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Cardiology > Hypertension > Flashcards

Hypertension Flashcards

1
Q

What conditions is hypertension a risk for?

A
  • Stroke
  • Ischaemic heart disease
  • Heart failure
  • Chronic kidney disease
  • Cognitive decline
  • Premature death
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2
Q

How do we manage BP that differs between arms?

A
  • If the difference in readings between arms is more than 15 mmHg, repeat the readings
  • If the readings between arms stay different by 15 mmHg, measure subsequent BP in the arm with the higher reading
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3
Q

How do we diagnose hypertension?

A
  • If the BP measured in clinic is 140/90 or more
  • 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 BP

  • If clinic BP is between 140/90 and 180/20, offer ambulatory BP monitoring to confirm the diagnosis of hypertension
  • If ABPM is unsuitable, offer home BP monitoring
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4
Q

What should we do whilst waiting for confirmation of a diagnosis of hypertension?

A
  • Investigations for target organ damage

- Formal assessment of cardiovascular risk using a CV risk assessment tool (QRISK3)

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5
Q

How should we measure blood pressure?

A
  • 2 consecutive measurements are taken, at least 60s apart and with the patient seated

If HBPM:

  • Blood pressure is recorded 2x a day, in the morning and evening
  • BP recording continues for at least 4 days, ideally 1 week
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6
Q

What BP is diagnostic of hypertension?

A
  • Clinic BP of 140/90 or higher
    and
  • ABPM daytime average or HBPM average of 135/85 or higher
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7
Q

What should we do if someone’s blood pressure is subclinical?

A

If hypertension is not diagnosed:
- Measure patient’s BP in clinic at least every 5 years, and measure it more frequently if the blood pressure is close to 140/90

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8
Q

How does ABPM work?

A
  • Ensure that at least 2 measurements per hour are taken during usual waking hours
  • Use the average value of at least 14 measurements taken to confirm a diagnosis of hypertension
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9
Q

What are the stages of hypertension?

A

Stages:

1: 140-159/90-99 (mild)
2: 160-179/100-109 (moderate)
3: >180/>110 (severe)

Isolated systolic hypertension: >140/<90

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10
Q

Why is staging of hypertension important?

A

Risk stratification of the patient

- Guides towards our next management steps

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11
Q

What is a hypertensive crisis?

A

Also known as malignant hypertension
Hypertensive urgency:
- BP elavated
- No target organ damage (heart, kidneys, brain)
- 180/110
- Symptoms: headache, shortness of breath, epistaxis, anxiety
Management: oral medication, outpatient setting

Hypertensive emergency (malignant hypertension):
- BP so high, target organs damaged
- 180/120
- Can happen at lower pressures
- Symptoms: cheat pan, shortness of breath, back pain, numbness, weakness, vision changes, difficulty speaking
- Can result in encephalopathy
- As BP rises causes cerebral oedema, builds pressure in skull and leads to dysfunction
Management: IV medication, vasodilator, calcium channel blocker or beta blocker
(relax arteries)

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12
Q

Which bloods should be done to assess cardiovascular risk when investigating suspected hypertension?

A
  • Bloods (RBC, U&Es, random blood gluocse, cholesterol)
  • Urine
  • ECG
  • CXR
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13
Q

What assessment tool is used to understand cardiovascular risk in suspected hypertension?

A

QRISK3

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14
Q

How do we calculate BP?

A

BP = cardiac output x peripheral resistance

CO = HR x SV

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15
Q

How does the RAAS work?

A
  • BP drops
  • Less blood flow to kidneys
  • Kidneys release renin
  • Angiotensinogen becomes Angiotensin I when renin is released
  • Angiotensin I becomes angiotensin II due to ACE (angiotensin converting enzyme)
  • Angiotensin II is the most potent vasconstrictor in the body
  • This causes vasoconstriction
  • Peripheral resistance increases
  • BP increases

Renin also causes the release of aldosterone

  • Aldosterone causes increase in Na+ reabsorption and H2O reabsorption
  • This increases blood volume
  • This increases BP

If BP increases too much, this damaged blood vessels and activated the sympathetic system, reducing blood flow to the kidneys

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16
Q

How is blood pressure controlled short-term?

A
  • Central nervous system response
  • Baroreceptors
  • Chemoreceptors
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17
Q

How is arterial pressure raised?

A
  • Sympathetic nervous system releases noradrenaline from nerve terminals
  • NA acts on the alpha adrenergic receptors of the VSMC
  • All arterioles constrict
  • Heart is directly stimulated

Not innervated: capillaries, precapillary sphincters and metarterioles

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18
Q

Which receptors does adrenaline affect, and what are its clinical uses?

A

Adrenaline

Receptors: β1 = β2 > α1* = α2*

Clinical uses: anaphylactic shock, cardiogenic shock, cardiac arrest

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19
Q

Which receptors does noradrenaline affect, and what are its clinical uses?

A

Noradrenaline

Receptors: β1 = α1 >
β2 = α2

Clinical uses: severe hypotension and septic shock

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20
Q

Which receptors does dopamine affect, and what are its clinical uses?

A

Dopamine

Receptors: β1 = β2 > α1*

Clinical use: acute heart failure, cardiogenic shock

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21
Q

Which receptors dobutamine affect, and what its clinical uses?

A

Dobutamine

Receptors: β1 > β2 > α1

Clinical use: acute heart failure, cardiogenic shock, refractors heart failure

22
Q

How do baroreceptors work?

A
  • Nerve endings in all large thoracic and neck arteries
  • Major populations: carotid sinus, arch of the aorta
  • Activated on stretch

If baroreceptors sense increased BP

  • Secondary signals from tractus solitarius
  • Inhibition of vasoconstrictor centre and excitation of vagal parasympathetic centre
23
Q

What are chemoreceptors?

A

Chemoreceptors

  • Sensitive to low O2, high CO2 and acidosis
    Chemoreceptor organs:
  • 2 carotid bodies (one each bifurcation)
  • 1-2 aortic bodies (adjacent to aorta)
  • Separate blood supply
  • Reduction in blood flow (reducation in pressure <80 mmHg) causes metabolic stimulation
  • Excitatory effect on vasomotor centre
24
Q

How is blood pressure controlled long term?

A
  • Renin angiotensine aldosterone system

- Vascular remodelling and contractility

25
Q

Where does aldosterone act and what does it do?

A

Aldosterone

  • Principal cells of the collecting tubules
  • Distal tubules
  • Collecting ducts
    Increases absorption of Na+ and secretion of K+ and H+
26
Q

What is primary hyperaldosteronism?

A

The body produces too much aldosterone
Leads to long-standing hypertension and hypokalaemia

Causes:

  • Unilateral aldosterone producing adenoma or Conn’s syndrome (50-60%)
  • Bilateral adrenal hyperplasia (40-50%)

Consequences: high aldosterone leads to low K+ and low H+
= hypokalaemic alkalosis
This is due to more Na/Cl reabsorption in the kidneys, which results in more K+ extretion

Presentation:

  • Hypokalaemia
  • Muscle weakness
  • Cramping
  • Palpitations

Hypokalaemia induced nephrogenic diabetes insipidus: polyruria + polydipsia
Complications of long standing hypertension

27
Q

What is Addison’s Disease?

A

Adrenal insufficency: the adrenal glands produce too little cortisol and aldosterone

Presentation:

  • Lethargy
  • Weight loss
  • Fainting
  • Hyperpigmenting skin creases
  • Postural hypotension
  • Dehydrated
  • Hyponatraemia
  • Hyperkalaemia
  • Acidotic

Investigations:

  • Short SynACTHen test
  • Tetracosactide (synacthen) 250µg IV/IM
  • Check blood cortisol at 0 mins and 30 mins
  • Cortisol at 30 mins should be >600nmol/L

Treatment:

  • Glucocorticoid, mineralocorticoid and sex steroid production are reduced!
  • Bracelet
  • Acutely ill -> hydrocortisone IV
28
Q

What changes are seen in the blood arterioles in essential hypertension?

A

Essential hypertension

  • Increase in wall thickness
  • Reduction in lumen diameter
  • Increase in wall to lumen ratio
  • Preservation or mild impairment of endothelial function
29
Q

What changes are seen in the blood arterioles in Type II diabetes and hypertension?

A

T2DM + Diabetes

  • Increase in wall thickness
  • No change/increase in lumen diameter
  • Impairment of endothelial function
30
Q

What is metabolic syndrome?

A

Metabolic syndrome:

  • Elevating blood pressure
  • Dyslipiaemia
  • Exacerbation of insulin resistance

All caused by adipose tissue causing increased vascular tone

31
Q

What is the first line treatment for hypertension?

A

Younger than 55 = ACEi/ARB
Older than 55 or black = CCB
Any age + T2DM = ACEi-ARB

32
Q

What is the second line treatment for hypertension?

A

Either:
ACEi/ARB + CCB
OR
ACEi/ARB + Diuretic

33
Q

What is the third line treatment for hypertension?

A

Always:

ACEi/ARB + CCB + Diuretic

34
Q

What is the fourth line treatment for hypertension?

A
  • Further diuretic therapy
  • Alpha blocker
  • Beta-blocker
    Consider seeking specialist advice
35
Q

What is seen in hypertensive retinopathy?

A

Hypertensive retinopathy

  • Flame haemorrhages
  • Hard exudates
  • Cotton wool spot
  • Papilloedema
36
Q

What end-organ damage is seen consequential to hypertension?

A

End-organ damage

  • Eyes: hypertensive retinopathy
  • Brain: hypertensive cerebrovascular disease
  • Heart: left ventricular hypertrophy, ischaemic heart disease, with or without heart failure
  • Kidneys: hypertensive nephropathy
37
Q

What are the causes of secondary hypertension?

A

10% of hypertension cases

Causes:
- Renal diseases
Kidneys don’t function well - struggle to regulate water and Na+, increases in fluid in body, and then BP
Ex: polycystic kidney disease - fluid filled cysts
- Glomerular disease
Poorer filtration of water and Na+
- Renovascular hypertension
Narrowing of arteries that supply kidneys with blood
Kidneys assume dehydration and hold onto more fluid

  • Cushing’s syndrome
    High levels of circulating glucocorticoids, facilitiate water and Na+ retention, increasing BP
  • Primary aldosteronism
    Too much aldosterone increases NA+ and water retention
  • Phaeochromocytoma
    Tumour growing on the adrenal glands, increase BP b release of epinephrine and norepinephrine
  • Sleep apnea
    Start stop breathing, reduced O2 intake, so blood pumps harder
    Blood flow increases at night, and so increases BP at night
  • Obesity
    Higher body weight increases blood volume, which increases flow and therefore BP
  • Brain tumours and encephalitis
    Reduced blood flow to parts of the brain, as the above increase the pressure in the skull the body increases BP in force more blood into the brain
38
Q

What clinical features are suggestive of secondary hypertension?

A
  • Severe or resistant hypertension
  • An acute rise in BP over a previously stable value
  • Proven age of onset before puberty
  • Age less than 30 years with no family history of hypertension and no obesity
39
Q

What clinical features are seen in renovascular disease?

A
  • Acute elevation in serum creatinine of at least 30% after administering ACEi or ARB
  • Moderate to severe hypertension in patient with
  • Diffuse atherosclerosis
  • Unilateral small kidney
  • Asymmetry in renal size of more than 1.5cm that cannot be explain by other reasons
  • Moderate to severe hypertension in patients with recurrent episodes of flash pulmonary oedema
  • Onset of stage II hypertension after 55 years
  • Systolic or diastolic abdominal bruit
40
Q

What clinical features are seen in primary renal disease?

A
  • Elavated serum creatinine concentration

- Abnormal urinanalysis

41
Q

Which drugs may cause elevations in BP?

A
  • Oral contraceptives
  • NSAIDS
  • Stimulants (eg cocaine, methyphenidate)
  • Calcineurin inhibitors
  • Antidepressants
42
Q

What clinical features are suggestive of phaeochromocytoma?

A
  • Paroxysmal elevations in BP (night time)

- Triad of headache (pounding), palpitations, and sweating

43
Q

What clinical features are suggestive of primary aldosteronism?

A
  • Unexplained hypokalaemia with urinary potassium wasting

- More than 50% patients are normokalaemic

44
Q

What clinical features are suggestive of Cushing’s syndrome?

A
  • Cushingoid faces
  • Central obseity
  • Proximal muscle weakness
  • Eccymoses
  • History of glucocorticoid use
45
Q

What clinical features are suggestive of sleep apnea syndrome?

A
  • Primarily obese men who snore loudly in sleep
  • Daytime somnolence
  • Fatigue
  • Morning confusion
46
Q

What clinical features are suggestive of coarctation of the aorta?

A
  • Hypertension in the arms with diminished or delayed femoral pulses
  • Low or unobtainable BP in the legs
47
Q

What clinical features are suggestive of hypothyroidism?

A
  • Symptoms of hypothyroidism
    (menorrhagia, weight gain, fatigue, lethargy, thinning hair, hoarse voice, dry skin, cold intolerance)
  • Elevated serum thyroid stimulating hormone
48
Q

What clinical features are suggestive of primary hyperparathyroidism?

A

Elevated serum calcium

49
Q

What lifestyle changes can help with hypertension?

A
  • Healthy diet
  • Reduced salt
  • Reduced coffee
  • Quitting smoking
  • Reduced alcohol intake
  • Regular exercise
  • Relaxation therapies and methods
50
Q

What are the risk factors for essential hypertension?

A
  • Being overweight
  • Being stressed
  • Eating too much salt
  • Excessive alcohol
  • Too much caffeine
  • Smoking cigarettes
  • Not enough fruit and veg
  • Not enough exercise
  • Family history
  • Caribbean or African descent

Cardiology (4 decks)

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