Hypertension Flashcards
Types of hypertension
- Primary or “essential” - no underlying cause
- Secondary - other pathology is causing it
- Malignant - syndrome involving severe elevation of arterial blood pressure, resulting in end-organ damage.
Aetiology of HTN
reduced elasticity of large arteries, due to age-related and atherosclerosis-related calcification, and degradation of arterial elastin - predominant form in adults
may also be present in conditions associated with increased cardiac output, such as anaemia, hyperthyroidism and aortic regurgitation.
Epidemiology
In 2015, it was reported that high blood pressure affected more than 1 in 4 adults in England (31% of men; 26% of women) – around 13.5 million people and contributed to 75,000 deaths.
Systolic vs diastolic pressure importance
Raised systolic pressure is more important than raised diastolic pressure as a risk factor for cardiovascular and renal disease
(Although the risk of cardiovascular disease increases progressively with increasing in either)
Complications
Increased risk of morbidity and mortality from all causes
Coronary artery disease
Heart failure
Renal failure
Stroke
Peripheral vascular disease
Hypertensive retinopathy
Investigations
Patients with a two measured BP >140/90 should be offered either ambulatory BP monitoring or home blood pressure monitoring
Assess for end organ damage including:
- Urine dip and albumin:creatinine level
- Blood glucose, lipids and renal function
- Fundoscopy for evidence of hypertensive retinopathy
- ECG - look for evidence of LV hypertrophy
Classification of HTN
Severity is classified by three stages:
- Single reading >140/90 mmHg and average ambulatory readings >135/85 mmHg
- Single reading >160/100 mmHg and average ambulatory readings >150/95 mmHg
- Single reading with systolic >180 mmHg or diastolic >110 mmHg.
Management: modifiable risk factors (5)
Controlling risk factors of cardiovascular disease:
Weight loss
Healthy diet (reduce salt and saturated fats)
Reduce alcohol and caffeine
Reduce stress
Stop smoking
Indications to start pharmacological management of essential hypertension
Stage 1 hypertensive patients + <80 years old +
- end organ damage, CVS disease, renal disease, diabetes or 10-year CVS risk >10%
OR
Anyone with Stage 2 hypertension
Step 1 of Pharmacological management
- ACE-inhibitor (e.g. Ramipril) if <=55 years old
- DHP-Calcium Channel Blocker (e.g. Nefedipine) if
> 55 years old
OR
African or Caribbean ethnicity
- If unable to tolerate ACE-inhibitor then switch to Angiotensin Receptor Blocker (e.g. Candesartan)
Step 2 of Pharmacological management
(If maximal dose of Step 1 has failed or not tolerated)
Combine CCB and ACE-I/ARB
Step 3 of Pharmacological management
(If maximal doses of Step 2 has failed or not tolerated):
Add thiazide-like diuretic (e.g. Indapamide)
Step 4 of Pharmacological management
- If blood potassium <4.5mmol/L then add Spironolactone (K+ sparing)
- If >4.5mmol/L increase thiazide-like diuretic dose (increase in K+ excretion)
- Other options at this point if the potassium is >4.5mmol/L include:
- Alpha blocker (e.g. Doxacosin)
- Beta blocker (e.g. Atenolol)
- Referral to cardiology for further advice
Malignant Hypertension features
- Blood pressure ≥180 mm Hg systolic and ≥120 mm Hg diastolic
- Evidence of end-organ damage
- Papilloedema and/or retinal haemorrhages
- New-onset confusion (encephalophathy)
- Seizure
- Chest pain
- Signs of heart failure
- Acute kidney injury
Malignant Hypertension Management
1. Aim
2. Oral or IV
1st line - CCB e.g. amlodipine or nifedipine PO
- Aim for controlled drop in blood pressure, to around 160/100mmHg over at least 24 hours.
Uncontrolled drops can lead to ischaemic stroke due to poor cerebral autoregulation and perfusion.
Oral medication is preferred to IV, unless there is encephalopathy, heart failure or aortic dissection.
Specific situations in treating hypertension: hypertensive encephalopathy
IV Labetalol or IV infusion Sodium Nitroprusside
Specific situations in treating hypertension: aortic dissection
IV Labetalol or IV infusion Sodium Nitroprusside, target 100-120mmHg systolic.
Specific situations in treating hypertension: pulmonary oedema
IV infusion GTN or Sodium Nitroprusside.
Beta blocker not recommended
Specific situations in treating hypertension: pregnancy-induced (pre-eclampsia)
IV Magnesium Sulphate with IV Labetalol/Hydralazine/Methyldopa.
Specific situations in treating hypertension: Phaeochromocytoma
IV Phentolamine/Phenoxybenzamine (α blockers) before beta blockade
Define secondary hypertension
Some common and uncommon medical conditions can increase blood pressure, leading to secondary hypertension
Clinical suspicion of secondary hypertension
- Younger patients with few comorbidities.
- Severe hypertension or hypertension resistant to treatment
- New hypertension in patients with previously stable or low readings.
- Hypertension with associated symptoms or electrolyte disturbances
Causes of secondary hypertension… (don’t memorise all of these please)
M/C: Primary intrinsic kidney disease (most common)
Renovascular disease (second most common) - RAS
Kidney
-Glomerulonephritis
-Chronic pyelonephritis
-Polycystic kidney disease
-Atheromatous renal artery stenosis in older co-morbid patients
Fibromuscular dysplasia in a younger patient group
Coarctation of the aorta is a potential cause of secondary hypertension in young children and adolescents.
Endocrine disease
- Cushing’s syndrome (raised cortisol)
- Conn’s syndrome(raised aldosterone)
- Phaeochromocytoma (catecholamine producing tumour)
Investigations in 2ndary HTN
1. Hypernatremia and hypokalaemia + raised aldosterone:renin ratio
2. Raised urea and creatinine
3. Raised 24 hour urinary cortisol or dexamethasone suppression test
4. Raised 24 hour metanephrine collection
5. Why renal ultrasound?
6. Why CT/MR angio
7. Why renal biopsy
Renal function (sodium, potassium, urea, creatinine)
1. Conn’s syndrome
2. intrinsic renal disease
3. in Cushing’s syndrome
4. pheochromocytoma
5. looking for evidence of kidney abnormalities (e.g. polycystic kidneys)
6. renovascular disease
7. intrinsic kidney disease