Hypertension Flashcards
Normal Blood pressure
120/80
Hypertension is worlds number 1 cause of preventable mortality/morbidity?
True
False
true
would a rise in 2mmHg cause an increase in mortality?
Yes
7% in mortality from ischaemic heart disease
10% in mortality from stroke
the graded relationship between BP and CVD
starts from 115/75
if the patient has sitting blood pressure 135/85 the risk of cardiovascular death is almost doubled regardless of age.
Blood pressure prevalence
>65
important risk for myocardial infarction, heart failure, stroke and cardiovascular disease.
accounts for 41% of all cardiovascular disease deaths.
organs hypertension affects on brain
Brain - cerebrovascular accident, stroke, haemorrhage
organs hypertension effects on heart
heart - lapidary hypertrophy. coronary heart disease, congestive heart failure, myocardial infarction
organs hypertension effects on eyes
eyes causing retinopathy
organs hypertension effects on blood vessels
peripheral vascular disease - blood supply to arms and legs, causing peripheral vascular disease.
organs hypertension effects on kidneys
renal failure, the requirement for transplantation, proteinuria.
risk factor for hypertension
smoking
can blood pressure vary throughout the day?
yes typically fluctuates during day likely due to:
stress physically
mental stress.
stage 1 hypertension
- clinic bp 140/90
Ambulatory bp (home) 135/85
stage 2 hypertension
- clinic bp 160/100
Ambulatory bp (home) 150/95
stage 3 or severe hypertension
- clinic bp 180/120
what is ABPM
ambulatory bp measurement - takes average 30 measurements both day time and night time
in 80-80% of cases no cause can be found - what hypertention type is this?
primary hypertension
what type of hypertension has a cause?
secondary hypertenion. e.g. chronic renal disease, renal artery stenosis
endocrine disease e.g. Cushings, primary hyperaldosteronism (Conns syndrome) phaeochromocytoma, Glucocorticoid-remediable aldosteronism (GRA)
Cushing’s syndrome
occurs when your body makes too much of the hormone cortisol over a long period of time.
Cortisol also helps maintain blood pressure and regulate blood glucose,
Primary aldosteronism (PA), also known as primary hyperaldosteronism or Conn’s
a hereditary form of primary hyperaldosteronism and the most common monogenic cause of hypertension
ectopic expression of aldosterone synthase activity hyperaldosteronism and suppression of angiotensin II-stimulated aldosterone production in the zona glomerulosa. (kidney)
pheochromocytoma
a noncancerous (benign) tumour that develops in an adrenal gland.
what age is likely for secondary hypertension?
younger - 20s
all under the age of 40 should be referred to a specialist to investigate ? secondary
risks of hypertension
smoking
diabetes
renal disease
males over females
hyperlipidaemia
previous myocardial infarction or stroke
left ventricular hypertrophy
what are contributors to blood pressure?
cardiac output - stroke volume, (amount blood pumped with each stroke) and heart rate
Peripheral vascular resistance - resistance that vasculature provides to slow cardiac output or blood flow.
sympathetic nervous system
* each can be manipulated by drug therapy*
How is the sympathetic nervous system in blood pressure?
SNS produces venoconstruction = peripheral resistance
reflex for tachycardia = increase stroke volume + cardiac output
stimulated RAAS - angiotensin 2 and aldosterone
SNS are rapid and account for second to second blood pressure control
importance of RAAS for blood pressure
RAAS pivotal for long term bp control
raas responsible for: maintaining sodium balance, controlling blood volume, control of blood pressure
what stimulates RAAS to do with blood pressure?
fall in bp; fall in circulating vol; sodium depletion
- stimulate renin release from juxtaglomerular apparatus
renin converts angiotensin to angiotensin 1
angiotensin 1 converts to angiotensin 2 by (ACE)
what factors would prompt us to think a patient has secondary hypertension?
severe/resistant hypertension (non-reactive to several medications given)
they are a child/adolescence
worsening of previous stable hypertension
malignant hypertension
no other risk factors identified and they are under age 30
investigations for secondary hypertension
renal function and urinalysis
renal imaging: ultrasound, MRA renal arteries
Aldosterone to renin ratio (ARR)
24-hour urine or catecholamines/metanephrines looking for pheochromocytoma or paraganglioma (only if clinical suspicion)
causes for secondary hypertension : renal
renal disease 20%) - chronic pyelonephritis (Kidney infection )
fibromuscular dysplasia
renal artery stenosis - common atherosclerotic disease; polycystic kidneys
causes for secondary hypertension - drug induced
drug-induced - NSAIDs, combined oral contraceptive
corticosteroids cocaine and other stimulants
causes for secondary hypertension - pregnancy
gestational hypertension
pre-eclampsia
causes for secondary hypertension - endocrine
- primary hyperaldosteronism (conns)
Cushings
pheochromocytoma
vascular - coarctation aorta
sleep apnoea
what age would you not expect to see coarctation of the aorta (cause secondary hypertension)
rarely over 35 as often died by then
focal fibromuscular dysplasia
- often young woman. no atherosclerotic disease
stenosis
treat single stent to affected kidney = normalise bp
what symptom/indigation on inspection would you expect of focal fubromuscular dysplasia?
bruit ofer the affected kidney
**bruit a sound, especially an abnormal one, heard through a stethoscope; a murmur. described as blowing sounds*
multifocal fibromuscular dysplasia
significant hypertension beaded appearance
requires triple therapy: angioplasty
bilateral 30% cases
polycystic kidney disease
often genetic
cysts form - necessary for remove kidneys and have transplant or dialysis
this is spontaneous (mutation)
pheochromocytoma
tumour adrenal gland (often benign)
may present accelerated hypertension, resistant hypertension, headaches, flushing, sweating, palpitations. Genetic predisposition.
essential to involve a multidisciplinary team with endocrinologists and surgeons
long term follow-up and monitoring essential
Cushings disease
malignant tumour on the left adrenal gland
treat chemotherapy and regular antihypertensive therapy.
what does differing blood pressures on either arm potential indicate?
e.g. 225/124 mmHg R 175/100 L
aortic coarctation
*rarely hear a murmur
not obvious on ECG
best to have MRI
nocturnal dip with prolonged hypertesnion
the problem if prolonged hypertension throughout the day will cause damage they will lose the nocturnal dip
Loss of nocturnal dip
persistently high even sleeping or higher.
cause = night worker? or person who had lost it.
high nocturnal poor prognostic
need night medications
masked hypertension
normal blood pressure leaves medical staff and rises.
carries significant cv event risk
first assessments for hypertensive patients
- History - previous MI, stroke - ischaemic heart disease
- smoker? - diabetic hypercholestraimia
- Family history - physical examination
hypertension - assessment for end-organ damage
ECH - for left ventricular hypertrophy
echocardiogram - for left ventricular hypertrophy
proteinuria - urine analysis
renal ultrasound
renal function test - creatinine, EGFR,
hypertension - what are the treatable causes (secondary)
common in young patients
- obesity - renal artery stenosis/FMD (Fibromuscular dysplasia)
- conns, cushings, pheochromocytoma
- coarction - drug-induced - sleep apnea
how to quantify risk hypertension
assign risk calculator/q risk
once assessed - set a target blood pressure
BHS suggest < 135/80-80mmHg
Treatment should be started at an overall CVD risk of 10%/10 years
treating hypertension
reasons
how?
reasons - reduced cerebrovascular disease by 40-50%
reduced MI by 16-30
treat - stepped approach
a low dose of several drugs
the approach minimises adverse events and maximises the patient outcome
What are NHS/BHS guidelines to reatment for hypertension?
Yong patients (high renin) A
Elderly (low renin) C D
A - ACE inhibitor/ARB
C - Calcium channel blocker
D- a diuretic - thiazide.
for stage 1 hypertension (135/85 abpm)
who do we offer hypertensive drug treatment to and what factors
under 80s with 135/85 and with:
target organ damage
- established cardiovascular disease
- renal disease
- diabetes
- 10 year vascular risk equivalent to or above 10%
for stage 2 hypertension (150/95)
who do we offer hypertensive drug treatment to and what factors
ABPM > 150/95
offer antihypertensive to any age with stage 2 hypertension
for elderly patients >80 with stage 1 hypertension and no other factors/comorbitities what do we do?
offer age 80 and over the same antihypertensive at age 55-80 taking into account comorbidities
but blood pressure target different in patients >80 years
target = 145/95
elderly more susceptible to side effects be pragmatic.
step 1 treatment hypertension in over 55 years and people of black/African or Caribbean family origin at any age
treatment =
calcium channel blocker
or a thiazide - like diuretic
step 1 treatment for patients under 55 years
(not African or Caribbean)
not child bearing age
offer ACE inhibitor or ARB
why would we avoid ACE1 /ARB treatment to under 55s who are:
African or Caribbean
childbearing age
African or Caribbean - less effective and significant risk angioedema (glottis, epiglottis, mouth face swelling of the area beneath the skin or mucosa) can be fatal
childbearing - teratogenic initial stages pregnancy and fetotoxic in later stages of pregnancy
step 2 treatment hypertension
add thiazide type diuretic such as (indapamide to CCD or ACE1/ARB)
pregnancy hypertension treatment?
Hydralazine
Methyldopa
Labetalol
Nifedipine
**Hypertensive Mums Love Nifedipine**
treat stage 3 hypertension (meds)
Add Calcium channel blocker, Ace1, diuretic together
treating resistant hypertension what treatment/considerations?
are there compliance issues (common)
higher dose thiazide-like diuretic if potassium level is higher than 4.5mmol
further diuretic therapy with low dose spironolactone (25mg once daily) if potassium is <4.5mmol
medications ACE inhibitors
ramipril
perindopril
competitively inhibit the action of angiotensin-converting enzyme
contraindications to ACE inhibitors
renal artery stenosis (renal failure or infarction)
impaired renal function
hyperkalaemia
hypotension
teratogenic in pregnancy
drug to drug interaction of ace inhibitors
NSAIDs - precipitate acute renal failure
potassium supplements - hyperkalaemia
potassium-sparing diuretic - hyperkalaemia
Angiotensin 2 antagonists (ARBS)
losartan, valsartan, candesartanm irbesartan
anhiotensin 2 antagonist competitively block action of angiotensin 2 at angiotensin 1 receptor.
advantage - fewer side effects e.g. cough.
Calcium channel blocker medications
adverse reactions + contraindications
Amlodipine felodipine - vasodilator - reduce peripheral resistance
verapamil diltiazem - reduce heart rate (rate-limiting) produces some vasodilation
block the l-type calcium channel in monocytes of vasculature and heart
drug reactions: flushing, headache, ankle oedema, indigestion reflux
contraindications - acute MI, Heart failure, bradycardia
- rate-limiting agents also cause - bradycardia - constipation
medication treatment thiazide type diuretics
reactions risk
indapamide, chlorthalidone
commonly first-line treatment in mild-moderate hypertension in people of African origin.
can be used in combination with any other antihypertensive agents
proven beneficial in reducing the risk of stroke and myocardial infarction
low dose not common side effects = gout and erectile dysfunction
low sodium
what are other less commonly used agents for hypertension (medications)
alpha-adrenoceptor antagonist - doxazosin
centrally acting agents - methyl dopa, moxonidine
vasodilator - hydralazine, minoxidil
best order treating hypertension ? 55 years
start calcium channel blocker
then thiazide-type diuretic
then add ace inhibitor
then add beta-blocker
then if not working add less common drug
first-generation beta blocker
beta 1 and 2 blockers
- timolol - propanolol (also treat migraines)
- nadolol - pindolol -sotalol (also blocks potassium)
side effect - increase intraoccular pressure = glaucoma
bronchoconstriction - asthma problem
2nd generation beta-blocker
beta 1 receptor
esmolol atenolol metopralol bisoprolol acebutalol
less likely to cause hypoglycaemia
ok for asthma COPD
what conditions can generation 1 and 2 beta-blockers also treat?
anxiety and thyroid storm
generation 3 beta-blockers
beta 1 and alpha 1 blocker
labetalol carvedilol
cause vasodilation
can be used for peripheral vascular disease and given in pregnancy
and hypertensive crisis
treatment of hypertension for young patients
start ACE1
(if childbearing age woman start calcium channel blocker or beta-blocker
then thiazide-type diuretic
then calcium channel blocker
then beta-blocker
signs of gestational hypertension
hypertension
no proteinuria
signs preeclampsia
bp rises severely from 20 weeks gestation
bp>40/90
and proteinuria >300mg/24hours
meds for chronic hypertension pre-pregnancy
hypertensive Mums love nifedipine
nifedipine methyl dopa labetalol atenolol
treating gestational hypertension
depends on the trimester of pregnancy
nifedipine modified release, methyl dopa, labetalol
treatment for preeclampsia
treatment for gestational methyl dopa, labetalol, nifedipine
plus iv labetalol or hydralazine or esmolol
acute severe hypertension types
hypertensive urgency
hypertensive emergency
acute severe hypertension types hypertensive emergency:
hypertensive urgency
hypertensive emergency - severely elevated bp >180/120 with evidence of acute target organ damage. require admission for bp reduction
called malignant hypertension
cardiac failure, retinopathy e.g.
acute severe hypertension types hypertensive urgency :
hypertensive urgency
severely elevated bp with NO evidence of acute target organ damage.
patients do not need admission and can be started on dual oral therapy and assessed after 24 hours
also called accelerated hypertension
(amlodipine 5 mg and atenolol 25 mg daily)
*pic below calcium channel blocker - dipine*
treatment of hypertensive emergency
lower systolic bp by 10-20% within the first hour and then to 160/100mmHg over subsequent 6 hours
more aggressive lowering associated with increased morbidity and mortality.
change to oral meds once target bo achieved wean off iv meds over next 12-24 hours
dont give ARB ACE either
what is indicator for rapid BP loweing?
normally you do NOT do this
you only do for ischaemic stroke whos bp > 195/110mmHg who are eligible for/who received thrombolysis within previous 24 hours OR bp 220/120mmHg and not ELIGIBLE FOR THROMBOLYSIS
aortic dissection - systolic bo should be rapidly lowered to target between 100-120mmHg systolic
what is orthostatic hypotension?
bp dro when shifting to a standing
decrease of 20mmGm systolic and/or a diastolic pressure of 10mmHg within 3 minutes of standing,.
what is constitutional hypotension
young people normally have
permanently low bp
causes of orthostatic hypotension
- age
diabetes
antihypertensive drugs
auto-immune systemic disease
neurological syndromes: pure autonomic failure, multiple systems atrophy, Parkinson’s disease
if you see ST elevation - what is the best move?
primary
reestablish blood flow - go to cath lab for stent PCI (percutaneous coronary intervention)
give thrombolysis blood thinner if you cannot get to cath lab.
risk of thrombolysis
bleeding
avoid when had recent stroke haemorrhage or intracranial bleed. recent surgery, on a blood thinner. outweigh the risks
investigations got MI
repeated ECg
check biomarkers - troponin renal function, cholesterol, harmoglobin
treatment for pain in MI
nitrates (GTN) - dilates or relaxes coronary artery (wont help complete blockage artery)
morphine for pain
treatments for MI (initial)
platelets
asprin + 2nd antiplatelet clopidogrel tecagrrlor presugel
anticoagulant - heparin or low molecular weight heparin or fondaparinux
other treatments to get patients started on for MI
beta-blockers - reduce work on heart, reduce risk of another event
statin - helps lower cholesterol
ace inhibitor - helps heart recover
normal blood flow is __
laminar
in blood cells where does the plasma flow and where do cells flow?
plasma on outer of lumen, cells central
is regard to blood flow, what is stasis?
stagnant blood flow
in regard to blood flow, what is turbulent flow?
abnormal, forceful and unpredictable flow
what is a thrombus
formation of solid mass from the constituents of blood within vascular system during life
normal artery
big lumen nothing wrong with intima, media or adventitia
atheromatous coronary artery
lumen is smaller at rest, reducesin size. lumen taken up by atheromatous plawue
part calcification causing destruction
what is the pathogenesis of thrombosis
endothelial injury
stasis or turbulent blood flow
hypercoagulability of blood
pathogenesis of thrombosis
atheromatous coronary artery turbulent blood flow loss of intimal cells, denuded plaque collagen exposed, platelets adhere fibrin meshwork RBCs trapped alternating bands (lines of Zahn) further turbulence and platelet deposition propagation consequences
the biggest risk for atherosclerosis
hypocholestraemia
histology fibrin buildup
what is ischaemia
lack of blood supply to tissuea leading to inadequate o2 supply (hypoxia)
types of hypoxia
hypoxic hypoxia
anaemic hypoxia
cytotoxic hypoxia
stagnant hypoxia
factors affecting 02 supply
1 inspired o2 2 pulmonary function 3 blood constituents 4 blood flow 5 integrity of vasculature 6 tissue mechanism
what is the cause of ischaemic heart disease in relation to blood flow
supply issues: coronary artery atheroma, cardiac failure (flow) pulmonary function - other disease or pulmonary oedema (left ventricular failure) anaemia, previous MI
Demand issues: heart has high intrinsic demand, exertion/stress
what is atheroma/atherosclerosis
localised accumulation of lipid and fibrous tissue in intima of arteries
effects of ischaemia
cell - different tissue variable 02 requirement and variably susceptible to ischaemia
cells with a high metabolic rate
cells with low metabolic rate
effects of ischaemia
dysfunction
pain
physical damage
specialised cells
infarction
what is infarction
ischaemic necrosis with a tissue/organ in living body produced by occlusion of either arterial supply or venous drainage
aetiological examples of infarction
thrombosis
embolism
strangulation e.g. guy
trauma - cut/ruptured vessel
appearance of infarcts after 24-48 hours?
pale infarcts: myocardium, spleen, kidney solid tissues
red infarcts: e.g. lung, liver, loose tissue, previously congested tissue; second/continuing blood supply, venous occlusion
immediate treatment for MI
