Priela, Noel Joseph S.

BSN 3-L1 GENERIC NAME adenisone BRAND NAME Adenocar d, Adenosca n DRUG CLASS Antiarrhythmic agent MECHANISM OF ACTION When administered intravenously, adenosine causes transient heart block in the Atrioventricular (AV) node. This is mediated via the A1 receptor, inhibiting adenylyl cyclase, reducing cAMP and so causing cell hyperpolarization by increasing outward K+ flux. It also causes endothelial dependent relaxation of smooth muscle as is found inside the artery walls. This causes dilation of the "normal" segments of arteries; i.e. where the endothelium is not separated from the tunica media by atherosclerotic plaque. Oral: Magnesium sulfate increases peristaltic activity by causing osmotic retention of fluids, thus resulting in bowel evacuation. Parenteral: Magnesium sulfate decreases levels of acetylcholine in motor nerve terminals. It also acts on the myocardium by decreasing the rate of SA node impulse formation and prolonging the conduction time. Adrenaline is used as a drug to treat cardiac arrest and other cardiac dysrhythmias resulting in diminished or absent cardiac output. Its actions are to increase peripheral resistance via 1receptor-dependent vasoconstriction and to increase cardiac output via its binding to 1receptors. AVP binds to V1 receptors on vascular smooth muscle to cause vasoconstriction via the IP3 signal transduction pathway, which increases arterial pressure; however, the normal physiological concentrations of AVP are below its vasoactive range. Studies have shown, nevertheless, that in severe hypovolemic shock, when AVP release is very high, AVP does contribute to the compensatory increase in systemic vascular resistance. STRUCTURE

magnesiu m sulfate

Magnesiu m sulfate

Antiepieptic, electrolyte, laxative

epinephrin e

Adrenalin

Sympathomimeti c, Vasopressor used in shock

arginine vasopressi n

Pitressin

antidiuretic hormones

Priela, Noel Joseph S. BSN 3-L1 amiodaron e Cordarone , Pacerone antiarrhythmic agent Amiodarone is categorized as a class III antiarrhythmic agent, and prolongs phase 3 of the cardiac action potential. It has numerous other effects however, including actions that are similar to those of antiarrhythmic classes Ia, II, and IV. Amiodarone shows beta blocker-like and potassium channel blocker-like actions on the SA and AV nodes, increases the refractory period via sodium- and potassium-channel effects, and slows intra-cardiac conduction of the cardiac action potential, via sodium-channel effects. Amiodarone resembles thyroid hormone, and its binding to the nuclear thyroid receptor might contribute to some of its pharmacologic and toxic actions AntiarrhythmicLidocaine decreases the depolarization, automaticity, and excitability in the ventricles during the diastolic phase by a direct action on the tissues, especially the Purkinje network, without involvement of the autonomic system. Neither contractility, systolic arterial blood pressure, atrioventricular (AV) conduction velocity, nor absolute refractory period is altered by usual therapeutic doses. In the Vaughan Williams classification of antiarrhythmics, lidocaine is a class IB agent. AtropineAn accumulation of acetylcholine at the sites of muscarinic cholinergic transmission occurs at the parasympathetic postganglionic receptors of the autonomic nervous system, which may cause parasympathomimetic side effects, such as bradycardia, bronchoconstriction, or increased secretions. The anticholinergic activity of atropine counteracts these muscarinic side effects. Digoxin binds to a site on the extracellular aspect of the -subunit of the Na+/K+ ATPase pump in the membranes of heart cells (myocytes) and

lidocaine

Xylocaine

Antiarrhythmic

atropine sulfate

Atropine

anticholinergic, parasympathetic antagonist, parasympathetic blocker

digoxin

Lanoxin

Cardiac glycoside

Priela, Noel Joseph S. BSN 3-L1 decreases its function. This causes an increase in the level of sodium ions in the myocytes, which leads to a rise in the level of intracellular calcium ions. This occurs because the sodium/calcium exchanger on the plasma membrane depends on a constant inward sodium gradient to pump out calcium. Digoxin decreases sodium concentration gradient and the subsequent calcium outflow, thus raising the calcium concentration in myocardiocytes and pacemaker cells. Increased intracellular calcium lengthens Phase 4 and Phase 0 of the cardiac action potential, which leads to a decrease in heart rate.[16] Increased amounts of Ca2+ also leads to increased storage of calcium in the sarcoplasmic reticulum, causing a corresponding increase in the release of calcium during each action potential. This leads to increased contractility, the force of contraction, of the heart. hydralazin e Apresolin e antihypertensive Hydralazine increases guanosine monophosphate levels, decreasing the action of the second messenger IP3, limiting calcium release from the sarcoplasmic reticulum of smooth muscle. This results in a vessel relaxation. It dilates arterioles more than veins. Intermediate dosages from 5 to 10 g/kg/min, known as the "cardiac dose", additionally have a positive inotropic and chronotropic effect through increased 1 receptor activation. Dopamine is used in patients with shock or heart failure to increase cardiac output and blood pressure. Dopamine begins to affect the heart at lower doses, from about 3 g/kg/min IV. High doses from 10 to 20 g/kg/min are the "pressor dose. This dose causes vasoconstriction,

dopamine

Dopastat, Intropin, Revimine

Autonomic nervous system agent, alphabeta- adrenergic agonist (symathomimetic )

Priela, Noel Joseph S. BSN 3-L1 increases systemic vascular resistance, and increases blood pressure through 1 receptor activation, but can cause the vessels in the kidneys to constrict to the point that urine output is reduced.