Arrhythemias Flashcards
What is susceptibility to an arrhythmia based on?
genetic abnormalities and acquired structural heart disease
What does how dangerous an arrhythmia is depend on?
how much it impairs cardiac output or how likely it is to deteriorate into a more serious disturbance
What increases susceptibility?
electrolyte abnormalities hormonal imbalances hypoxia drug effects myocardial ischemia
Classification of arrhythmias includes what?
those caused by
- disorders of impulse formation or automaticity
- abnormalities of conduction
- reentry
- triggered activity
heart rate under 60
sinus bradycardia
who is sinus bradycardia normal in? why?
athletes ; increase in vagal tone
what is sinus bradycardia assocaited with an increased risk for?
ectopic rhythms
heart rate >100 is _____ and occurs with what?
sinus tachycardia
occurs with fever, exercise, pain, emotion, shock, thyrotoxicosis, anemia, heart failure, and use of many drugs.
what beats are found in normal hearts, and do not alone constitute heart disease?
atrial premature beats
what is the most common paroxysmal tachycardia?
what persons does this occur in?
paroxysmal supraventricular tachycardia (PSVT)
usually occurs in persions without structural problems
what is the most common chronic arrhythmia?
atrial fibrillation
T/F incidence and prevalence of A-fib increases with age.
true
Who does atrial flutter usually occur in?
COPD (chronic obstructive pulmonary disorder)
CHF
Atrial Septal Defect
CAD (coronary artery disease)
Who do junctional rhythms occur in?
patients with normal hearts or those with myocarditis, CAD, or digitalis toxicity
transient failure of impulse formation into the sinus node
sinus pause
name 5 drugs that cause sinus bradycardia
digitalis
Bblockers
clacium channel blockers
antiarrhythmic agents such as sotalol and amiodarone
which causes sinus bradycardia?
hyperkalemia hypokalemia?
hyperthyroidism hypothyroidism
hyperthermia hypothermia?
hyperkalemia
hypothyroidism
hypothermia
when sinus pause (inactivity) is prolonged it is called?
sinus arrest
the result of abnormal transmission between the sinus node and the atrium
sinoatrial exit block
PR interval longer than .20
First degree AV Block
is p married to Q in first degree heart block?
yes
p-r interval >.2 with a narrow QRS
first degree AV block
progressive lengthening of the PR interval until a P wave is blocked
Second degree AV block Type 1
“starts out normal fast and then gets slower and slower until it decides it needs a break (dropped QRS)”
Wenckebach
-series of cycles with phrogressive blocking of AV Node conduction until the final P wave is totally blocked in the AV NOde, eliminating the QRS response.
-Each repeating Wenckebach series has a consistent P:QRS ratio like 3:2, 4:3, 5:4, etc. (one less QRS than P waves in the series)
P-R interval .12 - .2
series of cycles consisting of ONE normal PQRST cycle preceeded by a series of paced P waves that fail to conduct through the AV node (no QRS) response
Second Degree Heart Block Type 2 “Mobitz”
-Each repeating Mobitz series has a consistent P:QRS ratio
like 3:1 , 4:1, 5:1
type 2 av block with narrow QRS
site of block is usually in the His bundle above the bifercation but may occasionally be in the AV node
what are the finding that favor infrandoal AV block?
a history of near syncope or syncope
a QRS duration above .12
improved AV conduction during with carotid sinus massage
worsening AV conduction with atropine and exercise
Why is it important to know the site of the AV block in teh ASYMPTOMATIC patient with 2:1 AV block?
because infranodal block is assoc w/ worse prognosis and mandates the implantation of a pacemaker
T/F Mobitz 2:1 is less severe than Mobitz 3:1 & 4:1.
true
when mobitz blocks three atrial depolarizaitons (pwaves) producing a single ventricular response (QRS) this is written “3:1 block” , which describes the mechanism of conduction
these extremely slow ventricular rates may produce loss of consciousness (syncope)
how do you determine the difference between 2:1 AV block of Wenckebach and Mobitz?
Parasympathetic Vagal Maneuvers
- Wenchebach increases cycles/series to produce 3:2 or 4:3
- Mobitz - vagal maneuverse either eliminate the block, producing a 1:1 AV conduction, or they have no effect.
- *Explanation: av node is richly supplied with parasympathetic innervation, so vagal maneuvers inhibit the AV Node, making it more refractory
- Therefore, vagal maneuvers increase paraysmpathetic inhibition of the AV node, increasing the number of cylces/series to produce 3:2 or 4:3 Wenchkebach
- But if the 2:1 block is Mobitz (th eblock in the ventricular conduction system), vagal maneuvers either eliminate teh block, producing 1:1 AV conduction or they have no effect
name the dz: PR interval
- increased consistently
- progressively increases in each series of cycles
- totally variable
- decreased
- primary AV block
- Wenchebach
- tertiary AV block
- WPW and LGL syndrome
What has P without QRS response
Wenckebach and Mobitz secondary AV blocks
Tertiary AV block - independent atrial and ventricular rates
conduction of supraventricular depolarizations to the ventricles is TOTALLY BLOCKED… an automaticity focus ESCAPES to PACE the ventricles at its INHERENT rate.
Complete 3 degree block
-atrial conductions are NOT conducted to the ventricles
**ATRIOVENTRICULAR DISSOCIATION and an atrial rate that is faster than the ventricular rate
RR and PP intervals are usually constant
PR interval will vary because the P is independent of the QRS
joined QRS aka “rabbit ears”
prolonged QRS > .12 (3 boxes or more)
what leads do u look at?
Bundle Branch Block
R and R prime
look at V1 and V2 and V5 and V6
the presence of a full compensatory pause suggests =
aberrant APCs or VPCs
atrial vs ventricular premature complexes
VPC’s
full compensatory pause (RR interval surround the APC = twice teh sinus cycle length) suggests lack of sinus node resetiing, thus favoring a ventricular rather than an atrial site of origin
which bundle branch block are u more likely to see an atrial premature complex?
right b/c it has a longer refractory period
describe prevalence of APC’s
- increases with age
- freq. with structural ht dz such as chronic renal failure and chronic pulmonary dz
- increased in teh early stages of an MI with a subsequent decrease in frequency after 10 days (this characteristic may be related to atrial ischemia, increased filling pressures, or the increased catecholamine state often seen during MI.)
- appear to be freqent in PERICARDITIS
what are the symtpoms of APC
palpitations, or the sensations of skipped beats
dizziness and heart failure like symptoms might occurin the setting of ATRIAL BIGEMINY with nonconducted atrial premature beats
bigeminy = abnormal beats occur every other concurrent beat
what is the treatment for a pt with APC’s with no symptoms?
with if they have symptoms?
with no symptoms treat by removing underlying fators that are known to cause ectopic beats such as alcohol and caffeine intake. pt with symptoms = BETA BLOCKERS... followed by CCB and class IC agents such as flecainide and propafernone
P wave buried in QRS
describe the 3 locations
JPC - junctional premature complexes
1. perinodal = retrogradal atrial activation preceeds ventricular activation
2. His Bundle = retrograde atrial activation ALWAYS follows ventricular activation (P wave that follows the QRS)
3.
if a JPC impulse does not conduct in either antegrade nor retrograde activation, the result is what?
AV BLOCK
** CONCEALED JPC’S
What are the common settings of JPC
digitalis toxicity
high catecholamine states
hypokalemia
MI
wide QRS with a compensatory pause
VPC = ventricular premature complex
T/F VPCs have NO prognostic significance in patients with a normal heart, their presence in paitents with heart dz is often associated with poor outcome. in patients with a history of MI the presence of VPC’s increases MORTALITY.
true
what is the treatment of VPC’s in symptomatic patient
BetaBlocker 1st
if beta blocker therapy fails then amiodarone or catheter ablation should be considered.
when catheter ablation is performed, the VPC site of origin is identified and radiofrequency energy is applied to eleminate it
what is the rate of atrial tachycardia
what causes this
how do u read it on an EKG
100-250
caused by an ectopic atrial focus discharging at a rate faster than the sinus rate
different p-wave morphology
most commonly AV conduction is 1:1, however variable AV block might be seen
When atrial tachycardia occurs WITH Av BLOCK then what is expected?
digoxin toxicity
what is the treatment for atrial tachycardia?
when not a result of digoxin toxicity…. BB and CCB are the mainstays o ftherapy
-catheter ablation can eliminate this arrhythmia in 75-90% of pt
what is defined by the presence of three or more p wave morphologies and a rate greater than 100 beats/min
Multifocal atrial tachycardia
when do you commonly see MAT?
in pt with underlying lung dz; it is seen in the setting of an acute MI, hypokalemia, hypomagnesemia, and it may be precursor of a-fib
-Aminophylline use may also be a contributing factor
what is the treatment for MAT
rate control of this arrhythmia may be difficult but Verapamil is frequently effective
-treatment is directed at underlying dz
re-enterent tachycardial localized in the right atrium with passive activation of the left atrium
atrial flutter
if propagation of the impulse in atrial flutter is in what direction will it produce a negative p wave in the inferior leads with a sawtooth pattern?
counter clockwise
what is the rate of atrial flutter
250-350
what is the usual ventricular rate with a-flutter
usually 2:1 AV conduction with Ventricular rate of 150
AFL can result in the presence of an accessory pathway, teh ventricular rate can be rapid, resulting in hemodynamic compromise and V-fib.
when AFL is assoicated with hemodynamic compromise or angina, what is the treatment of choice?
IMMEDIATE CARDIOVERSION
Pt with A-Flutter who is hemodynamically stable, but remains symptomatic despite rate control drugs, what should be attempted?
rhythm control with drugs or catheter ablation when class IA anti-arrhythmic agents are used to convert AFL to sinus rhythm, the ventricular rate MUST first be controlled with digoxin, BB, or CCB.
most common sustained supraventricular tachycardia
atrial fibrillation
what is the rate of ventricle in Atrial Fib
irregularly irregular at rates between 120-170
EKG findings for A-fib
NO P WAVES
what is the physical examination of a pt with A-FIb
variation in the intensity of S1, an irregular cardiac rhythm, and absence of waves in the jugular venous pulsations
at the very short RR intervals tha toccur intermittently during rapid heart rates, the minimal diastolic filling time and subsequent low stroke volume fail to do what?
produce a palpable pulse
-a discrepancy may therefore exist between the ausculated heart rate and the palpable pulse rate, with the ausculated rate being more accurate reflection of the true ventricular rate
Treatment of A-Fib
warfarin to prevent thromboembolic event
digoxin, BB, or CCB for control of heart rate
if AF is assoc with hemodynamic compromise = CARDIOCONVERSION
