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CVR > Electrical Conduction > Flashcards

Electrical Conduction Flashcards

1
Q

What do ECGs record

A

Voltage over time

Show us magnitude of collective electrical impulse in specified directions
• Standard set up parameters
• provide information on rate, rhythm, axis, conduction, myocardial health

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2
Q

Typical ECG settings

A

Speed = 25 mm/s
Voltage = 10 mm/mV

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3
Q

1 big voltage square

A

0.5mV

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4
Q

1 big time square

A

0.2s

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5
Q

Voltage equation

A

Current x resistance
I x R

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6
Q

Rate (bpm)

A

300 / (number of large squares between cardiac cycles)

(cycles in 10s) x 6

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7
Q

Atrial fibrillation

A

• random atrial activity
• Random ventricular capture
• Irregularly irregular rhythm
• No discernible P wave

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8
Q

Atrial flutter

A

• organised atrial activity ~ 300/min
• Ventricular capture at ratio to atrial rate (usually 2:1 so 150 bpm)
• Usually regular
• Can be irregular if ratio varies

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9
Q

P wave

A

Arterial depolarisation

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10
Q

QRS wave

A

Ventricular depolarisation

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11
Q

T wave

A

Ventricular repolarisation

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12
Q

Positive deflection

A

Depolarisation waves moving towards electrode

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13
Q

Negative deflection

A

Depolarisation waves moving away from electrode

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14
Q

Isoelectric point

A

0 mV

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15
Q

PR interval

A

time for impulse to reach ventricles from SAN (AVN delay) - 120-200 ms (3-5 small squares)
• long PR interval- 1st degree heart block due to delayed AV conduction

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16
Q

Length of QRS complex

A

less than 120ms (3 small squares)
• prolonged QRS - >120 ms - bundle branch block most common cause, problems between left and right ventricle

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17
Q

QT interval

A

measure of time to ventricular repolarisation men = 350-440 ms / women = 350-460 ms. Most common cause is drugs

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18
Q

ST elevation

A

S wave does not come back to isoelectric point- important for patients with chest pain
• inferior - blocked right coronary artery

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19
Q

Electrode

A

Physical connection (stickers) to patient in order to measure potential at that point
• 10 electrodes to record a 12 lead ECG

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20
Q

Lead

A

Graphical representation of electrical activity in a particular ‘vector’
• Calculated by the machine from electrode signals- seen on ECG trace
• 12 leads for a 12 lead ECG (I-III, aVL, aVF, aVR, V1-6)

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21
Q

Rhythm strip

A

allows us to give a longer reading over time to allow to look at rhythm (copy of lead II)

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22
Q

Bipolar lead

A

Measures the potential difference (voltage) between two electrodes
• One electrode designated positive, the other negative- current flows to positive = positive deflection and vice versa

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23
Q

Unipolar lead

A

Measures the potential difference (voltage) between an electrode (positive) and a combined reference electrode (negative)
• Sometimes known as augmented leads

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24
Q

RL electrode

A

neutral electrode
• reduces artefact
• Not directly involved in ECG measurement

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25
Q

Normal axis

A

-30° to +90° of frontal plane

leads I and II positive

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26
Q

Lead I

A

RA (-ve) → LA (+ve) = positive deflection/ LA → RA = negative deflection

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27
Q

Lead II

A

RA (-ve) → LL (+ve) = positive deflection/ LL → RA =negative deflection

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28
Q

Lead III

A

LA (-ve)→LL (+ve) = positive deflection/ LL → LA = negative deflection

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29
Q

3 bipolar limb leads

A

: I, II, III

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30
Q

3 unipolar limb leads

A

aVL (towards LA), aVF (towards LL), aVR (towards RA)

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31
Q

6 unipolar chest leads

A

V1-6)- transverse plane
• V1/2 - septal wall of left ventricle
• V3/4 - anterior wall of left ventricle
• V5/6- lateral wall of left venticle

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32
Q

Which lead Yields complexes that are normally inverted compared to the anterior and inferior leads

A

aVR

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33
Q

size of one big square on ECG

A

0.5mm/0.5mm

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34
Q

Cardiac output

A

Mean blood pressure/ systemic vascular resistance
Heart rate x stroke volume

35
Q

Thrombosis is a major cause of coronary artery disease.

Occlusion of which artery below is most likely to result in a fatal heart attack?

A

Occlusion of the left main coronary artery - it supplies the largest area of heart muscle via its many branches including the left circumflex and LAD.

36
Q

A 72-year-old patient is diagnosed with severe mitral valve stenosis.

An increase in which of the following is consistent with mitral valve stenosis?

A

Mitral stenosis causes an increased resistance to blood flow across the valve therefore a higher pressure is required to force blood from atrium to ventricle i.e. a higher left atrial end systolic pressure.

37
Q

Acute heart failure can be a complication following myocardial infarction.

An increase in which of the following pressures signifies left heart failure?

A

In heart failure there is reduced contractility therefore there will be a reduction in stroke volume so end diastolic volume and end diastolic pressure will be increased.

38
Q

Which nerves innervate the pericardium

A

Phrenic nerves

39
Q

Signs and symptoms of left sided heart failure

A

Restlessness
Confusion
Tachycardia
Fatigue
Cyanosis
Exertion all dyspnea
Orthopnea
Pulmonary congestion (eg cough, wheezes)

40
Q

Signs and symptoms of right sided heart failure

A

Fatigue
Increased peripheral venous pressure
Ascites
Enlarged liver and spleen
Weight gain
Anorexia and complaints of GI distress
Distended jugular veins
Dependent oedema

41
Q

A 83 year old patient develops shortness of breath, severe peripheral oedema and ascites following a recent heart attack.

Which of the following best describes the aetiology of their signs and symptoms?

A

Right sided heart failure

42
Q

Patients with chronic obstructive pulmonary disease (COPD) can develop pulmonary hypertension.

Which of the following is most likely to complicate severe pulmonary hypertension?

A

Right heart failure
Severe pulmonary hypertension means the right ventricle has to work harder to pump blood through the pulmonary artery. Ultimately the right ventricle is unable to generate sufficient pressure and therefore starts to fail.

43
Q

The end diastolic volume (EDV) in the average healthy person’s left ventricle is 120mls.

If we assume normal ventricular function, what would you expect the end systolic volume (ESV) to be?

A

EDV of 120 mls.
Stroke volume of 70 mls in the average person
Leaving an ESV of 50 mls

44
Q

Cardiac arrythmias can complicate a myocardial infarction.

Which artery most frequently supplies the AVN?

A

The RCA supplies the area above including both SA & AV nodes.
The LAD supplies most of the area below the AV conducting system, the His-Purkinje system.

45
Q

The maintenance of blood pressure is an important homeostatic function of the cardiovascular system.

Which of the following best describes the relationships of blood pressure (BP) & systemic vascular resistance (SVR) with the sympathetic nervous system?

A

Sympathetic stimulation of the peripheral blood vessels causes vasoconstriction which decreases their diameter thus increasing their vascular resistance and increasing the blood pressure.
BP = CO x SVR

46
Q

Heart failure is a possible complication of myocardial damage.

Which of the following best describes the finding of pulmonary oedema in the presence of a normal central venous pressure?

A

A raised central venous pressure is a reflection of right sided heart failure. Respiratory failure can lead to right heart failure.
Left sided heart failure causes an increase in pulmonary pressure leading to pulmonary oedema.

47
Q

The maintenance of blood pressure is an important homeostatic function of the cardiovascular system.

Which of the following best describes the relationships of blood pressure (BP) & systemic vascular resistance (SVR) with the parasympathetic nervous system?

A

There is no parasympathetic innervation of blood vessels.

48
Q

During pregnancy the foetal circulation is adapted to developing in-utero.

What is the purpose of the Ductus Arteriosus in the foetal cardiovascular system?

A

allow blood to bypass the foetal lungs by shunting it from the Pulmonary Artery to the Aorta

49
Q

With regard to the normal cardiac cycle.

Which of these following statements is correct?
A.
Atrial contraction occurs before the P-wave on ECG
B.
Atrial systole corresponds to closure of the tricuspid valve
C.
For part of the cardiac cycle, both atrial and ventricular diastole occur together
D.
Ventricular systole corresponds to closure of the pulmonary valve
E.
Ventricular volume increases during ventricular systole

A

Both atria and ventricles are in diastole during the isovolumetric ventricular relaxation phase of the cardiac cycle.

50
Q

Sympathetic stimulation

A

• Increases heart rate (positively chronotropic)- up to 180-250 bpm
• Increases force of contraction (positively inotropic)
• Increases cardiac output- by up to 200%

51
Q

Parasympathetic stimulation

A

• Decreases heart rate (negatively chronotropic)- down to 30-40 bpm
• Decreases force of contraction (negatively inotropic)
• Decreases cardiac output- by up to 50%

52
Q

What is sympathetic stimulation of cardiac muscle controlled by

A

Adrenaline and noradrenaline + type 1 beta adrenoreceptors
• Increases adenylyl cyclase → increases cAMP

53
Q

What is parasympathetic stimulation of cardiac muscle controlled by

A

Acetylcholine
• M2 receptors – inhibit adenyl cyclase → reduced cAMP

54
Q

Automaticity

A

• spontaneous discharge rate of heart muscle cells decreases down heart
• SAN usually fastest
• Ventricular myocardium slowest
• Slow Na+ influx via ‘funny’ current
• Automaticity varies throughout the heart but all tissues capable of automaticity

55
Q

Sinoatrial node SAN

A

right atrium into Bachmann’s bundle for atrioatrial contraction)- pacemaker current release
Upsloping phase 4 affected by: autonomic tone, drugs, hypoxia, electrolytes, age
Less rapid phase 0
No discernible phase 1/2
SAN potential drifts towards threshold- Steeper the drift, the faster the pacemaker

56
Q

What is the upsloping phase 4 of SAN affected by

A

autonomic tone, drugs, hypoxia, electrolytes, age

57
Q

contraction of the heart muscle

A
  1. Ca2+ influx through surface ion channels in T-tubules
  2. Amplification of [Ca2+] with NaCa
  3. Calcium-induced calcium release from sarcoplasmic reticulin via ryanodine receptor (RvR)
  4. Calcium binds to troponin and a conformational change in tropomyosin reveals myosin binding sites
  5. Myosin head cross-links with actin
  6. Myosin head pivots causing muscle contraction
58
Q

Which channel proteins release calcium-induced calcium from sarcoplasmic reticulum

A

Ryanodine receptors

59
Q

Local current

A

Action potential propagation:
• local depolarisation activates nearby voltage gated Na+ channels
• Further influx of Na+
• Wave of depolarisation- action potential spreads across membrane
• Gap junctions allow cell-to-cel conduction and propagation of action potential through whole myocardium

60
Q

Atrial and ventricular muscle fibre velocity of conduction

A

0.3-0.5 m/s

61
Q

Purkinje fibre velocity of conduction

A

4m/s

62
Q

What does velocity of conduction depend on

A

amount of ions going into cell during action potential and interconnectedness of myocardial conduction cells (more gap junctions →less resistance to ion flow)

63
Q

Absolute refractory period

A

No stimulus can generate an action potential

64
Q

Effective refractory period

A

Large stimulus can generate an action potential but it is too weak to conduct

65
Q

Relative refractory period

A

Large stimulus can generate an action potential and it can be conducted

66
Q

Refractory period

A

Heart muscle-
• Refractory to further stimulation during the action potential
• Fast Na+ +/- slow Ca2+ channels closed (inactivating gates)
Normal refractory period of ventricle approx 0.25s
• Less for atria than for ventricles
Prevents excessively frequent contraction
Allows adequate time for heart to fill
After absolute refractory period- no stimulus can depolarise cell
• Some Na+ channels still inactivated
• K+ channels still open
Relative refractory period- Only strong stimuli can cause action potentials
Affected by heart rate

67
Q

Normal refractory period of ventricle

A

0.25 s

68
Q

Resting membrane potential

A

membrane of heart muscle cell normally only permeable to K+
• Potential determined only by ions that can cross membrane
Negative membrane potential:
• K+ ions diffuse outwards (high →low)
• Anions cannot follow
• Excess of anions inside the cell
• Generates negative potential inside the cell
Myocyte membrane pumps:
• 2 K+ pumped in to cells
• 3 Na+ and Ca2+ pumped out of cells
• Against their electrical and concentration gradients
• Requires active transport (Na+/K+ pump)

69
Q

Tachycardia

A

Fast heart rate
>100bpm

70
Q

Bradycardia

A

Slow heart rate
<50bpm

71
Q

Reasons for changes to cardiac axis

A

• Conduction diseases
• strain/ physical manipulation of the heart

72
Q

Main differences between SAN and cardiomyocytes

A

SAN: gradual depolarisation and no platea
Cardiomyocytes: flat membrane potential and plateau phase

73
Q

Pacemaker potential

A

SAN HCN Na+ channels always open
Spontaneous diastolic depolarisation
Automaticity of heart

74
Q

Sensory nervous system depolarisation of SAN

A

Noradrenaline binds to beta1 receptors
Increase Ca2+ channel opening
Faster depolarisation- steeper phase 4 slope
Reaches threshold earlier
Increases heart rate and stroke volume
Cardiac output increased by 200%

75
Q

Parasympathetic nervous system depolarisation of SAN

A

ACh binds to M2 receptors
Activates K+ channels
Hyperpolarisation- shallower phase 4 slope
Reaches threshold later
Decreased heart rate and stroke volume
Cardiac output decreases by 50%

76
Q

Cardiac AP vs skeletal muscle AP

A

Cardiac AP = 15 x skeletal muscle AP
Due to slow Ca2+ channels

77
Q

LV dilation/ fibrosis in RV

A

Delay in electrical activity going left

78
Q

Right axis deviation

A

Delay in depolarisation in right side

79
Q

Right bundle branch block

A

Conduction travels from AVN then to His- Purkinje system
Lose specialised tissue (due to heart attack or fibrosis)
Leads to delay in depolarisation of ventricles
QRS complex becomes wider
Posterior aspect of septum depolarised but delayed in anterior aspect

80
Q

Left bundle branch block

A

Left bundle damaged/lost
Depolarisation of septum from anterior to posterior aspect
Positive R in V6 and Q in VRV depolarised before left ventricle
Big R wave usually because of LV

81
Q

ST segment elevation

A

Acute heart attack/myocardial infarction
P wave positive in all (normal)
Negative in aVR so has sinus rhythm
QRS complex narrow and overall negative in V1/V2 and positive in V3-V6
ST segment elevation seen in aVR, aVF and V2
Give aspirin

82
Q

AV node block

A

Fibrosis in AV node can slow it down more than needed
1st degree- PR interval is prolonged
2nd degree- some P waves and sometimes no QRS- AVN complete electrical activity block
3rd degree- complete dissociation between activity in atria and ventricle- requires pacemaker

83
Q

At which stage in ventricular myocyte action potentials is there simultaneous outflow of potassium ions and inflow of calcium ions

A

Stage 2

CVR (22 decks)

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