<<
>>

Patent Ductus Arteriosus

History. A 3-month-old female Welsh corgi is brought to your clinic by its owner, who has noticed a ‘Tumbling noise” in the dogs chest. The dog is smaller than her Iittermates and less playful.

The dog coughs occasionally, but the cough does not produce fluid.

Clinical Examination. The dog appears to be in good health except for the occasional cough. The mucous mem­branes are pink, and the capillary refill time is normal (1.5 seconds). However, when you place your hand on the anterior left chest, you feel an abnormal vibration (thrill) with each heartbeat. With a stethoscope, you can auscultate a cardiac murmur that is loudest during systole but continues throughout both systole and diastole (continuous murmur). The murmur is heard most loudly at the ventral third inter­costal space on the left side. Expiratory sounds are slightly louder than normal. The pulse rate is 152 beats per minute, which you consider to be above normal for a dog of this size and age. While you are listening to the heart with the stethoscope, you palpate the femoral pulses, which are very strong.

The electrocardiogram indicates that the dog has sinus tachycardia; the atrial and ventricular rates are both 152 beats per minute. The R waves are abnormally large in leads II and III (2.5 and 3.5 mV, respectively). The QRS complex in lead I shows a large negative deflection followed immediately by a slightly larger positive deflection.

Thoracic radiographs show a generalized enlargement of the heart. The initial portion of the pulmonary artery is also substantially larger than normal, and the pulmonary blood vessels appear generally to be more prominent than normal.

An echocardiogram confirms the presence of a patent ductus arteriosus.

Comment. A murmur in a young, otherwise-healthy dog is most likely the result of a congenital cardiac abnormality. A continuous murmur can occur only if a defect causes tur­bulent flow throughout both diastole and systole.

Because flow can occur only when there is a pressure gradient, the defect in this dog must be in a location where there is a sub­stantial pressure gradient throughout the cardiac cycle. No single intracardiac defect meets this criterion; that is, a stenotic or regurgitant valve produces either a systolic murmur or a diastolic murmur, but not both. A valve that is both stenotic and regurgitant produces two murmurs: one in systole and one in diastole. In such a case, however, brief moments occur during the cardiac cycle when no pressure gradient exists across the valve, so there are moments of silence between the systolic murmur and the diastolic murmur. (Admittedly, if the heart rate is high, these moments of silence are very brief, and the two murmurs can be mistaken for a continuous murmur, particularly in the case of combined aortic stenosis and regurgitation.)

The most common cardiac defect that causes turbulent flow throughout both systole and diastole is a patent ductus arteriosus (PDA). This vessel is normal in the fetus but should close shortly after birth. The flow through a PDA is continuous because aortic pressure is higher than pul­monary artery pressure throughout the cardiac cycle. The resulting murmur is usually heard best in the left third intercostal space. All the other clinical signs in this dog are also consistent with the diagnosis of PDA. The prominence of the pulmonary vessels on the radiographs indicates that pressure and flow are abnormally high in the pulmonary artery and its branches. In a dog with a PDA the pulmonary artery receives blood flow from both the right ventricle and the aorta, which increases both pulmonary arterial pressure and pulmonary flow.

The radiographs and electrocardiograms indicate that this dog has both right and left ventricular hypertrophy. The large R waves in leads II and III indicate left ventricular hyper­trophy, and the large negative deflection during the QRS com­plex in lead I suggests that the right ventricle is hypertrophic as well. The left ventricle becomes hypertrophic in a dog with PDA because it is called on to pump three to five times the normal cardiac output.

(It pumps a near-normal volume to the organs of the systemic circulation and two to four times that much through the PDA.) The flow through the PDA is large because the PDA offers little resistance to flow. The demand on the left ventricle to pump so much blood (increased volume work) leads to left ventricular hypertrophy. The volume of blood pumped by the right ventricle is almost normal; it only needs to pump the blood that returns through the venae cavae from the systemic organs. However, the right ventricle must develop higher systolic pressures than normal to eject this blood into the pulmonary artery because pulmonary artery pres­sure is higher than normal, as explained earlier. This increase in pressure work often leads to right ventricular hypertrophy.

Because the PDA carries so much blood away from the aorta, dogs with PDA tend to have an abnormally low aortic pressure. Diastolic pressure is particularly reduced because of the rapid outflow of blood from the aorta during ven­tricular diastole. Therefore, PDA is typically associated with low mean aortic pressure but elevated pulse pressure (review Figure 22-9, G).

Two mechanisms work together to keep blood flow to the systemic organs almost normal despite the fact that a large fraction of cardiac output is uIostn through the PDA. First, reflex mechanisms (discussed in Chapter 25) increase sympathetic activity to the heart, which increases heart rate and contractility above normal. These sympathetic effects keep left ventricular output (and aortic pressure) sufficiently high to supply blood to the systemic organs, despite the PDA. Second, metabolic control mechanisms cause the systemic organs to vasodilate, which keeps their blood flow almost normal despite the subnormal aortic pressure.

The compensatory mechanisms just described allow most dogs with a PDA to maintain a nearly normal blood flow to the systemic organs at rest. Several months may pass before the dog’s owner notices limitations in the dog’s activity or growth.

Eventually, however, the heart cannot increase its output sufficiently to supply the systemic blood flow needed by the muscles during exercise, so a puppy with a PDA becomes less playful and energetic than its normal Iittermates. Also, if the heart is unable to supply the blood flow needed by metabolically active tissues, the owner may notice some stunting of growth. In any case, a dog with a widely open ductus has a poor long-term prognosis, unless treated.

Treatment. You show the dog’s owner a diagram of the fetal circulation and explain that the ductus arteriosus normally closes and seals itself within 1 to 6 weeks after birth, but that the ductus fails to close spontaneously in about 1 of every 700 newborns (the condition is four times more common in female pups than in male pups). Treat­ment involves closure of the ductus, either by ligation during open-chest surgery or by insertion of a specially designed plug during a cardiac catheterization procedure. Most dogs treated before age 6 months go on to lead completely normal lives. However, you inform the owner that PDA is hereditary and that this puppy should probably not be used for breeding.

The owner elects to have the dog treated surgically, and the surgery is successful. The murmur and cough disappear immediately. Within 1 week the dog is noticeably more energetic. At age 6 months, the dog has “grown into” her enlarged heart, and all physical findings are within normal limits.

<< | >>
Source: Cunningham J.G., Klein B.G.. Textbook of Veterinary Physiology. Elsevier Health Sciences,2007. — 720 đ.. 2007

More on the topic Patent Ductus Arteriosus: