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81 Cards in this Set
- Front
- Back
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list 7 differentials for poor performance
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musculoskeletal problems
resp tract conditions lack of fitness owner's unrealistic expectations of ability inappropriate training cardiovascular abnormalities other medical or neurological conditions |
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what is a horses cardiac reserve (rest and exercise)
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rest 35L/min, 350 L/min at exercise
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what indicates elevated central venous pressure?
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jugular distension above the lower 1/4 or 1/3
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what can cause jugular distension?
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cranial thoracic obstruction/mass
pericardial effusion right sided failure (murmur with tricuspid regurgitation) - more commonly develops secondary to left sided failure |
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what may reduced jugular filling indicate?
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hypovolaemia or low output failure
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why may right heart sided failure develop following left sided failure?
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because increased right ventricular workload occurs due to the pulmonary hypertension
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what may cause cardiac arrhythmias in horses?
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could e primary - e.g. atrial fibrillation or can be secondary to development of myocardial ischaemia or chamber dilatation as aresult of other cardiac disease
(a-fib can also develop secondary to left atrial enlargement caused by mitral regurg) |
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what happens to the pulse pressure in aortic insufficiency?
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the systolic pressure is raised due to the increased stroke volume
the diastolic pressure is low due to run off into left ventricle during diastole |
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what does the area under the pressure waveform of the pulse give a subjective assessment of?
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stroke volume
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what is a diastolic thrill on left hemithorax likely to be?
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aortic insufficiency
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what is a systolic thrill on left hemithorax likely to be?
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mitral regurgitation
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what is a systolic thrill on right hemithorax likely to be due to?
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tricuspid regurg or VSD
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what may be noted when palpating lower limbs in a horse with cardiac failure?
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cold extremities - cold in forward failure due to low CO
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what are considered normal arrhythmias?
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second degree AV block and sinus block - only abnormal if heart rate cannot increase in response to exercise
44% of horses have 2nd degree AV block hen recorded in holter monitor |
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what is the commonest cause of poor performance in racing TBs?
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atrial fibrillation
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what is the most common valvular regurgitation in TBs?
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tricuspid regurgitation (12%). followed by mitral (7%) and then aortic (0%).
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what is the most common valvular regurgitation in national hunt?
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tricuspid (54%), then mitral (21%) and then aortic (4%)
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do mitral and tricuspid regurg affect performance?
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cardiac murmurs due to valvular disease rarely affect performance unless they decompensate. most continue to compensate for the abnormal flow
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hat 2 things may cause toxic damage to myocardium? what do these toxins result in?
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monensin and salinomycin
--> fibrosis and acute myocardial necrosis diagnosis by demonstrating reduced myocardial contraction on echo |
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hat are the main forms of pericardial disease in horses?
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idiopathic fibrinous and idiopathic effusive pericarditis
neoplastic, traumatic and septic disease can also occur |
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what tends to be the cellular components of pericardial effusion in horses? what volume can the effusion be?
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up to 6L effusion
most cases serofibrinous but eosinophilic and histeocytic effusions reported |
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what may be heard on auscultation in pericardial effusion?
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friction rubs
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With regards to heart sounds (S1-S4) when does
1) atrial contraction 2) ventricular contraction 3) ventricular relaxation occur? |
1) S4 and S1
2) S1 and S2 3) S2 and S3 |
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how is pericardial effusion treated in non septic cases?
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drainage and corticosteroid treatment
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how are septic pericardial effusion cases treated?
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with aggressive antibiotics systemically and into pericardial sac plus pericardial lavage and use of indwelling drains
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where do you insert a drain for pericardiocentesis? describe procedure
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insert via left 5th intercostal space, below line level with point of shoulder and above lateral thoracic vein
- ECG on! 1) local beneath skin and into underlying muscle 2) 20-28 French catheter with trocar (due to problems with fibrin clots) lavage with 2 litres saline - leave in for 30-60 minutes (of antimicrobial or steroids to be given, a rftuerh 1-2 litres of saline with the medications are flushed into sac and left for 12 hours before draining) |
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what information does ECG supply in horses?
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heart rate and rhythm - no info on chamber size cf smallies
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where do you place electrodes to record base apex lead?
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left on cardiac apex, right (negtative elctrode) 2 thirds down the jugular on right (third electrode remote position from heart)
- record from lead 1 |
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what is the cause of atrial fibrillation? why is it seen in large horses?
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can be a result of high vagal tone
can be secondary to valvular dysfunction can be secondary toe lectrolyte abnormalities or peritonitis associated with administration of alpha2s (increase vagal tone --> occur in recovery of GA) large horses predisposed due to LARGE ATRIAL SIZE |
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what % of ventricular filling do the atria contribute?
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15-20%
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when is atrial contraction most needed?
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at high heart rates when diastole is short! - when A fib becomes a problem!
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what may be heard when auscultating chest of horse with a-fib?
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irregular rhythm
ther will be ong pauses greater than 2 preceding cardiac cycles with occasional beats occurring earlier than normal third heart sound may be loud will be no 4th heart sound if afib occurred secondary to mtiral regurg and horse is in heat failure, heart rate will be elevated |
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what is paroxysmal atrial fib?
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horses have fib during exercise but the rhythm spontaneously revers to normal sinus rhythm = difficult to diagnose
- may be clinically normal at exam. may have abnormal rhythm just after exercise but the horse may be in sinus hen presented for ECG |
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when may treatment of afib not be successful?
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when there is atrial dilatation secondary to valvular disease
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when can horses start being treated following diagnosis?
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3-4 days after diagnosis - may spontaneously revert to normal sinus!
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what is the quinidine sulphate treatment regime for a-fib?
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20mg/kg per os via indwelling nasogastric tube - repeat every 2 hours until sinus or signs of toxicity develop OR when max total dose of 60-90 grams achieved
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what are toxic signs of quinidine sulphate?
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nasal oedema and stertorous breathing and depression seen after a few doses
urticaria diarrhoea anorexia weakness ataxia tachycardia laminitis rare sudden death |
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what on ECG may indicate toxicity of quinidine sulphate?
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25% increase in RS width
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why should horses on quinidine not be moved?
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due to potential for producing hypotension and rapid SVT or VT
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what should you do if a horse starts to show mild signs of toxicity with quinidine sulphate?
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delay next dose of quinidine for up to 6 hours - allow time for side effects to resolve
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what can you treat SVT caused by quinidine sulphate?
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digoxin IV
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what can you do to decrease plasma quinidine levels for suspected toxicity?
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sodium bicarb IV with phenylephrine for severe hypotension
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what is the success rate for conversion of AF to normal sinus with quinidine?
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87%
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what should you do with horses that fail to respond to their initial course of quinidine?
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often respond to second treatment after 24 hours without drug administration
- if still fails to respond, administer quinidine every 6 hours - suggested that digoxin should be given every 12 hours until sinus rhythm restored |
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what has been suggested to do with horses that have gone back to normal sinus rhythm with quinidine treatment?
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check for presence of atrial premature systoles with 24 hour holter - indicate risk of recurrence of a-fib
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what should be done with horse with large number of atrial premature beats following quinidine treatment?
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rest for 1-2 months and possibly give anti-inflammatory therapy
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what is done following conversion to sinus with quinidine treatment with regards to training?
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rest them completely for 5-7 days and then gradually return to fast training over 3-4 weeks: advise owners to monitor rhythm by palpation of apex beat
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what may premature systoles be associated with?
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hypoxia, myocardial disease, electrolyte and metabolic disturbances, elevated sympathetic tone, fever and toxaemia
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when do VPC tend to occur?
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in immediate cardiac slowing period following fast exercise
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what should be done in cases of persistent ectopic activity?
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evaluate electrolyte status and other body systems before starting expensive cardiac examinations
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when may premature atrial systoles occur (in relation to ECG)?
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may occur after refractory period of ventricles = conducted normally with following QRS, just earlier than expected
may occur during refractory period: not conducted - may have different configuration may be lost in previous T wave --> abnormal T wave configuration |
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when are premature ventricular systoles of differing morphology?
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when there are multiple sites of ectopic activity
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What is an R on T phenomena and what does this indicate?
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it is when a premature QRS occurs during preceding T wave. This is a vulnerable period of the cells and may result in the development of V fib = poor prognosis
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what treatment may cases with active myocardial disease respond to?
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2-3 months of rest - may resolve arrhythmia: with or without steroid treatment
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which equids are pathological sinus bradycardias most commonly found in?
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elderly ponies and donkeys
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what does third degree AV block do after atropine administration?
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get increased P wave frequency with little or no increase in ventricular rate.
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what happens if escape beats (in 3rd AV block) if originating
1) high up in His purkinje network or 2) in ventricles |
1) QRS will be normal and rate ca 20-30bpm
2) QRS bizarre and rate 10-20bpm |
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what should you consider if detecting a murmur in horse during PPE?
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suitability/safety of horse for work
likely progression of disease resale value suitability for insurance costs of ongoing monitoring |
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what is character of mitral regurg in racing thoroughbreds?
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often low grade and crescendo in nature: suggestive of mitral prolapse
21% of 2yo TBS IN TRAINING HAVE IT DUE TO ECCENTRIC HYPERTROPHY AND INCREASED BLOOD VOLUME = does not progress |
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what may mitral valve regurgitation develop from?
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thickening/fibrosis of valve leaflets
rupture of one or more chordae tendinae secondary DCM, AI, VSD congenital dysplasia infective endocarditis |
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when may premature atrial systoles occur (in relation to ECG)?
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may occur after refractory period of ventricles = conducted normally with following QRS, just earlier than expected
may occur during refractory period: not conducted - may have different configuration may be lost in previous T wave --> abnormal T wave configuration |
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when are premature ventricular systoles of differing morphology?
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when there are multiple sites of ectopic activity
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What is an R on T phenomena and what does this indicate?
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it is when a premature QRS occurs during preceding T wave. This is a vulnerable period of the cells and may result in the development of V fib = poor prognosis
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what treatment may cases with active myocardial disease respond to?
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2-3 months of rest - may resolve arrhythmia: with or without steroid treatment
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which equids are pathological sinus bradycardias most commonly found in?
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elderly ponies and donkeys
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what does third degree AV block do after atropine administration?
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get increased P wave frequency with little or no increase in ventricular rate.
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what happens if escape beats (in 3rd AV block) if originating
1) high up in His purkinje network or 2) in ventricles |
1) QRS will be normal and rate ca 20-30bpm
2) QRS bizarre and rate 10-20bpm |
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what should you consider if detecting a murmur in horse during PPE?
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suitability/safety of horse for work
likely progression of disease resale value suitability for insurance costs of ongoing monitoring |
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what is character of mitral regurg in racing thoroughbreds?
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often low grade and crescendo in nature: suggestive of mitral prolapse
21% of 2yo TBS IN TRAINING HAVE IT DUE TO ECCENTRIC HYPERTROPHY AND INCREASED BLOOD VOLUME = does not progress |
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what may mitral valve regurgitation develop from?
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thickening/fibrosis of valve leaflets
rupture of one or more chordae tendinae secondary DCM, AI, VSD congenital dysplasia infective endocarditis |
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what type of murmur will you hear with rupture of minor chorda tendina of mitral valve? how do these cases tend to present?
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pansystolic 5-6/6 murmur --> little time for atrial dilatation as flow suddenly large: atrial pressure rise abruptly and get acute L sided failure and severe respiratory distress
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why may shifting lameness occur with endocarditis`
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due to immun emediated synovitis, or infection of joints or epiphyses
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how is infective endocarditis treated?
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ABs for 4-6 weeks based on culture - if not available give pen/gent, TMPS, enrofloxacin
if involving L heart valves prognosis poor |
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why may horse with mitral valve murmur/regurg be excluded from loss of use insurance policies?
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because may cause atrial enlargement, predispose to a-fib or progress to cardiac failure
but no icnreased risk of sudden death |
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how may tricuspid regurg develop?
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usually as a result of pulmonary hypertension caused by L ventricular failure
can develop as rupture chorda congenital dysplasia possible BUT NO THICKENING OF VALVE LEAFLETS |
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what causes aortic insufficiency?
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progressive thickening and fibrosis of valve leaflets: common in horses over 10 years of age
can be dilatation of aortic root or associated ith VSD in young horse |
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describe the pathogenesis/steps in aortic insufficiency
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volume overload of LV --> dilatation
may get mitral regurg due to dilatation --> may get cardiac failure |
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why may aortic insufficiency result in sudden death?
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gross dilatation of ventricle --> increased afterload and increased oxygen consumption. you also get decreased coronary perfusion due to reduced diastolic aortic pressure and therefore oxygen delivery to myocardium compromised:
INCREASED O2 DEMAND AND DECREASED CORONARY RESERVE INCREASES SUSCEPTIBILITY TO VENTRICULAR ARRHYTHMIAS --> SD! |
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where are VSDs usually located?
which breeds seen in? |
in membranous septum below aortic and tricuspid valves. can cause distortino of aortic valve leaflet --> AI!
shetland and welsh mountain ponies |
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where do VSDs tend to occur in Arabs or TBs?
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in muscular part of septum: if very large pressure in RV approaches or equals that of L: may be little flow across and may have no murmur - but will have murmur of tricuspid and mitral regurg secondary to dilation of annulus!
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which breeds tend to have a higher incidence of complex congenital heart disorders (e.g. tet of fallot)?
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arabs and TBs
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