Systemic HT by professor osman bukhari.ppt

Systemic hypertension

1. SYSTEMIC
HYPERTENSION
By Dr. Osman Bukhari

4. HTis:
-a major cause of premature vascular
disease(IHD, cerebrovascular and
peripheral vascular disease)
-a major cause of morbidity and mortality
which increases with rising age

5. Definition:
-WHOinternational society of HT defines
HT as Bp of 140/90 or more
-Prevalence10-15%; higher in blacks
-1 billion suffer from HTN worldwide

6. Measurement of BP :
-Clinicor office
-self measurement
-ambulatoryBP monitoring(to evaluate white
coat syndrome)
-intra-arterial
Sphygmomanometer
-cuff 12 cm wrapped round the arm 2.0 cm
above antecubital fossa)
BP is measured in
-Both arms, (Legsif femoral pulses are
diminished or delayed) Supine & erect specially in
elderly & diabetic

7. With white coat syndrome
confirm HTN by
ambulatory Bp monitoring

8. Mercury sphygmomanometer
Cuff
pump

9. Ambulatory BP monitoring

10. -BP= systolic
diastolic
-Systolic Bpwhen 1
st
korotkof sound is heard
-Diastolic Bpwhen korotkof sounds disappear
-Two measurementsat 5 minutes interval
with patient seated on chair, relaxed, feet on the
floor and arms supported at heart levelon the floor,
and arm supported at heart level or average BP at sepeate
measurements

11. Grading of HT:
-Optimal BP: < 120/80
-Pre HT: 120-139/80-89 (High normal)
-Stage 1 HT: 140-159/90-99
-Stage 2 HT: 160/100 or more
-Stage 3 HT:> 180/110

12. Causes:
1-Essential:(95 %):
-Rare before the age of 20 years
-Required life long TR.
2-Secondary:(5%):
-Reversible
-Most are due to renal causes

13. Essential Hypertension
Causes are multifactorial
-Genetic
-Enviromental factors:-obesity, alcohol,
smoking , salt intake, potassium intake,
and stress raise Bp in predisposed persons
-Humeral factors: sympathetic nervous
system over activity and renin-angiotensin-
aldosteron system activation.
-low birth weight.

14. -Insulin resistance(there is association between
diabetes mellitus and HTN)
-Metabolic syndrome(Syndrome X) : is a
major CV risk factor
In this syndrome there is association of
-HTN
-Hyperinsulinaemia
-glucose intolerance
-Reduced HDL cholesterol
-Hyper TG
-Central obesity.

16. Secondary HT
More likely in patients with:
1-age <30 year
2-accelerated HT
3-refractory HT
4-abnormal biochemistrye.g hypokalaemia
Causes of 2ry HT:
1-Renal diseases
2-Endocrine diseases
3-Co arcitation of aorta
4-Pregnancy (PIH)
5-Drugs

17. Renal (4%)
1-Glomerulonephritis
2-Polycystic kidney disease
3-Renovascular disease
4-Diabetic nephropathy
5-Interstitial nephropathy
6-Renal failure

18. Endocrine (1%)
1-Phaeochromocytoma
2-Pry hyperaldosteronsim
3-Cushing's syndrome
4-Adrenal hyperplasia
5-Acromegaly
6-Hyperthyroidism
7-Hyper parathyroidism

19. Drugs:
1-Corticosteroids
2-Oral contraceptive pills
3-NSAIDs
4-Cyclosporin
5-Vasopressin
These drugscause & aggravate
hypertension

20. Pathophysiology:
BP depends on CO & PR.
-Circulating catecholamines CO & PR
-PR: increased wall thickness and reduced
lumen diameter in chronic HT maintains
elevated BP.

21. Pathology:
HTN
-Arteriosclerosis e.g nephrosclerosis
-Atherosclerosis e.g CAD
-Left ventricular hypertrophy (LVH)

22. Complications of HT :
1-Cardiovascular disease
2-Cerebrovascular disease
3-Peripheral vascular disease
4-Renal vascular disease.
5-Retinopathy

23. Cardiovascular
1-LVH & LVF
2-CAD
3-Arrhythmias
4-Aortic dissection
5-Sudden death

24. LVH

25. Cerebrovascular dis
1-TIAs
2-HTN encephalopathy (from capillary congestion,
exudation & cerebral oedema)
3-Stroke (thrombosis or haemorrhage)
4-Dementia

28. Renal
1-Nephrosclerosis
2-Renal failure

29. Retinopathy
-Grade 1= increased tortuosity, thickening and
reflectiveness of retinal vessels (silver wiring)
-Grade 2= 1+ AV nipping.
-Grade 3= 2+ flamed shaped hage & soft
exudates (small infarcts).
-Grade 4= 3 + Papilledema (malign HTN)
Central retinal artery thrombosis
with optic atrophy
can occur in HT

30. Hypertensive retinopathy

32. MalignHTor accelerated (Rapidly
rising BP or DBP >140)leads to fibrinoid
necrosis of vessel wall and intravascular
thrombosis leading to death if
uncontrolledfrom:
-renal failure
-heart failure
-encephalopathy
-stroke.
Without treatment, 1 year survival is
less than 20%.

33. Hypertensive emergency
Hypertensive emergencies represent
severe HTN with TOD. In these
conditions, the BP should be lowered
aggressively over minutes to hours.
Hypertensive urgency
Hypertensive urgency is defined as a
severe elevation of BP, without evidence
of TOD. These patients require BP control
over several days to weeks .

34. Clinical features:
-Without complications HT is usually
asymptomaticand often diagnosed during
routine Ex or after complications
-Headache & Epistaxsisare rare.
-Symptoms of Target Organ Damage
-Features of secondary HTN.
-FH of HT
-Look for vascular risk factors

35. On examination:
-High Bpmay be the only abnormality
-Signs of complicationse.g. LVF, S3, S4
gallop rhythm & HF, CRF, retinopath
-Signs of underlying cause of HT
-Evidence of other vascular risk factors
e.g. xanthomas, diabetic retinopathy
-Retinopathy

36. Investigations (Assessment of HT)
The aim is to: :
1-Assess target organ damage (TOD)
2-Identify secondary HT.
3-Identify other vascular risk factors.
4-Identify co morbidities.
Target organ damageis assessed by
-Urine analysis, blood urea, electrolytes
serum creatinine.
-ECG, CXR, ECHO.

37. Left ventricular hypertrophy

38. LVH

40. If secondary HT is suspected
The following investigations are required:
-RenalUS , IVU, isotope & angiography
-Urine & serum epinephrine, norepineph
and VMA if the clinical picture suggest
phaeochromocytoma
-Urinary & serum cortisol if the clinical
picture suggests Cushing's syndrome
-CT & MRI abdomen in suspected adrenal
pathology

41. Vascular risk factors
-Blood sugar
-Lipid profile.
-CBC
-Others

42. Management of hypertension:
-Objectives:
1-To reduce risk of complication
2-To improve survival.
Theseshould be explained to the patient
-Goal of TR: BP < 140/90. (< 130/80 in
diabetics and chronic renal disease)
-The benefit of TRshould overweigh the
cost and SE.
-Management of HTN on individual basis

43. Management of HT include:
1-patient assessment
2-non pharmacological therapy
3-drug therapy
Patient assessment
1-Look for target organ damage
2-Identify:
-secondary HT
-cardiovascular risk factor
-co morbidities

44. Non pharmacological therapy
1-Life style modifications
in all HT and pre HT
1-Weight reduction
2-Dynamic exercise
3-Avoid alcohol
4-Low fat diet
5-Salt restriction
6-Increase fruits & vegetables intake (K).
2-Treatment of risk factors
1-Stopping smoking.
2-Treatment of dyslipidaemia.
3-Control of DM

45. Problem A
50 y old male who is diabetic & heavy smoker
presented to A & E unit with severe retro sternal
chest pain for 3 hours. The pain was crushing in
nature.
PH: HTN for 7y on Amlodipine
O/E he was in pain, sweaty & cold.
Pulse was rapid & BP 130/85
Systemic ex was normal
1-What is the clinical diag?
2-how do you confirm it?
3-What is the immediate management

46. 4-What is the pathogenesis of the underlying cinical
problem?
5-What are the risk factors?
6-What is the DD?
7-What is likely complications to happen to this patient?

47. Drug therapy
U suallystarted after a period of assessmentand
follow up.
-For all HT & pre HT=Non pharmacological TR
-Stage 2 & 3= drug therapy, usually in combin
-Stage 1 with TOD and/ or DM wz or without
CV risk factor=drug therapy,usually monotherapy
-Stage 1 without TOD or CV risk factors:
Life style modification only, assess monthly &
TR if HTN is sustained
-Pre HT= Reassess yearly. Drug treatment if
there is CV risk factor

48. Classification and Management
of BP for adults
BP
classification
SBP* DBP*
Lifestyle
modific
Initial drug therapy
Without compelling
indication
With compelling
indications
Normal <120 OR
<80
Encourage
Pre HTN 120-139OR
80-89
Yes No antihypertensive drug
indicated.
Drug(s) for
compelling
indications.
‡
Stage 1 HTN140–
159
OR
90–99
Yes Thiazide-type diuretics
for most. May consider
ACEI, ARB, BB, CCB, or
combination.
Drug(s) for the
compelling
indications.
‡
antihypertensive
drugs (diuretics,
ACEI, ARB, BB,
CCB) as needed.
Stage 2 HTN>160OR
>100
Yes2-drug comb for most
†
(usually thiazide-type
diuretic and ACEI or ARB
or BB or CCB).
*Treatment determined by highest BP
†
Initial combined therapy should be used cautiously in for orthostatic hypotension.
‡
Treat patients with chronic kidney disease or diabetes to BP goal of <130/80mmHg.

49. Drug used to treat HT :
-Diuretics
-Beta Blockers (BB)
-Angiotensin Converting Enzyme
Inhibitors (ACE-I)
-Angiotensin Receptor Blockers (ARBs)
-Calcium Channel Blockers (CCB)
-Alpha blockers
-Vasodilators
-Centrally acting drugs

50. First line drug TRdepends on:
-individual patient.
-compelling indications for specific drugs
-drug safety
-cost of the drug
-convenience of drug dosage
For the majority of HT patientsstart TR with
low dose thiazide diuretic or BB(if there is no
CI or compelling indicationsfor other antihypertensive)
For elderly patsstart with diureticsor long
acting dihydropyridine CCB(if there are no
compelling indication for BB)
Combination therapywill be required for many patients

52. Diuretics
They block reabsorption of sodium and
water diuresis & saluresis
hypovolemia & decreased CO
1-Thiazides: e.g. Hdrochlorothiazide(Esidrex)
Chlorthalidone, Indapamide.
SE Include: hypokalaemia
hyponatraemia
hypomagnesaemia
hypercholesterolemia
hyperuricemia
hyperglycemia (glucose intolerance)

53. 2-Loop diuretics: are potent diuretics and
preferred in:
-HF
-renal impairment
-combination with ACEI
e.g: frusemide(Lasix)and bumetanide.
3-Potassium sparing diureticse.g
spironolactone(Aldactone),amiloride and
triamterene.
They are not effective when used alone
except spironolactone in Con’s disease.

54. Beta-blocker
decrease HR & contractilityCO
and decrease Renin release & activity
decrease Angio II vasodilatation
PR
1-Cardio electives : e.g atenolol, metoprolol
andbisoprololwhich block B1 receptors
and not B2
2-Non cardio selective:e.g propranolol (lipid
soluble & crosses BBB CNS effects)

55. 3-Combined alpha & BBse.g. Labetalol which is
effective in malignant HT and used
in pregnancy.
* BB may aggravate asthma , HF, peripheral
vascular disease & can cause hypercholestrol
* SE:bradycardia, heart block, bronchospasm,
cold extremities, fatigue, hallucinations and
nightmaresandhallucinations
* CI:Bronchial asthma, Complete heart block
and severe heart failure.
.

56. ACE-Inhibitors
Block conversion of angiotensin 1 to
angiotensin 11 & Block degradation of
bradykinin which can lead to allergic reactions
including cough
Carewith its use in renal failure
CIin bilateral renal artery stenosis becauseit can
precipitate renal failure
Start with small dose& build up the dose
Add diuretic in black Africans

57. e.g captopril, enalapril, lisinopril, fosinopril and
ramipril
ACE-I slows diabetic nephropathy, LV dysfun
and improves survival.
* SE: First dose hypotensionspecially in
patients on diuretics , angio-edema,
cough, proteinuria , hyperkalaemia and
metallic taste.
Serum creatinine & electrolytesshould be
assessed before ACE-I therapy and 7-10 days
after start of treatment

58. Angiotensin Receptor Blockers
(ARBs)
-Similar effects to ACE-I but they do not
block bradykinin breakdowni.e. no cough
e.g losartan, valsartanand candisartan.

59. Calcium channel blockers
(CCB)
Mainly arteriolar vasodilaters
1-Dihydropyridine group e.g nifedipine,
amlodipine, filodipine.
2-Non-dihydropyridine group e.g Diltiazem
andverapamil. They decrease A-V
conduction, HR and force of contraction & CO
(caution with BB & HF)
CCB are specially useful when HT
coexist with angina

60. * SE include: flushing, palpitation,
fluid retention,
sweating, constipation.
Bradycardia with non
dihydropyridines

61. Alpha adreno rceptor blocker
Post synaptic alpha-1 receptor blockade
vasodilatation PR and CO
e.g.
prazocinand doxazocin (also used in BPH)
phentolamineis used for the diagnosis of
phaeochromocytoma
SE: First dose hypotension & dizziness.

62. Vasodilators
Used mainly in severe refractory HT
1-Hydralazine: Potent vasodilator (25-100 mg)
used in refractory HT& IV in emergency.
Can causeSLE like syndrome
2-Minoxidil:Directly acting potent arterial
vasodilator used in resistant HT(10-50 mg)
SE: first dose hypotension, tachycardia,
fluid retention & hirsuitism.
3-Na Nitroprusside: Arterial & venous
vasodilator for IV use in severe HT

63. Centrally acting drugs
They block alpha adrenergic receptors in
the CNS and decrease vasomotor tone.
They are cheap drugs
1-Methyl dopa(Aldomet)
-Safe in pregnancy.
-Causes postural hypotension , chronic
hepatitis & haemolysis.
2-Clonidine
Withdrawal causes rebound HT.

64. 3-Reserpine:Used in combination (Adelphan
esidrex & brinerdin)
4-Adrenergic neurone blockers
e.g. guanithidine) are no longer used.

65. Drug selection in HT
-Depends on the stage of HT, compelling
indications, cost and concomitant disease.
-TR Usually starts with monotherapywith a
goal BP< 140/90. Lower in diabetics.
-Start with one group & if it is ineffective
shift to the another group.
-If monotherapy is ineffective move to
combination therapy

67. Causes of resistant HTN
-improper BP measurement
-excess salt intake or inadequate diuretic
therapy
-inadequate doses
-drug interactions (NSAID, OCP,C/S)
-non compliance
-secondary HTN
-excessalcohol intake

68. Management of HTN emergency
Urgent parentral antihypertensivetherapy
needed in the following situations:
-Malignant HT
-HT encephalopathy
-Intra cranial bleeding
-Cardiac failure
-eclampsia
-Aortic dissection

69. Parentral antihypertensive therapyinclude:
-IV Labetalol(20 mg to maxim of 200 mg)
-IV Nitroprusside(0.3-1.0mg. / min.)
needs careful supervision in ICU.
-IM or IV hydralazine(5-10 mg and
repeated at ½ hr if no response)
-IVDiazoxide(150 mg.)

70. Very quick reduction will compromise
tissue perfusione.g coronary, renal and
cerebral
In most patients controlled reduction of BP to
150/90-100 over 24-36 hr is requiredwith bed
rest, then normalize over 2-3 days.

71. Hypertension in pregnancy
-Mild HT use aldomet or Labetalol
-PET use aldomet or Labetalol or
nifedipine or hydralazine & induce labour
if appropriate.
-Severe HT or eclampsia use IV
hydralazine or terminate pregnancy.
-Avoid ACE-I & ARBs in pregnancy

72. Generally
-Care with BB & thiazides in diabeticsand
in dyslipidaemia
-Care withthiazidesin gout.
-Care with BB & CCB in HF
-avoidBBin B asthma& peripheral
vascular disease.
-Avoid ACE-Iin renal artery stenosis and
in ARF
-Avoid combination of BB & non dihy CCB
-Avoid ACE-I & ARBs in pregnancy