Cardiology

1. Cardiology Ventricular Fibrillation/Pulseless Ventricular Tachycardia Algorithm Pharmacology

2. V. Fib/Pulseless V. Tach • Algorithm is the same for both situations. • Determine responsiveness • Assess airway, breathing and circulation status • Do CPR until monitor is ready • Apply Quick Patches, determine rhythm • If V. Fib/Pulseless V. Tach then: Defibrillate once at 120-200J (biphasic-energy based on manufacturer-if unknown, deliver 200J), 360J (monophasic) • Do 2 minutes (5 cycles) of CPR • Reanalyze, shock and resume CPR • Initiate IV access and consider advanced airway

3. V. Fib/Pulseless V. Tach • For the sake of brevity, please remember that after every drug you will defibrillate at the same energy you started with. • After every shock you will re-start 2 minutes of CPR. • 20 ml bolus of NSS is to follow all medications. • EMS providers who do not witness the arrest may do 2 minutes of CPR before defibrillation.

4. V. Fib/Pulseless V. Tach • After you have started your IV and maintained the airway (during second full round of CPR), it is now time for the first drug. • Standard Protocols: Epinephrine 1 mg IV/IO (1:10,000) q 3 to 5 minutes until you call the code or the patient regains spontaneous circulation. • Optional Approach: Vasopressin 1 time dose of 40 units as an alternative to the first or second dose of epinephrine.

5. V. Fib/Pulseless V. Tach Optional Antiarrhythmics (give during CPR): • Amiodarone: 300 mg IV/IO once, followed once after 3-5 minutes by a 150 mg dose Or 2) Lidocaine: 1-1.5 mg/kg first dose, followed by 0.5 to 0.75 mg/kg to a maximum of 3 mg/kg Special consideration meds: • Procainamide: 20-50 mg/min to a maximum of 17 mg/kg. Infusion for patients with recurrent VF/VT. • Magnesium Sulfate: 1-2 grams. Administered once only if Torsades de Pointes is suspected or known hypomagnesemia.

6. V. Fib/Pulseless V. Tach • Hypovolemia • Hypoxia • Hydrogen Ion (Acidosis) • Hypo/Hyperkalemia • Hypoglycemia • Hypothermia During CPR, consider and treat the causes. • Toxins (OD) • Tamponade (cardiac) • Tension Pneumothorax • Thrombosis (coronary or pulmonary) • Trauma

7. V. Fib/Pulseless V. Tach • These are your options. The actual working of the algorithm in lab will lay the sequence for you. • Also, remember that which ever antiarrhythmic broke the rhythm is the antiarrhythmic that is used in drip form. • This is always based on the last antiarrhythmic given. • If the patient converts prior to the administration of an antiarrhythmic, it is recommended to load the patient with 1-1.5 mg/kg of lidocaine and then hang a lidocaine drip (prophylactic protocol).

8. V. Fib/V. Tach AlgorithmPharmacology • Epinephrine • Vasopressin • Amiodarone • Lidocaine • Procainamide • Magnesium Sulfate

9. PharmacologyEpinephrine • Refer to previous medication sheets.

10. PharmacologyVasopressin • Generic Name: Vasopressin • Trade Name: Pitressin Synthetic • Classification: Pituitary hormone, antidiuretic • How Supplied: Injection: 20 units/ml

11. VasopressinMechanism of Action • Antidiuretic hormone • Acts at the tissue level by binding to specific receptors identified as V (vasopressin) receptors. There are two type of V receptors: V1 and V2. There are two subtypes of V1 receptors (V1a and V1b). • Stimulations of V1a receptors produces potent vasoconstrictor effects, in contrast to the vasodilator effect of V2-receptor stimulation. • Stimulation of V1a receptors in the liver results in glycogenolysis, and in the kidney, stimulation results in inhibition of renin secretion.

12. VasopressinMechanism of Action • V1a receptors in the brain appear to be involved in memory, BP regulation, and cerebrospinal fluid production. • Stimulation of V1b receptors in the pituitary results in secretion of corticotropin. • The V2 receptor is responsible for the antidiuretic effects of vasopressin, its vasodilator effects, its ability to increase factor VIII coagulant activity, and the concentration of von Willebrand factor in plasma.

13. VasopressinMechanism of Action • Stimulation of V1 receptors in vascular smooth muscle results in contraction in the coronary, splanchnic, GI, pancreatic, skin, and muscular vascular beds. • This effect is particularly prominent in the capillaries, small arterioles, and venules, with less effect on the smooth musculature of large veins.

14. VasopressinComparison: vasopressin vs. epinephrine • Vasopressin exerts a greater vasoconstrictive effect under conditions of hypoxia and acidosis than does epinephrine, and the effects of vasopressin last longer. • Vasopressin causes a greater increase in arterial tone than does epinephrine, an effect that correlates with greater myocardial perfusion. • Epinephrine increases myocardial oxygen consumption and lactate production in the arrest heart, and vasopressin does not.

15. VasopressinIndications • May be used as an alternative pressor to epinephrine in the treatment of adult shock-refractory pulseless VT/VF, asystole and PEA (Class IIb) • Hemodynamic support in vasodilatory shock (e.g., septic shock, sepsis syndrome) (Class IIb) • Adult cardiac arrest caused by pulseless VT/VF

16. VasopressinDosing (adult) • IV/IO: 40 units IV push (one-time dose)

17. VasopressinPrecautions • Because vasopressin can precipitate angina or myocardial infarction, it is not recommended for use in responsive patients with coronary artery disease or peripheral vascular disease.

18. VasopressinContraindications: • Hypersensitivity

19. VasopressinSpecial Considerations • Half-life: approximately 10 to 20 minutes

20. Amiodarone • Generic Name: Amiodarone Hydrochloride • Trade Name: Cordarone • Classification: Class III antiarrhythmic. Has electrophysiologic characteristics of all four classes of antiarrhythmics. Blocks sodium channels (class I ), inhibits sympathetic stimulation (class II), and blocks potassium channels (class III), as well as calcium channels (class IV). Nickname: Chemical Defibrillator. • How Supplied: Injection: 50 mg/ml

21. Amiodarone Mechanism of Action • Slows conduction in the His-Purkinje system and in accessory pathway of patients with Wolff-Parkinson-White Syndrome. • Inhibits alpha- and beta- receptors and possesses both vagolytic and calcium channel blocking properties. • Lengthens the action potential duration and increases the refractory period in all cardiac tissues, including the SA node, AV node, atrial cells, Purkinje fibers, and in the ventricular myocardium.

22. AmiodaroneMechanism of Action • At the SA node it slows the heart rate, slows conduction at the AV junction, and decreases ventricular response. • Hemodynamic effects: • Coronary and peripheral vasodilator • Mild decrease in myocardial contractility, however, cardiac output may actually increase because of decreased afterload. • Suppresses SA node function • Prolongs conduction at the AV junction

23. AmiodaroneIndications • Shock-refractory pulseless VT/VF (class IIb) • Polymorphic VT • Stable VT when cardioversion unsuccessful (class IIb) • Adjunct to electrical cardioversion of SVT (class IIa), atrial tachycardia (class IIb). • Ectopic or multifocal atrial tachycardia with normal LV function (class IIb) • Pharmacologic conversion of atrial fibrillation (class IIa) • Rate control of atrial fibrillation or flutter when other therapies ineffective (class IIb)

24. AmiodaroneDosing (adult) • Cardiac Arrest: pulseless VT/VF • Initial bolus – 300 mg IV bolus diluted in 20 to 30 ml of NS or D5W • Consider repeat dose (150 mg IV bolus) • If defibrillation successful, follow with 1 mg/min IV infusion for 6 hours (mix 900 mg in 500 ml NSS/hospital mix; field mix 100 mg in 100ml). Initially run at 1 mg/min for 6 hours, followed by 0.5 mg/min for 18 hours.

25. Amiodarone Other Indications: 150 mg bolus for tachycardias that are atrial, junctional, or ventricular in nature.

26. AmiodaronePrecautions • Hypotension most common side effect • Bradycardia and AV block  slow the infusion rate or discontinue if seen. Pacemaker may be required.

27. AmiodaroneContraindications • Known hypersensitivity • Severe sinus node dysfunction, causing marked sinus bradycardia • 2nd or 3rd degree AV block • Syncope caused by bradycardia (except when used in conjunction with a pacemaker) • Use with caution in patients with uncorrected electrolyte abnormalities, particularly hypokalemia and/or hypomagnesemia, because these conditions may predispose the patient to proarrhythmias.

28. AmiodaroneSpecial Considerations • Oral Amiodarone: half-life 26 to 70 days. • Forms a precipitate when mixed with sodium bicarbonate. • Infusion lasting more than 2 hours must be administer in polyolefin or glass bottles containing D5W. Use polyvinyl chloride (PVC) tubing during administration. Recommended dosing regimens for Amiodarone have considered the amount of Amiodarone adsorbed to PVC tubing. • Amiodarone IV must be delivered by a volumetric infusion pump.

29. AmiodaroneDrug Interactions • Additive effect with other medications that prolong the QR interval (Class Ia antiarrhythmics, phenothiazine, tricyclic antidepressant, thiazide diuretics, sotalol) • Can significantly impair the metabolism of digoxin, theophylline, and warfarin. Dosages of digoxin and warfarin should be decreased by one half when Amiodarone therapy is added. • Potentiates actions of oral anticoagulants

30. Lidocaine Hydrochloride Generic Name: Lidocaine Hydrochloride Trade Name: Xylocaine Classification: Class Ib Antiarrhythmic How Supplied: 100/mg/5 ml prefilled syringe 100 mg/10 mL prefilled syringe 1 g in 250 ml vials and prefilled syringes (IV infusion) 2 g in 500 ml D5W premixed bags

31. LidocaineMechanism of Action • Inhibits the influx of sodium through the fast channels of the myocardial cell membrane and decreases conduction in ischemic cardiac tissue without adversely affecting normal conduction. • Lidocaine raises the VF threshold • Decreases automaticity in phase 4 • Effects are on ventricular tissue only

32. LidocaineIndications • Monomorphic VT (Class IIb) • Polymorphic VT with normal QT interval (Class IIb) • Polymorphic VT with long QT interval (TdP) (Class indeterminate) • Pulseless VT/VF that persists after defibrillation and epinephrine administration (Class indeterminate) • Control of hemodynamically compromising PVCs (Class indeterminate)

33. LidocaineDosing (adult) Monomorphic VT with normal cardiac function, polymorphic VT with normal QT interval, polymorphic VT with long QT interval (TdP) • 1 to 1.5 mg/kg initial dose. Repeat dose, ½ initial dose every 5 to 10 minutes. Maximum total dose 3 mg/kg. Maintenance infusion 2-4 mg/min.

34. LidocaineDosing (adult) Monomorphic VT – impaired cardiac function (i.e., signs of shock) • 0.5 to 0.75 mg/kg IV push. May repeat every 5 to 10 minutes. Maximum total dose 3 mg/kg.

35. Lidocaine Dosing (adult) Pulseless VT/VF • Initial dose: 1 to 1.5 mg/kg IV bolus. • Subsequent doses: 0.5 to 0.75 mg/kg IV bolus, repeated every 5 to 10 minutes. Maximum IV bolus dose 3 mg/kg. • If pulse returns, begin maintenance infusion at 1 to 4 mg/min. • Endotracheal dose: 2 to 4 mg/kg

36. LidocainePrecautions • The maintenance infusion of lidocaine is 1 to 4 mg/min. This should be reduced after 24 hours (1 to 2 mg/min) or in the setting of altered metabolism (CHF, hepatic dysfunction, acute MI with hypotension or shock, patients > 70 years of age, poor peripheral perfusion), and as guided by blood level monitoring.

37. LidocainePrecautions • Renal dysfunction does not affect lidocaine kinetics but may increase the accumulation of metabolites. • Signs and symptoms of lidocaine toxicity are primarily CNS-related dizziness, drowsiness, mild agitation, tinnitus, slurred speech, hearing impairment, disorientation and confusion, muscle twitching, seizures, and respiratory arrest. These side effects are more common in patients with preexisting neurologic dysfunction and in those of advanced age.

38. LidocainePrecautions • In patients with sinus bradycardia or incomplete heart block, administration of IV lidocaine for the elimination of ventricular ectopic beats, without prior acceleration in heart rate (e.g. by atropine or pacing) may promote more frequent and serious ventricular dysrhythmias or complete heart block. ***Do not administer for PVCs in Bradycardic patients

39. LidocaineContraindications • Hypersensitivity to lidocaine or amide-type local anesthetics. • Severe degrees of sinoatrial, atrioventricular, or intraventricular block in the absence of an artificial pacemaker • Stokes-Adams syndrome (sudden recurring episodes of loss of consciousness caused by transient interruption of cardiac output by incomplete or complete heart block). • Wolff-Parkinson-White Syndrome

40. LidocaineSpecial Considerations • Routine prophylactic use in uncomplicated myocardial infarction or ischemia without PVCs is no longer recommended. • Lidocaine may be lethal in a bradycardia with a ventricular escape rhythm

41. LidocaineDrug Interactions • Use with caution in patients with digitalis toxicity accompanied by AV block. • Concomitant use of beta-blockers or cimetidine (Tagamet) may reduce hepatic blood flow, thereby reducing lidocaine clearance. • Lidocaine and Tocainide (Tonocard) are pharmacodynamically similar. Concomitant use may cause an increased incidence of adverse reactions, including seizures.

42. Procainamide Generic Name: Procainamide Trade Name: Pronestyl, Procan SR Classification: Class Ia antiarrhythmic How Supplied: Injection: 100 mg/ml, 500 mg/ml

43. ProcainamideMechanism of Action • In therapeutic doses, decreases conduction velocity in the atria, ventricles, and His-Purkinje system. • Prolongs the effective refractory period of the atria. • Shortens the effective refractory period of the AV node. • Decreases automaticity in the His-Purkinje system and ectopic pacemakers • Prolongs the PR and QR intervals • Exerts a peripheral vasodilatory effect • In therapeutic doses, myocardial contractility of the undamaged heart is usually not affected

44. ProcainamideIndications • Narrow-complex SVT when uncontrolled by Adenosine (Class IIa) • Control of rapid ventricular response Atrial fibrillation in Wolff-Parkinson-White (WPW) syndrome (Class IIb) • Stable wide complex monomorphic tachycardia of uncertain origin (Class IIb) • Recurrent Pulseless VT/VF

45. ProcainamideDosing (adult) • 20 mg/min IV infusion until one of the following occurs: • Dysrhythmia resolves • Hypotension • QRS widens by > 50% of original width • Total dose of 17 mg/kg administered • In life threatening situations you can administer 20 to 50 mg/min. • Maintenance infusion; 1 to 4 mg/min. Mix the same as lidocaine (1 g/250 ml)

46. ProcainamidePrecautions • Use with caution with other medications that prolong the QR interval (e.g., phenothiazines, cyclic antidepressants, thiazide diuretics, sotalol) • Conversion of atrial fibrillation to sinus rhythm may cause dislodgement of mural thrombi, leading embolization. • During administration, carefully monitor the patient’s ECG and BP. If the BP falls 15 mmHg or more, procainamide administration should be temporarily discontinued. Observe the ECG closely for increasing PR and QT intervals, widening of the QRS complex, heart block, and/or onset of TdP.

47. ProcainamidePrecautions • Reduce maintenance infusion rate in liver dysfunction (procainamide is metabolized by the liver), renal failure (procainamide is eliminated by the kidneys)

48. ProcainamideContraindications • Complete AV block in the absence of an artificial pacemaker • Patients sensitive to procaine • Patients with a prolonged QRS duration or QT interval because of the potential for heart block • Pre-existing QT prolongation/torsade de pointes • Digitalis toxicity (procainamide may further depress conduction)

49. ProcainamideSpecial Considerations • In conversion of atrial fibrillation to normal sinus rhythm by any means, dislodgement of mural thrombi may lead to embolization, which should be kept in mind.

50. ProcainamideDrug Interactions • Pharmacologic effects of procainamide may be increased if amiodarone is also administered. Amiodarone may inhibit the hepatic metabolism and renal clearance of procainamide • Procainamide has neuromuscular blocking properties that may counteract the action of the cholinergic drugs on skeletal muscle. Taking procainamide and a cholinergic concurrently may exacerbate symptoms of myasthenia gravis. • Additive cardiodepressant effects when lidocaine and procainamide are administered concurrently. Additive CNS toxicity has been reported.