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Block 13 - The Development of Cardiorespiratory Disease > ALS Lecture 11 - Hypertension and Heart Failure DONE > Flashcards

ALS Lecture 11 - Hypertension and Heart Failure DONE Flashcards

1
Q

what percent of the adult population in the UK have hypertension?

A

25%

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2
Q

what percent of 60+ people in the UK have hypertension?

A

50%

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3
Q

stage 1 hypertension clinic blood pressure requirement

A

140/90mmHg or higher

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4
Q

stage 1 hypertension ABPM or HBPM requirement

A

average 135/85mmHg or higher

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5
Q

stage 2 hypertension clinic blood pressure requirement

A

160/100mmHg or higher

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6
Q

stage 2 hypertension ABPM or HBPM requirement

A

daytime average 150/95mmHg or higher

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7
Q

severe hypertension requirement

A

clinic systolic = 180mmHg or higher

OR clinic diastolic = 110mmHg or higher

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8
Q

4 major determinants of blood pressure

A

baroreceptors, RAAS, Poiseuille’s law, renal function

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9
Q

Poiseuille’s law

A

flow = radius4

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10
Q

from moment to moment what is most important in bp control?

A

baroreceptors

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11
Q

baroreceptors alter

A

sympathetic outflow to all smooth muscle cells in arterioles

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12
Q

longer term blood pressure is controlled by (2)

A

kidneys, RAAS

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13
Q

label the diagram of RAAS (A)

A

done

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14
Q

primary hypertension is also known as

A

essential hypertension

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15
Q

what percentage of patients with hypertension have primary hypertension?

A

90-95%

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16
Q

primary hypertension means that there is

A

no known cause

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17
Q

things that can contribute to primary hypertension (6)

A

overweight, bad diet, lots of sodium, not much potassium, low physical activity, high alcohol intake

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18
Q

secondary hypertension

A

raised bp with identifiable cause

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19
Q

what percentage of patients with hypertension have secondary hypertension?

A

5-10%

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20
Q

most common causes of secondary hypertension (2)

A

renal, endocrine

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21
Q

secondary hypertension leads to increased (4)

A

cardiac output, vascular resistance, neurohumoral activation, blood volume

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22
Q

how does renal artery stenosis cause secondary hypertension? (4 steps)

A
  1. decreases pressure in afferent arteriole
  2. increased renin, angiotensin 2, aldosterone
  3. angiotensin 2 promotes cardiac and vascular hypertrophy
  4. increased blood volume, cardiac output, vascular resistance
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23
Q

how does chronic renal disease cause secondary hypertension? (4 steps)

A
  1. decreased Na+ excretion, so Na+ and H2O retention
  2. increased blood volume and cardiac output
  3. increased renin
  4. increased blood pressure in attempt to restore eGFR
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24
Q

primary hyperaldosteronism can be due to (2)

A

adrenal tumours, adrenal hyperplasia

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25
Q

how does how does primary hyperaldosteronism cause secondary hypertension? (4 steps)

A
  1. adrenal glands make too much aldosterone
  2. Na+ and H2O retention
  3. increased blood volume and cardiac output
  4. decreased renin and potassium
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26
Q

phaeochromocytoma are

A

adrenal medullary tumours

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27
Q

phaeochromocytomas secrete

A

catecholamines

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28
Q

phaeochromocytoma catecholamine release leads to (4)

A

a-mediated vasoconstriction, B-mediated cardiac stimulation, raised bp, tachycardia

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29
Q

coarctation of the aorta

A

birth defect where part of aorta is narrow

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30
Q

coarctation of the aorta leads to (3 steps)

A
  1. kidneys hypoperfused
  2. RAAS activated
  3. upper body hypertension, lower body normotension
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31
Q

other causes of secondary hypertension (5)

A

cushing’s, pregnancy, thyroid disease, sleep apnoea, alcohol

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32
Q

in the heart, hypertension can lead to (3)

A

coronary atheroma, pulmonary atheroma, concentric left ventricular hypertrophy

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33
Q

tall complexes on ECG indicate

A

left ventricle is under strain and hypertrophied

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34
Q

in the aorta, hypertension can lead to (3)

A

atheroma, aneurysm, dissecting aneurysm

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35
Q

in the brain, hypertension can lead to (2)

A

thrombotic stroke, haemorrhagic stroke

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36
Q

hypertension leads to thrombotic (ischaemic) stroke in the brain due to

A

increased carotid atheroma, small penetrating arteries

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37
Q

hypertension leads to haemorrhagic stroke in the brain in

A

small arteries, commonly Charcot-Bouchard aneurysms

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38
Q

in the brain, hypertension can lead to (2)

A

small vessel hypertensive disease = glomerular damage

large vessel atheromatous disease

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39
Q

in the eye, hypertension can lead to (3)

A

haemorrhage, papilloedema, hard exudates

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40
Q

the eye is the only area of the body where we can

A

see small blood vessels directly

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41
Q

accelerated hypertension

A

recent significant elevation over baseline blood pressure, associated with target organ damage

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42
Q

papilloedema indicates ___ ___ ___, so is called _____ ______

A

raised intracranial pressure, malignant hypertension

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43
Q

who is more vulnerable to accelerated hypertension?

A

men, smokers, secondary hypertension pts

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44
Q

acute heart failure

A

comes sharply to crisis

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45
Q

chronic heart failure

A

lasting, lingering

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46
Q

pre-load, a.k.a

A

filling pressure

47
Q

pre-load

A

pressure in ventricle just before it contracts

48
Q

after-load, a.k.a

A

peripheral resistance

49
Q

after-load

A

peripheral resistance, altered by state of blood vessels

50
Q

stroke volume

A

amount of blood ejected with each left ventricular contraction

51
Q

look at the pictures of the normal and heart failure hearts (B)

A

done

52
Q

frank-starling relationship is the relationship between the

A

pressure in left ventricle and what left ventricle is actually doing, i.e. stroke volume

53
Q

in a normal person, as __ _____ _____ increases, they can increase their ___ _____

A

end diastolic volume, stroke volume

54
Q

when a normal person exercises, stretch receptors in the heart are

A

activated so heart pumps harder, stronger

55
Q

in people with heart failure, the end diastolic volume increases but they have

A

limited myocardial reserve and contractility so develop breathlessness and pulmonary oedema

56
Q

label the diagram of the frank-starling relationship (C)

A

done

57
Q

acute heart failure leads to (4)

A

fluid in wrong place, pulmonary oedema, anasarca, cardiogenic shock

58
Q

heart failure is a significant risk factor for (1)

A

kidney disease

59
Q

how does heart failure lead to kidney disease? (6 steps)

A
  1. heart not pumping well so congested blood
  2. blood congestion in renal vein and kidneys
  3. kidney hypoperfusion
  4. RAAS overdrive trying to increase blood supply
  5. heart has to pump increased pressure, suffers
  6. kidney damaged by reduced O2
60
Q

label the flowchart of pulmonary oedema pathophysiology (D)

A

done

61
Q

acute pulmonary oedema pathophysiology (5 steps)

A
  1. drop in cardiac output, LV struggling
  2. increase LV end diastolic pressure to maintain output
  3. increased pulmonary vascular pressure
  4. end diastolic pressure above lymphatic drainage rate
  5. fluid leaks into interstitium and alveoli
62
Q

acute pulmonary oedema symptoms (5)

A

SOB, accessory muscle use, pink frothy sputum, sweating, cold/cyanosed

63
Q

pulmonary oedema causes (6)

A

acute ischaemia, arrhythmia, mechanical disaster, non-compliance, PE, drugs

64
Q

anasarca

A

massive, generalised oedema

65
Q

anasarca develops over

A

many days or weeks

66
Q

anasarca symptoms (4)

A

gradual weight gain (5kg+), pitting oedema, ascites, pleural effusion

67
Q

anasarca pathophysiology (7 steps)

A
  1. failure of LV pump
  2. fall in bp stimulates sympathetic nervous system
  3. increased hr and vasoconstriction = increased after-load
  4. also, fall in renal perfusion stimulates RAAS
  5. Na+ and H2O retention
  6. increased preload
  7. increased preload and afterload make LV struggle ven more
68
Q

label the diagram of anasarca pathophysiology (E)

A

done

69
Q

label the diagram of neuroendocrine response in heart failure (F)

A

done

70
Q

label the diagram of metabolic response in heart failure (G)

A

done

71
Q

pulmonary oedema treatment (7)

A

diamorphine, oxygen, diuretic, vasodilator, ventilatory support, inotropic support, treat precipitant

72
Q

diamorphine in treatment of pulmonary oedema

A

anxiety relief as distressing

73
Q

diuretic in treatment of pulmonary oedema

A

IV frusemide

74
Q

vasodilator in treatment of pulmonary oedema

A

IV nitrate titrated against bp

75
Q

ventilatory support in in treatment of pulmonary oedema

A

CPAP, IPPV

76
Q

inotropic support in treatment of pulmonary oedema

A

high mortality, only use in shock, usually dobutamine

77
Q

anasarca drug treatment (4)

A

diuretics, ACE inhibitors, beta blockers, aldosterone antagonists

78
Q

diuretics in treatment of anasarca

A

loop diuretics, loop + thiazide combination, reduce water

79
Q

ACE inhibitors in treatment of anasarca

A

inhibit RAAS

80
Q

beta blockers in treatment of anasarca

A

reduce activity of sympathetic nervous system

81
Q

aldosterone antagonists in treatment of anasarca

A

limit RAAS

82
Q

how can we induce diuresis in anasarca? (6)

A

bed rest, daily weigh-ins, fluid restriction, diuretics, inotropic support, mechanical help

83
Q

label the diagram of RAAS (H)

A

done

84
Q

explain RAAS (6 steps)

A
  1. drop in bp (perfusion to kidney)
  2. kidney produces renin
  3. renin converts angiotensinogen to angiotensin 1 in liver
  4. ACE (angiotensin converting enzyme) in the lungs converts angiotensin 1 to angiotensin 2
  5. angiotensin 2 stimulates aldosterone release
  6. aldosterone causes vasoconstriction, increased bp
85
Q

MOA beta-blockers (4)

A

protect cardiac myocytes, slow heart, increase diastolic coronary blood flow, decrease myocardial O2 demand

86
Q

beta blockers effect (3)

A

anti-ischaemic, anti-arrhythmic, reduced risk of recurrent MI

87
Q

beta blockers side effects (6)

A

worsen heart failure, fall in bp, fall in hr, cold peripheries, wheeze, fatigue

88
Q

ace inhibitors MOA (2 steps)

A
  1. inhibit ACE in RAAS

2. angiotensin 1 can’t be converted to angiotensin 2

89
Q

ACE inhibitors effect (2)

A

bp fall, potassium rise

90
Q

ACE inhibitors side effects (6)

A

affect kidneys, must check creatinine for rise, fall in Hb, cough, rash, angio-oedema

91
Q

types of diuretic (4)

A

loop, thiazide, potassium sparing, antidiuretic hormone antagonist

92
Q

label the sites of diuretic action diagram (I)

A

done

93
Q

loop diuretics MOA

A

block Na+/K+/2Cl- cotransporter in thick ascending loop of Henle

94
Q

thiazide diuretics MOA

A

block Na+/Cl- cotransporter in distal convoluted tubule

95
Q

potassium sparing diuretic MOA

A

prevent secretion of potassium in urine by blocking Na+/K+ pump and aldosterone

96
Q

ADH antagonist diuretic MOA

A

bind to vasopressin receptors, block action of ADH

97
Q

loop diuretics have a high ceiling, meaning the

A

higher the dose, the stronger the effect

98
Q

loop diuretics examples (3)

A

frusemide, bumetanide, torasemide

99
Q

loop diuretics side effects (3)

A

hyponatraemia, hypokalaemia, hyperuricaemia (can lead to gout)

100
Q

thiazide diuretics have a low ceiling, meaning that

A

increasing dose beyond certain point has no further diuretic effect

101
Q

thiazide diuretics examples (3)

A

bendroflumethiazide, metolazone, chlorthalidone

102
Q

thiazide diuretic side effects (2)

A

loss in sodium, potassium and magnesium. increase in urate and calcium.

103
Q

label the diagram (J)

A

done

104
Q

label the diagram of the typical clinical course for diuretics (K)

A

done

105
Q

typical clinical course for diuretics (4 steps)

A
  1. give IV frusemide
  2. ACE inhibitor
  3. switch to oral diuretic
  4. start beta blocker
106
Q

basic medications in hypertension are (4)

A

A - ACE inhibitors
B - beta blockers
C - calcium antagonists
D - diuretics

107
Q

calcium channel blocker type we must commonly use

A

dihydropyridines

108
Q

examples of dihydropyridines (2)

A

amlodipine, nefidipine

109
Q

MOA of calcium channel blockers

A

vasodilation, dihydropyridines slow hr so useful in angina

110
Q

calcium channel blockers side effects (3)

A

ankle swelling, tachycardia, flushing

111
Q

calcium channel blockers must not be used in people with (2)

A

LV dysfunction, heart failure

112
Q

in heart failure patients we measure

A

brain natriuretic peptide as it is a good measure of cardiac function

113
Q

natriuretic peptides lead to (3)

A

natriuresis, diuresis, lowered bp

Block 13 - The Development of Cardiorespiratory Disease (14 decks)

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