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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
Define: Arrhythmia
an abnormal rhythm of the myocardial action potentials
26
What are the two types of abnormal impulse generation?
1. triggered activity | 2. increased automaticity
27
What is triggered activity in an abnormal impulse generation arrhythmia?
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
28
How can triggered activity lead to tachycardia?
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
29
What is increased automaticity in an abnormal impulse generation arrhythmia?
ectopic activity, where the beat occurs in the wrong part of the heart
30
What are the two types of abnormal impulse propagation?
1. re-entry | 2. heart block/AV block
31
What is re-entry?
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
What is Circus Movement?
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
How does re-entry commonly caused?
scarring of the heart or through MI
34
What is the most common cause of arrhythmias?
re-entry through abnormal impulse propagation
35
What is 1st degree heart block?
delayed P-wave normally delay between P-wave and QRS complex is 200ms here the delay is longer that 200ms
36
What is 2nd degree heart block?
AV node completely refractory no QRS complex following the P wave resulting in a missing beat bradycardia
37
What is 3rd degree heart block?
``` 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
What occurs in a normal sinus rhythm?
P wave - atrial depolarisation QRS complex - ventricular depolarisation T wave - ventricular repolarisation
39
When are the atria contracted/relaxed?
contracted following P wave and atrial depolarisation | relaxed following the beginning of ventricular depolarisation
40
When are the ventricles contracted/relaxed?
contracted following completion of ventricular depolarisation / after S wave relaxed following ventricular depolarisation / after T wave
41
What are the four classification of arrhythmia origins?
1. sinus node 2. atrial 3. nodal 4. ventricular
42
What is atrial tachycardia?
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
What is ventricular tachycardia
more serious that atrial tachycardia produces a complex ventricular rhythm with a fast heart rate improper electrical activity in the ventricles
44
What is seen on an ECG showing atrial fibrillation? What does this result in?
no true P waves or atrial rhythm fibrillation waves irregular ventricular response no proper atrial output or atria contraction
45
What can occur as a result of atrial fibrillation?
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
What is seen on an ECG showing ventricular fibrillation? What does this result in?
``` no defined rhythm or output wide and complex ventricular waves irregular ventricular response variable morphology if not stabilised can result in patient death ```
47
How do you treat ventricular fibrillation?
defibrillator | electric shock to stabilise the heart rate
48
How does sympathetic stimulation affect heart rate?
``` increased heart rate with stimulation positive chronotropic effect release of NA activate flight-or-fight response increased slope of pacemaker potential increased automaticity ```
49
What is sympathetic stimulation mediated by?
beat-1 adrenoceptors
50
How does parasympathetic stimulation affect heart rate?
``` reduces heart rate with stimulation negative chronotropic effect AV conduction inhibited PR interval prolonged decreased slope of pacemaker potential decreased automaticity ```
51
What can prolongation of the PR interval lead to?
heart block
52
What is parasympathetic stimulation affect heart rate?
muscarinic (M2) acetylcholine receptors
53
Where are M2 receptors most commonly found?
nodal and atrial tissue
54
What are the four classes of Vaughan-Williams Antiarrhythmic drugs?
1. sodium channel blockers 2. beta-adrenoceptor antagonists 3. prolongation of action potential 4. calcium channel blockers
55
What are the three classes of sodium channel blockers and what do they treat?
1a. AF, atrial flutter, ventricular tachycardia 1b. ventricular tachycardia 1c. ventricular tachycardia
56
Give examples of 1a sodium channel blockers (x3)
disopyramide quinidine procainamide
57
Give examples of 1b sodium channel blockers (x2)
lidocaine | mexilitene
58
Give examples of 1c sodium channel blockers (x2)
flecainide | propafenone
59
What can lidocaine be used for?
a local anaesthetic | intravenous control of heart rhythm
60
What are the two types of beta-adrenoceptor antagonists?
1. non-selective | 2. beta1-selective
61
Give examples of non-selective beta-adrenoceptor antagonists (x3)
propranolol nadolol carvedilol
62
Give examples of beat1-selective beta-adrenoceptor antagonists (x2)
bisprolol | metaprolol
63
Give examples of drugs that prolong the cardiac action potential (x2)
amidarone | sotalol
64
What are calcium channel blockers used to treat?
hypertension and ventricular tachycardia
65
Give examples of calcium channel blockers (x2)
verapamil | diltiazem
66
What are the three states of ion channels?
resting, open and refractory
67
What state do drugs bind to ion channels in?
open
68
How does Digoxin work?
inhibition of sodium-potassium pump disrupting the resting membrane potential decreases sodium gradient across the cell decreases action of sodium-calcium pump
69
What effect does Digoxin have on the heart?
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
What is Digoxin used to treat?
atrial fibrillation | severe heart failure
71
What are the adverse effects of Digoxin?
narrow therapeutic window nausea and vomiting diarrhoea confusion
72
What are QT prolongation drugs used to prevent?
polymorphic ventricular tachycardia
73
Name two drugs that act to prolong the QT interval
amiodarone | sotalol
74
What are the adverse effects of Amiodarone?
``` 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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