Failing Heart 1 PDF (2022) - Veterinary Science

Failing Heart 1 Prof Kamalan Jeevaratnam DAHP, DVM, MMedSc (Mal); PhD (Cambridge), FRCVS (UK) School of Veterinary Medicine, Univeristy of Surrey [email protected]  Learning Outcomes Review normal anatomy and physiology of CVS...

Failing Heart 1 Prof Kamalan Jeevaratnam DAHP, DVM, MMedSc (Mal); PhD (Cambridge), FRCVS (UK) School of Veterinary Medicine, Univeristy of Surrey [email protected]  Learning Outcomes Review normal anatomy and physiology of CVS Understand the pathophysiology and principle causes of heart failure Describe the common clinical signs/presentation associated with the failing heart Describe the pathophysiological process leading to the observed clinical signs/presentation in the failing heart Understand and describe the use of classification schemes for heart failure #uniofsurrey 2 What are the roles of the cardiovascular system? » Functions of the cardiovascular system: Delivery of substances Oxygen, glucose, water, amino acids, fatty acids and other nutrients Removal of substances Carbon dioxide, hydrogen ions and other waste products Distribution Heat, hormones, cells and bioactive agents » Two fundamental mechanical functions of the heart: 1. Eject enough blood into the aorta and pulmonary arteries in order to meet perfusion requirements of tissues 2. To receive blood from the pulmonary and systemic veins in order to provide adequate drainage of capillary beds #uniofsurrey 3 Normal anatomy of the heart » 75% circulating blood in the systemic circulation » 25% circulating blood in the pulmonary circulation » Encased in pericardium » 4 chambers Left atrium and right atrium separated by the interatrial septum Left ventricle and right ventricle separated by the interventricular septum » 4 Valves Tricuspid valve (right atrioventricular valve) Mitral valve (left atrioventricular valve) Aortic valve Pulmonary valve » Major Vessels Coronary arteries Ware, 2007 ‘Cardiovascular Disease in Small Animal Medicine’ Pulmonary trunk Aorta #uniofsurrey 4 Normal anatomy of the heart The right atrium is filled by venous blood from the cranial The left atrium is filled with and caudal vena cavae and the oxygenated blood from the coronary sinus pulmonary veins (these vary in number) Tricuspid valve separates the The mitral valve separates the right atrium and ventricle left atrium and ventricle The chordae tendinae anchor valve cusps to papillary muscles From the left ventricle oxygenated blood flows through the Aortic valve and into the aorta The papillary muscles tense in early systole so that valves do The pulmonic valve opens into not prolapse Ware, 2007 ‘Cardiovascular Disease in Small Animal Medicine’ the pulmonary artery and caries deoxygenated blood to the lungs #uniofsurrey 5  Normal conduction system of the heart SA node (normal pacemaker of the heart) → spreads throughout the right and left atria via intermodal pathways → AV node → bundle of His → left and right bundle branches → Purkinje fibres → ventricular myocardium Ware, 2007 ‘Cardiovascular Disease in Small Animal Medicine’ #uniofsurrey 6 The heart as a pump The heart consists of two pumps that work in series: → Left heart draws oxygenated blood from the lungs and pumps it through the body LEFT = HIGH PRESSURE → Right heart draws blood from the veins and pumps this into the lung RIGHT = LOW PRESSURE #uniofsurrey https://www.slideshare.net/burhanumerchaudhry/heart-physiology-9002997 7 The heart as a pump https://www.slideshare.net/burhanumerchaudhry/heart-physiology-9002997 http://teachmephysiology.com/cardiovascular-system/cardiac-cycle-2/cardiac-cycle/ #uniofsurrey 8 Cardiac Physiology » PRELOAD: The volume of blood returning to the ventricle (ventricular end- diastolic volume) Affected by venous blood pressure and the rate of venous return, which are affected by venous tone and volume of circulating blood. » AFTERLOAD: The tension, force or stress acting on ventricular wall myocytes after onset of shortening. Affected by arterial and arteriolar vascular smooth muscle constriction or dilation » HEART RATE: Determined by the rate of spontaneous sinoatrial nodal discharge Under autonomic control Cardiac output = stroke volume x heart rate #uniofsurrey 9 Frank Starling Law » Greater amount of blood in the ventricles results in greater contractile strength of the ventricles and therefore increase in stroke volume. » Due to the more cross-bridges cycling, and a greater availability of Ca++ to initiate this cycling. https://www.cvphysiology.com/Cardiac%20Function/CF003 #uniofsurrey 10  Heart failure – pathophysiological state when it is unable to function to meet the animals requirements. Progression of heart failure involves: Neuroendocrine dysfunction Biomechanical dysfunction Dysfunction that leads to clinical syndrome of heart failure can either be systolic dysfunction or diastolic dysfunction. Cardiac failure Compensatory with clinical Cardiac injury mechanism signs of dysfunction #universityofsurrey 11 What are the principle causes of cardiac injury Myocardial failure Impaired contractility – primary (dilated cardiomyopathy) or secondary (related to causes below leading to myocardial failure) Nutritional deficiencies – taurine – cats and some breed of dogs (American Cocker Spaniel, Boxers, Welsh corgis, Dalmations, Newfoundlands) Metabolic cardiomyopathies – hyperthyroidism, hypothyroidism, chronic uremia Toxic cardiomyopathies – drugs (doxirubicin) Inflitrative cardiomyopathy – neoplasia, amyloidosis Atrial fibrillation – atrial remodelling over long term #universityofsurrey 12  Volume overload Valvular insufficiency Most common cause of volume overload Incompetence of atrio-ventricular valves (endocardiosis, endocarditis, congenital) – allow for regurgitation to occur Can be primary (myxomatous valve degeneration) or secondary (ventricular hypertrophy, ischemia, obstruction) Shunts Septal defects, persistent foramen are similar to valvular leaks in pathophysiology. Overloads a particular heart chamber #universityofsurrey 13  Excessive afterload/pressure overload Short increases in afterload helps with contractility but chronic increases will depress myocardial contractility. Overtime – reduced rate of ejection if afterload is always high, leads to also reduced volume of ejection. Pulmonary or systemic hypertension, obstruction of ventricular outflow tracts, stenosis cause increase afterload. #universityofsurrey 14  Inadequate preload & diastolic dysfunction Reduction in preload represent inability to adequately fill the heart and diastolic dysfunction represent the inability to relax (expand the chambers) – somewhat interrelated. Inadequate preload – pericarditis, pericardial effusion. Diastolic dysfunction – myocardial fibrosis, restrictive cardiomyopathy, failure of adequate ventricular relaxation. Increases in ventricular end diastolic pressure which exerts stress on the heart and lead to remodelling. #universityofsurrey 15 Algorithm of functional categories and etiologies of congestive heart failure in cats #universityofsurrey 16 Clinical signs and presentation Coughing Previously associated as the most common complaint in dogs with significant cardiac disease – recent research suggest concurrent respiratory disease. Cats with heart failure rarely cough – typically other airway disease --- they however do cough in feline heartworm (sometimes). Compress trachea and if cat has prolonged coughing after this then it is a problem in this cat. Horses cough in advanced or in acute heart failure. A cardiac cough typically would occur when there is pulmonary oedema and the fluid accumulates in the airway. Occurs together with tachypnoea and dyspnoea Acute onset, soft, moist and has blood tinged sputum (fulminant conditions – pink foam - heamoptysis). Enlarged atrium can cause coughing due to mechanical compression of trachea (anatomy of the heart in relation to the airways!). #universityofsurrey 17  Dyspnoea Defined as difficult, laboured or painful breathing – and can precede tachypnoea. Occurs in any pathology that increases the amount of air that needs to be breathed in. Different types of dyspnoea: Acute – pulmonary oedema (cardiac or non cardiac), pneumonia, airway obstruction, pneumothorax, pulmonary embolism. Chronic (progressive) – right sided heart failure with ascites, pleural effusion, pericardial disease, bronchial disease, anaemia. At rest – mix of the above depending on severity. Exertional/on exercise – cardiomyopathies, heart failure, obstructive lung disease.. Respiratory rate and breathing effort are good indicators of heart failure. Dyspnoea that resolve with diuretic therapy suggest a left sided heart failure. Dyspnoea that resolve with bronchodilators, steroids, antibiotics suggest respiratory disease. Dyspnoea can also be position related – occurs when lying down but not when standing – orthopnoea. #universityofsurrey 18 #universityofsurrey 19 Oedema/Ascites Pulmonary oedema Ascites – accumulation of fluid in the abdomen – typically seen in dogs less common in cats (is it right or left heart failure?) Ascites not so obvious in horses - in horses classic oedema sites ventrum, limbs, prepuce, throat latch and muzzle. In dogs sometimes decompensated heart failure can occur without a murmur – if ascites in seen – include RHF as differentials. Large volumes of fluid in abdomen causes dyspnoea or tachypnoea – WHY? #universityofsurrey 20 Cyanosis Associated with decreased oxygenation and blue tinged mucous membrane. Occurs secondary to left sided heart failure (in respiratory disease as well) – in heart failure this is a late finding. Insensitive indicator of deoxygenation and cardiac function – O2 saturation needs to be really low to see changes. Some animals have pigmented/dark mucous membrane – difficult to see. Heart muscles are unable to pump enough blood to lungs for oxygenation – so predominantly deoxygenated blood is circulating. Can be come worse with exercise – peripheral resistance drops but pulmonary vasculature pressure unchanged so more deoxygenated blood in systemically. http://www.petplace.com/article/dogs/diseases-conditions-of- dogs/symptoms/cyanosis-blue-coloration-in-dogs #universityofsurrey 21 Syncope Loss of consciousness due to reduction of cerebral blood flow – can recur and typically brief in duration. Animals fall over suddenly but able to get back up fairly quick (depending on severity of impeded blood flow). There maybe involuntary urination and vocalisation – brief confusion on waking up In heart failure it occurs because the muscles are weak and the heart is unable to pump blood effectively. Reduced pumping of blood to the brain leads to reduced oxygen supply to it thus the brain shuts down momentarily. Commonly associated with cardiac arrhythmia – atrio-ventricular blocks, sick sinus syndrome, sustained tachycardia (physiology?). Important to distinguish between syncope and seizure. #universityofsurrey 22 #universityofsurrey 23 Abnormal heart sounds and cardiac murmurs S1 and S2 should be present in all normal animals and must be identified during auscultation. Dogs, cats & horses: S1 and S2 heard (S2 can be split at lower heart rates in horses); S3 and S4 not heard in healthy dogs and cats but heard in horses (S3 and S4 commonly heard in Thoroughbred horses – intensity may vary in some pathological conditions such as atrial fibrillation). Changes to S1 in heart failure: splitting of S1 can occur if mitral and tricuspid don’t close at the same time – valvular stenosis, ventricular ectopic beats. can also be soft due to pleural effusion, decreased cardiac output in late stage failure. Changes to S2 in heart failure: splitting of S2 can occur when pulmonic valve closes after aortic valve – pulmonary hypertension, structural defects, stenosis. paradoxical splitting occurs when aortic valve closes after pulmonic – left ventricular failure, systemic hypertension. #universityofsurrey 24  S3 in dogs occurs with dilated cardiomyopathy, hyperthyroidism, decompensated valvular regurgitation. S4 in dogs & cats caused by atrial contraction into an over-distended/stiff ventricle – e.g hypertrophic cardiomyopathy. Gallop rhythm – merging S3 and S4 – low frequency, difficult to hear and an early sign of heart failure and precedes its clinical signs. Murmur - turbulent blood flow through blood and vessels – physiologic and pathologic – cause or consequence? #universityofsurrey 25 Weakness, exercise intolerance and weight loss Weakness and exercise intolerance: Non specific clinical signs – associated with many disease but typically associated with a change in activity (Owners feel animal is slowing down). Early sign of decompensated heart failure – heart cannot pump as normal to meet demand Weight loss Tends to occur in dogs with chronic , severe right sided heart failure (RHF) - Weight loss not so much in cats. Cardiac cachexia – loss of total body fat and lean mass despite normal appetite and adequate therapy. RHF causes congestion of pancreas – disrupt enzyme secretion – altered digestion. Malabsorptive disorders leading to ascites as well. Systemic venous and lymphatic hypertension – lymphangiectasia leading to protein losing enteropathy #universityofsurrey 26  Venous distension Key part of the physical examination. Jugular vein examined whilst animal is standing with head in neutral position. Pulse extending above lower third of neck – abnormal and could be related to heart failure(right) – tricuspid regurgitation (as primary issue). Pulsation not typical of chronic heart failure – normally persistent distension in heart failure. Generalized jugular distension can occur – indicative of systemic hypertension secondary to right sided heart failure. Horses with right heart failure – jugular or lateral thoracic distension #universityofsurrey 27 Classification of heart failure Patients with asymptomatic heart disease (e.g – Class I chronic valvular heart disease (CVHD) is present but no clinical signs are evident with exercise Patients with heart disease that causes clinical Class II signs only during strenuous exercise Patients with heart disease that causes clinical Class III signs with routine daily activities or mild exercise Patients with heart disease that causes severe Class IV clinical signs even at rest #universityofsurrey 28  Animals at high risk for developing heart disease but currently have no identifiable disorder of the heart Stage A Animal with structural heart disease (e.g. typical murmur of mitral valve regurgitation is present), but have never developed clinical signs caused by heart failure B1:Asymptomatic animals that have no radiographic or echocardiographic evidence of cardiac remodelling in response to CVHD B2: Asymptomatic animals that have hemodynamically significant valve regurgitation, as evidenced by radiographic or echocardiographic findings of left sided Stage B heart enlargement Animals with past or current clinical signs of heart failure associated with structural heart disease. May or may not require hospitalisation and aggressive anti- congestive therapy Stage C Animal with end stage disease with clinical signs of heart failure caused by CVHD that are refractory to standard therapy. Such patients require advance or specialised treatment strategies in order to remain clinically comfortable with their disease. As with Stage C, some animals in Stage D will require acute, hospital based therapy and others can be managed as an outpatient. Stage D #universityofsurrey 29 Causes of the failing heart…some of it! When these conditions go really wrong...the animal almost certainly ends up with heart failure Acquired valvular disease Degenerative mitral valve disease Endocarditis Endocardiosis Equine valvular regurgitation (aortic, mitral, tricuspid and pulmonic) Pericardial disease Pericarditis Traumatic reticulo-pericarditis Hypertension Pulmonary hypertension Systemic hypertension Cardiomyopathies Canine dilated cardiomyopathy Arrhythmogenic right ventricular cardiomyopathy Hypertrophic cardiomyopathy Feline cardiomyopathy Heartworm disease Cardiac arrhythmia Atrial fibrillation #universityofsurrey 30 References Figures, diagrams and other related resources were acquired from the following books: Manual of canine and feline cardiology – 5th edition – Smith, Tilley, Oyama & Sleeper - Elsevier Cardiology of the horse – 2nd edition – Marr & Bowen – Saunders Feline cardiology – 1st edition Cote, Macdonald, Meurs & Sleeper – Wiley Blackwell BSAVA Manual of canine and feline emergency and critical care Clinical medicine of the dog and cat – 3rd edition – Schaer & Gaschen – CRC Press Rapid interpretation of the heart and lung sounds – 3rd edition – Keene, Smith, Tilley & Hansen Monday, 21 November 31