicAntagonists
Atenolol
a
Selective 50mgPOdaily 25–100
Betaxolol
a
Selective 10mgPOdaily 5–40
Bisoprolol
a
Selective 5mgPOdaily 2.5–20
Metoprolol Selective 50mgPObid 50–450
MetoprololXL Selective 50–100mgPOdaily 50–400
Nebivolol
a
Selectivewith
vasodilatoryproperties
5mgPOdaily 5–40
Nadolol
a
Nonselective 40mgPOdaily 20–240
Propranolol Nonselective 40mgPObid 40–240
PropranololLA Nonselective 80mgPOdaily 60–240
Timolol Nonselective 10mgPObid 20–40
Pindolol ISA 5mgPOdaily 10–60
Labetalol α-andβ-antagonist
properties
100mgPObid 200–1200
Carvedilol α-andβ-antagonist
properties
6.25mgPObid 12.5–50
CarvedilolCR α-andβ-antagonist
properties
10mgPOdaily 10–80
Acebutolol
a
ISA,selective 200mgPObid,400mgPO
daily
200–1200
CalciumChannelAntagonists
Amlodipine DHP 5mgPOdaily 2.5–10
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Diltiazem 30mgPOqid 90–360
DiltiazemLA 180mgPOdaily 120–540
DiltiazemCD 180mgPOdaily 120–480
DiltiazemXR 180mgPOdaily 120–540
DiltiazemXT 180mgPOdaily 120–480
Isradipine DHP 2.5mgPObid 2.5–10
Nicardipine DHP 20mgPOtid 60–120
Nifedipine DHP 10mgPOtid 30–120
NifedipineXL(or
CC)
DHP 30mgPOdaily 30–90
Nisoldipine DHP 20mgPOdaily 20–40
Verapamil 80mgPOtid 80–480
VerapamilSR 120mgPOdaily 120–480
Angiotensin-ConvertingEnzymeInhibitors
c
Benazepril 10mgPObid 10–40
Captopril 25mgPObid–tid 12.5–450
Enalapril 5mgPOdaily 2.5–40
Fosinopril 10mgPOdaily 10–40
Lisinopril 10mgPOdaily 5–40
Moexipril 7.5mgPOdaily 7.5–30
Quinapril 10mgPOdaily 5–80
Ramipril 2.5mgPOdaily 1.25–20
Trandolapril 1–2mgPOdaily 1–4
Perindopril 4mgPOdaily 2–16
AngiotensinIIReceptorBlockers
c
Azilsartan
b
40mgPOdaily 40–80
Candesartan 8mgPOdaily 8–32
Eprosartan 600mgPOdaily 600–800
Irbesartan 150mgPOdaily 150–300
Olmesartan 20mgPOdaily 20–40
Losartan 50mgPOdaily 25–100
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