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CDL301 > Lecture 02 Heart Physiology 1 > Flashcards

Lecture 02 Heart Physiology 1 Flashcards

1. Describe the heart rate and rhythm, and the physiology of myocardial blood flow in detail 2. understand arrhythmias and the use of anti-arrhythmic drugs

1
Q

What is an echocardiogram?

A

an ultrasound of the heart

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2
Q

Why are valves important?

A

they control the directional flow of the blood (in and out flow of the heart)

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3
Q

Can the heart control its own rhythm?

A

yes, it is made of excitable tissue and will spontaneously on its own without any external influence

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4
Q

What are the three key ions involved in balancing membrane potential?

A

sodium, potassium and calcium

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5
Q

Why is the heart rate of firing limited?

A

limited by the refractory period of the ion channels

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6
Q

What are the five phases of the cardiac action potential?

A
  1. rapid depolarisation
  2. partial repolarisation
  3. plateau phase
  4. repolarisation
  5. pacemaker potential
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7
Q

What happens during Phase 0?

A

rapid depolarisation
when membrane potential reaches -60mV an action potential will occur
voltage-dependent sodium ion channels snap open causing large, rapid influx of sodium

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8
Q

How can you describe the type of action potential seen in the myocardium?

A

an all-or-nothing depolarisation or degenerative response

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9
Q

What is the resting potential of the myocardium?

A

-70mV

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10
Q

What happens during Phase 1?

A

partial repolarisation
sodium channels become refractory
causes a small depolarisation

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11
Q

What happens during Phase 2?

A

plateau phase
slow, inward calcium current making the cell more positive
initial fall in outward potassium current

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12
Q

Why is Phase 2 important?

A

allows widening of the action potential and maintaining the depolarised state, preventing another action potential from occurring

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13
Q

What happens during Phase 3?

A

repolarisation
calcium channels become refractory
outward potassium current increases to achieve a negative membrane potential

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14
Q

What happens during Phase 4?

A

pacemaker potential
a gradual depolarisation during diastole through sodium and calcium
small inward increase in membrane potential and decreasing outward potassium current
once reach critical point, another action potential will fire

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15
Q

What is the critical point?

A

the point at which an action potential will occur

-60mV

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16
Q

Where is the pacemaker potential found?

A

in the nodal and conducting tissue

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17
Q

What is the main pacemaker and where is it found?

A

sinoatrial (SA) node found in the right atrium

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18
Q

What order does the electric impulse move through the heart?

A

SA node - atrium - AV node - bundle of His - purkinje fibres - ventricle

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19
Q

Why is the AV node important?

A

causes a delay between atrial and ventricular contraction, allowing the ventricles to fill with blood from the atria

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20
Q

Which parts of the heart have pacemaker activity?

A

SA node, AV node and Purkinje Fibres

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21
Q

What is the ion activity in the SA and AV nodes?

A

absence of fast sodium currents

presence of slow calcium currents - which in nodal tissue cause depolarisation

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22
Q

Which node is dominant?

A

SA node is dominant but if it fails the AV node can taken over producing a slower, ectopic rhythm

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23
Q

Why are drugs affecting calcium important in the heart?

A

characteristically long action potentials and refractory periods for nodal/pacemaker tissue due to calcium influx during the plateau phase

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24
Q

What are the two mechanisms of arrhythmias?

A
  1. abnormal impulse generation

2. abnormal impulse propagation

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25
Q

Define: Arrhythmia

A

an abnormal rhythm of the myocardial action potentials

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26
Q

What are the two types of abnormal impulse generation?

A
  1. triggered activity

2. increased automaticity

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27
Q

What is triggered activity in an abnormal impulse generation arrhythmia?

A

delayed after-depolarisation and increase in intracellular calcium
triggers abnormal impulse to occur after depolarisation is completed (phase 4)
elevated intracellular calcium concentrations may occur in disease states/digoxin toxicity

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28
Q

How can triggered activity lead to tachycardia?

A

overloading of the SR causing spontaneous calcium release after repolarisation
calcium leaves the cell through the 3Na/2Ca exchanger resulting in a net depolarising current
one stimuli provides a small depolarising current
closer the stimuli are together, the larger the after-depolarisation
given enough stimulation, the heart goes over the threshold and produces a train of impulses - tachycardia

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29
Q

What is increased automaticity in an abnormal impulse generation arrhythmia?

A

ectopic activity, where the beat occurs in the wrong part of the heart

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30
Q

What are the two types of abnormal impulse propagation?

A
  1. re-entry

2. heart block/AV block

31
Q

What is re-entry?

A

a problem with the refractory tissue
normally impulse can only pass in one direction as the tissue behind it is refractory
can be a uni- or bi-directional block preventing the passing of the current

32
Q

What is Circus Movement?

A

a re-entrance circuit in a unidirectional block which can lead to tachycardia
a time delay allows the impulse to depolarise tissue that has already depolarised, propagating the current

33
Q

How does re-entry commonly caused?

A

scarring of the heart or through MI

34
Q

What is the most common cause of arrhythmias?

A

re-entry through abnormal impulse propagation

35
Q

What is 1st degree heart block?

A

delayed P-wave
normally delay between P-wave and QRS complex is 200ms
here the delay is longer that 200ms

36
Q

What is 2nd degree heart block?

A

AV node completely refractory
no QRS complex following the P wave resulting in a missing beat
bradycardia

37
Q

What is 3rd degree heart block?

A 
complete heart block 
atria and ventricles aren't connecting 
atria firing in the background 
AV node takes over ventricular rhythm (more spaced out)
P wave and ventricular beats independent
38
Q

What occurs in a normal sinus rhythm?

A

P wave - atrial depolarisation
QRS complex - ventricular depolarisation
T wave - ventricular repolarisation

39
Q

When are the atria contracted/relaxed?

A

contracted following P wave and atrial depolarisation

relaxed following the beginning of ventricular depolarisation

40
Q

When are the ventricles contracted/relaxed?

A

contracted following completion of ventricular depolarisation / after S wave
relaxed following ventricular depolarisation / after T wave

41
Q

What are the four classification of arrhythmia origins?

A
  1. sinus node
  2. atrial
  3. nodal
  4. ventricular
42
Q

What is atrial tachycardia?

A

atrial contract very rapidly with multiple atrial waves
due to delay at AV node not all impulses get through to the ventricles
offers some protection to the heart - can beat faster than 220bpm

43
Q

What is ventricular tachycardia

A

more serious that atrial tachycardia
produces a complex ventricular rhythm with a fast heart rate
improper electrical activity in the ventricles

44
Q

What is seen on an ECG showing atrial fibrillation? What does this result in?

A

no true P waves or atrial rhythm
fibrillation waves
irregular ventricular response
no proper atrial output or atria contraction

45
Q

What can occur as a result of atrial fibrillation?

A

atrial thrombosis
blood clot collects in the atria due to standstill of blood
passing of the clot around the body can lead to a stroke and travels to cerebral circulation
treat with anti-coagulants

46
Q

What is seen on an ECG showing ventricular fibrillation? What does this result in?

A 
no defined rhythm or output 
wide and complex ventricular waves 
irregular ventricular response 
variable morphology 
if not stabilised can result in patient death
47
Q

How do you treat ventricular fibrillation?

A

defibrillator

electric shock to stabilise the heart rate

48
Q

How does sympathetic stimulation affect heart rate?

A 
increased heart rate with stimulation
positive chronotropic effect
release of NA activate flight-or-fight response 
increased slope of pacemaker potential 
increased automaticity
49
Q

What is sympathetic stimulation mediated by?

A

beat-1 adrenoceptors

50
Q

How does parasympathetic stimulation affect heart rate?

A 
reduces heart rate with stimulation 
negative chronotropic effect 
AV conduction inhibited
PR interval prolonged
decreased slope of pacemaker potential 
decreased automaticity
51
Q

What can prolongation of the PR interval lead to?

A

heart block

52
Q

What is parasympathetic stimulation affect heart rate?

A

muscarinic (M2) acetylcholine receptors

53
Q

Where are M2 receptors most commonly found?

A

nodal and atrial tissue

54
Q

What are the four classes of Vaughan-Williams Antiarrhythmic drugs?

A
  1. sodium channel blockers
  2. beta-adrenoceptor antagonists
  3. prolongation of action potential
  4. calcium channel blockers
55
Q

What are the three classes of sodium channel blockers and what do they treat?

A

1a. AF, atrial flutter, ventricular tachycardia
1b. ventricular tachycardia
1c. ventricular tachycardia

56
Q

Give examples of 1a sodium channel blockers (x3)

A

disopyramide
quinidine
procainamide

57
Q

Give examples of 1b sodium channel blockers (x2)

A

lidocaine

mexilitene

58
Q

Give examples of 1c sodium channel blockers (x2)

A

flecainide

propafenone

59
Q

What can lidocaine be used for?

A

a local anaesthetic

intravenous control of heart rhythm

60
Q

What are the two types of beta-adrenoceptor antagonists?

A
  1. non-selective

2. beta1-selective

61
Q

Give examples of non-selective beta-adrenoceptor antagonists (x3)

A

propranolol
nadolol
carvedilol

62
Q

Give examples of beat1-selective beta-adrenoceptor antagonists (x2)

A

bisprolol

metaprolol

63
Q

Give examples of drugs that prolong the cardiac action potential (x2)

A

amidarone

sotalol

64
Q

What are calcium channel blockers used to treat?

A

hypertension and ventricular tachycardia

65
Q

Give examples of calcium channel blockers (x2)

A

verapamil

diltiazem

66
Q

What are the three states of ion channels?

A

resting, open and refractory

67
Q

What state do drugs bind to ion channels in?

A

open

68
Q

How does Digoxin work?

A

inhibition of sodium-potassium pump disrupting the resting membrane potential
decreases sodium gradient across the cell
decreases action of sodium-calcium pump

69
Q

What effect does Digoxin have on the heart?

A

increased vagal tone - bradycardia and slowing AV conduction
increased ectopic activity - pro-arrhythmia
increased force of contraction - increased IC calcium
positive inotropic effect
reduced ventricular rate

70
Q

What is Digoxin used to treat?

A

atrial fibrillation

severe heart failure

71
Q

What are the adverse effects of Digoxin?

A

narrow therapeutic window
nausea and vomiting
diarrhoea
confusion

72
Q

What are QT prolongation drugs used to prevent?

A

polymorphic ventricular tachycardia

73
Q

Name two drugs that act to prolong the QT interval

A

amiodarone

sotalol

74
Q

What are the adverse effects of Amiodarone?

A 
large drug distribution
interstitial pneumonitis
abnormal liver function 
hyper/hypo-thyroidism 
increased sun sensitivity 
slate grey skin discolouration
corneal micro deposits 
optic neuropathy 
multiple drug interactions

CDL301 (14 decks)

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