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T1 - Integrated (Full Review) > Physiology - Cardiology Block (I) > Flashcards

Physiology - Cardiology Block (I) Flashcards

1
Q

In a normal heart, what percentage of cardiac output comes from atrial contraction?

A

10%

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2
Q

The AV node has less of what type of channel and what type of cell junction than surrounding ventricular myocytes?

A

Sodium channels (those that are present are mostly inactive);

gap junctions

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3
Q

True/False.

Gap junctions are opened and closed based on intracellular conditions?

A

True

(they are regulated by intracellular pH and Ca2+ levels)

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4
Q

What intracellular conditions cause closure of cardiac connexons (gap junctions)?

A

High calcium levels;

low pH

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5
Q

What intracellular conditions cause opening of cardiac connexons (gap junctions)?

A

Low calcium;

normal pH

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6
Q

Describe the structure of a gap junction.

A

6 connexins coming together to make one connexon

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7
Q

In what state will cardiac gap junctions (connexons) be if the cell is at normal physiological conditions (e.g. low calcium levels, pH of 7.2)?

A

Open

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8
Q

In what state will cardiac gap junctions (connexons) be if the cell is undergoing ischemic conditions (e.g. high calcium levels, pH of ~6.4)?

A

Closed

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9
Q

What structure is responsible for the electrocardiogram P-R interval?

A

The AV node

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10
Q

The AV node is responsible for what part of a normal EKG reading?

A

The P-R interval

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11
Q

What type of cholinergic receptor do the vagal nerves activate on the heart?

What effect does it have on ion channels?

A

M2 (G-protein);

activating K+ leak channels (promoting K+ efflux),

inhibiting adenylyl cyclase (and thus inhibiting Ca2+ influx)

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12
Q

What type of adrenergic receptor do sympathetic nerves activate on the heart?

What effect does it have on ion channels?

A

β1 (G-protein);

activating adenylyl cyclase (promoting Ca2+ influx)

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13
Q

Vagal nerves activate M2 receptors on the heart. These receptors activate what type of G-protein subunits?

A

Gi

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14
Q

Sympathetic nerves activate β1 receptors on the heart. These receptors activate what type of G-protein subunits?

A

Gs

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15
Q

The channels in the AV node are mostly:

A

L-type calcium channels

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16
Q

What is a normal time range for the PR interval?

What is the normal time value for the QRS complex?

A

0.12 - 0.20 sec;

< 0.12 sec

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17
Q

What prevents atrial depolarization from bypassing the AV node and directly leading to depolarization of the ventricles?

A

A fibrous ‘skeletal’ ring separating the atria from the ventricles

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18
Q

Why is it important that gap junctions close during ischemic conditions?

A

To try to isolate the ischemic tissues from the healthy

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19
Q

Where does repolarization occur first, the epicardium or endocardium?

A

Epicardium

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20
Q

Describe the differences in action potential between the following:

SA node pacemaker cells

Atrial myocytes

AV node pacemaker cells

Purkinje fibers

Ventricular myocytes (epicardium and endocardium)

A
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21
Q

What type of cell are SA node and AV node pacemaker cells?

A

Modified cardiomyocytes

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22
Q

Arrange the following types of cell from longest to shortest action potential:

Atrial

Purkinje

Ventricular

A

Purkinje > Ventricular >>> Atrial

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23
Q

Which has more of a phase 1 ‘notch,’ the epicardium or endocardium?

A

Epicardium

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24
Q

Arrange the following types of cell from most to least unstable disatolic potential:

SA node pacemakers

AV node pacemakers

Purkinje fibers

A

SA node pacemakers >

AV node pacemakers >

Purkinje fibers

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25
Q

Describe when each of the following types of ionic channel in the cardiac myocytes is active during an action potential.

A
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26
Q

Name the ionic channel responsible for each of the following segments of the cardiac myocyte action potential.

A
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27
Q

What is the specific name of the ionic channel responsible for phase 0 of the cardiac myocyte action potential shown below?

A

Na channel

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28
Q

What is the specific name of the ionic channel responsible for phase 1 of the cardiac myocyte action potential shown below?

A

Transient outward channel

(K+)

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29
Q

What is the specific name of the ionic channel responsible for phase 2 of the cardiac myocyte action potential shown below?

A

L-type Ca2+ channel

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30
Q

What are the specific names of the ionic channel responsible for phases 3, early 4, and late 4 of the cardiac myocyte action potential shown below?

A

Delayed inward rectifier (K+);

Inward rectifier (K+)

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31
Q

Conduction velocity in the cardiac myocytes is proportional to the flow of which ion?

This will affect the steepness of which phase?

A

Na+;

phase 0

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32
Q

What is the effective refractory period (ERP) in terms of cardiac myocyte action potentials?

A

The inexcitable period until ~50% of Na channels are able to reopen

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33
Q

If a cardiac myocyte is stimulated during the effective refractory period (ERP), what occurs?

If a cardiac myocyte is stimulated during the relative refractory period (RRP), what occurs?

If a cardiac myocyte is stimulated after the relative refractory period (RRP), what occurs?

A

Nothing;

a blunt, shortened action potential;

a normal action potential

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34
Q

What parts of the heart are influenced by vagal stimulation?

A

SA node (right vagus n.)

AV node + Purkinje fibers (left vagus n.)

(Note: ventricular myocytes are not directly innervated by the parasympathetic system)

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35
Q

The right vagus nerve innervates which particular portion(s) of the heart?

A

The SA node

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36
Q

The left vagus nerve innervates which particular portion(s) of the heart?

A

The AV node and Purkinje fibers

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37
Q

Which vagus nerve (right or left), or neither or both, innervates the ventricular myocytes?

A

Neither

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38
Q

What parts of the heart are influenced by sympathetic stimulation?

A

Virtually all portions

(SA node, AV node, Purkinje fibers, ventricular myocytes)

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39
Q

What cardiac GPCR is activated by norepinephrine?

What cardiac GPCR is activated by acetylcholine?

A

β1

M2

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40
Q

SA and AV node pacemaker cells have action potentials that are missing which phases normally found in other contractile myocytes?

A

Phases 1 and 2

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41
Q

AV nodal conduction is centered around flow of what ion?

A

Ca2+

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42
Q

What effect will sympathetic stimulation have on the PR interval?

A

Shorter PR

(increased ICa)

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43
Q

What effect will vagal stimulation have on the PR interval?

A

Longer PR

(increased IK; decreased ICa)

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44
Q

What effect does adenylyl cyclase activation have on cardiac calcium channels?

A

They are phosphorylated and activated

(allowing calcium influx)

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45
Q

Are cardiac calcium channels similar to sodium channels?

How are they different in regards to time?

How are they different in regards to refractory periods?

A

Yes;

they are open longer;

the refractory period lasts longer than repolarization

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46
Q

Increased potassium conductance (IK) will have what effect on effective refractory periods in cardiac tissue?

What might cause this increase in IK?

A

The ERP increases;

vagal simulation

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47
Q

Why is it so important that the AV node be regulated by calcium conductance?

A

It slows down the current –> this allows time for ventricular filling

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48
Q

Which parts of the heart have automaticity?

At how many BPM each?

A

SA node (60 - 90 min-1)

AV node (40 - 60 min-1)

Purkinje fibers (15 - 40 min-1)

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49
Q

What is the term for cardiac cells that have the potential for pacemaking but are not normally displaying automaticity?

What is the term for cardiac locations that are abnormal sites of pacemaking?

A

Latent pacemakers;

ectopic pacemakers

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50
Q

What is the importance of the If (Ih) channel in cardiac tissue in terms of what types of ion it allows through?

A

It allows for either Na+ influx or K+ efflux

(either monovalent cation, depending on which is needed)

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51
Q

At an Em close to EK, will the If channel allow sodium or potassium through?

A

Sodium (slowly depolarizing the cell)

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52
Q

What differentiates the SA node from the Purkinje fiber pacemaker cells in terms of types of channel?

A

There are very few IK1 channels.

If thus becomes much more important

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53
Q

If the SA node (60 - 90 min-1) pacemakers fail, what pacemaker cells take over?

If the SA node pacemakers and the backup above fail, what pacemakers take over?

A

The AV node (40 - 60 min-1);

Purkinje fibers (15 - 40 min-1)

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54
Q

Acetylcholine has what effect on cardiac If channels and IKAch channels?

A

Decreased functional If channels (dephosphoylated);

increased functional IKAch channels

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55
Q

An increase in PK (via IKAch) has what effect on cardiac automaticity?

An increase in PNa (via If) (or PCa) has what effect on cardiac automaticity?

A

A decrease in automaticity (typically acetylcholine-induced);

an increase in automaticity (typically norepinephrine-induced)

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56
Q

Changes in which phase of the cardiac action potential will change heart rate?

A

Phase 4

(from repolarization leading up to threshold)

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57
Q

What effect does hyperkalemia have on SA node automaticity?

What effect does hyperkalemia have on Purkinje fiber automaticity?

A

Little to no effect (fail-safe mechanisms);

decrease in automaticity

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58
Q

What effect does hyperkalemia have on cardiac automaticity?

What effect does hypokalemia have on cardiac automaticity?

A

Decrease;

increase

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59
Q

What change in extracellular potassium causes a decrease in cardiac automaticity?

What change in extracellular potassium causes an increase in cardiac automaticity?

A

Hyperkalemia;

hypokalemia

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60
Q

Incoming calcium causes what to happen in cardiac muscle?

A

Sarcoplasmic reticulum release of calcium

(calcium-induced calcium release)

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61
Q

Hyperkalemia stimulates which transmembrane protein(s) on the heart (in particular, the one that digoxin inhibits)?

What effect does this have on the Na/Ca exchanger?

What effect does this have on contractility?

A

The Na/K pump;

increases activity (calcium is ejected);

less intracellular calcium = myocyte contractility decreases;

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62
Q

What drug inhibits the cardiac Na/K pump (thus increasing intracellular calcium via blockage of the Na/Ca exchanger)?

What effect does this have on contractility?

A

Digoxin;

increased

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63
Q

In considering hyper- or hypokalemia, what two ion transporters are most important to consider?

A

The Na/K pump;

the Na/Ca exchanger

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64
Q

Whether calcium entering a cardiac myocyte is due to any of the following: (1) sympathetic activation of calcium channels, (2) influx from neighboring myocytes through gap junctions (3) decreased activity of the Na/Ca exchanger, what will the effect be?

A

Calcium-induced calcium release from the SR

(increased contractility)

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65
Q

Identify which of the following will result in increased cardiac myocyte contractility:

Increase in intracellular calcium

Increase in extracellular calcium

Either

A

Either

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66
Q

How does inhibition of the Na/K pump lead to increased cardiac myocyte contractility?

What drug has this effect?

What endogenous substance has this effect?

A

Decreased Na/Ca exchange

(intracellular calcium increases);

digoxin,

ouabain

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67
Q

What is the most basic setup for an electrocardiogram (EKG)?

A

A lead

(a pair of bipolar electrodes - one positive, one negative)

+

a voltimeter

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68
Q

Einthoven’s triangle is made of leads in which locations?

A

The right wrist,

the left wrist,

the left leg

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69
Q

In Einthoven’s triangle, identify if the left wrist has positive electrodes, negative electrodes, or one of each.

A

One of each

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70
Q

In Einthoven’s triangle, identify if the right wrist has positive electrodes, negative electrodes, or one of each.

A

Both negative

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71
Q

In Einthoven’s triangle, identify if the left foot has positive electrodes, negative electrodes, or one of each.

A

Both positive

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72
Q

In Einthoven’s triangle, identify if the following locations each has positive electrodes, negative electrodes, or one of each.

Left foot

Right wrist

Left wrist

A

Left foot - both positive

Right wrist - both negative

Left wrist - one of each

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73
Q

In Einthoven’s triangle, lead _ connects the wrists.

In Einthoven’s triangle, lead _ connects the left wrist and left foot.

In Einthoven’s triangle, lead _ connects the right wrist and left foot.

A

I (left arm to right arm)

III (left arm to left leg)

II (right arm to left leg)

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74
Q

Describe how a single PQRST complex on an EKG relates to which part of the heart is being stimulated at any given time.

A
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75
Q

Depolarization towards the positive electrode results in what on an EKG?

A

Upwards deflection

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76
Q

Repolarization towards the positive electrode results in what on an EKG?

A

Downwards deflection

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77
Q

Depolarization away from the positive electrode results in what on an EKG?

A

Downwards deflection

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78
Q

Repolarization away from the positive electrode results in what on an EKG?

A

Upwards deflection

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79
Q

What changes in depolarization and repolarization (in relation to a positive electrode) will cause upward deflection on EKG?

A

Depolarization towards;

repolarization away from

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80
Q

What changes in depolarization and repolarization (in relation to a positive electrode) will cause downward deflection on EKG?

A

Depolarization away from;

repolarization towards

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81
Q

What three factors affect the amplitude of EKG deflection?

A
  1. Amount of muscle tissue involved
  2. Synchrony of the tissue
  3. Angle of the polarization events relative to the leads
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82
Q

Depolarization of cardiac tissue begins in which layer, the endocardium or epicardium?

Repolarization of cardiac tissue begins in which layer, the endocardium or epicardium?

A

Endocardium;

epicardium

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83
Q

True/False.

The QRS complex is analogous to a ventricular myocyte’s action potential.

A

False.

The QRS complex is only indicating the depolarizing phase

(the T wave shows the repolarizing phase)

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84
Q

Is depolarization of cardiac tissue from:

  1. endocardium to epicardium (in to out)

OR

  1. epicardium to endocardium (out to in)?
A
  1. endocardium to epicardium (in to out)
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85
Q

Is repolarization of cardiac tissue from:

  1. endocardium to epicardium (in to out)

OR

  1. epicardium to endocardium (out to in)?
A
  1. epicardium to endocardium (out to in)
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86
Q

What does the PR interval tell us?

What does the QT interval tell us?

A

Time between the atrial and ventricular action potentials

(AV node conduction);

duration of the ventricular muscle action potential

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87
Q

Why does the S wave exist (downward deflection after R)?

A

A few small ventricular areas are activated at a late stage

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88
Q

Which portion of the cardiac ventricular septum is activated first?

A

The left half (via the left bundle branch)

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89
Q

Describe the differences in timing between the endocardium and the epicardium for depolarization and repolarization.

A
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90
Q

Which EKG leads are in the frontal plane?

(I.e. in a coronal plane)

A

Leads I - III

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91
Q

What is the mean electrical axis (MEA)?

A

The average of the electrical vectors of the heart

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92
Q

Even the slightest discrepencies in cardiac output between the right and left sides of the heart can have what effects?

A

Very quick overload of either the pulmonary circuit or systemic circuit

(an uninhibited 1% difference would empty out one of the circuits in 100 minutes)

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93
Q

If both propranolol and atropine are administered to an individual (blocking both parasympathetic and sympathetic influences on cardiac tissue), what will occur?

A

The heart rate will increase to the intrinsic rate of SA node automaticity (~100 BPM)

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94
Q

Which has a stronger effect on heart activity during normal physiological conditions, vagal or sympathetic outflow?

A

Vagal

(note in the image how blocking parasympathetic outflow has larger effects than blocking sympathetic outflow)

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95
Q

In ‘forward’ heart failure, the heart does not produce enough cardiac output to what?

In ‘backward’ heart failure, the heart does not produce enough cardiac output to what?

A

Meet bodily demands (e.g. reduced pump activity in an AMI);

sufficiently empty the ventricles (congestive failure)

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96
Q

True/False.

Forward and backward heart failures are mutually exclusive of one another.

A

False.

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97
Q

True/False.

The forward heart failure (insufficient output to meet bodily demands) can lead to backward failure in chronic situations.

A

True.

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98
Q

What is the difference between systolic and diastolic congestive heart failures in terms of cardiac structural changes?

(Note: the terms are not mutually exclusive.)

A
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99
Q

What are the two most common causes of heart failure?

A
  1. AMI
  2. Chronic hypertension
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100
Q

If the heart can’t contract forcefully enough, this is termed _________ dysfunction.

If the heart can’t fill enough (due to hypertrophy or other reasons), this is termed _________ dysfunction.

A

Systolic;

diastolic

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101
Q

How is stroke volume calculated?

A

EDV- ESV

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102
Q

How is cardiac output calculated?

A

SV x HR

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103
Q

How is the cardiac ejection fraction calculated?

A

SV / EDV

(SV = EDV - ESV)

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104
Q

What three factors affect cardiac pump activity?

A

Contractility

Afterload

Preload

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105
Q

How is stroke volume affected by preload?

A

Frank-Starling mechanism

(contractility increases as fiber length increases as preload increases)

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106
Q

If aortic or pulmonic pressures are elevated, this will affect what factor determining stroke volume (contractility, preload, afterload)?

A

Afterload

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107
Q

Preload = end-________ volume.

Afterload = the _________ against which the ventricles contract

A

Diastolic;

pressure

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108
Q

What is the most important factor for determining stroke volume?

(Factors affecting SV: contractility, preload, afterload)

A

Preload

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109
Q

Describe the Frank-Starling curve.

A

(more of a hockey stick than a curve)

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110
Q

Why do very high preloads not result in increased stroke volumes?

A

The actin-myosin fibers are stretched out past one another to a poor relationship of actin:myosin

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111
Q

Describe the normal operating range of the heart in terms of preload and stroke volume.

A

P: 100 - 150 mL

SV: 60 - 100 mL

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112
Q

The stroke volume is directly proportional to:

A

Cardiac myofiber length (determined by end-diastolic volume).

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113
Q

What is the major mechanism by which left ventricular output and right ventricular output are kept equal with one another?

A

The Frank-Starling law

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114
Q

True/False.

Contractility as a factor of stroke volume is independent of preload and afterload and refers more to the ionic state of the myocytes.

A

True.

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115
Q

What is the normal value for cardiac ejection fraction?

A

60 - 65%

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116
Q

An increase in afterload has what effect on stroke volume?

An increase in preload has what effect on stroke volume?

An increase in contractility has what effect on stroke volume?

A

Increased afterload = decreased SV

Increased preload = increased SV

Increased contractility = increased SV

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117
Q

What are a few causes of rightward deviation in mean electrical axis?

A

Right ventricular hypertrophy

Acute right strain

Left posterior fascicular block

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118
Q

What are a few causes of leftward deviation in mean electrical axis?

A

Left ventricular hypertrophy (sometimes)

Inferior wall MI

Left anterior fascicular block

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119
Q

What do absent P waves indicate?

A

Lack of SA pacemaking –> some other portion of the heart takes on pacemaking activity

120
Q

What does a prolonged PR interval indicate?

What does a shortened PR interval indicate?

A

AV node blockage (or just increased parasympathetic activity);

abnormal route bypassing the AV node

(e.g. Wolf-Parkinson-White syndrome)

121
Q

What does a prolonged QRS complex indicate?

A

Abnormal conduction and/or delay through the ventricles

122
Q

What do a pronounced Q wave and ST elevation indicate?

A

Transmural infarct

(STEMI)

123
Q

What does ST segment depression indicate?

A

Ischemia / angina

124
Q

Describe how a normal Frank-Starling curve will change if an individual has heart failure.

Describe how a normal Frank-Starling curve will change if norepinephrine levels increase in a healthy individual.

A
125
Q

In terms of contractility and stroke volume, what effect can digitalis have on an individual with heart failure?

A
126
Q

What change in afterload causes an increase in stroke volume?

What change in preload causes an increase in stroke volume?

What change in contractility causes an increase in stroke volume?

A

Decreased afterload = increased SV

Increased preload = increased SV

Increased contractility = increased SV

127
Q

What is the definition of afterload?

A

“It is systolic load on the ventricle after contraction has begun. It is the resistance that must be overcome in order for the ventricle to eject its contents during contraction.”

128
Q

Of the three factors affecting stroke volume [preload, afterload, contractility], which is the most influential?

A

Preload

(Frank-Starling law)

129
Q

Why might an individual with left-sided heart failure be short of breath?

A

Fluid accumulation in the lungs

130
Q

Why might an individual with heart failure be tachycardic?

A

Compensatory increase in HR to make up for the decrease in stroke volume and maintain cardiac output

(baroreceptor reflex)

(CO = SV x HR)

131
Q

What is one cardiac cycle?

A

The time from the beginning of systole to the beginning of the next systole

132
Q

List the six steps of the cardiac cycle.

(assume the mitral and tricuspid valves have just closed)

A

Isovolumetric contraction (systole)

Rapid ejection (systole)

Reduced ejection (systole)

Isovolumetric relaxation (diastole)

Rapid filling (diastole)

Reduced filling (diastole)

– followed by atrial systole –

133
Q

What three steps of the cardiac cycle make up systole?

A

Isovolumetric contraction

Rapid ejection

Reduced ejection

134
Q

What three steps of the cardiac cycle make up diastole?

A

Isovolumetric relaxation

Rapid filling

Reduced filling

135
Q

When in the cardiac cycle does S1 occur?

When in the cardiac cycle does S2 occur?

When in the cardiac cycle can an S3 (sometimes pathologic) sometimes be heard?

When in the cardiac cycle can an S4 (pathologic) sometimes be heard?

A

Closure of the AV valves –> isovolumetric contraction

Closure of the semilunar valves –> isovolumetric relaxation

Increased ventricular filling –> rapid filling

Forced flow into stiff ventricle –> atrial systole

136
Q

When in the cardiac cycle can an S3 (sometimes pathologic) sometimes be heard?

When in the cardiac cycle can an S4 (pathologic) sometimes be heard?

A

Increased ventricular filling –> rapid filling

Forced flow into stiff ventricle –> atrial systole

137
Q

In the attached Wigger’s diagram, identify the point (a, b, c, or d) on the pressure lines where, respectively, the mitral valve opens, the mitral valve closes, the aortic valve opens, and the aortic valve closes.

A

Mitral valve

opens - d

closes - a

Aortic valve

opens - b

closes - c

138
Q

In the attached Wigger’s diagram, describe what valvular events occur at points a, b, c, and d.

A

a - mitral valve closes

b - aortic valve opens

c - aortic valve closes

d - mitral valve opens

139
Q

Identify what occurs at each corner in this pressure-volume diagram for the left ventricle.

A
140
Q

Which line on a left ventricular pressure-volume diagram indicates preload?

Which line on a left ventricular pressure-volume diagram indicates the end-systolic volume?

What on the diagram represents stroke volume?

A

EDV - red

ESV - blue

the space between the two

141
Q

Describe how an increase in preload would affect a pressure-volume diagram for the left ventricle.

A

(dashed line = change)

142
Q

Describe how an increase in afterload would affect a pressure-volume diagram for the left ventricle.

A

(dashed line = change)

143
Q

Describe how an increase in contractility would affect a pressure-volume diagram for the left ventricle.

A

(dashed line = change)

144
Q

What does a notched P wave indicate?

A

Left atrial dilation/enlargement

(typically due to mitral stenosis)

145
Q

What does the QT interval best represent about the myocardium?

A

Ventricular repolarization

146
Q

What rhythym is shown here?

A

Normal sinus rhythym

(P –> QRS –> T

every time)

147
Q

What rhythym is shown here?

A

Sinus tachycardia

149
Q

How much time is represented by each 1 mm box on an EKG?

How much time is represented by each 5 mm box on an EKG?

How much time is represented by five 5 mm boxes on an EKG?

A
  1. 04 second
  2. 2 second

1 second

151
Q

If there is one large box (five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?

A

300 BPM

(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)

152
Q

If there are two large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?

A

150 BPM

(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)

153
Q

If there are three large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?

A

100 BPM

(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)

154
Q

If there are four large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?

A

75 BPM

(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)

155
Q

If there are five large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?

A

60 BPM

(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)

156
Q

If there are six large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?

A

50 BPM

(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)

157
Q

If there are seven large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?

A

43 BPM

(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)

158
Q

Name the heart rate indicated by each of the following intervals of space between adjacent QRS complexes:

4 large boxes (twenty 1 mm boxes)

2 large boxes (ten 1 mm boxes)

1 large box (five 1 mm boxes)

3 large boxes (fifteen 1 mm boxes)

A

(Just 300 divided by the number of large boxes between adjacent QRS complexes)

75 BPM

150 BPM

300 BPM

100 BPM

159
Q

Name the heart rate indicated by each of the following intervals of space between adjacent QRS complexes:

1 large box (five 1 mm boxes)

2 large boxes (ten 1 mm boxes)

3 large boxes (fifteen 1 mm boxes)

4 large boxes (twenty 1 mm boxes)

5 large boxes (twenty-five 1 mm boxes)

6 large boxes (thirty 1 mm boxes)

A

(Just 300 divided by the number of large boxes between adjacent QRS complexes)

300

150

100

75

60

50

160
Q

What arrythmia is shown here?

A

Atrial fibrillation

161
Q

What arrythmia is shown here?

A

Atrial flutter

162
Q

What arrythmia is shown here?

A

Third degree AV block

163
Q

What arrythmia is shown here?

A

Premature ventricular beat

(ectopic ventricular beat –> this explains why it is opposite in polarity. It may be starting in the right ventricle)

164
Q

What is a normal PR interval?

What is a normal QRS interval?

A

0.12 - 0.20 sec

≤ 0.12 sec

166
Q

What is the internationally standardized speed at which EKG paper moves?

A

25 mm / sec

(so five large boxes = 1 sec)

168
Q

What is an example arrhythmia that could result in the following finding on EKG examination?

A

An ectopic site in the left atrium

(the green star in the attached diagram)

169
Q

What is an example arrhythmia that could result in either of the following findings on EKG examination?

A

A supraventricular ectopic site firing

[either in the AV node (no P wave) or adjacent to it]

(the purple circle in the attached diagram)

170
Q

What is an example arrhythmia that could result in the following finding on EKG examination?

(Note: the QRS is prolonged and the T wave inverted.)

A

An ectopic ventricular firing site

(the red star in the attached diagram)

172
Q

If you see multiple morphologies in the same EKG strip, what may be going on?

(See attached image for a simplified version.)

A

Multifocal ectopic firing

173
Q

What arrhythmia is shown here?

A

Ventricular tachycardia

174
Q

What arrhythmia is shown here?

A

Torsade de Pointes

[a polymorphic (multifocal) v. tach.]

175
Q

What is Torsade de Pointes?

A

A polymorphic (multifocal) ventricular tachycardia

177
Q

What arrhythmia is shown here?

A

Ventricular fibrillation

178
Q

≥80% of all clinically relevant arrhythmias are due to what mechanism type?

A

Reentrant excitation

(or just, reentry)

179
Q

What are two common causes of reentrant excitation in cardiac tissue?

A

disturbance in conduction (e.g. MI);

dispersion of ERPs (effective refractory periods) (e.g. due to atrial stretching in CHF)

181
Q

Name the mechanism common to each of the following arrhythmias:

Ventricular tachycardia (VTach),

atrial fibrillation (AFib),

ventricular fibrillation (VFib),

paroxysmal supraventricular tachycardia (PSVTs),

premature ventricular contractions (PVCs)

A

Reentrant excitation

(reentry)

182
Q

What type of reentrant excitation is associated with ventricular fibrillation and atrial fibrillation?

A

Multifocal

(many simultaneous rentrant loops)

(atrial shown in the attached image)

183
Q

What type of reentrant excitation is associated with paroxysmal supraventricular tachycardia (PSVT)?

A

AV nodal reentry

184
Q

What is a ‘dispersion of ERPs’ in regards to reentrant excitation in cardiac tissue?

A

Different sections of cardiac tissue have varying effective refractory periods

(flow is not even through the tissue and may loop around and ‘reenter’ slower tissues)

187
Q

Describe the changes in extracellular potassium and intracellular pH in infarcted cardiac tissue in the following timeframes after infarction has occurred:

the first 0 - 5 minutes

15 - 40 minutes

≥ 40 minutes

A

The first 0 - 5 minutes

Rapid efflux of potassium; rapid decrease in pH

15 - 40 minutes

Plateaued potassium level; rapid decrease in pH

≥ 40 minutes

Continued efflux of potassium; plateaued pH

188
Q

In the graph below, cardiac intracellular pH and extracellular potassium are shown plotted against time after infarction.

What is the significance of the potassium plateau between 10 and 40 minutes?

What is the significance of the rising levels of potassium after 40 minutes?

A

The changes are reversible;

cell necrosis has begun

189
Q

How long does it typically take for cardiac myocytes to begin to die in ischemic conditions?

A

30 - 40 minutes

193
Q

What effect do ischemic conditions have on cardiac myocyte resting potentials?

A

Depolarization;

Na+ channel inactivation

194
Q

What effect do ischemic conditions have on Na+ channels?

What is the result?

A

Depolarization –> Na+ channel inactivation

–>

conduction block

196
Q

The attached image shows a subendocardial infarction in the apex of the heart.

Indicate the accepted route that might be taken for a reentrant excitation (reentry) arrhythmia to take place.

A
197
Q

What are the three requirements that must be met for a reentrant excitation (reentry) arrhythmia to occur?

A
  1. ≥ Two parallel pathways
  2. Unidirectional block
  3. Conduction time of the circuit > ERP for the circuit
    * (Basically, all just requirements so that the action potential(s) can double back from its normal route and circle around between healthy and affected tissues)*
198
Q

Why is each of the following necessary to the development of a reentrant excitation (reentry) arrhythmia?

  1. ≥ Two parallel pathways
  2. Unidirectional block
  3. Conduction time of the circuit > ERP for the circuit
A
  1. So there is an unrefractory path ‘backwards’ if the action potential swings around and goes back the way it came
  2. So that when the action potential swings around to go back, it isn’t blocked going backwards
  3. If the effective refractory periods (ERPs) of some cells were longer, the circuit action potentials would simply hit them and dissipate (i.e. the circuit would not keep flowing around and around)
199
Q

For a slow-moving reentrant excitation (reentry) arrhythmia in the ventricles (as shown in the apex in the attached image), what might the resulting EKG look like?

A

(Single or multiple) premature ventricular contractions (PVCs)

(the current can get caught in this loop)

200
Q

For a _fast-movin_g reentrant excitation (reentry) arrhythmia in the ventricles (as shown in the apex in the attached image), what might the resulting EKG look like?

A

Ventricular tachycardia

(the current can get caught in this loop)

201
Q

Describe the mechanism by which atrial or ventricular tachycardia operate.

How does this differ from non-sustained ventricular tachycardia (> 2 beats; < 30 sec)?

A

A single loop of quick conduction goes around in a reentry (reentrant excitation) pathway

(the attached image shows an example in the ventricles);

NSVT = one transient circuit

203
Q

What is the accepted mechanism for paroxsymal supraventricular tachycardia?

A

AV nodal reentrant excitation

(reentry arrhythmia –> the conduction current goes around some differential in conduction speen and keeps reexciting its circuit by traveling back up the faster end)

204
Q

What predisposes individuals to paroxysmal supraventricular tachycardias (PSVTs)?

A

Large differences in speed and effective refractory period (dispersion of refractoriness) between at least two pathways in the AV node

205
Q

How do paroxysmal supraventricular tachycardias (PVSTs) often present?

How are they treated? Why?

A

Palpitations, dizziness — no P waves on EKG;

calcium channel-blockers — AV nodal dysfunction

206
Q

In atrial flutter (a macroreentry arrhythmia), why is the atrial rate so much higher than the ventricular rate (i.e., why doesn’t each atrial action potential make it to the ventricles)?

A

The AV node acts as a filter, only letting through 1 for every 3 or 4 atrial beats

(3:1 or 4:1)

208
Q

What tissues are ablated to try and treat atrial fibrillation?

A

Areas with especially short effective refractory periods (ERPs)

209
Q

How will a patient with ventricular fibrillation present?

Why?

A

Unconscious (cardiac arrest);

no successful systole –> virtually no blood being pumped

211
Q

What are some ways by which arrythmias are classified?

A

Origin

(SA, atrial, supraventricular, ventricular, etc.)

Pattern & rate

(tachycardia, bradycardia, fibrillation, flutter, etc.)

# of ectopic sites

(unifocal or multifocal)

212
Q

How can arrhythmias be classified based on their origin?

A

Sinus, atrial, supraventricular, ventricular, etc.

213
Q

How can arrhythmias be classified based on their pattern and rate?

A

Tachycardia, bradycardia;

flutter, fibrillation, etc.

214
Q

How can arrhythmias be classified based on their number of ectopic sites?

A

Either unifocal or multifocal

216
Q

What arrhythmia is shown here?

A

Mobitz type I 2° AV block

217
Q

What arrhythmia is shown here?

A

Atrial fibrillation

218
Q
A

Third degree (complete) AV block

221
Q

Early after-depolarizations (EADs) occur when in the cardiac cycle?

A

Phase 3

222
Q

What is the basic pathophysiology of an early after-depolarization (EAD)?

A

A prolonged repolarization (slow or blocked IKR channels) allows incoming ion flow (L-type calcium channels, sodium channels, sodium-calcium exchangers) to create extra upbeats during phase 3

223
Q

Describe the pattern and rate of each of the following:

tachycardia

bradycardia

fibrillation

flutter

A

T > 100 BPM; regular

B < 60 BPM; regular

Fibrillation 300 - 600 BPM; chaotic and irregular

Flutter 250 - 400 BPM; regular

224
Q

True/False.

Torsade de Pointes is a type of delayed after-polarization (DAD).

A

False.

Torsade de Pointes is a type of early after-depolarization (EAD).

225
Q

Early after-depolarizations (EADs) are most likely to occur in what cardiac cells?

A

Purkinje fibers

228
Q

What is the basic pathophysiology of a delayed after-polarization (DAD)?

(Note: the DAD is the small bump in the EKG strip after the previous beats)

A

Increased intracellular calcium (often due to blockage of the sodium-calcium exchanger)

–>

SR overloads and ejects calcium

229
Q

Describe delayed after-polarizations (DADs) in terms of:

intracellular ions

heart rate

phase involved

A

Increased intracellular calcium –> mechanism

Tachycardia –> increases severity

Phase 4 event

230
Q

Describe the differences in early after-polarizations (EADs) and delayed after-polarizations (DADs) in terms of:

major ions involved

phase involved

heart rate

A
231
Q
A

D. Tissue hyperkalemia

232
Q

Physiological levels of enhanced vagal tone, such as that produced by carotid artery massage or a Valsalva maneuver can reproducibly produce this condition.

A

B. First degree AV block

233
Q

A condition that can enhance Purkinje fiber (ectopic) automaticity more than automaticity of the SA node. A cause for ventricular tachyarrhythmias.

A

C. Hypokalemia

(causes more hyperpolarization-activated (Ih or If) pacemaker current to be activated)

234
Q

If a portion of cardiac tissue has a conduction defect that does not prevent conduction in either direction (bidirectional conduction block), will this be a potential site for reentrant excitation (reentry) arrhythmias?

A

No;

the site must have a unidirectional block

(so the conduction can swing around and enter from the opposite side)

235
Q

Conditions of intracellular calcium overload caused by hypercalcemia or excessive catecholamine stimulation (e.g. in a patient on digoxin or toxic levels of amphetamines) can result in arrhythmias due to:

A

A. Delayed after-depolarizations (DADs)

236
Q

Drugs or ion channel mutations that reduce the rate of phase 3 repolarization and prolong the QT interval can result in an arrhythmia associated with sudden death. A cellular mechanism believed to be responsible for this type of arrhythmia is:

A

B. Early after-depolarization (EADs)

239
Q

What is a very common cause of Torsade de Pointes?

A

Many, many medications can cause this

240
Q

How many ions does the cardiac sodium-calcium exchanger move and in what directions?

A

Three sodium ions in;

one calcium ion out

241
Q

The patient with the EKG results below mentions during his history & physical that he inhaled an excessive amount of organophosphate insecticide (cholinesterase inhibitor) an hour before arriving at the hospital.

What drug could you give to increase his heart rate & provide relief from his symptoms?

A. Acetylcholine

B. Atropine

C. Lidocaine

D. Norepinephrine

E. Nicotine

A

B. Atropine

242
Q

A patient on sotalol (a class III antiarrhythmic) for atrial fibrillation presents with the following EKG reading.

What is your diagnosis?

A

Torsade de Pointes

(medication-induced)

246
Q

How is the intensity of a systolic heart murmur described?

How is the intensity of a diastolic heart murmur described?

A

On a scale of 1/6 - 6/6.

On a scale of 1/4 - 4/4.

247
Q

What is 1/6 heart murmur?

What is 2/6 heart murmur?

What is 3/6 heart murmur?

What is 6/6 heart murmur?

(Note: all systolic)

A

Difficult to hear

Clearly audible (S1 and/or S2 is(are) still louder)

Louder than S1 and S2

Audible without a stethoscope

248
Q

What are some examples of arrhythmias for which the mechanism is often reentrant excitation (reentry)?

A

Ventricular tachycardia (VTach),

atrial fibrillation (AFib),

ventricular fibrillation (VFib),

paroxysmal supraventricular tachycardia (PSVTs),

premature ventricular contractions (PVCs)

253
Q

What are EADs (early after-depolarizations) and DADs (delayed after-depolarizations)?

A

Abnormal automaticity in cardiac tissue

(i.e. ectopic pacemaker(s) that is(are) repeatedly firing)

254
Q

Describe the murmur associated with aortic or pulmonic stenosis.

A

Crescendo-descendo during systole

255
Q

What is the cause for most EADs (early after-depolarizations) and DADs (delayed after-depolarizations)?

A

Medications;

they are most commonly drug-induced arrhythmias

256
Q

Describe the murmur associated with aortic or pulmonic regurgitation.

A

Normal S1, descendo following S2

258
Q

How can a murmur associated with left-sided valve stenosis be increased in intensity?

A

Squatting

259
Q

How can a murmur associated with right-sided valves be increased in intensity?

A

Inspiration

260
Q

What method can be used to increase forward flow over the left-sided cardiac valves?

What method can be used to increase forward flow over the right-sided cardiac valves?

A

Squatting;

inspiration

261
Q

What method can be used to resist forward flow over the cardiac valves?

A

Hand grip

262
Q

What murmur can be increased by increasing hand grip?

A

Aortic regurgitation

(increased TPR)

263
Q

The valsalva manuever (increasing intraabdominal pressure) increases what cardiac murmur?

A

Hypertrophic cardiomyopathy

264
Q

Describe both the effect of each of the following on heart murmurs and also the mechanism by which it occurs:

Hand grip

Valsalva maneuver

Squatting

Inspiration

A

Aortic regurgitation - Increases TPR that the LV is pushing against

Hypertrophic cardiomyopathy - Increases intraabdominal pressure

Left-sided valve stenosis - Brings the heart closer to the periphery

Right-sided valve murmurs - Increased venous return to the RA

265
Q

What clinical maneuver can increase the murmur of hypertrophic cardiomyopathy?

A

The Valsalva maneuver (bear down)

266
Q

What clinical maneuver can increase the murmur associated with aortic regurgitation?

A

Hand grip (increase TPR)

267
Q

What clinical maneuver can increase the murmurs associated with right-sided valves?

A

Inspiration

268
Q

What clinical maneuver can increase the murmur associated with left-sided stenosis?

A

Squatting

269
Q

Identify the heart sound(s).

(Point out any abnormalities)

A

Normal S1 and S2

270
Q

Identify the heart sound(s).

(Point out any abnormalities)

A

Normal S1 and S2;

physiological S3

271
Q

Identify the heart sound(s).

(Point out any abnormalities)

A

Pathologic S3

272
Q

Identify the heart sound(s).

(Point out any abnormalities)

A

S4

273
Q

Identify the heart sound(s).

(Point out any abnormalities)

A

The murmur associated with a VSD

274
Q

Identify the heart sound(s).

(Point out any abnormalities)

A

The murmur associated with Tetralogy of Fallot

275
Q

Identify the heart sound(s).

(Point out any abnormalities)

A

The murmur associated with an ASD

276
Q

Identify the heart sound(s).

(Point out any abnormalities)

A

The murmur associated with tricuspid regurgitation

277
Q

Identify the heart sound(s).

(Point out any abnormalities)

A

The murmur associated with PDA

278
Q

Identify the heart sound(s).

(Point out any abnormalities)

A

The murmur associated with mitral regurgitation

279
Q

Identify the heart sound(s).

(Point out any abnormalities)

A

The murmur associated with mitral regurgitation

280
Q

Identify the heart sound(s).

(Point out any abnormalities)

A

The murmur associated with mitral prolapse

281
Q

Identify the heart sound(s).

(Point out any abnormalities)

A

The murmur associated with an ASD

282
Q

Identify the heart sound(s).

(Point out any abnormalities)

A

The murmur associated with aortic stenosis

283
Q

Identify the heart sound(s).

(Point out any abnormalities)

A

The murmur associated with aortic stenosis

284
Q

Describe the following in terms of what you might hear through your stethoscope:

Normal S1 and S2

A

Identify the heart sound(s).

(Point out any abnormalities)

285
Q

Describe the following in terms of what you might hear through your stethoscope:

Normal S1 and S2;

physiological S3

A

Identify the heart sound(s).

(Point out any abnormalities)

286
Q

Describe the following in terms of what you might hear through your stethoscope:

Pathologic S3

A

Identify the heart sound(s).

(Point out any abnormalities)

287
Q

Describe the following in terms of what you might hear through your stethoscope:

S4

A

Identify the heart sound(s).

(Point out any abnormalities)

288
Q

Describe the following in terms of what you might hear through your stethoscope:

The murmur associated with a VSD

A

Identify the heart sound(s).

(Point out any abnormalities)

289
Q

Describe the following in terms of what you might hear through your stethoscope:

The murmur associated with Tetralogy of Fallot

A

Identify the heart sound(s).

(Point out any abnormalities)

290
Q

Describe the following in terms of what you might hear through your stethoscope:

The murmur associated with an ASD

A

Identify the heart sound(s).

(Point out any abnormalities)

291
Q

Describe the following in terms of what you might hear through your stethoscope:

The murmur associated with tricuspid regurgitation

A

Identify the heart sound(s).

(Point out any abnormalities)

292
Q

Describe the following in terms of what you might hear through your stethoscope:

The murmur associated with PDA

A

Identify the heart sound(s).

(Point out any abnormalities)

293
Q

Describe the following in terms of what you might hear through your stethoscope:

The murmur associated with mitral regurgitation

A

Identify the heart sound(s).

(Point out any abnormalities)

294
Q

Describe the following in terms of what you might hear through your stethoscope:

The murmur associated with mitral regurgitation

A

Identify the heart sound(s).

(Point out any abnormalities)

295
Q

Describe the following in terms of what you might hear through your stethoscope:

The murmur associated with mitral prolapse

A

Identify the heart sound(s).

(Point out any abnormalities)

296
Q

Describe the following in terms of what you might hear through your stethoscope:

The murmur associated with an ASD

A

Identify the heart sound(s).

(Point out any abnormalities)

297
Q

Describe the following in terms of what you might hear through your stethoscope:

The murmur associated with aortic stenosis

A

Identify the heart sound(s).

(Point out any abnormalities)

300
Q

What happens to extracellular K+ levels during infarction?

Why?

A

They increase;

lack of ATP –> no inhibition of KATP channels;

301
Q

What type of channel are KATP channels?

Where are they found?

A

K+ channels that are inhibited by ATP;

cardiac tissue, the pancreas, smooth muscle

302
Q

What happens to KATP channels if ATP levels fall?

A

They are unihibited;

massive efflux of potassium out of cardiac cells

305
Q

What happens when cardiac tissue action potentials run headlong into one another?

A

They extinguish one another

(due to ERPs)

312
Q

What is the simple mechanism for atrial or ventricular fibrillation?

What is atrial flutter’s simple mechanism?

A

Large number of reentry circuits (reentrant excitation)

a single, large reentry circuit (reentrant excitation)

317
Q

What arrhythmia is known for relapsing and recurring?

A

Atrial fibrillation

(“Afib begets afib”)

320
Q

Are the atrial contractions in atrial fibrillation regular?

Are the ventricular contractions in atrial fibrillation regular?

A

No;

no (occur at irregular, random rates –> but may appear regular at first glance!)

321
Q

In first degree AV node block, how prolonged is the PR interval?

A

> 0.20 sec

(larger than 1 large box on the EKG strip)

322
Q

True/False.

First degree AV blocks can devolve into third degree AV block without passing through second degree block.

A

True.

323
Q

Which type of AV block is most likely to devolve into third degree AV block?

A

Mobitz type II second degree AV block

(dropped QRS complexes with no change in PR interval)

324
Q

True/False.

Wenckebach AV block (Mobitz type I second degree AV block) is more likely to devolve into third degree than Mobitz type II second degree AV blocks.

A

False.

Mobitz type II second degree AV blocks is more likely to become third degree.

325
Q

In what disorder are atrial depolarization and ventricular depolarization regular but completely out of sync with one another?

A

Third degree AV block

329
Q

Describe the conditions that are risk factors for Torsade de Pointes in regards to the following:

Extracellular ionic concentrations

Gender

Heart rate

QT interval

A

Hypomagnesia

Hypokalemia

Female

Bradycardia

Prolonged QT interval

330
Q

Drugs that block what channel can predispose an individual to Torsade de Pointes?

How?

A

IKR

(Inward-rectifier potassium channel);

the QT interval is lengthened

333
Q

Congenital early after-depolarizations (EADs) are most often due to:

Acquired early after-depolarizations (EADs) are most often due to:

A

Long QT syndromes;

medication use (e.g. quinidine)

336
Q

Delayed after-depolarizations (DADs) occur when in the cardiac cycle?

A

Phase 4

337
Q

Delayed after-depolarizations (DADs) occur when in the cardiac cycle?

Early after-depolarizations (EADs) occur when in the cardiac cycle?

A

Phase 4;

phase 3

347
Q

Torsade de pointes is a potentially fatal arrhythmia that can be caused by more than 40 different drugs. Which of the following clinical conditions is also associated with an increased risk of this arrhythmia?

Female gender

Hyperkalema

Hypermagnesia

Tachycardia

A

Female gender

(and hypokalemia, hypomagnesia, and bradycardia)

348
Q

Do men or women typically have a longer QT syndrome?

A

Women

349
Q

Delayed after-depolarizations (DADs) result from activation of which transport mechanism?

L-type Ca channel

Na/Ca exchange

Na/K pump

Sodium channels

A

Na/Ca exchange

353
Q

True/False.

Even though it results in calcium efflux, increased Na/Ca exchanger activity can result in diastolic depolarization (resulting in DADs).

A

True.

354
Q

True/False.

Cardiac disease can be due to either issues in the electrical system or the pump system of the heart.

A

True.

355
Q

The S1 heart sound is caused by:

The S2 heart sound is caused by:

The S3 heart sound is caused by:

The S4 heart sound is caused by:

A

Closure of the AV valves

Closure of the aortic-pulmonic valves

Increased ventricular filling

Forced blood flow into stiff ventricle

358
Q

What is a cardiac murmur?

What is a gallop?

A

Turbulence over the heart valves;

extra heart sounds (S3, S4)

359
Q

Highly irregular S1 sounds might indicate what condition?

A

Atrial fibrillation

360
Q

Murmurs indicate problems in the:

Gallops (extra heart sounds) indicate problems in the:

A

Valves;

chambers (stiff or floppy)

361
Q

A pathologic S3 sound indicates what about the ventricles?

When in the cardiac cycle is it heard?

A

They are enlarged and floppy;

in early diastole

(bum, bum-bum)

362
Q

Which is sometimes normal, an S3 or an S4 heart sound?

A

S3

(pregnant women, children, athletes after exercise)

363
Q

Dilated cardiomyopathy often presents with what gallop?

A

S3

365
Q

S4 heart sounds are due to what change in the ventricle(s)?

When in the cardiac cycle does it occur?

A

They are stiff;

late diastole

(bu-dum, bum)

367
Q

When does the S3 gallop occur in the cardiac cycle?

When does the S4 gallop occur in the cardiac cycle?

A

Early diastole (bum, bu-dum);

late diastole (bu-dum, bum)

T1 - Integrated (Full Review) (29 decks)

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