Physiology - The Cardiac Cycle Flashcards

1
Q

Where does excitation of the heart normally originate?

A

Sino-Atrial Node

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2
Q

Where is the SA node located?

A

Upper right atrium

Close to where the SVC enters

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3
Q

What is Sinus Rhythm?

A

A heart controlled by the sino-atrial node

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4
Q

How does cardiac excitation normally originate?

A

The cells in the SA node exhibit spontaneous pacemaker potential. The membrane potential gradually drifts towards a threshold to generate an action potential

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5
Q

What is the pacemaker potential?

A

The gradual drift of the membrane potential to depolarisation

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6
Q

Ionic Basis for the Pacemaker Potential

A

Decrease in K+ efflux
Slow Na+ influx
(known as the funny current)
NET movement of positive ions into the cell

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7
Q

Ionic Basis for Pacemaker Action Potential - Depolarisation

A

Caused by voltage-gated Ca++ channels resulting in Ca++ influx

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8
Q

Ionic Basis for Pacemaker Action Potential - Repolarisation

A

Activation of K+ channels resulting in K+ efflux

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9
Q

How does the cardiac excitation spread across the heart?

A

SA to AV node

AV node to Bundle of His, left and right branches then Purkinje Fibres

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10
Q

Where does cell to cell spread of excitation occur?

A

SA node to AV node
SA node through both atria
Within ventricles

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11
Q

How does cell to cell conduction occur?

A

Through gap junctions (low resistant protein channels)

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12
Q

Where is the AV node located?

A

The base of the right atrium, just above the junction of the atria and ventricles

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13
Q

What kind of cells make up the AV node?

A

Specialised cardiac cells

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14
Q

What is the function of the slow conduction velocity of the AV node?

A

Allows the atria to contract before the ventricles

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15
Q

What is special about the AV node?

A

The only point of electrical contact between the atria and ventricles

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16
Q

Electrical conduction through Bundle of His and Purkinje Fibres

A

Rapid

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17
Q

Electrical conduction through ventricular muscle

A

Cell to cell conduction

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18
Q

Ionic Basis for Ventricular Muscle Action Potential - Phase 0

A

Depolarisation
Fast Na+ influx
Moves membrane potential to +30

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19
Q

Ionic Basis for Ventricular Muscle Action Potential - Phase 1

A

Closure of Na+ channels and transient K+ efflux

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20
Q

Ionic Basis for Ventricular Muscle Action Potential - Phase 2

A

Plateau Phase
Mainly Ca++ influx through voltage gated Ca++ channels
Unique to contractile cardiac muscle cells

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21
Q

Ionic Basis for Ventricular Muscle Action Potential - Phase 3

A

Falling Phase - Repolarisation

Closure of Ca++ channels and K+ efflux due to activation of K+ channels

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22
Q

Ionic Basis for Ventricular Muscle Action Potential - Phase 4

A

Resting Membrane Potential

-90

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23
Q

What effect does the autonomic nervous system have on heart rate?

A
Sympathetic = Increases 
Parasympathetic = Decreases
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24
Q

How does the vagus nerve influence the normal resting heart rate?

A

Exerts a continous influence on the SA node
Vagal tone dominates
Slows the intrinsic rate from ~100 bpm to ~70 bpm

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25
Q

Normal Resting Heart Rate

A

60-100 bpm

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26
Q

What is a Slow Heart Rate?

A

Bradycardia

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27
Q

What is Fast Heart Rate?

A

Tachycardia

>100 bpm

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28
Q

Parasympathetic Supply of the Heart

A

Supplies SA node and AV node Vagal supply
Stimulation slows heart rate ad increases AV nodal delay
Neurotransmitter is ACh acting through M2 receptor

29
Q

What is Atropine?

A

Competitive inhibitor of ACh

Used in to speed up heart rate in extreme bradycardia

30
Q

Effect of Vagal Stimulation on Pacemaker Potentials

A

Slope of pacemaker potential decreases
Takes longer to reach threshold
Frequency of AP decreases
Negative chronotropic effect

31
Q

Sympathetic Supply of the Heart

A

Cardiac sympathetic nerves supply SA node, AV node and myocardium
Stimulation increases heart rate, decreases AV nodal delay and increases force of contraction
Neurotransmitter is noradrenaline acting through beta1 adrenoceptors

32
Q

Effect of Sympathetic Stimulation on Pacemaker Potentials

A

Slope of pacemaker potential increases
Pacemaker potential reaches threshold quicker
Frequency of AP increases
Positive chronotropic effect

33
Q

What is Autorhymicity with respect to the Heart?

A

Th heart can stimulate its own rhythm

34
Q

What is an ECG a record of?

A

The depolarisation and depolarisation cycle of cardiac muscle obtained from the skin surface

35
Q

What is the “All-or-none” Law of the heart?

A

Electrical excitation reaches all the cardiac myocytes

This is by gap junctions forming low resistance electrical pathways between neighbouring myocytes

36
Q

What is the purpose of Desmosomes between cardiac cells?

A

Provide mechanical adhesion between adjacent cardiac cells

Ensure that tension developed by one cell is passed to the next

37
Q

What are the contractile units of muscle?

A

Myofibrils

38
Q

What is the structure of a myofibril?

A

Actin = Thin, lighter filaments
Myocin = Thick, darker filaments
Within each myofibril, actin and myosin are arranged into sarcomeres

39
Q

How is muscle tension produced by the myofibril?

A

Sliding of actin filaments on myosin filaments

40
Q

Which two things are necessary for contraction and relaxation?

A

ATP

Calcium

41
Q

What is the importance of calcium in cross bridge formation?

A

Calcium binds to troponin on the actin filament
Causes a conformational change to the troponin-tropomyosin complex, freeing up the cross bridge binding site
Myosin cross bridge can now bind to the actin filament
The filaments slide over each other

42
Q

How does the action potential switch on ventricular systole?

A

Ca++ influx during the plateau phase of the AP provides enough Ca++ to stimulate release of Ca++ from the SR
This provides sufficient Ca++ to go on to activate the contract machinery and cause contraction

43
Q

What is the refractory period?

A

A period following an AP in who it is not possible to produce another AP

44
Q

What is the benefit of a long refractory period?

A

Protective for the heart

Prevents generation of tetanic contractions in the cardiac muscle

45
Q

What is Stroke Volume?

A

The volume of blood ejected by each ventricle per heart beat
SV = End Diastolic Volume - End Systolic Volume

46
Q

What regulates the Stroke Volume?

A

Intrinsic mechanisms = Within the heart

Extrinsic mechanisms = Outwith the heart

47
Q

Intrinsic Control of Stoke Volume

A

Changes in diastolic length of myocardial fibres
This alters the end diastolic volume which determines cardiac preload
End diastolic volume is determined by the venous return to the heart

48
Q

Frank Starling Law of the Heart

A

The more the ventricle is filled with blood during diastole (EDV) the greater the volume of ejected blood will be during the resulting systolic contraction (SV)

49
Q

What is Afterload?

A

The resistance into which the heart is pumping

50
Q

How does the hear compensate for continue increased afterload?

A

Ventricular hypertrophy

51
Q

Extrinsic Control of Stroke Volume

A

Involves nerves and hormones
Ventricular muscle supplied by sympathetic nerve fibres - noradrenaline is the neurotransmitter. Increases force of contraction

52
Q

Effect of Sympathetic Stimulation on Ventricular Contraction

A

Activation of Ca++ channels mediated greater Ca++ influx, so increased force of contraction
cAMP mediated
Peak ventricular pressure rises, rate of pressure during systole increases, reducing the duration of systole
Rate of ventricular relaxation increases, reducing duration of diastole

53
Q

Effect of Parasympathetic Nerves on Ventricular Contraction

A

Very little vagus nervation of ventricles in man

Little if any direct effect on SV

54
Q

Hormonal Control of Stroke Volume

A

Adrenaline and noradrenaline released from the adrenal medulla have inotropic and chronotropic effect
Effects normally minor compared to sympathetic stimulation

55
Q

What is Cardiac Output?

A

The volume of blood pumped by each ventricle per minute
CO = SV x HR
Usually around 5 litres per minute

56
Q

What is the Cardiac Cycle?

A

All events that occur form the beginning of one heart beat to the beginning of the next

57
Q

Which five events occur during the Cardiac Cycle?

A
Passive filling 
Atrial contraction 
Isovolumetric ventricular contraction 
Ventricular ejection 
Isovolumetric ventricular relaxation
58
Q

What occurs during Passive Filling?

A

Pressure in atria and ventricles is close to zero
AV valves open so venous return flows into ventricles
Aortic/pulmonary valves are closed
Ventricles become ~80% full

59
Q

What occurs during Atrial Contraction?

A

P wave in the ECG signals depolarisation
Atria contract between P wave and QRS
Atrial contraction completes the end diastolic volume

60
Q

What occurs during Isovolumetric Ventricular Contraction?

A

Ventricular contraction starts after the QRS
Ventricular pressure rises
When ventricular pressure exceeds atrial pressure, AV valves shut
Aortic/pulmonary valves are still closed, so blood is contained within ventricles
Tension rises steeply around a closed volume

61
Q

What happens during Ventricular Ejection?

A

When ventricular pressure excess aorta/pulmonary artery pressure, aortic/pulmonary valves open
SV is ejected by each ventricle, leaving behind ESV
Aortic pressure rises
T wave in ECG signals ventricular repolarisation
Ventricles relax and ventricular pressure falls below aortic/pulmonary pressure
Aortic/pulmonary valves shut
Valve vibration produces dicrotic notch in aortic pressure curve

62
Q

What happens during Isovolumetric Ventricular Relaxation?

A

Closure of aortic/pulmonary valves
Ventricle is again a closed box
Tension falls around a closed volume
When ventricular pressure falls below atrial pressure, AV valves open

63
Q

What causes the Heart Sounds?

A
S1 = Closure of mitral and tricuspid valves. Start of systole. "Lub"
S2 = Closure of aortic and pulmonary valves. Start of diastole.  "Dub"
64
Q

Where is the aortic area on the chest wall?

A

Second intercostal space, right sternal edge

65
Q

Where is the pulmonary area on the chest wall?

A

Second intercostal space, left sternal edge

66
Q

Where is the tricuspid area on the chest wall?

A

Fourth intercostal space, left sternal edge

67
Q

Where is the mitral area on the chest wall?

A

Fifth intercostal space, mid-clavicular line, left side

68
Q

When does the JVP occur during the heart cycle?

A

After the right atrial pressure wave