Dysrhythmias and Blocks
BKN
1/24/02
How to crack a rhythm
 What is the atrial rate and what is the
source?
 What is the ventricular rate and what is the
source?
 What is the relationship between the atria
and the ventricles? (Who’s in charge here?)
 Is there conducting system blockade?
And after you crack it
 What is the underlying cause?
 Is the the rhythm hurting the patient?
 What should be done?
Rules of the road
 No arrests, you’ve all taken ACLS, you
know how to treat VF. Asystole and PEA
are dead people
 “It’s 2 a.m., there’s noone in the place. . .”
– PG1 or 2 assigned as senior resident
– PG3 assigned assigned as attending
 No kibbutzing from the crowd until I ok it.
Case 1: Dr. Nelson’s Happy New
Year
 51 y/o M complaining of palpitations
 Drunk on homemade wine (ETOH = 225)
 PE unremarkable
 Intermittent episodes of rapid pulse and
pallor with BP 95/60 lasting up to 1/2
minute
 Rhythm strips follow; not continuous
Happy New Year! What to do?
 At next episode, cardiovert with 50j (YES!)
 Amiodoarone or Lidocaine
 Magnesium sulfate 4 gm
 BAL 5 mg/kg
 Adenosine 12 mg IVB
 Leave him alone, we never liked him much
anyway and we see a possible end to
pimping
Happy New Year
 What’s the rhythm?
 Is it hurting him?
 What’s the cause?
V tach vs SVT with aberrancy
 Clinical features
 Physical
 EKG
 Specific QRS patterns
 Brugada’s Criteria for 4 step quick process
– MANY PATIENTS IN VT HAVE NORMAL BP AND
MENTATION. DX OF SUSTAINED VT REQUIRES
>30 SEC OF RHYTHM
Clinical Features
Favors V Tach
Favors SVT
Age > 50
Age<35
Organic Heart Disease None
Hx V Tach
Hx SVT
Physical Exam
V Tach
SVT
Cannon A waves
Absent
Pulse Variation
No variation
Variable heart sound
No variation
EKG
V Tach
SVT
Fusion Beats
None
AV dissociation
P waves precede QRS
QRS> .14 sec
QRS<.14 sec
Extreme LAD (<-30)
Normal Axis
No response to vagal
Vagal slows or stops
Specific QRS patterns
V tach
SVT
V1: R, qR. RS
V1: RsR’
V6: S, rS, qR
V6: qRs
Identical to previous Identical to previous
VT
SVT
Concordance of QRS
in V1 – V6
Brugada’s criteria: any Yes = VT
 1. Absence of RS complex in all precordial?
 2. R to S interval >100 ms in one
precordial?
 3. Atrioventricular Dissociation?
 4. Morphology criteria for VT present in
both leads V1-2 and V6?
Is there anything wrong with. . .?
 Cardioversion if in sustianed wide complex
tachycardia? Go ahead if patient metastable
or worse. Be sure you reassure the patient
that it doesn’t mean he’s dieing (if he’s not)
 Adenosine? Probably safe, has a very short
1/2 life
Holiday Heart
 Supraventricular tachycardias (most often
Atrial Fibrillation)
 Transient Ventricular Tachycardia
 Seen in chronic alcoholics on a binge
Alcoholic Heart Disease
 Holiday Heart
 Alcoholic Cardiomyopathy
 Acute intoxication has cardiodepressant,
vasodilatory and diuretic effects even in those
with a normal heart (keep in mind for that drunk
mildly hypotensive trauma victim)
 In those with coronary disease, >2 oz can decrease
exercise tolerance and increase ST depression
after angina
Treating Dr. Nelson
 Abstinence will lead to conversion to sinus
 Do not treat unless hemodynamically
unstable
Case 2: Aunt Jane ain’t right
 76 y/o F noted to be increasingly confused
by family over last several days
 Her Doctor is not available
 Family doesn’t know details of medical
history
 Patient complains of being weak
Aunt Jane’s physical
 Elderly female, oriented x 1, mod
respiratory distress
 BP 80/p, P 150, T 97 R, RR 24, SaO2 88%
RA
 JVD, Rales in bases
 ECG follows
Case 2: Aunt Jane ain’t right
 What’s the rhythm?
 What’s the underlying cause?
 Is it hurting her?
 What to do?
What’s the rhythm?
 Atrial rate 180, probably sinus
 Ventricular rate 150, alternates between ventricles
(LBBB pattern, RBBB pattern)
 Complete AV dissociation
 Apparent complete heart block
 Complete rhythm diagnosis: atrial tachycardia, bi-
directional V Tach, AV dissociation
Aunt Jane’s rhythm problems
 PAT with AVB and Bidirectional V Tach are both
almost pathognomonic of Digitalis toxicity
 Is it hurting her? Clearly yes, we probably need to
treat while waiting for the Fab frags to arrive, be
administered and take effect
 What to do? Cardiovert her? Overdrive pacing?
Diurese her? Use antidysrhythmics?
Cardiovert?
 Cardioversion generally considered
contraindicated for Dig toxic rhythms. The heart is
irritable due to increased catecholamine sensitivity
 Fear cardioversion to refractory VF, VT and
asystole
 Most of that literature is very old and is talking
about cardioverting AF. Applicability to VT
unclear.
 Is Aunt Jane an exception because she’s so sick
we don’t think we’ll make her worse?
Overdrive Pacing?
 Transvenous pacing in dig toxicitycarries
same dangers as cardioversion (Induces
ventricular dysrhymias, mortality 13%)
 Transthoracic pacing may be safer, but the
pacer would need to be capable of higher
rates than the intrinsic rhythm
Diuresis?
 Most patients in chronic dig toxicity are
already on diuretics and hypokalemic.
Hypokalemia worsens Dig toxicity.Must
check K and supplement as necessary if
going to diurese
Antidysrhythmics
 Most antidysrhythmics are contraindicated
in Dig toxicity
 Magnesium indicated for dig induced
tachydysrhythmias. 1-2 gm over 2 minutes
then 1-2 gm/hr
 Lidocaine or phenytoin are considered
safest
Anti digitalis Fab fragments
 Expensive
 Indicated for severe ventricular
dysrhythmias, atropine refractory
progessive hemodynamically sig
bradydysrhythmias, severe hyperkalemia,
rapidly progressive dysrhythmias,
cardiotoxic coingestants, plant cardiac
glycosides + severe dysrhythmias, high
levels plus any of the above
Case #3: Bloody Awful
 A 52 yo male presents with weakness,
melena, and palpitations. H/O heavy ETOH
intake chronically.
 BP 80-100 P fast and weak, monitor heart
rate 205, SaO2 = 78%, patient stuporous, no
ETOH odor
 Heart: very fast Abdomen soft, stool black,
NG grossly bloody
Bloody awful
 Initial lab:
 Glucometer = 500
 ABGs =7.25/20/55, BE = -15, Hgb = 7,
Wassup?
 What’s the rhythm?
 What’s the underlying cause?
 Do we need more info?
 Is it hurting him?
Wassup?
 Rhythm Atrial fibrillation with rapid ventricular
response
 Underlying causes: hypovolemic shock, alcoholic
heart disease, possible DKA
 Addl info: CXR borderline cardiomegaly without
failure
 Is it hurting him? In this clinical scenario, of
course. Combination of rate, blood loss, base
deficit, anemia suggest that cardiac arrest is
imminent
What to do?
 Define possible strategies
What to do?
 Cardiovert? (electrically or chemically)
 Slow Vent Response?
 Correct hypovolemia, anemia, DKA and
hope he gets better from this alone?
Cardioversion
 Pro: rapid return to a rate allowing ventricular
filling, adequate cardiac output
 Con: In presence of chronic AF, atrial thrombus
may exist. Cardioversion may lead to arterial
embolism (stroke, mesenteric infarct, etc)
 Do we think this is acute or chronic AF?
Acute or chronic?
 The rate and the clinical scenario suggests
acute, but you never really know.
 How to do it? Electrical or chemical?
Electrical or Chemical
 Electrical is quick and except in the dig toxic is
unlikely to have side effects. However, the
underlying condition leading to AF is unchanged.
The heart may go right back into the rhythm
 Chemical conversion is slower, but leads to
conditions more likely to allow permanent
conversion. However the drugs used (class 1a and
3) can all cause major dysrhythmias and
cardiodepression. Digoxin is slower but won’t
cause cardiodepression
Summary of recs (most pts
hemodynamically stable)
 For acute AF in patient without failure or
cardiomyopathy: use class 3 agent (Ibutilide
has highest success rate and quickest action,
but can cause dysrhythmias after single
dose)
 Chronic AF usually with cardiomyopathy:
rate control, anticoagulation for 3 weeks (or
TEE) followed by electrical cardioversion
Slow ventricular rate
 Calcium channel blockers are preferred for
the patient in absence of ventricular
dysfunction.
 Digoxin for the hemodynamically unstable
may take longer to have effect.
 Note reading the studies, it appears that the
differentiation between “rate-control” and
“cardioversion” is probably not real
Correct conditions: always
 MI, Ischemia, valvular disease, pericarditis,
hyperthyroidism, SSS, contusion, holiday,
idiopathic, hypertensive heart,
cardiomyopathy, cardiac surgery,
catecholamine excess, PE, CHF, WPW
For this patient
 It was felt that arrest was imminent and
acute AF was most likely, The patient was
cardioverted with 200 j. He converted to
sinus and within 3 seconds reverted to AF
 Class 1a, 3, and Ca blockers were rejected
because of patient’s probable
cardiomyopathy and hypotension/shock
For this patient
 O2 and fluid resuscitation were started
 Type specific blood was ordered
 Digoxin 0.5 mg was given IV
 Within 5 minutes the patient converted
spontaneously to sinus tach. Blood and
octriatide started, Pt admitted to ICU, GI
consulted.
Case 4: I fainted (4 p.m.)
 14 y/o female brought by mother and teacher.
Child reportedly was in Biology lab, dissecting a
frog which upset her
 The biology teacher reports she fell to the ground
suddenly, had few jerks of extremities, and awoke,
fully concious in about a minute.
 Child has no memory of falling and had no
prodromal sympotoms
I fainted
 Child is awake and alert
 VS are normal, glucometer is 110,
SaO2=98%
 Complete neuro exam is normal
 General physical exam is normal
 Should we quit? If not, what would you like
to do?
I might quit, but
 You could easily argue for a b-hcg, bmp,
cbc, and a CT/EEG to r/o
pregnancy/ectopic, anemia, seizure disorder
and subarachnoid bleed
 An ECG is harder to justify, but this is a
cardiology lecture, so:
What to do?
 Is there a problem?
 What will you recommend?
Course
 Child is admitted to telemetry, Cardiology
consult is planned for the AM
 The code team is called at 2 am as the child
has arrested
 Rhythm strip follows
What to do?
 What’s the rhythm?
 What’s the immediate treatment?
 In the short term?
 In the long term?
 Would it have been different if the child had
been taking erythromicin?
Long QT syndrome
 Adrenergic dependent or pause dependent
 Both can cause sudden death from
Polymorphic V Tach
 Pause dependent requires slowing of heart,
is generally acquired
 Adrenergic requires tachycardia and is
mostly congenital (thus the more
dangerous)
Causes of long QT: pause dep
 Class 1a, 3 antidysrhythmics
 Psych drugs: TCA, phenothiazines
 Antibiotics: erythromicin, ampicillin, pentamidine
 Antihistamines: terfenidine, astemizole
 misc: cocaine, organophosphates, cisapride,
 Electrolytes disorders: lo K, lo Ca, Lo Mg
 Severe ischemia
 Normal heart/ no drugs
Causes of Long QT: adrenergic
 Congenital
– Jervell and Lange-Nielsen (deafness, recessive)
– Romano-Ward (normal hearing, dominant)
– Sporadic (normal hearing, no family tendency)
– Mitral Valve Prolapse
 Acquired
– Cerebrovascular disease (particularly SAH)
– Autonomic surgery (radical neck, CEA, truncal
vagotomy)
Immediate treatment for PMVT
 Cardioversion in same manner as
monomorphic VT
Intermediate treatment
 Pause dependent
– stop offending medication
– Mg infusion
– Overdrive pacing or isoproterenol drip to rate of 100 to
120 bpm
– correct electrolytes
 Adrenergic dependent
– Beta blockade
Long term treatment-refractory
cases
 Adrenergic dependent
– left cervicosympathectomy
– cardiac pacing with maximum beta blockade
– implantable defibrillator
 Pause dependent
– permanent pacer
– implantable defibrillator
Case 5: Weak and Dizzy
 70 y/o women presents with occasional
episodes of near syncope
 PMH: HTN, angina
 PE: VS nl, CNS nl.
 CVS: S4,
 BMP, CBC nl
 ECG follows
What to do
 Diagnosis
 treatment
Weak and dizzy
 Sinus arrest, intermittent ventricular escape
rhythm, incomplete AV dissociation
 Treatment: trans thoracic pacing, EPS
referral
 While hooking up the pacer, the following
strips are collected
Weak and Dizzy
 What additional diagnoses added?
 Any additional therapy?
Weak and dizzy
 Brady-tachycardia syndrome, an advanced
manifestation of Sick Sinus syndrome
 May have to use antidysrhythmics to slow
rate. This increases block and necessitates a
permanent pacer
Case 6: My heart is running away
 30 y/o m presents with rapid heart beat,
dyspnea and weakness. Has had similar
episodes in past but no treatment
 PE: Pulse rapid, weak. BP 60/p, monitor
heart rate 220
 ECG follows
What’s next?
 Rhythym is Wolfe-Parkinson-White
syndrome with Atrial Fibrillation
What’s next
 Cardioversion gives following rhythm
change. Now what?
WPW with alternating
conduction
 Orthodromic tachycardia when conduction
down AV node and reciprocates up Bundle
of Kent
 Antidromic tachycardia when conduction
down Bundle of Kent and back up AV node
WPW with tachydysrhythmias
 Antidromic regular tachycardia or any
irregular tachycardia, regardless of QRS
duration at high risk for V Fib
 All drugs that block the AV node are
contraindicated as they may increase rate of
conduction through the accessory pathway,
accelerating rate of dysrhythmia leading to
V Fib
No-Nos
 No Digitalis, Ca channel Blockers, Beta-
blockers, or adenosine
 Regimen of choice: cardioversion if
unstable, procainamide, referral for catheter
radioablation of pathway
 Second line drugs: other 1a and 1c
Case 7: I need a doctor for Med Control
 56 y/o had a syncopal episode, feels well
now, wants to refuse therapy
 The paramedics fax this ECG, what do you
think?
Not so fast buddy
 Patient has First degree AV block, RBBB
and intermittent LAHB
 Consider this a “Partial Trifasicular Blcok”
Trifasicular Block
 When RBBB, LAHB and LPHB present one sees CHB
with VER (can be either from right or left ventricle).
 But there are five fasicles: His bundle, Right Bundle, Left
Bundle, Left Anterior, Left Posterior. If incomplete TFB
can be difficult to differentiate from surface ECG
 Refer all patients with BBB, BFB or HB with any degree
of AVB for EPS
 Admit all symptomatic patients with above findings
 Another example
Quickie no 1
 83 yo bedridden male found to be less responsive
than usual
 FMS finds in V tach with pulse, under med control
gives lido with conversion, during transport BVM
ventilated, aspirates.
 On hospital arrival RSI performed, SaO2
improves from 60% to 95%. % minute later V tach
recurs, pt cardioverted. Now what meds?
Quickie #1
 Pt given lidocaine boluses 100 and 50 while
procainamide loading dose prepared
 While being loaded, qrs changes, here’s the
rhythm strip, what’s going on?
Quickie #1
 Sinus mechanism with wide complex,
suggestion of j point elevation. Given the
clinical situation (elderly, bedridden).
Patient may be hypothermic.
 Check a temp, If temp below 94 no more
carediodepressant antidysrhythmics.
 Warm the patient (passive or active internal,
not active external)
Quickie #2
 73 y/o male, no symptoms
 What’s the ECG diagnosis?
Quickic #2
 Alternating RBBB and LBBB. What looks
like a second P on half the beats is really the
initial deflection of a RBBB
 Dig toxic rhythm?
 Needs EPS?
Quickie #3
 58 y/o female feels weak
 No PMH, doesn’t like Doctors
 Glucometer 450
 ECG follows: findings? Probable cause?
RX?
Quickie #3
 ECG findings: Diffuse Intraventricular
block (RBBB with LAHB?), flattened p
waves. Beginning to look like a sine wave
 Probable cause: Hyperkalemia sec to renal
failure
 Immediate Rx: CaCl2 10 ml slow push,
Insulin 10 units (don’t need D50 since
hyperglycemic), Kayexalate
Quickie #4
 58 y/o in 1 vehicle accident on Saturday
Night, smells of ETOH, BP 80/p, patient
comatose: PE, FAST, Xrays, Head CT
 What are the ECG findings?
 What should you do to confirm the probable
diagnosis?
 If confirmed, what should be done now?
Quickie #4
 ECG findings: Atrial flutter-fib advanced
AV block, diffuse intraventricular block,
PVCs, Osborne waves
 Take a rectal temp
 Do nothing but passive rewarming,
hypothermia <90 f explains all clinical and
ECG findings
Causes of Diffuse Intraventricular Block
 MI
 Severe Hypertensive Heart Disease
 Cardiomyopathy
 Hyperkalemia
 Elderly (senile fibroelastosis?)
 Hypothermia
Quickie #5
 48 y/o male feels dizzy and weak. BP 90/p
 ECG findings?
 Probable cause?
 Rx?
Quickie #5
 ECG findings: Multifocal atrial tachycardia, aberrant




conduction
Cor pulmonale with hypoxia, prescribed beta agonists or
methylxanthines may be contributing, may be dig toxic
Correct hypoxia, withdraw offending agents, electrical
cardioveriosn unlikely to be successful until underlying
condition treated
Rate control, if needed by Ca channel blockers, Mg second
line
Dig toxicity treated in usual manner
Quickie #6
 47 y/o male with idiopathic cardiomyopathy
 What’s the rhythm?
Quickie #6
 Wide complex tachycardia, confirmed as V
tach by AV dissociation by p waves before
the 4th and 13th QRS and after the 5th
Quickie #7
 80 y/o F, confused, BP 80/p, pulse 167
 ECG diagnosis?
 What can you do?
Quickie #7
 Dx: Pacemaker mediated tachycardia and
malpositioned electrode (RBBB pattern suggests
anode in Left Ventricle
 Try to convert to fixed rate output 70 bpm with
magnet
 Overdrive it with transthoracic and try to slow it
 Open the pocket and disconnect the wires or cut
them
 Find out where the tip is: Left ventricle?
Pulmonary outflow track? Pericardial sac?
Summary: immediate therapy
 If it’s too slow, pace it
 If it’s too fast, cardiovert it
 Correct underlying problems: ischemia,
electrolytes, drug toxicities, etc
 All antidysrhythmics are poisons, some are
useful poisons
 Understand special cases: Dig toxicity,
WPW with antidromic conduction, PMVT
Summary: long term
 Everybody with a significant dysrhythmia
deserves a EPS consult.
– Most recurrent, hemodynamically important
SVTs should be treated with catheter
radioablation
– Significant bradycardias, not responding to Bblocker withdrawal need a pacemaker
– V Tach and fib get mapping and
ventriculotomy or drugs plus defibrillator