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122 Cards in this Set
- Front
- Back
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Heart uses what type of metabolism |
Oxidative metabolism - requires air The heart does not tolerate periods of hypoxia or anaoxia well |
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Cardiovascular disease is less significant in animals than humans because |
Domestic animals live shorter lives Infectious diseases are a bigger killer of animals than humans Lipid abnormalities are rare in animals Idiopathic hypertension is less common in animals Secondary hypertension is common but usually less significant than primary lesions (eg renal failure) |
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Right side of the heart pumps blood to |
The lungs |
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Left side of the heart pumps blood to |
The systemic circulation |
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The left side of the heart is bigger and more muscular than the right because |
the blood pressure is higher in the systemic circulation than in the lungs |
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Normal healthy ratio of muscularity between left and right sides of the heart |
3:1 ratio |
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Cardio myocytes have poor regenerative capabilities and injury results in |
Fibrosis or scar formation This can result in disruption of electrical flow and contraction of the heart |
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Three layers to the heart consist of |
Pericardium - fibroblastic sac enveloping the heart muscle Myocardium - muscle Endocardium - innermost layer consisting of endothelium and fibrous tissue |
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Pericardial fat |
Expect a good bit of fat on the pericardium of domestic animals Lean wild animals would not have this amount of pericardial fat |
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Pericardial sac is |
A thin translucent membrane covering the heart - if it is not translucent that indicates and abnormality (likely inflammation) A normal pericardial sac contains no free fluid |
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Normal heart shapes |
Dog hearts are slightly rounded Avian hearts tend to be slim and quite pointy Rabbit hearts are very rounded |
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Thickening of the atrioventricular valves can result in |
Less efficient closing of the valve |
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Chordae tendineae |
Attachments of the AV valve to the wall of the heart |
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Causes of congenital abnormalities of the heart |
Usually noticed in young animals - occur in both small and large animals Many are heritable and are thus more common in purebred animals Fetal hypoxia, spontaneous, nutritional deficiencies, viral, chemical teratogens Teratogens are an important cause in people but less commonly diagnosed in animals |
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Three broad groups of congenital disease |
1. Failure of fetal structures to close 2. Abnormal valve development 3. Abnormal blood vessels Combination defects can also occur |
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Most common congenital abnormalities in the heart of dogs |
Aortic stenosis Atrial septal defect Patent ductus arteriosus Pulmonic stenosis Ventricular septal defect |
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Failure of closure of fetal cardiovascular shunts |
Atrial septal defect Ventricular septal defects (Most common) Patent ductus arteriosus |
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Atrial septal defect |
Failure of the foramen ovale to close Opening between the left and right atrium No oxygen in the lung at birth means capillaries are depressed and pressure is too high for much blood to reach there If flap doesn't come down or the foramen ovale is so large it cant be covered you result in septal defect |
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Clinical effects of atrial septal defect |
Dilation of the right atrium, right ventricle, and pulmonary artery Blood gets pushed back into the right atrium from the left ventricle which can cause dilation of both right atrium and right ventricle |
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Ventricular septal defect |
Opening between the left and right ventricles A common defect of domestic animals due to incomplete closure of the interventricular septum Exact position of the defect can vary A high defect just beneath the AV valves is more common |
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Clinical effects of ventricular septal defect |
Left to right shunt Left and right ventricular hypertrophy |
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Patent ductus arteriosus |
In the fetus blood bypasses the lungs by blood being shunted from the pulmonary to the systemic circulation (pulmonary artery to aorta) Once the lungs are inflated this shunt must close If it remains open, blood passes from high pressure aorta into the low pressure pulmonary artery This can read to pulmonary hypertension |
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Clinical effects of patent ductus arteriosus |
Hypertrophy of both ventricles Due to turbulent flow through the patent ductus it has a predisposition to thrombosis development |
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Pulmonic stenosis |
Narrowing of the outflow of the pulmonary artery Can occur: Just above the pulmonic valve At the pulmonic valve (most common) Just below the pulmonic valve |
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Clinical effects of pulmonic stenosis |
Hypertrophy of the right ventricle is a common sequelae to this condition due to increased effort of trying to push blood through a narrowed outflow Proximal pulmonary artery dilated due to increased pressure Mild cases often live normal lives |
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Subaortic stenosis |
Narrowing of the outflow of the aorta More common in pigs than in dogs |
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Clinical effects of subaortic stenosis |
Secondary left ventricular hypertophy Post-stenotic aortic dilation Altered blood flow can result in ischemic myocardial necrosis - can result in spontaneous heart failure |
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Mitral and tricuspid valve dysplasias |
Focal or diffuse thickening of valve leaflets, fusion of the valves with the cardiac walls, or shortening of the chordae tendineae or papillary muscles Left AV dysplasias are more common in cats |
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Clinical effects of mitral and tricuspid valve dysplasias |
Valve dysplasia result in leaking valves End result is usually dilation of the atria of the affected side and secondary dilation of the ventricle of the same side |
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Valvular hematocyst |
Abnormal valve development Incidental lesions, most often seen in young ruminants Can be quite spectacular but often dont have any clinical signs and spontaneously regress |
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Valvular lymphocyst |
Abnormal valve development Incidental lesions, most often seen in young ruminants |
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Persistent right aortic arch |
The ductus arteriosus entraps the oesophagus against the trachea Post-natally as the animal progresses to solid food there is obstruction of food passage through the oesophagus resulting in dysphagia, regurgitation, and megaesophagus |
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Transposition of the aorta and pulmonary artery |
A groupd of anomalies with the aorta being to the right of its normal position - there are 3 degrees of malposition 1. Overriding aorta 2. Partial transposition 3. Overriding pulmonary artery 4. Complete transposition |
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Transposition of the aorta and pulmonary artery Overidding aorta |
Aorta straddles the interventricular septum (which itself is defective), aorta receives blood from both ventricles. Pulmonary artery exits from right ventricle as normal |
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Transposition of the aorta and pulmonary artery Partial Transposition |
Both aorta and pulmonary artery exit from the right ventricle |
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Transposition of the aorta and pulmonary artery Overriding pulmonary artery |
Pulmonary artery straddles the defective ventricular septum, and the aorta exits the right ventricle |
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Transposition of the aorta and pulmonary artery Complete transposition |
The aorta exits from the right ventricle and the pulmonary artery exits from the left ventricle Not compatible with life |
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Tetralogy of Fallot |
Consists of 4 features: Ventricular septal defect Pulmonary valve stenosis Aortic transposition Secondary right ventricular hypertrophy |
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Clinicsl effects of tetralogy of fallot |
Affected animals will always have clinical signs Degree of pulmonary stenosis will determine the degree of shunting of blood from left to right side of the heart and thus pulmonary perfusion Poor pulmonary perfusion results in cyanosis and polycythemia Growth rates retarded Right ventricular hypertrophy will progress to heart failure |
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Polycythemia |
Increase in the fraction of red blood cells in response to tissue hypoxia |
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Cyanosis |
Blue or plum discoloration of the mucus membranes due to poorly oxygenated systemic blood Most commonly seen in anomalies with a large right to left shunt of blood (shunts that bypass the lungs) |
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Circulatory failure |
Failure to maintain blood flow to tissues |
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Heart failure develops when |
The heart can no longer adequately propel blood forward |
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Primary heart failure |
Damage to the heart muscle itself Genetic, toxic, nutritional, viral, bacterial, protozoal |
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Secondary heart failure |
Primary disease is a system other than the heart Systemic hypertension, pulmonary disease, pericardial disease, conduction system problem |
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Classifying types of heart failure into |
Acute vs chronic heart failure Left vs right heart failure |
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Heart failure that develops quickly is |
Acute heart failure What leads to acute heart failure in one animal may cause chronic heart failure in another Can easily go unnoticed by owners of misinterpreted as something else |
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Heart failure that develops over a longer time period |
Chronic heart failure What leads to chronic heart failure in one animal may cause acute heart failure in another Most common situation seen in practice |
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Causes of acute heart failure |
Arrythmias, chordae rupture, shock, hypovolaemia, acute cardiac tamponade |
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Causes of chronic heart failure |
myocarditis, pericarditis, endocarditis, endocardiosis etc. |
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Acute left ventricular failure causes |
Immediate drop in systemic blood pressure due to reduced output of left ventricle |
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Process of left sided heart failure |
Decreased blood pressure --> increased sympathetic nervous system --> increased adrenaline --> increased peripheral arterial constriction --> pallor of extremities |
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Left sided heart failure When the heart is unable to maintain outflow |
Accumulation of blood in left ventricle and atria --> pulmonary congestion and oedema --> dyspnea |
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Macrophages containing hemosiderin |
Macrophages that have phagocytosed red blood cells Known as heart failure cells |
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Increased pulmonary pressure from chronic left sided heart failure can result in |
Interstitial lung fibrosis with subsequent right sided heart damage and failure (cor pulmonale) |
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Causes of left sided heart failure |
Valve defects (eg. endocardiosis), myocarditis, pericarditis, endocarditis, cadiac tamponade, cardiomyopathies, systemic hypertension, infarction (not common in most domestic species) |
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Right sided heart failure results in |
Reduced output to the pulmonary circulation with damming back of blood in the venous system including liver Also results in reduced output from the left ventricle due to inadequate throughout put from pulmonary circulation Dont see pulmonary congestion because reduced blood flow to lungs |
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Damming of blood in liver from chronic right sided heart failure can result in |
Hepatocyte degeneration and necrosis with subsequent fibrosis Appearance of liver often referred to a nutmeg liver do ti the mix of light and darker zones |
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Causes of right sided heart failure |
Valve defects Pulmonary disease Myocarditis, pericarditis, endocarditis Cardiac tamponade Cardiomyopathies Infarction (no common) |
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Heart failure compensatory mechanisms |
Increased heart rate Increased contractility (increased effort) Increased peripheral vascular resistance Redistribution of blood flow Decompensation occurs when compensatory mechanisms are inadequate to maintain peripheral blood flow |
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Signs of heart failure |
Exercise intolerance Breathing difficulties - coughing, wheezing General weakness Syncope Tachycardia Irregular heartbeat oedema (subQ, hydrothorax, ascites) Weight loss |
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Signs of left sided failure vs right sided failure |
Left sided - lung oedema, dyspnea Right sided - liver congestion, ascites (dogs show ascites more than cats) |
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Consequences of chronic heart failure on the kidneys |
Reduced blood flow to kidneys (peripheral arteriolar constriction) Stimulates juxtaglomerular appuratus Renin + angiotensinogen = angiotensin 1 angiotensin I --> angiotensin II --> increased vascular resistance Angiotensin II --> adrenal cortex --> aldosterone released --> increased sodium/water retention increased sodium/water retention = increased blood volume Cannot utilize increased venous return - congestion in systemic circulation and liver - tissue oedema |
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To recover of maintain heart function from chronic heart failure you need |
Increased heart rate Increased venous return Increased blood pressure Improved contractility of myocardium |
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Hydropericardium |
Accumulation of sterile clear fluid within the pericardial sac |
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Causes of hydropericardium |
Generalized oedema (ex. chronic heart failure, hypoproteinemia) Pulmonary hypotension Loss of blood vessel integrity (eg. anaphylaxis, toxemias) Virus - African swine sickness, african horse sickness |
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Hemopericardium |
Accumulation of blood within the pericardial sac |
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Causes of hemopericardium |
Hemangiosarcomas Heart based tumors Ruptured aorta Idiopathic |
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Pericarditis |
Inflammation of the pericardium |
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Causes of pericarditis |
Hematogenous route Extension from myocardial lesion Extension from mediastinum, lungs Traumatic penetration of pericardium |
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Pericarditis classification |
Based on exudates - serous, fibrinous, suppurative, or combinations Based on causative agent - tuberculosis, streptococcus, trueperella |
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Hardware disease in suppurative pericarditis |
Foreign body in reticulum --> reticulum contractions --> penetrates reticulum and diaphragm --> migration to pericardium May also penetrate abdominal wall and cause peritonitis |
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Non-hardware causes of pericarditis |
Horse: strep Dogs: Staph, strep Cats: FIP, Strep, Staph Pigs: Haemophilus parasuis (glasser's disease), strep, mannheimia haemolytica, salmonella Sheep: Pasteurella, strep, clostridial enterotoxaemia, mannheimia haemolytica Cattle: mannheimia haemolytica, clostridium chauvoei (blackleg), trueperella pyogenes |
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Heart failure |
Any condition whereby cardiac output is insufficient to deliver adequate blood to meet metabolic demand |
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Heart disease is not the same thing as |
Heart failure |
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% of heart disease in small animal cases |
Approx 10% of all cases have heart disease 9% have acquired 1% have congenital condition |
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Signalment of heart disease: Age |
Congenital disease: young Acquired disease: middle aged to older |
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Signalment of heart disease: Gender |
Little clinical value Males: Mitral valve disease, DCM Females: PDA |
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Signalment of heart disease: Breed |
Boxers: subaortic stenosis Cavalier, Dachshund: mitral valve endocardiosis Doberman, St. bernard, great dane, irish wolfhound: Dilated cardiomyopathy |
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Common presenting complaints (history) for animals with heart disease |
Cough (dog > cat) Dyspnea or tachypnia - pulmonary oedema, plueral effusion Syncope Exercise intolerance, poor growth, weight loass Ascites Cyanosis, poor perfusion Blindness |
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Investigation of cardiac disease |
1. General physical examination 2. Complete cardiac assessment 3. Ancillary diagnostic tests - echocardiography, electocardiography, radiographs, blood pressure measurement, blood tests |
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Physical exam in heart disease cases |
Complete physical exam essential Confirm heart disease/ failure Identify other diseases that may exacerbate or explain clinical signs (anaemia, pyrexia, hypovolaemia) |
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Failure of the heart as a pump leads to |
Poor cardiac output ("forward" failure) Congestion ("backward" failure) |
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Compensatory mechanisms in heart failure |
1. Sympathetic nervous system 2. Renin-angiotensin-aldosterone system |
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Compensatory mechanism of the sympathetic nervous system in heart failure results in |
Increased heart rate Increased contractility Vasoconstriction |
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Signs of poor cardiac output/ poor peripheral perfusion |
Tachycardia Weak peripheral pulses Cold extremities Prolonged CRT Pale mucus membranes |
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Signs of left sided congestive heart failure |
Pulmonary oedema Pleural effusion (cats) Respiratory rate and pattern (restrictive not obstructive) Cyanosis Crackles |
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Signs of right sided congestive heart failure |
Jugular pulses Ascites Hepatomegaly Pleural effusion (dogs) Cyanosis Hepatojugular reflex |
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Examination of thorax for heart disease |
Palpation of pericardium Percussion at intercostal spaces Reduced resonance = increased tissue (masses, fluid, consolidated lung tissue) Increased resonance = increased air (emphysematous lung, pneumothorax) |
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Auscultation of the thorax in heart disease cases |
Always auscultate: Both sides Base and apex of heart Thoracic inlet Ventral (sternum) (cats) Whilst palpating femoral pulses - look for pulse deficits Whilst assessing respiratory pattern - to identify sinus arrhythmias |
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Descriptions of cardiac finding on auscultation should include |
Rate, rhthym, area, audibility, adventitious sounds |
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Normal Heart rate in dogs |
70-160 bpm Can change with breed, size, athleticism, stress, pain, other illness |
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Normal heart rate in cats |
150-180 bpm Can change with breed, size, athleticism, stress, pain, other illness |
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Sinus arrhythmia |
Physiological Increased heart rate during inspiration and decreased during expiration Seen in fit and calm dogs with low heart rate Seen with high vagal tone Not present in dogs with heart failure Rare in healthy cats |
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Abnormal heart rhythms |
Bradyarrhythmia Tachyarrhythmia Intermittent arrhythmias ("trips" in rhythms) ECG required for definitive classification |
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Audibility of heart sounds on auscultation Decreased |
When there's something between the stethoscope and the heart Pericardial effusion Intrathoracic neoplasia Obecity Pleural effusion |
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Audibility of heart sounds on auscultation Increased |
Sympathetic activation Emaciation |
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Normal heart sounds: S1 |
"Lubb" Closure of AV valves Corresponds to onset of ventricular systole |
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Normal heart sounds: S2 |
"Dupp" Closure of semilunar valves and vibrations in great arteries Corresponds to the onset of ventricular diastole |
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Abnormal heart sounds: Split S1 ("Lubb") |
Splitting of the "Lubb" portion into multiple sounds Asynchronous closure of the AV valves Often associated with abnormal conduction (ventricular complexes, bundle branch blocks) Differentials: S4 gallop |
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Abnormal heart sounds Split S2 ("Dupp") |
Asynchronous closure of the semilunar valves Usually delayed closure of pulmonary valve Causes: pulmonary hypertension, pulmonic stenosis, may be normal in large breed dogs |
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Abnormal heart sounds S3 |
Corresponds to rapid ventricular filling Usually pathologic in small animals Appears shortly after S2 (protodiastolic) May be associated with DCM, HCM, severe MVR |
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Abnormal heart sounds S4 |
Corresponds to atrial contraction Shortly before S1 (presystolic) May be normal in giant breed dogs May be pathologic (cardiomyopathy, hypertension) |
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Abnormal heart sounds Gallop rhythm |
Presence of a pronounced third heart sound Intensified S3, S4 or both (extra diastolic sound with similar intensity to S1/S2) Sounds like a horse's gallop at high rates Low frequency - bell > diaphragm |
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Abnormal heart sounds Pathological murmurs |
Ejection - during systole through a narrowed exit Regurgitation - through a 'hole' such as leaky valve, septal defect or anomalous vessel |
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Heart murmurs classified by |
Loudness, Timing, Location |
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Heart murmur loudness Grade I |
Very soft murmur heard in quiet surroundings after careful listening |
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Heart murmur loudness Grade II |
Soft but easily heard |
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Heart murmur loudness Grade III |
Moderate intensity murmur |
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Heart murmur loudness Grade IV |
Loud murmur but no precordial thrill (Thrill = vibrations generated by turbulent flow sufficiently strong to be detected by palpation) |
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Heart murmur loudness Grade V |
Loud murmur with a precordial thrill (Thrill = vibrations generated by turbulent flow sufficiently strong to be detected by palpation) |
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Heart murmur loudness Grade VI |
Very loud murmur that can be heard with the stethoscope off the chest wall and precordial thrill (Thrill = vibrations generated by turbulent flow sufficiently strong to be detected by palpation) |
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Abnormal heart sounds: timing Systolic |
Additional sound comes between the "Lubb" and the "Dupp" |
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Abnormal heart sounds: timing Diastolic |
The abnormal sound occurs after the "Dupp" "Lubb Dupp humm" |
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Abnormal heart sounds: timing Continuous |
A constant humming noise occurring - 'machinery murmur' |
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Examination of the heart on thoracic radiographs |
Take at the peak of inspiration - lateral and DV views Cardiac silhouette - size and shape (valentines heart in cats indicates atrial enlargement) Pulmonary patterns Major vessels Airways Pleural space |
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Decreased systolic blood pressure indicates |
Poor cardiac output (heart failure) Subaortic stenosis - prior to heart failure Monitor response to treatment - if sufficient to may start to see blood pressure rise |
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Increased systolic blood pressure can lead to |
Hypertrophic cardiomyopathy |
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Laboratory assessment: Cardiac biomarkers |
Cardiac troponin I (cTnl) Brain Natriuretic Peptide (BNP) No biomarkers have shown better performance compared to a thorough clinical exam and routine diagnostic imaging |
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Electrocardiography |
Identify cardiac rhythm and conduction disturbances Not commonly used for assessment of chamber size (echocardiography more accurate) |
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Echocardiography |
2D Mode: Measure chamber size and anatomy (valves, heart base, pericardial space, myocardium) M Mode: Measure motion - systolic function and mitral valve motion - can add color |
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Advanced heart disease diagnostic techniques |
24-hour ECG (holter) monitoring Angiography Event recorders Endomyocardial biopsy Direct cauterization and pressure measurement (jugular vein for right side of the heart, femoral artery for left) Tissue doppler analysis |
