Cardiovascular Physiology Quiz

Physiopathology I - Course Information

• Course title: Physiopathology I
• Instructor: Dr. Rana CHAAYA
• Semester: Fall 2021
• University: Université Libanaise - Faculté d'agronomie Et de médecine Vétérinaire

References for Animal Pathophysiology

• Pathologic Basis of Veterinary Disease: 5th edition, Edited by James F. Zachary DVM PhD (Editor), M. Donald McGavin MVSc PhD FACVSC, Published by Elsevier.
• Essentials of Pathophysiology: 3rd edition, by Carol Mattson Porth, Published by Wolters Kluwer.
• Veterinary Pathophysiology: Edited by Robert H. Dunlop and Charles-Henri Malbert, Published by Blackwell Publishing.

Cardiovascular Diseases

• Pathophysiology I: Pathology of Organ Systems: This section covers various diseases related to organ systems, including cardiovascular diseases.
• Topics covered include: Cardiovascular Diseases, Respiratory Diseases, Nervous Diseases, Urinary Diseases.

Part 1: Cardiovascular Diseases

• Chapter 1: Dysfunction/Responses to Injury
• Chapter 2: Congenital Heart Defects
• Chapter 3: Endocardial and valvular disorders
• Chapter 4: Disorders of the Pericardium & Cardiomyopathies

Chapter 1: Dysfunction/Responses to Injury

• Blood Circulation: Describes systemic and pulmonary circulations. Diagram illustrates the flow of blood through the heart and the rest of the body excluding the lungs, showing pulmonary arteries, pulmonary veins, systemic arteries, left atrium, and right ventricle etc.

Heart Anatomy

• The heart wall has three layers: the epicardium (visceral pericardium—outer serous covering), the myocardium (thickest part, cardiac muscle), and the endocardium (inner layer of endothelium).
• Cardiac muscle fiber contraction results in the heartbeat.

What is Heart Disease?

• Cardiovascular disease is any condition affecting the heart and blood vessels that disrupt the delivery of oxygenated blood to the body.
• Heart disease can be congenital (present at birth) or acquired (develop later).
• Many heart diseases are hereditary and are common in specific breeds of animals.

Pathophysiologic Mechanisms of Cardiovascular Dysfunction

• Pump failure: Weak contractility and emptying of heart chambers, impaired filling of chambers.
• Obstruction to forward blood flow: Valvular stenosis, vascular narrowing, systemic or pulmonary hypertension.
• Regurgitant blood flow: Volume overload of the chamber behind a failing valve.
• Shunted blood flow: From congenital defects (e.g., septal defects).
• Rupture of the heart or a major vessel: Cardiac tamponade, massive internal hemorrhage.
• Cardiac conduction disorders (arrhythmias): Failure of synchronized cardiac contraction.

Dysfunction: Heart Failure

• Heart failure is a progressive clinical syndrome involving impaired pumping leading to decreased ventricular ejection and venous return.
• Heart failure can involve low-output (decreased blood pumping) or it can involve congestion (inability to empty venous reservoirs).
• Low cardiac output can cause lethargy, syncope, and hypotension.
• Congestive heart failure can cause ascites, pleural effusion, and pulmonary edema.

Syndromes of Cardiac Failure or Decompensation:

• Congestive Heart Failure (CHF) can be right-sided, left-sided, or bilateral, and can occur with cardiac dilation and/or hypertrophy.
• Right-sided CHF usually manifests with signs of systemic congestion (ascites and peripheral edema).
• Left-sided CHF presents with pulmonary congestion (pulmonary edema and dyspnea). This often shows up in small animals with pleural effusion.

Cardiac Anatomy and Dysfunction

• Cardiac Dilation and Hypertrophy: Illustrates visual and structural differences in normal, dilated, and hypertrophied hearts with diagrams (transected ventricles)
• Responses of the Myocardium to Injury: Discusses disorders resulting from circulation impairment, growth disturbances (atrophy (dilation), hypertrophy, genesis (aplasia), hypoplasia, dysplasia (dysgenesis)), cellular degeneration (cell and metabolic dysfunction, oncotic necrosis apoptosis), and inflammation
• Cardiac Output: Explains the relationship between heart rate, stroke volume, and cardiac output. Increases in heart rate initially increase cardiac output proportionally, but eventually, further increases in heart rate lower cardiac output due to insufficient diastolic filling time.

Regulation of Stroke Volume

• Preload: Volume of blood in the ventricles at the end of diastole. Increased preload stretches the heart, making contractions more efficient (Frank-Starling law),
• Afterload: Resistance the ventricle must overcome to circulate blood. Increase in afterload reduces stroke volume, as it takes more effort for the ventricle to eject blood. Causes include hypertension or vascular narrowing (e.g., arteriosclerosis).

Regulation of Stroke Volume: Contractility

• Factors increasing contractility: positive inotropic agents (e.g., glucagon, thyroxine, norepinephrine) that increase Ca2+ flow
• Factors decreasing contractility: negative inotropic agents (e.g., anoxia, acidosis, increased extracellular K+ levels, calcium channel blockers)

Regulation of Stroke Volume: Afterload

• Afterload is the pressure the heart must overcome to eject blood from the ventricles during systole.
• Factors that increase afterload (e.g., hypertension, vascular narrowing) decrease stroke volume by increasing the workload.

Systolic and Diastolic Heart Failure

• Systolic Heart Failure: Occurs when the heart has impaired ability to contract enough for proper blood ejection (ejection fraction decreased). This can be caused by Myocardial failure (primary or secondary), and volume overload. Common causes for pressure overload include aortic/pulmonic stenosis, as well as hypertension.
• Diastolic Heart Failure: The heart is unable to properly relax and fill with blood, and subsequent reduced cardiac output. This is categorized by Impaired Energy Dependent Relaxation, Obstruction, and Pericardial Abnormalities

A-Concentric Hypertrophy, B-Eccentric Hypertrophy

• Concentric hypertrophy: Occurs in pressure overload, resulting in increased resistance which leads to ventricular wall thickening and smaller chamber size to regulate wall stress.
• Eccentric hypertrophy: Occurs in volume overload, increasing chamber size and causing lesser increase in wall stress compared to concentric hypertrophy.

Neuroendocrine Compensatory Mechanisms in Heart Failure

• Chronic activation of the neuroendocrine system in heart failure causes vasoconstriction, sodium and water retention for restoring and maintaining blood pressure (ABP), leading eventually to myocardial and vascular remodeling contributing to further cardiac dysfunction and persistent neuroendocrine activation.

Role of Catecholamines in the Progression of Heart Failure

• Increased norepinephrine (NE) in the plasma is a common result of CHF.
• The increase in norepinephrine leads to depletion of NE stores in the atria and ventricles, reducing the effect of sympathetic stimulation on the myocardium.
• Changes in receptor sensitivity and decreased stores of NE result in reduced contractility and positive chronotropy, which are commonly seen progressing left heart failure.

Summary of Pathophysiology of Heart Failure

• Long-term overloaded heart leads to cardiac hypertrophy, myocardial cell death, and fibrosis (cardiomyopathy).
• Ischemia from hypertrophy and expansion can cause further issues, such as loss of contractile strength.
• These issues lead to cardiac atrophy and myocardial fibrosis, impacting diastolic function.
• Chronic heart failure (CHF) involves both systolic and diastolic dysfunction and is ultimately a progressive and irreversible disease leading to death.

Pathophysiological cycles of progressive left heart failure

• Increased vascular resistance causes Myocardial Hypertrophy
• Water and Sodium retention leads to increased preload and vascular congestion.
• Neuroendocrine activation results in myocardium and vascular remodeling

Pathophysiology of heart failure

• Shows the interconnectedness of different cycles and their cumulative effects on the heart, leading to progressively severe heart failure.