Cardiology - Physiology Flashcards

1
Q

Cardiac Action Potential: Phase 0 (first upstroke)

A

Phase 0: Rapid Depolarisation

  • At threshold voltage-gated Na channels open
  • Rapid influx of Na
  • These channels automatically close after a few milliseconds
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2
Q

Cardiac Action Potential: Phase 1 (peak at top)

A

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
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3
Q

Cardiac Action Potential: Phase 2 (plateau)

A

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
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4
Q

Cardiac Action Potential: Phase 3 (downstroke)

A

Calcium channels close

More K channels open with rapid K efflux

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5
Q

Cardiac Action Potential: Phase 4 (floor)

A

Phase 4: Resting Potential

- Slow entry of Na into cell until threshold is reached

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6
Q

Cardiac Action Potential Conduction Velocity:

A

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

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7
Q

Parasympathetic effect on Conduction:

A

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

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8
Q

Sympathetic effect on Conduction:

A

Increased catecholamine concentrates
Activation of Beta-1 receptors which augment L-type calcium channels so Calcium enters cells and REACHES THRESHOLD FASTER

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9
Q

What supplies the ANTEROSEPTAL territory?

What ECG leads?

A

Left anterior descending

V1-V4

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10
Q

What supplies the INFERIOR territory?

What ECG leads?

A

Right coronary artery

II, III, aVF

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11
Q

What supplies the ANTEROLATERAL territory?

What ECG leads?

A

Left anterior descending
AND
Left circumflex

V4-V6, I and aVL

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12
Q

What supplies the LATERAL territory?

What ECG leads?

A

Left circumflex

I, aVL, V5-V6

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13
Q

What supplies the POSTERIOR territory?

What ECG leads?

A

Left circumflex
AND
Right coronary

TALL R waves in V1-V2

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14
Q

Left anterior descending supplies what?

A

Anteroseptal

Anterolateral

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15
Q

Right coronary supplies what?

A

Inferior and Posterior

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16
Q

Left circumflex supplies what?

A

Anterolateral
Lateral
Posterior

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17
Q

Left aortic sinus feeds into what?

A

The left coronary artery

Then go LAD and LCx

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18
Q

Right aortic sinus drains into where?

A

Into right coronary artery

Then into posterior descending

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19
Q

What nodes does the RCA supply?

A

SA node in 60%

AV node in 90%

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20
Q

How do you calculate the Rate of ECG?

A

Normal: 300/no. of large squares in R-R

Fast: 1500/no. of small squares in R-R

Slow: number of complexes x 6

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21
Q

Causes of Right Axis Deviation?

A
  • 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
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22
Q

Causes of Left Axis Deviation?

A
  • LVH
  • LBBB
  • Inferior MI
  • WPW with R sided accessory pathway
  • Primum ASD
  • Hyperkalaemia
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23
Q

Causes of tall P wave?

A

Right atrial enlargement

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24
Q

Causes of wide P wave?

A

Left atrial enlargement

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25
Q

P mitrale?

A

= bifid P waves

Caused by left atrial enlargement, classically due to mitral stenosis

26
Q

P pulmonale?

A

= peaked tall P in lead II

Due to Right atrial enlargement usually due to pulmonary hypertension

27
Q

How can you tell a multifocal atrial rhythm from p waves?

A

Variable morphology with >3 morphologies being defined as multifocal atrial rhythm

28
Q

DDx for Q waves on ECG?

A
  • MI
  • cardiomyopathy (HOCM or infiltrative)
  • rotation of the heart
29
Q

ECG features of dextrocardia?

A

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

30
Q

Hyperacute T waves?

A

= broad, asymmetrically peaked
Often seen in early STEMI before ST elevation
Also seen in Prinzmetal’s angina

31
Q

Inverted T waves?

A

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

32
Q

Classic PE findings on ECG?

A

S1Q3T3

–> S wave in lead I, Q wave in lead III, T wave inversion in lead III

33
Q

Causes of biphasic T waves?

A

Myocardial ischaemia
–> T waves go UP then DOWN

Hypokalaemia
–> T waves go DOWN then UP

34
Q

Wellen’s Syndrome?

A

= pattern of inverted or biphasic T waves in V2-3 with ischaemic chest pain
HIGHLY SPECIFIC for critical stenosis of LAD

35
Q

Camel Hump T waves?

A

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)

36
Q

What are U waves?

A

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
37
Q

Inverted U waves?

A

Highly specific for heart disease and myocardial ischaemia

38
Q

What are J waves?

A

= positive deflection at the J point, usually most prominent in precordial leads

Causes:

  • hypothermia (classic)
  • hypercalcaemia
  • neurological insult
39
Q

What are delta waves?

A

Characteristic finding of WPW

= slurred upstroke to the QRS

40
Q

What are the characteristic ECG findings of WPW?

A

Short PR <120ms
Broad QRS >100ms
Delta wave

41
Q

What is an epsilon wave?

A

= small positive ‘blip’ at the end of hte QRS

Characteristic of ARVD (arrhthymogenic right ventricular dysplasia)

42
Q

ECG findings of ARVD?

A

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

43
Q

Importance of PR depression or elevation in patients with MI?

A

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
44
Q

Heart Sounds:

What causes S1?

A

Closure of MITRAL and TRICUSPID valves

45
Q

Heart Sounds:

What causes a SOFT S1

A

Long PR

Mitral regurgitation

46
Q

Heart Sounds:

What causes a LOUD S1

A

Mitral stenosis
L to R shunt
Hyperdynamic states

47
Q

Heart Sounds:

What causes S2?

A

Closure of AORTIC and PULMONARY valves

48
Q

Heart Sounds:

What causes a SOFT S2?

A

Aortic stenosis

49
Q

Heart Sounds:

What causes a LOUD S2

A

Hypertension:
systemic HTN –> loud A2
pulmonary HTN –> loud P2

50
Q

Heart Sounds:

What causes a fixed S2?

A

Atrial septal defect

51
Q

Heart Sounds:

What causes a widely split S2?

A

RBBB

Deep inspiration

52
Q

Heart Sounds:

What causes a reverse split S2?

A

LBBB

Severe aortic stenosis

53
Q

Heart Sounds:

What makes the sound S3?

A

Due to diastolic filling of the ventricle

54
Q

Heart Sounds:

Causes of an S3?

A

Normal in aged <30yrs
LV failure (ie dilated CM)
Constrictive pericarditis (‘pericardial knock’
Mitral regurgitation

55
Q

Heart Sounds:

What makes the sound S4?

A

Due to atrial contraction against a stiff ventricle

56
Q

Heart Sounds:

Causes of an S4?

A

Aortic stenosis
HOCM (may feel the S4 as a double impulse)
Hypertension

57
Q

What important condition would mean an S4 will NOT be present?

A

Atrial fibrillation

58
Q

Name an alpha-1 antagonist

A

Doxazosin

59
Q

Name an alpha-1a antagonist

A

Tamsulosin

Acts mainly on urogenital tract

60
Q

Name an alpha2 antagonist

A

Yohimbine

61
Q

Which two medications are classically mixed alpha and beta antagonists?

A

Carvedilol and labetolol