Sie sind auf Seite 1von 10

Cardiovascular Drugs

Drugs Affecting Cardiac and Renal Systems

Inotropic Drugs Drugs that increase the force of myocardial contractions. effects influence myocardial contractility Chronotropic Drugs Drugs that increase the rate at which the heat beats. action affects cardiac rate Dromotropic Drugs Drugs that accelerate conduction. affects the conduction velocity through specialized conducting tissues Congestive Heart Failure CHF) Signs and Symptoms of Heart Failure Often no symptoms at rest Dyspnea (difficulty breathing) and fatigue occur with increased activity Edema of ankles and feet Distention of jugular veins In acute cases pulmonary edema cough and shortness of breath Drugs in first-line treatment Digoxin Diuretics ACE Angiotension-converting enzyme inhibitors Cardiac Glycosides o DIGITALIS - Oldest and most effective group of cardiac drugs. Comes from the plant fox glove (+) inotropic effect (-) chronotropic effect (-) dromotropic Cardiac Glycosides or Digoxin Rapid acting: Deslanoside action within 5 to 30 minutes Digoxin action within 5 to 30 mins Long acting: Digitoxin action within 1 to 4 hours Digoxin or Lanoxin is the only commonly used digitalis glycoside. digoxin (Lanoxin, Digitek) Classification Pharmacologic: digitalis, glycoside Classification Therapeutic: antiarrhythmic, inotropic Actions Digoxin improves the pumping ability of the heart Increases the force of myocardial contraction by inhibiting the Na, K-adenosine triphosphatase, an enzyme in cardiac cell membrane that decreases the movement of sodium out of myocardial cell after contraction. Calcium enter the cell in exchange for sodium. The calcium activates the contractile proteins and increased myocardial contractility. These will result to: Decrease venous pressure Decreased pulmonary and systemic congestion Enhanced cardiac circulation Decrease cardiac size Administration: Can be given orally or IV IV peaks within 10 to 30 minutes PO peaks within 1 to 2 hours Serum Blood Levels Maximum drug action occurs when steady tissue concentration has been achieved takes about 1 week Loading dose or digitalizing dosage will be higher until the therapeutic level has been reached. Dosage 0.75 to 1.5 mg every 6 to 8 hours When adequate levels have been reached than a maintenance dose can be started Chem 209 Pharmacology Ma. Christina B. Celdran Oraa, RN MAN Page 1

Cardiovascular Drugs
Maintenance Dose Dosing is 0.125 0.5 mg Average dose is 0.25 mg Take daily at same time of day Give with food or after meals Nursing Responsibilities Take apical pulse for one full minute before giving the medication listen for any irregular heart beats Specific guidelines for holding the drug and notifying physician Adults: apical pulse less than 60 Older child: apical pulse less than 60 Infant or younger child: apical pulse less than 100 Notify physician if bradycardia (heart rate less than 60 bpm) or new arrhythmias occur. Assess for peripheral edema and auscultate lunge for rales/crackles. Check kidney function since you want to know they can excrete excess digoxin and avoid build up in body. Digoxin Toxicity Anorexia, nausea, and confusion are symptoms of digoxin toxicity dysrhythmias HR below 60 in adults and 100 in infants and small children Digoxin should be discontinued by MD only takes about 1 week for drug to be eliminated from the body. Predisposing factors for digitalis toxicity: low potassium level Evaluation of Effectiveness Increased urinary output Decreased edema Decreased shortness of breath, dyspnea and crackles Decreased fatigue Improved peripheral pulses, skin color and temperature Serum digoxin levels 0.5 to 2 ng/mL digoxin Overdose: digoxin immune Fab or DigiFab (Ovine, Digibind) Therapeutic classification: antidotes Pharmacologic classification: antibody fragments Indications: serious life-threatening over dosage with digoxin. Action: An antibody produced in sheep that binds anti-genetically to unbound digoxin in serum. Therapeutic effect: Binding and subsequent removal of digoxin, preventing toxic effects in overdose. Nursing Responsibilities discontinue drug if causing dysrhythmias WOF: respiratory diseases, the drug may cause bronchoconstriction give potassium supplement drug should not be given with meals rich in fiber, binds with fiber and reduces absorption check pulse rate before and after giving the drug weigh every other day

Antianginal Drugs Vasodilators Coronary Arteries Arteries that deliver oxygen to the heart muscle.

Angina Pectoris Chest pain occurring when the hearts supply of blood carrying oxygen and energy-rich nutrients is insufficient to meet demands of the heart. sensory response to a temporary insufficiency of oxygen (ischemia) in the heart Ischemia Poor blood flow to an organ Ischemic heart disease = poor blood flow to heart Myocardial infarct = damage done to heart muscle after an ischemic event Angina pectoris is a clinical symptoms characterized by episodes of chest pain. Page 2

Chem 209 Pharmacology Ma. Christina B. Celdran Oraa, RN MAN

Cardiovascular Drugs
There is deficit in myocardial oxygen supply (myocardial ischemia) in relation to myocardial oxygen demand. Pain can be caused by coronary vasospasm

Anti-anginal Drugs Nitrates are used to treat and prevent attack of angina. Nitroglycerin (Nitrostat, Nitrobid, Nitrolingual, Nitrodisc, Transderm-Nitro) Only nitrates can be used in the acute treatment of angina pectoris. Calcium channel blockers and beta blockers are used prophylactically or in long-term management of angina. Isosorbide dinitrate (Isordil, Sorbitrate, Isobid) Nitroglycerin Most widely used nitrate Used to relieve acute angina Classification Pharmacologic: nitrates Classification Therapeutic: antianginals Action: Increases coronary blood flow by dilating coronary arteries and improving collateral flow to ischemic regions. Decreases left ventricular end-diastolic pressure and left ventricular end-diastolic volume. Reduces myocardial oxygen consumption/demand. At low doses, cause dilation of veins over arterioles Results to pooling of blood in the periphery Reduces preload At high doses, dilate arteriolar tissues and venous smooth muscles Therapeutic effects: Relief or prevention of anginal attacks. Reduction of blood pressure. Dosing: Oral dosage is rapidly metabolized in the liver and only small doses reach the systemic circulatory system For more effective absorption drug is given: Sublingually under the tongue acts in 1 to 3 minutes PO: sustained-released tablet Transdermal ointments applied on hairless area on back, chest or upper arm Patches takes a 40 minutes to an hour to start working Sublingual Administration Tablet should be held under tongue until dissolved. Avoid eating, drinking, or smoking until tablet is dissolved. Acute anginal attacks: Advise patient to sit down. Relief should occur in 5 minutes May be repeated every 5 minutes for 3 doses. If no relief call 911. Sustained Released Tablet Administer dose 1 hour before or 2 hours after meal with a full glass of water for faster absorption. Note: Sustained released preparations should be swallowed whole, do not crush, break or chew. Nitroglycerine Patch Place the patch on a hairless area of chest or upper arm each day. Move patch to a different place on your body each day to prevent skin irritation. Remove the patch for 8 to 12 hours each night and put on a fresh patch each day. Do not leave on all the time. Remove for defibrillation Nitroglycerine Ointment Comes with paper with a ruled line for measuring the dose Squeeze ointment onto the paper, carefully measuring the amount specified on the prescription label Use the paper to spread ointment in a thin layer on a hair-free area of skin (2 by 3 inches) Keep paper in place with bandage or tape Ointment is applied three or four times a day Side Effects: - Flushing of face and neck - Dizziness or light-headedness - Increased heart rate Chem 209 Pharmacology Ma. Christina B. Celdran Oraa, RN MAN Page 3

Cardiovascular Drugs
- Restlessness Rare side effects: - Blurred vision Dry mouth Weakness Fatigue

B-adrenergic Blockers : B-blockers (beta 1) Primary drug effect is related to the cardiovascular system. When Used: Angina Myocardial infarct Dysrhythmias Hypertension 4 Beta Blockers approved for Dysrhythmias: Propanolol (nonselective) Acebutolol (cardioselective) Esmolol (cardioselective) Sotalol blocks potassium channels Action of Beta 1 Blockers Decrease energy demands on heart to decrease angina attacks, decreasing myocardial contractility. Block the B receptors on the SA node to slow heart rate (decreases automaticity) Block the harmful release of catecholamines (epinephrine and norepinephrine) Blocks the release of renin a potent vasoconstrictor in the kidney to decrease blood pressure. Beneficial Effects: Suppression of excessive discharge of SA node Slowing of ventricular rate by decreasing transmission of atrial impulses through the AV node Contraindications: Systolic heart failure Systolic cardiac (heart) dysfunction (or systolic heart failure) occurs when the heart muscle doesn't contract with enough force, so there is not enough oxygen-rich blood to be pumped throughout the body. Conductive disturbances Bronchial asthma Diabetes: blocks hypo-glycemic induced tachycardia. Reduced metal alertness Peripheral vascular disease Adverse Effects: Decrease in HR blow the 60 bpm Decreased cardiac output Bronchocontriction in patients with asthma or COPD. Cardiac rhythm problems due to decreased SA or AV node conduction Hypo or hyperglycemia Beta Blocker Drugs- Three most common drugs used carvedilol or Coreg metoprolol or Lopressor atenolol or Tenormin Drug Interaction: alcohol calcium channel blockers beta blockers antidepressants Nursing Responsibilities: avoid alcohol take drug on an empty stomach advise to make position changes slowly stinging or biting sensation present avoid prolong standing protect drug from light Calcium Channel Blockers Three chemical classifications - Phenylalkylamines - Verapamil (isoptin) - Benzothiazepines - Diltiazem (Cardizem) - Dihydrophyridines

ANTIHYPERTENSIVE DRUGS: Chem 209 Pharmacology Ma. Christina B. Celdran Oraa, RN MAN

Page 4

Cardiovascular Drugs
2 Primary Mechanisms to Control Blood Pressure: Baroreceptor Reflex Renin-Angiotensin-Aldosterone Mechanism

3 Main Functions of the Kidneys: Cleansing of ECF and maintains volume and composition effects of diuretics Maintains acid and base balance Excretion of metabolic wastes Action of Diuretics: Loss of excess salt and water from the body by renal excretion The increase in urine flow is dependent upon the amount of Na and Cl that it blocks Drugs that block solute reabsorption to the highest degree produce profound diuresis The decrease in plasma and ECF volume depresses vascular reactivity to sympathetic stimulation causes vasodilation Adverse Effects: Acid base imbalance Hypovolemia Disturbances of electrolyte levels THIAZIDE and THIAZIDE LIKE DIURETICS: Drugs: Chlorthiazide (Diuril) Hydrochlorothiazide (Esidrix, Microxide, Oretic) Hydroflumethiazide (Diucardin, Saluron) Methylchlorothiazide (Enduron, Aquatensen) Polythiazide (Renese) Trichlorothiazide (Metahydrin, Naqua) Action: Inhibits renal tubular reabsorption of water, Na, Cl and K Causes diuresis reduce arterial blood pressure Effects not seen in patients without hypertension Often used in combination with other antihypertensive drugs Increases levels of uric acid and glucose Not effective in scant urine flow Only 10% of sodium and chloride is blocked in the early segment Beta Blockers with Diuretics: Atenolol with Chlorthalidone (Tenoretic) Bisoprolol with Hydrochlorothiazide (Ziac) ACE Inhibitors with Diuretics: Benazepril with hydrochlorothiazide (Lotensin HT) Captopril with hydrochlorothiazide (Capozide) Angiotensin II Blockers with Diuretics: Candesartan with hydrochlorothiazide (Atecand HCT) Telmisartan with hydrochlorothiazide (Micardis HCT) Adverse Reactions and Contraindications: Fluid and electrolyte imbalance Inhibits uric acid excretion LOOP DIURETICS: Drugs: Bumetanide (Bumex) Ethacrynic acid (Edecrin) Action: Primary site is the loop of Henle cause calcium excretion May lead to hypokalemia and metabolic acidosis Chem 209 Pharmacology Ma. Christina B. Celdran Oraa, RN MAN

Crosses placental barrier

Furosemide (Lasix, Novosemide) Torsemide (Demadex) IV only Inhibit symporters of Na, K, Cl

Page 5

Cardiovascular Drugs
Bumetanide is more potent than Furosemide (1mg of Bumetanide is equivalent to 40 mg of Furosemide) Most effective drug in mobilizing edema fluid Diuresis occurs in 5 to 10 minutes (if given IV) Diuresis occurs in 1 hour (if given oral) Ethacrynic acid is NOT given IM or SC causes pain and irritation

POTASSIUM-SPARING DIURETICS: Drugs: Amiloride (Midamor) Spironolactone (Aldactone) Triamterene (Dyrenium) Actions: Also known as aldosterone antagonists (spironolactone); or non-aldosterone antagonist Excrete Na but retains K 48 hours to take effect aldosterone stimulate cells to synthesize proteins necessary for sodium and potassium transport Spironolactone will block synthesis of new proteins but not the existing proteins Proteins complete their cycle in 1-2 days Uses: Control edema in heart failure, liver cirrhosis, and nephritic syndrome Treat HPN Reverse hypokalemia Spironolactone may lessen the effects of excessive aldosterone levels in patients with hyperaldosteronism Adverse Reactions: Patients with impaired renal function may have hyperkalemia watch carefully if given with ACEI Because the drug resembles mineralocorticoids, androgens and progestins; may cause: Menstrual irregularities Hirsutism Deepening of voice Gynecomastia (in males) Penile dysfunction CARBONIC ANHYDRASE INHIBITORS: Drugs: Acetazolamide (Diamox) Dichlorphenamide (Daranide) Methazolamide (Neptazane) Action: Forces elimination of the bicarbonate ions into the urine (along with water and Na) Causes mild metabolic acidosis with the excretion of alkaline urine Usually given on alternate days to prevent the kidneys from developing resistance to the drug (to give time to acetazolamide to be cleared form the body and bicarbonate levels in the blood to be replenished) Carbonic anhydrase inhibitors are sulfonamide derivatives OSMOTIC DIURETICS: Drugs: Mannitol (Osmitrol) Urea (Ureaphil, Urevert) Action: Nonelectrolyte which are filtered by the glolerulus Not significantly reabsorbed and metabolized High osmolality in tubules reduce reabsorption of water which increases production of urine With small excretion of Na, K, Ca, Cl and bicarbonate Given IV Adverse Reactions: Pulmonary congestion Seizures Acidosis Vomiting and diarrhea Blurred vision Tachycardia Chem 209 Pharmacology Ma. Christina B. Celdran Oraa, RN MAN Page 6

Cardiovascular Drugs
Angina-like pain

Nursing Responsibilities: (for diuretics) Diet increase K for all except Spironolactone Monitor I & O Review HR, bp, and electrolytes Careful in administering to elderly; evening is not recommended Take with or PC and in the morning May increase risk of orthostatic hypotension Avoid alcohol and cigarettes BETA BLOCKERS or BETA RECEPTOR ANTAGONISTS: DRUGS: - Acebutolol (Sectral) - Carteolol (Cartrol) - Penbutolol (Levatol) - Propanolol (Inderal) - Bisoprolol (Zebeta) - Nadolol (Corgard) - Betaxolol (Kerlone) - Metoprolol (Lopressor) - Timolol (Biocardren) - Atenolol (Tenormin) - Labetalol (Trandate) - Pindolol (Visken)

Beta 1 blockers affect the beta 1 receptors in the heart. They decrease excitability, workload, oxygen consumption, rennin release and lower bp Beta 2 blockers affect the lungs. Beta 2 blockers stimulate the beta receptors in the lung, relax bronchial muscles, increase vital capacity and decrease airway resistance. Higher doses may cause undesirable cardiac effects

Action: as first line drugs against HPN Patients with plasma rennin level respond best to BB and are generally unresponsive to diuretics Inhibit the release of rennin from the kidneys Decreases HR at rest but limits the cardiac stimulation seen during the SNS activation such as exercise and emotional stress Cardioselective BB produce greater effects on beta 1 receptors of the heart and beta 2 receptors of the lungs Nonselective BB produce effects on beta 1 and 2 receptor sites Uses: treat angina Who had heart attacks to protect the heart HPN as montherapy from SNS stimulation Arrhythmias (because it affects K channels) Adverse Reactions and Contraindications: Bradycardia Provoke heart failure (in normal functioning hearts) Bronchospasms or asthmatic attacks CNS effects: Fatigue Bradycardia Depression Blood Pressure too low BLOCKER outlines undesirable effects of Bronchial constriction Beta Blockers Blood sugar too low CALCIUM CHANNEL BLOCKERS: Diltiazem (Cardizem) Felodipine (Plendil) Isradipine (Dynacirc) Nicardipine (Cardene) Action: Prevents the contractile capacity reduces vascular tone Reduces peripheral resistance and bp Chem 209 Pharmacology Ma. Christina B. Celdran Oraa, RN MAN

Nifedipine (Adalat) Nisoldipine (Sular) Verapamil (Verelan)

Slows HR and conduction of impulses depress Ca channel current in SA node and conductive tissues in AV node vasodilation Page 7

Cardiovascular Drugs
Uses: Effective as a monotherapy for reducing bp in patients with angina Alternative to diuretics, nitrates and BB as first line drugs against HPN Provide long term protection against angina attacks by reducing the cardiac workload Safe in patients with asthma, hyperlipidemia, DM, and renal dysfunction or those who cannot tolerate BB Use to treat arrhythmias Adverse Reactions: Reflex tachycardia Peripheral edema can occur because of bradycardia reduced arterial pressure and reduced renal Hypotension perfusion Arrhythmias constipation Chest pain (because of inhibition of Sa and AV node with Verapamil and Diltiazem) Vasodilating effects: Headache - Dizziness Flushing - Weakness tachycardia ANGIOTENSIN-CONVERTING ENZYME (ACE) INHIBITORS: Benzapril (Lotensin) Captopril (Capoten) Enalapril (Vasotec) Fosinopril (Monopril) Lisinopril (Prinivil, Zestril) Moexipril (Univasc) Perindopril (Aceon) Quinilapril (Accupril) Ramipril (Altace) Trandolapril (Mavik) Action: Effective in treating HPN Given as initial therapy for all age groups Blocks the conversion of Angiotensin I to Angiotensin II Limit the damage to the renal blood vessels seen in DM patients Improves coronary artery blood flow by inhibiting the breakdown of bradykinin (vasodilator) Increased bradykinin stimulate production of prostaglandins and nitric oxide which causes COUGH Uses: first line drugs for heart failure and left ventricular dysfunction Decrease preload and afterload Adverse reactions: Hypotension Persistent dry cough Sodium or volume depletion Risk of induction of angioedema Interactions: K-sparing diuretics may lead to hypokalemia Diuretics may worsen hypotensive effects ANGIOTENSIN II RECEPTOR ANTAGONISTS or ANGIOTENSIN II RECEPTOR BLOCKERS Candesartan (Atacand) Administer without regard to meals Irbesartan (Avapro) Renal function tests review Telmisartan (Micardis) Blocks vasoconstriction effect of rennin Eprosartan (Taveten) angiotensin system Losartan (Cozaar) Salt distribution or potassium supplements Valsartan (Dilovan) do not use Action: As effective as ACE inhibitors in reducing activation of AT1 receptors AT1 subtype of all Angiotensin II receptors; these receptors are responsible for the effects of angiotensin in the heart, blood vessels, kidneys and adrenal glands relax vascular smooth muscles Cause vasodilation and reduced bp Reduce salt and water retention (by preventing aldosterone secretion) Difference between ACE Inhibitors and ARBs: ARBs do not cause cough; ACE Inhibitors do Do not increase levels of bradykinin Chem 209 Pharmacology Ma. Christina B. Celdran Oraa, RN MAN

Page 8

Cardiovascular Drugs
Nursing Responsibilities: Report any sign of infection Avoid taking cold preparations or decongestants Avoid K supplements Caution exercising to prevent dehydration VASODILATORS Diaxozide (Hyperstat) Hydralazine (Apresoline) Sildenafil (Viagra) Fenoldopam (Corlopam) Minoxidil (Rogaine, Loniten) Nitroprusside Na (Nipride) Action: Relaxation of smooth muscles by stimulating calcium binding processes Decreases peripheral resistance Decreases bp The decrease in bp stimulates the SNS and activates the baroreceptor reflexes; increases HR and CO and rennin release Increases renal and cerebral blood flow Take with food Review blood pressure Undesirable effects Lupus like reactions (fever, facial rash, muscle and joint pain, splenomegaly) Assess for peripheral edema of hands and feet headache, dizziness, anorexia, tachycardia and hypotension 2 Types of Vasodilators Arterial Dilators: - Hydralazine (Apresoline) - Diaxozide (Hyperstat IV) - Minoxidil (loniten) - Fenoldopam - Sildenafil Arteriolar and Venous Dilators - Nitroprusside (Nipride) -Biotransformed in endothelial cells to the powerful vasodilator (Nitric oxide); Potent direct vasodilator Adverse Reactions: Toxicity: - Nitroprusside accumulation of cyanide (drug is rapidly biotransformed into nitric oxide and cyanide; the cyanide is converted into thiocyanate by hepatic rhodanase and is eliminated in the urine) Administration of sodium thiosulfate as a sulfur donor which aids in the metabolism of cyanide Nursing Responsibilities IV solution must be wrapped in foil or other opague material Monitor bp to prevent hypotension ANTILIPEMIC DRUGS Coronary Artery Atherosclerosis - Causes fatty streaks (high cholesterol level) Fibrous plaques Thrombus formations precursor of steroid hormones manufactured by the liver from saturated fats Major Classes of Lipoproteins 1. BILE ACID RESINS Cholestyramine (Questran, Questran light) Colestipol (Colestid) reduce LDL levels by binding bile salts in exchange for chloride ions Chem 209 Pharmacology Ma. Christina B. Celdran Oraa, RN MAN

Page 9

Cardiovascular Drugs
Form an insoluble complex with the bile acids in the intestines which prevent reabsorption of the bile acids from the gut Increases elimination through the feces Onset occurs in 24 to 48 hours Peaks in 2-3 weeks Uses: Reduces LDL level by 15% to 20% when used in conjunction with low cholesterol diet Use in patients with risk for CAD For Type II hypercholesterolemia Adverse Reactions and Contraindications May cause bloating Hyperchloremia because of the exchange of Nausea and vomiting chloride ions Indigestion Metabolic acidosis Nursing Responsibilities Resins are insoluble powder; mix with fluids Not given to patients with steatorrhea or preexisting constipation 2. FIBRIC ACID DERIVATIVES Fenofibrate Gemofibrozil (Lopid) Action Alters the rate of synthesis of specific lipoproteins Formation of HDL increases Inhibits the biosynthesis of LDL and VLDL With antiplatelet effects Onset 2-5 days; peak in 1-2 hours Uses: Used to treat types III, IV and V hyperlipoproteinemia For triglycerides exceeding 750 mg/dl 3. HMG-CoA (3-hydroxymethylglutaril Co-enzyme A) Reductase Inhibitors Atorvastatin (Lipitor) Fluvastatin (Lescol) Lovastatin (Mevacor) Prevastatin (Prevachol) Simvastatin (Zocor) Action: Lowers total cholesterol Food reduces the bioavailability but not the drugs efficacy especially Simvastatin and Lovastatin Has antiplatelet properties Decreases the progression of CAD Adverse Reactions and Contraindications: 4. NICOTINIC ACID Niacin (Nia-Bid, Niacor, Nicobid) Action: Lipid lowering action is independent of its vitamin activity Requires higher dosage to lower lipids (more than 1000 mg/day) Reduces LDL, VLDL and elevation of HDL May produce peripheral dilation which causes flushing Lowers in several weeks Aspirin 325 mg 30 minutes before Niacin administration to prevent the synthesis of prostaglandins

Chem 209 Pharmacology Ma. Christina B. Celdran Oraa, RN MAN

Page 10