Glossary of ACLS 2
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- What is the preferred route of administration for ACLS?
- IV (Hard to absorb due to poor circulation and hypotension).
- Which type of IV is preferred in ACLS?
- Central placement. If you have it, use it, most patients don't and you CANNOT stop CPR to do it
- What is our 2nd choice for IV access?
- Intraosseous given via large bore needle into bone marrow (since lots of vasculature and has good absorption)
- Do you stop CPR to administer vital drugs?
- What should follow each drug after administration in IV?
- 20ml of Iv fluids or flush (NS)
- What should be done besides a flush after administering drugs to a patient?
- Elevate extremity to help deliver meds quicker to central circulation
- What is the 3rd choice for administering drugs in ACLS?
- Endotracheal (ONLY if not able to give IV/IO).
Use 2-2.5x the dose, follow with water flush(10-20ml)
- Which drugs can be put down the ETT?
- Naloxone, Atropine, Valium, Epi, Lidocaine
Vasopressin can, but not approved yet
- Ventricular fibrillation, what do you do?
- Out of hospital unwitnessed arrest: Assess breathing...
1. 5 cycles CPR
2. Attempt Defib x one
Autodefib will read rhythm to you, if VT or VF, biphasic 200J (Mono 360J)
Continue CPR for 5 cycles until need to shock again, then reassess rhythm
Do not need to check pulse after shock
- When should you use a pressor in VF? Which one?
- After 2 attempts to shock.
EPI or Vasopressin
When VF/VT persists after 2-3 shocks, consider amiadarone (second line)
- All ________ are pro-arrhythmic
- Is multi-drug therapy for treatment of arrhythmias recommeded?
- After a heart attack, discuss the efficacy of anti-arrhythmics
- Most will make cardiac function worse, Amiodarone indicated first, if unavailable, then use lidocaine
- Describe Pulseless electrical activity/Asystole
- Several different rhythms
Associated mechanical contractions are not strong enough to circulate blood.
-Caused by reversible conditiosn (evaluate and treat these)
- Describe the causes of pulseless arrest, the H's
Hydrogen ion excess
- Describe the causes of pulseless arrest, the T's
Tamponade, cardiac (fluid in sac around heart)
Tension pneumothorax (on ventilator, too much oxygen)
Thrombosis (coronary or pulmonary)
- Describe steps to be taken upon presentation with ACS
- ECG for Dx (W/I 15min of entering hospital)
Evaluate for fibrinolytic or cath lab
- Describe initial treatment for patient presenting with ACS
- -Oxygen 4L/min titrate to SaO2 >90%
ASA 160-325mg PO/SL
NG 0.4mg SL, spray or IV 2mcg/min to desired BP, pain relief or side effects
Morphine 2-8mg IVP divided dose for pain relief/anxiety/venodilatation
- Describe drugs to be used for STEMI
- Beta Blocker
Heparin (LMWH or UFH)
Reperfusion : door to balloon 90min, door to fibrinolytic 30min
HMG CoA reductase inhibitor
- UA/NSTEMI drugs to be used
Heparin LMWH or UFH
Evaluate for medical vs interventional Rxs
- Stroke management
- 1.Triage stroke quickly as AMI
2.Establish time of Sx onset (Very important for choosing Sx, if woke up with Sx, can't determine)
5.IV access and blood work
6.Neuro exam and stroke team
7.Emergent Brain CT, 12 lead ECG
8.Evaluate CT for hemorrhage
9.Early stroke (<3hr), evaluate for administration of fibrinolytic (no CI/Appropriate time window)
10.rTPA 0.9mg/kg to max of 90mg
NO BLOOD DRAWS OR ANTICOAG FOR 24 HOURS
- Epinephrine MOA
- Hits Beta 1 and 2, alpha receptors (Remember its dose dependent)
- Epi Indications
- Asystole, Bradycardia, PEA
- EPI Dose
- 1mg IVP q 3 -5 min
- Describe EPI efficacy in terms of survival
- No studies show epi improves survival, little evidence for return of spontaneous circulation and no evidence for improving neurological outcomes
- Vasopressin MOA
- Potent vasoconstrictor, ADH analogue
- Vasopressin Indication
- Same as EPI for refractory VF/pulseless VT; vasopressor
- Describe how vasopressin can displace EPI doses
- A dose of vasopressin can replace a dose of Epi (1st or 2nd)
- Vasopressin DOSE
- 40 U IVP x 1, may repeat x 1
Much longer duration 10-20 min, BUT don't wait, give A drug q 3 - 5 min
- Describe Vasopressin in terms of efficacy
- Found to improve survival vs Epi but no improvement of neurologic outcomes
- Dopamine DOA
- Dose dependent stimulation of Beta1 and Beta2 receptors and alpha at higher dose
Increases HR and CO
Stimulates DA receptors in renal vascular bed. Does not improve renal blood flow,d espite we've used it for this for years.
- Dopamine Indication
- Vascular support, Hypotension, Bradycardia
- Dopamine DOSE
- 2-10 mcg/kg/min continuous infusion (use central line when possible)
- NE MOA
- Predominantly hits alpha receptors to increase BP
- NE dose
- 0.5-1 mcg/min, titrate to effect
- Isoproterenol MOA
- Hits beta receptors, increases CO and HR
- Isopreterenol Indications
- Atropine MOA
- Anti-cholinergic, increases conduction via AV node, increase SA nodal discharge
- Atropine Indication
- Bradycardia, asystole, slow PEA
- Amiadarone MOA
- Blocks beta, alpha, Na+, K+ and Ca+ in heart
- Why is Amiodarone the best anti-arrhythmic?
- Doesn't really cause heart dysfunction
- Amiodarone Indcations
- STable VT, Refractory VF/Pulseless VT, recommended over lidocaine
- Amiodarone DOSE
- 300mg IVP, rapid infusion
- Administration concern of Amiodarone
- Foams if drawn up too quickly
- Preparation concerns of Amiodarone
- MUST DILUTE!
Dilute further in syringe with NS (20ml) OR Administer IVP then follow with rapid IVP NS 20ml Bolus
- One major advantage of Amiodarone
- Improves defibrillation response
- Lidocaine MOA
- Class 1b anti-arrythmic, decrease automaticity, decrease conduction velocity, increase vent. threshold
- Lidocaine Indcation
- 2nd line agent for persistant/recurrent V.fib/V.tach; stable VT
- Lidocaine DOSE
- 1-1.5 mg/kg IVP, may repeat in 10 minutes; 1-2mg/min continuous
- Procainamide MOA
- Class IIa anti-arryhtmic, supresses atrial and ventricular arrythmias (can convert to NSR)
- Procainamide indcation
- Persistant/recurrent v.fib/v.tach
- Why can procainamide cause hypotension?
- Blocks alpha receptor
- Mag Sulfate MOA
- Electrolyte with multiple functions throughout entire body, works as anti-arrythmic when hypomagnesemic
- Mag Sulfate Indications
- Refractory V.Fib,V.tach; TORSADES
- Mag sulfate Dose
- 1-2 GM IVP, may repeat
- Adenosine MOA
- Naturally occurring nucleoside that decreases AV node and SA node activity
- Adenosine Indication
- Adenosine Dose
- 6mg IVP rapid, repeat with 12mg IVP rapid in 1-2 min if no repsonse.
Use lower dose, 3mg if patient is taking dipyridamole or carbamazepine, transplanted hearts or given via central line.
Higher dose, 6mg may be required in patient on theophylline or large amounts of caffeine
- Na Bicarb MOA
- Neutralizes acidotic state
- Na Bicarb Indication
- Documented Acidosis
- Sodium Bicarb Dosing
- 1 mEq/Kg, typically 50 IVP
- Describe some incompatibilities of Bicarb
- Calcium, EPI, Atropine, isoprotenerenol, NE
- Calcium Salts MOA
- Enhance myocardial contractile force
- Calcium salts Indication
- No benefit in cardiac arrest, exception would be CCB overdose, hyperkalemia or hypocalcemia
- Calcium salts DOSE
- 2-4 mg/kg IVP slow
- Dobutamine MOA
- Beta1 stimulation to improve CO
- Dobutamine Indication
- Acute decompensated CHF
- Dobutamine Dose
- 5-20 mcg/kg/min
- Which beta blockers are cardioselective
- In which population of patients would a cardioselective betablocker be preferred?
- Asthma, COPD, PVD, DM
- Indications for Beta Blockers
- HTN, post-MI, CHF, cardiac arrhythmias, angina, intraoperative and postoperative tachycardia and hypertension
- Beta Blocker ADR
Precipitation of CHF
Cold extremities/exacerbation of intermittent claudication or Raynauds
Abrupt discontinuation may cause rebound tachycardia, UA, MI or even death
- ACEI MOA
- Blocks angiotensin converting enzyme or ACE and relax arterial walls and lower blood pressure
- Indications ACEI
- HTN, CHF
- ADR of ACEI
- Cough, rash, angioedema, fatigue, headache
- ARB Indications
- ARB ADR
- Angioedema, rash, HA dizziness
- Describe inotropic effects of ARBs
- All negative except amlodipine
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