The resp system in the equine athlete

What factors contribute to successful performance?

How does equine performance rely on the oxygen pathway?

• Relies mostly on aerobic (70% in 1000m sprint)

  • Inc distance inc aerobic capacity

• Problem anywhere along pathway will affect O2 delivery and gas exchange

What factors can you measure to determine how effective the oxygen pathway is?

VO₂ = volume of O₂ absorption

VO_2max= max rate of O₂ consumption during exercise (aka max aerobic capacity)- speed of reaching this correlated to endurance- can change with training

• Correlates with endurance ability so can assess these

How do you calculate minute ventilation?

• Tidal volume x breaths/min

How are ventilation and perfusion interrelated in terms of equine performance?

• If ventilation: perfusion ratio is mismatched then no matter how good the ventilation is there will be a 'limit'

(shunting —> reduced perfusion of poorly ventilated alveoli)

What effects the rate of perfusion in resp gas exchange?

• Resistance

• Pressure

• Shunting

What factors does diffusion in respiratory gas exchange depend on?

• Pressure gradient

• Transit time

• Alveolar-capillary barrier thickness

  • Species differences, disease (EIPH)

What can create resistance to airflow in the URT?

• Proportional to radius⁴

• Larynx has a high resistance (can get paralysis, diseases etc.)

  • Also nasal obstruction

  • most resistance from URT

By how much does minute ventilation increase in horses during exercise?

80L/min to 1800L/min

How can respiration be a limitation to exercise?

• Resp related to stride pattern

• CS see more frequently with exercise as exacerbated

• Exercise induced hypoxaemia (normal during max performance in atheltic breeds)

  • Pulmonary vascular pressure is high bc of thick diffusion barrier

• Obligate nasal breather so pulmonary resistance doubles during heavy exercise

What are the general resp changes that can cause poor performance?

• Inc pulmonary resistance

  • e.g.- URT disorders, resistance, turbulence, small airways (hypersecretion, blood, inflm)

• Dec alveolar/ pulmonary compliance

  • e.g.- oedema, hypertension, fibrosis, interstitial disease

  • thicker diffusion barrier

List some respiratory causes of poor performace

• Dynamic airway collapse

  • Inflammatory airway disease

  • Tracheal collapse

• Resp muscle/ chest wall disease

• Decrease CO

  • Dec lung or tissue perfusion, V/Q inequality

• Dec haemoglobin (chronic dz, anaemia)

(Unlikely to see muscle metabolism problems)

What is EIPH?

Equine induced pulmonary haemorrhage caused by 'capillary stress failure at intense exercise

• Highly prevalent

Describe the pathogenesis of EIPH

• CO and blood pressure inc

• Negative pressure inc in dorsal lung during insp

• Causes capillary wall rupture and haemorrhage (in caudo dorsal lung area)

• Progressive and irreversible 'veno-occlusive remodelling'

more likely to reoccur

What are the risk factors identified for EIPH?

• Speed

• Light jockeys

• Previous EIPH

• Number of years in training

• Hard ground/bar shoes

• Cold external temperatures

• Upper airway disorders

How is EIPH graded?

• Grades 1-4

  • 1 and 2 ass. with normal performance

  • 3 and 4 ass. with poor performance

epistaxis = sign of severe EIPH

How does EIPH present clinically?

• Typically within 4 hours of intense exercise

• Bursts of speed +/- breath holding (show jumpers may breathhold while jumping)

• Bilateral epistaxis

• Poor performance

• Caudo dorsal lungield

  

cranioventral = aspiration pneumonia

How do you diagnose EIPH?

• CE

• Tracheal endoscopy <2 hours post race

  • Presence of blood, grading

• BAL <14 days post race

  • RBCs, haemosiderophages and low grade inflm

• Imaging but rarely required

What are haemosiderophages?

specific macrophages that ingest RBCs + have iron pigmentation

How is EIPH treated?

• Rest and supportive care

• Anti inflammatories (NSAIDs)

• If severe- blood transfusion (rarely required)

What are the consequences of EIPH?

• Intrapulmonary blood provokes macrophage influx and activation. • The influx of inflammatory cells results in reversible disruption of the alveolar septal architecture.

• The chronic macrophage activity coincides with the development of alveolar septal wall thickening and fibrosis.

• Results in permanent alterations in alveolar blood-air barrier and pulmonary compliance

How is EIPH managed?

• Rest after episode

• Adjust training

• No evidence to justify many attempted treatments (steroids, bronchodilators etc.)

Furosemide (diuretic) 4 hours prior to intense exercise (not in UK)

What are the 2 types of exertional rhabdomyolysis?

• sporadic

• chronic

When may you suspect exertional rhabdomyolysis?

• history

• sweating

• stiffness/muscle soreness

• colic

• dark urine (more myoglobin)

• poor performance

What would be seen on bloods and urinanalysis in a case of exertional rhabdomyolysis?

• high CK + AST

• can exercise + see if CK increase in response

• urine will remain dark when centrifuge (where as if whole blood was present would seperate)

What is sporadic exertional rhabdomyolysis associated with?

• Exercise (vs level of fitness)

  • Overexertion

• High non-structural carbohydrates and low forage content

• Electrolyte deficiencies

• Low Selenium/Vitamin E

When is recurrent exertional rhabdomyolysis seen?

• thoroughbreds

• young nervous/stressed

• fillies

• hereditary

What is recurrent exertional rhabdomyolysis associated with?

excessive Ca release

(can use meds to decrease Ca release + manage by reduce triggers)

What is polysaccharide storage myopathy?

Excess polysaccharide storage in muscle leads to muscle damage

What are the different types of polysaccharide storage myopathy?

PSSM 1

• genetic (GYS1 gene)

• european draught ponies

• high non-structural carbohydrates predispose

• genetic testing or muscle biopsy to dx

PSSM 2

• no genetic tests

• myofibrillar myopathy

• more common in warm bloods