Clinical Heart PDF

Clinical Manifestations Veterinary Cardiology Brady Little, DVM, MSc Objectives: The following topics will be covered (be able to analyze, describe, and apply these topics): 1) Understand the fundamentals of cardiac auscultation 2) Identify the common causes of audible heart murmurs and their charac...

Clinical Manifestations Veterinary Cardiology Brady Little, DVM, MSc Objectives: The following topics will be covered (be able to analyze, describe, and apply these topics): 1) Understand the fundamentals of cardiac auscultation 2) Identify the common causes of audible heart murmurs and their characteristics 3) Recognize the pathophysiology of valvular insufficiencies 4) Be familiar with common cardiomyopathies 5) Comprehend the value in cardiac radiology Cardiac Auscultation Four Heart Sounds Possible Only 2 typically heard in normal small animals (may be more audible in Large) S1 = Closure of the AV valves (L&R) at the onset of ventricular Systole S2 = Closure of the Semilunar valves (Pulmonary and Aortic) at the end of ventricular systole S3 = Rapid ventricular filling during diastole. NOT normally ausculted in small animals Associated with congestive heart failure and cardiomyopathy S4 = Sound of Atrial systole. NOT normally ausculted in small animals Associated with filling of non-compliant ventricles (hypertrophic cardiomyopathy) Murmur: The sound of turbulent blood flow (ABNORMAL) 1) Abnormal flow pattern - Ex: Valvular insufficiency (valve does not close completely – allowing regurgitation) 2) Abnormal vessel diameter - Ex: narrowing (aortic stenosis) 3) Abnormal blood viscosity - Ex: Anemia causes low viscosity The Severity of Cardiac disease is NOT always linked to Severity of the murmur Some Physiology is needed to understand cardiac pathology: The volume of blood moving in circulation is the responsibility of the Heart AND the Kidneys cardiac output = Heart Rate X Stroke Volume Stroke volume can be altered by contractility AND / OR Changes in Blood volume Mitral Insufficiency - Some of the blood leaks through the valve back into the left atrium - Cardiac output (CO) goes down - Body responds by increasing HR. Initially, this is enough to bring cardiac output back to normal … but dz progresses - Now Kidneys compensate by retaining water and electrolytes → increasing blood volume and pressure → Increasing pre-load (end diastolic volume) - This will also help in short term (CO goes up), but will also increase the amount of blood regurgitated through the faulty valve - The Heart must compensate to the increased “work” → Left Ventricle enlarges to hold more volume = “Dilated Cardiomyopathy” snowball effect - End Result without therapy: - 1st Congestive heart failure - Left side of the heart cannot enlarge any more. Blood pressure continues to rise → more regurgitation occurs → pressure in the lungs increase → eventually causes fluid build up called “pulmonary edema” - 2nd Myocardial failure - Heart muscle fails to pump fluid forward. Mitral Valve insufficiency: Eventually causes a reduction of flow to the left side of the heart. - Draw it in! Right side of the heart is still pumping well R L Pulmonary circulation is congested → increase pressure of vessels inside the lungs → Pulmonary edema (fluid in the lungs) Respiratory rate and effort / Coughing Exercise tolerance Schematic drawing: 1, Left ventricle; 2, aorta; 3, capillary bed of head, neck, and forelimb; 4, abdominal aorta; 5, liver; 6, capillary bed of intestines; 7, portal vein; 8, capillary bed of kidneys; 9, capillary bed of caudal part of the body; 10, caudal vena cava; 11, cranial vena cava; 12, right ventricle; 13, pulmonary trunk; 14, capillary bed of lungs; 15, pulmonary vein; 16, hepatic veins. Tricuspid insufficiency (regurgitation) - Very similar disease process (pathophysiology) as mitral dz - Instead of Left congestion, we have RIGHT sided heart congestion - Pressures of the systemic circulation increase and start “leaking” The lining of the cavities of our bodies (thorax / abdomen) have tiny vessels that can become “leaky” under stress of high pressure. - Abdominal cavity and organs are lined by Peritoneum. Between the body wall and organs is the peritoneal space. - Excessive fluid in the peritoneal space = “Ascites” - Thoracic cavity and organs are lined by Pleura. Between the body wall and organs is the pleural space. - Excessive fluid in the plural space = “Plural Effusion” Tricuspid valve insufficiency Eventually causes a reduction in flow to the right side of the heart - Draw it in! LEFT side of the heart is still pumping well SYSTEMIC circulation is congested → high pressure in vessels of body cavity linings (abdomen and chest) R L Abdomen is lined by peritoneum. Accumulation of fluid in the peritoneal space is called “Ascites” → Distended abdomen Chest is lined by plura. Accumulation of fluid in the plural space is called “Plural effusion” → Increased Respiratory effort and rate Schematic drawing: 1, Left ventricle; 2, aorta; 3, capillary bed of head, neck, and forelimb; 4, abdominal aorta; 5, liver; 6, capillary bed of intestines; 7, portal vein; 8, capillary bed of kidneys; 9, capillary bed of caudal part of the body; 10, caudal vena cava; 11, cranial vena cava; 12, right ventricle; 13, pulmonary trunk; 14, capillary bed of lungs; 15, pulmonary vein; 16, hepatic veins. Dilated Cardiomyopathy - Boxers and Doberman Pinchers most frequently in contractility of cardiac muscle Initially compensate by increasing HR Eventually the orientation of the mitral valve is effected Mitral valve insufficiency ensues Dilated cardiomyopathy can also happen in cats! - Directly related to Taurine deficiency in diet - Very rare in household cats due to commercially available balanced nutrition Feline Hypertrophic Cardiomyopathy - Exact cause unknown - there is a definitive genetic predisposition (Ragdoll, Maincoon) - Ventricular walls become thickened - Pumps well, but cannot relax during diastole - Decreased Cardiac Output (CO) - Malalignment of valves (especially the mitral) Normal Hypertrophied