Physiology - Cardiology Block (I) Flashcards
(297 cards)
1
Q
In a normal heart, what percentage of cardiac output comes from atrial contraction?
A
10%
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
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)
4
Q
What intracellular conditions cause closure of cardiac connexons (gap junctions)?
A
High calcium levels;
low pH
5
Q
What intracellular conditions cause opening of cardiac connexons (gap junctions)?
A
Low calcium;
normal pH
6
Q
Describe the structure of a gap junction.
A
6 connexins coming together to make one connexon
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
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
9
Q
What structure is responsible for the electrocardiogram P-R interval?
A
The AV node
10
Q
The AV node is responsible for what part of a normal EKG reading?
A
The P-R interval
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)
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)
13
Q
Vagal nerves activate M2 receptors on the heart. These receptors activate what type of G-protein subunits?
A
Gi
14
Q
Sympathetic nerves activate β1 receptors on the heart. These receptors activate what type of G-protein subunits?
A
Gs
15
Q
The channels in the AV node are mostly:
A
L-type calcium channels
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
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
18
Q
Why is it important that gap junctions close during ischemic conditions?
A
To try to isolate the ischemic tissues from the healthy
19
Q
Where does repolarization occur first, the epicardium or endocardium?
A
Epicardium
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
21
Q
What type of cell are SA node and AV node pacemaker cells?
A
Modified cardiomyocytes
22
Q
Arrange the following types of cell from longest to shortest action potential:
Atrial
Purkinje
Ventricular
A
Purkinje > Ventricular >>> Atrial
23
Q
Which has more of a phase 1 ‘notch,’ the epicardium or endocardium?
A
Epicardium
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
25
Describe when each of the following types of ionic channel in the cardiac myocytes is active during an action potential.
26
Name the ionic channel responsible for each of the following segments of the cardiac myocyte action potential.
27
What is the specific name of the ionic channel responsible for phase 0 of the cardiac myocyte action potential shown below?
Na channel
28
What is the specific name of the ionic channel responsible for phase 1 of the cardiac myocyte action potential shown below?
Transient outward channel
| (K+)
29
What is the specific name of the ionic channel responsible for phase 2 of the cardiac myocyte action potential shown below?
L-type Ca2+ channel
30
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?
Delayed inward rectifier (K+);
Inward rectifier (K+)
31
Conduction velocity in the cardiac myocytes is proportional to the flow of which ion?
This will affect the steepness of which phase?
Na+;
phase 0
32
What is the effective refractory period (ERP) in terms of cardiac myocyte action potentials?
The inexcitable period until ~50% of Na channels are able to reopen
33
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?
Nothing;
a blunt, shortened action potential;
a normal action potential
34
What parts of the heart are influenced by vagal stimulation?
SA node (right vagus n.)
AV node + Purkinje fibers (left vagus n.)
*(Note: ventricular myocytes are not directly innervated by the parasympathetic system)*
35
The right vagus nerve innervates which particular portion(s) of the heart?
The SA node
36
The left vagus nerve innervates which particular portion(s) of the heart?
The AV node and Purkinje fibers
37
Which vagus nerve (right or left), or neither or both, innervates the ventricular myocytes?
Neither
38
What parts of the heart are influenced by sympathetic stimulation?
Virtually all portions
(SA node, AV node, Purkinje fibers, ventricular myocytes)
39
What cardiac GPCR is activated by norepinephrine?
What cardiac GPCR is activated by acetylcholine?
β1
M2
40
SA and AV node pacemaker cells have action potentials that are missing which phases normally found in other contractile myocytes?
Phases 1 and 2
41
AV nodal conduction is centered around flow of what ion?
Ca2+
42
What effect will sympathetic stimulation have on the PR interval?
Shorter PR
| (increased ICa)
43
What effect will vagal stimulation have on the PR interval?
Longer PR
| (increased IK; decreased ICa)
44
What effect does adenylyl cyclase activation have on cardiac calcium channels?
They are phosphorylated and activated
| (allowing calcium influx)
45
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?
Yes;
they are open longer;
the refractory period lasts longer than repolarization
46
Increased potassium conductance (IK) will have what effect on effective refractory periods in cardiac tissue?
What might cause this increase in IK?
The ERP increases;
vagal simulation
47
Why is it so important that the AV node be regulated by calcium conductance?
It slows down the current --\> this allows time for ventricular filling
48
Which parts of the heart have automaticity?
At how many BPM each?
**SA node** (60 - 90 min-1)
**AV node** (40 - 60 min-1)
**Purkinje fibers** (15 - 40 min-1)
49
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?
Latent pacemakers;
ectopic pacemakers
50
What is the importance of the If (Ih) channel in cardiac tissue in terms of what types of ion it allows through?
It allows for either Na+ influx or K+ efflux
(either monovalent cation, depending on which is needed)
51
At an Em close to EK, will the If channel allow sodium or potassium through?
Sodium (**slowly** depolarizing the cell)
52
What differentiates the SA node from the Purkinje fiber pacemaker cells in terms of types of channel?
There are very few IK1 channels.
If thus becomes much more important
53
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?
The AV node (40 - 60 min-1);
Purkinje fibers (15 - 40 min-1)
54
Acetylcholine has what effect on cardiac If channels and IKAch channels?
Decreased functional If channels (dephosphoylated);
increased functional IKAch channels
55
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 decrease in automaticity (typically acetylcholine-induced);
an increase in automaticity (typically norepinephrine-induced)
56
Changes in which phase of the cardiac action potential will change heart rate?
Phase 4
(from repolarization leading up to threshold)
57
What effect does hyperkalemia have on SA node automaticity?
What effect does hyperkalemia have on Purkinje fiber automaticity?
Little to no effect (fail-safe mechanisms);
decrease in automaticity
58
What effect does hyperkalemia have on cardiac automaticity?
What effect does hypokalemia have on cardiac automaticity?
Decrease;
increase
59
What change in extracellular potassium causes a decrease in cardiac automaticity?
What change in extracellular potassium causes an increase in cardiac automaticity?
Hyperkalemia;
hypokalemia
60
Incoming calcium causes what to happen in cardiac muscle?
Sarcoplasmic reticulum release of calcium
(calcium-induced calcium release)
61
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?
The Na/K pump;
increases activity (calcium is ejected);
less intracellular calcium = myocyte **contractility decreases**;
62
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?
Digoxin;
increased
63
In considering hyper- or hypokalemia, what two ion transporters are most important to consider?
The Na/K pump;
the Na/Ca exchanger
64
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?
Calcium-induced calcium release from the SR
(increased contractility)
65
Identify which of the following will result in increased cardiac myocyte contractility:
Increase in intracellular calcium
Increase in extracellular calcium
Either
Either
66
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?
Decreased Na/Ca exchange
(intracellular calcium increases);
digoxin,
ouabain
67
What is the most basic setup for an electrocardiogram (EKG)?
A lead
(a pair of bipolar electrodes - one positive, one negative)
**+**
a voltimeter
68
Einthoven's triangle is made of leads in which locations?
The right wrist,
the left wrist,
the left leg
69
In Einthoven's triangle, identify if the left wrist has positive electrodes, negative electrodes, or one of each.
One of each
70
In Einthoven's triangle, identify if the right wrist has positive electrodes, negative electrodes, or one of each.
Both negative
71
In Einthoven's triangle, identify if the left foot has positive electrodes, negative electrodes, or one of each.
Both positive
72
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
Left foot - both positive
Right wrist - both negative
Left wrist - one of each
73
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.
I (**_l_**eft arm to right arm)
III (**_l_**eft arm to **_l_**eft **_l_**eg)
II (right arm to **_l_**eft **_l_**eg)
74
Describe how a single PQRST complex on an EKG relates to which part of the heart is being stimulated at any given time.
75
Depolarization towards the positive electrode results in what on an EKG?
Upwards deflection
76
Repolarization towards the positive electrode results in what on an EKG?
Downwards deflection
77
Depolarization away from the positive electrode results in what on an EKG?
Downwards deflection
78
Repolarization away from the positive electrode results in what on an EKG?
Upwards deflection
79
What changes in depolarization and repolarization (in relation to a positive electrode) will cause upward deflection on EKG?
Depolarization towards;
repolarization away from
80
What changes in depolarization and repolarization (in relation to a positive electrode) will cause downward deflection on EKG?
Depolarization away from;
repolarization towards
81
What three factors affect the _amplitude_ of EKG deflection?
1. **Amount** of muscle tissue involved
2. **Synchrony** of the tissue
3. **Angle** of the polarization events relative to the leads
82
Depolarization of cardiac tissue begins in which layer, the endocardium or epicardium?
Repolarization of cardiac tissue begins in which layer, the endocardium or epicardium?
Endocardium;
epicardium
83
**True/False.**
The QRS complex is analogous to a ventricular myocyte's action potential.
**False**.
The QRS complex is only indicating the *depolarizing* phase
*(the T wave shows the* repolarizing *phase)*
84
Is depolarization of cardiac tissue from:
1. endocardium to epicardium (in to out)
**OR**
2. epicardium to endocardium (out to in)?
1. endocardium to epicardium (in to out)
85
Is repolarization of cardiac tissue from:
1. endocardium to epicardium (in to out)
OR
2. epicardium to endocardium (out to in)?
2. epicardium to endocardium (out to in)
86
What does the PR interval tell us?
What does the QT interval tell us?
Time between the atrial and ventricular action potentials
(AV node conduction);
duration of the ventricular muscle action potential
87
Why does the S wave exist (downward deflection after R)?
A few small ventricular areas are activated at a late stage
88
Which portion of the cardiac ventricular septum is activated first?
The left half (via the left bundle branch)
89
Describe the differences in timing between the endocardium and the epicardium for depolarization and repolarization.
90
Which EKG leads are in the frontal plane?
(I.e. in a coronal plane)
Leads I - III
91
What is the mean electrical axis (MEA)?
The average of the electrical vectors of the heart
92
Even the slightest discrepencies in cardiac output between the right and left sides of the heart can have what effects?
Very quick overload of either the pulmonary circuit or systemic circuit
## Footnote
*(an uninhibited 1% difference would empty out one of the circuits in 100 minutes)*
93
If both propranolol and atropine are administered to an individual (blocking both parasympathetic and sympathetic influences on cardiac tissue), what will occur?
The heart rate will increase to the intrinsic rate of SA node automaticity (~100 BPM)
94
Which has a stronger effect on heart activity during normal physiological conditions, vagal or sympathetic outflow?
Vagal
## Footnote
*(note in the image how blocking parasympathetic outflow has larger effects than blocking sympathetic outflow)*
95
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?
Meet bodily demands *(e.g. reduced pump activity in an AMI)*;
sufficiently empty the ventricles *(congestive failure)*
96
**True/False.**
Forward and backward heart failures are mutually exclusive of one another.
False.
97
**True/False.**
The forward heart failure (insufficient output to meet bodily demands) can lead to backward failure in chronic situations.
True.
98
What is the difference between systolic and diastolic congestive heart failures in terms of cardiac structural changes?
## Footnote
*(Note: the terms are _not_ mutually exclusive.)*
99
What are the two most common causes of heart failure?
1. AMI
2. Chronic hypertension
100
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.
Systolic;
diastolic
101
How is stroke volume calculated?
EDV- ESV
102
How is cardiac output calculated?
SV x HR
103
How is the cardiac ejection fraction calculated?
SV / EDV
(SV = EDV - ESV)
104
What three factors affect cardiac pump activity?
Contractility
Afterload
Preload
105
How is stroke volume affected by preload?
Frank-Starling mechanism
(contractility increases as fiber length increases as preload increases)
106
If aortic or pulmonic pressures are elevated, this will affect what factor determining stroke volume (contractility, preload, afterload)?
Afterload
107
Preload = end-\_\_\_\_\_\_\_\_ volume.
Afterload = the _________ against which the ventricles contract
Diastolic;
pressure
108
What is the most important factor for determining stroke volume?
(Factors affecting SV: contractility, preload, afterload)
Preload
109
Describe the Frank-Starling curve.
(more of a hockey stick than a curve)
110
Why do _very_ high preloads not result in increased stroke volumes?
The actin-myosin fibers are stretched out past one another to a poor relationship of actin:myosin
111
Describe the normal operating range of the heart in terms of preload and stroke volume.
P: 100 - 150 mL
SV: 60 - 100 mL
112
The stroke volume is directly proportional to:
Cardiac myofiber length (determined by end-diastolic volume).
113
What is the major mechanism by which left ventricular output and right ventricular output are kept equal with one another?
The Frank-Starling law
114
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.
True.
115
What is the normal value for cardiac ejection fraction?
60 - 65%
116
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?
Increased afterload = **decreased** SV
Increased preload = **increased** SV
Increased contractility = **increased** SV
117
What are a few causes of rightward deviation in mean electrical axis?
Right ventricular hypertrophy
Acute right strain
Left posterior fascicular block
118
What are a few causes of leftward deviation in mean electrical axis?
Left ventricular hypertrophy (sometimes)
Inferior wall MI
Left anterior fascicular block
119
What do absent P waves indicate?
Lack of SA pacemaking --\> some other portion of the heart takes on pacemaking activity
120
What does a prolonged PR interval indicate?
What does a shortened PR interval indicate?
AV node blockage (or just increased parasympathetic activity);
abnormal route bypassing the AV node
(e.g. Wolf-Parkinson-White syndrome)
121
What does a prolonged QRS complex indicate?
Abnormal conduction and/or delay through the ventricles
122
What do a pronounced Q wave and ST elevation indicate?
Transmural infarct
| (STEMI)
123
What does ST segment depression indicate?
Ischemia / angina
124
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.
125
In terms of contractility and stroke volume, what effect can digitalis have on an individual with heart failure?
126
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?
Decreased afterload = increased SV
Increased preload = increased SV
Increased contractility = increased SV
127
What is the definition of afterload?
*"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
Of the three factors affecting stroke volume [preload, afterload, contractility], which is the most influential?
Preload
| (Frank-Starling law)
129
Why might an individual with left-sided heart failure be short of breath?
Fluid accumulation in the lungs
130
Why might an individual with heart failure be tachycardic?
Compensatory increase in HR to make up for the decrease in stroke volume and maintain cardiac output
**(baroreceptor reflex)**
(CO = SV x HR)
131
What is one cardiac cycle?
The time from the beginning of systole to the beginning of the next systole
132
List the six steps of the cardiac cycle.
(assume the mitral and tricuspid valves have just closed)
Isovolumetric contraction (systole)
Rapid ejection (systole)
Reduced ejection (systole)
Isovolumetric relaxation (diastole)
Rapid filling (diastole)
Reduced filling (diastole)
*-- followed by atrial systole --*
133
What three steps of the cardiac cycle make up systole?
Isovolumetric contraction
Rapid ejection
Reduced ejection
134
What three steps of the cardiac cycle make up diastole?
Isovolumetric relaxation
Rapid filling
Reduced filling
135
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?
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
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?
Increased ventricular filling --\> **rapid filling**
Forced flow into stiff ventricle --\> **atrial systole**
137
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.
**Mitral valve**
opens - d
closes - a
**Aortic valve**
opens - b
closes - c
138
In the attached Wigger's diagram, describe what valvular events occur at points a, b, c, and d.
**a** - mitral valve closes
**b** - aortic valve opens
**c** - aortic valve closes
**d** - mitral valve opens
139
Identify what occurs at each corner in this pressure-volume diagram for the left ventricle.
140
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?
EDV - red
ESV - blue
the space between the two
141
Describe how an increase in preload would affect a pressure-volume diagram for the left ventricle.
(dashed line = change)
142
Describe how an increase in afterload would affect a pressure-volume diagram for the left ventricle.
(dashed line = change)
143
Describe how an increase in contractility would affect a pressure-volume diagram for the left ventricle.
(dashed line = change)
144
What does a notched P wave indicate?
Left atrial dilation/enlargement
| (typically due to **mitral stenosis**)
145
What does the QT interval best represent about the myocardium?
Ventricular repolarization
146
What rhythym is shown here?
Normal sinus rhythym
(P --\> QRS --\> T
every time)
147
What rhythym is shown here?
Sinus tachycardia
149
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?
0. 04 second
0. 2 second
1 second
151
If there is one large box (five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?
300 BPM
*(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)*
152
If there are two large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?
150 BPM
*(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)*
153
If there are three large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?
100 BPM
*(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)*
154
If there are four large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?
75 BPM
*(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)*
155
If there are five large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?
60 BPM
*(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)*
156
If there are six large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?
50 BPM
*(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)*
157
If there are seven large boxes (each of which is five 1 mm boxes) between adjacent QRS complexes, what is the heart rate?
43 BPM
*(Note: divide 300 by the number of large boxes between adjacent QRS complexes to get the HR)*
158
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)
*(Just 300 divided by the number of large boxes between adjacent QRS complexes)*
**75 BPM**
**150 BPM**
**300 BPM**
**100 BPM**
159
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)
*(Just 300 divided by the number of large boxes between adjacent QRS complexes)*
**300**
**150**
**100**
**75**
**60**
**50**
160
What arrythmia is shown here?
Atrial fibrillation
161
What arrythmia is shown here?
Atrial flutter
162
What arrythmia is shown here?
Third degree AV block
163
What arrythmia is shown here?
Premature ventricular beat
## Footnote
*(ectopic ventricular beat --\> this explains why it is opposite in polarity. It may be starting in the right ventricle)*
164
What is a normal PR interval?
What is a normal QRS interval?
0.12 - 0.20 sec
≤ 0.12 sec
166
What is the internationally standardized speed at which EKG paper moves?
25 mm / sec
| (so five large boxes = 1 sec)
168
What is an example arrhythmia that could result in the following finding on EKG examination?
An ectopic site in the left atrium
## Footnote
*(the green star in the attached diagram)*
169
What is an example arrhythmia that could result in either of the following findings on EKG examination?
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
What is an example arrhythmia that could result in the following finding on EKG examination?
## Footnote
*(Note: the QRS is prolonged and the T wave inverted.)*
An ectopic ventricular firing site
## Footnote
*(the red star in the attached diagram)*
172
If you see multiple morphologies in the same EKG strip, what may be going on?
## Footnote
*(See attached image for a simplified version.)*
Multifocal ectopic firing
173
What arrhythmia is shown here?
Ventricular tachycardia
174
What arrhythmia is shown here?
Torsade de Pointes
## Footnote
*[a polymorphic (multifocal) v. tach.]*
175
What is Torsade de Pointes?
A polymorphic (multifocal) ventricular tachycardia
177
What arrhythmia is shown here?
Ventricular fibrillation
178
≥80% of all clinically relevant arrhythmias are due to what mechanism type?
Reentrant excitation
| (or just, *reentry*)
179
What are two common causes of reentrant excitation in cardiac tissue?
**disturbance in conduction** *(e.g. MI)*;
**dispersion of ERPs** (effective refractory periods) *(e.g. due to atrial stretching in CHF)*
181
Name the mechanism common to each of the following arrhythmias:
## Footnote
Ventricular tachycardia (VTach),
atrial fibrillation (AFib),
ventricular fibrillation (VFib),
paroxysmal supraventricular tachycardia (PSVTs),
premature ventricular contractions (PVCs)
Reentrant excitation
| (reentry)
182
What type of reentrant excitation is associated with ventricular fibrillation and atrial fibrillation?
Multifocal
(many simultaneous rentrant loops)
*(atrial shown in the attached image)*
183
What type of reentrant excitation is associated with paroxysmal supraventricular tachycardia (PSVT)?
AV nodal reentry
184
What is a 'dispersion of ERPs' in regards to reentrant excitation in cardiac tissue?
Different sections of cardiac tissue have varying effective refractory periods
## Footnote
*(flow is not even through the tissue and may loop around and 'reenter' slower tissues)*
187
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
**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
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?
The changes are reversible;
cell necrosis has begun
189
How long does it typically take for cardiac myocytes to begin to die in ischemic conditions?
30 - 40 minutes
193
What effect do ischemic conditions have on cardiac myocyte resting potentials?
Depolarization;
Na+ channel inactivation
194
What effect do ischemic conditions have on Na+ channels?
What is the result?
Depolarization --\> Na+ channel inactivation
--\>
conduction block
196
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.
197
What are the three requirements that must be met for a reentrant excitation (reentry) arrhythmia to occur?
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
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
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
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?
(Single or multiple) premature ventricular contractions (PVCs)
*(the current can get caught in this loop)*
200
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?
Ventricular tachycardia
*(the current can get caught in this loop)*
201
Describe the mechanism by which atrial or ventricular tachycardia operate.
How does this differ from non-sustained ventricular tachycardia (\> 2 beats; \< 30 sec)?
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
What is the accepted mechanism for paroxsymal supraventricular tachycardia?
AV nodal reentrant excitation
## Footnote
*(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
What predisposes individuals to paroxysmal supraventricular tachycardias (PSVTs)?
Large differences in speed and effective refractory period (dispersion of refractoriness) between at least two pathways in the AV node
205
How do paroxysmal supraventricular tachycardias (PVSTs) often present?
How are they treated? Why?
Palpitations, dizziness --- no P waves on EKG;
calcium channel-blockers --- AV nodal dysfunction
206
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)?
The AV node acts as a filter, only letting through 1 for every 3 or 4 atrial beats
(3:1 or 4:1)
208
What tissues are ablated to try and treat atrial fibrillation?
Areas with especially short effective refractory periods (ERPs)
209
How will a patient with ventricular fibrillation present?
Why?
Unconscious (cardiac arrest);
no successful systole --\> virtually no blood being pumped
211
What are some ways by which arrythmias are classified?
**Origin**
(SA, atrial, supraventricular, ventricular, etc.)
**Pattern & rate**
(tachycardia, bradycardia, fibrillation, flutter, etc.)
**# of ectopic sites**
(unifocal or multifocal)
212
How can arrhythmias be classified based on their origin?
Sinus, atrial, supraventricular, ventricular, etc.
213
How can arrhythmias be classified based on their pattern and rate?
Tachycardia, bradycardia;
flutter, fibrillation, etc.
214
How can arrhythmias be classified based on their number of ectopic sites?
Either unifocal or multifocal
216
What arrhythmia is shown here?
Mobitz type I 2° AV block
217
What arrhythmia is shown here?
Atrial fibrillation
218
Third degree (complete) AV block
221
Early after-depolarizations (EADs) occur when in the cardiac cycle?
Phase 3
222
What is the basic pathophysiology of an early after-depolarization (EAD)?
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
Describe the pattern and rate of each of the following:
tachycardia
bradycardia
fibrillation
flutter
T \> 100 BPM; regular
B \< 60 BPM; regular
Fibrillation 300 - 600 BPM; chaotic and irregular
Flutter 250 - 400 BPM; regular
224
**True/False.**
Torsade de Pointes is a type of delayed after-polarization (DAD).
**False**.
Torsade de Pointes is a type of _early_ after-depolarization (EAD).
225
Early after-depolarizations (EADs) are most likely to occur in what cardiac cells?
Purkinje fibers
228
What is the basic pathophysiology of a delayed after-polarization (DAD)?
## Footnote
*(Note: the DAD is the small bump in the EKG strip after the previous beats)*
Increased intracellular calcium (often due to blockage of the sodium-calcium exchanger)
--\>
SR overloads and ejects calcium
229
Describe delayed after-polarizations (DADs) in terms of:
intracellular ions
heart rate
phase involved
Increased intracellular calcium --\> mechanism
Tachycardia --\> increases severity
Phase 4 event
230
Describe the differences in early after-polarizations (EADs) and delayed after-polarizations (DADs) in terms of:
major ions involved
phase involved
heart rate
231
D. Tissue hyperkalemia
232
Physiological levels of enhanced vagal tone, such as that produced by carotid artery massage or a Valsalva maneuver can reproducibly produce this condition.
B. First degree AV block
233
A condition that can enhance Purkinje fiber (ectopic) automaticity more than automaticity of the SA node. A cause for ventricular tachyarrhythmias.
C. Hypokalemia
*(causes more hyperpolarization-activated (Ih or If) pacemaker current to be activated)*
234
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?
No;
the site must have a **_uni_**directional block
(so the conduction can swing around and enter from the opposite side)
235
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. Delayed after-depolarizations (DADs)
236
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:
B. Early after-depolarization (EADs)
239
What is a very common cause of Torsade de Pointes?
Many, many medications can cause this
240
How many ions does the cardiac sodium-calcium exchanger move and in what directions?
Three sodium ions in;
one calcium ion out
241
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
B. Atropine
242
A patient on sotalol (a class III antiarrhythmic) for atrial fibrillation presents with the following EKG reading.
What is your diagnosis?
Torsade de Pointes
| (medication-induced)
246
How is the intensity of a systolic heart murmur described?
How is the intensity of a diastolic heart murmur described?
On a scale of 1/6 - 6/6.
On a scale of 1/4 - 4/4.
247
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)
Difficult to hear
Clearly audible (S1 and/or S2 is(are) still louder)
Louder than S1 and S2
Audible without a stethoscope
248
What are some examples of arrhythmias for which the mechanism is often reentrant excitation (reentry)?
Ventricular tachycardia (VTach),
atrial fibrillation (AFib),
ventricular fibrillation (VFib),
paroxysmal supraventricular tachycardia (PSVTs),
premature ventricular contractions (PVCs)
253
What are EADs (early after-depolarizations) and DADs (delayed after-depolarizations)?
Abnormal automaticity in cardiac tissue
(i.e. ectopic pacemaker(s) that is(are) repeatedly firing)
254
Describe the murmur associated with aortic or pulmonic stenosis.
Crescendo-descendo during systole
255
What is the cause for most EADs (early after-depolarizations) and DADs (delayed after-depolarizations)?
Medications;
they are most commonly drug-induced arrhythmias
256
Describe the murmur associated with aortic or pulmonic regurgitation.
Normal S1, descendo following S2
258
How can a murmur associated with left-sided valve stenosis be increased in intensity?
Squatting
259
How can a murmur associated with right-sided valves be increased in intensity?
Inspiration
260
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?
Squatting;
inspiration
261
What method can be used to resist forward flow over the cardiac valves?
Hand grip
262
What murmur can be increased by increasing hand grip?
Aortic regurgitation
| (increased TPR)
263
The valsalva manuever (increasing intraabdominal pressure) increases what cardiac murmur?
Hypertrophic cardiomyopathy
264
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
**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
What clinical maneuver can increase the murmur of hypertrophic cardiomyopathy?
The Valsalva maneuver (bear down)
266
What clinical maneuver can increase the murmur associated with aortic regurgitation?
Hand grip (increase TPR)
267
What clinical maneuver can increase the murmurs associated with right-sided valves?
Inspiration
268
What clinical maneuver can increase the murmur associated with left-sided stenosis?
Squatting
269
Identify the heart sound(s).
(Point out any abnormalities)
Normal S1 and S2
270
Identify the heart sound(s).
(Point out any abnormalities)
Normal S1 and S2;
## Footnote
**physiological S3**
271
Identify the heart sound(s).
| (Point out any abnormalities)
**Pathologic S3**
272
Identify the heart sound(s).
(Point out any abnormalities)
**S4**
273
Identify the heart sound(s).
(Point out any abnormalities)
The murmur associated with a **VSD**
274
Identify the heart sound(s).
(Point out any abnormalities)
The murmur associated with **Tetralogy of Fallot**
275
Identify the heart sound(s).
(Point out any abnormalities)
The murmur associated with an **ASD**
276
Identify the heart sound(s).
(Point out any abnormalities)
The murmur associated with **tricuspid regurgitation**
277
Identify the heart sound(s).
(Point out any abnormalities)
The murmur associated with **PDA**
278
Identify the heart sound(s).
(Point out any abnormalities)
The murmur associated with **mitral regurgitation**
279
Identify the heart sound(s).
(Point out any abnormalities)
The murmur associated with **mitral regurgitation**
280
Identify the heart sound(s).
(Point out any abnormalities)
The murmur associated with **mitral prolapse**
281
Identify the heart sound(s).
(Point out any abnormalities)
The murmur associated with an **ASD**
282
Identify the heart sound(s).
(Point out any abnormalities)
The murmur associated with **aortic stenosis**
283
Identify the heart sound(s).
(Point out any abnormalities)
The murmur associated with **aortic stenosis**
284
# Describe the following in terms of what you might hear through your stethoscope:
Normal S1 and S2
Identify the heart sound(s).
(Point out any abnormalities)
285
# Describe the following in terms of what you might hear through your stethoscope:
Normal S1 and S2;
## Footnote
**physiological S3**
Identify the heart sound(s).
(Point out any abnormalities)
286
# Describe the following in terms of what you might hear through your stethoscope:
**Pathologic S3**
Identify the heart sound(s).
| (Point out any abnormalities)
287
# Describe the following in terms of what you might hear through your stethoscope:
**S4**
Identify the heart sound(s).
(Point out any abnormalities)
288
# Describe the following in terms of what you might hear through your stethoscope:
The murmur associated with a **VSD**
Identify the heart sound(s).
(Point out any abnormalities)
289
# Describe the following in terms of what you might hear through your stethoscope:
The murmur associated with **Tetralogy of Fallot**
Identify the heart sound(s).
(Point out any abnormalities)
290
# Describe the following in terms of what you might hear through your stethoscope:
The murmur associated with an ASD
Identify the heart sound(s).
(Point out any abnormalities)
291
# Describe the following in terms of what you might hear through your stethoscope:
The murmur associated with **tricuspid regurgitation**
Identify the heart sound(s).
(Point out any abnormalities)
292
# Describe the following in terms of what you might hear through your stethoscope:
The murmur associated with **PDA**
Identify the heart sound(s).
(Point out any abnormalities)
293
# Describe the following in terms of what you might hear through your stethoscope:
The murmur associated with **mitral regurgitation**
Identify the heart sound(s).
(Point out any abnormalities)
294
# Describe the following in terms of what you might hear through your stethoscope:
The murmur associated with **mitral regurgitation**
Identify the heart sound(s).
(Point out any abnormalities)
295
# Describe the following in terms of what you might hear through your stethoscope:
The murmur associated with **mitral prolapse**
Identify the heart sound(s).
(Point out any abnormalities)
296
# Describe the following in terms of what you might hear through your stethoscope:
The murmur associated with an **ASD**
Identify the heart sound(s).
(Point out any abnormalities)
297
# Describe the following in terms of what you might hear through your stethoscope:
The murmur associated with **aortic stenosis**
Identify the heart sound(s).
(Point out any abnormalities)
300
What happens to extracellular K+ levels during infarction?
Why?
They increase;
lack of ATP --\> no inhibition of KATP channels;
301
What type of channel are KATP channels?
Where are they found?
K+ channels that are inhibited by ATP;
cardiac tissue, the pancreas, smooth muscle
302
What happens to KATP channels if ATP levels fall?
They are unihibited;
massive efflux of potassium out of cardiac cells
305
What happens when cardiac tissue action potentials run headlong into one another?
They extinguish one another
| (due to ERPs)
312
What is the simple mechanism for atrial or ventricular fibrillation?
What is atrial flutter's simple mechanism?
Large number of reentry circuits (reentrant excitation)
a single, large reentry circuit (reentrant excitation)
317
What arrhythmia is known for relapsing and recurring?
Atrial fibrillation
## Footnote
*("Afib begets afib")*
320
Are the atrial contractions in atrial fibrillation regular?
Are the ventricular contractions in atrial fibrillation regular?
**No**;
**no** (occur at irregular, random rates --\> but may appear regular at first glance!)
321
In first degree AV node block, how prolonged is the PR interval?
\> 0.20 sec
(larger than 1 large box on the EKG strip)
322
**True/False.**
First degree AV blocks can devolve into third degree AV block without passing through second degree block.
True.
323
Which type of AV block is most likely to devolve into third degree AV block?
Mobitz type II second degree AV block
## Footnote
*(dropped QRS complexes with no change in PR interval)*
324
**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.
**False**.
Mobitz type II second degree AV blocks is more likely to become third degree.
325
In what disorder are atrial depolarization and ventricular depolarization regular but completely out of sync with one another?
Third degree AV block
329
Describe the conditions that are risk factors for Torsade de Pointes in regards to the following:
Extracellular ionic concentrations
Gender
Heart rate
QT interval
**Hypo**magnesia
**Hypo**kalemia
Female
Bradycardia
Prolonged QT interval
330
Drugs that block what channel can predispose an individual to Torsade de Pointes?
How?
IKR
(Inward-rectifier potassium channel);
the QT interval is lengthened
333
Congenital early after-depolarizations (EADs) are most often due to:
Acquired early after-depolarizations (EADs) are most often due to:
Long QT syndromes;
medication use (e.g. quinidine)
336
Delayed after-depolarizations (DADs) occur when in the cardiac cycle?
Phase 4
337
Delayed after-depolarizations (DADs) occur when in the cardiac cycle?
Early after-depolarizations (EADs) occur when in the cardiac cycle?
Phase 4;
phase 3
347
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
Female gender
(and **hypo**kalemia, **hypo**magnesia, and **brady**cardia)
348
Do men or women typically have a longer QT syndrome?
Women
349
Delayed after-depolarizations (DADs) result from activation of which transport mechanism?
## Footnote
**L-type Ca channel**
**Na/Ca exchange**
**Na/K pump**
**Sodium channels**
**Na/Ca exchange**
353
**True/False.**
Even though it results in calcium efflux, increased Na/Ca exchanger activity can result in diastolic depolarization (resulting in DADs).
True.
354
**True/False.**
Cardiac disease can be due to either issues in the electrical system or the pump system of the heart.
True.
355
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:
Closure of the AV valves
Closure of the aortic-pulmonic valves
Increased ventricular filling
Forced blood flow into stiff ventricle
358
What is a cardiac murmur?
What is a gallop?
Turbulence over the heart valves;
extra heart sounds (S3, S4)
359
Highly irregular S1 sounds might indicate what condition?
Atrial fibrillation
360
Murmurs indicate problems in the:
Gallops (extra heart sounds) indicate problems in the:
Valves;
chambers (stiff or floppy)
361
A pathologic S3 sound indicates what about the ventricles?
When in the cardiac cycle is it heard?
They are enlarged and floppy;
in early diastole
*(bum, bum-bum)*
362
Which is sometimes normal, an S3 or an S4 heart sound?
S3
(pregnant women, children, athletes after exercise)
363
Dilated cardiomyopathy often presents with what gallop?
S3
365
S4 heart sounds are due to what change in the ventricle(s)?
When in the cardiac cycle does it occur?
They are stiff;
late diastole
(bu-dum, bum)
367
When does the S3 gallop occur in the cardiac cycle?
When does the S4 gallop occur in the cardiac cycle?
Early diastole (**bum, bu**-dum);
late diastole (bu-**dum, bum**)
