Lecture 8: Hypertension Flashcards
1
Q
What is hypertension?
A
- Persistent raised blood pressure
- Normal blood pressure: 120/80 mm Hg
- Treat when systolic > 140
- Diastolic > 90
2
Q
How do we measure BP?
A
Measure in the brachial artery in the arm
3
Q
What is white coat hypertension?
A
- BP may be artificially high bc you are being checked medically, making you nervous
- Can be circumvented via ambulatory blood pressure monitoring (ABPM)
- Inflates once an hour during the day n night
- BP measured automatically n transferred onto a disk
- Can also be overcome w home BP measurement but they’re not calibrated
4
Q
Describe the diagnosis of hypertension in the clinic
A
- High BP -> 140/90 mmHg or higher
- ABPM: ensure at least 2 measurements per hour during person’s waking hours
- Average value of at least 14 measurements taken during person’s waking hours
5
Q
Describe the diagnosis of hypertension in the home blood pressure monitoring (HBPM)
A
- For each BP recording, 2 consecutive measurements are taken, at least 1 minute apart n with the person seated
- BP is recorded twice daily, morning n evening
- BP recording continues for at least 4 days, ideally for 7 days
6
Q
What are you measuring when you take a blood pressure?
A
- Ausculation
- Listening to any sounds from the body (e.g. heart)
- Korotkoff sounds
- Inflate cuff n use statoscope to listen to brachial artery
- Inflate cuff so high to stop blood flow -> no sound
- Slowly let pressure off -> pressure falls
- Point when you hear the first sound (systolic BP)
- Pressure in cuff is low enough to allow blood to go thru = systolic BP
- Sound increases in volume [more blood blow]
- Turn pressure down further -> hear no more sound [no more turbulence] = diastolic pressure
7
Q
What is mean arterial pressure?
A
- MAP = (SP + (2 * DP)/3)
- Not just average BP as uneven amount of time spent at rest
- ~2/3 diastolic and ~1/3 systolic
- Mean closer to diastolic
8
Q
What are the causes of hypertension?
A
- 90-95% primary essential hypertension
- Probably a complex genetic disorder
- Secondary hypertension
- Renal causes [increase BP -> not providing volume of liquid]
- Endocrine disorders [hormones that cauese artery restriction]
- Aortic coarctation [part of the aorta is occluded]
- Preeclampsia (pregnancy)
- Neurogenic hypertension (overactivity of the SNS)
- Endocrine tumours: primary hyperaldosteronism, phaeochromocytoma, renin secreting tumour
- Drug induced: amphetamines, NSAIDS, steroids
9
Q
Why treat hypertension?
A
- Hypertension increases the risk of
- Stroke (occlusion in the brain)
- Coronary events (myocardial infarction, angina)
- Aortic aneurysm (bulging in blood vessel, aorta [pressure] -> fatal)
- Heart failure
- Renal failure
- End organ damage
10
Q
Symptoms of hypertension
A
- Headaches [high pressure]
- Dizzy
- Flushing
- Awareness of heart beat
- Nosebleeds
- None (most common): silent killer
11
Q
Signs of hypertension
A
- Level of blood pressure
- Cardiomegaly/left ventricular hypertrophy [heart has to work w high pressure -> increase in muscle mass]
- Can be observed in an echocardiogram
- Abnormal renal function
- Blood test
- Proteinuria or haematuria
- Urine test
- Hypertensive retinopathy
12
Q
How is hypertension managed?
A
- Patient education/lifestyle changes
- Stop smoking
- Loss of weight
- Exercise
- Reduce salt intake
- Diet
- Relaxation therapy
- Drug treatment
- Surgery
13
Q
What is the effect of excess weight on BP?
A
- Weight n BP are linked
- Likely that wight interacts w various factors controlling BP at different points over lifetime
14
Q
What determines BP?
A
- How much blood is ejected
- Determined by cardiac output
- Heart rate
- Stroke volume
- Filing pressure (Starling Law’s: more blood that comes back to heart, stretches the fibers in heart -> bigger CO)
- Contractility (determined by SNS)
- Total peripheral resistance
- Diameter of arterioles
- Small lumen -> higher pressure
- Determined by cardiac output
15
Q
What are the 2 major mechanisms for controlling BP?
A
- Baroreceptor/SNS
- Controls BP minute to minute
- ECF volume/plasma renin activity
- Longer term effects
16
Q
Describe the baroreceptor reflex
A
- Baroreceptors are located in the carotid sinus n aortic arch
- When there is a fall in BP -> decrease frequency of nerve impulse in baroreceptors -> inhibit parasympathetic nervous system n stimulate SNS -> increase in heart rate
- RESULT
- Increases heart rate n artery contraction [β receptors in the heart] ->increase in CO n total periphery resistance -> increase in BP
- Increase in venous return -> stretching of heart muscle -> increase cardiac output
- EXAMPLE
- Hemorrhage/loss of blood, baroreceptors keep alive
- Fast heart rate -> try to increase BP to maintain organs
- Hemorrhage/loss of blood, baroreceptors keep alive
17
Q
What things can you aim to change to reduce BP?
A
- Cardiac output (stroke volume * heart rate)
- Diuretics: reduce BP
- ACE inhibitors: reduce blood volume
- Angiotensin II receptor antagonists: reduce blood volume
- β-blockers: reduce heart rate n contractility
- Reduce total peripheral resistance
- Vasodilators
- Calcium channel antagonists
- ACE inhibitors
- Angiotensin II receptor antagonists
- α-adrenoreceptor blockers
- Some drugs do both: ACE inhibitors, angiotensin II receptor antagonists
18
Q
How do ACE inhibitors n angiotensin II receptor antagonists work?
A
- Renin-angiotensin-aldosterone system
- Liver secretes angiotensinogen (inactive) into blood stream
- Converted by renin, which is secreted by the kidney, into angiotensin I (inactive)
- Angiotensin I converted to angiotensin II (active)
- Causes adrenal cortex to cause aldosterone release
- Acts on BP
19
Q
What are the effects of angiotensin II?
A
- Vasoconstriction of arterioles
- Stimulates Na+ reabsorption in PCT
- Cl- and water follow passively
- Stimulates aldosterone secretion (adrenal cortex)
- Stimulates vasopressin secretion from posterior pituitary gland
- Stimulates thirst
20
Q
What are ACE inhibitors?
A
- All ACE inhibitors end w “pril” suffix
- Reduce arterial resistance n blood volume
- Causes rapid fall in BP n persistent dry cough
- Block the breakdown of bradykinin (mediator released in response to inflammation)
- Bradykinin is broken down to inactive peptides via ACE
- Thus ACE inhibitors block this process -> buildup of bradykinin -> can persist in throat -> dry cough
21
Q
What are angiotensin II receptor antaogonists?
A
- Angiotensin II receptor antagonists
- End w “sartan” suffix
- Osartan, candesartan, valsartan
- Well tolerated side effect profile
- Once daily dosing
- No significant adverse effects
- Cost effects
22
Q
What are Ca channel antagonists?
A
- Block L-type Ca channels
- Dihydropyridines end w “dine”
- Vasodilators -> reduce TPR
- Blocking Ca channels in muscles -> prevents contractions
- Unwanted side effects
- Headaches
- Flushing
- Ankle swelling
23
Q
What are β-adrenoreceptor blockers?
A
- e.g. atenolol (lol suffix)
- Used to be first line therapy but not anymore [significant reduction in blood pressure but ppl were still dying, other agents are more effective at reducing the incidence of stroke n CVS mortality]
- Mode of action unclear but reduce cardiac output, alter baroreceptor reflex sensitivity
- May also suppress renin secretion
- Contra-indicated: asthma sufferers
- β-receptors in lungs that cause dilation in bronchioles, block receptors -> more likely to get asthma attack
- Can cause peripheral vasoconstriction -> cold hands n feet
23
Q
Explain the reflex tachycardia
A
- Alpha 1 are in blood vessels
- Alpha 2 are presynaptic n inhibit noradrenaline release
- Non-selective alpha antagonists block both alpha 1 n alpha 2 -> more noradrenaline -> activates β receptors -> increase in heart rate
23
What are thiazide diuretics?
- Cause mild diuresis
- Bendroflumethiazide
- Work at the beginning of the distal convoluted tubule in kidneys to increase water n sodium loss
- Work to reduce blood volume, CO n mean arterial pressure [more excretion from the kidney]
- Take in the morning to avoid nocturnal diuresis
- Use low doses
- Cause hypokalemia
- Most effective in elderly or patients of African origin
24
What is malignant (accelerated) hypertension?
- V high BP (diastolic > 140 mm Hg)
- Medical emergency
- Symptoms
- Nausea
- Dizziness
- Headache
- Blurred vision
- Kidney failure
- Retinopathy
- Heart failure
- Treatment
- IV vasodilators
- Oral β blockers
- Calcium antagonists
- Not ACE inhibitors (immediately) as rapid fall in BP could lead to cerebral infarction n blindness
