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Cardiopulmonary > Electrocardiography > Flashcards

Electrocardiography Flashcards

1
Q

What are the 3 unique properties of cardiac muscle cells

A
  • Automaticity: ability to discharge an electrical stimulus w/o stimulation from a nerve
  • Rhythmicity: regularity of pacemaking activity
  • Conductivity: the ability to spread impulses to adjoining cells very quickly
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2
Q

ECG represents electrical impulses of the heart and reflects activity of 4 types of myocytes

A
  • Typical working myocytes: respond to electrical stimulus to contract & pump the blood
  • Nodal: have the highest rate of rhythmicity but slow impulse conduction rates
  • Transitional: conduct impulses 2x as fast as nodal cells
  • Purkinji cells: have a low rate of rhythmicity yet a high rate of conductivity
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3
Q

What occurs when the electrical impulse is generated

A
  • Potassium (K+) is prominent on the inside of the cell & sodium (Na+) on the outside
  • Sodium ions flow inward (fast channel)
  • Potassium ions start to flow outward (slow channel)
  • As the cell becomes positive on the inside/interior the myocardial cells are stimulated to contract
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4
Q

Define depolarization

A
  • Depolarization: electrical stimulation of specialized cells that causes contraction
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5
Q

Define repolarization

A
  • Repolarization: cells return to a negative interior and a positive exterior, and muscle relaxation occurs.
  • Begins when the potassium ion flow outward exceeds the sodium flow inward
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6
Q

Describe sympathetic and parasympathetic impact on the heart

A
  • Sympathetic: increases HR, conduction velocity throughout AV node, contractility, & irritability; norepinephrine and epinephrine release
  • Parasympathetic: general inhibitor on the rate of impulse formation & conduction velocity; acetylcholine release; Vagus nerve
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7
Q

Conduction system pathway through the heart

A
  • Electrical pulse initiated in the SA node in right atrium -> internodal pathways
  • Travels to the left atrium via the Bachmann bundle
  • P wave on ECG = atrial depolarization
  • Travels to AV node; atrial kick = PR interval on ECG
  • Travels to His bundle and bundle branches
  • Travels to Purkinje fibers, stimulating contraction; ventricular depolarization = QRS complex on ECG
  • Repolarization= ST segment phase of ECG
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8
Q

Describe the 3 internal tracts

A
  • Bachman (b/w R & L atrium, may be implicated in AFib)
  • Wenkebach (middle)
  • Thorel (posterior)
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9
Q

A single-lead tracing (rhythm strip) is assessed for ______________, _________, and presence of ______________.

A
  • Heart rate
  • Rhythm
  • Arrhythmias
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10
Q

If hypertrophy, ischemia, or infarction is suspected, a ________ ECG should be obtained.

A
  • 12 lead
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11
Q

Twelve-lead ECG assesses the following elements

A
  • Heart rate
  • Heart rhythm
  • Hypertrophy
  • Ischemia and/or infarction
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12
Q

Heart rate on ECG is determined by

A
  • Six-second tracing
  • R wave measurement
  • Counting boxes
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13
Q

Describe how to determine HR when counting boxes on ECG

A
  • Find an R wave
  • Count off 300, 150, 100, 75, 60, & 50 for each black line that follows until the next R wave falls
  • Take the difference between the two numbers the 2nd R wave follows between and divide by 5
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14
Q

How can you determine heart rate using the QRS Complexes

A
  • On a 6 second strip
  • Count the number of QRS Complexes shown
  • Multiply by 10
  • Gives you the BPM
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15
Q

Single-lead monitoring can accurately assess only ____ and ______.
It cannot diagnose _________ (ST-segment changes) and __________ (Q waves).

A
  • Rate and rhythm
  • Ischemia and infarction
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16
Q

Waveforms that represent depolarization of the myocardium are labeled

A
  • P
  • QRS
  • T
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17
Q

What questions should you ask yourself when assessing rhythm on ECG

A
  • Is there a P wave before each QRS Complex?
  • Are the QRS Complexes regular or irregular?
  • Best to check lead II on 12-lead ECG
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18
Q

What is the systematic approach to assess rate and rhythm

A
  • Evaluate the P wave. (Is it normal and upright, and is there a P wave before every QRS? Do all the P waves look alike?)
    Evaluate the PR interval. (Normal duration is 0.12–0.20 seconds.)
  • Evaluate the QRS complex. (Do all QRS complexes look alike?)
  • Evaluate the QRS interval. (Normal duration is 0.06–0.10 seconds. >0.12 seconds is abnormal)
  • Evaluate the QT interval. (Normal is <0.45 sec, if prolonged risk for arrhythmia is increased)
  • Evaluate the T wave. (Is it upright and normal in appearance?)
  • Evaluate the R to R wave interval. (Is it regular?)
  • Evaluate the heart rate (6-second strip if regular rhythm; normal rate is 60–100 beats per minute).
  • Observe the patient and evaluate any symptoms. (Do the observation, symptoms, or both correlate with the arrhythmia?)
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19
Q

How to assess intervals on ECG

A
  • QRS interval should be <.120 (more than 3 small boxes is concerning)
  • QTc should be <500
  • > 500 is risk for spontaneous torsades
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20
Q

Normal sinus rhythm (NSR) is normal cardiac rhythm indicated by the following

A
  • All P waves upright, normal, identical
  • P wave exists before every QRS complex
  • PR interval is between 0.12 and 0.2 second
  • QRS complexes are identical
  • QRS duration is between 0.06 to 0.10 second
  • RR interval is regular
  • Heart rate is between 60 and 100 bpm
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21
Q

Sinus bradycardia differs from NSR only by heart rate

A
  • HR <60 bpm
  • Individuals often asymptomatic
  • Common in athletes & individuals taking β-blocking medications
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22
Q

Sinus tachycardia differs from NSR only by rate

A
  • HR >100 bpm
  • Usually benign
  • Possible causes: exercise, anxiety, hypovolemia, anemia, fever or infection, medications (stimulants), and low cardiac output
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23
Q

Causes of bradycardia use the acronym DIE

A
  • Drugs
  • Ischemia
  • Electrolytes
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24
Q

What are the 5 common causes of tachycardia

A
  • Decreased O2 delivery; anemia, hypoxia, PE
  • Infection
  • Decreased volume: bleeding, dehydration
  • Drugs: stimulants or alcohol (ETOH) withdrawal
  • Adrenaline: pain, anxiety, nerves
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25
Q

Define Sinus arrhythmia

A
  • Irregularity in rhythm; impulse is initiated by the SA node, but with a phasic quickening and slowing of the impulse formation
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26
Q

Signs one ECG of a sinus arrhythmia

A
  • RR interval varies throughout
  • HR b/w 40-100 bpm
  • Respiratory type: related to respiratory cycle; rate increases with inspiration & decreases with expiration
  • Non-respiratory type: may occur with infection, medication (toxicity associated with digoxin and morphine), and fever
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27
Q

When does an artifact appear on ECG

A
  • Occurs when we are moving
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28
Q

Sinus pause or block occurs when

A
  • When the SA node fails to initiate an impulse, usually for only one cycle
  • Pause will be more than 2x the previous cardiac cycle of the underlying rhythm
  • Overall HR = 70
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29
Q

Define Wandering atrial pacemaker

A
  • Pacemaking in wandering pacemaker shifts from focus to focus, leading to irregular rhythm with an inconsistent pattern
30
Q

Signs on ECG of a Wandering atrial pacemaker

A
  • P waves are present but vary in configuration; each P-wave may look different
  • PR intervals may vary but are usually within normal width
  • QRS complexes are identical
  • RR intervals vary
  • HR is usually <100 bpm
31
Q

Define premature atrial complex

A
  • Defined as an ectopic focus in either atria that initiates an impulse before the next impulse is initiated by the SA node
  • Often a pause follows the premature atrial complex but it may be compensatory
32
Q

Define atrial tachycardia

A
  • 3 or more premature atrial complexes in a row
  • HR usually greater than 100 bpm; may be as fast as 200 bpm
33
Q

Define paroxysmal (supraventricular) atrial tachycardia

A
  • Sudden onset of atrial tachycardia or repetitive firing from an atrial focus
  • Underlying rhythm is usually NSR, followed by an episodic burst of atrial tachycardia that eventually returns to sinus rhythm
  • Patient may report “all of the sudden, my heart went racing”
34
Q

Describe atrial flutter

A
  • Usually there is more than one P wave for every QRS complex
  • RR intervals may vary depending on the atrial firing and number of P waves before each QRS complex
  • Rapid succession of atrial depolarization caused by an ectopic focus in the atria that depolarizes at a rate of 250 to 350 times per minute
  • P waves are called flutter waves and look identical to one another, with a “sawtooth” pattern
35
Q

Describe Atrial fibrillation (A-fib)

A
  • An erratic quivering or twitching of the atrial muscle caused by multiple ectopic foci in the atria that emit electrical impulses constantly
  • No true P waves and totally irregular rhythm
  • RR interval is characteristically defined as irregularly irregular
  • Rate varies but is called ventricular response.
  • If ventricular response is below 100, atrial fibrillation is considered controlled atrial fibrillation.
  • If ventricular response is more than 100, atrial fibrillation is considered uncontrolled. - If ventricular response is more than 120, this is considered rapid ventricular response (RVR) atrial fibrillation.
36
Q

Define premature junctional or nodal complexes arrhythmia

A
  • Premature impulses that arise from AV node or junctional tissue
  • AV node becomes irritated & initiates an early beat
  • Similar to premature atrial complexes, except an inverted, an absent, or a retrograde (wave that follows the QRS) P-wave is present
37
Q

Define junctional (or nodal) rhythm

A
  • AV junction takes over as pacemaker of heart
  • Rate b/w 40-60 bpm
  • Absence of P-waves before the QRS complex, but a retrograde P-wave may be identified
  • RR intervals are regular
  • If HR is too slow, symptoms of cardiac output decompensation can occur
38
Q

Describe nodal (junctional) tachycardia

A
  • AV junctional tissue acts as the pacemaker, but rate of discharge is accelerated.
  • P waves are absent, but retrograde P wave may be present
  • The RR interval is regular..
  • Rate is usually greater than 100 beats per minute.
39
Q

Describe a first-degree atrioventricular heart block

A
  • Impulse may be initiated in SA node but delayed on way to AV node, or initiated in the AV node itself, and the AV conduction time is prolonged.
  • PR interval is prolonged (>0.20 second/more than one big box)
40
Q

Describe a Second-degree atrioventricular block, type I (Wenckebach or Mobitz I heart block)

A
  • A benign, transient disturbance occurring high in the AV junction, preventing conduction of some impulses through the AV node.
  • Typical appearance: a progressive prolongation of the PR interval until finally one impulse is not conducted through to the ventricles (no QRS complex following a P wave).
  • The cycle then repeats itself.
  • Usually asymptomatic and requires no intervention in asymptomatic patients.
41
Q

Describe a Second-degree atrioventricular block, type II (Mobitz II)

A
  • A ratio of P waves to QRS complexes that is greater than 1:1 and may vary from 2 to 4 P waves for every QRS complex
  • Nonconduction of an impulse to the ventricles without a change in the PR interval
  • Site of the block usually below the bundle of His and may be a bilateral bundle branch block
  • Danger of progressing to complete heart block (third-degree AV block), a life-threatening condition
  • Transvenous pacemaker is usually indicated even in patients without symptoms.
  • The heart rate is usually below 100 and may be below 60 beats per minute.
42
Q

Describe a Third-degree atrioventricular block

A
  • Complete block in which all impulses that are initiated above the ventricle are not conducted to the ventricle
  • No relation between P waves and QRS complex because the atria are firing at their own inherent rate
  • Usual causes: acute myocardial infarction, digoxin toxicity, or degeneration of the conduction system
  • QRS duration may be wider than 0.10 seconds if the latent pacemaker is in the ventricles.
  • The heart rate depends on the latent ventricular pacemaker and may range from 30 to 50 beats per minute
  • Requires permanent pacemaker insertion, with atropine and isoproterenol injection or infusion in acute situation
  • Considered a medical emergency
43
Q

The characteristic ECG findings for right bundle branch block are as follows

A
  • QRS duration is greater than or equal to 120 milliseconds
  • In lead V1 and V2, there is an RSR` (“bunny ears”) in leads V1 and V2
  • In Leads 1 and V6, the S wave is of greater duration than the R wave, or the S wave is greater than 40 milliseconds
  • In Leads V5 and V6, there is a normal R wave peak time
  • In Lead V1, the R wave peak time is greater than 50 milliseconds
44
Q

Describe premature ventricular complexes (PVCs) arrhythmias

A
  • Ectopic focus originates an impulse from somewhere in one of the ventricles
  • Easily recognized on ECG—impulse originates in muscle of heart, and conduction is very slow
  • Absence of P waves in premature beat, with all other beats usually of sinus rhythm
  • QRS complex of premature beat is wide and bizarre
  • QRS duration of early beat is >0.10 second
    ST segment and T wave often slope in opposite direction from normal complexes
  • PVC is followed by a compensatory pause
45
Q

PVCs are considered serious or possibly life-threatening when they

A
  • Are paired together
  • Are multifocal in origin
  • Are more frequent than six per minute
  • Land directly on the T wave
  • Are present in triplets (considered to be V Tach) or more
46
Q

Describe ventricular tachycardia (V-tachy)

A
  • Series of three or more PVCs in a row.
  • P waves are absent.
  • QRS complexes are wide and bizarre.
  • Ventricular rate is 100 to 250 bpm.
  • Can be precursor to ventricular fibrillation.
  • Medical emergency: indicates increased irritability, with greatly diminished cardiac output and blood pressure
  • Can progress to ventricular fibrillation and death
47
Q

Define/describe Torsade de pointes

A
  • Unique configuration of ventricular tachycardia called the “twisting of the points”
  • Associated with prolonged Q-T interval (>0.5 second)
  • Identified only in individuals receiving antiarrhythmic therapy and for whom the medication is toxic.
  • Treatment is usually cardioversion.
48
Q

Describe ventricular fibrillation (V-fib)

A
  • Erratic quivering of ventricular muscle, resulting in no cardiac output
  • Usually the sequel to ventricular tachycardia
  • ECG shows grossly irregular up and down fluctuations of the baseline in an irregular zigzag pattern
49
Q

The three standard limb leads are defined as follows

A
  1. Lead I is created by making the left arm positive and the right arm negative. Its angle of orientation is 0°.
  2. Lead II is created by making the legs positive and the right arm negative. Its angle of orientation is 60°.
  3. Lead III is created by making the legs positive and the left arm negative. Its angle of orientation is 120°
50
Q

The three augmented limb leads are defined as follows

A
  1. Lead aVL is created by making the left arm positive and the other limbs negative. Its angle of orientation is −30°.
  2. Lead aVR is created by making the right arm positive and the other limbs negative. Its angle of orientation is −150°.
  3. Lead aVF is created by making the legs positive and the other limbs negative. Its angle of orientation is +90°, that is, toward the feet.
51
Q

Where are each of the precordial leads placed

A
  • V1 is placed in the fourth intercostal space to the right of the sternum.
  • V2 is placed in the fourth intercostal space to the left of the sternum.
  • V3 is placed between V2 and V4.
  • V4 is placed in the fifth intercostal space in the midclavicular line.
  • V5 is placed between V4 and V6.
  • V6 is placed in the fifth intercostal space in the midaxillary line.
52
Q

What region of the heart is each lead placed

A
  • V2, V3, V4 = Anterior
  • I, aVL, V5, V6 = Left lateral
  • II, II, aVF = Inferior
  • aVR, V1 = Right ventricular
53
Q

What vascular territories are each of the leads placed

A
  • Right coronary artery: II, III, aVF (may lead to blocks & bradycardia
  • Left anterior descending: V1-V6
  • Circumflex: I, aVL
54
Q

What do you see on ECG with right ventricular hypertrophy

A
  • V1 has a large R-wave and an S-wave smaller than the R-wave
  • R-wave becomes progressively smaller in the successive chest leads (V2, V3, V4, V5)
55
Q

What do you see on ECG with left ventricular hypertrophy

A
  • A deep S-wave occurs in V1 and a large R-wave in V5
  • If, when the depth of the S-wave in V1 is added to the height of the R-wave in V5 the resulting number is greater than 35, then L ventricular hypertrophy is present
56
Q

Define ischemia, infarction, and injury

A
  • Ischemia—reduced blood flow to myocardium from occlusion of coronary arteries
  • Infarction—cell death resulting from complete occlusion of coronary artery
  • Injury—indicates acuteness of the infarction
57
Q

Ischemia is demonstrated on 12-lead ECG with T wave __________ or ST segment ___________

A
  • Inversion and depression
  • T wave is sensitive indication of changes in repolarization activity within the ventricles
58
Q

During an acute STEMI, the EKG evolves through three stages

A
  1. T-wave peaking followed by T-wave inversion (A and B, below)
  2. ST-segment elevation (C)
  3. The appearance of new Q waves (D)
59
Q

T waves of myocardial ischemia are inverted ________________, whereas in most other circumstances, they are ____________, with a gentle ________slope and rapid ________slope

A
  • Symmetrically and asymmetric
  • Downslope and upslope
60
Q

When a region of myocardium dies it becomes electrically silent directing all electrical forces away from the area of infarction, therefore, an electrode overlying the infarct will record

A
  • A deep negative deflection (Q-wave)
  • aVR should not be considered when using Q-waves to look for possible infarction due to its orientation on the frontal plane
61
Q

How to identify a pathologic Q-wave on ECG

A
  • > 40ms (1 mm) wide (one small box)
  • > 2mm deep (2 small boxes)
  • > 25% of depth of QRS complex
  • Any Q-wave in leads V1-3
  • Present in 2 contiguous leads
62
Q

A significant Q-wave is defined as a minimum of

A
  • One small square wide and one-third the height of the QRS
63
Q

What ECG findings may indicate a subendocardial injury (signs of ischemia)

A
  • T-wave inversion
  • ST segment depression with no T-wave
64
Q

Describe a subendocardial infarction

A
  • An acute injury to the myocardial wall that does not extend through the full thickness of the ventricular wall; injury is only to the subendocardium
  • ECG shows ST-segment depression while the patient is at rest in the presence of chest pain or of suspected coronary ischemia.
  • Indicates that a transmural (also called STEMI or Q-wave) infarction could be pending
65
Q

Describe ST segment elevation

A
  • Elevation of the ST segment above the baseline when following part of an R wave indicates acute transmural injury.
  • In the presence of acute infarction, the ST segment elevates and then later returns to baseline (within 24–48 hours).
  • ST-segment elevation may also occur in the presence of a ventricular aneurysm (ballooning out of the ventricular wall).
66
Q

Describe normal, right, and left axis deviations

A
  • Normal = upward QRS in I and aVF
  • R axis deviation = downward QRS in I and upward QRS in aVF
  • L axis deviation = upward QRS in II and downward QRS in aVF
67
Q

What are the 2 main/serious causes of right axis deviation

A
  • Right ventricular hypertrophy
  • Lateral wall myocardial infarction
68
Q

What are the 2 main/serious causes of left axis deviation

A
  • Left ventricular hypertrophy
  • Inferior wall myocardial infarction
69
Q

Define acute pericarditis

A
  • Inflammation of the pericardial sac
  • Often a complication following myocardial infarction and/or open heart surgery
  • Pericardial pain is intense and can mimic angina
70
Q

What ECG changes can you see with acute pericarditis

A
  • Widespread distribution of ST-T changes without reciprocal depression distinguishes acute pericarditis from early myocardial infarction

Cardiopulmonary (18 decks)

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