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Alan's lecture - Pharmacology > CVS 4 > Flashcards

CVS 4 Flashcards

1
Q

hwo is blodd circulated in the heart?

A
  • Vena cava
  • Right atrium
  • Righet ventricle
  • to lungs
  • Return left atrium
  • Left ventricle
  • To periphery
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2
Q

what is the pacemaker?

A
  • The SA node
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3
Q

why are the ventricles forced to contract after the atria?

A
  • Because of the slowed signal in the AV node
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4
Q

what does the P wave represent on ECG trace/

A
  • Atrial depolarisation
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5
Q

what does the QRS complex represent ECG trace?

A
  • Ventricular depolarisation
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6
Q

by measuring P-R interval what does it tell?

A
  • How the the atria is functioning

- it measured the time the atria are contracting and when ventricles start to contract

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7
Q

what does the T wave represent in ECG trace?

A
  • Ventricles repolarising
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8
Q

what does the ST interval suggetsed?

A
  • how long the ventricels are depolarised for
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9
Q

what does the QT interval tell you?

A
  • How long ti takes for ventricles to start depolarising and to fully recovering
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10
Q

why is the SA node the pacemaker?

A
  • It fires the highest frequency
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11
Q

what happens in phase 4 nodel cells?

A
  • Slow depolarisation due to na+ influx (na+ channels open)
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12
Q

what occurs at phase 0 of nodel cells?

A
  • ca2+ channels open and ca2+ flood in leading to cell depolarising
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13
Q

what occurs at phase 3 of nodel cells?

A
  • Ca2+ and Na+ channels close and K+ channels open and k+ floods out of the cell repolarising the cell
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14
Q

what is the refractotry period?

A
  • The point at which another action potential can cause another contraction of the cells, this usually occurs at phase 1-2 in ventricular myocytes
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15
Q

what occurs in phase 0 in the ventricualr myocytes?

A
  • na+ channels open and membrane depolarises as na+ influx occurs
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16
Q

what occurs in phase 1 of the ventricualr myocytes?

A
  • na+ channels inactivate
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17
Q

what occurs in phase 2 of the ventricualr myocytes?

A
  • K+ and ca2+ channels

- ca2+ channels inactive eventually

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18
Q

what occurs in phase 3 of the ventricular myocytes?

A
  • K+ channel still open so cell repolarises
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19
Q

why does arrythmias occur?

A
  • M.I
  • Heart failure
  • Hyperthyrodism
  • Drugs B antagonist
  • Genetics
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20
Q

what are the abnormalities that can occur leading to arrythmias?

A
  • Conudction of impulse
  • Automaticity
  • These lead to non-coordination of contraction
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21
Q

what is automaticity?

A
  • Site of origin of impulse, regulation of pacemaker and rate
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22
Q

What is the goal of treating arrythmia?

A
  • Treating the electrical abnormalities
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23
Q

additional impulses caused due to slowed SA node firing and AV node becoming the dominant pacemaker can lead to arrythmias. TREU RO FALSE?

A

TRUE

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24
Q

describe how signal bypass can cause arrythmias?

A
  • additional signals can come from SA node to atria and straight ot the ventricles bypassing the AV node
  • Leading to additional signals
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25
Q

explain re-entry leading to arrymthmia?

A
  • the electric circuit is not complete so it creates an alternative route upon itself
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26
Q

explain conduction block leading to arrythmia?

A
  • When SA node is block for example the tissue below can take over as the pacemaker leading to bradykardia
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27
Q

explain afterdepolarization leading to arrythmia?

A
  • You can get additional signals early
  • Or you can get additional signals after depolarization which is also known as delayed
  • extra oscillations driven by action potential
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28
Q

what are the different classes of arrythmias and where do they originate from?

A
  • Supraventricular : orginates from SA, AV nodes or atria
  • Ventricular: originates in ventricles
  • Heart block: Pacemaker impulse is delayed or fails to reach ventricles
29
Q

what are the different types of supraventricular arrythmias?

A
  • sinus tachycardia/bradicardia: altered SA firing
  • atrial fibrillation: re-entry impulses in the atrium
  • atrial tachycardia: atrial pacemaker other SA node
  • atrial flutters: atrial rate too fast ventricles cant respond
30
Q

what are the different types of ventricular arrythmia?

A
  • Ventricular tachycardia:

- Ventricular fibrillation: re-entry to impulse/ fatal

31
Q

ventricular tachycardia can be either monomorphic or polymorphic whih relates ot the regularity of the beats. TREU RO FALSE? (mono is normal but polymorphic is irregular)

A

TRUE

32
Q

what is monomorphic and polymorphic ventricular tachucardia?

A
  • Monomorphic: ventricular pacemaker causes additonal systole

Polymorphic: Torsades de pointes caused by sustained early after depolarisation

33
Q

what are treatment goals for arrythmia?

A
  • Restore normal cardiac function
  • prevent reccurence of arrythmias
  • prevent more sever arrythmia
  • deal with haemodynamic consequences (e.g CO)
34
Q

what are the actions of anti-arrytmic drugs?

A
  • Alter the baseline in SA cells
  • The rate of phase 4 repolarization
  • Alter the baseline in contractile cells
  • Duration of action potential (alter refractory period)
35
Q

what are the different classes of anti-arrythmic drugs? (vaughan william classification)

A
  • Class 1 : (na+channel blockers)
  • Class 2 : b adrenergic receptor antagonists -
  • Class 3: K+ channel blockers
  • Class 4: ca2+ channel blockers
36
Q

what are the subgroups of class 1 antiarrythmic drugs and what does each do?

A
  • Class 1a : bind open na+ channel and blocks k+ channels
  • Class 1b: bind open as well as refractory na+ channel
  • Class 1c: not rate dependant
37
Q

How do class 1 antiarrythmic drugs work?

A
  • decreases slope phase 4

- decreases re-entry in contractile tissue - slows down phase 0 so refractory for longer

38
Q

all antiarrythmic drugs can precipitate arrythmia. TRUE RO FALSE?

A

TRUE

39
Q

Many drugs which prolong QT increases risk of torsade depointes. TREU RO FALSE?

A

TRUE

40
Q

Class 1a drugs are also cholinergic antagonists so they block parasympathetic inhibition of AV node. TREU RO FALSE?

A

TRUE

41
Q

give ana example of a class 1a drug?

A
  • Disopyramide
42
Q

what is Disopyramide indicated for?

A
  • Ventricular tachycardia following MI
43
Q

what are some ADRs of class 1a drugs?

A
  • Negative inotropic agent

- cholinergic antagonist so Causes dry mouth, blurred vision constipation

44
Q

what are some drug interactions with class 1a?

A
  • Avoid drugs that increase QT

- Avoid giving with drugs that are negative inotrops

45
Q

disporymide reduced cardiac output. TRUE OR FALSE?

A

TRUE

46
Q

class 1b is most effective on frequently depolarising tissue. TREU RO FALSE?

A

TRUE

47
Q

lidocaine is a class 1b antiarrythmic drug inicated for ventricular tachycardi and local anaesthesia. TREU RO FALSE?

A

TREU

48
Q

lidocaine is not effective in supraventricular arrythmia. TRUE RO FALSE?

A

TRUE

49
Q

lower doses of lidocaine should be given to patients with hepatoic impairment or haert failure. TREU RO FALSE?

A
  • TRUE
50
Q

why is Lidocaine is a contranidicated in AV block?

A

because it slows down AV conduction

51
Q

which of the class 1 antiarrythmic drugs are the most potent?

A
  • Class 1c - they are marked effective in phase 0 but not effect on duration
52
Q

what does class 1c do?

A
  • Slows conduction in all cardiac tissue
  • suppresse premature ventricular contraction
  • Increases PR and QRS intervals
53
Q

give an example of class 1c drug name and its indication?

A
  • Flecainide

- Atrial fibrillation and tachycardia

54
Q

what are ADRs for flecainide?

A
  • Negative inotropic agent
  • CNS toxicity
  • arrythmia by prolonging QT
55
Q

what is flecaidine contraindicated againts and waht are some drug interactions?

A
  • Contrai
  • HF
  • Previous MI

dRUG INTRECATIONS

  • patients using duiretics risk of arrythmia
  • avoid with ther negative iontropes
56
Q

class 2 antiarrytmic drugs are indicated for supraventricular arrythmia because decreases SA rate and AV conduction. TRUE OR FALSE?

A

TRUE

57
Q

give an example of a class 2 antiarrytmic drug?

A
  • propanolol
58
Q

Class 2 have been shown to reduce sudden death post M.I. TREU RO FALSE?

A

TRUE

59
Q

how does amiodarone a class 3 drug work?

A
  • prolongs action potential and QT interval
60
Q

Satolol is a B adrenergic antagonist with class 2 and 3 activity. TREU RO FALSE?

A

TRUE

61
Q

class 3 is contrainidcated agiants bradycardia, heart block, iodine sensitivity. TRE OR FALSE?

A

TREU

62
Q

What are some ADRs for class 3 drugs?

A
  • Pulmonary fibrosis
  • grey skin dicoloration
  • hyperthyroidism (inhibits conversation of T4 to T3 )
63
Q

what are some drug interactions?

A
  • Inhibits CYP3A4
  • Inhibits renal excretion of digoxin
  • Avoid with other drugs that prolong QT
64
Q

class 4 drugs slows phase 0 in AV node which slows conduction velocity through AV nod eincreasing its refractory period. TREU OR FALSE?

A

TRUE

65
Q

high doses of class 4 drugs can cause complete AV block. TRUE OR FALSE?

A

TREU

66
Q

name a class 4 drug?

A
  • Verapamil
67
Q

dihydropyridines tend to be less effective on cardiac tissue. TREU OR FLASE?

A

TREU

68
Q

Co administartion of dihydropyridines and B antagonists can cause asystole. TREU RO FALSE?

A

TRUE

Alan's lecture - Pharmacology (16 decks)

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