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Gen Med Cardiology > ACLS > Flashcards

ACLS Flashcards

1
Q

Increases SA node Firing by blocking Parasympathetic (Vagus) rate control

A

Atropine

Anticholinergic

CAUTION in MI & Hypoxia- Atropine increases cardiac O2 consumption and can worsen Ischemia

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2
Q

Avoid Atropine for Bradycardia in:

A

MI &/or Hypoxia
Hypothermia
Mobitz II or 3rd Degree Block

Atropine speeds the SA Node ONLY. If the SA impulse is blocked, it does nothing in the ventricle.

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3
Q

Max Atropine Dose & Dosing

A

Max is 3mg (Adult)

0.5mg IV every 3-5min until Max is reached.

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4
Q

First Line for Bradycardia

A

Atropine

Unless contraindicated

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5
Q

Second Line for Bradycardia

A

TransCutaneous Pacing

Dopamine & Epinephrine - These Vasopressors Increase Coronary Perfusion Pressure which increases myocardial blood flow.

Beta Adrenergic Agonists

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6
Q

Epinephrine Infusion Dosing

A

2-10 mcg/min titrated to pts response

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7
Q

Dopamine Infusion Dosing

A

2-10 mcg/KG/min

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8
Q

Mild Hypoxemia

A

90-94% O2 Sat

No Cognitive Impairment, Likely Pale

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9
Q

Severe Hypoxemia

A

Below 75% O2 Sat
Loss of Consciousness and
Brain Injury Likely

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10
Q

Moderate Hypoxemia

A

75- 89% O2 Sat
Cognition Impaired
Coloring Ashen, even Perioral bluing.

Cap Refill poor

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11
Q

Normal Oxygenation

A

95-99% O2 Sat

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12
Q

What is the treatment in common for Torsades, VFib, Eclamptic Seizure and Pulseless VTach?

A

Magnesium Sulfate

A CNS Depressant that reduces AcH release at the neuromuscular junction

Is 1st line for Torsades & Eclamptic Seizure

3rd line for VFib if already refractory to Defibrillation and Amiodarone or Lidocaine

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13
Q

The definitive Rx for VFib?

A

Defibrillation

Biphasic - Zoll
120 Joules then resume CPR then
150 Joules & resume CPR then
200 Joules & resume CPR

Monophasic:
200 J then resume CPR
360 J then resume CPR
360J then resume CPR

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14
Q

Max Joules for Biphasic & Monophasic:

A

200 Joules for Biphasic and

360 for Monophasic

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15
Q

Synchronized Cardioversion

A

The “shock” is delivered at the peak of the QRS, at “R”

If the synchronization button is engaged and you press the shock button there will be a pause as he machine orients itself on the host.

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16
Q

Compensatory Tachycardia caused by systemic conditions such as: Fever, Blood Loss, Anemia, Dehydration, Low BP

A

Sinus Tachycardia

100 - 220bpm

Usually less than 130 though

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17
Q

Bring Sinus Tach down with:

A

Rx the underlying systemic cause. Bring down the fever, bring up the blood volume, bump up the [O2]

DON’T use beta blockers to lower sinus tach, its COMPENSATING for something. FIX the something.

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18
Q

Normal QRS width

A

is NARROW:

  1. 5 - 3 boxes
  2. 06 - .12 seconds
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19
Q

Normal PR is

A

WIDER than QRS:

3-5 sm boxes

0.12 - .2 seconds

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20
Q

Effect of Tachycardia on PR Interval

A

Shortens it

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21
Q

QRS in VTACH is

A

Wide (over 3 boxes or .12sec) & can be irregular

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22
Q

QRS in SVT is

A

Narrow (less than 3 boxes) & very very regular

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23
Q

Onset & termination of Sinus Tach vs SVT

A

Sinus is grad onset + termination

SVT is abrupt onset + termination

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24
Q

Common SVT rate

A

160-220 but can go close to 300.

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25
Q

Delta Wave, think…

A

WPW Re-entry SVT

Cardiovert, don’t use Rx!!!

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26
Q

Brugada Sign

A

“Coved” ST elevation in V1-V3

Deep S, ST Elevation followed by an inverted T.

The ONLY potentially diagnostic sign for Brugada Syndrome but, in isolation, not really helpful

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27
Q

Brugada Syndrome

A

Genetic Na+ Channel Defect that causes sudden MI & Death in males under 40, esp. in South East Asians

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28
Q

South East Asians

A

Philippines
Thailand
Japan

South of China, North of Australia, West of New Guinea and East of India

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29
Q

Rx for Brugada Syndrome

A

If pt survives initial MI, implanted defibrillator is needed.

Entire family needs to be genetically tested and have defibrillators implanted as the first attach with Brugada is usually the last. Patients often die in their sleep.

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30
Q

Required to Dx Brugada Syndrome:

A

Brugada Sign in V1,2 or 2 WITH one of the following:

VTach - Polymorphic
VFib
Syncope
Night Time Agonal Breathing
"Coved-Type" ECG in Fam Memb
Electrically inducible VTACH
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31
Q

ACLS Team Leader

A

Organizes the effort of the group

The paramedic on scene organizing the EMTs & Firefighters.

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32
Q

Closed Loop Communication

A

Leader give message
Eye Contact/Clear Response + Verbal Acknowledgement that Message/Order is UNDERSTOOD

Leader opens the loop, Team Member closes it with Verbal Acknowledgement freeing Leader to issue next Order.

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33
Q

Name the SIX ACLS Team Positions

A
  1. Airway
  2. Compressor doing CPR
  3. IV/IO Meds
  4. Observer/Recorder
  5. Defibrillator
  6. Team Leader @ Pts Feet
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34
Q

When Rescuscitation isn’t working..

A

Go back to ABCs, check airway, pulses, Bp and ensure you’re giving quality CPR

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35
Q

Steps in the ADULT Chain of SURVIVAL:

A 
Call 911
Early CPR, Compressions 1st!
Rapid Defibrillation
Effective ALS on scene
Integrated post arrest care inhosp
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36
Q

MET/RRT

A

Medical Emergency Team
Rapid Response Teams
Respond and intervene In Hosp BEFORE Cardiac/Respiratory Arrest.

Alerted by staff nursing or families bedside who note deterioration in vitals.

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37
Q

Code Team

A

ALS Team administers CPR, Airway resuscitation, defibrillation and drugs to restore sinus rhythm or independent respirations.

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38
Q

Critical Care Team

A

Post Arrest Care providers

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39
Q

Theraputic Hypothermia

A

Post Cardiac Arrest cooling to between 93.2F (34C) to as low as 89.6F (32C) for 12 to 24 hours.

Initiated as soon after ROSC (return of spontaneous circulation) as possible and rewarming no more than 24 hrs from beginning of cooling.

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40
Q

Theraputic Cooling Methods

A

The intravascular Heat Exchanger is best. Inserted into the femoral vein blood is pumped over a cooled saline heat exchanger and back into the body. Rapid cooling and raising of temperature, minimizes shivering as skin warming is allowed.

Onscene, you can run in cooled saline or Ringers at 30ml/Kg. That’s why we have the refrigerated saline in the rig - so we can start cooling right after ROSC

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41
Q

Ventilation Optimization

A

Titrate [O2] to the lowest volume needed to maintain spO2 @ 94% to avoid O2 toxicity.

Avoid excessive Ventillation during CPR as compressions alter thoracic pressures and decrease atrial filling, reducing CO. Get Waveform Capnograpy in place and ventilate ONLY to 35-40 PetCO2, (PaCO2 of 40-45mmHg is using ABG)

Get MAP to at least 65 mmHg

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42
Q

MAP Formula

A

= 2/3 DP + 1/3 SP

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43
Q

PCI

A

Percutaneous Coronary Intervention (Reperfusion)

“Coronary Catheterization”

ACLS should transport pt directly to the cathlab whenever possible.

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44
Q

ACS

A

Acute Coronary Syndromes

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45
Q

Goals for ACS Pts

A

Reduce Myocardial Necrosis by ensuring best possible perfusion

  1. O2 delivery
  2. Quality CPR
  3. Rapid Defibrillation
  4. Hypothermia on RUSC
  5. Rapid PCI/Cath
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46
Q

STEMI-Alert

A

EMS calls in ST elevations so ER can prep for management/ PCI on arrival.

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47
Q

TPA

A

Tissue Plasminogen Activator

Alteplase, releplase, tenecteplase

ReOpro is the MAB (Abciximab) that

Given just before PCI, in PE or up to 5 hrs after non-hemorrhagic stroke. DO confirm blockage/no bleed by CT scan FIRST.

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48
Q

TPA vs Abciximab

A

TPA breaks down existing Blood Clots

Abciximab prevents new ones forming or existing clots growing.

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49
Q

Alteplase vs Reteplase vs Tenecteplase

A

Tenecteplase causes less unintended bleeding than does Alteplace in trials. Better for emergency MI.

Reteplase is Fastest of all three and easiest to administer

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50
Q

Mortality Rate after Cardiac Arrest

A

80% even with great CPR

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51
Q

Activate Rapid Response Team If:

A
  1. Respirations below 6 or over 30
  2. HR under 40 or above 140
  3. SBP under 90
  4. Symptomatic hyPERtension
  5. Altered Mental Status
  6. Unexplained Agitation
  7. Seizure
  8. Urine Output falls significantly
  9. Subjective concern for Pt
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52
Q

STEMI Definition

A

ST Elevation of greater than 1mm in TWO or more CONTIGUOUS leads:

II,III & aVF = Inferior STEMI
V1 + V2 = Septal STEMI
I, aVL,V5 + V6 = Left Lateral MI
V3 + V4 = Anterior Wall MI

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53
Q

Dominant S-Wave in V1

A

RBBB with bigger right rabbit ear

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54
Q

Dominant R-Wave in V1

A

LBBB with bigger Left rabbit ear

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55
Q

Rabbit Ears in General indicate:

A

Ventricles are depolarizing at different rates due to some sort of blockage in the electrical pathway of one ventricle.

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56
Q

3 Consecutive PVCs is technically:

A

VTACH

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57
Q

“Skipped Beat” felt when taking a pulse

A
  • Usually a PVC or a PAC
  • Heart didn’t really skip a beat but the early ventricular or atrial contraction didn’t allow for normal filling and thus Cardiac Output for that beat can’t be felt at the wrist since it didn’t push enough blood.

Then, of course there is the compensatory pause after the PVC/PAC, so the pulse was missed. THEN it took an extra moment for the SA Node to reassert control and that Compensatory Pause can seem like forever.

58
Q

PVC/PAC symptoms are felt more when the patient is….

A

At rest/at night

When the SA node is slower due to reduced demand, it isn’t overriding the ectopic ventricular pacemakers that cause the PVC/PACs, so they sneak off a beat while the SA snoozes.

59
Q

PVC on the ECG

A

a WIDE funny looking QRS followed by a COMPENSATORY PAUSE.

Often there is a P-Wave at the bottom of the PVC made as the atria contract but the blood they are pushing is blocked from entering the ventricle by the still contracting walls of the ventricle. This throws the atria off, resulting in the pause while the SA resets.

60
Q

Your Patient on Warfarin for AFib or Post-Stroke is having chest pain and SOB - do you give her Aspirin?

A

Yes

In Acute Coronary Syndrome you do give the 4 baby aspirin. Long term they may not take Aspirin but in THAT moment, so long as they’re not allergic, give it to them.

61
Q

PAC vs PVC on ECG

A

PAC is usually a P-Wave too close (on the tail of) the T-Wave. It’s just too early, then there’s a pause after it.

PVC usually looks like an extra wide QRS, often with a P-Wave at the bottom of the S-Wave. Then there’s a compensatory pause afterwards.

62
Q

Biphasic P

A

Atrial “Enlargement”

Left Side Up = Left Atrium Enlarged

Peaky P = Rt Atrium Enlarged

63
Q

peaked P Wave

A

Rt Atrial Enlargement

64
Q

Notched P

A

Mitral Stenosis which leads, of course, to LEFT Atrial Enlargement

65
Q

These are symptoms of what?

SOB, Altered Level of Consciousness (ALC), pre/syncope, weakness, lightheadedness/dizziness & fatigue

A

Bradycardia

66
Q

These are signs of what?

Orthostatic HypOtension
Diaphoresis
Pulmonary congestion/edema
Ankle edema
Frequent PVCs and/or VTach
A

Bradycardia

67
Q

How does Bradycardia predispose to VTach and/or VFib?

A

Two Ways:

Sinus Bradycardia leaves gaps in SA Node primacy which allows ectopic ventricular & junctional cells to kick off PVCs and PJCs. If one of these falls on a TWave just so, VTach or VFib can result

In the setting of MI where there is an “Ischemic Zone” Bradycardia highly correlates to VTach/VFib. The ischemic zone itself may allow REENTRY of a/serial PVCs/PJCs. creating an SVT-like re-entry situation down in the damaged ventricle.

68
Q

Heart Rate below which we have Bradycardia and initiate the ACLS Bradycardia (with pulse) Algorithm.

A

50bpm

Trick! Really Bradycardia exists below 60bpm but the ACLS Algorithm uses 50 for the cut off.

69
Q

ACLS Bradycardia Algorithm

A 
Pulse less than 50bpm
Oxygenate + Assist Ventillation
     if below 12/min or if pt 
     exhibits other signs of shock
Use the monitor to track Bp, Hr
      and SpO2
Gain IV Access
Get a 12 lead but don't delay 
     therapy to do it.
If Bradycardia is not symptomatic 
     (no hypotension, ALC, Shock
     chest discomfort) then 
     continue to monitor and 
     observe
If Brady IS Symptomatic:
    1.  Atropine 0.5mg Bolus
            q3-5min, max dose 
             3mg.  Dose until
             pulse exceeds 50bpm
 2.  If Atropine ineffective
  a)Transcutaneous Pacing TCP
      OR
  b) Dopamine Infusion:
         2-10mcg/Kg/min  OR
   c)  Epi Infusion:
         2-10mcg/min

 3.  You TCP for up to 60 min but you need to get Transvenous Pacing in place by then.  You NEED anxiolytic/analgesic to TCP though (Fentanyl IV 1-2mcg/Kg + Midazopam 0.1mcg/Kg)
70
Q

The INITIAL Treatment for Bradycardia is:

A

ATROPINE

0.5mg Bolus q3-5 min until pulse exceeds 50bpm OR max dose is reached (3mcg)

71
Q

Transcutaneous Pacing (TCP)

A

Non-Invasive SHORT TERM Pacing option (up to 1 hr, after which Transvenous Pacing should be in place) using the Defibrillator/Monitor on “Pacing” Setting:

Give Sedative AND Analgesia if there is time. Pacing is uncomfortable and lasts up to 1hr!!

  1. Place electrodes @ RU, LU & Left Sternal Border 4th ICS OR on all 4 limbs if your monitor only has limb leads.
  2. Place shock pads either Anterior/Apex or Ant/Post as pads direct. DO make sure your pads are connected to the monitor (0;

Turn Monitor On - confirm Brady.

  1. Select “Pacing” option
  2. Select Rate (80 pulses/min)
  3. Select Amperage
    a) Increase by 10 until you see
    capture on the ECG readout
    b) Capture is a pacer spike
    immediately followed by
    a QRS complex.
    c) Once captured, lock mAmp
    if your monitor amps lock
  4. Check pulse & Observe Pt
    Get Vitals q 5 minutes with
    current and pt’s rxn to pacing.

TCP Sedative/Analgesics should not drop BP (your patient is already unstable due to bradycardia)

IV Fentanyl and a tiny bit of Benzo
Fentanyl: 1-2mcg/Kg Slow Push
Midazopam: 0.1 mcg/Kg
Both have 30-60min half lives perfect for transcutaneous pacing.

72
Q

How does Epi work in Hypotension and in Bradycardia/Pulselessness?

A

Hypotension: Epi binds Alpha1 receptors constricting peripheral vessels, increasing Bp + improving heart and brain perfusion.

Bradycardia/Pulselessness:
Epi Binds Beta 2 Receptors in the heart Increasing Rate and Force of Contractions.

73
Q

Epinephrine is the antidote for what kinds of overdose?

A

Beta Blocker and Calcium Channel Blocker

74
Q

What are the results of Dopamine Infusion at Low, Med & High Doses

A

Low Dose Dopamine (

75
Q

Why can’t you dilute Dopamine in BiCarb before administering it?

A

Alkaline Solutions in general InActivate Dopamine

76
Q

Extravasation of IV Medication:

A

Missing the blood vessel and infesting the tissue

77
Q

Why is extravasation of Dopamine particularly bad?

A

Dopamine is a POWERFUL vasoconstrictor and can shut down blood supply to tissues into which it is mistakenly released.

Stop the infusion.
Resite to a larger vessel
Infiltrate the contaminated tissue with Phentolamine, a powerful enough vasodilator to counteract the local effect of dopamine.

78
Q

Why cautions with Dopamine in Cardiogenic Shock/CHF?

A

Even at low - moderate doses (below 5 mcg/Kg/min) Dopamine can increase heart rate and contractility BUT… it also increases oxygen consumption so if there is a blockage or very low blood pressure or a very tired heart, Dopamine can worsen ischemia.

79
Q

Drugs you CAN give via ET Tube

A

NAVEL: Adults

N - Naloxone
A - Atropine
V - Vasopressin (ADH) Adults
E - Epi
L - Lidocaine

LEAN: PEDS

L - Lidocaine
E - Epi
A - Atropine
N - Naloxone

        (No Vasopressin for Kids
         via ET Tube!!!)
80
Q

Epi for/dose?

A 
Cardiac Arrest (VF, VT, Asys,PEA)
     IV/IO 1mg q 3-5 min
         -10ml of 1:10 000 soon
         -Follow each dose w/20ml
          saline flush & elevate arm

BradyCardia 2-10 mcg/min raise
dosage to Pt response

Beta/Calcium Blocker Overdose

 - Requires HIGH dose
 - 0.2mg/Kg

ET Dose: 2-2.5 mg in 10ml
Normal Saline

81
Q

PreMedication Check List (6)

A
  1. Soln Clear + Not Expired
  2. RIGHT Patient
  3. Right Medication
  4. Right Dose
  5. Right Route
  6. Right Time
82
Q

ET Tube Drug Delivery

A

-Intubate w/ET Tube
-Ensure Correct Placement!!!
-Dilute Med to 3-5ml w/N Saline
in a syringe w/o needle (remove
needle if you used one to draw
up the medication into syringe)

  1. PreOxygenate w/3 Respirations
  2. Remove BVM
  3. Inject Med directly into ET Tube
  4. Reconnect BVM
  5. Ventilate 12-20 resp/min
  6. Monitor Pt for
    a) Desired Effect, increase
    med if not noted
    b) Undesired effects
83
Q

Unstable Tachycardia

Definition and Rx:

A

Pulse over 100 that is causing sxs of poor perfusion such as:

Dizzy/Lt Headedness
Altered mental status
SOB
Chest Pain
Shocky
Hypoxemia

Rx: Hook up to monitor
- Narrow QRS: SVT Rx:
-Try Vagal Maneuvers 1st
a) Push like you’re having a BM
b) Carotid massage
1. NOT if you hear Bruit or
pt has had a stroke
2. ONLY one side
3. Pt supine, Massage Carotid
Sinus below mandible for
1 Min Only. Can Switch sides
if unsuccessful.
-IV Access with TWO ports. Clamp above
Ports
a)Measure up 6mg Adenosine in
one Syringe and 20 ml NS in other
b) Unclamp & inject Adenosine. Keep
plunger depressed and inject saline.
- Adenosine 6mg followed
RAPIDLY by 20ml NS bolus
to PUSH it to the heart
before the Adenosine gets
taken up by RBCs and
blood vessel endothelium.
-If rhythm doesn’t convert in 2
min, give 2nd dose but
make it 12mg
-If rhythm doesn’t convert in 2
min, give Calcium Channel
Blocker (Diltiazem) or Beta
Blocker (

84
Q

How does Adenosine Work?

A

Its an AV Nodal Blocker when given in High Dose Rapid Push Bolus.

It slows Tachy Rhythms & Reentry that originate ABOVE the AV Node.

VTACH/VFIB doesn’t utilize the AV Node so it doesn’t work if you really do have a ventricular rhythm - BUT… we can “try” it on a stable, monomorphic wide complex tachycardia to DIFFERENTIATE SVT from VTACH - which is sometimes very difficult to do on the monitor as any P Waves get covered by the rapid QRS complexes.

Adenosine won’t hurt in V-Tach, it just won’t work as the AV Node isn’t much involved.

85
Q

Most common causes of Cardiac Arrest in Adults/Peds

A

Adult: VFIB

PEDS: Respiratory Arrest

86
Q

ETCO2 @

Initial Arrest
During CPR
At ROSC

A

Initial Arrest: Often High due to built up CO2 in lung following arrest

Usually falls, though if CPR is effective, it may level off

ET CO2 rises at ROSC - it is perhaps the earliest indication of ROSC

87
Q

Earliest Indication of ROSC

A

Increase in ET CO2

88
Q

Induced Hypothermia, WHO, WHY & HOW to induce?

A

WHO: Pt who remains comatose or unable to respond to verbal commands following Cardiac Arrest & ROSC

WHY: To reduce O2 demand of Brain and vital organs

HOW: Normal Temp is 37C (98.6F) Cool Pt to 34-32 C (93.2-89.6F) with :

  • Axillary/Groin/Cervical Cold Packs
  • Cold IV infusion of NON GLUCOSE containing isotonic fluid
  • Cooling Blanket ….

Gold Std is Intravascular Heat Exchanger

89
Q

What is a “PUSH?”

A

IV Med delivery followed by a 20ml bolus of Normal Saline to “PUSH” it toward the heart.

Adenosine is a rapid push as it is quickly taken up by RBCs and vascular endothelial cells so you need to give a HIGH dose and PUSH it toward the heart to ensure enough arrives to block the AV Node & convert the SVT.

90
Q

Synchronized vs UnSynchronized Cardioversion

A 
SYNCHRONIZED delivers a LOW ENERGY shock AT the PEAK of the next QRS complex.  This ensures that the shock doesn't fall on a T-Wave and tip the pt into VFIB.
          Use Synchronized For Unstable:
                 -SVT
                - AFib
                -AFlutter
                -Atrial Tach
UNSYNCHRONIZED delivers HIGH ENERGY shock anywhere because the cardiac cycle is already so out of whack it doesn't matter and we need enough energy to STOP the heart briefly, in the hope that it will then convert to Normal Sinus Rhythm or something better than:
                 Unstable VTACH
                 VFib
                 PEA
                 Asystole
91
Q

Epi or VasoPressin (ADH) in the unconscious pulseless patient?

A

Epi increases rate and contractility by binding Beta 1 Receptors in the heart. But Epi can increase heart O2 consumption, a demand that a damaged heart might not be able to meet - so Epi is associated with significant risk of post arrest arrhythmia.

Vasopressin binds V1 receptors in the periphery, constricting vessels and raising Bp while simultaneously stopping diuresis, increasing blood volume and thereby Bp. It is also thought that Vasopressin dilates cerebral vessels and improves brain perfusion.

ACLS says they’re essentially interchangeable & to

92
Q

Indications for use of Lidocaine in Pulseless VT

A

Lidocaine is under scrutiny for effectiveness but is still considered an option for pulseless VT when three shocks + Amiodarone have been unsuccessful

Initial Dose: 1-1.5mg/Kg IV
Refractory Dose: 0.5 -0.75 mg/Kg IV Push
You can repeat this q 5-10 min until
Max dose of 3mg/kg

93
Q

Max Dose of Lidocaine

A

3mg/Kg

94
Q

Lidocaine Toxicity follows a predictable pattern as follows:

A
  1. Tongue Numbness
  2. Lightheadedness
  3. Visual disturbances
  4. Muscle Twitching
  5. Unconsciousness
  6. Coma
  7. Respiratory Arrest
  8. Cardiovascular Depression
95
Q

Conditions that may precipitate Lidocaine Toxicity at below Max dose:

A

Liver Dysfunction - it is conjugated in the liver for excretion and is inactive when conjugated

Low Protein - If blood protein concentrations are low, it can’t be conjugated and thus remains active in the blood.

Acidosis - low pH frees drug from it’s protein binder and permits unconjugated drug to exert its action.

Be wary in pts w/edema & signs of ketoacidosis.

96
Q

Why is pulseless VT pulselsess

A

The ventricles are beating so fast they are not pushing enough blood to cause either carotid or femoral pulses.

Pulseless VT is therefore the equivalent of VF in terms of the ACLS Algorhythm. It must immediately be shocked and the monitor gets set to Unsynchronized whereas in a

VT WITH PULSE, the monitor would be set to SYNCHRONIZED

97
Q

When to use SYNCH Setting on the monitor?

A

SVT or VTach WITH a Pulse

98
Q

When to use UNSYNCHRONIZED setting on monitor

A

VTach WithOUT Pulse
VFIB

Asystole & PEA are not shockable rhythms. Continue CPR while obtaining IV/IO access and an advanced airway.

Then give 1mg EPI or 40 Units Vasopressin & resume CPR. Continue in this manner dosing with EPI (only use Vasopressin 1X) every 3-5 min

99
Q

Can you give EPI straight from the vial as an iV Bolus in Cardiac Arrest? Recall, Cardiac Arrest is VF

A

No. Epinephrine comes too concentrated for that and too much Epi in a bolus can induce VFIB or worse.

ALWAYS dilute your 1mg (1ml) EPI to a PUSH for Cardiac Arrest.

It comes 1:1000 (1mg/ml). Dilute it to 1:10,000 by diluting 1ml (aka 1mg) of the reagent with 9ml Normal Saline. You still have the 1mg dose but it’s diluted over 10ml of fluid.

If you are using an infusion (ACLS approved for Bradycardia) you would dilute 1mg (1ml of 1:1000 epinephrine) in 500 ml of NSL or 5% Dextrose and run it at 2-10mcg/minute.

100
Q

“Liquid Pacing” refers to what

A

High concentration Epi Infusion.

This is not ACLS protocol but is used in the ER and by some paramedics with permission from medical control

https://acls-algorithms.com/acls-drugs/acls-and-epinephrine/ These guys convert Asystole (Not Shockable) into VFIB (Shockable) by running 30mg (30ml) of Epi in 250ml of Saline at 125/hr (

The 1mg/10ml soln is a 1% and the 30mg/250ml is a 12% soon so it’s much stronger for converting Asystole to VFIB than for converting VTACH/VFIB to sinus.

101
Q

Reversible Causes of Cardiac Arrest

A

H5-T5

Hypovolemia
HypoThermia
Hypo/Hyper Kalemia
Hydrogen Ion Acidosis
Hypoxia
Tension Pneumo
Tamponade
Toxins
Thrombosis, Pulmonary
Thrombosis, Coronary
102
Q

What IS Cardiac Arrest

A

Heart pumping insufficient to sustain life:

VFIB, Asystole & PEA

103
Q

ROSC Post Arrest Care

ALWAYS begin with ABCs and RETURN to ABCs…

A
  1. Maintain Ventilation & Oxygenation
    a) spO2 @ 94% or above
    b) Consider Advanced Airway & ETCO2
    Wave Form Capnography
  2. DON’T Hyperventillate!! You can cause an alkalosis!!
  3. Rx Hypotension
    a) Vasopressin Infusion
    b) If hypotension cause is obvious, fix it
  4. Get a 12 Lead EKG and figure out what’s wrong with this heart!
  5. If Pt canNOT follow verbal commands
    INDUCE HYPOTHERMIA
  6. IF STEMI OR AMI (acute MI) Get Pt to
    Cath Lab for PCI (percutaneous intervention)
  7. If no stem, deliver pt to ER for Advanced Critical Care.
104
Q

How many boxes/seconds SHOULD a QRS be?

A

Under 3 sm boxes or under 0.12sec

105
Q

How wide should a PR Interval be:

From beginning of P to R the full P-wave

A

3-5 sm boxes or 0.12-0.2 seconds

106
Q

1st Degree Heart Block, describe:

A

Wide PR, over 0.2 seconds (5 sm boxes)

107
Q

Mobitz I

A

Going Going Gone

108
Q

Mobitz II

A

Fine Fine Fine Fine… Dropped QRS

109
Q

3rd Degree Heart Block, describe

A

Ps march out separate from QRS

110
Q

WPW sign on EKG

A

Delta Wave

No DRUGS for DELTA
Cardiovert instead of using Adenosine even though this looks like Stable SVT

111
Q

Old drug you can use in pulseless VT or VF if you don’t have Amiodarone and ROSC hasn’t occurred before the 3rd shock?

A

Lidocaine

112
Q

Drug used for Torsades and or HypoMagnesia?

A

Magnesium Sulfate

Cardiac Arrest dose = 1-2 grams

Always dilute MgSO4 in 10ml D5W then Flush with 20ml of NS

113
Q

Types of PULSELESS Cardiac Arrest

A

VTach (w/o Pulse)
VFib (never has pulse)
PEA (can look fine on monitor but no pulse)
Asystole

114
Q

High Peaky Ts

A

High Potassium (over 5)

115
Q

Pneumonic for HyperKalemia Rx:

Use this when you see peaky Ts on your EKG and your patient is unwell, look for low BP & Thready Pulse, fatigue & possibly weakness and neural deficits

A

C Big K Drop

C- Calcium Carbonate or Calcium Gluconate

B- B2 Agonist (albuterol inhaled) Or
BiCarb (IV good if in acidosis anyway)
I- Insulin
G- Glucose

K - Kayexalate - oral binds K in GI & removes to feces
Drop- Diuretic (Choose Loop/Furosamide to waste K+)
or chose Dialysis if the kidneys are working

Calcium just protects the heart
Beta Agonists, Bicarb and the Insulin/Glucose combo
actually MOVE the K+ into the cells & OUT of the
interstitial space where it’s screwing up muscle
contraction (most importantly in the heart!)
Then you have to get RID of the extra K+ so you can
BIND it in the Gut & excrete OR, if the kidneys work,
you can use a K+ Wasting Loop Diuretic. OR you could
use dialysis.

116
Q

Flattened Ts and Prominent U-Waves signal:

A

HYPOKalemia (under 3.5, severe under 2.5)

You may see severe bradycardia or arrythmias on EKG

Mild HypoK = you might just give oral K+ supplements
from 2.5-3.5 the Pt may be asymptomatic
though you can see EKG changes.

Severe HypoK = you’ll need to run in K+ IV
Always dilute to an infusion
This takes hours, has to be slow and
monitored carefully so as not to tip into
Hyper K+

Mg+ usually follows K+ so you’ll need to replenish both. Both values should show on your lab results.

117
Q

Common TOXINS that cause pulseless Arrest:

A

Beta Blockers
Calcium Channel Blockers
Digoxin
These get out of whack when Kidney function
Nosedives, which can happen easily in
elderly people

  Dig toxicity has the slopey/smiley R wave
  Betas & CCBs just cause Bradycardia and are 
  reversed by Atropine. Sotalol may cause 
  Torsades Tricyclics Cocaine
118
Q

Types of Wave Form Capnography Tubing

A

Nasal Lines - have CO2 detectors in the chamber between the nasal probes on a specialized nasal canula. You attach the Capnography canula just like one for O2 and insert the other end into the CO2 port on your monitor, then provide O2 via NRB over the capnography canula.

ET-Filter Lines - attach to the end of the ET Tube as it protrudes from Pts mouth, between the ET and the Ambu Bag. Plug the other end of the ET-filter line into the CO2 port on the monitor.

119
Q

Capnography Wave Shapes

A

Normal is a rectangular plateau 12-20/min proceeding left to right just like an EKG
- left Height of the rectangle is the fast increase in CO2
detected in early exhalation.
- The plateau Length of the wave is the steady end of the
exhalation emptying the alveoli into the trachea
- The right drop in height is the sharp decrease in CO2
as inhalation of O2 displaces CO2 from the breath

Shark Fin - usually means bronchospasm as in asthma
- give albuterol via nebulization until wave form
returns to normal

Short/shallow waves indicate poor circulation. If waves are
below 10mm Hg (very short & squat) try to improve CPR
until waves get taller (between 10 & 20 mmHg).

ROSC in a pt receiving CPR will show as increase in height
to 35-45 mmHg and hopefully an increase in waves/min

If your Wave is flat after intubation, first check that your Capnography tubing is properly placed and plugged in, the check chest for bilateral breath sounds on ventilation and, if absent, resituate the ET Tube - its in the esophagus

120
Q

Adenosine isn’t just for SVT anymore!!

Describe 2 uses for Adenosine Push

A

1) SVT - so long as there is no WPW delta wave on your
QRS complexes you can use 6mg Adenosine
followed by 20ml of NS to convert SVT.
CPR 5 cycles
Check Rate, ID SVT with no deltas
CPR 5 Cycles - during CPR give
6mg Adenosine Pushed by 20ml NS
Check Rate, if not converted…
Continue CPR 5- Cycles
Check Rate - if not converted
Continue CPR & give
12 mg Adenosine Pushed by 20ml NS
Continue CPR 5 Cycles
Check Rate, if not converted
Synchronised Defibrillation at 150J
A biphasic machine will automatically
measure the impedance in the Pt and
will adjust Joules DOWN if needed but
it won’t adjust UP, so set it higher than
120.
One synchronized defibrillation usually converts SVT to Something, hopefully NSR. If not, and you get a ventricular arrhythmia, continue CPR & switch to Unsynchronized shock and prepare to head down the pulseless VTach/VFib algorithm.

2) IF you have a STABLE Wide Complex Tachycardia, Usually this would be Monomorphic VTach with a pulse, you can use Adenosine to convert it

121
Q

VTach rate ranges

A

Usually above 120 and below 220

VTach under 150 may be asymptomatic and your patient may be hemodynamically stable BUT he won’t stay that way long…

122
Q

Difference between Vasopressors and Vasopressin?

A

Vasopressors are a class of medications that increase blood pressure by constricting periperhal blood vessels.

VASOPRESSIN is another name for Anti Diuretic Hormone (ADH) a hormone released by the posterior pituitary in response to increased osmolarity (saltiness) of the blood and/or low blood volume. It shuts down filtration of water out of the blood into the urine and has some vasoconstrictive effect at high concentrations.

Vasopressin 40 units can be substituted for the 1st or 2nd dose of epinephrine in a pulseless arrest situation. It has the advantage of not stressing out the heart like Epi does while still raising the Bp. Epi raises Bp mainly by making the heart beat faster and more forcefully though it does have peripheral vasoconstrictive properties as well. Epi does nothing to stop water being lost from blood to urine.

123
Q

What is the half life of Vasopressin? Epi?

A

Vasopressin is 20 minutes - that’s why you only give it once during a Code and then fall back to Epi

Epi is 2 minutes, that why you give it frequently in a code

124
Q

Witnessed vs Unwitnessed Cardiac Arrest, first action in each?

A

If Witnessed (and you have a Defibrillator/AED) SHOCK 1st.

If not witnessed, do 5 cycles of CPR then shock

125
Q

WHEN do you give the first dose of EPI in pulseless VT/VF?

A

1st Dose of Epi (or Vasopressin) is administered during CPR after the 2nd shock.

Thereafter medications technically proceed on a time schedule while shocks proceed on a CPR cycle.
Epi every 3-5 min if rhythm warrants NO MAX for EPI
Vasopressin is just given once in place of Epi1# or 2
Amiodarone is give if rhythm hasn’t converted
after shock #3. It is ONLY given twice but you
DONE shocking if you’re giving Amiodarone, so
you GIVE IT then wait
- 300 mg D5W Push

As a practical matter though, you check the rate at the end of the 5 CPR cycles and you need to check the rate before deciding to give more medication too, so Shock/CPR/Check Rate/ Shock/ CPR-give medication. You can’t give meds during a shock.

126
Q

DON’T use Amiodarone in:

A

Polymorphic VTACH. It can tip PM VTach right over into Torsades by prolonging the QT interval.

So… don’t give Amiodarone to Torsades either.

Just shock polymorphic VT and/or Torsades, right off. Then give Torsades MgSO3 if it didn’t convert.

127
Q

How does AMIODARONE work

A

It blocks primarily K+ channels, S-L-O-W-I-N-G down depolarization But…

Amiodarone is a quadruple whammy. It also blocks:

- Beta 1 Receptors
- Na+ Channels    - Ca++ Channels

That’s why we use it last. It can really do a number on the myocytes. It beats Lidocaine for survival to hospital but compared even to placebo it did not improve survival to hospital discharge.

Amiodarone changed its formulation to remove two additives that kept it in solution. Both ingredients independently reduced heart contractility. The new formulation is called “Aqueous Amiodarone” and it out performs Lidocaine for to hospital and 24hr survival. We await results (Sept 2015?) of a large randomized trial by the Rescusitation Outcomes Consortium as to whether Aq Amiodarone’s survival to Hospital Discharge stats are an improvement over those of original Amiodarone.

128
Q

How does LIDOCAINE work

A

Its a Na+ Channel Blocker, thus it prevents the myocytes from depolarizing and slows their contractions.

Not First Line anymore but you “CAN” use it after EPI/ADH if you don’t have Amiodarone in the pulseless VT/VF algorithm.

129
Q

Amiodarone Dosing

A

pVT/VF Refractory to 3 Shocks & 2 Epi Doses:
-300mg dil in D5W followed by 20ml NS PUSH
if no conversion then
-150mg dil in D5W followed by 20ml NS PUSH

          PUSH IT FAST!!!!!!

For paroxysmal ventricular arrhythmia after ROSC, start an Amiodarone infusion 1mg/min

Max 24Hr Dose of Amiodarone is 2.2 grams

130
Q

Only dilute Amiodarone in

A

D5W and use an In Line FILTER

PUSH it still with 20 ml of NS and PUSH it FAST!!!

131
Q

Atropine doesn’t work well in:

A

The COLD, don’t use in hypothermic Brady. Your heart is
beating slowly in this condition as COMPENSATION
and that just might save your life.

DON’T SPEED A COLD HEART

Also DON’T PACE A COLD HEART

Heart Block (Mobitz II or 3rd Degree). Atropine only takes the parasympathetic governor OFF the SA Node. if you have serious blockage at the AV Node, it doesn’t really matter how fast the SA Node is going - not much will get through. Switch to EPI/Dopamine and/or Transcutaneous Pacing.

132
Q

PACING start rate?

A

Start at 60 and adjust up in accordance with perfusion requirements.

Don’t forget to sedate and anesthetize pt before pacing!

133
Q

What to do for Sinus Tachycardia?

A

Fix the UNDERLYING CAUSE

Don’t try to convert it or use adenosine/epi/dopamine. Sinus Tach is compensatory and usually not over 130bpm.

STOP the blood/fluid leak 
Rx the INFECTION
Calm the person down
STOP the hyperventilation
GIVE 02 to hypoventillation
134
Q

Describe 3rd degree heart block and how to treat it

A

Regular QRS complexes and P-waves but the P’s are not driving the QRSs

If you have dropped QRS complexes, you have a Mobitz II, not 3rd Degree

Pace the 3rd degree; if it isn’t symptomatic yet, it soon will be.

If you can’t pace, use Epi or Dopamine infusion

135
Q

1st line Treatment for polymorphic VT?

A

UNsynchronized Defibrillation

Do NOT give amiodarone

Give MgSO4 if Torsades does’t convert after one shock

136
Q

Stable SVT including Aflutter

AFlutter and Sinus Tachycardia are included in SVT with the AV Nodal ReEntry Tachs. These are RAPID and REGULAR and originate ABOVE the VENTRICLES

A

STABLE = No sign of reduced cardiac output yet, though pt may feel palpitations or racing heart.

Seek Consult for Stable unless on Anticoagulants for at least a month or you can do an emergency TEE.

If on Warfarin or TEE is clear, you can Cardiovert, Synchronized 50-100J. It won’t usually stick for long but it might. If it doesn’t stick, you’ll need to schedule them for electrical studies and ablation.

Unstable SVT/FLUTTER is dizzy, possibly syncope & SOB with other signs of hypoxia.

Get an airway, High Flow O2 & Synchronized Cardioversion @ 50-100 J for UnStable.

137
Q

A Flutter is an AVT is AFIB?

A

AFib is Not an SVT. It is not organized. Unstable AFIB does get Cardioverted like SVT but… the voltage is higher. SVT is 50-100J and

Symptomatic (Unstable) AFIB gets Synchronized Cardioversion @ 120-200 J

138
Q

If you use Lidocaine instead of Amiodarone after the 3rd shock in pVT/VF, what is the dose?

A

1-1.5 mg/kg for 1st dose then

0.5-0.75mg/Kg for 2nd dose

Note: Lidocaine dosing is more complicated than Amiodarone and Amiodarone has better to hospital and 24hr survival rates than Lidocaine - so USE AMIODARONE

139
Q

Extreme Axis Deviation

A 
QRS is (+) in aVR [where it should be negative] and
it is (-) in leads I and aVF [where it should be +]

This is common in VT and is a way one might discriminate VT from SVT with aberrancy (SVT that is not super regular due to bundle branch block or some other anomaly)

140
Q

Left ear taller on the bunny ear

A

Left bundle branch block - this makes a tachycardia ventricular. The right bunny ear or right BBB won’t help distinguish VT from SVT but the left one is diagnostic of VT

141
Q

Positive concordance

A

V1-V6 QRS complexes are ALL positive with no S waves.

Negative concordance is the opposite, they’re all (V1-V6) negative.

Gen Med Cardiology (2 decks)

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