Arrhythmias Flashcards
Premature Atrial Complexes, the beat arises from…
within the atria
What do premature atrial complexes look like on ECG?
Early P waves with different morphology than the normal sinus P wave; QRS is normal
Premature Atrial Complexes are usually asymptomatic but when symptomatic may cause….
palpitations or give rise to PSVTs
If premature atrial complexes are symptomatic, how can they be treated?
Beta Blockers
Causes of premature atrial complexes:
Adrenergic excess drugs alcohol tobacco electrolyte imbalance ischemia infection
Premature Ventricular complexes
Early beat from a focus in the ventricle that then spreads to the other ventricle. PVCs can occur in patients with or without structural heart disease
Causes of premature ventricular complexes:
Hypoxia electrolyte abnormalities stimulants caffeine medications structural heart disease
Premature Ventricular complexes on ECG
Wide, bizarre QRS followed by a compensatory pause
***Wide QRS because conduction is slower because it is not going through the normal conduction pathways, but through ventricular muscle
Most patients with premature ventricular complexes are asymptomatic, but if symptomatic experience:
palpitations
dizziness
If PVCs are symptomatic, may treat with
Beta Blockers
Patients with frequent PVCs and underlying heart disease are at increased risk of
Sudden death due to cardiac arrhythmia, especially VFib and may benefit from an ICD
PVC couplet
2 successive PVCs
PVC Bigeminy
Sinus beat followed by a PVC
PVC Trigeminy
2 sinus eats followed by a PVC
Atrial Fibrillation
multiple foci in atria fire continuously in chaotic pattern leading to Irregular, rapid ventricular rate
In aFib the atrial rate is
> 400 bpm (most beats are inhibited at the AV node so the ventricular rate is about 75-175 bpm)
aFib plus underlying heart disease equals marked increased risk of …
thromboembolism and hemodynamic compromise
Signs and Symptoms of aFib
Fatigue and exertional dyspnea
Palpitations, dizziness, angina, syncope
Irregularly irregular pulse
thromboembolism
How does aFib contribute to thromboembolic events?
Due to ineffective contraction, blood stasis occurs which leads to formation of intramural thrombi that can then embolize to brain
ECG findings in aFib:
Irregular RR intervals with tiny erratic spikes with wavy baseline. No identifiable p waves.
Irregularly irregular rhythm
Treatment for aFib in a hemodynamically unstable patient
Immediate electrical cardioversion to sinus rhythm
Treatment of aFib in hemodynamically stable patient
Rate control (60-100 bpm) with Beta blocker or calcium channel blocker
Cardioversion (electrical preferred over pharm)
Anticoagulation to prevent embolic cerebrovascular accident
What are choice pharmacologic agents for cardioversion?
Ibutilide Procainamide flecainide sotalol amiodarone
why must a patient in aFib receive anticoagulation prior to cardioversion?
risk of embolization during cardioversion is significant, especially if aFib has been present for >48 hours
How long should aFib patients be anticoagulated for?
3 weeks before cardioversion and 4 weeks after cardioversion
What is the goal INR range for aFib patients?
INR of 2-3 is goal
Treatment of chronic aFib includes
Beta Blocker or CCB for rate control
Anticoagulation with warfarin (unless under age 60 with lone-aFib)
Cardioversion delivery
delivers shock in synchrony wiht QRS so that it does not hit T wave which could result in VFib
Purpose of Cardioversion
terminate certain dysrhytmias like PSVT or VT
Indications for cardioversion include:
aFib
Atrial flutter
VT with pulse
SVT
defibrillation delivery
delivers shock that is not in synchrony with QRS complex
purpose of defibrillation
convert dysrhythmia to normal sinus rhythm
indications for defibrillation
VFib
VT without pulse
indications for Automatic implantable defibrillator
VFib and/or VT not controlled by medial therapy
atrial flutter pathophysiology
irritable automaticity focus in atria fires about 250-300 bpm leading to regular atrial contractions
AV node allows only 1 out of every 2-3 flutter waves to conduct to ventricles
Causes of atrial flutter
HF (most common) Rheumatic heart disease CAD COPD ASD
Atrial flutter on ECG
saw tooth baseline
QRS every 2-3 teeth/p waves
Best seen in inferior leads ( II, III, aVF)
Treatment for atrial flutter
rate control: beta blocker or CCB
restore NSR (cardioversion)
assess need for anticoagulatin
Diagnosis of multifocal atrial tachycardia requires
at least three different p wave morphologies on ECG
ECG finding in multifocal atrial tachycardia
variable p wave morphology
variable PR and RR intervals
Multifocal atrial tachycardia usually occurs in patients with …
severe pulmonary disease (COPD)
what has a similar diagnostic criteria to multifocal atrial tachycardia, except that HR is between 60-100 bpm (not tachycardic)?
Wandering Atrial Pacemaker
Paroxysmal Supraventricular Tachycardia is most often due to….
Re-entry pathology:
AV nodal re-entrant tachycardia
Orthodromic AV re-entrant tachycardia
What is the most common cause of supraventricular tachyarrhythmias
AV nodal re-entrant tachycardia
What is AV nodal re-entrant tachycardia?
2 pathways are present within AV node; 1 fast, the other slow.
Re-entrant circuit is within AV node
AV nodal re-entrant tachycardia is initiated and terminated by…
premature atrial complexes
ECG with AV nodal re-entrant tachycardia
Narrow QRS with no discernible P waves
Circuit is short and conduction rapid leading to impulses exiting to activate atria and ventricle simultaneously, P wave is buried within the QRS
What is orthodromic AV re-entrant tachycardia?
accessory pathway between the atria and ventricles that conducts retrogradely
orthodromic AV re-entrant tachycardia is initiated or terminated by….
Premature atrial complexes or
premature ventricular complexes
ECG with orthodromic AV re-entrant tachycardia
Narrow QRS complexes with P waves which may or may not be discernible depending on the rate
Accessory pathway is some distance from the AV node, thus re-entrant circuit is longer leading to a difference in timing of activation of atria and ventricles
What is the most common arrhythmia associated with digoxin toxicity?
paroxysmal atrial tachycardia with 2:1 block
Causes of paroxysmal supraventricular tachycardia
Ischemic heart disease
digoxin toxicity
AV node re-entry
atrial flutter with rapid ventricular response
AV reciprocating tachycardia (accessory pathway)
excessive caffeine or alcohol consumption
What is the agent of choice for terminating SVTs?
IV adenosine (decreases SA and AV node activity)
other agents that can be used for acute treatment of SVTs
Verapamil (CCB)
Esmolol (beta blocker)
digoxin
what maneuvers help block re-entry mechanism in SVTs?
those that stimulate the vagus nerve that lead to a delay in AV conduction and blocks re-entry
Maneuvers include valsalva, carotid sinus massage, breath holding, head immersion in cold water
side effects of adenosine
headaches flushing SOB chest pressure nausea
Wolff-Parkinson-White syndrome:
accessory conduction pathway from atria to ventricles through bundle of Kent
causes premature ventricular excitation and may lead to paroxysmal tachycardia
ECG with WPW syndrome:
Narrow complex tachycardia
Short PR interval
Delta wave: upward deflections seen before QRS
Treatment for WPW syndrome:
radiofrequency catheter ablation of accessory pathway
Medical options: procainamide, quinidine
which drugs should be avoided in WPW?
those that are active on the AV node: digoxin, verapamil, beta blockers
*these may accelerate conduction through accessory pathway
which antiarrhythmics are better choices in WPW?
Type IA or IC antiarrhythmics
define Ventricular tachycardia
rapid repetitive firing of three or more PVCs in a row at a rate of 100-250 bpm
AV dissociation is present
Originate below bundle of His
sustained ventricular tachycardia
VT lasts longer than 30 seconds and is almost always symptomatic
*LIFE THREATENING arrhythmia that can progress to VFib if untreated
Non-sustained VT
brief, self-limited runs of VT, that is usually asymptomatic
what is associated with poor prognosis in VT?
If post-MI, especially if VT is sustained-VT
Physical findings with VT
Cannon A Waves in the neck
S1 varies in intensity
what arrhythmias account for most episodes of cardiac arrest?
VT and VFib causes 75% of cardiac arrests episodes
Torsades de Pointes
Rapid polymorphic VT, that can often lead to VFib
Associated with prolongation of QT interval
Treatment for Torsades de Pointes
IV magnesium provides cardiac stabilization
Why is VT especially worrisome in patients with underlying heart disease and LV dysfunction?
These patients are at high-risk of sudden death
VT on ECG
Wide and Bizarre QRS
QRS may be monomorphic or polymorphic
Unlike PSVT, VT does not respond to ___________
Vagal Maneuvers or Adenosine
Treatment of sustained VT in hemodynamically stable patients (BP >90):
ACLS recommends IV amiodarone, rocainamide, or sotalol
Treatmnt of sustained VT in hemodynamically unstable patients:
Immediate synchronous DC conversion
Followed by IV amiodarone to maintain sinus rhythm
All patients with sustained VT should undergo…..
placement of an ICD unless the ejection fraction is normal (then consider amiodarone)
Treatment of nonsustained VT in patient with no underlying heart disease
Do NOT treat
*not at increased risk of sudden death
Treatment of nonsustained VT in patients with underlying heart disease
order electrophysiologic study, if inducible, sustained VT consider ICD placement
Pharmacotherapy is second line (amiodarone has best results)
What should be suspected in a patient with QRS tachycardia >0.12 second
Always suspect VT
Cardiac Arrest
sudden loss of CO; potentially reversible if circulation and oxygen delivery are promptly restored
Sudden Cardiac Death
unexpected death within one hour of symptom onset secondary to a cardiac cause
Narrow complex tachycardias originate….
above the ventricles
Wide complex tachycardias originate…
within the ventricles
*more ominous because more likely to progress to VFib
Ventricular Fibrillation
Multiple Foci in ventricles fire rapidly, leading to chaotic quivering of the ventricles and no cardiac output
Most episodes of VFib begin with…..
VT
How is recurrence of VFib related to acute MI?
If VFib episode was NOT a/w acute MI, recurrence rate is high and chronic therapy is indicated.
If VFib develops within 48 hours of acute MI, recurrence rate is low
Chronic therapy of VFib
prophylactic antiarrhythmic treatment with amiodarone or implantation of automatic defibrillator
What is the most common cause of VFib?
Ischemic Heart Disease
Clinical Features of VFib
Unconscious patient
cannot measure BP
Absent heart sounds and pulses
VFib on ECG
no P waves
no QRS can be identified
Very irregular rhythm
Treatment of VFib
immediate defibrillation and CPR: unsynchronized DC cardioversion (up to 3 sequential shocks)
If persistent: epinephrine every 3- minutes attemtp defibrillation again
Treatment of refractory VFib
IV amiodarone followed by shock
Alternative second line: lidocaine, magnesium, procainamide
What is the key to treatment of VFib?
Defibrillation!!!!
Also CPR and Epi
**Drugs cannot convert VFib by themselves
Defibrillation does not work for….
asystole
perform CPR and administer Epi
What is pulseless electrical activity? How do you treat?
Electrical activity on the monitor, but no pulses, even with doppler.
*grim prognosis
Treat the possible causes of asystole: hypoxia, hypovolemia, PE, tamponade, etc.
Sinus Bradycardia
Sinus Rate
Treatment for Sinus Bradycardia
Atropine can increase sinus rate by inhibiting vagal stimulation to the SA node
Cardiac Pacemaker if persistent
Sick Sinus Syndrome
Sinus node dysfunction characterized by persistent spontaneous sinus bradycardia
Usually Elderly
First Degree AV Block: PR interval? QRS? Delay location? Treatment?
PR interval prolonged: >0.20 second
QRS follows each P wave
Delay usually in AV node
Benign, no treatment required
What are the second degree AV block types?
Mobitz Type I = Wenckebach
Mobitz Type II
Which AV blocks require pacemaker implantation?
second degree AV block Mobitz type II
3rd degree AV block
2nd degree AV block Mobitz Type I
progressive prolongation of PR interval until P wave fails to conduct
Site of block usually in AV node
Benign, no treatment required
2nd degree AV block Mobitz Type II
P wave fails to conduct suddenly without preceding PR prolongation
QRS also drops suddenly
Often leads to complete heart block (3rd degree)
Site of block is within the His-Purkinje system
3rd degree AV block (complete heart block)
Absence of conduction of atrial impulses to ventricles
There is no correspondence between P waves and QRS
AV dissociation
Ventricular Rate of 25-40 bpm
