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cardiac arrest
heart electrical dysfunction resulting in abnormal heart beating
can be classified as shockable or not

shockable rhythms
1. V fib
life threatening arrhythmia, leads to loss of consciousness + death if not quickly
treated
on ECG:

irregular waves, varying morphology and amplitude;

irregularly irregular rhythm;

No P waves, QRS complexes or T waves;

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 2. pulseless V tach
very fast V rate dissociated from underlying A contraction
why pulseless? rapid ventricular contraction does not enable heart to effectively
pump blood into the circulation
on ECG:

irregular morphology of QRS at regular intervals

high ventricular rate

regular rhythm

defibrillation is performed to stop heart conduction system when an abnormal rhythm

is present
It is indicated in the “shockable rhythms” to restore a normal sinus rhythm whereas they
are not indicated in the non-shockable arrhythmias

non shockable
1. pulseless electrical activity - PEA
aka electromechanical dissociation, pt who have cardiac electrical activity without a
palpable pulse (always check for central pulse instead of perypheral!!!)
why? absent mechanical contractions result from depleted myocyte energy stores
due to hypoxia, ischemia, met. acidosis. electrolyte alterations (mostly K and Ca2+)
on ECG:

may show complete P, QRS, T waves but no pulse

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 2. asystole
no electrical activity, no A/V depolarization
must guarantee organ perfusion → start compressions
on ECG: flatline

cardiac arrest protocol

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 1. no pulse or breathing unconscious pt? start CPR 100-120/min, fast hard
compressions (5cm) , allow chest to recoil
give oxygen + attach monitor/defibrillator
if no advanced airways keep 30:2 compressions/ventilation ratio if one
compressor, if 2 compressors 15:2

2. shockable rhythm? charge defibrillation and resume CPR while waiting

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 3. shock giving warning!

4. immediately resume CPR for 2 mins, if possible get IV access

after 2 mins recheck rhythm/pulse stopping compressions for no longer than 10
sec! is it shockable? NO

if pt returns to spontaneous circulation administer post cardiac care

if pulseless non shockable rhythm go to 10-11

5. YES → second shock

6. resume CPR for 2 mins, administer vasopressor every 3-5 min, consider
advanced airway + capnography
give 1 breath every 6 sec
reassess rhythm + pulse every 2 min. is it shockable? NO

if pt returns to spontaneous circulation administer post cardiac care*

if pulseless non shockable rhythm go to 10-11

7. YES → new shock

8. resume CPR for 2 min, considere administering antiarrhythmic and treating

reversible causes

🫀 rule of Hs and Ts to remember the possible causes underlying a cardiac

arrest:

H→ hypovolemia, hypoxia, hydrogen ions (acidosis),

hypo/hyperkalemia and hypothermia

T → tension pneumothorax, cardiac tamponade, toxins, and

thrombosis.

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 pharmacotherapy in shockable rhythms
action dosage timing

peripheral - given after 2nd and 4th

vasoconstrictor, to 1 mg every 3-5 shock (3 -5 interval) - after
epinephrine
restore perfusion and mins 2nd dose of amiodarone
avoid organ damage continue with epi

antiarrhythmic, used 1st dose: 300 mg

when arrhythmias are bolus 2nd: 150 mg
amiodarone after 3rd and 5th shock
resisting to no more than 2
defibrillation dosages

lidocaine in place of 1st: 1-1.5 mg/kg

amiodarone if not 2nd: 0.5-0.75

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 action dosage timing
available mg/kg

antyarrhythmic only
Mg sulfate used in torsade des
pointes or hypoMg

epi and amiodarone are only given AFTER the SECOND SHOCK, if the rhythm is
not responding to the shocks alone and requires medication.
in cardiac arrest the catecholamine of choice is epinephrine, NE is used as a
pressor even in severely decompensated patients but ONLY if the patient has a
pulse.

defibrillation
high energy non synchronized shock to depolarize heart cells and recover normal
electrical activity, only indicated in shockable rhythms
2 types of defibrillators: monophasic and biphasic
difference is in the way the current passes through the paddles
biphasic defibrillator allows shocking utilizing a lower amount of energy
standard energy:

monophasic: 360 J (initial dose)

biphasic: 120 or 200 J (initial dose)

rescuer should always utilize max energy when not sure if defibrillator is mono or
biphasic
for biphasic defibrillator it’s advised to utilize first 120 J to restore a normal rhythm
reducing damage of the cardiac cells

before shocking give a warning alarm, make sure no touching the patient and no
oxygen around
what to do:

1. Turn on monitor

2. Put patches on

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 3. Perform an analysis of the rhythm

4. Give the shock

back to the algorhythm

10. you found asystole or PEA
resume CPR for 2 mins, establish IV access, administer vasopressor, consider
advance airway + capnography
reassess rhythm + pulse every 2 min. is it shockable? YES, shock

11. NO → if unshockable rhythm with no pulse

resume CPR for 2 mins, treat reversible causes (Hs, Ts)

reversible causes
after 3rd CPR cycle focus on these! they’re always important but in the context of a
non-shockable rhythm there’s NOTHING else one can do
H

check for blood loss IV + fluids (maybe in bolus) NB

hypovolemia
physiological response to hypoV is sinus tachycardia

airway is patent? ventilation? O2 is connected? target sat >94%

hypoxia
and >90% in ACS

BGA, consider causes (DKA, hypoperfusion, hemorrhage,

H (acidosis)
hypoxia)

check ECG signs espetially in pt on antiarrhythmics or elderly

hypo/hyperK dehydrated pt hyperK → tall T waves, wide QRS; hypoK → flat
ST and T, prominent U waves

hypothermia core T should be raised > 30°

hypoglycaemia only in pediatric pt

T → tension PTX, tamponade, toxins

in case of hyperK administer Ca chloride, antagonises the bradycardic effect of
potassium, stronger and faster than calcium gluconate

MOA: It increases threshold potential at the level of the cardiac myocyte membrane
through unclear mechanism , restoring normal gradient between threshold potential

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 and resting membrane potential
in hypoK → KCL 40mEq, IV bolus (40mg in a 10ml syringe + 20ml NS flush)
side effects (overdose or rapid injection) include paraesthesia, cardiac conduction
block, fibrillation, arrhythmias.
in a stable pt KCL vile is administered in 500ml of NS

periarrest management
arrhyrhmias are common in peri arrest period, important to treat so they don’t
evolve into V fib or asystole

tachyarrhythmias
HR > 100 bpm, symptomatic above 150
identify cause, treat, give O2 if needed, monitor rhythm/BP/PaO2
in persistent tachy determine hemodynamic instability through ODDIO
SI/NO:

Obnubilation

Dyspnea

Dolore thoracic (chest pain)

Ipotensione (hypotension)

Others

if one of these is present you are instable → CARDIOVERSION to

synchronize rhthm
performed with different energies (J) according to the QRS morphology:

Narrow regular QRS: 50-100 J

Narrow irregular QRS: 120 – 200 J

Wide regular QRS: 100 J

Wide irregular QRS – defibrillation dose is given because the

rhythm is too irregular to allow synchronization (360 J)

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 before cardioversion pt is sedated since it is uncomfortable
drugs used are midazolam or propofol
like bdz, propofol is also a GABA receptor agonist, but also binds to
glycine, nicotinic, and muscuranic receptors in CNS
If pt has narrow regular QRS complexes,consider giving adenosine →
absolutely contraindicated in asthmatic patients due to its bronchoconstrictor
effect!!!

[aminophylline can counteract the bronchoconstrictor effect and promote

airway dilation]

If pt has wide QRS complexes, consider a drug acting at ventricular level

such as amiodarone
SYNC MODE (utilized in synchronized cardioversion) – allows the monitor to
detect the R waves of the patient and to synchronize to all of them.

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 avoids delivering the shock into the ST segment which is a vulnerable period
in which malignant arrhythmias may arise.

bradyarrhythmias
HR < 60 bpm, symptomatic below 50
airway patency + breathing, give O2 if needed, monitor rhythm/BP/PaO2,
get IV, ECG

assess signs/symptoms of hemodynamic instability

If hemodynamically stable,monitoring and observation

If hemodynamically unstable give atropine.

If not working, try to restore a normal rhythm with transcutaneous
pacing or infuse other drugs (dopamine or epinephrine)→ dopamine

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 is preferred over epinephrine as second line drug (in old pts epinephrine
can trigger arrythmia so you prefer to use dopamine, whereas in young
patients both are the same)

these are not treatment, just buying time

0.5 mg IV every 3-5minutes as needed Total max dose

atropine
– 0.04 mg/kg (3mg)

infusion rate is 2-20 mcg/kg per minute titrate to patient

dopamine response; taper slowly: first minimum effective dose:
2mcg and increase until response

epinephrine 2-10 mcg/minute infusion titrate to patient response

transcutaneous pacing
Cardioversion 🡪 conversion of an abnormally high rhythm into a slower one /
Transcutaneous pacing 🡪 increase the heart rhythm

1. attach patches

2. select rate you want to achieve and current (amount of energy)

3. assess if the heart is contracting effectively → check femoral pulse! there

may be electrical activity but no effective contraction of the heart
If no pulse (= no mechanical contraction) attempt new transcutaneous
pacing, changing the current or HR to have an improvement

Torsades de pointes ventricular tachycardia is a specific form of polymorphic

ventricular tachycardia in patients with a long QT interval. It is characterized by
rapid, irregular QRS complexes, which appear to be twisting around the
electrocardiogram (ECG) baseline. This arrhythmia may cease spontaneously or
degenerate into ventricular fibrillation. It causes significant hemodynamic
compromise and often death. Diagnosis is by ECG. Treatment is with IV
magnesium, measures to shorten the QT interval, and direct current defibrillation
when ventricular fibrillation is precipitated.
(magnesium sulfate 2 g IV over 1 to 2 minutes, correction of hypokalemia,

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 pacing or isoproterenol to increase heart rate, and correction of the
cause.)

questions

Gave me a scenario about a patient arriving with cardiac arrest, what do I

do? I just ran through the entire algorithm with drug dosages etc. and he
said that he keeps remaining in a shockable rhythm, but nothing is working,
so I said the epi, amiodarone, lidocaine etc. but also went through all of the
Hs and Ts and how I could possibly check for them and rule them out. The
guy was negative for all of them and kept remaining in that rhythm so I said
I don't know what you're looking for because unfortunately I don't remember
learning something specifically about that from the algorithms, so he said
he was in arrhythmic storm which I had never heard of, and kept pushing
for something that I "should know since I would do it in residency if I was
considering anesthesiology" (god please make it make sense). Regardless,
from talking to other people he seems to ask weirdly specific things, like
another student got asked the specifics of ventilation settings in a TBI.

cardiac arrest protocol !!!

young man presenting to the ER with palpitations, asked me what I would

do. So I went through the ODDIO SI/ODDIO NO algorithm. It was an
ODDIO NO situation. Went through that algorithm, he told me "this is his
ECG" and showed me an ECG with AFib. So I spoke of the AFib algorithm.
Out of that algorithm, we discussed the fact that even though the patient
could swear his palpitations started within that day, nevertheless we can't
be sure of when AFib started (didn't have an ECG performed within the prior
48 h), so before proceding to cardioversion, either 3 weeks of
anticoagulants or a TEE is necessary. Discussed about which could be the
best option in this case. Also discussed whether, once proceding to
cardioversion, pharmacological or electric cardioversion would be better in
this case. Electric cardioversion to be preferred + we should bear in mind
antiarrhythmics' side effects

arrhythmias management and doses

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 14yo patient with a heart rate of 200bpm, normal BP, normal saturation, no
ODDIO symptoms/signs. How would you proceed? What would be the
treatment? What is the diagnosis?

Then we quickly spoke about synchronized cardioversion, Joules, why we

give defibrillation dose in wide irregular QRS. and lastly he wanted to know
the most important contraindication for adenosine --> asthma patient

84 yo bradycardic patient management. he wanted to know the flowchart,

drugs (atropine, dopamine, epinephrine), transcutaneous pacing. He dived
into the details of when dopamine is preferred over epinephrine as second
line drug (in old pts epinephrine can trigger arrythmia so you prefer to use
dopamine, whereas in young patients both are the same). He also asked
about transcutaneous pacing, how do you do it, what button do you press
(pace) what do you modify on the machine (ampere), and what ecg pattern
are you trying to look for (broad tall T, wide QRS, spike followed by QRS).

what if the patient has bradycardia - what do you do? (I talked about oddio
symptoms and the different management in case he is stable/unstable -
including all drugs and doses!)

treatment of 3rd degree AV Block in the setting of bradycardia

tratment of torsade de pointes

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