HTN

Question 1

What are are some factors that involved in essential HTN?

Answer 1

Most common – 90+% cases

No single underlying cause, is multifactorial:

Genetics – 40-50% familial links

Foetal – low birth weight

Environmental

• Obesity – large = higher; BP overestimated with small cuff; also sleep disordered breathing
• Alcohol – more = higher; though small amounts can lower
• Salt – not causal, just exacerbating
• Stress – acute mainly i.e. white coat, possible effects of chronic stress
• Insulin intolerance

Question 2

What are some causes of secondary HTN?

Answer 2

5-10%

Renal disease
- Chronic glomerulonephritis/pyelonephritis, PKD, renal artery stenosis etc

Endocrine
- Cushing’s, conns, adrenal hyperplasia, acromegaly, phaeochromocytoma, exogenous steroid treatment

Congenital
- Coactation of the aorta

Neurological
- Raised ICP, brainstem lesion

Pregnancy
- Pre-eclampsia

Drugs
- Oral contraceptives, steroids, NSAIDs etc

Question 3

What is the difference between benign and malignant HTN?

Answer 3

Benign

i) Stable elevation of BP over many years
ii) Most common over 40yrs

Malignant

i) Acute, severe BP elevation – rare but if undiagnosed can kill in <2yrs due to renal/heart failure or stroke
ii) Retinal signs common – papilloedema, haemorrhage etc

Question 4

What is the epidemiology of HTN?

Answer 4

BP rises with age up to 70’s , rise is more pronounced in systolic

More common in men

Present in 30-40% of the population

More common in black Africans – 40-45%

Question 5

What is the pathophysiology of HTN?

Answer 5

Increase in peripheral vascular resistance due to

• Vasoconstriction
• Hypertrophy of arterial wall – reduced compliance
• Endothelial dysfunction – less NO
• Atherosclerosis

Cardio-renal axis dysfunction - RAAS system etc

Baroreceptors reset to high pressure - if you drop BP too quickly you’ll suffer cerebral ischemia

Question 6

What is end organ damage and give some examples?

Answer 6

Causes structural changes in the heart and cardiovascular system leading to complications = end organ damage

Cerebrovascular
i) Aneurysm formation – stroke

Cardiovascular

i) Systemic/left sided hypertensive heart disease, LVH then eventual myocyte death and LV dilatation
ii) Heart failure AF etc

Pulmonary
i) Pulmonary HTN then congestive HF

Question 7

How does HTN present?

Answer 7

Usually asymptomatic Possible headache (uncommon)
Nosebleeds – only if very very high

?Coarctation of aorta – radio-femoral delay
?Renal artery bruits

Macrovascular complications

Question 8

How do you take blood pressure to investigate HTN?

Answer 8

Patient relaxed, not talking 
Remove tight clothing from arm 
Support arm at the level of the heart 
Read to nearest 2mmHg 
Repeat after 5 mins if first reading raised then on 2 separate GP visits if still raised

Home readings tend to be lower and a more accurate representation of BP - encourage people to buy home BP monitors if chronically hypertensive

24hr ambulatory BP monitoring

Question 9

What other investigations might be indicated for?

Answer 9

Bloods

i) Glucose
ii) FBC – Hb
iii) U+E- for secondary endo causes
iv) Aldosterone – for primary HTN

Urinalysis

i) Proteinuria
ii) Creatinine
iii) Urea (eGFR)

CXR – coarctation
ECG – LVH

Question 10

When do you offer treatment for HTN?

Answer 10

New BP >180/120 = needs assessment for end organ damage (fundoscopy, bloods, urine dip, ECG)

One off >160/100

Two consecutive GP visits >140/90

Systolic >160

> 140/90 + 10yr CVD risk of >20% OR existing CVD organ damage

Question 11

What is the target BP for chronically hypertensive patients?

Answer 11

<140/90

Treatment worthwhile if BP lowering but not lower than target

Annual review is necessary to check BP, medication, lifestyle, symptoms etc

Question 12

What are some lifestyle changes that can improve HTN?

Answer 12

Weight loss 
Smoking cessation 
Low Na diet 
More exercise 
Reduce alcohol consumption 
Reduce caffeinated products

Question 13

What is the treatment pathway for a non black patient udner 55yrs?

Answer 13

Step 1 - ACE-I ie Ramipril or ARB ie Losartan

Step 2 - combine step 1 with a CaB ie Amlodipine OR a thiazide diuretic ie Indapamide

Step 3 - combine all three classes

Step 4 - add aldosterone antagonist ie Spironalactone OR a BB ie Propanolol OR an AB ie Doxazosin and consider specialist advice

Question 14

What is the treatment pathway for patients aged over 55 or of African/Caribbean ethnicity?

Answer 14

Step 1 - start with CaB or thiazide

Step 2 - add ARB (ACEI less efficacious)

Step 3 - add other drug not included in step 1

Step 4 - add spironolactone/propanolol/doxazocin etc + specialist advice

Question 15

What use do betablockers have in HTN treatment?

Answer 15

Less effective at reducing macrovascular complications than other drugs and does not reduce DM risk

Considered in - women of child bearing age; those intolerant to ACEi’s and ARBs

If on BB and need more control, dont stop (especially if other indications ie angina), add CaB as reduces DM risk

Question 16

What monitoring is required with HTN?

Answer 16

Regular BPs - home monitor encouraged

ACE-I’s require U+E 2 weeks after prescribing/titration to monitor renal function ; ARBs do not

Question 17

What is a hypertensive emergency and how do you manage it?

Answer 17

> 200/120 + presence of end organ damage:
- Always confirm BP yourself with appropriate cuff

• CNS - low GCS, headache, confusion, vomiting, new motor weakness, seizure, coma = CT head ?haemorrhage
• Eyes - visual disturbance = fundoscopy for retinal haemorrhages +/- papilloedema
• Heart - chest pain, orthopnoea = ECG - changes; elevated cardiac enzymes; pulmonary oedema on CXR
• Aorta - sudden tearing chest pain radiating to back, collapse = Echo or CT ?dissection or aneurysm rupture
• Kidneys - haematuria, lethargy, anorexia = rapidly worsening renal function, proteinuria, red cell casts on urine micro

Admit to HDU/ICU if end organ damage for close monitoring

Commence antihypertensives:
- If no end organ damage = ACEi or CaB 
If EO damage =
- Labetalol (PO/IV) if no LVF
- Furosemide (IV) +/- hydralazine if LVF 
\+/- ACE

DO NOT REDUCE TOO QUICKLY

• As can lead to cerebral hypoperfusion; only necessary in acute MI or aortic dissection
• Reduce diastolic to 100mmHg or by 25%, whichever higher, over 24hrs