Severe pulmonary hypertension and cardiovascular sequelae in dogs - Veterinary Medicine
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Severe pulmonary hypertension and cardiovascular sequelae in dogs
Once thought to be caused mostly by dirofilariasis, pulmonary hypertension is still being seen despite heartworm preventive measures, signifying additional important causes. Technologic advances may help us recognize the signs in time.


VETERINARY MEDICINE


Review of the presented cases

The two cases presented in this article are part of a group of nearly 54 dogs with various degrees of pulmonary hypertension (15 were severe) studied over two and a half years at the Virginia-Maryland Regional College of Veterinary Medicine. The prognosis and cardiac changes in the 54 dogs parallel the underlying severity of the pulmonary hypertension problem. The presented cases represent the severe form of pulmonary hypertension and reveal the difficulty in identifying the problem before it becomes irreversible. In addition, there is the challenge of understanding the pathophysiology in each case. Control of pulmonary vascular resistance and pressure is a finely tuned and complex system that can become imbalanced in many ways. To appropriately treat animals with the more severe forms of pulmonary hypertension, comprehensive physiologic monitoring could be of great benefit; however, the invasive procedures needed to monitor intracardiac pressures, cardiac output, and vascular resistance may be difficult to accomplish in critically ill patients.

At necropsy, the two dogs in this study had no evidence of heartworm disease or major pulmonary embolism. There was evidence of in situ thrombosis in the Labrador retriever.

Presumably, the pulmonary vascular hypertension in these dogs was related secondarily to pulmonary parenchymal disease. Both dogs had pathologic evidence of inflammatory pulmonary disease; however, the chronicity is open to question, particularly in the 14-year-old mixed-breed dog. This dog presented with an acute history of dyspnea and coughing and was referred quickly to Virginia Tech. The Labrador retriever had a much more chronic history and was referred many months after initial presentation to the referring veterinarian. The severity of the laryngeal paralysis and accompanying hypoxia could have played an important role in this animal's clinical course and development of pulmonary hypertension. Clearly, both dogs had documented hypoxemia, and it is well-known that this can promote pulmonary vasoconstriction; however, beyond the direct effect of hypoxia-induced vasoconstriction through potassium and calcium availability to the vascular smooth muscle cells, it is not known what other vascular control factors might have been disturbed. Disequilibrium of the vasoconstrictors and vasodilators that were discussed above could have played a principal role, but assessing this is not easily done in the clinical setting.

It is tempting to speculate on what effect abnormal pulmonary vascular function might have on other vessels. The systemic vessels, including the coronary arteries, are controlled in a manner similar to the pulmonary vessels. Perhaps the disequilibrium in the pulmonary vessels might liberate substances or trigger mechanisms that could influence systemic vessels. For example, endothelin is a potent vasoconstrictor with a long half-life and is important in pulmonary vascular control. Increased production of this circulating substance could cause constriction of systemic vessels, including the coronary arteries. Coronary vasoconstriction concurrent with a stressed right ventricle in a dog with severe pulmonary hypertension could be devastating. The frequent and long-standing premature ventricular contractions seen in the Labrador retriever could have been the result of reduced coronary blood flow associated with a stressed right ventricle trying to deal with an enormously increased afterload.

Finally, these two cases illustrate the challenge of trying to successfully treat the severe form of pulmonary hypertension. By examining the original group of 15 severe cases (including the two in this report), it is apparent that such dogs have a grave prognosis, irrespective of the therapeutic plan, and usually survive a few days to a few weeks.

Future considerations

Dealing with severe pulmonary hypertension in dogs is rewarding from the recognition perspective. The technology behind echocardiography, including transesophageal studies, is constantly improving, and it will become easier to recognize the vascular and cardiac manifestations of pulmonary hypertension. The frustrating aspect of this problem is to understand the pathogenesis and pathophysiology. While we assume that pulmonary parenchymal disease precedes pulmonary vascular disease, this is not always obvious. Some dogs have no physical or radiographic signs of pulmonary parenchymal disease but have severe pulmonary hypertension. The lack of necropsy studies in many cases makes final judgments about parenchymal disease difficult at best.

Developing a rational therapeutic plan is essential in these cases, and providing oxygen is clearly a reasonable step. However, the complex cascade of events involved in controlling pulmonary vascular tone could easily be disturbed in a number of ways. In the clinical setting, there is no practical way to evaluate the pulmonary vascular tone or assay the substances that play a principal role in controlling pulmonary vascular tone, so each case becomes an experiment in finding a plan that will substantially reverse the pulmonary hypertension.

A better understanding of nonheartworm pulmonary hypertension in dogs will result from appropriate research. Further characterization of parenchymal diseases of the lung as well as a comprehensive evaluation of the pulmonary vascular abnormalities will be critical. Assays of control substances and histochemical studies of the pulmonary vessels may be particularly rewarding. Progress is being made through multispecies studies, and this is likely to continue. In time, the treatment and management of canine pulmonary hypertension may be less empirical and more rational.

R. Lee Pyle, VMD, MS, DACVIM (cardiology)
Jonathan Abbott, DVM, DACVIM (cardiology)
Heidi MacLean, DVM
Department of Small Animal Clinical Sciences
Virginia-Maryland Regional College of Veterinary Medicine
Virginia Tech
Blacksburg, VA 24061

REFERENCES

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