Hypertension Flashcards
What are the prime contributors to blood pressure?
CO = SV x HR
PVR (high PVR = high BP)
Aetiology of HPT
Polygenic: major genes and polygenes (obesity, race, BP)
Polyfactorial: environment, individual and shared (stress, oral contraceptive, physical inactivity)
What is Primary HPT
Idiopathic
- Genetics
- Obesity
- Alcohol
- Na intake
- Stress
What is Secondary HPT
Occurs due to disease
- Renal
- Endocrine - Cushing’s syndrome, Conn’s syndrome
- Congenital - coarctation of aorta
- Pregnancy - pre-eclamsia
- Drugs - oral contraceptive, steroids, NSAIDs
- Sleep Apnoea
Symptoms
Usually asymptomatic but sustained HPT produces end organ damage to vessels, heart and kidney
Ideal BP
Between 120/80 - 140/90
Investigation to assess end-organ damage
ECG (LVH) Echo (LVH) Proteinuria Renal ultrasound Renal function
Risk factors
Previous MI stroke Smoking Diabetes Mellitus Hypercholesterolaemia Renal disease LVH Male
What treatable causes should be screened for
Renal artery stenosis
Cushing’s syndromes
Conn’s syndrome
Sleep apnoea
First Treatment for under 55yrs
ACE Inhibitor/ARBs - not afrocaribbean or women of child bearing age
If single agent doesn’t control BP, then use two together
If child bearing age: CCB or Beta Blocker
First treatment of over 55yrs
CCB and to afrocaribbean of any age
If not suitable offer thiazide (diuretic) - oedema, intolerance, HF
Step 2 treatment
Add Diuretic - clortalidone or indapamide
Step 3 treatment
Add CCB, ACEi, Diuretic together
Step 4 treatment
For resistant HPT:
Low dose diuretic spironolactone (25mg) if K level < 4.5 mmol/l
or
High dose thiazide-like diuretic if K level > 4.5mmol/l
Mechanism of ACEi
I.e. Rampiril
Inhibits angiotensin converting enzyme (ACE) which converts angiotensin I -> angiotensin II (vasoconstrictor and hypertrophic agent)
Mechanism of CCB
I.e. amlodipine
Blocks L type Ca channels prevent Ca from entering myocytes and blood vessel walls - lower BP
Relax and widen blood vessels by affecting the muscle cells in the arterial walls - reduces TPR
List possible complications of HPT
Stroke
LVH
MI
Renal failure
Define Stage 1
Clinic BP: 140/90mmHg or higher
ABPM average: 135/85 mmHg or higher
Define Stage 2
Clinic BP: 160/100mmHg or higher
ABPM average: 155/95 mmHg or higher
Define sever HPT
Clinic systolic 180 mmHg or higher
Clinic diastolic 110 mmHg or higher
Control of BP by the sympathetic nervous system
Vasoconstriction
Reflex tachycardia
Increased CO
All increase BP
Control of BP by the renin-angiotensin-asdosterone system (RAAS)
Stimulated by :
Low BP (low MAP)
Low circulating volume
Low Na
Released by the juxtaglomerular and converts angiotensinogen to angiotensin I
Angiotensin I to angiotensin II by ACE
Why are myocyte and smooth muscle hypertrophy poor prognostic factors?
Hypertrophy makes blood vessels stiff so that they can’t relax which increases bp and if the heart can’t relax, myocytes become ischaemic and start to fibres causing loss of function
Action of Angiotensin II
Vasoconstriction
Anti-natriuretic peptide
Stimulator of aldosterone release from the adrenal glands
Hypertrophy of myocytes and smooth muscle