Avian Cardiology Essentials

Abstract

Cardiovascular disease commonly occurs in companion birds and poses a serious threat to the quality of life and longevity of many avian species. Successful intervention requires a foundational understanding of relevant anatomy and physiology, as well as heightened awareness of risk factors and recognition of clinical disease states, including atherosclerosis, congestive heart failure, and pericardial disease and effusion. This lecture reviews key features of avian cardiovascular anatomy, disease states commonly encountered in practice, essential elements of a diagnostic workup, and current treatment approaches that can improve longevity and quality of life for these patients.

 

Outline

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Photo credit: Dr. Minh Huynh

Anatomy and physiology of the avian cardiovascular system Cardiac features Vasculature Relevant respiratory anatomy Cardiovascular control systems and hemodynamics Cardiovascular disease states  Atherosclerosis Pathophysiology and lesion characterization Clinical manifestations and sequelae Prevalence and risk factors Congestive heart failure Pathophysiology Clinical manifestations Pericardial disease and effusion Pathophysiology Clinical manifestations

• Diagnosis of cardiovascular disease
  • History, clinical signs, and physical examination findings
  • Clinical pathology
  • Electrocardiography and blood pressure
  • Radiography
  • Ultrasonography

• Treatment approaches to cardiovascular disease in the avian patient

• • Atherosclerotic disease
  • Congestive heart failure
  • Pericardial effusion and cardiac tamponade

• Prognostic considerations and follow-up

 

About the presenter

Dr. Brenna Fitzgerald is an associate veterinarian at Homestead Animal Hospital in Centennial, Colorado. Dr. Fitzgerald is a 2007 graduate of Texas A&M University College of Veterinary Medicine. She then worked as an associate in a private, multi-doctor practice in Dallas, Texas, where she practiced small animal, avian, and exotic animal medicine. Dr. Fitzgerald then completed both a clinical internship and residency at Dr. Brian Speer’s Medical Center for Birds in Oakley, California. She earned Diplomate status in avian practice in 2012. Dr. Fitzgerald has both published and presented on topics related to avian cardiology, including… [MORE]

 

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Expert Q&A

Dr. Fitzgerald answered remaining questions during a separate meeting and a transcript of her answers are posted below in italics. Each individual attendee also received their answer via email.

 

ANATOMY/PHYSIOLOGY

Is the shape of the avian red blood cell of significance?

Editor’s reply:  Slide 34 of Dr. Fitzgerald’s presentation includes a note that the reduced deformability of the nucleated red blood cell is one factor that makes birds more prone to pulmonary hypertension and right-sided congestive heart failure. I have attached a screenshot of that slide. (Click image to enlarge).

The attendee then wrote:  Thank you for the reply, what I wished to understand why the birds have nucleated RBC any evolutionary advantage. This class actually informs that it’s a major disadvantage. So is it a genetic defect or an evolutionary error or something else?

Editor’s follow-up reply:  I have since met with Dr. Fitzgerald and she did not have an answer for you regarding this conundrum.

Losing the nucleus does allow the red blood cell to contain more hemoglobin, which of course boosts the oxygen-carrying capacity of cells. However, the mechanism by which maturing red cells eject their nucleus is poorly understood. Presumably this process was part of an evolutionary “jump” or improvement, but I don’t think we can call it an evolutionary error per se. So many life forms have made this system work for them.

Thank you for sharing this thought-provoking question.

 

SPECIFIC DISEASE CONDITIONS

Is atherosclerosis mainly seen in old birds only?  What are the typical ages you see with atherosclerosis? 

Atherosclerosis is seen more in older birds, and there have been statistics done and it does seem as they start to get older, they’re more likely to have atherosclerosis.

Beaufrère H, Ammersbach M, Reavill DR, et al. Prevalence of and risk factors associated with atherosclerosis in psittacine birds. J Am Vet Med Assoc. 2013;242(12):1696-704. doi: 10.2460/javma.242.12.1696. PMID: 23725433.

What is considered old age will vary by species:

• For example, when medium-sized parrots, like African grey parrots and Amazon parrots, get into their 20s and 30s, we start to see clinical signs related to atherosclerosis. Although there are outliers that can be a lot younger when they start showing signs… 
• When we’re talking about smaller birds, like lovebirds or cockatiels, you might start seeing issues in those guys—at least in lovebirds—when you get past 10 years of age. And then in cockatiels, when in their teens, certainly 20s. 
• For larger parrots, like cockatoos and macaws, we’re seeing issues probably in their 30s and 40s, but it does vary quite a bit.  

Is [atherosclerosis] common in both sexes?

The short answer is yes.

Atherosclerosis can occur in both male and female birds, but the statistics that we have indicate that there is a higher risk of atherosclerosis if the bird is female, particularly in birds with a great deal of egg laying activity. The theory is that changes in cholesterol levels related to all of the metabolic changes and the production of egg yolks may hasten the development of atherosclerosis in female birds .  

Beaufrère H, Ammersbach M, Reavill DR, etal. Prevalence of and risk factors associated with atherosclerosis in psittacine birds. J Am Vet Med Assoc. 2013;242(12):1696-704. doi: 10.2460/javma.242.12.1696. PMID: 23725433.

Is atherosclerosis associated with [an] overweight [body condition] in pet birds?

It seems to be, yes. There are not any studies or statistics to support that but obesity does, at least anecdotally, seem to be a risk factor. Like people, bird that have been chronically obese can be more predisposed to atherosclerosis.

Is atherosclerosis an issue in chickens since they have a much shorter lifespan?

Atherosclerosis is known to occur in birds other than parrots, including chickens. These lesions are generally not as significant in chickens. For instance, we definitely do not see as large a degree of blockages or complete blockages, but [chickens] definitely do get atherosclerosis. 

Is it caused mostly by environmental factors (diets, lifestyle, etc.)?

The limited research that exists suggests that diets that are high in fat, certainly diets that are high in cholesterol or animal-based food, are definitely a risk factor. Companion birds ultimately diagnosed with advanced lesions often have a long-term history of eating animal-based foods, like meat, cheese, egg, or at least egg yolk, or the marrow out of chicken bones. 

There’s also a suggestion that lack of exercise might play role in the development of atherosclerosis, the same way that it might for human. Pet birds tend to be very sedentary. Free-ranging birds may fly for miles and miles every day and birds don’t in captivity…

Those are probably the biggest environmental factors:  diet and exercise. 

Beaufrère H. Atherosclerosis: Comparative pathogenesis, lipoprotein metabolism, and avian and exotic companion mammal models. J Exotic Pet Med. 2013: 22(4):  320-335. doi:  10.1053/j.jepm.2013.10.016.

 

CLINICAL PICTURE

Gut peristalsis is reduced in cardiac disease. What is the normal peristalsis rhythm so we can detect alterations?

Another attendee replied via chat:  Gastrointestinal (GI) peristalsis is best evaluated with a barium series. In decreased perfusion cases it is quite marked.

Dr. Fitzgerald added:  Normally when you’re observing GI peristalsis through ultrasound or a barium series on fluoroscopy, and you’re watching peristalsis in real time there are very regular contractions of the ventriculus or gizzard. Also, the intestinal tract is constantly moving with those peristaltic waves. So the attendee who answered via chat is correct. You can have a kind of generalized ileus or you can have more segmental hypomotility, but normally the gut is moving very actively all the time.

Pulmonary edema affects differently air sacs and lungs?

I think you are asking if [edema] is a phenomenon that affects the air sacs. If that’s what you mean, the answer is no.

Fluid does not collect in the air sacs. The air sacs can become compressed by fluid in the coelomic cavities but pulmonary edema really only refers to fluid [congestion] in the lungs.

Editor’s note:  Remember also that the air sacs are avascular structures. So there are no (or few) vessels from which fluid can exude. Learn more about the air sac system with the RACE-approved webinar recording Avian Respiratory Anatomy, Physiology & Diseases:  An Overview.

Do birds exhibit dysphagia or dysmetria from low cardiac output or hypertension?

For dysphagia, I would say no. If you’re referring to gastrointestinal function, then yes, hypomotility can be seen as a sequela of reduced blood flow.

Editor’s note:  Dysmetria, or cerebellar ataxia, is not associated with cardiovascular disease per se however cardiovascular disease can manifest as weakness, falling, or collapse. Slide 41 of Dr. Fitzgerald’s presentation lists clinical signs seen with atherosclerosis and reduced perfusion. (Click image to enlarge).

 

DIAGNOSTICS

In case of valvular insufficiency, is it possible to detect a murmur at auscultation?

Editor’s reply:  Dr. Fitzgerald discusses auscultation tips, including detection of murmurs, at Slide 40. This slide can be found at approximately timestamp 1:09:13.

What is her recommended sedation protocol for suspected cardiovascular disease patients? What sedative do you use for echos? Do you have a favorite sedative to use for taking x-rays?

The sedation protocol that I use for most cardiovascular patients includes two drugs, butorphanol and midazolam, both given intramuscularly.

• Butorphanol is dosed at 2 mg/kg.
• The midazolam dose range is 0.5-2.0 mg/kg. I usually use 1 mg/kg but in unstable patients, I might be more likely to choose 0.5 mg/kg.
• Sedation is reversed with flumazenil.*

…In most cases, this protocol is going to allow me to get x-rays taken and then get an echo done. However, sometimes the patient is too unstable OR too uncooperative and unstable to be held down for x-rays and then I might start with an echo instead.  

Editor’s note:  In most species, the dose for the benzodiazepene antagonist, flumazenil, is 0.02-0.1 mg/kg IM, IV (Exotic Animal Formulary, 4^th ed).

How are you positioning these birds for ultrasound? Are they awake?

Editor’s reply:  Slide 70 of Dr. Fitzgerald’s presentation summarizes recommended positioning. (Click image to enlarge).

Since the heart is surrounded by air sacs, how to use echocardiography to evaluate the heart?

Editor’s reply:  Please visit Slide 71 of Dr. Fitzgerald’s presentation, which summarizes how the liver is used as an acoustic window via the ventromedian approach. (Click image to enlarge).

What frames per second do you usually use ?

I don’t have an exact frames per second. We try to keep that high, on the higher end…You have to make certain adjustments to try to get enough penetration to target the heart. And sometimes you have to turn your frame rate frequency down in order to get that…

Any good references for normal pulmonary pressures based on tricuspid regurgitation (TR) on echo or what your category is for mild-moderate-severe pressure half-time (PHT)?

It’s very difficult normally to get pulmonary pressures. There is a case report in which pulmonary hypertension was determined by measurement of right AV valve velocity.

Sedacca CD, Campbell TW, Bright JM, Webb BT, Aboellail TA. Chronic cor pulmonale secondary to pulmonary atherosclerosis in an African Grey parrot. J Am Vet Med Assoc. 2009;234(8):1055-9. doi: 10.2460/javma.234.8.1055. PMID: 19366339.

In this case report the authors estimated pulmonary pressure at 90 mmHg. The authors commented that there were no published reference ranges for normal pulmonary pressures in birds, but they concluded that the bird in this case had pulmonary hypertension based on mammalian normals and the confluence of abnormalities documented in the case.

I’ve dug around the literature trying to find any normals for pulmonary arterial pressure (PAP) in birds or definitions for what’s considered mildly, moderately, or markedly elevated. It doesn’t seem that there are any accepted standard definitions of what PAPs correspond with different grades of severity of pulmonary hypertension. There are many old studies when people were first looking at these sorts of things, and from what I’ve found, “normal” in chickens and ducks is 20-30 mmHg. Most investigation has been in the context of pulmonary hypertension (causing so-called “ascites syndrome”) in broiler chickens, which is influenced, among other things, by genetics and altitude (hypoxia). One paper characterized lowest PAP values in susceptible broilers as 12-22.9 mmHg, intermediate PAP values as 23-32.9 mmHg, and highest PAP values as 33-62 mmHg. The birds with elevated PAPs consistently exhibited hemodynamic characteristics of pulmonary hypertension. That seems to fit with what you’ve observed with birds having effusions at >55 mmHg. I think it’s entirely fair to consider numbers >50 mmHg to be elevated and consistent with pulmonary hypertension especially if there is supporting evidence (effusions, RV hypertrophy and dilatation, etc, pulmonary artery disease, etc). I tend to use sildenafil in any case with such abnormalities suggestive of pulmonary hypertension and have seen some excellent clinical response.

Is it possible that the large most cranial vessel on the lateral view is in part the thoracic caudal vena cavas and summated with the brachiocephalic trunk(s)?

You pose an excellent question. I’ve performed a few dissections with the objective of determining the position of these structures and how/where they would appear radiographically. What I’ve learned from these dissections, together with CT scans, is that the cranial venae cavae are situated dorsolaterally relative to the brachiocephalic trunks, do not overlap them, and do not summate with them on the lateral view. The cranial venae cavae do, however, cross paths (somewhat perpendicularly) with the ascending aorta, pulmonary arteries, and pulmonary veins at the dorsal aspect of the heart and this would produce some (though I think minor) summation on the lateral radiograph. 

Have you used the thoracic inlet window to visualize greater vessels?

As for using the thoracic window inlet to visualize the great vessels, I have done so endoscopically, if I understand your question correctly. 

Do you have access to CT scan? What do you recommend equipment wise?

Epica Animal Health manufactures the VIMAGO ^TM Systems and these are really ideal for this kind of work.

Any suggestions of how or where to find a cardiologist that will assist with work-up of avian patients? Ones I’ve approached are hesitant to look at a bird.

That is definitely a problem because small animal cardiologists are not necessarily that comfortable with birds or that knowledgeable about birds. They’re just so different. I think for most veterinary practitioners they are going to need the input of a cardiologist in conjunction with the input of an avian specialist, therefore referral to a veterinary teaching hospital is generally your best bet. A cardiology service working in conjunction with an exotic animal medicine service may be able to do the best job.

 

THERAPY

Is your sildenafil a compounded oral liquid?

Yes, sildenafil is compounded into an oral liquid.

Any experience with torasemide in birds?

No. I’m not familiar with this diuretic.

Can telmisartan also be used to block the renin-angiotensin-aldosterone system (RAAS)?

Telmisartan is an angiotensin II receptor blocker, but I’m not really familiar with this drug.  

Editor’s note:  Here are a few resources that may be of interest:

Akhrass PR, McFarlane SI. Telmisartan and cardioprotection. Vasc Health Risk Manag. 2011;7:677-83. doi: 10.2147/VHRM.S9447. PMID: 22140319; PMCID: PMC3225351.

Konta M, Nagakawa M, Sakatani A, Akabane R, Miyagawa Y, Takemura N. Evaluation of the inhibitory effects of telmisartan on drug-induced renin-angiotensin-aldosterone system activation in normal dogs. J Vet Cardiol. 2018;20(5):376-383. doi: 10.1016/j.jvc.2018.07.009. PMID: 30126722.

Veterinary Specialist Services. Telmisartan – Fighting that RAAS from a different angle. Veterinary Specialist Services website. Available at https://s3-ap-southeast-2.amazonaws.com/wh1.thewebconsole.com/wh/8191/images/I-R-F-Telmisartan–1-.pdf. Accessed June 13, 2022.

Do you like to use NSAIDs in atherosclerosis cases for the inflammatory component of the disease?

I don’t do that because I don’t think anybody knows how effective NSAIDs are at addressing that particular type of inflammation.

I’m more apt to reach for omega fatty acid supplementation, which is thought to have anti-inflammatory effects. And what I use is essentially a flaxseed oil supplement called VetOmega^®. The dose is 0.1-0.2 ml/kg BW once a day. I think this is a really good supplement to give these guys that we’re suspecting of having atherosclerosis.

Isoxsuprine availability has been problematic recently, if becomes unavailable is pentoxifylline an alternative?  Other options?

Dr. Fitzgerald did address this issue during her live presentation at slide 96. (Click image to enlarge).

Dr. Fitzgerald added:  …There was a period of time when the compounding pharmacies were having trouble getting the isoxsuprine bulk powder. We were still able to score some tablets, and for a time we compounded our own. So I never really had zero access to isoxsuprine. And I’m glad I didn’t because who’s to say, we don’t know, how effective pentoxifylline is at all and we don’t know if it can be considered a stand in for a vasodilator like isoxsuprine.

Now it seems, at least this is true in the US, that the bulk powder has become available again and so I haven’t had any problems getting [isoxsuprine] from the compounding pharmacy. But there was a period of at least a year, where we sourced 20-mg tablets and compounded our own.

Are there any advanced treatment options like stenting arteriosclerotic lesions? Or is vasculature too small for catheter access?

I am unaware of stenting ever being tried, or at least published, in avian medicine. I can imagine this being possible in a larger bird, perhaps even something like a large raptor. But at least at this point in veterinary medicine, I am not aware of that being possible in small parrots.

Editor’s note: A literature search confirms that rodents (mice, rats) have been used as a laboratory model for stenting. Miniaturized stents were used in the mice studies.

Cornelissen A, Florescu R, Schaaps N, et al. Implantation of human-sized coronary stents into rat abdominal aorta using a trans-femoral access. J Vis Exp. 2020;(165). doi: 10.3791/61442. PMID: 33283790.

Iqbal J, Chamberlain J, Francis SE, Gunn J. Role of animal models in coronary stenting. Ann Biomed Eng. 2016;44(2):453-65. doi: 10.1007/s10439-015-1414-4. PMID: 26259974.

Rodriguez-Menocal L, Wei Y, Pham SM, et al. A novel mouse model of in-stent restenosis. Atherosclerosis. 2010;209(2):359-66. doi: 10.1016/j.atherosclerosis.2009.09.071. PMID: 19875114; PMCID: PMC2846184.

 

RACE approval

This program is approved by the American Association of Veterinary State Boards (AAVSB) Registry of Continuing Education (RACE) to offer a total of 1.00 CE credits to any one veterinarian and/or 1.00 veterinary technician CE credit.

 

References