CVS 4 Flashcards
hwo is blodd circulated in the heart?
- Vena cava
- Right atrium
- Righet ventricle
- to lungs
- Return left atrium
- Left ventricle
- To periphery
what is the pacemaker?
- The SA node
why are the ventricles forced to contract after the atria?
- Because of the slowed signal in the AV node
what does the P wave represent on ECG trace/
- Atrial depolarisation
what does the QRS complex represent ECG trace?
- Ventricular depolarisation
by measuring P-R interval what does it tell?
- How the the atria is functioning
- it measured the time the atria are contracting and when ventricles start to contract
what does the T wave represent in ECG trace?
- Ventricles repolarising
what does the ST interval suggetsed?
- how long the ventricels are depolarised for
what does the QT interval tell you?
- How long ti takes for ventricles to start depolarising and to fully recovering
why is the SA node the pacemaker?
- It fires the highest frequency
what happens in phase 4 nodel cells?
- Slow depolarisation due to na+ influx (na+ channels open)
what occurs at phase 0 of nodel cells?
- ca2+ channels open and ca2+ flood in leading to cell depolarising
what occurs at phase 3 of nodel cells?
- Ca2+ and Na+ channels close and K+ channels open and k+ floods out of the cell repolarising the cell
what is the refractotry period?
- The point at which another action potential can cause another contraction of the cells, this usually occurs at phase 1-2 in ventricular myocytes
what occurs in phase 0 in the ventricualr myocytes?
- na+ channels open and membrane depolarises as na+ influx occurs
what occurs in phase 1 of the ventricualr myocytes?
- na+ channels inactivate
what occurs in phase 2 of the ventricualr myocytes?
- K+ and ca2+ channels
- ca2+ channels inactive eventually
what occurs in phase 3 of the ventricular myocytes?
- K+ channel still open so cell repolarises
why does arrythmias occur?
- M.I
- Heart failure
- Hyperthyrodism
- Drugs B antagonist
- Genetics
what are the abnormalities that can occur leading to arrythmias?
- Conudction of impulse
- Automaticity
- These lead to non-coordination of contraction
what is automaticity?
- Site of origin of impulse, regulation of pacemaker and rate
What is the goal of treating arrythmia?
- Treating the electrical abnormalities
additional impulses caused due to slowed SA node firing and AV node becoming the dominant pacemaker can lead to arrythmias. TREU RO FALSE?
TRUE
describe how signal bypass can cause arrythmias?
- additional signals can come from SA node to atria and straight ot the ventricles bypassing the AV node
- Leading to additional signals
explain re-entry leading to arrymthmia?
- the electric circuit is not complete so it creates an alternative route upon itself
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
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
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
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
what are the different types of ventricular arrythmia?
- Ventricular tachycardia:
- Ventricular fibrillation: re-entry to impulse/ fatal
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
what is monomorphic and polymorphic ventricular tachucardia?
- Monomorphic: ventricular pacemaker causes additonal systole
Polymorphic: Torsades de pointes caused by sustained early after depolarisation
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)
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)
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
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
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
all antiarrythmic drugs can precipitate arrythmia. TRUE RO FALSE?
TRUE
Many drugs which prolong QT increases risk of torsade depointes. TREU RO FALSE?
TRUE
Class 1a drugs are also cholinergic antagonists so they block parasympathetic inhibition of AV node. TREU RO FALSE?
TRUE
give ana example of a class 1a drug?
- Disopyramide
what is Disopyramide indicated for?
- Ventricular tachycardia following MI
what are some ADRs of class 1a drugs?
- Negative inotropic agent
- cholinergic antagonist so Causes dry mouth, blurred vision constipation
what are some drug interactions with class 1a?
- Avoid drugs that increase QT
- Avoid giving with drugs that are negative inotrops
disporymide reduced cardiac output. TRUE OR FALSE?
TRUE
class 1b is most effective on frequently depolarising tissue. TREU RO FALSE?
TRUE
lidocaine is a class 1b antiarrythmic drug inicated for ventricular tachycardi and local anaesthesia. TREU RO FALSE?
TREU
lidocaine is not effective in supraventricular arrythmia. TRUE RO FALSE?
TRUE
lower doses of lidocaine should be given to patients with hepatoic impairment or haert failure. TREU RO FALSE?
- TRUE
why is Lidocaine is a contranidicated in AV block?
because it slows down AV conduction
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
what does class 1c do?
- Slows conduction in all cardiac tissue
- suppresse premature ventricular contraction
- Increases PR and QRS intervals
give an example of class 1c drug name and its indication?
- Flecainide
- Atrial fibrillation and tachycardia
what are ADRs for flecainide?
- Negative inotropic agent
- CNS toxicity
- arrythmia by prolonging QT
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
class 2 antiarrytmic drugs are indicated for supraventricular arrythmia because decreases SA rate and AV conduction. TRUE OR FALSE?
TRUE
give an example of a class 2 antiarrytmic drug?
- propanolol
Class 2 have been shown to reduce sudden death post M.I. TREU RO FALSE?
TRUE
how does amiodarone a class 3 drug work?
- prolongs action potential and QT interval
Satolol is a B adrenergic antagonist with class 2 and 3 activity. TREU RO FALSE?
TRUE
class 3 is contrainidcated agiants bradycardia, heart block, iodine sensitivity. TRE OR FALSE?
TREU
What are some ADRs for class 3 drugs?
- Pulmonary fibrosis
- grey skin dicoloration
- hyperthyroidism (inhibits conversation of T4 to T3 )
what are some drug interactions?
- Inhibits CYP3A4
- Inhibits renal excretion of digoxin
- Avoid with other drugs that prolong QT
class 4 drugs slows phase 0 in AV node which slows conduction velocity through AV nod eincreasing its refractory period. TREU OR FALSE?
TRUE
high doses of class 4 drugs can cause complete AV block. TRUE OR FALSE?
TREU
name a class 4 drug?
- Verapamil
dihydropyridines tend to be less effective on cardiac tissue. TREU OR FLASE?
TREU
Co administartion of dihydropyridines and B antagonists can cause asystole. TREU RO FALSE?
TRUE
