Arrhythmias Flashcards
1
Q
Goals of evaluation and treatment of arrhythmias
A
- eliminate or attenute sx
- prevent death or injury
- offset long-term risk
2
Q
Primary care approach to the patient with an arrhythmia
A
- ID of the arrhythmia
- Does it cause symptoms?
- Does it have prognostic significance?
- Is it life-threatening?
- Is treatment needed?
- Does the patient need to be in the hospital?
- Does cardiology need to be involved? How urgently?
3
Q
Arrhythmia symptoms
A
- Can be asymptomatic
- Palpitations
- Dizziness
- Chest pain
- Dyspnea
- Weakness
- Anxiety
- Symptoms may be due to underlying heart disease e.g. HF, ischemia
4
Q
Initial evaluation of arrhythmias consists of:
A
- Thorough HX and PE
- 12-lead ECG, ideally:
- in the presence and absence of symptoms
- in sinus rhythm and during the arrhythmia - In selected patients:
- Ambulatory monitoring (using a Holter or event monitor)
- Referral to an electrophysiologist
5
Q
describe risk assessment in an asymptomatic pt and one w/ known CAD
A
- Be very careful with arrhythmias in patients with known coronary artery disease
- Asymptomatic arrhythmias rarely require urgent intervention
*risk assessment often requires a cardiologist
6
Q
Tissues along the conduction pathway have inherent rates. In the absence of any external stimuli, these tissues will generate spontaneous impulses in the following ranges:
SA node:
AV junction:
Ventricle:
A
SA node: 60-100
AV junction: 40-60
Ventricle: 20-40
7
Q
describe the phenomenon of “escape”
A
If the SA node drops below its inherent rate, fails, or impulses are blocked, the site with the next-highest inherent rate (e.g. the AV junction) will take over the pacemaking role.
8
Q
describe the phenomenon of “irritability”
A
“Irritable” conduction site discharges impulses at a faster-than-normal rate and takes over the role of pacemaker.
9
Q
describe the phenomenon of “reentry”
A
An extra conduction pathway creates a circuit that can lead to rapid cycling, causing a “re-entrant” tachycardia
10
Q
Types of reentry tachycardias
A
- AVNRT (most common type of SVT)
- AV reciprocating tachycardia (or AVRT) (2nd most common)
- WPW (accessory pathwaying causing pSVT)
11
Q
due to a circuit created by an abnormal accessory pathway between the atrium and ventricle that is more distant from the AV node
A
AVRT (AV reciprocating tachycardia)
12
Q
Describe the PR interval
A
- beginning of the P wave to beginning of QRS
- normal is 0.12-0.2 (3-5 small boxes)
13
Q
Describe the QRS interval
A
-normal is less than 0.12 sec (3 small boxes)
14
Q
Describe the ST segment
A
-end of QRS to start of T wave
15
Q
Describe the QT interval
A
-beginning of QRS To end of T wave
16
Q
each small box = __
each large box = __
A
small = 0.04 sec big= 0.2 sec
*5 big boxes = 1 sec
17
Q
definition of sinus brady and sinus tachy
A
rate less than 60bpm
rate over 100bpm (rates over 140 may have P waves that are “buried”
18
Q
causes of sinus bradycardia
A
- Can be normal, particularly in athletes– unless accompanied by sx
- Sinus node dysfunction (aka SSS if has sx too)
- Metabolic (hyper-, hypo-kalemia, hypercalcemia, hyper-, hypo-thyroidism)
- Drugs (BB, CCB, lithium)
- Neurogenic, vagal stimulation (tight collar, cough, defecation, cold water to face)
- Cardiac ischemia, acute MI, AV conduction disturbance
- Obstructive sleep apnea
- Infection
- Increased intracranial pressure
19
Q
Symptoms of bradycardia
A
- Usually asymptomatic
- Lightheadedness
- Presyncope, syncope
- Worsening of angina pectoris
20
Q
Treatment of bradycardia
A
*Not indicated in asymptomatic patients
- If symptomatic:
1. Change or eliminate meds
2. Long-term drug therapy usually ineffective
3. May require pacemaker (50% of all pacemakers are for bradycardia)
21
Q
causes of sinus tachycardia
A
- Fever
- Sepsis
- Anemia (volume change)
- Hypotension and shock (volume change)
- Acute coronary ischemia and MI
- Heart failure
- Chronic pulmonary disease
- Hypoxia
- Pulmonary embolism
- Stimulants or illicit drugs (nicotine, caffeine, OTC decongestants, cocaine)
- Anxiety
- Pheochromocytoma
22
Q
Symptoms of sinus tachycardia
A
- Often asymptomatic
- Awareness of a rapid heartbeat (“palpitations“)
- shortness of breath,
- dizziness,
- syncope,
- chest pain,
- anxiety
23
Q
Treatment of sinus tachycardia
A
- Treat underlying disease
- Beta-blockers if underlying diseases ruled-out or treated
- Don’t miss acute MI or PE!
24
Q
how does HR change with inspiration and expiration
A
increase w/ inspiration
decrease w/ expiration
25
Atrial rhythms
1. wandering pacemaker (WAP)
2. APBs
3. AT
4. Aflutter
5. Afib
26
What is a wandering pacemaker (WAP) rhythm?
-Pacemaker site wanders between the sinus node, different ectopic sites within the atria (and, in some cases, the AV junction)
- Rhythm: Typically, slightly irregular 2º to changing atrial pacemaker sites
- P wave morphology changes (3 or more distinct p waves)
27
how does one dx WAP
1. Sometimes noted on exam as an irregularly irregular pulse
| 2. Usually an isolated finding on ECG and does not require treatment
28
What are APBs?
- An irritable focus within the atrium fires prematurely and produces a single ectopic beat
- Formerly called PACs
- P wave: P wave associated with the APB will have a different morphology (or may be hidden in preceding T wave)
- PRI: .12-.20 sec, may vary slightly in APB
*maybe be preceded by a shorted R-R interval
29
APBs can be triggered by:
1. caffeine
2. nicotine
3. alcohol
4. sympathomimetics (pseudoephedrine)
30
symptoms and tx of APBs
1. usually asymptomatic and require no tx
2. palpitations or 'skipping a beat"
tx for pt w/ uncomfortable sx, d/c potential triggers, and consider a BB
31
What are the different types of SVT
1. re-entry
- AVNRT
- AVRT (accessory pathway)
2. abnormal automaticity
- (unifocal) AT
*can be chronic, persistent, or paroxysmal
32
How does SVT look like on an EKG
Typically a narrow QRS complex tachycardia with a regular rate and no discernable P wave
33
Describe pSVT
1. Usually benign and self-limited and can be managed conservatively
2. Episodes begin and end abruptly, last from seconds to hours
3. Most common symptom is awareness of rapid pulse (also mild chest pain and SOB)
4. HR is typically 160-220 bpm
34
treatment of pSVT
1. avoid triggers (caffeine, alcohol, nicotine, stress)
2. vagal maneuvers to increase parasympathetic tone (valsalva, gag reflex, water on face, coughing, carotid massage)
3. Meds: best managed under supervision of cadiologist
4. radiofrequency ablation
5. pacemaker
35
Describe what WPW is
Accessory pathway from atrium to ventricle that bypasses usual delay at the AV node causing rapid pSVT
EKG: short PR interval w/ slurred QRRS upstroke (delta wave)
36
Risks of WPW
1. prone to SVT with may lead to Afib
2. can develop life-threating arrhythmias
*all should be monitored by cardiologists
37
How does unifocal AT occur
when a single irritable focus in the atrium fires repetitively at a rapid rate
38
How is unifocal AT treated
- meds
| - less commonly catheter ablation
39
describe what AT looks like on EKG
Rhythm: Regular
Rate: Typically 150-250 bpm
Atrial and ventricular rates are equal
P wave: Morphology different from sinus P wave, can be “buried” in T waves
-nl PR and QRS interval
40
How does atrial flutter occur
A single irritable focus within the atrium issues an impulse that is conducted in a rapid, repetitive fashion. The AV node blocks some of these impulses from being conducted through to the ventricles.
41
What is the main distinction between Aflutter and and AT?
in atrial flutter, the AV node blocks some of these singular irritable focus impulses from being conducted
42
describe what Aflutter looks like on EKG
- Rhythm: Atrial rhythm is regular. Ventricular rhythm may be regular or irregular.
- Rate: Atrial rate: 250-350 bpm, ventricular rate depends on conduction of atrial impulses
- P wave: Sawtooth appearance
- PRI: Not measured in this condition
- QRS: normal
43
atrial flutter is caused by/associated with:
1. HF
2. MV prolapse
3. ASD
4. hyperthyroidism
5. COPD
6. MI
44
Describe the management of atrial flutter
1. always prompt consult with cardio
2. DC cardioversion is often very effective at very low energies (less than 50 joules)
3. Chronic meds rarely effective
4. Catheter ablation 85% successful (usually the treatment of choice)
45
How does atrial fibrillation occur?
when atrial irritability leads to multiple foci initiating impulses, causing the atria to depolarize repeatedly (fibrillate). AV node blocks most of the impulses, allowing a limited number through to the ventricles
46
How does Afib look on an EKG
- Rhythm:Atrial rhythm unmeasurable, ventricular rhythm is irregularly irregular
- Rate: less than 100 = “controlled” A fib, over 100 = A fib with “rapid ventricular response”
- P wave: Not discernable
- PRI: Unmeasurable
- QRS: nl
47
What is the most common arrhythmia
Afib
*more common with advancing age (median age is 75)
48
paroxysmal Afib is characterized by ___ and is exacerbated with ____
1. episodes that self-terminate in less than 7 days
| 2. associated w/ emotional stress, following surgery, exercise, EtOH, hot tubs, caffeine, nicotine, fever
49
persistent Afib is characterized by __ and associated with ____
1. Fails to self-terminate in 7 days
2. associated w/ cardiovascular disease (rheumatic heart, mitral valve, hypertensive, chronic lung, ASD, etc.), thyrotoxicosis
50
How does Afib present?
1. Can be asymptomatic, found incidentally
2. Syncope, weakness, dizziness, fatigue, palpitations, irregularly irregular pulse
3. CVA
4. Ischemic heart disease, MI
5. CHF
51
describe the evaluation of Afib
1. PE: CV focus, signs/sx of CHF, severe hypotension
2. ECG
3. CXR
4. Echo
5. Thyroid tests, electrolytes
52
describe the management goals of Afib
1. must address associated conditions (ex. organic heart disease, hyperthyroidism)
2. rate control
3. rhythm control
4. prevention of systemic embolization
53
describe appropriate rate control for afib
1. Goal: 70-100 bpm
2. If severe failure, angina, hypotension--> electrical cardioversion
3. If stable--> Use drugs (Verapamil, Diltiazem, Beta-blockers)
54
describe appropriate rhythm control for afib (restore NSR)
1. Anti-arrhythmic drugs - IA (e.g. procainamide), IC (e.g. flecainide), and III (e.g. amiodarone)
OR
2. Direct-current cardioversion
55
which is more important in rate vs rhythm control in AFib?
- Rhythm control was the preferred approach until the results of several major clinical trials (e.g AFFIRM) found:
- Embolic events are just as likely with a rhythm control approach
- Rate control was associated with better mortality outcomes
*Thus, rate control is the preferred initial approach
56
Afib rhythm control approach should be considered it:
1. persistent sx despite rate control
2. there is an inability to attain rate control
3. patient prefers this approach
57
describe moderate and high risk factors for thromboembolism with afib
moderate: over 75, HTN, HF, DM
high: CVA, TIA, embolism, prosthetic valve
58
Describe the need for anticoagulation for Afib
*based on stroke risk
1. daily ASA (81-325mg) if no RF
2. ASA or coumadin (warfarin) if 1 moderate RF
3. coumadin if more than 1 moderate RF or 1 high RF
*coumadin to achieve INR of 2.0-3.0
59
When should you refer Afib?
1. New dx
2. If RVR: hospital admission for rate control is critical (send by ambulance)
3. Usually need 2-3 weeks of anti-coagulation before cardioversion
4. When in doubt: consult, consult, consult
60
when does junctional tachycardia occur?
Irritable focus in the AV junction overrides the SA node. Atria depolarized via retrograde conduction, ventricular depolarization is normal.
61
how does junctional tachycardia look on an EKG?
1. rate: 100-180
2. P waves can be before, buried within, or after QRS
- if before QRS, PRI is less than 0.12 (SHORT)
62
How are AV blocks acquired?
1. rarely congenital
2. MI
3. surgery
4. RFA trauma
5. meds (digoxin, CCBs, BB, Class 3 antiarrhythmics)
6. infections
7. common in trained athletes
*rarely of prognostic significance
63
symptoms of AV blocks
1. asymptomatic
2. weakness
3. fatigue
4. syncope
5. exercise intolerance
64
What is 1st degree AV block
Not a true block, actually a delay at the AV node. Each atrial impulse is conducted to the ventricles.
65
describe what 1st degree AV block looks like on an EKG
- Rhythm: Depends on underlying rhythm
- Rate: Depends on underlying rhythm
- P wave: Upright, uniform, each followed by a QRS
- PRI: Over .20 sec**** (LONG and Fixed)
- QRS: less than .12 sec (nl)
66
tx of 1st degree AV blocks
Does not require treatment but in some individuals can progress to 2nd degree AV block
67
Describe 2nd degree AV block type 1
Wenckebach
Each impulse is delayed at the AV node a little longer than the preceding impulse, until one impulse is blocked completely
68
how does 2nd degree AV block type 1 look on an EKG?
- Rhythm: Irregular R-R**
- Rate: Atrial rate is usually normal (60-100), ventricular rate is usually slow**
- P wave:Upright, uniform, some not followed by a QRS
- PRI: Get progressively longer until one P wave is not followed by a QRS***
- QRS: less than .12 sec (nl)
69
Describe the management of Wenckebach
1. Unlikely to progress or lead to asystole
2. Medication review and appropriate changes
3. Thorough cardiac evaluation
4. Patients with symptomatic bradycardia (syncope, pre-syncope, hypotension) usually benefit from pacing
70
describe 2nd degree AV block type 2
AV node selectively allows conduction of some impulses to the ventricles while blocking others
71
how does 2nd degree AV block type 2 look on an EKG?
- Rhythm: Atrial rhythm usually regular, ventricular rhythm can be regular or not, depending on conduction ratio*
- Rate: Atrial rate usually 60-100, ventricular rate typically bradycardic (less than 60bpm)*
- P wave:Upright, uniform, more P waves than QRS
- PRI:Constant on conducted beats
- QRS: less than .12 sec
72
What is 2nd degree AV block type 2 associated with?
1. Almost always due to disease within the AV node
| 2. High risk of progression and can lead (sometimes rapidly!) to asystole
73
Management of 2nd degree AV block type 2
all pts need pacers
74
describe 3rd degree heart block
Complete block of impulses at the AV node. The atria and ventricles function independently
-Complete AV dissociation
Impulses originate at SA and -AV node separately
75
how does 3rd degree heart block look on an EKG
- Rhythm: P-P and R-R intervals are constant but not related
- Rate: Atrial rate is typically 60-100, Ventricular rate can be junctional (40-60) or ventricular (20-40)**
- P wave: Upright, uniform, more P waves than QRS**
- PRI: None
- QRS: less than .12 sec if controlled by a junctional focus, .12 sec or greater if a ventricular focus**
76
3rd degree AV block can lead to ___. Tx includes ___
failure if significantly decreased CO from bradycardia
-tx: pacing
77
What is a BBB
- Abnormal ventricular depolarization
- Normal conduction down unblocked branch; opposite branch slowly depolarized via myocardial tissue (slower than conductive pathways)
78
causes of RBBB
1. Degenerative conduction system disease (fibrosis),
2. ischemic cardiac disease,
3. acute PE (big ones)
4. can be seen in a normal heart
5. RBB is a thin bundle of fibers, block can be due to a small lesion
79
What are the EKG characteristics of a RBBB
1. QRS greater than 0.12 sec
2. wide S wave in lead I, V5, and V6
3. R-S-R' in V1
4. "M" in V2
80
Causes of LBBB
1. widespread cardiac disease
2. LVH
3. degenerative disease
4. Aortic stenosis
5. ischemic disease
6. cardiomyopathy
* * cannot rule out infarctio in the presences of LBBB-- need other studies
81
What are the EKG characteristics of a LBBB
1. QRS: over 0.12 s
2. Wide S wave in leads V1 and V2
3. Wide R wave in V5 and V6, usually seen as R-R'
82
Management of BBB
1. newly dx, needs thorough eval
2. all new LBBB deserve stress test (persantine thallium)
3. tx underlying disease
4. if accompanied by syncope, will likely require pacemaker
83
what are VPBs
premature ventricular beats
- single irritable focus in the ventricle that fires prematurely
- Very common, increased incidence with age
- usually benign ectopic ventricular impulses
- May alternate with sinus beats (bigeminy) or after every two sinus beats (trigeminy)
84
how do VPBs appear on EKGS
- Rhythm: Depends on underlying rhythm
- Rate: Determined by underlying rhythm
- P wave: VPB not preceded by a P wave
- PRI: None associated with VPB
- QRS: Premature, bizarre, wide (over .12 sec) QRS with compensatory pause (early -QRS penetrates AV node, making it refractory to next impulse.)
85
___ or more consecutive VPBs is Vtach
3
86
VPBs are associated with
1. increased caffeine
2. EtOH
3. nicotine
*VPBs in the post-MI patient can influence prognosis
87
Management of VPBs
1. thorough H/P
2. VPBs and non-sustained Vtach (terminates in less than 30 sec) and no structural heart disease: no therapy is needed. Treat symptoms if desired (beta-blockers for 2 weeks)
3. if occurs during exercise-- cardiology referal (sudden cardiac death can occur w/ VPBs in the setting of ischemic heart disease)
88
describe what Vtach is
Irritable focus in the ventricle that fires regularly at a rate of 150-250 bpm and overrides higher sites
*difficult to differentiate from SVT w/ aberrancy
89
How does Vtach appear on an EKG
-Rhythm: Regular or slightly irregular
- Rate: 150-250 bpm
- P wave: None discernable
- PRI: None
- QRS: over .12 sec and bizarre, often cannot distinguish between QRS and T wave
90
what is considered slow VT and ventricular flutter
slow VT: less than 150bpm
Vflutter: over 250
91
Management of Vtach
1. often requires emergent treatment
2. thorough cardiac eval
3. ID Presence, type, severity of cardiac disease
4. Medication use is very important: proarrhythmics (digoxin, diuretics, erythromycin, class I antiarrhythmics, others)
92
tx of hemodynamically unstable VT
synchronized cardioversion (ACLS protocol)
93
tx of hemodynamically stable VT
1. meds: state w amiodarone.. if no response, procainamide.. if no response, lidocaine
* *NO verapamil
2. consider synchronized cardioversion
3. some will require ICDs
94
Why can you not use verapamil w/ VT
it can initiate Vfib in VT
-should only be considered if you are certain that it is SVT w/ abberancy
95
What is VFib
Multiple irritable foci in the ventricles generate chaotic, uncoordinated impulses that cause the heart to fibrillate rather than contract
96
how does vfib look on an EKG
- Rhythm: Baseline is chaotic, no discernable waves
- Rate: Can not be determined
- P wave: None discernable
- PRI: None
- QRS: None discernable
97
what is vfib associated w/
1. no effective pumping= death
| 2. most commonly seen w/ acute MI
98
tx of vfib
1. shock w/ electrical current
| 2. treat underlying disease
99
what is an idioventricular rhythm
A ventricular escape rhythm. In the absence of a higher pacemaker, the ventricles initiate a regular impulse.
100
what does an idioventricular rhythm look like on an EKG
- Rhythm: Usually regular, can gradually slow as death nears
- Rate: 20-40 bpm, can gradually slow as death nears
- P wave: None
- PRI: None
- QRS: over .12 and bizarre
