Cardiac Disease Flashcards
Differentials for cardiac murmur
Physiological
Congenital
When is a horse hypoxic on blood gas
PaO2 < 80mmHg
What classes as hypercapnia on blood gas
PaCa2 >45mmHg
What does jugular distension suggest
Reduced cardiac return
Right sided cardiac disease
Thoracic disease
Pericardial disease
What does peripheral oedema suggest
Right sided heart failure - vascular disease
Hypoproteinemia
Chronic endocardial disease
Signs of left sided heart failure
Pulmonary oedema
Ruptured chorda tendineae
Bacterial endocarditis
Congenital cardiac disease
Usually bilateral
Signs of left sided heart failure
Chronic endocardial disease
Where do you auscultate the mitral valve
5th left intercostal space halfway between elbow and shoulder
Where do you auscultate the aortic valve
Left side 4th intercostal space
What sound is lub
S1 onset of ventricular systole
Closure of AV valves and opening of semilunar valves
What sound is dub
Onset of diastole
Closure of semilunar valves and opening of AV
Changes with fever, adrenaline and anaemia
What sound is shhh
S4 only audible in 60% thoroughbreds
Onset of atrial systole
What sound is De
S3 - only audible in 40% skinny thoroughbreds
Rapid ventricular filling
Loudest over cardiac apex
What presents are a regularly irregular rythmn that goes away with exercise
Second degree AV block
How does atrial fibrillation present
Irregularly irregular rythmn
Inaudible S4 (active atrial contraction)
Absence of p waves
QRS normal but irregular
Abnormally high HR at exercise
Grades of murmur
1 quiet hard to identify murmur
2 murmur quieter than heart sounds
3 murmur as loud as s1/S2
4 murmur louder than s1/S2
5 cardiac murmur with precordial thrill
6 murmur audible with stethoscope off of thoracic wall
When is a holosystolic murmur
Between cardiac sounds
When is a pansystolic murmur
Across heart sounds
When is a midsystolic murmur
Between heart sounds
How does endocarditis present
Acute onset congestive heart failure with fever, tachycardia, tachypnea and cardiac murmur
Caused by secondary bacteremia to dental/respiratory/thrombophlebitis disease
What is endocardiosis
Progressive valvular degeneration
Treatment/prognosis of endocarditis
Broad spectrum antibiotics on sensitivity
Guarded prognosis as permanent damage to valve, right sided can return to performance
Organisms causing endocarditis
Pasteurella
Actinobacillus
Streptococci
Rhodococcus equi
Area of endocardial infection
Mitral valve more than aortic
Can include aortic route
Right side associated with thrombophlebitis
What is echocardiography used to assess
Doppler - valvular regurgitation
2d/m - valve structure/disease
Assess chamber size
What are the congenital cardiac defects
Atrial septal defect
Ventricular septal defect
What types of jugular thrombosis can occur
Non-septic - thickening/cording of the vein, reducing patency
Septic - hot and painful with discharging tracts
What occurs with jugular thrombosis
Venous occlusion
Supraorbital, cheek, lips and tongue swelling leading to dysphagia
Upper airway t
Proximal venous distension
Aetiology of jugular thrombosis
Intravenous catheterisation - poor placement, use and care
Predisposed by SIRD, MODS, irritant drugs
What is thrombophlebitis
Blood clot with vein inflammation
Diagnosis of thrombophlebitis
Ultrasonography - assess extent of thrombus, identify sepsis, assess vein, distinguish perivenous swelling from thrombosis, select site for aspiration
Culture - catheter tip, ultrasound guided aspirate from thrombus, Swab discharging tracts, blood
Treatment of thrombophlebitis
Broad spectrum antibiotics
Systemic and topical anti inflammatories
- aspirin, nsaids
- DMSO and hot packs
Heparin (or analogues)
Vasodilators (glyceryltrinitrate)
Raise head
Complications of thrombophlebitis
Embolic disease
- bacterial endocarditis, septic pneumonia
Long term poor performance
- recurrent laryngeal neuropathy
- upper airway oedema in exercise
Care for IV catheterisation
Insertion - sterile with minimal trauma
Catheter material - polyurethane is less thrombogenic
Flexible less thrombogenic
Use catheter with appropriate time length
Use extension set to avoid manipulation
What is aorto-illiac thrombosis
Partial or complete occlusion of the terminal aorta and external and internal iliac arteries
Exercise induced hindlimb lameness, cold limbs, weak pulses
Palpate on rectal exam - visualise ultrasound
Treatment - nsaids,aspirin, fenbendazole
What is the most common form of sudden death during exercise
Vascular rupture - aorta and pulmonary artery most common sites
Aetiology of vascular rupture
Pre existing aneurysm
Medial degeneration
Congenital
Parasitic
Uterine vessels - periparturient
Management of vascular rupture
Reduce movement
Support circulation - transexamic acid
Analgesia
Aortocardiac fistula
Congenital or acquired hole in aortic wall
Sudden death, distress, ventricular tachycardia, loud continuous murmur
Intact makes more common
Hopeless prognosis
Points of description for murmurs
Point of maximum intensity
Radiation
Shape
Character
Mitral regurgitation character
All age groups
Incidental finding with collapse and sudden death
Timing - holosystolic, pansystolic or mid-late systolic
Grade 1-6
PMI - left mitral valve
Radiation - caudo-dorsally
Shape - band/plateau and crescendo
Tricuspid regurgitation character
All age groups - racing TB and SB more common
Incidental finding with collapse and sudden death
Timing - holosystolic and pansystolic
Grade 1-6
PMI - right tricuspid
Radiation cranio-dordally
Shape - band/plateau and crescendo
Aortic regurgitation character
Middle age to older horses
Incidental, progressive to clinical when older
Holodiastolic and pandiastolic timing
Grade 1-6
PMI left aortic valve
Radiation caudoventrally
Decrescendo and musical
Which murmurs are well tolerated
Physiological
Tricuspid and mitral without structural lesions
Slow progressive aortic regurgitation in middle aged
Poorly tolerated murmurs
Acute onset - ruptured chordae tendineae, bacterial endocarditis, valvular disease
Murmur+ concurrent arrhythmias
Clinical signs of pericarditis
Venous distension
Ventral oedema
Muffled heart sounds
Pericardial friction rubs
Pleural effusion
Aetiology and pathology of pericarditis
Majority idiopathic - eva, flu, strep.pneumoniae, e.coli, actinobacillus
Tend to develop fibrinous effusion
Diagnosis of pericarditis
Echocardiography - fluid/fibrin in pericardial sac and compression of chambers
Electrocardiography - small complexes
Pericardiocentesis - cytology
Treatment of pericarditis
Pericardial drainage and lavage indicated if RA collapse
Indwelling drain and 2x daily lavage with antibiotics
Good prognosis with early aggressive treatment
What is myocardial disease
Disruption to action potential propagation leading to abnormalities in contraction
Manifestations of myocardial disease
No clinical t
Poor performance - AF, VPDs (ventricular premature depolarization)
Collapse - multiple VPDs, VT
rarely death - VT to VF
Indications for blood transfusion
Fast loss
O2 extraction ratio (vo2/do2) normal is 30%
Tachycardia/tachypnoea
Decreased pulse quality
Cool extremities
Pale MM
Mentation changes
Increased blood lactate
Decreased PCV
Causes of myocardial dysfunction
Electrolyte abnormalities
Increased myocardial muscle mass
Increased chamber size - cardiomyopathy
Myocarditis
How do you evaluate the LA myocardium
Pathology
Proteins - cardiac troponin 1 - cell membrane disruption
Enzymes - release by cell membrane dysfunction
Creatinine kinase - myocardial isoenzyme
Causes of myocarditis
Bacterial - staph aureus, strep equi, clostridium chauvoei, mycobacterium spp, secondary to sepsis
Viral - FMD, EIA, EVA, EIV, AHS
Parasites - large strongyles, toxoplasma, sarcocystis
Types of cardiomyopathy in equine
Only DCM reported - subacute/chronic with dilated ventricle
Myocarditis
Toxic
Myocardial evaluation
Echocardiography - long/short axis appearance
Fractional shortening
- resting equipment cheap and available
- telemetric/holter - 24h or exercising ecgs
Dobutamine-atropine stress echo
Myocardial biopsy
How does 2nd degree AV block look on ecg
Considered normal due to high vagal tone
Missed beats on auscultation that don’t occur at exercise
Atrial fibrillation cause
Lack of coordination in electrical activity
Can be triggered by electrolyte imbalai
Pathophysiology of atrial fibrillation
Larger horses more susceptible - tbs, sbs, draughts
High vagal tone, low heart rate
Clinical signs of atrial fibrillation
None
Exercise intolerance
Epistaxis
Rare - weakness, myopathy, colic, CHF
Types of atrial fibrillation
Paroxysmal - only 24-48h duration, spontaneous conversion, associated with K+ depletion
Sustained - longer than 24-48h
Diagnosis of atrial fibrillation
Auscultation and PE
Resting ECG - no p waves, normal QRS, f waves
Further diagnostics prior to treatment
- electrolytes and acid base abnormalities
- echocardiography for cause/chamber size
- exercising ecg
Treatment of atrial fibrillation
Quinidine sulphate - use with caution, Negative inotrope, side effects include - fatal dysrhythmias, colitis, laminitis
Use with caution - need repeat physical exams/auscultation/continuous ecg monitoring.
Monitor toxicity with QRS complexes
TVEC - one wire into left pulmonary artery and other into vein and shock
Prognosis of atrial fibrillation
Paroxysmal - good to excellent (unless reoccurring)
Sustained - no underlying disease - good
Sustained - underlying disease - average
Sustained, heart failure - poor to grave
What dysrhythmias are not compatible with life
Asystole
Ventricular fibrillation (unusual)
Ventricular dysrhythmia treatment
Lidocaine - first line, CRI 50mg/kg/min prolonged or boluses 0.5mg/kg every 5 mins up to 4mg/kg. SE - nystagmus, muscle twitching, disorientation, excitement, convulsions
Magnesium - can be effective for refractory ventricular dysrhythmias - action not understood
Procainamide
Amiodarone
Management of bradyarrhythmias
Causes - drug administration, electrolyte derangements, intestinal disease, primary myocardial disease
Treatment -
- anticholinergics - glycopyrrolate, atropine, hyoscine
- ventricular packing
blood types
A,C,D,K,P,Q,U with allelic factors
important for transfusion reaction and neonatal isoerythrolysis
donors - geldings
Aa, Qa and Ca most immunogenic
Aa and Qa common donors
cross matching essential
