ECG/EKG Flashcards
Primary heart block
(AV Node) results in prolonged P-R interval due to an abnormally lengthened conduction time within the AV node and/or bundle of His
One atrial to ventricular conduction
Secondary Heart Block
(AV Node)
- results from increased refractory pd of AV nodal tissue or His system, thus making it less excitable
- not every impulse is relayed through AV node/His to ventricles
- thus, ratio of P:QRS is greater than 1:1
Third degree heart block
“Complete heart block” - AV dissociation
- no atrial impulses reach the ventricles
- can occur within AV node or beyond
- escape rhythms form without proper relay ssytem (subsidary pacemakers assume control of cardiac rate and rhyth)
- If block in AV Node: AV jxn resumes role: ~50bpm; relatively stable rate/rhythm; maintains hemodynamic stability
- Blocks distal to the AV node result in inherently unstable and ventricular escape rhythm consisting of about 30-40 bpm
- occurs while artia continue to beat independently at intrinsic rate of 60-100 bpm
- ECG: multiple P waves, superimposed P and QRS complexes (due to non-coordinated myocardial contractions)
Fibrillation
- arrhythmia that prevents effectual contraction of atrial and/or ventricular mycardum
- may represent a reentry phenomenon: reentry loop fragments into multiple irregular circuits within the myocardium; degeneratinginto non-coordinated and inefficient myocardial contractions
A fib
- most common cardiac arrhythmic disorder
- basic prob: the normal orderly seq of electrical conduction (depol/repol) through atrial myocardium is disrupted
- no coordinated, uniform atrial contractions, instead, rapid charotic fibrilation
- irregularity can be transmitted to AV node –> irreguar ventricualr response
- no P wave
- fibrillatory waves ( waves of varying size, shape, and rhythm)
- irregularly irrectular rhythm
- Sx: postural lightheadedness; atrial thrombus –> systemic arterial embolism
- Stages:
- recurrnt: self terminate
- paroxymal: once sinus rhythm is spontaneously restored
- persistent: paroxysmal episode that does not spontaneously end
- requires cardioversion
- permanent
V fib
- fatal if untreated
- widespread irregular contractions (fibrillations) of ventricular myocardium –> blood cannot be effectively pumped from ventrciles
- can result from hypoxic ischemia, eletrocution and certain drubs
- vulnerable period that occurs during downslope of the T wave (end period of ventricular repol)
Sinus Arrhythmia
normal but
- exremely minimal increase in HR during inspiration andexremely minimal decrease in HR during expiration
- (due to SNS stimulation of SA node during inspiration and PSNS stimulation during expiration)*
Bachmann’s Bundle
originates in SA node and distributes depol to LA
His Bundle and Bundle Branches makeup and signal on EKG
- rapidly conducting Purkinje fibers
- depol passing through Pfibers is too week to record on EKG: concealed conduction
QRS curve represents
rapid depol via terminal Purkinje filaments to the endocardial surface of the ventricular myocardium
(ventricular myocardium depol)
QT interval
ventricular contraction begins and ends
T wave
end of ventricular repol
(however repol of Purkinje fibers takes a little longer, so Pfiber depol ends beyond the end of the T wave; final phase of the Purkinje repol may record a small hump: U wave - after T on EKG)
Entrance Block
any incoming depol is blocked (protecting them from passive depol by any other source, but NOT healthy protection bc by being insensitive to passive depol, the cannot be overdrive suppressed: while their own automaticity is still conducted to surrounding tissue)
(ie: in hearts with structural pathology/ hypoxia)
Wandering Pacemaker
- irregular rhythm
- P’ wave shape varies
- atrial rate < 100
- irregualr ventricualr rhythm
Multifocal Atrial Tachycardia (MAT)
- Common in pts with COPD
- HR > 100 bpm
- P’ wave shape varies
- each individual atrial focus paces at its own inherent rate
- each foci has different P morphology (so P’s look different)
- irregular ventricular rhythm
Hypocalcemia
- prolongs duration of contraction
- lengthes QT interval
Ca2+ plays role in depol:
- fast depol in pacemaker
- plateau phase in myocyte AP
Physiology:
- Type L Ca2+ Channel are regulated by amt of EC Ca2+
- if Ca2+ levels are too low, the channels become sluggish (open and stay open for longer than normal)
- allow for long infusion of Ca2+
Hypercalcemia
- Type L Ca2+ channels open and shut quickly
- lots of EC Ca2+
- QT intervals very short
Hyperkalemia
- SA node and atrial depol are dependent on K+
-
no p waves (bc atria and SA node depend on K+
- gradient is messed up: K+ doesn’t want to go EC bc there is already too much out there
- Tented T waves (high T waves)
- rate and rhythm are fine
RAD
- lead I: -
- AVF: +
- lead II: isolelectric
axis > 100 degrees
LAD
- lead I: +
- Lead aVF and II: -
Hypokalemia
- ST depression
- flattened T
- increased P duration and amplitude
- prolonged QT interval
PVC
- uncoordinated ventricular depols which arise form irritable focus within the ventricle
- no p waves associated with aberrant QRS complex
Bundle Branch Block
widdened QRS
- RBBB: wide QTS in lead III
- R-R’ in V1 - V2
- LBBB: R-R’ in I, II, V5, V6
MI
Localizing an MI
Compare peaking MI to Irreversible Myocardial Death
Leads Showing Left Circumflex A Occlusion
- I
- aVL
- V5
- V6
Leads Showing Left Anterior Descending A Occlusion
V1-V6
Leads Showing Right Coronary Artery Damage
This artery can affect both interior and posterior parts:
- Inferior: II, III, aVF
- Posterior: reciprocal changes in V1
- ie: a prominent R wave which is not present in a ECG from a healthy heart
Aortic Valve Stenosis
LVH:
Pulmonic Valve Stenosis
RVH
Mitral Stenosis
Left Atrial Enlargement:
- increased amplitude of LA component of P waves (Leads II and V1)
Mitral Regurgitation
Left Atrial Enlargement:
increased amplitude of LA component of P waves (Leads II and V1)
Aortic Insufficiency
LVH
