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Cardiovascular System > Electricity and the heart > Flashcards

Electricity and the heart Flashcards

1
Q

3 types of muscle

A

Smooth, skeletal and cardiac

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2
Q

Na+ extra and intra cellular

A

E: 120
I: 10

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3
Q

Ca2+ extra and intra cellular

A

2 and 0

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4
Q

K+ extra and intra cellular

A

4 and 140

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5
Q

What is resting potential of nerve cell?

A

-70 mV

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6
Q

What causes depolarisation?

A

Sodium entering

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7
Q

What causes depolarisation?

A

Potassium leaving

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8
Q

Potential of cardiac myocyte

A

-85 to -90 mV

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9
Q

How is potential in cardiac myocyte regulated?

A
  • ATP driven pump exchanges sodium and potassium - high Na+ outside cell and high K+ inside
  • Antiport system: establishes Ca2+ gradient - exchange of sodium and calcium needed
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10
Q

Phase 0

A

Depolarisation

  • Fast sodium channels open
  • When cardiac cell is stimulated and depolarises, the membrane potential is more positive
  • Voltage gated sodium channels open and allow Na+ into cell = depolarisation
  • Membrane potential reaches +20 mV before Na+ channels close
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11
Q

Phase 1

A

Repolarisation

Na+ channels close and cell repolarises, K+ leaves cell through K+ channels

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12
Q

Phase 2

A

Plateau

  • Ca2+ channels open and fast K+ channels close
  • After initial repolarisation occurs, AP plateaus as a result of increased Ca2+ permeability and decreased K+ permeability
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13
Q

Phase 3

A

Rapid repolarisation

  • Ca2+ channels close
  • Slow K+ channels open, K+ exits cell
  • Plateau ends and resting level is re-established
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14
Q

Phase 4

A

Resting potential

Averages -80 to -90 mVW

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15
Q

Why is there a prolonged resting potential in cardiac myocytes?

A

Ion channel inactivation and prevents tetany

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16
Q

Features of pacemaker cells

A
  • Specialised cells in atria, especially SAN and AVN
  • Autonomic firing without stimulus
  • Results from continuous slow ionic leak
  • Natural highest rate in SAN - others become active if SAN fails
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17
Q

What does pacemaker AP start at?

A

-60 mv

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18
Q

What causes depolarisation of pacemaker cells?

A

Ca2+ influx

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19
Q

Sympathetic influence on HR

A

Slow Na+ channel permeability increases
Slope of phase 4 steeper
Threshold reached sooner, increasing HR

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20
Q

Parasympathetic influence on HR

A

Increases resting K+ permeability
Trough potential is lowered and slope of phase 4 flatter
Threshold reached later, decreasing HR

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21
Q

Intra-cardiac conduction

A
  • Non-specific conduction in atria
  • AVN: gate in firewall between atria and ventricles - slows conduction and allows time for atrial emptying, protects ventricles from atrial tachyarrhythmias, also affected by autonomic NS
  • His-Purkinje system - ventricles - depolarise of myometrium from in to out (opposite of perfusion)
  • Branching nature of cardiac muscle also enables synchronous ventricular contraction
22
Q

What are ECGs?

A

Surface recording of electrical activity

Polarity of impulses is +ve if moving towards electrode, -ve if away

23
Q

Axis of ECGs

A

Lead iii at 90 degrees to axis = isoelectric trace

24
Q

Characteristics of ischaemia/infarction on ECH

A
  • Typically produces ST segment (with/without T wave) changes acutely
  • Damaged cells repolarise early so ST segment is out of step with normal areas
  • Division between ischaemia and infarction is now less clear (acute coronary syndrome can be reversible) but classically:
  • Full thickness damage (ST elevation)
  • Subendocardial damage (ST depression)
25
Q

Full thickness STEMI on ECH

A

ST elevation

Q wave

26
Q

Subendocardial damage on ECG

A

ST wave depression

With or without T wave inversion

27
Q

Coronary artery to inferior heart

A

Right

28
Q

Coronary artery to antero-septal heart

A

Left anterior descending

29
Q

Coronary artery to antero-apical heart

A

Left anterior descending - distal

30
Q

Coronary artery to antero-lateral heart

A

Circumflex

31
Q

Coronary artery to posterior heart

A

Right

32
Q

Inferior MI on ECG

A

ST elevation in leads II, III and aVF (inferior leads)

33
Q

Anterior/septal MI on ECH

A

ST elevation in V2/3/4 - tombstoning

34
Q

What is the Q wave?

A

First downwards deflection in PQRS pathology

Seen in lateral leads as septal depolarisation

35
Q

What does deep Q wave indicate?

A

STEMI

36
Q

Hyperkalaemia on ECG

A

High, peaked T waves and QRS widening

37
Q

Hypertrophy on ECG

A
  • LVH = large amplitude QRS complexes
  • Negative deflection in V1, positive deflection in V5
  • Add the negative deflection to the positive deflection, want it to be less than 35
38
Q

Fibrillation on ECG

A
  • Rapid, uncoordinated contraction
  • Atrial fibrillation: AVN prevents VF, cardiac output less than 30%, thrombo-embolism risk
  • Ventricular fibrillation: No cardiac output, fatal if not treated quickly
39
Q

AF on ECG

A
  • No P waves
  • QRS normal but irregularly irregular
  • To confirm irregularity, mark consecutive r peaks on paper and compare down the line
40
Q

Management of AF

A
  • Anti-thrombotics: warfarin, dabigatran, rivaroxaben, aspirin
  • Rhythm: cardioversion (synchronised shock to prevent VF), rate control ( beta blocker, Ca2+ antagonist, amiodarone, digoxin)
  • Plus any underlying causes
41
Q

Mechanism of digoxin

A
  • Slows conduction through AVN - reduces ventricular rate in AF
  • Increases myocardial contractility
  • Na+/K+ pump inhibited, increasing [Na+]
  • Na+/Ca2+ exchange mechanism now less efficient, raising [Ca2+] - stored in sarcoplasmic reticulum
  • Force of subsequent contraction enhanced
42
Q

Ventricular fibrillation

A
  • Continuous, bizarre, irregular trace

- No P wave

43
Q

Management of VF

A
  • Defibrillation: unsynchronised (150-200J, biphasic)
  • Treat underlying causes
  • Automated function - AED (paramedics, airports) and AID (implanted, high risk patients)
  • Sudden death is often VF
44
Q

Conduction defects

A
  • SAN: pacemaker failure, lower site normally takes over
  • AVN: heart block
  • Intra-ventricular - bundle branch block
  • Heart block:
  • Problem with conduction through AVN
45
Q

1st degree block

A

PR interval, prolonged but all eventually conducted

46
Q

2nd degree block

A

Some P waves not conducted, here in 2:1 ratio (type ii)

47
Q

3rd degree block

A

P waves unrelated to QRS complexes, usually bizarre in nature

48
Q

Bundle branch blockages

A
  • Problem with circulation through R or L branch
  • 1 ventricle depolarises after the other
  • Wide QRS complex after normal P wave
  • RBBB: M pattern in V1, W pattern in V6
  • LBBB: M pattern in V6
49
Q

ventricular ectopic

A
  • One-off can be normal
  • Ventricle contracts after stimulus transported throughout heart
  • Wide QRS complex
  • Abnormalities in repolarisation
  • No P wave
50
Q

Pacing impulse

A
  • Very brief impulse external impulse stimulates ventricle (with or without atrium)
  • Wide QRS
  • Short, sharp pacing spike

Cardiovascular System (21 decks)

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