Cardiology - Hypertension Flashcards Preview

Year 4 - SPM > Cardiology - Hypertension > Flashcards

Flashcards in Cardiology - Hypertension Deck (37):
1

What is hypertension?

There is a continuous relationship between high blood pressure and cardiovascular risk. Clinically, hypertension is levels of blood pressure above which the risk increases significantly and treatment can provide a clear cut benefit.

The average of two readings at each of a number of visits should be used to define the blood pressure.

2

What causes hypertension?

Majority of patients (>95%) have essential (primary) hypertension in which an underlying cause of the hypertension is NOT FOUND.

There are many causes of secondary hypertension.

3

Give some causes of secondary hypertension?

1) Renal disease - diabetic nephropathy, renovascular disease (e.g renal artery stenosis), glomerulonephritis, vasculitis, chronic pyelonephritis, polycystic kidneys

2) Endocrine disease - Conn's syndrome, Cushings syndrome, glucocorticoid remediable hypertension, phaeochromocytoma, acromegaly, hyperparathyroidism

3) Other - aortic coarctation, pregnancy and pre-eclampsia, obesity, excessive dietary salt, drugs (e.g. NSAIDs, sympathomimetics, illicit stimulates esp amphetamine, MDMA and cocaine)

4

What are the symptoms of hypertension?

Usually asymptomatic (except malignant hypertension). Headache is no more common than in the general population. Always examine the CVS fully and check for retinopathy. Are there features of an underlying cause, signs of renal disease, radiofemoral delay, or weak femoral pulses (coarctation), renal bruits, palpable kidneys or Cushing's syndrome?

5

Clinical signs of hypertension

Signs that are present may point to the underlying cause, for example radiofemoral delay or weak femoral pulses, renal enlargement or bruit or cushingoid features.

Evidence of end organ damage (heart failure, retinopathy, aortic aneurysm, carotid or femoral bruit) should also be sought because this indicates severity and duration of hypertension and associated with a poor prognosis.

6

What is malignant hypertension?

This refers to a rapid rise in BP leading to vascular damage (pathological hallmark is fibrinoid necrosis). It is is diagnosed when severe hypertension (systolic blood pressure >200mmHg +/- diastolic blood pressure >130mmHG) is identified, together with grade III-IV retinopathy.

7

What are the clinical features of malignant hypertension?

The patient often complains of a headache and occasionally visual disturbance.
There is proteinuria and haematuria.

It is a medical emergency requiring immediate treatment to prevent progression to renal failure, heart failure or stroke. Untreated, 1 year mortality is approximately 90%.

8

How should hypertension be investigated?

To help quantify overall cardiac risk - fasting glucose, cholesterol profile (total, HDL, LDL, and triglycerides)

To look for end organ damage - ECG (any LVH? past MI?), urine analysis (protein, blood)

To exclude secondary causes - U&E, Ca++ (hyperparathyroidism)

Special tests - If secondary hypertension is suspected, further investigation should focus on the possible underlying cause (e.g. urinary cortisol, plasma renin aldosterone levels, renal ultrasound, MRA of renal arteries, MAG3 renogram and 24 hour urinary catecholamines or VMA)

9

How is hypertensive retinopathy treated?

I - Tortuous arteries, with thickened bright walls ("silver wiring")
II - Arteriovenous nipping (narrowing in a vein where crossed by an artery)
III - Flame haemorrhages and cotton wool spots (small retinal bleeds and exudates)
IV - Papilloedema

10

Which patients should be treated for hypertension?

All patients with BP >160/100mmHg. For those >140/90mmHg the decision depends on the risk of a coronary event, presence of diabetes or end organ damage. HYVET study showed there is even substantial benefit in treating the over 80s.

NICE recommend:
1) Clinic BP <140/90mmHg = normotensive

2) Clinic BP >140/90mmHg = offer ABPM, calculate CV risk and look for end organ damage
- if ABPM >135/85 then this is stage 1 hypertension and Rx is only required if CV risk >20% at 10 years or end organ damage
- if ABPM >150/95 then this is stage 2 hypertension and requires treatment

3) Clinic BP >180/110mmHg = consider starting antihypertensive drug treatment immediately. Consider referral.

11

What is a target blood pressure for hypertensive patients?

Most patients should have their BP lowered to a target of <140/85mmHg.

Patients with diabetes have been shown to benefit from more aggressive BP reduction and a target of <130/80mmHg is more appropriate.

12

What lifestyle measures can be used before medical therapy to treat hypertension?

1) Minimise daily salt intake
2) Reduce alcohol to <21 units (for a man) and <14 units (for a woman) per week
3) Take regular aerobic exercise if not contraindicated
4) Achieve and maintain a healthy BMI (20-25)
5) Increase fruit and veg intake
6) Stop smoking, and reduce dietary fat content especially unsaturated and trans-fatty acids

13

Why are antihypertensive drugs combined?

Combining drugs at an earlier stage in the up-titration of therapy often results in better control with fever side effects than maximizing the dose of individual agents.

14

How should antihypertensive agents be combined?

British Hypertension Society (BHS) recommends the ABCD principle (A - ACEi, B-beta blocker, C-calcium channel blocker, D-diuretic)

A or B are effective first line drugs in the young who typically have high renin hypertension that responses well to these classes.

C or D are more effective first line agents in the elderly and black individuals, who typically have lower levels of renin and are less responsive to these agents.

Drugs can be substituted or added in a stepwise fashion according to the response.

15

Why should care be used when prescribing a beta blocker and a diuretic together?

This combination may slightly increase the incidence of type 2 diabetes. ACE-i and ARB therapy can both reduce risk of developing this condition.

16

Outline the stages of BHS hypertension management

Stage 1 - A or B for <55 years and non black (C or D if >55 years or black)

Stage 2 - A + C or D

Stage 3 - A (or B) + C + D

Stage 4 - Add beta blocker/ sprionolactone or other diuretic

17

What other agents should be used in hypertensive patients?

Patients with hypertension and average cholesterol may benefit from atorvastatin 10mg daily for less than 4 years (ASCOT study).

Aspirin 75mg daily is recommended in hypertensive patients with evidence of clinical atheroslcerotic disease or >20% 10 year cardiovascular risk after adequate BP control is achieved. Stating therapy should also be initiated in high risk individuals, regardless of baseline cholesterol levels.

18

What is the mechanism by which thiazide diuretics lower blood pressure?

Thiazide diuretics are considered first line diuretic therapy for hypertension in some patients. But the mechanism by which they lower BP is not fully understood. Initially, BP falls because of a decrease in blood volume, venous return and cardiac output. Gradually, the cardiac output returns to normal but the antihypertensive effect remains because the peripheral resistance has, in the meantime, decreased. Diuretics have no direct effect on vascular smooth muscle and the vasodilation they seem to cause seems to be associated with a small but persistent reduction in body Na+.

19

What are the side effects of thiazide diuretics?

Thiazide diuretics (e.g. bendroflumethiazide) may cause hypokalaemia, diabetic mellitus, and gout. But they have a flat dose response curve and a low dose of thiazides currently used to lower blood pressure cause insignificant metabolic side effects. Thiazides seem to be particularly effective in older people (>55).

20

What beta blockers can be used to treat hypertension?

Non selective beta blockers include propranolol. Beta 1 selective antagonists (located on the heart) include atenolol, metoprolol and bisoprolol.

Most beta blockers used in the treatment of hypertension lower blood pressure by reducing cardiac output (negative inotropic effect). With continued treatment the cardiac output returns to normal, but the blood pressure remains low by an unknown mechanism.

21

What are the side effects of beta blockers?

Cold hands and fatigue are very common. Less common, but serious, is provocation of asthma. Beta blockers also tend to raise serum triglyceride and decrease high density lipoprotein cholesterol levels. All of the beta blockers lower blood pressure, but at least some of the side effects can be reduced by using cardioselective hydrophillic drugs (i.e. those without liver metabolism or brain penetration) such as atenolol.

22

What vasodilator drugs are used in the treatment of hypertension?

1) ACEi / ARBs
2) CCBs
3) Alpha 1 adrenoceptor antagonists
4) Others - hydralazine, minoxidil

23

Why doe angiotensin converting enzyme inhibitors decrease blood pressure?

Angiotensin II is a powerful circulating vasoconstrictor and inhibition of its synthesis in a hypertensive patient results in a fall in peripheral vascular resistance and a lowering of blood pressure.

ACE inhibitors do not impair cardiovascular reflexes or share the common side effects of beta blockers.

24

What are the side effects of ACE inhibitors?

A common and unwanted side effect of ACEi's is a dry cough caused by increased bradykinin (ACE also metabolises bradykinin). Rare but serious adverse side effects of ACE inhibitors include angioedema, proteinuria, and neutropenia. The first dose may cause a very sharp drop in blood pressure, especially on patients taking diuretics (because they are Na+ deplete).

ACEi may also cause renal failure in patients with bilateral renal artery stenosis, because in this condition angiotensin II is apparently required to constrict postglomerular arterioles and maintain adequate glomerular filtration.

Inhibition of angiotensin II reduces but does not seriously impair aldosterone secretion and hyperkalaemia only occurs in patients taking potassium supplements or potassium sparing diuretics (aldosterone increases Na+ reabsorption and K+ excretion).

25

What is the mechanism of action of the ARBs?

The ARBs are angiotensin receptor blockers/ antagonists (e.g. losartan, cadesartan). These lower the blood pressure by blocking AT1 receptors. They have similar properties to ACEi's but do not cause cough, perhaps because they do not prevent bradykinin breakdown.

26

How do calcium channel blockers lower blood pressure?

The tone of vascular smooth muscle is determined by the cytosolic calcium concentration. This is increased by alpha 1 adrenoceptor activation (resulting from sympathetic tone), which triggers Ca++ release from the sarcoplasmic reticulum via the IP3 second messenger system. There are also ligand gated ion channels that are important, because the entry of cations through them depolarizes the cell, opening voltage dependent L type Ca++ channels and causing additional Ca++ to enter the cell. CCBs (e.g. nifedipine, amlodipine) bind to L type channels and by blocking the entry of Ca++ into the cell cause relaxation of vascular smooth muscle. This reduces the peripheral resistance and causes a fall in arterial blood pressure.

27

What are the side effects of CCBs?

Their most common side effects are caused by excessive vasodilation and include dizziness, hypotension, flushing and ankle oedema.

28

Briefly outline how the different types of adrenoceptors affect vascular tone?

Alpha 1 adrenoceptors are located post synaptically and cause vasoconstriction (think of the alpha shape like a rope and pulling on the ends constricts the hole in the middle). This is via Ca++ release via the IP3 pathway.

Alpha 2 adrenoceptors are located post synaptically and cause vasoconstriction by inhibiting cAMP formation leading to MLCK activation and smooth muscle contraction.

Beta 1 adrenoceptors are located on myocardium and increase intracellular cAMP levels which activates PKA. This increases intracellular Ca++ leading to contraction.

Beta 2 adrenoceptors are located on vascular smooth muscle and have the same second messenger system as beta 1 receptors. But increased cAMP inhibits MLCK in vascular smooth muscle caused vasodilatation.

29

What alpha 1 antagonist is used to treat hypertension?

Doxazosin causes vasodilation by selectively blocking vascular alpha 1 adrenoceptors. Unlike non selective alpha blockers, alpha 1 antagonists are unlikely to cause tachycardia, but they may cause postural hypotension. They are used with other antihypertensives in cases of resistant hypertension.

30

What is the mechanism of action of hydralazine? What are the side effects?

The mechanism is unknown, but it is used in combination with a beta blocker and a diuretic. Side effects include reflex tachycardia, which may provoke angina, headaches and fluid retention (as a result of secondary hyperaldosteronism). In slow acetylators in particular, hydralazine may induce a lupus syndrome resulting in fever, arthralgia, malaise and hepatitis.

31

What is minoxidil?

This is a potent vasodilator that causes severe fluid retention and oedema. However, when given with a beta blocker and a loop diuretic, it is effective in severe hypertension resistant to other drug combinations.

32

What centrally acting drugs are used to treat hypertension?

Methyldopa is converted in adrenergic nerve endings to the false transmitter alpha methylnorepinephrine which stimulates alpha 2 adrenoceptors in the medulla and reduces sympathetic outflow. Drowsiness is common and in 20% of patients it causes a positive antiglobin (Coomb's) test, and rarely haemolytic anaemia.

Clonidine causes rebound hypertension if the drug is suddenly withdrawn.

33

How is malignant hypertension managed?

In general, oral therapy is used unless there is encephalopathy or CCF. The aim is for controlled reduction in blood pressure over days, not hours. Avoid sudden drops in BP as cerebral autoregulation is poor (so stroke risk increases). There is no ideal hypotensive, but atenolol or long acting Ca++ blockers may be used PO.

If encephalopathy is present (headache, focal CNS signs, seizure, coma) aim to reduce BP to 110mmHg over 4h. Sodium nitroprusside infusion is used after furosemide bolus.

34

What are the cardiovascular changes caused by hypertension?

1) Heart - undergoes concentric left ventricular hypertrophy due to increased afterload
2) Large arteries - although not causative, atheroma is potentiated by hypertension, particularly in the aorta, coronary and cerebral vessels
3) Muscular arteries - medial hypertrophy and intimal thickening
4) Small arteries - undergo arteriolar sclerosis characterised by
a) hyaline thickening of the wall
b) increased elastic tissue with reduplication of the elastic lamina

35

How are the kidneys affected by hypertension?

The kidneys undergo hypertensive nephosclerosis (a type of arteriolar sclerosis). Macroscopically the kidneys are small and pale with a pale grey and narrow cortex and a decrease in medullary size. The arcuate arteries are particularly affected in hypertension with wall thickening.

Microscopically, the glomeruli show extracapsular glomerulofibrosis with wrinkling of the basement membrane and fibrosis. Blood vessels develop thick walls with decreased lumen due to hyaline material which replaces the muscle of the media.

36

What are the most common causes of death in hypertensive patients?

1) Congestive cardiac failure - 45%
2) Coronary insufficiency or infarction - 35%
3) Cerebral vascular accident - 15%
4) Renal failure - 5%

37

What are the pathological organ changes seen in malignant hypertension?

Cardiovascular:
1) Heart - degree of left ventricular hypertrophy depends upon the duration of the disease. In rapidly progressive cases it may be minimal with dilatation instead
2) Vessels - usually uncomplicated by any significant degree of atheroma. The small arteries show malignant arteriolar sclerosis with
a) fibrinoid necrosis
b) hyperplasia of the "onion skin" type

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