Unit III (9-13)- The Heart Flashcards

1
Q

Parasympathetic innervation of the heart is provided by what nerves

A

Vagus nerve

Pre-ganglionic fibers of of the recurrent laryngeal n.

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2
Q

Sympathetic innervation of the heart is provided by what nerves

A

Cardiac nerves that originate from the cervicothoracic/middle and 1st few thoracic ganglion

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3
Q

What mechanical event is represented by a P-wave?

A

Atrial depolarization

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4
Q

What mechanical event is represented by a QRS complex?

A

Ventricular depolarization

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5
Q

What mechanical event is represented by a T wave?

A

Ventricular repolarization

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6
Q

What mechanical event is represented by a QT interval?

A

Ventricular contraction and relaxation

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7
Q

What mechanical event is represented by a PR interval?

A

Atrial contraction and relaxation

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8
Q

What does S1 sound represent?

A

Lub - Closure of mitral and tricuspid valves

Usually occurs at the end of QRS complex

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9
Q

What does S2 sound represent?

A

Dub - Closure of semilunar valves

Usually occurs at the end of T wave

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10
Q

What does S3 sound represent?

A

Early ventricular filling

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11
Q

What does S4 sound represent?

A

Atrial contraction

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12
Q

At what stage of the cardiac cycle do gallop sounds occur?

A

Diastole

low frequency in dogs; higher frequency in cats

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13
Q

What pathology is usually associated with S3 sounds?

A

DCM

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14
Q

What pathology is usually associated with S4 sounds?

A

HCM

pushing blood into a stiff non compliant ventricle

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15
Q

What do systolic clicks represent?

A

Primary AV valve prolapse

(usually higher amplitude, just as loud or louder than S1 and S2) would occur between S1 and S2

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16
Q

What do split sounds represent?

A

Delay between closure and opening of valves
S1 - Mitral and tricuspid valves
S2 - semilunar valves

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17
Q

ECG paper speed of 25mm/sec

1 small box = ___

A

0.04 seconds

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18
Q

ECG paper speed of 50mm/sec

1 small box = ___

A

0.02 seconds

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19
Q

ECG paper speed of 25mm/sec

30 big boxes x ____ = beats per pen

A

10

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20
Q

ECG paper speed of 50mm/sec

30 big boxes x ____ = beats per pen

A

20

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21
Q

What are the ECG characteristics of sinus block? sinus arrest?

A

Abrupt pause in rhythm
Block - 2x longer than the previous R-R interval
Arrest - more than 2x longer than previous R-R interval

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22
Q

What are the ECG characteristics of atrial standstill?

A

No P waves

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23
Q

What diseases are associated with atrial standstill?

A

Hyperkalemia

Atrial fibrosis - english springer spaniels, old english sheepdogs

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24
Q

What are the ECG characteristics of 1st degree AV block?

A

Prolonged P-R interval

There is a P for every QRS

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25
Q

What are the causes of 1st degree AV block?

A

increased vagal tone - resting and digestion

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26
Q

What are the ECG characteristics of 2nd degree AV block Type 1?

A

Gradually prolonged PR interval

P without QRS complex

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27
Q

What is the cause of 2nd degree AV block Type I?

A

High vagal tone

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28
Q

What are the ECG characteristics of 2nd degree AV block Type 2?

A

Fixed P-R interval

P without a QRS

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29
Q

What are the causes of 2nd degree AV block Type 2?

A

AV nodal disease (myocarditis, tumors, age related fibrosis)

more likely to go into 3rd degree AV block

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30
Q

What are the ECG characteristics of 3rd degree AV block?

A

Complete dissociation between P and QRS complex

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31
Q

What is the mechanism behind atrial tachycardia?

A

increased automaticity of ectopic foci with re-entry

32
Q

What are the ECG characteristics of atrial tachycardia?

A

Abnormal P wave morphology

Normal QRS complex with regular R-R interval

33
Q

What is the mechanism behind atrial fibrillation?

A

Micro-reentry

34
Q

What are the ECG characteristics of atrial fibrillation?

A

No P waves
Irregularly irregular of R-R interval
Normal QRS complex

35
Q

What is the mechanism behind atrial flutter?

A

Macro-reentry

36
Q

What are the ECG characteristics of atrial flutter?

A

Flutter waves - saw tooth appearance to the baseline
Regular R-R interval
Normal QRS complex

37
Q

A VPC with positive deflection originates from what side?

A

Right

38
Q

A VPC with negative deflection originates from what side?

A

Left

39
Q

How does cardiac muscle differ from skeletal?

A

Cardiac muscle is a syncytium - muscle fibres separated by intercalated discs

40
Q

What are 2 differences in action potentials in cardiac/skeletal muscle?

A

1 - cardiac muscle action potential caused by opening of fast sodium and slow calcium channels (vs fast sodium only)
2 - in cardiac muscle, after onset of action potential membrane potassium permeability decreases until calcium channels close
Both cause plateau in action potential

41
Q

Describe the stages of cardiac muscle action potential

A

0 - fast sodium channels open
1 - fast sodium channels close
2 - slow calcium channels open. K+ channels close
3 - calcium channels close, k+ channels open

42
Q

What is a difference in excitation-contraction coupling between cardiac and skeletal muscle?

A

In cardiac muscle calcium diffuse into the sarcoplasm from the T tubules, as well as the sarcoplasmic reticulum

43
Q

Where is the sinus node located?

A

In the right atrium

44
Q

How much of ventricular filling is active/passive?

A

80% passive
20% active

45
Q

What are the pressure changes in the atria known as?

A

a wave - atrial contraction
c wave - ventricular contraction
w wave - flow of blood from veins

46
Q

What is preload?

A

End diastolic pressure

47
Q

What is afterload?

A

Pressure in aorta

48
Q

Where does the energy for cardiac contraction come from?

A

70-90% fat metabolism
10-30% glucose/lactate

49
Q

What is the Bainbridge reflex?

A

Stretch of the right atrial wall increases HR by 40-60%

50
Q

What are the effects of vagal stimulation on the heart?

A

Mostly decrease in HR, slight reduction in contractility (vagus innervates atria not ventricles)

51
Q

What are the effects of sympathetic stimulation on the heart?

A

Increase in HR and contractility

52
Q

What are the effects of excess potassium ions on the heart?

A

Dilated, flaccid, reduced HR
High extracellular potassium decreases membrane potential - less negative, reduced intensity of action potential

53
Q

What are the effects of excess calcium ions on the heart?

A

Spastic contraction - direct effect of ions to initiate contraction

54
Q

What are the effects of deficiency of calcium ions on the heart?

A

Cardiac weakness

55
Q

What is the effect of increased body temperature on the heart?

A

Increased HR - increased permeability of cardiac membrane

56
Q

What are the effects of increased arterial blood pressure on cardiac output?

A

Minimal up to 160mmHg - cardiac output determined by venous return

57
Q

How is the tissue of the sinus node different to other heart muscle fibre?

A

Resting potential -55-60mV (vs -85-90mV)
Due to cell membrane being leaky to sodium and calcium
At less negative resting potential fast sodium channels blocked - only slow sodium channels open

58
Q

How does the sinus node self excite?

A

Sodium ions leak through membrane - funny currents
Resting potential slowly rises until L-type calcium channels activate
L-type channels inactivate and potassium channels open - repolarisation

59
Q

Which parts of the heart can exhibit intrinsic rhythmical activity?

A

Sinus node, AV node, Purkinje fibres

60
Q

What is the mechanism of vagal effects on the heart?

A

ACh increases permeability to potassium => hyperpolarisation

61
Q

Where is the majority of energy needed for heart contraction derived from?

A

Oxidative metabolism of fatty acids

62
Q

How does high atrial stretch increase heart rate?

A

Directly increased by 10-20%
Bainbridge reflex (vagus) - increases an additional 40-60%

63
Q

What causes respiratory sinus arrhythmia?

A

Spillover of signals from the medullary respiratory centre into the adjacent vasomotor centre

64
Q

What are the possible causes of a SA block?

A

Myocardial ischaemia, myocarditis, medication, fitness

65
Q

What are the possible causes of a SA block?

A

Ischaemia of the AV node/bundle
Compression of the AV bundle with scar tissue
Inflammation of the AV node/bundle
Extreme vagus stimulation
Degeneration of the AV conduction system
Medication (digitalis, beta blockers)

66
Q

What are the types of second degree AV block?
What causes them

A

Mobitz type I (Wenckeback periodicity) - progressive prolongation of PR until ventricular beat dropped. Usually abnormal AV node, normally benign
Mobitz type II - fixed number of non-conducted P-waves. Usually associated with issue with His-Purkinje system, may require pacing

67
Q

What is electrical alternans and what causes it?

A

Partial intraventricular block every other heartbeat
Tachycardia, ischaemia, myocarditis, digitalis toxicity

68
Q

What are the causes of premature contractions?

A

Ischaemia
Calcified plaques
Toxic irritation of AV node, purkinje system or myocardium

69
Q

What are the classical features of VPCs?

A

Prolonged QRS
High voltage QRS
T wave has opposite electrical potential polarity opposite to QRS

70
Q

What is long QT syndrome and why are they of potential concern?

A

Delayed depolarisation of ventricles
Increased susceptibility to torsades de pointes

71
Q

What are the possible causes of long QT?

A

Congenital - mutations of Na or K channels
Acquired - hypomagnesaemia, hypokalaemia, hypocalcaemia, drugs (quinidine, fluoroquinolone, erythromycin)

72
Q

What causes ventricular tachycardia?

A

Usually considerable damage to ventricles
Digitalis

73
Q

How can ventricular tachycardia be treated?

A

Lidocaine
Amiodarone

74
Q

What is the MOA of lidocaine?

A

Reduced sodium permeability of cardiac muscle membrane

75
Q

What is the MOA of amiodarone?

A

Prolongs action potential and refractory period in cardiac muscle
Slows AV conduction

76
Q

What factors can predispose to circus movements?

A

Cardiac dilation
Delayed velocity of contraction - blockage of Purkinje, ischaemia, hyperkalaemia
Short refractory period - epinephrine, repeated stimulation