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Yr 2 - Cardiology System > Cardiovascular Response to Stress > Flashcards

Cardiovascular Response to Stress Flashcards

1
Q

What is systemic arterial blood pressure?

What is the equation for ‘mean systemic arterial pressure’?

A

Refers to the pressure measured within large arteries in the systemic circulation (pressure exerted upon arteries during heart contractions). This number splits into systolic blood pressure and diastolic blood pressure.

Cardiac Output x Total Peripheral Resistance

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2
Q

What does the Frank-Starling curve say about preload?

A
  • Increase in preload increases stroke volume - Decrease in preload decreases stroke volume - High levels of preload eventually leads to decreased stroke volume (downstroke of curve)
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3
Q

What is preload best measured as?

A

End diastolic volume (echo)

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4
Q

What can preload be defined as?

A

The initial stretching of the cardiac myocytes prior to contraction related to ventriuclar filling. (i.e. strength of ventricular contraction increased when ventricle stretched prior to contraction)

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5
Q

How does increased venous return to the heart affect the stroke volume?

A
  • Increasing venous return increases filling pressure of ventricle (LVEDP: left ventricular end diastolic pressure) –> this stretches sacromeres and increases preload
  • Leads to increased stroke volume
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6
Q

What factors increase preload?

A
  1. Increased central venous pressure that can result from decreased venous compliance or increased thoracic blood volume 2. Increased ventricular compliance 3. Increased atrial force of contraction / increased filling of atria 4. Reduced heart rate 5. Increased aortic / pulmonary pressure
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7
Q

What can decreased venous compliance be caused by?

A

Sympathetic activation of venous smooth muscle

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8
Q

How does increased ventricular compliance lead to increased preload?

A

Greater expansion of the chamber during filling at a given filling pressure

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9
Q

What can cause increased atrial force of contraction?

A

Sympathetic stimulation of the atria or from increased filling of the atria

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10
Q

How can reduced heart rate increase preload?

A

Prolongs diastole

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11
Q

How does increased aortic pressure increase preload?

A

Increases the afterload on the ventricle, reduces stroke volume by increasing end-systolic volume, and leads to a secondary increase in ventricular preload

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12
Q

How does the ‘Bowditch Effect’ relate to heart rate?

A
  • Increase in heart rate increases force of contraction - Decrease in heart rate decreases force of contraction - High levels of heart rate eventually leads to decreased force of contraction
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13
Q

Why is the Bowditch (Treppe) Effect independent of Frank-Starling?

A

Length of muscle not affected

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14
Q

What is the Bainbridge reflex?

A

An increase in heart rate due to an increase in central venous pressure

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15
Q

What are baroreceptors? What do they detect?

A

Stretch receptors –> detect increased stretch (caused by increase in blood volume) Many individual baroreceptors are inactive at normal resting pressures and only become activated when their stretch or pressure threshold is exceeded.

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16
Q

What is effect of baroreceptors in atria detecting increased stretch?

A

Heart rate increased via sympathetic simulation to SA node

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17
Q

What are direct cardiac sympathetic actions?

A
  1. Positive chronotropy (speeds up heart rate) 2. Positive dromotropy (increases speed of conduction) 3. Positive ionotropy (better contraction) 4. Positive lusitropy (better relaxation of ventricles and atria)
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18
Q

What is effect of dobutamine? How does it work? What type of drug is it? What is it used to treat?

A
  • B-agonist
  • A cardiac stimulant which acts on beta1 receptors in cardiac muscle, and increases contractility.

Activates sympathetic system (acts as mimic), increasing heart rate and force of contraction

Used to treat: cardiogenic shock and severe heart failure

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19
Q

How does activation of RAAS affect central venous pressure?

A

Increases central venous pressure –> increases stroke volume

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20
Q

Describe RAAS

A
  1. Angiotensinogen produced in liver 2. Angiotensiogen converted to angiotensin I by renin (produced by kidney) 3. Angiotensin I converted to angiotensin II by ACE (in lungs and kidneys) 4. Angiotensin II stimulates release of aldosterone by adrenals
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21
Q

What is effect of angiotensin II on: 1. Arterioles 2. Kidneys 3. Sympathetic nervous system 4. Adrenals 5. Hypothalamus

A
  1. Vasoconstriction 2. Increased Na+ and H20 reabsorption 3. Increased release of noradrenaline 4. Aldosterone 5. Stimulates anti-diuretic hormone (ADH) release
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22
Q

What are the effects of increased aldosterone?

A

Increased Na+ and H20 retention

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23
Q

What is vasopressin? What is its effect?

A

ADH - promotes H20 retention

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24
Q

What is effect of this vasoconstriction and increased H20 and Na+ reabsorption due to a stimulation of the RAAS?

A
  1. Increased central venous pressure –> increases stroke volume 2. Vasoconstriction –> increases total peripheral resistance
25
Q

What are catecholamines?

A

Hormones made by adrenal glands (dopamine, adrenaline, noradrenaline)

26
Q

Where are adrenal glands located?

A

On top of kidneys

27
Q

What are catecholamines released by?

A

Adrenal medulla

28
Q

When are catecholamines released?

A

In response to stress –> trigger a fight or flight response

29
Q

What are effects of catecholamines?

A

Increased heart rate (and stroke volume), blood pressure, breathing rate, mental alertness, vasoconstriction Also lower blood going to skin and intestines but increase blood going to major organs (brain, heart, kidneys)

30
Q

What are parasympathetic actions: 1. Heart rate 2. AV conduction 3. Atrial contractility 4. Ventricular contractility 5. RAAS

A
  1. Decrease heart rate (chronotropy) 2. Decrease AV conduction (dromotropy) 3. Decrease atrial contractility (inotropy) 4. No major effect 5. No major effect
31
Q

Where are baroreceptors located?

A

Carotid sinuses, aortic arch

32
Q

What effect does a decreased/increased arterial pressure have on baroreceptors?

A

Decreased/increase firing

33
Q

What is effect of increased baroreceptor firing (as a result of an increased blood pressure)?

A

Decreases sympathetic tone and increases parasympathetic (vagal) tone

  • Reduced HR
  • Reduced SV
  • Vasodilation
34
Q

What is effect of decreased baroreceptor firing (as a result of decreased blood pressure)?

A

Increases sympathetic tone and decreases parasympathetic tone

35
Q

In clinical case of significant blood loss, what effect would this have on blood pressure and how would baroreceptors respond?

A

Blood loss –> decreased central venous pressure –> decreased preload –> decreased stroke volume and cardiac output –> decreased blood pressure Baroreceptors sense this –> decrease firing –> increases sympathetic and decreases parasympathetic to try and increase BP

36
Q

During CPX, what is the anaerobic threshold?

A

The level of exercise when the exercising muscles being to have anaerobic metabolism and release copious amounts of lactic acid

37
Q

What does CPX measure?

A

Measure of aerobic exercise capacity and fitness

38
Q

Effect of blood loss on RAAS and catecholamines

A
39
Q

What is afterload?

A

The pressure against which the heart is contracting when it ejects blood (increased afterload in hypertension)

40
Q

What do baroceptors detect?

A

Arterial stretch

41
Q

What does the Frank-Starling law represent?

A

The relationship between stroke volume and end diastolic volume –> states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction, when all other factors remain constant

The ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return is called the Frank-Starling mechanism

42
Q

How does decreased venous return affect stroke volume?

A

Leads to decreased stroke volume due to decreased preload

43
Q

What is inotropy?

A

Myocardial contractility

44
Q

What shifts Frank-Starling starling curve down and to the right?

A
  • Increasing afterload
  • Decreasing inotropy

Results in lower SV

45
Q

What shifts Frank-Starling curve up and to the left?

A
  • Decreasing afterload
  • Increasing inotropy

Increases SV

46
Q

In summary, how does venous return affect curve and how does afterload/inotropy affect curve?

A

Changes in venous return cause the ventricle to move up or down along a single Frank-Starling curve; however, the slope of that curve is defined by the existing conditions of afterload and inotropy.

47
Q

What is the slope of the Frank-Starling curve defined by?

A

Existing conditions of afterload and inotropy

48
Q

What is end diastolic volume?

A

refers to the quantity of blood in the left or right ventricle at the end of diastole, just before systole starts.

49
Q

How does increased venous return affect EDV?

A

Increases it (increased preload)

50
Q

How is SV defined?

A

EDV - ESV

51
Q

What is ESV?

A

volume of blood in a ventricle at the end of contraction (systole)

52
Q

What are the 2 ways by which increased venous return increase preload?

A
  1. Increases stretching of cardiac myocytes prior to contraction
  2. This increases sacromere length
  3. Causes increases in force generation –> increases stroke volume
  4. Also increases ventricular filling (EDV)
  5. Therefore increases preload
53
Q

Explain how preload influences contractile force using the troponin C mechanism

A
  1. increasing the sarcomere length increases troponin C calcium sensitivity
  2. which increases the rate of cross-bridge attachment and detachment
  3. increases the amount of tension developed by the muscle fibre
54
Q

How does sympathetic effect fibres to the heart affect:

  1. Chronotropy (heart rate)
  2. Inotropy (contractility)
  3. Lusitropy (rate of relaxation)
  4. Dromotropy (conduction velocity)
A
  1. Positive chronotropy (increases heart rate)
  2. Positive inotropy (increases contractility)
  3. Increased lusitropy (increased rate of relaxation)
  4. Positive dromotropy (increased rate of conduction velocity)
55
Q

What is sympathetic activity effect on blood vessels? How does this affect blood pressure?

A
  1. sympathetic activation constricts arteries and arterioles (resistance vessels)
  2. this increases vascular resistance and decreases distal blood flow
  3. the increased vascular resistance causes arterial pressure to increase
56
Q

How does sympathetic activity affect venous return?

A

Sympathetic-induced constriction of veins decreases venous compliance (more stiff) and blood volume, and thereby increases venous pressure.

57
Q

How does sympathetic activity overall affect:

  1. Cardiac output
  2. Systemic vascular resistance
  3. Arterial blood pressure
A

The overall effect of sympathetic activation is to increase cardiac output, systemic vascular resistance (both arteries and veins), and arterial blood pressure.

58
Q

What is effect of parasympathetic activity on:

  1. Chronotropy (heart rate)
  2. Inotropy (contracility)
  3. Lusitropy (rate of relaxation)
  4. Dromotropy (conduction velocity)
A
  1. Negative chronotropy (heart rate)
  2. Negative inotropy (contractility) –> more pronounced in atria than ventricles
  3. Negative lusitropy (rate of relaxation) –> more pronounced in atria than ventricles
  4. Negative dromotropy (conduction velocity)

Yr 2 - Cardiology System (25 decks)

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