Arrythmia Flashcards
ectopic beats
potentials reached by myocardial cells outside normal conduction system
spontaneously depolarize
escape rhythm
SA node fails and latent pacemakers take over
PAC
increased sympathetic activity depolarizes atria outside SA node
typically asymptomatic, may have palpitations
early beat on an otherwise normal rhythm
causes of PAC symptoms
EtOH
caffeine
emotional stress
bradycardia arrhythmia causes
issue is with the SA node
- sinus bradycardia
- sick sinus syndrome
sinus bradycardia
heart rate slowed bc of decreases SA node firing
intrinsic issue or extrinsic
often benign, only treat if symptoms
intrinsic causes of sinus bradycardia
aging
ischemic heart disease
cardiomyopathy
athletes
extrinsic suppression of SA node causes
pharm (beta blockers)
metabolic causes (thyroid, DM)
vasovagal PNS stimulation (fear, pain)
secondary to shock (hemorrhagic or neurogenic)
symptoms of bradycardia
fatigue light headedness syncope change in mental staus chest pain
tx of bradycardia
atropine 0.5 mg IV (temp. speeds up HR)
transcutaneous or transvenous pacing (central line)
definitive tx is implantation of pacemaker
Paces of SA node, AV node, ventricular escapes
SA: 60-100
AV: 40-60
ventricular escape: 20-40
junctional escape rhythm
arises from AV node or His
narrow QRS no P wave
HR 40-60
ventricular escape rhythm
HR 20-40
wide QRS
tx of escape rhythms
same as bradycardia
- atropine
- transcutaneous or transvenous pacemaker
first degree AV block
prolonged PR
P wave for each complex
transient or fixed
no need for tx, but can progress
transient first degree AV block causes
vagal tone increase
transient local ischemia
drugs that depress conduction
fixed first degree AV block causes
MI and or degeneration due to age
second degree AV block
intermittent failure of AV node conduction
two types (Wekenbach/Mobitz I and Mobitz II)
Mobitz I
AV delay gradually increases until impulse is blocked
PR segment increases between each beat until blockage and then is reset
population with Mobitz I
type I 2nd degree AV block
children, athletes, increased vagal tone, during sleep
2nd degree AV block Type I treatment
almost never needed
can be benign but also could be due to MI
if symptomatic treat like bradycardia (atropine, transcutaneous pacer/transvenous pacer, permanent pacemaker)
Mobitz II
PR interval is unchanged prior to a P wave with no QRS
predictable cadence
treatment regardless of symptoms is pacemaker
3rd degree AV block
complete heart block
no association between atrial contraction and ventricular contraction
SA node passes to AV node but doesnt get to ventricle - escape beat controls ventricles
common causes of 3rd degree AV block
MI
drug toxicity
chronic degeneration
third degree AV block symptoms
lightheadedness syncope chest pain hypotension AMS
Completely unstable
sick sinus syndrome
intrinsic SA node dysfunction
brief periods of episodic bradycardia
decreased CO = sx of bradycardia
sick sinus syndrome symptoms + treatment
dizziness, confusion, syncope, altered mental status
treatment: transcutaneous pacemaker + permanent pacemaker
tachycardia mechanisms
HR >100
- enhanced cellular automaticity
- triggered activity
- unidirectional block and re-entry
factors to consider with tachycardia
is it above ventricle (narrow QRS) ?
P wave association with QRS complex
P wave morphology
sinus tachycardia
100-160 bpm
p wave for every QRS (can be difficult)
secondary to increased sympathetic tone and decreased vagal stimulation
probably causes of sinus tachycardia
exercise
fever
dehydration
hypoxemia
atrial flutter
fast atrial rate (250-350) with different ventricular rate
“saw tooth pattern”
causes of atrial flutter
re-entry impulse
saw tooth P waves (atria depolarized thru out cycle)
pre existing heart condition
can be transient, persistent, permanent
symptoms of atrial flutter
palpitations
SOB
generalized weakenss
vague (feel ill, nausea)
atrial flutter tx
unstable
synchronized cardioversion
atrial flutter tx
asymptomatic but stable
pharmacological
Non-DHP CCB
anti-arrythmics
consider synchronized cardio version
atrial fibrillation
very common
atrial quiver or anarchy in atria
atrial rate 350-600
very erratic baseline w.o. recognizable p waves
atrial fibrillation symptoms
palpitations
SOB
weaknesss
chest pain
atrial fibrillation common in its with
HTN CAD EtOH intoxication thyrotoxicosis pulmonary disease
atrial fibrillation is dangerous bc
- decreased CO
2. blood stasis, causing increased clot risk
unstable AFib with RVR tx
systolic BP less than 90
chest pain
altered mental status
synchronized cardio version
tx of stable AFib with RVR
control ventricle rate to restore sinus rhythm
CCB (BB if needed)
stable asymptomatic persistent AFIB tx
CCB
Beta blocker
Start on anticoagulant
MAT
stimuli does not come from one foci from several foci
isoelectric baseline which is more discernible between P waves (can see the P wave)
MAT commonly associated
Pulmonary disease
Hypoxemia
MAT tx
non-DHP
two types of re-entrant tachycardias
AV nodal reentrant Tachycardia
AVRT
Paroxyxsmal SVT
sudden onset and termination
atrial rates b/t 160-180
narrow QRS
PSVT symtoms and epidemiology
mc effects young adults, if elderly will have syncope
palpitations, light headedness, SOB, can be asymptomatic
PSVT treatment
non pharm
vagal maneuvers
- carotid massage
- Ice pack to the face
valsalva maneuvers
-classical and REVERT techniques
PSVT tx pharm
adenosine (adenocard) 6mg IB fish
theophylline may inhibit adenosine
mc form of AV nodal re-entrant tachycardia
PSVT
AVRT Ventricular pre-excitation syndrome
only one bypass tract (typically bundle of kent)
impulses travel to ventricles thru accessory pathway AND AV node
AKA WPW
distinct EKG of wolfe parkinson white syndrome
shortened PR
delta wave
widened QRS
WPW orthodromic conduction tx
narrow QRS, more common
vagal maneuvers, adenosine and procanamide if stable
synchronized cardio version if stable
WPW Antidromic conduction
wide complex QRS
less common
tx with procainamide
DONT GIVE CCB, BB, adenosine
PVCs origination and EKG shows
ectopic ventricular foci
widened QRS complex (No P wave)
PVCs are issue
not dangerous in those W/O heart disease
increased risk of VTach or VFib in those WITH heart disease
commonly follows MI
increased risk if >10/min or couplet/triplet
Bigeminal PVCs
when every alternate beat is a PVC
trigeminy PVCs
two normal beats precede a PVC
PVC every third beat
PVC tx
reassurance, BB if >10/min
V Tach
> 3 + consecutive beats
HR > 100-250
Non-sustained V Tach
3 or more PVCs, last less than 30 seconds, self-limiting
dont usually treat (anti-arrythmics can cause VFib)
consider beta blocker for tx
sustained V Tach
lasts > 30 seconds and requires termination
can be stable or unstable
stable V Tach vitals + tx
Pt has: Pulse, normal BP, no chest pain, normal mental status
tx with: 1. IV access 2. EKG 3. Cardio consult consider anti-arrhythmic (Procainamide)
unstable VTach vitals + tx
1 of: pulseless, chest pain, hypotension, LOC
WITH Pulse: tx is synchronized cardio version + ICD
NO pulse: defibrillation
defibrillation steps in unstable V Tach
PULSELESS
- CPR + defibrillate
- CPR 2 min, IV/IO access
- defibrillate again
- Epinephrine + CPR 2 min
- Defib (3rd time)
- Amiodarone + CPR
- Defibrillation
monomorphic V Tach
rate is regular and QRS complexes are the same
single origin of arrhythmia in ventricle
polymorphic V Tach
rate is irregular and QRS complexes are variable in shape
cyclic alteration of impulse from ventricle
gives appearance of twisted QRS - TORSADES
Torsades des Pointes
long QT syndrome is a cause (can be congenital)
can be caused by underlying metabolic abnormalities (hypo-K, Mg) or medications
initial tx of Torsades des Pointes
CPR
non synchronized cardio version
amiodarone and Epi
Mg 2gm IV drip over 5-15 min while treating
long term: BB + ICD
definitive pharm tx of Torsades
Mg IV drip
how is V Tach differentiated from SVT
wide QRS in v tach
most life threatening form of arrhythmia
V Fib
severe drop in cardiac output that leads to death
treatment of VFib
electrical defibrillation
CPR + Defib between Epi and Amiodarone
pulseless electrical activity
presence of rhythm without a pulse or electrical activity without perfusion
PEA treatment
CPR + Epi + H&Ts
success depends on patient’s baseline and speed when started
what do we do for patients who have ROSC following V Tach, V Fib, or PEA
RAVEL
fluid management
airway management
vasopressors
evaluate H & T
H & Ts
H: hypovolemia, Hypoxia, Hyponatremia, Hyperkalemia, Hypothermia
T: thrombosis, tension pneumothorax, tamponade, toxins
RAVEL
Responsive Airway Vitals Ekg Labs
done after return of SR in Vtach/VFib
Asystole management
- CPR
- 1 Epi ever 3-5 min
- H & Ts
physiological monitoring during CPR
PeTCO2 (end tidal CO2 device connected to endotracheal tube, measures CO2 exhalation)
Arterial one (radial artery, monitors BP and ABG)
when an IV site is not available in cardiac arrest…
IO
can give drugs, fluids, all ages, quick
found in PROXIMAL TIBIA, distal femur, proximal humors, distal tibia)
