Electrocardiographic Assessment Flashcards
1
Q
Be able to describe the specific ions responsible for cardiac contraction, conduction through the heart, repolarization of the heart and conduction through the AV node.
A
-
Phase 0: Rapid depolarization (inflow of Na+)
Phase 1: Partial repolarization (inwards Na+ current deactivated, outflow of K+) - Phase 2: Plateau (slow inward Ca++ current)
- Phase 3: Repolarization (Ca++ current inactivated, K+ outflow)
- Phase 4: Pacemaker potential (Slow Na+ inflow, slowing of K+ outflow) Autorhythmicity
Refractory period: Phases 1-3
2
Q
Which leads assess the heart in the frontal plane** versus the **horizontal plane?
A
- *Limb leads**: Frontal plane. Used for determining axis.
- *Precordial leads**: Horizontal plane.
3
Q
What is the concern with a prolonged QT?
A
Prolonged QT is associated with risk of developing Torsade’s de pointes – Ventricular fibrillation (deadly dysrhythmia)
4
Q
What are causes of prolonged QT?
A
Hypomagnesemia
Hypokalemia
Antidepressants
Antipsychotics
Antifungals
Antibiotics
Fluoroquinolone
Antiarrhytmics
Digitalis (Foxglove)
5
Q
What are automaticity foci?
A
Pacemaker sites within the heart. Helpful when SA node fails to pace or there is a block somewhere in the conduction system that does not allow electrical activity to be conducted.
6
Q
What are causes of increased foci irritability that increases one’s susceptibility to a dysrhythmia?
A
Sympathetic stimulation (drugs, caffeine, alcohol), inflammation, infection, dehydration/electrolyte abnormalities, stress, atrial enlargement/ventricular hypertrophy, beta blockers, calcium channel blockers
7
Q
What are symptoms of a dysrhythmia?
A
Palpitations, syncope, sudden death, angina
8
Q
What labs might one order to assess a dysrhythmia?
A
CBC, comprehensive metabolic panel, TSH
9
Q
What “imaging” might one consider to assess a dysrhythmia?
A
ECG, Holter monitor, ambulatory telemetry monitoring, implant event recorders, echo
10
Q
What is sudden cardiac death and what is the most common cause?
A
SCD is an unexpected death from cardiac causes either without symptoms or within 1-24 hours of symptom onset. Most common cause = Coronary artery disease (80-90%)
11
Q
What is the definition of bradycardia versus tachycardia?
A
- *Bradycardia**: <60 bpm
- *Tachycardia**: >100 bpm
12
Q
Describe the autonomic nervous system’s role in the regulation of heart rate, contractility, and irritability.
A
- *Sympathetic**:
- (NE) β-1 adrenergic receptors -> stimulate cardiac activity
- Also stimulates α-1 adrenergic receptors on arteries
- Affect on atria and junctional foci; minimal effect on ventricular foci
- *Parasympathetic**
- (vagus nerve) ACh -> cholinergic receptors -> inhibit cardiac activity
- Affect on atrial and junctional foci; no effect on ventricular foci
These two branches also have an effect on systemic arteries to control blood flow and pressure
13
Q
Be able to describe the theory behind the acetylcholine protocol, the supplements used, and in which patients it may be indicated and contraindicated for treatment.
A
MAP treatment is to give 2 essential nutrient precursors for endogenous production of Ach
(Choline + pantetheine)
- *Indications**: Any tachydysrhythmias, any ectopic dysrhythmias
- *Contraindicated**: Any bradydysrhythmias, any AV blocks
14
Q
Be able to describe the views of the heart from each of the leads.
A
15
Q
Define: Arrhythmia/dysrhythmia
A
Abnormal cardiac rhythm – any disturbance in rate, regularity, site or origin, or conduction of the cardiac electrical impulse
Arrhythmia: without rhythm
16
Q
What is the amplitude of a wave
A
Amplitude of a wave is the magnitude of deflection and is a measure of voltage
17
Q
Segment vs Interval
A
Segment: straight line between two waves
Interval: a straight line + at least one wave
18
Q
Sinus bradycardia symptoms
A
Asymptomatic
Presyncope/syncope
Unexplained falls
Fatigue
Exercise intolerance
19
Q
Sinus bradycardia labs
A
Comprehensive metabolic panel
TSH
20
Q
Sinus bradycardia pathophsiology
A
- Normal during sleep
- Medications (beta blockers, non-dihydropyridine calcium channel blockers, opioids)
- Hypothyroidism
- Anorexia nervosa
- Parasympathetic excess (athletes at rest)
21
Q
Sinus tachycardia sxs
A
Palpitations
22
Q
Sinus tachycardia pathophysiology
A
- Fever
- Hypovolemia
- Anemia
- Pain
- Anxiety
- Caffeine/nicotine
- Amphetamines
- Hyperthyroidism
- Sympathetic stimulation (exercise)
23
Q
Sinus tachycardia labs
A
- CBC
- Comprehensive metabolic panel
- TSH
24
Q
Sinus arrhythmia
A
Rate increases with inspiration and decreases with expiration
25
Name these rhythms:
Sinus tachycardia
Sinus bradycardia
26
Define **Premature Atrial Complexes** (PAC)
Early beat typically due to an irritable focus in the atrium.
PAC may come at a time when the ventricles have yet to be repolarized, resulting in a longer PR interval
27
Define **Premature Junctional Complexes** (PJC)
P waves inverted as the atria depolarize via retrograde conduction
P wave can come before or after the QRS complex, or can be lost entirely within QRS complex. If visible, P wave will be inverted.
28
Premature beats: Identify (PAC or PJC)?
PJC - No P wave at 4th beat
29
Premature beats: Identify (PAC or PJC)?
PAC - 3rd beat premature
30
Premature beats: Identify (PAC or PJC)?
PAC - 3rd is a premature beat
31
Premature beats: Identify (PAC or PJC)?
PJC - 3rd beat is premature. No P wave
32
Premature beats:
* Pathophysiology
* SXS
* Treatment
* **Pathophysiology**:
* Structural heart disease - Valvular disease (mitral stenosis)
* Hypertrophic cardiomyopathy
* Smoking/alcohol/coffee
* **SXS**
* Asymptomatic
* Skipping sensation
* Irregular rhythm palpitated at radial pulse
* **Treatment**
* Often benign do not need tx
* Frequent PACs may degenerate intro atrial fibrillation:
* Avoid triggers/beta blockers/ nervine herbs
33
Define: **Atrial flutter**
Impulses travel in circular course in atria, setting up regular, rapid (220-300/min) flutter (F) waves without any isoelectric baseline.
An irritable focus initiates an impulse that is conducted in a repetitive, cyclic pattern, creating atrial waves with sawtooth appearance called flutter waves.
34
Atrial Flutter with Block
Regularly irregular
* With the heart rate this rapid, the ventricles do not have adequate time to fill:
* AV node prevents this from occurring by blocking some impulses from reaching ventricles
* The AV node doesn't have enough time to repolarize; therefore not all atrial depolarizations are conducted to the ventricles
* Observe that not every flutter wave is followed by a QRS complex
35
Atrial Fibrillation
Multiple atrial foci firing at \>350x/min the AV node allows ventricular depolarization at variable intervals - often producing a irregularly irregular rhythm
•[https://www.youtube.com/watch?v=1pOVk1hZjv8](https://www.youtube.com/watch?v=1pOVk1hZjv8)
Most common sustained dysrhythmia. Increased prevalence with age. Over 8% in pt over 80YO
36
Tachycardia induced cardiomyopathy
(bpm) Atria to ventricles ratio:
Atria to ventricles ratio 2:1
37
(T or F) There are no discernable P waves in **atrial fibrillation**, and conduction is **irregularly irregular**.
True
38
Who is she?
**A fib**
* Irregularly irregular
* P waves are lost and replaced by fibrillatory waves
39
**Atrial Fibrillation** pathophysiology
* Often associated w history of rheumatic heart disease affecting mitral valve (structural abnormalities)
* Hyperthyroidism
* Obstructive sleep apnea (low O2 irritates atria)
* Post-op inflammation, oxidative stress, fibrosis
40
(T or F) Post-op for a fib is significantly associated with increased risk of neurocognitive disorders and septicemia
True
41
\_\_\_\_\_\_ supplementation was associated with a significantly reduced risk of post-op a fib in coronary artery bypass graft surgery.
Vitamin C
42
Labs for a fib
* CBC
* Comprehensive metabolic panel
* TSH
43
Imaging for a fib
* Transthoracic echocardiogram
* Transesophageal echocardiogram (evaluate for presence of a left atrial thrombus prior)
44
Complications of a fib
* Atrial remodeling
* Tachycardia induced cardiomyopathy
* As atria fibrillate, blood pools in the atria and a clot may form increasing the risk of **embolic stroke**
45
Types of a fib (3)
* **Paroxysmal**: Episodic and resolve spontaneously or with intervention within 7 days
* **Persistent**: Lasts \>7 days
* **Permanent**: Attempts to restore or maintain normal sinus rhythm have been discontinues. (Causes atrial remodeling)
46
Treatment of A fib
* Cardioversion
* Rate control (beta blockers)
* Anticoagulation
* Ablation therapy
* Left atrial appendage obliteration (LAA)
47
What is Virchow's Triad?
Factors important in the development of thrombosis.
* Abnormal blood flow (stasis/turbulence)
* Endothelial injury (inflammation/hypercholesterolemia)
* Hypercoagulability (inherited/acquired)
48
Supraventricular tachycardia (SVT)
* Heart rates are so fast that the p wave often is not visible as it may be hidden in the preceding T wave:
* Rates: 150-250 beats-per-minute
* Rhythm: regular without visible p waves
* Often called paroxysmal supraventricular tachycardia PSVT as a very irritable focus _suddenly_ paces very rapidly and the termination is _abrupt_
* Typically SVT is due to AV node reentrant tachycardia (above the ventricles)
* Technically atrial flutter and atrial fibrillation are considered SVT but it is more precise to call them by their respective names
49
SXS and triggers of SVT
Sudden (paroxysmal) onset of symptoms: (Start and stop quickly vs gradual onset of sinus tachycardia)
* Palpitations
* Dyspnea
* Presyncope/syncope
* Chest discomfort
* Anxiety
Triggers: Caffeine, stress, exercise
50
SVT: Wolff-Parkinson-White Syndrome
Abnormal accessory AV conduction pathway
* **Delta wave**
* **Short PR interval**
51
Atrial tachycardia
52
SVT treatment
* Valsalva maneuver
* Adenosine (short acting AV node blocking agent)
* Beta blockers (metoprolol)
* Non-dihydropyridine calcium channel blockers (varapamil, diltiazem)
* Cardioversion (if unstable)
* Chronic setting: Pharm agent or catheter ablation (95% success rate)
53
Premature Ventricular Complexes (PVCs)
Ventricles made irritable by low O2
54
PVC (unifocal or multifocal) ?
Unifocal
55
PVC (unifocal or multifocal) ?
Multifocal
56
Who is she? Name this pattern of PVC
Unifocal bigeminy
57
PVC labs and imaging
* CBC
* Comprehensive metabolic panel
* TSH
* Echocardiogram
58
(T or F) You should be concerned if there are \> 6 PVC/min.
True. \>10% of beats = pathologic
\> 3 PVCS in a row = ventricular tachycardia
59
Ventricular Tachycardia presents on an ECG as \_\_\_\_\_\_\_.
Tombstones
60
Ventricular Tachycardia (VT) pathophysiology and SXS
* Ischemia/infarction
* Structural heart disease
* Heart failure
* Electrolyte imbalance
SXS:
* Palpitations
* Dyspnea
* Chest pain
* Presyncope/syncope
61
Who is she?
Ventricular Tachycardia
4+ beats = V tach
\> 30 seconds = sustained v tach
62
Ventricular Fibrillation definition and treatment
Chaotic depolarization in the ventricle causes loss of organized QRS complexes and loss of organized ventricular contractions
* circulatory arrest begins within second
* Cause of most sudden cardiac deaths
Treatment: Defibrillation and CPR
63
Asystole
No detectable cardiac activity on ECG
64
Atrial flutter
P wave without a QRS, regular, 2:1 block, 3:1 block, 4:1 block (2 flutter 1 QRS)
65
Atrial Fibrillation
Irregularly irregular rhythm, no P wave
66
What are the signs and symptoms of atrial flutter or atrial fibrillation?
Asymptomatic, palpitations, dyspnea, heart failure, stroke
67
What are common conditions associated with atrial fibrillation?
* Epicardial, myocardial, and endocardial disease
* Lactogenic conditions
* Structural heart disease
* Electrolyte abnormalities
* Illicit drugs
* Sleep apnea
* Hyperthyroidism
68
What are appropriate blood tests and imaging for evaluating someone with atrial fibrillation?
* CBC
* CMP
* TSH
* Transthoracic echocardiogram
* Transesophageal echocardiogram
69
What are complications of atrial fibrillation?
Atrial remodeling
Tachycardia induced cardiomyopathy
Embolic stroke
70
What is the left atrial appendage?
Small pouch shaped like a windsock found in the L atrium which can fill with blood and form a clot that can lead to a stroke
71
What are CHADsVASC and HASBLED scoring systems used for?
CHADsVASc is used for measuring stroke risk
HAS-BLED is used for measuring bleeding risk
72
How do patients typically describe their symptoms when they have SVT?
Sudden (paroxysmal) onset of:
* Palpations
* Dyspnea
* Presyncope/syncope
* Chest discomfort
* Anxiety
73
What is the pathophysiology of SVT?
AV node depolarizes down the alpha pathway once it reaches the bottom of AV node it travels retrograde and renters the AV node via the beta pathway
74
What are the treatments used to abort an acute episode of SVT?
* Valsalva maneuver
* Medication: adenosine, beta blockers, non-dihydropyridine calcium channel blockers
* Cardioversion
75
Why are ventricular rhythms concerning?
Ventricles don’t have enough time to fill, and the brain is deprived of oxygen
76
What is the definition of **ventricular tachycardia**?
When the ventricles beat too fast to pump enough oxygenated blood to the body
77
What is the pathophysiology and causes of VT and VF?
_VT_:
* Ischemia/infarction
* Heart failure
* Electrolyte imbalances
* Structural heart disease
* Cardiomyopathies:
* Hypertrophic cardiomyopathy
* Dilated cardiomyopathy
* Infiltrative cardiomyopathy
VF:
* Chaotic depolarization in ventricle causes los of organized QRS complexes and loss of organized ventricular contractions, VT lasting \>30 seconds
* Ischemia/infarction
* Heart failure
* Electrolyte imbalances
* Structural heart disease
* Cardiomyopathies
* Hypertrophic cardiomyopathy
* Dilated cardiomyopathy
* Infiltrative cardiomyopathy
78
At what point is ventricular tachycardia considered sustained and at risk of ventricular fibrillation?
What is the treatment of sustained VT and VF?
VT lasting \>30 seconds
Treatment: Implantable cardioverter defibrillator
79
What does axis assess on ECG?
Direction of movement of depolarization through the heart
80
What leads are used to assess axis?
Limb leads
81
What are the causes of axis deviation?
Ventricular hypertrophy and infarction
82
What is a hemiblock? How does a left anterior versus left posterior hemiblock impact axis?
Hemiblock is a block in either the left anterior or posterior fascicle
Left anterior hemiblock: shifts the axis to the left
Left posterior hemiblock: shifts the axis to the right
83
What is the differential diagnosis of left axis deviation versus right axis deviation?
**Left axis deviation:**
* Left ventricular hypertrophy:
* Hypertension
* Aortic stenosis
* Left anterior hemiblock
**Right axis deviation:**
* Right ventricular hypertrophy:
* Chronic obstructive pulmonary disease
* Pulmonary emboli
* Certain types of congenital heart disease
* Pulmonary hypertension
* Left posterior hemiblock
84
How does right atrial enlargement versus a left atrial enlargement appear on ECG? What are respective causes of right atrial enlargement and left atrial enlargement?
Right atrial enlargement: Tall narrow P wave in leads, II, III, and aVF
* Chronic obstructive pulmonary disease
* Pulmonary emboli
* Pulmonary hypertension
* Pulmonary valve disease
* Some congenital disorders
* Tricuspid stenosis
* Tricuspid regurgitation
Left atrial enlargement: Wide and notched P wave in I, II, and aVL
* Mitral stenosis
* Left ventricular failure
* Aortic valve disease
* Systemic hypertension
* Mitral regurgitation
85
How does right ventricular hypertrophy versus left ventricular hypertrophy appear on ECG?
Right ventricular hypertrophy R \>S in V1 or deep S in I, aVL, V5, V6
Left ventricular hypertrophy: deep S waves V1 or V2 and large R waves V5 and V6
86
What ECG manifestation is associated with **ischemia**
ST Depression
87
What ECG manifestation is associated with **injury**
ST Elevation
88
What ECG manifestation is associated with **infarction**
Deep Q Wave
89
What ST abnormality is associated with a transmural infarct versus a subendocardial infarct?
Transmural: ST segment is shifted toward the epicardial layer, ST elevation
Subendocardial infarction: no Q wave, ST depression
90
How do you assess for ST elevation or depression?
Find the S wave go two small boxes over and then look to see if the segment is elevated or depressed compared to baseline
91
Rank from most specific to least specific the ST segment depression morphology associated with ischemia.
Least to most
92
What are some examples of non-ischemic causes of ST depression?
Right and left ventricular hypertrophy
Right and left bundle branch blocks
93
What are some examples of non-infarction causes of ST elevation?
Early repolarization
Pericarditis
94
What are tall T waves associated with?
Acute MI, hyperkalemia, injury
95
How might potassium levels impact the T wave?
96
What is the criteria for a Q wave to be significant?
Greater than one small box or more, Q wave dominates the R wave
97
What is the pathophysiology for a Q wave after an infarct?
When infarct tissue is dead it can no longer depolarize, so only one side is being shown on the EKG and shown as a negative deflection creating a **bigger Q wave**
