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BRS (RF) > Coronary disorders > Flashcards

Coronary disorders Flashcards

1
Q

What is the definition of heart failure?

A

Heart failure is defined as the inability of the heart to accommodate adequate systemic circulation to maintain the metabolic requirements to supply the organs of the body

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2
Q

What ejection fraction parameter defines preserved ejection fraction (HFpEF)?

A

Less than 50%

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3
Q

What is HFpEF affiliated with?

A

Reduction in diastolic function

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4
Q

What arrangement of muscle is configured by cardiomyocytes in HFpEF?

A

Concentric development

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5
Q

What state is ventricular muscle in during HfPEF?

A

Contractile state (Inability to relax

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6
Q

Why is there a reduction in cardiac output for preserved EFHf?

A

Ventricular diastole cannot proceed effectively, pressure gradient unable o be established (AV valves opening time has decreased)
Reduced EDV & preload

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7
Q

What are the causes of preserved EFHf?

A

Hypertension, increases afterload and thus the development cardiac muscle through hypertrophy

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8
Q

What ejection fraction parameter defines reduced EFHf?

A

Less than 40%

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9
Q

What is reduce EFHf associated with?

A

Reduction in systolic function

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10
Q

Why is there a reduction in cardiac output associated with reduced EFHf?

A

Left ventricle is more dilated, reduced contractility, and decreases ejection of blood (Laplaces law, high radius = greater wall stress, therefore lower pressures can be sustained = less contractility)

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11
Q

What are the underlying causes of Reduced EFHf?

A

Cardiac damage, ischaemia, myopathy, hypertension, valve disease

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12
Q

What are the ECG findings for heart failure?

A

Enlarged QRS complex

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13
Q

Why is there an enlarged QRS complex associated with heart failure?

A

Hypertrophy –> greater depolarisation of the muscle, (amplitude and width increases)
Time taken to depolarise all ventricular cells increases

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14
Q

What other diagnostic measures are used for Heart failure?

A

Echocardiography

Elevated ANP levels (Atrial-natriuereitc peptide)

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15
Q

What are the symptoms associated with heart failure?

A

Breathlessness, fatigue, fluid retention

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16
Q

What other non-specific findings coincide with heart failure ECGs?

A

Hypertrophy

Atrial fibrillation

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17
Q

What is dilated cardiomyopathy?

A

Cardiomegaly. and dilation of ventricular myocardiocytes

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18
Q

What is associated with dilated cardiomyopathy?

A

Hypo-contraction and systolic dysfunction, reducing stroke volume

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19
Q

What ECG findings reflect dilated cardiomyopathy?

A

Enlarged QRS complex

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20
Q

What is Tako-Tsubo Syndrome?

A

Left ventricular enlargement in a specific arrangement (Architecture expresses resemblance to pot), apical ballooning of the ventricles

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21
Q

Why does ventricular enlargement cause reduced cardiac output?

A

Reduced diastolic filling, and preload, this decreases the stroke volume.
Apical ballooning reduces contractility

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22
Q

Why does Tako-Tsubo syndrome cause myocardial infarction?

A

Coronary vessels arise from aortic sinuses, therefore reduction in coronary arteriole flow causes cardiac necrosis via ischaemic mechanism

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23
Q

What is the pathophysiology associated with Tako-Tsubo syndrome?

A

Stress induced event

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24
Q

Which demographic is more at risk of Tako-Tsubo Syndrome?

A

Widowed females

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25
Q

What ECG findings are associated with Tako-TS Syndrome?

A

ST-Segment Elevation (STEMI)

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26
Q

What is STEMI?

A

Early onset of depolarisation of ventricular cardiomyocytes in response to hypertrophy

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27
Q

What is the ST-segment?

A

The isoelectric line, the interval between depolarisation and depolarisation of ventricles

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28
Q

What can be associated with Tako-tsubo syndrome?

A

Chest pain

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29
Q

What is hypertrophic cardiomyopathy?

A

Unexplained left ventricular hypertrophy

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30
Q

Which ventricular feature does hypertrophic cardiomyopathy affect?

A

Interventricular septum

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31
Q

What type of inheritance pattern is demonstrated by hypertrophic cardiomyopathy?

A

Autosomal dominant

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32
Q

What can occur during exercise with patients suffering from hypertrophic cardiomyopathy?

A

Sudden death

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33
Q

What are the symptoms associated with hypertrophic cardiomyopathy?

A

Dyspnoea, fatigue

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34
Q

What are the ECG findings with Hypertrophic cardiomyopathy?

A

Enlarged QRS complex

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35
Q

What is a P wave?

A

Represents atrial depolarisation

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36
Q

What is the QRS complex?

A

Represents ventricular depolarisation, requires greater electrical amplitude (larger ventricular cardiac muscle)

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37
Q

When does ventricular contraction occur?

A

R wave

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38
Q

What is the ST segment?

A

Baseline, interval between ventricular depolarisation and repolarisation, it is isoelectric

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39
Q

What is the QT interval?

A

The total duration of ventricular depolarisation and repolarisation

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40
Q

What is the RR interval?

A

Duration between ventricular depolarisations (heart rate)

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41
Q

What is the T wave?

A

Represents the depolarisation of the ventricles

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42
Q

How is atrial Repolarisation shown on an ECG?

A

None, the QRS complex masks the atrial repolarisation

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43
Q

What is a segment on an ECG?

A

Defined as the regions between two waves

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44
Q

What is more clinically relevant the PR segment or PR interval?

A

PR interval

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45
Q

What is the PR interval?

A

Starts at the P wave, ends at the beginning of the QRS complex

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46
Q

What is the typical time for the PR interval?

A

120-200ms

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47
Q

What factors influence the PR segment?

A

Electrical conductance through the atrioventricular node

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48
Q

How would delayed impulse passage from SAN to AVN influence the ECG PR interval?

A

Longer PR interval

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49
Q

Which ECG lead results in the greatest QRS complex?

A

V5 (lateral view)

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50
Q

Which ECG leads provide a septal view?

A

V1 and V2

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51
Q

Which region of the heart generates electrical activity the fastest?

A

The sinoatrial node (SAN)

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52
Q

Why is it important that there is slower conduction of the electrical signal through the AV node (and its extension, the Bundle of His)?

A

The delay allows the atria to contract completely before a ventricular contraction begins.

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53
Q

Movement of depolarisation towards the lead will produce which type of deflection?

A

A wave of depolarization moving towards a lead produces a positive deflection (i.e., movement above isoelectric line). The magnitude of this deflection is greatest when the wave is moving directly towards the lead.

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54
Q

Movement of depolarisation away from the lead produced what type of deflection?

A

Depolarization away from the lead produces a negative deflection.

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55
Q

Which type of movement in comparison to the leads will lead to no deflection?

A

Perpendicular movements

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56
Q

Waves of repolarisation moving away from the lead will produce which type of deflection?

A

Positive deflection
Waves of repolarization produce a signal opposite to that seen with a depolarizing wave (e.g., a repolarizing wave moving away from the positive lead causes a positive deflection on the ECG trace

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57
Q

What is Einthoven’s Triangle?

A

Einthoven’s Triangle is a useful imaginary triangle spanning the trunk which can quickly give an idea about which lead will best show certain electrical activity.

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58
Q

What is the direction of lead one?

A

Left-arm –> Right arm

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59
Q

What is the direction of lead three?

A

Left arm –> Left foot

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60
Q

What is the direction of lead 2?

A

Left foot –> Right arm

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61
Q

Which wave has the largest R wave?

A

Lead II

62
Q

Which lead is unipolar?

A

AvR (Negative)

63
Q

Where do V3 and V4 lie?

A

Near the interventricular septum

64
Q

Where do V1 and v2 reside?

A

Near the right ventricle

65
Q

Which electrodes have prominent R & S waves?

A

V3 and v4

66
Q

Which electrodes always depict positive T waves?

A

V3-6

67
Q

What is right axial deviation?

A

QRS complex is predominantly negative in lead 1 and positive in lead aVF , axis is rightward. The direction of depolarisation is distorted to the right (1 to 7 o clock)

68
Q

Which lead has a negative deflection in right axial deviation?

A

Lead 1

69
Q

Which lead has positive deflection in right axial deviation?

A

AvF

70
Q

What are the main causes for right axial deviation?

A 
Right bundle branch block (RBBB)
Right ventricular hypertrophy 
Left posterior fasciuolar block
Dextrocardia
Wolff-Parkinson-white syndrome
71
Q

Which lead becomes deflected in left axis deviation?

A

Lead III

72
Q

Which axis angles are defined for left axis deviation?

A

-30 to -90

73
Q

What are the main causes for left axial deviation?

A

Left anterior fascicular block, left bundle branch block (LBBB),mechanical shift, inferior myocardial infarction, Wolf-Parkinson-White syndrome.

74
Q

What is arrhythmia?

A

Describes abnormal heartbeat (Too slow, too rapid, irregular too early)
Sinoatrial node spontaneously generates action potentials resulting in coordinated rhythmic electrical activity . Impulse generation or conduction is disrupted - detectable on ECG

75
Q

What is tachycardia?

A

Resting heart rate greater than 100bpm

76
Q

What is bradycardia?

A

Heart rate slower than 50bpm

77
Q

Which node initiates the spread of electrical activity to begin atrial systole?

A

Sinoatrial node

78
Q

What is the role perfumed by the SAN?

A

Results in coordinated and rhythmic contractionn

79
Q

What is an ectopic foci?

A

Cardiac muscle fibres initiate waves of exception to stimulate cardiac contraction
Appear when own rate of action potential generations become enhanced when the rhythmicity of SAN is reduced, conduction pathways from the SAN are blocked

80
Q

What is supraventricular arrhythmia:

A

Tachycardias/premature contractions occurring rapidly as a result of abnormal electrical activity of the atria. Atrial tachycardias and premature atrial contractions.

81
Q

What is the ECG finding for a supra ventricular arrhythmia?

A

Absence of p waves in the aberrant ECG

82
Q

What is respiratory sinus arrhythmia?

A

Cyclic change in the heart rate during breathing

83
Q

What is sinus tachycardia?

A

SAN is firing at a faster rate than compared to normal

84
Q

What is sinus Bradycardia?

A

The sinoatrial node is firing at a reduced rate.

85
Q

What is atrial flutter?

A

Rapidly repetitive atrial depolarisations causing the atrial muscles to contract rapidly.

86
Q

What is atrial fibrillation?

A

Atrial cells depolarise in an uncoordinated manner. Atria no longer contract. Electrical activity is conducted to the ventricles in a random fashion determined by the excitatory state of AVN.

87
Q

What is known as disorganised electrical activity and contraction?

A

Atrial fibrillation

88
Q

What is the pathophysiology of atrial fibrillation?

A

Spontaneously active cells throughout the atria (ectopic) can be associated with pulmonary veins. In AF the electrical waves of excitation is uncoordinated and generated from multiple regions

89
Q

What are the effects on cardiac output due to atrial fibrillation?

A

Decline cardiac output attributed to reduced diastolic filling
Insufficient cardiac output and flow through the atrioventricular orifice into the ventricles result in atrial blood accumulation - causes blood clotting

90
Q

Why do blood clots form in atrial fibrillation?

A

Insufficient cardiac put and flow through the atrioventricular orifice into the ventricles results in blood accumulation

91
Q

What are the associated risks with blood clots due to atrial fibrillation?

A

Can embolism as a pulmonary embolism

92
Q

What are the clinical investigations of atrial fibrillation?

A

Palpitations
Chest pain
ECG findings: Absent P waves

93
Q

What are the main ECG findings for atrial fibrillation?

A

Absent p waves

94
Q

Why are there absent p waves in atrial fibrillation?

A

Due to AVN nodal stimulation

95
Q

What is Wolff-Parkinson white?

A

Syndrome causing tachycardia and abnormal cardiac electrical conductance

96
Q

What is the pathophysiology of Wolff-Parkinson white?

A

Accessory conduction pathway through the Bundle of Kent, between the atria and ventricles.
Accessory pathway is in addition to the intraventircular pathway. The accessory pathway communicates between the atria & the ventricles, in addition to the AVN

97
Q

Which Bundle forms the accessory pathway in Wolff-Parkinson white?

A

Bundle of Kent

98
Q

Where does the Bundle of Kent reside?

A

Resides within the ventricular wall

99
Q

What is the difference between the Bundle of Kent and AVN in terms of electrical activity?

A

Does not express rate slowing properties of the AVN, therefore conducting electrical activity at a higher rate significantly

100
Q

Why is there pre-excitation in Wolff-Parkinson white?

A

no AV block, the depolarisation of ventricles occurs earlier

101
Q

What is the effect on cardiac output for Wolff-parkinson white?

A

Cardiac output is unchanged.

102
Q

What are the main ECG findings for patients with Wolff-Parkinson White?

A

Pre-Excitation of QRS complex

Biphasic/inverted T wave

103
Q

Where does ventricular fibrillation originate?

A

From the His-Purkinje system or ventricular myocytes due to disorganised ventricular activity

104
Q

What is the average ventricular contraction rate during ventricular fibrillation?

A

150-400bpm

105
Q

What is the pathophysiology of ventricular fibrillation in terms of an acute myocardial infarction?

A

Ectopic beat or ishcaemia occurs due to scar tissue
Re-entry: Waves of excitation returning to original ventricular cardiomyocytes  Occurs due to non-conductive scar tissue (anatomical re-entry) formed from MI directing waves back to cause further depolarisation.

106
Q

What is tissue heterogeneity?

A

Tissue is electrically changed. Intracellular calcium accumulation and ionic balance. Elevated external potassium ion concentration or decreased sodium ion reduced negativity of th e maximum diastolic potential (closer to threshold potential) _ cellular depolarisation is more susceptible

107
Q

What is the effect on cardiac output by ventricular fibrillation?

A

Decreased ventricular contraction results in insufficient contractility due to dysfunction non-uniformed isotonic contraction reduces stroke volume = complete loss of cardiac output

108
Q

What is the main risk of ventricular fibrillation that leads to death?

A

Ventricular fibrillation results in hypoxia, reduction in oxygenated blood towards brain, death within seconds-minutes

109
Q

Why does syncope occur during ventricular fibrillation?

A

Due to reduced oxygenation to brain

110
Q

What are the ECG findings for ventricular fibrillation?

A

Irregular deflections, difficult to identify PQRST waves. During the refractory period, ventricular repolarisation occurs, there is a distribution in the available ventricular myocytes to depolarise, thus a proportion do (uncoordinated).

111
Q

What is Torsade Des Pointes?

A

Long Q-T syndrome, ventricular repolarisation is pronged within ventricular myocytes due to disturbed ion channel movements –> Cardiac action potential within ventricular myocytes triggered non-uniformly

112
Q

What happens during the plateau phase in terms of ion movements?

A

Potassium ion channels are open, causing potassium efflux, L-type calcium channels open equalises membrane potential as the isoelectric line.

113
Q

What happens during phase 3 in terms of cardiac action potential?

A

The L-type calcium channels close, enabling repolarisation of ventricular myocytes

114
Q

Why is there a long-QT in Torsade des pointes?

A

L-type calcium channels open for longer, therefore longer plateau phase.
result gin in-early afterdepolarsaition (membrane more positive) . It takes longer for the ventricles to depolarise

115
Q

What is the consequence of reduced depolarisation in Torsade Des Pointes?

A

Premature ventricular contraction arises, waves of depolarisation propagated by depolarised myocytes - - re-entrance circuit stimulated by prolonged depolarised cells

116
Q

What are the effects on Cardiac output with Tornado des pointes?

A

Reduced cardiac output

117
Q

Can Torsade Des pointes resolve?

A

Resolves automatically

118
Q

What are the general symptoms of Torsade Des Pointes?

A

Chest pain

Syncope

119
Q

What are the ECG findings for Torsade Des Pointes?

A

Long Q-T

Characteristic twisting around the point

120
Q

What is the average atrial tachycardia rate?

A

100-250bpm

121
Q

With sinus tachycardia what is the pattern with P waves?

A

P waves followed by QRS complex. PQRST complex is standard (increased frequency

122
Q

Which type of tachycardia has p waves that are not always followed by a QRS complex?

A

Atrial tachycardia

123
Q

Why are there solitary p waves within Atach?

A

Concerned with ectopic source of atrial beat

124
Q

Which type of tachycardia is associated with ectopic source of atria beat?

A

Attach

125
Q

What is an AV block?

A

Impaired electrical conduction through the atrioventricular node. AV block occurs when the electrical transmission of waves of excitation travelling from the atria to the ventricles is impaired. SAN transmission electrical signal to control the heart rate -> AVN -> AV block signal is delayed or completely blocked

126
Q

What is produced in order to compensate from blocked electrical signal?

A

Ventricular escape beat, as the ventricles generate an independent signal

127
Q

What is a first degree AV block?

A

Occurs when there is a delay through the AV node (Minimal disruption as the signal moves from the atrium to the ventricles)
THERE ARE NO DROPPED BEATS

128
Q

Why is there a delay through the AV node in a first degree AV block?

A

Fibrosis of the AV node results in the formation of non-conductive scar tissue, this delays and interrupts electrical conduct through node

129
Q

What are the ECG findings for a first degree AV block?

A

PR interval > 200ms Prolonged

There are no dropped beats

130
Q

What is a Mobitz 1 second degree block?

A

Characterised by a progressive reversible block of the AV node. There is a progressive prolongation of the PR interval resulting in a dropped beat (PR interval longer until beat is dropped considering ventricular depolarisation is not initiated)

131
Q

In a Mobitz II block which cells are affected?

A

There is a sudden failure the His-Purkinje cells to conduct an electrical impulse

132
Q

On an ECG is the PR interval affected for a Mobitz-II block?

A

The PR interval is unchanged from the heat, however there is a sudden failure to conduct the signal to the ventricles

133
Q

Why is a mobitz-II block lethal?

A

Random skipped beat can result in a complete heart block

134
Q

What is a type III block?

A

Complete signal block between the atria and ventricles, there is no communication.
There is no relationship between P waves or QRA complex not a 1:1 ratio

135
Q

What is a bundle branch block?

A

A bundle branch block is a defect of the bundle branches of fascicles in the electrical conduction system of the heart (left and right)

136
Q

What happens when bundles/fascicles are disrupted?

A

Cease to conduct electrical impulse, therefore resulting in altered pathways for ventricular depolarisation considering the electrical impulses cannot be transmitted through the interventricular septum to the ventricles across the bundle branch.
Traverses through cardiac muscle fibres, educes transmission speed and direction propagation of the impulses

137
Q

How is the cardiac output affected in a bundle branch block?

A

There is a loss of ventricular synchrony, ventricular depolarisation is prolonged

138
Q

What is a right bundle branch block?

A

The right ventricle is not directly activated by impulses travelling through the right bundle branch,
the left ventricle is activated by the left bundle normally

139
Q

During a right bundle branch block how is the right ventricle activated?

A

Impulses move through the myocardium of the left ventricle tot he right ventricle –> Method of depolarisation. Conduction through th myocardium is slow than conduction through the bundle of His, therefore there is a widened QRS complex

140
Q

Why is the QRS complex widened in a right bundle branch block?

A

Conduction through the myocardium is slow than conduction through the bundle of His

141
Q

What are the ECG findings for a right bundle branch block?

A

QRS complex is widened
Extra deflection that reflex rapid depolarisation of left ventricle followed by slower depolarisation of the right ventricle
Right axial deviation

142
Q

What are the main causes for a right bundle branch block?

A

Right ventricular hypertrophy
Pulmonary embolism
Cardiomyopathy
Hypertension

143
Q

What are the symptoms of a right bundle branch block?

A

Asymptomatic & benign

144
Q

What is a left bundle branch block?

A

Activation of the left ventricle is delayed, causes left ventricle to contact later than the right ventricle -> reduces cardiac output (consequence of ischaemia or heart disease)

145
Q

What are the ECG findings for a left bundle branch block?

A

Widened QRS complex > 120msec.

Hemiblock of fascicle blockage, alteration in a cardiac axis -> left axis deviation

146
Q

What is the clinical diagnostic blood pressure reading for hypertension?

A

140/90mmHg

135/85mmHg (Ambulatory)

147
Q

What is the effect of hypertension on cardiac output?

A

Decreases cardiac output and increases the likelihood of heart disease, in addition to end-organ damage.
Hypertension in creases after load onto the left ventricle, thus requiring greater contractility to overcome

148
Q

What the ECG findings for patients with hypertension?

A

No specific ECG features

149
Q

What is a myocardial infarction?

A

Acute coronary syndrome results in cardiac tissue damage to coronary artery blockage

150
Q

What is angina?

A

Pain or discomfort that typically radiates from the chest at rest (unstable), or brought on by physical exertion or emotional stress (stress)

151
Q

What is the pathophysiology of a myocardial infarction?

A

Myocardial ischaemia/cell necrosis due to vascular occlusion of coronary arteries

152
Q

What are the ECG findings for a myocardial infarction?

A

ST-segment elevation (STEMI) - unstable

Normal ST-segment elevation (NSTEMI)

BRS (RF) (38 decks)

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