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M103 T3 > M103 T3 L6 > Flashcards

M103 T3 L6 Flashcards

1
Q

Which organ is a functional synctium and why?

A

the heart bc it is gap junctions that electrically couple cells

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2
Q

What are the three types of cardiomyocytes?

A

Pacemaker cells – set the heart’s rhythm
Conducting cells – transmit rhythm throughout the heart
Contractile cells – contract to the rhythm set by the conducting cells (most numerous)

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3
Q

What are the speeds of propagation in contractile cells, purkinje fibres, the fastest neurons and the AV node?

A

Contractile - 0.3-0.5 m/s
Purkinje fibres - up to 5 m/s
fastest neurons ~100 m/s
AV node 0.05 m/s

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4
Q

What is the effect of cardiomyocytes being linked by low resistance pathways associated with gap junctions at the intercalated discs?

A

When an actpt depolarises one cell, it initiates an actpt in the adjacent cell

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5
Q

Where does the electrical impulse go when its travelling through the heart?

A

starts in the SA node - AV bundles
atrium - AV node
travels through a hole in the fibrous skeleton
enters the conducting system (the CS starts at the bundle of his, goes on either side of the heart, bundle branches, towards the valves)

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6
Q

What is the function of internodal bundles?

A

to conduct impulse from SA node to AV node

to ensure synchronous contraction of the atria

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7
Q

What are the conducting speeds through the atrial muscle and through bundles?

A

atrial muscle - slow at 0.3-0.5 m/s

bundles - much faster at 1.0 m/s

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8
Q

How many specialised bundles are there in the atria?

A

4 bundles that are all in direct contact with atrial muscle

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9
Q

How long is the electrical delay at the AV node and why is it useful?

A

AV node delays wave of excitation from atria to ventricles by 0.1 - 0.2 s
it means that ventricles contract after atria to permit longer and more effective ventricular filling

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10
Q

What is the electrical delay at the AV node caused by?

A

the actpt is conducted very slowly in AV node (0.05 m/s) bc the AV node composed of small modified myocytes
AAR the electrical connection between adjoining cells is weaker

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11
Q

Where does the AV node lead on to?

A

AV node - purkinje fibres - ventricles - contractile myocytes
the AV node connects to the bundle of His followed by Purkinje fibre system
Purkinje fibres transmit the impulse rapidly to the main mass of the ventricles
from there slower conduction between contractile myocytes can occur

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12
Q

In what order are the areas of the ventricular wall depolarised by the electrical signal?

A

septum, apex, AV groove

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13
Q

Why do the purkinje fibres conduct relatively fast?

A

bc they have a larger diameter

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14
Q

From where is the electrical activity of the heart measured and how is this possible?

A

on the skin
The individual currents of cardiac myocytes are tiny - a few nano-amps
These currents can be detected from the wrist and the ankle, nearly one metre from the heart
this is possible because the heart is a “functional syncytium” in which large groups of cells all make electrical changes simultaneously

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15
Q

What are the medical benefits of the ECG?

A

Excellent for heart rate rather than just taking a pulse
Especially useful when the atrial rate ≠ ventricular rate
is very fast and affordable

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16
Q

What are the medical disadvantages of the ECG?

A

Many subtleties
Not a one-stop-diagnosis
Patient Hx essential for interpretation
a full diagnosis requires other techniques

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17
Q

Where are the leads placed on Lead II?

A

positive electrode on left leg
negative electrode on right arm
ground electrode on the right leg (although the ground could be almost anywhere)

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18
Q

What are the 12 standard leads?

A

three bipolar leads - I, II, III
three augmented leads (on the frontal plane)
six precordial (V1-6)

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19
Q

What is the interpretation if the QRS is wide or mishapen?

A

the ventricular conduction is abnormal

e.g. ectopic pacemaker or bundle branch block

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20
Q

What will lead to a bigger contribution to the ECG?

A

more cells acting together

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21
Q

What cells are the primary drivers of the QRS and how do the G fibres and the conduction system compare?

A

the contractile cells are the primary drivers of the QRS complex
whereas there are only a tiny number of G fibres in the heart, which have almost no contribution to the ECG
the conduction system have such small electrical signals that it’s impossible to detect them from the wrist and from the leg

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22
Q

What is a large (deep) Q wave a sign of?

A

dead tissue (old MI)

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23
Q

What criteria is required IOT recognise sinus rhythm (normal)?

A

Each P wave is followed by a QRS complex

When PR interval is always normal (3-5 little boxes)

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24
Q

What are the normal PR / QRS / QT durations in boxes and ms?

A

PR interval duration = 3-5 boxes / 120 – 200 ms
QRS complex duration = 2-3 boxes / 80 – 120 ms
QT interval duration = 9-11.5 boxes / 360 – 460 ms

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25
Q

What is the horizontal scale in cm/sec on an ECG for one little box and one big box?

A

Horizontal scale is 2.5 cm/sec.
One little box = 1 mm = 40 ms (milliseconds)
A big box = 5 little boxes = 200 ms

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26
Q

How is the rate and ventricular rate calculated on an ECG?

A

rate - count how many boxes occur between two P waves

ventricular rate - how many boxes between R waves

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27
Q

What is the bpm for the first 10 boxes?

A 
1 big box = 300 bpm
2 boxes = 150 bpm
3 boxes = 100 bpm
4 boxes = 75 bpm
5 boxes = 60 bpm
6 boxes = 50 bpm
10 boxes = 30 bpm
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28
Q

How do you calculate the bpm for a big box on an ECG?

A

300 / big boxes

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29
Q

What three things does a parasympathetic withdrawal cause an increase in?

A

heart rate
contractility
conduction velocity

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30
Q

How does sympathetic input to heart work?

A

travels via the stellate nerves

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31
Q

Which two types of drugs will increase and decrease the heart rate?

A

Beta agonists - increased rate

Beta blockers - decreased rate

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32
Q

What are the four different categories of severity for heart blocks?

A

1st degree heart block (asymptomatic)
2nd degree heart block (Mobitz T1&2, asymptomatic or mild symptoms)
3rd degree heart block (serious symptoms)

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33
Q

What conditions will you have to read ECGs on?

A 
1st & 3rd degree heart block
Mobitz Types 1&2 block
Premature Ventricular contractions
AV heart block
Bundle Branch Block
AF
Respiratory Sinus Arrhythmia
Acute MI (STEMI)
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34
Q

How can a first degree heart block be identified from an ECG?

A

Delayed AV node transmission
PR interval > 5 little boxes (200 ms), normal PR < 5 little boxes
But all P’s followed by QRS and vv

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35
Q

What are the clinical features of first degree heart block?

A

Almost always asymptomatic
Often young people (adolescents)
Rarely treated

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36
Q

How can Mobitz Type I and Type 2 blocks be identified from an ECG?

A

type 1: increased PR interval (AV damage)

type 2: stable PR interval (BoH issue), some P waves blocked, aren’t followed by QRS complex

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37
Q

What is Mobitz Type I block caused by?

A

AV damage, so usually the ventricle picks up the slack when the bundle of His creates its own signal

38
Q

Is Mobitz Type I usually treated and why (not)?

A

no treatment bc it’s the least serious type of 2nd degree heart block - it may occasionally cause symptoms of mild dizziness and does not usually require treatment

39
Q

What is Mobitz Type II block caused by?

A

normally, a problem in the Bundle of His

40
Q

Is Mobitz Type II usually treated and why (not)?

A

yes (implant pacemaker) bc it’s a high risk condition - can progress to 3rd degree heart block

41
Q

What are the features of an ECG for a patient with Third Degree Heart Block?

A

PR interval varies radically – sometimes > 12 boxes
intrinsic ventricular rate is consistent but slow (30-40 bpm)
the time between atrial beats and ventricular beats is variable

42
Q

What is Third Degree Heart Block caused by?

A

atrial signals consistently fail to arrive at ventricles

the only reason the ventricles continue to beat is bc they have escape beats

43
Q

What are the symptoms of Third Degree Heart Block?

A

dizziness, malaise, syncope, risk of sudden death

44
Q

What are the features of the ECG of premature ventricular contractions?

A

ventricular electrical activity that is unusually wide and weird looking
No S wave, instead a wide negative dip where the T wave should be

45
Q

From where do premature ventricular contractions originate?

A

in the middle of myocardium

46
Q

How does the purkinje system affect the synchronisation of the two ventricles contracting?

A

Normally, the two ventricles are beating simultaneously because of the his purkinje system
The two ventricles will be electrically unsynchronised
AAR the PVC has a delayed and inefficient conduction (non-Purkinje)
Width is determined by slowed conduction velocity

47
Q

What group of patients is AF very common in?

A

elderly patients

48
Q

Why is the ventricular rate fast and irregular in atrial fibrillation?

A

too many disorganised unregulated signals reach AV node
the AV node will let through some of the signals but not all of them - it won’t let the heart beat any faster than a certain rate, usually not any faster than 150

49
Q

What can AF lead to?

A

thrombus formation in the atrium due to the slow flow of blood
increased stroke risk

50
Q

What are the features of an ECG for a patient with AF?

A

No P wave - instead, flat line or wiggly line instead of P

51
Q

In what groups is respiratory sinus arrhythmia present in?

A

Usually only present in children & athletes

52
Q

What is respiratory sinus arrhythmia caused by and how does it affect the ventricular rate?

A

respiratory centres in brain’s medulla

ventricular rate: inverse of RR interval

53
Q

What is most numerous type of cardiomyocyte?

A

contractile cells

54
Q

How are Escape beats caused?

A

when the ventricles spontaneously produces electrical impulses, acting as the pacemaker because they aren’t receiving the sinus rhythm because of Mobitz Type II

55
Q

How do escape beats occur and why?

A

they are late or are triggered by the natural rhythmicity of non-atrial tissue
when the ventricles spontaneously produces electrical impulses, acting as the pacemaker because they aren’t receiving the sinus rhythm bc of Mobitz Type II

56
Q

What are the two types of unipolar leads?

A

augmented and chest

57
Q

How long is the conduction of depolarisation waves delayed by the AV node?

A

Total of 160 ms delay in AV network

30 ms to AV node
90 ms delay before enters penetrating portion of AV bundle
40 ms delay in penetrating bundle

58
Q

How and why does the AV node delay conduction of waves of depolarisation?

A

Mostly due to increased resistance
(i) diminished numbers of gap junctions between modified myocytes per cross sectional area, (ii) smaller fibres, (iii) more cell junctions per length distance travelled

59
Q

What are the causes of AV Heart Block?

A

Ischaemia of AV node or AV bundle
Compression of AV bundle by scar or calcified tissue
Inflammation of the AV node or bundle

60
Q

What are the symptoms of 2nd degree AV Heart Block?

A

dizziness, fainting, tiredness and shortness of breath

61
Q

What is the sign of an acute MI on an ECG?

A

ST segment elevation

62
Q

What are the two different types of myocardial infarction?

A

STEMI - if the myocardial infarction has an ST-elevation on the patient’s ECG (ST elevated MI)
NSTEMI - if there is no ST-elevation on the patient’s ECG, but there is elevation of the blood markers suggesting heart damage (non-ST elevated MI)

63
Q

What are the characteristics of an NSTEMI on an ECG ?

A

depressed ST wave or T-wave inversion.

no progression to Q wave

64
Q

What is the measurement of hypertension in adults?

A

anything over 130/90 mmHg

65
Q

What is the range of hypertension for over 80s?

A

anything over 150/90

66
Q

By what mechanisms can cardiac output be decreased?

A

dcs symp / ics parasymp NS activity
dcs peripheral resistance
prevent ACh breakdown
prevent noradrenaline release

67
Q

What drug types can be used to decrease cardiac output?

A 
muscarinic agonists
ACh'ase inhibitors
adrenoceptor antagonists
noradrenaline 
selective alpha or beta antagonists
non selective beta antagonists
68
Q

What’s an example of a muscarinic agonist?

A

ACh

69
Q

What are two analogues of ACh?

A

carbachol or pilocarpine

70
Q

What’s an example of a ACh’ase inhibitor? )

A

​neostigmine

71
Q

What are the side effects of ACh’ase inhibitors?

A

visual disturbances
lacrimation and salivation
bronchoconstriction

72
Q

What receptors does Noradrenaline act on?

A

alpha and beta adrenoceptors

73
Q

What is the difference between alpha and beta adrenergic receptors?

A

alpha causes vasoconstriction, ics bp & HR
beta 1 - vasodilation, dcs bp & HR
beta 2 - vasoconstriction, ics bp & HR

74
Q

Where are beta-adrenergic receptors located?

A

b1 - in the heart

b2 - bronchioles and skeletal muscle arteries (very few in heart)

75
Q

What do b-adrenergic receptors primarily bind to?

A

norepinephrine released from symp adrenergic nerves

76
Q

What’s an example of a selective b1 antagonist?

A

atenolol

77
Q

What is the effect of nonselective beta antagonists?

A

decreased cardiac output (due to increased peripheral resistance)

78
Q

What are nonselective beta blockers used to treat?

A

hypertension, arrhythmia, etc

79
Q

What are the side effects of nonselective beta blockers?

A

bronchoconstriction

muscle weakness

80
Q

What receptor is atropine an antagonist of?

A

muscarinic receptors

81
Q

What is the role of atropine when administered as a drug?

A

it inhibits the effects of excessive vagal (parasymp) activation on the heart

82
Q

What conditions is atropine used to treat

A

bradycardia and astyole

83
Q

What type of drug can be used to prevent the breakdown of acetylcholine?

A

an acetylcholinesterase inhibitor

84
Q

What is an example of an acetylcholinesterase inhibitor?

A

neostigmine

85
Q

What is the effect of adrenoceptor antagonists?

A

dcs in symp NS activity, CO & peripheral resistance (by blocking the symp innervation of blood vessels)

86
Q

What are the normal ranges for RR duration at 50 - 90 bpm?

A

1200 ms to 667 ms

87
Q

Where is the QT interval actually measured from?

A

from the start of P to the start of Q

88
Q

What are the normal values for RR duration at 60 and 75 bpm specifically?

A

60 bpm = 1000 ms

75 bpm = 800 ms

89
Q

What is normal resting bpm?

A

technically 60-100 bpm
but over 80bpm = higher chance of developing CVS disease
under 60 is dangerous

90
Q

What is the normal PP interval range?

A

for 50 - 90 bpm = 1200 - 667 ms

91
Q

What are the PP interval values for 60 and 75 bpm?

A

60 bpm, 1000 ms

75 bpm, 800 ms (75 pbm - normal sinus rhythm)

M103 T3 (21 decks)

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