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CR1 > Heart and ECG > Flashcards

Heart and ECG Flashcards

1
Q

How is cardiac muscle similar to skeletal muscle?

A

Both are striated

Both have distinct bands of actin and myosin fibres – increase their overlap during contraction

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2
Q

In which two crucial ways does cardiac muscle differ from skeletal muscle?

A

Cardiac muscle cells in both atria and ventricles are joined together mechanically by INTERCALATED DISCS. Hold the cells together into a mechanically interconnected 3D network.
GAP JUNCTIONS within the intercalated discs link adjacent cardiac muscle cells electrically so that an action potential in any one cell spreads into the adjacent cells.

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3
Q

What do gap junctions enable? What does this produce? What name does this give atria and ventricular tissue?

A

Gap junctions enable an action potential in one cardiac cell to spread throughout entire atria or ventricle and produce a SYNCHRONOUS CONTRACTION OF THE WHOLE TISSUE.
Produces a powerful even tension in the tissue.
Atria or ventricular tissue is known as a SYNCYTIUM because of this electrical and mechanical connectivity.

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4
Q

What are the other names for the sino-atrial node?

A

SA node, SAN, or sinus node

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5
Q

What is the sino-atrial node? What does it do?

A

Group of cells positioned on wall of right atrium, near entrance of superior vena cava
This is the impulse generating (pacemaker) tissue

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6
Q

What type of cells are in the SAN? How are they connected to the adjacent atrial cells?

A

These nodal cells are MODIFIED CARDIAC MUSCLE CELLS, not nerve cells
Connected to adjacent atrial cells by gap junctions

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7
Q

Where does cardiac electrical activity start? Where does it spread to?

A

Cardiac electrical activity starts in SA node and spreads across atria to the ATRIO-VENTRICULAR (AV) node, where it stops (it is not directly transmitted to the ventricles)
The AV node is located on the inter-atrial septum close to the tricuspid valve

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8
Q

What is the normal resting potential in all cells? How is this maintained?

A

-70 to -90 mV

Maintained by tonically open potassium channels

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9
Q

What happens to the membrane potential if some of the potassium channels in a cell close?

A

The membrane potential will become less negative, i.e. become DEPOLARISED

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10
Q

How is an action potential generated in the pacemaker cells of the SAN?

A

Pacemaker cells in the SA node are spontaneously active
Action potentials are initiated by opening of sodium (and calcium) channels
After each action potential, potassium channels (which open during action potential) slowly spontaneously close (‘funny current’)
This causes a progressive depolarisation (prepotential or pacemaker potential) which eventually reaches threshold for the Na+ action potential channels to open and a new action potential is generated

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11
Q

What nerves innervate the SA node?

A

SA node is richly innervated by vagal and sympathetic autonomic nerve fibres

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12
Q

What is the effect of the parasympathetic nerves on the SA node?

A

PARASYMPATHETIC nerves from the vagus act via interneurons in the node to INHIBIT THE CLOSURE of one set of potassium channels via (cholinergic) MUSCARINIC RECEPTORS
Makes the receptor cells SLOW DOWN

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13
Q

What is the effect of the sympathetic nerves on the SA node?

A

SYMPATHETIC nerves at the SA node INCREASE RATE OF CLOSURE of other potassium channels by beta adrenoreceptor actions
This makes pacemaker rate INCREASE

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14
Q

What is the character of the input to the AV node of the para-/sympathetic systems?

A

Weaker than to the SA node

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15
Q

How does blood-borne adrenaline affect the heart?

A

Blood-borne adrenaline does not increase heart rate but acts on beta adrenoreceptors in the cardiac muscle to produce an INCREASED FORCE OF ATTRACTION

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16
Q

What can cause a normal ‘sinus arrhythmia’? What drug can make this disappear?

A

Parasympathetic outflow in vagus nerve increases during expiration and decreases during inspiration
Leads to a normal sinus arrhythmia - i.e. DECREASE IN HEART RATE DURING EXPIRATION
Administration of atropine (which blocks parasympathetic effects) can make sinus arrhythmia disappear

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17
Q

How does action potential spread in the heart? What does this allow for?

A

Action potential will have spread all over both atria and the AV node by ~60 ms after the SA node is activated
However, the AV node does not start to transmit action potentials down into the ventricles the bundle of His until 120 ms after the start of the SA node action potential
The delay of 60 ms at the AV node allows time for the atria to physically contract and so to push their blood into the ventricles before the ventricles start to contract

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18
Q

What are the Purkinje fibres? How many are there?

A

Large diameter muscle fibres (specialised for speed of conduction)
that leave the AV node and travel down the interventricular septum to activate the ventricles
There are two bundles of Purkinje fibres known as the left bundle and right bundle

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19
Q

What are the top of the left and right bundle called?

A

Bundle of His

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20
Q

What can damage conduction through the bundles? What happens if conduction fails at the top? What about the left/right bundles?

A

Ischaemia damages conduction
If conduction fails, we get BUNDLE BRANCH BLOCK
Further down we can get LEFT BUNDLE BRANCH BLOCK where the left ventricle is not activated, or RIGHT BUNDLE BRANCH BLOCK where the right ventricle is activated late or not activated

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21
Q

What are the first parts of the ventricle to contract? What does this contraction cause?

A

The first parts of the ventricle to contract are the papillary muscles – this contraction closes the AV valves before main ventricular contraction

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22
Q

When is contraction at the base of the heart delayed until?

A

Contraction at the base of the heart is delayed until ~180 ms

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23
Q

What do the papillary muscles pull on? What does this cause?

A

The papillary muscles pull on tendinous filaments called the chordae tendinea (like parachute strings) to pull the AV valves together and close them

24
Q

What is the unusual shape of action potential in the ventricular muscle?

A

Starts like a normal nerve action potential with sodium influx
However, this is followed by a prolonged depolarisation phase called the plateau

25
Q

What causes the plateau in action potential in the ventricular muscles? What does this help the muscle to do?

A

The plateau is due to a prolonged entry of calcium into the cell which helps the muscle contract for a much longer time than ordinary skeletal muscle

26
Q

What affect does adrenaline have on contraction of the heart? What is this called?

A

Adrenaline in the blood increases calcium entry during the plateau and thus INCREASES THE FORCE OF CONTRACTION of the heart
This is called an inotropic effect

27
Q

How do calcium ion enter the cardiac cells? What drugs block this, and what effect do these have?

A

The calcium ions enter through slow (L type) calcium channels found in the membranes of cardiac cells.
Drugs like amlodipine or verapamil which block these calcium channels REDUCE the force of ventricular contraction and thus the work (and oxygen demand) of the heart

28
Q

What are the four classes of drugs affecting the cardiac action potential? (give examples)

A 
o	sodium channel blockers (1a/moderate=Quinidine and Procainamide, 1b/weak=Lidocaine and Phenytoin, 1c/strong=Flecainide and Propafenone)
o	beta (adrenaline) blockers (Verapamil and Diltiazem)
o	calcium channel blockers (Amiodarone and Sotalol)
o	potassium channel blockers (Propranolol, Metoprolol)
29
Q

Why do myocardial cells have a long refractory period before the action potential?

A

This prevents the muscle contracting prematurely and keeps all the cells synchronous
If cells get ‘out of synchronisation’ then fibrillation can occur, when different parts of the ventricle are contracting at different times
Ventricular pressure does not rise enough to generate any cardiac output and death results

30
Q

How does a defibrillator work?

A

A defibrillator shocks all the muscle and makes it contract synchronously, all cells then go into refractory period together and rhythm is restored

31
Q

What does an Electrocardiogram (ECG) detect?

A

The action potentials in the cardiac muscle cells generate electrical voltages outside the heart which can be detected on the surface of the body.

32
Q

How many skin electrodes are used in a standard ECG? How many recording leads does this result in?

A

There are ten skin electrodes used in a standard ECG; four on the limbs and six on the chest. From these ten electrodes 12 recording ‘leads’ are obtained: Each lead shows a slightly different picture. The relative sizes (amplitudes) of the ECG on different leads gives us information about heart function.

33
Q

What is an ECG lead?

A

An ECG ‘lead’ is not a physical wire, but the VOLTAGE recorded between two points on the body

34
Q

What does leads I, II and III record?

A

Lead I records the signal voltage occurring between the left and right axillae
Lead II records the voltage between the right axilla and leg
Lead III records the voltage between the left axilla and leg
These leads give you a picture of the electrical activity of the heart in a frontal plane

35
Q

What are the names of the 3 augmented leads? Where do these point to? How is a reading given from these?

A

As well as the three basic limb leads I,II,III there are three augmented limb leads:
o aVR
o aVL
o aVF
aVR points up to the right axilla, aVL points up to the left axilla, aVF points down to the groin
The ECG machine automatically calculates the values on these leads and gives a reading

36
Q

How many limb leads are there in total? What are these called?

A

There are six limb leads in total: I,II, III, aVR, aVL, aVF

37
Q

Why are augmented leads helpful?

A

Augmented leads are useful as they are used with the main leads to help identify the locus of an abnormality in the heart

38
Q

Which lead is the ‘standard’ ECG recorded from? Why?

A

The ‘standard’ ECG is recorded from lead II. This lead normally gives the largest signal of the three limb leads

39
Q

How many deflections are usually visible in the ECG of a healthy subject?

A

Four or five deflections (PQRST) are usually visible in healthy subjects. (Q may not be present). The QRS wave is often called the QRS ‘complex’ and should last 60-100 ms

40
Q

How is the PR interval measured?

A

The PR interval is actually measured from start of P wave to start of QRS complex; it should be 120-200 ms. (However in most cases a Q wave is negligible and so start of QRS complex is effectively start of R wave)

41
Q

What must be remembered about an ECG?

A

Remember that the ECG is caused by the cardiac action potentials but is not the same shape as the cardiac action potentials and is much smaller (~1 mv) than the cardiac action potentials. As a general rule, the ECG is mainly generated at the start and end of cardiac action potentials. In particular, THE ‘R’ WAVE SIGNALS THE START OF VENTRICULAR DEPOLARISATION.

42
Q

What is the usual scale of the horizontal axis of an ECG? What about the vertical axis?

A

Horizontal: normally 25mm/s (i.e. one large square is 0.2 sec, one small sqaure is 40 ms)
Vertical: 1 mv is normally ten small squares

43
Q

What is the P wave?

A

Occurs at start of atrial depolarisation
P wave should be smooth and rounded
Should be positive in leads I, II, sometimes also in III

44
Q

What is the QRS complex?

A

Start of depolarisation of ventricles

45
Q

What is the Q wave?

A

The Q wave is negative by definition
No Q wave present if QRS signal starts upwards
Q wave due to earlier depolarisation of left side of interventricular septum
Normally small or absent on lead II
Small ‘septal’ Q waves typically seen in the left-sided leads (I, aVL, V5 and V6)

46
Q

What are the R & S waves?

A

QR wave is due to start of depolarisation of apex of ventricles
It is positive by definition. R wave usually present on leads I, II and III
RS S wave due to spread of depolarisation to rest of ventricles
It is negative by definition.
The polarity of the QRS complex depends on which lead is viewed - it may be positive, negative or bipolar

47
Q

What is the ST segment?

A

Represents period when whole of ventricles are depolarised
Normal ST segment starts flat and curves upwards into T wave
ST segment changes are very important for diagnosis of Acute Myocardial Infarcation (AMI)

48
Q

What is the T wave?

A

Normally stated as due to repolarisation of ventricles
Actually due to fact that base of ventricles normally repolarises earlier than apex, creating an upwards wave
Normally oriented in same direction as preceding QRS complex?

49
Q

How many chest (‘precordial’) leads are there? What are they called?

A

6 chest leads

V1-V6

50
Q

Where is each precordial lead located?

A

V1 = Right sternal edge, 4th intercostal space
V2 = Left sternal edge, 4th intercostal space
V3 = Halfway between V2 and V4
V4 = Apex beat
V5 = Anterior axillary line
V6 = Mid-axillary line
(V4, V5 and V6 all on same horizontal plane)

51
Q

How in particular are chest leads different to limb leads?

A

QRS complex in chest leads is usually bipolar

52
Q

What are the characteristics of each chest lead on an ECG reading?

A

V1 and V2 normally mainly negative (i.e. small R but large S wave)
V3 normally bipolar
V4 similar to lead 2
V5 and V6 normally mainly positive (i.e. large R wave but small S wave)

53
Q

Why do we have 12 different recordings in the ECG?

A

Different leads are affected by electrical activity in physically different parts of the heart
We say that different leads ‘view’ different regions of the heart (e.g. V3 and V4 view anterior heart wall so would selectively pick up abnormalities in this area of the heart)

54
Q

Which leads give which ‘views’ of the heart?

A 
Inferior = II, III, aVF
Lateral = I, aVL, V5, V6
Anterior = V3, V4
Septal = V1, V2
55
Q

What are the 3 most important things to remember about an ECG?

A

The normal appearance of lead II
The normal range of values of the PR interval
The normal duration of the QRS wave

CR1 (23 decks)

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