CVPR 04-01-14 09-10am Clinical Treatment of Arrhythmias - Nguyen Flashcards Preview

CVPR Unit 1 > CVPR 04-01-14 09-10am Clinical Treatment of Arrhythmias - Nguyen > Flashcards

Flashcards in CVPR 04-01-14 09-10am Clinical Treatment of Arrhythmias - Nguyen Deck (66):

Bradyarrhythmias – sources

Sinus node dysfunction; AV & infranodal blocks


Sinus node dysfunction - cause

Eventually manifested by everyone (may not be symptomatic), as sinus node myocutes are replaced overtime during the normal aging process or as a result of an underlying process (infiltrative cardiomyopathy, HF, etc.)


Sinus node dysfunction – treatment

In symptomatic pts, pacemakers can improve symptoms; Limited role of drugs, except for withdrawal of potentially causative agents such as beta-blockers or anti-arrhythmic drugs


Atrioventricular block – causes

Disease in AV node or below (His-Purkinje system)… location determines urgency of treatment


Atriventricular block –types

Incomplete (occasional or frequent dropped beats) or Complete (no association between atrial & ventricular depolarizations…. Incomplete AV block is further delineated into Mobitz I and II varieties (type II more serious)


First degree AV block

No actual block occurs, just an AV conduction delay ---> prolonged PR interval (>200 ms / 0.2 s)


Second degree AV block - Mobitz I AV block (Wencheback)

Characterized by progressive prolongation of the PR interval on ECG until a ventricular beat is blocked ….. Underlying PR interval is usually prolonged at the beginning of the cycle, indicating underlying problem in the actual AV node…. Irregular ventricular rate


Second degree AV block - Mobitz II AV block

Usually results from disease below the level of the AV node, in the His-Purkinje system (later in the PR interval)….. Much more unpredictable that Mobitz type I and urgent action is required to avoid potential asystole


Complete heart block (3rd degree AV block)

When there is no association between atrial& ventricular depolarizations….. No impulse conduction from atria to ventricles (slower ventricular rate and faster atrial rate, with variable PR interval)


When should you be concerned about AV block?

When pt is symptomatic (no matter which part of the conduction system is blocked)…. When the rhythm is infranodal (below AV node)….. they can both progress to unreliable heart rhythms


Escape rhythm from blocked AV node

1. Usually block in the AV node will permit for a reliable escape rhythm from the AV junction ---> IDed w/a regular (34-45bpm), narrow QRS complex, indicating its origination from the junction….. 2. Infranodal AV block is more unreliable, with escape rhythms originating from the Purkinje system or ventricular myocardium ---> IDed by wide QRS with very low, often irregular HR (15-30bpm)


AV block treatment

Remove underlying causes (drugs, ischemia/infarct, hypothyroidism, Lyme disease, neurologic)….. For potentially reversible causes, drugs w/chronotropic effect on AV junction (isoproterenol, dopamine) can be useful to temporarily relieve symptoms in AV block involving the AV node; However, such drugs may exacerbate symptoms in pts w/infranodal AV block, worsening the block as a result of the increase in AV nodal conduction and underlying HR…. No great long-term treatment for bradyarrhythmias, so usually require Pacemaker


Cardiac pacemakers

Implantable device which acts to restore normal cardiac rhythm, by acting as a timer which senses electrical activity in one chamber & either delivers or withholds an electrical impulse….. May be single (atrial or ventricular) or dual chamber….. Usually consist of pulse generator implanted over pectoral muscle + one or more leads implanted transvenously


Simple pacemakers

Single chamber device set to a back-up pacing mode….If impulse is not sensed above a baseline pacing rate, then the device will send an electrical impulse to the chamber, causing it to depolarize….. The device times in milliseconds (such as 1000 msec, the equivalent of 60bpm); the timer resets and inhibits pacing if there is an impulse w/in 1000 mscec of the prior impulse & acts as if nothing is sensed in the 1000 msec window


Tachyarrhythmias – source

Above ventricle (supraventricular tachycardia, SVT) or from the ventricle (ventricular tachycardia/fibrillation)


Acute Treatment of Supraventricular Tachycardias

If pt is unstable, shock or cardiovert ….. If stable, treat medically….. (1) For irregular SVTs, control rates w/antiarrhythmics or cardiovert them…… (2) For regular SVTs, the 1st step is both a diagnostic & treatment option, which is to use ADENOSINE, a drug that blocks the AV node very transiently.


Adenosine - action & use

Simple & safe med; Acts on AV node to slow down; helps w/Dx (slows down enough to see pattern) as well as treat


Sinus tachycardia

Not an arrhythmia itself, but can be an abnormal finding; important not to ignore if discovered clinically….. Often a manifestation of important underlying process, such as poor pain control, volume depletion, anemia, bacteremia/sepsis, hypoxia/hypercarbia, etc……Rarely, variants of sinus tachycardia are NOT due to an underlying cause & are pathologic unto themselves (ex: inappropriate sinus tachycardia, postural orthostatic tachycardia syndrome)


Atrial fibrillation – qu’est-ce que c’est ?

Most common arrhythmia in US; Due to chaotic electrical activity in the atria, with multiple micro-reentrant wavelets existing simultaneously ---> effective atrial rate of >300 bpm….. There is often a trigger that initiates tachycardia and the underlying substrate to maintain arrhythmia


Atrial fibrillation – characteristics

Paroxysmal (occurs intermittently & terminates spontaneously)….. Persistance (recurs w/out spontaneous conversion)….. Permanent (can’t restore sinus rhythm)


Three Tenets of Treatment for Atrial Fibrillation

1. Rate control….. 2. Rhythm control….. 3. Anticoagulation
5C’s: Cause reversal…. Control rate…. antiCoagulation…. Control rhythm…. Cure(?) via ablation


Rate control in Atrial Fibrillation

AV nodal blockade OR (when refractory) ablation of AV node….. BB, Digoxin (not good for exercise), Verapamil, Diltiazem, Amiodarone


Rhythm control in Atrial Fibrillation

For symptomatic cases: (1) Pharmacologic agents (class I and III anti-arrhythmic drugs); may also use these drugs at lower doses for maintenance, (2) Cardioversion (acutely successful, but w/varying degrees of recurrence depending on underlying substrate), or (3) Ablation of triggers (usually w/in pulmonary veins; decreased recurrence in 70-75% success in paroxysmal pts, 40-50% in permanent pts… but, risks such a stroke preclude its 1st line use)


Anticoagulation in Atrial Fibrillation

To minimize risk of stroke & overall morbidity; even after rhythm has been controlled….. Embolic events risks quantified via CHADS (Congestive HF, HTN, Age >75, Diabetes, Stroke – 2 pts each) ---> Daily aspirin for 0 points, aspirin or warfarin for 1 pts, warfarin for 2+ points


Atrial flutter

Prototypical reentrant arrhythmia & illustration of reentry as a tachycardia mechanism….. Typical right atrial flutter involves unidirectional electrical conduction around the tricuspid valve, utilizing an area of slow conduction (critical isthmus)


Critical isthmus

An area of slow conduction between two electrically unexcitable structures (myocardial scar, valves, veins, etc.)


Mechanism of Tachycardia in Atrial Flutter

In sinus rhythm, activation around the valve takes place in both clockwise & counterclockwise directions, causing the two wave fronts to eventually collid e& extinguish each other….. If a premature atrial stimulus arrives at the lateral or septal aspect of the valve, the cavotricuspid isthmus (slow conduction area & slow link in the circuit) may be refractory & unable to propagate an impulse ---> Conduction will simultaneously proceed around the tricuspid valve, allowing time for recovery of the critical isthmus ---> when the wave front reaches the critical isthmus once more, it can be conducted unidirectionally, completing one cycle of the tachycardia circuit = reentry


Rate of Tachycardia in Atrial Flutter

Governed by the ability of the tissue to conduct the impulse…the slow link in the chain is the cavotricuspid (critical) isthmus (a small rim of tissue between the tricuspid valve & inferior vena cava)


Diagnosis of Atrial Flutter

Usually diagnosed based on characteristic “sawtooth” pattern in the inferior EGC leads (II, III, aVF), using a 12-lead ECG…. This pattern is generated b/c activation proceed towards the inferior leads for the first half of the cycle (positive deflection), then away for the second half of the cycle (negative deflection)


Atrial Rate in Atrial Flutter

Normally around 200 ms (300 bpm); May be longer depending on presence of right atrial dilation or scar (dilation stretches tricuspid valve & elongates the circuit; scarring/other myopathic processes from right atrial disease affects tissue conduction of electrical signals)


Ventricular rate in Atrial Flutter

Typically 150 bpm in the absence of rate-controlling agents (which act through AV node)
& conduction takes place in a 2:1 manner from atrium to ventricle


Treatment of Atrial Flutter

Pharmacologic (AV node blockers & anti-arrhythmic drugs) = not too successful….. Electrical cardioversion (initially successful but high recurrence rate)….. Ablation of the arrhythmia have good long-term success - CURE (targets cavotricuspid isthmus between IVC and tricuspid valve, to prevent propagation of wave around the valve)


Pharmacologic Treatment of Atrial Flutter

Controlling HR is hard w/out high doses of AV nodal blockers & is nearly impossible during exertion unless there is an underlying AV nodal disease….. Anti-arrhythmic drugs can minimize premature atrial beats, which initiate tachycardia….. Once tachycardia as been established, anti-arrhythmic drugs (class I or III) can help terminate tachycardia, or may be harmful by helping to maintain the arrhythmia….. Long-term, pharmacologic treatment is successful in only 50%


Actions of Anti-arrhythmic drugs (Class I & III) in Atrial Fluter – Help or Harm

HELP: If depolarization/recovery along leading edge is slow by the drug more than the trailing edge is, conduction will catch up & tachycardia will be terminated b/c excitable gap is bridged….. HARM: If depolarization/recovery is affected more along trailing edge, excitable gap is widened & tachycardia is more likely to continue


Atrial Flutter Pts on Anti-Arrhythmic Drugs should also be on…

...AV nodal blockers like beta-blockers or Ca2+ channel blockers, b/c AADs may slow conduction enough to facilitate 1:1 AV conduction at a rate causing significant symptoms like syncope


Cardioversion – defn.

Application of DC energy in a single rapid shock across the precordium


Ablation – defn

Application of radio frequency energy, transferred to the tissue in the form of heat, which destroys myocytes & causes scar ---> stops its ability to conduct


Regular supraventricular tachycardias w/predominant 1:1 AV association – DDx

Atrial tachycardia (10%), AV nodal reentrant tachycardia (AVNRT – 65%), and AV reentrant tachycardia (AVRT) mediated by accessory pathway (25%)


Atrial tachycardia - characteristics

An arrhythmia analogous to sinus tachycardia, but distinguished by a rapid onset & offset….. 1:1 AV conduction (unless arrhythmia is fast or there is an underlying AV nodal conduction disease)


Atrial tachycardia – mechanism/cause

Abnormal focus of atrial tissue which possesses its own automaticity & which thus can generate atrial beats…. Often occurs w/a trigger (catecholamine surge, caffeine, HF)…. May be in structurally normal heat or underlying cardiac disease


Atrial tachycardia – treatment

Antiarrhythmic drugs (beta-blockers, Ca2+ channel blockers, Class I & III antiarrhythmics) = 30% 1 year success rate….. Ablation targeting abnormal focus = 70-90% success rates


AV Nodal Reentrant Tachycardia (AVNRT) – pathway characteristics

Involves a reentrant circuit around the AV node…. ~10-20% of ppl posses two different pathways w/in the AV node – “fast” & “slow” pathways (FP & SP)….. The pathways are electrically connected at their proximal and distal ends…. The fast pathway conducts faster, but recovers more slowly than the slow pathway


AV Nodal Reentrant Tachycardia (AVNRT) –mechanism

During sinus rhythm, conduction is propagated down both FP & SP, but faster down FP (duh)….. Upon reaching His, the electrical activation of FP goes down the ventricle as well as returns up to SP, which collides w/& extinguishes the wave already traveling down the slow pathway….. HOWEVER, if a premature atrial beat occurs, it will find the FP still refractory from its previous activation and thus conduction will proceed solely down the SP, to activate His and the ventricle, and then return up the FP to conduct again down the SP in a reentrant manner ---> circuit ---> continued electrical activation leads to AVNRT


AV Reentrant Tachycardia (AVRT) – mechanism

Mediated via conduction through an accessory pathway (AP) = abnormal electrical connection btwn atrium & ventricle = may conduct antegrade (atrium to ventricle) and retrograde (ventricle to atrium), or only retrograde…. Rare cases of APs conduct only antegrade & possess AV node-like properties


Wolff-Parkinson-White syndrome

Rare type of AV reentrant tachycardia (AVRT) where there is only antegrade conduction down an accessory pathway (AP)…..the only SVT (suprventricular tachycardia) associated w/sudden death….. On surface activation, the AP conduction can be seen by the “delta wave,” which represents activation of the ventricle via the AP prior to its activation via the AV node = “ventricular preexcitation”


Mechanisms of Tachycardia in AV reentrant tachycardia (AVRT)

With AP (accessory pathway) conduction, conduction can occur (1) Down the AV node to the ventricle, back to the atrium via the AP, and then repeat = “normal” ventricular activation via AV node = “orthodromic reciprocating tachycardia (ORT) = MOST COMMON MECHANISM….. (2) Activation down the AP and retrograde through the AV node = “antigrade reciprocating tachycardia….. (3) Atrial fibrillation in the presence of antegrade conducting AP = APs can conduct much faster than the AV node’s max rate & thus activate the ventricle at rates >300bpm (ventricular fibrillation) ---> sudden cardiac death if lasts over several seconds = MOST DANGEROUS MECHANISM


ECG findings of different Accessory Pathway Mechanism utilized in AVRT (AV reentrant tachycardia)

(1) Orthodromic reciprocating tachycardia (ORT): narrow QRS….. (2) Antidromic reciprocating tachycardia (ART) = wide QRS due to ventricular activation via the myocardium rather than via the normal conduction system….. (3) Atrial & ventricular fibrillation (rates >240bpm)


Treatment Strategies of AV Nodal Reentrant Tachycardia (AVNRT) & AV Reentrant Tachycardia (AVRT)

Treatment depends on acute vs. chronic nature…. ACUTE: Try to break arrhythmia by slowing conduction through one or both pathways or halting conduction altogether temporarily (AV nodal blockers like BBs, CCBs to slow conduction; Adenosine to temporarily halt conduction)….. Can also perform vagal maneuvers to increase endogenous adenosine (carotid sinus massage, clenching abdominal muscles by bearing down, cold water immersion)….. CHRONIC: May be minimal to invasive, to treat symptoms (vagal maneuvers, AV nodal blockers) or to stop the arrhythmia (catheter ablation cures in most)


Adenosine Mechanism

Adenosine (often in escalating doses) ---> transient AV nodal blockade ---> terminates arrhythmia


Considerations when using Adenosine for AV reentrant tachycardia (AVRT)

Adenosine should be withheld if AP is known to be present (otherwise, can lead to 1. AP nodal block & conduction solely down the AP; 2. Atrial fibrillation when there is rapid AP conduction)….. Rather, Procainamide can be used safely b/c it affects conduction down both the AV node & AP


Ventricular tachycardia (VT) – defn.

In contrast to SVT (supraventricular tachycardias), VT relies entirely on the ventricle for arrhythmia origination & propagation… More V’s (QRS) than A’s (P) = VA dissociation (ventrical & atria dissociated)
….. Usually dangerous & often life-threatening, esp. in pts w/structural heart disease (HF, CAD, etc.)


Ventricular tachycardia (VT) – mechanisms

(1) Reentrant arrhythmia using prior scar or (2) an Automatic or Triggered focus


Ventricular tachycardia (VT) – QRS morphology

Usually QRS during VT has a single morphology, but can occasionally have alternating morphologies due to drugs (digoxin) ro alternating reentry circuits


Therapy for Ventricular Tachycardia (VT) - factors

Depends on pt’s status & underlying heart function/disease (if known)….. For awake & non-hypotensive pts, administer meds (1st Amiodarone as bolus then as IV drip – few contraindications for short term administration)….. For pts that are NOT hemodynamically stable, cardioversion is used to restore normal rhythm


Ventricular Tachycardia (VT) in Pts w/Structually Normal Hearts

Two main types of VT might be seen: (1) Ventricular outflow tract tachycardias (most originate from RV outflow tract right below the pulmonic valve; minority originate from LV outflow tract, including aortic cusps)….. (2) Idiopathic VT or verapamil-sensitive VT = reentrant rhythm utilizing the left posterior fascicle, w/characteristic ECG pattern


Long-term therapy for Ventricular Tachycardia (VT) in Pts w/Structually Normal Hearts

Usually benign… May use medications (PRN or not; BBs, CCB[verapamil, diltiazen], Class I or III anti-arrhythmics) or ablation


Ventricular Tachycardia (VT) in Pts with Structural Heart Disease/Coronary Artery Disease

VT is considered life-threatening in such patients …. Most episodes result from reentry; the rest from triggered/automatic foci


Acute Treatment of Ventricular Tachycardia (VT) in Pts with Structural Heart/Coronary Artery Disease

Determined by hemodynamic stability of pt…. Amiodarone can be used for stable patients, but cardioversion should be considered even for them as hemodynamic status can deteriorate quickly


Long-term Treatment of Ventricular Tachycardia (VT) in Pts with Structural Heart/Coronary Artery Disease

Focuses on reduction of mortality and reduction of symptomatic events….. MORTALITY IMPROVEMENT: Implantable Cardioverter-Defibrillator (ICD) = only therapy to improve mortality ….. SYMPTOMATIC EPISODE REDUCTION: Antiarrhythmic drugs to minimize symptoms (esp. those from an ICD shock) = limited options due to underlying cardiac disease, but can use: (1) Amiodarone & sotalol, (2) BBs


Implantable Cardioverter-Defibrillator (ICD) – qu’est-ce que c’est

Similar to a pacemaker but instead detects rapid heart rhythms & distinguish normal from arrhythmic heart rhythms (normal sinus tachycardia during exercise vs. ventricular tachycardia)…. Treats ventricular arrhythmias w/a shock or rapid pacing design to suppress/terminate the arrhythmia


When is a defibrillator needed?

Secondary prevention after sudden cardiac arrest due to VT or VF w/out reversible cause (don’t want it to happen again!)….. Primary prevention when at significant risk (ischemia heart disease w/low EF despite therapy or with inducible VT, or w/structural heart disease w/high risk of cardiac arrest [hypertrophic cardiomyopathy, cardiac sarcoid, congentical heart disease, ARVC])


Implantable Cardioverter-Defibrillator (ICD) & Mortality

Superior to drugs/ablation, but more risk….. Only therapy successful in to improving mortality in pt w/VT and structural heart/coronary artery disease….. also successful for anyone w/heart disease who has survived a ventricular arrhythmia outside of the setting of MI, in those w/left ventricular ejection fraction <35%


Sudden cardiac death

Good at IDing pts at high risk, but vast majority who die of sudden death are in general population and aren’t well-IDed….. Most common reason for death in US, mostly from ventricular arrhythmias, with very poor prognosis for morbidity/mortality….. best treatment is AED defibrillator (w/in 5 min!)


Types of Tachyarrhythmias

Divided into supraventricular arrhythmias and those coming from the ventricle.


Danger of unstable tachyarrhythmia



Treatment strategy of tachyarrhythmias

Treat & reverse the underlying causes…. SVT treatment is individualized according to the specific mechanism so MAKE THE DIAGNOSIS (Adenosine to see p waves)

Decks in CVPR Unit 1 Class (28):