Arrhythmias Flashcards
a fib
rapid, irregular, atrial activation (atria quiver instead of contracting properly, causes blood to pool & form a clot –> increased r/o stroke)
-very common
-increased risk w/ age
a fib sx
-may be asx
-palpitations (all arrhythmias), tachycardia (100-200 bpm), fatigue, weakness, mild dyspnea
-irregularly irregular pulse
others: stroke, thromboembolism
Dx studies for a fib
EKG: no p waves, ventricular rhythm lacks a repetitive pattern
ECHO: should be done on all pts w/ new onset a. fib to look for clots
Labs: CBC, electrolytes, renal fxn
a fib tx (address rhythm)
-cardiac ablation: better than drugs but higher r/o stroke (ex. atrioventricular junction ablation w/ cardiac resynchronization therapy - destroys link btwn LA and LV, f/b pacemaker implantation)
-drugs: AMIODARONE has least cardiotoxic AEs & is more effective than sotalol, donedarone, propafenone, flecainide; start in hosp to closely monitor!
-cardioversion: must be on AC for 3 wks and have TEE prior
A fib: tx of rate vs rhythm
-for decades, rate control was deemed most important d/t AEs of anti-arrhythmics and “noninferiority” of rate control agents
-recent studies, lean towards prioritizing rhythm control
-there are times when both are important
a fib tx (address rate)
-indications: asx, elderly, long-standing afib, markedly enlarged left atrium
-1st line: B-blockers and non-DHP (CCB) ***avoid CCB in pts w/ CHF
-less aggressive rate control (<110bpm) is preferred over more intense rate control (<80bpm)
a fib tx (address stroke risk)
Calc CHA2DS2-VASc score –>
-start oral AC if 2+ in men or 3+ in women
-may consider LAA closure (i.e. WATCHMAN device) depending on score
What does CHA2DS-VASc score stand for/consider
CHF
HTN
Age 75+ (doubled)
DM
Stroke (prior stroke, TIA, or thromboembolism) (doubled)
Vascular dz
Age 65-74
Sex category
*each is worth 1 pt unless it says “doubled”
Stroke risk AC: new oral AC (NOACs) that are now recommended over warfarin
-Dabigatran (Pradaxa)
-Apixaban (Eliquis)
-Rivaroxaban (Xarelto)
-Edoxaban
When is warfarin still recommended over other NOACs
if pt has moderate/severe mitral stenosis, advanced kidney dz, or if pt has an artificial heart valve
Supraventricular tachycardias
-caused by premature signaling in atria
-often paroxysmal (PSVT)
Supraventricular tachycardia S/S
- > 100 bmp (often 150-200)
-narrow QRS
-palpitations, dyspnea, dizziness, chest discomfort, syncope
3 types of supraventricular tachycardia (most to least common) and their changes on EKG
- AVNRT (atrioventricular node reentry): retrograde p wave falls w/in or just after QRS
- AVRT: reentry involving an accessory pathway (i.e. WPW - short PR interval)
- Focal & Multifocal Atrial tachycardia: p waves immediately in from of QRS complex
*supraventricular –> think above ventricles, which lies the atria; on EKG the p wave represents the atria, therefore these will have p wave abnormalities
AVNRT (AV nodal reentrant tachycardia)
-MC type of PSVT
-reentry circuit involving the AV node & nearby atrial tissue –> leads to separate pathways w/in the AV node, resulting in tachycardia d/t premature beats
-usu presents after age 20
Dx of AVNRT (s/s, dx test results)
-HR of 150-250 bpm
-palpitations, lightheadedness, dizziness, dyspnea
-neck pounding secondary to CANNON WAVES is pathognomonic
-EKG (PAC w/ prolonged PR at beginning, p wave in or just after QRS - may be superimposed (“pseudo-r”))
*pathognomonic = specifically typical of that disease
*cannon waves are d/t atria & ventricles contracting simultaneously causing waves in the blood
what are cannon waves and what condition is this associated with?
cannon waves are d/t atria & ventricles contracting simultaneously causing waves in the blood
associated with AVNRT
AVNRT: acute management tx
-if hemodynamically stable, try vagal maneuvers (Valsalva)
-if Valsalva doesn’t work, give IV adenosine
-If adenosine is ineffective, give IV verapamil or IV metoprolol
-If all fails, OR if pt is hypotensive, has angina pectoris, or has CHF, then cardioversion is performed
*if refractory (resistant to tx) then perform advanced CV life support (ACLS)
how does the Valsalva maneuver work
holding your breath and bearing down decreases blood return to the heart –> stim symNS –> increased HR and contractility –> stim parasymNS to compensate for overstim of symNS –> decreased HR and contractility
AVNRT: preventative therapy
depends on frequency of arrhythmia, severity, pt preference, etc.
Tx for recurrent AVNRT (Cure rate)
catheter ablation
-95% cure rate
*if pt can’t undergo ablation, then use B-blockers, non-DHP (CCB), anti-arrhythmics
WPW
<1% of population
-accessory pathways connect the atria and ventricles; AV node is bypassed
-dx in teenager/early adulthood
Sx of WPW
dizziness
syncope
SOB
weakness
chest pain
EKG findings w/ WPW
short PR interval
delta wave
WPW: Tx
-Goals: reduce sx and prevent life-threatening arrhythmia
-urgent cardioversion if hemodynamically unstable (low BP, elevated HR)
-Vagal maneuvers
-Adenosine 1st choice if vagal maneuvers fail; Verapamil 2nd line
-Long-term management: catheter ablation
Focal Atrial Tachycardia (what is it, what causes it, EKG findings, long-term therapy)
-small area in atria generates impulses that override SA node
-can be d/t meds, caffeine, alcohol, or idiopathic
-EKG: abnormal p wave morphology, QRS is normal
-Long-term therapy: uncertain, drugs (???), catheter ablation may be effective in 70-90%
Multifocal Atrial Tachycardia (MAT)
100-130bpm
-3+ morphologically distinct p waves
-irregular
-multiple areas of the atria are sending electrical impulse randomly
(same sx as other arrhythmias)
what diseases are MAT associated with
respiratory dz (MAT is secondary to COPD, hypoxia, pulm HTN)
CHF
MAT: Tx
tx underlying problems (oxygen)
rate control w/ Metoprolol or Verapamil
atrial flutter
rapid, circular (more organized than a fib), reentrant atrial arrhythmia
clinical presentation of atrial flutter (s/s)
-unusual in pts w/o cardiac dz (a fib, valvular dz, cardiomyopathy) or pulm dz
-palpitations, fatigue, dizziness, dyspnea
-tachycardia, hypotension, diaphoresis
Atrial flutter: Dx tests
EKG: ventricular rate ~150bpm, p waves absent, “sawtooth” pattern in II, III, aVF
Echo: perform in all new diagnoses
Atrial flutter: Tx/Management
-rate control
-AC
comparing presentation and tx of a fib and a flutter
presentation is the same
tx for both is rate control and AC but for a fib you can consider cardioversion & anti-arrhythmics
Ventricular tachyarrhythmias (organized re-entry vs disorganized re-entry)
Organized re-entry (>120bpm): non-sustained VT (<30 secs, may be asx) and sustained VT (lasts 30+ secs)
Disorganized re-entry: V fib (350-450 bpm), Torsades de Pointes(250-350 bpm)
*all except non-sustained VT can lead to cardiac arrest
Ventricular tachycardia: monomorphic vs polymorphic
Monomorphic: single focus or reentrant pathway; regular identical QRS complexes
Polymorphic: several foci or pathways; irregular, varying QRS complexes
Ventricular tachycardia
3+ consecutive ventricular beats at 120+ bpm
-occurs MC in pts w/ past MI or cardiomyopathy
-frequently deteriorates to ventricular fibrillation (scary!)
Sx of VT
variable
-if sustained, pt may have palpitations, hemodynamic compromise (decreased BF to body/shock), or sudden cardiac death
Dx of VT
any wide QRS complex tachycardia should be considered VT until proven otherwise
VT: Tx depending on type of VT
Non-sustained VT: no immediate tx unless sx occur; if sx occur drugs are usually used
Hemodynamically stable sustained VT: cardioversion or antiarrhythmics (lidocaine, procainamide, amiodarone)
Pulseless VT (hemodynamically unstable): defibrillation
ICD is often used for long-term prevention of sudden death
What may occur if CCB are used in a pt w/ VT
hemodynamic collapse, so AVOID CCB!!!
Cardioversion
different from defibrillation in that the shock is synchronized (given at certain time) and has less energy
Long Q-T syndrome causes
can be congenital or acquired (d/t drugs, hypokalemia, or hypomagnesemia)
Long-QT syndrome: Sx
most acquired cases are asymptomatic
sometimes pts have palpitations, syncope, cardiac arrest
**pay attention to hx of syncope
Long-QT syndrome: Prognosis
-increased r/o sudden death if have congenital deafness, h/o syncope, female, and VT during monitoring
What is your biggest fear with long QT syndrome
Torsades de Pointes (bc long QT synd messes w/ how your heart relaxes and recharges)
What may be the result of untreated long QT syndrome
if untreated, 50% have experienced LOC or cardiac arrest by age 12
Long QT syndrome: Tx
-B-blockers
-Surgical sympathectomy if unresponsive to drugs (removal of ganglion)
Torsades de Pointes (“twisting of the points”)
a polymorphic VT w/ a long QT
-may degenerate into v fib (scary!)
-points & curves alternate up and down on EKG
Torsades de Pointes: Tx
-MAGNESIUM in the short-term
-B-blockers (propranolol) in the long-term
V fib
-uncoordinated quivering of ventricles
-results in no useful contractions (lethal bc no CO)
-on EKG rate and rhythm are fast and irregular, p waves and QRS are absent
What % of cardiac arrest pts present with V fib
70%
V fib Tx
-requires CPR and defibrillation, Epi q3-5minutes
commonality of PVCs (premature ventricular contractions)
1/2 of all people have them
more likely in older pts
If PVCs are found post-MI what does this mean
higher risk of death
Increased risk of ____ if EF is <50% in conjunction w/ PVCs
cardiac arrest
PVC Sx
mostly asymptomatic
-may have palpitations (MC), dizziness (uncommon)
PVC signs
exam is usually normal, may be an irregular pulse during PVCs
Dx tests for PVCs
EKG
ECHO if significant sx or suspicious of structural dz
Tx of PVCs
-eliminate triggers if possible (alcohol, caffeine, thyroid dz, anemia, stress/anxiety)
-B-blockers, CCBs, ablation if medical therapy doesn’t work
EKG findings for PVCs
P wave: usu doesn’t precede QRS; may be seen after QRS causing distortion of ST segment
QRS: wide, abnormal
ST segment & T wave: inverted
R-R interval: usu f/b a full compensatory pause
bigeminy, trigeminy, couplet
Bigeminy: PVC after every normal beat
Trigeminy: PVC after every 2 normal beats
Couplet: Two PVCs in a row
What % of pts >50yo have at least one PAC/hr
99% of pts over 50 have at least 1 PAC/hr
PAC EKG findings
abnormal (shape) p waves
atria contract early so may have p wave early
sinus bradycardia
sinus rhythm w/ <60 bpm
Cause of sinus bradycardia
-may be normal in many healthy adults and children, particularly during sleep and in endurance athletes
-Pathological causes: dysfunctional SA node, meds (B-blockers), AMI, OSA, infectious diseases
Sinus bradycardia: Sx
if sx occur, they include lightheadedness, fatigue, syncope
Sinus bradycardia: Tx
-if no sx, then no tx required
-if tx is necessary, IV atropine is often used
*If atropine doesn’t help, then pacing is performed
1st, 2nd, and 3rd degree Heart Block (poem)
If the R is far from P (slow transmission, long PR interval), then you have a 1st degree
Long, longer, longest, drop! Then you have a Wenkebach (Mobitz I)
If some Ps don’t get through (missing QRS-T), then you have Mobitz II (more likely to have sx and need tx)
If Ps (atria) and Qs (ventricles) don’t agree, then you have a 3rd degree
Heart Block Sx (based on degree)
1st degree & Wenkebach: typically asx
Mobitz II (sometimes Wenkebach: palpitations
3rd degree: palpitations & syncope
Heart block tx
Pacemaker for Mobitz II and 3rd degree blocks
