Transcript MEDICATIONS USED IN ADVANCED CARDIAC LIFE SUPPORT

Overview of ACLS
Pharmacology
and
Update on New ACLS
Guidelines
Krista Piekos, Pharm.D.
Clinical Pharmacy Specialist - Critical Care
Harper University Hospital
Adjunct Assistant Professor
Wayne State University
Objectives
• Pharmacists should be able to identify:
Why?
…we use an agent
When?
…to use an agent
How?
…to use an agent
What?
...to watch for
• To familiarize the pharmacist with the ACLS
algorithms
• To help the pharmacist become comfortable with the
crash cart
• To introduce the needless delivery system
Outline
• Present conclusions of the International Guidelines
2000 ACLS objectives with 2003 updates
• Classification of recommendations
• ACLS Algorithms
• Pharmacology of agents used in algorithms
• Overview of crash cart revisions
• Overview of needless system
Background
• In Seattle 43% of patients in VF survived to
hospital discharge if CPR w/in 4 min and
defibrillation w/in 8 min
• These figures are higher than national
average - due to AED’s throughout public
• Overall survival from CPR is poor 5-15%
• Survival for in-patient CPR to discharge is
<10%
Guidelines 2000 for
Cardiopulmonary Resuscitation and
Emergency Cardiovascular Care
•
•
1st international consensus on resuscitation
guidelines
Experts from around the world
• Identified issues
• Gathered scientific evidence; level (quality) of evidence
• Integrate into a class of recommendation
• Revised guidelines
Classification of Therapeutic
Interventions
Class I: definitely helpful, excellent
 Class II:
Class II a -probably helpful;
good to very good
Class II b -possibly helpful; fair
to good
• Class Indeterminate: insufficient evidence; no
harm, but no benefit
 Class III: possibly harmful

New Goals
1. Early Defibrillation - Public Access Defibrillation (PAD)
Probability of successful defibrillation and survival is negatively
related to the time from onset of VF to delivery of first shock
“PAD has the potential to be the single greatest advance in the
treatment of prehospital sudden cardiac death since the invention of
CPR”
Circulation August 22, 2000
2. Establishing a specific diagnosis by ECG
3. Antiarrhythmic agents are just as likely to be
proarrhythmic as they are antiarrhythmic.
One, and only one antiarrhythmic should be used.
Routes of Administration
Intravenous
• Preferred route
Endotracheal
·
·
·
·
2-2.5 X’s IV dose in 10ml volume
Each dose is followed by 10 ml NS flush down the ET tube
(Ex. epinephrine, atropine, lidocaine, diazepam, naloxone)
Absorption occurs at alveolar capillary interface
Intraosseous (active bone marrow)
· Pediatric patients without IV access
Other: Sublingual, intracardiac, IM, SC (poor absorption)
ACLS
Algorithm
Approach
Universal Algorithm
Epinephrine
WHY?
• Natural catecholamine with  and ß-adrenergic agonist activity
•
Results in:
•  flow to heart and brain
•  SVR, SBP, DBP
•  electrical activity in the myocardium & automaticity ( success with
defibrillation)
• myocardial contraction (for refractory circulatory shock (CABG))
•  increases myocardial oxygen requirements
• Primary benefit: -vasoconstriction
• ß-adrenergic activity controversial b/c  myocardial work
WHEN?
• VF/VT, asystole, PEA, bradycardias
Epinephrine
HOW?
• High dose versus standard dose?
• Higher ROSC with high dose, but no change in survival
• High doses may exacerbate postresuscitation myocardial dysfunction
Recommendations:
•
•
•
•
Class I: 1 mg IV q 3 - 5 min
Class IIb: 2-5mg IVP q3-5min, or 1mg-3mg-5mg
Class Indeterminate: high-dose 0.1mg/kg IVP q3-5min
Infusion for  HR & BP (IIb)
• 1mg in 250ml NS or D5W - infuse @ 1-10 mcg/min
• ET Dose=2-2.5 times IV dose
What to watch for?
•
Tachycardia, hypertension, myocardial ischemia, acidosis
Incompatible with Ca, HCO3, aminophylline & PHY. Alkaline solutions cause auto-oxidation.
Vasopressin
WHEN?
• Alternative to epinephrine for shock-refractory VT/VF
WHY?
• Natural antidiuretic hormone
• Potent vasoconstrictor by stimulation of SM -V1 receptors :
•  BP & SVR;  CO, HR, myocardial O2 consumption and contractility
• Does not  myocardial oxygen consumption
• Not affected by severe acidosis
• Class IIb for shock-refractory VF
• Class Indeterminate for PEA, asystole
• Half life = 10-20 minutes
Dose?
• 40 Units IVP - one time only!!!
Why Vasopressin?




During CPR, plasma ADH levels are higher in patients with
return of spontaneous circulation (ROSC)
During CPR patients may be severely acidotic
Epinephrine compared to vasopressin pre-hospital CPR (20
patients/study group)
Multiple animal studies showing  ROSC
Survival to hospital
24 hour survival
Discharge alive
EPI (n=20)
VP (n=20)
35%
20%
15%
70%
60%
40%
(p=0.06)
(p=0.02)
(p=0.16)
ILCOR Universal Algorithm
(International Liaison Committee on Resuscitation)
Medication changes in 2000:
• Emphasis on identification of all possible stroke
victims for IV fibrinolytics
• Epinephrine has become Class Indeterminate
• High-dose epinephrine no longer recommended
• For shock-refractory VT/VF: Epinephrine 1 mg q 3-5 min
• Vasopressin 40 Units IVP one time
• Epinephrine alone for non-VT/VF
Pulseless Ventricular Fibrillation
or Tachycardia
• In ACLS, always assume VF - most common
• 85%-95% of survivors have VF
• Survival dependant on early defibrillation
• Medications indicated only after 3 failed shocks
VFib/Pulseless VT Algorithm
“Please Shock-Shock-Shock, EVerybody Shock, And Let's Make Patients
Better”
Please - Precordial Thump If pulse-less with no defibrillator
Shock 200J*
Shock 200-300J*
Shock 360J* (*only consecutive, if persistent)
EVerybody - Epinephrine 1 mg IV q3-5 min or Vasopressin 40 U IVP
If VF/PVT persists, "CONSIDER" antiarrhythmics and sodium bicarb. NOTE: always "max
out" one agent before proceeding to the next in order to limit pro-arrhythmic drug-drug
interactions
Shock 360J
And - Amiodarone (First Choice) 300mg IV push. May repeat once at
150mg in 3-5 min. (max. cumulative dose: 2.2g IV/24hrs)
Drug-shock-drug-shock sequence
(continued)
“Please Shock-Shock-Shock, EVerybody Shock, And Let's Make Patients
Better”
Let's - Lidocaine 1.0-1.5 mg/kg IV. May repeat in 3-5 min (max=3 mg/kg)
Make - Magnesium Sulfate 1-2 g slow IVP for suspected  Mg or TdP
Patients- Procainamide 30 mg/min, or 100 mg IV q 5 min. for refractory VF.
(max. dose: 17 mg/kg)
NOTE: Besides having a pro-arrhythmic drug-drug interaction with amiodarone, procainamide is of
limited value in an arrest situation due to a lengthy administration time
Better (consider buffers) - Bicarbonate 1 mEq/kg IV for:
•
•
•
•
•
preexisting  K+
bicarb-responsive acidosis
some drug overdoses
protracted code (intubated)
ROSC after long code with effective ventilation.
Drugs for VF/PVT
• Epinephrine - Why? How? What?
• Vasopressin - Why? How? What?
• Amiodarone
• Magnesium
• Procainamide
• Lidocaine
• Buffers
Classification of Antiarrhythmics
Class
Drug
Ia
Quinidine
Procainamide
Disopyramide
Ib
Lidocaine
Mexiletine
Tocainide
Ic
Conduction Velocity
Refractory Period
Automaticity
Ion Block
Sodium
Sodium
(fast on-off)
0/
Flecainide
Propafenone
Moricizine
Sodium
(slow on-off)
0
II
Beta-Blockers
Calcium
III
Amiodarone
Bretylium
Sotalol
Potassium
IV
Verapamil
Diltiazem
0
0
Calcium
Drugs Used for Heart Rhythm and Rate
Amiodarone
WHY?
• Class III antiarrhythmic (characteristics of all classes)
• Na, K and Ca channel blocker &  & -adrenergic blocker
• Prolongs AP and RP
• Decreases AV conduction velocity & SN function
New Recommendations (WHEN?):
• pulseless VT or VF (IIb)
• hemodynamically stable VT (IIb), polymorphic VT (IIb),
wide-complex tachycardia uncertain origin (IIb)
• refractory PSVT (preserved function, IIa; impaired function
IIb)
• atrial tachycardia (IIb)
• cardioversion of AF (IIa)
Amiodarone
HOW?
• Cardiac arrest (PVT/VF) - 300mg IVP diluted in 2030ml, may repeat with 150mg in 10 minutes, or start
infusion (max=2..2 g/24h)
• Atrial & ventricular arrhythmias in impaired hearts
•
•
150mg IVP over 10 min
May repeat q10-15 min, or start gtt 1mg/min x 6 hours,
then 0.5mg/min x 18 h
WHAT?
• Hypotension, bradycardia (slow rate, fluids)
Why Amiodarone?
ARREST Trial
Objective:
Efficacy of IV amiodarone in out-of-hospital cardiac arrest
due to ventricular fibrillation or pulseless ventricular
tachycardia
Endpoints:
Hospital admission with perfusing rhythm
Survival to discharge
Functional neurologic status at discharge
*Insufficiently powered to detect survival to discharge and functional neurologic
status*
ARREST Trial: Amiodarone in the
Resuscitation of Refractory Sustained
Ventricular Tachyarrhythmias
• Prospective, randomized, DB, PC trial
• 504 patients, who failed >/= 3 shocks
• Randomized to placebo or 300mg IV amiodarone
• Amiodarone Dosing:
• 300mg diluted with 5% D5W to 20mL
• Rapid IV bolus
• Found a statistically significant increase in the number of
patients who arrived to hospital alive (p=0.03)
• Consistent results regardless of presenting rhythm
This is the only antiarrhythmic agent which has shown definitive benefit in cardiac
arrest!
ARREST Trial - Subgroup Analysis
Amiodarone
Placebo
% Surviving to
Admission
70
60
50
40
30
20
10
0
All Patients
VF
Asystol e or PEA
ROSC
No ROSC
Drugs Used for Heart Rhythm and Rate
Magnesium Sulfate
WHY?
Magnesium deficiency causes arrhythmias
Facilitates ventricular repolarization by enhancing
intracellular potassium flux, dilates coronary
arteries
WHEN?
Suspected hypomagnesemia, pulseless VT/VF,
torsade de pointes
HOW?
Class IIa in suspected hypomagnesemia, TdP, and
Class IIb in VF/VT: 1 - 2gm slow IVP in 100ml
WHAT?Hypotension at large doses
Drugs Used for Heart Rhythm and Rate
Procainamide
WHY?
•
•
•
Suppresses both ventricular and atrial arrhythmias
Type Ia antiarrhythmic, affects fast Na+channels-slowing
conduction velocity, prolongs RP, and decreases automaticity
Phase IV depolarization
WHEN?
•
•
•
Refractory/recurrent VF/VT
Control of rapid ventricular response (IIb)
Conversion SVT (AF/Fl) (IIa)
Drugs Used for Heart Rhythm and Rate
Procainamide
HOW?
VF: 20-30 mg/min slow infusion (max=17 mg/kg)
AF with rapid vent. response: 100 mg over 5 min
then infuse@ 1 - 4 mg/min
1-2 gm/250ml D5W
WHAT?Stop infusion if patient hypotensive, widened QRS >50%,
arrhythmia suppression, or dose=17mg/kg
Dose reduction in renal failure
SLE syndrome
Levels: PA=4-12 µg/ml
NAPA=7-15 µg/ml (active metabolite-Class III)
Drugs Used for Heart Rhythm and Rate
Lidocaine
WHY?
•
•
•
•
•
Type IB antiarrhythmic
Affects fast Na+ channels, shortens refractory period
Suppresses spontaneous depolarization
Local anesthetic, increases fibrillation threshold
Suppresses ventricular ectopy post-MI
•
Without effecting myocardial contractility, BP or AV nodal conduction
WHEN?
• SECOND-CHOICE agent
• VT/VF refractory to electrical countershock and epinephrine
(Indeterminate)
• Control of PVC’s (Indeterminate)
• Hemodynamically stable VT (IIb)
•
Not for routine prophylaxis post-MI, however, accepted in high-risk patients
(hypokalemia, myocardial ishchemia, LV dysfunction)
Drugs Used for Heart Rhythm and Rate
Lidocaine
HOW?
Class IIa: 1 - 1.5 mg/kg IVP q5 - 10 min (max=3mg/kg)
Infusion (with pulse): 1 - 4 mg/min (if pulse is regained)
Therapeutic Levels: 1.5-6 µg/ml
ET Dose: 2-2.5 times IV dose
Preparation: 1-2 gm/250 ml D5W or NS
WHAT?Hepatic metabolism, renal elimination
Bradycardia, cardiac arrest, seizures
Lidocaine toxicity/neurotoxicity - twitching, LOC, seizures,
coma
Lidocaine levels persist in low CO states
Drugs Used to Improve Cardiac Output and Blood Pressure
Sodium Bicarbonate
WHY?
Enhances sodium shift intracellularly, buffers acidosis, decreases
toxicity of TCA’s, increases clearance of acidic drugs
WHEN?
Class I - hyperkalemia
Class IIa - bicarbonate-responsive acidosis metabolic acidosis
secondary to loss of bicarb (renal/GI); overdoses (TCAs,
phenobarbital, aspirin)
Class IIb - protracted arrest in intubated patients
Class III - hypoxic lactic acidosis
HOW?
1 mEq/kg IVP, 0.5mEq/kg q10 min prn
WHAT?
May worsen outcome if not intubated/ventilated.
Metabolic alkalosis, decreased O2 delivery to tissues, hypokalemia,
CNS acidosis, hypernatremia, hyperosmolarity
Incompatible with calcium, epinephrine, atropine, norepinephrine, isoproterenol
Summary
V.Fib and Pulseless V.Tach
Changes:
• Vasopressin added - Class IIb 40 U IVP x 1
• Epinephrine - Class Indeterminate 1mg IVP q 3-5 min
• Amiodarone added - Class IIb
• 300mg IVP (cardiac arrest dose). May repeat 150mg x 1
• Lidocaine - Class Indeterminate 1-1.5 mg/kg IVP q 3-5
min (Max = 3mg/kg)
• Procainamide is acceptable but not recommended due to
long administration times
• Bretylium fell off algorithm due manufacturing problems
The Tachycardia Algorithms
Major New Concepts:
• Make a specific rhythm diagnosis
• Identify patients with significantly impaired
cardiac function (EF<40%, overt HF)
• Only use one antiarrhythmic, especially in
damaged hearts
• Resulted in 3 new algorithms
The Tachycardia Overview Algorithm
Is the patient stable or unstable?
Stable
Identify 1 of 4 types of tachycardia
Unstable
Cardioversion
(premedicate)
AF/Aflutter
Narrow-complex tachycardia
Stable wide-complex tachycardia
Stable monomorphic VT
VT, PSVT,
100J, 200J,
300J, 360J
Tachycardia - Atrial Fibrillation/Flutter
4 Clinical Features:
• Unstable?
• Impaired cardiac function?
• WPW?
• Duration? <48h, or > 48h?
• Focus - treat unstable patients urgently
• Control ventricular response  convert 
anticoagulate
Atrial Fibrillation/Flutter
Condition
Rate Control
EF > 40%
CCB (I)
-Blocker (I)
EF < 40%
Digoxin (IIb)
Diltiazem (IIb)
Amiodarone (IIb)
WPW
Preserved heart
fxn:
DC Cardioversion
Amiodarone(IIb)
Flecainide (IIb)
Procainamide (IIb)
Propafenone (IIb)
Sotalol (IIb)
Impaired
EF<40%:
DC Cardioversion
Amiodarone(IIb)
Conversion
> 48h
DC Cardioversion
Amiodarone (IIa)
Ibutilide (IIa)
Flecainide (IIa)
Propafenone (IIa)
Procainamide (IIa)
DC Cardioversion
OR
Amiodarone (IIb)
Conversion
< 48h
No DC Cardioversion
Anticoagulation x 3
weeks, then CV, then
anticoagulation x 4 wk
OR r/o clot by TEE,
CV, then AC x 4 wk
(See above)
DC Cardioversion
Amiodarone (IIb)
Flecainide (IIb)
Propafenone (IIb)
Procainamide (IIb)
Sotalol (IIb)
(See above)
Drugs Used in Afib/AFlutter
•
•
•
•
•
•
•
Calcium channel blockers
Beta-blockers
Digoxin
Amiodarone
Procainamide
Flecainide (IV form in ACLS -not available in US)
Propafenone (IV form in ACLS -not available in
US)
• Sotalol (IV form in ACLS -not available in US)
Drugs Used for Heart Rhythm and Rate
Calcium Channel Blockers
WHY?
Blocks inward flow of Ca and Na, slows conduction, RP in AVN
Terminate reentrant arrhythmias requiring AVN conduction
Control ventricular response rate in AF/AFl
Coronary vasodilation
May exacerbate CHF
Verapamil:
Negative inotrope & chronotrope (good anti-ischemic)
Class I for acute and preventative SVT
Diltiazem:
Direct negative chronotropic effect, mild negative inotrope
Highly effective in controlling ventricular response in A Fib
WHEN?
Control ventricular response rate in patients with AF/Fl, or MAT
Verapamil: PSVT not requiring cardioversion
Drugs Used for Heart Rhythm and Rate
Calcium Channel Blockers
HOW?
Verapamil:
2.5 - 5 mg IVP, over 2 min (max=30mg)
Inf @ 5-10 mg/hr
Diltiazem:
0.25 mg/kg IVP, may repeat with
0.35mg/kg in 15 min
Infuse @ 5-15 mg/hr
WHAT?Contraindicated in wide QRS complex tachycardias and
ventricular tachycardias, exacerbation of CHF in patients
with LV dysfunction
Transient decrease in BP
Avoid in sick sinus syndrome of AV block (w/out pacer)
May potentiate digoxin toxicity.
Incompatible with bicarbonate, epinephrine, furosemide
Drugs Used for Heart Rhythm and Rate
Beta - Blockers
WHY?
B-adrenergic blockade, slows conduction and
increases refractory period in AV node
WHEN?
AMI (reduces rate of reinfarction), reduces
recurrent ischemia and incidence of VF in postMI patients, USA
HOW?
Atenolol:
Metoprolol:
Propranolol:
Esmolol:
2.5-5 mg IV over 5 min
5 - 10 mg IVP q 5 min
0.1 mg/kg IV divided into 3
doses @ 2 - 3 min intervals
500 mcg/kg over 1 min
Inf @ 50 mcg/kg/min
WHAT?Hypotension, bradycardia, AV block, overt heart
failure or severe bronchospasm/COPD
Stable Monomorphic Ventricular Tachycardia
Preserved
Cardiac
Function
NOTE!
May go directly to
cardioversion
Medications: any one
•Procainamide (IIA)
•Sotalol (IIA)*
•Amiodarone (IIB)
•Lidocaine (IIB)
*Not yet available in the US.
Impaired LV
EF<40% or
CHF
Amiodarone (IIB)
•150 mg IV bolus over 10 min
•may repeat 150mg q10-15min or
start infusion
OR
Lidocaine (IIB)
•0.5 to 0.75 mg/kg IV push
Then use
•Synchronized cardioversion
Narrow-Complex Supraventricular
Tachycardia
• Vagal stimulation
• Adenosine
• Junctional
• 1. EF > 40% - Amiodarone, B-blocker, CCB
• 2. EF <40%, CHF - Amiodarone
• PSVT
• EF>40% - CCB, BB, digoxin, DC cardioversion
(procainamide, amiodarone, sotalol)
• EF<40%, CHF - no DC cardioversion; digoxin,
amiodarone, diltiazem
• MAT
• EF>40% -No DC cardioversion; CCB, BB, amiodarone
• EF<40% -No DC cardioversion; amiodaonre, diltiazem
Wide-Complex Tachycardia
• “Wide” …. Prolonged QRS or QRST interval
• HR > 120 bpm (ex. VT, sinus tachycardia, A.flutter)
• OLD - Lidocaine
• NEW • Establish diagnosis - 12-lead ECG
• Adenosine if SVT- slows AV conduction. Short-lived
hypotension
• Amiodarone (IIa) normal LV function
• Amiodarone (IIb) impaired LV function
• Procainamide (IIa)- terminates SVT due to altering
conduction across accessory pathways
• Lidocaine if VT
• Sotalol, propafenone, flecainide
Drugs Used for Heart Rhythm and Rate
Adenosine
WHY?
Endogenous nucleoside, slows conduction through the
AV node and can interrupt AV nodal reentry pathways
WHEN?
PSVT (half-life=10 sec)
If PSVT persists may want longer acting agent
(verapamil or diltiazem)
HOW?
6 mg rapid IV over 1 - 3 sec, followed by 20 ml
NS flush. May repeat in 1-2min with 12 mg dose.
Max.=30 mg
WHAT?Flushing, dyspnea, chest pain, post-conversion bradycardia
Drug interaction with theophylline, dipyridamole
Pulseless Electrical Activity
• PEA… no pulse with + electrical activity (not VF/VT)
• Reversible if underlying cause is reversed (5 H’s, 5 T’s)
• Hypovolemia, hypoxia, hydrogen ion (acidosis), hyper/hypokalemia,
hyper/hypothermia
• Tablets, tamponade, tension pneumothorax, thrombosis (ACS),
thrombosis (PE)
Intervention
Comments/Dose
Problem
Search for the probable cause and intervene
(HCO3)
Epinephrine
1 mg IV q3-5 min.
Atropine
With slow heart rate, 1 mg IV q3-5 min.
(max. dose 0.04 mg/kg)
Atropine
WHY?
Anticholinergic/direct vagolytic
Enhances sinus node automaticity and AVN conduction
WHEN?
PEA, symptomatic sinus bradycardia, asystole,
HOW?
Bradycardia: 0.5 -1 mg IV q3-5 min
Asystole: 1 mg IV q 3-5 min
Max = 0.04 mg/kg or 3 mg
ET Dose=1-2mg diluted in 10ml
Paradoxical bradycardia with insufficient dose (<0.5mg)
WHAT?Tachycardia; 2nd or 3rd degree AV block (paradoxical
slowing may occur), MI (may worsen ischemia/HR)
Incompatible with bicarbonate, epinephrine & norepinephrine
Bradycardia
“All Patients Deserve Empathy”
(The sequence reflects interventions for increasingly severe bradycardia)
•
•
Absolute (< 60 BPM) or relative
Serious signs and symptoms (CP, SOB, hypotension, mental status changes)
Mnemonic
Intervention
Comments/Dose
All
mg/kg)
Atropine
0.5-1.0 mg IVP q 3-5 min (max 0.03-0.04
Patients
Pacing
Use Transcutaneous Pacing if severe S/S
Deserve
Dopamine
5-20 µg/kg/min.
Empathy
Epinephrine
2-10 µg/min.
Medications for Bradycardia
•
•
•
Atropine - Why? How?
Dopamine
Epinephrine infusion
•1mg/250 ml @ 1-4 mcg/min
Note: Lidocaine can be lethal if  HR is due to ventricular escape
rhythm
Dopamine
WHY?
related)
hypotension
NE precursor
Stimulates DA,  & -adrenergic receptors (doseWant  -stimulation, for bradycardia-induced
WHEN?
Hypotension/shock
HOW?
renal:
2 - 5 mcg/kg/min
cardiac: 5 - 10 mcg/kg/min (B1 & alpha)
vascular: 10 - 20 mcg/kg/min (alpha)
Preparation:
400 mg/250 ml D5W or NS
WHAT?
Tachycardia, tachyphylaxis, proarrhythmic
If requiring > 20mcg/kg/min consider adding NE
ACLS Algorithms
Asystole
• Consider possible causes and treat accordingly (ex.hypoxemia,
hyper/hypokalemia, acidosis)
Acronym “TEA”
T
Transcutaneous Pacing (TCP) (Class IIb) Only
effective with early implementation along
with
appropriate interventions and
medications
E
Epinephrine 1 mg IV q3-5 min.
A
mg/kg)
Atropine 1 mg IV q3-5 min. (max. dose 0.04
• Discourage shocking due to excess parasympathetic discharge
• Consider Na Bicarbonate 1 mEq/kg
Drugs Used for Myocardial
Ischemia/Pain
•
•
•
Oxygen
Nitroglycerin
Morphine Sulfate
•
AMI - Aspirin, thrombolytics, heparin, lidocaine,
beta-blockers
• Glycoprotein IIb/IIIa receptor antagonists
Acute Myocardial Infarction
•
•
•
•
•
•
“Call first, call fast, call 911”
Oxygen 4L/min
NTG SL, paste or spray; if BP > 90 mm Hg, IV NTG
Morphine IV
ASA PO (I)
Thrombolytics? (I) - within 6 hours of symptoms,
(II) if > 6hr
• IV heparin
• B-blockers
• Magnesium (if  Mg)
Oxygen
Why?
increases hemoglobin saturation, improves tissue
oxygenation
•  supply to ischemic tissues
• 16-17% oxygen from mouth-to-mouth
When?
• Must give supplemental oxygen in ACLS
• Always for MI
How?
• NC 4 L/min, intubation, etc
• Goal - Osat=97-98%
• Confirm tube placement
•
Drugs Used for Myocardial Ischemia/Pain
Nitroglycerin
WHY?
•
•
•
•
•
•
•
binds to receptors on vascular smooth muscle vasodilation (venous > arterial)
 venous BF to heart (preload) & O2 consumption
dilates coronary arteries -  myocardial blood supply
antagonizes vasospasm
increases collateral flow to ischemic myocardium
inhibits infarct expansion
decreases pain
Drugs Used for Myocardial Ischemia/Pain
Nitroglycerin
WHEN?
Ischemic CP; USA; pulmonary edema (when SBP>100); AMI
SL NTG -drug of choice for angina
IV NTG - drug of choice for unstable angina or AMI
Congestive heart failure with ischemia
HOW?
IV: 10-20 mcg/min, increase by 5-10 mcg/min q5-10 min until desired
effect or hemodynamic compromise
SL: 1 tablet (0.4mg) SL q5min times 3
Spray: 1 spray onto oral mucosa
Ointment 2%: 1-2 inches over 2-4 inch area
Patches: no role in acute therapy
Drugs Used for Myocardial Ischemia/Pain
Nitroglycerin
Preparation:
50 mg/250 ml D5W or NS
Must be in glass bottle
Cautions:
•
•
•
•
hypotension - treat with fluids, and rate reduction/elimination
bradycardia - vasovagal reflex to hypotension
• treat with fluids, rate reduction, atropine
• reflex tachycardia also a concern
headache, dizziness - may be diminished by laying down
patients develop tachyphylaxis to effects - promote nitrate-free
periods, intermittent dosing and lowest-possible doses
Drugs Used for Myocardial Ischemia/Pain
Morphine Sulfate
WHY? (Pain can  catecholamines - BP, HR, O2 demands)
Opiate analgesic
 pain,  preload and afterload,  SVR,  anxiety
Relieves pulmonary congestion,  myocardial oxygen demand
WHEN?
Pain, pulmonary edema, BP > 90 mm Hg
HOW?
1-3mg IVP (2-15 mg IVP q15-30 min prn)
CAUTION?
Respiratory & CNS depression, bradycardia, hypotension, N/V
Drugs Used for Myocardial Ischemia/Pain
(Continued)
• Aspirin
• Heparin
• Thrombolytics - reteplase, alteplase, TNK
• B Blockers
• Magnesium
• Lidocaine - not for prophylaxis
Hypotension/Shock/Pulmonary
Edema
Identify Problem? Volume; Pump; Rate?
• Volume:
• fluids, blood, vasopressors
• Pump:
• s/s of shock - vasopressors; no s/s shock -
dobutamine
•  BP (>100 mm Hg) - NTG, Nitroprusside
• pulmonary edema -furosemide 0.5-1mg/kg,
morphine 1-3mg, NTG SL, oxygen/intubate
• Rate: see algorithms
Drugs Used to Improve Cardiac Output
and Blood Pressure
Norepinephrine
Action:
Alpha & ß-adrenergic stimulation, increases
contractility and HR, vasoconstriction, improves
coronary blood flow
Indication:
Shock refractory to fluid replacement, severe
hypotension
Dose:
0.5 - 1 mcg/min
refractory shock = 8 - 30 mcg/min
Preparation:
4-8mg/250 ml D5W or NS
Caution:
Hypertension, myocardial ischemia, cardiac arrest,
palpitations
Drugs Used to Improve Cardiac Output
and Blood Pressure
Dobutamine
Action:
B1- adrenergic activity
Indication:
Inotrope in heart failure/hypotension
Dose:
2 - 20 mcg/kg/min
Preparation:
250 mg/250 ml D5W or NS
Caution:
tachyarrhythmias,worsens myocardial ischemia
Drugs Used to Improve Cardiac Output
and Blood Pressure
Inamrinone and Milrinone
Action:
Phosphodiesterase inhibitors, positive inotropes and
vasodilator
Indication:
Refractory heart failure
Dose:
Inamrinone:
Milrinone:
Caution:
750 mcg/kg over 2 - 3 min
Inf @ 5 - 15 mcg/kg/min
50 mcg/kg over 10 min
Inf @ 0.375 - 0.75 mcg/kg/min
Thrombocytopenia, worsens myocardial ischemia,
SV and ventricular arrhythmias
Drugs Used for Heart Rhythm and Rate
Isoproterenol
WHY?
Synthetic sympathomimetic amine
Pure B-adrenergic activity +inotropic& chronotrope
 HR/CO, contractility;  MAP secondary vasodilation
WHEN? Symptomatic bradycardia
Refractory torsades de pointes
HOW? Class II - 2 - 10 mcg/min
Class III - higher doses
Preparation: 1 mg/ 250 ml D5W or NS
WHAT?  mycocardial O2 consumption & peripheral vasodilation
Avoid in ischemic heart disease; arrhythmogenic
Drugs Used to Improve Cardiac Output
and Blood Pressure
Sodium Nitroprusside
Action:
Antihypertensive, peripheral vasodilator, reduces
afterload, increases CO and relieves pulmonary
congestion
Indication:
Hypertension, AMI, CHF
Dose:
0.1 - 5 mcg/kg/min, and titrate up to 10mcg/kg/min
Preparation:
50 mg/250 ml D5W
Caution:
Cyanide and thiocyanate toxicity, hypotension
Summary of 2000 Changes
•
NEW AGENTS - Amiodarone & Vasopressin
•
Amiodarone (Class IIb) & Procainamide (Class IIb) hemodynamically stable wide-complex tachycardia (esp. in poor
cardiac fxn)
VT - amiodarone & sotalol (Class IIa)
Vasopressin (Class IIb) - alternative to epinephrine
Bretylium acceptable, but not recommended
Lidocaine for VT/VF (Class Indeterminate) & Class III for prophylaxis
of ventricular arrhythmias in AMI
Magnesium (Class IIb) -  Mg or TdP
High-dose epinephrine (Class Indeterminate)
Fibrinolytics for AMI & Stroke
•
•
•
•
•
•
•
Crash Cart Revisions
Summary of Changes:
Additions:
5 amps of amiodarone 150mg/3ml (were 3)
3 vials of vasopressin (20 Units/vial)
1 bag of premixed dopamine 400mg in 250ml
4 Na Bicarbonate syringes (were 3)
5 filter needles
20 blunt cannulas
Deletions:
1 dopamine vial (new total=1)
Remove 5 epinephrine syringes (new total=10)
Remove 1 lidocaine syringe (new total=2)
Remove metoprolol
Needless System/Cannulas
Questions ?