Cardiac Pathology I PDF

Cardiac Pathology I Geoffrey Talmon, M.D., M.Ed. [email protected] Overview ◼ 1st hour: ◼ Congestive Heart Failure ◼ Cor Pulmonale ◼ Ischemic Heart Disease ◼ 2nd hour: ◼ Hypertensive Heart Disease ◼ Valvular Heart Disease ◼ 3rd hour: ◼ Primary Myocardial Dis...

Cardiac Pathology I Geoffrey Talmon, M.D., M.Ed. [email protected] Overview ◼ 1st hour: ◼ Congestive Heart Failure ◼ Cor Pulmonale ◼ Ischemic Heart Disease ◼ 2nd hour: ◼ Hypertensive Heart Disease ◼ Valvular Heart Disease ◼ 3rd hour: ◼ Primary Myocardial Diseases ◼ Congenital Heart Diseases ◼ Pericardial Diseases ◼ Cardiac Tumors The Heart of the Matter A Review of Basic Anatomy and Function The heart is a muscular pump with one responsibility: Providing adequate blood flow to all tissues of the body. It is located within the mediastinum. It is encased in a fibrous sac (pericardium). Wall has three layers: ▪ Epicardium (outer surface) ▪ Myocardium (muscle) ▪ Endocardium (inner surface) >86,000 beats per day ~ 6000L of blood circulated per day The Heart of the Matter A Review of Basic Anatomy and Function There are four cardiac chambers separated by valves. Two connected, but independent sides. Right Side: ▪Low Pressure System / Low Oxygen ▪Outflow to Lungs Left Side: ▪ High Pressure System / High Oxygen ▪ Outflow to Body The amount of blood pumped by both sides per unit time is equal and the heart can usually pump all of the blood that is returned to it. The Cardiovascular System 02 C02 waste “Afterload" “Preload" Systemic Circulation *Preload = Afterload Rules of Cardiac Pathology ◼ The harder the heart works (more pressure), the moreblood supply it needs ◼ When subjected to increased volume or pressure for extended periods of time, cardiac muscle enlarges (like your biceps) ◼ In adulthood the heart may grow in size, but its blood supply does not ◼ A ventricle can only hypertrophy so much before it dilates and becomes dysfunctional ◼ Any structural disease to the heart makes it electrically unstable and prone to arrhythmias Congestive Heart Failure (CHF) ◼ Symptom complex (descriptive term) ◼ “CHF” tells you nothing of the cause ◼ Heart failure means: Heart cannot provide enough flow to meet the demands of the body And/Or Heart cannot pump all of the blood that is returned to it Congestive Heart Failure (CHF) ◼ Symptoms develop due to: ◼ Forward Failure: not enough blood flow to tissues resulting in fatigue, renal insufficiency, tissue hypoxia, etc. ◼ Reverse Failure: back up of venous return (“congestion”) with expression of fluid into surrounding tissue (edema) ◼ Clinically divided into right heart failure and left heart failure: ◼ Right Sided Failure: peripheral edema, ascites, pleural effusions, stasis dermatitis ◼ Left Sided Failure: pulmonary edema with dyspnea, cough, hemoptysis, “paroxysmal nocturnal dyspnea,” orthopnea Causes of Congestive Heart Failure (CHF) (Mechanisms to be Discussed Later) ◼ Left Sided Heart Failure: ◼ Hypertension ◼ Valvular disease ◼ Ischemic heart disease (coronary artery disease) ◼ Cardiomyopathies ◼ Right Sided Heart Failure: ◼ Left Sided Heart Failure ◼ Lung Disease (“Cor Pulmonale”) ◼ Congenital Heart Disease Progression of CHF ◼ Compensation– make the pump “better” ◼ Increased sympathetic tone (Epinephrine/Norepinephrine) ◼ Increased contraction force (“inotropic”) ◼ Increased preload (venous return) ◼ Stretch the muscle = more pumping power (for a while) ◼ Aldosterone: increase amount of fluid in blood vessels ◼ Hypertrophy ◼ more muscle myofibrils = more pumping power ◼ Decompensation– (the above was not enough) ◼ Ventricular dilation too much, heart becomes flabby ◼ Dilation of the heart causes and extra heart sound (S3) ◼ A dilated heart is electrically unstable (seelater) Why does increasing Preload work? Normal Compensated Decompensated Increased preload Too much stretch Increased stretch Decreased power Increased power Onset of CHF C02 waste 02 “Afterload" “Preload" Systemic Circulation *Preload > Afterload Compensated CHF C02 waste 02 “Afterload" “Preload" Systemic Circulation *Preload > Afterload Output is back to normal Decompensated CHF C02 waste 02 “Preload" “Afterload" Systemic Circulation *Preload > Afterload Too Much Back Up/Stretch Decreased Output Cor Pulmonale ◼ Heart disease caused by lung disease ◼ Therefore, LV is usually not affected ◼ Elevations in pulmonary circulation pressure (right sided) lead to right ventricular hypertrophy, then dilation, then failure ◼ Disorders that predispose to cor pulmonale ◼ diseases of the lung ◼ diseases of pulmonary vessels ◼ disorders affecting chest movement ◼ disorders inducing pulmonary arteriolar constriction ◼ Most common cause is chronic obstructive pulmonary disease Cor Pulmonale Ischemic Heart Disease ◼ Damage to myocardium caused when supply of blood not adequate to meet needs (demand > supply) ◼ Most commonly caused by occlusion of coronary arteries, usually by atherosclerosis (90%)-- a.k.a.- “coronary artery disease” ◼ Other causes– hypovolemia, emboli, drugs, infection, etc. Ischemic Heart Disease 02 C02 waste “Afterload" “Preload" Systemic Circulation *Preload = Afterload The Coronary Arteries ◼ Heart supplied by three main coronary arteries: ◼ LAD- anterior wall, anterior 2/3 of IVS, apex ◼ LCX- lateral LVFW ◼ RCA- RV, post. 1/3 IVS, conduction system ◼ The artery affected dictates damage location and presentation ◼ In atherosclerosis, often >1 artery affected Ischemic Heart Disease ◼ Why do we care? ◼ Leading cause of death for adult men and women ◼ 1.5 M people have a myocardial infarction per year ◼ 500,000 per year die of IHD ◼ 250,000 per year die before reaching the hospital Ischemic Heart Disease ◼ Usually long-standing narrowing of coronary arteries by atherosclerotic plaque before presentation. ◼ Four presentations: ◼ Angina pectoris ◼ Stable ◼ Unstable ◼ Acute myocardial infarction ◼ Sudden cardiac death ◼ Congestive heart failure Ischemic Heart Disease ◼ Symptoms appear when artery is >75% occluded ◼ 2 months Complications of AMI ◼ 80-90% of patients suffer some complication ◼ 25% suffer “sudden cardiac death” (see later) ◼ Arrhythmias (most common in 24-48 hours)– 75-95% of patients ◼ sinus bradycardia ◼ Ventricular tachycardia/fibrillation ◼ asystole ◼ Myocardial rupture-- 4-8% of patients ◼ mechanical weakening of necrotic/inflamed myocardium ◼ Most common at 7-10 days after infarct ◼ rupture of the ventricular free wall (most common) or ventricular septum ◼ papillary muscle rupture (least common) Complications of AMI Rupture of the Ventricular Papillary Muscle Rupture of Ventricular Free Wall Rupture Septum Complications of AMI ◼ Pericarditis ◼ A fibrinous or fibrohemorrhagic pericarditis ~2-3 days post AMI ◼ Mural thrombus ◼ Due to inability to pump efficiently, stasis of blood may occur. ◼ The damaged endocardial surface is a thrombogenic surface which may foster mural thrombi and possible thromboemboli ◼ Ventricular aneurysm ◼ Usually a result of a large transmural anteroseptal infarct that heals into a thin piece of tissue ◼ Papillary muscle dysfunction ◼ Resulting in post infarct regurgitation Clinical Features of AMI ◼ Angina >30 minutes (20-30% are “silent”) ◼ Dyspnea ◼ Tachycardia ◼ Diaphoresis ◼ Acute-onset congestive heart failure ◼ Cardiogenic shock ◼ Usually when 40% of LV affected ◼ Arrhythmias Clinical Features of AMI ◼ EKG changes: ◼ Q waves (old AMI) ◼ ST-segment elevation (acute MI) ◼ T wave inversion ◼ Cardiac enzyme elevations ◼ Change in a defined sequence/timeframe ◼ Measured serially every 8 hours x 3 ◼ Usually positive within 4-6 hours ◼ Troponin I is most specific Chronic Ischemic Heart Disease ◼ Progressive myocardial damage caused by moderate to severe atherosclerosis (years) ◼ Can be punctuated by AMI(s) ◼ Leads to progressive heart failure– common cause of transplantation ◼ Features: ◼ Dilation of all cardiac chambers ◼ Myocardial fibrosis ◼ Hypertrophy Sudden Cardiac Death ◼ Death within 24 hours of symptom onset ◼ Often no preceding symptoms ◼ Often no proximate cause– patient “went down in the community” ◼ Attributed to sudden onset of arrhythmia that does not allow for sufficient cardiac output to support life. ◼ Rule out other causes of sudden death: ◼ Pulmonary embolism ◼ Ruptured cerebral aneurysm ◼ Ruptured aortic aneurysm Sudden Cardiac Death ◼ AMI (“heart attack”) is not synonymous with SCD ◼ Any structural heart lesion can predispose to arrhythmia ◼ Scars, interstitial fibrosis, inflammation, ventricular dilation, areas of myocardial infarction ◼ Lesions related to coronary artery disease or HTN are the most common etiologies Rules of Cardiac Pathology ◼ The harder the heart works (more pressure), the moreblood supply it needs ◼ When subjected to increased volume or pressure for extended periods of time, cardiac muscle enlarges like your biceps ◼ In adulthood the heart may grow in size, but its blood supply does not ◼ A ventricle can only hypertrophy so much before it dilates and becomes dysfunctional ◼ Any structural disease to the heart makes it electrically unstable and prone to arrhythmias University of Nebraska Medical Center·M BREAKTHROUGHS FORLIFE.® NeoiasKa MedicalCenter