ALS Lecture 11 - Hypertension and Heart Failure DONE Flashcards
what percent of the adult population in the UK have hypertension?
25%
what percent of 60+ people in the UK have hypertension?
50%
stage 1 hypertension clinic blood pressure requirement
140/90mmHg or higher
stage 1 hypertension ABPM or HBPM requirement
average 135/85mmHg or higher
stage 2 hypertension clinic blood pressure requirement
160/100mmHg or higher
stage 2 hypertension ABPM or HBPM requirement
daytime average 150/95mmHg or higher
severe hypertension requirement
clinic systolic = 180mmHg or higher
OR clinic diastolic = 110mmHg or higher
4 major determinants of blood pressure
baroreceptors, RAAS, Poiseuille’s law, renal function
Poiseuille’s law
flow = radius4
from moment to moment what is most important in bp control?
baroreceptors
baroreceptors alter
sympathetic outflow to all smooth muscle cells in arterioles
longer term blood pressure is controlled by (2)
kidneys, RAAS
label the diagram of RAAS (A)
done
primary hypertension is also known as
essential hypertension
what percentage of patients with hypertension have primary hypertension?
90-95%
primary hypertension means that there is
no known cause
things that can contribute to primary hypertension (6)
overweight, bad diet, lots of sodium, not much potassium, low physical activity, high alcohol intake
secondary hypertension
raised bp with identifiable cause
what percentage of patients with hypertension have secondary hypertension?
5-10%
most common causes of secondary hypertension (2)
renal, endocrine
secondary hypertension leads to increased (4)
cardiac output, vascular resistance, neurohumoral activation, blood volume
how does renal artery stenosis cause secondary hypertension? (4 steps)
- decreases pressure in afferent arteriole
- increased renin, angiotensin 2, aldosterone
- angiotensin 2 promotes cardiac and vascular hypertrophy
- increased blood volume, cardiac output, vascular resistance
how does chronic renal disease cause secondary hypertension? (4 steps)
- decreased Na+ excretion, so Na+ and H2O retention
- increased blood volume and cardiac output
- increased renin
- increased blood pressure in attempt to restore eGFR
primary hyperaldosteronism can be due to (2)
adrenal tumours, adrenal hyperplasia
how does how does primary hyperaldosteronism cause secondary hypertension? (4 steps)
- adrenal glands make too much aldosterone
- Na+ and H2O retention
- increased blood volume and cardiac output
- decreased renin and potassium
phaeochromocytoma are
adrenal medullary tumours
phaeochromocytomas secrete
catecholamines
phaeochromocytoma catecholamine release leads to (4)
a-mediated vasoconstriction, B-mediated cardiac stimulation, raised bp, tachycardia
coarctation of the aorta
birth defect where part of aorta is narrow
coarctation of the aorta leads to (3 steps)
- kidneys hypoperfused
- RAAS activated
- upper body hypertension, lower body normotension
other causes of secondary hypertension (5)
cushing’s, pregnancy, thyroid disease, sleep apnoea, alcohol
in the heart, hypertension can lead to (3)
coronary atheroma, pulmonary atheroma, concentric left ventricular hypertrophy
tall complexes on ECG indicate
left ventricle is under strain and hypertrophied
in the aorta, hypertension can lead to (3)
atheroma, aneurysm, dissecting aneurysm
in the brain, hypertension can lead to (2)
thrombotic stroke, haemorrhagic stroke
hypertension leads to thrombotic (ischaemic) stroke in the brain due to
increased carotid atheroma, small penetrating arteries
hypertension leads to haemorrhagic stroke in the brain in
small arteries, commonly Charcot-Bouchard aneurysms
in the brain, hypertension can lead to (2)
small vessel hypertensive disease = glomerular damage
large vessel atheromatous disease
in the eye, hypertension can lead to (3)
haemorrhage, papilloedema, hard exudates
the eye is the only area of the body where we can
see small blood vessels directly
accelerated hypertension
recent significant elevation over baseline blood pressure, associated with target organ damage
papilloedema indicates ___ ___ ___, so is called _____ ______
raised intracranial pressure, malignant hypertension
who is more vulnerable to accelerated hypertension?
men, smokers, secondary hypertension pts
acute heart failure
comes sharply to crisis
chronic heart failure
lasting, lingering
pre-load, a.k.a
filling pressure
pre-load
pressure in ventricle just before it contracts
after-load, a.k.a
peripheral resistance
after-load
peripheral resistance, altered by state of blood vessels
stroke volume
amount of blood ejected with each left ventricular contraction
look at the pictures of the normal and heart failure hearts (B)
done
frank-starling relationship is the relationship between the
pressure in left ventricle and what left ventricle is actually doing, i.e. stroke volume
in a normal person, as __ _____ _____ increases, they can increase their ___ _____
end diastolic volume, stroke volume
when a normal person exercises, stretch receptors in the heart are
activated so heart pumps harder, stronger
in people with heart failure, the end diastolic volume increases but they have
limited myocardial reserve and contractility so develop breathlessness and pulmonary oedema
label the diagram of the frank-starling relationship (C)
done
acute heart failure leads to (4)
fluid in wrong place, pulmonary oedema, anasarca, cardiogenic shock
heart failure is a significant risk factor for (1)
kidney disease
how does heart failure lead to kidney disease? (6 steps)
- heart not pumping well so congested blood
- blood congestion in renal vein and kidneys
- kidney hypoperfusion
- RAAS overdrive trying to increase blood supply
- heart has to pump increased pressure, suffers
- kidney damaged by reduced O2
label the flowchart of pulmonary oedema pathophysiology (D)
done
acute pulmonary oedema pathophysiology (5 steps)
- drop in cardiac output, LV struggling
- increase LV end diastolic pressure to maintain output
- increased pulmonary vascular pressure
- end diastolic pressure above lymphatic drainage rate
- fluid leaks into interstitium and alveoli
acute pulmonary oedema symptoms (5)
SOB, accessory muscle use, pink frothy sputum, sweating, cold/cyanosed
pulmonary oedema causes (6)
acute ischaemia, arrhythmia, mechanical disaster, non-compliance, PE, drugs
anasarca
massive, generalised oedema
anasarca develops over
many days or weeks
anasarca symptoms (4)
gradual weight gain (5kg+), pitting oedema, ascites, pleural effusion
anasarca pathophysiology (7 steps)
- failure of LV pump
- fall in bp stimulates sympathetic nervous system
- increased hr and vasoconstriction = increased after-load
- also, fall in renal perfusion stimulates RAAS
- Na+ and H2O retention
- increased preload
- increased preload and afterload make LV struggle ven more
label the diagram of anasarca pathophysiology (E)
done
label the diagram of neuroendocrine response in heart failure (F)
done
label the diagram of metabolic response in heart failure (G)
done
pulmonary oedema treatment (7)
diamorphine, oxygen, diuretic, vasodilator, ventilatory support, inotropic support, treat precipitant
diamorphine in treatment of pulmonary oedema
anxiety relief as distressing
diuretic in treatment of pulmonary oedema
IV frusemide
vasodilator in treatment of pulmonary oedema
IV nitrate titrated against bp
ventilatory support in in treatment of pulmonary oedema
CPAP, IPPV
inotropic support in treatment of pulmonary oedema
high mortality, only use in shock, usually dobutamine
anasarca drug treatment (4)
diuretics, ACE inhibitors, beta blockers, aldosterone antagonists
diuretics in treatment of anasarca
loop diuretics, loop + thiazide combination, reduce water
ACE inhibitors in treatment of anasarca
inhibit RAAS
beta blockers in treatment of anasarca
reduce activity of sympathetic nervous system
aldosterone antagonists in treatment of anasarca
limit RAAS
how can we induce diuresis in anasarca? (6)
bed rest, daily weigh-ins, fluid restriction, diuretics, inotropic support, mechanical help
label the diagram of RAAS (H)
done
explain RAAS (6 steps)
- drop in bp (perfusion to kidney)
- kidney produces renin
- renin converts angiotensinogen to angiotensin 1 in liver
- ACE (angiotensin converting enzyme) in the lungs converts angiotensin 1 to angiotensin 2
- angiotensin 2 stimulates aldosterone release
- aldosterone causes vasoconstriction, increased bp
MOA beta-blockers (4)
protect cardiac myocytes, slow heart, increase diastolic coronary blood flow, decrease myocardial O2 demand
beta blockers effect (3)
anti-ischaemic, anti-arrhythmic, reduced risk of recurrent MI
beta blockers side effects (6)
worsen heart failure, fall in bp, fall in hr, cold peripheries, wheeze, fatigue
ace inhibitors MOA (2 steps)
- inhibit ACE in RAAS
2. angiotensin 1 can’t be converted to angiotensin 2
ACE inhibitors effect (2)
bp fall, potassium rise
ACE inhibitors side effects (6)
affect kidneys, must check creatinine for rise, fall in Hb, cough, rash, angio-oedema
types of diuretic (4)
loop, thiazide, potassium sparing, antidiuretic hormone antagonist
label the sites of diuretic action diagram (I)
done
loop diuretics MOA
block Na+/K+/2Cl- cotransporter in thick ascending loop of Henle
thiazide diuretics MOA
block Na+/Cl- cotransporter in distal convoluted tubule
potassium sparing diuretic MOA
prevent secretion of potassium in urine by blocking Na+/K+ pump and aldosterone
ADH antagonist diuretic MOA
bind to vasopressin receptors, block action of ADH
loop diuretics have a high ceiling, meaning the
higher the dose, the stronger the effect
loop diuretics examples (3)
frusemide, bumetanide, torasemide
loop diuretics side effects (3)
hyponatraemia, hypokalaemia, hyperuricaemia (can lead to gout)
thiazide diuretics have a low ceiling, meaning that
increasing dose beyond certain point has no further diuretic effect
thiazide diuretics examples (3)
bendroflumethiazide, metolazone, chlorthalidone
thiazide diuretic side effects (2)
loss in sodium, potassium and magnesium. increase in urate and calcium.
label the diagram (J)
done
label the diagram of the typical clinical course for diuretics (K)
done
typical clinical course for diuretics (4 steps)
- give IV frusemide
- ACE inhibitor
- switch to oral diuretic
- start beta blocker
basic medications in hypertension are (4)
A - ACE inhibitors
B - beta blockers
C - calcium antagonists
D - diuretics
calcium channel blocker type we must commonly use
dihydropyridines
examples of dihydropyridines (2)
amlodipine, nefidipine
MOA of calcium channel blockers
vasodilation, dihydropyridines slow hr so useful in angina
calcium channel blockers side effects (3)
ankle swelling, tachycardia, flushing
calcium channel blockers must not be used in people with (2)
LV dysfunction, heart failure
in heart failure patients we measure
brain natriuretic peptide as it is a good measure of cardiac function
natriuretic peptides lead to (3)
natriuresis, diuresis, lowered bp
