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ToDay's VeTeriNary PracTice | November/December 2015 | tvpjournal.com aHs HearTWorM HoTLiNe Peer reviewed 66 Obstructive Pulmonary Disease The effects of arterial obstruction on pulmonary arterial fow and its resulting impact on worm location in dogs heavily infected with heartworms were studied by Kitagawa and colleagues, who artifcially induced obstructive disease by surgically placing silicone tubes, similar in size to adult heartworms, into the pulmonary arteries of infected dogs. 8 a similar study utilized dead adult worms placed in the pulmonary arteries to mimic a more natural thromboembolic episode. in both scenarios, obstruction of the distal pulmonary arteries caused increased vascular resistance, reduction in blood fow, and resultant decrease in cardiac output. The live adult worm population subsequently moved or were forced, in a retrograde manner, toward the right atrium, thereby inducing cs. Cardiovascular Collapse The retrograde movement of heartworms and development of cs were similarly observed when cardiovascular collapse was experimentally induced. • a whole-worm extract concocted from dead worms was administered intravenously and, through an unexplained mechanism, profound vasodilation resulted in circulatory collapse. 8 • in a separate study, when milbemycin D was administered to heartworm-infected dogs with high microfilaria numbers, anaphylaxis was induced. 9 • in a third study, a dramatic reduction in cardiac output was induced by administration of a potent beta-1 blocker. 10 in each of these studies, a resultant shock-like reaction led to cardiovascular collapse, and as cardiac output decreased, worms moved into the right atrium. Role of Blood Flow although obstructive pulmonary vascular disease and cardiovascular collapse are entirely different disease processes, both lead to a dramatic decrease in pulmonary fow. if blood fow is indeed responsible for keeping adult heartworms constrained to the pulmonary arteries, it is plausible that the development of cs may be potentiated by any condition that causes a reduction in the normal velocity and/or volume of pulmonary blood fow. WHAT CONTRIBUTES TO CAVAL SYNDROME? Etiology once believed to be the consequence of "too many worms to ft in the pulmonary arteries," we now know that factors other than worm numbers are involved in the etiology of cs. 4 The diffculty has been in defning these other "factors," especially in dogs with natural infection. Based on the study fndings discussed earlier, the relationship between blood fow and location of adult worms must be considered. Normal pulmonary arterial fow facilitates location of worms almost exclusively within the pulmonary arteries. as pulmonary arterial fow was decreased by artifcially creating obstructive disease or by cardiac insuffciency, worms relocated to the proximal right heart. 8-11 These experimental scenarios correlate directly with the progressive disease observed in natural infection as HWi-induced pulmonary vascular obstruction and cardiac insuffciency progress. 7,12,13 Vascular Obstruction Vascular obstruction commonly occurs in HWD and can result from several disease processes (Table 2, page 64). 7,13-15 individually, each of these obstructive conditions can cause increased resistance to blood fow, but when they occur in combination, the additive effect can be quite dramatic. Cardiac Insuffciency cardiac insuffciency can be a pathologic consequence of advanced HWD. even without overt signs of right-sided heart failure, reduction in cardiac output can signifcantly impact hemodynamics, decreasing the ejected volume of blood. 13 While many unrelated diseases can Potential development of Caval syndrome 1. Heartworms mature in the pulmonary arteries, prompting formation of antigen:antibody complexes and resulting in microvascular disease and, thus, increased vascular resistance. 14 2. Adult worms incite intimal thickening; the combination of worm mass along with a narrowed vascular lumen continue to increase pulmonary vascular resistance. 13,16,17 3. An adult worm spontaneously dies, causing a thromboembolic event, which further increases vascular resistance. 4. Dead worm vasomediators are released, impacting cardiac function. 8 5. Arterial blood fow is reduced, allowing heartworms to migrate toward the heart. 8 6. One or more worms move into the right ventricle, interfering with the tricuspid valve and simultaneously causing tricuspid regurgitation and infow tract obstruction. 2,4,10 7. Cardiac output falls and acute signs of CS ensue. 10 P o t e