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93 Cards in this Set

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  • Back
what route of administration is preferred for ACLS?
IV (due to poor circulation, hard to absorb things)
what is the preferred placement for an IV line?
central placement is preferred; if pt has it, use it. do not stop CPR to place a central line though.
what is another preferred route of administration during ACLS (2nd line)?
intraosseous via large bore needle into bone marrow (long bones of arms and legs)
which routes of parenteral administration should be avoided during ACLS?
IM or SQ
what should NOT be stopped to insert lines or administer drugs?
CPR - good CPR compressions is more important than drugs!
what should be administered prior to and after drug administration?
20 mL of IV fluids or NS flush
what can be done to deliver meds to central circulation faster?
elevate the extremity
when is endotracheal tube (ETT) used? what should be kept in mind when administering drugs through ETT?
only if not able to give IV/IO - 3rd choice;
use 2-2.5 x dose, follow w/ 10-20 mLs of water flush
which drugs CAN be placed down an ETT?
NAVEL - naloxone, atropine, valium, Epi, lidocaine (maybe eventually vasopressin)
describe the initial management of VF/VT
out of hospital unwitnessed arrest: assess breathing, etc.
give 5 cycles of CPR
attempt defibrillation x ONE
continue CPR for 5 cycles until need to shock again, then reasses rhythm
do NOT check pulse after shock
when are drugs used in the treatment of VF/VT? which drugs are used?
after 2 attempts to shock, start administration of a pressor: epi or vasopressin (equal efficacy)
when VT/VF persists after 2-3 shocks, consider amiodarone (lidocane = second line)
describe the arrhythmia principles
all anti-arrhythmics are pro-arrhythmics
use of more than one agent per episode is not recommended
post AMI, most anti-arryth will make cardiac fx worse: amiodarone is indicated first, if unavailable, use lidocaine
describe the initial management of PEA/asystole
give 5 cycles of CPR; if rhythm is PEA/asystole, administer Epi or vaso and resume CPR x 5 cycles; then, consider administering atropine
last: transvenous pacing?
what is PEA/asystole?
pulseless electcial activity/asystole: several different rhythms (NOT SHOCKABLE); associated mechanical contractions are not strong enough to circulate blood; usually caused by reversible conditions: evaluate and treat these!!! (Hs and Ts)
what are the "Hs and Ts" that cause PEA/asystole?
hydrogen ion excess
toxins (overdose/suicide/abuse)
tamponade, cardiac (fluid in the pericardial sack)
tension pneumothorax (too much O2 given while on ventilator)
thrombosis (coronary, pulmonary)
trauma (hypovolemia, increased ICP)
define and describe the management of bradycardia
HR < 60 and inadequate for clincial condition
1. maintain airway and assist breating, give oxygen, monitor EKG, BP, oximetry, estalish IV acess
2. asses for s/sx of poor perfusion caused by bradycardia (ms changes, CP, hypotension)
3. if no s/sx - observe/monitor
4. if sx of poor perfusion: prepare for transcutaneous pacing; use w/o delay for high degree block; consider atropine 0.5 mg IV while awaiting pacer, may repeat to a total dose of 3mg; if ineffective, begin pacing
consider epinephrine (2-10mcg/min) or DA (2-10mcg/kg/min) infusion while awaiting pacer of if pacing ineffective
4. prepare transvenous pacing, treat contributing causes, consider consultation
describe the steps to manage Acute coronary syndrome
ECG for diagnosis (w/in 15 min of entering hospital)
IV access
brief hx
evaluate for fibrinolytic (w/in 30m) or cath lab (w/in 90m)
lab studies
O2 4L/min titrate to SaO2 >90%
ASA 160-325 mg PO/SL
NTG: 0.4 mg SL, spray, IV 2 mcg/min to desired BP, pain relief or side effects
morphine 2-8mg IVP in divided doses for pain relief/anxiety/venodilation
how is STEMI treated?
Heparin, LMWH, or UFH
reperfusion: balloon w/in 90 minutes of entering hospital
(or fibrinolytic w/in 30m of entering)
ACE/ARB (earlier the better)
HMG-CoA reductase inhibitor
how is UA/NSTEMI treated?
heparin LMWH or UFH
glycoprotein IIb/IIIa1
evaluate for medical vs. interventional Rx
describe the steps in the management of stroke?
triage stroke as quickly as AMI
establish time of sx onset***
IV access and blood work
Neuro exam and stroke team
emergent brain CT, 12 lead EKG
evaluate CT for hemorrhage
early stroke (<3 hr) eval for administration of fibrinolytic (no CI/appropriate time window)
rTPA 0.9mg/kg to max of 90mg
no blood draws or anticoag for 24 hours
when is it appropriate to stop CPR?
no set time, based on clinical judgement
respect the pts dignity
respect the pts wishes
what is the pre-arrest quality of life, other med conditions, etc.
what is the MOA of epinephrine?
stimulates B1, B2 and alpha receptors
what are the indications for epinehprine?
asystole, bradycardia, PEA (VT/VF? its in the algorithm)
what is the dose of epi used in ACLS?
1 mg IVP q 3-5 minutes (VT/VF)
- de-emphasis on high or escalating doses
- probably induces more harm than good
- continuous infusion 2-10 mcg/min (bradycardia)
what forms does epinephrine come in?
1 mg/1ml amp, 1 mg/10mL syringe, 1 mg/1ml 30 mL vial
true or false: use of epi for ACLS improves survival
false - no evidence to prove this
little evidence of return of spontaneous circulation(ROSC)
no evidence of improvement in neuro outcomes
what is the moa of vasopressin?
potent vasoconstrictor, ADH analog
when is vasopressin used in ACLS?
to replace 1 dose of epi (either 1st or 2nd)
what is the dose of vasopressin used in ACLS?
40U IVP x 1, may repeat x 1
has a longer duration than epi, but still give A drug every 3-5 min
true or false: vasopressin has shown improvement in survival to hospital discharge over epi, but no improvement in neuro outcomes?
what is the moa of dopamine?
dose dependent stimulation of B1 and B2 receptors, alpha at higher dose
increase in HR and CO
stimulates DA recpt in renal vascular bed - does NOT improve renal blood flow
what are the indications for DA?
vascular support, hypotension, bradycardia
what are the indication for vasopressin?
equivalent to Epi for refractory VF/VT; vasopressor
what is the dose of dopamine used for ACLS?
2-10 mcg/kg/min continuous infusion (should be in central line when possible)
what forms does DA come in?
4mg/4ml amp, dilute in 250mL of D5W
when is isoproterenol indicated for ACLS?
no longer recommended for use in ACLS
what is the moa of atropine?
anticholinergic, increases conduction via the AV node, increases SA nodal discharge
what are the indications for atropine?
bradycardia, PEA, asystole
what doses are used for atropine for bradycardia and for asystole or PEA?
bradycardia: 0.5 mg IVP q 3-5 min to a total of 3mg
asystole/PEA: 1mg IVP q 3-5 min to a total of 3 mg
what forms is atropine available in?
1 mg/10 mL syringe
what happens if doses less then 0.5mg of atropine are given?
heart rate slows - not good if being used to treat bradycardia, or PEA/asystole
what is the MOA of amiodarone?
blocks beta, alpha, Na, K, and Ca channels
what are the indications for amiodarone?
stable VT
refractory VF/VT
recommended over lidocaine
what is the dose of amiodarone used for ACLS?
300 mg IVP rapid infusion; may give a repeat bolus 150-300 mg IVP x 1
what are the available forms of amiodarone?
150mg/3ml vials, must be filtered for standing drips (not for bolus); foams if drawn up to quickly
what special considerations must be given when administering amiodarone?
must be diluted
dilute further in syringe w/ 20 mL NS
or, administer IVP, then follow w/ rapid IVP NS (20mL) bolus
do NOT hang infusion post-bolus
true or false: amio vs lido - amio increases survival to hospital admission but not overall survival for ACLS
what is the moa of lidocaine?
class Ib anti-arrhythmic, decreases automaticity, decreases conduction velocity, increases ventricular threshold
what is the indication for using lidocaine in ACLS?
persistant/recurrent V.fib/V.tach, stable VT
what is the dose of lidocaine used for ACLS?
1-1.5 mg/kg IVP, may repeat in 10 minutes; 1-2 mg/min continuous infusion
what are the available forms of lidocaine?
100mg/10 mL syringe, 2 gm in D5W 250 mL premade drip
what is the moa of procainamide?
class IIa anti-arrhyth, suppresses atrial and vent arrhythmias, can convert atrial arrhyth to NSR
what are the indications for procainamide?
persistant/recurrent V.fib/V.tach
what is the dose of procainamide used in ACLS?
20 mg/min until:
rhythm supressed
>50% increase in QRS complex
total dose of 17 mg/kg
continuous infusion drip 1-4 mg/min
what forms are available for procainamide?
100mg/ml 10 mL; 500mg/mL 2 mL vial
what is the MOA of magnesium sulfate?
electrolye w/ multiple fx throughout the body, works as anti-arrhythmic when hypomagnesemic
what are the indications for magnesium sulfate?
refractory vfib/vtach, torsades***
what is the dose of mg sulfate used for ACLS/
1-2 g IVP, may repeat
what are the available forms of Mg sulfate?
1g/2ml (50% sol'n); dilute to minimum of 10% sol'n (multiply total vol x 5 and infuse over 1-2 minutes)
what is the MOA of adenosine?
naturally occuring nucleoside that decreases AV node and SA node activity (atrial activity only)
what is the indication for adenosine?
what is the dose of adenosine used?
6 mg IVP rapid, repeat w/ 12 mg IVP rapid in 1-2 minutes if no response
lower dose to 3 mg if pt taking dipyridamole, cbz, transplanted heart, or given via central line
higher doses may be given in pts on theophylline or large amt of caffeine
what are the available form of adenosine?
6mg/2ml syringe
what is the moa of sodium bicarb?
neutralizes acidotic state
what is the indication for bicarb?
what is the dose of bicarb used?
1 mEq/kg, typically 50 mEg IVP
what are some incompatabilities associated w/ bicarb?
calcium, epi, atropine, isoproterenol, norepi
what are the available forms of bicarb?
4.2% 10mEq/10mL, 8.4% 50mEq/50mL syringe
what is the moa for calcium salts (choloride/gluconate)
enhance myocardial contractile force
what is the indication for calcium salts?
no benefit in cardiac arrest, exception would be CaB overdose, hyperkalemia, hypocalcemia
what is the dose of calcium salts used for ACLS?
2-4 mg/kg (500-1000mg) slow IVP
what are the available forms of calcium salts?
1 g/10mL amps and vials
what is the moa of dobutamine?
stimulation of B1 receptors to improve CO
what are the indications for dobutamine?
acute decompensated CHF
what is the dose of dobutamine used for ACLS?
5-20 mcg/kg/min
what are the available dosage forms of dobutamine?
250mg/20mL vials, mix 500 mg in D5W 250 mL
what are the actions of BBs?
block both B1 and B2 receptors, preventing the activity of NE and Epi; decreases HR, myocardial contraction, CO, BP (and thus myocardial O2 demand).
slows conduction through AV node and prolongs refactory period, reduces renin levels and ATII conc - decreases cardiovascular risk
cardioselective (atenolol, metoprolol, bisoprolol, acebututolol) block only B1 recpt but at high dose may block B2 - safer for pts w/ asthma, COPD, PVD, and DM
what are the indications for BBs (lots!)
HTN, post-MI, CHF, arrhythmia, angina, intraoperative and postop tachycardia and HTN
shown to reduce mortality in pts w/ HTN
reduction in nonfatal reinfarction and death when used post AMI
what are the ADRs associated w/ BBs?
bradycardia, precipitation of heart failure, bronchoconstriction, fatigue, cold extremeties/exacerbation of intermittent claudication/raynauds
abrupt d/c may cause rebound tachycard, UA, MI or death, must taper over 14 days
what is the moa of ACE-Is?
block ACE and relax arterial walls and lower pressure
what are the indications for ACE-Is?
what are the ADRs associated w/ ACE-Is?
cough, rash, angioedema, fatigue, HA
what is the moa of ARBs?
block the effect of ATII by binding AT1 recpt; help blood vessels stay open and lower blood pressure
what are the indications for ARBs?
what are the ADRs of ARBs?
angioedema, rash, HA, dizziness
what is the moa of CCBs?
blocks the release of Ca ions into cardiac and vascular smooth muscle - inhibits activation of ATPase on muscle contraction
causes depression of mechanical contraction of myocardial and smooth muscle and depression of both impulse formation (automaticity) and conduction velocity
reduces intracellular Ca levels in cardiac and smooth muscle cells of the coronary and peripheral vasculature, resulting in dilation of coronary and peripheral arteries and arterioles
results in an increased supply of blood and oxygen to the heart and reduces afterload
CCBs have antiarrhythmic, antianginal, and antihypertensive effects
both types are similar in their antihypertensive effects, but differ in other clinical effects
all (except amlodipine) have negative inotropic effects
what are some effects of DHP CCBs?
cause reflex increase in HR, less likely to call a fall in CO
may exacerbate sx of angina, do not alter AV nodal conduction
norvasc is the only CCB included in the AHA/CHF guidelines as safe in CHF management
which CCB is used for CHF management?
Norvasc (amlopdipine)
what are the effects of verapamil?
decreases HR and slows AV nodal conduction, less vasodilation than nifedipine
what are the effects of diltiazem?
decreases AV conduction and HR, but to a lesser extent than verapamil
which of the following is a more potent negative inotrope? verapamil or diltiazem?
in which pts must the effects of negative inotropy be taken into account?
pts w/ LVEF <30%
what are the ADRs associated w/CCBs?
pronounced vasodilation causes a decrease in BP, monitor for orhtostatic hypotension; do not use IR nifedipine for HTN
HA, dizziness, constipation (esp w/ verapamil)
dose dependent edema
gingival hyperplasia