Cardiology - Physiology Flashcards
Cardiac Action Potential: Phase 0 (first upstroke)
Phase 0: Rapid Depolarisation
- At threshold voltage-gated Na channels open
- Rapid influx of Na
- These channels automatically close after a few milliseconds
Cardiac Action Potential: Phase 1 (peak at top)
Phase 1: Early Repolarisation
- Once transmembrane potential reaches +30mV the voltage-gated Na channels all close until the potential reaches -60mV
- Active efflux of Na begins
- Slow voltage gated K channels and also open for K efflux
Cardiac Action Potential: Phase 2 (plateau)
Phase 2: Plateau
- Slow voltage gated Ca channels open and Ca enters the cell, balancing the efflux of Na and K
- these channels remain open for 175ms
Cardiac Action Potential: Phase 3 (downstroke)
Calcium channels close
More K channels open with rapid K efflux
Cardiac Action Potential: Phase 4 (floor)
Phase 4: Resting Potential
- Slow entry of Na into cell until threshold is reached
Cardiac Action Potential Conduction Velocity:
SA Node through Atria: 50msec
Delay at AV node: 100msec
AV Node to AV Bundle of His, Bundle Branches to Purkinje Fibers: 25msec
Purkinje Fibres through Ventricular Myocardium: 50msec
Parasympathetic effect on Conduction:
ACh binds to muscarinic receptors
–> results in activation of K channels so phase 4 is slowed and it takes LONGER to reach threshold for depolarisation
Sympathetic effect on Conduction:
Increased catecholamine concentrates
Activation of Beta-1 receptors which augment L-type calcium channels so Calcium enters cells and REACHES THRESHOLD FASTER
What supplies the ANTEROSEPTAL territory?
What ECG leads?
Left anterior descending
V1-V4
What supplies the INFERIOR territory?
What ECG leads?
Right coronary artery
II, III, aVF
What supplies the ANTEROLATERAL territory?
What ECG leads?
Left anterior descending
AND
Left circumflex
V4-V6, I and aVL
What supplies the LATERAL territory?
What ECG leads?
Left circumflex
I, aVL, V5-V6
What supplies the POSTERIOR territory?
What ECG leads?
Left circumflex
AND
Right coronary
TALL R waves in V1-V2
Left anterior descending supplies what?
Anteroseptal
Anterolateral
Right coronary supplies what?
Inferior and Posterior
Left circumflex supplies what?
Anterolateral
Lateral
Posterior
Left aortic sinus feeds into what?
The left coronary artery
Then go LAD and LCx
Right aortic sinus drains into where?
Into right coronary artery
Then into posterior descending
What nodes does the RCA supply?
SA node in 60%
AV node in 90%
How do you calculate the Rate of ECG?
Normal: 300/no. of large squares in R-R
Fast: 1500/no. of small squares in R-R
Slow: number of complexes x 6
Causes of Right Axis Deviation?
- RVH
- Acute RV strain
- Lateral STEMI
- WPW with L sided accessory pathway
- Sodium channel blockade (ie TCA poisoning)
- Secundum ASD
- Chronic lung disease with cor pulmonale
- Dextrocardia
Causes of Left Axis Deviation?
- LVH
- LBBB
- Inferior MI
- WPW with R sided accessory pathway
- Primum ASD
- Hyperkalaemia
Causes of tall P wave?
Right atrial enlargement
Causes of wide P wave?
Left atrial enlargement
P mitrale?
= bifid P waves
Caused by left atrial enlargement, classically due to mitral stenosis
P pulmonale?
= peaked tall P in lead II
Due to Right atrial enlargement usually due to pulmonary hypertension
How can you tell a multifocal atrial rhythm from p waves?
Variable morphology with >3 morphologies being defined as multifocal atrial rhythm
DDx for Q waves on ECG?
- MI
- cardiomyopathy (HOCM or infiltrative)
- rotation of the heart
ECG features of dextrocardia?
Positive QRS complex in aVR (upright P and T)
Negative QRS in lead I
Marked R axis deviation
Dominant S waves (downside) throughout V1-V6
Hyperacute T waves?
= broad, asymmetrically peaked
Often seen in early STEMI before ST elevation
Also seen in Prinzmetal’s angina
Inverted T waves?
Usually inverted (ie is NORMAL) in aVR and V1
Abnormal TWI DDx:
1) Myocardial ischaemia/infarction
2) BBB (RBBB produces TWI in V1-3)
3) Ventricular hypertrophy
- -> LVH causes TWI in I, aVL and V5-6
- -> RVH causes TWI in V1-3 and inferior leads
4) PE (TWI in V1-3 and inferior leads)
5) HOCM (deep TWI in all leads)
6) Raised ICP
Classic PE findings on ECG?
S1Q3T3
–> S wave in lead I, Q wave in lead III, T wave inversion in lead III
Causes of biphasic T waves?
Myocardial ischaemia
–> T waves go UP then DOWN
Hypokalaemia
–> T waves go DOWN then UP
Wellen’s Syndrome?
= pattern of inverted or biphasic T waves in V2-3 with ischaemic chest pain
HIGHLY SPECIFIC for critical stenosis of LAD
Camel Hump T waves?
May be either prominent U waves fused to end of T waves (ie severe hypokalaemia)
OR
Hidden P waves in T wave (ie sinus tachy or heart blocks)
What are U waves?
Small deflection immediately after T wave, usually in same direction of T wave, best in V2-V3
Causes:
- bradycardia (most common cause)
- severe Hypokalaemia
- Hypocalcaemia
- Hypomagnesaemia
- Hypothermia
- RAISED ICP
- LVH
- HOCM
Inverted U waves?
Highly specific for heart disease and myocardial ischaemia
What are J waves?
= positive deflection at the J point, usually most prominent in precordial leads
Causes:
- hypothermia (classic)
- hypercalcaemia
- neurological insult
What are delta waves?
Characteristic finding of WPW
= slurred upstroke to the QRS
What are the characteristic ECG findings of WPW?
Short PR <120ms
Broad QRS >100ms
Delta wave
What is an epsilon wave?
= small positive ‘blip’ at the end of hte QRS
Characteristic of ARVD (arrhthymogenic right ventricular dysplasia)
ECG findings of ARVD?
Epsilon wave is MOST SPECIFIC but is NOT SENSITIVE
TWI in V1-3
Prolonged S wave upstroke
Localised QRS widening in V1-3
Paroxysmal episodes of VT with LBBB morphology
Importance of PR depression or elevation in patients with MI?
Indicates concurrent atrial ischaemia or infarction
Assoc with:
- poorer outcomes post MI
- increased risk of AV block and supraventricular arrythmias
- increased cardiac free wall rupture
Heart Sounds:
What causes S1?
Closure of MITRAL and TRICUSPID valves
Heart Sounds:
What causes a SOFT S1
Long PR
Mitral regurgitation
Heart Sounds:
What causes a LOUD S1
Mitral stenosis
L to R shunt
Hyperdynamic states
Heart Sounds:
What causes S2?
Closure of AORTIC and PULMONARY valves
Heart Sounds:
What causes a SOFT S2?
Aortic stenosis
Heart Sounds:
What causes a LOUD S2
Hypertension:
systemic HTN –> loud A2
pulmonary HTN –> loud P2
Heart Sounds:
What causes a fixed S2?
Atrial septal defect
Heart Sounds:
What causes a widely split S2?
RBBB
Deep inspiration
Heart Sounds:
What causes a reverse split S2?
LBBB
Severe aortic stenosis
Heart Sounds:
What makes the sound S3?
Due to diastolic filling of the ventricle
Heart Sounds:
Causes of an S3?
Normal in aged <30yrs
LV failure (ie dilated CM)
Constrictive pericarditis (‘pericardial knock’
Mitral regurgitation
Heart Sounds:
What makes the sound S4?
Due to atrial contraction against a stiff ventricle
Heart Sounds:
Causes of an S4?
Aortic stenosis
HOCM (may feel the S4 as a double impulse)
Hypertension
What important condition would mean an S4 will NOT be present?
Atrial fibrillation
Name an alpha-1 antagonist
Doxazosin
Name an alpha-1a antagonist
Tamsulosin
Acts mainly on urogenital tract
Name an alpha2 antagonist
Yohimbine
Which two medications are classically mixed alpha and beta antagonists?
Carvedilol and labetolol
