HI!
Basically, elevated left

HI!

Basically, elevated left atrial pressures automatically lead to increased PA pressures because otherwise the blood would flow into the wrong direction across the pulmonary circuit. When a dog is in left heart failure, LA pressures are usually around 40 mm Hg. Given the normal driving pressure across the pulmonary circuit, this would lead to a PA pressure of around 50 mm Hg. Means that if you notice PA pressures of 100 mm Hg, increased LA pressures can’t be the only single reason. When the dog has chronic hypoxia from whatever reason (pulmonary edema, chronic lung or airway disease) then the so-called Euler-Liljestrand-Mechanism causes vasoconstriction – and this can cause much higher pressures. Other reasons are obstructive disease, compression of vessels or embolic disease (also heart worms etc). The basic work-up consists of urine sampling (proteinuria is one important reason for PTE due to loss of antithrombinIII – this is also the reason why heparin does not work in these cases because it needs antithrombin III), chest radiographs, abdominal scan (tumor? HAC?), bloods (albumine? angiostrongylus (!), heart worm testing), maybe CT if lung or airway disease is seen on chest radiographs.

Regarding tricuspid dysplasia: I know the discussion about why PHT is sometimes detected with TD. From a pathophysiological standpoint, pressures >40 mm Hg are very unlikely to be caused by TD. TD leads to underperfusion of the lungs. One could argue that underperfusion can cause central hypoxia because of reduced blood volumes that take over the oxygen from the lungs. From experimental studys, we know, that mixed venous oxygen saturation does not really influence PA pressures – alveolar oxygen saturation does!. What I frequently see with TD is malformation of the right ventricular papillary muscles that leads to intra-ventricular obstruction. This could be the reasons why we sometimes measure high pressure gradients across the tricuspid valve in patients with TD. But jobrags case is different: He also measures high diastolic gradients across the pulmonic valve: This proves pulmonary arterial hypertension because a right venrticular intraventricular obstruction cannot be responsible for this. 

I completely agree with Eric: There are changes of the TV that would match with vegetations (infectious) or neoplasia. 

As you said, Furosemide, ACEI, Spiro, Pimo and Sildenafil are options apart from oxygen. Prognosis is bad – but I would still try and find a possible reason for this condition, because is simply cool to find it!

Peter