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78 Cards in this Set

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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?
NO
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
Anti-arrythmics
Is multi-drug therapy for treatment of arrhythmias recommeded?
No
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
Hypoxia
Hypovolemia
Hydrogen ion excess
Hypo/Hyperkalemia
Hypoglycemia
Hypothermia
Describe the causes of pulseless arrest, the T's
Toxins
Tamponade, cardiac (fluid in sac around heart)
Tension pneumothorax (on ventilator, too much oxygen)
Thrombosis (coronary or pulmonary)
Trauma
Describe steps to be taken upon presentation with ACS
ECG for Dx (W/I 15min of entering hospital)
IV access
Brief history
Evaluate for fibrinolytic or cath lab
Lab studies
CXR
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
Clopidogrel
Heparin (LMWH or UFH)
Reperfusion : door to balloon 90min, door to fibrinolytic 30min
ACE/ARB
HMG CoA reductase inhibitor
UA/NSTEMI drugs to be used
NG
Beta Blocker
Clopidogrel
Heparin LMWH or UFH
Glycoprotein IIb/IIIAI
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)
3.ABC's
4.Oxygen
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
Continuous 2-10mcg/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
None
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
PSVT
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
Atenolol
Metoprolol
Bisporolol
Acebutolol
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
Bradycardia
Precipitation of CHF
Bronchoconstriction
Fatigue
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
HTN/CHF
ARB ADR
Angioedema, rash, HA dizziness
Describe inotropic effects of ARBs
All negative except amlodipine