3. Heartbeat & ECG Flashcards
Where is the SAN?
Wall of R atrium, near entrance of superior vena cava
Where is the AVN?
On the inter-atrial septum
Give the conduction pathway
Pacemaker cells in SAN -> electrical impulse -> AVN -> 60ms delay before AVN transmits to ventricles via bundle of His -> purkinje fibres -> contracts apex up
NB. delay = “weak link”
Where does the SAN usually receive blood from?
What does this mean?
RCA
If MI occludes RCA there has to be a good anastamosis for the LCA or else cell death will stop SAN triggering heartbeat.
How long is a cardiac mucle AP?
200 milliseconds
Describe how pacemaker cells work
Constant Na+ in at rest and K+ out so current balance at -70mv.
K+ out decays with time and depolarises cell (-40mv) causing AP.
K+ is reset to high level again.
Thus HR depends on rate of K+ out.
What is the SAN innervated by?
Parasympathetic vagal fibres inhibit K+ channel closure via muscarinic cells
Sympathetic cardiac plexus fibres increase K+ channel closure via beta-adrenoreceptors
(NB. blood-bourne adrenaline acts on beta receptors throughout myocardium)
What is first degree AV block?
PR interval is lengthened beyond 200ms (prevalence in normal young pop of 1%), so cardiac output limited.
What is happening at A, B & C in this ventricular muscle AP?
A: Na+ enters cell, depolarisation
B: Ca2+ enters cell, contraction initiation
C: K+ exits cell, repolarisation
What is the plateau in a ventricular muscle AP due to?
Why is there such a long refractory period?
Late prolonged entry of Ca2+ which helps muscle contract longer than skeletal muscle. Ca2+ enter through slow L type channels on cardiac cell membranes.
To keep cells synchronous
How does amylodapine work?
Blocks Ca2+ channels on cardiac cell membranes and thus reduces force of ventricular contraction and work/O2 demand of heart.
What happens if cardiac cells get out of synchronisation?
How does a defibrilator work?
Fibrillation - different parts of ventricle contracting at different times and ventricular pressure does not rise enough to generate any cardiac output -> death
It shocks all muscle and makes it contract simultaneously, then the cells all go into refractory period together and rhythm is restored.
What do the P,Q,R,S, and T waves show?
P: atrial depolarisatin
QRS: ventricular depolarisation
T: due to differences in time of ventricular repolarisation
What are the ECG leads and where do they go?
3 limb leads show I, II, III
3 augmented leads show aVR, aVL, aVF (unipolar - virtual reference point in middle of chest)
6 chest leads show V1-V6
Which lead is the standard ECG recorded from?
How long should the QRS complex last?
How long should the PR interval be? (And what does higher values indicate?)
When do you hear the first heart sound?
II
<100ms
120-200ms, heart block
QRS
What could a notched/peaked P wave indicate?
What is one small box on ECG trace?
How does the Q wave appear on lead II?
What are ST segment changes important for diagnosing?
COPD, CHF
40ms
Small/absent
Acute MI (STEMI)
What are the normal appearances of aVR and aVL?
Where is V1 placed?
How are V1-V6 described?
aVR = large Q wave and small/non-existant R wave, aVL = v. small
4th intercostal space to right of sternum
V1 = mainly -ve, V5,6 = mainly +ve, transition between -ve and +ve
What leads would you look at for the following views of the herart:
Inferior
Lateral
Anterior
Septal
I,III,aVF
I,aVL,V5,V6
V3,V4
V1,V2
What does this ECG show and why?
No P wave - atrial fibrillation (pacemaker cells firing at different times = asynchronised and no electrical activity)
What does this ECG show and why?
Extra P waves - atrial flutter (look at V1), often due to poor blood supply to SAN
What does this ECG show and why?
S-T elevation = acute ischaemia (but most common cause = AMI)
What does this ECG show and why?
S-T depression, can be sign of chronic ischaemia
What can you see in leads II and III?
S-T elevation
What does this ECG show and why?
Ventricular fibrillation - grossly abnormal ECG with no clear QRS complexes
What is the electrical axis of the heart?
How do you calculate the electrical axis of the heart?
How does the axis deviate with damage?
Electrical vector showing different depolarisation in different parts of the heart at the same time.
Measure size of QRS complex (R height - S height) on two leafds and draw them to scale on a triangle.
If R ventricle damaged = L axis deviation and vice versa. (Swings TOWARDS HYPERTROPHIC tissue and AWAY from DAMAGED tissue).
