Lecture 25 Flashcards
how prevalent are congenital anomalies of CVS
low. dogs-1% camelids/pigs-4%
Most common congenital anomaly in dogs, cats, pigs, horse, cow
dog-PDA, pulmonic or subaortic stenosis cat- tricuspid or mitral valve dysplasia pig- subaortic stenosis,endocardial cushion defect horse- VSD cow- ASD,VSD, valvular hematocysts
Why more prevalence in purebred dogs?
requires inheritance of several genes at different loci (polygenic inheritance)
Most common location for an ectopic heart
cattle- pre sternal subcutaneous
clinical significance of congenital absence of parietal pericardium
usually asymptomatic
congenital peritoneopericardial diaphragmatic hernia
triangular defect in ventral diaphragm and in parietal pericardium->abdominal viscera into pericardial sac (often clinically silent)
significant changes to fetal blood flow at birth
vasoconstriction of umbilical veins->dec venous return to RA and dec RA vol and pressure
- post natal lung inflationand O2 induced vasodilation of pulmonary arteries->dec pulmonary pressure->inc vol and pressure in LA and LV and aorta
- Closure of Ductus venosus, ductus arteriosus, and foramen ovale
Which species is PDA most often detected
dogs (especially females)
consequences of PDA (uncomplicated and complicated)
uncomplicated- L to R shunt during systole and diastole->inc volume in pulmonary artery and inc vol load on LA (dilation) and LV(dilation->chronic eccentric hypertrophy)
Complicated- pulmonary pressure inc and exceeds aortic-> shunt reversal (now R to L)->venous blood bypasses lungs-> hindquarter peripheral cyanosis (cranial blood supply before shunt)
Patent foramen ovale common in what species> Significant? Why?
common in ruminants
not a true atrial septal defect, does not permit shunting (functionally closed)
potential post natal consequences of atrial septal defect (ASD)
shunting-> L to R-> inc central venous pressure and volume overload on RA (dilation) and RV (dilation then chronic eccentric hypertrophy) also vol overload on LA due to return of extra blood from lungs
Potential post natal consequences of VSD
depend on diameter and degree of pulmonary vascular resistance
small may be clinically insignificant
large-> L to R shunting of blood->vol overload on RV during diastole and equilibration of pressures between RV and LV->pressure overload on RV during systole
Why do some VSD’s eventually close
reparative fibrosis induced by blood turbulence
which animals are likely to develop shunt reversal and at what age?(3 at the same age)
PDA, ASD, or VSD within first 6 months of post natal life
large defects that allow L to R shunting of large vol of blood
Possible defects associated with abnormal development of endocardial cushions (4 and common in)
high VSD or low ASD
tricuspid or mitral valve dysplasia
common AV canal
common in pigs and cats