DA5 Flashcards
Fetal circulation starting from placenta (high oxygen content)
- Placenta
- Umbilical veins
- passes the liver, ductus venosus
- Caudal vena cava
- RA
- Foramen ovale
- LA
- LV
- Aorta
- Fetal tissues
Fetal circulation (non oxygenated blood) starting from venae cavae
- Venae cavae
- RA
- RV
- Pulmonary trunk
- Ductus arteriosus
- Aorta
- Umbilical arteries
- placenta
Main changes of postnatal circulation
- Closure of umbilical vessels, umbilical arteries and veins
- Closure of ductus arteriosus
- Closure of foramen ovale
- Complete separation of heart chambers is a progressive event
Cardiac anomalies occur in all domestic animals because ….
- complex developmental processes and dramatic circulatory changes at birth
- Incidence is higher in pedigree dogs than mixed breeds
- In humans they make up the largest category of birth defects
Cardiac anomalies are due to
- Abnormal partitioning of cardiac chambers
- Abnormal formation of cushions
- Abnormal division of aortic and pulmonary channels
- Abnormal transformation of aortic arches
What are easy targets for genetic and teratogenic influences?
Nueral crest cells, because they form endocardial cushions and formation of aoritc and pulmonary channels. They have great inductive powers.
Most cardiac anomalies are associated with _____
Craniofacial anomalies
Hereditary cardiac defect often involves ….
Same antomic site in a group of related animals; genetic testing is useful in selective breeding
Degree of severity to cardiac anomalies are proportional with
- the defect
- some defects are lethal, others limit peak performance or reproductive value of animal
This type of cardiac anomaly allows enough oxygenated blood to tissues for normal functions
Acyanotic
This type of cardiac anomaly does not have enough oxygenated blood in peripheral tissues.
It is diagnosed by dark bluish color of gums and oral mucosa.
Cyanotic
Common secondary changes in heart anomalies
- Dilation: abnormal increases in size of heart chambers due to increased blood volume
- Hypertrophy: thickening of walls of chambers due to increased contraction force to empty a chamber
Definition of shunt pathophysiology
Deviation of blood flow between systemic (L) and pulmonary (R)
Result and symptoms of L-R shunt
- Volume overload due to increased pulmonary arterial flow and venous retun –> pulmonary hypertension
- Exercise interolerance, dyspnea (rapid and shallow breathing), pulmonary edema, venous distention, ventral edema, shunted growth
Causes and symptoms of R-L shunt
- Causes: secondary to chronic pulmonary hypertension
- Symptoms: cyanosis, dyspnea, exercise interolerance, occasional syncope
- Shunt reversal: L side chambers are small and R side is hypertrophied to sustain the systemic blood pressure
Common L –> R shunt anomalies
ASD, VSD, PDA
Common R–>L shunt anomalies
PDA, tetralogy of fallot, persistent right aortic arch
Acyanotic anomalies: atrial septal defect (ASD/PFO)
- Causes: defective formation of septa
- Lack of closure of foramen ovale
- Severity: proporitonal to size of defect
- Result: R side dilation and hypertrophy (L –>R shunt)
- Management: surgical closure
- Reportings: in all domestic animals, rare in horses
Acyanotic anomalies: ventricular septal defect (VSD)
- Causes: presence of opening in interventricular septum (membranous part most commonly)
- Outcome: L –> R shunt (OR bidirectional) and pulmonary hypertension
- Management: surgical correction
- Reportings: most common in CHD human, most common in large domestic animals, usually extensive and fatal in cats and horses (die before weaning)
Acyanotic anomalies: Patent Ductus arteriosus (PDA)
- L –> R shunt
- Causes: lack of closure of ductus arteriosus
- Severeity: proprotional to size of patency
- Abnormal heart sounds
- Outcome: L –> R shunt
- L side will eventually hypertrophy, pulmonary hyerptension, over time it becomes a R –> L shunt –> heart failure
- Management: ligation if no secondary changes
- Reportings: dogs - breed predisposition
- Diagnosed primarily in premature infants
Cyanotic anomalies: teratology of fallot
- Classical cyanotic multiple defect in domestic animals and humans
- Causes: unequal division of bulbus cordis
- Defects: pulmonary stenosis, interventricular septal defect, overriding aorta, RV hypertrophy (secondary defect)
- R –>L shunt
- Symptoms: cyanosis after exercise, dyspnea, exercise intolerance, syncope
- Management: articial PDA to increase pulmonary blood flow (done by anastomosing R subclavian A. to R pulmonary A.)
- Reportings: all domest animals, humans
- Prognosis: poor survival due to chronic complications
Cyanotic Anomalies:Persistent Truncus Arteriosus
- Causes: lack of division of conus cordis into pulmonary and aortic channels and a coexisting VSD
- Outcome: early onset of heart failure
- Management: correction by cunduit revision (separate pulmonary trunk from the aorta, and then connect it to the normal right ventrical)
- Reportings: humans, dogs, pigs
- Lethal condition without early correction
Persistent Right aortic arch
- 4th aortic arch becomes brachiocephalic turnk on the right, and on the left it forms the adult aorta
- Sometimes this arch persists and wraps around trachea and esophagus
- Cause: abnormal retention of R fourth aortic arch
- Result: vascular ring constricting trachea and esophagus –> esophageal dilation and regurgitation of solid foods
- Diagnosis: contrast radiographs
- Management: surgical removal of offending vessel
Anomalies: venous system
Congentical Porto-Systemic Shunt (Portal - caval shunt)
- Cause: persistence of ductus venosus (blood bypasses liver sinusoids and doesn’t get filtered)
- Result: blood from GI tract passes into systemic circulation
- Symptoms: neurological (seizures), vomiting, diarrhea, anorexia, polyuria
- Reportings: cats and dogs and most common
- Management: conservative - low protein diet
Dextrocardia
Heart looks reversed
Anomaly of malpositioning
