Cardio-Drugs-Summary (1) PDF

Summary on Drugs Acting on the Cardiovascular System Prep red by: Yvette M. B t r, RN, MAN, DM For det iled inform tion & expl n tion, refer to PLP & recorded PPT Reference: Focus on Nursing Pharmacology by Amy M. Karch...

Summary on Drugs Acting on the Cardiovascular System Prep red by: Yvette M. B t r, RN, MAN, DM For det iled inform tion & expl n tion, refer to PLP & recorded PPT Reference: Focus on Nursing Pharmacology by Amy M. Karch (Chapters 43, 44, 45) a a a a a a a  Drugs Affecting Blood Pressure - Chapter 43 REVIEW OF BP CONTROL BARORECEPTORS Are specialized cells located in the 3 Elements that Determine carotid sinus & in the aortic arch that Pressure of Cardiovascular (CV) serve as BP sensors, mediating thru System: ANS. Heart Rate - the number of times Sensory input is received by Medulla each minute that the heart beats in an area called Cardiovascular/ Stroke Volume - the amount of Vasomotor center. blood that is pumped out of the ventricle Total Peripheral Resistance - the resistance of the muscular arteries to the blood being pumped  Drugs Affecting Blood Pressure HYPERTENSION - “Silent Killer” If untreated may risk for: CAD & cardiac death, stroke, RF, & vision loss. Essential Hypertension With no known cause Total Peripheral Resistance is elevated; Organs are effectively perfused; No symptoms Secondary Hypertension From known cause Left ventricle thickens bec muscle must constantly work hard to expel blood at greater force  Drugs Affecting Blood Pressure HYPOTENSION ANTIHYPERTENSIVE AGENTS Can occur in following situations: Altering the body’s regulatory When mechanisms is the best tx Heart muscle is damage & currently available for HPN unable to pump effectively. considering its unknown cause. Blood volume drops dramatically Tx does not cure HPN but aimed due to severe blood or fluid loss. at maintaining BP w/in normal There’s extreme stress & the limits to px damage. body’s levels of norepinephrine Not all patients respond in same are depleted, leaving the body way due to varied factors that unable to respond to stimuli to raise BP. contribute to each person’s HPN. Drugs Affecting Blood Pressure  Agents for Treating Heart Failure Drug Classi ication Name of Drugs Benazepril (Lotensin), Captopril (Capoten), Enalapril (Vaster), Enalaprilat (generic), Ace Inhibitors Fosinopril (generic), Lisinopril (Prinivil), Moexipril (Univasc), Perindopril (Aceon), Quinapril (Accupril), Ramipril (Altace), Trandolapril (Mavik) Renin Inhibitor Aliskerin (Tekuna) Angiotensin II Receptor Azilsartan (Edarbi), Candesartan (Candez), Eprosartan (Teveten), Irbesartan (Avapro), Blockers Losartan (Cozaar), Olmesartan (Benicar), Telmisartan (Micardis), Valsartan (Diovan) Amlodipine (Norvasc), Clevidipine (Cleviprex), Felodipine (Plendil), Isradipine (generic), Calcium-Channel Nicardipine (Cardene), Nifedipine (Procardia XL), Nisoldipine (Sulfar), Diltiazem Blockers (Cardizem), Verapamil (Calan SR) Vasodilators Hydralazine (generic), Minoxidil (generic), Nitroprusside (Nitropress) Other Hypertensive Diuretic Agents - to be discussed in Chapter 51 Agents Sympathetic Nervous Blockers discussed in Chapter 31 f Drug Classi ication Therapeutic Actions Act in the lungs to prevent ACE from converting angiotensin I to angiotensin II, leading to Ace Inhibitors decrease BP, a decrease in aldosterone production, & slight increase in serum potassium levels, along with sodium & luid loss. Directly inhibits renin, leading to decreased plasma renin activity & inhibiting the conversion Renin Inhibitor of angiotensinogen to angiotensin 1. This inhibition of of RAS leads to decrease BP, decrease aldosterone release, & decrease sodium reabsorption. Selectively blocks the binding of angiotensin II to speci ic tissue receptors found in the Angiotensin II Receptor vascular smooth muscle & adrenal glands; blocks the vasoconstriction & release of Blockers (ARBs) aldosterone associated with the RAS. Calcium-Channel Decrease the workload of the heart and decrease the heart’s oxygen demands and are used Blockers to treat variant angina pectoris. Reduce cardiac afterload, which increases cardiac output. Vasodilators Dilate the arterioles of the kidneys to improve renal perfusion and increase luid loss. Improve circulation to the skeletal muscles. Other Hypertensive Diuretics promote sodium depletion, which decreases extracellular luid volume. It is the irst- Agents line drug for treating mild hypertension. f f f f f f  Side Effects ARBs “CANDESARTAN” ACE Inhibitor Renin Inhibitor “CAPTOPRIL” “ALISKERIN” Cough Aching head, stomach, & back Aching head, dizziness, & weakness Loose stools (diarrhea) Nausea In esophagus stomach acid Drop in BP, Dizziness, Dry mouth & skin (heartburn) E ectiveness loss if taken w/ phenobarbital Severe hypotension Syncope Kough (cough) Abdominal pain Experience dizziness Respi infection (upper), Rash, Renal damage Rask Tooth pain Increase potassium (hyperkalemia) Alopecia Nausea & vomiting Not used w/ ACE & Renin Inhibitors ff  C lcium-Ch nnel Blockers “AMLODIPINE” Side Effects Diuretics V sodil tors “DIURETIC” Aching head & fatigue “HYDRALASINE” Dizziness Dehydration; Dysfunction of Mild rashes & skin ushing kidney; Decrease BP Re ex tachycardia, Rapid HR, & Low BP & bradycardia Redness of skin Increased blood sugar levels Oral grapefruit juice intake Anxiety (thiazide); Issues in GIT Dizziness Lesion & skin rash Urinate frequently Injury of liver (hepatic injury) Aching head Rashes in skin Peripheral edema Swelling of extremities Electrolyte imbalances Increase toxicity of cyclosporine if taken w/ In pain chest & heart failure Tinnitus, hearing loss (w/ Lasix) diltiazem Nasal congestion, nausea & vomiting Increase uric acid Nausea Evaluate grape juice intake if w/ Excessive hair growth (with Cholesterol level elevation toxic e ects minoxidil) a a fl ff a a fl  STEPPED CARE MANAGEMENT OF HYPERTENSION Weight Reduction Step 1: Lifestyle Smoking cessation Modi cation are Moderation of alcohol intake Instituted Reduction of salt in diet Increase in physical activity Continue lifestyle modi cations in step 1. If not su cient to lower BP to an acceptable level, then drug therapy is added: Diuretic (decreases serum Na+ levels & blood volume) Step 2: Inadequate ACE inhibitor (blocks the conversion of angiotensin I Response to angiotensin II) Calcium-channel blocker (relaxes muscle contraction) or other autonomic blockers Angiotensin II receptor blocker (blocks the e ects of angiotensin in blood vessels Drugs A ecting Renin-Angiotensin-Aldosterone System Consider change in drug dose or class, or addition of 3 Drugs that Alter RAS Step 3: Inadequate another drug for combined e ect. (Note: Fixed Response combination drugs should only be used when the Ace Inhibitors - block conversion of angiotensin I to patient has been stabilized on each drug separately. angiotensin II. ARBs - block angiotensin receptor site on blood vessels. All of the above measures are continued. Step 4: Inadequate Renin Inhibitor - blocks the reflex at the beginning by A 2nd or 3rd agent or diuretic is added if not already Response prescribed. inhibiting renin. ffi fi ff fi ff ff  Antihypotensive Agents Drug Classi ication Name of Drugs Alpha-speci ic Adrenergic Midodrine (ProAmatine), Droxidopa (Northera) Agents Discussed in chapter 30; 1st choice drugs for treatment of hypotension or shock. Sympathetic Adrenergic Dopamine (Intropin), Dobutamine (Dobutrex), Ephedrine (generic), Epinephrine Agonist or Vasopressors (Adrenalin, Epi-Pen), Isoproterenol (Isuprel), Metaraminol (Aramine), N orepinephrine (Levophed), and phenylephrine (Neo-Synephrine). Drug Classi ication Therapeutic Actions Alpha-speci ic Activates alpha-receptors in arteries & veins to produce an increase in vascular tone & an Adrenergic Agents increase in BP. React w/ sympathetic adrenergic receptors to cause e ects of sympathetic stress response: Sympathetic Adrenergic increased BP, blood volume, & strength of cardiac muscle contraction. Agonist or Vasopressors These actions increase BP & may restore balance to the cardiovascular system while the underlying cause of the shock (e.g., volume depletion, blood loss) is treated. f f f f ff  Side Effects Alph -speci ic Adrenergic Agents Symp thetic Adrenergic Agonist or V sopressors “MILODRINE” “DOPAMINE” My aching head w/ vertigo Decreased GI activity (constipation) Increase BP (hypertension) Occurrence of breath shortness Living on nervousness & chills Peripheral blood ow changes On urination problems or changes (urinary (numbness, tingling, necrosis) retention) Aching head Decrease HR, Dizziness & vision changes Rash Motor uctuations Itching of scalp Increased RR & BP Numbness Nausea & vomiting Erection of end of hair (piloerection or Extravasation; Excessive diuresis goosebumps) a a fl f fl a Agents for Treating Heart Failure Chapter 44  Heart Failure (HF) Also called “dropsy” or decompensation A syndrome that involves dysfunction cardiac muscle, of w/c sarcomere is the basic unit. Can occur in any disorders below: - Coronary Artery Disease (CAD) - Cardiomyopathy or Valvular Heart Disease - Hypertension - Valvular Heart Disease  Disorders that Lead to HF Coronary Artery Disease (CAD) Hypertension Leading cause of HF (95% of cases) Leads to enlarged cardiac muscle bec heart must work harder than normal to pump against the Results in insu cient supply of blood to meet high pressure in arteries. O2 demands of myocardium. Puts constant, increased demands for O2 on the Muscles become hypoxic & can no longer system bec heart is pumping so forcibly. function e ciently. When evolves into MI, muscle cells die or are Valvular Heart Disease damaged, leading to ine cient pumping e ort. Leads to overload of ventricles bec valves do not close tightly, allowing blood to leak backward Cardiomyopathy into the ventricles. Overloading leads to muscle stretching & A disease of heart muscle that leads to an increased demand for O2 & energy as heart enlarged heart & eventually to complete muscle muscle must constantly contract harder. failure & death. ff ffi ffi ffi  Compensatory Mechanisms in HF Decreased CO stimulates baroreceptors in aortic arch & the carotid arteries, causing a sympathetic stimulation. Sympathetic stimulation causes an increase in HR, BP, & rate & depth of respirations, as well as a positive inotropic e ect (increased force of contraction) on the heart & an increase in blood volume (through the release of aldosterone). Decrease in CO also stimulates release of renin from kidneys & activates RAS w/c further increases BP & blood volume. ff  Cellular Changes & Clinical Manifestations of HF Cellular Changes Reflecting increase central occurs as body stimulates venous pressure sympathetic stress reaction Myocardial cells are changed with Enlargement is Pulmonary vein engorgement w/c leads to DOB prolonged HF. due to blood congestion Pulmonary Edema in severe cases Cells of failing heart seem to lack Rales signals presence of fluid in the ability to produce energy lung tissue needed for e ective contractions. Due to decrease blood flow Movement of calcium ions into & out of cell is no longer e ective, Reflecting fluid leading to further deterioration bec pooling in tissues muscle contracts ine ectively & is unable to deliver blood to the cardiac muscle. SIGNS & SYMPTOMS OF HF ff ff ff  Treatments for Heart Failure Decrease cardiac workload, relax vascular smooth muscle to decrease afterload, & allow pooling in the veins, thereby decreasing preload of heart & helping to improve function (Chap 43) Vasodilators In 2005, a combination drug containing a nitrate & vasodilator was approved speci cally for treating HF (ACE inhibitors & in African American patients (Box 44.1). Nitrates) Diuretics decrease blood volume, w/c decreases venous return & BP, resulting in decreased afterload, preload, & cardiac workload (Chap 51). Stimulate beta receptors in SNS, increasing Ca+ ow into myocardial cells & causing increased Beta-adrenergic contraction, a positive inotropic e ect. Antagonists Other sympathetic stimulation e ects can cause increased HF bec heart’s workload is increased by most sympathetic activity. (Chap 30) Normally produced by myocardial cells as a compensatory response to increased cardiac workload & increased stimulation by the stress hormones. Bind to endothelial cells, leading to dilation & resulting in decreased venous return, peripheral Human B-type resistance, & cardiac workload. Natriuretic Also suppress body’s response to stress hormones, leading to increased uid loss & further decrease in Peptides cardiac workload. Nesiritide (Natrecor) is the only drug currently available in a class of drugs called human B-type natri- uretic peptides. (Chap 50) ff ff fl fl fi  Drugs in Focus Drug Classi ication Name of Drugs Digoxin (Lanoxin) Cardiac Glycoside Antidote: Digoxin immune Fab (DigiFab) Inamrinone (Inocor), Milrinone Phosphodiesterase (Primacor) HCN Blockers Ivabradine (Corlanor) f  Drug Classi ication Therapeutic Actions Digoxin increases intracellular calcium & allows more Ca+ to enter myocardial cells during depolarization causing the following e ects: Increased force of myocardial contraction (a positive inotropic e ect). Increased CO & renal perfusion (w/c has a diuretic e ect, increasing urine output & decreasing Cardiac Glycoside blood volume while decreasing renin release and activa- tion of the renin–angiotensin– aldosterone system). Slowed heart rate, owing to slowing of the rate of cellular repolarization (a negative chronotropic e ect). Decreased conduction velocity through the atrioventricular node. Blocks the enzyme phosphodiesterase, w/c leads to increase in myocardial cell cAMP, w/c Phosphodiesterase increases calcium levels in the cell, causing a stronger contraction & prolonged response to sympathetic stimulation; directly relaxes vascular smooth muscle. Slows heart’s pacemaker, the sinus node, in the depolarizing phase of the action potential Hyperpolarization- that leads to HR’s reduction. Slowing HR allows more time for ventricular illing & improves activated Cyclic CO. Nucleotide-gated Systemic e ects seen in beta-blockers are not seen in this drug. No e ects on ventricular Channel (HCN) Blockers repolarization or on ventricular contractility. This action also e ects channels in retina, w/c may alter the retinal response to bright light & explain some of the adverse e ects seen with this drug. ff ff f ff ff ff ff ff ff f  C rdi c Glycoside “DIGOXIN” Side Effects HCN Blockers Phosphodiester se “IVABRADINE” Drowsiness & vision changes “MILRINONE” Memory loss (rare) Increase BP (hypertension) Increased e ects if taken w/ verapamil, amiodarone, quinidine, Irregular heart beat Visual eld changes (luminous quinine, erythromycin, tetracycline or cyclosporine Low BP (hypotension) phenomena: sudden changes GIT upset & anorexia Radiating chest pain & in parts of visual eld, colored abdominal pain bright lights, image Oral form should not be taken with food or antacid to avoid Itis: vasculitis, pericarditis, decomposition, multiple absorption delay pleuritis, & ascitis images) Xcreted largely in urine Nausea & vomiting Atrial brillation unchanged On injection site burning Bradycardia Immune Fab is its antidote Not normal platelet (low or Nausea, vomiting, malaise, thrombocytopenia) depression, & irregular heart rhythm are signs of toxicity Epistaxis & Erythema a a fi fi ff a fi Anti-arrhythmic Agents Chapter 45 ARRHYTHMIAS Conductivity Involve changes to automaticity or With normal heart function, each cycle of conductivity of the heart cells. cardiac contraction & relaxation is Changes can result from: electrolyte controlled by impulses arising imbalances that alter the action potential, spontaneously in the sinoatrial (SA) node & decreased O2 delivery to cells that changes transmitted via a specialized conducting their action potential, structural damage system to activate all parts of the heart that changes conduction pathway, or muscle almost simultaneously. acidosis or waste product accumulation These continuous, rhythmic contractions that alters the action potential. are controlled by the heart itself. In some cases, changes to the heart’s This property allows the heart to beat as automaticity or conductivity may result long as it has enough nutrients & O2 to from drugs that alter the action potential or survive, regardless of the status of the rest cardiac conduction. of the body.  Automaticity 5 Phases of Action Potential of Cardiac Muscle Cell Occurs when cell reaches a point of stimulation. Sodium gates open along cell membrane, & Na+ rushes into Phase 0 cell; this positive low of electrons into cell results in an electrical potential called depolarization (no charge di erence b/n inside & outside of membrane). A very short period during which the sodium ion Phase 1 concentration equalizes inside and outside of the cell. Or Plateau Stage, occurs as the cell membrane becomes less permeable to Na+, Ca+ slowly enters the cell,& Phase 2 potassium begins to leave the cell. Cell membrane is trying to return to its resting state, a process called repolarization. A time of rapid repolarization as the sodium gates are Phase 3 closed and potassium lows out of the cell. Occurs when the cell comes to rest; the sodium– potassium Phase 4 pump returns the membrane to its resting membrane potential, and spontaneous depolarization begins again. ff f f  Hemodyn mics Types of Arrhythmi s The study of forces that move Tachycardia blood throughout the Bradycardia cardiovascular system. Premature Atrial Contractions (PACs) or Premature Ventricular Contractions Hemodynamic alterations cause (PVCs) serious complications: lack of Atrial lutter suf icient blood low to the brain Atrial ibrillation cause syncope or precipitate stroke; lack of suf icient blood low to the Note: Arrhythmias are discussed in chap 42 myocardium can exacerbate atherosclerosis & cause angina or myocardial infarction (MI). f f f f a f f a Drug Classi ication Name of Drugs (Anti-arrhythmics) Class Ia: Disopyramide (Norpace), Procainamide (Pronestyl), Class I Anti- Quinidine (Generic) arrhythmic Class Ib: Lidocaine (Xylocaine); Mexiletine (Mixitil) Class Ic: Feicainide (Tambocor), Propafenone (Rythmol) Class II Anti- Acebutolol (Sectral), Esmolol (Brevibloc), Propanolol (Inderal) arrhythmic Class III Anti- Amiodarone (Cordarone), Dofetilide (Tikosyn), Ibutilide (Corvert), arrhythmic Sotalol (Betapace), (Betapace AF) Class IV Anti- Diltiazem (Cardizem), Verapamil (Calan, Covera - HS) arrhythmic Other Anti- Adenosine (Adeconard), Digoxin (Lanoxin) arrhythmic f Drug Classi ication Therapeutic Actions Stabilize cell membrane by binding to sodium channels, depressing phase 0 of Class I Anti- the action potential and changing the duration of the action potential. Class Ia prolong the duration of the action potential; Class Ib shorten the duration arrhythmic of the action potential; Class Ic extreme slowing of conduction, but have little e ect on the duration of the action potential. Competitively block beta-receptor sites in heart & kidneys resulting to decrease Class II Anti- HR, cardiac excitability, & CO that stabilizes excitable cardiac tissue & decrease arrhythmic BP w/c decrease heart’s workload & further stabilize hypoxic cardiac tissue. Block potassium (K) channels & slow outward movement of K during phase 3 of Class III Anti- action potential, prolonging it. These drugs are proarrhythmic & have the arrhythmic potential of inducing arrhythmias. Block movement of Ca+ ions across cell membrane, depressing the generation Class IV Anti- of action potentials & delaying phases 1 & 2 of repolarization, which slows arrhythmic automaticity and conduction f ff  Side Effects Cl ss I Anti- rrhythmic “LIDOCAINE” Long duration of action potential for class Ia In short duration of action potential for class Ib Digoxin toxicity increased if combined w/ quinidine Other e ects: rash, hypersensitivity reactions, loss of hair, & potential bone marrow depression. Cardio e ects: proarrhythmic e ects leading to development of arrhythmias (including heart blocks), hypotension, vasodilation, & potential cardiac arrest. Respiratory depression progressing to respi arrest. Avoid grapefruit juice & foods that alkalinize urine (increase toxicity) Intestinal & gastro symptoms: changes in taste, nausea, & vomiting. Nervous system e ects: dizziness, drowsiness, fatigue, twitching, mouth numbness, slurred speech, vision changes, & tremors that can progress to convulsions. Extreme slowing of conduction with class 1c a ff ff a ff ff  Cl ss II Anti- rrhythmic Side Effects Cl ss III Anti- rrhythmic “PROPANOLOL” Cl ss III Anti- rrhythmic “DILTIASEM” Peripheral perfusion altered “AMIODARONE” Depression, Dizziness & Arrhythmia (common) Respi e ects: bronchospasm & weakness dyspnea Metabolized in liver Injury in liver Intestinal & gastro distress Out of sleep (insomnia) Ocular abnormalities Low BP Possible constipation & diarrhea Dizziness & weakness Total cessation of heart function AV block, arrhythmia, & (heart failure) Absorption of sotalol decreased by bradycardia presence of food Intestinal & gasto upset (nausea Nausea & vomiting Risk of proarrythmias is increased if & vomiting) combined w/ antihistamine, Out of sexual desire (loss of libido) Aching head phenothiazines, or tricyclic Low BP (hypotension) antidepressants Shock, Shortness of breath, On decrease exercise tolerance, Others: Hypotension, Heart Failure, liver Sudden weight gain toxicity fatigue, & dizziness Edema (peripheral) Nausea & Vomiting Loss of appetite (anorexia) Excreted in urine Milder side e ects than verapamil a a a ff ff a a a