Cardiovascular Drugs PDF

THE HEART as assessed through the IPPA (Inspection, Palpation, Percussion, Auscultation) technique,  REGULATION OF HEART FUNCTION Cardiac Output (CO): This is the total volume of blood pumped by the heart per minute. It’s a measure of how efficiently the heart is meeting the body's demand fo...

THE HEART as assessed through the IPPA (Inspection, Palpation, Percussion, Auscultation) technique,  REGULATION OF HEART FUNCTION Cardiac Output (CO): This is the total volume of blood pumped by the heart per minute. It’s a measure of how efficiently the heart is meeting the body's demand for oxygenated blood and is calculated by multiplying stroke volume by heart rate:CO=SV×HR Stroke Volume (SV): Stroke volume is the amount of blood ejected by the left ventricle with each heartbeat. It’s typically measured in milliliters (mL) Heart Rate (HR): Heart rate is the number of heartbeats per minute, generally measured in beats per minute (bpm).  Three Factors affecting Stroke Volume : 1. PRELOAD the volume of blood in the ventricle at the end of diastole 2. AFTERLOAD the resistance the heart must pump against 3. CONTRACTILITY - the strength of the heart's contraction P Wave: 0.08-0.10 seconds PR Interval: 0.12-0.20 seconds QRS Complex: 0.06-0.10 seconds QT Interval: 0.36-0.44 seconds (rate-dependent) ST Segment: Should be isoelectric (flat) Prolonged P wave: Indicates atrial enlargement (e.g., right atrial enlargement in pulmonary hypertension). Absent P wave: Seen in atrial fibrillation or junctional rhythms. Prolonged PR interval: May suggest first-degree AV block. Wide QRS (>0.12 seconds): Seen in bundle branch blocks, ventricular rhythms, or hyperkalemia. Elevated ST segment: Can indicate myocardial injury or infarction. Peaked T wave: Often seen in hyperkalemia. Sinus Rhythm: Originates in the SA node with a consistent rate of 60-100 bpm. Each P wave (atrial contraction) is followed by a QRS complex (ventricular contraction), with an even spacing between beats. Heart Rate: Bradycardia: Sinus rhythm with a rate 100 bpm. TYPES OF ARRYTHMIAS Atrial Fibrillation (AFib): Rapid, irregular contractions of the atria. Atrial Flutter: Similar to AFib but with a more regular and "saw-tooth" pattern of atrial contractions. Ventricular Tachycardia (VT): A fast, regular rhythm originating in the ventricles. Ventricular Fibrillation (VF): A severe, life-threatening arrhythmia where the ventricles quiver instead of contracting, effectively stopping blood flow Heart Blocks (Atrioventricular Blocks) Occur when electrical impulses are delayed or blocked as they travel from the atria to the ventricles.  ANTIHYPERTENSIVE AGENTS Hypertension – an increase in BP such that systolic pressure is greater than 140 mmHg & diastolic pressure is greater than 90 Essential hypertension…. Secondary hypertension…. 1. DIURETICS – promote sodium depletion which decreases ECFV (Extracellular Fluid Volume) - first line drugs for mild hypertension - may be used with other antihypertensive drugs. - Ex. Thiazides & loop diuretics (Hydrochlorothiazide, Furosemide) 2. SYMPATHOLYTIC DRUGS (Sympathetic depressants) 5 Groups: A. Beta adrenergic blockers - reduce CO by diminishing the SNS response thereby decreasing basal sympathetic tone - reduce HR, contractility & renin release Ex.: Propranolol, Carvedilol (non-selective), Acebutolol, Atenolol, Betaxolol, Bisoprolol, Metoprolol (cardioselective) S/E: decreased PR, decreased BP, bronchospasm, hypoglycemic symptoms, dizziness  B. ALPHA 2 AGONISTS 📫Decrease sympathetic response from brainstem to peripheral vessels 📫Stimulate alpha 2 receptors → decreases sympathetic activity - increase vagus activity, decrease CO decrease serum epinephrine, norepinephrine & renin release Examples: Methyldopa (Aldomet), Clonidine (Catapres), Guanfacine (Tenex) S/E: drowsiness, dizziness, dry mouth & slow HR  C. ALPHA ADRENERGIC BLOCKERS 📫Blocks the alpha-adrenergic receptors→vasodilation & ↓BP 📫Help maintain the renal blood flow rate 📫Useful in treating hypertension with lipid abnormalities Ex.: Prazosin, Terazosin, Doxazosin S/E: dizziness, faintness, light-headedness, ↑HR, orthostatic hypotension, reflex tachycardia DRUG-DRUG INTERACTION Prazosin + anti-inflammatory drug = intensifies peripheral edema Prazosin + nitroglycerin = syncope  D. PERIPHERALLY ACTING SYMPATHOLYTIC (Adrenergic Neuron Blocker) 📫…blocks NE release from sympathetic nerve endings → ↓BP Ex.: Reserpine for severe hypertension S/E: orthostatic hypotension, may cause vivid dreams, nightmares, & suicidal ideation 📫 Can cause sodium & water retention (can be taken alone or with a diuretic) E. ALPHA I & BETA I BLOCKERS Block both Alpha I & Beta I receptors Ex.: labetalol S/E: orthostatic hypotension, GI disturbances, nervousness, dry mouth & fatigue  3. DIRECT ACTING ARTERIOLAR VASODILATORS 📫Acts by relaxing the smooth muscles of the blood vessels, mainly arteries causing vasodilation →↑ blood flow to brain & kidneys, ↓ BP 📫 may cause Na & water retention - Usually combined with beta-blockers Ex.: Hydralazine, Minoxidil, Nitroprusside (for acute hypertensive emergency) S/E: tachycardia, palpitations, edema, nasal congestion, h/a, dizziness, GI bleeding, neurologic symptoms (tingling, numbness)  4. ANGIOTENSIN ANTAGONISTS (ACE INHIBITORS) 📫Antagonist of renin-angiotensin system 📫Inhibit angiotensin-converting enzyme (ACE) → inhibits formation of angiotensin II (vasoconstrictor) & blocks release of aldosterone → dilation of peripheral blood vessels & reduction of BP Ex.: Captopril (Capoten), Benazepril (Lotensin), Enalapril maleate, Fosinopril, Moexipril, Perindopril, Quinapril, Ramipril 4. ANGIOTENSIN ANTAGONISTS (ACE INHIBITORS) S/E: constant irritating cough (primary side effect), N/V, diarrhea, H/A, dizziness, fatigue, insomnia, excess serum K, & tachycardia **Should not be given during pregnancy.  5. ANGIOTENSIN II RECEPTOR ANTAGONISTS (ARBs) 📫Block the binding of angiotensin II on its receptors → reduced aldosterone (sodium retaining hormone) →↓ BP 📫Cause vasodilation & decrease peripheral vascular resistance Ex.: Losartan (Cozaar), Valsartan (Diovan), Irbesartan (Avapro), Candesartan (Atacand), Eprosartan (Teveten), Telmisartan (Micardis). Esartan medoxomil (Benicar) S/E: Dizziness, light-headedness 6. CALCIUM CHANNEL BLOCKERS Block Ca in the vascular smooth muscles promoting vasodilation Reduced arterial BP at rest & during exercise by dilating peripheral arterioles & decreasing systemic Peripheral Vascular Resistance Ex.: verapamil, diltiazem, amlodipine, nifedipine S/E: flushing, H/A, dizziness, ankle edema (common S/E) bradycardia, & AV block 7. Direct Renin Inhibitors New class of antihypertensives Effectively treat mild-to-moderate hypertension Cause vasodilation through directly blocking the renin part Aliskiren hemifumarate (Tekturna) – currently, only one agent approved Side effects: diarrhea, skin rash, cough & hypotension Non-pharmacologic management Stress reduction techniques Exercise Salt restriction Decrease alcohol ingestion Quit smoking Weight reduction ANTIANGINAL DRUGS ANGINA PECTORIS – a condition of acute cardiac pain caused by inadequate blood flow to the myocardium resulting from either plaque occlusions within or spasms of the coronary arteries. Decreased blood flow, decreased oxygen to myocardium leading to PAIN lasting for a few minutes S/sx: tightness, pressure in the center of the chest & pain radiating down the left arm, neck Angina Pectoris  3 TYPES OF ANGINA PECTORIS: 1. CLASSIC (STABLE) – occurs with stress or exertion 2. UNSTABLE (PREINFARCTION) – occurs frequently over the course of a day with progressive severity 3. VARIANT (PRINZMETAL, VASOSPASTIC) – occurs during rest ANTI-ANGINAL DRUGS: Increase blood flow either by increasing oxygen supply or by decreasing oxygen demand by the myocardium  1. NITRATES 📫 act on smooth muscles at the blood vessels causing relaxation & dilation 📫Decreases preload & afterload & reduces myocardial oxygen demand 📫Reduces myocardial ischemia but can cause hypotension 📫developed in 1840s 📫1st agent used to relieve angina Pharmacokinetics: Nitroglycerin – SL, topical (ointment, transdermal patch), IV NTG SL --- internal jugular vein---right atrium Onset of action: SL, IV – rapid (1-3 minutes) Transderm Nitro patch: 24 hours Nitro bid ointment: 6 – 8 hours (3-4x a day) Ex: Isosorbide Dinitrate (Isordil, Sorbitrate), Isosorbide Mononitrate (Monoket, Imdur), Transderm Nitro, Nitro-bid ointment S/E: h/a, postural (orthostatic) hypotension, dizziness, weakness & faintness, myocardial ischemia (rebound effect), reflex tachycardia  Examples: Nitrostat, Nitro-bid, Transderm Nitro, Isosorbide Dinitrate (Isordil), Isosorbide Mononitrate (Monoket, Imdur) Nitroglycerin (SL, topical ointment, transdermal patch), IV Onset of action: SL, IV – rapid (1-3 minutes) Transdermal Nitro patch: 24 hours Nitroglycerin ointment: 6 – 8 hours (3-4x a day)  Side effects: headache (most common), orthostatic hypotension, dizziness, weakness, faintness, myocardial ischemia (rebound effect), reflex tachycardia  Nursing Responsibilities: 1. Monitor vital signs 2. Have client sit & lie down during administration 3. Offer sips of water before giving sublingual nitroglycerin 4. If chest pain persists after 3 doses of NTG SL, instruct client to go to nearest hospital 5. Tolerance to nitrates may develop due to continued increase in dosage & prolonged use 6. Ointment: do not use finger, instead use gloves or tongue depressor Transderm patch: do not touch the medicated portion 7. Do not apply on the chest in the vicinity of defibrillator- cardioverter paddle  8. Avoid alcohol ingestion 9. Store bottle away from light 10. Burning & stinging sensation means drug is potent 11. Rotate sites: thighs & arms can be used 12. Avoid hairy areas 13. Instruct client not to discontinue these drugs without healthcare provider’s approval. Withdrawal symptoms may be severe Non-pharmacologic ways of decreasing angina: 1. Avoid heavy meals, smoking, extremes of weather changes, strenuous exercise, emotional upset 2. Moderate exercise, rest, relaxation techniques  2. BETA BLOCKERS Block B1 receptors → decrease effects of sympathetic NS → block release of catecholamines (NE/Epi) → decrease HR, decrease BP For classic angina (anti-angina) decrease HR, decrease myocardial contractility---- decrease oxygen consumption----decrease pain of angina Non-selective beta blockers 📫blocks beta 1, beta 2 📫Decrease HR, bronchoconstriction Ex: Propanolol (Inderal), Nadolol (Cogard), Pindolol (Visken) CI: asthma S/E: bronchospasm, psychotic response, impotence, bradycardia, hypotension  Selective beta blockers (Cardioselective) - blocks beta 1, decreases HR Ex: Atenolol (Tenormin), Metoprolol (Neobloc, Lopressor) S/E: decrease HR (bradycardia), decrease BP (hypotension)  3. CALCIUM CHANNEL BLOCKERS Calcium 📫 increases myocardial contractions 📫 increases workload of the heart 📫 increases oxygen need/consumption Calcium-channel blockers – blocks Ca 📫 exert dilating effect on coronary arteries & peripheral blood vessels by inhibiting calcium → coronary vasodilation & ↑ blood flow & lower BP  Examples: Amlodipine (Norvasc), Biperidil HCl (Vascor), Diltiazem HCl) (Cardizem), Nicardipine HCl (Cardene), Nifedipine (Procardia, Adalat),Verapamil Side effects: H/A, hypotension, dizziness, flushing of the skin, changes in liver & kidney functions CONGESTIVE HEART FAILURE HEART – pumping organ Heart failure – pump failure Pumping chambers - VENTRICLES  Due to cardiac abnormalities or conditions that place increase demand on the heart; heart compensates Heart muscle weakens and enlarges Loses its ability to pump blood to the lungs & systemic circulation Left or right failure Continuous increase, forceful contractions Compensatory mechanism fails CONGESTIVE HEART FAILURE CARDIAC ARREST  Left – sided CHF dyspnea, orthopnea, fatigue, restlessness, crackles, peripheral cyanosis, dry non-productive cough, frothy blood tinged mucus  Right – sided CHF Abdominal pain, fatigue, bloating, nausea, dependent pitting edema, ankle edema, ascites, jaundice, hepatomegaly, decreased urine output, increased CVP, HPN  STAGES OF HEART FAILURE Stage Characteristics according to Stage A High risk to heart failure without symptoms of structural heart disease B Some cardiac changes such as decreased ejection fraction without symptoms of heart failure C Structural disease with symptoms of heart failure such as fatigue, SOB, edema, & decrease in physical activity D Severe structural heart disease & marked symptoms of heart failure at rest  AGENTS FOR TREATING HEART FAILURE A. Cardiac Glycosides (Digitalis, Digitalis Glycosides) Inhibit Na – K pump thus increasing intracellular calcium w/c causes the cardiac muscle fibers to contract more efficiently Inhibition of Na-K Pump leads to influx of Calcium. Cardiac muscles contract more efficiently as a result. Cardiac glycosides are also used to correct Atrial Fibrillation and Atrial Flutter  Three Effects of Cardiac Glycosides 1. (+) INOTROPIC action – increases force of ventricular contraction 2. (-) CHRONOTROPIC action – decreases HR 3. (-) DROMOTROPIC action – decrease conduction of heart cells through AV node Increases myocardial contractility Increase cardiac, peripheral & kidney function 1. Increase CO 2. Decrease preload 3. Improving blood flow to the periphery & kidneys 4. Decrease edema 5. Increase fluid excretion 6. Decrease fluid retention in the lungs Pharmacokinetics: Cardiac Glycosides Digoxin (Lanoxin) Absorption: oral tablet form 70%, liquid prep 90% t ½ : 36 hours low protein binding power 30% metabolized by the liver 65% excreted by the kidneys unchanged Digitoxin (Crystodigin) – a potent cardiac glycoside that has a very long half life & is highly protein bound. (seldom prescribed) Therapeutic serum level: Digoxin: 0.5 – 2 ng/ml Digitoxin: 10 – 35 ng/ml  Digoxin Toxic level: > 2-3 ng/ml Can be administered orally or by IV route  DIGITALIS TOXICITY Also known as cardiotoxicity due to overdose or accumulation of Digoxin. Gastrointestinal distress: (n/v, anorexia &/or diarrhea (earliest signs), salivation & abdominal pain Neurological effects: ( restlessness, irritability, headache, weakness, lethargy, drowsiness &/or confusion. Visual disturbances (blurred or colored vision, halo vision, amblyopia & diplopia)  DIGITALIS TOXICITY Cardio effects: bradycardia, Premature ventricular contractions, cardiac dysrhythmias, DIGITALIS TOXICITY Cardiotoxicity is a serious adverse reaction to digoxin & ventricular dysrhythmias result Treatment: Phenytoin & Lidocaine ANTIDOTE: Digoxin immune fab (Digibind, DigiFab) Digibind binds to digoxin molecules, reducing free digoxin.  Drug-drug Interaction: 1. Diuretics – Furosemide (Lasix), Hydrochlorothiazide (Hydrodiuril) - promote the loss of K from the body (Hypokalemia – numbness and tingling, muscle weakness, hypotension, dysrythmias) 2. Cortisone preparation - when taken systematically promote Na retention & K excretion or loss (Hypokalemia) 3. Antacids, bulk forming laxatives - can decrease digitalis absorption  Nursing Responsibilities: 1. Obtain drug history 2. Check apical pulse before giving digoxin 3. Instruct patient to eat foods rich in K. (Bananas, raisins, oranges, prunes, most vegetables) 4. Read drug labels carefully 5. Check serum level of Digoxin 6. Instruct to report signs & symptoms of toxicity Other Agents Vasodilators ACE inhibitors Diuretics Nonpharmacologic Measures 1. Limit salt intake to 2 g/day (1 tsp.) 2. Alcohol intake should be either decreased to 1 drink/day or completely be avoided 3. Fluid intake may be restricted 4. Smoking should be avoided 5. Control of weight 6. Mild exercise  ANTIARRHYTHMIC AGENTS Cardiac dysrhythmia (arrhythmia) – any deviation from the normal rate or pattern of the heartbeat; bradycardia, tachycardia, irregular heart rhythm Dysrhythmia (disturbed heart rhythm) Arrhythmia (absence of rhythm) Atrial dysrhythmias – prevent proper filling of the ATRIA & decrease the cardiac output by one third. Ventricular dysrhythmias – life-threatening, ineffective filling of the ventricles results in decreased or absent CO.  TYPES OF ANTIARRHYTHMIC AGENTS (VAUGHAN-WILLIAMS CLASSIFICATION) CLASS 1: SODIUM CHANNEL BLOCKERS > decrease the fast sodium influx to the cardiac cell thereby stabilizing neuronal cardiac membrane > Na⁺ channels play a key role in initiating these electrical impulses. By blocking these channels, we can slow down the rate of electrical signaling in the heart, helping to restore a regular rhythm. Class I ANTI ARRHYTHMIC DRUGS > primarily block sodium channels, affecting the way electrical impulses are conducted in the heart. Class IA: Moderate Na⁺ channel blockade and prolongation of the action potential duration Quinidine Procainamide Disopyramide These drugs are commonly used to treat atrial and ventricular arrhythmias because they slow conduction and extend the action potential, stabilizing the heart rhythm. Class IB: Mild Na⁺ channel blockade and shortening of the action potential duration Lidocaine Mexiletine Phenytoin Class IB drugs are typically used for ventricular arrhythmias, especially after a heart attack, as they target the damaged heart tissue and reduce abnormal electrical activity. Class IC: Strong Na⁺ channel blockade with minimal effect on the action potential duration Flecainide Propafenone These drugs are effective for both atrial and ventricular arrhythmias and are often used when other antiarrhythmics are not effective. They slow conduction significantly but don’t alter the action potential duration as much. CLASS II: BETA BLOCKERS Decrease conduction velocity & recovery time (refractory period)) Ex: Acetabulol, Esmolol, Metoprolol, Propanol CLASS III: DRUGS THAT PROLONG REPOLARIZATION Prolong repolarization & is used in emergency treatment of ventricular dysrhythmia Ex.: Amiodarone increases refractory period & prolongs action potential duration CLASS IV: CALCIUM CHANNEL BLOCKERS Inhibit movement of calcium ions decreasing excitability & contractility of the myocardium Most effective at the SA & AV nodes to reduce rate of contraction Dilate coronary arteries & increase blood flow to the myocardium Examples: verapamil (Calan), diltiazem (Cardizem) S/E: n/v, diarrhea, confusion, hypotension, heart block, neurologic & psychotic symptoms, blurred vision, double vision,lightheadedness & dizziness Nursing Responsibilities Obtain apical pulse for 1 full minute… Administer the drug over 2-3 minutes or as prescribed if given through push or bolus Clients receiving continuous infusion of anti-dysrhythmics should be placed on hemodynamic monitoring program Nursing Responsibilities Continuous IV infusion antidysrhythmic agents should be accomplished with the use of a volumetric infusion device Check vital signs… Monitor carefully for drug interactions…