Pathology of CV system Flashcards
1
Q
Hypertrophy
A
- Inc mechanical work from pressure or volume overload
- causes myocytes to inc in size
- Causes an inc in size and weight of heart
- dependant on inc protein synthesis
- requires healthy myocardium
2
Q
Inc pressure (hypertension/aortic stenosis) causes
A
- Pressure-overload hypertrophy
- causes a concentric inc in wall thickness
3
Q
Volume-overload hypertrophy
A
- Ventricular dilation
- wall thickness may be increased, normal, or less than normal
4
Q
Cardiac Compensation
Dilation
A
- Stretching myofibers
- Maintain connections and architecture
- Often degenerative in nature
- Results from chronic volume overload
5
Q
Result of Dilation
A
- gradual inc in chamber pressures occurs as chamber volume increases
- not as profound a change as seen with outflow obstructions
- dilation dec pressures in chamber by increasing surface area
6
Q
Supply of oxygen and nutrients to hypertrophied heart
A
More tenuous than the normal heart
7
Q
Hypertrophy often accompanied by
A
deposition of fibrous tissue
8
Q
Cardiac hypertrophy associated with
A
- heightened metabolic demands due to
- inc wall tension
- inc heart rate and contractility
9
Q
Hypertrophied heart vulnerable to
A
- Decompensation
- can evolve to cardiac failure => death
- Sequence of compensation initially beneficial, later harmful
10
Q
CHF characterized by
A
- dec cardiac output
- dec tissue perfusion (forward failure)
- pooling of blood in the venous system (backward failure)
- may cause pulmonary edema, peripheral edema, or both
11
Q
Right-to-left shunts
A
- Tetralogy of Fallot
- Transposition of great arteries
- Persistent truncus arteriosus
*Hypoxemia and cyanosis result because of mixture of poorly oxygenated venous blood w/ systemic arterial blood b/c it bypasses the lungs
12
Q
Left-to-right shunts
A
- ASD, VSD, PDA, septal defects
- inc pulmonary blood flow
- no cyanosis initially
13
Q
Consequences of left-to-right shunts
A
- raise flow and pressures in pulmonary circulation
- normally low pressure system
- right ventricular hypertrophy and pulmonary vasculature changes
- When pulmonary vasculature approaches systemic levels
- new right-to-left shunt introduces unoxygenated blood into systemic circulation
- eventually cyanosis
14
Q
PDA
A
- shunt L to R, overloads R ventricle and inc pulmonary pressures
- To compensate
- total blood volume increases
- left ventricle forced to increase output above normal levels
15
Q
PDA Pathologic findings
A
- Compensatory hypertrophy of both LV & RV, with left atrial dilation due to inc pulmonary blood flow
- Dilation of PA and AA due to turbulence and altered pressure
- Slowly developing hypertrophy if the shunt is < 3mm, and pulmonary hypertension and congestive heart failure if its > 5mm
- Prone to thrombosis (Virchow’s triad)
16
Q
Septal Defects
A
- VSD most common
- most common congenital defect in horses
- Pulmonary hypertension from blood shunting L to R
- R ventricular hypertrophy
- Inc in pulmonary hypertension can lead to eventual compensatory R to L shunting
- shunts blood past lungs
17
Q
Atrial septal defects
A
- patent foramen ovale
- may be probe patent but functionally closed
- R ventricular hypertrophy and L to R shunts
- Equalization of pressures may cause R to L shunts cyanosis
18
Q
Tetralogy of Fallot
A
- VSD
- R Ventricular Hypertrophy (secondary)
- Pulmonary Stenosis
- Dextroaorta
19
Q
Abnormalities of the Aortic Arch
A
- May be incidental findings
- Clinical signs are from compression of trachea and esophagus
- Persistent right aortic arch - something about megaesophagus
- Double aortic arch
- Anomalous subclavian arteries
20
Q
Ectopia cordis
A
- heart enclosed w/in pericardium outside of thorax
21
Q
Endocardial fibroelastosis
A
- Left ventricle
- Inc collagen and elastin
- can affect conduction
