04 Patient With Hypertension

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PATIENT WITH HYPERTENSIONPATIENT WITH HYPERTENSIONPATIENT WITH HYPERTENSIONPATIENT WITH HYPERTENSION

2004-20052004-2005


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Case presentation 1Case presentation 1

D.A. 45 years

Female

Risk factors:

Family history: mother - HT

smoker

Obesity (BMI = 30)

Asymptomatic

BP= 135/85 mmHg, HR= 62 b/min (medicated)

D.A. 45 years

Female

Risk factors:

Family history: mother - HT

smoker

Obesity (BMI = 30)

Asymptomatic

BP= 135/85 mmHg, HR= 62 b/min (medicated)


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Associated risk factors

Dislipidemia

Associated risk factors

Dislipidemia

Total Colesterol = 220 mg/dL

LDL = 152 mg/dL

HDL = 32 mg/dL

Total Colesterol = 220 mg/dL

LDL = 152 mg/dL

HDL = 32 mg/dL


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45 years

high normal HT, obesity

High normal HTN isassociated with an increased

cardiovascular risk

The risk for 1o years?

HIGH RISK!HIGH RISK!

45 years

high normal HT, obesity

High normal HTN isassociated with an increased

cardiovascular risk

The risk for 1o years?

HIGH RISK!HIGH RISK!

Vasan RS, Larson MG, Leip EP, et al. N Engl J Med. 2001;345:1291-1297.Vasan RS, Larson MG, Leip EP, et al. N Engl J Med. 2001;345:1291-1297.

Vasan RS, Beiser A, Seshadri S, et al. JAMA. 2002;287:1003-1010.Vasan RS, Beiser A, Seshadri S, et al. JAMA. 2002;287:1003-1010.

High normal

Normal

Optimal

0 2 4 6 8 10 12 14

TimeTime

(years))(years))

10

8

6

4

2

0

Cum

ulativecardiova

scularincidents(%)

Cum

ulativ

ecardiova

scula

rincidents(%)

10 years cardiovascular events rate in women

with obesity and HT

A. What is the risk of a 45 year old woman

with high normal hypertension?

A.What is the risk of a 45 year old woman

with high normal hypertension?


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BP increases with aging

diastolic BP increases with aging, but reaches maximal values between 55

and 60 years

Arterial stiffness: leads to high systolic BP, but also low diastolic BP

BP increases with aging

diastolic BP increases with aging, but reaches maximal values between 55

and 60 years

Arterial stiffness: leads to high systolic BP, but also low diastolic BP

Diastolic

4

3

2

1

95

90

85

80

75

70

65

BP(mm

Hg

)

30

-3

4

35

-3

9

40

-4

4

45

-4

9

50

-5

4

55

-5

9

60

-6

4

65

-6

9

70

-7

4

75

-7

9

80

-8

4

Age

(years)

30

-3

4

35

-3

9

40

-4

4

45

-4

9

50

-5

4

55

-5

9

60

-6

4

65

-6

9

70

-7

4

75

-7

9

80

-8

4

Age

(years)

Systolic175

165

155

145

135

125

115

105

BP(mm

Hg)

Cohort study

Franklin SS, Fustin W 4th, Wong ND, et al. Circulation. 1997;96:308-315.Franklin SS, Fustin W 4th, Wong ND, et al. Circulation. 1997;96:308-315.

B. Does BP normally increase with aging?BP normally increase with aging?B. Does BP normally increase with aging?BP normally increase with aging?


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C. What is the proper treatment?C. What is the proper treatment?

Does she need associated medication?Does she need associated medication?

C. What is the proper treatment?C. What is the proper treatment?

Does she need associated medication?Does she need associated medication?

1. Lifestyle change:

- diet (low sodium, low cholesterol intake,hypocaloric)

- daily exercise

2. ACEI (or Dihydropirydine or Sartan or Diuretic)

3. Aspirin 100 mg /zi

4. Dislipidemia - Statin

1. Lifestyle change:

- diet (low sodium, low cholesterol intake,hypocaloric)

- daily exercise

2. ACEI (or Dihydropirydine or Sartan or Diuretic)

3. Aspirin 100 mg /zi

4. Dislipidemia - Statin


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B.P. 50 years

Male

Type 2 DM (for 8 years, treated with gliclazid andmetformin)

HbA1C 8.2% 1 month ago

no retinopathy or neuropathy

Obesity (BMI 32)

BP 140/85 mm Hg, HR 64 b/ min (treated withdihydropirydine)

B.P. 50 years

Male

Type 2 DM (for 8 years, treated with gliclazid andmetformin)

HbA1C 8.2% 1 month ago

no retinopathy or neuropathy

Obesity (BMI 32) BP 140/85 mm Hg, HR 64 b/ min (treated with

dihydropirydine)

CASE PRESENTATION 2CASE PRESENTATION 2


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Cholesterol 220 mg/dL, HDL 32 mg/dL, LDL 144 mg/dL

TG 200 mg/dL

Albuminuria

Cholesterol 220 mg/dL, HDL 32 mg/dL, LDL 144 mg/dL

TG 200 mg/dL

Albuminuria

Associated risk factorsAssociated risk factors


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A.Connection between HT and DMA.Connection between HT and DM

HT is more frequent in

type 2 diabetes

HIGH RISK!

HT is more frequent in

type 2 diabetes

HIGH RISK!

Grundy SM, Benjamin IJ, Burke GL, et al. Circulation. 1999;100:1134-1146.Grundy SM, Benjamin IJ, Burke GL, et al. Circulation. 1999;100:1134-1146.

Excessive

caloric intake

Inherited

genetic

disorders

Obesity Diabetes (NIDDM)

Insulinresistance

Hyperinsulinemia

Hypertension

HyperTG

Hyper CT

LowHDL

Atherosclerosis


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B. Which risk factor should be monitored?B. Which risk factor should be monitored?

UK Prospective Diabetes Study Group. BMJ. 1998;317:703-713.UK Prospective Diabetes Study Group. BMJ. 1998;317:703-713.

High incidence of vascular diseases

(stroke, CAD, peripheric vascular

disease) in type 2 diabetes

Does the patient have metabolic

syndrome?

High incidence of vascular diseases

(stroke, CAD, peripheric vascular

disease) in type 2 diabetes

Does the patient have metabolic

syndrome?

Metabolic syndrome

Obesity

Hypertension

Glucose tolerance

impairment

Dislipidemia

Insulinresistance


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C. Comments regarding the assessment and

management

C. Comments regarding the assessment and

management

HT treatment reduces CV death

in diabetics

Goals of treatment:

Lifestyle changes- diet

- exercise

control glycemia (HbA1C


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The proper therapy should consider ACEI or

AT1 blockers

ACEI are superior to calcium channel blockers

in elderly and in diabetics (they decrease

morbidity and mortality)

ACEI and AT1 blockers: renoprotective effects

The proper therapy should consider ACEI or

AT1 blockers

ACEI are superior to calcium channel blockers

in elderly and in diabetics (they decrease

morbidity and mortality)

ACEI and AT1 blockers: renoprotective effects

C. Comments regarding the assessment

and management

C. Comments regarding the assessment

and management


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CARDIOVASCULAR RISK FACTORSCARDIOVASCULAR RISK FACTORSCARDIOVASCULAR RISK FACTORSCARDIOVASCULAR RISK FACTORS

x 1.6 x 3

x 4

x 4.5

x 6 x 9

x 16

Cholesterol

Smoking

HT


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DIAGNOSTIC STEPS IN HTDIAGNOSTIC STEPS IN HTDIAGNOSTIC STEPS IN HTDIAGNOSTIC STEPS IN HT

(1) ASSESS BP(1) ASSESS BP

HT should be defined depending on the way of BP assessing(mmHg)

(1) ASSESS BP(1) ASSESS BP

HT should be defined depending on the way of BP assessing(mmHg)

SBP DBP

Hospital 140 90

Holter monitor 125 80

At home (self) 135 85


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DIAGNOSTIC STEPSDIAGNOSTIC STEPSDIAGNOSTIC STEPSDIAGNOSTIC STEPS

- Duration of high BP

- Possible secondary HT:

- family history of polycystic kidney

- personal history of kidney disorder: hematuria, urinary infections,

analgetics abuse

- intake of: oral contraceptives, amphetamines, cocaine, steroids,

NSAIDS etc.

- episodes of headache-anxiety-palpitations (feocromocitoma)

- episodes of muscular fatigue, tetany (hyperaldosteronism)

- Risk Factors : High lipid level

Smoking

Diabetes mellitus

Obesity-Sedentary lifeEating habits

- Signs that suggest target organ damage

- Use of BP lowering medication (type/doses/effectiveness /adverse reactions)

- Duration of high BP

- Possible secondary HT:

- family history of polycystic kidney

- personal history of kidney disorder: hematuria, urinary infections,

analgetics abuse

- intake of: oral contraceptives, amphetamines, cocaine, steroids,

NSAIDS etc.

- episodes of headache-anxiety-palpitations (feocromocitoma)

- episodes of muscular fatigue, tetany (hyperaldosteronism)

- Risk Factors : High lipid level

Smoking

Diabetes mellitus

Obesity-Sedentary lifeEating habits

- Signs that suggest target organ damage

- Use of BP lowering medication (type/doses/effectiveness /adverse reactions)

(2)(2) Personal and family historyPersonal and family history


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Routine tests: fasting glycemia

CT

HDL

TG

creatinin

K+

Hb, Ht

urine exam

ECG

Routine tests: fasting glycemia

CTHDL

TG

creatinin

K+

Hb, Ht

urine exam

ECG

(3) Investigations(3) Investigations


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Specific tests: EchocardiographyCarotid / femural ultrasound

C reactive protein

Microalbuminuria (D.M.)

Quantitative proteinuria

Funduscopy


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Extended evaluation (specialist)

- Complicated HT: tests to assess cardiac function

renal function

cerebral function

- secondary HT: measurement of renin

aldosteronecatecholamines

arteriography

renal and adrenal ultrasound

CT / MRI


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- LVH: ECG Sokolow-Lyon > 38mm

ECHO LV mass index

- IVS LVPP

- LV dysfunction- Ultrasound evidence of arterial wall thickening (carotid IMT

0.9 mm) or atherosclerotic plaque

- Serum creatinine 1,0-1,2 mg/dl

- microalbuminuria 30-300 mg/24 hours

- LVH: ECG Sokolow-Lyon > 38mm

ECHO LV mass index

- IVS LVPP

- LV dysfunction- Ultrasound evidence of arterial wall thickening (carotid IMT

0.9 mm) or atherosclerotic plaque

- Serum creatinine 1,0-1,2 mg/dl

- microalbuminuria 30-300 mg/24 hours


(4)(4).. Target organ damage (TOD)Target organ damage (TOD)


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- Cerebrovascular disease: - ischemic stroke

- transient ischemic attack

- cerebral haemorrhage

- Heart disease - myocardial infarction

- angina

- coronary revascularization

- congestive heart failure

- Renal d. - diabetic nephropathy

- renal impairment: serum creatinine > 1,5mg/dl

- proteinuria > 300mg/24 hours

- Peripheral vascular disease

- Advanced retinopathy

- Cerebrovascular disease: - ischemic stroke

- transient ischemic attack

- cerebral haemorrhage

- Heart disease - myocardial infarction

- angina

- coronary revascularization

- congestive heart failure

- Renal d. - diabetic nephropathy

- renal impairment: serum creatinine > 1,5mg/dl

- proteinuria > 300mg/24 hours

- Peripheral vascular disease

- Advanced retinopathy


(5)(5).. Associated clinical conditions (ACC)-complicationsAssociated clinical conditions (ACC)-complications


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CLASSIFICATION OF BP LEVELS (mm Hg)CLASSIFICATION OF BP LEVELS (mm Hg)CLASSIFICATION OF BP LEVELS (mm Hg)CLASSIFICATION OF BP LEVELS (mm Hg)

ESH-ESC Guidelines, 2003

Category SBP DBP

Optimal < 120 < 80

Normal 120-129 80-84

High normal 130-139 85-89

Grade 1 HT (mild) 140-159 90-99

Grade 2 HT (moderate) 160-179 100-109

Grade 3 HT (severe) 180 110

Isolated systolic HT 140 < 90


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STRATIFICATION OF RISKSTRATIFICATION OF RISKSTRATIFICATION OF RISKSTRATIFICATION OF RISK

RF

BP (mmHg)

Normal

SBP 120-129 or

DBP80-84

High normal

SBP 130-139 or

DBP 85-89

Grade 1

SBP 140-159 or

DBP 90-99

Grade 2

SBP 160-179 or

DBP 100-109

Grade 3

SBP 180 or

DBP 110

No other RF Average risk Average risk Low added risk Moderate added

risk

High added risk

1-2 RF Low added risk Low added risk Moderate addedrisk

Moderate addedrisk

Very high addedrisk

3 or more RF or TOD

or diabetes

Moderate added

risk

High added risk High added risk High added risk Very high added

risk

ACC High added risk Very high addedrisk

Very high addedrisk

Very high addedrisk

Very high addedrisk

ACC associated clinical conditions; TOD target organ damage; SBP systolic blood pressure; DBP

diastolic blood pressure


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White-coat HTWhite-coat HTWhite-coat HTWhite-coat HT

- Diagnosis : BP 140/90 mmHg (at several visits)

BP < 125/80 mmHg (Holter)

- Investigation - possible metabolic syndrome

- possible target organ damage (TOD)

- Prescription: - lifestyle changes

- pharmacological treatment (TOD)

- Diagnosis : BP 140/90 mmHg (at several visits)

BP < 125/80 mmHg (Holter)

- Investigation - possible metabolic syndrome

- possible target organ damage (TOD)

- Prescription: - lifestyle changes

- pharmacological treatment (TOD)


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THERAPEUTIC APPROACHTHERAPEUTIC APPROACHTHERAPEUTIC APPROACHTHERAPEUTIC APPROACH

(1)(1) High normal BPHigh normal BP

STRATIFY ABSOLUTE RISK

- very high drug treatment

- high drug treatment

- moderate monitor BP frequently

- low lifestyle change


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(2)(2) Grades 1 and 2 HTGrades 1 and 2 HT

- STRATIFY ABSOLUTE RISK

(a) very high: drug treatment promptly

(b) high : drug treatment promptly

(c) moderate : monitor BP and RF (3 months)-SBP 140 or TAD 90 drug treatment

-SBO < 140 and DBP < 90 continue to monitor

(d) low : monitor BP and RF (3-12 months)

-SBP 140-159 and DBP 90-93 consider drug treatment

-SBP < 140 and DBP < 90 continue to monitor


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(3)(3) Grade 3 HTGrade 3 HT

BEGIN DRUG TREATMENT IMMEDIATELY!

Assess - other RF

- Diabetes mellitus

- Target organ damage

- Associated clinical conditions

Add: lifestyle changes and correction of other RF and diseases


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GOALS of treatmentGOALS of treatmentGOALS of treatmentGOALS of treatment

a) Maximum reduction in the long-term total risk:

* CV morbidity reduction

* CV mortality reduction

Treatment of all reversible RF

Treatment of ACC

b) Recommended BP:

BP < 140/90 mmHg

BP < 130/80 mmHg (diabetics)

a) Maximum reduction in the long-term total risk:

* CV morbidity reduction

* CV mortality reduction

Treatment of all reversible RF

Treatment of ACC

b) Recommended BP:

BP < 140/90 mmHg

BP < 130/80 mmHg (diabetics)


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DIURETICSDIURETICSDIURETICSDIURETICS


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DIURETICSDIURETICSDIURETICSDIURETICS

(A) THIAZIDES AND ANALOGSHydroclorothiazid Butizid Chlortalidon Clopamid

Mefrusin Metazolon Xipamid Indapamid

(B) LOOP DIURETICS

Furosemid Piretanid Torasemid Bumetanid

(C) ANTI-ALDOSTERONE DIURETICS

Spironolacton Triamteren Amilorid

(D) FIX COMBINATIONS

Triamteren + Butizid or/Hydroclorothiazid or/Xipamid or/Furosemid Amilorid + Hydroclorothiazid or/Furosemid or/Trichlormethiazid

Spironolacton + Furosemid or/Hydroclorothiazid or/Butizid

(A) THIAZIDES AND ANALOGSHydroclorothiazid Butizid Chlortalidon Clopamid

Mefrusin Metazolon Xipamid Indapamid

(B) LOOP DIURETICS

Furosemid Piretanid Torasemid Bumetanid

(C) ANTI-ALDOSTERONE DIURETICS

Spironolacton Triamteren Amilorid

(D) FIX COMBINATIONS

Triamteren + Butizid or/Hydroclorothiazid or/Xipamid or/Furosemid Amilorid + Hydroclorothiazid or/Furosemid or/Trichlormethiazid

Spironolacton + Furosemid or/Hydroclorothiazid or/Butizid

BETA BLOCKERS


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(A )NON-SELECTIVE:

Alprenolol Bopindolol Bupranolol Carazolol Carteolol

Carvedilol Mepindolol Nadolol Oxprenolol Penbutolol

Pindolol Sotalol Tertataolol

(B) SELECTIVE:Acebutolol Atenolol Betaxolol Bisoprolol Celiprolol

Metoprolol Nebivolol Talinolol

(C) FIX COMBINATIONS:

DIRETICS + BETA-BLOCKERS

C1 SELECTIVE: Hydrochlorothiazid + Metoprolol

Hydrochlorothiazid + Bisoprolol

Chlortalidon + Metoprolol

Chlortalidon + Atenolol

C2 NON-SELECTIVE: Hydrochlorothiazid + Mepindolol

Piretanid + Penbutolol

Furosemid + Penbutolol

Hydrochlorothiazid + Propranolol

Bendroflumethiazid + Propranolol

Butizid + Metipranolol

Chlortalidon + Oxprenolol

Clopamid + Pindolol

Hydrochlorothiazid + Triamteren + Propranolol

Hydrochlorothiazid + Amilorid + Timolol

BETA-BLOCKER + CALCIUM-BLOCKER

Metoprolol + Phelodipin SR Metoprolol + Nifedipin

Atenolol + Nifedipin retard Acebutolol + Nifedipin

BETA-BLOCKER + DIURETIC + DIHYDRALAZIN

C3 SELECTIVE: Metoprolol + Hydrochlorothiazid + Hydralazin

Atenolol + Chlortalidon + Hydralazin

C4 NON-SELECTIVE: Propranolol + Dihydralazin

Propranolol + Bendroflumethaizid + HydralazinOxprenolol + Hydralazin + Chlortalidon

(A )NON-SELECTIVE:

Alprenolol Bopindolol Bupranolol Carazolol Carteolol

Carvedilol Mepindolol Nadolol Oxprenolol Penbutolol

Pindolol Sotalol Tertataolol

(B) SELECTIVE:Acebutolol Atenolol Betaxolol Bisoprolol Celiprolol

Metoprolol Nebivolol Talinolol

(C) FIX COMBINATIONS:

DIRETICS + BETA-BLOCKERS

C1 SELECTIVE: Hydrochlorothiazid + Metoprolol

Hydrochlorothiazid + Bisoprolol

Chlortalidon + Metoprolol

Chlortalidon + Atenolol

C2 NON-SELECTIVE: Hydrochlorothiazid + Mepindolol

Piretanid + Penbutolol

Furosemid + Penbutolol

Hydrochlorothiazid + Propranolol

Bendroflumethiazid + Propranolol

Butizid + Metipranolol

Chlortalidon + Oxprenolol

Clopamid + Pindolol

Hydrochlorothiazid + Triamteren + Propranolol

Hydrochlorothiazid + Amilorid + Timolol

BETA-BLOCKER + CALCIUM-BLOCKER

Metoprolol + Phelodipin SR Metoprolol + Nifedipin

Atenolol + Nifedipin retard Acebutolol + Nifedipin

BETA-BLOCKER + DIURETIC + DIHYDRALAZIN

C3 SELECTIVE: Metoprolol + Hydrochlorothiazid + Hydralazin

Atenolol + Chlortalidon + Hydralazin

C4 NON-SELECTIVE: Propranolol + Dihydralazin

Propranolol + Bendroflumethaizid + HydralazinOxprenolol + Hydralazin + Chlortalidon

BETA-BLOCKERS

ANGIOTENSIN CONVERTING ENZYME


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(A) Captopril Enalapril Lisinopril Cilazapril Perindopril

Ramipril Trandolapril Fosinopril Benazepril Quinapril

Moexipril Spirapril

(B) FIX COMBINATIONS:

ACE + DIURETICS

Hydroclorothiazid + Captopril or/Enalapril or/Cilazapril or/Lisinopril or/Ramiprilor/Quinapril or/Benazepril or/Fosinopril or/Moexipril

ACE + CALCIUM-BLOCKERS

Trandolapril + Verapamil Ramipril + Phelodipin

AT1-BLOCKERS

(A)Candesartan Eprosartan Irbesartan

Losartan Telmisartan Valsartan


Hydrochlorothiazid + Losartan or/Valsatran or/Irbesartan

(A) Captopril Enalapril Lisinopril Cilazapril Perindopril

Ramipril Trandolapril Fosinopril Benazepril Quinapril

Moexipril Spirapril


ACE + DIURETICS

Hydroclorothiazid + Captopril or/Enalapril or/Cilazapril or/Lisinopril or/Ramiprilor/Quinapril or/Benazepril or/Fosinopril or/Moexipril

ACE + CALCIUM-BLOCKERS

Trandolapril + Verapamil Ramipril + Phelodipin

AT1-BLOCKERS

(A)Candesartan Eprosartan Irbesartan

Losartan Telmisartan Valsartan


Hydrochlorothiazid + Losartan or/Valsatran or/Irbesartan

ANGIOTENSIN-CONVERTING ENZYME

INHIBITORS


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(A) DIHYDROPYRIDINES:

GENERATION I Nifedipin

Nicardipin

GENERATION II Phelodipin Nimodipin

Nifedipin SR

Nisoldipin Nitrendipin

GENERATION III Lercanidipin

Lacidipin Amlodipin

(B) Verapamil SR

(C) Diltiazem

(A) DIHYDROPYRIDINES:

GENERATION I Nifedipin

Nicardipin

GENERATION II Phelodipin Nimodipin

Nifedipin SR

Nisoldipin Nitrendipin

GENERATION III Lercanidipin

Lacidipin Amlodipin

(B) Verapamil SR

(C) Diltiazem

CALCIUM CHANNEL BLOCKERS

ALFA-1 BLOCKERSALFA-1 BLOCKERS


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ALFA-1 BLOCKERS

(A) Alpha 1 selective: Prazosin Doxazosin Terazosin

(B) Non-selective: Phenoxybenzamin

Urapidil

CENTRAL SYMPATHETIC INHIBITORS

(A) IMIDAZOLINIC RECEPTOR : Moxonidin(B) ALPHA-RECEPTOR: Alpha-metil Dopa(C) IMIDAZOLINIC RECEPTOR+ALPHA 2-AGONIST: Clonidin

DIRECT VASODILATORS

(A) (Di)Hydralazin

(B) Minoxidil

(C) Diazoxid

(D) Sodium nitroprussideE Nitro l cerine

ALFA-1 BLOCKERS

(A) Alpha 1 selective: Prazosin Doxazosin Terazosin

(B) Non-selective: Phenoxybenzamin

Urapidil

CENTRAL SYMPATHETIC INHIBITORS

(A) IMIDAZOLINIC RECEPTOR : Moxonidin(B) ALPHA-RECEPTOR: Alpha-metil Dopa(C) IMIDAZOLINIC RECEPTOR+ALPHA 2-AGONIST: Clonidin

DIRECT VASODILATORS

(A) (Di)Hydralazin

(B) Minoxidil

(C) Diazoxid

(D) Sodium nitroprussideE Nitro l cerine


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24 hours effect in monodosis

Better protection against major cardiovascular events andagainst target organ damage.

Calcium antagonists are effective in stroke prevention

ACEI proved their efficiency in primary and/or secondaryprevention of myocardial infarction.

24 hours effect in monodosis

Better protection against major cardiovascular events andagainst target organ damage.

Calcium antagonists are effective in stroke prevention

ACEI proved their efficiency in primary and/or secondaryprevention of myocardial infarction.

Antihypertensive drugs with long-term action:


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MONOTHERAPY vs. COMBINATION THERAPYMONOTHERAPY vs. COMBINATION THERAPYMONOTHERAPY vs. COMBINATION THERAPYMONOTHERAPY vs. COMBINATION THERAPY

Consider untreated BP level

Assess the absence / presence of RF and target organ damage

Choose between

SINGLE AGENT TWO-DRUG COMBINATION

at low dose at low dose

Goal BP not achieved

Prev. agent Switch to Prev. combin Add a 3rd drug

(full dose) diff. agent (full dose) (at low dose)

(at low dose)

Goal BP not achievedTwo-three-drug Full dose THREE-DRUG COMBINATION

combination monotherapy at effective doses

Consider untreated BP level

Assess the absence / presence of RF and target organ damage

Choose between

SINGLE AGENT TWO-DRUG COMBINATION

at low dose at low dose

Goal BP not achieved

Prev. agent Switch to Prev. combin Add a 3rd drug

(full dose) diff. agent (full dose) (at low dose)

(at low dose)

Goal BP not achievedTwo-three-drug Full dose THREE-DRUG COMBINATION

combination monotherapy at effective doses

POSSIBLE COMBINATIONSPOSSIBLE COMBINATIONSPOSSIBLE COMBINATIONSPOSSIBLE COMBINATIONS


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POSSIBLE COMBINATIONSPOSSIBLE COMBINATIONSPOSSIBLE COMBINATIONSPOSSIBLE COMBINATIONS

Diuretics

ACE inhibitors

BB

-Blockers

AT1-receptor

blockers

Calcium antagonists


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CHOICE OF ANTIHYPERTENSIVE DRUGSCHOICE OF ANTIHYPERTENSIVE DRUGSCHOICE OF ANTIHYPERTENSIVE DRUGSCHOICE OF ANTIHYPERTENSIVE DRUGS

1. Previous experience (favourable/unfavourable) of the individual patient

with a given class of drugs

2. Cost of drugs

3. Cardiovascular risk profile of the individual patient

4. Presence of target organ damage

5. Presence of other coexisting disorders

6. Possibility of interactions with drugs used for other conditions present in

the patient

1. Previous experience (favourable/unfavourable) of the individual patient

with a given class of drugs

2. Cost of drugs

3. Cardiovascular risk profile of the individual patient

4. Presence of target organ damage

5. Presence of other coexisting disorders

6. Possibility of interactions with drugs used for other conditions present in

the patient


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ANTIHYPERTENSIVE THERAPY INANTIHYPERTENSIVE THERAPY IN

DIABETICSDIABETICSANTIHYPERTENSIVE THERAPY INANTIHYPERTENSIVE THERAPY IN

DIABETICSDIABETICS

Goal BP: < 130/80 mmHg

Type 1 DM- without albuminuria : diuretics

beta-blockers

- with albuminuria : ACE inhibitors

Type 2 DM : AT1-receptor antagonists

Goal BP: < 130/80 mmHg

Type 1 DM- without albuminuria : diuretics

beta-blockers

- with albuminuria : ACE inhibitors

Type 2 DM : AT1-receptor antagonists

S S i h


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1st choice therapy : ACE inhibitors or AT1-receptor blockers

2nd choice therapy: combination

- loop diuretic (creatinine > 2 mg/dl)

- Calcium antagonist

Recent evidence : in advanced stages of renal impairment

ACE inhibitors + AT1-receptor blockers

1st choice therapy : ACE inhibitors or AT1-receptor blockers

2nd choice therapy: combination

- loop diuretic (creatinine > 2 mg/dl)

- Calcium antagonist Recent evidence : in advanced stages of renal impairment

ACE inhibitors + AT1-receptor blockers

THERAPY IN HYPERTENSIVES withTHERAPY IN HYPERTENSIVES with

IMPAIRED RENAL FUNCTIONIMPAIRED RENAL FUNCTIONTHERAPY IN HYPERTENSIVES withTHERAPY IN HYPERTENSIVES with

IMPAIRED RENAL FUNCTIONIMPAIRED RENAL FUNCTION

THERAPY IN HYPERTENSIVES ithTHERAPY IN HYPERTENSIVES ithTHERAPY IN HYPERTENSIVES ithTHERAPY IN HYPERTENSIVES with


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CAD and CONGESTIVE HEARTCAD and CONGESTIVE HEART

FAILUREFAILURE


CAD and CONGESTIVE HEARTCAD and CONGESTIVE HEART

FAILUREFAILURE

The risk of a recurrent event in patients with CAD is significantlyaffected by the BP level

Usual antihypertensive agents:- Beta-blockers

- ACE inhibitors

- Anti-aldosterones

Recent data:

- AT1-receptors (as an alternative to ACE inhibitors orin combination)

- dihydropiridines with long-term action (coronaryevents prevention)

The risk of a recurrent event in patients with CAD is significantlyaffected by the BP level

Usual antihypertensive agents:- Beta-blockers

- ACE inhibitors

- Anti-aldosterones

Recent data:

- AT1-receptors (as an alternative to ACE inhibitors orin combination)

- dihydropiridines with long-term action (coronaryevents prevention)

ANTIHYPERTENSIVE THERAPY IN THESANTIHYPERTENSIVE THERAPY IN THE


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Benefit in all types of HT (isolated systolic HT)

Treated :

SBP = 140 mmHg

DBP < 60 mmHg bad prognosis

Choice:

- diuretics

- dihydropiridines

- ACE inhibitors or AT1-receptor blockers

- beta-blockers

Benefit in all types of HT (isolated systolic HT)

Treated :

SBP = 140 mmHg

DBP < 60 mmHg bad prognosis

Choice:

- diuretics

- dihydropiridines

- ACE inhibitors or AT1-receptor blockers

- beta-blockers

ANTIHYPERTENSIVE THERAPY IN THEANTIHYPERTENSIVE THERAPY IN THE

ELDERLYELDERLYANTIHYPERTENSIVE THERAPY IN THEANTIHYPERTENSIVE THERAPY IN THE

ELDERLYELDERLY

Hypertension in pregnancyHypertension in pregnancyHypertension in pregnancyHypertension in pregnancy


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Hypertension in pregnancyHypertension in pregnancyHypertension in pregnancyHypertension in pregnancy

1. PRE-EXISTING HT BP 140/90 mmHg proteinuria

- before week 20 of gestation

- persists > 40 days postpartum

2. GESTATIONAL HT

a) without proteinuria

b) with significant proteinuria (> 500 mg/day)

= PRE-ECLAMPSIA

- develops after 20 weeks of gestation

- it resolves within 40 days postpartum

3. PRE-EXISTING HT + SUPERIMPOSED GESTATIONAL HT withproteinuria

1. PRE-EXISTING HT BP 140/90 mmHg proteinuria

- before week 20 of gestation

- persists > 40 days postpartum

2. GESTATIONAL HT

a) without proteinuria

b) with significant proteinuria (> 500 mg/day)

= PRE-ECLAMPSIA

- develops after 20 weeks of gestation

- it resolves within 40 days postpartum

3. PRE-EXISTING HT + SUPERIMPOSED GESTATIONAL HT withproteinuria

C O C G CTHERAPY CHOICE IN PREGNANCY


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THERAPY CHOICE IN PREGNANCYTHERAPY CHOICE IN PREGNANCYTHERAPY CHOICE IN PREGNANCYTHERAPY CHOICE IN PREGNANCY

- Normal diet, without salt restriction!- Not recommended: weight reduction!

- Level of SBP 170 mmHg or DBP 110 mmHg

- emergency admission !

- pharmacological therapy - Labetalol I.V.

- MetilDOPA p.o.

- Nifedipin

- Pharmacological management

* Gestational HT without proteinurie

* Pre-existing HT before 20 weeks of gestation

* gestational HT with proteinuria

Used agents : - MetilDOPA

- Labetalol

- Calcium antagonists

- BB

- Normal diet, without salt restriction!- Not recommended: weight reduction!

- Level of SBP 170 mmHg or DBP 110 mmHg

- emergency admission !

- pharmacological therapy - Labetalol I.V.

- MetilDOPA p.o.

- Nifedipin

- Pharmacological management

* Gestational HT without proteinurie

* Pre-existing HT before 20 weeks of gestation

* gestational HT with proteinuria

Used agents : - MetilDOPA

- Labetalol

- Calcium antagonists

- BB

HYPERTENSIVE EMERGENCIESHYPERTENSIVE EMERGENCIESHYPERTENSIVE EMERGENCIESHYPERTENSIVE EMERGENCIES


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HYPERTENSIVE EMERGENCIESHYPERTENSIVE EMERGENCIESHYPERTENSIVE EMERGENCIESHYPERTENSIVE EMERGENCIES

1. MALIGNANT HT

Onset : hypertensive encephalopathy

Convulsive crises

DBP > 140 mmHg

Severe hypertensive retinopathy

Spontaneous evolution : death/ cerebral, cardiac , renal damage

Assessment: clinic: BP, diuresis

lab: urea, creatinine, ions

Therapy: loop diuretics

arteriolar vasodilators: Hydralazin/Diazoxid/Na nitoprusside

ACE inhibitors

haemodialysis

2. PAROXISTIC HT


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2. PAROXISTIC HT

Etiology: - Phaeochromocytoma

- Aortic dissection

- Abrupt cessation of antihypertensive agents- Brainstem tumors

Therapy:

* Regitin

* Loop diuretic

* Diazoxid or - Na nitroprusside

- Labetalol

- Clonidin

3. HT CRISIS and ACUTE CORONARY SYNDROME

* Na nitroprusside

* ACE inhibitors

* Sympathetic central inhibitors (Guanfacine)

* Nitrates

Antihypertensive agents in HTAntihypertensive agents in HTAntihypertensive agents in HTAntihypertensive agents in HT


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Antihypertensive agents in HTAntihypertensive agents in HT

emergency - dosisemergency - dosisAntihypertensive agents in HTAntihypertensive agents in HT

emergency - dosisemergency - dosis

1. Nitroprusiat Na: 0.25 - 10 g/kg/min

2. Nitroglycerin: 5 - 100 g/min

3. Diazoxid: 10 - 30 mg/min/30 min

4. Hydralazin: 10 - 20 mg

5. Labetalol: 2 - 4 mg/min

6. Urapidil: 12.5 - 25 mg bolus

7. Regitin: 5 - 10 mg bolus

8. Enalapril: 0.625 - 1.25 mg

1. Nitroprusiat Na: 0.25 - 10 g/kg/min

2. Nitroglycerin: 5 - 100 g/min

3. Diazoxid: 10 - 30 mg/min/30 min

4. Hydralazin: 10 - 20 mg

5. Labetalol: 2 - 4 mg/min

6. Urapidil: 12.5 - 25 mg bolus

7. Regitin: 5 - 10 mg bolus

8. Enalapril: 0.625 - 1.25 mg


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Resistant HypertensionResistant HypertensionResistant HypertensionResistant HypertensionDEFINITION:

Lifestyle changes and three-combination agents fail to lower systolic and diastolic BP sufficiently

DEFINITION:

Lifestyle changes and three-combination agents fail to lower systolic and diastolic BP sufficiently

Causes of resistant HTN:

-Unsuspected secondary cause

-Poor adherence to therapeutic plan

-Continued intake of drugs that rise blood pressure

-Failure to modify lifestyle (weight gain, heavy alcohol intake)

-Volume overload due to:

-Inadequate diuretic therapy

-Progressive renal insufficiency

-High sodium intake

04 Patient With Hypertension

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