Cardiology Flashcards
What are the normal heart sounds possible in a normal equine?
2-4 sounds
Bah (S4) —lub (S1)————dub(S2)———-ahh(S3)
- S1= closeure of AV valves; long, loud, low-pitched*
- S2=Closure of semilunar valves (can be split), shorter, softer, higher-pitched*
- S3=End of rapid filling phase*
- S4= Atrial contraction*
How would you descirbe a classic physiological pulse of a horse?
No higher than the junction of middle to lower third of the neck with the horses head in a neutral position
How would you desribe a classic physiologic arrythmia in a horse?
Mobitz 1 Second Degree AV block (Wrenkebach)
Longer, longer, longer drop. Then you have a Wrenkebach!
What are the possible types of normal ausculations in terms of rhyhtm?
2 types of gallop rhythms:
S4-S1-S2 (Bah-lub-dub) - more common
S1-S2-S3
Why are radiographs done in equine cardiac evaluation?
To assess the effect of the cardiac function/dysfunction on the lungs
What are the common features of an equine ECG?
Notched P (/F) wave
Negative QRS complex
Large T wave
How can you determine whether the arrythmia you are heading is physiologic or not?
Exercise or scare the horse
A horse HR can increase from a resting rate of ___-___ bpm to ____-_____bpm in flight/while exercising . This corresponds to an increase in CO from ___ L/min to ___L/min.
A horse HR can increase from a resting rate of 26-32 bpm to 220-250 bpm in flight/while exercising . This corresponds to an increase in CO from 25 L/min to 300 L/min.
What is the most common pathologic arrythmia in horses?
Atrial fibrillation
Describe the 2 factors affecting the pathophysiology for atrial fibrillation in horses.
-
Cardiac mass
Horses have a large cardiac mass and thus high vagal tone which causes asynchrony of repolarization of atrial mass (this asynchrony does not affect the horse at rest because their HR is so slow (~30bpm)) - Myocardial disruption (accomapnying a disease state)
What are the 2 presentations for a-fib in horses?
Paroxysmal: Single episode of poor performance, usually disappears spontaneously within 24-48hrs ; difficullt to diagnose- must use halter monitor
Sustained: can diagnose by ausculation, classical presentation
What are the 3 possible clinical manifestations of a-fib?
- Most common: Primary arrhythmia without identifyable stuctural heart disease
- Secondary arrhythmia in absence of structural heart disease but in presence of systemic abnormality (e.g. e-yle or A/B disturbances) that predipose to the arrhythmia
- Secondary arrythmia associated w/cardiac disease affecting the atria
What are the clinical signs seen with a-fib?
How will the ausculation sound and what will the pulse quality be?
Exercise intolerance - quitting at the 3/4 post (problem when at maximum intensity), racing poorly (Cardiac output problem- missing atrial kick
Others dependent on underlying cause:
- EIPH
- Myopathy
- Colic
- Collapse
- CHF
Auscultation- irregularly irregular (tennis shoe in a dryer)
Pulses- variable strength
In the equine patient what is the most valuable tool to evaluate the heart? What is it used to assess?
Echocardiographic evaluation
To assess:
- Valvular size
- Chamber size (LA:aoertid width ratio 1.2:1)
- Cardiac contractility (fractional shortening, ejection fraction)
What is the difference between complicated and uncomplicated a-fib?
Presence vs absense of cardiac dysfunction
Your horse patient has a-fib, a normal physical exam, normal echo, but a heart rate < 60 bpm. How do you treat?
Quinidine (to convert to normal sinus rhythm)
Oral formulation (Quinidine sulfate) via NG tube preferred to IV
Your horse patient has a-fib, a normal physical exam, normal echo, but a heart rate >60 bpm. How do you treat?
Digoxin until HR is normal
and then Quinidine
Must normalize HR because quinidine is tachyarrythmogenic
What complications do you need to watch for when treating with digoxin and quinidine?
Digoxin toxicity potential is increased by quinidine
(Also must be careful if giving phenylbutazone because it too is highly protein bound and can increase potential for drug toxicity
Quinidine toxicity: GIT sings, neuro (behavioral) signs, widened QRS complex
Idiosynchratic reaction: rapid supreventricular tachycardia (Tx= Digoxin +/- bcarb)
If quinidine does not convert your patient from a-fib, what can you try?
Electocardioversion
Usually transvenous (TVEC) under general anesthesia
Amioderone (limited success, class III AA)
Flecanide (not a good choice)
What are possible etiologies for VPCs in horses? What are the therapies indicated to manage VPCs?
Edx: E-lyte abnormalities, endotoxemia, myocardial inflammation, hypoxia (E.g. Surgical colic cases)
Tx: Lidocaine (treat underlying disease first)
How would you describe the typical physiologic/functional murmur of a horse?
Less than Grade 3-4/6
Low intensity
Soft decrescendo or cresendo-decresendo
Left Heart base (over pulmonic and aoertic valve areas)
Systolic
Ejection murmur
Absence of precordial thrill
How can you confirm that a murmur is physiologic?
Echocardiographic assessment
What are the most common pathologic murmurs in horses?
VSD (most common)
ASD
PDA
T/F: Horses rarely develop stenosis.
True
