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
Other causes of HPT
Over reactive resistance vessels - increases PVR due to defect in Na transporter of smooth muscle
Na effect - if kidneys unable to excrete Na, it builds up in vessels and fluid retained -> high BP
Age effect in hypertension
BP rises with age due to decreased arterial compliance
Environment effect in HPT
Mental and physical stress increase BP
Genetic effect in HPT
FH of HPT common
Sodium intake and diet effect in HPT
Reducing salt intake can reduce BP in hypertensive individuals
Alcohol effect in HPT
Small amount of alcohol tend to decrease BP
Large amounts of alcohol tend to increase BP
If alcohol reduced, BP will fall over several days to weeks
Weight effect in HPT
Weight reduction is most important non-pharmalogical measure - loss of weight will reduce BP
Lower birth weight, higher chance of developing HPT and heart disease
Race effect in HPT
Caucasians have lower BP than black population in same environment
Rural living has lower BP than in towns
Black population genetically salt retainers, so are more sensitive to an increase in diet salt
Treatment of Stage 1 HPT
Antihypertensive drug to people < 80yrs with ABPM > 135/85 with: Target organ damage CVD Renal disease Diabetes
Treatment of Stage 2 HPT
Drug treatment to any age with ABPM > 150/95
Treatment of > 80yrs
Same drugs as people 55-80yrs, taking into account co-morbidities
BP target is different: < 145/85
Contraindication to ACEI and drug-drug interactions
Renal artery stenosis
Renal failure - NSAIDs
Hyperkalaemia - Potassium supplements or potassium sparing diuretics
Action of ARB
I.e. losartan, valsartan
Angiotensin II antagonists competitively block the actions of angiotensin II at the angiotensin AT1 receptor
What drug do you add if combination of CCB, diuretic and ACEi cause incomplete effect?
Beta blocker
HPT in pregnancy
During normal pregnancy, BP falls but if patient has existing HPT it can cause primary HPT -pre-eclampsia
Do not treat with ARB or ACEi, use: nifedipine MR, methyl dopa, atenolol
then add diuretic and/or amlodipine
