Pathology of the Cardiovascular System Flashcards
What are the 4 normal functions of the heart?
- maintain adequate blood flow (cardiac output)
- delivery oxygen, nutrients, and hormones to peripheral tissues
- remove carbon dioxide and other metabolic waste products
- maintain normal thermoregulation and glomerular filtration rates —> urine output
What are 5 common compensatory mechanisms available to maintain cardiac function?
- cardiac dilatation - stretching of cardiac muscle to increase contractile force and stroke volume, necessary to maintain normal cardiac output
- myocardial hypertrophy - caused by increased workload
- increased heart rate
- increase in peripheral resistance - shunts blood from periphery to necessary organs
- blood flow redistribution
Normal heart:
(thick left ventricle to pump blood to organs and periphery)
Myocardium:
- striated
- central nucleus
- intercalated discs
What are the 4 reversible changes in cardiac muscle in response to injury? 2 irreversible?
REVERSIBLE
1. vacuolar degeneration
2. fatty degeneration
3. fatty infiltrations (causing atrophy)
4. myocytolysis (partial loss of proteins)
IRREVERSIBLE
1. lipofuscinosis (wear and tear —> common in older animals or cachexic)
2. neoplasia
What are the 4 steps to the general response of cardiomyocytes to injury? What is another possible (but rare) outcome?
- normal cardiac muscle cells are injured (toxic insult, nutritional deficiency, physical insult, infection)
- hyaline necrosis
- macrophage invasion
- healing with fibrosis, where fibroblasts proliferate, causing scar (connective tissue) formation
regeneration is not common - BM is commonly ruptured, not allowing satellite cells to differentiate into myoblasts, and since connective tissue replaces cardiomyocytes, the heart is left more susceptible to subsequent injury
What is the normal ventricle thickness ratio?
1:3 ratio of RV and LV thickness
How does blood flow from the placenta through the fetus?
umbilical vein carries oxygenated blood to the fetus and umbilical arteries carry deoxygenated blood to the placenta
- lungs are developing and do not need as much blood, so the foramen ovale allows atria to communicate and mix blood, and the ductus arteriosus is the only blood supply to the lungs
What does serous atrophy of the heart look like grossly? What is the most common cause?
yellow and gelatinous due to fat mobilization
- remember: the coronary groove is usually fatty to protect vessels!
poor nutrition
- dental disease
- insufficient/unbalanced diet
- GI disturbance
Epicardial hemorrhage, cow:
- endotoxemia
- anoxic/hypoxic
- terminal hypoxia (stunning, hanging)
(petechia/ecchymosis)
What causes cardiac failure/decompensation?
the heart cannot keep up with increased physiological needs and compensatory mechanisms fail
What’s the difference between cardiac syncope and congestive heart failure?
CARDIAC SYNCOPE: acute onset of cardiac failure causing collapse and unconscious, commonly caused by abnormal heart rhythm, defective heart valves, etc.
CHF: develops slowly from gradual loss of cardiac output due to pressure or volume overload or myocardial injury
How does congestive heart failure typically manifest in bulls? What is the most common cause?
brisket edema, swelling near sternum
increased altitude results in less oxygen in the air, making the heart have to compensate by pumping blood to the lungs —> pulmonary hypertension
Idiopathic pulmonary hypertension leading to CHF, heifer:
recovered from severe pneumonia, causing connective tissue to replace and compress pulmonary veins which leads to pulmonary edema and hydrothorax
- blood pools on pulmonary side in the caudal vena cava, which can also cause hepatic congestion (nutmeg liver)
Ascites (hydroperitoneum), dog:
- right-sided CHF
- hypoproteinemia from renal disease or protein-losing enteropathy
What 4 things are we looking for during a postmortem examination of the heart?
- shape change - bigger, rounded, ventricle thickness
- valves - inflammation
- ventricular/atrial communication defects
- size of aorta and pulmonary veins
Normal tricuspid valve:
(right AV valve)
- thin and transleucent
Mitral valve, chordae tendineae:
can rupture with increased pressure due to chest trauma
What do congenital anomalies in the cardiovascular system involve? How does this tend to affect the animal?
heart or blood vessels
- die in utero (stillborn, aborted)
- present clinical signs after birth, like exercise intolerance, cyanosis, and stunted body growth
What are valvular hematocysts?
congenital valvular anomaly that manifests as a nodule filled with blood on/near valves (typically no vessels on valve in adults, since they get nutrition from osmosis)
- (typically no clinical signs and will disappear with age)
What is the tetralogy of Fallot? In what dogs is it most common? How does it present in humans?
- ventricular septal defect (opening between RV and LV)
- overriding aorta (dextroposition over the septal defect)
- pulmonic stenosis
- right ventricle hypertrophy
- Keeshonds
- English Bulldogs
- “blue babies” (blood on right side will be pushed to the periphery before it is oxygenated)
What is right ventricular hypertrophy commonly secondary to?
pulmonic stenosis - compensatory for pressure overload and to ensure the lungs still get proper blood supply
(prominent RV makes heart seem round)
What does subvalvular aortic stenosis result in?
compensatory concentric hypertrophy of the left ventricle and post-stenotic dilation of the aorta (fibrous band constricts aorta)
BLUE = aortic valve
GREEN = fibrous band
In what species is tricuspid dysplasia most common? What does this lead to?
cats
valvular insufficiency —> animals usually born dead
What are ventricular septal defects? What does this cause?
communication between RV and LV - LV is more powerful, so it pushes blood from LV to RV, causing the RV to overload and undergo hypertrophy which can then push deoxygenated blood into the LV —> cyanosis
- exercise intolerance
- heart failure
Ventricular septal defect, calf:
- stunted growth
- murmur
(view from right ventricle - tricuspid valve)
How can ventricular septal defects affect the endocardium?
increased turbulence causes the development of a fibrotic and thickened endocardium —> jet lesions, typically on the right ventricular free wall