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
explain re-entry leading to arrymthmia?
- the electric circuit is not complete so it creates an alternative route upon itself
26
explain conduction block leading to arrythmia?
- When SA node is block for example the tissue below can take over as the pacemaker leading to bradykardia
27
explain afterdepolarization leading to arrythmia?
- 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
28
what are the different classes of arrythmias and where do they originate from?
- Supraventricular : orginates from SA, AV nodes or atria - Ventricular: originates in ventricles - Heart block: Pacemaker impulse is delayed or fails to reach ventricles
29
what are the different types of supraventricular arrythmias?
- 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
what are the different types of ventricular arrythmia?
- Ventricular tachycardia: | - Ventricular fibrillation: re-entry to impulse/ fatal
31
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)
TRUE
32
what is monomorphic and polymorphic ventricular tachucardia?
- Monomorphic: ventricular pacemaker causes additonal systole Polymorphic: Torsades de pointes caused by sustained early after depolarisation
33
what are treatment goals for arrythmia?
- Restore normal cardiac function - prevent reccurence of arrythmias - prevent more sever arrythmia - deal with haemodynamic consequences (e.g CO)
34
what are the actions of anti-arrytmic drugs?
- 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
what are the different classes of anti-arrythmic drugs? (vaughan william classification)
- Class 1 : (na+channel blockers) - Class 2 : b adrenergic receptor antagonists - - Class 3: K+ channel blockers - Class 4: ca2+ channel blockers
36
what are the subgroups of class 1 antiarrythmic drugs and what does each do?
- 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
How do class 1 antiarrythmic drugs work?
- decreases slope phase 4 | - decreases re-entry in contractile tissue - slows down phase 0 so refractory for longer
38
all antiarrythmic drugs can precipitate arrythmia. TRUE RO FALSE?
TRUE
39
Many drugs which prolong QT increases risk of torsade depointes. TREU RO FALSE?
TRUE
40
Class 1a drugs are also cholinergic antagonists so they block parasympathetic inhibition of AV node. TREU RO FALSE?
TRUE
41
give ana example of a class 1a drug?
- Disopyramide
42
what is Disopyramide indicated for?
- Ventricular tachycardia following MI
43
what are some ADRs of class 1a drugs?
- Negative inotropic agent | - cholinergic antagonist so Causes dry mouth, blurred vision constipation
44
what are some drug interactions with class 1a?
- Avoid drugs that increase QT | - Avoid giving with drugs that are negative inotrops
45
disporymide reduced cardiac output. TRUE OR FALSE?
TRUE
46
class 1b is most effective on frequently depolarising tissue. TREU RO FALSE?
TRUE
47
lidocaine is a class 1b antiarrythmic drug inicated for ventricular tachycardi and local anaesthesia. TREU RO FALSE?
TREU
48
lidocaine is not effective in supraventricular arrythmia. TRUE RO FALSE?
TRUE
49
lower doses of lidocaine should be given to patients with hepatoic impairment or haert failure. TREU RO FALSE?
- TRUE
50
why is Lidocaine is a contranidicated in AV block?
because it slows down AV conduction
51
which of the class 1 antiarrythmic drugs are the most potent?
- Class 1c - they are marked effective in phase 0 but not effect on duration
52
what does class 1c do?
- Slows conduction in all cardiac tissue - suppresse premature ventricular contraction - Increases PR and QRS intervals
53
give an example of class 1c drug name and its indication?
- Flecainide | - Atrial fibrillation and tachycardia
54
what are ADRs for flecainide?
- Negative inotropic agent - CNS toxicity - arrythmia by prolonging QT
55
what is flecaidine contraindicated againts and waht are some drug interactions?
- Contrai - HF - Previous MI dRUG INTRECATIONS - patients using duiretics risk of arrythmia - avoid with ther negative iontropes
56
class 2 antiarrytmic drugs are indicated for supraventricular arrythmia because decreases SA rate and AV conduction. TRUE OR FALSE?
TRUE
57
give an example of a class 2 antiarrytmic drug?
- propanolol
58
Class 2 have been shown to reduce sudden death post M.I. TREU RO FALSE?
TRUE
59
how does amiodarone a class 3 drug work?
- prolongs action potential and QT interval
60
Satolol is a B adrenergic antagonist with class 2 and 3 activity. TREU RO FALSE?
TRUE
61
class 3 is contrainidcated agiants bradycardia, heart block, iodine sensitivity. TRE OR FALSE?
TREU
62
What are some ADRs for class 3 drugs?
- Pulmonary fibrosis - grey skin dicoloration - hyperthyroidism (inhibits conversation of T4 to T3 )
63
what are some drug interactions?
- Inhibits CYP3A4 - Inhibits renal excretion of digoxin - Avoid with other drugs that prolong QT
64
class 4 drugs slows phase 0 in AV node which slows conduction velocity through AV nod eincreasing its refractory period. TREU OR FALSE?
TRUE
65
high doses of class 4 drugs can cause complete AV block. TRUE OR FALSE?
TREU
66
name a class 4 drug?
- Verapamil
67
dihydropyridines tend to be less effective on cardiac tissue. TREU OR FLASE?
TREU
68
Co administartion of dihydropyridines and B antagonists can cause asystole. TREU RO FALSE?
TRUE