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Cardiovascular > Physiology 2 + 3 > Flashcards

Physiology 2 + 3 Flashcards

1
Q

What is striation of cardiac muscle caused by?

A

Regular arrangement of contractile protein

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2
Q

Why are there no neuromuscular junctions in cardiac muscle?

A

Heart capable of generating its own action potentials

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3
Q

How are myocytes electrically coupled?

A

Gap junctions

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4
Q

What are gap junctions?

A

Protein channels that form electrical communication pathways between myocytes

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5
Q

What is the all-or-none law of the heart?

A

Gap junctions ensure electrical excitation reaches all the cardiac myocytes

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6
Q

Where are desmosomes and gap junctions located?

A

Within intercalated discs

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7
Q

What are desmosomes?

A

Provide mechanical adhesion between myocytes ensuring tension developed by one cell is transmitted to the next

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8
Q

What are the contractile units of muscle?

A

Myofibrils (found in each muscle cell)

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9
Q

What are myofibrils made up of?

A
  • Thin (actin) filaments which cause lighter appearance

* Thick (myosin) filaments which cause darker appearance

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10
Q

Within each myofibril, what are actin and myosin arranged into?

A

Sacromeres (functional unit of the muscle)

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11
Q

How is muscle tension produced?

A

Sliding of actin filaments on myosin filaments

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12
Q

What does force generation depend on?

A

ATP-dependent interaction between myosin and actin filaments i.e. cross bridge formation

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13
Q

What do both contraction and relaxation require?

A

ATP

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14
Q

When will interaction of actin and myosin not occur even when ATP is present?

A

In the absence of calcium

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15
Q

Why is calcium required for formation of cross bridge in addition to ATP?

A
  • When muscle relaxed, myosin binding sites on actin are covered with regulatory proteins like tropomyosin and troponin
  • Calcium binds to troponin, removing troponin-tropomyosin complex and allowing binding of myosin
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16
Q

How does action potential switch on cardiac muscle contraction?

A

Ca+ released from sarcoplasmic reticulum

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17
Q

What is release of Ca+ from SR dependent on in cardiac muscle?

A

Presence of extra-cellular Ca+

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18
Q

Explain the process of contraction from action potential in cardiac muscle (3)

A
  • Phase 2: Ca+ influx through L-type Ca+ channels
  • Ca+-induced Ca+ release from SR
  • Increased intra-cellular calcium stimulates formation of cross bridges by removal of troponin-tropomyosin complex
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19
Q

How does heart muscle relax once action potential has passed? (2)

A
  • Ca+ influx ceases

* Ca+ re-sequestered in SR by Ca+ ATPase

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20
Q

What is the importance of a long refractory period to normal cardiac function?

A

Prevents generation of tetanic contraction

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21
Q

What is the refractory period?

A

Period following an action potential where it is not possible to produce another action potential

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22
Q

What are the components of the long refractory period?

A
  • Plateau phase: Na+ channels are in closed state

* Descending phase: K+ channels are open so membrane cannot be depolarised

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23
Q

What is stroke volume?

A

Volume of blood ejected by each ventricle per heart beat

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24
Q

Equation for stroke volume?

A

SV = end diastolic volume (EDV) - end systolic volume (ESV)

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25
Q

How is stroke volume regulated? (2)

A
  • Intrinsic mechanisms: within heart muscle itself

* Extrinsic mechanisms: nervous and hormonal control

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26
Q

What is end systolic volume?

A

Volume of blood in ventricle at the end of contraction

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27
Q

What is intrinsic control of stroke volume?

A

Changes in SV caused by changes in diastolic length of myocardial fibres

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28
Q

What is diastolic length of myocardial fibers determined by?

A

End diastolic volume

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29
Q

What is end diastolic volume?

A

Volume of blood in ventricle at end of diastole

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30
Q

What determines the cardiac preload?

A

End diastolic volume

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31
Q

What is cardiac preload?

A

How much of heart is loaded with blood before it contracts

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32
Q

What is end diastolic volume determined by?

A

Venous return to heart i.e. the higher the venous return, the higher the EDV

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33
Q

What is the Frank-Starling Mechanism or Starling’s law of the Heart?

A

The more blood ventricle is filled with during diastole (EDV), the greater the volume of ejected blood during systole (stroke volume)

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34
Q

What does stretch of myocardial fibres also do?

A

Increases affinity of troponin for Ca+

35
Q

When do skeletal muscles reach optimum fibre length?

A

Under resting conditions

36
Q

When do cardiac muscles reach optimal fibre length?

A

Stretching the muscle (Frank-Starling Mechanism)

37
Q

How does Starling’s Law match the stroke volume of RV and LV?

A
  • If venous return to right atrium increases, EDV of right ventricle increases so increased SV into pulmonary artery
  • Increased venous return to left atrium from pulmonary vein increases, EDV of left ventricle increases so increased SV into aorta
38
Q

What is afterload?

A

Resistance into which heart is pumping

39
Q

How does Frank-Sterling mechanism partially compensate for decreased SV caused by increased afterload?

A
  • If afterload increases, heart unable to eject full SV so EDV increases
  • Force of contraction increased by Frank-Sterling mechanism
40
Q

What happens if increased afterload continues to exist e.g. in untreated hypertension?

A

Ventricular hypertrophy to overcome resistance

41
Q

What is extrinsic control of SV?

A

Involves nerves and hormones

42
Q

What effect does stimulation of sympathetic nerves have on force of contraction?

A

Increases force of contraction

43
Q

What is anything that increases force of contraction the heart known as?

A

Positive inotropic effect

44
Q

How does sympathetic stimulation increase force of contraction?

A

Activation of Ca+ channels - greater Ca+ influx

45
Q

What happens to peak ventricular pressure during sympathetic stimulation?

A

Rises

46
Q

How does sympathetic stimulation reduce the duration of systole?

A

Rate of pressure change (dP/dt) during systole increases

47
Q

How does sympathetic stimulation reduce the duration of diastole?

A

Rate of ventricular relaxation increases (increased rate of Ca++ pumping)

48
Q

What is the effect of peak ventricular pressure rising?

A

Contractility of heart at given EDV rises

49
Q

What happens to Frank-Sterling curve in sympathetic nerve stimulation?

A

Shifted to left

50
Q

What will a negative inotropic effect (e.g. heart failure) do to Frank-Sterling curve?

A

Shift to right

51
Q

What is the effect of parasympathetic innervation on force of contraction?

A
  • Very little direct effect on SV

* Vagal stimulation has major influence on rate, not force of contraction

52
Q

What is the effect of adrenaline and noradrenaline released from ADRENAL MEDULLA (not neurotransmitters) on the heart?

A

Positive Inotropic and chronotropic effect

53
Q

Cardiac output?

A

Volume of blood pumped by each ventricle per minute

54
Q

Equation for cardiac output

A

CO = SV x HR

55
Q

What is resting CO in a healthy adult?

A

5 litres per minute

56
Q

How is cardiac output regulated?

A

Regulating heart rate and stroke volume

57
Q

When do heart valves produce sound?

A

When they shut

58
Q

What is cardiac cycle?

A

All events that occur from beginning of one heart beat to beginning of next

59
Q

What is ventricular diastole?

A

Heart ventricles are relaxed and fill with blood

60
Q

What is ventricular systole?

A

Heart ventricles contract and pump blood into aorta/pulmonary artery

61
Q

At a heart rate of 75 bpm what is the length of ventricular systole and diastole? (2)

A
  • Systole: 0.3 sec

* Diastole: 0.5 sec

62
Q

What are the events of the cardiac cycle? (5)

A

1) Passive Filling
2) Atrial Contraction
3) Isovolumetric ventricular Contraction
4) Ventricular Ejection
5) Isovolumetric ventricular Relaxation

63
Q

What is passive filling?

A
  • Pressure in atria and ventricles almost 0 but atrial pressure slightly higher than ventricular pressure
  • AV valves open so venous return flows into ventricles via pressure gradient
64
Q

What is aortic pressure during passive filling? Is aortic valve closed or open?

A

~80 mmHg

Closed

65
Q

What percentage of ventricles are filled by passive filling?

A

80%

66
Q

At what point on an ECG do the atria contract?

A

Between P-wave and QRS

67
Q

What completes the end diastolic volume?

A

Atrial contraction (20%)

68
Q

What is EDV in normal resting adult?

A

~130 ml

69
Q

At what point on ECG do ventricles contract?

A

After QRS

70
Q

What happens when ventricular pressure exceeds atrial pressure?

A

AV valves shut producing first heart sound (LUB)

71
Q

What is isovolumatric ventricular contraction?

A
  • Ventricular pressure rises and AV valves shut
  • Aortic valve/pulmonary valve still shut
  • There is a closed volume as no blood can enter or leave the ventricle
72
Q

What happens in ventricular ejection? (2)

A
  • Ventricular pressure exceeds aorta/pulmonary artery pressure causing aortic/pulmonary valves to open
  • SV is ejected by each ventricle leaving behind the ESV
73
Q

Explain the vents of ventricular repolarisation (2)

A
  • Ventricles relax and ventricular pressure falls
  • When ventricular pressure falls below aortic/pulmonary pressure aortic/pulmonary valves shut, producing second heart sound (DUB)
74
Q

What are LUB and DUB heart sounds produced by?

A
  • LUB - AV valve closure

* DUB - Aortic/pulmonary valve closure

75
Q

What does valve vibration produce?

A

Dicrotic notch in aortic pressure curve

76
Q

What marks the start of isovolumetric relaxation?

A

Closure of aortic/pulmonary valves

77
Q

Explain the events of isovolumetric relaxation (3)

A
  • Tension falls around a closed volume as AV valves and pulmonary/aortic valves are shut
  • When ventricular pressure falls below atrial pressure, AV valves open and new cardiac cycle begins
78
Q

What does first heart sound (S1) herald the beginning of? S2?

A

S1 - systole

S2 - diastole

79
Q

What valves are auscultated in a cardiac exam?

A 
In order of position:
All - Aortic
Physicians - Pulmonary 
Take - Tricuspid 
Money - Mitral
80
Q

Why does arterial pressure not fall to zero during diastole?

A

Elastic recoil of elastic arteries

81
Q

When does jugular venous pulse (JVP) occur?

A

After right atrial pressure waves

82
Q

What is a, c and v in the following diagram? (3)

A
  • a - atrial contraction
  • c - bulging of tricuspid valve into atrium during ventricular contraction
  • v - rise of atrial pressure during atrial filling (release once AV valves open)
83
Q

What do pressure changes in JVP reflect?

A

Pressure changes in the right atrium

Cardiovascular (28 decks)

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