normal heart rhythm
What does each aspect of the ECG mean? i.e.
P wave
QRS complex
T wave
PR interval
P wave = atrial depolarisation
QRS complex = ventricular depolarisation
T wave = ventricular repolarisation
PR interval = beginning of P wave -> beginning of QRS. Represents time taken for excitation to spread from the SA node to the ventricles
How does atrial fibrillation look on ECG?
No P waves
Disorganised atrial activity
Irregular QRS complex distribution
what is atheroma?
Fibrous plaque with a lipid rich core. The core can become necrotic and rupture
How do class IV antiarrhythmics work? + give an example
L-type Ca2+ channel blockers, affecting SA and AV node depolarisation
e.g. verapamil, diltiazem
What is disability?
The impact of the disease on the patient's life. Often relates to work and arises from environmental and societal barriers.
What is sinus rhythm?
The two rules of sinus rhythm:
1. every P wave is followed by a QRS
2. every QRS is preceded by a P wave
What is bundle branch block?
DELAYED conduction, NOT blocked
Right bundle - delayed RV contraction
Left bundle - delayed LV contraction
why is distinction between STEMI and NSTEMI crucial?
How do class I antiarrhythmics work? + give an example
- block the rapid sodium channels but in varying degrees
e.g. Lidocaine - shortens duration of action potential and decreases refractoriness
other examples:
quinidine, procainamide, disopyramide, phenytoin, tocainide, mexiletine, flecainide, encainide, propafenone
How might grief be experienced in cardiac and respiratory disease?
- health and stamina
- employment
- identity
- expected future
what is the difference in AP duration between atria, ventricles and purkinje fibres?
Atrial myocytes have the shortest AP duration
Ventricular myocytes have a longer AP duration for strong contraction
Purkinje fibres have the longest AP duration to ensure effective conduction.
What is supraventricular tachycardia?
tachycardia that originates above the ventricles, in or above the AV node
Includes:
- AF
- AVRT and AVNRT (atrioventricular re-entrant tachycardia, atrioventricular nodal re-entrant tachycardia)
- atrial flutter
What are the 4 stages of atheroma development?
1. damage to tunica intima
2. foam cells
3. fatty streak
4. atheroma
How do Class II antiarrhythmics work? + give an example
Beta blockers
Block beta receptors, causing a decrease in sympathetic nervous system stimulation. This reduces pacemaker activity in the SA/AV nodes, lowers heart rate, slows AV node conduction and increases the refractory period
examples - atenolol, bisoprolol, labetalol, metoprolol
1. Denial
2. Anger
3. Bargaining
4. Depression
5. Acceptance
Describe slow response action potential (SA and AV nodes)
1. Phase 4 - pacemaker potential. Slow depolarisation. T type and L type Ca2+ channels also contribute
2. Phase 0 - depolarisation. L type Ca2+ channels open, causing a slower upstroke (compared to Na+ dependent depolarisation in fast AP)
3. Phase 3 - repolarisation. K+ efflux restores the negative membrane potential.
What are ectopic beats and what causes them?
- heart beat that originates from outside the normal conduction system - not the SAN
- benign
- due to transient abnormalities in myocytes e.g. electrolytes, SNS and PSNS activation, chemicals - caffeine, alcohol
What are some short term and long term complications of MI?
short term - ventricular arrythmia, myocardial rupture, ischaemic MR
long term - ventricular aneurysm, heart failure, ventricular arrythmia
Give an example of a class V antiarrhythmic drug and how it works
- Digoxin - causes increase in parasympathetic activity and slowed conduction in AV node
- adenosine - activation of K+ channels and subsequently inhibiting Ca2+ current causing shortened action potential duration and slowed AV conduction
- atropine - competitive, reversible antagonist of muscarinic receptors which leads to parasympathetic inhibition
- Ivabradine - selectively block If channel blockade, reducing the rate of depolarisation in SA node
- magnesium sulfate - affects K+ and Ca2+ flow
Describe the dual process model
- Oscillation between loss-focused and restoration-focused coping
- concept of chronic grief in relapsing conditions
- emotional distress may fluctuate with exacerbations or hospital admissions
Describe the phases of fast response action potential (atria, ventricles and purkinje fibres) (phase 0 to phase 4)
1. Phase 0 - depolarisation. Rapid Na+ influx through voltage gated Na+ channels. Membrane potential rises to +30mV
2. Phase 1 - initial repolarisation. Inactivation of Na+ channels, opening of K+ channels
3. Phase 2 - plateau phase. Balance between inward Ca2+ and outward K+. Prolongs depolarisation, crucial for sustained contraction
4. Phase 3 - repolarisation. Ca2+ channels close. K+ efflux through delayed rectifier channels restores resting potential
5. Phase 4 - resting membrane potential. Maintained by Na+K+ATPase pump and background K+ currents (~ -90mV in ventricles)
What is the difference between first, second and third degree heart block in terms of ECG?
First degree - all P waves are conducted
Second degree - some P waves are conducted
Third degree - no P waves are conducted
How is acute coronary syndrome classified?
1. History - central chest pain, radiating to neck and jaw, at rest or very mild exertion, some relief but not resolving with nitrates
2. ECG - ST elevation (STEMI) or no ST elevation
3. if no ST elevation - bloods - raised Troponin T (TnT) (nSTEMI) or normal TnT (unstable angina)
How do class III antiarrhythmics work? + give an example
predominantly block K+ channels. Increase the action potential duration and increase refractory periods.
e.g. amiodarone, sotalol, dronedarone