HYPERTENSION

TD Chawana
 Epidemiology
1/3 of the global adult population affected
Females > males
Common finding in African ancestry
Occurs at a younger age in blacks vs whites
Blacks 3-5X more likely to develop renal
complications
Blacks more vulnerable to strokes than whites
 Definition
Raised blood pressure (BP)
BP= Cardiac output (CO)x total peripheral
resistance (TPR)
Factors that can increase BP:
-increased CO
-reduced lumen diameter of arteries
CO-
TPR-
 Definition
18-60 years:
Systolic 140mmHg
Diastolic 90mmHg
Or both
>60 years:
Systolic >150mmHg
NB-systolic BP more important, and is basis of
diagnosis in most patients
 Risk factors
Age (>45)- men develop HTN earlier than women
Race-blacks>whites
Excess sodium (salt) intake
Potassium deficiency
Excess alcohol intake
Lipid abnormalities
Glucose intolerance
Diabetes mellitus
Positive family history
Obesity
Cigarette smoking or chewing tobacco
Stress
Pregnancy
 Risk factors
3 phenomena driving HTN:

1. Increasing life span

2. Obesity

3. Increased salt intake

 Risk factors
Low risk of complications at BPs around
115/75mmHg

For each 20mmHg rise in systolic BP or

10mmHg rise in diastolic BP, risk of major CV
and stroke events doubles
 Causes
2 types of HTN:

Primary

Secondary
 Primary HTN
Aka essential HTN
95% of adults
Aetiology not known
Genetic and environmental factors are thought to
contribute
Environmental- salt, obesity, sedentary lifestyle
Stiffening of aorta with increasing age (high
systolic often with normal diastolic)
 Secondary HTN
5% of adults
Cause can be identified and sometimes
treated
Causes- chronic kidney dzz
-renal artery stenosis
-excess aldosterone secretion
-phaeochromocytoma
-sleep apnea
 Classification
Normal- systolic <120mmHg; diastolic <80mmHg

Pre-HTN- systolic 120-139mmHg; diastolic 80-89mmHg

Stage 1- systolic 140-159mmHg; diastolic 90-99mmHg

Stage 2- systolic 160mmHg; diastolic 100mmHg

Isolated systolic HTN- systolic 140mmHg with

diastolic <90mmHg
 Symptoms
Usually asymptomatic- but body damage
being done

Non-specific symptoms- dull headache, dizzy

spells, more than usual nosebleeds, confusion,
blurred vision- advanced disease
 Diagnosis
1.History- prior raised BPs, CV events, renal
conditions, DM, medications (NSAIDs, TCAs,
OCs) , recreational drugs etc
2.Physical exam- BP, BMI, waist circumference
(>102 cm men & >88cm women), eyes, signs
of CCF and stroke, renal failure
3.Investigations- RBS, lipid profile, U n Es, FBC,
LFTs, urinalysis, ECG
 Management
Goal of treatment:
To lower BP to below levels used for diagnosi
To deal with risk factors
Target systolic <140mmHg, diastolic <90mmHg
Target systolic <130mmHg, diastolic <80mmHg
in pts with end-organ damage and DM
Rx- non-pharmacologic and pharmacologic
 Non-pharmacologic interventions
12 weeks in mild HTN, reassess monthly
Weight loss, fresh fruit and vegetables
Reduction of total and saturated fat
Salt reduction
Exercise
Reduce to stop alcohol consumption
Stopping cigarette smoking
Relaxation
 Pharmacologic interventions
Moderate to severe
If non-pharma hasnt worked in mild HTN
Blacks- 1st line diuretics or beta blockers
Whites- 1st line ACEI or ARB or beta blockers
Treatment is lifelong
Single agents often not adequate
Start with lowest dose
Use both pharma and non-pharma measures
 Drug classes
First-line-thiazide diuretics
-beta blockers
Second-line- ACE inhibitors
-ARBs
-calcium channel blockers
-alpha blockers
-loop diuretics
 Feasible combinations
Diuretic Beta blocker Ca channel ACE inhibitor Alpha blocker
antagonist

Diuretic Yes Yes Yes

Beta blocker Yes Yes Yes

Ca channel Yes Yes Yes

antagonist

ACE inhibitor Yes Yes Yes

Alpha blocker Yes Yes Yes Yes

 Thiazide diuretics
Thiazides- HCT, bendroflumethiazide

Thiazide related cpds- chlortalidone, metolazone,

xipamide, indapamide

Indications- alone in mild to moderate HTN, or in

combination in moderate to severe HTN, edema

Can impair glucose tolerance, and in diabetics can

exacerbate hyperglycemia and hyperlipidermia.
 Mechanism of action
Inhibit Na re-absorption at the distal
convoluted tubule
Onset of action per oral 1-2 hours
Duration of action 12-24 hours
Better given am to avoid disturbing sleep
Routes of admin- oral
 Unwanted effects
Postural hypotension
Hypokalaemia, hypomagnesaemia,
hyponatraemia, hypochloraemic alkalosis
Hypercalcaemia, hyperglycaemia,
hyperuricaemia and gout
Mild GI disturbances
Contra-indications- refractory hypokalaemia,
hyponatraemia, hypercalcaemia,
hyperuricaemia, Addisons dzz
 Loop diuretics
Furosemide, bumetamide, torasemide

Indications- pulmonary edema from left

ventricular failure, chronic heart failure,
diuretic-resistant edema
 Mechanism of action
Inhibit reabsorption from ascending limb of
loop of Henle in the renal tubules
Powerful diuretics
Onset of action per oral 1 hr
Duration of action 6 hrs
Peak effect within 30 mins if given IV
Routes of admin- oral, IV
 Unwanted effects
Hyperglycaemia (lesslikely than with thiazides)
Hyperuricaemia
Hypotension
Hypovolaemia
Hyponatraemia, hypokalaemia, hypocalcaemia,
hypochloraemia, hypomagnesaemia, metabolic
alkalosis
Contra-indications- severe hypokalaemia, ,
hyponatraemia, anuria
 Potassium sparing diuretics and
aldosterone antagonists
Amiloride, triamterene- weak diuretics
Aldosterone antagonists- spironolactone
Diuretics that cause potassium retention
Can be given with thiazide or loop diuretics as
an alternative to potassium supplements
Cannot be given with ACEI or ARBs- severe
hyperkalaemia
 Aldosterone antagonists
Block the effect of aldosterone
Indications- oedema, ascites from liver
cirrhosis, heart failure, primary
hyperaldosteronism
Must not be given with potassium
supplements
 Angiotensin-converting enzyme
inhibitors (ACEI)
Captopril, enalapril, lisinopril, cilazapril
Indications- HTN, symptomatic heart failure
Mech of action- inhibit conversion of AT 1 to AT 2
by inhibiting angiotensin converting enzyme,
inhibit breakdown of bradykinin and other kinins
AT 2 is a powerful vasoconstrictor
Helpful in diabetic nephropathy and HTN co-
morbidity
Blacks respond poorly to ACEI when used alone,
but in combination with a diuretic
 Unwanted effects
Hypotension
Persistent dry cough
Angio-edema
Rashes
Angiotensin-ll receptor blockers (ARB)
Losartan, candesartan, valsartan, telmisartan
Properties similar to ACEI, but do not inhibit
breakdown of kinin and other kinins
Also helpful in diabetic nephropathy and HTN
co-morbidity
Alternative to ACEI if there is persistent dry
cough
 Calcium channel blockers (CCB)
Nifedipine, amlodipine
Block entry of calcium into myocardial
vascular cells
Hence reduce myocardial contractility
Relax myocardial and vascular smooth muscle
Indications- HTN, heart failure, arrhythmias,
angina
 Unwanted effects
Headache, dizziness, lightheadness,
hypotension, constipation
 Beta blockers
Atenolol, labetalol, carvedilol
Block adrenaline from binding to beta 1 and 2
receptors on nerves
Results in slowed heart rate and vasodilation
Blacks respond poorly to beta blockers when
used alone, but in combination with a diuretic
 Complications of untreated HTN
CVS-myocardial infarction, aneurysm, heart
failure
CNS- cerebro-vascular accidents (stroke)
Renal- reduced renal perfusion
Eyes- loss of vision