The cardiac cycle Flashcards

1
Q

What is the pacemaker impulse in the lobster heart?

A

The pacemaker impulse in the lobster heart comes from the cardiac ganglion (neurogenic).

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2
Q

What is the pacemaker impulse in the human heart?

A

The pacemaker impulse in the human heart is built in (myogenic).

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3
Q

What did Stannius discover about pacemakers in the frog heart?

A

Stannius demonstrated that there is a hierarchy of pacemakers in the frog heart. The primary pacemaker is located in the sinus venosus, and there are secondary pacemakers in the atria and ventricles, which are slower.

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4
Q

What happened when Stannius tied a ligature between the sinus venosus and atria in the frog heart?

A

Tying a ligature between the sinus venosus and atria slowed the heart rate, showing that the sinus venosus is the primary pacemaker.

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5
Q

What was the result of Stannius tying a second ligature between the atria and ventricle in the frog heart?

A

The heart rate slowed further, indicating that the atria contain a secondary, slower pacemaker.

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6
Q

What is the hierarchy of pacemakers in the frog heart as demonstrated by Stannius’s experiment?

A

The hierarchy is:
Primary pacemaker: Sinus venosus

Secondary pacemaker: Atria

Tertiary pacemaker: Ventricles (driven by Purkinje fibers)

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7
Q

What is the primary pacemaker of the mammalian heart?

A

The primary pacemaker is the sinoatrial (SA) node, located at the top corner of the right atrium just below the superior vena cava.

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8
Q

What characteristic do the muscle cells in the sinoatrial (SA) node have?

A

The muscle cells in the SA node have an action potential with a sloping diastolic potential. This means the membrane potential is unstable and depolarizes up to a threshold before firing the next action potential.

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9
Q

How does the wave of excitation spread in the heart after the sinoatrial node?

A

The wave of excitation spreads from the SA node through the right atrium to the atrioventricular (AV) node, and then through the Bundle of His, the right and left bundle branches, and the Purkinje fibers in the ventricles.

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10
Q

Which structures in the mammalian heart have intrinsic pacemaker activity?

A

The sinoatrial node, atrioventricular node, Bundle of His, right and left bundle branches, and Purkinje fibers all have intrinsic pacemaker activity, meaning they beat regularly without external stimulus

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11
Q

How do the action potentials in the atrium and ventricles differ from the pacemaker structures?

A

The action potentials in the atrium and ventricles have a flat, stable resting membrane potential between beats, unlike the pacemaker structures that have a sloping resting membrane potential and can generate action potentials without external stimuli.

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12
Q

Which pacemaker structure in the mammalian heart has the fastest intrinsic rate?

A

The sinoatrial (SA) node has the fastest intrinsic rate and determines the rate of all the other structures in the heart.

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13
Q

How does the SA node control the heart rate in relation to other pacemaker structures?

A

The SA node sets the tempo, and the other pacemaker structures (AV node, Bundle of His, Purkinje fibers) follow the rhythm it generates, even though they each have their own intrinsic rates.

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14
Q

What is the hierarchy of pacemaker structures in terms of their intrinsic rate?

A
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15
Q

What happens if pacemaker structures in the heart start firing off at faster rates or abnormal intervals?

A

If pacemaker structures fire at abnormal rates or intervals, it can lead to cardiac arrhythmias.

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16
Q

Where is the sinoatrial (SA) node located in the heart?

A

The SA node is located at the top of the right atrium, at the junction of the superior and inferior vena cavae

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17
Q

what is the sinoatrial node bounded by

A

thick ridge of atrial muscle called the crista terminalis

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18
Q

What 3 types of cells are found in the SA node?

A

The SA node contains a mixture of specialized nodal cells, atrial cells, and connective tissue.

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19
Q

How much connective tissue is present in the SA node?

A

The SA node contains up to 50-90% connective tissue, depending on the species and age.

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20
Q

Why is the mixture of cell types in the SA node important?

A

The heterogeneous mixture of cell types in the SA node is essential for the normal functioning of the pacemaker.

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21
Q

What are the three types of cells found in the sinoatrial (SA) node?

A

The three types of cells in the SA node are:
- Spindle cells (from the center of the node)
- Elongated spindle cells (probably from the periphery)
- Spider cells

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22
Q

where are spindle cells located

A

Spindle cells – located in the center of the node.

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23
Q

where is an elongated spindle cell located

A

likely from the periphery.

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24
Q

what is the location of spider cells

A

location unclear.

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25
Q

What is a characteristic of SA node cells?

A

SA node cells have a nucleus surrounded by membrane with very little cytoplasm, specialized to generate action potentials but not to function as muscle cells.

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26
Q

How do the cells in the periphery of the SA node differ from those in the center?

A

Peripherally, SA node cells resemble typical atrial muscle cells, with clear intracellular contents and well-defined muscle fibers. Cells in the center (spindle cells) are more specialized for pacemaking.

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27
Q

What is a key feature of the SA node action potential?

A

The key feature is the region of diastolic depolarisation (also called pacemaker depolarisation or phase 4), which is the sloping baseline between action potentials.

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28
Q

What generates the pacemaker potential in SA node cells?

A

The pacemaker potential is generated by a combination of increasing inward currents and decreasing outward currents.

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29
Q

What happens when the membrane potential reaches threshold in SA node cells?

A

When the membrane potential hits threshold, sodium and/or calcium channels open, generating the upstroke of the action potential.

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30
Q

What occurs after sodium and calcium channels close in SA node cells?

A

After the sodium and calcium channels shut, potassium channels open, repolarizing the membrane back to its minimum diastolic level.

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31
Q

How does the SA node action potential repeat?

A

The process of action potential generation in SA node cells repeats with a regular clock-like rhythm.

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32
Q

What is the characteristic feature of the SA node action potential?

A

The characteristic feature is slow diastolic depolarization

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33
Q

What happens during the diastolic depolarization phase of the SA node action potential?

A

During diastolic depolarization, the resting membrane potential starts at about -65 to -70 mV and slowly depolarizes until it reaches the threshold, triggering the next action potential.

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34
Q

How does the rate of diastolic depolarization affect heart rate?

A

Faster diastolic depolarization (steeper slope) results in a faster intrinsic rate and heart rate, while slower depolarization leads to a slower heart rate.

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35
Q

What is the funny current (pacemaker current) and what role does it play in diastolic depolarization?

A

The funny current (or pacemaker current) is carried by HCN channels, which open during diastolic depolarization, allowing sodium ions into the cell and contributing to the slow depolarization

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36
Q

How does the size of the funny current affect the heart rate?

A

Increasing the size of the funny current makes depolarization faster, leading to a higher heart rate, while decreasing the funny current makes depolarization slower, leading to a slower heart rate.

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37
Q

What is chronotropy and how does it affect heart rate?

A

Chronotropy refers to the influence on heart rate.

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38
Q

effect of positive and negative chronotropy on heart rate

A

Positive chronotropes increase heart rate, while negative chronotropes decrease heart rate.

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39
Q

What is inotropy

A

Inotropy refers to the strength of contraction.

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40
Q

difference between positive intropes and neagtive intropes

A

Positive inotropes increase the strength of contraction, while negative inotropes decrease it.

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41
Q

What is lusitropy

A

Lusitropy refers to the rate of relaxation of the heart muscle

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42
Q

what is the difference between positive lusitropes and negative lusitropes

A

Positive lusitropes increase the rate of relaxation, while negative lusitropes decrease it.

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43
Q

What are positive chronotropic agents?

A

Positive chronotropic agents include adrenaline and noradrenaline, which increase heart rate.

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44
Q

How do positive chronotropic agents affect the SA node action potential?

A

Positive chronotropic agents cause faster diastolic depolarization, leading to an increase in heart rate.

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45
Q

What is the effect of sympathetic stimulation on the SA node action potential?

A

Sympathetic stimulation (via adrenaline and noradrenaline) speeds up diastolic depolarization, causing the action potential to reach threshold faster.

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46
Q

What are negative chronotropic agents?

A

Negative chronotropic agents include acetylcholine and adenosine, which decrease heart rate.

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47
Q

How do negative chronotropic agents affect the SA node action potential?

A

Negative chronotropic agents cause slower diastolic depolarization, resulting in a slower heart rate.

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48
Q

What is the effect of parasympathetic stimulation on the SA node action potential?

A

Parasympathetic stimulation (via acetylcholine and adenosine) slows down diastolic depolarization, causing the action potential to reach threshold more slowly.

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49
Q

How does sympathetic stimulation affect heart rate?

A

Sympathetic stimulation, via noradrenaline, increases heart rate by raising cAMP, which enhances the funny current and activates downstream signaling pathways.

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50
Q

How does parasympathetic stimulation affect heart rate?

A

Parasympathetic stimulation, via acetylcholine, lowers heart rate by reducing cAMP and directly activating the IK(ACh) potassium channel.

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51
Q

What happens when acetylcholine binds to muscarinic receptors in the heart?

A

Acetylcholine binding to muscarinic receptors directly activates the IK(ACh) potassium channel, lowering heart rate without involving second messengers.

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52
Q

What role does cAMP play in sympathetic stimulation of the heart?

A

cAMP increases heart rate by:
1. Enhancing the funny current (If) channel.
2. Activating Protein Kinase A (PKA), which phosphorylates substrates like the L-type calcium channel, phospholamban, and ryanodine receptor in the sarcoplasmic reticulum, accelerating diastolic depolarization.

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53
Q

How does the calcium clock influence the heart rate?

A

The calcium clock influences the heart rate by regulating the membrane clock, with phosphorylation of substrates in the sarcoplasmic reticulum playing a key role in this regulation.

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54
Q

What is the role of the sympathetic nervous system?

A

The sympathetic nervous system is responsible for “fight or flight” responses, which prepare the body for action and increase heart rate.

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55
Q

What is the role of the parasympathetic nervous system?

A

The parasympathetic nervous system is responsible for “rest and digest” responses, promoting relaxation and lowering heart rate.

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56
Q

which nerve does the sympathetic nervous system use

A

sympathetic nerves

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57
Q

which nerve does the parasympathetic nervous system use

A

the vagus nerve

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58
Q

Which neurotransmitters are associated with the sympathetic and parasympathetic nervous systems?

A

The sympathetic nervous system uses noradrenaline,

while the parasympathetic nervous system uses acetylcholine.

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59
Q

How does the sympathetic nervous system affect heart rate and AV node conduction?

A

The sympathetic nervous system raises heart rate (tachycardia) and speeds conduction through the AV node via noradrenaline.

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60
Q

How does the parasympathetic nervous system affect heart rate and AV node conduction?

A

The parasympathetic nervous system, via the Vagus nerve (acetylcholine), slows heart rate (bradycardia) and slows AV conduction.

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61
Q

What are the two branches of the autonomic nervous system that innervate the heart?

A

The sympathetic nervous system and the parasympathetic nervous system innervate the SA and AV nodes.

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62
Q

Normal resting heart rate

A

72bpm

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63
Q

What happens if beta-blocking drugs are administered?

A

Beta-blocking drugs lower heart rate to about 60 bpm by reducing sympathetic stimulation (accelerator effect).

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64
Q

What is the effect of atropine or cutting the Vagus nerve?

A

Atropine or cutting the Vagus nerve increases heart rate to around 90 bpm by reducing parasympathetic stimulation (brake effect).

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65
Q

What is the relationship between heart rate and vagal tone during initial exercise?

A

During the initial phase of exercise, the increase in heart rate from rest to about 90 bpm is entirely due to the withdrawal of vagal tone (removing the “foot off the brake”).

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66
Q

What happens when heart rate increases from rest to 90 bpm during light exercise

A

The increase in heart rate from rest (around 72 bpm) to 90 bpm during light exercise is primarily due to reduced vagal tone (the brake being released).

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67
Q

What is required to raise heart rate above 90 bpm during exercise?

A

To raise heart rate above 90 bpm during more intense exercise, sympathetic activation (via adrenaline and noradrenaline release) is required.

68
Q

How does the autonomic nervous system regulate heart rate during daily activities and mild exercise?

A

During daily activities and mild exercise, changes in heart rate are mainly mediated by alterations in vagal tone, allowing the heart rate to increase or decrease slightly.

69
Q

How is the conduction from the SA node to the AV node different from other parts of the cardiac conduction system?

A

Conduction from the SA node to the AV node is slow, as it passes through the atrial muscle without specialized conducting pathways.

70
Q

What is the purpose of the AV pause?

A

The AV pause allows time for the ventricles to fill before the electrical impulse is passed to the ventricle and also prevents the transmission of high heart rates from the atria to the ventricles.

71
Q

How does the AV pause help in pathological conditions

A

The AV pause prevents very high heart rates from reaching the ventricles during conditions like atrial fibrillation, allowing the ventricles time to fill properly and avoiding ineffective pumping.

72
Q

Why is the conduction through the ventricular conduction system fast?

A

Conduction through the ventricular conduction system is fast to allow the apex of the ventricle to contract before the rest of the ventricle, efficiently pushing blood towards the outflow tracts.

73
Q
A
74
Q

How does the fast conduction through the ventricular conduction system benefit blood ejection?

A

Fast conduction allows for apex-to-base contraction, ensuring that the ventricle contracts from the apex to the base, which optimally ejects blood towards the aortic and pulmonary arteries.

75
Q

how are Cardiac myocytes arranged

A

Cardiac myocytes are arranged like bricks in a wall, and the ends of the cells interdigitate to form intercalated disks, which are tight junctions that facilitate electrical conduction along the cardiac fibres.

76
Q

What are intercalated disks in ventricular muscle?

A

Intercalated disks contain gap junctions, which are low-resistance pathways coupling adjacent cells in the heart muscle.

77
Q

What are connexons and where are they located?

A

Connexons (also known as hemi-channels) are located in the intercalated disks, one in each cell

78
Q

what are connexons made up of

A

made up of 6 proteins called connexins.

79
Q

What do connexons allow to pass between cells?

A

Connexons allow the passage of ions, electrons (electro-tonic currents), and small molecules between cells, facilitating cell-to-cell conduction.

80
Q

What happens when connexons malfunction?

A

Malfunction of connexons can occur in pathologies like heart failure, affecting cell-to-cell conduction and disrupting normal heart function.

81
Q

another word for connexons

A

hemi-channels

82
Q

What is anisotropic conduction in the heart muscle?

A

Anisotropic conduction refers to the electrical impulse traveling faster along the fibres of the cardiac muscle and slower across the fibres.

83
Q

Where are connexons located in the cardiac muscle cells ? how does it benefit the cell?

A

Connexons are located at the ends of cardiac muscle cells and facilitate fast conduction along the fibres.

84
Q

what is conduction in connexons like along the fibre, compared to across the fibre

A

along fibre = fast

across fibre = slow

85
Q

what determines conduction through cardiac muscle?

A

fibre orientation

along = fast
across = slow

86
Q

What is measured by electrodes placed on either side of the heart?

A

Electrodes measure the spread of excitation from the top (base) to the apex of the heart, recorded as a potential difference in the electrocardiogram (ECG).

87
Q

What is the electrical dipole in electrocardiography?

A

The electrical dipole consists of a wave of positiveness followed by a wave of negativeness, representing the depolarization (upstroke) and repolarization of the heart muscle.

88
Q

What does the positive wave in the ECG represent?

A

The positive wave represents the upstroke of the action potential as it spreads from the top (base) of the heart towards the apex.

89
Q

What does the negative wave in the ECG represent?

A

The negative wave represents repolarization, following the depolarization (upstroke) of the heart muscle.

90
Q

Why is measuring the ECG complex?

A

Measuring the ECG is complex because it involves not only the depolarization and repolarization of ventricular muscle cells but also the three-dimensional geometry of the heart and how excitation spreads down to the apex and around the walls of the ventricles.

91
Q

What was Augustus Waller’s contribution to ECG measurement?

A

In 1887, Augustus Waller was the first to record an ECG, using newly developed equipment. He recorded the ECG from his dog, Jimmy, and amusingly labeled the waves to spell out “BEST WISHES.” This experiment sparked controversy, with debates in Parliament about animal experimentation.

92
Q

How did Augustus Waller first measure the ECG in humans?

A

Waller used an early ECG machine with electrodes connected to a subject’s hands and foot in saline buckets. This setup allowed the recording of the ECG on a mercury electrometer.

93
Q

What is a mercury electrometer and how did it work?

A

A mercury electrometer uses a column of mercury that moves up and down in response to electrical potential changes. This movement was either visualized or recorded on a trace.

94
Q

Why was the mercury electrometer system slow in recording the ECG?

A

The mercury column was sluggish, causing the recorded ECG trace to be slow and not faithfully reproduce the rapid waves of the modern ECG.

95
Q

Who was Willem Einthoven and what was his contribution to ECG measurement?

A

Willem Einthoven, present at one of Waller’s lectures, realized that he could build a more sensitive ECG machine that would provide better resolution and accuracy in ECG measurements.

96
Q

What was Willem Einthoven’s contribution to ECG measurement?

A

Willem Einthoven improved ECG recording with a better recording device and introduced Einthoven’s Triangle to define electrode placement.

97
Q

What is Einthoven’s Triangle?

A

Einthoven’s Triangle is formed by the right shoulder, left shoulder, and groin, with the heart at the approximate center. It provides a consistent convention for electrode placement.

98
Q

What did Willem Einthoven standardize about ECG waveforms?

A

Einthoven standardized the naming of ECG waves, introducing the letters PQRST to represent the different phases of the ECG waveform.

99
Q

Why didn’t Augustus Waller share the Nobel Prize with Willem Einthoven?

A

Waller was nominated for the Nobel Prize, but he died in 1922, and Nobel Prizes are never awarded posthumously, so the prize went solely to Einthoven in 1924.

100
Q

What does the ECG measure?

A

The ECG measures the electrical activity of the heart by recording the potential difference between electrodes placed on the body.

101
Q

What is Limb Lead I in Einthoven’s Triangle?

A

Limb Lead I in Einthoven’s Triangle uses a reference electrode on the right shoulder (RA) and a recording electrode on the left leg (LF), following Einthoven’s conventions.

102
Q

What does the P wave represent on the ECG?

A

The P wave represents atrial depolarization, the wave of excitation spreading from the sinoatrial node across the atria, causing an upward deflection on the ECG.

103
Q

Why does the ECG show an upward deflection during atrial depolarization?

A

The upward deflection occurs because the wave of excitation spreads away from the reference electrode (RA) and towards the recording electrode (LF), causing a positive potential change.

104
Q

What does the Q wave on the ECG represent?

A

The Q wave represents depolarization of the septum, specifically the headward depolarization from the middle of the septum toward the atria, seen as a downward deflection on the ECG.

105
Q

Why don’t we see the excitation of the Hiss Bundle and Bundle Branches on the ECG?

A

The Hiss Bundle and Bundle Branches are small structures with minimal tissue mass, so their excitation is not detectable on the ECG

106
Q

What causes the negative deflection of the Q wave on the ECG?

A

The negative deflection of the Q wave occurs because the depolarization of the septum spreads towards the reference electrode (headward), which results in a downward deflection on the ECG.

107
Q

What does the R wave in the ECG represent?

A

The R wave represents the depolarization of the ventricles as the excitation spreads towards the apex of the heart, resulting in a large upward deflection.

108
Q

What causes the large upward deflection of the R wave in the ECG?

A

The large upward deflection of the R wave is caused by the depolarization of the ventricular muscle towards the apex, which has a large muscle mass.

109
Q

What phase of the ECG is associated with ventricular depolarization

A

The QR interval (QR phase) of the ECG is associated with ventricular depolarization towards the apex.

110
Q

What does the S wave in the ECG represent?

A

The S wave represents the depolarization of the ventricles as the wave of excitation moves away from the recording electrode and towards the isoelectric line, overshooting slightly.

111
Q

Why does the S wave appear in the ECG?

A

The S wave appears as the excitation spreads from the apex back up through the free walls of the ventricles, moving away from the recording electrode, and then overshoots toward the isoelectric line.

112
Q

What phase is represented by PQRS in the ECG?

A

PQRS represents the entire process of ventricular depolarization, from the initial depolarization of the septum (Q) to the completion of ventricular depolarization (S wave).

113
Q

What does the T wave represent in the ECG?

A

The T wave represents ventricular repolarization, which occurs as a wave of negativeness spreads back through the ventricles, towards the endocardium.

114
Q

What are the main components of the ECG according to Einthoven’s convention?

A

The ECG consists of the P wave (atrial depolarization), the QRS complex (ventricular depolarization), and the T wave (ventricular repolarization). Atrial repolarization is not visible as it is hidden by the QRS complex.

115
Q

Why is atrial repolarization not seen in the ECG?

A

Atrial repolarization is hidden by the QRS complex because the depolarization of the ventricles (QRS) is much larger in magnitude than the repolarization of the atria.

116
Q

What does the P-R interval on the ECG represent?

A

The P-R interval represents atrial conduction and A-V nodal delay. It measures how fast the wave of excitation spreads from the sinus node to the AV node. Example pathology: AV block (longer P-R interval indicates a conduction problem).

117
Q

What does the QRS duration on the ECG tell us?

A

The QRS duration indicates ventricular conduction velocity, showing how fast the wave of depolarization spreads through the ventricles. Example pathology: Bundle branch block (longer QRS duration indicates slower conduction).

118
Q

What does the S-T segment on the ECG indicate?

A

The S-T segment represents when the ventricles are fully depolarized (plateau phase of the ventricular action potential). Changes in the S-T segment (e.g., ST elevation or ST depression) indicate myocardial ischemia or myocardial infarction.

119
Q

What is the significance of the Q-T interval on the ECG?

A

The Q-T interval measures ventricular action potential duration. A prolonged Q-T interval can be indicative of Long QT syndrome, a genetic channelopathy that can be life-threatening.

120
Q

Why is atrial repolarization not visible on the ECG?

A

Atrial repolarization is hidden by the QRS complex, as it occurs during ventricular depolarization, which is much larger in magnitude.

121
Q
A
122
Q
A
123
Q
A
124
Q

What is the name of the valve between the left atrium and the left ventricle?

A

The valve between the left atrium and left ventricle is called the Mitral valve (also known as the bicuspid valve due to its two leaflets).

125
Q

What is the name of the valve between the right atrium and the right ventricle?

A

The valve between the right atrium and right ventricle is called the Tricuspid valve, due to its three leaflets.

126
Q

What are the two valves that separate the ventricles from their outflow tracts?

A

The valves separating the ventricles from the outflow tracts are the Aortic valve (left ventricle to aorta) and the Pulmonary valve (right ventricle to pulmonary artery). Both are semi-lunar valves

127
Q

What is the common feature of healthy heart valves?

A

Healthy heart valves have very little resistance to flow. A small pressure gradient (a few mmHg) across them is sufficient for them to open or close easily.

128
Q

What is the difference between diastole and systole in the cardiac cycle?

A

Diastole is the phase between heartbeats, when the heart relaxes and fills with blood. Systole is the contraction phase, when the heart pumps blood.

129
Q

What happens at Point #1 on the Wiggers diagram?

A

At Point #1, left atrial pressure (brown) is higher than left ventricular pressure (purple), causing the mitral valve to open. Blood flows from the left atrium into the left ventricle.

130
Q

What is the “atrial kick” and when does it occur in the cardiac cycle?

A

The atrial kick occurs at Point #2, when the left atrium contracts, adding a small amount of blood to the left ventricle. It happens just after the P wave on the ECG.

131
Q

What is the volume status of the left ventricle at Point #1?

A

At Point #1, the left ventricle is almost full of blood, as the mitral valve has opened and blood has flowed in from the left atrium.

132
Q

What happens at Point #3 in the cardiac cycle on the Wiggers diagram? (insert digram of this from slide 41 at later date)

A

At Point #3, the left ventricle is full of blood, and electrical excitation spreads through the ventricle (seen in the QRS complex of the ECG), causing ventricular contraction.

133
Q

What is isovolumic contraction and when does it occur?

A

Isovolumic contraction occurs at Point #4, where the left ventricle contracts, raising pressure but the volume remains unchanged because the aortic valve is still closed.

134
Q

When does the aortic valve open in the cardiac cycle?

A

The aortic valve opens at Point #5 when the left ventricular pressure exceeds the aortic pressure, allowing blood to begin flowing out of the left ventricle.

135
Q

What is the phase called when blood is ejected from the left ventricle?

A

The phase when blood is ejected from the left ventricle is called ventricular ejection, occurring at Point #6. It is marked by a drop in left ventricular volume.

136
Q

What happens at Point #7 in the cardiac cycle?

A

At Point #7, left ventricular pressure begins to fall as the ventricle stops contracting.

137
Q

What causes the dichotic notch in the aortic pressure curve?

A

The dichotic notch occurs at Point #8, when the left ventricular pressure falls below aortic pressure, causing the aortic valve to shut. This creates a characteristic bump in the aortic pressure.

138
Q

What is isovolumic relaxation in the cardiac cycle?

A

Isovolumic relaxation occurs at Point #9, when the left ventricular pressure falls while the volume remains constant (since the aortic valve is closed).

139
Q

When does the mitral valve open during the cardiac cycle?

A

The mitral valve opens at Point #10 when left ventricular pressure falls below left atrial pressure, allowing blood to flow from the left atrium into the left ventricle.

140
Q

What happens to the left ventricular volume during Point #10 of the cardiac cycle?

A

At Point #10, as the mitral valve opens, the left ventricular volume increases as blood flows from the left atrium into the left ventricle, starting the refilling phase.

141
Q

We can put a catheter into the left ventricle of the heart in the Cardiology Catheter Lab. We can measure the?

A

pressure-volume loop - measures the pressure and volume changes that occur in a single cardiac cycle.

142
Q

What is measured on the X and Y axes of a Pressure-Volume (P-V) loop?

A

X-axis: Left ventricular volume (ml)
Y-axis: Left ventricular pressure (mmHg)

143
Q

Where does the Pressure-Volume loop start, and what is this point called?

A

It starts at the bottom left-hand corner, called the End-Systolic Point, where the ventricle is fully contracted.

144
Q

What is the End-Systolic Volume (ESV) in the cardiac cycle?

A

The volume of blood remaining in the left ventricle after contraction, about 50 ml.

145
Q

What happens during the period of ventricular filling?

A

The mitral valve opens.

Blood flows from the left atrium to the left ventricle.

The ventricular volume increases from about 50 ml to 120 ml (End-Diastolic Volume, EDV).

146
Q

What happens at the End-Diastolic Volume (EDV) point?

A

The ventricle is full of blood (120 ml).
The mitral valve closes as the left ventricular pressure rises above the left atrial pressure.

147
Q

Describe the phase of isovolumic contraction.

A

The volume remains constant at 120 ml.
Pressure rises from 20 mmHg to 80 mmHg, preparing to open the aortic valve.

148
Q

At what pressure does the aortic valve open, and what phase begins?

A

The aortic valve opens at 80 mmHg.
The period of ejection begins, where blood flows from the ventricle to the systemic circulation.

149
Q

What is the systolic maximum pressure in the left ventricle?

A

120 mmHg, which corresponds to the peak systolic blood pressure.

150
Q

What triggers the closure of the aortic valve?

A

When the left ventricular pressure falls below the aortic pressure, the aortic valve closes.

151
Q

What happens during isovolumic relaxation?

A

The aortic valve is closed.
Volume remains constant at 50 ml (ESV).
Pressure falls from 100 mmHg to 20 mmHg.

152
Q

What information can a Pressure-Volume loop provide?

A

It helps measure the contractile and relaxation phases of the cardiac cycle, including pressures and volumes during each phase.

153
Q

to measure pressure and volume which ventricle is the catheter inserted into?

A

left ventricle

154
Q

What is stroke volume and how is it calculated?

A

Stroke volume is the amount of blood ejected from the heart with each beat.

End-Diastolic Volume (EDV) - End-Systolic Volume (ESV).

155
Q

What does the width of the Pressure-Volume (P-V) loop represent?

A

The width of the loop represents the stroke volume

156
Q

What is stroke work and how is it measured?

A

Stroke work is the work the heart does to move blood into the peripheral circulation.

It is measured by the area of the P-V loop.

Larger loop = heart working harder.
Smaller loop = heart working less.

157
Q

How is ejection fraction (EF) calculated, and what does it measure?

A

EF is the fraction of blood in the ventricle at end-diastole that is ejected with each beat.

158
Q

What is the normal range for ejection fraction (EF), and what indicates heart failure?

A

Normal EF: 55-75%
Heart failure: EF < 40%
Severe heart failure: EF ~30-35%

159
Q

What units are used to measure stroke work?

A

Units can vary and include mmHg cm³ or Joules (J). Often used as relative measures rather than absolute values

160
Q

What aspects of heart function can be assessed using a Pressure-Volume (P-V) loop?

A

Systolic function: Strength of contraction (contractility).
Diastolic function: Relaxation between beats (compliance or stiffness).

161
Q

Why is compliance/stiffness important in evaluating heart function?

A

It reflects the ability of the ventricle to relax and fill properly, which is critical in diagnosing conditions like heart failure.

162
Q

What does End Systolic Pressure Volume Relationship (ESPVR) indicate?

A

It represents systolic function (contractility) and is shown by the upper blue dashed line.

163
Q

What does End Diastolic Pressure Volume Relationship (EDPVR) indicate?

A

It represents diastolic function (stiffness) and is shown by the lower blue dashed line.

164
Q

How can P-V loops be used to differentiate between systolic and diastolic dysfunction?

A

Systolic dysfunction: Decrease in ESPVR slope (contractility).
Diastolic dysfunction: Alteration in EDPVR curve (stiffness or compliance).

165
Q

What happens to the P-V loops during vena cava occlusion?

A

The loops shift left as preload (ventricular volume) decreases.