Hypertension Flashcards
Hypertension stages
Stage 1: CBP 140/90 + ABPM or HBPM > 135/85
Stage 2: CBP > 160/100 + ABPM or HBPM > 150/95
Stage 3/severe: > 180/120
Accelerated/malignant HTN
Severe increase in BP to > 180/120 with signs of:
- retinal haemorrhage +/or papilloedema
- usually associated with TOD
White coat HTN
15-30%
> 20/10mmHg discrepancy between clinic and ABPM or HBPM at diagnosis
Masked HTN
Clinic BP < 140/90 but BP higher on HBPM or ABPM
RFs for HTN
1) Age
2) < 65y -men, 65-74y -women
3) African and black Caribbean
4) FH
5) Social deprivation
6) DM, CKD
7) Smoking, alcohol, salt, diet, obesity, lack of exercise
8) anxiety and stress
Most common cause of secondary HTN
Renal disorders:
1) CKD - most common cause
2) Chronic pyelonephritis
3) DM nephropathy - proteinuria
4) Glomerulonephritis - haematuria
5) PCKD - mass, haematuria, FH
6) Obstructive uropathy -mass
7) Renal cell carcinoma - haematuria, loin pain, mass
Other causes:
1) Vascular:
- coarctation of the aorta
- renal artery stenosis
2) Endocrine:
- Primary hyperaldosteronism: most common curable cause of HTN
- phaeochromocytoma
- Cushing’s syndrome
- Acromegaly
- Hypothyroidism: increased diastolic BP
- Hyperthyroidism: increased systolic BP
3) Drugs:
- Alcohol: most common individual secondary cause of HTN
- ciclosporin
- cocaine, amphetamine, stimulants
- COCP / HRT
- steroids
- liquorice
- NSAIDs
- venlafaxine
4) Other conditions:
- pregnancy
- SLE, scleroderma, PAN
- OSA
Coarctation of aorta findings
1) Difference in BP R & L arm
2) Absent/weak femoral pulses
3) R-F delay
40 suprasternal murmur radiating to back
Renal artery stenosis findings
1) History of PVD
2) Abdominal bruit
3) BP resistant to treatment
4) Raised renin
Primary hyperaldosteronism
Most common curable cause of HTN
Adrenal adenoma
Presentation:
1) HypoK, raised bicarbonate (alkalosis), Na > 140 or larger than expected decrease in K when using thiazide diuretic
2) Tetany, muscle weakness, nocturia, polyuria
3) CCB can mask features
Phaemochromocytoma
Presentation:
1) Intermittently high or labile BP
2) Postural hypotension
3) Headaches
4) Sweating attacks, diaphoresis
5) Palpitations
6) Unexplained fever or abdominal pains
7) or asymptomatic
Can become malignant or have catastrophic haemorrhage
Risks reduced for every 10mmhg reduction in BP
1) 17% reduction in CHD
2) 27% reduction in stroke
3) 28% reduction in heart failure
4) 13% reduction in all cause mortality
5% reduction in systolic BP reduces risk of major CVE by 10% even at normal BP
Measuring clinic BP
If difference in BP > 15mmHg between both arms x 2, then measure BP on highest arm
Automated devices may give inaccurate measurement if pulse irregularity therefore always feel pulse first
If symptoms of postural hypotension and drop in 20mmHg on standing for 1 minute, then measure subsequent BPs standing
ABPM
2 measurements/hour during waking hours
Use average of at least 14 measurements
HBPM
For each recording, 2 consecutive measurements at least 1 minute apart, twice daily.
4-7 days
Discard first day of measurements
BP > 180/120
Same day specialist assessment:
- accelerated HTN (retinal haemorrhage/papilloedema)
- life-threatening symptoms: new onset confusion, chest pain, signs of HF or AKI
No symptoms:
- **urgent investigations for TOD **
- consider starting antihypertensive drug without waiting for ABPM/HBPM result
- if no TOD identified, repeat BP in 7 days
Investigations for TOD
1) Urine dip: haematuria and Urine A:Cr
2) U&E, HbA1c, lipids
3) ECG
Management stage 1 HTN
< 80y + ToD/QRisk > 10%, renal disease, DM, CVD:
- discuss starting antiHTN + lifestyle advice
Consider starting antiHTN if < 60y and QRisk < 10% or > 80y with CBP > 150/90
< 40y and no TOD - refer to secondary care to exclude secondary causes of HTN
Management of stage 2 HTN
Offer antiHTN + lifestyle advice regardless of age
AntiHTN if black African or Afro-Caribbean origin
CCB first line if no T2DM
Offer ARB over ACEI (increased risk of side effects)
Management of HTN
Step 1:
1) ACEi/ARB if:
- < 55y and not black A/AC
- have T2DM of any age/race
- titrate every 4 weeks, check U&E 1-2 weeks after every dose increase
2) CCB if:
- > 55y and no T2DM
- black A/AC and no T2DM
- if CCB not tolerated off thiazide-like diuretic (indapamide)
- If HF - indapamide
Step 2:
1) A + C or D
2) C + A or D
Step 3:
1) A + C + D
Step 4: resistant HTN
- check for postural hypotension.
- confirm using ABPM/HBPM
1) K <=4.5 - low dose spironolactone - measure U&E within 1m
2) > 4.5 - a-blocker/BB
HTN targets
1) Use CBP to monitor response to lifestyle or drugs
2) T2DM, symptoms of postural hypotension or > 80y - measure standing BP too and use standing BP if significant drop. If > 20 drop - review medications/advice
3) If white coat/masked HTN, then consider ABPM or HBPM in addition to CBP
4) Targets:
- < 80y - < 140/90 (HBPM < 135/85)
- > 80y - < 150/90 ( < 145/85)
Annual review
1) Check BP:
- if raised, recheck 2-3x over next few weeks
- if suspect raised due to white-coat HTN, then for HBPM/ABPM
2) Can consider withdrawing if lifestyle changes, low BP, single drug
- wean
- review 4 weekly for 6 months then 2-3x/year to check for recurrence
3) U&E + urine ACR :
- if eGFR < 60 or ACR > 3mg/mmol - CKD
4) Lipids and QRisk
ACEi / ARB
MOA:
1) reduce AI –> AII –> reduced aldosterone secretion –> reduced Na + H20 retention
2) AII constricts efferent arterioles - reduced constriction reduces pressure on glomerular capillaries - renoprotective
CI:
- angio-oedema
- If on aliskerin + DM/CKD
- pregnancy & breastfeeding
- renovascular disease
Caution:
- HOCM
- PVD - risk of silent renovascular disease
**- severe HF/AS **
- furosemide > 80mg/day -increases hypotension
SE:
- HyperK
- Cough
- Angio-oedema (also avoid ARBs)
- arrhythmia, sleep, taste
Interactions:
- NSAIDs - increased risk of renal impairment and hypotension
- Antacid - reduced absorption
- Heparin - HyperK
- Spironolactione - HyperK, use lowest dose of both drugs
-Lithium -toxicity, monitor levels
Monitoring
- U&E before and at 1-2 weeks, then annually
Abnormal test results - ACEi
eGFR reduces by < 25% or creatinine by < 30% - continue, recheck in 1-2 weeks
eGFR reduces by >=25% or Cr increases by >=30%:
- ?volume depletion
- Reduce/stop NSAIDs, CCB, nitrates, K supplements, diuretics
- if persists - stop ACEI or reduce to lower dose and recheck in 5-7 days
K >= 5:
- Stop of reduce K-sparing diuretics, nephrotoxic drugs ( NSAID)
K 5-5.9 despite above changes - reduce ACEi and re-check in 5-7 days
K >= 6 despite measures - stop
Or K >=5.5 - stop
Thiazide-like diuretics
Avoid in:
- HypoNa/HypoK/HyperCa
- Addison’s
- eGFR < 30
- pregnancy - neonatal thrombocytopenia, BM suppression, jaundice, electrolyte disturbance, reduced placental perfusion
Caution in:
- DM, gout, SLE - exacerbate these
- CVD + glucosides - risk of hypoK
Monitoring:
- U&E and LFT before
- U&E - Na and K during first week
CCB
CCB, except amlodipine, should be avoided in heart failure
Angina, if BB contraindicated, may prefer rate-limiting CCB
Spironolactone
Step 4 + K <=4.5
Dose 225mg OD
Monitor U&E within 1 month
CI:
- Addison’s
- AKI
- HyperK
SE:
- AKI
- agranulocytosis, leucopenia, thrombocytopenia
- alopecia
- benign breast tumour/pain/gynaecomastia
- libido change
- hyperK (stop), hypoNa
- leg cramps
- pruritis
- SJS
Interactions:
- ACEI - lowest doses of both
- digoxin
-lithium
B-blockers
HTN + HF: bisoprolol, carvedilol, nebivolol
HTN + angina: atenolol, bisoprolol, metoprolol
HTN + previous MI (no HF) : metoprolol, propranolol, timolol, atenolol
Alpha-blockers
Doxazosin or Terazosin
CI:
- postural hypotension
- micturition syncope - BPH
- do not use MR if GI obstruction as outer membrane not digested
- caution in HF
- pregnant/breast feeding
Risk of intraoperative Floppy Iris Syndrome during cataract surgery
Doxazosin SR - titrate 1mg/day, double dose after 1-2 weeks up to max 16mg/day (usually 4mg)
Which combination of antiHTN should be avoided in DM?
BB + thiazide like diuretic
At what point do thiazide diuretics become ineffective in CKD?
eGFR < 30 - avoid as not effective
Why has use of BBs declined sharply in past 5 years to treat HTN?
Less likely to prevent stroke and potential impairment of glucose tolerance
