Download Deadly Arrhythmia and ECGs

DEADLY ARRHYTHMIAS
LMHER Oct 25, 2016
or…
DEADLY RHYTHMS AND
ECGS YOU DON’T WANT TO
MISS IN THE ER
DISCLAIMER !
These are obviously not all the deadly ECGs and rhythms
you can see in an ER.
However, they are some of the ones you could realistically
come across in a rural ER.
GOALS
To identify and know the treatment for some deadly
arrhythmias and ECGs in the Emergency Room
WHICH ARRHYTHMIAS CAN BE DEADLY?
Generally ANY rhythm that leads to cardiovascular compromise.
Ones covered here are:
• Atrial Fibrillation/Flutter- Decompensated
• Profound Bradycardia
• Supraventricular Tachycardia
• Ventricular Fibrillation/ Pulseless Ventricular Tachycardia
• AVR – the forgotten lead in ECGs
• All that ‘QT interval stuff’
• “Electrical alternans”
WHICH ARRHYTHMIAS CAN BE DEADLY?
Generally ANY rhythm that leads to cardiovascular compromise.
Ones covered here are:
• Atrial Fibrillation/Flutter- Decompensated
• Profound Bradycardia
• Supraventricular Tachycardia
• Ventricular Fibrillation/ Pulseless Ventricular Tachycardia
• AVR – the forgotten lead in ECGs
• All that ‘QT interval stuff’
• “Electrical alternans”
ATRIAL FIBRILLATION/FLUTTERDECOMPENSATED
• Normally Atrial Fibrillation only drops cardiac output by
5+/- %.
• Subsequently most patients are only mildly symptomatic.
• However if the ventricular rate is vey rapid and the patient
has some underlying cardiac disease, atrial fibrillation can
be life threatening.
ATRIAL FIBRILLATION/FLUTTERDECOMPENSATED
78 year old woman presents in Atrial Fibrillation with a
ventricular rate of 185.
BP 82/45.
Patient looks unwell.
Treatment?
ATRIAL FIBRILLATION/FLUTTERDECOMPENSATED
Shock ? 100 - 200 J
May work if new Atrial Fib, but if chronic rarely works.
Pre medicate the patient. ? Ketamine 0.3-0.5 mg/kg
Synchronized biphasic shock 200 J.
If that doesn’t work, you need to get the rate down, but
only after you get the BP up!
ATRIAL FIBRILLATION/FLUTTERDECOMPENSATED
Phenylephrine 50-200 mcg every minute.
Keep giving until the diastolic is over 60 or MAP over 65.
Now slow the rate.
Calcium channel blocker:
Diltiazem 2.5 mg/min (ie slowly) (max 50 mg)
or Verapamil 1 mg/min (max 25 mg)
ATRIAL FIBRILLATION/FLUTTERDECOMPENSATED
If rate not coming down, consider
Magnesium
Re-shocking
Call cardiology!
WHICH ARRHYTHMIAS CAN BE DEADLY?
Generally ANY rhythm that leads to cardiovascular compromise.
Ones covered here are:
• Atrial Fibrillation/Flutter- Decompensated
• Profound Bradycardia
• Supraventricular Tachycardia
• Ventricular Fibrillation/ Pulseless Ventricular Tachycardia
• AVR – the forgotten lead in ECGs
• All that ‘QT interval stuff’
• “Electrical alternans”
PROFOUND BRADYCARDIA
• ACLS teaches that bradycardias are treated with
atropine, external pacing and pacemakers.
• That treats the ‘symptom’ but not the cause.
CAUSES OF BRADYCARDIA
What are the common causes of bradycardia?
• Heart tissue damage related to aging or heart attack
• Infection of heart tissue (myocarditis)
• Hypothyroidism
• Electrolyte imbalance – hyperkalemia
• Medications – CCB, beta blockers
CAUSES OF BRADYCARDIA
What are the common causes of bradycardia?
In the ER, with acute Bradycardia ALWAYS look for:
Electrolytes (hyperkalemia)
Drug Toxicity (CCB, BBlockers)
CASE OF BRADYCARDIA
63 year old male presents to the ER feeling short of breath
and fatigued.
The nurse says ‘this fellow doesn’t look well’.
His vitals are 88/60, HR ~ 30bpm, Sats 97% on 2 liters.
Afebrile
“take a look at his ECG”
CASE OF BRADYCARDIA
CASE OF BRADYCARDIA
What do you see on his ECG?
- Severe bradycardia (HR ~ 30)
- Barely visible P waves
- Broad QRS complexes
- Peaked T waves V2-5
CAUSE OF THIS BRADYCARDIA?
Hyperkalemia
TREATMENT OF SYMPTOMATIC
HYPERKALEMIA
1. Calcium Gluconate (1000 mg = 10 ml of a 10% solution)
over 2-3 minutes.
(try to avoid Calcium Chloride unless you have a
central vein access)
2. Then 10 units regular insulin in 500 ml 10% dextrose given
IV over 60 minutes. Monitor serum glucose.
Onset 15 minutes, peaks 30-60 minutes, last 4-6 hours.
3. Kayexalate 15 gm qid po. (at this point be calling for help)
WHICH ARRHYTHMIAS CAN BE DEADLY?
Generally ANY rhythm that leads to cardiovascular compromise.
Ones covered here are:
• Atrial Fibrillation/Flutter- Decompensated
• Profound Bradycardia
• Supraventricular Tachycardia
• Ventricular Fibrillation/ Pulseless Ventricular Tachycardia
• AVR – the forgotten lead in ECGs
• All that ‘QT interval stuff’
• “Electrical alternans”
NARROW COMPLEX
TACHYARRHYTHMIAS
• By far the most common narrow complex
tachyarrhythmia is Supraventricular Tachycardia.
• However always consider:
Regular narrow complex:
- Sinus tachycardia, AV reentrant tachycardia,
Atrial flutter
Irregular narrow complex:
- Atrial Fibrillation, Multifocal atrial tachycardia
NARROW COMPLEX
TACHYARRHYTHMIAS
Supraventricular Tachycardia.
• SVT more common in women. Mean age of onset is ~ 30
years.
• Most common symptoms are palpitation (HR ~ 120-240),
dizziness, dyspnea and chest pain.
• 20 – 50 % patients may have ST depression on ECG,
which is usually due to repolarization changes, not
ischemia.
SUPRAVENTRICULAR
TACHYCARDIA
TREATMENT
If unstable, shock.
Pre-medicate
Synchronized Biphasic 200 j.
SUPRAVENTRICULAR
TACHYCARDIA
TREATMENT
If stable:
Vagal maneuvers ?
SUPRAVENTRICULAR
TACHYCARDIA
Adenosine 6 mg IV push, repeat x 1 of 12 mg IV. ?Mix
(Use cautiously in patients with severe bronchospastic asthma and severe CAD
Or
Verapamil 5-10 mg IV over 2 minutes.
Diltiazem 15-20 mg IV over 2 minutes.
Or
Metoprolol 2.5 – 5 mg IV over 2 minutes
Digoxin 0.25-0.5 mg IV
WHICH ARRHYTHMIAS CAN BE DEADLY?
Generally ANY rhythm that leads to cardiovascular compromise.
Ones covered here are:
• Atrial Fibrillation/Flutter- Decompensated
• Profound Bradycardia
• Supraventricular Tachycardia
• Ventricular Fibrillation/ Pulseless Ventricular Tachycardia
• AVR – the forgotten lead in ECGs
• All that ‘QT interval stuff’
• “Electrical alternans”
VENTRICULAR FIBRILLATION
& PULSELESS V. TACH
These should NEVER be diagnosed by an ECG!
A patient with either of these rhythms is dead.
‘Treatment’
Start CPR
Shock !
WHICH ARRHYTHMIAS CAN BE DEADLY?
Generally ANY rhythm that leads to cardiovascular compromise.
Ones covered here are:
• Atrial Fibrillation/Flutter- Decompensated
• Profound Bradycardia
• Supraventricular Tachycardia
• Ventricular Fibrillation/ Pulseless Ventricular Tachycardia
• AVR – the forgotten lead in ECGs
• All that ‘QT interval stuff’
• “Electrical alternans”
THE aVR LEAD
“all the waves are negative in lead AVR”
THE aVR LEAD
So when is AVR ‘abnormal’ and so what?
Wide QRS (> 120 ms or 3 small squares)
and prominent R wave in AVR
26 YEAR OLD WITH
DROWSINESS.
26 YEAR OLD WITH
DROWSINESS.
Wide QRS, Prominent R wave in aVR
= Tricyclic Overdose
26 YEAR OLD WITH
DROWSINESS.
A QRS of > 100 ms is a predictor of seizures
and arrhythmias in these patients
And an R wave of 3 mm or more is even more of a predictor
of seizures and arrhythmias than the QRS width
THE aVR LEAD
So when is AVR ‘abnormal’ and so what?
ST elevation in AVR > V1
ST elevation in aVR of > 0.5 mm is a strong
predictor of LAD occlusion or 3 vessel disease or
diffuse subendocardial ischemia
(all of these are BAD)
ST ELEVATION IN a VR IS
GREATER THAN IN V1
ANOTHER ST ELEVATION IN aVR
WHICH ARRHYTHMIAS CAN BE DEADLY?
Generally ANY rhythm that leads to cardiovascular compromise.
Ones covered here are:
• Atrial Fibrillation/Flutter- Decompensated
• Profound Bradycardia
• Supraventricular Tachycardia
• Ventricular Fibrillation/ Pulseless Ventricular Tachycardia
• AVR – the forgotten lead in ECGs
• All that ‘QT interval stuff’
• “Electrical alternans”
QT INTERVAL
QT INTERVAL
The QT interval is from the start of the Q wave to the end of
the T wave = ventricular depolarization and repolarization.
The QT interval is inversely proportional to the heart rate.
So the faster the rate, the shorter the QT and vice versa.
So we calculate the “corrected QT” or QTc which estimates
the QT interval at a heart rate of 60 bpm.
Thankfully, this is done digitally on the new ECG machines!
QT INTERVAL
QTc is ‘prolonged’ if > 440ms in men or 460ms in women.
QTc > 500 ms is associated with risk of torsade's de pointes.
A shortened QTc < 350 ms is associated with increased risk
of Paroxysmal Atrial and Ventricular Fibrillation and
sudden cardiac death. (this is a congenital syndrome)
CAUSES OF PROLONGED QT
Drugs
Hypo:
kalemia
magnesemia
calcemia
thermia
Ischemia
Raised ICP
DRUGS CAUSING PROLONGED QT
Antipsychotics – basically all of them!
Tricyclic antidepressants
Most other antidepressants (SSRI, NSSRI)
Antihistamines
Others: macrolides, quinine, chloroquine.
HYPOKALEMIA – QT 500MS AND
PROMINENT U WAVES IN V1-4
HYPOCALCEMIA – QT 500MS
INCREASES ICP
On ECG:
QTc prolongation
Widespread giant T-wave inversions (“cerebral T waves”)
Bradycardia (Cushing reflex)
INCREASES ICP
INCREASES ICP
MORE SUBTLE ECG
WHICH ARRHYTHMIAS CAN BE DEADLY?
Generally ANY rhythm that leads to cardiovascular compromise.
Ones covered here are:
• Atrial Fibrillation/Flutter- Decompensated
• Profound Bradycardia
• Supraventricular Tachycardia
• Ventricular Fibrillation/ Pulseless Ventricular Tachycardia
• AVR – the forgotten lead in ECGs
• All that ‘QT interval stuff’
• “Electrical Alternans”
ELECTRICAL ALTERNANS
This is alternating tall and short QRS complexes.
Usually will also be seen with tachycardia and low voltage
QRS complexes.
58 YEAR OLD WITH SOB AND
CHEST PAIN
58 YEAR OLD WITH SOB AND
CHEST PAIN
Large pericardial effusion
ELECTRICAL ALTERNANS
The alternating tall and short QRS complexes is thought
to be due to the heart swinging back and forth within the
fluid filled pericardial sac.
The small QRS are again due to the surrounding fluid
interference with the ECG.
TAKE HOME POINTS
1. Decompensated Atrial Fib. Don’t go trying to control
the rate right away, get the BP up! Phenylephrine.
2. Profound Bradycardia. Don’t just treat the brady, look
for causes. Do electrolytes stat! Think of meds as cause.
3. SVT – know your drugs – adenosine, CCB
4. V Fib/Pulseless V Tach. You better know this cold!
TAKE HOME POINTS
5. aVR lead. Usually waves are all negative. Wide QRS with
prominent R = TCA overdose.
ST elevation (especially if > ST in V1) think LAD occlusion or
bad ischemia generally.
6. QTc prolonged – worry about torsade de pointes (TdP).
Think of the causes. “electrolytes hypos, ischemia, ICP,
drugs”
7. QTc shortened – worry about congenital QT and sudden
death.
TAKE HOME POINTS
8. If you see Electrical Alternans, assess hemodynamic status, do
a cardiac EDE stat. Be prepared to do a pericardiocentesis.
THE END