Cardiology Review PDF

CARDIOLOGY REVIEW: THE HEART  Primarily a muscle that acts as a pump to deliver blood to  The heart valves assist in controlling the direction of flow the body tissues of the...

CARDIOLOGY REVIEW: THE HEART  Primarily a muscle that acts as a pump to deliver blood to  The heart valves assist in controlling the direction of flow the body tissues of the blood into the systemic and pulmonary  The walls of the four chambers of the heart are very circulations muscular and provide the ability to generate enough force  Blood supply to the cardiac muscle (myocardium) is during contraction to circulate blood provided by the coronary arteries and collateral vessels THE HEART Cardiovascular Physiology Three components to a working heart: Conduction System  Muscle (myocardium)  Specialized muscle fibers located in specific locations in  Conduction system (impulses) the myocardium that deliver electrical impulses that  Nerve supply initiate and sustain heart contraction  Conduction tissues have auto rhythmicity which allows the heart to initiate its own electrical stimulation Conduction System  The correct order of the impulse is very important as this  Under normal circumstances the electrical impulse begins coordinates the contraction of the heart chambers and in the sino-atrial node (SA node) continues through the allows the pumping action to occur atrio-ventricular node (AV node), is distributed through the  The electrical activity of the heart can be monitored with Bundle of His, left and right bundle branches and along the an electrocardiogram (ECG) the wave form illustrates the Purkinje Fibers to the ventricles depolarization (sodium influx) and repolarization (potassium efflux) phases of conduction NERVE SUPPLY  Myocardium (heart muscle) is controlled by both branches of the autonomic nervous system  Sympathetic (fight or flight)  Norepinephrine  Increase heart rate and force of contraction  Parasympathetic (rest)  Acetylcholine  Decreases heart rate and force of contraction  Therefore, nervous system controls both the rate of contraction (chronotropic effect) and the force of contraction (inotropic effect) Main Diseases of the Heart  Congestive/Chronic Heart Failure (CHF)  Coronary Artery Disease (CAD) o Arteriosclerosis o Atherosclerosis o Angina Pectoris o Myocardial Infarction (an event) Next Class Patients: Arteriosclerosis, Angina, MI, Arrhythmias, CHF  Congestive Heart Failure  Failure of the heart as a pump  Blood returned to the heart via the pulmonary circulation is greater in volume than the blood being pumped out into the peripheral circulation via the aorta  Blood accumulates in the chamber of the heart and ejection fraction is reduced  CHF may be right sided/left sided or both  Since distribution of oxygenated blood to organs is reduced, the kidney retains more salt and fluid to compensate leading to edema and fluid retention  Symptoms – peripheral edema, pulmonary edema, SOB, fatigue, cyanosis, exertional dyspnea Coronary Artery Disease (CAD)  Insufficient blood flow to myocardium via the coronary arteries Arteriosclerosis (happens to everyone eventually)  Often not diagnosed in early stages due to development of  Aging process collateral circulation – small vessels communicate  Hardening or fibrosis of the arteries  Further classified as:  Stiffness and loss of elasticity  Arteriosclerosis  Narrowing of vessels  Atherosclerosis Atherosclerosis (danger)  Angina  Fatty deposits (plaques) within artery walls,  MI narrowing of vessels CAD - Angina Pectoris CAD - Angina Pectoris  Chest pain that results from insufficient blood flow to the Classic: myocardium ¨ exertional angina caused by fixed obstruction of  Caused by: coronary arteries  Coronary artery disease (CAD) Variant:  atherosclerosis or arteriosclerosis ¨ vasospastic angina  transient myocardial ischemia Unstable:  coronary artery spasm ¨ between classic angina and myocardial infarct  Attacks may be triggered by exertion or stress ¨ atherosclerotic plaque disruption increases  Three types : obstruction of coronary vessels – pre-infarction Classic, variant, and unstable angina CAD - Myocardial Infarction (MI)  Leading cause of death in industrialized world  Ischemia (lack of blood supply) occurs  Tissue becomes necrotic (dead) muscle cells  Blockage, thrombosis of coronary artery is usual cause  Prognosis depends on size of infarcted area ( how much heart damage has been done?)  Muscle is replaced by scar tissue  Lack of muscle mass – less cardiac reserve, more susceptible to arrhythmias, CHF due to left ventricular hypertrophy  LECTURE 10 Congestive Heart Failure  Failure of the heart as a pump  Blood returned to the heart via the pulmonary circulation is greater in volume than the blood being pumped out into the peripheral circulation via the aorta  Blood accumulates in the chamber of the heart and ejection fraction is reduced  CHF may be right sided/left sided or both  Since distribution of oxygenated blood to organs is reduced, the kidney retains more salt and fluid to compensate leading to edema and fluid retention  Symptoms – peripheral edema, pulmonary edema, SOB, fatigue, cyanosis, exertional dyspnea Similar to COPD Coronary Artery Disease (CAD)  Insufficient blood flow to myocardium via the coronary arteries  Often not diagnosed in early stages due to development of collateral circulation – small vessels communicate  Further classified as: ◼ Arteriosclerosis ◼ Atherosclerosis ◼ Angina ◼ MI Arteriosclerosis  Aging process  Hardening or fibrosis of the arteries  Stiffness and loss of elasticity  Narrowing of vessels Atherosclerosis  Fatty deposits (plaques) within artery walls, narrowing of vessels CAD - Angina Pectoris When muscle die, you feel a lot of pain (MI)  Chest pain that results from insufficient blood flow to the myocardium  Caused by:  Coronary artery disease (CAD) ◼ atherosclerosis or arteriosclerosis  transient myocardial ischemia ( no oxygen is being transfer to that area) ◼ coronary artery spasm  Attacks may be triggered by exertion or stress  Three types : Classic, variant, and unstable Classic: ¨ exertional angina caused by fixed obstruction of coronary arteries = Variant: ¨ vasospastic angina = irregular Unstable: to full blown of MI ¨ between classic angina and myocardial infarct ¨ atherosclerotic plaque disruption increases obstruction of coronary vessels – pre-infarction angina CAD - Myocardial Infarction (MI)  Leading cause of death in industrialized world  Ischemia (lack of blood supply) occurs  Tissue becomes necrotic (dead) muscle cells  Blockage (narrowing) , thrombosis of coronary artery is usual cause (CHF)  Prognosis depends on size of infarcted area  Muscle is replaced by scar tissue  Lack of muscle mass – less cardiac reserve, more susceptible to arrhythmias, CHF due to left ventricular hypertrophy = once you get CHF, your more likely to get heart attack =leading cause of death ANTIANGINAL DRUGS Pharmacotherapy of Angina Classes: 1. Nitrates 2. Beta Blocking Agents 3. Calcium Channel Blockers NITRATES:  Nitroglycerin (OPEN UP THE BLOOD VESSEL)  Isosorbide Dinitrate  Isosorbide Mononitrate Nitroglycerin - INDICATIONS Nitro-Dur, Nitrostat, Nitrong SR, Nitrolingual, Nitrol, Minitran, Transderm Nitro 1. Prevention of angina  Drugs used prophylactically as maintenance 2. Treatment of angina  Used PRN for acute attacks, relieves intense pain Nitroglycerin – MOA  Vasodilation in peripheral circulation  Nitrate or Nitrite from drug changed to nitric oxide (NO)  NO is a potent, short-acting vasodilator  Tends to have a greater effect on venous rather than arterial side  Less blood returning to heart (PRELOAD) and decreased blood pressure (AFTERLOAD)  Reduces work of heart  Reduces oxygen consumption  Reduces chest pain Nitroglycerin – SUPPLIED  Sublingual tablets - acute anginal attacks  Sublingual spray - acute anginal attacks  Ointment – prophylaxis/treatment  Oral SR tablets - prophylaxis  Topical patches – prophylaxis ( 12 HOURS )  IV solution in glass bottle - emergency/surgery Nitroglycerin – ADVERSE EFFECTS  Vasodilation  Headache  Flushing  Dizziness  Fainting  Decreased blood pressure  Reflex tachycardia Nitroglycerin – Education Nitro SL (tabs or spray)  Carry medication with them – original containers  Patient should sit down before use  Place tablet under tongue or spray on/under tongue  Allow tablet to dissolve or spray to be absorbed  no eating, drinking, or smoking  May repeat every 5 minutes to maximum of 3 times  If no relief seek assistance - hospital = after 3 times, its fully blocked and they need to seek assistant right away! (after second spray call 911 right away) =do not shake the ones with tablet (it can break) , or the bottle (it creates bubbles) Isosorbide Dinitrate/Mononitrate Isosorbide Dinitrate (Isordil, Cedocard SR) Isosorbide Mononitrate (Imdur) Indications  Maintenance of angina – oral tabs and SR tabs MOA and Adverse Effects  Same as nitroglycerin Daily Nitrate Administration Tip  For patients on daily/maintenance nitrate therapy, encouraged to have a “nitrate break” of about 10-12 hours per day to avoid potential tolerance  Ensure directions appropriate on Rx labels to allow for required break, especially for patches, oint, and daily oral meds 2. Beta Blocking Agents  Propranolol (Inderal) (non selective)  Atenolol (Tenormin) (selective)  Nadolol (Corgard) (non selective)  Metoprolol (Betaloc, Lopressor) (selective)  Acebutolol (Monitan, Sectral) (selective)  Bisoprolol (Monocor) (selective)  Pindolol (Visken) (non selective) Indications  Long-term (chronic) management of angina  Treatment of hypertension Many others Nonselective = affect the heart, lungs, vascular smooth muscles, kidneys, GI, etc. Selective = predominantly heart Nonselective is used when people are nervous, or high rate and other. while selective is indicated for just the heart. MOA  Block cardiac Beta Sympathomimetic receptor (B1)  Reduce heart rate (chronotropic)  Reduce force of contraction (inotropic)  Therefore, reduction in oxygen consumption and cardiac work  Also act as vasodilators Supplied Tablets (and a few as injections) Adverse Effects  Vasodilation, bradycardia and hypotension  Others often drug specific  Nausea, vomiting, diarrhea CNS – drowsiness, depression Vasodilation = headache, flushing, faint, dizziness, low BP, slower HR 3. Calcium Channel Blockers  Diltiazem (Cardizem/Tiazac) – non-DHP  Amlodipine (Norvasc) DHP  Nifedipine (Adalat) DHP  Verapamil (Isoptin) – non-DHP  Felodipine (Plendil, Renedil) DHP DHP very specific to the blood vessel, more to potent to the vasodilator (blood pressure) Non-DHP, Dihydropyridine CCBs have predominantly peripheral vasodilatory actions, whereas nondihydropyridine CCBs have significant sinoatrial (SA) and AV node depressant effects and possible myocardial depressant effects with lesser amounts of peripheral vasodilation. Dihydropyridine (DHP) CCBs tend to be more potent vasodilators than non-dihydropyridine (non-DHP) agents, whereas the latter have more marked negative inotropic effects. Indications  Preventative treatment of angina  Oftern preferred for vasospastic angina  Hypertension and other related conditions MOA  Inhibits calcium influx  Reduces vascular tone and produces a vasodilating effect  Vasodilation – reduces preload and afterload thus decrease in cardiac work and oxygen consumption Supplied  Tablets/capsules  XR strengths  Injection Adverse Effects  Vasodilation, bradycardia, hypotension  GI disturbances  Verapamil – constipation, bradycardia (CHF)  Nifedipine – reflex tachycardia  Diltiazem – bradycardia (CHF)  Antiarrhythmic Drugs Arrhythmias ( your heart is not beating In sync)  Disorder of cardiac conduction  Usually occurs in a diseased heart as a result of:  Congestive heart failure  Coronary artery disease  Myocardial infarction  Or due to drug therapy and/or drug interactions  Could also be genetic or unknown cause  Symptoms may range from palpitations to cardiac arrest Terminology  Arrhythmias that originate in the atria or AV nodal area are termed supraventricular  Arrhythmias that originate below the AV node are referred to as ventricular arrhythmias  Ectopic Foci – when regular conduction pathways are blocked or delayed, areas of abnormal impulse generation may become excitable and produce a heartbeat  Tachycardia – rapid heart rate (150-250 bpm)  Bradycardia – slow heart rate (< 60 bpm)  Atrial flutter – 200-350 bpm  Atrial fibrillation - >350 bpm  Ventricular fibrillation  Uncoordinated contractions  350-450 bpm  Most serious arrhythmia – cardiac arrest Antiarrhythmic Drugs  Do not cure the underlying disease process  Attempt to restore the normal cardiac rhythm (sinus rhythm)  There are 4 Antiarrhythmic Drug Classes: ◼ Class I – sodium channel blockers ◼ Class 2 – beta blockers (as seen before) ◼ Class 3 – “amiodarone” Class 4 – calcium channel blockers (as seen before) Class 1 Antiarrhythmics Possess local anesthetic activity  Interfere with the movement of sodium ions during excitation and depolarization  Excitability of heart is reduced  Slow down conduction velocity  Prolong refractory period  Decrease automaticity of the heart  Many side effects, specific to each drug CLASS 1 – SPECIFIC AGENTS Flecanide (Tambocor tablets) Procainamide (Pronestyl, Pronestyl SR, Procan SR)  Supplied – capsules, tablets, IV Disopyramide (Rythmodan capsules and LA tabs) Propafenone (Rythmol tablets) Lidocaine (Xylocaine)  Supplied – IV, IM (Emergency – ventricular arrhythmias) = non often use, but there’s a time and place for it. Class 2 Antiarrhythmics  Beta-adrenergic blocking drugs (beta blockers)  Antagonize the effects of epinephrine/norepinephrine  Decrease conduction velocity  Decrease excitability  Decrease automaticity  Prolong refractory period  Common side effects include bradycardia and hypotension Class 2 – Specific Agents Sotalol (Sotacor)  Supplied as tablets Propranolol (Inderal) ( also good for stage right)  Supplied – tablets, IV = they don’t bring down the heart to low and keep it in range. Class 3 Antiarrhythmics Amiodarone (Cordarone – Tablet and IV) Indication  Ventricular arrhythmias ( 350-450 bpm) ◼ Very potent, used when other drugs not effective ◼ Interferes with efflux of potassium ions during repolarization ◼ This prolongs refractory period and decreases frequency of arrhythmias Adverse Effects  Potentially serious: interferes with thyroid function, corneal deposits, pulmonary fibrosis, liver dysfunction, dermatitis, skin discolouration Class 4 Antiarrhythmics  Calcium Channel Blockers (antagonists)  Decrease entry of calcium into cells  Decrease conduction velocity in nodes  Decrease heart rate  Decrease inotropic effect – force of contraction Class 4 Specific Agents Verapamil (Isoptin) Diltiazem (Cardizem/Tiazac)  Indications  supraventricular tachycardias  also hypertension and angina  Supplied – tablets, capsules, injection  Adverse Effects  Vasodilation (bradycardia, hypotension, headache, dizziness and reflex tachycardia )  Verapamil: constipation  Diltiazem: arrhythmias, N/V, skin rash = non DHP use  Congestive Heart Failure Congestive Heart Failure (CHF)  Let’s hear from our “patient” with CHF…  Condition in which the heart is unable to pump sufficient blood to tissues of the body  Signs & Symptoms  Blood pools in heart  Swelling in lungs (pulmonary edema) and veins of lower extremities (peripheral edema)  Leads to clotting, trouble breathing, cardiac arrhythmias, death  Typical symptoms include: tiredness, SOB, rapid heartbeat, edema =Often patients think they have lung condition CHF – primary treatments  Vasodilators and Beta Blockers  Lower peripheral resistance and blood pressure  This decreases cardiac work and O2 consumption  Leads to increased cardiac output with less effort  Vasodilators may include ACE-I’s etc.  Diuretics  Eliminate excess Na and H2O from urinary tract  This reduces blood volume and edema and work of the heart When is digoxin used?  Considered third line therapy  Digoxin is considered when diuretic and vasodilator therapy are unable to effectively control symptoms and when myocardial contractility is weak and unable to maintain cardiac output Cardiac Glycosides  Group of compounds from plant leaves of Digitalis purpurea and Digitalis lanata  Indications:  CHF  some cases of Atrial Fibrillation  Therapeutic Effects:  Increase the force of myocardial contractions in CHF without effect on oxygen consumption  More forceful contractions within a shorter period of time – more blood pumped by the heart Cardiac Glycosides – Administration  Digoxin  Available PO and IV  Digitalization  Method of quick interval dosing with cardiac glycosides that rapidly produces effective drug levels  Maintenance Dose  Daily dose that maintains effective drug levels in blood  Narrow therapeutic index: What does this mean? Cardiac Glycosides - Adverse Effects  Usually caused by overdose  N/V, headache, visual disturbances, rash ◼ Can be relieved by dose reduction  Cardiac arrhythmias ◼ Ectopic beats: extra beats ◼ Can lead to ventricular tachycardia, ventricular fibrillation and cardiac arrest ◼ Treatment: stop glycoside, administer K and antiarrhythmics  Antidote for overdose: Digibind (Digifab) Cardiac Glycosides and Serum Electrolytes  Glycosides are affected by changes in serum electrolytes  If hypokalemia: sensitizes heart to drug toxicity  If hyperkalemia: antagonizes therapeutic effect  If hypercalcemia: enhances drug action =General idea that electrolytes highly affect muscle and heart functions, that an imbalance can cause symptoms and can also affect drug use Cardiac Glycosides - Drug Interactions  Digoxin absorption decreased by:  antacids, laxatives, kaopectate, cholestyramine  Opposite actions with other meds:  beta blockers and Calcium channel blockers  Increased toxicity of digoxin when:  potassium lowered by diuretics (thiazides and organic acids)