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Sophie - Applied Physiology & Pharmacology Year 2 > 52.1 The Control of Systemic Arterial Blood Pressure > Flashcards

52.1 The Control of Systemic Arterial Blood Pressure Flashcards

1
Q

What provides short-term regulation for arterial blood pressure?

A

Baroreceptor reflex
circulation as a closed system

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2
Q

Describe the receptors, ganglia and afferent nerves involved in the baroreflex.

A

Carotid sinus baroreceptors:

  • Via the petrosal ganglia
  • Glossopharyngeal nerve (IX)

Aortic arch baroreceptors:

  • Via the nodose ganglia
  • Vagus nerve (X)
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3
Q

What type of receptors are involved in the baroreflex?

A

Baroreceptors -> These detect transmural pressure, not flow

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4
Q

What are the atrial baroreceptors?

A

↑-pressure receptors in carotid sinus + aortic arch
*Innervated by glossopharyngeal/ vagus nerve respectively

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5
Q

What are the cardiopulmonary baroreceptors?

A

↓-pressure receptors in atria + adjacent large veins.

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6
Q

What does stimulation of the low pressure baroreceptors lead to?

A

Triggers secretion of ADH, angiotensin and aldosterone (increase salt and water reabsorption in the kidney to raise BP)

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7
Q

Where do the afferent nerves of the baroreflex synapse in the brain?

A

Nucleus tractus soltarius (NTS) -> This is in the medulla

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8
Q

Describe the efferent target organs of the baroreflex.

A

Parasympathetic:

  • Heart

Sympathetic:

  • Heart
  • Blood vessels
  • Kidney
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9
Q

Is the normal stability of ABP independent or dependent of local flows to organs and tissues?

A

It is independent of local flows to organs and tissues.

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10
Q

How is ABP regulated in the long term?

A

By renal pressure natriuresis (sodium excretion) and diuresis (water loss) to keep blood volume at 5L with circulation as an open system.

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11
Q

What is Guyton’s hypothesis/ physical equilibrium model?

A

Guyton’s hypothesis → ↑ renal perfusion pressure → ↑ Na+ excretion → ↑ water loss → ↓ ECF → ↓ BP

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12
Q

What is the mechanism of Guyton’s hypothesis?

A

Mechanism unclear → 2 hypotheses:
*↑ renal perfusion → ↑ GFR + Tubular flow rate → ↓ time for water/ Na+ reabsorption → ↑ excretion.
*↑ renal perfusion pressure → ↑ shear stress → ↑ NO production → ↑ medullary washout

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13
Q

Which system is in control of long term blood pressure regulation?

A

Renin-angiotensin-aldosterone axis (RAAS)

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14
Q

What is typical blood pressure?

A

120/80mmHg

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15
Q

Which blood pressure is defined as being hypertensive?

A

Three consecutive readings of over 140/90 at home (monitored 24 hours at home where two readings are taken every day)

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16
Q

What are the BP targets for those > 80, and <80?

A
  • <140/90 mmHg in patients aged <80
    *<150/90 in patients aged ≥ 80
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17
Q

How can hypertension be classified?

A

1o → essential HT (95%)
*Heterogeneous disease
*Precise + ultimate causes undetermined despite multiple genetic, hormonal, nervous, + environmental factors + lifestyle linked to HT.
2o → 5%. Known cause
*Renal disease (e.g. renal stenosis/ diabetic nephropathy)
*Endocrine disorders (e.g. Conn’s syndrome - 1o hyperaldosteronism/ Cushing’s disease - pituitary adenoma → ↑ ACTH → ↑ cortisol)

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18
Q

What are type 1 and type 2 HT according to NICE?

A

*Type 1 HT
<55 y/o
associated w ↑ renin levels + vasoconstriction
*Type 2 HT
>55y/o or African-Caribbean family origin
associated w/ ↓ renin levels + ↑ circulating volume

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19
Q

What is the first and second line treatment in hypertension to someone under 55 or a diabetic?

A

1) ACE inhibitor
2) Calcium channel blocker (amlodipine)
LOWERS TOTAL PERIPHERAL RESISTANCE

20
Q

What is the first and second line treatment for hypertension in someone who is over 55 or black and not diabetic?

A

1) Calcium channel blocker (amlodipine)
2) Thiazide like diuretic

21
Q

What are the other treatments that can be used alongside the specific first and second line treatments for hypertension?

A

USED AFTER FIRST AND SECOND LINE
Beta blockers
alpha blocker
spironolactone (antagonist of aldosterone receptor to stop increased reabsorption of sodium)

22
Q

What are the risk factors for hypertension? Why?

A

*Age: ↑ age → ↑ stiffness of arterioles → ↓ vascular compliance. Also nephron count ↓ w/ age → p-n curve shifted to right.
*Obesity: ↑ sympathetic activity
*Lifestyle: smoking/ alcohol
*Ethnicity: African-Caribbean heritage at ↑er risk (lower nephron count? Substitution in ENaC?)
*↑er Na+ intake
*Genetic: rare, some linkage analyses in familial HT have identified some rare monogenic HT causes
Genes associated w/ essential HT include ACE polymorphisms, AT-1 receptor gene, etc.

23
Q

How can you tell if someone has end organ damage as a result of hypertension?

A

ECG hypertrophy (enlarged QRS wave)
Looking at the back of the eye (haemorrhage of retinal blood vessels)

24
Q

Give an example of a tumour which can cause hypertension?

A

Pheochromocytoma

25
Q

How does pheochromocytoma lead to hypertension?

A
  • Phaeochromocytoma = tumour of chromaffin cells in the adrenal medulla –> significantly increased circulating levels of adrenaline and other catecholamines

-This can be severe enough to push the body into a hypertensive crisis, where blood pressure becomes so high (often >200mmHg systolic) as heart cannot effectively pump blood against the dramatically elevated systemic resistance

(vascular smooth muscle responding to α1 stimulation, dramatic stimulation of tachycardia and positive inotropy)

–> crashing organ perfusion for significant damage to multiple systems if not treated with adrenergic antagonists such as prazosin, and diuretics to help reduce blood pressure over time

26
Q

Why do individuals with Conn’s syndrome often have a high blood pressure?

A

Conn’s is caused by the overproduction of aldosterone, causing increased salt and water retention

27
Q

How does blood pressure change with age?

A

A reasonable approximation is:

  • Healthy systolic pressure increases linearly with age
  • Healthy diastolic pressure rises between the age of 20 and 50 and then progressively declines.
28
Q

What classifies as hypertension?

A

According to NICE, hypertension is confirmed when a patient has:

  • Clinic blood pressure of 140/90 mmHg or higher and
  • ABPM daytime average or HBPM average of 135/85 mmHg or higher (these are measures of blood pressure throughout the day)
29
Q

What are the benefits and disadvantages of treating hypertension?

A

The benefits of treatment are due to the fact that hypertension is associated with other diseases:

  • Stroke (both haemorrhagic and embolic)
  • Heart attack
  • Heart failure
  • Renal disease
  • Retinal disease

The disadvantages are that hypertension itself is usually asymptomatic and treatment often has side effects.

30
Q

Describe the changes in the cardiovascular system that lead to hypertension.

A
  • Remember: BP = SVR x CO
  • It has been observed that patients with pre-hypertension typically have a high cardiac output but normal systemic resistance
  • However, in patients with hypertension, there is usually normal cardiac output but increased systemic resistance
  • Thus, it has been suggested that the first event in the pathophysiology is usually an increase in cardiac output
  • This results in an increased ratio of wall : lumen in systemic blood vessels, to combat the change in wall stress
  • This leads to an increase in systemic vascular resistance

(Note: This might be controversial)

31
Q

What are the main afferent pathways that feed into the brain and are involved in cardiovascular control (aside from the baroreceptors in the aortic arch and carotid sinus)?

[IMPORTANT]

A
  • Cardiopulmonary receptors
    • In great veins, pulmonary artery and right atrium/ventricle
    • Detect filling of the heart
    • Inhibit heart rate and cause vasodilation, plus increased renal excretion -> Causing blood pressure and volume to fall
  • Arterial baroreceptors
    • In aortic arch and carotid sinus
    • Detect arterial pressure
    • Inhibit heart rate and cause vasodilation -> Causing blood pressure to fall
  • Muscle work receptors
    • Involve C fibres that are activated upon muscle activity (e.g. by potassium)
    • Increase heart rate -> Causing blood pressure to rise
  • Arterial chemoreceptors
    • In aortic arch and carotid sinus
    • Respond to decreased pO2 and pH, and increased pCO2
    • Increase heart rate and sympathetic stimulation of vasculature -> Causing blood pressure to rise
32
Q

When is the only time that the cortex of the brain is involved in the cardiovascular system?

A

It is indirectly involved via fainting. When you are shocked/scared by something, there is a massive drop in the vagus activity, so that blood pressure drops very much and you may faint.

33
Q

How does renal perfusion affect natiuresis?

A

Higher perfusion leads to higher salt excretion.

34
Q

How is the left ventricle affected in hypertension?

A
  • The left ventricle has a thick wall, and so it is dependent on the coronary arteries and their transmural branches for its oxygen supply.
  • The blood flow in these vessels is at its greatest during diastole, when the ventricular wall is relaxed and not compressing the coronary arteries.
  • In hypertension, the left ventricle hypertrophies to overcome the increased resistance.
  • This increases the risk of myocardial ischaemia for two reasons:
    • Decreased perfusion of the left ventricle since the wall compresses the coronary arteries
    • Increased metabolic demand of the heart to overcome the systemic resistance

(Note that this ventricular hypertrophy is not the same as ventricular dilation, which occurs when the ventricle cannot clear all of its blood in systole, so that it remains partly filled. If the ventricular hypertrophy leads to ischaemia, both may occur simultaneously.)

35
Q

How are arteries affected in hypertension?

A
  • There is a bidirectional causal relationship between hypertension and atherosclerosis:
    • Hypertension increases the risk of atherosclerosis (due to increased turbulence of blood flow)
    • Atherosclerosis increases the risk of hypertension (due to reduced elasticity of the wall)
  • There is a similar bidirectional relationship between hypertension and arterial wall thickening, where the muscular arterial wall thickens to sustain the increased pressure, which in turn leads to increased blood pressure due to reduced elasticity
36
Q

What kind of hypertension is most common in the elderly and why?

[IMPORTANT]

A
  • Isolated systolic hypertension -> This is where the systolic pressure is classed as high, but diastolic is normal or even low.
  • This is commonly seen among the elderly as there is increased deposition of calcium and collagen to the arterial wall, which reduces the compliance of the arterial vessels, decreased lumen-to-wall ratio, and increased thickening and fibrotic remodeling of the vascular intima and media.
37
Q

When the body wants to change blood flow to a certain tissue, does the ABP change?

[IMPORTANT]

A

No, it remains relatively constant. It can be seen as a reservoir of driving force, which can be distributed locally to different tissues by local regulation.

38
Q

What are the two main types of hypertension?

[IMPORTANT]

A
  • Primary hypertension (a.k.a. ‘essential hypertension’) -> Hypertension with an unknown underlying cause
  • Secondary hypertension -> Hypertension with a known disease causing it
39
Q

Give some factors that the spec says are associated with long-term increases in blood pressure.

[IMPORTANT}

A
  • ‘Essential hypertension’ -> Unknown cause
  • Renal disease
  • Phaeochromocytoma -> Rare tumor of adrenal gland tissue. It results in the release of too much epinephrine and norepinephrine.
40
Q

What is the relationship between the radius of a blood vessel and its resistance?

A

R ∝ 1/r4

41
Q

Juxtaglomerular cells are modified … cells.

A

Smooth muscle

42
Q

Describe the mechanism of renin secretion.

A

This is unusual because the calcium is an inhibitor of release.

43
Q

How does the macula densa influence renin secretion from the juxtaglomerular cells?

A
  • When there is reduced sodium detected by the macula densa, renin secretion is stimulated.
  • Prostaglandins are used to stimulate release
  • Adenosine is used to inhibit release
44
Q

List and describe the consequences associated with hypertension?

A

-Left ventricular hypertrophy –> ischemia –> angina –> MI (coronary atery perfusion reduced as the wall is too thick too allow proper relaxation and filling)
-Stroke (haemorrhaigic or embolic-athersclerotic plaque)
-Renal damage due to stenosis of smaller arterioles or fibrosis of nephrons following shear stress here
-Atherosclerosis due to increased turbulence and endothelial damage –> inflammatory response
-Arterial aneurysm
-Retinal damage from haemorrhage of blood vessels F

45
Q

What are the potential treatments for hypertension?

A

LIFESTYLE CHANGE: increased exercise, weight loss, dietary manipulation (limit salt and cholesterol intake)
DRUG THERAPY

46
Q

Draw and reference a graph to show the relative risk of mortality (from CHD and stroke) according to arterial blood pressure.

[IMPORTANT]

A

(Lipp, 2015)

Sophie - Applied Physiology & Pharmacology Year 2 (32 decks)

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