Cardiovascular Flashcards
Nodules of Arantius
Normal nodules on semilunar valves
Sinus of valsalva
Origin of coronary arteries
Common site to sample to diagnose cardiomyopathy
Mid-ventricle
Best sample to look for cardiac degeneration
Papillary muscle
Characteristics of heart failure
Decreased myocardial contractility
Decreased compliance (fibrosis)
Dysrhythmias/arrhythmias
Best/most common compensatory method of heart
Hypertrophy
Development of hypertrophy requires
Time
Healthy myocardium
Adequate nutrition and oxygenation
What happens when limit of hypertrophy is reached
Dilation
Dilation
Stretching of myofibers as a result of chronic volume overload
Maintain connections and architecture
Cardiac syncope
Acute cardiac failure
Sudden onset of extreme changes in BP and HR
May or may not have gross or histo lesions
Congestive heart failure
Chronic loss of pumping ability
Syndrome NOT a disease
Can be forward (decreased flow to peripheral tissues) or backward (accumulation behind the failing chamber)
Cardiac decompensation/embarrassment
Failing heart has to pump a greater volume of thicker fluid
Cardiac decompensation -> hypoxia
- > renin release from kidneys -> aldosterone release from adrenals -> Na and H2O retention -> increased plasma volume -> edema
- > stimulation of EPO -> polycythemia -> increased blood viscocity
What does septal thickening indicate
HCM
Causes of right ventricular hypertrophy
Pulmonary hypertension
Congenital abnormalities
Tricuspid (right AV) incompetence
Mechanical obstruction (HW)
Cor Pulmonale
Right ventricular hypertrophy +/- failure due to long-term pulmonary hypertension
Causes of left ventricular hypertrophy
Systemic hypertension
Congenital abnormalities
Mitral incompetence
Endocrine disease (hyperthyroidism, acromegaly)
Causes of right heart failure
Valvular insufficiency (tricuspid or pulmonary valves)
Pulmonary hypertension
Cardiomyopathy
Sequelae of right heart failure
Hepatic congestion (“nutmeg liver”)
Ascites
Hydrothorax
Pleural and pericardial effusion
Causes of left heart failure
Myocardial loss of contractility (myocarditis, myocardial necrosis, cardiomyopathy)
Valvular insufficiency (mitral or aortic valves)
Congenital defects (PDA)
Sequelae of left heart failure
Pulmonary congestion
Pulmonary edema
Pulmonary fibrosis
Hemosiderosis (“heart failure cells”)
Common differentials for cardiac disease in dogs vs cats
Dogs: congenital, endocardiosis, DCM, hemopericardium
Cats: congenital, HCM, hyperthyroidism-associated hypertrophy
Granular, crystalline deposits on endocardial curface
Euthanasia solution artifact
PDA
Connection between pulmonary artery and aorta normally closes up to 5 days after birth
Breeds- poodles, collies, poms, chi, maltese
Aortic stenosis
Valvular, subvalvular, supravalvular
Breeds- Newfoundland, boxer, GSD, golden
Pathologic findings: concentric hypertrophy of L ventricle, endocardial thickening, post-stenotic dilation of aorta, jet lesions, myocardial necrosis/fibrosis
Can cause sudden death due to arrhythmias
Pulmonic stenosis
Infundibulum, pulmonary artery, pulmonary valve
Breeds- beagle, english bulldog, chi, westies
Right ventricular hypertrophy, post-stenotic dilation of pulmonary artery
Muscular hypertrophy of RV outflow tract can complicate stenosis
Valvular dysplasia
Tricuspid, mitral
Malformation of valve leaflets (may be attached to septum)
Thickened cordae tendinae
Labs- tricuspid (autosomal dominant)*
Malformations causing L -> R shunting
Atrial septal defect
Atrioventricular septal defect
Ventricular septal defect
PDA
Atrial septal defect
Pressure in RV overcomes LV
Ventricular septal defect
High most common (membranous portion)
Pulmonary hypertension from blood shunting from L -> R
Causes RV hypertrophy, increase in pulmonary hypertension can lead to eventual compensatory R -> L shunting
Eisenmenger complex
VSD cases with reversal of shunting
