Lecture 14 CH11 Cardiovascular System.pptx.pdf

The Cardiovascular System Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com. Learning Objectives Explain the basic anatomy and physiology of the heart and relate information to the common types of heart disease. 2. How is the heart beat generated?...

The Cardiovascular System Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com. Learning Objectives Explain the basic anatomy and physiology of the heart and relate information to the common types of heart disease. 2. How is the heart beat generated? 3. Describe the common causes of congenital heart disease and valvular heart disease. Explain the effects of these diseases. Describe the methods of treating congenital and acquired valvular heart disease. 4. Describe the pathogenesis of primary myocardial disease. 5. Describe the development and treatment of cardiac arrhythmias. 6. Describe the pathogenesis of myocardial ischemia. Describe the clinical manifestations of coronary heart disease. Explain the methods of treatment and their rationales. 7. List the major complications of myocardial infarction and describe their clinical manifestations. Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com 1. Learning Objectives Explain the general principles applied to the diagnosis and treatment of coronary heart disease and myocardial infarction. 9. Compare and contrast myocardial ischemia and myocardial infarct. 10. Discuss drugs used in the prevention and treatment of cardiovascular disease. Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com 8. Cardiac Structure and Function Function: Muscular pump; propels blood through the lungs to the tissues Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Transport: Nutrients, oxygen, carbon dioxide, hormones, blood cells (immunity, hemostasis) Heart disease: Disturbance of function(s) Location: Within mediastinum; extends obliquely about 5 inches from second rib to fifth intercostal space; rests on the diaphragm; anterior to vertebral column and posterior to sternum ▪ Two thirds of heart mass lies left of midsternal line ▪ Apex of heart points downward toward the left hip https://en.wikipedia.org/wiki/Circulatory_system Heart Anatomy Layers of the heart wall ▪ Epicardium: Outer layer of connective tissue, coronary arteries ▪ Myocardium: Middle layer, muscular, thickest layer, workhorse of the heart ▪ Endocardium: Thin endothelial layer- Innermost layer, smooth membrane, covers heart valves - part of endocardium Layers form a fibrous framework tissue – provides support (acts as skeleton) and divides atria/ventricles so they can function independently -also provides support for valve attachment Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Heart covering ▪ Pericardium: Double-walled fibrous sac, outer layer of tough connective tissue (mesothelial cells) ▪ Continuous with layer of cells of epicardium (mesothelial): Visceral layer of pericardium covering myocardium Heart Anatomy Chambers: No direct communication between right and left halves Atria receive blood returning to heart, Ventricles pump blood away to lungs/aorta ▪ Right half: Right atrium (RA) and right ventricle (RV) ▪ Pulmonary pump, circulates blood into pulmonary artery, lungs ▪ Left half: Left atrium (LA) and left ventricle (LV) ▪ Systemic pump, circulates blood into aorta, organs, and tissues Systole – during contraction of Ventricles Diastole – during relaxation as ventricle refill Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Divided by septum Cardiac Valves 4 Cardiac valves permit flow of blood in only one direction Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Atrioventricular (AV) valves (Lub): Flap-like valves between atria and ventricles; prevent back flow of blood into atria when ventricles contract ▪ Tricuspid valve: Three flexible flaps; directs blood flow from RA to RV, prevents backflow to RA when RV contracts ▪ Bicuspid valve or mitral valve: Directs blood flow from LA to LV; prevents backflow to LA when LV contracts ▪ Chordae attach/support flaps Diastole – causes tension on valves through chordae, causing them to open Systole – no tension, blood flow forces closure Cardiac Valves Pulmonary valve: From RV to pulmonary trunk Aortic valve: From LV to aorta Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Semilunar valves – dub (Aortic/Pulmonary) ▪ Cup shaped – 3 cusps on both ▪ Aorta and pulmonary artery ▪ Free margins of valves face upward ▪ Prevent backflow of blood into ventricles during diastole ▪ Force of Ventricular contraction forces opening ▪ Ventricular contraction coordinates valve functions – Closure of AV valves and opening of semilunar valves Blood Supply to the Heart Coronary arteries ▪ Shortest circulation in the body ▪ Myocardium is too thick for the diffusion of nutrients ▪ Aorta branches (aortic sinus) to right and left coronary arteries that carry arterial blood to the heart when relaxed ▪ Blood passes through capillary beds of myocardium ▪ Venous blood collected by cardiac veins Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Main blood supply of the heart Blood Supply to the Heart Cardiac veins join together and form the coronary sinus that empties blood into the RA Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Blood supply to the heart ▪ Right coronary artery (RCA) ▪ Supplies posterior wall and posterior part of interventricular septum ▪ Left coronary artery (LCA) and branches ▪ Left anterior descending artery (LADA) ▪ Supplies anterior wall, anterior part of interventricular septum ▪ Left circumflex artery (LCA) supplies lateral wall Blood Supply to the Heart ▪ Blockage of an artery – some blood flow can compensate to form other communicating artery through these connections. ▪ Adult cardiac muscle does not proliferate to replace damaged (due ischemia) or destroyed muscle fibers (necrosis – cardiac infarct) ▪ Most areas of cell death repaired with noncontractile scar tissue Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Terminal branches of coronary arteries communicate though connections (anastomoses) Conduction System ▪ A group of specialized muscle cells that initiate electrical impulses through depolarization ▪ SA node controls normal cardiac rhythm “cardiac pacemaker” – initiates atrial contraction ▪ Intranodal tracts connect SA to AV node/bundle of His ▪ AV node (though bundle of His) transmits signals to ventricles (right/left branches) ▪ Terminate in perkinje fibers that active heart muscle contraction ▪ Ability of cardiac muscle to depolarize and contract is intrinsic; does not depend on the nervous system ▪ Depolarization rate can be influenced by Autonomic NS Sympathetic – increase Parasympathetic - decrease Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Impulses are generated/ initiated in the sinoatrial (SA) node in RA near opening of the superior vena cava Cardiac Cycle ▪ Atrial systole → atrial diastole → ventricular systole → ventricular diastole Ventricles fill passively in Diastole (120ml) Late in Diastole, atria contract to expel final 30 ml (important during incr HR) ▪ Systole: Ventricular Contraction period ▪ Diastole: Ventricular Relaxation period ▪ Cardiac output: Typically 5L/min pumped out by each ventricle (70ml/contraction x 72 bpm) Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Consists of all events associated with blood flow through the heart during one complete heartbeat Cardiac Cycle ▪ Blood enters RA via three veins ▪ Superior vena cava (from body regions above diaphragm) ▪ Inferior vena cava (from body areas below diaphragm) ▪ Coronary sinus (collects blood that drains from myocardium) ▪ Blood enters LA via four pulmonary veins Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Atria (singular is atrium): Receiving chambers, thin walled; RA; LA Cardiac Cycle ▪ Pulmonary circulation ▪ Oxygen-poor blood enters RA → RV through tricuspid valve → pulmonary artery → lungs ▪ Systemic circulation ▪ Freshly oxygenated blood leaves lungs through pulmonary veins → LA → LV through mitral valve → aorta → rest of the body Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Blood, which is low in oxygen and high in carbon dioxide, returns to the heart Blood Pressure Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Blood flow in the arteries results from the force of ventricular contraction ▪ Pressure is highest when ventricles contract (systolic pressure) ▪ Pressure is lowest when ventricles relax (diastolic pressure) ▪ Pressure is decreased due to elasticity of blood vessels ▪ Loss of elasticity (Atherosclerosis) leads to increased BP Tools to Examine Cardiovascular Function: ECG – electrocardiogram Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Measures electrical activity of heart; diagnostic tool ▪ P wave: Atrial depolarization, atrial systole ▪ QRS complex: Ventricular depolarization, ventricular systole ▪ T wave: Ventricular diastole ▪ PR interval: Time for depolarization to pass from atria to ventricles via AV bundle Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Purkinje conduction - QRS AV node conduction – P-R interval SA node conduction – P wave Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Detects disturbances in rate, rhythm, conduction, muscle injury, extent of muscle damage Tools to Examine Cardiovascular Function ▪Ultrasound imaging of heart ▪Identify valve/chamber/blood flow abnormalities https://sifsof.com/clinical-apps/tte-transthoracic-echocardiogram/ Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Echocardiogram Angiogram by Radiography or CT https://emedicine.medscape.com/article/153647-overview Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com coronary angiography in the left panel shows severe left anterior descending coronary artery stenosis. This lesion was treated with stent placement in the left anterior descending coronary artery, as observed in the right panel. https://www.ahajournals.org/doi/full/10.1161/circulationaha.113.002835 Congenital Heart Disease ▪ During development heart goes through many stages Ductus arteriosus (pulmonary artery-aorta) – redirects blood from lungs Foramen ovale – maintains blood flow between RA to LA(one way valve) while heart is developing Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Fetal circulation has lung bypass regions Congenital Heart Disease ▪ Atrial, ventricular, or combined septal defects (Heart murmurs) Shunts – mixing of blood (oxygenated) and pressures ▪ Abnormalities obstructing flow: Pulmonary stenosis, aortic stenosis, coarctation of the aorta ▪ Abnormal formation of aorta and pulmonary artery or abnormal connection of vessels: Tetralogy of Fallot, transposition of great vessels Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Causes: German measles (viral infections), Down syndrome, drugs, genetic factors, undetermined causes ▪ Fetal bypass channels fail to close normally Patent ductus arteriosus; patent foramen ovale Common Congenital Cardiovascular Abnormalities ▪ Atrial and ventricular septal defects – usually cause by non-closure of foramen ovale ▪ Pulmonary or aortic valve stenosis – obstructed/narrowed valve ▪ Coarctation (narrowing) of the aorta ▪ Tetralogy of Fallot – ventricular septal defect Correction is though surgical interventions Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Patent ductus arteriosus –shunts blood from aorta into pulmonary artery Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Primary Myocardial Disease – diseases that effect heart muscle Cardiomyopathy: No evidence of inflammation ▪ Dilated cardiomyopathy: Enlargement of heart and dilatation of chambers; impaired ventricular action leads to chronic heart failure; cause uncertain; no treatment – complex hereditary susceptibility (50 genes identified) ▪ Hypertrophic cardiomyopathy: Hereditary, transmitted as dominant trait, muscle fibers in disarray with marked hypertrophy of heart muscle Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Two types: Myocarditis: Inflammation; injury and necrosis of individual muscle fibers ▪ Cause: Viruses, parasites (Trichinella), fungi (Histoplasma), or hypersensitivity (acute rheumatic fever); abrupt onset; may lead to acute heart failure ▪ Tx underlying cause, most time subsides without permanent damage Primary Myocardial Disease ▪ Septal muscles more hypertrophied than rest of myocardium; impedes flow into aorta ▪ Thick septum impinges on anterior mitral valve leaflet; intermittently blocks outflow from left ventricle ▪ Genetic screening available B-myosin heavy chain and Myosin binding protein G mutations Beta blockers (reduce force/rate) can be used to slow the heart Calcium channel blockers to reduce contractility of cardiac muscle (reduce contraction) Surgical resection of blocking septum also option Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Hypertrophic cardiomyopathy ▪ Hypertrophy reduces size of ventricles, which do not readily dilate in diastole Valvular Heart Disease: Rheumatic Fever ▪A response to a bacterial infection; an immunologic reaction that develops weeks after initial streptococcal infection ▪Complication of group A beta hemolytic streptococcal infection (causes sore throat and scarlet fever) ▪Antistreptococcal antibodies against strep antigens cross react with similar antigens in tissues “molecular mimicry Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪Commonly encountered in children Molecular Mimicry Any given TCR/BCR is generated randomly and can recognize different antigens with varying efficiencies with potential to “cross-react” Infection awakens these self reactive cells and provides necessary inflammatory environment. (inhibits Peripheral Tolerance) Autoimmune diseases frequently follow bacterial or viral infections probably due to predisposing conditions (genetic/environment) combined with Immune activation (provides co-stimulation that would otherwise be absent) Rheumatic heart disease: T cells that recognize streptococcal antigens cross react with tissues of the mitral valve of the heart. Viral antigen Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Potential for certain self antigens to also be recognized by cells that also recognize pathogens Rheumatic Heart Disease Scarring of heart valves following rheumatic inflammation ▪ Clinical outcome: Valve regurgitation or stenosis; impairs cardiac function, increases strain on heart, eventually leads to heart failure, flare ups with future strep infections ▪ Prevention ▪ Treat beta strep infection promptly ▪ Prophylactic penicillin throughout childhood and young adulthood to prevent strep infections and reduce risk of recurrent rheumatic fever and further heart valve damage ▪ Surgical removal and replacement (artificial) of valve if severely damaged Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Causes inflammation in connective tissues throughout the body: Primarily affects mitral and aortic valves (left side of heart) and joint tissues Aortic Stenosis ▪ aortic stenosis secondary to bicuspid aortic valve ▪ Works for a time, increased stress causes thickening and calcification and valve rigidity (many years) due to increased strain on valve, leads to heart failure ▪ Similar risk factors to heart disease promote development Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com 2% of population have bicuspid instead of tricuspid aortic valve Valvular Heart Disease: Aortic Stenosis Leaflets undergo connective tissue degenerative changes (fibrotic, calcified, rigid); restricts valve mobility Also occurs with deposits of lipids and macrophages, as in coronary atherosclerosis ▪ Clinical outcomes: Increased strain leads to left ventricular hypertrophy and heart failure ▪ Prevention: Control risk factors (high cholesterol, diabetes, hypertension) ▪ Tx – surgical repair/replacement Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Aortic stenosis can also occur due to aging Valvular Heart Disease: Mitral Valve Prolapse ▪ Common, but only a few patients develop problems ▪ Prolapsing leaflets may not fit together tightly; blood leaks back into LA; mitral regurgitation ▪ On auscultation: Clicking sound on systole followed by a faint systolic murmur from reflux of blood between closed valve leaflets ▪ Can cause excess strain on chordae leading to ventricular arrythmia, or chordae rupture ▪ Diagnosis made with echocardiogram ▪ Surgical repair/replacement may be necessary Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ One or both leaflets enlarge, stretch, and prolapse into LA during ventricular systole Infective Endocarditis Abnormal or damaged mitral and aortic valves are susceptible to develop active disease Platelets and fibrin may deposit on abnormal or damaged valves then serve as sites for bacteria to implant or for thrombi to form, casing valve inflammation, followed by emboli and tissue infarct ▪ In susceptible patients with diagnosed heart valve damage -Prophylactic antibiotics given prior to dental or surgical procedures to prevent transient bacteremia and resulting endocarditis Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Under normal conditions it manifests as subacute infective endocarditis (usually bacterial) ▪ Caused by organisms of low virulence ▪ Complication of any valvular heart disease ▪ Mild symptoms of infection Infective Endocarditis ▪ Severe symptoms of infection and valve destruction ▪ Affects normal heart valves At-risk groups ▪ Intravenous drug users; affect tricuspid valve instead of mitral or aortic valves ▪ Unsterile materials or contaminants enter right side of heart, form large bacteria-laden growths on valves, can dislodge into pulmonary circulation and cause pulmonary infarct Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Acute infective endocarditis caused by highly pathogenic organisms, commonly staphylococci Cardiac Arrhythmias Ventricular fibrillation (VF) ▪ Ventricles unable to contract normally, incompatible with life- no blood circulation ▪ Heart block (complete or incomplete) ▪ Delay or interruption of impulse transmission from atria to ventricles ▪ Usually caused by arteriosclerosis when parts of conduction system loses blood supply ▪ Heart block will not allow conduction to AV node, can cause arrythmias ▪ Tx- pacemaker to stimulate ventricular contraction at a determined rate. Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Disturbances in heart rate or rhythm Atrial fibrillation (AF) ▪ Atria contract in irregular pattern: 400bpm- “quiver” versus normal contraction ▪ Can also affect ventricular rate and Ventricles beat irregularly and fast (140-160), shortening diastole (pulse deficit due to inadequate ventricular filling) Decreased circulating blood volume leads to hypotension and pulmonary congestion (blood pooling in lungs) ECG – lack of P wave, variable QRS complex Disorganized electrical activity Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com lack of P wave Acute Coronary Syndrome Cardiac arrest may result from: ▪ Arrhythmia from prolonged or severe myocardial ischemia that disrupts ventricular contraction; most common and rapidly fatal is ventricular fibrillation ▪ Asystole is complete cessation of cardiac contractions Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Basic mechanisms that trigger a heart attack ▪ Sudden blockage of a coronary artery from a thrombus or atheromatous debris ▪ Hemorrhage from an atheromatous plaque rupture ▪ Arterial spasm Exacerbated by: sudden greatly increased myocardial oxygen requirements (vigorous physical activities) Acute Coronary Syndrome Partial chronic blockage – Stable angina (temporary chest pain relieved by vasodilator (nitroglycerine) or rest. Unstable angina, needs anticoagulation and antithrombotic drugs Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Cause: Arteriosclerosis of coronary arteries ▪ Narrowing and hardening of arteries from an atheroma (plaque) containing lipid deposits (neutral fat and cholesterol) by diffusion from bloodstream ▪ Changes in atheroma lead to platelet accumulation, inflammation and formation of a thrombus ▪ Thrombosed coronary artery can not supply sufficient blood to cardiac muscle cells ▪ Severe myocardial ischemia occurs Myocardial Ischemia: Heart Attack Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Caused by inadequate blood supply to the heart muscle -precipitated by atherosclerosis, thrombosis Myocardial Infarction: Location Depend on location of obstruction and collateral flow • Anterior wall: Left anterior descending artery distribution • Lateral wall: Circumflex artery distribution • Posterior wall: Right coronary artery distribution • anterior and lateral wall: Main left coronary distribution, frequently fatal Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Often involves muscles of left ventricle and septum Thicker walls require rich blood supply; work harder to pump blood into systemic circulation; rarely involves atria or right ventricle Myocardial Ischemia Manifestations Clinical manifestations are variable ▪ Asymptomatic (free of symptoms) ▪ Angina pectoris (pain of the chest) bouts of oppressive chest pain that may radiate into neck or arms; caused by myocardial ischemia ▪ Myocardial infarction: Actual necrosis of heart muscle ▪ Cardiac arrest: Cessation of normal cardiac contractions Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Due to decreased blood supply to heart muscle from narrowing or obstruction of the coronary arteries (chronic myocardial ischemia) Pathophysiology: Results in partial thickness damage to cardiac muscle STEMI – complete occlusion of major coronary artery Results in full thickness damage ST elevation reflects myocardial necrosis – can be Reversed if treated promptly with thrombolytics Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com NSTEMI – complete occlusion of minor coronary artery or partial occlusion of major MI ACS – Acute Coronary Syndrome Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Cocaine-Induced Arrhythmias and Infarcts ▪ Increases heart rate: Increased oxygen demand ▪ Increased muscle irritability: Predisposes to arrhythmias ▪ Increased peripheral vasoconstriction and coronary artery spasm: High blood pressure ▪ Fatal arrhythmias and MI can occur even among those with normal coronary arteries Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Prolongs and intensifies effects of sympathetic nervous system Myocardial Infarction: Diagnosis ▪ Pain of severe angina may be similar to pain of MI ▪ Possible mild symptoms of subendocardial infarct Physical examination usually not abnormal unless patient exhibits evidence of shock, heart failure, murmur Laboratory data ▪ ECG, Cardiac imaging ▪ Enzyme tests; enzymes leak out from necrotic cells after an infarct ▪ The larger the infarct, the longer for elevated levels to return to normal Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Medical history may be inconclusive Myocardial Infarction: Diagnosis Troponin T and Troponin I ▪ Specific to heart, slight heart damage causes levels to rise ▪ Appears in 3h, peaks in 24 hours, remains high for 10 to 14 days ▪ Pattern reflects cardiac muscle necrosis Creatine kinase - myocardial band (CK-MB) Enzyme present in muscle ▪ Rises a few hours after MI, peaks in 24 hours Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Enzyme tests Myocardial Infarction: Treatment In addition to drug treatments (nitro, beta blockers), 2 methods to re-establish blood flow to the heart muscle. Angioplasty - Requires specialized medical center ▪ May be undertaken after immediate thrombolytic therapy ▪ Catheter (femoral vein) passed into stenotic vessel – balloon/stent ▪ Widens coronary artery in areas of blockage ▪ Better success rate (90%) compared to thrombolytics (70-80%) Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Thrombolytic therapy ▪ Effective, but clot may not dissolve completely ▪ Better outcome the sooner medication is provided (within 1 hour of first MI symptoms, no use after 6h) ▪ May cause bleeding problems (making it unsuitable for 30% of cases) Myocardial Infarction: Treatment ▪ Stroke or diseases of cerebral blood vessels ▪ Severe hypertension ▪ Recent operation ▪ Bleeding disorder or condition (gastric or duodenal ulcer) Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Contraindications for thrombolytic therapy Myocardial Infarction: Complications ▪ Arrhythmias from irritability of ischemic heart muscle adjacent to the infarct or from conduction disturbance (heart block) ▪ Heart failure due to badly damaged ventricles ▪ Intracardiac thrombi: Mural thrombus forms on ventricular wall; bits of clot embolize into systemic circulation causing infarct in brain, kidneys, spleen ▪ Pericarditis: Infarct extends to epicardial surface, leads to inflammation and fluid accumulation in pericardial sac; may cause chest pain Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com In addition to damage to heart muscle/cardiac function and associated problems: Myocardial Infarction: Treatment Recovery – greatest risk of subsequent attack in first 6 months ▪ Anti-arrhythmic drugs: Reduce irritability of heart muscle ▪ Cardiac pacemaker: If complete heart block develops ▪ Possible insertion of a cardioverter-defibrillator ▪ Control or eliminate risk factors such as hypertension and smoking ▪ Use of drugs including beta blockers (slow down nerve impulses through heart muscle) and antiplatelet agents (anticoagulant), lower cholesterol (statins) ▪ Aspirin: Reduces tendency of platelets to aggregate Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com ▪ Bed rest advancing to graded activity Aspirin and Reduced Cardiovascular Disease Risk ▪ Rapidly absorbed from stomach and small intestines ▪ Inhibits platelet function within 1 hour of ingestion ▪ 30 mg per day can inactivate thromboxane A2 for the entire 10-day life span of platelets ▪ Reduces risk of cardiovascular disease and stroke ▪ Increases risk of bleeding in the brain if person has stroke ▪ Prophylactic use without indication is controversial Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Action: Interferes with platelet function by permanently inactivating thromboxane A2 that causes platelets to aggregate and start clotting process Myocardial Infarction: Severe complications Papillary muscle dysfunction: Infarcted papillary muscle unable to control mitral valve leaflet, resulting in mitral valve prolapse and mitral insufficiency Ventricular aneurysm: Late complication; outward bulging of healing infarct during ventricular systole; reduces left ventricular function and cardiac output; rather than being ejected, blood fills aneurysm sac Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Cardiac rupture: Blood leaks into pericardial sac from perforation in necrotic muscle, prevents ventricular filling (cardiac tamponade); rupture may occur in ventricular septum or papillary muscle Myocardial Infarction: Survival ▪ Mortality rates: 6% for small infarcts without heart failure to 50% or more for large infarcts with severe heart failure ▪ Causes of death following MI: Arrhythmia, heart failure, cardiac rupture Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Factors affecting survival ▪ Size of infarct ▪ Age of patient ▪ Complications ▪ Other diseases Heart Failure May result from any type of heart disease Chronic heart failure: Develops slowly and insidiously Acute heart failure: Rapidly failing heart ▪ Forward failure (Left): Reduced blood flow to tissues → reduced renal blood flow → salt and water retention to increase blood volume and venous pressure → edema ▪ Backward failure (Right): Blood backups in veins drain to the heart → increased venous pressure, congestion, edema ▪ Both types are present to some degree in patients with heart failure Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com No longer able to pump adequate amount of blood Heart Failure: Treatment Diet/ lifestyle modification Cardiac/ Arrythmia Drugs – wide variety ▪ Digitalis - Increases efficiency of ventricular contraction Angiotensin-converting enzyme (ACE) inhibitors ▪ Promote retention of salt and water to increase blood pressure ▪ Treat congestive heart failure Use of a ventricular assist device - pacemaker Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com Diuretic drugs ▪ Promote excretion of excess salt and water by kidneys to lower blood pressure (Lasix) The Cardiovascular System Copyright © 2021 by Jones & Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com.