EKG Flashcards
(120 cards)
1
Q
Types of cardiac cells
A
- Pacemaker cells
- Electrical conducting cells
- Myocardial cells
2
Q
Pacemaker cells
A
SA node
AV node
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
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
5
Q
Cardiac conduction pathway
A
- Sinoatrial (SA) node
- Internodal fascicles
- Atrioventricular (AV) node
- Bundle of HIS
- Right Bundle Branch
- Left Bundle Branch
- Purkinje Fibers
6
Q
5 large boxes = ?? time
A
1 second
7
Q
300 large boxes = ?? time
A
1 minute
8
Q
P wave characteristics
A
Atrial depolarization
Normal duration <120 ms (3 small boxes)
9
Q
Upright P wave characteristics
A
Normal
Beat originated from SA node or atria and traveled antegrade (down the normal pathway)
10
Q
Inverted P wave characteristics
A
Beat originated in AV node
Depolarizes atria in retrograde
Junctional beats
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
12
Q
Narrow QRS complex
Absent or inverted P wave
A
Junctional rhythm
13
Q
Wide QRS complex
Absent P wave
A
Ventricular rhythm
14
Q
Absent P wave
Narrow QRS complex
Irregular rhythm
A
Afib
15
Q
Ventricular depolarization
A
QRS complex
Normal <120 ms
16
Q
Slow depolarization, likely coming from the ventricular myocardium
A
Wide QRS
17
Q
Potential causes of wide QRS complexes
A
- The myocardium gets irritated (common with pH imbalance, caffeine, stress, ischemia, electrolyte abnormality
- The ventricles must take over as the pacemaker
- Wolf Parkinson White Syndrome (WPW)
- RBBB/LBBB
18
Q
Ventricular repolarization
A
T wave
<5 mm height in leads I, II, III
19
Q
When would you see a U wave?
A
With hypokalemia
20
Q
The point at which the S wave returns to baseline
A
the J point
21
Q
Upward slurring of the Q wave, commonly seen with WPW syndrome
A
Delta wave
22
Q
J wave
A
“bump” on the S wave. Commonly seen with hypothermia
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
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
25
May cause prolonged QT
Zofran and Phenergan
26
Characteristics of PR segment
"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
27
Start and end of ST segment
Starts at the J point, ends at the start of the T wave
28
a heart beat that happens before it is expected to
premature beat
29
a heart beat that comes after a long pause
escape beat
30
What happens during systole?
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
31
What happens during diastole?
The heart relaxes, aortic valve closes, blood rushes into the coronary arteries to perfuse the heart
32
True/false: The faster the heart rate, the better coronary perfusion
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
33
True/false: Stroke volume is reduced when ventricular filling is reduced
True
34
Describe active vs passive ventricular filling
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
35
Heart conditions that can reduce ventricular filling
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)
36
Detects the electrical difference/voltage between two limbs
EKG leads
37
Provides a picture of the heart from a 0-180 degree angle
Lead I
38
Provides a picture of the heart from a 60 degree angle
Lead II
39
Provides a picture of the heart from a 120 degree angle
Lead III
40
Limitation of a 3 lead EKG
Not as sensitive for detecting myocardial ischemia in the L ventricle
41
Where is lead I located?
```
R arm (-) to L arm (+)
White to black
```
42
Where is lead II located?
```
R arm (-) to L foot (+)
White to red
```
43
Where is lead III located?
```
L arm (-) to L foot (+)
Black to red
```
44
The neutral/ground lead in a 5 lead EKG
Green
45
Precordial lead in a 5 lead EKG that makes it more sensitive to pick up myocardial ischemia in the L ventricle
Brown (V5)
46
Heart rate is faster during inspiration and slower during expiration
Irregular sinus rhythm
47
How does your HR increase during inspiration?
Intrathoracic pressure decreases and preload increases
48
How does your HR decrease during expiration?
Intrathoracic pressure increases and preload decreases
49
EKG description of sinus tachycardia
P wave present
| >100 bpm
50
Etiologies of sinus tachycardia
Hypovolemia/hypotension
| Pain/light anesthesia
51
Anesthetic concerns for sinus tach
Increased cardiac oxygen demand
Decrease cardiac oxygen supply
Possible hypovolemia
52
Treatment for sinus tachycardia
Fluids
Deepen anesthetic
Beta blocker
53
EKG description of sinus bradycardia
P wave present
| <60 bpm
54
Benefits of sinus bradycardia
1. Healthy patients that exercise regularly (typically have higher stroke volume)
2. Patients with CAD (increased oxygen supply, decreased oxygen demand)
55
Anesthetic concerns for bradycardia
1. Age of the patient (particularly kids)
2. Severity of bradycardia
3. How fast the heart rate drops
56
Treatment for sinus bradycardia
1. Robinul, atropine, epinephrine
| 2. Pacemaker (temporary transcutaneous pacing or permanent implantable pacemaker)
57
Slow, complex rhythms that precede asystole
Agonal rhythm
58
True/false: You should defibrillate patients in asystole
False! Perform CPR, administer Epinephrine and treat any reversible causes
59
EKG description of pulseless electrical activity (PEA)
EKG strip shows electrical activity but the patient has no pulse
60
Physiology of PEA
1. The heart does not contract
| 2. There is an insufficient cardiac output to generate a pulse and supply blood to the organs
61
Treatment for PEA
1. CPR
2. Epinephrine administration
3. Treat any reversible causes
NOT DEFIBRILLATION
62
Any heart beat that originates outside the SA node
Ectopy
63
Types of ectopy
1. Premature beats
2. Supraventricular ectopic rhythms
3. Escape beats
4. Ventricular ectopic rhythms
64
EKG description for PACs
1. Upright P wave
| 2. Normal/narrow QRS complex
65
Physiology of premature beats
The specific myocardium was irritated (atrial, junctional or ventricular) and decided to initiate a heartbeat prior to the signal from the SA node
66
Anesthetic concerns for premature beats
No concern unless they occur frequently due to less ventricular filling/low stroke volume/cardiac output
67
EKG description of PJC
Missing or inverted P wave
| Normal QRS complex
68
EKG description of PVC
No P wave
| Wide, "bizzare/different" QRS complex
69
Treatment of PVCs
1. Antiarrhythmics (lidocaine, amiodarone)
| 2. Robinul, atropine
70
EKG description of junctional escape beat
1. Inverted or absent P wave
2. Normal/narrow QRS complex
Occurs after a long pause
71
Physiology of escape beats
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
Anesthetic concerns with escape beats
If it occurs multiple times or pauses are prolonged, consider robinul/atropine/pacing
73
EKG description for ventricular escape beats
1. Long pause followed by wide QRS complex
| 2. No P wave
74
EKG description for aflutter (atrial flutter)
1. "Saw tooth pattern" 250-350 P waves/min
| 2. More P waves than QRS complexes
75
Physiology of aflutter
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
Anesthetic concerns for aflutter
1. Ventricular filling and cardiac output is reduced
2. Heart is burning more oxygen than normal
Needs evaluated by cardiologist first
77
Treatment for aflutter
1. Medications (Amiodarone, Sotalol, Digoxin)
| 2. Synchronized cardioversion
78
Difference between pacing and cardioversion
Pacing treats unstable slow rhythms while cardioversion/defibrillation treats unstable fast rhythms
79
EKG description of atrial fibrillation (afib)
No P waves
| Irregularly irregular rhythm
80
Physiology of afib
Atria are chaotically "quivering" up to 500 atrial impulses/min
81
Clinical implications of afib
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
Anesthetic concerns of afib
Only with acute onset
83
Treatments for afib
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
EKG description for junctional rhythm
Inverted or absent P wave
Normal QRS complex
Regular rate
85
Normal junctional rhythm (bpm)
40-60 bpm
86
Accelerated junctional rhythm (bpm)
60-100 bpm
87
Junctional tachycardia (bpm)
>100 bpm
88
Physiology of junctional rhythm
SA node isn't working, so the AV node takes over
| Atrial contraction is slightly delayed
89
Anesthetic concerns with junctional rhythms
Less ventricular filling, can be concerning with low BP
| May convert to sinus after Robinul
90
EKG description of SVT
1. HR >150 bpm
2. Normal QRS complex
3. Difficult to differentiate between sinus and junctional
91
Anesthetic concerns with SVT
Decreased ventricular filling. Should treat promptly
92
Treatment of SVT
1. Vagal maneuvers
2. Adenosine
3. Synchronized cardioversion
93
EKG description for ventricular escape rhythms
1. No P wave
2. Wide QRS complex
3. Slow heart rate <60 bpm
94
Physiology of ventricular escape rhythms
1. Both the SA node and AV node have failed
| 2. Ventricular myocardium starts initiating beats
95
Anesthetic concerns with idioventricular rhythm
1. There is no active ventricular filling
2. Low HR
3. Low cardiac output
96
Treatment for ventricular escape rhythm
1. Cardiac pacing
2. Potentially epinephrine if pt is unstable
AVOID LIDOCAINE (it suppresses ventricular ectopy)
97
Rates of idioventricular rhythm, accelerated idioventricular rhythm and vtach
1. <60 bpm for idioventricular rhythm
2. 60-100 bpm for accelerated idioventricular rhythm
3. >100 bpm for vtach
98
EKG description for monomorphic vtach
1. No P waves
2. Wide QRS complexes of the same shape
3. Heart rate >100 bpm
99
EKG description for polymorphic vtach (Torsades de Pointes)
R wave alternate in polarity and amplitude
| Prolonged QT interval
100
Physiology of vtach
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
Anesthetic concerns with vtach
Medical emergency!!!
| Requires immediate cardioversion/defibrillation
102
Treatment of vtach
Antiarrhythmics (amiodarone, lidocaine)
| Electrical cardioversion
103
EKG description for ventricular fibrillation
No real P waves or QRS complexes
| Scribbles
104
Physiology of Vfib
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
Anesthetic concerns with vfib
Immediate defibrillation!!!!
106
Treatment for vfib
1. Defibrillation
| 2. CPR until perfusing rhythm returns
107
EKG description for 1st degree AV block
Prolonged PR interval (>0.2s, or one large box)
108
Physiology of 1st degree AV block
For some reason conduction through AV node is slower than normal
109
Anesthetic concerns with 1st degree AV block
Not really
110
EKG description of 2nd degree AV block
```
Dropped QRS complexes
Type I (Wenckebach): Increasingly longer PR intervals
Type II: Constant PR interval
```
111
Physiology of Type I 2nd degree AV block
Partial block within the AV node that's bad enough to completely block some of the impulses going through
112
Physiology of Type II 2nd degree AV block
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
Anesthetic concerns with 2nd degree AV block
Yes, concerning. May require cardiac pacing
114
EKG description for 3rd degree AV block
P waves and QRS complexes are not associated with each other
| Slow ventricular rate (30-40bpm)
115
Physiology of 3rd degree AV block
Atria are contracting, but the AV node is blocked and no impulses are coming through
The ventricles must initiate their own beat
116
Clinical effects of complete heart block
- The atria may try to empty into full ventricles
- Ventricles may attempt to contract when empty
- Serious reduction in cardiac output
117
Treatment for complete heart block
1. Cardiac pacing
2. Epinephrine if pt is unstable
AVOID LIDOCAINE
118
Signs of ischemia/infarction
1. ST segment changes (depression is more ischemia, elevation is more infarction)
2. Abnormal T waves
3. Abnormal Q waves
119
Myocardial ischemia treatment
1. Increased oxygen supply
| 2. Decrease oxygen demand
120
Anesthetic concerns with signs of ischemia/infarction
Compare to old EKGs, if acute onset, very concerning
