ALS Lecture 11 - Hypertension and Heart Failure DONE Flashcards
(113 cards)
1
Q
what percent of the adult population in the UK have hypertension?
A
25%
2
Q
what percent of 60+ people in the UK have hypertension?
A
50%
3
Q
stage 1 hypertension clinic blood pressure requirement
A
140/90mmHg or higher
4
Q
stage 1 hypertension ABPM or HBPM requirement
A
average 135/85mmHg or higher
5
Q
stage 2 hypertension clinic blood pressure requirement
A
160/100mmHg or higher
6
Q
stage 2 hypertension ABPM or HBPM requirement
A
daytime average 150/95mmHg or higher
7
Q
severe hypertension requirement
A
clinic systolic = 180mmHg or higher
OR clinic diastolic = 110mmHg or higher
8
Q
4 major determinants of blood pressure
A
baroreceptors, RAAS, Poiseuille’s law, renal function
9
Q
Poiseuille’s law
A
flow = radius4
10
Q
from moment to moment what is most important in bp control?
A
baroreceptors
11
Q
baroreceptors alter
A
sympathetic outflow to all smooth muscle cells in arterioles
12
Q
longer term blood pressure is controlled by (2)
A
kidneys, RAAS
13
Q
label the diagram of RAAS (A)
A
done
14
Q
primary hypertension is also known as
A
essential hypertension
15
Q
what percentage of patients with hypertension have primary hypertension?
A
90-95%
16
Q
primary hypertension means that there is
A
no known cause
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
18
Q
secondary hypertension
A
raised bp with identifiable cause
19
Q
what percentage of patients with hypertension have secondary hypertension?
A
5-10%
20
Q
most common causes of secondary hypertension (2)
A
renal, endocrine
21
Q
secondary hypertension leads to increased (4)
A
cardiac output, vascular resistance, neurohumoral activation, blood volume
22
Q
how does renal artery stenosis cause secondary hypertension? (4 steps)
A
- decreases pressure in afferent arteriole
- increased renin, angiotensin 2, aldosterone
- angiotensin 2 promotes cardiac and vascular hypertrophy
- increased blood volume, cardiac output, vascular resistance
23
Q
how does chronic renal disease cause secondary hypertension? (4 steps)
A
- decreased Na+ excretion, so Na+ and H2O retention
- increased blood volume and cardiac output
- increased renin
- increased blood pressure in attempt to restore eGFR
24
Q
primary hyperaldosteronism can be due to (2)
A
adrenal tumours, adrenal hyperplasia
25
how does how does primary hyperaldosteronism cause secondary hypertension? (4 steps)
1. adrenal glands make too much aldosterone
2. Na+ and H2O retention
3. increased blood volume and cardiac output
4. decreased renin and potassium
26
phaeochromocytoma are
adrenal medullary tumours
27
phaeochromocytomas secrete
catecholamines
28
phaeochromocytoma catecholamine release leads to (4)
a-mediated vasoconstriction, B-mediated cardiac stimulation, raised bp, tachycardia
29
coarctation of the aorta
birth defect where part of aorta is narrow
30
coarctation of the aorta leads to (3 steps)
1. kidneys hypoperfused
2. RAAS activated
3. upper body hypertension, lower body normotension
31
other causes of secondary hypertension (5)
cushing's, pregnancy, thyroid disease, sleep apnoea, alcohol
32
in the heart, hypertension can lead to (3)
coronary atheroma, pulmonary atheroma, concentric left ventricular hypertrophy
33
tall complexes on ECG indicate
left ventricle is under strain and hypertrophied
34
in the aorta, hypertension can lead to (3)
atheroma, aneurysm, dissecting aneurysm
35
in the brain, hypertension can lead to (2)
thrombotic stroke, haemorrhagic stroke
36
hypertension leads to thrombotic (ischaemic) stroke in the brain due to
increased carotid atheroma, small penetrating arteries
37
hypertension leads to haemorrhagic stroke in the brain in
small arteries, commonly Charcot-Bouchard aneurysms
38
in the brain, hypertension can lead to (2)
small vessel hypertensive disease = glomerular damage
| large vessel atheromatous disease
39
in the eye, hypertension can lead to (3)
haemorrhage, papilloedema, hard exudates
40
the eye is the only area of the body where we can
see small blood vessels directly
41
accelerated hypertension
recent significant elevation over baseline blood pressure, associated with target organ damage
42
papilloedema indicates ___ ___ ___, so is called _____ ______
raised intracranial pressure, malignant hypertension
43
who is more vulnerable to accelerated hypertension?
men, smokers, secondary hypertension pts
44
acute heart failure
comes sharply to crisis
45
chronic heart failure
lasting, lingering
46
pre-load, a.k.a
filling pressure
47
pre-load
pressure in ventricle just before it contracts
48
after-load, a.k.a
peripheral resistance
49
after-load
peripheral resistance, altered by state of blood vessels
50
stroke volume
amount of blood ejected with each left ventricular contraction
51
look at the pictures of the normal and heart failure hearts (B)
done
52
frank-starling relationship is the relationship between the
pressure in left ventricle and what left ventricle is actually doing, i.e. stroke volume
53
in a normal person, as __ _____ _____ increases, they can increase their ___ _____
end diastolic volume, stroke volume
54
when a normal person exercises, stretch receptors in the heart are
activated so heart pumps harder, stronger
55
in people with heart failure, the end diastolic volume increases but they have
limited myocardial reserve and contractility so develop breathlessness and pulmonary oedema
56
label the diagram of the frank-starling relationship (C)
done
57
acute heart failure leads to (4)
fluid in wrong place, pulmonary oedema, anasarca, cardiogenic shock
58
heart failure is a significant risk factor for (1)
kidney disease
59
how does heart failure lead to kidney disease? (6 steps)
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
label the flowchart of pulmonary oedema pathophysiology (D)
done
61
acute pulmonary oedema pathophysiology (5 steps)
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
acute pulmonary oedema symptoms (5)
SOB, accessory muscle use, pink frothy sputum, sweating, cold/cyanosed
63
pulmonary oedema causes (6)
acute ischaemia, arrhythmia, mechanical disaster, non-compliance, PE, drugs
64
anasarca
massive, generalised oedema
65
anasarca develops over
many days or weeks
66
anasarca symptoms (4)
gradual weight gain (5kg+), pitting oedema, ascites, pleural effusion
67
anasarca pathophysiology (7 steps)
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
label the diagram of anasarca pathophysiology (E)
done
69
label the diagram of neuroendocrine response in heart failure (F)
done
70
label the diagram of metabolic response in heart failure (G)
done
71
pulmonary oedema treatment (7)
diamorphine, oxygen, diuretic, vasodilator, ventilatory support, inotropic support, treat precipitant
72
diamorphine in treatment of pulmonary oedema
anxiety relief as distressing
73
diuretic in treatment of pulmonary oedema
IV frusemide
74
vasodilator in treatment of pulmonary oedema
IV nitrate titrated against bp
75
ventilatory support in in treatment of pulmonary oedema
CPAP, IPPV
76
inotropic support in treatment of pulmonary oedema
high mortality, only use in shock, usually dobutamine
77
anasarca drug treatment (4)
diuretics, ACE inhibitors, beta blockers, aldosterone antagonists
78
diuretics in treatment of anasarca
loop diuretics, loop + thiazide combination, reduce water
79
ACE inhibitors in treatment of anasarca
inhibit RAAS
80
beta blockers in treatment of anasarca
reduce activity of sympathetic nervous system
81
aldosterone antagonists in treatment of anasarca
limit RAAS
82
how can we induce diuresis in anasarca? (6)
bed rest, daily weigh-ins, fluid restriction, diuretics, inotropic support, mechanical help
83
label the diagram of RAAS (H)
done
84
explain RAAS (6 steps)
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
MOA beta-blockers (4)
protect cardiac myocytes, slow heart, increase diastolic coronary blood flow, decrease myocardial O2 demand
86
beta blockers effect (3)
anti-ischaemic, anti-arrhythmic, reduced risk of recurrent MI
87
beta blockers side effects (6)
worsen heart failure, fall in bp, fall in hr, cold peripheries, wheeze, fatigue
88
ace inhibitors MOA (2 steps)
1. inhibit ACE in RAAS
| 2. angiotensin 1 can't be converted to angiotensin 2
89
ACE inhibitors effect (2)
bp fall, potassium rise
90
ACE inhibitors side effects (6)
affect kidneys, must check creatinine for rise, fall in Hb, cough, rash, angio-oedema
91
types of diuretic (4)
loop, thiazide, potassium sparing, antidiuretic hormone antagonist
92
label the sites of diuretic action diagram (I)
done
93
loop diuretics MOA
block Na+/K+/2Cl- cotransporter in thick ascending loop of Henle
94
thiazide diuretics MOA
block Na+/Cl- cotransporter in distal convoluted tubule
95
potassium sparing diuretic MOA
prevent secretion of potassium in urine by blocking Na+/K+ pump and aldosterone
96
ADH antagonist diuretic MOA
bind to vasopressin receptors, block action of ADH
97
loop diuretics have a high ceiling, meaning the
higher the dose, the stronger the effect
98
loop diuretics examples (3)
frusemide, bumetanide, torasemide
99
loop diuretics side effects (3)
hyponatraemia, hypokalaemia, hyperuricaemia (can lead to gout)
100
thiazide diuretics have a low ceiling, meaning that
increasing dose beyond certain point has no further diuretic effect
101
thiazide diuretics examples (3)
bendroflumethiazide, metolazone, chlorthalidone
102
thiazide diuretic side effects (2)
loss in sodium, potassium and magnesium. increase in urate and calcium.
103
label the diagram (J)
done
104
label the diagram of the typical clinical course for diuretics (K)
done
105
typical clinical course for diuretics (4 steps)
1. give IV frusemide
2. ACE inhibitor
3. switch to oral diuretic
4. start beta blocker
106
basic medications in hypertension are (4)
A - ACE inhibitors
B - beta blockers
C - calcium antagonists
D - diuretics
107
calcium channel blocker type we must commonly use
dihydropyridines
108
examples of dihydropyridines (2)
amlodipine, nefidipine
109
MOA of calcium channel blockers
vasodilation, dihydropyridines slow hr so useful in angina
110
calcium channel blockers side effects (3)
ankle swelling, tachycardia, flushing
111
calcium channel blockers must not be used in people with (2)
LV dysfunction, heart failure
112
in heart failure patients we measure
brain natriuretic peptide as it is a good measure of cardiac function
113
natriuretic peptides lead to (3)
natriuresis, diuresis, lowered bp
