Advanced Cardiac Life Support

Transcription

1 Advanced Cardiac Life Support

2 Algorithm

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13 Drugs

14 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

15 Epinephrine - Why? How? What? Vasopressin - Why? How? What? Amiodarone Magnesium Procainamide Lidocaine

16 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

17 WHEN? Alternative to epinephrine for shock-refractory VT/VF WHY? Natural antidiuretic hormone Potent vasoconstrictor by stimulation of SM -V 1 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 = minutes Dose? 40 Units IVP - one time only!!!

18 Class Drug Conduction Velocity Ia Ib Quinidine Procainamide Disopyramide Lidocaine Mexiletine Tocainide 0/ Refractory Period Automaticity Ion Block Sodium Sodium (fast on-off) Ic Flecainide Propafenone Moricizine 0 Sodium (slow on-off) II Beta-Blockers Calcium III IV Amiodarone Bretylium Sotalol 0 0 Verapamil Diltiazem Potassium Calcium

19 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), widecomplex tachycardia uncertain origin (IIb) refractory PSVT (preserved function, IIa; impaired function IIb) atrial tachycardia (IIb) cardioversion of AF (IIa)

20 HOW? Cardiac arrest (PVT/VF) - 300mg IVP diluted in 20-30ml, may repeat with 150mg in 10 minutes, or start infusion (max=2..2 g/24h) Atrial & ventricular arrhythmias in impaired hearts WHAT? 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 Hypotension, bradycardia (slow rate, fluids)

21 WHY? WHEN? HOW? WHAT? Magnesium deficiency causes arrhythmias Facilitates ventricular repolarization by enhancing intracellular potassium flux, dilates coronary arteries Suspected hypomagnesemia, pulseless VT/VF, torsade de pointes Class IIa in suspected hypomagnesemia, TdP, and Class IIb in VF/VT: 1-2gm slow IVP in 100ml Hypotension at large doses

22 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 nodalconduction 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)

23 HOW? WHAT? Class IIa: mg/kg IVP q5-10 min (max=3mg/kg) Infusion (with pulse): 1-4 mg/min (if pulse is regained) Therapeutic Levels: µg/ml ET Dose: times IV dose Preparation: 1-2 gm/250 ml D5W or NS Hepatic metabolism, renal elimination Bradycardia, cardiac arrest, seizures Lidocaine toxicity/neurotoxicity - twitching, LOC, seizures, coma Lidocaine levels persist in low CO states

24 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)

25 WHY? Verapamil: Diltiazem: WHEN? 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 Negative inotrope & chronotrope (good anti-ischemic) Class I for acute and preventative SVT Direct negative chronotropic effect, mild negative inotrope Highly effective in controlling ventricular response in A Fib Control ventricular response rate in patients with AF/Fl, or MAT Verapamil: PSVT not requiring cardioversion

26 HOW? Verapamil: mg IVP, over 2 min (max=30mg) 5-10 mg/hr Diltiazem: 0.25 mg/kg IVP, may repeat with 0.35mg/kg in 15 min 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

27 WHY? WHEN? B-adrenergic blockade, slows conduction and increases refractory period in AV node AMI (reduces rate of reinfarction), reduces recurrent ischemia and incidence of VF in post- MI patients, USA HOW? Atenolol: mg IV over 5 min Metoprolol: 5-10 mg IVP q 5 min Propranolol: 0.1 mg/kg IV divided into min intervals Esmolol: 500 mcg/kg over 1 min 50 mcg/kg/min WHAT? Hypotension, bradycardia, AV block, overt heart failure or severe bronchospasm/copd

28 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) Problem Epinephrine Atropine Search for the probable cause and intervene (HCO3) 1 mg IV q3-5 min. With slow heart rate, 1 mg IV q3-5 min. (max. dose 0.04 mg/kg)

29 WHY? Anticholinergic/direct vagolytic Enhances sinus node automaticity and AVN conduction WHEN? PEA, symptomatic sinus bradycardia, asystole, HOW? Bradycardia: 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

30 Vagal stimulation Adenosine

31 WHY? WHEN? HOW? WHAT? Endogenous nucleoside, slows conduction through the AV node and can interrupt AV nodal reentry pathways PSVT (half-life=10 sec) If PSVT persists may want longer acting agent (verapamil or diltiazem) 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 Flushing, dyspnea, chest pain, post-conversion bradycardia Drug interaction with theophylline, dipyridamole

32 Atropine Dopamine Epinephrine

33 WHY? WHEN? NE precursor Stimulates DA, & -adrenergic receptors (doserelated) Want -stimulation, for bradycardia-induced hypotension Hypotension/shock HOW? renal: 2-5 mcg/kg/min cardiac: 5-10 mcg/kg/min (B 1 & alpha) vascular: mcg/kg/min (alpha) Preparation: WHAT? 400 mg/250 ml D5W or NS Tachycardia, tachyphylaxis, proarrhythmic If requiring > 20mcg/kg/min consider adding NE

34 Oxygen Nitroglycerin Morphine Sulfate Aspirin Clopidogrel Thrombolytics Heparin Beta-blockers Glycoprotein IIb/IIIa receptor antagonists ACE inhibitor HMG CoA reductase

35 Why? increases hemoglobin saturation, improves tissue oxygenation supply to ischemic tissues 16-17% oxygen from mouth-to-mouth When? How? Must give supplemental oxygen in ACLS Always for MI NC 4 L/min, intubation, etc Goal - Osat=97-98% Confirm tube placement

36 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

37 WHEN? Ischemic chest pain; 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: 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

38 Preparation: 50 mg/250 ml D5W or NS 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

39 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

40 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

41 Action: Indication: Dose: Preparation: Caution: Alpha & ß-adrenergic stimulation, increases contractility and HR, vasoconstriction, improves coronary blood flow Shock refractory to fluid replacement, severe hypotension mcg/min refractory shock = 8-30 mcg/min 4-8mg/250 ml D5W or NS Hypertension, myocardial ischemia, cardiac arrest, palpitations

42 Action: Indication: Dose: Preparation: Caution: B1- adrenergic activity Inotrope in heart failure/hypotension 2-20 mcg/kg/min 250 mg/250 ml D5W or NS tachyarrhythmias,worsens myocardial ischemia

43 Action: Indication: Dose: Preparation: Caution: Antihypertensive, peripheral vasodilator, reduces afterload, increases CO and relieves pulmonary congestion Hypertension, AMI, CHF mcg/kg/min, and titrate up to 10mcg/kg/min 50 mg/250 ml D5W Cyanide and thiocyanate toxicity, hypotension

44 WHY? WHEN? HOW? WHAT? Enhances sodium shift intracellularly, buffers acidosis, decreases toxicity of TCA s, increases clearance of acidic drugs 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 1 meq/kg IVP, 0.5mEq/kg q10 min prn 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

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