Pulmonary hypertension frequently accompanies respiratory disorders, heartworm disease and chronic degenerative mitral valve disease in dogs (Tai and Huang, 2013). Mitral valve disease is reported as the most common cause of canine pulmonary hypertension, but when it is found in association with respiratory disorders or heartworm disease, it tends to be of greater severity.
This canine patient was referred for echocardiography with a high suspicion of pulmonary hypertension.
2D signs that confirmed this diagnosis:
LONG AXIS VIEW
– Dilated right ventricle (and right atrium). The right ventricle in the parasternal long-axis view should occupy approximately 1/3, and the left ventricle approximately 2/3 of the image. In this instance, the right ventricle completely dominates the left.
– Hypertrophied right ventricle. The walls of the right ventricle in this dog are thick – thicker, in fact, than the walls of the left ventricle. This is indicative of very high right ventricular systolic pressure.
– Impaired right ventricle. Both longitudinal and radial function in this dog are severely impaired. The walls barely move. Orientating the image to the longitudinal motion of the right ventricle, TAPSE could have been used to quantify this. Unlike in cats (Spalla et al., 2017), TAPSE should always be adjusted for body weight in dogs (Pariaut et al., 2012) at 0.6cm per kg (Chetboul et al., 2018), but 1.2cm can be crudely used as a lower cutoff (Chetboul et al., 2018) in instances where significant dysfunction is obvious.
SHORT AXIS VIEW
– Compression of the left ventricle. The pressure in the right ventricle is so high that it exceeds the pressure in the left, resulting in a ‘flattening’ of the interventricular septum. The eccentricity index would quantify this and is particularly useful in heartworm disease assessments where it has significant prognostic implications (see Tai and Huang, 2013), but the obvious septal flattening here is more than sufficient to confirm the elevated pressures on the right side of the heart.
– The right ventricular outflow tract and pulmonary artery were markedly dilated in this dog, and another measurement that could be performed is the main pulmonary artery to aortic root ratio (Tai and Huang, 2013), taken at valve closure.
Above: The main pulmonary artery is visually dilated in comparison with surrounding structures.
– The moderate-severe tricuspid regurgitation here is to be expected, secondary to annular dilatation, and is another hallmark of chronically elevated pressures in the right side of the heart.
– Velocity of the regurgitant jet. The large amount of tricuspid regurgitation lends itself well to the estimation of pulmonary pressures. Continuous Wave Doppler would be invaluable here. In the absence of this, we actually tried Pulsed Wave Doppler, but unsurprisingly, the velocity of the jet far exceeded the scale/pulse repetition frequency (PRF). This means that the velocity of the jet is so high that we simply cannot sample it rapidly enough to obtain an accurate measurement. The only way to do so would be with continuous sampling.
If CW Doppler was available, we could place the sampling line through the jet (trying to find the most parallel alignment possible) and obtain a waveform trace. The simplest rule of thumb to use is >1.5m/s indicates mild pulmonary hypertension, 2m/s or more is moderate, and 3m/s or greater would be severe pulmonary hypertension (Serres et al. 2007).
It is possible to convert this into a pressure gradient by using the simplified Bernoulli equation, simply squaring the peak velocity and multiplying it by 4. In the absence of pulmonary stenosis, pulmonary artery systolic pressure can then be estimated by adding on an estimated right atrial pressure, which in dogs, is best estimated by assessing the size of the right atrium (Soydan et al., 2015).
One situation where it may be important to calculate PASP as opposed to relying solely on the tricuspuid regurgitant jet velocity would be where there is severe, free-flow tricuspid regurgitation, with almost complete equalisation of pressure between the right atrium and right ventricle. This will result in a much lower velocity of the TR regurgitant jet (as the pressure difference between the two chambers is low), so relying on this velocity alone would greatly underestimate the severity of the pulmonary hypertension.
Example of free-flow tricuspid regurgitation:
Extreme tricuspid annular dilatation can result in severe tricuspid regurgitation (TR), but perhaps the most extreme example of free-flow TR is when there is a primary valve lesion. In this example from a human patient with carcinoid heart disease, the tricuspid valve leaflets are fixed in the open position, so that there is practically no gradient between the right ventricle and right atrium:
With this severity of TR, you might expect to be getting velocities of over 3m/s, whereas in fact, the peak velocity was only 2.4m/s, – within the normal range for humans. If the high right atrial pressure was ignored and only the TR velocity was used, one would erroneously conclude that this patient did not have elevated pulmonary pressures.
Above: In this case of severe tricuspid regurgitation, the pressure gradient between the right ventricle and right atrium is only 23mmHg (velocity is 2.4m/s).
In canine echocardiography, right atrial pressure is subjectively estimated based primarily on the size of the right atrium. Kittleson and Kienle (2014) suggest adding 5mmHg if the right atrium appears normal in size, 10mmHg if it appears enlarged but without any other signs of right sided heart failure, and 15mmHg if it’s enlarged and accompanied by signs of right sided heart failure (Soydan et al., 2015). This is then added to the pressure gradient obtained from the CW Doppler trace through the tricuspid regurgitant jet.
Another important use of CW Doppler would be in ruling out pulmonary stenosis. By ruling out pulmonary stenosis, we can safely assume that right ventricular systolic pressure (RVSP) = pulmonary artery systolic pressure (PASP), and can therefore quote our calculated RVSP as PASP.
Chetboul, V., Damoiseaux, C., Lefebvre, H. et al. (2018). Quantitative assessment of systolic and diastolic right ventricular function by echocardiography and speckle-tracking imaging: a prospective study in 104 dogs. J Vet Sci, 19(8):683-692.
Kittleson M., Kienle R. (2014). Pulmonary arterial and systemic arterial hypertension. Small Animal Cardiovascular Medicine. 433–449.
Pariaut, R., Sealinger, C., Strickland, K., et al. (2012). Tricuspid Annular Plane Systolic Excursion (TAPSE) in Dogs: Reference Values and Impact of Pulmonary Hypertension. Journal of Veterinary Internal Medicine.
Serres, F., Chetboul, V., Gouni, V., et al. (2007). Diagnostic value of echo-Doppler and tissue Doppler imaging in dogs with pulmonary arterial hypertension. J Vet Intern Med, 21(6):1280-9.
Soydan, L., Kellihan, H., Bates, M., et al. (2015). Accuracy of Doppler echocardiographic estimates of pulmonary artery pressures in a canine model of pulmonary hypertension. J Vet Cardiol, 17(1):13-24.
Spalla, I., Payne, J., Borgeat, K. et al. (2017). Mitral Annular Plane Systolic Excursion and Tricuspid Annular Plane Systolic Excursion in Cats with Hypertrophic Cardiomyopathy. J Vet Intern Med, 31(3):691-699.
Tai, T., Huang, H. (2013). Echocardiographic assessment of right heart indices in dogs with elevated pulmonary artery pressure associated with chronic respiratory disorders, heartworm disease, and chronic degenerative mitral valvular disease. Veterinarni Medicina, 58, 2013 (12): 613–620.