14/08/2013 by admin | Cardiology


  1. Hypotension: <90 / <60
  2. Normal: 90-139 / 60-89
  3. Mild HTN: 140-159 / 90-99
  4. Moderate HTN: 160-179 / 100-109
  5. Severe HTN: >180 / >110
  6. Malignant HTN (and imminent secondary organ damage): >200 / >140



  1. 20-30% of the adult population (urban, western disease)
  2. 40-45% in black African population (=low renin HTN)



  1. Elevated blood pressure
  2. LVH
  3. loud A2 sound (S2)
  4. In cardiac failure = sinus tachycardia and S3 (= passive flow between atria nd ventricles in hypertensive states).


Fundoscopy is an essential part of the examination of any hypertensive patient.

The abnormalities are graded to the Keith-Wagener classification:

  1. 1. Tortuosity of the retinal arteries with increased reflectiveness
  2. 2. Grade 1 plus the appearance of arteriovenous nipping produced when thickened retinal arteries pass over the retinal veins
  3. 3. Grade 2 plus flame-shaped haemorrhages and soft “cotton wool” exudates due to small infarcts
  4. 4. Grade 3 plus papilloedema


Grades 3 and 4 are diagnostic of malignant hypertension.


  1. ECG for LVH/RVH (increased amplitude and deep QRS complexes)
  2. Urine Stix test for protein and blood (=renal impairment and end organ damage)
  3. Fasting blood for lipids and glucose
  4. Serum urea, creatinine and electrolytes


Aetiology – cause, risk factors

Age – blood pressure changes with age.

  1. o Systolic rises, but diastolic decreases with age (=increased pulse pressure)
  2. o More pronounced in men



  1. o Obese have higher blood pressure than normal people
  2. o Sleep disordered breathing may be an additional risk factor (PND=develops over hours of lying flat [coughing/wheezing], orthopnoea=occurs instantly when lay flat, sleep apnoea=obstructive airways)


Excessive alcohol intake

  1. o But subjects who consume small amounts of alcohol seem to have lower blood pressure level than those who consume no alcohol.


High salt intake

  1. o High sodium intake has been suggested to be a major determinant of blood pressure differences.
  2. o High sodium = high blood pressure (reduce Na to reduce BP)!
  1. o Migration from rural to urban environment is associated with increase in blood pressure in relation to amount of salt in diet.



  1. o Acute pain and stress can raise blood pressure


Genetic susceptibility

Foetal factors

  1. o Low birth weight is associated with subsequent high blood pressure
  2. o May be due to fetal adaptation to intrauterine undernutrition with long-term changes in blood vessel structure or in the function of crucial hormonal systems.



  1. Primary hypertension = 90-95%
  2. Secondary hypertension = 5-10% (=renal disease, endocrine, coarctation, drugs, pregnancy…)
    1. o 25% = renovascular (atheromatous)
    2. o 75% = intrinsic (GN, polyarteritis nodosa, systemic sclerosis, pyelonephritis, polycystic kidney disease)
    3. o Endocrine: cushing’s, conn’s, phaechromocytoma, acromegaly, hyperparathyroidism.


Humoral mechanisms

  1. Autonomic nervous system (renin-angiotensis-aldosterone, natriuretic peptide and kallikrein-kinin system [not well understood but group of protein sthat moderate BP]) plays a role in short-term changes in blood pressure


Insulin resistance

  1. Association between diabetes and hypertension has been recognised.
  2. Metabolic syndrome: hyperinsulinaemia, glucose intolerance, reduced levels of HDL cholesterol, hypertriglyceridaemia and central obesity in association with hypertension. = Metabolic syndrome.


Pathogenesis remains unclear.

  1. In some young hypertensive patients, there is an early increase in cardiac output, in association with increased pulse rate and circulating catecholamines.
  2. Could result in changes in baroreceptor sensitivity which would then operate at a higher blood pressure level.


In chronic hypertension.

  1. Cardiac output is normal
  2.  ↑ total peripheral resistance - maintains the elevated blood pressure.
  3. Resistance vessels (small arteries and arterioles) show structural changes in hypertension.
    1. o Some evidence of rarefaction (decreased density) of these vessels
  4. Mechanisms result in overall peripheral vascular resistance.


Hypertension also causes changes in the large arteries:

  1. Thickening of the media
  2. Increase in collagen
  3. Secondary deposition of calcium
  4. Result in loss of arterial compliance, which in turn leads to a more pronounced arterial SBP waves.


total peripheral vascular resistance, left ventricular load leads to left ventricular hypertrophy.

Is a significant prognostic indicator of future cardiovascular events.

Changes in renal vasculature eventually lead to:

  1.  ↓ renal perfusion
    1. o Leads to activation of renin-angiotensin system, with increased aldosterone and sodium and water retention.
  2.  ↓ glomerular filtration rate (GFR)
  3.  ↓ in sodium and water excretion = bodies attempt to increase BP to compensate for failing CO and contractility. OEDEMA.



Use of non-pharmacological therapy (lifestyle advice) in all hypertensive and borderline hypertensive people:

  1. Weight reduction – BMI should be <25kg/m2
  2. Low fat and saturated fat diet
  3. Low sodium diet – <6g sodium chloride per day
  4. Limited alcohol consumption – <21 units/week for men and <14 units/week for women
  5. Dynamic exercise
  6. Reduced cardiovascular risk by stopping smoking and increased oily fish consumption.


Start anti-hypertensives in:

  1. Non-diabetics: >160 / >100
  2. Diabetics: >140 / >90


Most hypertensive patients will require a combination of antihypertensive drugs to achieve the recommended targets.

The decision to commence specific drug therapy should usually be made only after a careful period of assessment, of up to 6 months, with repeated measurements of blood pressure.

Aims of treatment:

  1. Reduce cardiac output and total peripheral resistance


Younger (<55yrs) and non-black (have high renin HTN)

Older (>55yrs) or black (have low renin HTN)

Step 1


C or D

Step 2

A + C or D

Step 3

A + C + D

Step 4

Resistant hypertension

Add: either alpha-blocker or spironolactone or other diuretic

A: ACE inhibitor or angiotensin receptor blocker

B: Beta-blocker

C: Calcium channel blocker

D: Diuretic (Thiazide)

Step 1:

Young Caucasians are more likely to have high renin hypertension, and older patients and blacks usually have low renin hypertension.

Step 2:

Involves combining one drug from each group.

Not advised to combine a diuretic with a beta-blocker since both aggravate diabetes.

Step 3:

ACE inhibitor is combined with a calcium channel blocker and diuretic.

Mechanism: Block conversion of angiotensin I to angiotensin II, which is a potent vasoconstrictor.

Also block the degradation of bradykinin, a potent vasodilator = bradykinin accumulation = COUGH

Particularly useful in diabetics with nephropathy as slows disease progression.

Drug Side effects





Hypotension following the first dose, seen in:

  1. Sodium-depleted patients
  2. On treatment with large doses of diuretics
  3. Deterioration of renal function in those with severe bilateral renovascular disease (RAS)


Mild dry cough

  1. o Due to effect on bradykinin


Caution: in AS, hypovolaemia, dehydration

ACEi are teratogenic and also cause angioedema.


Mechanism: Selectively block angiotensin-II AT1 receptors.

No effect on bradykinin

Used for patients who can’t tolerate ACE inhibitors.

Drug Side effects




  1. Teratogenic
  2. Hyperkalaemia
  3. Orthostatic hypotension


No benefit to combining ACEi and ARB.


Aliskiren (‘Rasilez’) = direct renin inhibitor. Expensive. Rarely used.

Mechanism: Block sympathetic activity in the heart (central: beta1 = most cardio-selective), peripheral vasculature (beta2) and bronchi (beta2).

heart rate and myocardial contractility.

cardiac output.

Via negative inotropic and chronotropic effects (slow contractility and HR – by blocking adrenergic input)

May also block beta-receptors on juxtaglomerular granule cells in the kidney – reduce renin.

Inhibit renin release and reduce plasma levels of angiotensin II and aldosterone.


Drug Side effects
ATENOLOL – Beta 1 selective (cardioselective) BISOPROLOL – Beta 1 selective ( ,, )

METOPROLOL – Beta 1 selective ( ,, )

PROPANOLOL – Non-selective, block both beta 1 and beta 2

CARVEDILOL – non-selective, block alpha1 and beta1&2

SOTOLOL – half non-selective beta-blocker, half class III potassium channel blocker. s/e – fatigue.

Alpha-adrenoceptor agonists: prazosin, tamulosin, doxazosin – constrict arteries and arterioles and increase TPR and so decrease CO. s/e postural hypotension.

  1. Bronchoconstriction, leading to worsening asthma or chronic obstructive airways disease – worse in non-selectives
  2. Bradycardia
  3. Hypoglycaemia
  4. Fatigue and lethargy
  5. Impotence
  6. Sleep disturbance, nightmares, and vivid dreams – particularly propranolol
  7. Rebound hypertension if stopped suddenly.
  8. Cold extremities


Beta blockers, main contraindications, cautions


  1. Asthma
  2. Block (heart block)
  3. COPD
  4. Diabetes mellitus
  5. Electrolyte disturbance (hyperkalaemia)
  6. HF
  7. PVD
  8. Raynauds



Mechanism: Block voltage-gated calcium channels in myocardium and vascular smooth muscle – stop influx of calcium.

PHENYLALKYLAMINES (others): ↓in myocardial contractility and electrical conductance

DIHYDROPYRIDINES (…dipines): ↓vascular tone.

Interfere with the action of various vasoconstrictor agonists (noradrenaline, angiotensin II, thrombin).

All may precipitate heart failure.

Drug Side effects
  1.  ↓cardiac output and heart rate
  2. Not to be used with beta-blockers because causes hypotension and may lead to asystole.
  3. Main side effect is constipation.
  4. Gingival hyperplasia


  1. Relax smooth muscle, dilating arteries
  2. Main side effects are headache and ankle oedema.


  1. Decreases vascular tone.
  2. Effective in angina
  3. Main side effect is bradycardia.




  1. Inhibit sodium reabsorption in the distal renal tubule



  1. salt and water excretion (water follows by osmosis)
  2.  ↓ blood volume
  3.  ↓blood pressure
  4. Act within 12-24hours
  5. Useful in low renin HTN pts who do not react to ACEi / ARBs


Drug Side effects
  1. Hypokalaemia leading to arrhythmia and muscle fatigue
  2. Hyperuricaemia causing gout
  3. Hyperglycaemia
  4.  ↑ LDL and VLDL leading to atherosclerosis



Mechanism: Cause postsynaptic block of alpha1-adrenoceptors which prevents sympathetic tonic drive and leads to vasodilation.

total peripheral resistance

blood pressure

Drug Side effects
  1. Postural hypotension caused by loss of sympathetic vasoconstriction
  2. First dose phenomenon of rapid hypotension when initially administered.



Mechanism: Open ATP dependent K+ channels,

Hyperpolarises vascular smooth muscle cells.

Making depolarisation harder to achieve.

Reduces the stimulation of vasoconstricting agonists on the muscle cells.

Used only in severe hypertension.

Usually used with a beta-blocker and thiazide diuretic to counteract side effects.

Drugs Side effects
MINOXIDIL (s/e – hypertrichosis, can be used topically to tx alopecia) DIAZOXIDE

SPIRONOLACTONE: aldosterone antagonist. s/e: gynecomastia

SODIUM NITROPRUSSIDE: emergency / malignant HTN only!

HYDRALAZINE: s/e: SLE-like syndrome

  1. Increased hair growth with Minoxidil
  2. Salt and water retention leading to oedema
  3. Reflex sympathetic activation causing tachycardia




HTN linked to:

  1. Atherosclerosis
  2. Intracerebral haemorrhage from berry aneurysm
  3. Aortic aneurysm
  4. Cardiac failure = LVH
  5. Atrial fibrillation = due to stretching of atria
  6. Renal failure and renal artery stenosis
  7. Visual disturbance – papilloedema



  1. Cerebrovascular disease and coronary artery disease are most common causes of death.
  2. Hypertensive patients also prone to renal failure and peripheral vascular disease.
  3. 6x increase in stroke risk.
  4. 3x increase in cardiac disease. 
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