Avian Cardiology

Question 1

What are some unique features of the avian cardiovascular system?

Identify at least ten ways the avian cardiovascular system differs from mammals.

Answer 1

1. Unique Avian Features
   
   1. HR relative to body mass is lower in birds vs mammals
   2. Heart is relatively larger and stroke volume and CO greater
   3. HR can increase 2-4 X during flight (ex: budgerigar in flight has CO 7X dog in max. exercise)
   4. MAP higher vs mammals, but total peripheral resistance is lower

Question 2

Where is the avian heart located anatomically?

What air sacs surround the heart?

What species ahve a sinus venosus prior to right atrium?

What is unique about the right AV valve in birds?

How do avian cardiomyocytes differ from ammalian ones?

Answer 2

1. Heart
   
   1. Located in cranioventral coelom next to sternum, tracheal bifurcation, esophagus, proventriculus
   2. Surrounded by cervical, clavicular, and cranial thoracic air sacs
   3. Intrathoracic diverticula of the unpaired clavicular air sac surrounds the heart and great vessels
      
      1. Also pneumatize the sternum and suspend the esophagus, trachea, syrinx
   4. 4 chambered heart (LA, RA, LV, RV) composed of endocardium, myocardium, epicardium
      
      1. Cardiac cartilage forms fibrous rings around aorta and pulm. arteries
      2. Some spp. have sinus venosus prior to RA (ex: chickens, crows, ostriches, kiwis)
   5. Right AV valve lacks chordae tendinae (unique to birds)
      
      1. Has a spiral muscular flap composed (atrial myocardium and ventricular myocardium)
   6. Avian cardiomyocytes are smaller and more numerous than mammalian
      
      1. T-tubule system is absent lacking in birds
      2. Sarcolemma and sarcoplasmic reticulum occur at cell surface
      3. Lack M-bands that connect myosin filaments in mammalian cardiac muscle

Question 3

How is cardiac size measured in avian species?

What factors inluence these measurements?

Answer 3

Question 4

Describe the conduction system of the avian heart.

How is it different from mammals?

Answer 4

1. Cardiac conduction system
   
   1. Three bundle branches (left, right, middle)
   2. AV ring of Purkinje fibers surrounding the right AV opening and connecting to the right AV valve
   3. Ventricular depolarization begins subepicardially and spreads to endocardial surface
      
      1. Reason for negative ECG in lead II
      2. Different from mammals whose depolarization starts at endocardium

Question 5

Describe the anatomy of the avian pericardium.

Answer 5

1. Pericardium = non-compliant sac
   
   1. Outer layer is continuous with adventitia of great vessels
   2. Attachments exist to sternal plate, hilus of lungs, adjacent air sacs, and liver

Question 6

Describe the vascular anatomy of avian species.

What is the structure of the vena cava as it enters the heart?

Where do the coronary arteries originate?

What vessels arise from the ascending aorta? What areas are supplied by it?

What are the major branches of teh descending aorta? What areas are supplied by it?

How do the gonads receive blood?

Describe the pulmonary vasculature.

What is the renal portal system? How is it controlled?

Answer 6

1. Vascular Anatomy
   
   1. Vena Cava
      
      1. Paired crania venae cavae enter at sinoatrial valve
      2. Septum sinus venosi separates LCrVC and RCrVC
2. Single caudal vena cava empties into right atrium
3. Coronary Arteries and Cardiac Veins
   
   1. Unlike in mammals, the ascending aorta immediately gives rise to L and R coronary arteries
   2. R coronary is largest in most spp. and anastomose frequently
   3. Left, right, middle, and left circumflex cardiac veins (middle and left circumflex = largest)
4. Ascending aorta – supply of head, neck and thoracic limbs
   
   1. Large, paired brachiocephalic trunks brach simultaneously from ascending aorta
   2. Subclavian arteries supply flight muscles, so they are larger than aorta
   3. Intercarotid anastomosis at base of brain, present in virtually all bird spp. 🡪 no circle of Willis
5. Descending aorta – supply of trunk, viscera and pelvic limbs
   
   1. Major branches: Coeliac, cranial mesenteric, pair cranial renal, external iliac, ischiatic, caudal mesenteric, internal iliac
   2. Testicular arteries arise from cranial renal arteries
   3. Single or multiple ovarian arteries arise from either left cranial renal artery or from aorta
6. Pulmonary vasculature
   
   1. RV → pulmonary trunk → R and L pulmonary arteries 🡪 intraparabronchial arteries 🡪 intraparabronchial arterioles
7. Venous System
   
   1. Right jugular is larger than left and receives blood from the left via anastomosis at base of head
8. Renal Portal System = ring formed by cranial and caudal renal portal veins ventral to kidneys
   
   1. Receives blood from gut and pelvic region
   2. Passes through renal parenchyma mixing with post-glomerular efferent arteriolar blood 🡪 renal veins 🡪 common iliac veins and CdVC
   3. Renal portal valve = smooth muscle sphincter in external iliac v.
      
      1. Sympathetic and parasympathetic control of venous blood that enters kidney tissue\
   4. Venous flow can be shunted into internal vertebral venous sinus or to hepatic portal system
      
      1. Through caudal mesenteric vein (bidirectional flow)
9. Vascular microanatomy
   
   1. 2 classifications for arterial structure: elastic and muscular arteries
   2. Resilience of avian elastic arteries are superior to mammals

Question 7

How is the avian cardiovascular system mediated?

Which catecholamine is the more potent stimulant in birds?

Answer 7

1. Cardiovascular Control Systems
   
   1. Systemic arterial blood pressure is function of cardiac output and resistance of arterial system
   2. Both epinephrine and norepinephrine act on beta-adrenergic receptors
   3. Positive inotropic, chronotropic, and lusitropic effects
   4. Unlike in mammals, norepinephrine believed to be more potent stimulant

Question 8

What is atherosclerosis?

What are some potential complicatiosn from this disorder?

Describe the pathophysiology of this disease.

Answer 8

1. Atherosclerosis
   
   1. Definition: chronic inflammatory and degenerative disease of arterial wall where the lumen narrows by progressive accumulation of inflammatory cells, fat, cholesterol, calcium, cellular debris that forms fibrofatty atheromatous plaques within the intima
   2. Potential complications: stenosis, ischemia, thrombosis, hemorrhage, aneurysm
   3. Pathophysiology
      
      1. Endothelial dysfunction, damage and oxidative stress which promotes increased endothelial permeability to lipoproteins and intimal adherence and migration of inflammatory cells
      2. Attracts monocytes 🡪 macrophages (internalize lipoproteins, store cholesterol) 🡪 foam cells
      3. foam cells die by necrosis or apoptosis = further accumulation of lipid and necrotic debris = necrotic core
      4. Smooth muscle cells proliferate and migrate into intima/subintimal space producing extracellular matrix
      5. Fibrous cap overlays lipid and necrotic core
      6. Smooth muscle cells also form foam cells

Question 9

What are the common gross and histologic lesions of atherosclerosis in avian species?

Describe the grading scale used for lesion characterization.

How does disease differ between mammalian and avian species?

Why is acute myocardial infarction less likely in birds?

What sites are most affected?

Answer 9

Gross

• Vascular intima thickening with mural lipid accumulation
• Particularly in the aorta, brachiocephalic trunks, pectoral and carotid arteries
• Thickened artery walls and yellow plaques

Histo -

• macrophages wtihin intima, vacuolated smooth muscle
• Mineralizaiton less ommon in birds than in mammals

1. Lesion Characterization
   
   1. I and II: early – increased foam cells, extracellular lipids and Ca, no arterial wall disruption
   2. III: intermediate – mild arterial wall architectural disruption
   3. IV-V: advanced – formation of fibroatheromatous plaque by accumulation of lipid and cell debris
   4. VI and VII – fissure, hematoma, thrombosis and VII is calcific lesion (osseous metaplasia)
   5. Unlike in humans, avian clinical dz primarily progressive flow-limiting arterial stenosis in birds, rather than thrombosis and hemorrhage of disrupted plaques
   6. Acute myocardial infarction less likely in birds because:
      
      1. Differences in coronary vasculature
      2. Greater collateral circulation
2. Lesion Location
   
   1. Most frequently: ascending aorta, brachiocephalic trunks, pulmonary arteries
   2. Coronary and aortic aneurysms secondary to atherosclerosis d/t decreased compliance of vessels
3. 1. 1. Inability of avian thrombocyte to form shear-resistant arterial thrombi

Question 10

What psittacine genera are predisposed to atherosclerosis?

How prevalent is atherosclerosis in psittacines?

What are some risk factors for developing atherosclerosis? (Seven)

What galliform species are susceptible? What risk factors exist for them?

How prevalent is atherosclerosis in raptors? What risk factors exist for them?

What other species are susceptible?

Answer 10

Psittacus, Nymphicus, Amazona

• Prevalence
  
  • Prevalence (2 to 92%) varies with highest reported in Amazons and Grey parrots
  • Advanced lesions most common in Grey parrots > Amazons > cockatiels
    
    • Cockatiels and macaws are least susceptible
• Risk Factors
  
  • Increasing Age
  • Female sex
    
    • Estrogen → lipoproteins used to transport lipid from liver to yolk
  • High cholesterol and dyslipidemia
    
    • Grey parrots, Amazons, cockatiels >>>> cockatoos >macaws
    • High HDL is not protective because most cholesterol in birds is transported as HDL
  • High calorie and fat diets
  • Limited physical activity
  • Reproductive disease
  • Hepatic disease
  • Concurrent myocardial fibrosis
  • Low intake of omega-3 fatty acids protect
    
    • Severity of atherosclerosis negatively correlates with muscle and adipose tissue content of linolenic acid in parrots
• Non-psittacine species
  
  • Galliformes
    
    • Chickens/Turkeys – males more prone vs female
    • Turkeys can get dissecting aortic aneurysms with copper deficiency and atherosclerosis
  • Raptors
    
    • Common in lder captive birds and free-ranging
    • Falconiformes and Accipitriformes: 8%; Strigiformes: 16%
    • Risk factors – inactivity in captivity, increasing age, obesity, rapid wgt loss
    • Common practice of feeding day-old chicks may potentiate atherosclerosis
  • Also seen in Columbiformes, Spheniscifomes, and Ciconiiformes

Question 11

What are the common changes to the heart following atherosclerosi?

Answer 11

Left vetnricular dilatation, Dilation of LA, right heart dilatation, right heart failure

Terio ZP 32 - Psittaciformes

Question 12

What are some potential causes of non-atherosclerotic aneurysm and aterial rupture in avian species?

What species are particularly at risk?

What dietary components may be causing issues?

Answer 12

1. Non-atherosclerotic Aneurysm and Arterial Rupture
   
   1. Copper deficiency, hypertension, fungal infection, spontaneous/idiopathic
   2. Mainly seen in ostriches and turkeys – systemic hypertension, genetics, connective tissue disorders, peas in the ration (toxin beta aminopropionitrile in the peas can cause interference with collagen formation), dietary deficiencies (copper deficiency)
   3. Copper dependent enzyme is needed for connective cross-linking collagen & elastin in artery wall

Question 13

Describe heart failure in avian species.

What clinical signs present with right sided CHF?

What about left sided CHF?

Describe the pathophysiology of heart failure in birds. How does myocardial hypertrophy lead to heart failure?

What does heart failure difffer between birds adn mammals?

Answer 13

• Heart Failure
  
  • Right-sided CHF – venous congestion, hepatic congestion, ascites, pericardial effusion
  • Left-sided CHF – pulmonary edema and congestion of pulmonary veins
  • Pathophysiology
    
    • CHF is not primary disease, but it is a frequent clinical endpoint to CV dz in companion birds
    • Myocardial failure – primary dz of myocardium or 2ndary to chronic pressure or volume overload
    • Hypertrophy initially decreases wall stress and increases contractility but eventual ischemia of hypertrophied myocardium 🡪 fibrosis and increased collagen content impairing bot hsystolic and diastolic function
    • Eccentric hypertrophy characterized by chamber enlargement and increased myocardial mass with little increase in wall thickness
    • Birds = greater propensity for developing pulmonary hypertension and R-sided CHF vs mammals
    • Due to morphology of right AV valve, less deformable nucleated erythrocytes, rigid non-distensible lungs which limit blood capillary expansion and accommodate greater blood flow

Question 14

Describe common causes of myocardial disease in avian species.

What species are prone to spontaneous DCM?

How does atherosclerosis lead to myocardial changes?

What are three viruses that cause myocardial damage? What lesions are typically seen?

What dietary issues can lead to myocardial damage?

What toxins?

What neoplasia?

Answer 14

• Primary myocardial disease
  
  • DCM – ventricular dilation, thinning of myocardium, systolic and diastolic dysfunction
    
    • 4 wk old turkey poults – spontaneous DCM
  • Myocardial changes consistent with ischemic injury assoc with atherosclerosis in psittacines
    
    • Potential to produce arrhythmias, risk of sudden death
    • Acute myocardial infarction rare
      
      • Difference in coronary artery and greater collateral circulation vs humans
  • Proventricular Dilatation Disease PDD caused by Avian Bornavirus (ABV) characterized by lymphoplasmacytic infiltration of nerve ganglia.
    
    • Inflammatory infiltrates found in epicardium and myocardium, esp Purkinje fibers
    • Potentially precipitates arrhythmias and sudden death
    • Study: 70% PDD cases had cardiac lesions
  • Polyomavirus produces myocarditis with necrosis and hemorrhage
    
    • Intranuclear inclusion bodies within cardiomyocytes
  • WNV, parasites (protozoal, filaroid nematodes)
  • Visceral gout – inflammatory reaction accompanies urate deposition
  • Deficiencies of vit E/selenium – myocardial degeneration, white streaks
  • Dietary Ca-Phos imbalance, vitamin D toxicity - cardiac and vascular mineralization
  • Cardiotoxins – furazolidone induces DCM in turkey poults (used as model for human DCM)
  • Lead toxicosis in waterfowl – myocardial degeneration, necrosis, subsequent thrombosis/infarction
  • Neoplasia – hemangioma, hemangiosarcoma, rhabdomyoma, rhabdomyosarcoma, fibrosarcoma, melanosarcoma, lymphoma
  • Poultry – oncogenic viruses – lymphoma (diffuse or nodular)
  • Traumatic injury
  • Congenital defect

Question 15

How does heart disease lead to pressure overload in avian species?

What diseases commonly result in this sequela?

Pulmonary hypertension commonly affects what species?

Answer 15

• Pressure overload
  
  • HCM – arterial luminal stenosis and decreased compliance from atherosclerosis or pulmonary hypertension 2ndary to atherosclerosis, chronic pulmonary dz or L-sided CHF
  • The incidence of fibrotic changes increases in proportion to atherosclerotic lesion severity
  • Systemic hypertension has not been defined in psittacines
  • Iron storage dz in mynah and yellow-billed magpie -> severe hepatic fibrosis with cardiomegaly or CHF
  • Cor pulmonale – Grey parrot d/t pulmonary arterial atherosclerosis and severe pulmonary hypertension
  • Pulmonary hypertension plays key role in ascites syndrome of broilers
    
    • Primary cause of pulmonary hypertension and hypoxemia -> inadequate cardiac output related to relatively small LV and poor systolic function
    • Environmental conditions that contribute: high altitude, hot/cold temps that increase O2 demand

Question 16

Describe the mechanisms resulting in volume overload of the avian heart.

Are there any species with a higher incidence of septal defects?

Answer 16

• Volume Overload
  
  • Endocardiosis – non-inflammatory nodular thickening of valves
    
    • Idiopathic, mostly affecting left AV valve
  • Congenital – ventricular or atrial septal defects in 7% Mississippi Sandhill Cranes
    
    • Cockatoos overrepresented with ventricular septal defects

Question 17

What are the clinical signs of heart arrhythmias in avian species?

What arrhythmias have been documented in birds? And in what species?

Answer 17

1. Arrhythmias
   
   1. C/S: absent OR weakness, syncope, sudden death
   2. Supraventricular and VPCs reported in chickens, Amazons, Grey parrots
   3. First-degree AV block, 2nd degree AV block – may be found in healthy individuals
   4. Mobitz type 2 2nd degree AV block has potential to progress to 3rd degree AV block

Question 18

How do mammals compensate physiologically during heart failure?

HOw does this differ in birds?

Answer 18

• Compensatory mechanisms in heart failure
  
  • In mammals – AII and aldosterone – mediators of inflammation, oxidative stress, myocardial and vascular remodeling and fibrosis
  • AVT product of posterior pituitary homologous to mammalian antidiuretic hormone ADH
    
    • Released in response to increases in plasma osmolality, hypotension, and AII
    • Induces vasoconstriction, decreases GFR by constriction of afferent glomerular arterioles and promotes tubular water resorption
  • Prevalence
    
    • Cardiac dz in 10% of 269 psittacines (path survey at Ohio State – 1991-1995)
    • 58% CHF, 42% systemic infectious diseases
  • Another study 36% of 107 psittacines had grossly visible heart abnormalities (99% had histo changes)
    
    • 60% inflammatory infiltrates
    • Majority of noninfectious CV dz = atherosclerosis and CHF
    • Atherosclerosis in 13%

Question 19

What are some causes of pericardial effusion in avian species?

Cardiac tamponade is likely to affect which side of the heart first? Why?

Fibrinous pericarditis is commonly caused by what organism?

What type of inflammation is associated with visceral gout?

Answer 19

• Pericardial Disease and Effusion
  
  • Pathophysiology
    
    • Causes of pericardial effusion - pericarditis, trauma or aneurysmal rupture, cardiac or pericardial neoplasia, metabolic derangement, toxicity, R-sided CHF, idiopathic
    • Cardiac tamponade – thinner walled RV overcome by the pressure of pericardial effusion more rapidly than left 🡪 R-sided CHF occurs first
      
      • Clinical severity depends on the rate that the pericardial effusion develops
• Pericarditis and Visceral Gout
  
  • Fibrinous pericarditis in 10% of C. psittaci infected psittacines
  • Pericarditis = most severe and persistent lesion in domestic turkeys infected with virulent C psittaci
  • Mycotic infections (Aspergillus) – pericardial dz by extension from resp tract or hematogenous spread
  • Viral etiologies (ex: psittacid herpesevirus, polyomavirus, adenovirus, avian influenza…)
  • Visceral gout frequently affects pericardium and causes heterophilic inflamm response
    
    • Gout = smooth white plaques vs infectious = yellow rough exudates

Question 20

What are teh typical clinical signs that a bird has heart disease?

What findings might be appreciated on physical examination?

What signs are suggestive of diminished blood flow through stenotic arteries?

What signs and exam findings are consistent with CHF in birds?

What baseline diagnostic should be performed in birds for diagnostics for heart disease?

What findings might be seen on bloodwork?

Answer 20

Diagnostic Methods

• History, Clinical Signs, Exam Findings
  
  • C/S: subtle insidious onset with owner report progressively declining activity, reduced appetite, waning interest in house-hold activities, toys, vocalizations
    
    • Many subclinical and go unrecognized
    • No premonitory signs appreciated prior to sudden death
  • Presenting complaint: lethargy, depression, weakness, reduced appetite, respiratory distress, exercise intolerance
  • PE findings: cachexia, tachypnea, dyspnea, harsh lung sounds, pallor or cyanosis, tachycardia, arrhythmia, systolic murmur, poor pulse quality or deficits, coelomic distension, acites, peripheral edema, peripheral venous congestion, altered mentation
  • Cardiac auscultation relatively insensitive tool, absence of audible murmur does not r/o CV pathology
  • Arterial pulses best palpated proximal antebrachium and relative warmth of each extremity
• Atherosclerosis
  
  • C/S: diminished blood flow through stenotic arteries; vary based on artery affected, severity and any concurrent disease, falling, weakness, dysfunction of one or more limbs, +/- altered mentation
    
    • Sudden death as result of cerebral infarct, aneurysmal rupture, lethal cardiac arrhythmia
    • Recurrent or non-resolving derm conditions (axillary feather loss) 🡪 atherosclerotic lesions in vessels supplying these areas
• a)Tissue hypoperfusion or pain/numb/tingling sensation
• Congestive Heart Failure
  
  • Present most consistently w/ respiratory embarrassment as a results of intracoelomic air sac compression
    
    • Ascites and organomegaly, pulmonary edema or combination
  • Hepatomegaly (palpation beyond sternal margin), venous congestion (jugular and cutaneous ulnar veins), edema of hocks/feet, delayed absorption of SQ fluids (>48 hrs)
  • Pericardial effusion = muffled heart sounds, pulmonary edema (increased resp noise cranial dorsum parallel to spine; rare to hear cough, severe cases crackles and wheezes)
• Baseline Diagnostic for Birds with Signs of Cardiovascular Disease
  
  • CBC, Chem, rads, U/S, ECG, BP, Endoscopy, CT, MRI
  • CBC low sensitivity for CV dz – leukocytosis, heterophilia, lymphopenia, polycythemia
    
    • Polycythemia can result from chronic hypoxemia resulting from persistent ventilation/perfusion mismatch and increased oxygen demands
  • Chem – elevations in AST, CK, LDH; cardiac troponins T and I sensitive and specific in humans but no reference range established for birds
  • Diagnostic value of plasma lipid profile not established; hypercholesterolemia neither necessary nor sufficient for diagnosis of atherosclerosis
    
    • Birds with normal plasma cholesterol may have atherosclerotic dz, while those with hypercholesterolemia may not

Question 21

What is unique about electrocardiography in birds?

Where are leads placed in birds?

Describe the morphology of the electrocardiogram in a bird. What’s different from mammals?

Hoes avian blood pressure differ from mammalian blood pressure?

How can blood pressure be measured in birds?

What are the cutoffs for hypotension?

Answer 21

1. Electrocardiography
   
   1. Severe pathology and mechanical dysfunction can exist in absence of ECG changes
   2. Benzodiazepines used with increasing regularity in companion birds of unknown effect on ECG
   3. Right thoracic limb (RA – white), left thoracic limb (LA – black), left pelvic limb (LL – red)
   4. P wave followed in some birds by small depression in beginning of PR interval = Ta wave
   5. rS complex negative in lead II (prominent deflection); Q typically absent
   6. ST is short or absent and S merges into T wave (ST slurring), elevated above baseline
      
      1. May have P-on-T phenomenon which can be normal in some Amazons and Greys
   7. Unlike in mammals, ventricular MEA is negative in most birds (-90 degrees)
      
      1. Except: broiler chickens, Pekin ducks
2. Blood Pressure
   
   1. Arterial BP higher in birds than in most other vertebrates
   2. Direct BP = arterial catheter in superficial ulnar artery, deep radial artery or external carotid artery
   3. Indirect BP = Doppler and sphygmo 🡪 cuff 30-40% limb circumference
      
      1. Don’t usually agree with direct BP but monitor trends
      2. Oscillometric method is unreliable
   4. Hypotension defined as: systolic < 90 mmHg, MAP < 60 mmHg

Question 22

Describe the various imaging modalities for evaluating the avian heart.

• How can radiography be used to measure the heart?
  
  • What is a typical size of the heart for psittacines?
  • What lesions are suggestive of atherosclerosis?
• How can ultrasound be sued to evaluate the heart?
  
  • Why is ultrasound so difficult in birds?
  • What are the two main approaches?
• How can CT or MRI be used to evaluate the heart?
  
  • What are some difficulties in avian species with this approach?
  • What are some benefits to this approach?
• How can coelioscopy be used to evaluate the heart?
  
  • What are the two main approaches?
  • What sites are best appreciated from each?

Answer 22

• Radiography
  
  • Most practical = measurement of cardiac silhouette at widest point on VD view and comparison with both thoracic width at same level and length of sternum
    
    • Medium sized psittacines: 51-61% of thoracic width, 35-41% length of sternum
  • Increasing radiodensity and tortuosity of great vessels suggestive of atherosclerosis (not conclusive)
    
    • Most often along ascending and descending aorta, brachiocephalic trunk, occasionally along smaller arteries incl coeliac artery
  • Fluoroscopy may be considered – does not require patient restraint, sedation or anesthesia
• Ultrasound
  
  • 2D (B mode) – Motion-mode (M-mode) not useful - only longitudinal and semitransverse views attainable
  • presence of large sternal plate and air sacs substantially limits acoustic windows
  • 2 approaches for transcoelomic U/S
    
    • ventromedian – most commonly used for psittacine and raptors; liver is acoustic window
      
      • 2 longitudinal views (horizontal 4 chamber view) and vertical (2 chamber view)
      • reflection off ultrasound beam may produce mirror artifact 🡪 false impression of chamber dilation or aneurysm
    • parasternal – right lateral approach to avoid ventriculus
      
      • birds that do not have ribs with caudal extension ex: pigeons, gallinaceous birds
    • transesophageal U/S: 5 consistent views of cardiac structures, can use M-mode
      
      • size limitation b/c of narrow thoracic inlet, risk of esophageal perforation
    • some reference values available
    • accuracy and precision questionable with rapid HR, current resolution of equipment, and different observer can add up to 30% variability
• CT and MRI
  
  • seldom used to image heart because cannot be gated to fast cardiac cycle in birds to reduce motion artifacts and improve diagnostic value
  • CT can be used to image vasculature – investigate arterial calcification associated with advanced arteriosclerosis, cardiomegaly, ventricular dilation, pericardial effusion, effusion, ascites, pulmonary edema, venous congestion, cerebral complications (ischemic and hemorrhagic strokes)
• Endoscopy
  
  • Interclavicular approach – best for visualizing heart base, ascending aorta, brachiocephalic trunks, carotid and subclavian arteries, pulmonary arteries and jugular veins
  • Ventral midline approach – pericardiocentesis and pericardial biopsy; preferred if ascites because does not require entry to air sacs, minimizing fluid leakage into respiratory tract

Question 23

Discuss the therapeutic options for atherosclerosis in avian species.

What is the mechanism of isoxuprine? How does it help these cases?

How do ACE inhibitors help?

what about pentoxifylline?

Are statins usable in birds?

What dietary supplements can be helpful?

Answer 23

1. Atherosclerosis
   
   1. controlling risk factors and managing sequelae
   2. Isoxsuprine – peripheral vasodilator causing vascular smooth muscle relaxation via alpha-adrenoreceptor blockade
   3. ACE inhibitors – blocks formation of AII which promotes vasoconstriction by mediating release of catecholamines
   4. Pentoxifylline – promotes passage of erythrocytes through damaged microvasculature by increasing flexibility -> used in mammals
   5. Statins – group of lipid lowering drugs for atherosclerotic effects via inhibition of cholesterol synthesis
      
      1. Efficacy in birds questionable
         
         1. Hispaniolan Amazons: 10 and 25 mg/kg PO -> plasma levels below limit of quantitation
   6. Omega-3 fatty acids – improve lipid metabolism, reduce inflammation, minimize devmt of atherosclerosis

Question 24

What are the mainstays of treating congestive heart failure in avian patients?

How effective is furosemide in avian species? What doses have been used in avian species?

What is an advantage of spironolactone?

How are ACE inhibitors used in avian species? What dose and interval is supported by PK studies?

When are positive inotropes contraindicated in avian heart failure?

Answer 24

• Congestive Heart Failure (prognosis is poor)
  
  • Mainstays similar to small animal medicine 🡪 diuretics, ACE inhibitors, positive inotropes, beta blockers
  • Furosemide – potent loop diuretic inhibits Na, , and Cl co-transporter in ascending limb of loop of Henle promoting diuresis and excretion of Na and Cl
    
    • Efficaceous and has rapid onset of action in birds DESPITE the presence of only 10 – 30 % of looped nephrons in avian kidney
    • Dose and administration based on clinical effect 🡪 ultimate goal is for lowest dose that controls the congestive signs
    • Oral bioavailability assumed poor (60-75% in humans), so dose increased at least 2 fold
      
      • Chickens – 2.5 mg/kg SQ or 5 mg/kg PO q8-12h
    • Must monitor renal functional status and electrolytes given potential for dehydration and hypoK+
      
      • Lories and lorikeets – extremely susceptible to adverse effects of furosemide
  • Spironolactone – aldosterone antagonist 🡪 K+ sparing diuretic that can be used concurrently with furosemide to offset K+ loss (not expected to be efficacious as sole agent)
  • ACE-inhibitor – essential management for CHF long-term by blunting effects of RAAS
    
    • Enalapril most commonly used in birds and empirically appears safe and effective
      
      • PK supports 1.25 mg/kg PO q8-12h in pigeons and Amazons
      • Shorter half=life and lower max plasma concentration in Amazons vs pigeons
    • Potential AE: hypotension, renal dysfunction, hyperkalemia
  • Positive inotropes – enhance myocardial contractility 🡪 use if systolic dysfunction
    
    • Contraindicated: HCM where diastolic dysfunction is primary problem and outflow obstruction
    • Digoxin – digitalis glycoside: weak positive inotrope and negative chronotrope (slows sinus rate and decreases AV nodal conduction) – increases myocardial contractility by directly inhibiting the Na-K-ATPase pump resulting in intracellular Ca accumulation via activation of Na/Ca exchanger
      
      • Controversial in small animal and human medicine because failure to reduce overall mortality and proarrhythmic and GI side effects
      • Risks of digoxin toxicity 🡪 require therapeutic drug monitoring and ECG follow up
        
        • Arrhythmia further potentiated by hypoK+ from diuretic use
    • Pimobendan – calcium sensitizer and phosphodiesterase inhibitor: positive inotrope, vasodilator, positive lusitrope – enhances myocardial contractility via Ca sensitization of cardiac myofibrils and by phosphodiesterase III inhibition without increasing myocardial O2 consumption
      
      • Increases survival time and QoL in dogs with DCM and heart failure 2ndary to mitral valve disease
      • PK in Hispaniolan Amazons: 10 mg/kg PO required to reach peak plasma levels considered therapeutic in dogs and humans
      • AE: GI upset, potential for proarrhythmic effects

Question 25

What is the treatment for hypertrophic cardiomyopathy in avian species?

How is systemic hypertension managed in avian species?

Answer 25

1. Hypertrophic Cardiomyopathy
   
   1. Mostly secondary to pressure overload states
   2. Beta blockers to reduce HR and myocardial O2 consumption, improve diastolic coronary artery flow
2. Systemic Hypertension
   
   1. Beta blockers reduce arterial BP by decreasing CO and inhibiting RAAS activation
   2. Amlodipine is treatment of choice in cats
   3. No established definition of hypertension in avians

Question 26

When is lidocaine useful for avian arrythmias? What is teh effective dose?

When are atropine or glycopyrrolate indicated? When are they contraindicated?

Answer 26

1. Arrhythmias
   
   1. Lidocaine – parenteral antiarrhythmic agent to control life-threatening ventricular tachyarrhythmias
      
      1. Contraindications: SA or AV block
      2. AE: neuro dysfunction
      3. ED 50 6.3 mg/kg in chickens
   2. Antimuscurinic agents – atropine and glycopyrrolate – competitively inhibit binding of acetylcholine to muscarinic receptors
      
      1. Antidote for organophosphate and carbamate intoxication
      2. Contraindication: tachycardia or tachyarrhythmias, use cautiously if heart failure