EKGs & arrhythmia Flashcards
Sinus rhythm if….
P wave followed by QRS (+vv)
P wave upright in leads I/II (also sometimes aVF/III but they’re beyond 75 degrees)
PR interval 0.12-0.2 seconds (3-5 small boxes)
Irregularly irregular rhythm is almost always…
AFib
HR = ___/small boxes or ___/large boxes
1500/small
300/large
Rates always refer to ____
Ventricular
Normal PR interval
0.12-0.2 seconds (3-5 small boxes)
Normal QRS interval
Normal QRS amplitude
<=0.1 seconds (<=2.5 small boxes)
Amp > 0.5 mV in at least 1 standard lead, >1.0 mV in at least one precordial lead
Upper limit of amp = 2.5-3 mV
Normal QT interval
Corrected QT <=0.44 sec (male) <=0.46 (female)
If HR normal (60-100), QT <50% interval between QRS complexes is okay
Normal mean QRS axis
-30 –> +90
positive deflection of leads I/II
What is the isoelectric complex? What can occur in the T wave following this?
Upward/downward deflections of QRS complex are equal magnitude
(T wave may cancel itself out)
Voltage calibration: 1 mm vertical =
0.1 mV
Decrease PR interval: 2 differentials
Preexcitation syndrome
Junctional rhythm
Increased PR interval differential
1st-degree AV block
Increased QRS interval: 4 differentials
BBBs
Ventricular ectopic beat
Toxic drug effect (e.g. certain antiarrhythmic drugs)
Severe hyperkalemia
Decreased QT interval: 2 differentials
Hypercalcemia Tachycardia (QT interval varies with HR (shorter for faster) so need to correct based on RR interval)
6 differentials for increased QT interval
Hypocalcemia Hypokalemia (QU interval) Hypomagesia Myocardial ischemia Congenital prolongation of QT Toxic drug effect
What is a U wave
small, rounded deflection sometimes seen after the T wave (see Fig. 2-2). As noted previously, its exact significance is not known. Functionally, U waves represent the last phase of ventricular repolarization. Prominent U waves are characteristic of hypokalemia
What quick check automatically tells you that the QRS axis is normal?
Primarily upward in leads I & II
If leads I/II aren’t primarily upward, how do you determine the mean axis? (2 steps)
Perpendicular to the lead with the most isoelectric complex
Then if it’s primarily up then the mean axis points to the + pole of that lead, and vice versa
Is the R or L side of the heart more anterior
R
Which atrium depolarizes first?
RA (helpful for differentiating RA vs LA enlargement when the P wave isn’t smooth)
In V1 what does the P wave look like
Small positive then negative deflection
Positive = RA (anterior)
Negative = LA (posteriod)
d. Solkolow-Lyon criteria: add the S wave in V1 plus R wave in V5 or V6; if sum > 35…
LVH is present! (too high amplitude)
R axis deviation could indicate…
RV hypertrophy or acute right heart strain
What happens to QRS in an incomplete/complete BBB?
Incomplete: 0.1-0.12 sec
complete: >0.12 sec
RBBB EKG diagnostic criteria (3)
QRS duration > 120ms
RSR’ pattern in V1-3 (“M-shaped” QRS complex)
Wide, slurred S wave in lateral leads (I, aVL, V5-6)
LBBB ECG diagnostic criteria (5 things)
QRS duration > 120ms
Dominant S wave in V1
Broad monophasic R wave in lateral leads (I, aVL, V5-6)
Absence of Q waves in lateral leads
Prolonged R wave peak time > 60ms in leads V5-6
LBBB vs RBBB - which one starts normally in the QRS?
RBBB because L always depolarizes first
Bundle blocks are typically detected in the ___ leads
Fasicular blocks are typically detected in the ___ leads
BBBs - chest (precordial)
Fasicular - Limb leads
Fasciular blocks aka?
Can markedly alter ___ but don’t significatly alter ___
Change QRS axis but don’t significantly widen QRS
Evidence of past STEMI can include ____
Or if it was posterior infarction could be ____ on ___ leads
Pathological Q waves
Tall R wave on V1/V2
What changes on EKG happen ~1 day after stemi
Elevation disappears
T wave inversion begins
Q wave deepens
NSTEMI and unstable angina typically cause ST segment depressions, which are frequently accompanied by ….
inverted or flat T waves
T wave inversion in lead III is…
a normal variant (unless suddenly new)
T wave deflection should be in the same direction as the QRS complex in at least…
5/6 limb leads
T wave should be ___ in leads V2-V6, ___ in aVR
Upright in V2-V6
Inverted in aVR
T wave should have amplitude of at least _ mV in leads V3 and V4 and at least __mV in leads V5 and V6
V3/V4: 0.2 mV
V5/V6: 0.1 mV
• isolated T wave inversion in an asymptomatic adult is generally…
a normal variant
Hyperkalemia leads to what T wave alteration?
Tall “peaked” T wave
(K+ is involved in repolarization. Lots of potassium total flux will increase (net amount of K moving) Peaked T wave)
R wave becomes progressively taller from V1 --> V6 Transition lead (where height R > depth S) is usually which?
V3 or V4
Normal ejection fraction = __/___ = ___%
SV/EDV = ~55%
Name 5 pacemakers of heart (native/latent) and their bpm
SA node = 60-100 bpm
Atria = <60
AV node, bundle of His = 50-60
Purkinje = 30-40
Parasympathetic (vagal) tone impacts ___ most, then ___, then ___
o Mod vagal stim –> ____
o Strong vagal stim —> _____
Parasympathetic (vagal) tone impacts SA node most, then AV, then ventricular system
o Mod vagal stim –> AV node becomes pacemaker
o Strong vagal stim —> ventricular escape rhythm
Escape beat/rhythm vs ectopic beat/rhythm
Escape beat/rhythm= initiated by latent pacemaker because SA firing slowed
Ectopic beat/rhythm = latent pacemaker develops intrinsic rate > SA
(rhythm = many beats)
Possible causes of ectopic rhythms
High catecholamines, ischemia/hypoxemia, drug toxicities, electrolyte imbalance
Cardiac injury can lead to leaky cell membranes which can lead to…
Gradual depolarization in cells that don’t have pacemaker channels –> abnormal automaticity –> ectopic rhythms (if rate of depol > SA node)
_____ is more likely in conditions that prolong AP duration/QT interval; can be self-perpetuating –> tachyarrhythmia
Example:
Early afterdepolarization
Torsades de pointes (polymorphic ventricular tachycardia)
2 varieties of conduction blocks
Functional (refractory period)
Fixed (fibrosis, ischemic scarring)
Wolff-Parkinson-White syndrome involves the presence of _____
Leading to what EKG appearance and why?
Congenital accessory bypass tract (Bundles of Kent) b/w A & V
EKG has PR <0.12 (“preexcited ventricles”) & wide QRS w/ delta wave because impulse passed both through AV/purkinje system and myocardium via bypass tract
WPW sets up ideal conditions for…
Anatomic reentry + monomorphic tachycardia
Premature beat can trigger the reentry circuit
Polymorphic ventricular tachycardia can result from what type of re-entry? Can lead to ___ if very disorganized
Functional reentry w/ spiral waves
can lead to AFib or VFib
The heart block poem
If the R is far from P, then you have a first degree
Longer, longer, longer, drop! Then you have a Wenckebach (Mobitz I)
If some Ps don’t get through, then you have a Mobitz II
If Ps and Qs don’t agree, then you have a 3rd degree!
A Mobitz I heart block would be what kind of rhythm?
Regularly irregular
Mobitz I and Mobitz II blocks are usually issues with __ and ___ respectively
Mobitz I = AV node issue
Mobitz II = usually distal to AV node (His/Purkinje, e.g. LBBB/RBBB)
An AV block where multiple Ps in a row are not followed by QRS
“High grade” AV block (Mobitz II)
What is the rate like in a complete heart block? Width of QRS?
Depend on source of escape rhythm
Often slow (lightheadedness/syncope)
If block is in AV node, escape pacemaker may be in distal AV or common Bundle of His before bifurcation –> normal QRS + not super slow
SVT is characterized by ___ QRS. Why?
Narrow because His-Purkinje system normal (originates in AV node or above)
Treatment for atrial premature beats?
If symptomatic, can use B-blockers; otherwise treatment not necessary (common in healthy hearts)
2 pharmalogical classes used to treat bradyarrhythmias + examples
1) Anticholinergics (e.g. atropine) - decrease vagal effect via competitive inhibition of muscarinic receptors
2) B1-receptor agonists (isoproterenol) - mimic catecholamines
(both are IV, not suitable long-term)
What does carotid sinus massage do?
Triggers baroreceptor reflex –> increased vagal tone, decreased symp tone –> reduce SA node activity + AV blocking “unmasks” atrial activity, SVT termination
Adenosine blocks what?
Nodes, NOT accessory pathways (so don’t use when the issue is an accessory pathway)
Totally stops heart temporarily, have cardiac resus ready
Cardioversion is synced to _____. If that’s not present (e.g. ____), then perform ____
QRS complex
Not present in VFib –> external defibrillation (asynchronous)
Sick Sinus Syndrome =
Intrinsic SA node dysfunction –> bradycardia
cell’s automaticity is decreased when the cell is driven to depolarize more frequently than its intrinsic discharge rate
- Increases hyperpolarizing current of Na/K-ATPase
What is this called?
Example of arrhythmia where this is seen in action?
Overdrive suppression
Bradycardia-tachycardia syndrome
Junctional escape rhythms come from where? About how many bpm? Wide or narrow QRS?
AV node or bundle of His
40-60
Narrow QRS
A pacemaker for AFlutter could do what?
Burst pacing (rapid atrial stimulation)
Cardiac glycosides: mechanism/effects, example
Digoxin
Inhibit Na/K ATPase
–> positive inotropic effect (increased contractility),
–> negative chronotropic effect (SA node depression, reduced HR)
–> negative dromotropic effect (reduced velocity of conduction via AV node depression)
Visual disturbance common in digoxin overdose
Blurry vision + yellow tint/halos
Digoxin has a ___ therapeutic index
Narrow
Main indications for digoxin treatment:
Afib
Treatment-resistant heart failure
Atrial fibrillation has a _____ ______ rhythm
Regularly irregular
AFib is associated w/ atrial ___ e.g.
atrial enlargement
HF, hypertension, CAD, pulmonary disease
Examples of paroxysmal supraventricular tachycardias (PSVTs)
AVNRT = AV nodal reentrant tachy
AVRT (bypass tract, e.g. WPW syndrome)
WPW syndrome usually leads to ___ AVRT. What’s the other type. EKGs?
Orthodromic (down the AV node, retrograde up bypass tract)
vs antidromic (vv)
*both EKGs have retrograde P waves
Orthodromic has narrow QRS, antidromic has widened QRS
First-line long-term treatment for WPW
Catheter ablation of accessory pathway
What is the specific treatment consideration for WPW syndrome (ventricular preexcitation) & tachyarrhythmia
AV node blocking agents or vagal maneuvers–> unrestricted ventricular conduction of rapid atrial impulses through accessory pathway –> Vtach (BAD)
Rhythm control (cardioversion, IV procainamide = Na-blocker) are safer
EKG shows irregular rhythm, each QRS preceded by P wave of varying morphology
Pt has severe COPD
Atrial rate > 100
Probable arrhythmia =
Multifocal atrial tachycardia
What is bigeminy? Trigeminy? What happens after that?
Every 2nd beat is a Ventricular Premature Beat
every 3rd beat
3+ consecutive VPBs = ventricular tachycardia
Atrial flutter is usually ___ over a _______ circuit
Reentry over a large, fixed circuit
Polymorphic VT w/ varying QRS amplitude =
Results from ____
Risk factor?
Torsades de pointes
Early afterdepolarizations
RF = long WT interval
3 EKG characteristics of VTach
Change in axis
Change in QRS morphology (often wide)
AV dissociation
Why is the change in QRS axis a more convincing feature of VTach than wide QRS?
SVT can cause wide QRS if aberrant conditions (e.g. BBB)
Change in axis of QRS means the SOURCE of conduction has changed
Vtach such as torsades de pointes can degenerated into….
Vfib + Cardiac arrest
Ventricular Fib –> ____ if not quickly reversed
CO cessation + death
Characteristics of pulse in Vfib?
PULSELESS
Name 2 shockable rhythms & 2 NONshockable rhythms
Shock: Vfib, pulseless Vtach
Nonshockable: Ventricular asystole, pulseless electrical activity
CPR: ratio of compressions:breaths
30:2
Describe pulseless electrical activity
Although an electrocardiographic rhythm is present, there is no meaningful ventricular activity (also referred to as electromechanical dissociation).
Amiodarone blocks ___ and is used to treat ____ and ___ after unsuccessful defib and ___ long-term
Blocks VG K+ channels –> prolonged repolarization
Vtach + Vfib
AFib long-term
Lung fibrosis & chronic interstitial pneumonitis are rare but serious side effects of…
amiodarone
Beta blockers = class ___ antiarrhythmic
II
Metoprolol, atenolol, esmolol,, bisoprolol = ___ beta blockers
Cardioselective (B1 only)
Mnemonic for CAUSAL factors of arrhythmia
HIS DEBS Hypoxia (pulmonary disorders) Ischemia Sympathetic stimulation Drugs (incld anti-arrhythmics!) Electrolyte disturbances (hypokalemia, Ca/Mg imbalances) Bradycardia Stretch
Recommended drugs for rate control in AFib
Beta-blockers
ND-CCBs
Digoxin
Amiodarone (rare)
What is “Pill-in-the-Pocket” Antiarrhythmic drug therapy?
Who is this indicated for?
Symptomatic patients w/ sustained AF episodes (>2hrs) that occur <1/month
No severe/disabling Sx during episodes
Can reliably comply w/ med instructions
Basically use immeidate release oral AV nodal blocker (ND-CCB or BB) followed by class Ic antiarrhythmic (Flecainide, propafenone)
We recommend ____ of AF in patients who remain symptomatic after an adequate trial of antiarrhythmic drug therapy and in whom a rhythm control strategy remains desire
catheter ablation
Most patients should receive ____ for anticoagulation rather than _____
DOAC (apixaban, rivaroxaban, dabigatran, edoxaban) rather than warfarin
(at least as effective + less bleeding complications, easier to dose
Stable vascular disease and AF in patients at high risk of stroke/systemic thromboembolism –> treatment?
OAC therapy
AF patients at higher risk of stroke undergoing elective PCI without high-risk features for thrombotic CV events –> treatment?
Dual therapy: OAC + P2Y12 (clopidogrel)
AF patients at higher risk of stroke undergoing PCI for ACS or elective PCI with high-risk features –> treatment
Triple therapy (OAC + ASA + P2Y12) for up to 1 month, then dual therapy for up to 12 months
In what AF patients is therapeutic OAC for 3+ weeks REQUIRED before cardioversion?
- Valvular AF (any duration), or
- NVAF Duration <12 hours and recent stroke/TIA, or 3. 3. NVAF Duration 12-48 hours and CHADS2≥2, or
- NVAF Duration >48 hours
Alternative to 3 weeks of anticoagulation before cardioversion in hemodynamically stable AF patients?
TEE to rule out thrombus
2 circumstances where cardioversion may be performed w/out preceding anticoagulation
i) patients with non-valvular AF who present with a clear AF onset within 12 hours in the absence of recent stroke or TIA;
ii) patients with non-valvular AF and a CHADS2 score 0 (men) or 0-1 (women) who present after 12 hours but within 48 hours of AF onset.
In the absence of strong contraindication, all patients who undergo cardioversion of AF should receive____ afterward for ____ long
Anticoagulation for at least 4 weeks
In what context would a patient w/ AF and CAD be NOT put on OAC? what would they be put on?
ASA only if they have stable CAD and CHADS2 = 0
What do you do in an unstable patient with Afib >48hrs
Don’t delay electrical cardioversion but anticoagulate w./ heparin/DOAC ASAP
Validated scoring system for assessing risk of stroke in nonvalvular Afib
CHA2DS2-VASc Congestive HF or LV dysfunction Hypertension Age 75+ (2) Diabetes Prior stroke/TIA/TE (2) Vascular disease Age 65-74 Sex: female
Scoring system used to assess risk of bleeding in patients starting anticoagulation
HAS-BLED Hypertension uncontrolled (1 pt) Abnormal renal/liver function (1 each) Stroke Hx (1) Bleeding Hx (1) Labile INR (1) (in therapeutic range <60% of time) Elderly (>65, 1) Drugs predisposing to bleeding or alcohol use (1 each) 0 = low risk, 1-2 = mod, 3+ = high
When is heparin indicated as an anticoagulant in AFib/AFlutter? (2)
Pregnancy
Anticoagulation prior to immediate unplanned cardioversion (may also use DOACs in this case)
We suggest that, in the absence of a strong contraindication, ALL patients who undergo cardioversion of AF ______ after cardioversion
We suggest that, in the absence of a strong contraindication, all patients who undergo cardioversion of AF receive at least 4 weeks of therapeutic anticoagulation (adjusted-dose VKA or a DOAC) after cardioversion
Does Mobitz I or Mobitz II have a worse prognosis?
Mobitz II because tends to progress to 3rd degree
Mobitz 1 generally doesn’t progress to a more advanced block
What is a high-grade Mobitz II?
Sequential QRS complexes are blocked
What is the most common EKG finding during pulmonary embolism? What is a very characteristic finding but that only one occurs in 10-20% of patients?
Most common = sinus tachycardia
~10% = S1Q3T3 (wide S in lead 1 + Q and inverted T in lead III) = McGinn-White Sign
