CVS Physiology Flashcards

(128 cards)

1
Q

What triggers contraction of cariac muscle cells?

A

An action potential

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2
Q

What is autorhythmicity?

A

The ability of the heart to contract itself

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3
Q

What are the two types specialised cardiac cells?

A

Contractile and autorhythmic

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4
Q

What is the function of contractile cells?

A

To pump blood, they don’t initiate an AP

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5
Q

What is the function of autorhythmic cells?

A

They disply pacemaker activity

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6
Q

What is the pacemaker potential?

A

The slow drift of autorhythmic cells to threshold

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7
Q

How do autorythmic cells trigger contractile cells?

A

By cyclically initiating an AP that spreads through the heart

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8
Q

What areas of the heart contain autorhythmic cells?

A

The SA node, AV node, bunle of His and the Purkinje fibres

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9
Q

What is linked by the internodal pathway?

A

The SA node and AV node

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10
Q

Why does the SA node set the heart rate?

A

It has the fastest rate of AP discharge

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11
Q

What will happen if the SA node fails?

A

The AV node will take over

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12
Q

What branc of the nervous system alters heart rate?

A

The ANS

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13
Q

What is the pathway of cardiac excitation?

A

SA noe -> AV node -> Bundle of His -> Purkinje Fibres

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14
Q

At what point is the AP spread from atria to ventricles?

A

At the AV node

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15
Q

Why is the delay of excitation at the AV node necessary?

A

As it allows time for the blood to move from the atria to ventricles

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16
Q

When does cardiac depolarisation occur?

A

When the membrane potential is -40 mV

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17
Q

When does pacemaker potential occur?

A

After the AP is induced

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18
Q

What occurs in the early phase of the pacemaker potential?

A

The voltage gated Na (funny) channels open and Na enter the cell down its concentration gradient. Depolarisation begins.

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19
Q

What occurs in the late phase of the pacemaker potential?

A

The funny channels close and transient-type Ca channels open. Ca enters the cell down its concentration graient which causes furher depolarisation and brings the Em to threshold. Ca channels close and the AP occurs.

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20
Q

What occurs at pacemaker potential peak upstroke?

A

K channels open and K ions move out of the cell. This causes repolarisation and K channels close. Downstroke occurs

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21
Q

What does repolarisation of the AP stimulate?

A

Opening of the funny channels which triggers nect pacemaker potential

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22
Q

What are the five steps of the cardiac myocyte cycle?

A
  1. Depolarisation of ventricular AP
  2. Early repolarisation
  3. Plateau phase
  4. Late reploarisation
  5. Resting potential
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23
Q

What drives stage 1 of the cardiac myocyte cycle?

A

Na (fast)

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24
Q

What drives stage 2 of the cardiac myocytes cycle?

A

K (fast)

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25
What drives stage 3 of the cardiac myocyte cycle?
Ca L-type channels opening (slow)
26
What drives stage 4 of the cardiac myocyte cycle?
K leaving the cell restoring the resting potential
27
What must happen before another AP can be triggered?
The cardiac myocyte exciteable membrane must recover
28
What does an ECG record?
Overall sprea of activity through the heart
29
What is the p wave of an ECG?
Atrial depolarisation
30
What is the QRS complex of an ECG?
Ventricular depolariation, atrial reploarisation
31
What is the T wave of an ECG?
Ventricular repolarisation
32
What is the PR segment of an ECG?
AV node delay
33
What is the ST segment of an ECG?
Plateau phase. The time during which ventricles are contracting and emptyng. Ventricles fully depolarised.
34
What is the TP interval of an ECG?
The heart is fully depolarised and the ventricls are filling
35
What is a lead in an ECG?
A pair of connections
36
How many leads are used for an ECG?
12: 6 limb, 6 chest
37
How are leads arranged?
In an inverted triangle over the thorax
38
What are the 6 limb leads?
I, II, III, aVL, aVF
39
What three leads are bipolar?
I,II,III
40
What does the electrode on the right leg serve as?
The ground eleectrode
41
What do exploring electrodes record?
Electrical potential of cardiac musculature by measuring beneath the electroe and in six different locaion around the heart
42
When ECG are waves recorded?
When the potential is changing across cell membranes
43
When is the ECG flat?
During diastole and plateau phases
44
What is cardiac output?
The volume of blood pumed by each ventricle individually per minute
45
What is th equation for cardiac output?
CO = HRxSV
46
What is stroke volume?
The vlume of blood ejected per contraction (ml)
47
How is SV calculated?
SV = En diatolic volume - end systolic volume
48
Why is the end diastolic volume highr at lower heart rates?
As the time spent in diastole is longer
49
What are the methods of stroke volume control?
Intrinsic and extrinsic control
50
What initiates intrinsic control of SV?
EDV and so initial length ventricular muscle fibres
51
What stimulates extrinisc control of the SV?
Sympathetic stimulation
52
What is the principle of the Frank-Starling Law?
Increased ventricular filling (EDV) increases length and stretch of the venriclar fibres which increases the SV
53
What does increased stretch allow for?
Longer initial cardiac fibre length before contraction
54
What does increased ventricular fibre length allow for?
Increased force and so increased SV
55
WHat does increase venous return result in?
Increased SV
56
What are the advantages of the Frank Starling Law?
Equalises output between left and right ventricles so blood evenly distribued between pulmonary and systemic circuits. It allows for a larger cardiac output when requred by increasing venous return.
57
How is Ca involved in increasing SV?
Grater initial fibre lengthincrases sensitivity of contractile proteins to Ca. Increased inital fibre length increases Ca release from Ca
58
What neurotransmitter is used to enhance contractility in extrinsic control?
Adrenaline
59
What effect does adrenalne have on contractile fibres?
Makes them contract more forcefully
60
How dos extrinsic control increase rate of relaxation?
By stimulating Ca pumps ad shortening systole
61
Hw does extrinisc control shift the Frak Starling Curve?
Shifts to left
62
How does extrinisc control affect EDV and ESV?
Increases EDV and decreases ESV so overall SV is increased
63
How does adrenaline affec Ca concentration in te heart?
It causes as influx in the plateau phase
64
When do semilunar valves open to allow ejection?
When ventricular pressure is higher than that of the arteries
65
What is afterload?
Arterial blood pressure
66
How does the heart compensate for sustained increase in afterload?
By hypertrophy - enlargement
67
When does heart failure occur?
When the hear can’t compensate for afterload
68
What is dP/dt?
Change in pressure/change in time
69
What is dP/dt used for?
To estimate the contractile state of the myocardium and determine severity of valve disfunction
70
What is the isometric phase?
When the LVis contracting but the AV and SL alves are still closed so there is nowhere for the blood to go
71
When id dP/dt used to measure contractility?
When the heart is in isometric phase
72
Why is dP/dt measured at isometric phase?
As this phase occurs independently of afterload
73
What is tachycardia?
An increase in heart rate
74
What is bradychardia?
A decrease in heart rate
75
What is a chronotropic effect?
An effect that causes a change in heart rate
76
What neurotransmitter is released by the parasypathetic NS and acts via MAChR?
ACh
77
Which branch of the ANS is asociated with the vagus nerve?
Parasympathetic NS
78
Which parts of the heart are innervated by the vagus nerve?
The SA and AV nodes
79
Which adrenoceptor does noradrenaline work on?
B1
80
WHat are the two main ways the parasympathetic NS affects heart rate?
Hyperpolarisation of SA node and decrease of spontaneous depolarisation
81
How does ACh effect levels of K in the cell?
By increasing K permeability by slowing the closure of K channels
82
What is the result of increased K permeability?
Hyperpolariation
83
How does increasing K permeability increase the time taken to reach threshold?
It makes the cells starting point furter from the threshold
84
How does the parasympathtic NS slow depolariation?
ACh inhibits the c-AMP pathway which in turn reduces Na entry through funny channels and Ca through t-type channels.
85
How is AV node delay lengthened by the parasympathetic NS?
K permeability is increased, hyperpolarising the membrane and slowing excitation
86
Why does the parasympathetic system have little effect on the ventricles?
As the ventricles are unaffecte by the vagus nerve
87
How does the parasympatehtic system shrten the plateau phase?
By reducing Ca current which weakens atrial contraction
88
Why does the parasympathetic NS not affect the ventricles?
As the vagus nerve doesn’t innervate the ventricles
89
What is the main mechanism employed by the sympathetic NS to incease heart rate?
Speed up depolarisation so the threshold is reached more rapidly
90
What is the neurotransmitter released by the sympatehtic NS?
Noradrenaline
91
How is speed of depolarisation increased by the sympathetic NS?
Pacemaker cells increase their permability in t-type and funny channels, increasing intracellular levels of Ca and Na whch increases speed of depolarisation
92
How does the sympathetic NS decrase nodal delay?
By increasing conduction velocity
93
How is contactile strength increased by the sympathetic NS?
Ca permeability is increaed by opening L-type channels. More Ca, greater force of contraction
94
How does the sympathetic NS speed up relaxation?
By enhancing Ca pumps in the SR to take up Ca
95
What is the function of arterioles?
They resist blood flow, are responsible for pattern of blood distrubution and participate in regulation of arterial blood pressure
96
What is the function of capillaries?
They are sites of nutrient and waste exchange
97
What is the function of veins?
Low resistance vessels that return blood to the heart
98
What is the tunica intima layer of arteries composed of?
Endothelial and connective tissue
99
What is the tunica media layer of arteries composed of?
Smooth muscle and often elastin
100
WHat is the tinca adventitia layer of arteries composed of?
Supporting connective tissue
101
Why do arterioles have a high proportion of smooth muscle?
To regulate blood flow
102
Why do veins have a high proportion of smooth muscle?
To alter the venous resevoir and venous return
103
What is hydrostatic pressure?
The pressure exerted by a fluid
104
What are the measurements of blood flow?
L/min or ml/min
105
What are the units of pressure difference (dP)?
MmHg
106
What’s required to calculate flow rate?
Pressure difference and resistance to flow
107
What is resistance?
The measure of difficulty of blood to flow between two points given pressure differences
108
What drives blood flow through vessels?
Pressure from heart contraction
109
What is flow rate dependent on?
Pressure gradient an vascular resistance?
110
What is the equation for flow?
F=dP/R
111
What happens to flow as resistance increases?
Decreases
112
How is theoretical maximum HR calculated?
220 - age in years
113
Which heart phase is longer at rest?
Diastole
114
What happens to valvs under forward presure?
The valve opens
115
What happens to valves under backwards pressure?
They close
116
What are the normal fluctuations of aortic pressure?
80-120 mmHg
117
What is normal left ventricular pressure?
0-120 mmHg
118
What is normal left ventricular EDV?
135 ml
119
What is left ventricular ESV?
65 ml
120
Does the left ventricle ever fully empty?
No
121
What are the main events of Mid-diastole?
Ventricles are relaxed In flow of blood into atria AV valves open and so passive filling Aortic and pulmonary valves closed
122
What are the main stages of late diastole?
``` AP generated AP conducted across atrial tissue via internodal pathway Atrial muscle cells depolarised Atrial contraction Increased ventricular pressure AV valves open ```
123
What are the main events of early systole?
``` EDV reached AP excites ventricular muscle via AV node Ventricles contract at end of QRS AV valves shut Isometric phase ```
124
What are the main events in the ejection period?
Ventricular pressure exceeds arterial Aortic valve opens Blood ejected ESV reached - 65ml
125
What are the main events of the end of systole?
``` Ventricles depolarised Ventricular pressure less than aortic Aortic valve shuts Dicrotic notch occurs AV valves shut Isometric ventricular relaxation ```
126
What is responsable for the first heart sound?
The close of the AV valves at the start of systole
127
What is responsible for the second heart sound?
The closure of the SL valves at the onset of diastole
128
What are heart murmurs?
Abnormal sounds of the heart that indicate an issue with the valves.