Cardiac Electrical Function & Dysfunction Flashcards
1
Q
Depolarization of atrial cells is fast or slow?
A
Slow wave of depolarization
2
Q
How is the electrical conducting system divided?
A
Atrial Conducting System, Ventricular Conducting System
3
Q
What constitutes the atrial conducting system? (4)
A
SA node, Bachman’s bundle, Intranodal pathways, AV Node
4
Q
What constitutes the ventricular conducting system? (4)
A
Bundle of His, Left bundle branch, Right bundle branch, Purkinje fibers
5
Q
What is the cardiac skeleton? (What is it made of and what is its function? What does it contain?)
A
Band of fibrous tissue that does NOT conduct electrical activity. Only the Bundle of His pierces it (normally) and carries signal into ventricular conducting system. It is responsible for the delay, so that nothing happens while the atria contracts.
6
Q
What characteristics allow the conducting systems to work? (2)
A
Gap junctions, large diameter
7
Q
What is different about the AV node versus other components of conducting system?
A
AV node has small diameter, and few gap junctions (delays signal)
8
Q
The electrical conducting system contains what type of cells?
A
Specialized muscle cells. They are NOT nerve cells!
9
Q
T/F: All conducting cells are capable of self-depolarizing.
A
True
10
Q
What are the inherent rates of self depolarization in the SA node, the AV node, and the ventricles?
A
SA node - 60-100BPM, AV node - 45-50BPM, ventricles - 35-40BPM
11
Q
The inherent rate of self depolarization (SLOWS/SPEEDS UP) as distance away from SA node?
A
SLOWS
12
Q
What happens if SA node is blocked?
A
AV node will spontaneously depolarize at the slower (inherent) rate. May conduct back to SA node/atria, but slower
13
Q
Einthoven’s Triangle is outlined by 3 leads called?
A
Bipolar Limb Leads; Lead I, II, III
14
Q
Describe +/- of Lead I
A
Left Arm (LA): + Right Arm (RA): -
15
Q
Describe +/- of Lead II
A
Left Leg (LL): + Right Arm (RA) -
16
Q
Describe +/- of Lead III
A
Left Leg (LL): + Left Arm (LA): -
17
Q
What are ways of remembering leads and polarity?
A
- More L’s = More positive
- Lead I = 1 L, Lead II = 2 L’s, Lead III = 3 L’s
18
Q
What are the Unipolar Limb Leads?
A
aVR, aVL, aVF; they compare the positive end to a reference of 0 at the heart.
19
Q
Describe +/- of aVR:
A
RA +, LA & LL -
20
Q
Describe +/- of aVL:
A
LA + , RA & LL -
21
Q
Describe +/- of aVF:
A
LL +, RA & LA -
22
Q
Bipolar & unipolar limb leads measure ECG in which plane?
A
Frontal
23
Q
Precordial (chest) leads are bipolar or unipolar?
A
Unipolar
24
Q
Chest leads measure ECG in which plane?
A
Horizontal (anterior to posterior)
25
If a wave of depolarization moves toward the positive end of the lead, which way does the pen deflect? Give an example of a common wave form.
Upwards (away from isoelectric line). Eg. R Wave
26
What does the P wave represent in an ECG?
Atrial depolarization
27
What does the QRS wave represent in an ECG?
Ventricular depolarization
28
What does the T wave represent in an ECG
Ventricular repolarization
29
What happens when there is no electrical activity detected by recording electrodes?
Flat line / iso-electric line
30
The simple wave form (P wave) is which direction in lead I? II? III?
All upward (positive)
31
Why does repolarization also result in an upward pen deflection?
The wave of repolarization is in the opposite direction; last cells to depolarize are first to repolarize.
32
What are characteristics of normal sinus rhythm? (4)
- Every P wave followed by QRS
- Every QRS preceded by P
- P is upright in I, II, and III
- PR interval is 3-5 small spaces
33
What are two factors that cause bradyarrhythmia?
1) Altered Impulse Formation --> Decreased automaticity
| 2) Altered Impulse Conduction --> Conduction Block
34
What (physiologic) reasons cause sinus bradycardia?
- Increased parasympathetic drive via vagal nerve
- Decreased phase 4 slope
- More positive threshold for action potential (less frequently reached)
- More negative resting membrane potential (RMP)
35
What phase of the cardiac cycle of the SA node determines HR?
Phase 4
36
What does stimulation of the parasympathetic nervous system do to the slope of phase 4?
Flatten
37
What is the characteristic ECG finding of 1st degree block?
Constant, prolonged PR interval (> 3-5 little squares)
38
What is the characteristic ECG finding of 2nd degree Type 1 block?
Increasing length of PR interval with an occasionally dropped beat; may not lead to bradyarrhythmia - depends on frequency of dropped beats
39
What is the characteristic ECG finding of 2nd degree Type 2 block?
Constant PR interval with dropped QRS
40
What is the characteristic ECG finding of 3rd degree block
Complete dissociation of atrial & ventricular electrical activity. Usually bradycardic with ventricular rate of ~45bpm. Atrial rate about 100bpm. Often can find a P wave buried in between 2 "absolutely certain" P waves
41
What is a narrow QRS interval and what does it signify?
<3 small squares. Shows that tachycardia (if any) is supra-ventricular in origin. It is narrow as the conduction goes down the normal system - less time needed to conduct.
42
What is a wide QRS interval and what does it signify?
>3 small squares. Shows that the tachycardia originates in the ventricles of His Purkinje system. More time is needed for a contraction, so a wider complex is formed (x-axis is time).
43
How does altered impulse conduction manifest as tachyarrhythmia?
Through re-entry pathways
44
How does altered impulse formation manifest as tachyarrhythmia?
Through increased automaticity and triggered activity
45
What are signs of anti-cholinergic overdose?
- Red as a beet (cutaneous vasodilation)
- Hot as a hare (no PSN sweating)
- Dry as a bone
- Blind as a bat (no PSN pupillary dilation or visual accommodation)
- Mad as a hatter (Blocked muscarinic effects on CNS)
46
How does overstimulation of the anticholinergic system affect automaticity? What is the mechanism?
It decreases parasympathetic drive and therefore increases the slope of the phase 4 slope, leading to increased heart rate. In addition, the threshold is lowered (more negative), and resting membrane potential (RMP) is elevated. It increases automaticity.
47
What is reentry?
An alteration in AP conduction that results in generation of circular electrical activity leading to tachyarrhythmias
48
Describe the 2 parallel pathways in the AV node and its significance in cardiovascular physiology.
There is a fast pathway with a long refractory period and a slow pathway with a short refractory period. Normally the fast pathway is responsible for conducting the impulse to the Bundle of His & downstream. The slow pathway is halted when the 2 pathways converge as the fast pathway is in its refractory period when the short pathway impulse arrives. When there is a unidirectional block in the fast pathway, the impulse is forced to be conducted in the slow pathway with a short refractory period, and goes through the retrograde direction in the fast pathway (as there is no impulse due to the block, and therefore no refractory period), and a circuit has been created for re-entry of the impulse into the slow pathway through the retrograde direction of the fast pathway.
49
What can predispose a reentry tachycardia?
Atrial premature beat
50
What is the connection between re-entry circuits and atrial fibrillation?
Atrial fibrillation is when there are multiple re-entry circuits within the atria
51
What are the 4 classes of antiarrhythmics? What is each's mechanism?
Class I: Na channel blocker
Class II: Beta blocker
Class III: K channel blocker
Class IV: Ca channel blocker
52
Which phase influences conduction speed?
Phase 0
53
Phase 0 of the action potential influences which electrophysiological property of conduction?
Conduction speed
54
Which phase(s) influences refractory period?
Phase 2 & 3
55
Phase 2 of the action potential influences which electrophysiological property of conduction?
Refractory period
56
Phase 3 of the action potential influences which electrophysiological property of conduction?
Refractory period
57
Phase 4 of the action potential influences which electrophysiological property of conduction?
Rate of spontaneous depolarization (pacemaker rate)
58
Which phase influences the pacemaker rate?
Phase 4
59
How would you manipulate the phases to slow a physiological pacemaker? Which classes of drugs would you use?
Lengthen phase 4. Use a beta-blocker or calcium channel blocker.
60
How would you manipulate the phases to increase the refractory period in ventricular cells? Which classes of drugs would you use? Name one agent.
Lengthen phase 2/3. Use a potassium channel blocker (Class III agent). Amiodarone would be a good example.
61
How would you manipulate the phases to increase the heart rate? Which classes of drugs would you use?
Shorten phase 4. Beta agonist.
62
How would you manipulate the phases to slow down a re-entry circuit in the atria? Which classes of drugs would you use?
Lengthen phase 0. Sodium channel blocker (Class I)
63
What are 2 common mechanisms to speed up the SA node in sinus bradycardia? Name 3 dugs.
- Increase sympathetic activity
- Decrease parasympathetic activity
- Epinephrine (increase SNS)
- Dopamine (increase SNS)
- Atropine (decrease PNS)
64
What is the most common location for a heart block? How do you treat it
AV Node. Use an artificial pacemaker to increase ventricular rate.
65
What pathological processes may lead to sinus tachycardia? (2)
Hyperthyroidism, pain due to MI.
66
T/F: All atrial causes of tachycardia are pathological.
True
67
What is one concern with atrial tachycardia and how do we manage it?
Clots in the atrium due to poor contraction (esp. in atrial fibrillation). Need anti-coagulation before conversion to sinus rhythm
68
if you cannot break the re-entry circuit or have to wait for anticoagulation. What do you do?
Control ventricular rate = "rate control"
| - Drugs: beta blockers, CCBs, digoxin, adenosine
69
How does adenosine work?
It depresses the AV node and has a short onset and duration of action. Not useful for tachycardias of atrial origin.
70
Which types of re-entry circuits are easy to break?
AV node
71
What is the difference between AVNRT and AVRT?
- AVNRT = Circuit entirely within AV node
| - AVRT = Simply passes through AV node; associated with Wolff-Parkinson-White syndrome (accessory pathway)
72
What are 4 ways of breaking a AV node reentrant pathway?
1) Carotid massage
2) Adenosine
3) Beta blockers
4) Calcium channel blockers
73
What is carotid massage and how does it work?
Applying pressure on the carotid sinus stimulates the carotid baroreceptor. This tricks baroreceptor into thinking there is high BP, and so parasympathetic tone is increased to heart causing SA & AV node depression
74
How does adenosine work?
Shuts down AV node for a few seconds - breaks re-entrant circuit.
75
T/F: Suppressing the AV node will break a ventricular circuit.
False.
76
How to treat a ventricular tachycardia?
Terminate the pathological circuit by manipulating conduction speed (via class I antiarrhythmics) and refractory period (via class III antiarrhythmics).
77
How does cardioversion and defibrillation work?
Force all cells into depolarization & depolarization at the same time. This causes the entire heart to enter refractory period at same time and stops conducting any signals. Hopefully the sinus node will be first to send electrical signal and normalize.
78
What is the difference between cardioversion and defibrillation and why is this difference important?
Cardioversion - Shock is synchronized with underlying heart rhythm so the shock is not delivered on the T wave, which could precipitate ventricular fibrillation if it occurs.
79
What is ablation, and how does it work?
Act of burning tissue inside the heart with a radio frequency catheter. This permanently destroys the abnormal circuit.
Note - if the AV node is destroyed in its entirety, patient will have lifelong 3rd degree heart block.
80
How to treat a 3rd degree heart block?
Permanent pacemaker
81
What is the ventricular mean electrical axis?
Average direction of all the vectors in the ventricle that represent electrical depolarization.
82
What information do you need to estimate the ventricular mean electrical axis using the ECG?
- QRS waveforms from 2 perpendicular leads
| - The hex axial system circle
83
Lead I = Downward
aVF = Upward
What is VMEA?
Downward I = Left half of circle (signifying RIGHT HEART)
Upward aVF = Bottom half of circle
Summation = Bottom left = right axis deviation
84
Lead I = Upward
avF = Downward
What is VMEA?
Need a tie-breaker to determine whether it is left axis deviation. Examine Lead II.
If Lead II is upwards, means on lower half of circle (left heart) - this is normal axis.
If Lead II is downwards, means on upper half of circle - shows a left axis deviation.
85
What are characteristics of a left axis deviation?
Upward (positive) lead I
Downward (negative) lead aVF
Downward (negative) lead II
86
What is used to determine the baseline/isoelectric line
The PR segment
87
What does the isoelectric lead, and what is its significance?
Isoelectric lead is the lead where the QRS is equally positive (upward) as negative (downward). The ventricular mean electrical axis is perpendicular to that lead. It is always the lead with the smallest voltage for QRS. It DOESN'T tell you which direction the vector is heading. Need to find the lead whose axis is perpendicular to the isoelectric lead, and see if it is positive or negative.
88
How is current (I) defined in electrocardiac physiology?
The inward flow of positive charges into the cell is the direction of current.
89
What is the working myocardium? What is its resting membrane potential (no stimulus)?
All cells in the atria/ventricles responsible for producing force without an innate tendency to contract. It stays at -85 to -90mV in the absence of stimulation.
90
What happens in phase 0 of the action potential in the working myocardium?
Fast Na+ channels open. Membrane becomes more permeable to Na+ than K+. Membrane potential rises swiftly due to the INWARD NA+ CURRENT (INa). Towards Nernst equilibrium potential for Na, but is not reached as Na+ channels inactivate and outward K+ channels carrying the transient outward current opens for depolarization.
91
What happens in phase 1 of the action potential in the working myocardium?
Fast Na+ channels inactivated. TRANSIENT OUTWARD CURRENT carried by K+ (Ito) is active. Membrane potential depolarizes about 10mV
92
What happens in phase 2 of the action potential in the working myocardium?
Ca2+ channels open and membrane permeability to calcium is high. This is the SLOW INWARD CURRENT (Isi or ICa). Membrane potential attempts to reach ECa but cannot as it is opposed by outward K+ current (IKr = rapid, IKs = slow; delayed rectifiers)
93
What happens in phase 3 of the action potential in the working myocardium?
ICa inactivates. Membrane potential rapid returns to baseline as the DELAYED RECTIFIERS become fully active. In the latter part of phase 3, the INWARD RECTIFIER opens, which conducts an OUTWARD K+ CURRENT to complete depolarization. All inactivated channels begin to close.
94
What happens in phase 4 of the action potential in the working myocardium?
Inward rectifier is fully active and clamps membrane potential down to Ek. Remaining inactivated channels close.
95
How do the channels in the working myocardium work? (Ie. what causes them to open and close?)
Generally they open when the membrane is positive, and close when the membrane is negative. The exception is IKi or IKir, which functions in the opposite way and is the inward rectifier.
96
What is a pacemaker cell?
Cardiac muscle cells that are able to initiate contractions on its own. They include the SA node, AV node, Bundle of His, and Purkinje fibres. There is no resting potential as the membrane potential is always oscillating.
97
What happens in phase 0 of the action potential in the pacemaker cell?
This is the rising phase of the action potential. Entirely due to opening of calcium channels carrying the SLOW INWARD CURRENT (Isi). This is also why the rate of rise is slower than that of the working myocardium. ECa is never reached because the calcium channels inactivate, and delayed rectifiers (IKr & IKs) activate.
98
What happens in phase 3 of the action potential in the pacemaker cell?
Calcium channels inactivate. Delayed rectifiers (IKr, IKs) repolarize the membrane. The FUNNY CURRENT (If) activates and conducts both Na+ & K+ and opposes the depolarization. Funny current becomes more active as the membrane potential becomes more negative.
99
What happens in phase 4 of the action potential in the pacemaker cell?
Called diastolic depolarization. There is no resting membrane potential. Delayed rectifiers are open during this phase but close with time. As the delayed rectifiers close, the funny current depolarizes the membrane until threshold potential is reached at which point the calcium channels open.
100
The delayed rectifiers activate in which phase of the action potential?
Phase 3
101
The funny current activates in which type of cell, and what does it do?
In pacemaker cells. Conducts Na+ & K+ and opposes depolarization by delayed rectifiers.
102
T/F: Purkinje cells express If and act as pacemakers.
True
103
How are Purkinje fibers similar/different from pacemaker and working myocardium cells?
Express If and act like pacemakers, with a slower intrinsic frequency. The action potentials are like those of working myocardium, with a slow depolarization in phase 4.
104
Outline the channels in sequential order for the working myocardium.
INa (Na In) --> Ito (K+ out) --> Isi or ICa (Ca in) --> IKr & IKs (K+ out) --> IKi or IKir (K+ out; other channels close)
105
Outline the channels in sequential order for the working myocardium.
Isi or ICa (Ca in) --> IKr & IKs (K+ out) --> If (Na+ & K+; oppose repolarization)
106
Absolute refractory period involves the (inactivation/closure) of (____) channel?
Inactivation. Na+.
107
Describe the different states of the ion channels involved in action potential conduction.
Open --> Inactive --> Close. In that order. Cannot close until membrane potential is negative. Cannot open until closed.
108
How is conduction velocity controlled? (3)
1) The size of the cells; smaller = more resistance = slower
2) # of gap junctions; more quantity = easier flow = faster conduction
3) Rate of rise of action potential; faster rate of rise = faster seed of conduction
109
Which cells have the slowest rate of rise of action potential? Fastest?
```
Slowest = pacemaker cells
Fastest = Purkinje cells (so fastest conduction)
```
110
List the cells in conducting pathway in order of size (largest to smallest)
Purkinje > Bundle of His > Ventricle = atria > SA & AV nodes
111
Which phase of action potential corresponds to the refractory period?
Absolute refractory period = Phase 1, 2 & part of 3. Relative refractory period = end of phase 3. Basically corresponds to the amount of Na channels inactivated in those phases.
112
ST elevation of V1 & V2 on ECG indicates a:
Septal MI
113
ST elevation of V3 & V4 on ECG indicates a:
Anterior MI
114
ST elevation of V5 & V6, I & aVL on ECG indicates a:
Lateral MI
115
ST elevation of II, III, aVF on ECG indicates a:
Inferior MI
116
ST elevation of V1 & V4R on ECG indicates a:
Right ventricular MI
117
ST elevation of V7-V9 on ECG indicates a:
Posterior MI
118
What type of MI (anatomical location) is associated with an increased mortality risk?
Right ventricle MI
119
An inferior (& inferolateral/inferoposterior) MI is associated with occlusion of which coronary artery?
Right coronary artery
120
A posterior MI (& posterolateral/inferoposterior) MI is associated with occlusion of which coronary artery
Left circumflex artery
121
A septal/anterior/lateral MI is associated with occlusion of which coronary artery?
Left anterior descending artery
122
What is a key ECG finding in pericarditis?
ST elevation across many leads/anatomic territories
123
A patient's ECG shows ST elevation in many leads/anatomic territories. You would suspect a
Pericarditis
124
A patient's ECG shows a predominant S wave in V1 & V2, a predominant R wave in V5 and V6, an R wave getting larger from V2 to V4, and a positive T wave in leads with an R wave. This patient has
A normal ECG
125
"Rabbit ears" corresponds to?
A RSR' presentation of the "QRS complex" where there is no first dip (so no Q). This is characteristic of bundle branch block.
126
A patient's ECG shows a widening of QRS complex and a RSR' in V1/V2. The patient has:
Right bundle branch block
127
A patient's ECG shows a widening of QRS complex and a RSR' in V5/V6. The patient has:
Left bundle branch block
128
The sum of the largest R wave and the largest S wave is >35mm. This is characteristic of:
Left ventricular hypertrophy
129
ST depression in V4 to V6 and/or T wave inversion in V4 to V6. This is characteristic of:
Right ventricular hypertrophy
130
A progressively decreasing (in amplitude) R wave from V2 to V4 may signify a:
Right ventricular hypertrophy (this shows a decreasing R wave towards the left side)
131
The R wave in V1 is greater than 7mm shows:
Right ventricular hypertrophy
132
ST segment is measure from:
End of S wave (when it recovers from the dip) to beginning of T wave (before it goes up or down)
133
QT interval is measured from:
Beginning of Q wave (before it dips) to the end of the T wave
134
An ectopic pacemaker refers to
New beats originating from anywhere other than the sinus node
135
Premature beat refers to
A beat earlier than the next expected "normal" beat
136
Escape beat refers to
A beat occurring later than the expected beat (which can only occur if the expected normal beat doesn't happen)
137
Slowed conduction in the AV node presents on an ECG as
A long PR interval
138
The ECG approach taught in lecture tells us to look at: (5)
Rate --> Rhythm --> P wave --> PR interval --> QRS complex
139
Presence of a P wave suggests that
The pacemaker is supraventricular
140
A "sawtooth" pattern on an ECG is characteristic of:
| What is the sawtooth pattern?
Atrial flutter. More P waves than QRS complexes. (Atrium contracts but not all passed down to ventricle to cause ventricular contraction)
141
A patient presents with a regular rhythm and a normal heart rate. There is 1 P wave for every QRS complex and the PR interval is normal. Occasionally there is an early beat with no P wave preceding it, and the QRS complex for the early beat is wide. What does the patient have?
Premature ventricular beat
142
Wide and fast QRS. This shows:
Ventricular tachycardia
143
What are characteristics (on ECG) of Torsade de Pointes? What is physiological significance?
High heart rate, normal rhythm, no P waves/PR interval, wide QRS complexes with fluctuating amplitudes - "twisting". There is no cardiac output, no pulse, and no blood pressure, and is a form of cardiac arrest and cause sudden death.
144
What is Wolff-Parkinson-White Syndrome?
Extra electrical connection between atria & ventricles through an accessory pathway called Bundle of Kent. Short circuits the AV node - no delay between atrial/ventricular impulse so ventricle contracts prematurely, causing PR interval to be short. Patient will be at risk of developing large re-entry circuits.
