Horses 6 Flashcards
Tricuspid valve insufficiency what murmur present, when normal and when problematic, what causes severe and clinical signs
○ Murmur PMI R heart apex
§ Usually soft, grade 2-3/6 murmur - no worried at this point
§ No obvious leaflet abnormalities
○ Tricuspid regurgitation may increase with athletic training
○ Tricuspid murmur considered problematic if ≥ grade 4/6
○ Endocarditis may be secondary to jugular thrombophlebitis (colitis - SIRS)
○ Abnormal systolic jugular venous pulsations if severe
Aortic valve regurgitation what murmur present, how lesions common, performance effect, when more problematic and effects on the heart
○ Murmur (diastolic) PMI L heart base/aortic valve
○ Degenerative lesions common, esp. older horses (second most common)
○ Often mild, normal performance (may not be able to detect of exercise)
○ More problematic if moderate-severe regurgitation, younger horses - increased risk
§ L ventricular dilation, increased aortic root diameter
Bounding arterial pulse if significant LV volume overload
Aortic valve regurgitation diagnosis and monitoring
○ Diagnosis
§ Exercising ECG if poor performance, cardiac remodelling (presence VPCs, HR for level exercise)
§ 24 hour Holter - if worried about sporadic arrythmia
○ Monitor for progression, esp. moderate-severe AR
§ Monitor for development arrhythmias
□ VPCs
□ A fib
Pulmonic valve lesions common and treatment
- Pulmonic valve ○ Acquired valvular lesions uncommon ○ Relative stenosis –NORMAL valve, murmur systolic Treatment? - Benazepril - reduce volume overload - NOT LOTS OF TREATMENT OPTIONS
Ventricular septal defect what occurs with the murmur, common causes and what can lead to
- R-sided murmur = L→R shunt (loudest)
- L-sided murmur = relative pulmonic stenosis
- Most common congenital cardiac defect
○ Most are membranous - Some breed predispositions
○ Welsh Mountain Ponies
○ Standardbreds
○ Arabians - L-sided volume overload - increase venous return from pulmonary system - left sided congestive heart disease
Ventricular septal defect diagnosis and prognosis
- Diagnosis ○ Echocardiography - Prognosis ○ Unlikely to be a successful athlete ○ Size important
Lung disease when does it affect performance and the 2 main differentials
- Lung disease resulting in no changes at rest, but affects performance
○ Large respiratory reserve - Two main differential diagnoses
○ Exercise-induced pulmonary haemorrhage (EIPH)
○ Inflammatory airway disease (IAD)
Excercise induced pulmonary haemorrhage likely mechanism, what occurs and diagnosis
- Likely mechanism
○ Rupture alveolar capillary membranes as transmural pressures increase during exercise
○ Mucociliary clearance leads to blood in bronchi, trachea
○ Epistaxis in severe cases - Breeds that perform intense exercise predisposed
- Diagnosis
○ Epistaxis associated with exercise
○ Endoscopy - MOST IMPORTANT
§ Within 30-60 minutes of racing
○ BAL
Endoscopic grades for EIPH
○ 0: no blood in upper airway, trachea or bronchi
○ 1: flecks of blood in trachea taking up < 10% tracheal surface area and extending < ¼ tracheal length
○ 2: long stream of blood taking up < 1/3 trcaheal circumference and > ½ tracheal length
○ 3: multiple distinct streams blood covering > 1/3 tracheal circumference; no blood pooling
○ 4: multiple coalescing streams blood > 90% tracheal circumference, blood pooling in thoracic inlet
BAL cytology for EIPH and treatment
○ Haemosiderophages present for ≥ 21 days
○ RBCs/RBCs in macrophages if recent (< 7 days)
Treatment
○ None specific
○ Furosemide
§ OK for training
§ Cannot be given day of race
§ Consider effects on electrolytes
○ Possible association with IAD –treat that?
○ REST
IAD what is it, diagnosis, what see endoscopically, how do you mange the horse
- Diagnosis - BAL - - non-degenerative neutrophils, mast cells, eosinophils, mixed inflammatory
- What might you see endoscopically? - tracheal mucus
Management
○ Environmental management - NOT INDOORS, feed (wet it down, less dusty, not in hay nets), increase ventilation if in a barn
○ Inhaled or systemic corticosteroids
§ Break from racing until off these medications
Arrhythmia how common, causes and are some normal
- Most common of the cardiac causes of poor performance
- May be isolated electrical disorder or secondary to other factors
○ Structural heart disease
○ Metabolic/endocrine disorders
○ Systemic inflammation
○ Hypotension, haemorrhage, anaemia, ischaemia
○ Autonomic influences
○ Toxins
○ Drugs - Some arrhythmias “normal”, especially athletes
Normal arrhythmias what caused by, the 3 main ones and when normal
- Common in athletic horses –high vagal tone - vagally mediated brady arrythmias
○ Second degree AV block - more common
○ Sinus arrhythmia - increase length between p waves
○ Sinoatrial block - Normal at rest and immediately post-exercise
- May be due to cardiac disease on rare occasions (in which case not normal!)
Second degree AV bock is it normal or pathological, HR, rhythm, auscultation and when bad
- Low-normal HR
- Regularly irregular rhythm
○ Several conducted beats before “dropped” beat - S4 alone may be auscultated at dropped beats
- Abnormal if
○ P:QRS is 2:1 or greater - dropping every other beat or multiple beats
§ “high grade”
Pathologic arrhythmias what is the main effect what is the main one and 4 others
1) Atrial fibrillation - IMPORTANT Other arrhythmias (less common) 1. Atrial premature complexes (APCs) 2. Ventricular premature complexes (VPCs) 3. Ventricular tachycardia (VT) 4. AV block ○ 3rd degree
Atrial fibrillation how common, what occurs, HR, types and cause
- Most common cardiac cause of poor performance
- Loss of organised atrial conductivity; disorganised self-sustained electrical activity
- Resting HR usually normal
- Types -> “Lone” A fib (normal structural heart - TB after racing) vs. secondary (underlying heart disease)
- Electrolyte disturbances - bicarb, frusemide
Atrial fibrillation pathogenesis short and longer term
- Reduction of CO due to ↓ SV due to loss of atrial contribution to ventricular filling (15-20%)
○ No effect at rest (high cardiac reserve) - Inappropriately high HR for level of exercise
○ Compensate for decreased SV by increasing HR
○ Exercise reduces vagal tone and allows more conduction through AV node - Cardiac remodelling occurs if A fib longstanding
○ After 3 months becomes irreversible
Atrial fibrillation common history and physical exam findings
Common history
- Poor performance at high intensity exercise
- May not affect performance at low-level exercise
- May be sudden “pulling up” during fast work
- Development of A fib during fast work
Physical exam
- Cardiac auscultation
○ “Irregularly irregular” rhythm
○ Murmur, increased HR might suggest underlying cardiac disease
○ Absence S4
- Can be paroxysmal
○ Resolves spontaneously in minutes-hours-days after exercise
○ Exercising ECG can be important to detect in these cases
Atrial fibrillation what are the 4 important tests for diagnosis and the best one
- ECG
○ Exercising ECG (Certain circumstances) - Echocardiography - ideal
○ Determine presence of underlying heart disease
§ Structural normal heart or not? - changes prognosis - CTnl
- Electrolytes
In terms of trying to get atrial fibrillation to convert what are the main considerations and ideally what should you do
○ How long has horse been in A fib?
○ Is there any underlying cardiac disease?
○ Are there other underlying causes (e’lyte, acid-base disturbances)?
§ Ensure normal electrolytes and acid-base before treatment
○ CHF –not candidate for conversion
IDEALLY - refer
What are the 2 main options for conversion of atrial fibrillation and how works
1) Quinidine
§ Class 1A antiarrhythmic drug (sodium channel blocker)
§ Prolongs action potentials and lengthens myocardial cell refractory period
2) Transvenous electrocardioversion (TVEC)
§ Deliver
§ Whole atria refractory and so sinal node takes over again
§ Reserve for horses that develop complications during quinidine OR those who don’t convert with quinidine
Quinidine for atrial fibrillation conversion, how often successful, when don’t use and the 2 main types, which most common
§ Successful conversion in approx. 80-90% cases lone A fib -i.e. likely but NOT guaranteed
§ Don’t use if: complex VPCs, rapid ventricular rate, CHF
§ Types
1. Quinidine gluconate (IV) –only if A fib known to be < 2 weeks duration
® NOT IN AUS
2. Quinidine sulfate (via NGT) - most common- IMPORTANT
Quinidine sulfate for atrial fibrillation conversion, how to give, when stop, what monitoring for and common signs seen through treatment
® Repeat q 2 hours until convert to sinus rhythm –then STOP
® If no conversion after 4 treatments↓ frequency to q 6 hours
If signs of toxicosis develop –STOP!
Monitoring essential
◊ Heart rate
◊ ECG (ideally continuous) - or give ECG prior to give second dose (don’t want to go into ventricular tachycardia)
◊ Plasma quinidine concentrations
◊ Signs of toxicosis
® Commonly seen during quinidine treatment - NOT SIGNS OF TOXICOSIS
◊ Dull mentation
◊ Paraphimosis
What are the main signs of qunidine toxicosis
- Diarrhoea
- Ataxia
- Weakness
- Colic
- Anorexia
- Tachycardia
- Laminitis
- Nasal oedema
- Sudden death! Rare
- Prolongation of QRS > 25% baseline
- Development other arrhythmias (SVT, VPCs, VT)
- Plasma quinidine concentration > 4 μg/ml
Atrial fibrillation what to do post successful conversion and prognosis
After successful conversion ○ Rest (minimum one week) ○ Gradual return to work ○ Regular monitoring of HR and rhythm Prognosis - Depends on: ○ Presence underlying heart disease § 95% recurrence within short time period ○ Duration of A fib (cardiac remodelling) ○ How many times gone into A fib § The more you go into the more - Young racehorses with lone A fib have best prognosis
Atrial premature complexes what also called, how common, performance issues, diagnosis and treatment
supraventricular complexes SAME THING) ○ Occasional APCs occur not uncommonly ○ Rarely cause of poor performance if no underlying heart disease Diagnosis ○ Auscultation ○ ECG ○ Check for underlying heart disease § Echo § CTnI (Cardiac troponin) ○ Exercising ECG § Most disappear with exercise Treatment often not required § May need to treat underlying heart disease if present ○ Risk for A fib
Ventricular premature complexes what associated with, can lead to and when cause for concern
○ Most often associated with other disease
§ May be due to primary cardiac disease
○ Runs VPCs = ventricular tachycardia
○ Isolated VPCs common when HR slowing after exercise
○ VPCs during exercise
§ Cause for concern
§ May occur in normally performing horses
§ Further research needed…
