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Patient Monitoring/Instrumentation & SIM > EKG > Flashcards

EKG Flashcards

1
Q

Types of cardiac cells

A
  1. Pacemaker cells
  2. Electrical conducting cells
  3. Myocardial cells
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2
Q

Pacemaker cells

A

SA node

AV node

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3
Q

Electrical conducting cells

A 
*Transmit currents quickly and effectively
Anterior, posterior, middle fascicles
Bundle of HIS
Left Bundle Branch
Right Bundle Branch
Purkinje Fibers
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4
Q

Characteristics of myocardial cells

A

Transmits current slow
Contract and pump blood out of heart
Can initiate heart beats if the SA node fails or if the myocardium gets irritated

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5
Q

Cardiac conduction pathway

A
  1. Sinoatrial (SA) node
  2. Internodal fascicles
  3. Atrioventricular (AV) node
  4. Bundle of HIS
  5. Right Bundle Branch
  6. Left Bundle Branch
  7. Purkinje Fibers
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6
Q

5 large boxes = ?? time

A

1 second

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7
Q

300 large boxes = ?? time

A

1 minute

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8
Q

P wave characteristics

A

Atrial depolarization

Normal duration <120 ms (3 small boxes)

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9
Q

Upright P wave characteristics

A

Normal

Beat originated from SA node or atria and traveled antegrade (down the normal pathway)

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10
Q

Inverted P wave characteristics

A

Beat originated in AV node
Depolarizes atria in retrograde
Junctional beats

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11
Q

Absent P wave characteristics

A

Originates in the ventricular myocardium
Only the ventricles depolarize
Can occur in afib or junctional rhythm as well

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12
Q

Narrow QRS complex

Absent or inverted P wave

A

Junctional rhythm

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13
Q

Wide QRS complex

Absent P wave

A

Ventricular rhythm

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14
Q

Absent P wave
Narrow QRS complex
Irregular rhythm

A

Afib

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15
Q

Ventricular depolarization

A

QRS complex

Normal <120 ms

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16
Q

Slow depolarization, likely coming from the ventricular myocardium

A

Wide QRS

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17
Q

Potential causes of wide QRS complexes

A
  1. The myocardium gets irritated (common with pH imbalance, caffeine, stress, ischemia, electrolyte abnormality
  2. The ventricles must take over as the pacemaker
  3. Wolf Parkinson White Syndrome (WPW)
  4. RBBB/LBBB
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18
Q

Ventricular repolarization

A

T wave

<5 mm height in leads I, II, III

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19
Q

When would you see a U wave?

A

With hypokalemia

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20
Q

The point at which the S wave returns to baseline

A

the J point

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21
Q

Upward slurring of the Q wave, commonly seen with WPW syndrome

A

Delta wave

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22
Q

J wave

A

“bump” on the S wave. Commonly seen with hypothermia

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23
Q

Normal PR interval start, end and time

A

Starts at the beginning of the P wave and ends at the start of the Q wave
120-200 ms

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24
Q

Normal QT interval start, end and time

A

Starts at the Q wave, ends at the end of the T wave

400-440 ms

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25
Q

May cause prolonged QT

A

Zofran and Phenergan

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26
Q

Characteristics of PR segment

A

“pause” at the end of atrial depolarization to allow blood to fill the ventricles
starts at the end of the P wave and ends at the beginning of the Q wave

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27
Q

Start and end of ST segment

A

Starts at the J point, ends at the start of the T wave

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28
Q

a heart beat that happens before it is expected to

A

premature beat

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29
Q

a heart beat that comes after a long pause

A

escape beat

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30
Q

What happens during systole?

A

Heart contraction
Aortic valve opens and the valve leaflets close off the blood supply to the coronary arteries
Blood is ejected from the L ventricle and organs are perfused

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31
Q

What happens during diastole?

A

The heart relaxes, aortic valve closes, blood rushes into the coronary arteries to perfuse the heart

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32
Q

True/false: The faster the heart rate, the better coronary perfusion

A

False. The slower the heart rate, the longer the time that the coronary arteries are open, the greater the diastolic filling time and the better coronary perfusion

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33
Q

True/false: Stroke volume is reduced when ventricular filling is reduced

A

True

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34
Q

Describe active vs passive ventricular filling

A

Active filling occurs when the atria contract and force blood into the ventricles
Passive filling is when the atria don’t contract and the volume entering the ventricles is much lower

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35
Q

Heart conditions that can reduce ventricular filling

A
  1. When a heart beat occurs without atrial contraction (No P wave); afib, escape ventricular rhythm
  2. When there is a premature heartbeat (PAC, PVC)
  3. Rapid HR (SVT or Vtach)
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36
Q

Detects the electrical difference/voltage between two limbs

A

EKG leads

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37
Q

Provides a picture of the heart from a 0-180 degree angle

A

Lead I

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38
Q

Provides a picture of the heart from a 60 degree angle

A

Lead II

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39
Q

Provides a picture of the heart from a 120 degree angle

A

Lead III

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40
Q

Limitation of a 3 lead EKG

A

Not as sensitive for detecting myocardial ischemia in the L ventricle

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41
Q

Where is lead I located?

A 
R arm (-) to L arm (+)
White to black
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42
Q

Where is lead II located?

A 
R arm (-) to L foot (+)
White to red
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43
Q

Where is lead III located?

A 
L arm (-) to L foot (+)
Black to red
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44
Q

The neutral/ground lead in a 5 lead EKG

A

Green

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45
Q

Precordial lead in a 5 lead EKG that makes it more sensitive to pick up myocardial ischemia in the L ventricle

A

Brown (V5)

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46
Q

Heart rate is faster during inspiration and slower during expiration

A

Irregular sinus rhythm

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47
Q

How does your HR increase during inspiration?

A

Intrathoracic pressure decreases and preload increases

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48
Q

How does your HR decrease during expiration?

A

Intrathoracic pressure increases and preload decreases

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49
Q

EKG description of sinus tachycardia

A

P wave present

>100 bpm

50
Q

Etiologies of sinus tachycardia

A

Hypovolemia/hypotension

Pain/light anesthesia

51
Q

Anesthetic concerns for sinus tach

A

Increased cardiac oxygen demand
Decrease cardiac oxygen supply
Possible hypovolemia

52
Q

Treatment for sinus tachycardia

A

Fluids
Deepen anesthetic
Beta blocker

53
Q

EKG description of sinus bradycardia

A

P wave present

<60 bpm

54
Q

Benefits of sinus bradycardia

A
  1. Healthy patients that exercise regularly (typically have higher stroke volume)
  2. Patients with CAD (increased oxygen supply, decreased oxygen demand)
55
Q

Anesthetic concerns for bradycardia

A
  1. Age of the patient (particularly kids)
  2. Severity of bradycardia
  3. How fast the heart rate drops
56
Q

Treatment for sinus bradycardia

A
  1. Robinul, atropine, epinephrine

2. Pacemaker (temporary transcutaneous pacing or permanent implantable pacemaker)

57
Q

Slow, complex rhythms that precede asystole

A

Agonal rhythm

58
Q

True/false: You should defibrillate patients in asystole

A

False! Perform CPR, administer Epinephrine and treat any reversible causes

59
Q

EKG description of pulseless electrical activity (PEA)

A

EKG strip shows electrical activity but the patient has no pulse

60
Q

Physiology of PEA

A
  1. The heart does not contract

2. There is an insufficient cardiac output to generate a pulse and supply blood to the organs

61
Q

Treatment for PEA

A
  1. CPR
  2. Epinephrine administration
  3. Treat any reversible causes
    NOT DEFIBRILLATION
62
Q

Any heart beat that originates outside the SA node

A

Ectopy

63
Q

Types of ectopy

A
  1. Premature beats
  2. Supraventricular ectopic rhythms
  3. Escape beats
  4. Ventricular ectopic rhythms
64
Q

EKG description for PACs

A
  1. Upright P wave

2. Normal/narrow QRS complex

65
Q

Physiology of premature beats

A

The specific myocardium was irritated (atrial, junctional or ventricular) and decided to initiate a heartbeat prior to the signal from the SA node

66
Q

Anesthetic concerns for premature beats

A

No concern unless they occur frequently due to less ventricular filling/low stroke volume/cardiac output

67
Q

EKG description of PJC

A

Missing or inverted P wave

Normal QRS complex

68
Q

EKG description of PVC

A

No P wave

Wide, “bizzare/different” QRS complex

69
Q

Treatment of PVCs

A
  1. Antiarrhythmics (lidocaine, amiodarone)

2. Robinul, atropine

70
Q

EKG description of junctional escape beat

A
  1. Inverted or absent P wave
  2. Normal/narrow QRS complex
    Occurs after a long pause
71
Q

Physiology of escape beats

A

SA node fails temporarily, atrial, AV or ventricular nodes jump in for one beat before the SA node starts working again
Atrial will take over first, then AV, then ventricular

72
Q

Anesthetic concerns with escape beats

A

If it occurs multiple times or pauses are prolonged, consider robinul/atropine/pacing

73
Q

EKG description for ventricular escape beats

A
  1. Long pause followed by wide QRS complex

2. No P wave

74
Q

EKG description for aflutter (atrial flutter)

A
  1. “Saw tooth pattern” 250-350 P waves/min

2. More P waves than QRS complexes

75
Q

Physiology of aflutter

A

Atrial myocardium is contraction regularly at 250-350 times/min
Causes decreased ventricular filling and decreased cardiac output
AV node blocks impulses to control heart rate, leading to ventricular rate being slower than atrial rate

76
Q

Anesthetic concerns for aflutter

A
  1. Ventricular filling and cardiac output is reduced
  2. Heart is burning more oxygen than normal
    Needs evaluated by cardiologist first
77
Q

Treatment for aflutter

A
  1. Medications (Amiodarone, Sotalol, Digoxin)

2. Synchronized cardioversion

78
Q

Difference between pacing and cardioversion

A

Pacing treats unstable slow rhythms while cardioversion/defibrillation treats unstable fast rhythms

79
Q

EKG description of atrial fibrillation (afib)

A

No P waves

Irregularly irregular rhythm

80
Q

Physiology of afib

A

Atria are chaotically “quivering” up to 500 atrial impulses/min

81
Q

Clinical implications of afib

A
  1. Risk of clot formation in L atrium increases

2. Cardiac output can be decreased by 25-30% and can be decreased even more if ventricular rate is too fast

82
Q

Anesthetic concerns of afib

A

Only with acute onset

83
Q

Treatments for afib

A

Synchronized cardioversion
Medications (adenosine)
Blood thinners to prevent clots (if afib has been present for more than 2 days, they need anticoagulation for 3 weeks before cardioversion and for 4 weeks after)

84
Q

EKG description for junctional rhythm

A

Inverted or absent P wave
Normal QRS complex
Regular rate

85
Q

Normal junctional rhythm (bpm)

A

40-60 bpm

86
Q

Accelerated junctional rhythm (bpm)

A

60-100 bpm

87
Q

Junctional tachycardia (bpm)

A

> 100 bpm

88
Q

Physiology of junctional rhythm

A

SA node isn’t working, so the AV node takes over

Atrial contraction is slightly delayed

89
Q

Anesthetic concerns with junctional rhythms

A

Less ventricular filling, can be concerning with low BP

May convert to sinus after Robinul

90
Q

EKG description of SVT

A
  1. HR >150 bpm
  2. Normal QRS complex
  3. Difficult to differentiate between sinus and junctional
91
Q

Anesthetic concerns with SVT

A

Decreased ventricular filling. Should treat promptly

92
Q

Treatment of SVT

A
  1. Vagal maneuvers
  2. Adenosine
  3. Synchronized cardioversion
93
Q

EKG description for ventricular escape rhythms

A
  1. No P wave
  2. Wide QRS complex
  3. Slow heart rate <60 bpm
94
Q

Physiology of ventricular escape rhythms

A
  1. Both the SA node and AV node have failed

2. Ventricular myocardium starts initiating beats

95
Q

Anesthetic concerns with idioventricular rhythm

A
  1. There is no active ventricular filling
  2. Low HR
  3. Low cardiac output
96
Q

Treatment for ventricular escape rhythm

A
  1. Cardiac pacing
  2. Potentially epinephrine if pt is unstable
    AVOID LIDOCAINE (it suppresses ventricular ectopy)
97
Q

Rates of idioventricular rhythm, accelerated idioventricular rhythm and vtach

A
  1. <60 bpm for idioventricular rhythm
  2. 60-100 bpm for accelerated idioventricular rhythm
  3. > 100 bpm for vtach
98
Q

EKG description for monomorphic vtach

A
  1. No P waves
  2. Wide QRS complexes of the same shape
  3. Heart rate >100 bpm
99
Q

EKG description for polymorphic vtach (Torsades de Pointes)

A

R wave alternate in polarity and amplitude

Prolonged QT interval

100
Q

Physiology of vtach

A

Ventricular myocardium is initiating beats at a rapid rate, which leads to:

  1. High oxygen consumption
  2. Minimal ventricular filling (may or may not produce pulses)
101
Q

Anesthetic concerns with vtach

A

Medical emergency!!!

Requires immediate cardioversion/defibrillation

102
Q

Treatment of vtach

A

Antiarrhythmics (amiodarone, lidocaine)

Electrical cardioversion

103
Q

EKG description for ventricular fibrillation

A

No real P waves or QRS complexes

Scribbles

104
Q

Physiology of Vfib

A

Ventricles are not contracting, only quivering at a rapid rate

  1. Heart is consuming a lot of oxygen
  2. There is no pulse or cardiac output
105
Q

Anesthetic concerns with vfib

A

Immediate defibrillation!!!!

106
Q

Treatment for vfib

A
  1. Defibrillation

2. CPR until perfusing rhythm returns

107
Q

EKG description for 1st degree AV block

A

Prolonged PR interval (>0.2s, or one large box)

108
Q

Physiology of 1st degree AV block

A

For some reason conduction through AV node is slower than normal

109
Q

Anesthetic concerns with 1st degree AV block

A

Not really

110
Q

EKG description of 2nd degree AV block

A 
Dropped QRS complexes
Type I (Wenckebach): Increasingly longer PR intervals
Type II: Constant PR interval
111
Q

Physiology of Type I 2nd degree AV block

A

Partial block within the AV node that’s bad enough to completely block some of the impulses going through

112
Q

Physiology of Type II 2nd degree AV block

A

A block below the AV node (within the Bundle of His or the bundle branches) that’s bad enough to completely block the impulses

113
Q

Anesthetic concerns with 2nd degree AV block

A

Yes, concerning. May require cardiac pacing

114
Q

EKG description for 3rd degree AV block

A

P waves and QRS complexes are not associated with each other

Slow ventricular rate (30-40bpm)

115
Q

Physiology of 3rd degree AV block

A

Atria are contracting, but the AV node is blocked and no impulses are coming through
The ventricles must initiate their own beat

116
Q

Clinical effects of complete heart block

A
  • The atria may try to empty into full ventricles
  • Ventricles may attempt to contract when empty
  • Serious reduction in cardiac output
117
Q

Treatment for complete heart block

A
  1. Cardiac pacing
  2. Epinephrine if pt is unstable
    AVOID LIDOCAINE
118
Q

Signs of ischemia/infarction

A
  1. ST segment changes (depression is more ischemia, elevation is more infarction)
  2. Abnormal T waves
  3. Abnormal Q waves
119
Q

Myocardial ischemia treatment

A
  1. Increased oxygen supply

2. Decrease oxygen demand

120
Q

Anesthetic concerns with signs of ischemia/infarction

A

Compare to old EKGs, if acute onset, very concerning

Patient Monitoring/Instrumentation & SIM (12 decks)

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