Cardiovascular S+H Flashcards
Primary trigger for activation of RAAS in CV disease
Heart unable to provide adequate renal blood flow
Which hormone is released by the macula dense when there is decreased renal perfusion and sodium delivery to the distal portions of the nephron
Renin
Renin converts _____ to ____
Angiotensinogen to angiotensin I
Angiotensin converting enzyme (Ace) converts ____ to ____
Angiotensin I to angiotensin II
Chronic SNS activation leads to
Adrenergic receptor down regulation
Persistent tachycardia
Increased myocardial oxygen demand
Myocyte necrosis
What are the two main hormones that induce natriuresis, diuresis, and vasodilation?
Atrial natriuretic peptide and brain natriuretic peptide (ANP and BNP)
What induces production of ANP and BNP
Myocardial stretch/stress
Endothelin I causes ____ and is released by vascular endothelial cells in response to ____
Causes vasodilation
Released in response to shear stress, angiotensin II, and other various cytokines
Together with ____, endothelin I causes vasoconstriction and increased cardiac after load
Angiotensin II
In addition to its vascular effects, endothelin I alters normal ___ cycling within muscle cells and is directly toxic to ____
Alters normal calcium cycling within muscle cells and is directly toxic to cardiac myocytes
Arginine vasopressin, or ADH, is released in response to stimulation of ____ in response to decreased intravascular pressure
Stimulation of the baroreceptors in the aortic arch and carotid
Dilutional hyponatremia indicates ____
Excess free water and dilution of sodium despite entire body stores of sodium being elevated
Concentric hypertrophy is in response to increased ____ such as with _____
Increased pressure load
Increased after load - systemic hypertension, SAS
Increased after load triggers replication of _____ in parallel resulting in a relative increase in ___ of the ventricular wall
Sarcomeres
Increase in relative thickness
Conversely, in situations of volume overload (i.e. mitral regurgitation), the sarcomeres replicate in _____ which results in elongation of the myocytes and dilation of the ventricle.
In series (end to end)
Eccentric hypertrophy
Consequences of concentric hypertrophy
Increased myocardial oxygen demand, endocardial ischemia, fibrosis, collagen disruption, injury to small coronary vessels
Consequences of eccentric hypertrophy
Increased myocardial wall stress, myocyte injury and necrosis, and myocyte slippage
Main storage area of calcium in the heart muscle cells
Sarcomplasmic reticulum
During systole, calcium ions ____ which triggers release of additional calcium from the SR
Calcium ions enter the myocardial cell and trigger release of additional calcium ions from the SR
Channel that calcium flows through
Ryanodine channel
Calcium flows through the ryanodine channel and binds to _____
Troponin C located on the actin-myosin complex
What initiates the cascade of events that lead to sarcomere contraction
Calcium binding to troponin C
Once contraction is complete, calcium is released from troponin C and travels back to the SR via the _____ channel
Sarcomplasmic/endoplasmic reticulum Ca-ATPase (SERCA) channel
Another effector molecule in the cytoplasm that helps regulate calcium reuptake
Phospholamban
Myocyte mitochondria provide high-energy _____ molecules that fuel calcium and other ion pumps
Phosphate molecules
In dogs with myocardial disease, the _____ chain located within mitochondria lack critical cytochromes and enzymes needed for energy production
Oxidative phosphorylation chain
The heart can utilize ___ and ___ as its main substrates for energy production
Glucose and fatty acids
In cases of heart failure, the heart preferentially uses ___ which requires less oxygen to metabolize than ___
Preferentially uses glucose over fatty acids
Pulmonary venous pressures greater than ____ and systemic venous pressures >____ typically result in congestion
> 25 mmHg pulmonary venous
20 mmHg systemic venous
Why are dogs at less risk for coronary artery disease than humans
Extensive epicardial network of collateral vessels
In dogs with atherosclerosis, what are predisposing factors
Hypothyroidism
Hyperlipidemia
Hypercholesterolemia
HYPERCOAGULABILITY
In a case report of six dogs with snake envenomation, sepsis and SIRS, what ECG abnormality was seen associated with myocardial infarction?
Transient deep and negative T waves
During skeletal and cardiac muscle relaxation, ____ blocks the binding sites on actin
Tropomyosin
Once intracellular calcium levels rise and ATP is present, calcium will bind to ____, displacing it from tropomyosin allowing exposure of myosin binding sites on actin
Troponin
Three distinct proteins associated with troponin complex
I, T and C
Which two troponin play a role in diagnosis of myocardial injury, particularly infarction
I and T
Troponin T (cTnT) is present in four isoforms, of which only ____ is expressed in adults
One
Troponin I (cTnI) is present in three isoforms, with only ____ found in cardiac muscle
One
cTnI is/is not expressed in fetal tissue
NOT
_____ is inhibited by cTnI and thereby prevents interaction with myosin and actin binding sites
Actomyosin ATPase
When calcium binds to ____, ___ is displaced and a conformational change of tropomyosin results, allowing muscle contraction
When calcium binds to troponin C, cTnI is displaced and a conformational change of tropomyosin results, allowing muscle contraction
The majority of troponin is bound within _____ but a small amount is free in the cytosol
The thin filaments
When cardiac myocytes becomes damaged, ___ becomes released into circulation
Troponin
Circulating troponin increases ____ hours after injury with peak values occurring _____ after onset of symptoms, which can last up to ____ days
Increase 2-4 hours after injury
Peak in 18-24 hours
Can last up to 14 days
What other diseases can result in troponin elevation
Renal disease, sepsis, trauma, extreme exercise, infectious disease, inflammatory disease
In order for wall motion to be abnormal/segmental wall abnormality to be detected on echocardiogram, >____% of the myocardial wall must be affected
> 20%
____ foci have also been detected on echo and suggest myocardial infarction
HypERechoic foci within the myocardium
Vipera berus envenomation in dogs- ECG abnormalities and cTnI levels
All dogs survived. Twelve dogs (57%) developed arrhythmias, all of which were ventricular in origin. Severe complex ventricular arrhythmias (VAs) were observed in 6 dogs (29%). Eighty-one percent of dogs (n = 17) had increased cTnI concentrations at 1 or more time points. Dogs that developed arrhythmias had signifi- cantly higher concentrations of cTnI at 12 hours (1.67 [0.04-32.68] versus 0.03 [0.01-0.052]; P = .002), 24 hours (1.88 [0.2-14.23] versus 0.06 [0.01-2.06]; P = .009), and 36 hours (3.7 [0.02-16.62] versus 0.06 [0.01-1.33]; P = .006) after bite compared to those that did not.
Troponin and CRP levels in dogs with various snake envenomations
Concentrations of cardiac troponin I (cTnI), a marker of myocardial injury, and C-reactive protein (CRP), a marker of systemic inflammation, were measured in each blood sample. Evidence of myocardial injury was found in 58% of dogs envenomed by V. berus at one or more time points. A significant correlation between cTnI and CRP concentrations was found at all time points. Evidence of myocardial injury was found in 80% of dogs envenomed by B. arietans at one or more time points; however, no correlation was found between cTnI and CRP concentrations. Evidence of myocardial injury was found in 67% of dogs envenomed by N. annulifera at one or more time points. A significant correlation between cTnI and CRP concentrations was found at admission, but not at other time points.
Transient deep and negative T waves in dogs with myocardial injury (2021)
Six cases were diagnosed with MI associated with deep (n = 1) and giant (n = 5) transient NTWs. Myocardial injury was classified as acute in all cases and was due to snake envenomation (n = 3), sepsis (n = 2), and systemic inflammatory response syndrome (n = 1). At the time of deep/giant NTWs identification, all dogs had elevated cardiac troponin I and ≥1 echocardiographic abnormality of the left ventricular structure and/or function. Moreover, all dogs with giant NTWs had prolonged QT intervals. After the MI resolution, T-wave polarity and QT-interval duration became normalized in all dogs. Moreover, left ventricular morphological and functional parameters were completely normalized in four dogs. In contrast, ventricular echogenicity remained heterogeneous in two dogs, despite otherwise normalized ventricular parameters. Five dogs were still alive at the conclusion of the study.
Five cardiomyopathy phenotypes
- Hypertrophic
- Dilated
- Restricted - end-myocardial restrictive, myocardial restrictive
- ARVC
- Non-specific/unclassified
Characteristics of HCM
Segmental or diffuse left ventricular wall thickening
Sequela of HCM possible
CHF
Arterial thromboembolism
Ventricular arrhythmias +/- sudden death
Supraventricular arrhythmias
Normal lifespan possible
Characteristics of DCM
Primary reduction of left ventricular systolic function with normal or reduced LV wall thickness, and eventual LV and LA dilation
Potential sequela of DCM
Arterial thromboembolism
CHF
Ventricular arrhythmias +/- sudden death
Supraventricular arrhythmias
Normal lifespan UNLIKELY
Endomyocardial restrictive cardiomyopathy characteristics
Endocardial scar bridging the left ventricular septum and free wall with associated LA or biatrial enlargement
Characteristics of myocardial restrictive cardiomyopathy
Left or biatrial enlargement with normal LV dimensions
Sequela of restrictive cardiomyopathy
Arterial thromboembolism
CHF
Ventricular arrhythmias +/- sudden death
Supraventricular arrhythmias
Normal lifespan UNLIKELY
Characteristics of ARVC
Severe dilation of right heart with right ventricular systolic dysfunction and myocardial thinning
Sequela of ARVC
Right sided CHF
Ventricular and supra ventricular arrhythmias common - may cause sudden death
PULMONARY thromboembolism
Characteristics of non-specific cardiomyopathy
Any phenotype not fitting the others
Concomitant/underlying disease states contributing to feline cardiomyopathy phenotypes
Hypertension - HCM
Neoplastic myocardial infiltration - HCM
Transient myocardial thickening - HCM
Inflammatory myocardial infiltration - HCM
Acromegaly - HCM
Hyperthyroidism - HCM, RCM, UCM
Taurine deficiency - DCM
Chronic tachycardia - DCM
Suspected underlying mechanism of genetic HCM
Sarcomeric mutations involving either thick (myosin) or thin (actin) filaments causing a hyper contractile cardiac sarcomere
Genetic mutations detected predisposing cats to HCM
Two mutations in one gene (myosin binding protein C, MYBP3) - the A31P mutation in Maine Coon cats, and the R820W in Ragdolls
Most common complication of HCM and percentage of development
CHF, 23.9%
Approximately what percentage of cats with HCM develop ATE
~11%
Embolism to the right ____ artery can affect the front limbs
Brachial artery
The primary arterial occlusion results in release of vasoactive substances from activated platelets, such as ____, which results in vasoconstriction of collateral arteries
Serotonin
Burnout or end-stage HCM
Once systolic function starts to decrease
Dynamic LEFT ventricular outflow obstruction can occur in ____ % of cats with HCM
About 45-67% of cats with HCM will develop at some point
DLVOTO can result from
SAM - mitral valve moves out of place during systole, to make contact with the inter ventricular septum and impede blood flow through the LVOT. The mechanism of SAM involves anterior displacement of the anterior papillary muscle due to myocardial hypertrophy, which causes laxity of the anterior mitral chordae
T/F: A heart murmur is LESS likely to be heard once a cat develops heart failure, as compared to during the occult phase
TRUE
In cats a maximal LA dimension in long axis greater than ____ and a LA:Ao > ____ is suggestive of significant heart disease
> 16.5 mm
> 1.5
Normal fractional shortening
≥ 40%
NT-ProBNP can help differentiate cardiac from non-cardiac causes of respiratory distress in cats, with a ____ sensitivity and ____ specificity for diagnosis of CHF
93.9% sensitivity
72.2% specificity
Chronic activation of _____ in heart failure causes myocardial fibrosis, vascular remodeling, and endothelial dysfunction via ____ receptors on myocardial, vascular, and fibroblast cells
RAAS
Mineralocorticoid receptors
____ may potentially block some of the mineralocorticoid profibrotic effect
Spironolacton
Dogs with DCM and concurrent A-fib more often show signs of ___ sided heart failure, in addition to signs of ___ sided failure
Right sided in addition to left sided
Doberman DCM age of onset
6 years
Two autosomal dominant gene mutations in Dobermans associated with DCM
Splice site mutation in the gene encoding mitochondrial protein pyruvate dehydrogenase kinase 4
Missense mutation in the titin gene
Starting Pimobendan and ACE inhibitors in Dobermans with LVE detected and the occult stage of disease, shown to delay onset of CHF and sudden death by up to ___ and ___ months respectively
9 and 3 months
Sotalol- drug class, effects
Sotalol is a non-cardioselective β-blocker that possesses potassium channel-blocking properties. Due to the predominant potassium channel–blocking effect, this drug is classified as a class III agent
Used for ventricular arrhythmias
May worsen systolic dysfunction in some patients (beta blocking effects)
Mexiletine- drug class, effects
Mexiletine is a sodium channel blocker and further classified as a Class 1B antiarrhythmic
Ventricular arrhythmias
GI upset
Fish oil therapy for heart disease
May be used to help combat cardiac cachexia
DCM in Irish Wolfhounds
Familial
Not uncommon to diagnose A-fib prior to structural changes
Breeds with suspected genetic DCM
Great Dane
Doberman
Portuguese Water Dog
Toy Manchester Terrier
Newfoundland
Irish Wolfhounds
Standard Schnauzer
Goldens- muscular dystrophy
Dog breeds that seem more at risk for nutritional secondary DCM
Goldens
American Cocker Spaniels
Newfoundland
Dalmations
Boxers
Dogs with DCM related to nutrition are typically fed diets low in ____ and high in ___ and ___
Low in grain
High in potatoes and legumes
Causative mechanism of fibrofatty infiltration in the myocardium of Boxers (ARVC)
Mutation of the striatin gene
Three subcategories of ARVC
Type I: Dogs with subclinical ventricular arrhythmias
Type II: Dogs with ventricular arrhythmias and syncope
Type III: Dogs with structural cardiac changes identified on echo with a diagnosis of CHF
Diagnosis of >____ VPCs in a 24 hour period is consistent with ARVC
> 300 in 24 hours
Atrioventricular myopathy
Replacement fibrosis of the atrial myocardium with or without fatty degeneration, leading to atrial dilation and persistent atrial standstill.
Breeds: ESS, Labs
Need a pacemaker
Median time to CHF or cardiac death in untreated smaller dogs with clinically significant cardiomegaly can be as long as __-___ years
2-3 years
Hallmark of MMVD
Systolic mitral valve regurgitation
T/F: Vegetative endocardial lesions and significant inflammatory changes do not play a role in MMVD
True they do not
Forward stroke volume is initially maintained in MMVD via this mechanism of the Frank Starling
Enhanced LV filling (increased preload) and eccentric hypertrophy (chamber dilation)
Chronic LAE and weakening of the LA wall can lead to a LA tear which can result in two different things
A tear between atria resulting in a L–>R shunting defect
OR
A split and acute pericardial effusion
Development of PH associated with MMVD
Chronic post-capillary PH (pulmonary venous hypertension) can lead to a reactive pulmonary arterial vasoconstriction and pulmonary vascular disease (combined post and pre capillary PH)
Two other diseases which can increase NT-proBNP in dogs
Renal disease
Pulmonary hypertension
Seven proposed mechanisms of development of blunt cardiac injury
1) direct impact to the chest at the end of diastole when the ventricles are maximally distended, or impact at the end of systole when the atria are maximally distended
2) sudden increase cardiac preload secondary to increased venous return from impact applied to the peripheral or abdominal veins
3) bidirectional forces that compress the heart within the thoracic cage
4) forces of acceleration and deceleration that cause the heart to move, leading to myocardial damage and damage to the great vessels and coronary arteries
5) blast forces leading to cardiac contusion or rupture
6) concussive forces leading to development of arrhythmias
7) cardiac penetration from displaced fractures
When are heart valves most susceptible to injury from blunt cardiac injury
During time of closure
Aortic/pulmonary valves - most susceptible in diastole
Mitral/tricuspid valves - most susceptible during systole
Commotio cordis
Sudden cardiac death after BCI without any observable pathology
Basically it’s a traumatic precordial thump
Impact during ventricular repolarization within 15-30 milliseconds before the peak of the T wave, leading to acute R on T, which degenerates to V fib and death
Most arrhythmias associated with BCI
Happen within 24 hours
Ventricular
Happen in 96% of dogs following BCI
and may not be present on initial ECG
Which troponin is most sensitive for myocardial injury in dogs?
cTnI
Treatment of ventricular arrhythmias in cats
Sotalol
Causes of PCE
Idiopathic
Neoplastic (HSA, heart base > others)
Coagulopathy
Infectious (FIP)
CHF
LA split
Trauma
Chyle
Hypoalbuminemia
Chronic uremia
Pulses paradoxus
Fall in inspiratory arterial pressure of 10 mmHg or more
Hepatojugular reflex
Animal is standing with head in a normal position
Cranial abdominal pressure applied
If jugular vein remains distended (increased preload) during compression this is abnormal
Cardiac tamponade characterized by
Diastolic (and early systolic) compression or collapse of the right atrium and sometimes the right ventricle
Cardiac tamponade commonly raises the CVP to ____ or higher
10-12 cmH2O
Wandering pacemaker- ECG finding in sinus bradycardia secondary to increased vagal tone
P wave appears shorter during expiration when the heart is slower
P wave appears taller during inspiration when the heart rate is faster
Absence of a junctional or ventricular escape beat for more than _____ seconds suggests a disease process that is affecting more than just the SA node
3-4 seconds
First degree AV block
Impulses are conducted, just take longer (PR interval is prolonged)
AV nodal fibrosis, high vagal tone, drugs
Second degree AV block Mobitz type I (Wenkebach phenomenon)
Longer longer longer drop
AV nodal fibrosis and progressive vagal tone increase
Will get better with atropine
Second degree AV block Mobitz II
Unexpected occurrence of lone p Waves
PR interval of complexes before and after are normal
Area of block is below the bundle of His- QRS complexes wide
Atropine - unchanged or WORSE
Third degree AV block
Complete lack of transmitted P waves
Cardiac output dramatically reduced
Atrial and ventricular activity completely unrelated
QRS complexes wide and bizarre with rates of 20-60 bpm in dogs and 60-140 bpm in cats
Atrial rate may be elevated
Ventricular rate is normally regular unless VPCs are originating from an ischemic source
Myocardial fibrosis, inflammation or infiltration, drug toxicities most common. Dogs- age related fibrodegenerative disease; cats- structural heart disease
Syncope more common with _____ block
Paroxysmal second degree AV block
Atrial standstill
Complete loss of atrial activity on ECG
English springer spaniels (atrial myopathy)
How is lack of p waves on ECG with hyperkalemia different than atrial standstill
Atrial standstill- SA node isn’t firing
Hyperkalemia- SA node is firing, still conducts to the AV node - however, signal doesn’t propagate to remainder of atrial tissue which is why you can’t see the P wave on ECG
Supraventricular tachycardias require __ or __ nodal tissues for initiation and maintenance
SA and AV or both
SVT rate
180-300
Young or middle age dogs with no evidence of systemic illness and SVT present
Concerning for atrioventricular accessory pathway
SVTs with irregular RR intervals
A-fib
Atrial flutter with varying block
Multifocal atrial tachyardia
AV nodal tachycardias
AV nodal reentrant tachycardia
AV reentrant tachycardia (accessory pathway)
Junctional tachycardias
SVT with a ____ can look like a ventricular arrhythmia
Bundle branch block
A fib
No p waves
Irregular
Tachycardia
Slight fluctuations in baseline representing struggling atrial activity called fibrillation waves
Responses to vagal maneuvers
Sinus tach: may show some slowing
A-fib: no response
Atrial flutter: may slow transiently, allow visualization of F waves
Multifocal atrial tachycardia: may slow ventricular response rate transiently
Focal atrial tachycardia: transient positive response with abrupt cessation of SVT
AV re-entrant tachycardia mediated by accessory pathway: transient positive response with an abrupt cessation of SVT
Ventricular escape rate in dogs and cats
Dogs: 30-40 bpm
Cats: 60-130 bpm
What is overdrive suppression
The faster rhythm suppresses the slower one
What are three arrhythmogenic mechanism
Enhanced automaticity
Triggered activity
Reentry
Most commonly seen VT and mechanism
Monomorphic VT - most often reentry
Most common electrolyte abnormality associated with VT
Hypokalemia
How does hypokalemia precipitate VT
Increases phase 4 depolarization, increasing automaticity, and prolongs the action potential duration which promotes arrhythmias from triggered activity
Enhanced automaticity and triggered activity
Why does magnesium deficiency cause VT
Magnesium necessary for proper functioning of the Na-KATPase pump which maintains normal intracellular potassium
Dobermans with occult DCM
No clinical signs but indications of early LV function on echo and 30% chance of sudden death
Doberman pinscher DCM ECG
92% VT
Ventricular ectopies have a right bundle branch block morphology on lead II indicating the impulse originates in the left ventricle
Boxer ARVC
Ventricular ectopics typically have a left bundle branch block morphology indicating their origin in the right ventricle
May have faulty ryanodine receptor
Bulldog ARVC pheotype
Disease centered in region of the right ventricular outflow tract which is the site of origin of the ventricular tachycardia
Tetralogy of Fallot components
pulmonic stenosis
large ventricular septal defect
right ventricular hypertrophy
dextropositioning (overriding) of the aorta
Bulldog pulmonic stenosis
English Bulldogs are the most common breed to have pulmonic stenosis. Previous studies showed that this congenital heart abnormality in Bulldogs frequently is caused by a circumpulmonary left coronary artery originating from a single right coronary artery.
English Bulldogs (EB) with pulmonic stenosis (PS) sometimes have an aberrant coronary artery (CA) type R2A encircling the pulmonary artery (PA). Balloon valvuloplasty (BV) is treatment of choice for severe PS, but is considered to be contraindicated in dogs with aberrant CA.
R on T
When there is a superimposed ectopic beat over top of the preceding T wave during a “vulnerable period” and may progress to VF and death
Non infectious myocarditis causes
Doxorubicin in dogs
Heat stroke
Vasculitis
Allergic reactions
Radiation
NT-proBNP
Degrades less quickly than other BNPs
Three main categories of systemic hypertension
Situational
Idiopathic
Secondary
Most common causes of secondary hypertension in dogs and cats
1) CKD and AKI
2) Hyperadrenocorticism in dogs, hyperthyroidism in cats
3) Diabetes (high in dogs, low in cats)
4) Pheo/hyperaldosteronism
Goal of antihypertensive therapy- hypertensive EMERGENCY
For acute crisis - reduction in 10% BP in first hour, then 15% over next several hours.
Development of infective endocarditis
Mechanical lesion of the heart valve and disrupted endothelial surface –> extracellular matrix proteins, thromboplastin, and tissue factor exposed –> a coagulum consisting of fibrin, fibrinogen, platelet proteins forms and avidly binds bacteria
The primary attachment of bacteria to the disrupted endothelium
Fibrinogen binding
Subsequent fibronectin binding triggers endothelial cell internalization and local pronflammatory and procoagulant responses
Inflammation induces endothelial cell expression of _____ which bind bacteria and fibronectin to the extracellular matrix
Integrins
Some bacteria, like ______, carry fibronectin binding proteins and also can trigger active internalizations by host cells
Staphylococcus aureus
Organisms that commonly cause IE are those that have the greatest ability to adhere to the damaged valves because of specialized receptors called ____
Microbial surface components
Staph and Strep
Pattern of CHF with infective endocarditis
May be fulminant and cause pulmonary flooding, without massive LAE
Cytokines/biomarkers that are elevated in patients with IE
IgG
IgM
C3
Rheumatoid factor
Two immune mediated diseases which are commonly seen in dogs with IE
Polyarthritis (75%)
Glomerulonephritis (36%)
Thromboembolism (septic and aseptic) is seen commonly post mortem in dogs with IE, __-___% of them
70-80%
Dogs are more likely to suffer from thromboembolic disease if they have ____ valve IE
Mitral valve
Most frequent organ sites of thromboembolism
Infarction of the kidneys and spleen, followed by myocardium, brain, and limbs
Brain - middle cerebral eatery
Most common presenting complaint with IE
Lameness
Predisposing factors for IE in dogs
SAS - only structural heart abnormality associated with it
Endothelial dysfunction and bacteremia
Diskospondylitis
Prostatitis
Pneumonia
UTI
Pyoderma
Periodontal disease
Long term indwelling central lines
+/- Immunosuppression
Most common causes of IE in dogs (bacteria)
Staphylococcus spp. (S. aureus, S. pseudintermedius, and coagulase negative Staphylococcus)
Streptococcus spp. (S. Canis and S. bovis)
E. coli
Les common:
Enterococcus
Psueodomonas
Pasteurella
Enterobacter
Suggested MAJOR criteria for diagnosis of IE in dogs
- Echocardiogram: Vegetative, oscillating lesion; erosive lesions; abscess
- New valvular insufficiency
- More than mild AI in absence of SAS
- Positive blood culture ≥2 bottles with typical organism, ≥3 bottles with common skin contaminant, Persistent positive cultures over ≥12 hours
Suggested MINOR criteria for diagnosis of IE in dogs
- Fever
- New or worsening murmur
- Predisposing cardiac disease (SAS)
- Evidence of thromboembolic disease
- Evidence of autoimmune disease
- Microbiologic findings not meeting major criteria: Positive Bartonella serology, Blood cultures not meeting major criteria
Definite diagnosis of IE
Histopathology
Two major criteria
One major and two minor criteria
Possible and unlikely diagnosis of IE
Possible:
One major and one minor
Three minor
Unlikely:
Other diagnosis made
Resolved in <4 days treatment
No evidence on necropsy
Bartonella most commonly implicated in IE and dogs and where does it like to go
Bartonella vinsonii spp. berkhoffii
Likes to go to aortic valve
PE findings in dogs with IE
Murmur (89-96%); often may be diastolic, with bounding pulses
Fever (50-74%); Bartonella less likely to cause a fever
Arrhythmias (40-70%) including ventricular and supraventricular tachycardia, third degree AV block (periannular abscess from aortic IE)
–> dogs with aortic IE tend to be more likely to develop arrhythmias
CHF (almost 50%)
What additional test may identify bacteria in the blood in addition to blood cultuers
16S rDNA PCR
Testing for Bartonella
PCR - blood may be false negative; improved with a week culture on BAPGM
Culture on Bartonella alpha proteobacteria growth medium (BAPGM) for at least week, followed by plating on agar for up to 5 weeks may be needed for it to grow
Antibiotic therapy for IE
Ampicillin/sulbactam + amikacin if possible
Baytril + ampicillin silbactam
1-2 weeks of IV ABX
Will need weeks to months or longer of tx
Which antibiotic is associated with rapid development of resistance and Bartonella
Azithromycin
Dogs with ____ IE tend to have a far worse prognosis than dogs with ___ IE
Aortic way worse than mitral
