ECEIM 2009



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 Disorganised atrial electrical activity and loss of atrial contribution to ventricular filling

o Re-entrance rhythm disturbance

• Classification

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

o 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 Development of re-entrant pathways within the atrial myocardium

o 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.

o Once initiated, a critical mass is required to sustain fibrillation.

o Proposed mechanisms :

▪ Circus movement and re-entry

▪ Single or multiple foci of spontaneous activity

▪ Association of both

o Recently, the re-entrance theory has been superseded by evidence from complex electrophysiologic mapping studies that have suggested the waveforms actually originate from the uninterrupted periodic activity of a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 1. predominant vagal tone (leads to variable refractory periods

o 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 :

▪ 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)

o can occur in association with:

▪ Valves insufficiencies (mitral+++)

▪ Myocarditis

▪ endocarditis

• Changes associated with longstanding AF:

o focal and diffuse myocardial fibrosis

o thining and dilation of the atria

o fatty infiltration

o myocarditis with inflammatory infiltrates .

o 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 sub-headings (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 Totally irregular heart rhythm

o variable intensity heart sounds

o absent S4

o resting HR variable (17 to 120/min)

▪ in most of the cases in is normal ?

▪ resting heart rate usually higher than normal ?

• Pulse

o variable intensity

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 sub-headings (50 points):

(a) “classical” therapeutic approach (25 points)

• General treatment of AF

o Objective: return to previous perfomances

o 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 !)

o 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.

o Before: correct any electrolytic, acido-basic or fluid disturbance

• Classic treatment = quinidine sulfate PO

o Classification - class 1A anti-arrhythmic

▪ now difficult to obtain in some European countries

o Mode of action

▪ blocking the fast Na+-channel

▪ decrease in conductivity

▪ thus increasing the refractory period .

o Objective of the treatment - obtain a steady state plasma level of quinidine

o Under ECG monitoring

▪ drug-induced cardiac arrhythmias can occur and can be fatal if not treated

▪ measure the QRS duration

o 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

o 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 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 Enlargement of the left (> 14.8 cm) or right atrium

o High rest HR (= sign of CHF ?) ( limited significance in defining the prognosis for 2

o AF since a long time (> 4 months) (> 3 months for1)

o Prior bouts of AF

o No response to quinidine treatment

o Older and larger horses

o poor prognosis in complicated cases with other signs of cardiac disease

• Positive prognostic factors (quinidine)

o HR ≤ 60/min

o Murmurs ≤ III/VI

o AF since < 4 months

o Improvement of chances of permanent cardioversion: younger horses and in which AF occurred since a short time

• Risks of recurrence

o Difficult to predict

o 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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