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Cardiology > Myocardial disease NB: more being added > Flashcards

Myocardial disease NB: more being added Flashcards

1
Q

Signalment of DCM in dogs

A

Large and giant breed dogs esp Doberman, Great Dane, Irish Wolfhounds

+ exception to rule = cocker spaniels

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2
Q

What is DCM

A

A primary myocardial disease characterised by left ventricular systolic dysfunction

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3
Q

What is the aetiology of DCM

A

Assumed familial
Mutations have been found in Dobermans

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4
Q

Pathology of DCM

A

There is ventricular systolic dysfunction, leads to left ventricular dilation –> get progressive left atrial dilation
In same cases get dilation and dysfunction of the right ventricle too

There is eccentric hypertrophy with thinner ventricular walls that normal

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5
Q

What is the pathophysiology of DCM

A

Cellular level metabolic dysfunction and contractility defects
–> Get systolic dysfunction
–> Reduction in stroke volume and CO which activates RAAS and sympt system causing remodelling, increased myocardial O2 demand and cell death leading towards CHF

+ reduced function and ventricular dilation leads to increases in LV end diastolic pressures and therefore rise in left atrial and venous pressures

So get left sided CHF

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6
Q

What are some potential sequelae of DCM

A

Left sided congestive heart failure
Forward failure
RIght sided CHF because of arrhythmias
Arrhythmias

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7
Q

at what point of DCM is the dog at risk of congestive heart failure

A

When the left atrium is enlarged

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8
Q

What arrhythmias can occur in DCM

A

Atrial fibrillation esp in giant breeds
Ventricular arrhythmias and sudden death

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9
Q

Current staging of DCM

A

Pre-clin = have DCM but not in heart failure
Clnical = in heart failure

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10
Q

What does pre-clinical DCM mean

A

Either echo or electrical changes or both
No signs of congestive heart failure

= typically a slowly proressive disease

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11
Q

How prevalent is DCM in dobermans

A

Up to 60% have it

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12
Q

History and clinical exam of pre-clin DCM

A

History = asymptomatic usually, but often family history
May show exercise intolerance, or collapse

Clin exam may be unremarkable; may head soft murmur or arrhythmia

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13
Q

Why might we hear a soft murmur with pre-clinical DCM

A

Due to ventricular dilation causing stretching of the mitral valve and some regurgitation occuring

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14
Q

History of clinical DCM

A

= of congestive heart failure
- Exercise intolerance
- Lethargy, weakness
- Collapse/syncope
Tachypnoea, dyspnoea
Cough
Abdominal distension

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15
Q

What clinical exam signs can we see with clinical DCM

A

Murmur
Tachycardia
Tachyarrhythmias
Pulse deficits/reduced pulse quality
Dyspnoea
PUlmonary crackles
Weakness, collapse

+ in some cases have signs of right sided CHF - abdominal distension, jugular distension

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16
Q

What do we look for on echo with DCM evaluation

A

LV systolic function
Assess LV and LA size
Identify any murmurs
Assess right side size and function too

Hallmarks = LV systolic dysfunction and dilation

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17
Q

What do we use the ECG holter for in DCM analysis

A

Assess ventricular arrhythmias for burden i.e number of VPCs in 24hrs, severity of arrhythmias e.g couplets/triplets etc

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18
Q

What are the ECG criteria for DCM

A

> 300 VPCs Or two wtihin 12 months showing 50-300

Frequent couplets or triplets are assocaited with higher risk of sudden death

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19
Q

What is the gold standard way to diagnose pulmonary oedema

A

Thoracic radiographs

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20
Q

What two cardiac biomarkers can we look at

A

NT-proBNP: tells us about myocardial stretch and strain

Cardiac troponin 1: indicator of myocardial cell damage

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21
Q

Advantages/disadvantages of NT-proBNP as DCM biomarker

A

Predicts pre-clinical DCM with echo changes well but not those with just arryhtmias

Can get false +ves in renal disease, sepsis, hypertension

Takes a while so not good for emergency

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22
Q

What do very high values of cardiac troponin 1 suggest

A

Myocarditis

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23
Q

How do we treat pre-clinical DCM

A

Pimobendan; PDE III inhibitor should be introduced now
Advise monitoring of respiratory rate for increases that indicate moving into heart failure

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24
Q

What is different about resting respiratory rate monitoring in large dogs with DCM vs small ones with mitral valve

A

They go intro heart failure at much lower RRs so very important to have a base level to spot increase (Can’t jsut use over 30 rule)

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25
Q

What imaging signs do we see as DCM progresses to clinical stage

A

Echo shows worse ventricular dysfunction, atria now may be dilated
X rays show pulmonary oedema

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26
Q

What drugs do we use once in clinical DCM

A

[already should be on pimobendan]

Add in diuretics until stable
Then spironolactone, ACE inhibitors

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27
Q

What drugs should we use to treat atrial fibrillation in DCM

A

Want to get HR back until 125bpm
Diltiazem
Digoxin

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28
Q

What do we need to remember about digoxin

A

Very narrow therapeutic window

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29
Q

How to treat sustained ventricular tachycardia in DCM

A

Lidocaine
Amiodarone

Then can move to chronic oral therapy later; amiodarone, sotalol, mexiletine

30
Q

Primary vs secondary cardiomyopathy

A

Primary = no apparent cause; i.e genetic - this is most cases

Secondary = where systemic disease is causing damage to myocardium

31
Q

What systemic diseases can cause secondary cardiomyopathy cat HCM phenocopies

A

Hypertension, hyperthyroidism, acromegaly, lymphoma, nutritional

32
Q

What is the most common cardiomyopathy in cats

A

Hypertrophic cardiomyopathy
Up to 15% of cats have this and most are asymptomatic with normal life expectancy

33
Q

Basic complications of HCM in cats

A

~30% get complications
> Congestive heart failure
> Thromboembolic events
> Sudden cardiac death

34
Q

What is the aetiology of HCM

A

Disease of the sarcomere
Familial in several breeds and some mutations identified e.g in myosin binding protein

e.g Maine coon, ragdoll, DSH

35
Q

How do we diagnose HCM

A

Echocardiography showing left ventricular hypertrophy (wall thickness >6mm in diastole)

36
Q

What does a HCM phenocopy look like and what are the most common ones

A

Thick walls; but not necessarily hypertrophy could be oedema or infiltration

37
Q

What are the most common causes of HCM phenotype

A

First one is HCM

Then systemic hypertension and hyperthyroidism

38
Q

What are the categories of causes of increased left ventricular thickness

A
  • Myocardial hypertrophy: from aortic stenosis, hypertension, HCM, acromegaly, hyperthyroidism

Pseudohypertrophy due to dehydration

Accumulation of cells of fluid e.g TMT, lymphoma

39
Q

At what blood pressures can we get significant changes to the heart

A

> 180mmHg

40
Q

What condition are acromegalic cardiomyopathy cats frequently presented with

A

Diabetes mellitus

41
Q

If thick ventricular walls normalise after IV fluid therapy what does this tell us

A

It was pseudohypertrophy due to dehydration

42
Q

What tumour can cause thickened left ventricle and HCM phenotype

A

Cardiac lymphoma

43
Q

What is transient myocardial thickening

A

Present with thick walls and in congestive heart failure
- There is reverse remodelling over time to revert to normal

Good prognosis so can stop treatment evnetually unlike heart failure

44
Q

What is the key difference between HCM and TMT

A

Typically young cats
Reverts to normal over time

Classifcally there is an antecedent stressful event a couple of weeks before the presentation in heart failure

45
Q

What are two proposed ideas for transient myocardial thickening in cats

A

Acute myocarditis; causing myocardial oedema and cellular infiltration which makes walls thick causing acute dysfunction
- Then inflammation resolves

Broken heart syndrome = where severely stressful event causes catecholamine surge

46
Q

Murmur frequency in HCM cats

A

~50 have systolic murmur
Up to 70% have normal sounds

47
Q

What is systolic anterior motion of mitral valve

A

Where the mitral valve is pushed towards the outflow tract in systole, against the interventricular septum which creates an obstruction to blood flow

So blood accelerates to go round leaflet giving a murmur

+ this holds valve open so get regurgitation into atria

Also more likely in HCM bcecause ventricle very thick, longer leaflets and hypercontractive ventricle

48
Q

What is the most common cause of systolic anterior motion of mitral valve

A

HCM

49
Q

What other than HCM can cause SAM

A

Hypovolaemia because the empt ventricle creates conditions that can drag the vlve

MV dysplasia

Subaortic stenosis

50
Q

What is the classic pulmonary oedema lung pattern in dogs with congestive heart failure and how is it different in cats

A

Dogs show alveolar pattern in caudo-dorsal region
In cats no pattern is followed; so cannot exclude pulmonary oedema based on X ray distribution

51
Q

What is restrictive cardiomyopathy

A

= the second most common cardiomyopathy in cats
= due to replacement fibrosis in the ventircular walls so they are normal thickeness but fibrosed

This means high pressure in ventricles, atrial dilation, restrictive LV filling pattern

52
Q

What are the two phenotypes of restrictive cardiomyopathy

A

Myocardial form = where myocardium very fibrotic; normal wall thickness; very large atria

Endomyocardial form = where muscle/scar tissue bridge in the middle of the left ventricle

53
Q

What is the aetiology of restrictive cardiomyopathy

A

Unclear could be congenital, could be just very late stage HCM where walls become thinner due to fibrosis

54
Q

What is presentation of restrictive cardiomyopathy like and what must we be aware of

A

Middle age/older cats typically
Around half have systolic murmurs
Gallop rhythms or arrhythmias are more specific

NB: many cats have no abnormalities on auscultation

55
Q

Characteristics of dilated cardiomyopathy in cats

A

Severe LV dilation and systolic dysfunction (BUT there are other phenocopies of this e.g late stage HCM, L to R shunt, tachycardia induced]

56
Q

What has dilated cardiomyopathy classically been assocaited with in cats

A

Taurine deficiency

57
Q

What are the characteristics of arrhythmogenic RV cardiomyopathy

A

Fibrous and fatty infiltration into the right ventricle
Causes severe dilation of RV, thin RV wall
Associated with malignant ventricular arrhythmias due to scar tissue blocking normal conduction

58
Q

What does B1 vs B2 stage of feline cardiomyopathy mean

A

Both are subclinical
But B1 = low risk of complications
B2 = high risk

These complications = heart failure, thromboembolic disease

59
Q

How does a cat with thromboembolic disease from left atrium embolising into aorta often present

A

Suddenly paraparetic on hind limbs
Cold, painful legs with no pulse, pale toe MMs

60
Q

What does the appearance of smoke in the atrium on ultrasound mean

A

Blood is flowing slowly in the large atrium, allowing RBCs to aggregate and form mini thrombi

This means there is a high risk for thrombus formation and thromboembolic disease

61
Q

What should we do at stage B2 feline cardiomyopathy

A

Start clopidogrel blood thinner to reduce thromboembolism risk

Ask owners to start taking resting respiratory rates to help detect going into heart failure

62
Q

What do we do in stage C of feline cardiomyopathy

A

Congestive heart failurue treatment
Oxygen
Furosemide

63
Q

What should we do if a thromboembolic event has occured (e.g HCM in cats)

A

Antithrombotics e.g unfractionated heparin, clopidogrel etc
Pain management because this is very painful

But do NOT remove thrombus or attempt to lyse it; instead stop growth and give body time to make collateral circulation

64
Q

Risk factors for poorer prognosis in HCM

A

LA dilation
LA thormbus
Smoke on U/S

65
Q

Survival time of asymtomatic HCM cats

A

Normal i.e >10 years

66
Q

What things can cause a DCM phenotype in dogs

A

Hypothyroidism, hypoadrenocorticim
SIRS
Chronic volume overload e.g anaemia, high fluids
Chronic myocarditis
Taurine deficiency
Grain free/legume rich diets

Long term arrhythmias

67
Q

What is arrhythmogenic right ventricular cardiomyopathy and what breeds are commonly affected

A

Myocardiac disease mostly affecting right ventricle with progressive loss of myocytes and replacement with fatty/fibrous tissue

Can affect electrical systmon most and present with arrythmias

Seen in boxers and bulldogs

68
Q

Treatment of arrhythmogenic right ventircular cardiomyopathy

A

Sotalol = first line oral treatment to manage arrhythmias
If there is systolic function add in pimobendan

69
Q

What are the three forms of ARVC presentation

A

Asymptomatic; but see VPCs on holter
Symptomatic; synvope with arryhtmias but normal systolic function
DCM phenotype and arrhythmias

70
Q
A

Cardiology (6 decks)

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