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− | == Introduction<br> ==
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− | This cardiac defect is also known as PDA. It occurs in all animals, but young animals have a greater risk. It is a very common condition in dogs, although it is not very common in cats. Predisposed breeds include toy Breeds (Yorkshire Terrier, Pomeranian, Maltese, Toy Poodles); Miniature Poodles, Shetland Sheepdogs, German Shepherds, Collies. There has been found to be a greater occurrence in females.
| + | Also known as: '''''PDA''''' |
| + | == Introduction == |
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− | The condition is the persistence of the ductus arteriosus after birth. During fetal life, the ductus arteriosus connects the pulmonary artery to the descending aorta. This fetal vessel allows most of the blood to bypass the developing lungs and go directly to the aorta and systemic circulation. In fetal life oxygen is provided by the placenta while the lungs are developing. At birth, the animal takes a breath of air and uses its lungs for the first time. High levels of oxygen from the pulmonary vasculature enter the circulation and the ductus arteriosus responds by contracting the smooth muscles lining its vessel wall. The functional closure of the ductus arteriosus occurs within 2-3 days after birth and with time it will become an anatomical closure. However, some animals have a ductus arteriosus that doesn't respond to the increased oxygen at birth and remains open (patent). After birth PDA causes a reversal of blood flow from the higher pressure of the descending aorta through the ductus arteriosus to the pulmonary artery and into the lungs. This is known as left-to-right shunting. The shunting of blood in this manner overwhelms the pulmonary vasculature and the left side of the heart. The increased volume of blood from the lungs travels to the left atrium and left ventricle which respond to the added pressure by dilation and hypertrophy. As a result, PDA can eventually lead to pulmonary edema and left-sided congestive heart failure. Normally the pulmonary circulation is equipped to handle increased volumes of blood without pulmonary arterial pressure changes. However, sometimes the increased blood volume in the lungs causes gross changes to the pulmonary arterioles causing pulmonary hypertension and raised pulmonary arterial pressures. If the pressure is high enough, it can cause a reverse PDA (right-to-left shunt) and unoxygenated blood will bypass the lungs heading straight for the descending aorta and the systemic circulation.
| + | This cardiac defect occurs in all animals, but is more likely to be diagnosed in the young. |
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| + | The condition is the persistence of the ductus arteriosus after birth. During fetal life, the ductus arteriosus connects the pulmonary artery to the descending aorta. This fetal vessel allows most of the blood to bypass the developing lungs and go directly to the aorta and systemic circulation. In fetal life oxygen is provided by the placenta while the lungs are developing. At birth, the animal takes a breath of air and uses its lungs for the first time. High levels of oxygen from the pulmonary vasculature enter the circulation and the ductus arteriosus responds by contracting the smooth muscles lining its vessel wall. The functional closure of the ductus arteriosus occurs within 2-3 days after birth and with time it will become an anatomical closure. However, some animals have a ductus arteriosus that doesn't respond to the increased oxygen at birth and remains open (patent). After birth PDA causes a reversal of blood flow from the higher pressure of the descending aorta through the ductus arteriosus to the pulmonary artery and into the lungs. This is known as left-to-right shunting. The shunting of blood in this manner overwhelms the pulmonary vasculature and the left side of the heart. The increased volume of blood from the lungs travels to the left atrium and left ventricle which respond to the added pressure by dilation and hypertrophy. As a result, PDA can eventually lead to [[Pulmonay Oedema|pulmonary oedema]] and [[Heart Failure, Left-Sided|left-sided congestive heart failure]]. Normally the pulmonary circulation is equipped to handle increased volumes of blood without pulmonary arterial pressure changes. However, sometimes the increased blood volume in the lungs causes gross changes to the pulmonary arterioles causing [[Pulmonary Hypertension|pulmonary hypertension]] and raised pulmonary arterial pressures. If the pressure is high enough, it can cause a '''reverse PDA''' (right-to-left shunt) and unoxygenated blood will bypass the lungs heading straight for the descending aorta and the systemic circulation. |
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− | == Clinical Signs<br> ==
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− | Clinical signs include left sided congestive heart failure, exercise intolerance, differential cyanosis (Reverse PDA) and hindlimb weakness (Reverse PDA). Sometimes,depending on severity of defect there may be no clinical signs.<br>
| + | ==Signalment== |
| + | It is a very common condition in dogs and is not very common in cats. Predisposed breeds include toy breeds (Yorkshire Terrier, Pomeranian, Maltese, Toy Poodles); Miniature Poodles, Shetland |
| + | Sheepdogs, German Shepherds, Collies. There has been found to be a greater occurrence in females. |
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− | <br>
| + | == Clinical Signs == |
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− | == Diagnosis<br> ==
| + | Clinical signs include left sided congestive heart failure, exercise intolerance, differential cyanosis (reverse PDA) and hindlimb weakness (reverse PDA). Sometimes, depending on severity of defect, there may be no clinical signs. |
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− | Clinical signs and history may be indicative of the disease. Physical examination findings will include systolic and diastolic continuous machinery murmur (Left side of the heart is the loudest), a precordial thrill (Palpable after a murmur) and the presence of waterhammer pulses (A forceful pulse that immediately collapses).
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− | In a reverse PDA, differential cyanosis (Normal oral mucus membranes, cyanotic membranes everywhere else) and hyperviscosity (Increased PCV from hypoxia-mediated polycythemia) may be seen.<br>
| + | == Diagnosis== |
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− | On radiographs of the thorax, you may see left atrial & ventricular enlargement, pulmonary overcirculation, dorsoventral view shows three bulges: aorta (1 o’clock), pulmonary artery (2 o’clock), left auricle (3 o’clock) positions and signs of left-sided congestive heart failure (pulmonary congestion, edema). If there is a reverse PDA, you may see right ventricular enlargement, dilation of the pulmonary trunk and arteries and left ventricular enlargement. | + | Clinical signs and history may be indicative of the disease. Physical examination findings will include systolic and diastolic continuous machinery [[Heart Murmur|murmur]] (left side of the heart is the loudest), a precordial thrill (palpable after a murmur) and the presence of waterhammer pulses (a forceful pulse that immediately collapses). |
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| + | In a reverse PDA, differential cyanosis (normal oral mucus membranes, cyanotic membranes everywhere else) and hyperviscosity (increased PCV from hypoxia-mediated polycythemia) may be seen. |
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| + | On radiographs of the thorax, you may see left atrial & ventricular enlargement, pulmonary overcirculation, dorsoventral view shows '''three bulges''': aorta (1 o’clock), pulmonary artery (2 o’clock), left auricle (3 o’clock) positions and signs of left-sided congestive heart failure (pulmonary congestion, edema). If there is a reverse PDA, you may see right ventricular enlargement, dilation of the pulmonary trunk and arteries and left ventricular enlargement. |
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| On echocardiography you will see left atrial & ventricular enlargement, dilation of pulmonary artery and a PDA might be visualized. Doppler can show abnormal flow. In a reverse PDA you will see right ventricular enlargement and left ventricular enlargement. Doppler can show abnormal flow. | | On echocardiography you will see left atrial & ventricular enlargement, dilation of pulmonary artery and a PDA might be visualized. Doppler can show abnormal flow. In a reverse PDA you will see right ventricular enlargement and left ventricular enlargement. Doppler can show abnormal flow. |
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− | On electrocardiographic (ECG) you may see classsic signs for left atrial enlargement (wide P wave), classic signs for left ventricular enlargement (tall R wave, wide QRS) and atrial & ventricular arrhythmias may be present. In a reverse PDA you may see classic signs of right sided heart enlargement. | + | On electrocardiographic (ECG) you may see classic signs for left atrial enlargement (wide P wave), classic signs for left ventricular enlargement (tall R wave, wide QRS) and atrial & ventricular arrhythmias may be present. In a reverse PDA you may see classic signs of right sided heart enlargement. |
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| == Treatment == | | == Treatment == |
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− | For a PDA, surgical ligation of the ductus arteriosus (2-4 months of age) can be performed if reffered. Animals with congestive heart failure need stabilization of heart failure before surgery. | + | For a PDA, surgical ligation of the ductus arteriosus (2-4 months of age) can be performed if refered. Animals with congestive heart failure need stabilization of [[:Category:Heart Failure|heart failure]] before surgery. |
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− | For a reverse PDA surgery is contraindicated. Exercise restriction and palliative care may be all that can be done. Phlebotomy (Bleeding to keep PCV at normal levels) can be peformed on a regular basis to help treat the symptoms. | + | For a reverse PDA surgery is contraindicated. Exercise restriction and palliative care may be all that can be done. Phlebotomy (bleeding to keep PCV at normal levels) can be performed on a regular basis to help treat the symptoms. |
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| == Prognosis == | | == Prognosis == |
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− | '''PDA: '''Very good prognosis with surgical treatment.<br> '''Reverse PDA: '''Poor prognosis. | + | '''PDA: '''Very good prognosis with surgical treatment. |
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| + | '''Reverse PDA: '''Poor prognosis. |
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| + | == Test yourself with the Developmental Pathology Flashcards == |
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| + | [[Cardiovascular Developmental Pathology Flashcards]] |
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− | == References<br> == | + | == References == |
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− | Ettinger, S.J. and Feldman, E. C. (2000) Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2 (Fifth Edition) W.B. Saunders Company<br>Ettinger, S.J, Feldman, E.C. (2005) Textbook of Veterinary Internal Medicine (6th edition, volume 2)W.B. Saunders Company<br>Fossum, T. W. et. al. (2007) Small Animal Surgery (Third Edition) Mosby Elsevier <br>Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition) Merial<br>Nelson, R.W. and Couto, C.G. (2009) Small Animal Internal Medicine (Fourth Edition) Mosby Elsevier<br><br> | + | Ettinger, S.J. and Feldman, E. C. (2000) '''Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume''' 2 (Fifth Edition) ''W.B. Saunders Company'' |
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− | <br>
| + | Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2) ''W.B. Saunders Company'' |
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− | <br>
| + | Fossum, T. W. et. al. (2007) '''Small Animal Surgery '''(Third Edition) ''Mosby Elsevier'' |
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− | == Test yourself with the Developmental Pathology Flashcards ==
| + | Merck & Co (2008) '''The Merck Veterinary Manual '''(Eighth Edition)'' Merial'' |
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| + | Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine''' (Fourth Edition) ''Mosby Elsevier'' |
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− | [[Cardiovascular Developmental Pathology Flashcards]]
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− | [[Category:Cardiovascular_System_-_Developmental_Pathology]] [[Category:To_Do_-_Review]] [[Category:Cardiac_Diseases_-_Dog]] [[Category:Cardiac_Diseases_-_Horse]] [[Category:Cardiac_Diseases_-_Cattle]] [[Category:Cardiac_Diseases_-_Pig]] | + | [[Category:Cardiovascular_System_-_Developmental_Pathology]] [[Category:Expert_Review]] [[Category:Cardiac_Diseases_-_Dog]] [[Category:Cardiac_Diseases_-_Horse]] [[Category:Cardiac_Diseases_-_Cattle]] [[Category:Cardiac_Diseases_-_Pig]] |