DCC

radio frequency ablation

surgery

pharmacotherapy

symptomatic PSVT

destruction of the reentry pathway

Maze procedure

creating an stitching cuts in the atrium to create scar tissues in a pattern "maze"

What are the two drugs that are lacking in the Vaughan Williams classification?

And do you know any of the other limitations of this classification?

adenosine and digoxin

many agents have more than 1 class property

does not incorporate mechanisms of tachycardia termination/prevention, clinical indications, side effects

Agents "labeled" within a class

Electrocardiogram

Echocardiogram

Electrolytes

Thyroid function tests

Electrophysiological testing

Evidence of pre-excitation

Narrow or Wide QRS complex tachycardia

hypomagnesia or hypokalemia

Hyperthyroidism

anti  /  orth

anti passes through the accessory

vagal maneuvers  

Gentle massaging one of the carotid sinuses, located in the neck (in the vicinity of the carotid arteries) for about five seconds with a firm circular movement – Has to be under supervision of professionals and ECG monitoring

Stimulation of carotid sinus triggers baroreceptor reflex and increased vagal tone, affecting SA and AV nodes

Gagging, valsalva maneuver (holding breath and exerting or bearing down), immersing face in ice-cold water (diving reflex), and coughing

What are the acute treatment options for the following patients with PSVT with a wide QRS?

Hemodynamically unstable

hemodynamically stable with a regular rhythm

and stable with an irregular rhythm

DCC

regular rhythm (VT or antidromic AVRT) you should use antiarrhythmics (procainamide, ibultide, and flecanaide)

adenosine as well as other AV nodal blocking agents may be ineffective and deleterious

IRRegular (AF with accessory pathway) you should use antiarrhythmics (procainamide, ibultide, flecainide, propafenone, amiodarone, and sotalol

 what is the chronic managment of a patient with PSVT with a wide QRS

If these drugs cannot be used which drugs are available and when should they not b used?

AV nodal blocking agents

(nonhydropyridine CCB's, beta blockers, digoxin)

antiarrhythmic agents
(CLASS IC - flecainide and propafenone)

(class III - amiodarone or sotalol)

(class Ia - procainamide, quinidine, and disopyramide)

They should not be used in patients with Structural HD

The pill in the pocket therapy is available for the chronic managment of PSVT with (narrow or wide) QRS and what are the requirements?

In which patient pop. is it not indicated?

narrow, patients with infrequent, prolonged, well tolerated episodes of PSVT

LV dysfunction, sinus bradycardia, pre-excitation

What are the first line pharmaceutical agents for a patient with antidromic PSVT that is unresponsive to AV-node blocking agents?

Then what are the alternatives?

flecainide and propafenone

sotalol and amiodarone

BP

ECG (QT interval, HR, abnormal rhythm)

Electroytes

Renal function

Hepatic function

reentrant

AF - multiple atrial reentrant loop

AFL - single dominant reentrant substrate

What are the life threatening symptoms of AF/AFL?

What are the most serious complications?

Name a few of the transient with few symptoms.

Synocope or hemodynamic collapse (associated with HR > 200bpm and AF associated with an accessory pathway)

Thromboembolic events including cardioembolic stroke

Intermittent episodes of rapid HR/palpitations, Abruptly start and stop withot provocation, synocope (check or neck pressure), Worsening of HF signs and symptoms

How many types of atrial flutters are there and which one is faster?

Which is more common?

Which is found in small tissues while the other is in large?

2 and the second is faster

1 is more common

first is found in larger tissues

Is it in AF or AFL that there is an irregular ventricle activation?

And is it the atrial or ventricle that causes the symptoms?

AF

ventricle

What is the diffrence in acute or chronic/establish tacchycardias?

What is the diffrence in paroxysmal, persistent, permanent, and lone?

acute onset < 48 hrs / chronic > 7d

paroxysmal <7 days self limiting, persistent >7d requires treatment, permanent (is refractory to CV or accepted as final rhythm), and lone is in younger patiens without SHD

symptom control

stroke prevention

reduction in hosp.

Ventricular rate control at rest and excercise

Rhythm control

Prevention of thromboembolism

Acute ventricular rate control

What agents with LV function > 40

What agents with LV function < 40

IV Beta blockers and diltiazem and verapamil

IV digoxin and amiodarone is 1st line (amiodarone may convert patients to sinus rhythm and increase risk factor for thromboembolic events)

IV beta blockers (caution in ADHF)

AVOID CCB's due to neg. inotropic effects

low chance of recurrence - lone episode of AF in young pt

symptomatic pts despite adequate ventricular rate control

ventricular rate control cannot be achieved

TRUE or FALSE

Many AF cases spontaneously convert to sinus rhythm on their own.

In the case of an AF it is always necessary to use preventative measures to keep the sinus rhythm.

TRUE

FALSE

Normal electrolyte status

appropriate anticoagulation

AV nodal blockade prior to aa that dont have blockade

initiate therapy at low dose titrate up

What are the drugs that are effective for restoring the sinus rhythm? (5)

What are the drugs that are considered less effective or havent been studied enough? (3)

Which drugs should not be administered for restoring the sinus rhytm? (2)

flecainide, propafenone

amiodarone, ibultide, dolfetilide

Procainamide, quinidine, disopyramide

not needed if <48 hrs or no thrombus on TEE

indicated in pts with stroke risk factors or AF recurrence

4 wks after cardioversion

longer than 4 for high risk pts

pts with proarrhythmia risk factors for that agent

with sinus AV node dysfuncton unless pacemaker is present

What are the drugs we discussed from the maintenance of sinus rhythm?

Which of these drugs can only be initiated inpatient?

propafenone, flecanide, amiodarone, sotalol, dronedarone, and dofetililde

Dofetilide

What maintanence sinus rhythm drug can decrease the need for hosp. for cardiovascular events with paroxysmal AF or after conversion of persistent AF??

When is this drug contraindicated?

Dronedarone

Severe HF

ectopic atrial tachycardia

multifocal atrial tachcardia

what are the causes of automatic atrial tachycardias?

Which is the common cause?

severe pulmonary disease (common)

acute infection, sepsis, dilated cardiomyopathy

What is the treatment for automatic atrial tachycardias?

(1st line) and others

what should be corrected before initiating treatment?

(underlying causes)correct acid-base/electrolyte disorders

1st - CCB's

IV magnesium may be eff. at high doses

Type 1a occasionally eff.

IV beta blokers - CI due to bronchospastic disease

Digoxin - controversial increase atrial tissue automatic properties

What are the three most common ventricular arrhythmias?

What are the range of symptoms?

VT

VF
PVC

none, mild palpitations with PVC, life threatening hemodynamic collapse with VF necessitatin CPR

triggered activity

or

reentrant mechanisms

nonsustained clear within 30 secs (self terminting)

sustained last for > 30 secs or requires therapeutic intervention to restore normal rhythm

Incessant VT - more often VT than sinus rhythm

>3 consecutive PVC's at rate greater than 100bpm

Presence of AV dissociation (Hallmark)

(THe SA node causing the depolirization of the atrium at a rate slower than the ventricular rate)

(P-waves an QRS have their own rates)

(P wave may be visual or embedded in QRS)

monomorphic

may be irregular rhythm with varying QRS amp. and morphology

What can cause VT or PVC's?

(which electrolytes and others)

hypo mag. kal. cal.

ischemia

medications/illicit drugs

(digoxin toxicity, sympathomimetics, methamphetamine or cocaine use, and drugs that prolong QT interval)

What is the treatment for PVC for patients at risk for sudden cardiac death and if the patient has no history cardiac disease, isolated, asymptomatic ventricular ectopy? (2 answers)

Besides these two pt pops what else should be looked at?

Beta blockers

none

managment of electrolyte imbalance, eliminatino of triggers, rule out MI

Pt's in convalescense period of MI

with LV dysfunction

with complex PVC's

What are three examples of underlying causes that should be corrected in an acute episode of sustained VT with a pulse?

Treatment for severe symptoms, mild, and what i the chronic therapy?

Which drug should be used if pt has a long QT?

MI, drug toxicity, electrolyte imbalance

severe - DCC

mild - DCC or procainamide, sotalol, amiodarone

LIdocaine esp. if long QT

NO NEED FOR CHRONIC THERAPY

Pharm - amiodarone

non - more eff. and safer

(catheter ablation and implantable cardioverter defib ICD)

sinusoidal/incessant monomorphic VT - TYPE 1c

polymorphic VT (Tdp) - 1a, 3, and other non-cardiac drugs

• incessant monomorphic and polymorphic VT's are caused by blockade or what ion(s)?

Which of these can be hereditary?

mono (Na)

poly (K)

POLY

What is the drug of choice to prevent the recurrence of Tdp?

What do most pts require and respond appropriatly to for the managment of Tdp?  After this is it likely to recur?

IV magnesium sulf.

DCC, yes

What is the goal for sick sinus syndrome?

Long term treatment choices?

Medications should be used in cautin without _____.

side effect of digoxin /  B-blockers, CCB's, methyldopa, clonidine

eliminate symptomatic brady and manage alterna. tac

Permanent ventrcular pacemaker (why? improves symptoms and decreases chance of paroxysmal AF and embolism

pacemaker

digoxin - suppress AV nodal escape/rescue rhythms

others - may excaberate brady