Lecture 43 Coronary Artery Disease Pathophysiology Klassen INTRODUCTION: HEART: Pumps blood through 2 main circuits o Pulmonary circulation o Systemic circulation Supply (diastolic) vs. demand (systolic) Heart blood supply: coronary arteries o Oxygenated blood for heart function HEART ANATOMY: Triple (3) layer construction: o Endocardium: inner layer interacting with blood o Myocardium: muscular layer of cardiomyocytes o Epicardium: outer layer of support tissue Pericardium: double walled sac with minimal fluid b/w layers o Structural and nutritional support o Limit heart volume (overfilling) END CIRCULATION: limited redundancy in blood supply to heart Left coronary artery: left ventricle/atrium o Left anterior descending artery: anterior wall/septum (2/3 supply) o Left circumflex artery: left ventricle Right coronary artery: right ventricle/atrium o Right posterior descending artery: posterior of septum (1/3 supply) o Acute marginal arteries: whole right ventricle o Supply to pacemaker (sinoatrial and atrioventricular nodes) ISCHEMIC HEART DISEASE: MYOCARDIAL ISCHEMIA: Inadequate blood supply (O2) o Imbalance: ischemia = O2 supply < O2 demand Impact greatest on myocardium (highest O2 demand for function) o Demand: exercise, exertion o Supply: blockage/constriction o Both can occur simultaneously > 98% from coronary artery disease o Atherosclerosis of coronary artery wall thickening and blockage Impairment of heart function o Insufficient oxygen o Limited nutrients o Build of metabolites/waste IMBALANCE IN SUPPLY VS. DEMAND: RISK FACTORS: Lifestyle Disease Genetics Age (men > 60, women > 65) Stress Diet Inactivity Obesity Smoking Stroke Peripheral vascular disease (vascular damage) Hypertension (high systolic) Hypercholesteremia (cholesterol deposits/artery narrowing) Hyperglycemia (DM) Family history of CVD Ethnicity CLASSIFICATION: Acute coronary syndrome (ACS) o Unstable angina – changing/worsening chest pain o Myocardial infarction – heart attack o Sudden cardiac death – heart cessation Chronic coronary artery disease (CCAD) o Stable angina – chest pain after exertion o Coronary artery disease
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Pumps blood through 2 main circuits o Pulmonary circulation o Systemic circulation
Supply (diastolic) vs. demand (systolic)
Heart blood supply: coronary arteries o Oxygenated blood for heart
function
HEART ANATOMY:
Triple (3) layer construction: o Endocardium: inner layer interacting with blood o Myocardium: muscular layer of cardiomyocytes o Epicardium: outer layer of support tissue
Pericardium: double walled sac with minimal fluid b/w layers o Structural and nutritional support o Limit heart volume (overfilling)
END CIRCULATION: limited redundancy in blood supply to heart
Left coronary artery: left ventricle/atrium o Left anterior descending artery: anterior wall/septum (2/3 supply) o Left circumflex artery: left ventricle
Right coronary artery: right ventricle/atrium o Right posterior descending artery: posterior of septum (1/3 supply) o Acute marginal arteries: whole right ventricle o Supply to pacemaker (sinoatrial and atrioventricular nodes)
Impact greatest on myocardium (highest O2 demand for function) o Demand: exercise, exertion o Supply: blockage/constriction o Both can occur simultaneously
> 98% from coronary artery disease o Atherosclerosis of coronary artery wall
thickening and blockage
Impairment of heart function o Insufficient oxygen o Limited nutrients o Build of metabolites/waste
Transmural infarction: full thickness of ventricular wall; complete occlusion of blood supply to region
Subendocardial infarction: inner 1/3 to 1/2 of ventricular wall
MI SYMPTOMS:
Angina (chest pain) o Common sx BUT 20% are silent o Dull radiating pain (left side dominant)
Shortness of breath
Excessive sweating
Nausea/vomiting
FACTORS IMPACTING SIZE OF INFARCT REGION:
Severity & duration of ischemia
Location of block o Main vs. peripheral branches
Metabolic needs of region o Left ventricle requires more O2
Regions with fewer collateral blood vessels have > risk of damage
Heart rate/rhythm/blood pressure o Challenge supply/demand balance
MI CLINICAL COMPLICATIONS:
Contractile dysfunction: irreversible damage to myocardium
Arrhythmia: irregular contraction rhythm
Mural thrombus: perpetual clot on heart chambers that disrupt normal blood passage inefficient/working harder
Myocardial rupture: mechanical weakness in heart wall so there’s increased heart effort to accommodate O2 lack heart bursts/ruptures
Pericarditis: swollen pericardial sac that rubs on heart and chest with beats = chest pain (changes with body position) o Post infarct = 24 hrs post MI
Dressler’s Syndrome: onset week months post MI
CHRONIC MI CARDIAC FAILURE:
Progressive heart failure o Ischemic damage to myocardium o Hypertrophy: enlarged heart & ventricular walls
Compensation for absent/dead cardiomyocytes
Cardiac failure o Insufficient pumping to maintain blood flow to body
SUDDEN CARDIAC DEATH: natural, rapid and unexpected death (can occur w/o sx OR within 1 hr of sx onset) LETHAL VENTRICULAR ARRYTHMIA