EXAMPLE OF A CERTIFYING ESSAY QUESTION AND MODEL
ANSWER (in red)
Atrial fibrillation (AF) is a well recognised dysrhythmia in the horse.
A. Write SHORT NOTES on AF under the following sub-headings (25 points):
(a) definition and classification (5 points)
 Definition
o
o
Disorganised atrial electrical activity and loss of atrial contribution to
ventricular filling
Re-entrance rhythm disturbance
 Classification
o
o
Paroxysmal
 AF which appears and disappears spontaneously
 Single episode of exercise intolerance, AF spontaneously
disappear within 24-48 hours
 Can be associated with transient K depletion or Magnesium
 Can also develop postoperatively in surgical colics (spontaneous
resolution within 3-4 days)
 Occasionally in foals
Sustained
 Primary = uncomplicated cases of AF
 Secondary to another heart condition, most commonly mitral
regurgitation
(b) epidemiology (5 points)
 The most common cardiovascular cause of poor performance and exercise





intolerance in horses
The most common arrhythmia of clinical importance
Around 2.5 % (0.34 to 2.5 %) in selected population, probably lower in the general
population. 1 % in national hunt thoroughbreds
5.7 -6.2 % in horses referred for cardiovascular examination
Most common in adult horses
o reported in all ages but higher incidence in older horses
Higher incidence in standardbreds, draft horses, warmbloods
o higher in heavier and and larger breeds or types of horses
(c) pathogenesis / pathophysiology/ pathology (10 points)
 Mechanism
o
o
o
Development of re-entrant pathways within the atrial myocardium
Necessitates heterogenicity in the atrial myocytes refractory period:
adjacent areas of myocardium must be in a state of depolarization,
absolute refractory and relative refractory period at any given time.
Once initiated, a critical mass is required to sustain fibrillation.
o
Proposed mechanisms :



o
Circus movement and re-entry
Single or multiple foci of spontaneous activity
Association of both
Recently, the re-entrance theory has been superseded by evidence from
complex electrophysiologic mapping studies that have suggested the
waveforms actually originate from the uninterrupted periodic activity of a
small number of discrete re-entrant sites in the left atrium (rotors) possibly
in the region of pulmonary veins. It seems likely that the rhythm is
maintained because of differences in electrophysiologic characteristics
between anatomic sites in the atria and between the left and right atria
themselves.
 Predisposition in the horse:
o
o
1. predominant vagal tone leads to variable refractory periods
2. large myocardial mass  normal horse is capable of sustaining AF
o
AF can occur in normal horses without underlying heart disease or in
horses with enlarged atria
o
Predisposing factors :



o
larger atrial mass (especially secondary to mitral insufficiency)
high autonomic (vagal) tone (shortening of the refractory period 
promotes re-entry; slows the sinus rate  facilitates ectopic
activity)
Areas of damaged myocardium (path for re-entry)
can occur in association with:
 Valves insufficiencies (mitral+++)
 Myocarditis
 endocarditis
 Changes associated with longstanding AF:
o
o
o
o
o
focal and diffuse myocardial fibrosis
thining and dilation of the atria
fatty infiltration
myocarditis with inflammatory infiltrates .
also changes in the expression of membrane-bound ion channels .
(d) consequences of AF during exercise (5 points)
 Reduced SV due to loss of atrial contribution to ventricular filling.
 CO normal at rest but limited during exercise because of the lack of atrial contribution
to ventricular filling (most important at higher HR)
 LA pressure (Pulmonary wedge pressure) normally significantly increases during
heavy exercise; this increase is more marked in horses with AF because of loss of
active atrial transport function
 Greater elevation in HR in response to a submaximal exercise, more rapid rise in HR,
greater HRmax -peak HR exceeding 280/min;
B. Regarding the diagnosis of AF, write SHORT NOTES under the following subheadings (25 points)
(a) clinical signs (10 points)
 Can be incidental finding
o Affected horses may appear to work normally at submaximal intensity
 Poor performance
o tendency to tire at a level of work that the horse previously tolerated
o usually sudden – recurrent if paroxysmal AF
o the most common clinical sign, especially in horses engaged in vigorous
athletic activities ; generally poor performance at maximal exertion
 Others:
o Exercise-induced pulmonary haemorrhage
o respiratory distress
o CHF
o Ataxia
o Collapse
o Myopathy
o syncopal attacks (sometimes also syncopal attacks at rest)
 If AF develops suddenly, the decrease in CO is sudden and affected horses pull up
suddenly, sometimes with ataxia and distress
(b) physical examination findings (10 points)
 Auscultation
o
o
o
o
Totally irregular heart rhythm
variable intensity heart sounds
absent S4
resting HR variable (17 to 120/min)
 in most of the cases in is normal ?
 resting heart rate usually higher than normal ?
o
variable intensity
 Pulse
o pulse deficit sometimes present
 Biphasic jugular pulse can be present
 If AF secondary to MR, irregular rhythm + murmur + signs of heart failure
(c) additional diagnostic findings (5 points)
 ECG :
o
absence of P waves (replaced by large or small f waves-rate up to
500/min) – if f waves large and coarse, consistent in size and duration 
atrial flutter
o QRS normal morphology but irregular rhythm, sometimes some variation
in amplitude
o T waves can vary in amplitude
o Ventricular rate normal or slighthly increased
 Blood analysis:
o usually normal
o exclude low K, low K fractional excretion, red blood cell K
o isoLDH, cardiac troponin I usually normal
 Echocardiography
o to exclude underlying heart disease
o no abnormality except for a low fractional shortening of the LV (24-32%)
C. Regarding the treatment of AF, write SHORT NOTES under the following subheadings (50 points):
(a) “classical” therapeutic approach (25 points)
 General treatment of AF
o
o
o
o
Objective: return to previous perfomances
If not treated: could contribute to progressive myocardial and possibly
valvular deterioration - does not progress in HF - most horses with AF
are safe to ride, but they can develop paroxysmal ventricular tachycardia
and collapse (risk for the ridder !)
Do not perform if since less than 48 hours or in horses undergoing a
surgery because of a life-threatening situation. In such cases, do not use
2 drugs.
Before: correct any electrolytic, acido-basic or fluid disturbance
 Classic treatment = quinidine sulfate PO
o
o
o
o
Classification - class 1A anti-arrhythmic
 now difficult to obtain in some European countries
Mode of action
 blocking the fast Na+-channel
 decrease in conductivity
 thus increasing the refractory period .
Objective of the treatment - obtain a steady state plasma level of
quinidine
Under ECG monitoring
 drug-induced cardiac arrhythmias can occur and can be fatal if not
treated
o
 measure the QRS duration
Treatment regime
 Some authors recommend the use of a test dose before
proceeding to the treatment schedule - not necessary
 Quinidine sulfate via naso-gastric tube 20-22 mg/kg every 2 hours
to a 4 to 6 doses (60-80 g or 120 mg/kg , to conversion or to
toxicosis
 If unsuccessful, continue quinidine therapy with doses of 22 mg/kg
(or may be less ? 2) via naso-gastric tube every 6 hours for 2 to 3
days or to conversion or to toxicosis.
 For other authors: 22 mg/kg for up to 9 doses day 1 (increased
risks of toxicity after 6 doses) and recommence the day 2 if
unsuccessful
 BUT some horses convert 24 hours after the initial 2 hours
interval treatment  this treatment regime is questionable
 proposed modified technique :
o Day 1: 6 doses at 2 hours interval
o Wait for 24 hours
o 6 doses at 2 hours interval
o If unsuccessful, continue with the 6 hours interval
 Concurrent administration of digoxine (0.0055 to 0.011 mg/kg PO
BID; low doses because the concurrent administration of quinidine
increases the serum concentration of digoxine because the 2
drugs are highly protein bound)
 Controversial
 For certain authors
o administer if significant increase in HR with
quinidine
o if no conversion on day 2 of quinidine treatment
 Digoxine should be used in cases:
o With evidence of HF or reduced myocardial
performance on echocardiography
o With high resting HR
o With a history of marked tachycardia during
previous attempts to cardioversion
o With evidence of significant organic heart disease
(moderate to severe valve regurgitation+++)
o
Why?
 digoxine reduces some of the toxic effects
of quinidine:
 reduces the myocardial aesthetic
effects of quinidine
 limits the elevation in ventricular rate
induced through the vagolytic effects
of the quinidine
 digoxin slows AV nodal conduction
and hence offsets some of the
proarrhythmic effects of quinidine
o


BUT questionable because digoxin tends to
stabilize AF by increasing the number of wavelets
circulating in the atria and decreases their
wavelength
Monitor plasma level of quinidine if possible (better because of the
variable of the pharmacokinetics of the drug,1): therapeutic range
2-4 gr/ml (6.16-12.32 mol/L); toxic range >5 gr/ml
 Signs of toxicosis :
o Diarrhea (colitis)
o Depression
o paraphymosis: do not indicate to stop treatment
o Urticaria
o Laminitis: rare
o Ataxia
o colics unresponsive to NSAIDS
o nasal edema causing stridor
o Increased ventricular rate > 100/min
o Increased QRS duration (> 25 %)
o Tachyarrhythmias (torsades de pointe, multiform
ventricular tachycardia, multiform ventricular
complexes)
o Sudden death
 A relationship between high plasma levels of quinidine and
ataxia or respiratory stridor has been demonstrated, but
not for tachycardia, diarrhea and colic
 Cardiac toxic effects of quinidine due to
o vagolytic effects  can cause supraventricular
tachycardia
o Increases the atrioventricular nodal conduction 
can cause supraventricular or ventricular
tachycardia
o prolongation of the action potential (lengthening of
the myocardial cells refractory period) can cause
ventricular tachycardia
o -adrenorepctor antogonism  can cause
peripheral vasodilation and hypotension
 In case of toxicosis
o Stop quinidine administration or increase the
interval between administration
o Administer digoxin (to slow the conduction through
the AV node and reduces HR)  propanolol
o IV Fluids  Phenylephrine IV drip if sever
hypotension
o Sodium bicarbonate to bind free plasma quinidine
(if HR > 100/min)
o In case of ventricular arrhythmias: magnesium
sulfate and/or lidocaïne IV, procainamide IV
Rest the horse after conversion ? (controversial); recommended
rest duration: 1 to 2 weeks for certain authors
(b) “alternative” therapeutic options (15 points)
 Other treatments
o
Quinidine gluconate IV (or dihydroquinidine chlorhydrate, or
dihydroquinidine gluconate) (
 Appropriate if recent AF (since < 7 days) , during anesthesia or if
nasogastric delivery is impossible or difficult
 1 mg/kg IV every 5 to 10 minutes to a maximum of 10 mg/kg
cumulative dosis (4); 1,5 mg/kg every 10 minutes for a maximum
àf 6 treatements
 necessitaes continuous ECG monitoring
 Allows to obtain cardioversion more rapidely, but secondary
effects can develop much more rapidly: other arrhythmias, serious
tachycardia, fall in blood pressure
o
Other pharmacological drugs
 Under investigation but not developed yet
 Flecainide
 Class 1C antidysrhythmic agent
 Blocks fast sodium channels (idem quinidine)
 More efficient than quinidine in human patients with AF
 Effective in horses with AF induced by pacing (1.4 mg/kg
IV) (Ohmura et al, 2000)
 Failed to convert and induced potentially dangerous
ventricular dysrhythmias in horses with naturally occurring
chronic AF.
 Oral dose: 4-6 mg/kg
 T1/2 shorter than quinidine  shorter administration
intervals
 Higher pro-arrhythmic effects than quinidine
 Less bound to protein than quinidine  bicarbonate
administration less effective to control drug-induce side
effects
 Amiodarone, sotalol, dofetilide,ibutilide
 Class 3 antidysrhythmic agent (K+ channel blockers)
 Also lengthen action potential duration, used in humen
medicine
 Not fully investigated in horses
 IV infusion In 6 horses with chronic AF: 4 converted with
side effects (hind limbs weakness and weight shifting)
 Adapted IV infusion protocol: 6 horses with chronic AF: 3/6
converted without side effects, 3 others side effects
(diarrhea, 1 euthanasied)
 Sotalol
 Not associated with side effects but inefficient in converting
3 horses with AF
 Propafenone


tested in 2 horses with long term AF and in 4 horses with
chronic pacing-induced AF: unsuccessful in any of the
horses
Regardless of the used treatment, once cardioversion is obtained
it is not necessary to use an additional doses.
 Exception: horse with a propensity to relapse and in which
the cardioversion has been obtained just before the
administration of the following dose ?
o
External electrical cardioversion
 Necessitates general anesthesia and echocardiography to identify
optimal placement for the paddles
 Concurrent treatment with quinidine gluconate could be benefical
to prevent relapse
 Difficult in horses because of the transthoracic impedance
 unsucessful in 2 horses with AF – the smallest converted after
pretreatement with quinidine
o
Internal electrical stimulation
 Also necessitates general anetshesia
 Successful in several studies in horses
Radiofrequency ablation of tissue
 Can not be performed in horses for technical reasons (fluoroscopy
not available and echocardiographic positioning of the catheter not
faisable).
o
o
Return to exercise: variable-depends on authors and type of cases
 In uncomplicated cases, return to full work could be done within 2
weeks after cardioversion
 a more pragmatic approach should be to rest the horse completely
for 5-7 days (time necessary to eliminate the side effects of
quinidine), then gradually return to fast training over 3-4 weeks
with a close monitoring of the heart rhythm during this period .
 24 hours holter can be done to monitor the incidence of atrial
ectopy. If atrial premature beats are frequent (increases risks of
recurrence, rest for 1 month is recommended , or antiarrhythmic
therapy, anti-inflammatory therapy and prolonged rest (3-4
months) (efficiency of such approach not documented
scientifically)
(c) success of treatment, including factors affecting the rate of success and the
risks of recurrence (10 points)
 Negative prognostic factors (less chance to convert/more chances to revert to AF if
converted):
o CHF, dilated cardiomyopathy, valve regurgitation with CHF
o
o
o
o
o
o
Enlargement of the left (> 14.8 cm) or right atrium
High rest HR (= sign of CHF ?)  limited significance in defining the
prognosis for 2
AF since a long time (> 4 months) (> 3 months for1)
Prior bouts of AF
No response to quinidine treatment
Older and larger horses
o
poor prognosis in complicated cases with other signs of cardiac disease
 Positive prognostic factors (quinidine)
o
o
o
o
HR ≤ 60/min
Murmurs ≤ III/VI
AF since < 4 months
Improvement of chances of permanent cardioversion: younger horses
and in which AF occurred since a short time
 Risks of recurrence
o
o
Difficult to predict
If positive factors: risks of recurrence around 25 %, most frequently within
1 year, but sometimes longer – 15 % risks of recurrence if uncomplicated
cases since less than 3 months
 If recurrence: can be retreated; response to treatment can decrease with repeated
treatments
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ESSAY QUESTION 2
Ataxia is a common expression of disease of the nervous system in the horse. The
clinical presentation of many conditions that result in signs of ataxia may be similar and
achieving a diagnosis is difficult when relying on clinical findings alone.
1. DESCRIBE what neural pathways and tissues can be damaged that result in signs of
ataxia and outline their location in the nervous system. In your answer refer to both
general proprioception and special proprioception pathways. (25 points )
2. DESCRIBE an approach to investigation of a horse with signs of ataxia that includes
how lesion localisation and diagnosis are to be achieved. Consideration and mention of
differential diagnoses for ataxia should be integrated into your answer. (75 points)
Your approach should incorporate:
(i)
use of clinical history (8%)
(ii)
use of animal signalment (7%)
(iii)
consideration of geographical location (4%)
(iv)
general physical examination findings (6%)
(v)
neurological examination findings (20%)
(vi)
use of diagnostic aids (25%)
(vii)
human health considerations (5%)
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ESSAY QUESTION 3
Recurrent airway obstruction (RAO), a common cause of chronic coughing in horses in
temperate countries, is occasionally referred to as the equine equivalent to human
atopic (extrinsic) asthma.
1. DESCRIBE the aetiopathogenesis of RAO (15 points), highlighting published
evidence both supporting and refuting the involvement of a polarised Th-2 immune
response (15 points).
2. DESCRIBE how the clinical signs associated with RAO relate to the pathology of the
disease (20 points).
3. LIST the various drugs that may be utilised in the treatment of RAO (10 points). For
each drug:
(a) describe its mode of action (20 points)
(b) briefly highlight any practical and/or pharmacological advantages or
disadvantages associated with the use of the drug (20 points)
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