Cardiac Arrhythmias pt 2 Flashcards
Define bradyarrhythmias
Definition: Heart rate < 60 bpm • Arise from disorders of impulse formation or impaired conduction
Sinus bradycardia is decreased firing SA node; can be both phyisiologic and pathologic: what are some examples
intrinsic SA node disease and extrinsic factors like autonomic regulation SA node, medications, metabolic causes.
Pt was admited with a HR of 45bmp, she was dizzy, confused. No other irregularities on ECG.. Whats a possible Dx?
Sick sinus syndrome; which is an intrinsic SA node disease
Escape Rhythms originate from:
latent pacemakers: both junctional and ventricular
_________ escape beats arise from AV node or His bundle. Typically narrow, rate typically 40-60 bpm. Not preceded by normal P wave but retrograde P may be present (after QRS, inverted inferior leads)
Junctional
________escape slower (30-40 bpm), wide QRS with morphology determined by origin escape pacemaker cells.
Ventricular
First Degree AV Block:
– PR prolongation due to
prolongation of normal delay between atrial and ventricular depolarization
In first degree bundle block:
– PR =
_____AV relationship
– PR > 200 ms
– 1:1 AV relationship
What are the causes of 1st degree heart block, both reversible and irreversible?
Conduction delay usually within AV node
– Reversible causes: autonomic, transient AV nodal ischemia, drugs
– Irreversible causes: myocardial infarction, chronic degenerative disease often seen with aging
What treatment do we give to pt with 1st degree heart block?
– Usually benign and asymptomatic, requiring no specific therapy
What happens to the PR interval in Morbitz type I block (2nd degree block)
PR gradually increases until an impulse is completely blocked, after which PR shortens again to its initial length
In Morbitz type I, conduction is usually impairedin the _______
What symptoms do we expect and what are the causes?
Conduction is impaired in AV node.
• Usually benign and asymptomatic
• Causes include autonomic tone, acute MI either due to increased vagal tone or ischemia AVN
Sudden intermittent loss of AV conduction without preceding gradual PR lengthening.
Morbitz II: 2nd degree block
Where is the block located in Morbitz II?
Conduction block usually distal to AVN (His-Purkinje) and QRS often widened due to His Purkinje system disease
What is concerning about MOrbitz II?
May progress to third degree AVB without warning, typically requires pacemaker.
What is the cause of a Morbtiz II block?
Results for scar, myocardial infarct, chronic degenerative disease of conduction system
A second degree block is due to:
intermittent failure of AV Conduction
Complete failure of conduction between atria and ventricles.
• No relationship between P and QRS complexes
• Distal escape rhythm or asystole in ventricles.
Third degree heart block
Causes of third degree heart block
Causes include myocardial infarct, chronic degeneration of conductive pathways. Congenital form associated with neonatal lupus.
In thrid degree heart block: More proximal escape results in ________ QRS;
distal produces_____ QRS.
relatively narrow
wide
Symptoms and Tx for third degree heart block
Symptoms: lightheadedness, syncope, exercise intolerance.
• Treatment: Permanent pacemaker.
When figuring out what type of bradyarrhythmia your pts has, look at the relationship between P wave and QRS complex….
If its 1:1 it could be:
sinus bradycardia or first degree AV block
When figuring out what type of bradyarrhythmia your pts has, look at the relationship between P wave and QRS complex….
if it has an intermittent block:
Second degree AV block (morbitz I or II)
When figuring out what type of bradyarrhythmia your pts has, look at the relationship between P wave and QRS complex….
it its dissociated
Complete heart block
Definition of tachycardia
: Heart rate
> 100 bpm for 3 or more beats
Mechanism of tachycardia
enhanced automaticity, reentry and triggered activityf
How is tachycardia usually classified?
It’s origin
–origin above ventricle = supraventricular
origin w/in ventrcles = ventricular
Origin SA node, Rate > 100 bpm, P and QRS complexes normal in appearance
Sinus tachycardia
Causes of sinus tachycardia:
Results from increased sympathetic or decreased vagal tone.
May be appropriate (exercise, physiologic stress- fever, anemia, hypoxia,hypovolemia, hyperthyroidism) or inappropriate (inappopriate sinus tachycardia)
- Automaticity or reentry in an atrial focus outside SA node.
- May cause palpitations.
- Produce early P wave with abnormal shape, dissimilar to sinus rhythm P wave.
Atrial Premature Beats/Atrial
tachycardia
What do we see with the P wave in atrial tachycardia?
Produce early P wave with abnormal shape, dissimilar to sinus rhythm P wave.
If pt has atrial tachycardia, when do we give them B-blockers
If symptomatic, beta blockers often used to treat, usually benign
If automatic focus generates series of consecutive atrial premature beats with resulting HR > 100, we term this:
atrial tachycardia
Rapid regular atrial activation produced by reentry over a large fixed circuit.
SVT: Atrial Flutter
What’s the difference between counter clockwise and clockwise atrial flutter?
Counterclockwise typical flutter: circuit produces right atrialdepolarization up the septum, across the roof and down the RA free wall, then along the floor of RA between tricuspid valve and inferior vena cava “tricuspid-caval isthmus”, producing “saw tooth” pattern.
• Clockwise flutter: same circuit, opposite direction.
What kind of AV conduction do we see in atrial flutter?
AV conduction is variable, can be 1:1 but more commonly more flutter waves than QRS complexes.
Drugs that slow atrial flutter circuit (e.g. flecainide) may promote 1:1 AV conduction which will:
paradoxically increasing ventricular rate.
Atrial flutter can be asymptomatic or symptomatic: what are some symptoms?
May be asymptomatic or associated with palpitations, dyspnea, weakness, and stroke from atrial thrombus (loss atrial contractility d/t rapid A rates).
What are the predisposing factor for atrial flutter?
• Predisposing factors: prior heart surgery, coronary disease, cardiomyopathy.
What is this shit?
Atrial flutter: see there is sawtooth pattern with variable AV conduction
What abnormalities do we see in atrial flutter?
see more flutter waves then QRS complexes
What tx do we prescribe for RATE controle in atrial flutter?
Rate control: beta blockers, calcium channel blockers, digoxin
Pt has had atrial flutter for over 48 hours.. your attending asks you what the first step of action should be….
– Duration > 48 hours necessitates transesophageal echo to rule out left atrial thrombus or 3 weeks anticoagulation prior to conversion. Anticoagulation continued post cardioversion at
least 4 weeks (delay recovery mechanical atrial function).
What tx do we provide for pts with atrial flutter for rhythm control?
– Electrical cardioversion
– Pace termination
– Catheter ablation of tricuspid caval isthmus, curative 95%, thus preferred
– Antiarrhythmic drug therapy (class I, III agents) for sinus rhythm maintenance, occasional chemically convert, modestly effective.
What drug therapies are recommended for RHYTHM control in atrial flutter?
– Antiarrhythmic drug therapy (class I, III agents) for sinus rhythm maintenance, occasional chemically convert, modestly effective.
PT comes in with Chaotic rapid rhythm with atrial rates > 400 discharges/min).
• No distinct P waves.
• Most of P waves find AV node refractory, only some of the depolarizations are conducted to ventricle, resulting in “irregularly irregular” rhythm.
Whats going on?
Atrial fibrillation
What do we see in pt with atrial fibrillation;
P waves
atrial rate:
rhythm:
See no distinct P waves
chaotic rapid rhythm
atrial rates >400 discharges
Mechanism of atrial fibrillation
triggered by rapid firing from atrial foci often localized to atrial muscle extending into pulmonary veins.
How is atrial fibrillation sustained in the heart?
by multiple wandering reentrant circuits within the atria; minimum number of circuits required for AF, thus AF promoted by enlarged atrium.
What are the predisposing causes of atrial fibrillation?
Predisposing factors: ETOH, CHF, valvular disease, enlarged atria, hypertension, coronary disease, pulmonary disease, sleep apnea, hyperthyroidism, cardiothoracic surgery.
In atrial fibrillation, ventricular response rates may be rapid and lead to:
symptoms, hypotension or heart failure.
In atrial fibrillation, Rapid atrial activation results in
absence of organized atrial contraction, blood stasis in atrium and risk of thrombus formation, especially in left atrial appendage, with risk of embolization and stroke.
Treatment for acute atrial fibrillation you use anticoagulation, specifically in
acute:
chronic:
cardioversion
CHADSVasc score
What is key for rate control in atrial fibrillation?
AV nodal blockade (Beta blocker, calcium channel blocker, digoxin)
What are three key therapies to restore sinus rhythm in atrial fibrillation?
– Cardioversion (>48 hours, preceded by 3 weeks anticoagulation or TEE)
– Antiarrhythmic Drugs
– Catheter ablation
AF Is Associated With Increased Thromboembolic Risk
Major cause of stroke in elderly1
• 5-fold ↑ in risk of stroke
• 15% of strokes in US are attributable to AF
• Stroke severity (and mortality) is worse with AF than without AF
• Incidence of all-cause stroke in patients with AF: 5%
• Stroke risk persists even in asymptomatic AF
CHA2DS2-VASc Score
Past disease states that give you 1 point
Congestive HF
Hypertension
Diabetes
Vascular disease
CHA2DS2-VASc Score
What earns you 2 points?
Age over 75
having a stroke
What risk factors (non-disease states) will earn you 1 point in the CHA2DS2-VASc Score
being female and being over 65
CHA2DS2-VASc Score
Score of 0 =
Score of 1 =
**score of 2 or more = **
0= no therapy or aspirin (no therapy preferred)
1= aspirin or oral anticoagulation
2 or more = oral anticoagulation
Key management of AF stroke prevention is:
anticoagulation: use coumadin (warfarin) Dabigatran, Rivaroxaban, Apixaban
(or anti-platele; aspirin)
