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BRS > Introduction to heart,cardiac mechanics and cardiac cycle > Flashcards

Introduction to heart,cardiac mechanics and cardiac cycle Flashcards

1
Q

Describe the route of blood flow in the right side of the heart?

A

Vena cava, right atrium, right ventricle, pulmonary artery, lungs.

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2
Q

Describe the route of blood flow in the left side of the heart?

A

Pulmonary vein, left atrium, left ventricle, aorta, rest of body.

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3
Q

Valve in between left atrium and left ventricle?

A

Mitral valve.

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4
Q

Valve in between left ventricle and aorta?

A

Aortic valve.

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5
Q

Valve in between right atrium and right ventricle?

A

Tricuspid valve.

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6
Q

Valve in between right ventricle and pulmonary artery?

A

Pulmonary valve.

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7
Q

Explain the electrical activity in the heart?

A

Primary pacemaker signal is generated in the SAN. Electrical signals is transmitted across the myocardium of atrium along the internodal tracts. Slowing down of electrical signal at AV node. Transmission of electrical signals along bundle of his down intravetrincular septum to apex of heart. Transmission of electrical signals along the purkinje fibers cause contraction of ventricles.

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8
Q

What cause the P wave in ECG?

A

Electrical signals transmitting across the myocardium of atrium along the internodal tracts.

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9
Q

What causes the P-R interval?

A

Slowing down of electrical signal at AV node.

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10
Q

What are the 4 main coronary arteries?

A

The right coronary artery, the left main coronary, the left anterior descending, and the left circumflex artery.

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11
Q

What is the largest coronary vein?

A

Coronary sinus.

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12
Q

Where does muscle surface level depolarisation occur?

A

Sarcolemma.

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13
Q

What do T tubules do?

A

Carry surface depolarisation deep into cell.

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14
Q

Where are t tubules found?

A

Along each z line of every myofibril.

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15
Q

What mechanism triggers heart contraction?

A

Calcium induced calcium release.

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16
Q

Explain calcium induced calcium release?

A

Depolarisation occurs on the surface of a cardiomyocyte via sodium channels. Depolarisation opens voltage gated L-type calcium channels on the surface and in the T-tubules allowing calcium to enter the cell. Calcium acts as a ligand and binds to the ryanodine receptor on the sarcoplasmic reticulum and activates it. This triggers calcium release from sarcoplasmic reticulum which further increases calcium availability in the cell. Calcium release from SR results in contraction of myofilaments. As the contraction ends calcium is pumped back into the sarcoplasmic reticulum by SR Ca2+ ATPase (active transport). Calcium that entered the cell via the L-type calcium channel diffused out via the surface level Na+/Ca2+ exchanger; restoring calcium balance.

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17
Q

Cardiac vs skeletal muscle stretching ability?

A

Cardiac muscle is more resistant to stretching. Cardiac muscle therefore produces more passive force and so more overall force.

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18
Q

What affects the stretching ability of different types of muscle?

A

Different ECM and cytoskeleton.

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19
Q

Why can’t cardiac muscle be overstretched?

A

Pericardium sac prevents overstretching.

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20
Q

What is an isotonic contraction?

A

Muscle fibres shorten and movement occurs.

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21
Q

What is an isometric contraction?

A

Muscle fibres do not shorten but tension increases.

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22
Q

What is preload?

A

Weight that stretches the muscle before it is stimulated to contract.

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23
Q

What is afterload?

A

Weight encountered only when muscle starts to contract.

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24
Q

What does stretching do to the muscle?

A

More stretch. Increase in passive force. More powerful contraction.

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25
Q

What determines preload in the heart?

A

Venous return.

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26
Q

What determines afterload in the heart?

A

Aortic pressure.

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27
Q

What does an increase in afterload result in?

A

Decrease in isotonic shortening and velocity of shortening.

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28
Q

What is preload in the heart?

A

Volume of blood in ventricles at the end of diastole.

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29
Q

How do you measure preload in the heart?

A

End diastolic pressure, End diastolic volume and right atrial pressure.

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30
Q

When is preload increased in the heart?

A

Hypervolemia, regurgitation of aortic and pulmonary valve (leaky heart valves - don’t close fully), heart failure.

31
Q

What is the afterload in the heart?

A

The resistance that has to be overcome after opening of aortic valve in order to circulate blood.

32
Q

How is afterload measured?

A

Diastolic blood pressure. End systolic volume.

33
Q

What is end systolic volume?

A

The end-systolic volume (ESV) is referred to as the volume of blood in the left or right ventricle at the end of the systolic ejection phase immediately before the beginning of diastole or ventricular filling.

34
Q

When is afterload increased in the heart?

A

Hypertension and vasoconstriction.

35
Q

Why is high afterload in a heart bad?

A

Reduced stroke volume. More cardiac workload.

36
Q

What is starling’s law and why is it important?

A

Increased diastolic fibre length increases ventricular contraction. Ventricles pump greater stroke volume as venous return increases and so at equilibrium cardiac output exactly balances the augmented venous return.

37
Q

What are the theories to why increase the length of a fibre increases level of contraction?

A

More stretching of muscle fibres leads to decreased myofilament lattice spacing and so more likely to form myofilament cross bridges. More force for the same amount of activating calcium.

Longer sarcomere lengths increase affinity of troponin C for Ca2+ due to conformational change in protein. Less Ca2+ required for same force.

38
Q

What is myofilament lattice spacing?

A

Space between myosin and actin filaments.

39
Q

How to calculate stroke work?

A

Stroke volume (volume of blood ejected in each stroke) x pressure (at which the blood is ejected).

40
Q

What is stroke work?

A

Work done by heart to eject blood under pressure into aorta and pulmonary artery.

41
Q

What is law of laplace?

A

Wall tension = (pressure in vessel x radius of vessel) / wall thickness

42
Q

How does the left ventricle walls experience similar tension to right ventricles?

A

Left ventricles have a low radius of curvature (radius) and a higher pressure. Allows left ventricle to generate higher pressures with similar wall stress.

43
Q

Why do failing hearts have increased wall stress?

A

The ventricles become dilated.

44
Q

How to calculate stroke volume?

A

ESV - EDV.

45
Q

How to calculate ejection fraction

A

(Stroke volume / EDV) x 100

46
Q

How to calculate cardiac output?

A

Heart rate x stroke volume.

47
Q

What are the 7 stages of the cardiac cycle?

A

Atrial systole, Isovolumetric contraction, Rapid ejection, Reduced ejection, Isovolumetric relaxation, Rapid passive filling and reduced passive filling.

48
Q

What happens during atrial systole? Is there a trace on the ECG? What part of the cardiac cycle is it a part of?

A

Top up volume of blood in ventricles. P wave on ECG. Part of diastole.

49
Q

When would you have a 4th heart sound?

A

During atrial systole. In patients with congestive heart failure, pulmonary embolism or tricuspid incompetence (regurgitation).

50
Q

What happens during isovolumetric contraction? Is there a trace on the ECG? What part of the cardiac cycle is it a part of?

A

Start of ventricular contraction. Marked by QRS complex on ECG. Interval between AV valves closing and semi lunar valves opening - produces S1 sound. Contraction of ventricles with no change in volume; stretching of fibres.

51
Q

What happens during rapid ejection? Is there a trace on the ECG? What part of the cardiac cycle is it a part of?

A

Opening of aortic and pulmonary valves mark the start of the phase. Isotonic contraction - Pressure in ventricles exceed the pressure in aorta and pulmonary artery. Blood is pumped out (shortening of myofibrils), volume of ventricles decreases. No heart sounds.

52
Q

What happens during reduced ejection? Is there a trace on the ECG? What part of the cardiac cycle is it a part of?

A

Aortic and pulmonary valves begin to close. Blood flow from ventricles decreases and ventricular volume decreases more slowly. As pressure in ventricles falls below arteries, blood begins to flow backwards causing the semi lunar valves to shut. Ventricular muscle cells repolarize producing T wave. End of systole.

53
Q

What happens during isovolumetric relaxation? Is there a trace on the ECG? What part of the cardiac cycle is it a part of?

A

Aortic and pulmonary valves shut. Atrioventricular valves remain shut until ventricular pressure drops below atrial pressure. Dichrotic notch is present.

54
Q

What is dichrotic notch?

A

Caused by closure of the aortic valve. Rebound pressure as distended aortic wall relaxes.

55
Q

What happens during rapid passive filling? Is there a trace on the ECG? What part of the cardiac cycle is it a part of?

A

Isoelectric ECG trace. AV valves open and blood enters ventricles.

56
Q

When would you have a 3rd heart sound?

A

During rapid passive filling in patients with severe hypertension or mitral incompetence.

57
Q

What happens during reduced passive filling? Is there a trace on the ECG? What part of the cardiac cycle is it a part of?

A

Ventricular volume fills more slowly. Ventricles are able to fill considerably without atria.

58
Q

Another name for reduced passive filling?

A

Diastasis.

59
Q

Despite lower pressures right ventricle ejects same volume of blood. Why?

A

Pumping the same quantity of blood into a lower pressure circuit.

60
Q

Change in pressure volume loop when preload is increased?

A

Extended to right.

61
Q

Change in pressure volume loop when afterload is increased?

A

Extended upwards and decreased in width from the left inwards.

62
Q

Why does an increase in afterload extended pressure volume loop upwards?

A

Greater pressure required to open aortic valve.

63
Q

Why does an increase in afterload decrease width of the pressure volume loop?

A

Less shortening as working against increased afterload results in a decrease in stroke volume.

64
Q

Explain how noradrenaline or adrenaline can cause changes in cardiac contractility?

A

Noradrenaline or adrenaline bind to beta 1 or beta 2 receptors. This triggers a g protein to activate adenylyl cyclase. Adenylyl cyclase converts ATP to cAMP (cyclic adenosine monophosphate). cAMP activates PKA (protein kinase A). PKA phosphorylates the L-type calcium channel and the ryanodine receptor. This leads to more calcium entry and calcium release. More calcium delivery to myofilaments results in more force produced. PKA also phosphorylates SRCa2+ATPase allowing for more take up of calcium to prepare for next contraction.

65
Q

Why can very high tachycardia be a problem?

A

Can result in low diastolic filling time resulting in a lower EDV. This results in a lower stroke volume.

66
Q

What is ESPVR?

A

Maximal pressure developed by the LV at any given volume and is a measure of cardiac contractility.

67
Q

What does an increase in contractibility result in?

A

Increased ESPVR gradient.

68
Q

Change in pressure volume loop during exercise?

A

Extended to the left and right. Extended upwards.

69
Q

Why does the pressure volume loop extend to the right during exercise?

A

Increased venous return due to muscle pump system. Cycles of muscle contraction and relaxation result in veins being alternately compressed and decompressed.

70
Q

Why does the pressure volume loop extend to the left during exercise?

A

Sympathetic activation of the myocytes increases ventricular contractility, that decreases end-systolic volume.

71
Q

Why does the pressure volume loop extend upwards during exercise?

A

The increase in arterial pressure that occurs during exercise increases afterload.

72
Q

Why does an increase in afterload (arterial pressure) during exercise not result in an overall decrease in stroke volume?

A

Increase in contractibility and increase in preload (increase in venous return) offsets increase in afterload (arterial pressure). Overall there is a net increase in stroke volume.

73
Q

Longest phase of cardiac cycle?

A

Reduced passive filling.

74
Q

What slows the SA node rate at rest?

A

Parasympathetic stimulation is present at rest.

BRS (52 decks)

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