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ECVIM Certifier > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Functions of AT2 receptor?

A

Vasodilation, natriuresis, antigrowth factor, anti fibrosis, tissue regeneration

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2
Q

Functions of AT1 receptor?

A

Vasoconstriction, increased PVR, increased Na resorption, increased aldosterone and increased Na resorption in collecting ducts, increased vascular growth factors, atherogenesis, increased ADH, thirst, CO, decrease GFR, cardiac hypertrophy, fibrosis, ROS, inflamm cytokines

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3
Q

Sex bias in dogs for hypertension?

A

Males

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4
Q

Cats age and hypertension?

A

Increases with increasing age and with increasing HR

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5
Q

CKD and hypertension in cats?

A

20 - 60 %, 65 - 100 % of hypertensive cats with TOD have evidence renal dysfunction.

No corr with severity

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6
Q

Pathophys hypertension renal dz?

A 
RAAS 
Symp tone
Na retention
Excess free water
Structural arterial changes and endothelial dysfunction,. lack of local NO, increased ET
Ox stress/ROS
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7
Q

SDMA and BP?

A

? assoc with NO?

ADMA no corr with hypertension or TOD

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8
Q

What types of CKD more likely have hypertension dogs?

A

Glomerular

60 % of glomerular dz secondary to leishmania

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9
Q

T/F: cats with polycystic kidney disease have high BP?

A

False, not common

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10
Q

Evidence for antihypertensives in cats?

A

60 % cats with SHT reached 15 % decrease or less than 150 BP using amlodipine, cf 18 % placebo

Decreased clin manifestations too but no imp survival

May decrease aldosterone secretion

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11
Q

T/F: amlodipine is really excreted?

A

No - hepatic metab, no need to drop dose in renal disease

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12
Q

What glomerular arteriole does amlodipine preferentially dilate?

A

Afferent

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13
Q

Amlodipine and antifungals?

A

Azoles might decrease metabolism

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14
Q

When to use emergent BP management?

A

TOD and > 180

> 200

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15
Q

MAP calculation?

A

Diastolic + (systolic - diastolic)/3

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16
Q

Neural control of vascular tone?

A

Vasomotor centre, medulla oblongata, constrict tissue bed dilate muscle with sympathetic stim

Baroreceptors in carotid body and aortic arch lack of stretch
Atria and pulm artery lack of distension (stretch receptors)

Also hypoxaemia/hypercarbia via chemoreceptors carotid body and aortic arch

Also effects macula densa to decrease GFR and conserve sodium

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17
Q

Mechanism of hypotension in sepsis/SIRS?

A

NO production
Depletion vasopressin
Disrupted smooth muscle calcium
Downregulation catecholamine receptors

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18
Q

How much hypovolaemia to cause hypotension?

A

20 - 25 %

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19
Q

Cardiac effects of SNS activation?

A

Increased SA node firing
Beta adrenergic receptor activation - increase slow inward calcium current so increase SA node firing
Shift activation curve inward pacemaker current (If), more pos voltage, Gs adenyl cyclase

Adrenergic activity increases contractility - beta - SERCA2, ryanodine, L type calcium channels, phospholamban

Augmented calcium induced calcium release and reuptake into SR

PKA force and contraction myofilaments

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20
Q

Effect of cardiac disease on CO at increased HR?

A

CO drops off at lower HR than healthy

NB downreg/uncoupling (beta arrestin, beta receptor kinase) beta1 receptors in heart failure, diminished contractility
Depletion cardiac norepinephrine stores, reply on systemic

Decreased response to adrenergic stim

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21
Q

Why can’t peripheral nerves produce epinephrine?

A

No phenylethanolamine N methyltransferase

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22
Q

Catecholamines in heart failure?

A

NE and epi higher than controls for both DCM and valve dz, NE maybe higher in DCM, corr with severity

Cats - both increased in cardiac dz also cong and noncong

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23
Q

Heart disease SNS or RAAS 1st?

A

SNS

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24
Q

Stim for renin?

A

SNS beta 1 activation juxtaglomerular cells
Decreased renal perfusion
Decreased sodium absorption PCT

ATII inhibits renin release

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25
Q

ATII remodelling?

A

MAPK

NB activation chymase myocardium

ATIII less potent

ROS (ATII and aldosterone) myocardial hypertrophy

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26
Q

Where do the natriuretic peptides come from? Effects?

A

BNP ANP atria
CNP endothelium

More BNP in chronic cardiac as ventricles start to make

Counteract RAAS. A type natriuretic peptide receptor. Induce natriuresis/diuresis. Inhibit tubular sodium transit inner medullary collecting duct.

Vasorelaxation

Inhibit renin and aldosterone release

NPRB does vasodilation from CNP (local)

NPRC clears the natriuretic peptides from circulation (ANP > BNP)
N terminal fragments of pro forms renal excretion so longer

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27
Q

Use of BNP in diagnostics?

A

Cats - marked increase BNP in myocardial dz

More useful than ET1

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28
Q

What is conivaptan?

A

V1A/V2 blocker

Normalise sodium and help congestion

Tolavaptan = V2 specific

AVP increased in heart failure

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29
Q

What factors cause vasoconstriction when CO falls?

A

Norepi, vasopressin, ET, ATII - calcium mediated vasoconstriction (muscle hypertrophy when chronic)

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30
Q

What causes endothelin release?

A

Hypoxaemia, stretch, ATII AVP NE bradykinin

Growth factors cytokines tGFbeta

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31
Q

ET1 and NO?

A

ET 1 increases NO which then decreases ET1

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32
Q

When is ET1 increased?

A

Cardiac dz pulm hypertension renal disease not systemic hypertension

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33
Q

Cardiac remodelling?

A

Physiological reversible pathologic not.

Hypertrophy from increased wall stress, wall stress normalised by hypertrophy (compensation), exhaustion and death of cardiomyocytes, fibrosis, ventricular dilation, decreased CO

Fibroblast proliferation AT11 aldosterone

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34
Q

Law of Laplace?

A

Wall stress = pressure x radius/2x wall thickness

Pressure overload - compensate with increased wall thickness, still increased energy requiremenet

Volume overload - modest wall thickness inc with chamber enlargement - appropriate workload redistribution, less increase in total work

Concentric hypertrophy - parallel sarcomere replication

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35
Q

Most common cause of death aortic stenosis?

A

Sudden death vent arrhyth (hypoxia?)

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36
Q

Terminal concentric hypertrophy?

A

Initial decrease collagen breakdown (metalloproteinase inhibitor decrease MMP 1 and 9(

Then collagen breakdown increases and hypertrophied ventricle dilates and fails

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37
Q

When is pleural effusion in heart failure most likely?

A

Biventricular due to overload of lymphatic drainage

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38
Q

What nitrate vasodilators effect pre and afterload?

A

Nitroglycerin preload - venodilator, nb tachyphylaxis

Nitroprusside balanced vasodilator

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39
Q

ACEi in CHF?

A

No prospective evidence preclinical MVD, retrospective DCM though benazepril improved outcome

Use in chronic diuretic

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40
Q

Dobutamine mechanism of action?

A

Beta1 antagonist - inotrope and lusitrope

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41
Q

Beta blockers in feline myocardial disease?

A

Detrimental heart failure, neutral preclinical

Dog - detrimental heart failure

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42
Q

What is atropine used to predict?

A

Medical management for sick sinus syndrome, doesn’t predict well with AV block

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43
Q

What factors determine the impact of arrhythmia on animal?

A 
Rate
Length sustained for
Atrial ventricular temporal assoc
Sequence of ventricular activation
Myocardial/valvular function
Cycle length irregularity
Drug therapy
Extra cardiac influences
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44
Q

What causes wide QRS?

A

Macro reentry
BBB
Ventricular premature complex

Eg asynchronous ventricular depolarisation
T wave should also be abnormal

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45
Q

What does vagal predominance do to ECG?

A

Wandering pacemaker - increased P w/ increased HR on insp

Sinus arrhythmia

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46
Q

What is ventriculophasic sinus arrhythmia?

A

P-P interval longer during AV block cf surrounding - P-P interval flanking QRS (2nd or 3rd degree)

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47
Q

Differentiate wandering pacemaker or sinus arrhyth from atrial arrythmia?

A

HR < 150
P’s taller not narrower
Degree of prematurity

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48
Q

Criteria for APC?

A 
Premature timing
Normal QRS (v occasionally wide/absent if timing dose to repol of ventricle)
Non compensatory pause 
Diff amplitude P
Diff P-R interval

Often structural. Also HT4 digitalis atrial tumour.

Atrial tachycardia = three or more APC > sinus rate (160/220)

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49
Q

Criteria for atrial flutter?

A

Flutter waves (rhythmic monomorphic)
Lack fo return to baseline
Normal QRS
Variable R-R

Macroreentrant

Treat if many passing AV node (tachycardia mediated cardiomyopathy > 240 > 3w)

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50
Q

Atrial fibrillation?

A

15 % canine arrhythmias, present in 50 % DCM

Electrical disorganisation at atrial level

Chaotic fibrillation waves
Irregular R-R
No P waves
Normal QRS

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51
Q

Afib prognostic importance?

A

Cause impacts rate - lone then subclin then CHF

Lone better px

Afib worsen prognosis large dogs with MMVD and CHF

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52
Q

How to treat AFib?

A

Digoxin and diltiazem, change dose of latter, aim 130 - 145, ECG assessment

Better HR control together cf alone

Beta blockers inferior

Treatment improves survival time in CHF large breed MMVD dogs if add digoxin cf diltiazem alone

Conversion - defib, amiodarone, lidocaine

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53
Q

Atrial dissociation?

A

Larger P wave passes AV other one stays in atrium - no significance

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54
Q

VPC criteria?

A

Most common pathological rhythm disturbance

Wide QRS, different with different T and no P
Narrow R-R interval

Diagnostic of VT:
Fusion beat (normal and premature collide)
Capture beat (normal PQRST after VPCs)

Usually compensatory pause or interpolation

> 3 in a row vtach

Must differentiate from:
Escape complexes
Potassium disturbance 
Cardiomegaly
Bundle branch block
Motion

More commonly cardiac in cats than dogs

NB inherited sudden cardiac death GSD - myocardial depolarisation defect

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55
Q

Cut offs for ventricular arrhythmias?

A

< 70 idioventricular, < 160 accelerated idioventricular, > 160 vtach

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56
Q

What should accompany ventricular fibrillation?

A

Unconscious, no pulses

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57
Q

What is Torsades de Pointes?

A

Ventricular arrythmia, arises from Q-T interval prolongation

Rotation of peaks due to changing geometry of reentrant circuit

Diagnosis:
Slow rhythm with prolonged QT before
R on T extrasystole (R occurs during vulnerable T wave)
Rapid ventricular rhythm with QRS complexes more regular than VF but with changing amplitude and polarity

Causes:
Hypokalaemia and hypocalcaemia
Congenital long QT syndrome of dalmatians
Class 1A antiarrthythmics eg quinidine

Tx - magnesium

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58
Q

Describe AV blocks

A

1st degree: long PR interval - high vagal tone/digitalis/alpha2

2nd degree: complete transient AV conduction interruption.
Mobitz I - progressive lengthening, Wenckeback phenomenon. High AV node good prognosis. Rare clin signs.
II - sudden, more guarded/poor px (?). Essentially if high grade same as 3rd degree and need pacing.

3rd degree: complete sustained with escape rhythm.
Can be incidental 110 - 140 bpm cats, can be subclin, but most likely of the 3 to cause clin signs

Sometimes caused by atrial dilation

2/3 can be functional alpha 2 hyperkalaemia digitalis but more common structural age inflamm or degen

Low number 3rd degree resolve or convert to second degree spontaneously

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59
Q

Treatment of AV block?

A

Pacing high degree 2nd II/3rd degree, increase survival cf no pacing

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60
Q

Feline AV block?

A

More than half have cardiomyopathy, in general have long survival times with no pacing as incidental

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61
Q

What are bundle branch blocks?

A

Altered bundle of his conduction - not arrhythmias in and of themselves

Wide QRS due to ventricular desynchronisation

Duration QRS > 0.07 dog or > 0.04 cat

Lead II - polarity pos left neg right

Hypertrophy, dilation, inflammation

Right - no issue
Left - indicative of left ventricular enlargement

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62
Q

What block do cats with heart disease get?

A

Left anterior fascicle block- degeneration/fibrosis/osseous metaplasia of left bundles more common than right

Tall R wave lead 1
Deep S wave II and III

Left axis deviation

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63
Q

What causes atrial standstill?

A

Hyperkalaemia
Atrial myopathy eg marked stretch
ECG artifact

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64
Q

Cardiac effects of hypokalaemia?

A

Cardiomyocytes more negative and AP longer (prolonged repolarisation) therefore near threshold longer - proarrhythmic

Latter effect clinically dominates < 3.5

Prolonged QT, atrial dissoc

Class I antiarrhythmics eg lidocaine act on sodium channels which require K to function, so hypokal can cause refractoriness to antiarrhythmics

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65
Q

Cardiac effects of hyperkalaemia?

A

Increased membrane potassium permeability during depolarisation when mild - rhythm stabilising, this predominates over depolarising effects (makes cell more pos overall)

Mild - short Q-T, narrow tall T wave (only 15 % for latter)

Decrease activity normal pacemaker tissue/decrease slope phase 4 depolarisation - sinus bradycardia, however HR unreliable

Wide QRS and decreased R wave amplitude - interfere cell-cell transmission velocity in ventricles

P-R prolongation, absence of P waves

Atria more sensitive than ventricles, myocardium most in atria, - sinoventricular rhythm (don’t see P but SA is firing)

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66
Q

Cardiac effects of hypocalcaemia?

A

Alter myocyte AP threshold, not resting potential. Low decrease threshold and facilitate depol. This is most in skeletal muscle minimal in cardiac.

Prolongs initial ventricular depolarisation - prolong QT

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67
Q

Why is calcium cardio protective?

A

Potassium raise resting membrane potential, calcium raise depolarisation threshold - so more normal gradient

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68
Q

What should be monitored during calcium infusion?

A

Shortened QT, ventricular complexes, decrease HR

Calcium raises depol threshold and shortens ventricular repol

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69
Q

What is an orthodromic AV reentrant tachycardia?

A

Normograde transmission AV node retrograde through accessory - macroreentrant loop - WolffParkinsonWhite

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70
Q

Diagnosis of sick sinus syndrome?

A

Prolonged sinus pauses, 1st/2nd degree AV block, bursts of supra ventricular tachycardia/ventricular asystoles - get ECG during episode of syncope/stumbling etc - episodes occur during bradycardia

Atropine response predict response to medical management - eg theophylline controls 50 %

Sometimes only sinus bradycardia

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71
Q

Criteria to institute pacing?

A

High degree second or any third degree AV block

SSS/SND with clin signs HR < 50, sinus pauses >3s when awake

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72
Q

What congenital cardiac defect do Chartreux cats get?

A

ASD and TVD

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73
Q

Siamese?

A

Supravalvular mitral stenosis, endocardial fibroelastosis

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74
Q

Most common congenital cardiac dz cat/dog?

A

Dog - PDA, AS, PS

Cat - VSD, PDA, TVD, MVD

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75
Q

What congenital conditions can severity be predicted from murmur duration and intensity?

A

SAS, PS

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76
Q

Lesions in Eisenmenger’s syndrome?

A

R to L shunt

Pulmonary arterial intimal thickening, medial hypertrophy, plexiform lesions

+/- pulm vasoconstriction

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77
Q

Embryology of PDA?

A

Embryonic left sixth aortic arch

Should close 7 - 10 d

Only elastic no muscular fibres in ductal media

Tapering most common, non tapering more severe and uncommon (the latter assoc with pulm hypertension and r-l or bidirectional shunting

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78
Q

Name 3 breeds common PDA?

A

GSD, Lab, cocker

also poodle, bichon

female!

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79
Q

Ddx for continuous murmur?

A

PDA, aortopulm shunt, coronary AV fistula

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80
Q

ECG with right ventricular hypertrophy?

A

Right axis deviation, deep S wave

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81
Q

Difference cat PDA?

A

More common pulm hypertension development

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82
Q

What PDAs not amenable to amplatz?

A

Non tapering - type III

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83
Q

Genetic VSD?

A

Keeshond

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84
Q

Breeds ASD?

A

Boxer, Samoyed, Doberman

Chartreux, Persian

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85
Q

Breeds VSD?

A

English bulldog, WHWT, ESS

Maine coone

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86
Q

ECG VSD?

A

Notched/wide Q

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87
Q

TVD breeds?

A

Labrador - autosomal dominant mutation with incomplete penetrance

Gret, Gt Dane, GSD

male!

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88
Q

Mitral valve stenosis?

A

Bull terrier

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89
Q

Mitral valve dysplasia?

A

GSD, Get, Gt Dane

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90
Q

ECG TVD?

A

Splintered QRS

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91
Q

Pulmonic stenosis breeds?

A

Beagle, cocker, Lab

Supravalvular - giant schnauzer

Subvalvular - boxer and English bulldog, anomalous corony artery development - circles RVOT below pulmonic valve

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92
Q

Cause of pulmonic stenosis?

A

Subvalvular/valvular obstruction or valve dysplasia

Thickening, leaflet fusion, annular hypoplasia, tethered valves

Overproduction normal valve collagen

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93
Q

Pulmonic stenosis severity?

A

Mild < 50
Severe > 80

Mild/mod probably normal life
Severe > 125 frequent major consequences

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94
Q

Criteria for pulmonic stenosis intervention?

A

Severe > 100
Symptomatic
Tricuspid regurgitation

Balloon - decrease pressure 50 % + in 80 %
50 % reduction mortality

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95
Q

Breeds for SAS?

A

Boxer, rottie,
Bull terrier valvular

Newfie - autosomal dominant, PICALM gene

Dogue de Bordeaux auto recessive

GRet

Normal boxer aortic annulus is smaller cf other breeds

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96
Q

What other abnormality assoc with SAS?

A

Mitral valve lesions

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97
Q

SAS severity?

A

80 - 100 = mod

can overest if CO high

Mild around 2.3 - 2.4 m/s

< 50 normal life
> 125 severe consequence

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98
Q

SAS management?

A 
Prophylactic ABs (though evidence?)
Balloon - decrease severity 50 % but improvement attenuated over time, no sig diff survival cf atenolol

Beta blockers to decrease myocardial ischaemia, decrease HR, decrease myocardial o2 consumption, increase diastolic time

However again no sig survival benefit atenolol

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99
Q

Breed for ToF?

A

Keeshond, English bulldog

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100
Q

Abnormalities ToF?

A

Transposed aorta, right ventricular hypertrophy, VSD, RV outflow obstruction

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101
Q

MMVD signalment?

A

CKCS, dachshund, mini poodle, yorkie
Male > female
Males develop younger than female

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102
Q

What happens if breed two MMVD early onset dogs?

A

Earlier onset dz in pups, and vice versa

Gene loci 13 and 14 assoc with age of onset in CKCS

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103
Q

MMVD histopath?

A

Weakened/disturbed connective tissue, prominent spongiosa, disorganised collagen fibres iin fibrosa layer, increased mucopolysacharide/glycosaminoglycan, endothelial cells damaged esp edge

104
Q

Pathophys MMVD?

A

Endothelial damage > ET1 > valvular interstitial cells become myofibroblast/smooth muscle cells (serotonin driven - increased in CKCS), MMPs

105
Q

Which leaflet more likely to prolapse MMVD?

A

Anterior - more mobile, jet lesions laterally directed

106
Q

MMVD heart chamber enlargement?

A

Initially slow, fast in 6-12 months before CHF

107
Q

MMVD XR changes?

A

Elevation caudal trachea and left mainstream bronchus, bulge/straightening caudal border heart, bulge 2-3oclock

XR pulm oedema - dorsocaudal, perihilar, often RHS worse - cranial can be first in acute

108
Q

XR right heart enlargement?

A

Increased sternal contact, elevation trachea, straight cranial border, vena cava enlargement, bulge 9 - 12 - reverse D shape

109
Q

How to measure LA?

A

Right parasternal short axis view

110
Q

MMVD - why would regurgitant jet velocity be low?

A

Hypotension, myocardial failure, increased LA pressure, impending CHF

111
Q

Risk factors MMVD progression?

A

Large breed, older, male, severity of valve lesion, severity MR/LA/LV dilation, HR, NTproBNP, troponin, arrythmia, syncope

112
Q

Ddx for MMVD?

A

Endocarditis, DCM, congenital cardiac dz

Endocarditis lesions more isolated and echogenic

113
Q

Evidence for stage B MMVD tx?

A

ACEi mono therapy: no difference survival placebo control - SVEP/VETPROOF

Beta blocker: experimental? prospective placebo control trial terminated due to lack of efficacy

Amlodipine: ? imp echo?

Pimobendan: decrease cardiac size. EPIC delays onset CHF (doubles time) in B2 (LVIDD > 1.7, LA:Ao > 1.6, VHS > 10.5)

114
Q

Goals in management of stage C MMVD?

A

Reduce venous pressure
Maintain CO
reduce regurg and cardiac workload
Protect heart from negative neurohormonal effects

115
Q

Benefit of torasemide?

A

Longer duration of action, potency less affected by diuretic resistance, aldosterone antagonist properties

116
Q

Evidence for stage C MMVD?

A

Pimobendan: VETSCOPE/QUEST - adjunct to diuretic, less severe CHF and longer survival cf ACEi + diuretic. Decrease HR, decrease free water retention, decrease heart size, decrease regurg.

ACEi: less severe clin signs less exercise intolerance live longer. Counteract reflex RAAS stim when diuretics admin.

Spironolactone: decrease cardiac death/euthanasia/worsening CHF when add to other tx

Digoxin: weak pos inotrope, decrease baroreceptor reflex tachycardia/decrease central symp activity no evidence

117
Q

Prognostic factors after onset CHF?

A

Pos: pimo, ACEi,

Neg: higher furosemide dose, worsening exercise tolerance, cardiomegaly, worse MR, LVIDD, E wave velocity, worsening systolic function, decreasing creatinine (cachexia), complication development

118
Q

What drugs might reduce MR/LA size?

A

Pimobendan, afterload reducers (amlodipine hydralazine ACEi), diuretic

119
Q

Pulmonary hypertension in MMVD?

A

Pressure gradient > 55 neg prog factor

120
Q

Endocarditis signalment?

A

Male middle age medium to large purebreed

121
Q

Pathophys endocarditis?

A

Either direct bacterial contact or haematogenous (capillaries in valves) - bacteria usually req predisposing factors to colonise eg immune supp, endothelial damage/platelet-fibrin complex deposition - adhere to valve

Extracellular matrix protein, thromboplastin and tissue factor trigger coagulation, coagulum forms, inflamm starts

Inflamm and bacterial enzymes cause valve tissue degradation

122
Q

Endocarditis bacteria?

A

Staph (aureus, pseudintermedius, coagulation pos and neg)/Strepp (canis, bovis, beta haemolytic). Ability to adhere to valves.

Also - E coli, P aeruginosa, Corynebacterium

Staph aureus and Bartonella (henselae, clarridgeiae, washoensis) internalise in endothelium, evade immune system and antibacterials

Some no detectable infection elsewhere

123
Q

Consequences of endocarditis - what factors?

A

Bacteria - virulence/production of endocrine or exotoxins (gram neg paracute/acute, chronic subacute/chronic)
Site of infection and impact on valve function - necrosis/destruction of valve stroma/chordae tendinae peracute/acute with CHF
Sequelae eg immune complex deposition, vegetative thrombi/metastatic infection - thromboembolic 30 - 40 %, lungs then kidneys most common, then distal aorta

124
Q

Most common valves endocarditis?

A

Left heart, mitral > aorta, aortic more common Barttonella

Might involve wall (mural endocarditis) but rarely RHS

125
Q

What is an intracardiac vegetation made of?

A

Platelets, WBC, fibrin, bacteria, RBC - often covered by intact endothelium

126
Q

When to raise suspicion for endocarditis?

A 
Immunosuppression
Non-oral surgery within 3m
Trauma to or infections of oral or genital mucosa 
Indwelling catheters
Infected wounds
Abscess
Pyoderma
127
Q

Most common clin sign endocarditis?

A

Lameness 34 %, new heart murmur (diastolic with bounding pulses = aorta - aortic insufficiency)

Heart murmur 75 %

Ventricular arrythmia 60 % aortic, arrthymia 50 - 75 % overall

Fever 50 - 90 % (absence more common in aortic or Bartonella)

128
Q

Endocarditis echo?

A

Hyperechoic, independent movement, irregular outline

Erosive more difficult to identify - severe aortic regurg raise suspicion

However congenital SAS/systemic hypertension could also cause this/myxomatous valve/quadricuspid aortic valve

129
Q

Arrhythmias in endocarditis?

A

Ventricular most common

ST segment deviation (?myocardial hypoxia/embolism/ischaemia)

130
Q

CHF in endocarditis?

A

50 % - perihilar/caudodorsal pulm oedema - no diff with valve affected

LA enlargement not common (acute)

131
Q

Blood culture endocarditis?

A

Negative in up to 60 - 70 % of cases - ABs, encapsulated infection, non-infectious endocarditis, Bartonella/slow growing organisms

In positive cultures, 90 % pos in 72 h

132
Q

Bartonella in endocarditis?

A

28 % of cases in Cali, 50 % of those with neg culture
Also cause in cats
Concurrent pos serology for tick borne dz common (tick/flea vector)

133
Q

Criteria for canine endocarditis diagnosis?

A

Definitive: histopath of valve, 2 major, 1 major and 2 minor
Possible - 1 major 1 minor, 3 minor
Rejected - other disease, resolution valve abnormalities in 4d, no PM evidence

Major - pos echo (vegetative/erosive/abscess), new valvular insufficiency (> mild aortic, no SAS/annuloaortic ectasia), pos culture (>1 pos or > 2 if common skin contaminant)
Minor - fever, > 15 kg, thromboembolic or immune mediated disease, pos culture (other), pos bartonella serology > 1:1024

134
Q

What should you not use alongside aminoglycosides?

A

Diuretic - potentiate nephrotoxicity

135
Q

ABs for endocarditis?

A

Beta lactam and aminoglycoside (or enro but resistance poss)
Depends on organ involvement
Also seek source

IV AB 1-2w, 6w overall, apt blood culture after 1-2w AB and 1-2w after. stop

Repeat echo during and after too

Monitor Bartonella with serology 1m after start AB - increased = ineffective, decreased = effective

136
Q

Neg px endocarditis?

A

Late dx/late start tx
Aortic
Valvular vegetation
Bartonella
Gram neg
Heart/renal complications not responding to tx
Septic embolisation or metastatic infection
Throbocytopenia, increased ALP or hypoalb (70 % mort with latter)
Concurrent steroids
Bacteriostatic AB/premature AB termination

137
Q

Pos px endocarditis?

A 
Mitral valve (MST > 400 d)
G pos from skin/abscess/cellulitis/wound
138
Q

When to use prophylactic AB to prevent endocarditis?

A

SAS PDA VSD - also make sure treat any infection aggressively

Amoxi-clav/clindamycin

NOT MMVD even if doing dental

139
Q

Juvenile onset DCM?

A

Portuguese water dog (autosomal recessive chromosome 8, sudden death or CHF), toy Manchester terrier (sudden death) - < 1y

140
Q

Forms of DCM?

A

Occult/overt (former murmur/echo/arrhythmia, latter coughing weakness etc)

141
Q

DCM echo findings?

A

Decreased FS, ejection fraction, end. systolic diameter/volume

Many also diastolic dysfunction

No valve thickening

Systolic dysfunction or ventricular dilation can occur first

NB EPSS, sphericity index

142
Q

Biomarkers for DCM?

A

ANP in dobermann’s sig increased in occult and overt - other breeds not found sens/spec

Troponin - increased doberman overt/occult, not sens/spec

NTproBNP - increased in occult, quite sens, up to 1.5y pre-overt

143
Q

Structural changes DCM?

A

Eccentric hypertrophy
L > R
Attenuated. waxy myofibrils, vacuolated myocytes, collagen fibres replace myocytes, fibrosis, necrosis, fatty infiltration

144
Q

Specifics of cocker spaniel DCM?

A

ACS and ECS
Taurine ACS - supp taurine/l-carnitine and increase FS/decrease LVIDD in 4m (not completely normal) - blood better than plasma. cont supp for life. often can discont cardio meds 3-4m when FS > 20 %
ECS - familial? nutritional not identified. Marked LV enlargement. Variable dz course.

145
Q

Dalmatian DCM?

A

Males
Only left sided
Arrhythmias uncommon
Survival 1.5 - 30 m, no sudden death, refractory CHF
Low protein diet? No evidence carnitind/taurine def.

NB Dals occ get AV valve dz

146
Q

Doberman DCM?

A

Left/bivent (left > right), Afib/sudden death
Overt - Afb/VPC/CHF

If syncope do holter - Brady and tachyarrhythmias

Annual echo/holter = best predictors - increased LV end diastolic or systolic diameter; > 50 vpc/24h, couplets or triplets

147
Q

Genetic mutations in DCM?

A

Doberman - autosomal dominant. PDK4 splice site mutation. Incomplete penetrance. Genetic test avail. not sole cause and this is only US NOT European.

Great Dane - Xlinked

Irish wolfhound - autosomal recessive, sex specific male dogs overrep

Standard schnauzer - RNA binding motif protein 20 gene (RBM20), auto recessive, genetic test available

148
Q

Great Dane DCM?

A

Weight loss/coughing. Ascites. Afib. Occ VPC.

Afib before echo changes.

149
Q

Irish wolfhound DCM?

A

Males.

Afib before structural. Precede CHF 24m.

Sometimes VPC/LAFB

Occ sudden death. More CHF (bivent, sometimes chylothorax)

Low taurine?

150
Q

Newfie DCM?

A

No gender predip.

CHF, cough, bivent.

V few have heart murmur.

Afib most common.

151
Q

Taurine in DCM?

A

Less likely in dog than cat as cats can’t synthesise taurine dogs can.

ACS taurine/carnitine

Lamb meal/rice diet (rice bran/whole rice?)

GRet - familial taurine deficiency

Taurine blood < 150 plasma < 40

Supp might fix - reecho

152
Q

Evidence for DCM meds?

A

ACEi: delay onset of CHF in doberman with ventricular dilation (retrospective)

Beta blockers: 3m carvedilol no diff on anything

Pimobendan: PROTECT study placebo control, support use in doberman in occult phase - survival benefit and delay CHF/sudden death. Also increase survival symptomatic.

153
Q

Risk factor for cardiac death DCM?

A

Arrhythmias - rapid VT, complex ventricular, combination of vent arrhythmia, systolic dysfunction and chamber dilation - risk sudden death

But sudden death occurs without these factors

These are factors poss to treat arrhythmias - sotalol (beta blocker/potassium channel blocker) - dose cautiously if systolic dysfunction

Mexilitene

Amiodarone (cf neutropenia hepatic enzymes)

154
Q

Negative prognostic indicators DCM?

A

Age of onset, pleural effusion, pulm oedema, ascites, AFib, end systolic vol index, ejection fraction, restrictive transmittal flow pattern

155
Q

ARVC histopath?

A

Fibrous fatty infiltration RV wall, myocyte vacuolation and loss

156
Q

Features of ARVC?

A

Boxer
Vent arrhythmia/collapse/syncope/sudden death, some CHF (10 %, either left or bivent), some asymptomatic
Small number systolic dysfunction and ventricular dilation
Autosomal dominant inheritance with variable penetrance

157
Q

Genetic cause ARVC?

A

Striatin gene mutation - genetic test available

Homozygous severe - type III ARVC, structural heart disease variety and higher numbers of arrhythmias

HOWEVER can have without the mutation

158
Q

Type III ARVC?

A

Homozygous

Systolic murmur/gallop, ventricular dilation/systolic dysfunction

159
Q

What physiological murmurs do Boxers get?

A

Left basilar systolic (can also be aortic stenosis…)

NOT indication of ARVC

160
Q

Biomarkers for ARVC?

A

Troponin: increased, corr with VPC number and grade and arrythmia complexity BUT sensitivity lacking

BNP not useful

161
Q

ECG ARVC?

A

VPC single/pairs/paroxysmal runs
Left bundle branch block morphology to VPC due to right ventricle affected

> 100 VPC/24h or periods of couplets, triplets, runs VTach on holter considered suggestive, may have APC in vent dilation/systolic dysfunction

162
Q

Echo ARVC?

A

Usually normal - might find right vent enlargement

163
Q

When to treat ARVC?

A

> 1000 VPC/24h, vtach runs, RonT

Early if homozygous for striatin mutation?

Treatment:
Decreases vpc and syncopal episodes

Sotalol or mexiletene, sometimes need combo

Therapeutic effect = 85 % reduction VPC number (due to daily variation)

Fish oils decrease VPC? Not > variation…

Lcarnitine might imp systolic function/prognosis

Also standard cardiac

164
Q

ARVC px?

A

If no vent dilation or systolic dysfunction, comparable to non-ARVC - live to around 11y

165
Q

What is myocarditis?

A

Necrosis, degeneration, inflammation

Physical/chemical/infectious

May cause chamber dilation, arrhythmia, systolic dysfunction

Protozoal/viral most common in dog

Troponin often increased

166
Q

Possible infectious causes of myocarditis?

A

Trypanosoma cruzi (serology, circulating trypomastigotes - tx with cysteine protease inhibitor? for heart effects, arrhythmia and RCHF)

Leishmania (parasite in myocardium and assoc inflammation, AV block)

Toxo/Neo

Parvo (peracute, 3-8w puppies or < 1y DCM)

West Nile (RTPCR, IHA, serology, virus isolation)

Blastomyces (uncommon presentation and poor px)

Borrelia burgdorferi

167
Q

HCM in dogs?

A

HOCM in pointers, heritable

168
Q

T/F: doberman DCM is caused by hypoT4?

A

False, no link

169
Q

Difference between primary and secondary cardiomyopathies in cats?

A

Primary - confined to myocardium, genetic/non genetic/mixed

Secondary - myocardial involvement of systemic/multiorgan disorder

170
Q

Prevalence of the different cardiomyopathies?

A 
HCM 58 %
RCM 21 %
DCM 10 %
UCM 10 %
ARVC uncommon
171
Q

Left ventricular moderator bands?

A

Might be incidental

If dense network may have cardiac consequences - poss role in HOCM? More commonly in the outflow tract in HOCM than healthy or non obst HCM

172
Q

Types of HCM?

A

Either diffuse concentric left vent hypertrophy (2/3) - which can be asymmetric IVS/LVFS or one segment (basal IVS or apex)

OHCM - obstruction of LVOT often by protruding thickened basal IVS

Papillary hypertrophy can cause systolic mid ventricular cavity obstruction and endocardial contact plaques

Can get infarction LVFW

Right ventricle can also be thickened.

NB dilated stage with thin walls

173
Q

Breeds and HCM types?

A

OHCM Persian/Chartreux (44 % cf 18 % other breeds)

50 % Maine coone diffuse symmetric LVH

174
Q

HCM histopath?

A

Myocardial fibre disarray, fibrosis, arteriosclerosis

Inflammatory infiltrates in preclin

175
Q

Signalment HCM?

A

Male
DSH, DLH, BSH, Himalayan, sphinx
5-7y

Maine coone/sphynx/ragdoll younger?

176
Q

Genetic HCM?

A

Maine coone - myosin binding protein C sarcomeric gene (MyBPC3) auto dom but higher risk of HCM for homozygotes, incomplete penetrance hetero at middle age

Ragdoll - MyBP3 (diff mutation). homozygotes worse px.

Sphynx - auto dom incomplete penetrance

177
Q

Cats pleural effusion?

A

Can be caused by LHS dz as visceral pleural veins drain to LA

178
Q

What cardiac auscultation abnormalities are more common in symptomatic HCM cats?

A

Gallop and arrhythmia

179
Q

Clinical predictors of cardiac death in HCM?

A

Arrhythmia, gallop, CHF, ATE, syncope.

LA enlargement, severe LVH, decreased systolic function, decreased LA function, RV enlargement, regional wall hypokinesia, spontaneous contrast, restrictive diastolic filling pattern

Ragdolls (homozygote) and Maine coone more poor px

180
Q

Types of RCM?

A

Fibrosis in walls, fibrosis on walls, fibrosis between walls - myocardial/endomyocardial

Same histopath cf HCM (sarcomere mutation?)

181
Q

RCM signalment?

A

10y - older cf HCM
Conflicting studies on sex
DSH, Burmese, siamese, Persian, birman, maine coone

182
Q

Clin signs RCM?

A

Almost all clinical at presentation, cf HCM

183
Q

Px RCM?

A

Poor 200 d cf 1000 HCM

184
Q

DCM histopath?

A

Myocytolysis, fibrosis, coronary arteriosclerosis, inflamm infiltrates

185
Q

DCM signalment?

A

9y

Conflicting sex predilection

186
Q

Clin signs DCM?

A

Usually symptomatic, often hypotensive

187
Q

Px DCM?

A

Days, sl better (month) if add pimobendan tx to standard (taurine, furosemide, acei)

Negative - hypothermia, FS < 20 %

188
Q

What is striatin?

A

Located at intercalated disc cardiomyocytes, co localised with other desmosomal proteins involved in human ARVC

189
Q

ARVC in cats?

A

< 5 %

No genetic

Histopath - diffuse/segmental RV wall thinning, aneurysm, RA enlargement

Myocardial atrophy and fatty or fibrous tissue replacement

Usually CHF at presentation but can be asymptomatic

Poor px if overt - days/weeks survival

190
Q

ARVC signalment cats?

A

7Y
No breed/sex predilection
Familial?

191
Q

Taurine and feline myocardial disease?

A

Cats have low cysteine sulfinic acid decarboxylase so can’t synthesise much taurine from cysteine

Exclusively use taurine for bile acid conjugation (cf glycine)

25 % taurine deficient cats get myocardial failure (also retinal central degeneration, CNS, immune, repro)

DCM - check taurine and retina (1/3 and may be sign of past taurine def) and diet hx (whole blood taurine better but affected by fasting)

Diet - heat processing in canning, potassium depletion, acidification, rice brain/whole rice

Difficult to diagnose so supplement if DCM (rapid improvement if taurine deficient, some persistent signs but better and aymptomatic)

192
Q

UCM echo changes?

A

Segmental LVH, regional hypokinessia, marked LAE

Could be form of HCM or RCM

193
Q

Signalment UCM?

A

Female

8y

194
Q

Px UCM?

A

Better (900d, cf HCM 500, RCM 100, DCM 11)

195
Q

What should be ruled out when considering primary cardiomyopathy in cats?

A

HT4, lymphoma in wall, myocarditis, muscular dystrophy, hypersomatotropism, aortic stenosis, hypertension, taunt, doxorubicin, sustained tachyarrhythmia

196
Q

VHS in cats?

A

> 8 specific not sensitive, esp left dz

Acute dyspnoea - > 9 highly specific

197
Q

Significance of valentine heart?

A

Not spec for HCM or even cardiac disease, doesn’t predict biatrial enlargement

198
Q

What interferes with echo in cats?

A

Dehydration - increase wall thickness and decrease LV diameter
Volume - increase LV diameter, fractional shortening and LA:Ao, with appearance of a murmur

Less skilled echo overest wall thickness

Breed - sphinx 5 or 5.5 in < or > 5kg, > 6 others

199
Q

LA size in cats?

A

Prognostic and marker of chronicity

1.3 end diastole, 1.5 end systole

200
Q

Biomarkers feline myocardial disease?

A

Troponin: cTNI and TNT predictor of death in HCM but low sens/spec, TNI more sens. No corr echo.
TNI higher in cardiac dyspnoea cf non cardiac but overlap

NTproBNP: 90 % accurate to distinguish cardiac resp signs
70 % sens/100 % sens to identify occult dz cf healthy if > 99. Corr LV thickness and LA:Ao.

201
Q

Echo marker of decreased diastolic function?

A

Inversed E:A = relaxation pattern (<1 HCM), restrictive pattern (E:A increase > 2 with increased E decreased A)

202
Q

How to classify evidence levels?

A

Level 1 - at least 1 PRCT
Level 2 - at least one well designed clinical trial without randomisation, cohort/case controlled studies lab models, dramatic uncontrolled
Level 3 - opinion , pathophys justification

203
Q

Medication evidence in feline cardiac disease?

A

Beta blockers: atenolol - decrease HR/ increase diastole, decrease LVOTO, negative inotrope, decrease myocardial O2 demand which is antiarrhythmic

Ivabradine - inhibit If current in SA node so negative chronotrope - level 1 evidence for imp diastolic function in HEALTHY cats

Calcium channel blockers - negative chrono/inotrope, imp LV relaxation, coronary vasodilation, antiarrhythmic. Level 3 evidence to avoid dihydropyridine (amlodipine) because of excess vasodilation. Diltiazem (less potent negative inotrope/vasodilator cf verapamil) more commonly used.

ACEi\aldosterone blocker - stop myocardial hypertrophy, reverse lesions, vasodilatory and imp diastolic in LVH animal models

204
Q

Stage B feline cardiac dz management evidence?

A

80 % asymptomatic HCM die non cardiac dz

Atenolol: no survival benefit (level 1 evidence), no decrease in biomarker Maine coone (level 2), may be deleterious as decreases LA function and flow velocity in left auricle of healthy cats (risk factors for ATE) 0 ? deleterious? Use in LVOTO or vent arrhythmia?

Benazepril: level 1 for increase mitral E:A ratio cf diltiazem, but not sig

Ramipril/spironolactone: no imp diastolic function Maine coone

Spironolactone: facial dermatitis 1/3 @ 2.5m reversible when stop, dose 2mg/kg BID (level 1)

Clopidogrel: no evidence

205
Q

Stage C feline cardiac dz management evidence?

A

Furosemide, sedation, thoracocentesis, cage rest (level 3)

Diltiazem: imp clin signs and imaging with 94 % survival at 6m (level 2)

Benazepril: added to diltiazem, imp clin signs and LV (level 2)

Enalapril: with furosemide, survival longer cf diltiazem or placebo or atenolol (920, 227, 235, 72d) - level 1 with no stat sig

206
Q

Stage D feline cardiac dz management evidence?

A 
Spironolactone (level 3)
Hydrochlorthiazide added (level 3)
Pimobendan - LV systolic dysfunction (level 2), not OHCM due to worsening/hypotension (level 3)
207
Q

Other feline cardiac dz management evidence?

A

Taurine for DCM (level 1)
Pimobendan DCM (level 2 as increased MST)
ARVC - similar DCM, level 3 evidence

208
Q

Breed for PPDH?

A

Weimeraner

DLH, Main coone

209
Q

ECG in PPDH?

A

Low voltage complexes

Shift electrical axis

210
Q

What is cardiac tamponade?

A

Impairment of ventricular filling due to fluid accumulation in pericardial space, reducing SV and CO

Diastolic collapse of right heart

211
Q

What volume of pericardial fluid is required for cardiac tamponade?

A

Acute - 50 - 150 ml for 20 kg dog

Chronic - stretch allows for more fluid - can accommodate several hundred more litres

212
Q

Clinical presentation of cardiac tamponade?

A

Acute - arterial hypotension due to decreased diastolic filling of left heart due to decreased right heart output

Chronic - RCHF

Increase in diastolic pressure req to cause leaking of systemic capillaries is lower than that required for pulmonary - so pulm oedema not common

213
Q

Difference in neurohormonal activation pericardial effusion cf heart failure?

A

No ANP increase, limits natriuresis and contributes to volume overload - this is why chronic causes effusion

214
Q

Changes in stroke volume during inspiration?

A

Neg intrathoracic pressure causes pooling in RHS - compliant - and decreased LV preload, RV output higher LV lower (hence increased HR on inspiration)

215
Q

Pericardial effusion on inspiration?

A

Ventricular interdependence, increased right heart at expensive of left, so decreased LV output (pulsus paradoxus)

216
Q

How many dogs with cardiac HSA have concurrent splenic?

A

30 %

217
Q

Most common site of mesothelioma metastasis?

A

Intrathoracic LNs

218
Q

Metastasis heart base thyroid gland carcinoma?

A

Pericardium

219
Q

Idiopathic pericarditis aetiology?

A

Viral/immune mediated.
Mononuclear inflamm/fibrosis target pericardial blood vessels ad lymphatics.
Damaged blood vessels > bleeding.
Chronic. 50 % don’t recur. 50 % do days - years
Sequel = restrictive

220
Q

Infectious agents causing pericarditis?

A

Actinomyces, strep. bacteroides, pasteurella, coccidoises

221
Q

XR for pericardial eff?

A

Not sens or spec

222
Q

ECG pericardial effusion?

A

Electrical alternans
Decreased QRS voltage - also fat pleural eff etc
Ventricular arrhythmias

223
Q

pH of pericardial fluid for aetiology?

A

Not reliable

224
Q

Treatment of choice for recurrent idiopathic pericarditis?

A

Thoracotomy - 100 % survival MST not reached 3y

Thoracocoscopic window - disease free interval 11.6m, MST 13m

225
Q

Mesothelioma pericardial eff tx?

A

No sig diff surg vs window, approx 10m MST both

Chemo might imp survival

226
Q

Heart base mass and pericardial eff?

A

Partial pericardectomy MST 700d vs 42d w/out

Chemo didn’t help survival

This is for aortic body tumours

227
Q

Cardiac HSA?

A

Pericardectomy doesn’t prolong survival.
Resection and doxo prolongs survival. Doxo alone also.

Neg px mass size and decreased platelet but NOT mets

228
Q

What pericardial disease doesn’t have pulsus paradoxus?

A

Constrictive pericarditis

229
Q

D. immitis lifecycle in the dog?

A

Female worms produce L1, microfilariae, which circulate in the blood.
Female mosquito feeds, L1 molts to L3 over 8 - 17 d - temp and Wolbachia pipientis dependent
L3 infective, transmitted when mosquito feeds again
L3 > L4 in subq/muscle/adipose 1 - 12 d
L4 > S5 2 - 3 months post-infection

Juvenile adult migrates to right pulmonary vessels, matures (females bigger than males) and mates. Life cycle completes in 180 - 210 days. Live mostly in caudal pulmonary vascular tree.

Microfilaremia 6-7m post infection.

Microfilaria persist 30m, adults 5 - 7 y

230
Q

What determines severity of consequences of heart worm infection?

A

Burden of worms, duration of infection, interaction with immune system.

Worm toxic substance/physical trauma/immune stim

Dead worms severe inflamm reaction

exercise increases pulm hypertension?

231
Q

Occult heartworm disease?

A

Microfilaria immune mediated destruction in pulmonary circulation, amicrofilaraemia and eosinophilic pneumonitis

232
Q

Cytological difference between D immitus and its imitator?

A

D. immitus - many, stationary, larger, straight body and tail with tapered head

Dipetalonema reconditum - few, progressive motion, curved body blunt head curved tail, smaller

233
Q

Test for D. immitus in dogs?

A

Mod. Knott more sens than direct smear.

10 - 20 % amicrofilaraemic, macrocyclic lactones do this

Antigen test - only female adult - low worm burden false neg

234
Q

Macrocyclic lactones and heartworm?

A

Milbemycins and avermectins

Terminate L3/L4 larval development in 1st 2m infection

Minimal adverse reaction microfilaraemic dogs. Some adulticidal. Many microfilariacidal

Resistance reported

Moxidectin imidacloprid heartworm/microfilaria, render females sterile, kill adults

Ivermectin 3m reach back

doxycycline synergistic

235
Q

Adulticide therapy for heartworm?

A

Melarsomine, 90 % worm kill 70 % dogs cleared

Split dose safer - 50 % worm kill 1st then 100 % 1 month later

236
Q

Pro/con single dose/split dose protocol D. immitus?

A

Single - cheaper, don’t have to exercise restrict so long, less melarsomine exposure (better if hepatorenal dz)

Split - safer and more efficacious, better resolution proteinuria

Doxycycline also reduces severity of lung lesions on worm kill

237
Q

When to recheck antigen after adulticide tx in heartworm?

A

8m

238
Q

What dogs are most likely to get heartworm naval syndrome?

A

Males

239
Q

Differences in feline heartworm?

A

More resistant, often worms don’t mature, longer prepatent period, get pulmonary dz even if worms don’t mature.

50 % exposed get heartworm assoc resp dz

Pulmonary arterial response more marked (pulmonary interstitial macrophages) even though worm burden lower

Embolisation more significant as cats less pulm collaterals

Wollbachia might mediate bronchoconstriction

240
Q

Cytokines in feline heartworm dz?

A

PGE2 HARD, TXB2/LTB4 mature HW

241
Q

Differences between HARD and mature heartworm infection in cats?

A

HARD - clin signs 3m, due to immature heart worms in pulm arteries, resp signs, antigen neg AB pos filaria neg, bronchointerstitial with normal echo

Mature - > 7m, pulm and cardiac, neuro, emesis, more severe resp, Ag pos/neg, AB pos, microfilaria sometimes, variable XR with vessel changes, echo sometimes abnormal

242
Q

Difference between arterial thrombosis and. thromboembolism?

A

AT: made at site, shear stress and narrowed vessel

ATE: vessel normal, from diff site, due to stagnant flow

ATE common AT not

Venous > arterial uncommon (unless ASD) - exception is pulm venous emboli eg d/t neoplasia

243
Q

Coag changes in canine thrombosis

A

Low - AT, protein C
High - I, II, V, VII - X, XII
Platelet hypersensitivity

244
Q

Pathophys ATE?

A

In aorta, acute and release vasoactive substances from activates platelets causes vasoconstriction which inhibits development of collateral supply and get ischaemic neuromyopathy

NB serotonin

245
Q

Second most common vascular obstruction in feline cardiac dz?

A

Right subclavian

246
Q

Mechanism of heparin?

A

AT mediated II, X-XII, and thrombin catalysed V and VIII, inhibit thrombin platelet aggregation and vWF

247
Q

Reperfusion injury?

A

Metabolic acidosis and hyperkalaemia

40 - 70 % cats undergoing thrombolytic tx

Thrombolytics most dangerous aortic, less so cerebral/splanchnic/renal?

248
Q

Thrombolytic tx?

A

Streptokinase - activate plasminogen

  • one study all cats died
  • another 50 % return femoral pulses 24h, motor function 30 %, single limb better (80 % motor function), bleeding 1/4 and severe, 50 % reperf
  • dogs good response small number cases

Urokinase - more fibrin specific eg just fibrin bound plasminogen

  • LMW molecules bind greater affinity to lysine-plasminogen form which accumulate in thrombi
  • cats 50 % motor function 27 % pulse no bleeding, 1/4 reperf
  • dogs all dead

tPA: case reports, works in some

249
Q

How to improve collateral flow thromboembolism?

A

Aspirin (TXA2 inh, vasodilation)

Clopidogrel inh serotonin release

250
Q

Negative px indicator cat ATE?

A

Hypothermia two limbs bradycardia absent motor function

Around 30 % survival.
MST 50 - 350d.

251
Q

Feline thrombosis prevention?

A

Suggested if LA:Ao > 2 or spontaneous contrast

If have antithrombotic added on initial event, 17 - 75 % happen again, 25 - 50 % in a year

FAT CAT - clopidogrel decreases recurrence and increases time to recurrence versus aspirin - 443 vs 192 and reduced likelihood of recurrence/cardiac death = 346/128 d

252
Q

Aspirin mechanism of action?

A

Inhibits secondary platelet aggregation, reduce TXA2 and prostacyclin production (latter endothelium compensates for in vivo)

Lower dose no sig diff thromboembolic recurrence but less GI

Survival increased in IMHA dogs

253
Q

Clopidogrel mechanism of action?

A

ADP2Y12 blocker

Primary and secondary platelet aggregation

Inhibit ADP induced GPIIb/IIIa conformational change so no vWF/fibrinogen binding

Impairs platelet release reaction - decrease vasoconstriction/proaggregate serotonin/ADP

Hepatic biotransformation p450

No bleeding complications reported.

254
Q

LMW heparin?

A

Less II inhibition so aPTT normal

Similar recurrence/MST in cats cf warfarin with ATE - warfarin study 42 - 53 % and MST 471 d (vs 210d) - lots of bleeding

Infrequent bleeding LMW hep

255
Q

Lymphatic ducts?

A

Thoracic duct drains everything apart from that drained by the right lymphatic duct which drains the right heart/neck and right forelimb

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