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ACVECC Exam 2024 > Cardiovascular S+H > Flashcards

Cardiovascular S+H Flashcards

1
Q

Primary trigger for activation of RAAS in CV disease

A

Heart unable to provide adequate renal blood flow

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2
Q

Which hormone is released by the macula dense when there is decreased renal perfusion and sodium delivery to the distal portions of the nephron

A

Renin

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3
Q

Renin converts _____ to ____

A

Angiotensinogen to angiotensin I

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4
Q

Angiotensin converting enzyme (Ace) converts ____ to ____

A

Angiotensin I to angiotensin II

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5
Q

Chronic SNS activation leads to

A

Adrenergic receptor down regulation
Persistent tachycardia
Increased myocardial oxygen demand
Myocyte necrosis

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6
Q

What are the two main hormones that induce natriuresis, diuresis, and vasodilation?

A

Atrial natriuretic peptide and brain natriuretic peptide (ANP and BNP)

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7
Q

What induces production of ANP and BNP

A

Myocardial stretch/stress

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8
Q

Endothelin I causes ____ and is released by vascular endothelial cells in response to ____

A

Causes vasodilation

Released in response to shear stress, angiotensin II, and other various cytokines

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9
Q

Together with ____, endothelin I causes vasoconstriction and increased cardiac after load

A

Angiotensin II

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10
Q

In addition to its vascular effects, endothelin I alters normal ___ cycling within muscle cells and is directly toxic to ____

A

Alters normal calcium cycling within muscle cells and is directly toxic to cardiac myocytes

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11
Q

Arginine vasopressin, or ADH, is released in response to stimulation of ____ in response to decreased intravascular pressure

A

Stimulation of the baroreceptors in the aortic arch and carotid

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12
Q

Dilutional hyponatremia indicates ____

A

Excess free water and dilution of sodium despite entire body stores of sodium being elevated

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13
Q

Concentric hypertrophy is in response to increased ____ such as with _____

A

Increased pressure load

Increased after load - systemic hypertension, SAS

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14
Q

Increased after load triggers replication of _____ in parallel resulting in a relative increase in ___ of the ventricular wall

A

Sarcomeres

Increase in relative thickness

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15
Q

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.

A

In series (end to end)
Eccentric hypertrophy

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16
Q

Consequences of concentric hypertrophy

A

Increased myocardial oxygen demand, endocardial ischemia, fibrosis, collagen disruption, injury to small coronary vessels

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17
Q

Consequences of eccentric hypertrophy

A

Increased myocardial wall stress, myocyte injury and necrosis, and myocyte slippage

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18
Q

Main storage area of calcium in the heart muscle cells

A

Sarcomplasmic reticulum

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19
Q

During systole, calcium ions ____ which triggers release of additional calcium from the SR

A

Calcium ions enter the myocardial cell and trigger release of additional calcium ions from the SR

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20
Q

Channel that calcium flows through

A

Ryanodine channel

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21
Q

Calcium flows through the ryanodine channel and binds to _____

A

Troponin C located on the actin-myosin complex

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22
Q

What initiates the cascade of events that lead to sarcomere contraction

A

Calcium binding to troponin C

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23
Q

Once contraction is complete, calcium is released from troponin C and travels back to the SR via the _____ channel

A

Sarcomplasmic/endoplasmic reticulum Ca-ATPase (SERCA) channel

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24
Q

Another effector molecule in the cytoplasm that helps regulate calcium reuptake

A

Phospholamban

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25
Q

Myocyte mitochondria provide high-energy _____ molecules that fuel calcium and other ion pumps

A

Phosphate molecules

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26
Q

In dogs with myocardial disease, the _____ chain located within mitochondria lack critical cytochromes and enzymes needed for energy production

A

Oxidative phosphorylation chain

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27
Q

The heart can utilize ___ and ___ as its main substrates for energy production

A

Glucose and fatty acids

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28
Q

In cases of heart failure, the heart preferentially uses ___ which requires less oxygen to metabolize than ___

A

Preferentially uses glucose over fatty acids

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29
Q

Pulmonary venous pressures greater than ____ and systemic venous pressures >____ typically result in congestion

A

> 25 mmHg pulmonary venous
20 mmHg systemic venous

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30
Q

Why are dogs at less risk for coronary artery disease than humans

A

Extensive epicardial network of collateral vessels

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31
Q

In dogs with atherosclerosis, what are predisposing factors

A

Hypothyroidism
Hyperlipidemia
Hypercholesterolemia
HYPERCOAGULABILITY

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32
Q

In a case report of six dogs with snake envenomation, sepsis and SIRS, what ECG abnormality was seen associated with myocardial infarction?

A

Transient deep and negative T waves

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33
Q

During skeletal and cardiac muscle relaxation, ____ blocks the binding sites on actin

A

Tropomyosin

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34
Q

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

A

Troponin

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35
Q

Three distinct proteins associated with troponin complex

A

I, T and C

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36
Q

Which two troponin play a role in diagnosis of myocardial injury, particularly infarction

A

I and T

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37
Q

Troponin T (cTnT) is present in four isoforms, of which only ____ is expressed in adults

A

One

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38
Q

Troponin I (cTnI) is present in three isoforms, with only ____ found in cardiac muscle

A

One

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39
Q

cTnI is/is not expressed in fetal tissue

A

NOT

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40
Q

_____ is inhibited by cTnI and thereby prevents interaction with myosin and actin binding sites

A

Actomyosin ATPase

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41
Q

When calcium binds to ____, ___ is displaced and a conformational change of tropomyosin results, allowing muscle contraction

A

When calcium binds to troponin C, cTnI is displaced and a conformational change of tropomyosin results, allowing muscle contraction

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42
Q

The majority of troponin is bound within _____ but a small amount is free in the cytosol

A

The thin filaments

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43
Q

When cardiac myocytes becomes damaged, ___ becomes released into circulation

A

Troponin

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44
Q

Circulating troponin increases ____ hours after injury with peak values occurring _____ after onset of symptoms, which can last up to ____ days

A

Increase 2-4 hours after injury
Peak in 18-24 hours
Can last up to 14 days

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45
Q

What other diseases can result in troponin elevation

A

Renal disease, sepsis, trauma, extreme exercise, infectious disease, inflammatory disease

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46
Q

In order for wall motion to be abnormal/segmental wall abnormality to be detected on echocardiogram, >____% of the myocardial wall must be affected

A

> 20%

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47
Q

____ foci have also been detected on echo and suggest myocardial infarction

A

HypERechoic foci within the myocardium

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48
Q

Vipera berus envenomation in dogs- ECG abnormalities and cTnI levels

A

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.

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49
Q

Troponin and CRP levels in dogs with various snake envenomations

A

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.

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50
Q

Transient deep and negative T waves in dogs with myocardial injury (2021)

A

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.

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51
Q

Five cardiomyopathy phenotypes

A
  1. Hypertrophic
  2. Dilated
  3. Restricted - end-myocardial restrictive, myocardial restrictive
  4. ARVC
  5. Non-specific/unclassified
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52
Q

Characteristics of HCM

A

Segmental or diffuse left ventricular wall thickening

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53
Q

Sequela of HCM possible

A

CHF
Arterial thromboembolism
Ventricular arrhythmias +/- sudden death
Supraventricular arrhythmias
Normal lifespan possible

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54
Q

Characteristics of DCM

A

Primary reduction of left ventricular systolic function with normal or reduced LV wall thickness, and eventual LV and LA dilation

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55
Q

Potential sequela of DCM

A

Arterial thromboembolism
CHF
Ventricular arrhythmias +/- sudden death
Supraventricular arrhythmias
Normal lifespan UNLIKELY

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56
Q

Endomyocardial restrictive cardiomyopathy characteristics

A

Endocardial scar bridging the left ventricular septum and free wall with associated LA or biatrial enlargement

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57
Q

Characteristics of myocardial restrictive cardiomyopathy

A

Left or biatrial enlargement with normal LV dimensions

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58
Q

Sequela of restrictive cardiomyopathy

A

Arterial thromboembolism
CHF
Ventricular arrhythmias +/- sudden death
Supraventricular arrhythmias
Normal lifespan UNLIKELY

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59
Q

Characteristics of ARVC

A

Severe dilation of right heart with right ventricular systolic dysfunction and myocardial thinning

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60
Q

Sequela of ARVC

A

Right sided CHF
Ventricular and supra ventricular arrhythmias common - may cause sudden death
PULMONARY thromboembolism

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61
Q

Characteristics of non-specific cardiomyopathy

A

Any phenotype not fitting the others

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62
Q

Concomitant/underlying disease states contributing to feline cardiomyopathy phenotypes

A

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

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63
Q

Suspected underlying mechanism of genetic HCM

A

Sarcomeric mutations involving either thick (myosin) or thin (actin) filaments causing a hyper contractile cardiac sarcomere

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64
Q

Genetic mutations detected predisposing cats to HCM

A

Two mutations in one gene (myosin binding protein C, MYBP3) - the A31P mutation in Maine Coon cats, and the R820W in Ragdolls

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65
Q

Most common complication of HCM and percentage of development

A

CHF, 23.9%

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66
Q

Approximately what percentage of cats with HCM develop ATE

A

~11%

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67
Q

Embolism to the right ____ artery can affect the front limbs

A

Brachial artery

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68
Q

The primary arterial occlusion results in release of vasoactive substances from activated platelets, such as ____, which results in vasoconstriction of collateral arteries

A

Serotonin

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69
Q

Burnout or end-stage HCM

A

Once systolic function starts to decrease

70
Q

Dynamic LEFT ventricular outflow obstruction can occur in ____ % of cats with HCM

A

About 45-67% of cats with HCM will develop at some point

71
Q

DLVOTO can result from

A

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

72
Q

T/F: A heart murmur is LESS likely to be heard once a cat develops heart failure, as compared to during the occult phase

A

TRUE

73
Q

In cats a maximal LA dimension in long axis greater than ____ and a LA:Ao > ____ is suggestive of significant heart disease

A

> 16.5 mm

> 1.5

74
Q

Normal fractional shortening

A

≥ 40%

75
Q

NT-ProBNP can help differentiate cardiac from non-cardiac causes of respiratory distress in cats, with a ____ sensitivity and ____ specificity for diagnosis of CHF

A

93.9% sensitivity
72.2% specificity

76
Q

Chronic activation of _____ in heart failure causes myocardial fibrosis, vascular remodeling, and endothelial dysfunction via ____ receptors on myocardial, vascular, and fibroblast cells

A

RAAS
Mineralocorticoid receptors

77
Q

____ may potentially block some of the mineralocorticoid profibrotic effect

A

Spironolacton

78
Q

Dogs with DCM and concurrent A-fib more often show signs of ___ sided heart failure, in addition to signs of ___ sided failure

A

Right sided in addition to left sided

79
Q

Doberman DCM age of onset

A

6 years

80
Q

Two autosomal dominant gene mutations in Dobermans associated with DCM

A

Splice site mutation in the gene encoding mitochondrial protein pyruvate dehydrogenase kinase 4

Missense mutation in the titin gene

81
Q

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

A

9 and 3 months

82
Q

Sotalol- drug class, effects

A

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)

83
Q

Mexiletine- drug class, effects

A

Mexiletine is a sodium channel blocker and further classified as a Class 1B antiarrhythmic

Ventricular arrhythmias

GI upset

84
Q

Fish oil therapy for heart disease

A

May be used to help combat cardiac cachexia

85
Q

DCM in Irish Wolfhounds

A

Familial
Not uncommon to diagnose A-fib prior to structural changes

86
Q

Breeds with suspected genetic DCM

A

Great Dane
Doberman
Portuguese Water Dog
Toy Manchester Terrier
Newfoundland
Irish Wolfhounds
Standard Schnauzer

Goldens- muscular dystrophy

87
Q

Dog breeds that seem more at risk for nutritional secondary DCM

A

Goldens
American Cocker Spaniels
Newfoundland
Dalmations
Boxers

88
Q

Dogs with DCM related to nutrition are typically fed diets low in ____ and high in ___ and ___

A

Low in grain
High in potatoes and legumes

89
Q

Causative mechanism of fibrofatty infiltration in the myocardium of Boxers (ARVC)

A

Mutation of the striatin gene

90
Q

Three subcategories of ARVC

A

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

91
Q

Diagnosis of >____ VPCs in a 24 hour period is consistent with ARVC

A

> 300 in 24 hours

92
Q

Atrioventricular myopathy

A

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

93
Q

Median time to CHF or cardiac death in untreated smaller dogs with clinically significant cardiomegaly can be as long as __-___ years

A

2-3 years

94
Q

Hallmark of MMVD

A

Systolic mitral valve regurgitation

95
Q

T/F: Vegetative endocardial lesions and significant inflammatory changes do not play a role in MMVD

A

True they do not

96
Q

Forward stroke volume is initially maintained in MMVD via this mechanism of the Frank Starling

A

Enhanced LV filling (increased preload) and eccentric hypertrophy (chamber dilation)

97
Q

Chronic LAE and weakening of the LA wall can lead to a LA tear which can result in two different things

A

A tear between atria resulting in a L–>R shunting defect
OR
A split and acute pericardial effusion

98
Q

Development of PH associated with MMVD

A

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)

99
Q

Two other diseases which can increase NT-proBNP in dogs

A

Renal disease
Pulmonary hypertension

100
Q

Seven proposed mechanisms of development of blunt cardiac injury

A

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

101
Q

When are heart valves most susceptible to injury from blunt cardiac injury

A

During time of closure

Aortic/pulmonary valves - most susceptible in diastole

Mitral/tricuspid valves - most susceptible during systole

102
Q

Commotio cordis

A

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

103
Q

Most arrhythmias associated with BCI

A

Happen within 24 hours
Ventricular
Happen in 96% of dogs following BCI
and may not be present on initial ECG

104
Q

Which troponin is most sensitive for myocardial injury in dogs?

A

cTnI

105
Q

Treatment of ventricular arrhythmias in cats

A

Sotalol

106
Q

Causes of PCE

A

Idiopathic
Neoplastic (HSA, heart base > others)
Coagulopathy
Infectious (FIP)
CHF
LA split
Trauma
Chyle
Hypoalbuminemia
Chronic uremia

107
Q

Pulses paradoxus

A

Fall in inspiratory arterial pressure of 10 mmHg or more

108
Q

Hepatojugular reflex

A

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

109
Q

Cardiac tamponade characterized by

A

Diastolic (and early systolic) compression or collapse of the right atrium and sometimes the right ventricle

110
Q

Cardiac tamponade commonly raises the CVP to ____ or higher

A

10-12 cmH2O

111
Q

Wandering pacemaker- ECG finding in sinus bradycardia secondary to increased vagal tone

A

P wave appears shorter during expiration when the heart is slower

P wave appears taller during inspiration when the heart rate is faster

112
Q

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

A

3-4 seconds

113
Q

First degree AV block

A

Impulses are conducted, just take longer (PR interval is prolonged)

AV nodal fibrosis, high vagal tone, drugs

114
Q

Second degree AV block Mobitz type I (Wenkebach phenomenon)

A

Longer longer longer drop

AV nodal fibrosis and progressive vagal tone increase

Will get better with atropine

115
Q

Second degree AV block Mobitz II

A

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

116
Q

Third degree AV block

A

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

117
Q

Syncope more common with _____ block

A

Paroxysmal second degree AV block

118
Q

Atrial standstill

A

Complete loss of atrial activity on ECG
English springer spaniels (atrial myopathy)

119
Q

How is lack of p waves on ECG with hyperkalemia different than atrial standstill

A

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

120
Q

Supraventricular tachycardias require __ or __ nodal tissues for initiation and maintenance

A

SA and AV or both

121
Q

SVT rate

A

180-300

122
Q

Young or middle age dogs with no evidence of systemic illness and SVT present

A

Concerning for atrioventricular accessory pathway

123
Q

SVTs with irregular RR intervals

A

A-fib
Atrial flutter with varying block
Multifocal atrial tachyardia

124
Q

AV nodal tachycardias

A

AV nodal reentrant tachycardia
AV reentrant tachycardia (accessory pathway)
Junctional tachycardias

125
Q

SVT with a ____ can look like a ventricular arrhythmia

A

Bundle branch block

126
Q

A fib

A

No p waves
Irregular
Tachycardia
Slight fluctuations in baseline representing struggling atrial activity called fibrillation waves

127
Q

Responses to vagal maneuvers

A

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

128
Q

Ventricular escape rate in dogs and cats

A

Dogs: 30-40 bpm
Cats: 60-130 bpm

129
Q

What is overdrive suppression

A

The faster rhythm suppresses the slower one

130
Q

What are three arrhythmogenic mechanism

A

Enhanced automaticity
Triggered activity
Reentry

131
Q

Most commonly seen VT and mechanism

A

Monomorphic VT - most often reentry

132
Q

Most common electrolyte abnormality associated with VT

A

Hypokalemia

133
Q

How does hypokalemia precipitate VT

A

Increases phase 4 depolarization, increasing automaticity, and prolongs the action potential duration which promotes arrhythmias from triggered activity

Enhanced automaticity and triggered activity

134
Q

Why does magnesium deficiency cause VT

A

Magnesium necessary for proper functioning of the Na-KATPase pump which maintains normal intracellular potassium

135
Q

Dobermans with occult DCM

A

No clinical signs but indications of early LV function on echo and 30% chance of sudden death

136
Q

Doberman pinscher DCM ECG

A

92% VT
Ventricular ectopies have a right bundle branch block morphology on lead II indicating the impulse originates in the left ventricle

137
Q

Boxer ARVC

A

Ventricular ectopics typically have a left bundle branch block morphology indicating their origin in the right ventricle

May have faulty ryanodine receptor

138
Q

Bulldog ARVC pheotype

A

Disease centered in region of the right ventricular outflow tract which is the site of origin of the ventricular tachycardia

139
Q

Tetralogy of Fallot components

A

pulmonic stenosis
large ventricular septal defect
right ventricular hypertrophy
dextropositioning (overriding) of the aorta

140
Q

Bulldog pulmonic stenosis

A

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.

141
Q

R on T

A

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

142
Q

Non infectious myocarditis causes

A

Doxorubicin in dogs

Heat stroke
Vasculitis
Allergic reactions
Radiation

143
Q

NT-proBNP

A

Degrades less quickly than other BNPs

144
Q

Three main categories of systemic hypertension

A

Situational
Idiopathic
Secondary

145
Q

Most common causes of secondary hypertension in dogs and cats

A

1) CKD and AKI
2) Hyperadrenocorticism in dogs, hyperthyroidism in cats
3) Diabetes (high in dogs, low in cats)
4) Pheo/hyperaldosteronism

146
Q

Goal of antihypertensive therapy- hypertensive EMERGENCY

A

For acute crisis - reduction in 10% BP in first hour, then 15% over next several hours.

147
Q

Development of infective endocarditis

A

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

148
Q

The primary attachment of bacteria to the disrupted endothelium

A

Fibrinogen binding

Subsequent fibronectin binding triggers endothelial cell internalization and local pronflammatory and procoagulant responses

149
Q

Inflammation induces endothelial cell expression of _____ which bind bacteria and fibronectin to the extracellular matrix

A

Integrins

150
Q

Some bacteria, like ______, carry fibronectin binding proteins and also can trigger active internalizations by host cells

A

Staphylococcus aureus

151
Q

Organisms that commonly cause IE are those that have the greatest ability to adhere to the damaged valves because of specialized receptors called ____

A

Microbial surface components

Staph and Strep

152
Q

Pattern of CHF with infective endocarditis

A

May be fulminant and cause pulmonary flooding, without massive LAE

153
Q

Cytokines/biomarkers that are elevated in patients with IE

A

IgG
IgM
C3
Rheumatoid factor

153
Q

Two immune mediated diseases which are commonly seen in dogs with IE

A

Polyarthritis (75%)
Glomerulonephritis (36%)

154
Q

Thromboembolism (septic and aseptic) is seen commonly post mortem in dogs with IE, __-___% of them

A

70-80%

155
Q

Dogs are more likely to suffer from thromboembolic disease if they have ____ valve IE

A

Mitral valve

156
Q

Most frequent organ sites of thromboembolism

A

Infarction of the kidneys and spleen, followed by myocardium, brain, and limbs

Brain - middle cerebral eatery

157
Q

Most common presenting complaint with IE

A

Lameness

158
Q

Predisposing factors for IE in dogs

A

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

159
Q

Most common causes of IE in dogs (bacteria)

A

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

160
Q

Suggested MAJOR criteria for diagnosis of IE in dogs

A
  1. Echocardiogram: Vegetative, oscillating lesion; erosive lesions; abscess
  2. New valvular insufficiency
  3. More than mild AI in absence of SAS
  4. Positive blood culture ≥2 bottles with typical organism, ≥3 bottles with common skin contaminant, Persistent positive cultures over ≥12 hours
161
Q

Suggested MINOR criteria for diagnosis of IE in dogs

A
  1. Fever
  2. New or worsening murmur
  3. Predisposing cardiac disease (SAS)
  4. Evidence of thromboembolic disease
  5. Evidence of autoimmune disease
  6. Microbiologic findings not meeting major criteria: Positive Bartonella serology, Blood cultures not meeting major criteria
162
Q

Definite diagnosis of IE

A

Histopathology
Two major criteria
One major and two minor criteria

163
Q

Possible and unlikely diagnosis of IE

A

Possible:
One major and one minor
Three minor

Unlikely:
Other diagnosis made
Resolved in <4 days treatment
No evidence on necropsy

164
Q

Bartonella most commonly implicated in IE and dogs and where does it like to go

A

Bartonella vinsonii spp. berkhoffii

Likes to go to aortic valve

165
Q

PE findings in dogs with IE

A

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%)

166
Q

What additional test may identify bacteria in the blood in addition to blood cultuers

A

16S rDNA PCR

167
Q

Testing for Bartonella

A

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

168
Q

Antibiotic therapy for IE

A

Ampicillin/sulbactam + amikacin if possible
Baytril + ampicillin silbactam

1-2 weeks of IV ABX

Will need weeks to months or longer of tx

169
Q

Which antibiotic is associated with rapid development of resistance and Bartonella

A

Azithromycin

170
Q

Dogs with ____ IE tend to have a far worse prognosis than dogs with ___ IE

A

Aortic way worse than mitral

ACVECC Exam 2024 (26 decks)

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