Cardiovascular Systems Physiology and Pathophysiology III Flashcards
1
Q
The standard ECG consists of 12 leads. These 12 leads give a 3D representation of the hearts electrical activity. What represents the
- ) Frontal plane of the heart?
- ) Anterior and posterior directions?
A
- ) The 6 limb leads
2. ) The 6 precordial leads
2
Q
What are the 6 limb leads?
A
Inferior: II, III, and aVF
Left lateral: I and aVL
Right lateral: aVR
3
Q
When interpretting an ECG, what 5 things should be evaluated?
A
- ) Rate
- ) Rythm
- ) Electrical axis
- ) Intervals
- ) Segments
4
Q
In which wave do the 1st and 2nd halves represent the right and left atrial depolarization respectively?
A
P wave
5
Q
Atrial depolarization and the end of ventricular repolarization is represented by the
A
PR
6
Q
The duration of ventricular activation is represented on an ECG by
A
QRS complex
7
Q
Represents the end phase of ventricular depolarization in an ECG
A
S wave
8
Q
In an ECG, the end of ventricular depolarization and the beginning of ventricular repolarization is signified by the
A
ST segment
9
Q
In an ECG, ventricular repolarization is signified by the
A
T wave
10
Q
The isoelectric line of the ECG. Represents the electrically silent myocardium
A
TP
11
Q
The preponderant direction of current during ventricular depolarization
A
Cardiac electrical axis
12
Q
Collectively, leads I, II, and III enable construction of
A
Einthoven’s triangle
13
Q
A configuration translating into a geometric representation that indicates the electrical axis of the heart
A
Einthoven’s triangle
14
Q
The major vector of ventricular activation (i.e. depolarization)
A
The QRS axis
15
Q
When viewing ECGs it is a good habit to determine the
net QRS voltages from leads
A
I, II, and aVF
16
Q
The average cardiac electrical axis approximates 50-60 degrees, which means what for leads:
- ) I
- ) II
- ) aVF
A
- ) Positive
- ) Isoelectric (zero charge)
- ) Positive
17
Q
An axis between 0- (-30º) is considered a
A
Normal varient
18
Q
An axis between 0- (-30º) is considered a normal varient where leads
- ) I
- ) II
- ) aVF
A
- ) positive
- ) positive
- ) negative
19
Q
An axis greater than 100º shows right axis deviation. What does this mean for leads
- ) I
- ) II
- ) aVF
A
- ) Negative
- ) Isoelectric
- ) Positive
20
Q
An axis between -30º and -90º indicates left axis deviation. What does this mean for leads
- ) I
- ) II
- ) aVF
A
- ) Positive
- ) Negative
- ) Negative
21
Q
Some of the more common reasons for axis deviation are
A
Right or left ventricular hypertrophy and pregnancy
22
Q
Anything that disrupts the normal amount and/or timing of ionic flux in cardiac myocytes and/or nodal tissue can induce an
A
Arrythmia
23
Q
An alteration of the normal sinus rythym which guides coordinated myocyte contractility
A
Arrythmia
24
Q
Recall that cardiac depolarization and repolarization are substantially controlled by
A
Ca2+ and K+ respectively
25
What are some features of Hyperkalemia?
Tall peaked and narrow based T and QT interval shortening
26
Primary AV block, flattening/ widening P, ST depression, and QRS widening are features of
Hyperkalemia
27
No P, left/right bundle branch block, widened/diffuse conduction delay, and possible V tach, V fib, or asystole are features of an ECG of
Severe Hyperkalemia
28
Shows ST depression, flattened T, increased P duration and amplitude, and prolonged QT interval
Hypokalemia
29
Shortened ST segment, PR prolongation, and normal P, QRS, and T
Hypercalcimia
30
What are some features of an ECG of hypocalcemia?
Prolonged ST interval
31
Results from increased generation of SA node AP
Tachycardia
32
Results from decreased generation of SA node AP
Brachycardia
33
Strictly speaking, sinus rhythm refers only to the
Atrium
34
A normally conducting SA node and atrium with complete heart block is strictly speaking
Sinus rythym
35
Atrial depolarization follows SA nodal firing. These are shown by the
P wave
36
Note that the P wave is functionally split into two segments. What do the following represent?
1. ) The 1st half
2. ) The 2nd half
1. ) Right atrial depolarization
| 2. ) Left atrial depolarization
37
Episodes of tachycardia (HR > 100 bpm) are represented on the ECG by a severely decreased
P-P interval
38
Causes an increased P-P interval on an ECG
Sinus Brachycardia (HR < 60 BPM)
39
Causes a severely decreased P-P interval on an ECG
Sinus tachycardia (HR > 120 BPM)
40
Niether sinus tachycardia or sinus brachycardia substantially alter the physical properties of the
P wave or QRS complex
41
Rapid and regular atrial activity
Atrial Flutter
42
Atrial flutter is reflected within the ECG as rapid atrial activity, with P waves exhibiting a so-called
Saw-tooth appearance
43
Atrial flutter can result from reentry, and is usually generated from a large fixed region, which can often times be mapped to near the
Tricuspid valve annulus
44
Atrial beats can reach 300 BPM, however the relay of all atrial impulses to the ventricles is impeded by
AV delay
45
Malfunctions in the AV node are referred to as
Heart Block or Nodal Block
46
Results in a prolonged P-R interval due to an abnormally lengthened conduction time within the AV node and/or the bundle of His
Primary heart block
47
There is one atrial to ventricular conduction with
Primary heart block
48
Results from an increased refractory period of AV nodal tissue or His system, thus making it less excitable
Second degree heart block
49
During secondary heart block, not every impulse is
| relayed through the AV node and/or His to the ventricles; thus we see a
P : QRS ration greater than 1:1
50
Caused when no atrial impulses reach the ventricle
Third degree heart block (AKA complete heart block or AV dissociation)
51
In a third degree heart block, without the proper relay system, subsidiary pacemakers assume control of cardiac rate and rythym. This is known as an
Escape rythym
52
If the 3rd degree heart block resides in the AV node, a relatively stable rate (~50 BPM) and rythym maintains hemodynamic stability. This pacemaker function is at the
AV junction (called the junctional escape)
53
Result in an inherently unstable and slow ventricular escape rhythm consisting of about 30-40 bpm
Blocks distal to the AV node
54
The ECG during a third degree heart block can be distinguished by
Multiple P waves and superimposed QRS complexes
55
Used to re-establish the normal pattern of cardiac electrical activity resulting from third degree heart
block
Implantable pacemakers
56
An arrhythmia that prevents effectual contraction of atrial and/or ventricular myocardium
Fibrillation
57
May represent a reentry phenomenon in which a reentry loop fragments into multiple irregular circuits within the myocardium
Fibrillation
58
Fibrillation is characterized by non-coordinated and inefficient
Myocardial contractions
59
The most common cardiac arrythmia disorder
Atrial fibrillation (A Fib)
60
The abnormal electrical re-excitation of a region of the atrial myocardium that was previously excited
Reentry
61
A pathologic relationship exists between AP conduction velocity and refractoriness that allows for the formation of a
Self-sustained electrical circuit
62
Can spin-off from the circuit and depolarize regions of surrounding myocardium
-Often come from regions of superior and inferior pulmonary veins
Impulses
63
These rogue electrical signals travel in any manner of reentry type circuits so that we see resulting random islets of
Fibrillation
64
Is essentially atrial myocardial electrical chaos
A fib
65
This disruption results in very rapid bursts of electrical activity that induces small regions of the atrial myocardium to
Depolarize
66
The ensuing multiple wandering reentry wavelets collide and cause haphazard blocks and/or augmentations in
Atrial conduction
67
Hence, no coordinated, uniform atrial contractions
| occur; instead chaotic re-excitation occurs, and the atrial myocardium
Fibrillates
68
Rapid twitches or contractions of muscle fibrils, but not coordinated contraction of the entire muscle
Fibrillation
69
Without uniform atrial contraction (uniform depolarization) the ECG will show no
P wave
70
The absence of a P wave is a hallmark of
A fib
71
Furthermore, the random events of atrial electrical activity result in the formation of so-called
-waves of varying size, shape, and rythm within the ECG
Fibrillatory waves
72
Due to the unpredictable burts seen in A fib, the AV nodal conduction frequency is
Disrupted
73
During A fib, we can see fluctuations of AV nodal conduction frequency within a range of approximately
90-170 BPM
74
Collectively these abnormal signals are translated into an
Irregular ventricular rythm (supraventricular arrhythmia and supraventricular tachycardia (SVT)
75
The heart rate and pulse of a patient in A fib is described as
Irregularly irregular
-Evident in lead V5 of ECG
76
What are the 4 classifications of A fib?
1. ) Recurrent
2. ) Paroxysmal
3. ) Persistent
4. ) Permanent
77
Random episodes of A fib that self terminate
Recurrent A fib
78
Once sinus rythm is spontaneously restored, recurring episodes of A fib are identified as
Paroxysmal
79
A paroxysmal episode which does not spontaneously end is referred to as
Persistent A fib
80
Requires pharmacological or electrical stimulation (i.e. cardioversion) to restore normal sinus rythm
Persistent A Fib
81
If these interventions can not resolve the A fib, it is called
Permanent A fib
82
As a result of A fib, the atrial contribution to cardiac output is
Lost (which is about 20%)
83
Reduces ventricular filling time, and thus lowers cardiac output; this can explain the episodes of postural lightheadedness that patients can experience
Tachycardia
84
The serious risk associated with A fib in the development of an
Atrial thrombosus
85
An atrial thrombosus can form after approximately 48 hours from the onset of A fib and its eventual dislodgement causes a
Systemic arterial embolism
86
A systemic arterial embolism results in a
Pulmonary embolus or ischemic stroke
87
Characterized by wide-spread irregular contractions (fibrillations) of ventricular myocardium
-rapidly fatal if untreated
Ventricular fibrillation
88
Ventricular fibrilation can result from
Hypoxic ischemia, electrocution, and certain drugs
89
Often initiated by ventricular tachycardia in which multiple reentry wavelets chaotically excite the ventricular myocardium
Ventricular fibrillation
90
The cellular mechanism for V fib involves the stimulation of myocytes during the so-called vulnerable period that occurs during the
Down-slope of the T wave (end period of ventricular repolarization)
91
In order to cease ventricular fibrillation, electric current
| is applied to the heart in order to induce
Defibrillation
92
Causes the entire myocardium to undergo a brief period of refraction
-allows SA node to regain normal pacemaker control
Defibrillation
93
Results from a delay or block in conduction within the right or left branch of the bundle of His
-can be complete or incomplete as determined by changes in QRS duration
Bundle branch block (BBB)
94
As a result of the BBB, impulses must be relayed from the unaffected side to the blocked side via the
-causes a delay in conduction
Interventricular septum
95
In general, for an ECG, BBB will cause
Widened QRS and changes in the characteristics of the R waves in the right (RBBB) or left (LBBB) lateral leads
96
The most common of the ventricular arrhythmia, and are uncoordinated ventricular depolarizations which arise from an irritable focus within the ventricle
Premature ventricular contractions (PVC)
97
A PVC will show up on an ECG as
No P waves associated with an aberrant QRS complex
98
This arrhythmia is a result of an abnormal discharge from an ectopic ventricular focus
Ventricular tachycardia (Vtach)
99
Occurs when, for example, scarred myocardium can provide a platform for reentrant current enabling 3 or more consecutive contractions
PVC's
100
Within the ECG, ventricular tachycardia is evident by the presence of
Wide QRS complexes
101
Within the ECG, ventricular tachycardia is evident by the presence of wide QRS complexes which may be
Regular and rapid (monomorphic) or vary in shape and rythym (polymorphic)
