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TAS Cardiology > Cardiovascular Physiology > Flashcards

Cardiovascular Physiology Flashcards

1
Q

Does the heart fill actively or passively?

A

Passively

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2
Q

What limits the filling of the heart?

A

It’s limited pressure-volume compliance

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3
Q

What is the venous return?

A

The amount of blood flowing into the right atrium per minute from the systemic circulation

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4
Q

What drives venous return?

A
  • Peripheral vein compression from skeletal muscle activity
  • Respiration
  • Active ventricular contraction
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5
Q

How does peripheral vein compression from skeletal muscle activity drive venous return?

A

It pushes venous blood into vessel segments closer to the heart

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6
Q

How does respiration drive venous return?

A

It produces an alternating pressure gradient between the abdomen and thorax that favours venous return during inspiration

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7
Q

What opposes the opposite effect of respiration on venous return during expiration?

A

The presence of semilunar valves in the veins

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8
Q

How does active ventricular contraction drive venous return?

A

It shifts the atrioventricular border downwards in the direction of the cardiac apex and, as the atrioventricular valves are closed at this point, draws blood from the venae cavae and pulmonary veins into the atria

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9
Q

What is stroke volume defined as?

A

The volume ejected by each ventricle

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10
Q

What is the stroke volume in an adult?

A

About 70ml

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11
Q

What is cardiac output defined as?

A

The total volume of blood pumped out of each ventricle every minute

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12
Q

Does cardiac output refer to the volume pumped by the right or left ventricle?

A

Either, but not total amount pumped by both

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13
Q

How is cardiac output calculated?

A

Stroke volume (L) x heart rate (per min)

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14
Q

How can the heart modify its cardiac output?

A

By adjusting the number of contractions per unit of time, and by moderating the volume of blood pumped by each contraction (stroke volume)

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15
Q

How are the mechanisms for the heart modifying its cardiac output brought about?

A

Through a number of intrinsic biophysical pathways as well as extrinsic control

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16
Q

In terms of electrical activity of the heart, how can acceleration of the heart rate be achieved?

A

By decreasing the time taken to depolarise a pacemaker cell

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17
Q

What substances act as positive inotropes?

A

Catecholamines

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18
Q

Give 2 catecholamines?

A
  • Noradrenaline

- Adrenaline

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19
Q

What do catecholamines bind to when acting as positive inotropes?

A

Cardiac ß1-adrenoceptors

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20
Q

What is the effect of catecholamine binding to cardiac ß1-adrenoceptors?

A

It moves the threshold for action potential generation towards a more negative potential

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21
Q

What is the result of catecholeamines moving the threshold for action potential generation towards a more negative potential?

A

It increases the rate of diastolic depolarisation

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22
Q

What does acetylcholine bind to in the heart?

A

Muscarinic M2 receptors

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23
Q

What is the effect of acetylcholine binding to M2 receptors in the heart?

A

It slows the heart rate

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24
Q

Give 6 positive inotropic factors

A
  • Sympathetic nerve stimulation and catecholamines
  • Increase in extracellular calcium
  • Decrease in extracellular sodium
  • Increased pH
  • Drugs
25
Q

Give 3 drugs that are positive inotropic factors

A
  • Digoxin
  • Glucagon
  • L-thyroxine
26
Q

Give 7 negative inotropic factors

A
  • Hypoxia
  • Hypercapnoea
  • Decrease in extracellar calcium
  • Increase in extracellular sodium
  • Decreased pH
  • Decreased temperature
  • Drugs
27
Q

What can cause a decrease in extracellular calcium?

A

Calcium channel blockers

28
Q

Give 2 drugs with negative inotropic effects?

A
  • Beta blockers

- Anaesthetic agents

29
Q

How are changes in the heart rate initiated?

A

By the reticular formation in the brainstem

30
Q

Where does the reticular formation in the brainstem receive information from that indicates a need to change the heart rate?

A

Specialised nerve receptors that are constantly feeding back to the reticular formation

31
Q

Via what does the reticular formation initiate changes in the heart rate?

A

The glossopharyngeal and vagal nerve supply

32
Q

How are changes in blood pressure detected?

A

Baroreceptors

33
Q

Where are baroreceptors located?

A
  • Walls of internal carotid arteries

- Arch of aorta

34
Q

How is the amount of oxygen in the blood monitored?

A

Chemoreceptors

35
Q

Where are chemoreceptors located?

A

Carotid and aortic bodies

36
Q

What is meant by preload?

A

The end-diastolic volume loading of the heart

37
Q

What happens to the heart rate when the preload is increased?

A

It increases

38
Q

Why does the heart rate increase when preload is increased?

A

The increased preload stretches the sinuatrial (SA) node and increases the heart rate via a reflex pathway and local stretch-activated ion channels

39
Q

How do stretch activated ion channels in the heart work?

A

They depolarise the pacemaker cells and increase the rate of diastolic depolarisation

40
Q

What happens to the contractility of the myocardium when preload increases?

A

It increases

41
Q

Why does the contractility of the myocardium increase with an increasing preload?

A

Due to the Frank-Starling law

42
Q

What describes the relationship between the preload and the contractility of the myocardium?

A

The Frank-Starling law

43
Q

What is the Frank-Starling law?

A

The energy of contraction is proportional to the initial length of the cardiac muscle fibre, i.e. length dependent activation

44
Q

How does increasing the preload lead to an increased contractility?

A
  • Increases load experienced by each muscle fibre
  • Increases affinity of troponin C for calcium
  • Causes greater number of actin-myosin cross-bridges to form within the muscle fibres
45
Q

What is pre-load affected by?

A
  • Length of diastole
  • Venous return
  • Atrial systole
  • Myocardial compliance
46
Q

Give an example of a cause of increased preload?

A

Premature ventricular contraction

47
Q

What happens in premature ventricular contraction?

A

There is early emptying of the left ventricle

48
Q

How does premature ventricular contraction lead to increased preload?

A

It increases the filling time for the next regular ventricular contraction, and so increases left ventricular end-diastolic volume

49
Q

What is the result of the greater end-diastolic volume when there is a premature ventricular contraction?

A

The next ventricular contraction will be more forceful, causing the ejection of a larger than normal amount of blood, brining left ventricular end diastolic volume back to baseline

50
Q

What effect might pericardial effusion have on stroke volume?

A

Decrease it

51
Q

Why might pericardial effusion decrease stroke volume?

A

It reduces myocardial compliance

52
Q

What does the law of Laplace describe?

A

The relationship between;

  • The pressure difference across a wall
  • The radius of the cavity
  • The thickness of the cacity
53
Q

What is the law of Laplace?

A

The greater the pressure difference or larger the radius, the more tension there will be in a wall, but the tension is reduced the thicker the wall

54
Q

How can the law of Laplace be applied to dilated cardiomyopathy?

A

In dilated cardiomyopathy the heart becomes distended and the radius increases, and so the heart must increase cardiac tension produced by the cardiac muscle. The dilated heart therefore requires more energy to pump the same amount of blood compared to a heart of normal size.

55
Q

What is afterload?

A

The external load against which the ventricles must pump to eject blood

56
Q

What is the total peripheral vascular resistance determined by?

A
  • Vessel diameter, pressure, and tone
  • Aortic valve resistance
  • Ventricular cavity size
  • Haematocrit
57
Q

Which vessels are most important in determining total peripheral vascular resistance?

A

Resistance arterioles

58
Q

Why is haematocrit important in determining total peripheral vascular resistance?

A

Measures blood viscosity

59
Q

Give 5 factors causing constriction of arterioles

A
  • Increased sympathetic activity
  • Circulating catecholamines
  • Circulating angiotensin II
  • Locally released serotonin
  • Decreased local temperature

TAS Cardiology (7 decks)

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