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CardioRespiratory Year 1 > Physiology - Heartbeat and ECG > Flashcards

Physiology - Heartbeat and ECG Flashcards

1
Q

What is the Sino-atrial node

A
  • a group of impulse generating cells that are positioned in the right atrium near the entry of the superior vena cava
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2
Q

describe the structure of the Sino atrial node

A
  • they are nodal cells which are modified cardiac muscle cells (they are NOT nerve cells)
  • connected to adjacent atrial cells by gap junctions
  • death from affected cells will stop the SA from triggering the heartbeat - but the heart will not stop beating as atria can act as pacemaker this just means that the heart will go at a slower rate
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3
Q

What is the blood supply to the SA

A
  • right coronary artery
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4
Q

What happens if there is a blockage in the right coronary after

A
  • MI blocking in this artery will cause ischaemia in the SSA node unless there is a good anastomosis from the left coronary artery
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5
Q

describe the structure of the AV node

A
  • Located on the inter-atrial septum close to the tricuspid valve
  • The AV node gives rise to modified muscle fibres called the bundle of His that travels down the interventricular
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6
Q

the action potential of the heart is…

A

-100 times longer at 200ms compared to a nerve action potential

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7
Q

Why does the cardiac action potential last longer

A
  • In cardiac pacemaker cell there is a constant inward (leak) sodium influx into a cell at rest, this would normally depolarise the leaky potassium channels causes an outward potassium current which prevents the depolarisation, the membrane potential depends on the balance between the inward and outward currents
  • The outward potassium current decays with time therefore the inward sodium current gradually becomes dominant and the membrane potential slowly depolarises
  • Eventually cell is sufficiently depolarised to trigger an action potential
  • During the action potential the outward potassium current is reset to a higher level and then starts to decay again
  • Cells inside the SA node are spontaneously active due to the constant inward current - heart rate depends on the rate of decay of the outward potassium current
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8
Q

The heart rate depends on…

A

the rate of decay of the outward potassium current

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9
Q

What is the SA innervated by

A
  • parasympathetic (vagal) and sympathetic nerve fibres
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10
Q

describe the parasympathetic innervation to the SA node

A
  • from the vagus act via interneurons in the node inhibit the decay of potassium current via muscarinic receptors this slows the pacemaker down
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11
Q

describe the sympathetic innervation to the SA node

A
  • At the SA node accelerate the decay of the potassium current by beta-1 adrenoreceptor action making the pacemaker speed up
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12
Q

describe innervation to the AV node

A

parasympathetic and sympathetic have weaker inputs to the AV node, blood borne adrenaline acts on beta-1 receptors on cardiac muscle cells node to produce an increased force of contraction (inotropic action)

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13
Q

Describe the action of the SA and AV nodes

A
  1. The action potential form the SA nodes spread over both atria by 60ms after the SA node has been activated
  2. AV node does not start to transmit action potentials down into the ventricles the bundle of His until 120ms
  3. The 60ms delay at the start of the AV node allows the atria to physically contract and push blood into the ventricles before the ventricles contract, because of the delay the AV is called the weak leak
  4. Muscle fibres specialised for the speed of conduction levae the AV node and travel down the interventricular septum and cause the activation of the ventricles and cause the ventricles to contract
    - These are the purkinje fibres, there are two bundles there is the left and the right bundle
    - At the top of both bundle is the bundle of His
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14
Q

what happens when there is damage to the bundle of his

A
  • it is damaged by ischaemia so conduction is damaged
  • First degree AV block - This is when the PR interval is lengthened (increase in the delay) beyond to 200ms, not usually serious,
  • 1% of young adults have it
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15
Q

What is plateau

A
  • Ventricles action potential starts like a normal nerve action potential when sodium is being influxed and sodium is depolarising, but this is followed by the prolonger depolarisation phase called the plateau
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16
Q

What is plateau due to

A
  • Plateau is due to a late and prolonged entry of calcium into the cell which helps the muscle contract for a longer time than ordinary skeletal muscle
  • Calcium ions enter through slow (L type) calcium channels found at the membranes of cardiac cells
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17
Q

duration of the plateau affects…..

A

the force of contraction

- the longer the influx the more strong the contraction

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18
Q

atria have a ..

A

Shorter plateau than the ventricles

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19
Q

How do the drugs affect the ventricles

A
  • Drugs that block the calcium channels are used clinically to reduce the force of ventricular contraction and the work of the heart
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20
Q

Why do the heart have a refractory period

A
  • Prevents the muscles contracting prematurely and keeps all the cells synchronous
  • If cells get out of synchronisation this leads to fibrillation – different parts of the ventricles contracting at different times
  • Means that ventricular pressure does not rise enough to generate any cardiac output and death results
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21
Q

How does a defibrillator affect the refractory period

A
  • shocks all the muscles and makes it contract synchronously, all cells then go into the refractory period together and the rhythm is restored
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22
Q

What is an ECG

A
  • Action potetnials in the cardiac muscle generate electrical voltages outside the heart which can be detected on the surface of the body
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23
Q

How many leads are there

A

12

24
Q

what do the leads do

A
  • Amplitudes of the ECG on different leads gives information about heart function
25
Q

define a lead

A

lead is the voltage recorded between two points on the body

26
Q

what is the difference between ECG and cardiac action potentials

A
  • ECG is not the same shape as the cardiac action potential it is much smaller (1mv) than cardiac action potentials
  • ECG wave is generated at the start of cardiac action potential and is shorter lasting
  • The R wave signals the start of ventricular depolarisation
27
Q

What does lead I do

A
  • Records the signal between left and right axillae
28
Q

What does lead II do

A
  • Records signal between the right axilla and leg
29
Q

What does lead III do

A
  • Records signal between the left axilla and leg
30
Q

what view of the heart does the leads I II and III supply

A
  • picture of the electrical activity of the heart in the frontal plane
31
Q

where can leads I, II and III be placed

A

They can be placed anywhere on the arm and leg as these have no cardiac muscles so act as conductors

32
Q

what lead is the standard ECG recorded on and why

A

Lead II

- it gives the largest singal of the three limb leads meaning it shows a good picture

33
Q

What does PR tell you

A

tells you the delay of the AV node, should be 120 to 200ms, if it is greater than that then it can cause heart problems

34
Q

describe p wave

A
  • Due to atrial depoliarsation
  • Smooth and rounded
  • Positive in leads I II and sometimes III
  • Notched or peaked P waves are in COPD and CHF
  • Lasts 100ms
35
Q

Describe the QRS complex

A
  • Depolarisation of the ventricles
  • Polarity of the QRS complex depends on which lead is viewed, it could be positive, negative or bipolar
  • If there is no R wave then it is called an S wave
36
Q

describe the Q wave

A
  • Negative by definition, no Q wave is present if QRS signal starts upwards
  • Q wave size depends on which lead you are looking at
  • Absent in Lead I,III might be small or absent in lead II
37
Q

Describe R and S waves

A
  • R wave is positive by definition, present in Leads I,II and III
  • S waves are negative by definition
38
Q

describe the ST segment

A
  • Time when all ventricular muscles are contracting
  • Normal ST segment starts flat and curves upwards into the T wave
  • Called the iso electric point as there is no voltage between
  • Important for diagnosis of acute MI
39
Q

describe the T wave

A
  • Due to difference in time of repolarisation of the ventricles
  • Normally orientated in some direction as preceding QRS complex
40
Q

What are the 3 augmented leads

A
  • aVR
  • aVL
  • aVF
41
Q

what are the augmented leads

A
  • They are called unipolar leads as the amplitude of the signal is calculated between on physical recording point and a virtual reference point in the middle of the chest
  • The ECG machine automatically calculates the values of these and gives a reading
42
Q

How many limb leads are there

A

6

Therefore there are 6 limb leads these are I, II, III, aVR, aVL, aVF

43
Q

How many chest leads are there

A

6 precordial chest leads

V1-V6

44
Q

describe what the ECG looks like in an aVR

A
  • The aVR always has a large Q wave and a small or non existent R wave
  • Inverted T wave
  • Lead one is recording negative to positive where as aVR is recording positive to negative
  • S wave is what it is called not an inverted R wave
45
Q

Describe what the ECG looks like in the aVL

A
  • often small
46
Q

Where is V1 positioned

A
  • V1 is in the 4th intercostal space on the right
47
Q

Where is V2 positioned

A
  • V2 is in the 4th intercostal space on the left
48
Q

Describe the ECG in the chest leads

A

V1 is larger negative so has large S waves
V3, V4 has a bipolar this is the transition between V1 and V6
V5,6 is mainly positive and has a large R wave

49
Q

Why do we have 12 different recording leads

A
  • Electordes are affected more by electrical activity in physically nearer parts of the heart
  • Different leads view different regions of the heart
50
Q

what leads are needed for an inferior view of the heart

A

II
III
aVF

51
Q

What leads are needed for a lateral view of the heart

A

I
aVL
V5
V6

52
Q

What leads are needed for the anterior view of the heart

A

V3

V4

53
Q

What leads are needed for the septal view of the heart

A

V1

V2

54
Q

Describe what atrial fibrillation looks like on an ECG

A
  • No P wave as there is no synchronised electrical acivity
55
Q

Describe what atrial flutter looks like on an ECG

A
  • This is when there is extra P waves

- SA node is working but not at a regular rate so you get extra P waves

56
Q

Describe what a change in the ST segment looks like on an ECG

A
  • ST elevation on one or more leads is normally a sign of acute iscaemia in the viewed part of the heart, although the most common cause of ischaemia is acute mi this is not always the reason for ST elevation
  • ST depression can also be a sign of ischaemia but this time chronic rather than acute
57
Q

Describe what ventricular tachycardia looks like on an ECG

A
  • Ventricles are contracting synchrosly because you are getting discrete waves

CardioRespiratory Year 1 (28 decks)

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