normal P waves and VARRIED RR Intervals with ventricular rate <60 bpm, which is normal variant for Pts
A Fib
#1 common sustained cardiac arrhythmia where multiple atrial pacers depolarize but only some get through to ventricles, appearing as irregularly irregular rhythm with no identifiable P waves; ventricular rate can reach 150-170 bpm, but is limited by refractory period of AV node (cannot depolarize repolarizing tissue) - AKA ___ with rapid ventricular response (RVR); common in underlying heart disease, mitral disease, HTN
A Fib Etiology
precipitated by underlying disease including 1. Cardiac = HTN, mitral disease, MI, HF, pericarditis, cardiac surgery 2. Non-Cardiac = hypothyroidism, PE, pneumonia, COPD, alcoholism
A Fib Types
can be 1. Paroxysmal = >2 episodes that spontaneously ruminate within 24 hours 2. Persistent = fails to self-terminate in 7 days, requiring cardioversion 3. Long-standing = lasting >1 year 4. Permanent/Chronic = conscious decision to stay in A Fib
A Fib Presentation
may be asymptomatic, but can have 1. Mild symptoms = palpitations, fatigue, weakness, dizziness, DOE 2. Moderate symptoms = dyspnea at rest, angina, pre-syncope 3. Severe symptoms = R-sided HF, syncope, thromboembolic event 4. In SH = alcohol abuse, caffeine use, stimulants 5. On physical, IRREGULARLY IRREGULAR rhythm +/- irregular pulse
A Fib Eval
initially, get 1. CBC and CMP 2. Troponin 3. Mg 4. TSH/T4 5. PT/PTT 6. BNP 7. D Dimer 8. EKG = ABSENT P waves and irregular deflections called F WAVES - best seen in inferior leads (no P wave/PR interval, but normal QRS complexes with irregular ventricular rate between 120-160)
A Fib Tx
goals are 1. Thromboembolism prevention using Anticoagulation - prevent embolus from A Fib itself or dislodgment of 1 during treatment (ex: cardioversion) - more likely atrial thrombus with recent A Fib episode 2. Hemodynamic stabilization with Rate vs Rhythm Control - keep HR <100 OR put Pt back into sinus rhythm, but rate control is cheaper with comparable mortality rates
Anticoagulation
immediate part of A Fib thromboembolism prevention tx if new-onset and symptomatic, using Heparin OR LMWH if no renal disease; goal is to decrease risk of emboli, prep Pt if need to cardiovert, and to bridge to warfarin; long-term ___ can reduce CVA risk by a lot, so stratify who is at risk for CVA + evaluate who can tolerate ___ long-term using CHADS Score
CHADS Score
determines year thromboembolic risk by giving point for CHF, HTN, Age >75, DM, Stroke (2 pts); proven decreased risk of events on warfarin, so if ___ >2, use anticoagulation with WARFARIN for long-term A Fib tx
Warfarin
part of A Fib Tx that is best for long-term anticoagulation, inhibiting Vit K dependent clotting factors, II, VII, IX, X, protein S/C; only inhibits formation of NEW clotting factors, so "bridge" from Heparin to ___ until factors are dialed back; diet can alter INR, so must monitor with frequency depending on Pt - typical goal = 1. Typical anticoagulation = 2-3 2. For Pt with prior CVA and high risk for A Fib = 2.5-3.5 3. Pt with fall risks = 1.8-2 4. If supratherapeutic INR/signs of bleeding, can use Aquamephyton (Vit K) + get CBC
Diet
effects efficacy of warfarin as Vit K-heavy foods like spinach/brussels/swiss chard decrease efficacy while alcohol can increase effectiveness and lead to bleeding
High INR
guidelines exist for ___ + have Aquamephyton (Vit K) reversal agent; 1. Start IV and check INR and CBC 2. If significant bleeding, admit and depending on INR elevation, give ORAL Vit K - available IM but give PO if can 3. Risk of bleeding > risk of thromboembolic event 4. May just hold dose for 1-2 days and follow up with repeat INR
Cardioversion
rhythm control option for A Fib that has increased success, decreased incidence of recurrence, and avoids long-term anticoagulation if done EARLY within 48 hours (tipping point for thrombus formation); timing = only AFTER anticoagulation to avoid immediate ___ unless Pt is unstable - 1. If planning early ___ within 24 hours, obtain TEE to exclude clot 2. Preferred timing = DELAYED ___ after 3 weeks of anticoagulation 3. If unstable (hypotensive, respiratory distress, MI), give bolus of Heparin, sedate Pt, and SHOCK with Synchronized Cardioversion at 100 J 4. PEARL - spontaneous ___ is common in first 24 hours for most A Fib Pts (paroxysmal)
Chemical
Cardioversion type that is simple and does not require anesthesia/sedation, but less effective; 1. With NORMAL cardiac function = Amiodarone (preferred - Class III) or Procainamide (Class IA) 2. With compromised cardiac function = Amiodarone (or Electrical)
Electrical
Cardioversion type that is complicated and requires monitoring/sedation, but is very effective and can be used for compromised cardiac function
Rate Control
preferred hemodynamic stabilization technique for A Fib Tx with goal of ventricular response ~80 bpm; use meds that slow conduction through AV node such as #1 BB like Esmolol, CCBs like Diltiazem, or Digoxin
Permanent A Fib
if conscious decision to leave Pt in ___, medically manage with Rate Control and Anticoagulation - give BB (Esmolol) or CCB (Diltiazem) + warfarin
A Flutter
atrial depolarization rate of 250-350 bpm due to reentry mechanism with limited conduction to ventricles, resulting in SAW TOOTH pattern in Lead II
V Tach
can be 1. Non-sustained = runs <30s 2. Sustained = more prolonged episodes >30s 3. Monomorphic = consistent QRS appearance 4. Polymorphic = varied QRS appearance associated with Cardiomyopathy 5. Stable ___ = treat with Procainamide, Amiodarone, or Lidocaine 6. Unstable ___ = treat with synchronized cardioversion
V Fib
chaotic disorganized ventricular rhythm (fine or coarse) that is pulseless and with no CO due to MI, HF, prolonged QT, electrolyte issues, congenital heart disease; for each minute left untreated, chance of conversion to normal rhythm decreases 10%, so tx = requires 1. Immediate Defibrillation followed by CPR 2. Epi 3. Amiodarone or Lidocaine - used to suppress ventricular arrhythmias and raise fibrillation thresholds
PACs
single electrical impulse that originates outside SA node in atria and occurs earlier than next expected beat; looks like normal PQRST complexes of underlying rhythm and has incomplete, non-compensatory pause afterward, then underlying rhythm returns until next ___ occur; appear as 1. HR 60-100 bpm 2. Regular atrial/ventricular rhythms except when ___ occur 3. P wave differs in size/shape/location from normal underlying rhythm 4. PR interval is variable based on pacemaker site 5. QRS complex <0.12s and similar to underlying rhythm
Atrial Flutter
presence of regular atrial activity with sawtooth pattern due to SINGLE irritable site in atria initiating many electrical impulses at a rapid rate + no normal P wave produced (replaced by F waves); AV node becomes gatekeeper, deciding amount of stimulation to send to ventricles - ventricular response is established based on number of impulses AV node accepts; appears as 1. ___ with slow ventricular response - ventricular rate <60 bpm 2. ___ with rapid ventricular response - ventricular rate 100-150 bpm 3. Atrial rate 250+ bpm and variable ventricular rate 4. Atrial rhythm regular and ventricular rhythm regular or irregular 5. F waves replace P waves 6. PR interval immeasurable 7. QRS complexes <0.12s and appear alike
A Fib
irregularly irregular rhythm with indiscernible P waves replaced by F waves due to MULTIPLE ectopic atrial foci stimulating AV node - AV node unable to handle each impulse and randomly allows impulses to enter conduction system; appears as 1. Variable atrial/ventricular rates 2. Irregularly irregular rhythm 3. F waves replace P waves 4. PR interval immeasurable 5. QRS complex <0.12s and similar to underlying rhythm
SVT
any fast dysrhythmia with HR >100 bpm and originating above ventricles when rapid atrial ectopic focus overrides SA node to become primary pacemaker - rarely exceeds bpm >160; characterized as fast, regular, narrow, without P waves/measurable PR interval
Wolff Parkinson White
syndrome characterized by TWO AV conduction pathways that creates reentry circuitry as identified by DELTA wave on EKG + QRS >0.10s due to ventricular stimulation from abnormal conduction pathway
Ventricular Rhythms
least efficient representation of heart's pacemaker abilities; impulse can travel retrograde to depolarize atria or antegrade to depolarize ventricles, bypassing normal conduction pathway and resulting in WIDE QRS complexes >0.12s with bizarre appearances + P waves buried in QRS complexes
PVCs
SINGLE ectopic complex arising from irritable site in ventricles that occurs earlier than next expected complex; indicated by wide, bizarre, premature QRS complex in presence of compensatory pause with interruption of SA node - shape is based on site of origin of ectopic focus; appears as 1. HR depends on number of ___ and underlying rhythm 2. Irregular rhythm with PVC present unless Interpolated Beat 3. No P waves with ___ or P waves of underlying rhythm are present 4. No PR interval 5. Wide, bizarre QRS complex >= 0.12s 5. Unifocal if same morphology vs multifocal if different morphologies from different origin sites 6. PEARL - indicates MYOCARDIAL IRRITABILITY
Interpolated
occurs if PVC beat falls between 2 sinus beats without interfering with rhythm - PVC at regular rhythm
Salvos
3 PVCs in a row, which is considered a run of V Tach
V Tach
3+ PVCs arise in sequence at HR >100 bpm; occurs rapidly and is initiated by PVC or PVCs occurring in rapid succession; considered Sustained if run >30s vs Non-sustained if <30s; appears as 1. HR 100+ bpm - differentiates from Idioventricular rhythm 2. Usually regular ventricular rhythm + no atrial rhythm 3. No P waves or PR interval 4. Wide, bizarre QRS complexes that look alike
V Tach Tx
involves 1. If Pulseless, immediate defibrillation - same method for V Fib 2. If hemodynamically unstable, consider immediate synchronized cardioversion 3. If hemodynamically stable, drug intervention, O2, IVF
Torsades de Pointes
similar rhythm to V Tach with variations in width/shape of QRS complex morphology in crescendo-decrescendo pattern - "twisting motion" along baseline; tx = #1 Mg Sulfate
V Fib
#1 common initial rhythm in sudden cardiac arrest cases + common in hours following acute MI as result of MULTIPLE weak ectopic foci in ventricles; myocardial cells quiver without coordinated atrial/ventricular contraction due to lack of normal conduction pathway; creates disorganized, rapid, irregular waves with varying morphologies and no well-organized QRS complexes; considered 1. Fine = <3 mm amplitude 2. Coarse = >3 mm amplitude - usually more irregular looking 3. Indiscernible HR 4. Rapid, unorganized rhythm 5. No P waves, PR interval or QRS complexes
PJCs
initiated from SINGLE site in AV junction and arise earlier than next anticipated complex/beat of underlying rhythm; less common than PACs/PVCs; appear as 1. HR of underlying rhythm plus number of ___ 2. Regular rhythm except for when ___ occur 3. P waves are inverted or absent + occur before or after QRS 4. PR interval is short <0.12s if before QRS or absent if not before QRS 5. QRS complexes look alike and are <0.12s
First Degree
#1 common AV Block with delay at level of AV node, resulting in PROLONGED PR INTERVAL - NSR + PR Interval >0.20s; appears as 1. HR based on underlying rhythm 2. Regular rhythm 3. P waves before each QRS and upright/uniform 4. PR interval >0.20s 5. QRS complexes look alike and are <0.12s when conducted
Second Degree Type I
AV Block AKA Wenckebach phenomenon with progressive delay of impulse at AV node, producing increasing length of PR interval until impulse is not conducted and QRS complex is dropped; pattern is regular with regular atrial rhythm and irregular ventricular rhythm; appears as 1. Unaffected atrial HR + slower ventricular HR (less ventricular beats) 2. Regular atrial rhythm + irregular ventricular rhythm 3. P wave before each conducted QRS and upright/uniform 4. PR interval progressively prolongs until QRS is not conducted 5. QRS complexes look alike and are <0.12s
Second Degree Type II
AV Block that increases risk of progression to 3rd degree block; some P waves are not followed by QRS complex if impulse is blocked in one bundle branch as AV node prevents conduction through to ventricles; appears as 1. Regular atrial HR + slower ventricular HR (may be bradycardic) 2. Regular atrial rhythm + irregular ventricular rhythm 3. Some P waves are not followed by QRS complex and are upright/uniform 4. PR interval is constant whenever QRS complex is present 5. QRS complexes are intermittently absent and can be less or greater than 0.12s
Third Degree
most serious AV Block that is lethal dysrhythmia as atria and ventricles beat independently of each other - SA node fires at 60-100 bpm, while ventricles are paced at AV junction (narrow QRS at 40-60 bpm) or Purkinje network (wide QRS at 20-40 bpm); PR intervals are variable length since no relationship between atria/ventricles; appear as 1. Atria HR 60-100 bpm + ventricular rate based on site of escape pacemaker (AV junction vs ventricles) 2. Regular atrial and ventricular rhythms independently 3. No relationship between QRS complexes and P waves 4. No pattern to PR interval 5. QRS complex appearance is based on site of escape pacemaker - <0.12s if from AV node vs >0.12s if from ventricles
ST Segment Anomalies
change in J point by 1 mm above or below isoelectric line indicates ischemia/injury - 1. Early Ischemia = inverted T waves 2. Late Ischemia = ST depression 3. Injury/Infarction = ST elevation 4. PEARL - must print strip in order to interpret segment changes (cannot determine on monitor)
Inferior Wall
seen from left leg with leads II, III, aVF; indicates RCA or marginal branch (RV) involvement
Septal Wall
seen along sternal borders with leads V1 and V2; indicates some LAD involvement
Anterior Wall
seen along left anterior chest with leads V3 and V4; indicates definite LAD involvement
Lateral Wall
seen along left lateral chest with leads V5 and V6; indicates part of circumflex involvement
High Lateral Wall
seen with leads I and aVL; indicates definite circumflex involvement
Bundle Branch Block
conduction system block of L or R bundle branch, lowering CO and overall ejection fraction since ventricles are no longer in sync - takes longer for ventricles to depolarize, so QRS gets wider; if supraventricular in origin AND QRS >0.12s, ___ is present - like a traffic jam, so have to detour and take backroads instead of main highway; PEARL - watch the NITRATES since they reduce preload, afterload, and CO
Bundle Branch Block Determination
if supraventricular in origin AND QRS >0.12s, look at V1 for direction - use V1's QRS deflection to determine L (- QRS with left turn signal) vs R (+ QRS with right turn signal)
Hypertrophic Cardiomyopathy
autosomal dominant EKG change that can result in sudden cardiac death as LV wall thickens asymmetrically in the absence of obvious inciting hypertrophic stimulus; presents with #1 DYSPNEA + murmur gets louder with STANDING; on EKG, appears as asymmetrical septal hypertrophy producing deep narrow, DAGGER-LIKE Q waves in lateral (I, aVL, V5-V6) and inferior (II, III, aVF) leads; dx with ECHO then tx = total abstinence from strenuous exercise + Beta Blocker and AICD implantation
COPD
leads to 1. R axis deviation = negative QRS in I and positive QRS in aVF - due to lung hyperexpansion causing elongation/vertical orientation of heart and RVH from RA enlargement and RV increased workload 2. Reduced QRS amplitude due to increased retrosternal air = low voltage and muffled heart sounds 3. RBBB in V1 - always look for Brugada Syndrome too (wide QRS and ST elevation)
Pericarditis
results in sinus tachycardia with DIFFUSE CONCAVE ST ST DEPRESSION + PR DEPRESSION; diffuse involvement and concavity differentiate from MI
Sick Sinus Syndrome
rare dysrhythmia more commonly developed with increased age, Pts with heart disease, or s/p heart surgery that damages sinus node that affects SA node, resulting in slow heartbeats, pauses between beats, or irregular rhythm; usually asymptomatic, but can have intermittent S/S of palpitations, chest pain, SOB, dizziness, presyncope/syncope, fatigue, or memory loss/cognitive defects; EKG features = 1. Sinus bradycardia 2. Sinus arrest 3. Chronotropic incompetence = HR WNL at rest, but does not increase as much as it should during activity 4. Tachy-Brady Syndrome = alternates between slow and fast rhythms with long pause between beats 5. Second Degree AV Blocks 6. Supraventricular tachyarrhythmias = SVT, A Fib, A Flutter 7. Tx = Pacemaker (AICD) 8. PEARL - difficult to dx/distinguish as underlying cause of arrhythmia on EKG, but distinguishing feature is A Fib with slow ventricular rate in absence of meds that would cause bradycardia (BBs, Digoxin)
Middle