The main function of the circulatory system, which consists of the heart and blood vessels, is transport. The circulatory system delivers oxygen and nutrients needed for metabolic processes to the tissues, carries waste products from cellular metabolism to the kidneys and other excretory organs for elimination, and circulates electrolytes and hormones needed to regulate body function. This process of nutrient delivery is carried out with exquisite precision so that the blood flow to each tissue of the body is exactly matched to tissue need.
Coronary Circulation There are two main coronary arteries, the left and the right, which arise from the coronary sinus just above the aortic valve. The left coronary artery extends for approximately 3.5 cm as the left main coronary artery and then divides into the anterior descending and circumflex branches . The left anterior descending artery passes down through the groove between the two ventricles, giving off diagonal branches, which supply the left ventricle, and perforating branches, which supply the anterior portion of the interventricular septum and the anterior papillary muscle of the left ventricle. The circumflex branch of the left coronary artery passes to the left and moves posteriorly in the groove that separates the left atrium and ventricle, giving off branches that supply the left lateral wall of the left ventricle. The right coronary artery lies in the right atrioventricular groove, and its branches supply the right ventricle. The sinoatrial node usually is supplied by the right coronary artery. The right coronary artery usually moves to the back of the heart, where it forms the posterior descending artery , which supplies the posterior portion of the heart (the interventricular septum, atrioventricular [AV] node, and posterior papillary muscle). In 10% to 20% of persons, the left circumflex, rather than the right coronary artery, moves posteriorly to form the posterior descending artery. Although there are no connections between the large coronary arteries, there are anastomotic channels that join the small arteries. With gradual occlusion of the larger vessels, the smaller collateral vessels increase in size and provide alternative channels for blood flow. One of the reasons CHD does not produce symptoms until it is far advanced is that the collateral channels develop at the same time the atherosclerotic changes are occurring. The openings for the coronary arteries originate in the root of the aorta just outside the aortic valve; thus, the primary factor responsible for perfusion of the coronary arteries is the aortic blood pressure. Changes in aortic pressure produce parallel changes in coronary blood flow. In addition to generating the aortic pressure that moves blood through the coronary vessels, the contracting heart muscle influences its own blood supply by compressing the intramyocardial and subendocardial blood vessels. The large epicardial coronary arteries lie on the surface of the heart, with the smaller intramyocardial coronary arteries branching off and penetrating the myocardium before merging with a network or plexus of subendocardial vessels that supply the endocardium. During systole, contraction of the cardiac muscle compresses the intramyocardial vessels that feed the subendocardial plexus, and the increased pressure in the ventricle causes further compression of these vessels. As a result, blood flow through the subendocardial vessels occurs mainly during diastole. Thus, there is increased risk of subendocardial ischemia and infarction when diastolic pressure is low, when a rapid heart rate decreases the time spent in diastole, and when an elevation in diastolic intraventricular pressure is sufficient to compress the vessels in the subendocardial plexus. Heart muscle relies primarily on fatty acids and aerobic metabolism to meet its energy needs. Although the heart can engage in anaerobic metabolism, this process relies on the continuous delivery of glucose and results in the formation of large amounts of lactic acid. Blood flow usually is regulated by the need of the cardiac muscle for oxygen. Even under normal resting conditions, the heart extracts and uses 60% to 80% of oxygen in blood flowing through the coronary arteries, compared with the 25% to 30% extracted by skeletal muscle. Because there is little oxygen reserve in the blood, myocardial ischemia develops when the coronary arteries are unable to dilate and increase blood flow during periods of increased activity or stress.
Atherosclerosis is by far the most common cause of CHD, and atherosclerotic plaque disruption the most frequent cause of myocardial infarction and sudden death. More than 90% of persons with CHD have coronary atherosclerosis. Most, if not all, have one or more lesions causing at least 75% reduction in cross-sectional area, the point at which augmented blood flow provided by compensatory vasodilation no longer is able to keep pace with even moderate increases in metabolic demand. Atherosclerosis can affect one or all three of the major epicardial coronary arteries and their branches ( i.e. , one-, two-, or three-vessel disease). Clinically significant lesions may be located anywhere in these vessels but tend to predominate in the first several centimeters of the left anterior descending and left circumflex or the entire length of the right coronary artery. Sometimes the major secondary branches also are involved. There are two types of atherosclerotic lesions : the fixed or stable plaque , which obstructs blood flow, and the unstable or vulnerable plaque , which can rupture and cause platelet adhesion and thrombus formation. The fixed or stable plaque is commonly implicated in chronic ischemic heart disease (stable angina, variant or vasospastic angina, and silent myocardial ischemia) and the unstable plaque in unstable angina and myocardial infarction. Atherosclerotic plaques are made up of a soft lipid-rich core with a fibrous cap. Plaques with a thin fibrous cap overlying a large lipid core are at greatest risk for rupture. Plaque disruption may occur with or without thrombosis. When the plaque injury is mild, intermittent thrombotic occlusions may occur and cause episodes of anginal pain at rest. More extensive thrombus formation can progress until the coronary artery becomes occluded, leading to myocardial infarction. Platelets play a major role in linking plaque disruption to acute CHD. As a part of the response to plaque disruption, platelets aggregate and release substances that further propagate platelet aggregation, vasoconstriction, and thrombus formation. Because of the role that platelets play in the pathogenesis of CHD, antiplatelet drugs ( e.g. , low-dose aspirin) are frequently used for preventing heart attack. There are two types of thrombi formed as a result of plaque disruption: white platelet-containing thrombi and red fibrincontaining thrombi. The thrombi in unstable angina have been characterized as grayish-white and presumably platelet rich. Red thrombi, which develop with vessel occlusion in myocardial infarction, are rich in fibrin and red blood cells superimposed on the platelet component and extended by the stasis of blood flow. Coronary heart disease is commonly divided into two types of disorders: chronic ischemic heart disease and the acute coronary syndromes. There are three types of chronic ischemic heart disease: chronic stable angina, variant or vasospastic angina, and silent myocardial ischemia. The acute coronary syndromes represent the spectrum of ischemic coronary disease ranging from unstable angina through myocardial infarction. Cholesterol is a soft waxy substance found among the lipids in the bloodstream and in all of your body’s cells. Everybody needs cholesterol, it serves a vital function in the body. It is a component of the nerve tissue of the brain and spinal cord as well as other major organs. We get cholesterol from two ways. Our bodies make it and the rest comes from animal products we eat. It is frequently measured to promote health and prevent disease. Desirable levels of total cholesterol levels should be at 200 or less. 240 is considered high but it will depend on the HDL and LDL levels if at this level there is a risk to your health. It is a major component of the plaque that clogs arteries. Cholesterol and other fats can’t dissolve in the blood. They have to be transported to and from cells by special carriers called lipoproteins.
ISCHEMIC HEART DISEASE ■ The term ischemic heart disease refers to disorders in coronary blood flow due to stable or unstable atherosclerotic plaques. ■ Stable atherosclerotic plaques produce fixed obstruction of coronary blood flow, with myocardial ischemia occurring during periods of increased metabolic need, such as in stable angina. ■ Unstable atherosclerotic plaques tend to fissure or rupture, causing platelet aggregation and potential for thrombus formation with production of a spectrum of acute coronary syndromes of increasing severity, ranging from unstable angina, to non–ST-segment elevation myocardial infarction, to ST-segment elevation myocardial infarction.
Atherosclerosis, the process underlying most cardiovascular disease (CVD), has 3 distinct stages: Initiation, during which lipids are deposited on the vessel wall Progression, during which inflammation increases, plaque formation builds up in the intima, and fibrous caps are formed, increasing the potential for atheroma Clinical disease, when complications result from stenosis or unstable plaque rupture, leading to myocardial infarction (MI), stroke, or death. Libby P. Circulation. 2001;104:365-372.
Atherosclerosis is a progressive disease involving the development of arterial wall lesions. As they grow, these lesions may narrow or occlude the arterial lumen. Complex lesions may also become unstable and rupture, leading to acute coronary events, such as unstable angina, myocardial infarction, and stroke. Pepine CJ. The effects of angiotensin-converting enzyme inhibition on endothelial dysfunction: potential role in myocardial ischemia. Am J Cardiol . 1998; 82(suppl 10A):244-275.
Atherosclerosis is a LIFELONG, even childhood, process. This chart is worth knowing.
A very well constructed graphic understanding of the pathogenesis of atherosclerosis. Please be expected to not only KNOW these five items, but their correct ORDER too.
This slide shows an example where an atheroma, evident by IVUS, remains undetected by angiography as a result of coronary remodelling. On the left, the angiogram is completely normal. However, two sites in the anterior descending coronary artery, indicated by arrows, show a varying extent of atherosclerosis by IVUS. The more distal site (top right) has little disease, but the more proximal site (bottom right) has a large crescentic atheroma. The lumen size at both sites is similar because of remodelling, resulting in a false-negative angiogram. Reference Nissen SE, Yock P. Intravascular ultrasound: novel pathophysiological insights and current clinical applications. Circulation 2001; 103: 604–616. Abbreviation IVUS=intravascular ultrasound Reproduced from Circulation 2001; 103: 604–616, with permission from Lippincott Williams & Wilkins.
Why does the necrosis spread from the endocardium to the pericardium (i.e., epicardium)?
Cardiovascular pathology coronary heart disease finale
CONTENT1. Features of coronal circulation of blood and metabolism of cardiac muscle.2. Classification of coronary heart disease. CHD: determination, reasons and terms of origin, form.3. Ischemic heart disease. Definition of the notion, risk factors, mechanisms of development4. Sudden coronary death: reasons, mechanisms of origin.5. Angina pectoris: classification, pathogenesis of displays.6. Heart attack of myocardium: kinds, description of functional and biochemical violations in a cardiac muscle, mechanisms of pain syndrome.7. Mechanisms of origin of spasms of coronary vessels.8. Complication of heart attack of myocardium. Pathogenesis of cardiogenic shock.9. Experimental models of heart attack of myocardium.
ACTUALITY• The term coronary heart disease (CHD) describes heart disease caused by impaired coronary blood flow. In most cases, CHD is caused by atherosclerosis.• Diseases of the coronary arteries can cause angina, angina myocardial infarction or heart attack, cardiac attack dysrhythmias, conduction defects, heart failure, and dysrhythmias defects failure sudden death. death• During the past 50 years, there have been phenomenal advances in understanding the pathogenesis of CHD and in the development of diagnostic techniques and treatment methods for disease.• However, declines in morbidity and mortality have failed to keep pace with these scientific advances, probably because many of the outcomes are more dependent on lifestyle factors and age than on scientific advances. advances
FUNCTIONAL ORGANIZATION OF THE CIRCULATORY SYSTEM■ The circulatory system consists of the heart, heart which pumps blood; the arterial system, system which distributes oxygenated blood to the tissues; the venous system, which collects system deoxygenated blood from the tissues and returns it to the heart; and the capillaries, capillaries where exchange of gases, nutrients, and wastes occurs.■ The circulatory system is divided into two parts: the low-pressure pulmonary circulation, linking the transport function of circulation the circulation with the gas exchange function of the lungs; and the high-pressure systemic circulation, providing oxygen and circulation nutrients to the tissues.■ The circulation is a closed system, so the output of the right and left heart must be equal over time for effective functioning of the circulation.
Coronary Heart Disease The term coronary heart disease (CHD) describes heart disease caused by impaired coronary blood flow. In most cases, CHD is caused by atherosclerosis. Diseases of the coronary arteries can cause angina, myocardial infarction or heart attack, cardiac dysrhythmias, conduction defects, heart failure, and sudden death. Heart attack is the largest killer of American men and women, claiming more than 218,000 lives annually. Each year, 1.5 million Americans have new or recurrent heart attacks, and one third of those die within the first hour, usually as the result of cardiac arrest resulting from ventricular fibrillation.
Pathogenesis of Coronary Heart Disease • HDL (good) cholesterol removes excess cholesterol in the blood stream. • LDL (bad) cholesterol enters the arterial wall and is taken up by our body’s scavenger cells. • Subsequently, they will turn into fatty streaks which progress into atheromatous plaques. • Hence, LDL cholesterol is said to promote atherosclerosis.
Healthy LifestyleWell-Balanced Cholesterol Levels : HDL cholesterol Acceptable: ≥ 0.9 mmol/L Risky : < 0.9 mmol/L Triglyceride Desirable : < 2.3 mmol/L•A healthy person should have a higher level ofHDL and a low level of LDL and triglyceride .
Types of chronic ischemic heart disease and acute coronary syndromes Coronary heart diseaseChronic ischemic heart disease Acute coronary syndrome Stable Variant No ST-segment ST-segment angina angina elevation elevation Silent myocardial Unstable Q-wave ischemia angina AMI Non-ST-segment elevation AMI
The Normal Heart - Coronary Artery Anatomy Left Main CA Layers of the Arterial Wall Circumflex Adventitia Media Intima Right CALeft Anterior Descending CA Marginal Branch Intima composed of endothelial cells
Atherosclerosis: A Progressive Process Plaque Ischemia Occlusive Rupture/ Unstable Fibrous Fissure & Fatty Atherosclerotic Thrombosis Angina Normal Streak Plaque Plaque Thrombus formation MI Coronary vasospasm Coronary Death StrokePHASE I: Initiation PHASE II: Progression PHASE III: Complication Critical Leg Ischemia Disease progression Libby P. Circulation. 2001;104:365-372.
1) FATTY STREAK (non- palpable, but a visible YELLOW streak)2) ATHEROMA (plaque) (palpable)3) THROMBUS (non- functional, symptomati c)
Coronary Artery Pathology in Ischemic Heart Disease PlaqueSyndrome Stenoses Disruption Plaque-Associated ThrombusStable angina >75% No NoUnstable angina Variable Frequent Nonocclusive, often with thromboemboliTransmural Variable Frequent Occlusivemyocardial infarctionSubendocardial Variable Variable Widely variable, may be absent,myocardial infarction partial/complete, or lysed FrequentSudden death Usually Often small platelet aggregates or thrombi severe and/or thromboemboli
Correlation of CT angiography of thecoronary arteries with intravascular Non-calcified, soft, lipid-rich plaque inultrasound illustrates the ability of MDCT left anterior descending artery (arrow) .to demonstrate calcified and non-calcified The plaque was confirmed bycoronary plaques (Becker et al., Eur J intravascular ultrasound (Kopp et al.,Radiol 2000) Radiology 2004)
Pathophysiology of ISCHEMIA Ischemia of cardiac cells occurs when the oxygen supply is insufficient to meet metabolic demands. Myocardial cells are unable to store much energy in the form of adenosine triphosphate (ATP) and must therefore continuously receive a supply of oxygen for aerobic synthesis of ATP. ATP is essential for powering myocardial construction as well as for cell maintenance. Because the heart is unable to slow its activity when ATP supplies dwindle, it is essential that a steady flow of oxygen be provided.
Critical factors in meeting cellular demands for oxygen are: the rate of coronary perfusion the myocardial workload can be impaired in next ways depends on Large, stable Vasospasm Heart rateatherosclerotic plaque PreloadAcute platelet aggregation Poor perfusion and thrombosis pressure AfterloadFailure of autoregulation Contractility by the microcirculation
ANGINA PECTORIS• Par oxysmal (sudden)• Recur r ent• 15 sec.15 min.• Reduced perfusion, but NO infar ction• THREE TYPES • STABLE: relieved by rest or nitroglycerin • PRINZMETAL: SPASM is main feature, responds to nitro, S-T elevation • UNSTABLE (crescendo, PRE-infarction, Q-wave angina): perhaps some thrombosis, perhaps some non transmural necrosis, perhaps some embolization, but DISRUPTION of PLAQUE is universally agreed upon
Chest Pain First symptom of those suffering myocardial ischemia. Called angina pectoris (angina – “pain”) Feeling of heaviness, pressure Moderate to severe In substernal area Often mistaken for indigestion May radiate to neck, jaw, left arm/ shoulderDue to : Accumulation of lactic acid in myocytes or stretching of myocytes
Stable angina pectoris Caused by chronic coronary obstruction Recurrent predictable chest pain Gradual narrowing and hardening of vessels so that they cannot dilate in response to increased demand of physical exertion or emotional stress Lasts approx. 3-5 minutes Relieved by rest and nitrates Stress test shows ST segment depression > 1mm
Prinzmetal angina pectoris (Variant angina) Caused by abnormal vasospasm of normal vessels (15%) or near atherosclerotic narrowing (85%) Occurs unpredictably and almost exclusively at rest. Often occurs at night during REM sleep (rapid eye movement) May result from hyperactivity of sympathetic nervous system, increased calcium flux in muscle or impaired production of prostaglandin Vasoconstriction is due to platelet thromboxane A2 or an increase in endothelin This causes a pattern of ST elevation that is very similar to acute STEMI — i.e. localised ST elevation with reciprocal ST depression occurring during episodes of chest pain. However, unlike acute STEMI the ECG changes are transient, reversible with vasodilators and not usually associated with myocardial necrosis. They may be impossible to differentiate on the ECG. ST elevation myocardial infarction (STEMI)
Silent Ischemia Totally asymptomatic May be due abnormality in innervation Or due to lower level of inflammatory cytokines
blockers: Block sympathetic input, so Decrease heart rate, so Decrease oxygen demand Digitalis Increases the force of contraction Calcium channel blockers Antiplatelet agents (aspirin, etc.)
Surgical treatment• Angioplasty – mechanical opening of vessels• Revascularization – bypass • Replace or shut around occluded vessels
ACUTE CORONARY SYNDROMES “The acute coronary syndromes are frequently initiated by an unpredictable and abrupt conversion of a stable atherosclerotic plaque to an unstable and potentially life- threatening atherothrombotic lesion through superficial erosion, ulceration, fissuring, rupture, or deep hemorrhage, usually with superimposed thrombosis.”
Unstable Angina pectoris Lasts more than 20 minutes at rest, or rapid worsening of a pre-existing angina May indicate a progression to M.I.Pathogenesis: Severe, fixed, multivessel atherosclerotic disease Disrupted plaques with or without platelet nonocclusive thrombi
The ECG above belongs to a patient with unstable angina pectoris. Negative T pectoriswaves are observed in leads C2-C5 while negative U waves are seen in leads C2-C4. Additionally, the PR interval is above 200 msec (1st degree AV block).Coronary angiography showed significant stenosis of the LAD and Circumflex(Cx) arteries
Sudden cardiac death (SCD) 1. Inexpected death within 1 hour after the onset of symptoms2. Risk factors a. Obesity b. Glucose intolerance c. Hypertension d. Recent non-Q wave myocardial infarction e. Smoking3. Occurs more frequently in the morning hours when hypercoagiilability is at its peack4. Pathogenesis a. Severe atheroselerotic coronary artery disease b. Disrupted filimns plaques c. Absence of occlusive vessel thrombus (>80%; of cases) d. Cause of death is ventricular fibrillation. 5. Diagnosis of exclusion after the following causes are ruled out a. Mitral valve prolapse (MVP) b. Hypertrophic cardiomyopathy c. Calcific aortic stenosis d. Conduction system abnormalities e. Cocaine abuse
Acute myocardial infarction (AMI)1. Epidemiology a. Most common cause of death in adults in the United States. b. Prominent in males between 40 and 65 years old c. No predominant sex predilection after 65 years old d. At least 25% of AMIs are clinically unrecognized.
Myocar dial Ischemia Myocardial cell metabolic demands not met Time frame of coronary blockage: 10 seconds following coronary block Decreased strength of contractions Abnormal hemodynamics See a shift in metabolism, so within minutes: Anaerobic metabolism takes over Get build-up of lactic acid, which is toxic within the cell Electrolyte imbalances Loss of contractibility
20 minutes after blockage Myocytes are still viable, so If blood flow is restored, and increased aerobic metabolism, and cell repair, →Increased contractilityAbout 30-45 minutes after blockage, if no relief Cardiac infarct & cell death
Myocardial infarction Necrosis of cardiac myocytes – Irreversible – Commonly affects left ventricle – Follows after more than 20 minutes of ischemia
Pathogenesisa. Sequence 1) Sudden disniptinn of an atheromatous plaque 2) Subendothelial coliagen and thrombogenic necrotic material are exposed. 3) Platelets adhere to the exposed material and eventually form an occlusive platelet thrombus.b. Role of thromboxane A2 1) Contributes to formation of the platelet thrombus 2) Causes vasospasm of the artery to reduce blood flow
PATHOPHYSIOLOGY Coronary artery cannot supply enough blood to the heart in response to the demand due to CAD Within 10 seconds myocardial cells experience ischemia Ischemic cells cannot get enough oxygen or glucoseMyocardium Infarction Ischemic myocardial cells may have decreased electrical & muscular function Cells convert to anaerobic metabolism. Cells produce lactic acid as waste Pain develops from lactic acid accumulation Pt feels anginal symptoms until receiving demand increase 02 requirements of myocardial cells
Types of myocardial infarctiona. Transmural infarction (Qwave infarction)• 1) Involves the full thickness of the myocardium• 2) New Q waves develop in an electrocardiogram (ECG).b. Subendocardial infarction (non-Q wave infarction)• 1) Involves the inner third of the myocardium• 2) Q waves are absent.
Reperfusion injury a. Follows thrombolytic (fibrinolytic) therapy b. Early reperfusion salvages some injured but viable myocytes but destroys myocytes that are irreversibly damaged.1) Removal of irreversibly damaged myocytes improves short- and long-term function and survival.2) Prevents any further damage to myocardial cells3) Limits the size of the infarction c. Reperfusion histologically alters irreversibly damaged cells.1) Produces contraction band necrosis2) Caused by hyporcontraction of myofibrils in dying cells • Due to the influx of Ca-++ into the cytosol
RE-PERFUSION Thrombolysis PTCA CABG Reperfusion CANNOT restore necrotic or dead fibers, only reversibly injured ones REPERFUSION “INJURY” Free radicals Interleukins
Consequences after acute coronary artery occlusionBlood flow M. Ischemia Chest discomfort PMVT, VF M.stunning Heart failure STEMI NSTEMI ,UA Sudden Cardiogenic Elevated Death shock +CK,Trop-T Cardiovascular Research & Prevention Center, Bhumibol Adulyadej hospital
May hear extra, rapid Clinical Manifestations heart sounds ECG changes: T wave inversion ST segment depression
MYOCARDIAL INFARCTIONTransmural vs. Subendocardial (inner 1/3)DUH! EXACT SAME risk factors as atherosclerosisMost are TRANSMURAL, and MOST are caused bycoronary artery occlusionIn the 10% of transmural MIs NOT associated withatherosclerosis: Vasospasm Emboli UNexplained
Structural, functional changes Decreased contractility Decreased LV compliance Decreased stroke volume Dysrhythmias Inflammatory response is severe Scarring results – Strong, but stiff; can’t contract like healthy cells
Sign and Symptom Classic symptom of heart attack are chest pain radiating to neck, jaws, back of shoulder, or left arm The pain can be felt like: Squeezing or heavy pressure A tight band on the chest An elephant sitting on the chest
Other symptoms Cont include: Shortness of breath (SOB) Weakness and tiredness Anxiety Lightheadedness Dizziness Nausea vomiting Sweating, which may be profuse
Clinical manifestations Sudden, severe chest pain Similar to pain with ischemia, but stronger Not relieved by nitrates Radiates to neck, jaw, shoulder, left arm Indigestion, nausea, vomiting Fatigue, weakness, anxiety, restlessness and feelings of impending doom. Abnormal heart sounds possible (S3,S4)
Blood test show several markers: Leukocytosis Increased blood sugar Increased plasma enzymes Creatine kinase Lactic dehydrogenase Aspartate aminotransferase (AST or SGOT) Cardiac-specific troponin
Laboratory diagnosis of AMI I. Serial testing for creatine kinase isoenzyme MB (CK-MB)1) CK-MB appears within 4 to 8 hours; peaks at 24 hours; disappears within 1.5 to 3 days. • Sensitivity and specificity 95%,2) Reinfarction a) Occurs in 10% of AMIs b) Reappearance of CK-MB after 3 days II. Serial testing for cardiac troponins I (cTnl) and T (cTnT)1) Normally regulate calcium-mediated contraction2) cTnl and cTnT appear within 3 to 12 hours: peak at 24 hours; disappear within 7 to 10 days. a) Sensitivity 84% to 96%, specificity 80% to 95% b) False positive results are lisually related to ischemia (e.g., unstable angina),3) CK-MB is used in conjunction with troponins to diagnose an AMI. a) Detects reinfarction (troponins cannot) b) Improves overall sensitivity and specificiry in diagnosing an AMI III. Lactate dehydrogenase (LDH)1-2 "flip"1) Normally, LDH2 is higher than LDH1. • In AMI, LDH1 in cardiac muscle is released, causing the “flip,"2) LDH1-2 • Appears within 10 hours; peaks at 2 to 3 days: disappears within 7 days3) This test has been replaced by troponins I and T.
Treatment First 24 hours crucial Hospitalization, bed rest ECG monitoring for arrhythmias Pain relief (morphine, nitroglycerin) Thrombolytics to break down clots Administer oxygen Revascularization interventions: by- pass grafts, stents or balloon angioplasty
AMI DIAGNOSIS• SYMPTOMS• EKG• DIAPHORESIS• (10% of MIs are “SILENT” with Q-waves)• CKMB gold standard enzyme• Troponin-I, Troponin-T better• CRP predicts risk of AMI in angina patients
Primary Management Techniques• Heart Attack Treatment• First you must conduct a primary survey of the casualty;• A primary survey consists of following the DRABCD procedure, this involves; • D = DANGER – If I find a heart attack casualty I should check for any surrounding danger to myself first and for the casualty and others • R = Response – I should asses whether the person is conscious or unconscious using the COWS procedure; -Can you hear me, -Open your eyes, -What is your name, -Squeeze my hand. • A = Airways - After response if the casualty is unconscious I should then check the airways for any obstructions or blockages and if there is a blockage turn the victim onto his/her side and clear the airway. • B = Breathing – The next step if the patient is unconscious is to check for signs of life. Check for breathing by using look, listen and feel technique. If breathing place the casualty in recovery position, if not give 2 rescue breaths and... • C = Compressions - If the casualty is unconscious with no breathing, start compressions immediately! Give 30 compressions. At a rate of 100 compressions per minute (approx 2 compressions per second). At 1/3 depth of the casualty’s chest. • D = Defibrillation - If available use a defibrillator on the casualty as soon as possible.
Definitions• Cardiac Output: (Q) = HR X SV• Cardiac Index = Q / body surface area• Preload: (EDV) volume of the left ventricle at the end of diastole (dependent on venous return & stretch of the cardiac muscle cells)• Afterload: resistance to ventricular emptying during systole (the amount of pressure the left ventricle must generate to squeeze blood into the aorta)• Frank Starling Law of the Heart:the heart will contract with greater force when preload (EDV) is increased• Myocardial Contractility: the squeezing contractile force that theheart can develop at a given preload • regulated by: • sympathetic nerve activity (most influential) • catecholamines (epinephrine norepinephrine) • amount of contractile mass • drugs
Don’t wait for a heart attack to take an action ! Don’t wait for a second life we are not cats!
References1. General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin – Vinnytsia: Nova Knuha Publishers – 2011. – P.460–478.2. Russell J. Greene. Pathology and Therapeutics for Pharmacists. A basis for clinical pharmacy practice / Russell J. Greene, Norman D. Harris // Published by the Pharmaceutical Press An imprint of RPS Publishing 1 Lambeth High Street, London SE1 7JN, UK 100 South Atkinson Road, Suite 200, Greyslake, IL 60030-7820, 3rd edition, USA. – 2008. – Chapter 4. – P. 166–207, 235–269 .3. Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins), Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. – Chapters 14, 17, 18. – P. 231–303, 308–338.4. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publishing. – 2010. – P. 344–351.5. Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko, I.P. Gurcalova // Study guide for medical students and practitioners. Edited by prof.Zaporozan, OSMU. – Odessa. – 2005.– P. 207–221.6. Silbernagl S. Color Atlas of Pathophysiology / S. Silbernagl, F. Lang // Thieme. Stuttgart. New York. – 2000. – P. 194–205, 216–233.7. Corwin Elizabeth J. Handbook of Pathophysiology / Corwin Elizabeth J. – 3th edition. Copyright В. – Lippincott Williams & Wilkins – 2008. – Chapter 13. – P. 292–298, 345–347, 414–429, 447–462.8. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L. Banasic // Elsevier Inc. – 2010. – P. 396–427, 448–509.9. Robbins and Cotran Pathologic Basis of Disease 8th edition./ Kumar, Abbas, Fauto. – 2007. – Chapter 11. – P. 379–398, 400–420.10. Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn Matfin. – New York, Milwaukee. – 2009. – P. 536–553, 584–633.
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