Cardiac/Vascular Nurse Exam Secrets Study Guide (22 page)

Contraindications include allergy, bradycardia, sick sinus syndrome, atrioventricular block, shock, hypotension, and respiratory depression. Caution should be used when administering these agents in patients with congestive heart failure.

Anti-dysrhythmic agents

Class I anti-dysrhythmic agents inhibit sodium channels. Class II drugs include beta-adrenergic receptor antagonists, which slow heart rate and increase cardiac muscle contraction. Class III drugs inhibit potassium efflux during repolarization. Class IV agents include calcium channel blocker. Unclassified agents such as digoxin decrease conduction velocity and adenosine activates adenosine receptors that play a role in potassium conductance.

Therapeutic uses of anti-dysrhythmic agents include atrial dysrhythmia, ventricular tachycardia, life-threatening ventricular dysrhythmias, ventricular dysrhythmias, sinus tachycardia, atrioventricular reentry, Wolff-Parkinson White syndrome, premature ventricular contractions, atrial fibrillation, atrial flutter, and atrial tachycardia.

Nitrates/nitrites

Nitrates and/or nitrates act directly on vascular smooth muscle and increase vasodilation. This class of agents increases blood flow and increases oxygen supply to myocardial cells. This class of agents has been shown to be ineffective in patients with coronary artery disease. Nitrates and/or nitrates are used to treat acute and chronic angina.

Adverse events associated with nitrates and/or nitrites include cardiovascular events such as hypotension, rebound tachycardia, bradycardia, flushing, and sweating and central nervous system events such as headache and dizziness. Other adverse events include nausea, vomiting, incontinence, and contact dermatitis. Contraindications include head trauma, cerebral hemorrhage, pregnancy, and lactation. Sublingual administration of nitrates/nitrates is the most preferred method of administration due to low bioavailability of these agents. Patients may develop resistance to these agents over time and may require higher doses to get the same effect.

Phosphodiesterase inhibitors

Phosphodiesterase inhibitors increase calcium levels within myocardial cells. These agents increase cardiac muscle contractions and cardiac output. However, these inhibitors have little impact on heart rate and blood pressure.

Phosphodiesterase inhibitors are typically prescribed over short periods due to a high degree of toxicity associated with these agents. They are used to treat decompensated congestive heart failure in patients who fail first line treatment approaches. Adverse events associated with phosphodiesterase inhibitors include cardiovascular events such as dysrhythmia and gastrointestinal events such as nausea, vomiting, and liver enzyme changes. Other adverse events include thrombocytopenia and bone marrow toxicity. Contraindications include aortic or pulmonary valvular disease, myocardial infarction, and ventricular dysrhythmia.

Vasodilator group of drugs

Classes of agents include in the vasodilator group include beta-blockers such as acebutolol, atenolol, betaxolol, bisoprolol, carteolol, carvedilol, esmolol, labetalol, metoprolol, nadolol, penbutolol, pindolol, propranolol, sotalol, and timolol; nitrates/nitrites, also known as anti-anginal vasodilators, such as amyl nitrate, isosorbide dinitrate, isosorbide mononitrate, and nitroglycerin; antihypertensive vasodilators such as diazoxide, minoxidil, fenoldopam, nitroprusside, hydralazine, and tolazoline; and calcium channel blockers such as amlodipine, bepridil, diltiazem, felodipine, isradipine, nicardipine, nifedipine, nimodipine, nisoldipine, and verapamil.

Beta-adrenergic inhibitors can also be classified as adrenergic agents. Beta-adrenergic inhibitors and calcium channel blockers indirectly act as vasodilators, whereas anti-anginal vasodilators and antihypertensive vasodilators directly act on vasodilator mechanisms.

Calcium channel blockers

Calcium channel blockers act by antagonizing L-type calcium channels in vascular smooth muscle, which leads to reduced cardiac muscle contractility, decreased SA pacemaker rate, and decreased atrioventricular conduction velocity in cardiac tissue.

Therapeutic uses include angina, hypertension, congestive heart failure, bradycardia associated with angina, Raynaud’s phenomenon, atrial tachycardia, atrial flutter, and subarachnoid hemorrhage. Adverse events associated with calcium channel blockers include headache, dysrhythmias, edema, bleeding gums, agranulocytosis, dizziness, nausea, fatigue, severe gastrointestinal upset, constipation, tachycardia, flushing, diarrhea, hypotension, and myocardial depression.

Patients on concomitant calcium channel blocker and beta-blocker and/or nitrate should have their blood pressure monitored by a practicing clinician due to increased risk of hypotensive episodes. Degree of vasodilation should be monitored due to increased risk of edema.

Antihypertensive vasodilators

Antihypertensive vasodilators act directly on vascular smooth muscle and increase vasodilation. These agents decrease arteriolar resistance and decrease arterial blood pressure. Therapeutic uses include treatment of hypertension, hypertensive crisis, and pulmonary hypertension in newborns.

Adverse events associated with antihypertensive vasodilators include cardiovascular events such as sweating, flushing, edema, dizziness, hypotension, reflex tachycardia and central nervous system events such as headache. Other adverse events include systemic lupus like syndrome and hypertrichosis. Contraindications include pregnancy and lactation. Caution should be used when administering these agents in patients with peripheral vascular disease, coronary artery disease, congestive heart failure, and/or tachycardia. Practicing clinicians should take caution when administering nitroprusside in patients with renal failure.

Anticoagulant, antithrombotic, and thrombolytic group of drugs

The classes of agents within this group include anticoagulants, antithrombotic or antiplatelet agents, and thrombolytic or fibrinolytic agents. Anticoagulants include antithrombin III, heparin, lepirudin, warfarin, danaparoid, and low molecular weight heparins such as ardeparin, dalteparin, enoxaparin and tinzaparin, argatroban and bivalirudin. Antithrombotic or antiplatelet agents include abciximab, aspirin, ibuprofen, sulfinpyrazone, clopidogrel, dipyridamole, eptifibatide, ticlopidine, and tirofiban. Thrombolytic or fibrinolytic agents include alteplase, streptokinase, anistreplase, urokinase, reteplase, and TNK t-PA.

This group of agents, which include anticoagulants, antithrombotic or antiplatelet agents and thrombolytic or fibrinolytic agents, prevent inhibition of platelet aggregation and clot formation.

Anticoagulants

Anticoagulants prevent clot formation but each of the agents included in this class have various mechanisms of action. These agents prevent clot formation by depleting clotting factors, inhibiting their activity, and/or prolonging clotting times.

Antithrombin III prevents clotting, while heparin is a protein that inhibits the conversion of prothrombin to thrombin, which prevents fibrinogen being converted to fibrin. Lepirudin directly inhibits thrombin formation, while low molecular weight heparins block factors Xa and IIa, which inhibit thrombus and clot formation. Warfarin prevents clot formation by interfering with formation of vitamin K dependent clotting factors in the liver.

Practicing clinicians should not use warfarin during acute situations, as the onset of action is about 3 days and lasts for about 5 days. Heparin or low molecular weight heparins should be used during acute situations, but warfarin can be used over the long term due to the drug’s long-lasting effects. Warfarin should be administered with caution, as the drug is contraindicated with a variety of drugs to treat a number of different conditions. Practicing clinicians should keep antidotes on hand in case of overdose including protamine sulfate for heparin overdose and vitamin K for warfarin overdose.

Therapeutic uses of anticoagulants include hereditary antithrombin III deficiency with potential for thromboembolism, acute deep venous thrombosis, prevention of deep venous thrombosis, acute pulmonary embolism, prevention of pulmonary embolism, atrial fibrillation with embolism, prevention of clotting in blood samples, dialysis, venous tubing, diagnosis and treatment of disseminated intravascular coagulation, myocardial infarction, stroke, heparin-induced thrombocytopenia, artificial heart valves, and valvular damage.

Adverse effects associated with anticoagulants include bleeding complications, hemorrhage, nausea, gastrointestinal upset, thrombocytopenia, and hepatic dysfunction. Contraindications include hemorrhagic disorders, recent trauma, spinal puncture, gastrointestinal ulcers, recent surgery, intrauterine device placement, tuberculosis, indwelling catheters and threatened abortion. More specifically, warfarin is contraindicated during pregnancy. Caution should be taken if anticoagulants are prescribed in patients with congestive heart failure, thyrotoxicosis, diarrhea, and fever.

Antithrombotic agents

Therapeutic uses of antithrombotic, or antiplatelet agents, include ischemia, percutaneous coronary intervention, risk reduction of recurrent TIAs in men, risk reduction of myocardial infarction or death in patients with history of cardiovascular disease, reduction of embolization in rheumatic valve disease, atrial fibrillation, peripheral arterial disease, stroke, prevention of thromboembolism, acute coronary syndrome, and prevention of cardiac ischemic complications.

Caution should be taken when prescribing antithrombotic or antiplatelet agents in patients who underwent recent surgery, or who are at risk of excessive blood loss or closed head injuries. Patients undergoing treatment with antithrombotic or antiplatelet agents should avoid cutting themselves and contact sports.

Antithrombotic or antiplatelet agents inhibit platelet aggregation. Specifically, abciximab, tirofiban, and eptifibatide are glycoprotein IIb/IIIa inhibitors that block platelet aggregation. Aspirin, ibuprofen, and sulfinpyrazone are cyclooxygenase inhibitors that inhibit the formation of thromboxanes, thereby blocking platelet aggregation. Clopidogrel and ticlopidine interfere with the ADP receptor blockade and prevent ADP from binding to platelets, thus inhibiting platelet aggregation. Dipyridamole is a phosphodiesterase inhibitor that increases cAMP, activating prostacyclin, and inhibiting platelet aggregation.

Adverse events associated with antithrombotic or antiplatelet agents include bleeding, hemorrhage, gastrointestinal ulcerations, angina, dizziness, headache, syncope, rash, thrombocytopenia, neutropenia, nausea, and diarrhea.

Thrombolytic or fibrinolytic agents

Thrombolytic or fibrinolytic agents open blood vessels and restore blood flow to dependent organ systems. These agents induce the production of plasmin through the digestion of fibrin, thereby degrading fibrin clots within blood vessels.

Specifically, streptokinase, urokinase, and anistreplase inhibit the formation of fibrin by disrupting the conversion of plasminogen to plasmin. Alteplase, tenecteplase, and reteplase activate the conversion of fibrin-bound plasminogen to plasmin.

Therapeutic uses of thrombolytic and fibrinolytic agents include lysis of thrombi in coronary arteries after myocardial infarction, stroke, pulmonary embolism, deep venous thrombosis, occluded cannulas in dialysis patients and peripheral artery thrombosis.

Adverse effects associated with thrombolytic or fibrinolytic agents include bleeding, bruising, anaphylaxis, and hematoma. Contraindications associated with use of thrombolytic or fibrinolytic agents include any condition that could be compromised by dissolution of clots such as recurrent surgery, hemorrhage, recent cerebrovascular accident, aneurysm, obstetric delivery, organ biopsy, serious gastrointestinal bleeding, major trauma, or hypertension.

Aminocaproic acid inhibits fibrin formation and is typically administered to antagonize the action of thrombotic or fibrinolytic agents.

Patients should be monitored for blood loss. Also, practicing clinicians should initiate treatment with thrombolytic or fibrinolytic within 3 hours of experiencing an acute myocardial infarction to prevent further cardiovascular complications if percutaneous coronary intervention is not available.

Angiotensin-converting enzyme inhibitors

Angiotensin-converting enzyme inhibitors inhibit the converting enzyme that hydrolyzes angiotensin I to angiotensin II, which increases bradykinin that is a potent vasodilator. By inhibiting the renin-angiotensin system, angiotensin-converting enzyme inhibitors prevent vasoconstriction by blocking angiotensin II formation, decreasing sodium and water reabsorption in the kidneys, and indirectly inducing bradykinin.

The pharmacologic effect of angiotensin-converting enzyme inhibitors is to decrease blood pressure through vasodilation and inhibiting salt reuptake through aldosterone. Therapeutic uses of angiotensin-converting enzyme inhibitors include hypertension treatment, diabetic nephropathy, congestive heart failure after myocardial infarction, and preservation of left ventricular function after myocardial infarction.

The classes of drugs that influence the renin-angiotensin system include angiotensin-converting enzyme inhibitors and angiotensin II antagonists. Angiotensin-converting enzyme inhibitors, also known as ACE inhibitors, include benazepril, moexipril, captopril, perindopril, enalapril, quinapril, fosinopril, ramipril, lisinopril, and trandolapril. Angiotensin II antagonists include candesartan, losartan, eprosartan, telmisartan, irbesartan, and valsartan.