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Cardiovascular Lectures > L3: Hypertension: Mechanisms and Consequences > Flashcards

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
Q

What drugs affect CO?

A

Beta blockers –> heart rate
Diuretics –> preload, total body water –> stroke volume -venous return
Beta blockers + Ca2+ channel blockers –> contractility –> SV - venous return

26
Q

What is the ABCD treatment for hypertension?

A

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
Q

Second line treatment for hypertension

A
  • alpha-adrenoreceptor antagonists/ centrally acting sympatholytic agents
  • K+ channel agonists
  • Aldosterone antagonist
28
Q

What medicines can increase hypertension?

A
  • NSAIDs and oral contraceptives

- should not be given to hypertensives

29
Q

What are the general 3 steps to treat hypertension?

A

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
Q

Who should not be prescribed ACE or ARB? What is recommended instead?

A
  • Females of reproductive age should not be prescribed

- INSTEAD beta blockers (e.g. metoprolol) or calcium channel blockers (e.g. felodipine) are recommended

31
Q

When should beta blocker in combination be considered?

A

Ischaemic heart disease or heart failure present - reduce mortality
Atrial fibrillation present - for rate control

32
Q

What medication should be recommended if peripheral vascular disease is present?

A

ACE inhibitor - to slow disease progression

or Calcium channel blocker - vasodilate peripheral arteries

33
Q

What is role of ACE inhibitors?

A
  • 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
Q

Side effects of ACE inhibitors

- what can it be changed to?

A

Irritable dry cough - particularly in females

- can change to ang II receptor blockers (less side effects)

35
Q

What is the role of calcium channel blockers?

A

vasodilation

  • targets blood vessel
  • targets cardiac muscle
36
Q

When should ACE inhibitor be prescribed first line?

A

if patient has diabetes or evidence of end organ damage

Cardiovascular Lectures (2 decks)

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