L3: Hypertension: Mechanisms and Consequences Flashcards

1
Q

What is systemic arterial pressure?

A

Pressure coming out of left side of heart supplying oxygenated blood to all organs

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2
Q

What happens when you have hypertension?

A
  • increased wall tension
  • too much sympathetic activity and Ang II
  • remodelling of heart: thicker, stiffer wall, smaller lumen
  • poor supply to end organs - heart needs to work harder
  • increase in afterload, arterial damage
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3
Q

Risk factors for CVD

A
  • Asymptomatic w no known risks - 1st screening M 45 yrs, F 55 yrs
  • High risk (genetics or co-morbidities) - 1st screening M 35yr, F 45 yr

BP > 170/100 mmHg - treat regardless
Total CVD risk is 10>20% - treatment options, initiate lifestyle changes
Total CVD risk > 20% - strongly recommend BP lowering treatment

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4
Q

What are the determinants of mean blood pressure? Equation?

A

P = CO (cardiac output) x R (peripheral resistance)

CO: total blood flow
- determined by tissue/body needs
R: increasing total R leads to upstream increase in pressure to maintain flow

If CO increases, resistance must decrease to maintain arterial pressure

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5
Q

What is normal mean systemic arterial pressure? systolic? Diastolic?

A

Mean: 100mmHg
Systolic: 120 mmHg
Diastolic: 90 mmHg

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6
Q

What can change CO?

A
  • volume in the system (depends on kidneys) -
  • heart: how fast and strong its beating
  • nerves and hormones
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7
Q

What determines R?

A
  • SNS activity
  • hormones
  • local factors: O2, pH
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8
Q

What causes hypertension?

A

Increase in CO

increase in Systemic Vascular Resistance (SVR)

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9
Q

What determines resistance?

A

R is proportional to

  1. tube length
  2. viscosity of fluid

Inversely proportional to
3. radius raised to fourth power

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10
Q

r4 factor - relationship btwn radius and resistance

A

small change in radius of blood vessels = large effect on resistance
- doubling radius increases flow 16x

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11
Q

What controls contraction of vascular smooth muscle?

A
  1. Vascular endothelial cells
  2. mediators released locally from sympathetic nerve terminals (e.g. noradrenaline)
  3. Circulating hormones (e.g. vasopressin, ang II )
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12
Q

Equation for CO (cardiac output)

- what affects CO

A

CO = HR x SV

  • increasing HR = increases CO
  • increasing preload (filling of heart) = increases CO
  • increasing afterload (arterial pressure) = increases CO
  • increased sympathetic activity or Ca2+ availability = increases contractility and thus SV
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13
Q

What is the role of increased sympathetic activity ?

A
  • send info from brain to heart to contract more
  • increased heart CO
  • act on kidney : constrict blood vessels and secrete renin –> increase AngII –> increase blood volume –> increase CO
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14
Q

What do we target to reduce blood pressure?

A

reduce AngII
reduce sympathetic activities
reduce blood volume
- helps reduce CO and thus BP

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15
Q

What happens when Beta adrenergic receptors are stimulated?

A

Beta adrenergic receptor stimulation causes increased intracellular Ca2+ –> increases force development of heart (more contraction) –> increased SV (stroke volume)

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16
Q

What are the determinants of pulse pressure?

- equation

A

Pulse pressure (PP) = systolic pressure (Ps) - diastolic pressure (Pd)

Systolic pressure - depends on aortic compliance + SV

Diastolic pressure - depends on aortic compliance + diastolic run off:
Heart rate, TPR

17
Q

Aortic pulse pressure - importance of aorta and artery compliance

A

Systole: aorta stretches to absorb blood
Diastole: flow continues due to compliance (elastic recoil) of blood vessels

More compliant large blood vessels = smaller pulse pressure
Compliance of arteries - ensure capillary flow continues throughout cardiac cycle
Once reaching small arterioles = flow is non-pulsatile

18
Q

What happens to pulse pressure if you have poor compliance and stiff arteries?

A

larger pulse pressure - high systolic pressure but low diastolic pressure

19
Q

Relationship btwn compliance of aorta and age

A

Compliance of aorta decreases with age

  • pulse pressure increases
  • systolic pressure increases + diastolic pressure may decrease
20
Q

Effect of increased stroke volume on arterial pulse pressure

A

more volume = higher pulse pressure

21
Q

What is SV determined by?

A
  • preload
  • afterload
  • chronotropy
  • inotropy
22
Q

What is diastolic pressure determined by?

A

Determined by diastolic run off - ability of blood to flow forward
Dependent on:
TPR : increased resistance increases diastolic pressure
HR: increased HR increases DP

23
Q

Recommended lifestyle changes for treatment of hypertension

A
  1. weight reduction
  2. moderation of alcohol consumption
  3. Diet - high fruit + veges/low fat
  4. salt restriction
  5. Regular exercise
  6. Smoking cessation
24
Q

What drugs affect total TPR?

A
alpha-adrenergic blockers 
Ang II receptor blockers 
ACE inhibitors 
Ca2+ channel blockers 
Vasodilators (nitrates) 
Diuretics
25
What drugs affect CO?
Beta blockers --> heart rate Diuretics --> preload, total body water --> stroke volume -venous return Beta blockers + Ca2+ channel blockers --> contractility --> SV - venous return
26
What is the ABCD treatment for hypertension?
A: angiotensin pathway: ACE inhibitors or Angiotensin type 1 receptor blockers B: beta blockers (via effect on HR/CO) --> NOT recommended as first choice as they dont reduce risk of stroke and are poorly tolerated - not targeting vasculature that causes stroke only target heart - only for pregnant women or people with heart failure C: calcium channel blockers D: diuretic (thiazide) - caution in diabetics
27
Second line treatment for hypertension
- alpha-adrenoreceptor antagonists/ centrally acting sympatholytic agents - K+ channel agonists - Aldosterone antagonist
28
What medicines can increase hypertension?
- NSAIDs and oral contraceptives | - should not be given to hypertensives
29
What are the general 3 steps to treat hypertension?
Step 1: for primary prevention in patients w uncomplicated hypertension = ACE inhibitor or Calcium channel blocker Step 2: combine ACE inhibitor or ARB with Calcium channel blocker Step 3: Add thiazide diuretic e.g. indapamide (targets kidneys)
30
Who should not be prescribed ACE or ARB? What is recommended instead?
- Females of reproductive age should not be prescribed | - INSTEAD beta blockers (e.g. metoprolol) or calcium channel blockers (e.g. felodipine) are recommended
31
When should beta blocker in combination be considered?
Ischaemic heart disease or heart failure present - reduce mortality Atrial fibrillation present - for rate control
32
What medication should be recommended if peripheral vascular disease is present?
ACE inhibitor - to slow disease progression | or Calcium channel blocker - vasodilate peripheral arteries
33
What is role of ACE inhibitors?
- reduce production of AngII (vasoconstrictor) - reduces vasoconstriction - acts on kidneys to reduce sodium retention - reduce blood volume - act on heart long term --> prevent remodeling of heart
34
Side effects of ACE inhibitors | - what can it be changed to?
Irritable dry cough - particularly in females | - can change to ang II receptor blockers (less side effects)
35
What is the role of calcium channel blockers?
vasodilation - targets blood vessel - targets cardiac muscle
36
When should ACE inhibitor be prescribed first line?
if patient has diabetes or evidence of end organ damage