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Practical Cardiology Case Studies
Wendy Blount, DVM Nacogdoches TX
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Daisy Signalment 15 year old spayed female mixed terrier 11 pounds
Chief Complaint Became dyspneic while on vacation, as they drove over a mountain pass Come to think of it, she has been breathing hard at night for some time
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Daisy Exam T 100.2, P 185, R – 66, BP – 145, BCS – 3.5
Increased respiratory effort (heart sounds) 3/6 pansystolic murmur loudest at left apex Mucous membranes pale pink Crackles in the small airways Pulses weak, somewhat irregular, no pulse deficits CRT seconds
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Daisy CBC, mini-panel, electrolytes Normal
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Daisy CBC, mini-panel, electrolytes Normal
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Daisy ECG
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Daisy Calculating Instantaneous Heart Rate (iHR)
Measure R wave to R wave (9mm) Divide by paper speed (25 mm/sec) for time per beat 9mm x _sec_ = 0.36 sec per heart beat 25mm Calculate beats per minute _heart beat_ x _60 sec = 166 beats/minute 0.36 sec minute
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Daisy ECG Rate – 110 bpm Rhythm – sinus arrhythmia with VPCs
MEA – normal (lead II has tallest R waves) P, QRS and T waves – normal No evidence of enlarged LA and LV on the ECG VPC – abnormal QRS Comes too early (iHR 166 bpm) Wide and bizarre shape Not preceded by a P wave T wave opposite in polarity than normal QRS Compensatory pause after the VPC
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Daisy Initial Therapeutic Plan Lasix 25 mg IM, then 12.5 mg PO BID
Enalapril 2.5 mg PO BID Pimobendan 1.25 mg PO BID Owner is a med tech, and set up oxygen mask to use PRN at home
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Daisy When to treat VPCs VPCs unusual for MR
Did not treat in this case, because: MR dogs not predisposed to sudden death PS, SAS and DCM are more associated with sudden death due to arrhythmia Ectopic focus not firing at a fast rate (166 bpm) <200 bpm iHR is well away from the T wave No pulse deficits – did not affect hemodynamics Primary treatments for VPC are Sotalol or B blocker Negative inotropes not ideal for myocardial failure
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Daisy Recheck – 4 days Daisy’s breathing is much improved (30-40 at rest) Lateral chest x-ray Electrolytes normal BUN 52
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Daisy Recheck – 4 days Daisy’s breathing is much improved (30-40 at rest) Lateral chest x-ray Electrolytes normal BUN 52
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Daisy Diagnostic Plan - updated Recheck – 1 week
Decrease enalapril to SID Recheck BUN 1 week Recheck chest rads 1 week Recheck – 1 week BUN – 37 Thoracic rads no change Request recheck in 3 months, or sooner if respiratory rate at rest is above 35 per minute
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Daisy 2 months later Daisy is breathing hard again at night
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Daisy 2 months later Daisy is breathing hard again at night
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Daisy 2 months later Daisy is breathing hard again at night
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Daisy Bloodwork CBC, electrolytes normal BUN 88 Therapeutic Plan
Increase furosemide to mg PO BID Add hydralazine 2.5 mg PO BID Recheck chest rads, BUN, electrolytes, blood pressure 1 week
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Daisy Recheck – 1 week Clinically much improved – respiratory rate per minute at rest electrolytes normal BUN 58 Blood pressure 135
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Daisy Recheck – 1 week Clinically much improved – respiratory rate per minute at rest electrolytes normal BUN 58 Blood pressure 135
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Daisy Recheck – 6 months Daisy dyspneic again Exam
Similar to last crisis – BP 90
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Daisy Bloodwork CBC, electrolytes normal BUN 105, creat 2.1
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Daisy Bloodwork CBC, electrolytes normal BUN 105, creat 2.1
Chest x-rays
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Daisy Bloodwork CBC, electrolytes normal BUN 105, creat 2.1
Chest x-rays Similar to last crisis ECG Sinus tachycardia, wide P wave
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Daisy - Echo Short Axis – LV apex (video)
LV looks big Short Axis – LV papillary muscles IVSTD – 6.0 mm – low normal LVIDD – 35 mm (n ) LVPWD – 4.3 mm – low normal IVSTS – 9.4 mm – normal LVIDS – 25 mm (n ) LVPWS – 8.4 mm - normal
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Daisy - Echo Short Axis – LV papillary muscles
IVSTD – 6.0 mm – low normal LVIDD – 35 mm (n ) LVPWD – 4.3 mm – low normal IVSTS – 9.4 mm – normal LVIDS – 25 mm (n ) LVPWS – 8.4 mm – normal FS – (35-25)/35 = 29% (normal 30-46%)
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Daisy - Echo Short Axis - MV MV leaflets hyperechoic and thickened
EPSS – 8 mm (n 0-6) Short Axis – Aortic Valve/RVOT LA appears 2-3x normal size AoS – 13.0 – normal LAD – 33 mm (n ) LA/Ao = 2.5 (n )
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Daisy - Echo Long View – 4 Chamber LV and LA both appear large
MV is very thick and knobby, with some prolapse into the LA
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Daisy - Echo Long View – 4 Chamber LV and LA both appear large
MV is very thick and knobby, with some prolapse into the LA
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Daisy - Echo Long View – 4 Chamber LV and LA both appear large
MV is very thick and knobby, with some prolapse into the LA Pulmonary vein markedly enlarged Long View – LVOT Large LA, Large LV
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Daisy Therapeutic Plan Increase hydralazine to 5 mg PO BID
Add spironolactone 12.5 mg PO BID Increase furosemide to mg PO TID x 2 days, then decrease to BID if respiratory rate decreases to less than 40 per minute at rest. Recheck 1 week – BUN, creat, phos, electrolytes, chest rads, BP
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Daisy Recheck – 1 week Clinically improved again BP - 125
BUN 132, creat 2.6, phos 6.6 Electrolytes normal chest rads improved pulmonary edema Therapeutic Plan – Update Add aluminum hydroxide gel 2 cc PO BID
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Daisy 5 Months later Coughing getting worse
Chest rad show no pulmonary edema LA getting larger Therapeutic Plan – Update Add torbutrol 2.5 mg PO PRN to control cough
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Daisy 18 Months after initial presentation
Owner discontinue pimobendan due to GI upset 28 months after initial presentation Daisy finally took her final breath BUN >100 for 22 months
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Chronic MV Disease May be accompanied by similar TV disease (80%)
TV disease without MV disease possible but rare LHF and/or RHF can result Right heart enlargement can develop due to pulmonary hypertension, in turn due to LHF
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Chronic MV Disease Echo abnormalities: (doppler echo)
LA and/or RA dilation, LV and/or RV dilation Exaggerated IVS motion (toward RV in diastole) Increased FS first, then later decreased FS Thickened valve leaflets (video) (video 2) If TV only affected, left heart can appear compressed, small and perhaps artifactually thick Ruptured CT – MV flips around in diastole MV flies up into LA during systole – “MV flail” (video) May see trailing CT, or CT floating in the LV
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Chronic MV Disease Right Heart Failure Medications similar to LHF
Medications not as effective at eliminating fluid congestion More effective at preventing fluid accumulation, once controlled Periodic abdominocentesis and/or pleurocentesis required Prognosis for RHF and LHF is extremely variable
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Chronic MV Disease Classification of Chronic AV Valve Disease
Class I - small, discrete nodules along the edge of the valve leaflets Class II - free edges are thickened and the edges of the leaflets become irregular. Some CT are thickened. Class III - valve edges grossly thickened and nodular, extending to the base of the valve leaflets. There is redundant tissue, resulting in prolapse into the LA. CT are thickened and may rupture, resulting in mitral valve flail. CT to the septal leaflet can also elongate.
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(MR Client Handout) (ACVIM MVD Guidelines)
Chronic MV Disease LA Jet Lesions fibrous plaques in the endocardium in a region subjected to the impact of the high velocity MR jet. Endomyocardial splits or tears may also be identified. On occasion, a full thickness left atrial tear occurs resulting in hemopericardium, pericardial tamponade, and usually death. Rarely, a full thickness endomyocardial tear will involve the interatrial septum, causing an acquired atrial septal defect. (MR Client Handout) (ACVIM MVD Guidelines)
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MVD in Cavaliers Leading cause of death in Cavaliers
CHF can develop as young as 1-3 years old First sign of disease is mitral murmur Careful annual auscultation Radiographs should be done as soon as murmur is detected q6months when progressing annually for stable disease Sooner when respiratory rate exceeds per minute Doppler Echo when abnormalities are present on rads
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MVD in Cavaliers The median survival period from grade III CHF due to MVD is approximately seven months, with 75% of the dogs dead by one year Current recommendation is that no Cavalier be bred until after 5 years of age, with no murmur At this time, a majority of Cavaliers are affected (Client Handout)
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Trip Signalment 2 year old castrated male border collie
Chief Complaint/History Productive Cough, weight loss for 2 months Breathing hard for a 2 days Energy good; did well in agility 4 days ago Owner thinks has had lifelong PU-PD Has wanted to be in AC this summer – unlike last summer when he enjoyed being outside
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Trip Exam T 102.2, P 168, R 42, CRT 3 sec BCS 2.5 BP 100
Bounding pulses, notable in dorsal pedal artery Precordial – exaggerated left apical heave Lung sounds clear
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Trip Exam 3 murmurs: PMI left base (audio) To-and-fro murmur 3/6
aortic stenosis in systole, regurg in diastole 2. PMI left apex, but heard all over chest (link) Holosystolic murmur 3/6 Mitral regurgitation due to LHF 3. PMI Carotid artery (audio) 2/6 ejection murmur aortic stenosis
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Trip Differential Diagnoses Aortic endocarditis
SAS with aortic regurgitation Mitral regurgitation (endocarditis?) Diagnostic Plan Thoracic radiographs EKG Echocardiography
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Trip EKG Normal sinus rhythm for 10 minutes
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Trip EKG Normal sinus rhythm for 10 minutes
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Trip EKG Normal sinus rhythm for 10 minutes Thoracic Radiographs
Interstitial pattern caudal lung fields Vertebral heart score 10.5 Enlarged cranial pulmonary lobar vein Mildly enlarged left atrium Early left congestive heart failure
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Trip - Echo Short Axis – LV Apex No abnormalities noted
Short Axis – LV PM
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Trip - Echo Short Axis – LV Apex No abnormalities noted
Short Axis – LV PM
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Trip - Echo Short Axis – LV Apex No abnormalities noted
Short Axis – LV PM LVIDD – 57.3 (n ) IVSTS – 15.5 mm (n ) LVIDS – 41.1 mm ( ) FS = ( )/57.3 = 28% (n 30-46%) EF = 54% (n >70%)
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Trip - Echo Short Axis – MV EPSS – 8 mm (n 0-6) Short Axis – Ao/RVOT
AoS – 20.2 (normal) LAD – 27.8 (n ) LA/Ao – 27.8/20.2 = 1.38 (n ) Aortic valve leaflets are hyperechoic
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Trip - Echo Short Axis – MV EPSS – 8 mm (n 0-6) Short Axis – Ao/RVOT
AoS – 20.2 (normal) LAD – 27.8 (n ) LA/Ao – 27.8/20.2 = 1.38 (n ) Aortic valve leaflets are hyperechoic
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Trip - Echo Short Axis – MV EPSS – 8 mm (n 0-6) Short Axis – Ao/RVOT
AoS – 20.2 (normal) LAD – 27.8 (n ) LA/Ao – 27.8/20.2 = 1.38 (n ) Aortic valve leaflets are hyperechoic
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Trip - Echo Short Axis – PA No abnormalities noted
Long Axis – 4 Chamber
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Trip - Echo Short Axis – PA No abnormalities noted
Long Axis – 4 Chamber
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Trip - Echo Short Axis – PA No abnormalities noted
Long Axis – 4 Chamber LA appeared mildly enlarged IVS bowed anteriorly toward RV No evidence of mitral encodarditis or endocardiosis Vegetation on aortic valve
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Trip - Echo
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Trip - Echo Long Axis – LVOT (video)
Hyperechoic thickened aortic valve leaflets Diagnosis Aortic endocarditis Therapeutic Plan Elected euthanasia due to poor prognosis
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Trip
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Valvular Endocarditis
Clinical Features Present for FUO, weight loss or heart failure Aortic much more common than mitral Dogs much more common than cats Many bacteria including Bartonella Breed predisposition Rottweiler, Boxer, Golden retriever Newfoundland, German shepard
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Valvular Endocarditis
Clinical Features Abnormal valve + bacteremia = endocarditis Bacteremia caused routinely by: Dental cleaning Brushing your teeth (chewing) Constipation, any GI illness defecation Urinary catheterization infection
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Valvular Endocarditis
ECG abnormalities Tall, wide P wave (LA enlargement) Tall R wave (LV enlargement) Ventricular arrhythmias common Treat if multiform of >30 per minute Class I or III antiarrhythmic Sotalol 2-3 mg/kg PO BID Thoracic radiographs Left heart failure
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Valvular Endocarditis
ECG abnormalities Tall, wide P wave (LA enlargement) Tall R wave (LV enlargement) Ventricular arrhythmias common Treat if multiform of >30 per minute Class I or III antiarrhythmic Sotalol 2-3 mg/kg PO BID Thoracic radiographs Left heart failure
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Valvular Endocarditis
Echocardiographic abnormalities Thickened, hyperechoic valves Vegetation may flop around MV in diastole, AV in systole Variable LV dilation (more with time) FS normal to low normal until myocardial failure MV endocarditis can be difficult to distinguish from MV endocardiosis Endocarditis dogs are systemically ill
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Valvular Endocarditis
Treatment Based on urine and blood culture and sensitivity, Bartonella PCR Antibiotics IV 3-5 days – broad spectrum until culture results SC/IM 3-5 days Then PO long term – often for life Treat Heart failure (severe) Treat ventricular arrhythmia if present Watch for and treat bacterial embolization of abdominal organs, skin, IVDiscs, CNS, joints, etc. Watch for and treat immune complex disease
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Valvular Endocarditis
Prognosis <20% survival Antibiotic therapy often required for life Median survival is 6 days from diagnosis for aortic endocarditis Survival is longer for mitral endocarditis LHF due to MR not as severe as AoR (Client Handout)
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Maximus 18 month old male Boxer Chief Complaint
Drastic and rapid weight loss Not eating well Coughing up blood tinged fluid since yesterday Exam, Chest rads, ECG Similar to Trip, except temp 103.8 And BCS 2
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Maximus Urine culture Diagnostics Blood culture CBC
negative (2 samples 2 hours apart) Urine culture Enterobacter susceptible to all CBC neutrophilia 23,100/ul Mild anemia – PCV 35.5%
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Maximus Diagnostics General Health Profile, electrolytes Urinalysis
BUN – 55 (n 10-29) ALT – 225 (n ) Albumin – 2.2 (n ) Urinalysis USG – 1.045 WBC 7-10/hpf, rare bacteria seen
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Maximus Treatment (58 lbs, BCS 2, RR 66) Antibiotics Furosemide
IV - ampicillin 750 mg TID, Baytril 150 mg BID x 3 days IM – ampicillin 750 mg BID, Baytril 150 mg x 3 days PO – ampicillin 750 mg BID, Baytril 136 mg PO for life Furosemide 100 mg IV TID the first day - RR down to 28 Then 75 mg PO BID Enalapril – 15 mg PO BID Pimobendan – 5 mg PO BID
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Maximus Treatment – Day 3 – RR 30, eating well Chest x-rays
Pulmonary edema much improved, but mild amount still present Continue Furosemide, Enalapril, Pimobandan Added Spironolactone – 25 mg PO BID
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Maximus Diagnostics – Day 5 – RR 36, BP 150 Chest x-rays - No change
BUN – 43 Electrolytes - normal Treatment – Day 5 Continue Furosemide, Enalapril, Pimobendan Spironolactone – increased to 50 mg PO BID Added Hydralazine – 12.5 mg PO BID
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Maximus Diagnostics – Day 10 RR 30, BP 135, Wt 61.8, Temp 103
Chest x-rays – perihilar edema resolved BUN – 11, albumin 2.3 Electrolytes – normal CBC – neutrophilia 23,000/ul Continued this treatment for the rest of Max’s life – 3 months
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Summary PowerPoint – Cases – Valvular Disease
.pdf of PowerPoint – Valvular Disease All Audio and Video Files ACVIM Position Statement on CHF Client Handouts Endocarditis Valvular Dysplasia Congestive Heart Failure MVD in Cavaliers
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