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PATHOLOGY OF THE CARDIOVASCULAR SYSTEM Normal Structure and Function Response to Injury Shannon Martinson, 2017 VPM 222 – Systemic Pathology II http://people.upei.ca/smartinson/ PATHOLOGY OF THE CARDIOVASCULAR SYSTEM • There are excellent tutorials and quizzes available at : • http://people.upei.ca/lopez Miller, LM and Gal, A. Cardiovascular System and Lymphatic Vessels: In, Pathological Basis of Veterinary Disease, 6th Edition. Zachary Ed. Elsevier. 2017 INTRODUCTION: STRUCTURE AND FUNCTION RA LA • The heart is the first organ to form in the embryo • Mammalians and birds have 4 chambers: • Left atrium • Right atrium • Right ventricle • Left ventricle RV LV Reptiles – 1 ventricle INTRODUCTION: STRUCTURE AND FUNCTION Function - maintain adequate blood flow (cardiac output) to deliver oxygen and nutrients and remove waste INTRODUCTION: STRUCTURE AND FUNCTION The heart is composed of three layers: 1. Pericardium (Epicardium) 2. Myocardium (Heart muscle) 3. Endocardium (includes valves) Myocardium Endocardium Epicardium INTRODUCTION: STRUCTURE AND FUNCTION Epicardium and Pericardium Visceral Pericardium = Epicardium Parietal Pericardium INTRODUCTION: STRUCTURE AND FUNCTION Epicardium and Pericardium Epicardial surface – pericardial space Epicardium PBVD Zachary, 2017 Myocardium INTRODUCTION: STRUCTURE AND FUNCTION Myocardium Myocardium INTRODUCTION: STRUCTURE AND FUNCTION Myocardium • Myocardiocytes • Involuntary striated muscle • Arranged in sarcomeres • Branched fibers connect via intercalated discs • Contain↑ # mitochondria • Left ventricular myocardial thickness is ~ 2 – 4 times thicker than the right • Due to higher pressure on the left side • Purkinje cells • Modified myocardiocytes function in conduction INTRODUCTION: STRUCTURE AND FUNCTION Endocardium • Inner lining and the valves • Equivalent to the tunica intima of BV • Close contact with blood • Important in hemostasis Endocardium INTRODUCTION: STRUCTURE AND FUNCTION Endocardium • 3 layers 1. Endothelium 2. Basal lamina 3. Subendothelial connective tissue Endocardium Purkinje Fiber • Also contains part of the conductive system and Purkinje fibers Myocardium INTRODUCTION: STRUCTURE AND FUNCTION Endocardium • There are four cardiac valves: 1. Right atrio-ventricular (Tricuspid) 2. Pulmonic 3. Left atrio-ventricular (Mitral) 4. Aortic Right A-V valve Prevent backflow in the heart Right heart Pulmonic valve INTRODUCTION: STRUCTURE AND FUNCTION Endocardium Left A-V valve • There are four cardiac valves: 1. Right atrio-ventricular (Tricuspid) 2. Pulmonic 3. Left atrio-ventricular (Mitral) 4. Aortic Left heart Aortic valve INTRODUCTION: STRUCTURE AND FUNCTION Endocardium • Thin, translucent and shiny INTRODUCTION: STRUCTURE AND FUNCTION Endocardium • AV valves attach to the papillary muscles via the chordae tendineae Valve Chordae tendineae Papillary muscle POSTMORTEM EXAMINATION OF THE HEART Silhouette in situ Shape Size Weight Color Pericardial fluid Fat deposits Coronary vessels Wall thickness Valves Endocardium Great vessels POSTMORTEM EXAMINATION OF THE HEART Differentials for an enlarged cardiac silhouette: • Cardiomegaly • Tumor • Cardiac effusions • Hydropericardium • Hemopericardium • Pericarditis Pay attention to the relative size of the cardiac silhouette! POSTMORTEM EXAMINATION OF THE HEART Differentials for an enlarged cardiac silhouette: • Cardiomegaly • Tumor • Cardiac effusions • Hydropericardium • Hemopericardium • Pericarditis Pay attention to the relative size of the cardiac silhouette! POSTMORTEM EXAMINATION OF THE HEART When opening the pericardium – pay attention to the content. POSTMORTEM EXAMINATION OF THE HEART When opening the pericardium – pay attention to the content. POSTMORTEM EXAMINATION OF THE HEART • Examine the heart in situ before removing it • Pay careful attention in young animals to look for congenital defects • Check the epicardium, epicardial fat stores and great vessels Lymphatic vessels may be visible POSTMORTEM EXAMINATION OF THE HEART • Evaluate the myocardium and endocardium • Samples for histopathology • Routine: LV, RV and IVS • Full thickness • +/- Atria , +/- Valves/ +/- Conduction system RESPONSE TO INJURY • Healing is limited • Compensatory mechanisms: • Activation of neurohumoral mechanisms • Cardiac dilation • Cardiac hypertrophy Depression in Cardiac Output Release of norepinephrine Redistribution /↓ renal blood flow ↑ADH ↑ HR and contractility + vasoconstriction ↑Renin / Angiotensin /Aldosterone ↑Retention of water ↑Na water reabsorption + Vasoconstriction ↑blood volume Expansion of the blood volume induces secretion of atrial natriuretic peptide: Induces Na and water excretion and vasodilation RESPONSE TO INJURY Normal Increased Heart Rate (beats/min) Cardiac output = heart rate x stroke (blood) volume Cardiac Dilation -Increased stroke volume Myocardial hypertrophy - Greater contractility and ejection force Cardiac hypertrophy and dilation are beneficial to a point RESPONSE TO INJURY - CARDIAC DILATION • Myocardial fibers stretch: • ↑ Contractile force • ↑ Stroke volume • ↑ Cardiac output • ↑ Contractile force has a limit • ↑ stretch causes ↓ tension • Chronically - addition of sarcomeres and lengthening of myocytes. • Acute volume overload leads to dilation • Chronic volume overload causes hypertrophy Response to ↑ workload in both physiologic or pathologic states RESPONSE TO INJURY - CARDIAC HYPERTROPHY Increase in heart mass due to increased cell size • Primary cardiac hypertrophy (=cardiomyopathy) • Primary (idiopathic) disease of the myocardium • Secondary cardiac hypertrophy • Due to sustained ↑ in cardiac workload • Volume overload • Pressure overload • Due to trophic signals (hyperthyroidism) • Limited benefit – eventually develop: • Impaired intrinsic contractility • Impaired ventricular relaxation • Decreased compliance • Can be right or left sided or biventricular • Can also be classified as: • Eccentric • Concentric RESPONSE TO INJURY - CARDIAC HYPERTROPHY Eccentric Concentric Images: Maxie, Pathology of Domestic Animals, 2015 RESPONSE TO INJURY - CARDIAC HYPERTROPHY Eccentric Note thin ventricular wall (line) and distended ventricle (arrow) Concentric Note thick ventricular wall (line) and reduced ventricular space (arrow) RESPONSE TO INJURY - CARDIAC HYPERTROPHY Eccentric Note thin ventricular wall (line) and distended ventricle (arrow) Concentric Note thick ventricular wall (line) and reduced ventricular space (arrow) RESPONSE TO INJURY - CARDIAC HYPERTROPHY Gross changes Heart Side Right Left Bi-ventricular Normal Gross Changes Broad base Increased length Globose (rounded) Right Underlying cause (egs) Pulmonic stenosis, pulmonary hypertension Aortic stenosis, feline hyperthyroidism HCM, tetralogy of Fallot Left Biventricular RESPONSE TO INJURY - CARDIAC HYPERTROPHY Cellular stages in cardiac hypertrophy: 1. Initiation: Increase cell size (sarcomeres / mitochondria) 2. Compensation: Stable hyperfunction with no clinical signs 3. Deterioration: Degeneration of hypertrophied cardiomyocytes and loss of contractility followed by heart failure Histology • ↑ Size of cardiomyocytes • +/- Dissarray With chronicity: • Cardiomyocytes loss • Fibrosis CARDIAC DYSFUNCTION AND FAILURE No clinical disease Heart Disease Lesion at necropsy Clinically detectable but no heart failure Uncompensated Congestive heart failure (fluid accumulation, edema) Heart failure Acute heart failure (collapse, weakness) CONGESTIVE HEART FAILURE Decreased contractibility of myocardial fibres (myocardial failure) is the pathophysiological hallmark of clinical heart failure Retrograde component: Systemic/pulmonary venous stasis Anterograde component: Decreased cardiac output Often both occur together • Inability to empty the venous reservoirs ( = congestive heart failure) • Ascites • Pleural effusion • Pulmonary edema • Insufficient blood pumping into the aorta/pulmonary artery ( = low output heart failure) • Depression • Lethargy • Syncope • Hypotension CARDIAC DYSFUNCTION BASIC PATHOPHYSIOLOGICAL MECHANISMS OF CARDIAC DYSFUNCTION AND FAILURE Change Example Pump failure Weak contractility: ↓emptying of the chambers due to myocardial damage Outflow obstruction Vascular or valvular stenosis, systemic or pulmonic hypertension Blood flow regurgitation Valvular insufficiency, endocardiosis, endocarditis, volume overload Shunted blood Congenital heart defects Restricted atrial / ventricular filling Cardiac tamponade, pericarditis, tumour Conduction disorders Arrhythmias – die to functional or structural abnormalities in the conduction system CONGESTIVE HEART FAILURE • CHF occurs when the heart is unable to pump blood at a rate sufficient to meet the metabolic demands of tissues • Can occur at the end stage of many forms of chronic heart disease • Acute hemodynamic stresses can cause CHF to appear suddenly CONGESTIVE HEART FAILURE Heart failure can be right sided, left sided or bilateral: Pulmonic stenosis Pulmonary hypertension Brisket disease Hardware disease Pulmonary fibrosis Aortic stenosis Systemic hypertension Mitral endocardiosis Mitral dysplasia Feline hyperthyroidism Tetralogy of Fallot Hypertrophic Cardiomyopathy CONGESTIVE HEART FAILURE – EXTRACARDIAC LESIONS Right sided failure Left sided failure Systemic venous congestion Pulmonary venous congestion Edema and ascites Pulmonary edema and intra-alveolar macrophages Chronic passive hepatic congestion RBCs phagocytosed by alveolar macrophages Iron in alveolar macrophages Nutmeg liver Heart failure cells CONGESTIVE HEART FAILURE – RIGHT HEART FAILURE Right sided failure 3-yr-old dog • Presented for distended abdomen (ascites) and dyspnea • 2.5 L of fluid in the abdomen and 400 ml in the thorax • Liver dark with rounded margins (hepatic congestion) • Notably enlarged heart wide on the base • RV concentric hypertrophy • Final Diagnosis: Pulmonic valve stenosis CONGESTIVE HEART FAILURE – RIGHT HEART FAILURE Image: Noah’s arkive Right sided failure Chronic passive hepatic congestion “Nutmeg Liver” CONGESTIVE HEART FAILURE – LEFT HEART FAILURE Left sided failure Aged cat • Lethargy and anorexia • Difficulty breathing • Pulmonary edema and congestion, hydrothorax • LV eccentric hypertrophy • Final Diagnosis: LAV dysplasia CONGESTIVE HEART FAILURE – LEFT HEART FAILURE Left sided failure Aged cat • Lethargy and anorexia • Difficulty breathing • Pulmonary edema and congestion, hydrothorax • LV eccentric hypertrophy • Final Diagnosis: LAV dysplasia +/- excess moderator bands Heart failure cells I would like to thank Dr A Lopez and Dr E Aburto, Atlantic Veterinary College, for their contributions to this material.