hypertension Flashcards
hypertension definition
abnormal elevation of systolic and/or diastolic blood pressure.
Diagnosed by repeated BP of >140/90mmHg, confirmed on ambulatory BP recording.
generally asymptomatic for many years
secondary hypertension
when a specific cause of HTN is found, hence secondary to an underlying disease process
- renal disease, about 5% of cases
- many other causes, e.g. tumours secreting hormones, OCP, cocaine, preclampsia
primary ( essential hypertension)
- cause unknown (95%) of cases
- can be benign (slowly progressive) or Malignant (rapid onset and above 180/10)
proposed mechanisms:
issue with renal excretion of Na and water
Baroreceptor sensitivity- operates at higher set point
Renin secretion
- genetic component
risk factors for essential hypertension
Advancing age Low Birth weight Low Socio-economic class High salt diet (Nice recommends low salt diet) Obesity Sedentary Lifestyle Excessive Alcohol intake Stress & Anxiety (Relaxation therapies can reduce blood pressure) Smoking
diagnosing HTN
If blood pressure measured in the clinic is 140/90 mmHg or higher, take a second measurement during the consultation.
If the second measurement is substantially different from the first, take a third measurement.
Record the lower of the last 2 measurements as the clinic blood pressure.
If the person’s blood pressure is between 140/90 mmHg and 180/120 mmHg,offer ambulatory blood pressure monitoring (ABPM) to confirm the diagnosis of hypertension.If ABPM is unsuitable or the person is unable to tolerate it, offer home blood pressure monitoring (HBPM).
ABPM
ensure that at least 2measurements per hour are taken during the person’s usual waking hours (for example between 8am and 10pm). Use the average value of at least 14 measurements taken during the person’s usual waking hours to confirm a diagnosis of hypertension.
using HBPM
For each blood pressure recording, 2consecutive measurements are taken, at least 1 minute apart and with the person seated.
Blood pressure is recorded twice daily, ideally in the morning and evening.
Blood pressure recording continues for at least 4 days, ideally for 7 days — discard the measurements taken on the first day and use the average value of all the remaining measurements to confirm the diagnosis of hypertension.
what are the treatment aims
Reduce and maintain BP to the following targets:
Age <80 years:
Clinic BP <140/90 mmHg
ABPM/HBPM <135/85 mmHg
Age ≥80 years:
Clinic BP <150/90 mmHg
ABPM/HBPM <145/85 mmHg
Specific goals are:
Reduction in cardiovascular damage.
Preservation of renal function.
Limitation or reversal of left ventricular hypertrophy.
Prevention of Ischaemic Heart Disease.
Reduction in mortality due to stroke and myocardial infarction
ACE inhibitors
e.g. captopril, enalapril, lisinopril, ramipril
- for age <55 and not of black-african or african-caribbean family origin
- also for hypertension with type 2 diabetes
By inhibiting the ACE, they lead to reductions in angiotensin II, which leads to:
Reductions in arterial and venous vasoconstriction
Reduced aldosterone production leads to reductions in salt and water retention
Also potentiate bradykinin (is vasodilator)
Can increase potassium
Should be avoided in renovascular disease – renal artery stenosis.
Renin-dependent hypertension, ACEIs lead to renal underperfusion and severe hypotension
Paradoxically ACEIs are effective at the prevention of nephropathy in DM and may be agents of choice in pts with diabetes.
AT1 receptor antagonists
e.g. candesartan, losartan, valsartan
Block the action of Ang II at the AT1 receptor.
The AT1 subtype is found in the heart, blood vessels, kidney, adrenal cortex, lung and brain and mediates the vasoconstrictor effects
These agents have similar consequences as ACEIs but do not give rise to a cough.
calcium channel blockers
e.g. diltiazem, verapamil & dihydropyridines (amlodipine, felodipine, nifedipine)
Inhibit voltage operated Ca2+ channels on vascular smooth muscle
leading to vasodilatation and a reduction in BP
Rate-limiting (e.g. verapamil): greater effects on cardiac tissue
DHPs (e.g. amlodipine) more on vascular smooth muscle
thiazide-like diuretics
Thiazide-like (e.g. indapamide, chlortalidone)
Second line antihypertensives
Inhibit Na+/Cl- reuptake in distal convoluted tubule
Reduction in circulating volume hence reduction in SV MAP = (CO × SVR) + CVP
Important side effects
Hypokalaemia
Postural hypotension
Impaired glucose control
alpha-blockers
e.g. doxazosin, prazosin
These are competitive receptor antagonists of a1-adrenoceptors
Last choice antihypertensives
Widespread side effects, which makes them poorly tolerated
beta-blockers
2006: NICE no longer recommended as first line e.g. atenolol (most common), propranolol
Atenolol is b1-selective
Propranolol is b-nonselective
Mechanism of action unclear:
Reduction in sympathetic drive to the heart, reducing cardiac output
A reduction in sympathetically evoked renin release
Beta-blockers (even b1 selective agents) may block bronchial b2 receptors and are used with caution in asthma and caution in COPD
Blockade of peripheral b2-adrenoceptors opposes vasodilatation to skeletal muscle ~ cold extremities and fatigue