Dysrhythmias part 3 Flashcards
what are Junctional Arrhythmias
- Rhythm originating from junction/AV node
- gradual or abrupt onset, with change in rate, followed by abrupt termination
- 70-120 bpm
- Retrograde P waves either immediately preceding QRS, immediately following QRS, or buried in the QRS and not visible
causes of Junctional Arrhythmias
- Digoxin toxicity
- Electrolyte abnormalities
- Other AAD toxicities
- Ischemia, Myocarditis
presentation of junctional arrhythmias
May be asymptomatic
Palpitations, dizziness, near syncope
management for junctional arrhythmias
Treat underlying cause
Usually no need for pacemaker or other management
2 mechanisms of Accelerated Idioventricular Rhythm
- escape rhythm due to suppression of higher pacemakers resulting from sinoatrial and AV block or from depressed sinus node function
- slow ventricular tachycardia due to increased automaticity
causes of accelerated idioventricular rhythm
- In acute MI and following reperfusion with angioplasty or thrombolytics
- Also common with digoxin toxicity
tx for accelerated idioventricular rhythm is not indicated unless ?
there is hemodynamic compromise or more serious arrhythmias.
what is V tach?
- Defined as 3+ consecutive ventricular premature beats
- Nonsustained – < 30 s, terminates spontaneously
- Sustained – > 30 s - 160–240 bpm
causes of V tach
- Acute MI, CAD
- Cardiomyopathy, valvular disease, myocarditis
- May occur in structurally normal hearts
- Catecholaminergic Polymorphic VT
- Long QT syndromes, Brugada - Torsades de pointes - severe hypokalemia, hypomagnesemia, or after administration of a drug that prolongs the QT interval
what are Congenital Long QT Syndromes
- Rare in US – may be autosomal recessive or dominant, depending on underlying genetic disturbance
- Characterized by recurrent syncope, a long QT interval (0.5–0.7 s), documented ventricular arrhythmias, and sudden death.
- Specific genetic mutations affecting membrane potassium and sodium channels have been identified
Congenital Long QT Syndromes may occur in the ____ or ___ of congenital deafness.
What are the official syndrome names?
presence (Jervell-Lange-Nielsen syndrome) or absence (Romano-Ward syndrome)
Congenital Long QT Syndrome is mainly characterized by ____ that are often triggered by adrenergic stimulation, which can be brought about by physical exertion or mental or emotional stress.
episodes of torsades de pointes
MC forms of congenital LQTS are caused by ?
ion channel defects
which LQT is a Na channel mutation?
LQT 3
which LQT are K+ channel abnormalities
LQT1 and LQT2
Proposed as one of the causes of sudden infant death syndrome
Congenital Long QT Syndromes
which type of congential LQT is MC
LQT1and LQT2account for 80% of the cases.
Exercise and sudden auditory stimuli are triggers
which LQT is only seen in 10% of the cases, but it accounts for most of the lethal cases of LQTS.
Most of the events occur during sleep at slower heart rates
LQT 3
Characterized by sudden death associated with one of several ECG patterns characterized by incomplete RBBB and ST-segment elevations in the anterior precordial leads
Brugada Syndrome
Brugada Syndrome is MC in who?
The typical patient is young, male, and otherwise healthy, with normal general medical and CV PE.
Also more common in Asians (Philippines, Thailand, Japan)
Brugada syndrome has been associated with alterations in what gene?
SCN5Agene
management of congenital LQT/brugada
- Refer to Cardio or EP ASAP
- Long-term tx - BB - Propranolol & Nadolol preferred
-
ICD implantation, esp Brugada
- also recommended in recurrent syncope, sustained ventricular arrhythmias, or sudden cardiac death occurs despite medical therapy. - Avoid prolonging QT meds
s/s of v tach
- Patient may be asx, esp with nonsustained
- Majority with sustained VT have sx
- Palpitations, heart racing
- Near syncope, syncope
- Confusion, fatigue
- Chest pain, SOB
PE findings and diagnostic study results depend on the underlying cause
management for Acute Sustained VT
- hemodynamically unstable - immediate synchronized direct current cardioversion
-
stable – IV amiodarone
- IV Lidocaine if refractory
- IV magnesium replacement - Manage any underlying causes
long term therapy for v tach
ICD
Beta blockers
Amiodarone, Sotalol (Class III AAD)
Catheter ablation
management for nonsustained VT
If no heart disease – BB if sx only
If due to structural HD (low EF) - BB, even if no sx, d/t increased risk of sustained VT and sudden death
Over 75% of VFib victims of sudden cardiac death have what underlying condition
severe CAD
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Other conditions besides Vfib that predispose to sudden death include:
- Severe LVH, hypertrophic cardiomyopathy, dilated cardiomyopathy
- Severe AS
- Primary pulmonary hypertension, cyanotic congenital heart disease
- Hypoxia, electrolyte abnormalities
- Long QT, Brugada syndrome, ARVD, catecholaminergic VT
management for Vfib
- IMMEDIATE unsynchronized defibrillation
- Follow ACLS protocol, CPR, etc.
- Treat underlying condition
- Consider ICD if indicated
Intraventricular conduction defects are common in ?
individuals with otherwise normal hearts
Intraventricular Conduction Delays can also occur in many disease processes, including:
- ischemic heart disease
- inflammatory disease
- infiltrative disease
- cardiomyopathy
- postcardiotomy
LBBB most often occurs in patients with ?
- underlying heart disease and may be associated with progressive conducting system disease.
- However, LBBB can also be seen in asx pts with a structurally normal heart
which artery provides the primary blood supply for the LBB
left anterior descending artery
causes of LBBB
-
Structural Heart Disease
- not usually the result of a single clinical entity, except in acute MIs.
- conditions that contribute to myocardial fibrosis (HTN, CAD, cardiomyopathies) can contribute to LBBB.
- may result following acute myocardial insult = worse prognosis -
Functional LBBB
- Rate-related aberrancy
Evaluation of a patient with LBBB:
- In the setting of CP/ACS sx, MIs are difficult to determine with EKG alone
- Assume MI until proven otherwise, unless old LBBB - Thorough H&P to assess for causes: HTN, CAD, CM, Valve disease, Myocarditis
- Diagnostic testing should be based on H&P
- Echo
- Stress test or LHC
management for LBBB
- asx w/ isolated LBBB, no evidence of cardiac disease - no therapy required
- Otherwise, treat any underlying cause
- Sx pts w/ LBBB and low EF - CRT
The RBB receives most of its blood supply from ?
septal branches of L anterior descending coronary artery
RBBB conduction can be compromised by?
both structural and functional factors:
- Structural heart disease –
- Processes that increase RV pressure, like COPD, PE, Pulm HTN
- MI, HTN, CM, Myocarditis, Congenital heart defects - Rate-related aberrancy is possible
T/F: Patients with isolated chronic RBBB are generally asymptomatic and do not require further diagnostic evaluation or tx
T
presentation of bifascicular block
asymptomatic and fairly benign
- asx - no further diagnostic evaluation or therapy is required
- Pts should be screened carefully for s/s suggesting occult cardiac disease
management for symptomatic bifascicular blocks
present with presyncope or syncope and are noted to have bifascicular block on ECG
-
additional monitoring and eval are required - intermittent complete heart block may result occur
- Continuous ECG monitoring x 24-48 h - inpatient
- Echo - assess for underlying structural heart disease
- CHB is identified - PPM
Otherwise, if no sx and no underlying ischemia, then no tx is necessary
