Moa

Front 1

Adenosine

Back 1

Used to bring heart back to a normal rhythm, not for all irregular rhythms, test forCAD. Slows AV node, terminates PSVT (includes PSVT with WPW due to reentry), Produces transient AV/VA block in arrhythmia not due to reentry, helps clarify for diagnosis, A Flu, A Fib, AV tach, short lived half-life of 5s so PSVT may recur.

Front 2

Atropine

Back 2

Via direct vagolytic action enhances SA node automaticity, VA node conduction

Front 3

Epinephrine

Back 3

Endogenous catecholamine with alpha and beta adrenergic stimulation, vasoconstrictor.Improves coronary and cerebral perfusion, produces favorable redistribution of blood flow during arrest. When used in cardiac arrest will increase coronary/cerebral blood flow, inotropic state, automaticity, MVO2, SVR, BP andHR.

Front 4

Lidocaine Hydrochloride

Back 4

Decreases automaticity of purkinje fibers (suppress ventricular arrhythmias). May terminate reentrant ventricular arrhythmias. Shown to elevate the fibrillation threshold.Usually does not affect BP or myocardial contractility.

Front 5

Amiodarone

Back 5

Effects Na+, K+, Ca2+ channels. Alpha and beta adrenergic blockade. Coronary and peripheral vasodilation. CCB lengthens the effective refractory period in cardiac tissue and bypass tract. Na channel block inhibits inactivated Na channels at high stimulation frequencies.

Front 6

Procainamide (Pronestyl)

Back 6

Decreases the speed of electrical conduction through the heart muscle, prolongs the ARP for electrical and muscle cells of the heart, also RRP. Suppresses vent ectopy and may be effective when lidocaine has not suppressed it. In normal vent muscle and purkinje suppresses phase 4 depolarization reducing automaticity of ectopic pacemaker. Slows intraventricular conduction by reducing slope of phase0 action potential. If conduction is already slowed as in ischemic tissue,further slowing of the conduction may terminate reentry.

Front 7

Magnesium Sulfate

Back 7

May reduce incidence of post infarct vent arr. Hypomagnesaemia. Precipitate refractory Vfib. Hinder replenishment of intracellular K+. Mag deficiency is associated with cardiac arrhythmias and sudden cardiac death.

Front 8

Verapamil (Isoptin)

Back 8

CCB, affects amount of Ca found in heart and muscle. Relaxes blood vessels and reduce cardiac workload. Used to treat chest pain cause by angina. Hypertension and controls HR in certain conditions. Blocks Ca ions and possibly Na ions. Contractile cells, myocard cells, vascular muscle cells. Antiarr effect appears to be slow channel block of conduction cells. Vasodil effects appear to be due to blockade of: Ca channels, alpha receptors. Action is primarily on: SA/AV. Net effect is to lengthen refractory period of the AV node and limit response to Afib/flu, reduces afterload, decrease inotropy. 5-10mg will maintain CO in moderate disease.

Front 9

Diltiazem (Cardizem)

Back 9

Slow channel activity in cardiac and vascular smooth muscle can be inhibited by Ca channel blockers. Produces direct potent neg chronotropic effect with only mild direct inotropic effect. Fewer hemodynamic effects than verapamil. Less myocardial depression that verapamil in pts with dysfunction. Slow conduction and prolongs refractoriness in the AV node. Useful in terminating SVT.

Front 10

Procardia (Niphedipine)

Back 10

Dilates main coronary art and arterioles in normal and ischemic. Inhibits spasms of coronary arteries. Reduces myocardial O2 demand and afterload by peripheral arteriole dilation: negative inotropy, SA/AV conduction is slowed. Neg chronotropic effect is possible. Worsening of heart block has been observed.

Front 11

Propranolol

Back 11

Reduce and inhibit effects of catecholamines by blocking ability to bind beta adrenergic. Non selective, both beta 1 and 2. Reduce HR, BP, contractility, AV node conduction that causes a controlled ventricular response in SVTs.

Front 12

Metoprolol/Lopressor

Back 12

Metroprolol low dose beta-1 selective, in high dose selectivity is lost. Reduce HR, BP,contractility. AV node conduction that causes a controlled vent response in SVTs.

Front 13

Esmolol

Back 13

Reduce HR, BP, contractility, AV node conduction that causes a controlled ventricular response in SVTs.

Front 14

Atenolol

Back 14

Reduces:HR, CO, BO, MVO2. Redistributes blood flow from adequately supplied area of the heart to ischemic areas. Acts in 1-2min, last 3-4hrs.

Front 15

Calcium Chloride

Back 15

Ca ions increase inotropy. Ions in sarc retic are transferred to actin and myosin filament sites to initiate myofibril shortening. In normal heart: pos inotropy, vasoconstricting, raises arterial BP.

Front 16

Sodium Bicarbonate

Back 16

Alkalinizing agent, short acting antacid that neutralizes acid to produce sodium chloride, water and CO2.