Diseases of the Myocardium Flashcards
What are the main myocardial diseases?
DCM
HCM
RCM
ARVC
Myocarditis
secondary myocardial diseases
Neoplasm
** every cardiac disease will eventually lead to cardiac muscle damage!
HCM
Most common disease in CATS!! not in dogs
Enlargement of the muscle
Males have it more severe at an earlier age
Maine coone and ragdoll
Clinical signs of HCM
Sudden onset
When diagnosing in an older cat remember it could ahve been present for a ehile without any clinical symptoms
Exercise intolerance
Dyspnoea (usually bad before owner notices!)
Asphyxia
Cyanosis
(collpase and coughing)
Physical findings of HCM
only at the life threatening stage therefore cannot conduct a full phys exam!!
Signs of acute L sided HF– must determine the origin of the dyspnoea!!!! can either be pulm edema or hydrothorax (unknown! modified transudate, pseudochylus or chylus)
Tachycard
Murmur
Gallop rhythm
Arrhyth
Pulse deficit
Diagnosis of HCM
Radio: will not give an exact diagnosis but it will show the secondary pulm edema/hydrothorax
Blood and urine: only for diffs
BP: for differentials
*ECHO!!
- Thickened LV wall and septum, narrow chamber especially in systole!
- Dilated RA
- Systolic function: contractility and FS%
What are the differentials you must exclude when diagnosing HCM
The causes of Concentric LV hypertrophy
- High BP
- Hyperthyreoisis
- Aortic stenosis
Treatment of HCM
None until there are signs!
Goals: decr the congestive signs and HF
Acute: O2, thoracocentesis, for pulm edema can give furosemide or nitroglycerine (this ONLY for acute pulm edema!)
Chronic: FUROSEMIDE! and repeated thoracocentesis. (maybe ACE, Ca and Beta blockers)
Treatment of HCM: thrombus
Nearly always a consequence of HCM
Begins in auricle of LA
90% lodge at terminal part of the abd Ao by the ext iliac and femoral arerties– sudden HL paralysis!!
if lodges in mesenteric or kidney arteries- infarcts in different organs
Prox part of Ao– sudden death
After it lodges= STE systemic arterial thromboembolism
Can remain static in the LA: either dissolves or occludes intracardiac flow
Signs of thromboembolism in the terminal part of the Ao (also known as riding thrombus)
Caud limb paralysis
Vocalization because of pain
Differential cyanosis (*just remeber we encountered this with R - L shunt also)
Femoral pulse not palpable
Diagnosis, treatment and prognosis of thromboembolism in the terminal part of the Ao
US and angiography to diagnose
Usually euth!
Surgery- still high risk of thrombosis, reperfusion injury, pain management
Preventing thrombolysis: aspirin, streptokinase, low Mr heparins e.g deltaperin, clopidogrel
DCM
More common in dogs
Formerly caused by taurine deficiency
Large breeds, males, older
Causes of DCM
Viral, nutritional, toxic, genetic— but the etiology is usually undetermined therefore classified as idiopathic!
Carnithine/taurine def: American cocker spaniel, golden retriever, dalmation, boxer
Genetics: portugese water dog (juveile form)
Great-danes: recessive x-linked
Dobermans: autosomal dominant
Irish-woldhound-arrhythmias
New-foundland
History and Clinical signs of dogs with DCM
Tiredness, coughing, dyspnoe
Weak heart beats, cardiac dullness, systolic murmur, distension of jugular vein, SC edema, ascites, dyspnea, cyanosis, arrhyth
Diagnosis of DCM
Radio: cant diagnose but good for the secondary pulm edema and hydrothorax
Blood and urine: useful for BNP
ECG: NB for arrhyth,holter for monitoring of dobermans
- atrial fibrillation
- supraventric tachycard
- ventric extrasystoles and tachycard
- bundle-branch block
ECHO- can diagnose!!
- Enlargement of chambers,
- thin ventric wall and septum
- decr systolic function i.e contractility and FS%
- mitral ± tricuspid regurg
What is the FS%
End diastolic diameter minus end systolic diameter over the end diastolic diameter multiplied by 100
In healthy: >30%
DCM: < 15%
Serious stage: <10%
