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Cardiovascular and Pulmonary > Cardiovascular Systems Physiology and Pathophysiology III > Flashcards

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

  1. ) Frontal plane of the heart?
  2. ) Anterior and posterior directions?
A
  1. ) The 6 limb leads

2. ) The 6 precordial leads

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2
Q

What are the 6 limb leads?

A

Inferior: II, III, and aVF
Left lateral: I and aVL
Right lateral: aVR

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3
Q

When interpretting an ECG, what 5 things should be evaluated?

A
  1. ) Rate
  2. ) Rythm
  3. ) Electrical axis
  4. ) Intervals
  5. ) Segments
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4
Q

In which wave do the 1st and 2nd halves represent the right and left atrial depolarization respectively?

A

P wave

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5
Q

Atrial depolarization and the end of ventricular repolarization is represented by the

A

PR

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6
Q

The duration of ventricular activation is represented on an ECG by

A

QRS complex

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7
Q

Represents the end phase of ventricular depolarization in an ECG

A

S wave

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8
Q

In an ECG, the end of ventricular depolarization and the beginning of ventricular repolarization is signified by the

A

ST segment

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9
Q

In an ECG, ventricular repolarization is signified by the

A

T wave

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10
Q

The isoelectric line of the ECG. Represents the electrically silent myocardium

A

TP

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11
Q

The preponderant direction of current during ventricular depolarization

A

Cardiac electrical axis

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12
Q

Collectively, leads I, II, and III enable construction of

A

Einthoven’s triangle

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13
Q

A configuration translating into a geometric representation that indicates the electrical axis of the heart

A

Einthoven’s triangle

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14
Q

The major vector of ventricular activation (i.e. depolarization)

A

The QRS axis

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15
Q

When viewing ECGs it is a good habit to determine the

net QRS voltages from leads

A

I, II, and aVF

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16
Q

The average cardiac electrical axis approximates 50-60 degrees, which means what for leads:

  1. ) I
  2. ) II
  3. ) aVF
A
  1. ) Positive
  2. ) Isoelectric (zero charge)
  3. ) Positive
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17
Q

An axis between 0- (-30º) is considered a

A

Normal varient

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18
Q

An axis between 0- (-30º) is considered a normal varient where leads

  1. ) I
  2. ) II
  3. ) aVF
A
  1. ) positive
  2. ) positive
  3. ) negative
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19
Q

An axis greater than 100º shows right axis deviation. What does this mean for leads

  1. ) I
  2. ) II
  3. ) aVF
A
  1. ) Negative
  2. ) Isoelectric
  3. ) Positive
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20
Q

An axis between -30º and -90º indicates left axis deviation. What does this mean for leads

  1. ) I
  2. ) II
  3. ) aVF
A
  1. ) Positive
  2. ) Negative
  3. ) Negative
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21
Q

Some of the more common reasons for axis deviation are

A

Right or left ventricular hypertrophy and pregnancy

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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

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23
Q

An alteration of the normal sinus rythym which guides coordinated myocyte contractility

A

Arrythmia

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24
Q

Recall that cardiac depolarization and repolarization are substantially controlled by

A

Ca2+ and K+ respectively

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25
Q

What are some features of Hyperkalemia?

A

Tall peaked and narrow based T and QT interval shortening

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26
Q

Primary AV block, flattening/ widening P, ST depression, and QRS widening are features of

A

Hyperkalemia

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27
Q

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

A

Severe Hyperkalemia

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28
Q

Shows ST depression, flattened T, increased P duration and amplitude, and prolonged QT interval

A

Hypokalemia

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29
Q

Shortened ST segment, PR prolongation, and normal P, QRS, and T

A

Hypercalcimia

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30
Q

What are some features of an ECG of hypocalcemia?

A

Prolonged ST interval

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31
Q

Results from increased generation of SA node AP

A

Tachycardia

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32
Q

Results from decreased generation of SA node AP

A

Brachycardia

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33
Q

Strictly speaking, sinus rhythm refers only to the

A

Atrium

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34
Q

A normally conducting SA node and atrium with complete heart block is strictly speaking

A

Sinus rythym

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35
Q

Atrial depolarization follows SA nodal firing. These are shown by the

A

P wave

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36
Q

Note that the P wave is functionally split into two segments. What do the following represent?

  1. ) The 1st half
  2. ) The 2nd half
A
  1. ) Right atrial depolarization

2. ) Left atrial depolarization

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37
Q

Episodes of tachycardia (HR > 100 bpm) are represented on the ECG by a severely decreased

A

P-P interval

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38
Q

Causes an increased P-P interval on an ECG

A

Sinus Brachycardia (HR < 60 BPM)

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39
Q

Causes a severely decreased P-P interval on an ECG

A

Sinus tachycardia (HR > 120 BPM)

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40
Q

Niether sinus tachycardia or sinus brachycardia substantially alter the physical properties of the

A

P wave or QRS complex

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41
Q

Rapid and regular atrial activity

A

Atrial Flutter

42
Q

Atrial flutter is reflected within the ECG as rapid atrial activity, with P waves exhibiting a so-called

A

Saw-tooth appearance

43
Q

Atrial flutter can result from reentry, and is usually generated from a large fixed region, which can often times be mapped to near the

A

Tricuspid valve annulus

44
Q

Atrial beats can reach 300 BPM, however the relay of all atrial impulses to the ventricles is impeded by

A

AV delay

45
Q

Malfunctions in the AV node are referred to as

A

Heart Block or Nodal Block

46
Q

Results in a prolonged P-R interval due to an abnormally lengthened conduction time within the AV node and/or the bundle of His

A

Primary heart block

47
Q

There is one atrial to ventricular conduction with

A

Primary heart block

48
Q

Results from an increased refractory period of AV nodal tissue or His system, thus making it less excitable

A

Second degree heart block

49
Q

During secondary heart block, not every impulse is

relayed through the AV node and/or His to the ventricles; thus we see a

A

P : QRS ration greater than 1:1

50
Q

Caused when no atrial impulses reach the ventricle

A

Third degree heart block (AKA complete heart block or AV dissociation)

51
Q

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

A

Escape rythym

52
Q

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

A

AV junction (called the junctional escape)

53
Q

Result in an inherently unstable and slow ventricular escape rhythm consisting of about 30-40 bpm

A

Blocks distal to the AV node

54
Q

The ECG during a third degree heart block can be distinguished by

A

Multiple P waves and superimposed QRS complexes

55
Q

Used to re-establish the normal pattern of cardiac electrical activity resulting from third degree heart
block

A

Implantable pacemakers

56
Q

An arrhythmia that prevents effectual contraction of atrial and/or ventricular myocardium

A

Fibrillation

57
Q

May represent a reentry phenomenon in which a reentry loop fragments into multiple irregular circuits within the myocardium

A

Fibrillation

58
Q

Fibrillation is characterized by non-coordinated and inefficient

A

Myocardial contractions

59
Q

The most common cardiac arrythmia disorder

A

Atrial fibrillation (A Fib)

60
Q

The abnormal electrical re-excitation of a region of the atrial myocardium that was previously excited

A

Reentry

61
Q

A pathologic relationship exists between AP conduction velocity and refractoriness that allows for the formation of a

A

Self-sustained electrical circuit

62
Q

Can spin-off from the circuit and depolarize regions of surrounding myocardium

-Often come from regions of superior and inferior pulmonary veins

A

Impulses

63
Q

These rogue electrical signals travel in any manner of reentry type circuits so that we see resulting random islets of

A

Fibrillation

64
Q

Is essentially atrial myocardial electrical chaos

A

A fib

65
Q

This disruption results in very rapid bursts of electrical activity that induces small regions of the atrial myocardium to

A

Depolarize

66
Q

The ensuing multiple wandering reentry wavelets collide and cause haphazard blocks and/or augmentations in

A

Atrial conduction

67
Q

Hence, no coordinated, uniform atrial contractions

occur; instead chaotic re-excitation occurs, and the atrial myocardium

A

Fibrillates

68
Q

Rapid twitches or contractions of muscle fibrils, but not coordinated contraction of the entire muscle

A

Fibrillation

69
Q

Without uniform atrial contraction (uniform depolarization) the ECG will show no

A

P wave

70
Q

The absence of a P wave is a hallmark of

A

A fib

71
Q

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

A

Fibrillatory waves

72
Q

Due to the unpredictable burts seen in A fib, the AV nodal conduction frequency is

A

Disrupted

73
Q

During A fib, we can see fluctuations of AV nodal conduction frequency within a range of approximately

A

90-170 BPM

74
Q

Collectively these abnormal signals are translated into an

A

Irregular ventricular rythm (supraventricular arrhythmia and supraventricular tachycardia (SVT)

75
Q

The heart rate and pulse of a patient in A fib is described as

A

Irregularly irregular

-Evident in lead V5 of ECG

76
Q

What are the 4 classifications of A fib?

A
  1. ) Recurrent
  2. ) Paroxysmal
  3. ) Persistent
  4. ) Permanent
77
Q

Random episodes of A fib that self terminate

A

Recurrent A fib

78
Q

Once sinus rythm is spontaneously restored, recurring episodes of A fib are identified as

A

Paroxysmal

79
Q

A paroxysmal episode which does not spontaneously end is referred to as

A

Persistent A fib

80
Q

Requires pharmacological or electrical stimulation (i.e. cardioversion) to restore normal sinus rythm

A

Persistent A Fib

81
Q

If these interventions can not resolve the A fib, it is called

A

Permanent A fib

82
Q

As a result of A fib, the atrial contribution to cardiac output is

A

Lost (which is about 20%)

83
Q

Reduces ventricular filling time, and thus lowers cardiac output; this can explain the episodes of postural lightheadedness that patients can experience

A

Tachycardia

84
Q

The serious risk associated with A fib in the development of an

A

Atrial thrombosus

85
Q

An atrial thrombosus can form after approximately 48 hours from the onset of A fib and its eventual dislodgement causes a

A

Systemic arterial embolism

86
Q

A systemic arterial embolism results in a

A

Pulmonary embolus or ischemic stroke

87
Q

Characterized by wide-spread irregular contractions (fibrillations) of ventricular myocardium

-rapidly fatal if untreated

A

Ventricular fibrillation

88
Q

Ventricular fibrilation can result from

A

Hypoxic ischemia, electrocution, and certain drugs

89
Q

Often initiated by ventricular tachycardia in which multiple reentry wavelets chaotically excite the ventricular myocardium

A

Ventricular fibrillation

90
Q

The cellular mechanism for V fib involves the stimulation of myocytes during the so-called vulnerable period that occurs during the

A

Down-slope of the T wave (end period of ventricular repolarization)

91
Q

In order to cease ventricular fibrillation, electric current

is applied to the heart in order to induce

A

Defibrillation

92
Q

Causes the entire myocardium to undergo a brief period of refraction

-allows SA node to regain normal pacemaker control

A

Defibrillation

93
Q

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

A

Bundle branch block (BBB)

94
Q

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

A

Interventricular septum

95
Q

In general, for an ECG, BBB will cause

A

Widened QRS and changes in the characteristics of the R waves in the right (RBBB) or left (LBBB) lateral leads

96
Q

The most common of the ventricular arrhythmia, and are uncoordinated ventricular depolarizations which arise from an irritable focus within the ventricle

A

Premature ventricular contractions (PVC)

97
Q

A PVC will show up on an ECG as

A

No P waves associated with an aberrant QRS complex

98
Q

This arrhythmia is a result of an abnormal discharge from an ectopic ventricular focus

A

Ventricular tachycardia (Vtach)

99
Q

Occurs when, for example, scarred myocardium can provide a platform for reentrant current enabling 3 or more consecutive contractions

A

PVC’s

100
Q

Within the ECG, ventricular tachycardia is evident by the presence of

A

Wide QRS complexes

101
Q

Within the ECG, ventricular tachycardia is evident by the presence of wide QRS complexes which may be

A

Regular and rapid (monomorphic) or vary in shape and rythym (polymorphic)

Cardiovascular and Pulmonary (25 decks)

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