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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
Normal Resting Heart Rate
60-100 bpm
26
What is a Slow Heart Rate?
Bradycardia
27
What is Fast Heart Rate?
Tachycardia | >100 bpm
28
Parasympathetic Supply of the Heart
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
What is Atropine?
Competitive inhibitor of ACh | Used in to speed up heart rate in extreme bradycardia
30
Effect of Vagal Stimulation on Pacemaker Potentials
Slope of pacemaker potential decreases Takes longer to reach threshold Frequency of AP decreases Negative chronotropic effect
31
Sympathetic Supply of the Heart
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
Effect of Sympathetic Stimulation on Pacemaker Potentials
Slope of pacemaker potential increases Pacemaker potential reaches threshold quicker Frequency of AP increases Positive chronotropic effect
33
What is Autorhymicity with respect to the Heart?
Th heart can stimulate its own rhythm
34
What is an ECG a record of?
The depolarisation and depolarisation cycle of cardiac muscle obtained from the skin surface
35
What is the "All-or-none" Law of the heart?
Electrical excitation reaches all the cardiac myocytes | This is by gap junctions forming low resistance electrical pathways between neighbouring myocytes
36
What is the purpose of Desmosomes between cardiac cells?
Provide mechanical adhesion between adjacent cardiac cells | Ensure that tension developed by one cell is passed to the next
37
What are the contractile units of muscle?
Myofibrils
38
What is the structure of a myofibril?
Actin = Thin, lighter filaments Myocin = Thick, darker filaments Within each myofibril, actin and myosin are arranged into sarcomeres
39
How is muscle tension produced by the myofibril?
Sliding of actin filaments on myosin filaments
40
Which two things are necessary for contraction and relaxation?
ATP | Calcium
41
What is the importance of calcium in cross bridge formation?
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
How does the action potential switch on ventricular systole?
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
What is the refractory period?
A period following an AP in who it is not possible to produce another AP
44
What is the benefit of a long refractory period?
Protective for the heart | Prevents generation of tetanic contractions in the cardiac muscle
45
What is Stroke Volume?
The volume of blood ejected by each ventricle per heart beat SV = End Diastolic Volume - End Systolic Volume
46
What regulates the Stroke Volume?
Intrinsic mechanisms = Within the heart | Extrinsic mechanisms = Outwith the heart
47
Intrinsic Control of Stoke Volume
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
Frank Starling Law of the Heart
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
What is Afterload?
The resistance into which the heart is pumping
50
How does the hear compensate for continue increased afterload?
Ventricular hypertrophy
51
Extrinsic Control of Stroke Volume
Involves nerves and hormones Ventricular muscle supplied by sympathetic nerve fibres - noradrenaline is the neurotransmitter. Increases force of contraction
52
Effect of Sympathetic Stimulation on Ventricular Contraction
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
Effect of Parasympathetic Nerves on Ventricular Contraction
Very little vagus nervation of ventricles in man | Little if any direct effect on SV
54
Hormonal Control of Stroke Volume
Adrenaline and noradrenaline released from the adrenal medulla have inotropic and chronotropic effect Effects normally minor compared to sympathetic stimulation
55
What is Cardiac Output?
The volume of blood pumped by each ventricle per minute CO = SV x HR Usually around 5 litres per minute
56
What is the Cardiac Cycle?
All events that occur form the beginning of one heart beat to the beginning of the next
57
Which five events occur during the Cardiac Cycle?
``` Passive filling Atrial contraction Isovolumetric ventricular contraction Ventricular ejection Isovolumetric ventricular relaxation ```
58
What occurs during Passive Filling?
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
What occurs during Atrial Contraction?
P wave in the ECG signals depolarisation Atria contract between P wave and QRS Atrial contraction completes the end diastolic volume
60
What occurs during Isovolumetric Ventricular Contraction?
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
What happens during Ventricular Ejection?
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
What happens during Isovolumetric Ventricular Relaxation?
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
What causes the Heart Sounds?
``` S1 = Closure of mitral and tricuspid valves. Start of systole. "Lub" S2 = Closure of aortic and pulmonary valves. Start of diastole. "Dub" ```
64
Where is the aortic area on the chest wall?
Second intercostal space, right sternal edge
65
Where is the pulmonary area on the chest wall?
Second intercostal space, left sternal edge
66
Where is the tricuspid area on the chest wall?
Fourth intercostal space, left sternal edge
67
Where is the mitral area on the chest wall?
Fifth intercostal space, mid-clavicular line, left side
68
When does the JVP occur during the heart cycle?
After the right atrial pressure wave

Cardio (19 decks)

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