antiarrythmics/random/hypertrophy/BBB Flashcards
Class 1a action
sodium channel blockers; depress phase 0 polarization; slow conduction; prolong polarization
Class 1b action
Shorten repolarization
Class 1c action
Depress phase 0 repolarization; slow conduction
Class II action
BB, slow AV conduction
Class III action
K channel blockers, prolong action potential
Class IV action
slow calcium channel blockers
Class V action
Adenosine: slows conduction time through AV node, interrupts reeentry pathways
digoxin: direct action on cardiac muscle and indirect action on cardiovascular system via ANS
Class Ia indications
SVT, Vtach, prevent Vfib, symptomatice ventricular premature beats
1b indications
Vtach, prevention of vfib, symptomatic ventricular premature beats
1c indications
life threatening vtach or vfib, refractory SVT
II indication
SVT, prevent Vfib
III indication
refractory Vtach, SVT
IV indication
SVT
V indication
SVT
1a examples
Quinidine, procainamide, disopyramide, moricizine
1b
lidocain, mexiletine
1c
flecainide, propafenone
II
esmolol, propanolol, metoprolol
III
amiodarone, sotalol, dofetilide, ibutilide
IV
verapamil, diltiazem
V
adenosine, digoxin
supraventricular arrhythmias
sinus bradycardia, sinus tachy, atrial premature beats, PSVT, afib, aflutter, junctional rhythms
sinus brady.
symptoms less than 50,
Weakness, pre-syncope/syncope, SOB
tx with atropine (vagolytic) or postivie chronotropic (epi or dopamine)
sinsus tachy (regular, narrow complex)
sx: palpitations, dizzy, SOB, angina
stable-valsalva , 1s push adenosine, then BB or CCB
Unstalbe- synchronized cardioversion
stable tachy with wide QRS
antiarrhytime infusion of procainamide, amiodarone or sotatlol
afib
most common, “holiday heart” excessive alcohol use or withdrawal
unstable- cardiovert at 200J
stable- 1) rate control w/BB , then CCB, then digoxin 2) anticoag (heparin or enoxaparin and warfarine or dibigatran, and rate control for 3-4 weeks prior to converstion
chemical converstion-flecanimide, propafenone, amiodarone, dronedrone or ibutilide
aflutter
unstable: cardioversion w/ 50 J
stable- anticoags, and rate control (metoprolol, esmolol, diltiazem or verapamil) prior to conversion
chemical conversion w/ IV ibultilide or synchronized cardioverstion w. 5 to 50 J can also be effective
chronic a flutter
dofetilide is primary choice, but dronedarone, amiodarone, sotalol, procainamide, and flecainide
ventriculare premature beats (PVC)
tx w/ BB
may be benign or lead to sudden death; can occure w/ increasing frequency if myocardium is irritated by facots such as ischemia or electrolyte disturbance
vtach
three or more consecutive ventricular premature beats; frequent complication of actue MI or dilated cardiomyopathy
unstable- shock! pulseless=unsynchronized,
pulse=synchronized
torsades de pointes
polymoprhic vtac- continually changing axis; I V Mg
Long QT
causes recurrent syncope; AT interval 0.5-0.7 sec long; ;tx- correct electorolyep abnormality, stop offending drug
Brugada’s
think Asains and men; implantable defibrillator
vfib
no effective pumping action
***Main cuase of sudden cardiac death
tx-non-synchronized defibrillation 120-200 J; amiodarone for 28-48 hours
conduction disorders
sick sinus syndrome, AV blocks
sick sinus syndrome
found in elderly, made worse by digitalis, CCB, BB, sympatholytic agents; collagen vasculare or metastaic dz, surgical injury, coronary artery dz; scarring of heart
tx permanent pacing
AV block
delay or inerupption in the transmission of an ipulse from the atria to the ventericles
**key is the PR interval
AV blokc symptoms
weakness, fatigue, light-headedness, syncope
first degree
if the Ris far from the P, then you have a first degree. no tx really needed
mobitz I (or a wekenbach)
longer, longer, longer, drop, then you have a wenckebach.
regular irregular, type 1 conduction delay usually in AV node
think athletes, elderly, ischemia, drugs (BB, CCB, anti-arrhythmics)
tx- is symptomatice and signs of hypoperfusion use atropine
mobitz II
block usually in bundle of his,; almost always secondary to organic dz in infranodal system, almost always will progress to a complete heart block
(if some ps get through, then you have a mobitz II)
tx with pacemaker
3rd degree
if p’s and q’s dont agree, then you have a 3rd degree
what are sx of sick sinus syndrome?
mostly asx, but pt may have syncope, dizziness, confusion, heart failure, palpitations, decreased exercise intolerance
what can cause a shortened PR interval?
junctional rhythm if inverted p wave
wolff-parkinson-white sydrome
what can use a prolonged PR interval
AV blocks
what affects the height and amplitude of a QRS complex?
size and direction of vectors in relations to the lead
what would hypertrophy do to a QRS complex?
increase it bc more muscle to conduct through
what would an infarct do to a QRS complex?
you would see higher voltage on the unopposed wave (other side)
how do you calculate the axis?
look at I and AVF
if both negative=extreme R, if both positive then normal
what is a RBBB
RV depolarization is delayed
what is the criteria for reading a RBBB?
XRS prolongation >.12
slurred S wave in leads i and V6
RSR pattern in lead 1
criteria for LBBB
QRS prolongations > .12
Broad monomorphic R waves in I and V6
Broad monomorphic S waves in V1
what do you need to think of if there is a LBBB
AMI until proven otherwise
criterai for a LPH
right axis deviation
s wave in lead 1 and q in III
how to see left atrial enlargement
P wave in lead II: > .12
M shape=P mitrale
camel humpts
P wave in V1: v=biphasic second half of wave neg and deeper/wider
what can cause LAE?
MS/MR, AS/AR, systemic HTN
Right atrial enlargement
P in lead II: > 2.5 mm, Peak shape= P pulmonale
P in lead V1: IF biphasic, + half taller and wider than neg half
causes of RAE
TS/R
pulmonary HTN,
Pulmonary embolism
left ventricular hypertrophy
causd by pressure or volume overlad
**will see increased amplitude on EKG bc more cells=more action potentials
what is LVH w/ strain
ST depression and or inverted T waves that are actually abnormal repolarization
criteral for LVH
deepest S wave in V1 or V2 + tallest R wave in V5 or V6 = >/= 35 mm
Right Ventricualr hypertrophy
Look at leads V1 and V2
R wave in these leads at least as tall as the depth of S wave (R:S ratio ≥ 1)
Early transition zone
what can cuase RVH?
Pressure overload: Pulmonary HTN, PE Pulmonic stenosis/regurgitation Ventricular septal defect Tricuspid regurgitation Severe mitral stenosis
why would you see a flipped Twave in an MI
Zone of injury does not repolarize completely
Remains more positive than surrounding tissue, leading to ST elevation
T remains flipped
what is the idea of a reciprocal change?
, the recording made by the lead on the wall exactly opposite an AMI is registering the reciprocal change of that AMI
what is an example of a reciprocal change?
Inferior MI’s = Reciprocal changes in Anterior and Lateral Leads
Lateral MI’s = Reciprocal Changes in I, avL, V5, V6
what EKG change is seen in hopthermia?
rounded osborn wave at the J point
how to determie if pace maker is atrial or ventricular
look at pacer spikes
if where P wave should be- atrium
if where Q wave should be- ventricle
what is sinus arrhythmia?
Representation of normal respiratory variation
Slower during exhalation and faster upon inhalation
Inhalation increases venous return by lowering intrathoracic pressure
Common in both young and elderly
Symptoms: usually none, occasionally palpitations
Evaluation: EKG
Treatment: None, normal clinical finding
