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CV System - Alex's Cards (ESA2) > Session 5 Lectures > Flashcards

Session 5 Lectures Flashcards

1
Q

What is the calculation for working out mean arterial bp ?

A

mean arterial BP = CO x TPR
and
mean arterial BP = diastole + 1/3 (systole - diastole)

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2
Q

What is the calculation for working out cardiac output?

A

CO = HR x SV

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3
Q

What are 3 locations of baroreceptors?

A
  1. Carotid sinus
  2. Aortic arch
  3. Afferent arteriole of kidney
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4
Q

How long does the baroreceptor help deal with hypertension?

A

For up to 15 minutes
It then resets back to the level it was previously at
Only works for acute changes in BP

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5
Q

What 4 neurohumoral pathways control circulating volume and BP?

A
  1. RAAS
  2. Sympathetic nervous system
  3. Anti-diuretic hormone (ADH)
  4. Atrial natriuretic peptide (ANP)
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6
Q

Where is renin released from?

A

From granular cells of juxtaglomerular apparatus

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7
Q

Give 3 factors that stimulate renin release

A
  1. Reduced sodium delivery into kidney
  2. Reduced pressure in the afferent arteriole (indicative of low blood volume)
  3. Sympathetic stimulation
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8
Q

What is the function of renin?

A

Converts angiotensinogen to angiotensin I

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9
Q

What converts angiotensin I to angiotensin II?

A

ACE (angiotensin converting enzymes)

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10
Q

Where are the main 2 types of angiontensin receptors?

Which produces main actions?

A

AT1 and AT2

AT1 receptor is where main actions produced from

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11
Q

Name the 5 sites of angiontensin receptors

A
  1. Kidney
  2. Arterioles
  3. Sympathetic NS
  4. Adrenal cortex
  5. Hypothalamus
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12
Q

What is the effect of angiotensin on arterioles?

A

Acts on smooth muscle receptors to cause vasoconstriction = increasing arterial BP

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13
Q

What is the effect of angiotensin on the kidney?

A

Increases sodium reabsorption and therefore water = increasing plasma volume and BP

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14
Q

What is the effect of angiotensin on the sympathetic NS?

A

Causing more noradrenaline to be released = increasing actions of sympathetic NS (increases renin release)

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15
Q

What is the effect of angiotensin on the adrenal cortex?

A

Stimulates aldosterone release

Aldosterone acts to increase sodium reabsorption by the kidneys

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16
Q

What is the effect of angiotensin on the hypothalamus?

A

Increases thirst sensation

Encourages fluid intake

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17
Q

What channel does aldosterone act on to increase sodium intake?

A

ENaC

Epithelial Sodium Channel

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18
Q

What effect do ACE have as well as conversion of angiotensin I to II?

A

They stimulate the breakdown of bradykinin to peptide fragments
This effects the vasodilation action of bradykinin

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19
Q

If bradykinin is not broken down what symptoms might a person
get?

A

Dry cough

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20
Q

How does stimulation of sympathetic nervous system increase BP?

A

It acts on smooth muscle receptors to cause vasoconstriction
Blood flow is reduced to kidney which stimulates renin release

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21
Q

When is anti-diuretic hormone stimulated?

A

When plasma osmolality increases or in severe hypovolaemia

It stimulates sodium reabsorption and water retention to increase plasma volume

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22
Q

Where is atrial natriuretic peptide synthesised and stored?

When is ANP released and what does it do?

A

In the atrial myocytes
They are released in response to stretch = the less the heart is filled the less they stretch and the less ANP released
ANP stimulates sodium excretion and prevents reabsorption

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23
Q

What effect do prostaglandins have?

Are they effective for a hypertensive patient?

A

They are vasodilators
They reduce sodium reabsorption and act as a buffer against excessive vasoconstriction to prevent damage to blood vessels
Not effective long term as they have a short half life

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24
Q

What effect does dopamine have?

In what condition is it often used?

A

It is a vasodilator
It reduces reabsorption of sodium into the kidney
It is used to treat patients with Parkinson’s

25
Q

What blood pressure (in clinic) is stage 1 hypertension?

A

140/90 mmHg

26
Q

What is accelerated hypertension?

A

Where a significant and sudden rise in BP causes accelerated damage to the blood vessels

27
Q

What is primary hypertension?

A

Hypertension where the cause is unknown or it is multi-factorial

28
Q

What is secondary hypertension?

A

Where the cause can be identified

29
Q

What is renovascular disease?

A

Occlusion of renal artery (renal artery stenosis) causes a fall in perfusion pressure and increased renin production

30
Q

What is renal parenchymal disease?

A

Chronic kidney disease

The kidneys inadequately filter so you get increased sodium and water retention

31
Q

What is Conn’s syndrome?

A

A benign tumour in adrenal gland that secretes aldosterone

Causes a high BP

32
Q

What is Cushing’s syndrome?

A

Effect of long term steroid use

Causes sodium and water retention

33
Q

What 2 effects can hypertension have?

A 
Increased afterload (increasing work of the heart)
Arterial damage
34
Q

Name the 5 main locations that can be affected by hypertension

A
  1. Eyes
  2. Heart
  3. Kidney
  4. Brain
  5. Arteries
35
Q

Is BP = SV x HR x TPR correct?

A

Yes
BP = CO x TPR
CO = HR x SV

36
Q

Does smoking affect BP?

A

No!

It does impact on CV disease

37
Q

What are the 2 main drugs of RAAS system for treating hypertension?

A
  1. ACE inhibitors

2. Angiontensin receptor antagonists/blockers

38
Q

Give 2 examples of drugs to cause vasodilation

A
  1. L-type Ca channel blockers

2. A1 receptor blockers (found in vascular smooth muscle)

39
Q

What effect do diuretics have?

Give an example of one

A

They reduce circulating volume by inhibiting sodium reabsorption and water retention
Thiazide diurectics

40
Q

Why might beta blockers not always be used to treat hypertension?
What receptor would they work at?

A

Work at beta 1 receptors in heart
They would reduce force and contractility of heart so would only be used if other reasons such as previous myocardial infarction

41
Q

What is haemodynamic shock?

A

Acute condition of inadequate blood flow throughout body

Can be caused by reduced CO or reduced TPR (causing reduction in mean arterial pressure)

42
Q

What is cardiogenic shock?

A

When the ventricle can’t empty properly

Heart fills but unable to pump properly

43
Q

What is mechanical shock?

A

When the ventricles can’t fill properly

44
Q

Suggest a reason for cardiogenic shock

Does it alter CO or TPR?

A

Following a myocardial infarction heart may not be able to pump out enough blood to maintain BP
CO is affected

45
Q

What is cardiac arrest?

A

Unresponsiveness associated with a lack of pulse (no cardiac output)

46
Q

What is the most common form of cardiac arrest?

A

Ventricular fibrillation

47
Q

What is pulseless electrical activity?

A

When you still have electrical activity but no mechanical activity = still a form of cardiac arrest

48
Q

Name 3 ways to treat cardiac arrest

A
  1. Basic life support (chest compression
  2. Advanced life support (defibrillator) - delivers electric current to heart and depolarises all the cells (putting them into refractory period to allow coordinated activity to restart)
  3. Adrenaline - increases TPR
49
Q

What affect does a pulmonary embolism have on venous and arterial BP?

A 
Venous = increases (block in pulmonary artery means backlog of blood in venous system as RV can't empty)
Arterial = decreases (blood not reaching LV so reduced left atrial pressure)
50
Q

What % of blood loss leads to a serious shock response?

A

30-40% of blood lost

51
Q

BP = CO x TPR
CO = HR x SV
How are these equations affected following a haemorrhage?

A

Haemorrhage = blood loss
This reduces venous pressure because the is reduction in blood filling the heart
The stroke volume is decreased so cardiac output decreases
When cardiac output falls, BP falls too (so mean arterial BP drops)

52
Q

What is the compensatory response?

A

Response to hypovolaemic shock by increased sympathetic stimulation
Trying to maintain the same venous pressure and stroke volume by increasing heart rate as well as venoconstriction

53
Q

What are the 2 long term responses to hypovalaemia?

A
  1. RAAS

2. Anti-diuretic hormone (to increase blood volume and BP)

54
Q

What is distributive shock?

A

Shock that is due to reduction in TPR

Vasodilation has occurred so there is an increase in volume of circulation (more vessel space available)

55
Q

What is the cause of septic shock?

A

Endotoxins are released by bacteria which produce inflammatory response
Produce vasodilation (fall in TPR and arterial pressure)
Impaired perfusion of vital organs
Also capillaries becomes leaky which reduces blood volume

56
Q

What is septic shock?

A

Persisting hypotension requiring treatment to maintain BP despite fluid resuscitation
(capillaries are leaky so the fluid providing is not enough to combat this)

57
Q

What happens in anaphylactic shock?

A

Histamine is released from mast cells which have a powerful vasodilator effect as well as bronchoconstriction

58
Q

How can you help a person having an anaphylactic shock?

A

Give them adrenaline

This causes vasoconstriction via actions at a1 adrenoreceptors

CV System - Alex's Cards (ESA2) (9 decks)

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