Cardiology Flashcards
degenerative valve disease predisposition
older dogs, mostly pure breeds, can also be large (GSD), small> large, males> female
- king Charles, dachshund, mini poodle, chihuahuas
cause degenerative valve disease
dogs mitral valve is most effected, cats not considered a common cause of valvular insufficiency
pathogenesis of degenerative valve disease
- connective tissue disease
- loss of valvular endothelial cells
- activation of valvular interstitial cells
- deposition of glycosaminoglycans (GAGs)
- dissolution of ECM, oxidative damage
- end result thickening and elongation of the valve with loss of valvular function
symptoms of degenerative disease
- respiratory distress: pulmonary edema, pleural effusion, pulmonary hypertension, expiratory airways collapse
- cough: bronchial compression, pulmonary edema
- syncope: arrhythmia, exertional/vasovagal
- sudden cardiac death (rare)
diagnosis of degenerative valve disease
- auscultation: detection of a typical heart murmur
- (pan/holo) systolic murmur
- point of maximal intensity : left apical area
- murmur intensity increases with severity
staging of degenerative valve disease
Asymptomatic:
- A (high risk of developing), B1 (mild), B2 (moderate)
- B1 – murmur present, no cardiac remodelling
- B2 – murmur present cardiac remodelling
Symptomatic:
- C (severe with CHF)
- D (worst with refractory CHF)
treatment of degenerative valve disease
- Stage A + B1 nothing
- B2 – pimobendane (ace inhibitor)
- C – diet Na + restric, furosemide, spironolactone, pimobendane, ACE inhibitor, sedation, oxygen
- D - same as C but higher dose of pimobendane and furosemide torsemide
- surgical treatment – mitral valve repair or hybrid procedures – transcatheter edge to edge repair
predisposition of canine DCM
sex, Dobermans, German boxers, huge breeds, cocker spaniels, dalmatians
cause of DCM canine
mostly idiopathic, but can be genetic basis too
canine pathogenesis of DCM
characterised by poor myocardial contractility with or without arrhythmia
canine signs of DCM
reduced exercise tolerance, weakness, syncope, lethargy, tachypnoea, cough, loss of muscle mass, anorexia, ascites
canine diagnosis of DCM
ECG and Holter, gallop sound, murmur
- radiography = generalised cardiomegaly
canine treatment of DCM
antiarrhythmic drug (lidocaine), with CHF: furosemide, long term therapy (pimobendane)
canine prognosis of DCM
generally guarded
predisposition of PDA
poodle, cocker spaniel, German spitz, German + Scottish shepherd, Shetland sheepdog, 3x more common in female than male
cause o PDA
genetic defect in structure of the ductus arteriosus
pathogenesis of PDA
with the birth the ductus remains open which leads to the shunting of the blood from the aorta to pulmonary artery during systole and diastole
- essence PDA leads to volume overload of the heart
- 1. decrease in stroke volume/CO
- 2. RAAS activation
- 3. Volume overload of the left ventricle
signs of PDA
asymptomatic when first diagnosed (usually)
- reduced exercise ability, tachypnoea, cough occurs sometimes
Continuous (systolic-diastolic heart murmur)
- best auscultated left cranially, over the axillary region
- systolic component of the murmur is louder than diastolic component
- precordial thrill
Hyperdynamic/kinetic (bounding) pulse – Corrigan pulse
- pulse pressure = SAP – DAP
- greater the difference between SAP and DAP pulse is stronger
diagnosis of PDA
- Radiograph = cardiac elongation, LA and auricular enlargement and pulmonary over circulation
- ECG = wide P waves, tall R waves and deep Q waves
treatment of PDA
Prevention of the CHF
Surgical - transthoracic approach – thoracotomy, ductal ligation
prognosis of PDA
patients with CHF, prognosis is worse
cause of reverse PDA + pathogenesis
present already at birth, or developing during the 1st several weeks of life
in which the flow Is directed from the pulmonary artery to the aorta. Occurs when the resistance in the pulmonary artery is higher than in the aorta
sub aortic stenosis predisposition
German boxer, golden retriever, German shepherd, Rottweiler, Newfoundland
types of sub aortic stenosis predisposition
subvalvualr (most common), valvular, supravalvular, subaortic stenosis (during first 12 months of life)
pathogenesis of sub aortic stenosis predisposition
leads to pressure overload because of the stenosis making it difficult for blood to flow, concentric hypertrophy of LV
signs of sub aortic stenosis predisposition
- weak pulses in severe cases
- (holo)systolic ejection heart murmur best heard over left heart base
- hypodynamic/kinetic (weak) pulse in cases of severe stenosis, precordial thrill
diagnosis of sub aortic stenosis
ECG: elevated R waves, elevation of ST segment, premature ventricular contractions
- Radiographs: show left atrial + ventricular enlargement, wide cranial cardiac waist (dilated ascending aorta)
treatment of sub aortic stenosis
- Medical - beta blockers (reduce myocardial oxygen demand)
- interventional – cutting and high pressure valvuloplasty
- surgical – open heart surgery
prognosis of sub aortic stenosis
- mild stenosis – normal life span
- moderate – most dogs normal, some have occurrence of ventricular arrhythmia and SC
- severe – most dogs die within 3 years
predisposition of pulmonic stenosis
small dogs (whereas subaortic is large) and brachycephalic
types of pulmonic stenosis
subvalvualr (rare), valvular (most common), supravalvular (rare)
pathogenesis of pulmonic stenosis
pulmonic stenosis leads to overload, same as subaortic stenosis but concentric hypertrophy
signs of pulmonic stenosis
normal pulse
diagnosis of pulmonic stenosis
ECG – right axis shift, deep S-wave in lead 1, narrow QRS complex (hypertrophy of RV), wide QRS complex (bundle branch block)
- radiographs: pulmonary trunk bulge, RAE and RVE
treatment of pulmonic stenosis
Balloon valvuloplasty
- success defined as reduction of pressure gradient for 50% from the starting pressure gradient
- possible complications:
o acute: arrhythmias and sudden cardiac death: perforation or rupture of PA
o chronic: restenosis (rare)
prognosis of pulmonic stenosis
depends on severity of stenosis. Mild may have normal life, but severe stenosis often die within 3 years of diagnosis
predisposition of ventricular septal defect
Very common in cats, in dogs seen most in WHWT, Lakeland terriers, English bulldogs
types of ventricular septal defect
Restrictive
- small defects
- no equalisation of the pressures
- blood flows in the direction of the pressure gradient, from left to right
Non-restrictive
- large defects
- equal pressures L R
- blood flow dependent on the pressure gradient:
o from left to right, from right to left, no flow-balance
pathogenesis of ventricular septal defect
- most often located high in the membranous part of septum, just below aortic valve and under the septal tricuspid leaflet
- typically, volume overload of the left heart
- Underfilling of the systemic vasculature
- RAAS activation
- Volume overload of the left heart
symptoms of ventricular septal defect
- exercise intolerance and sides of L heart failure
- holosystolic heart murmur can be heard
- point of maximal intensity is dependent on the location of the defect:
o over the right hemithorax – defect under the tricuspid valve
o Parasternally – an RV inlet/outlet tract defect
o over the left hemithorax, in the area of the heart – defect in the vicinity of pulmonary artery
diagnosis of ventricular septal defect
- Radiographs - L – R shunt cause left heart enlargement and pulmonary over circulation
- ECG – normal or suggest LA or LV enlargement
treatment of ventricular septal defect
- cardiopulmonary bypass or transcatheter coil
VSD with normal heart dimensions - yearly re-checks and monitoring of progression
VSD with enlarged hearts and/or heart failure - medical therapy of heart failure
- surgical treatment
prognosis of ventricular septal defect
with moderate sized defect, often have normal life span
predisposition of HCM
middle – older cats, more common in male, Maine coon, American shorthair, BSH, Persian, Bengal, most common in domestic
cause of HCM
genetic mutation
pathogenesis of HCM
- Increased thickness of left ventricular myocardium, in absence of congenital aortic stenosis or systemic arterial hypertension
- dynamic left ventricular outflow tract obstruction often accompanies hypertrophic cardiomyopathy as well as mitral valve apparatus and papillary muscle abnormalities
- end stage hypertrophic cardiomyopathy
signs of ventricular septal defect
heart murmur, cardiac gallop, respiratory distress, pulmonary edema, pleural effusion, arrhythmias
diagnosis of ventricular septal defect HCM?
Thoracic x-ray
- not suitable for diagnosis of HCM
- impossible to determine the type of cardiomyopathy
- suitable for diagnosis of pulmonary edema or pleural effusion
ECG
- neither sensitive, neither specific for diagnosis of HCM
- gold standard for diagnosis of arrhythmias
Biomarkers
- natriuretic peptides – arterial and B-type
- NT-pro BNP
o feline 1-step SNAP test, fast
o if positive in asymptomatic cat – follow with ECHO
o positive in respiratory distress – emergency and ECHO
treatment of ventricular septal defect
enhance myocardial relaxation and ventricular filling, control pulmonary edema and suppress arrhythmias
- beta blockers (atenolol), diltiazem (ACEI), spironolactone
prognosis of HCM
variable, asymptomatic cats is 5 years, median survival time with CHF 1-2 years
predisposition of restrictive CM
older cats (2nd most common feline CM)
cause of RCM
multifactorial
pathogenesis of RCM
normal/decreased volume of the left ventricle, dilation of both atria, normal left ventricular myocardium thickness and severe diastolic
signs of RCM
heart murmur, cardiac gallop, arrhythmias, body cavity effusion, pulmonary edema, arterial thromboembolism, poor appetite, vomiting and weight loss
diagnosis of RCM
- physical exam can show systolic murmur or mitral or tricuspid regurgitation
- NT-proBNP may be helpful
- radiographs: show LA or biatrial enlargement and LV or generalised heart enlargement
treatment of RCM
pimobendane, atenolol or diltiazem
prognosis of RCM
guarded to poor, some cats survive more than a year after diagnosis
feline DCM predisposition
older cats, uncommon
cause feline DCM
taurine deficienct
pathogenesis of feline DCM
poor myocardial contractility
signs of feline DCM
anorexia, lethargy, increased respiratory effort, hypothermia, jugular venous distension, bradycardia, increased lung sounds and pulmonary crackles
diagnosis of feline DCM
- Radiographs: generalised cardiomegaly with rounding of the cardiac apex
- pleural effusion is common and may obscure the heart shadow
- variable ECG: ventricular/supraventricular tachyarrhythmias, AV conduction disturbance and an LV enlargement pattern
- plasma or whole blood taurine concentration measure to see if deficiency
treatment of feline DCM
B2 – anticoagulation therapy
C – diuretics and anticoagulation therapy
D- diuretics, anticoagulation therapy and pimobendane
supplemental taurine
prognosis of feline DCM
cats without deficiency of taurine prognosis is guarded to poor, with median survival time of 49 days even with pimobendane treatment
complication of feline DCM
acute CHF, cardiogenic arterial thromboembolism, sudden cardiac death
cariogenic arterial thromboembolism predisposition
not common in dogs
cause of cariogenic arterial thromboembolism
HCM most common underlying disease in cats with arterial thromboembolism
pathogenesis of cariogenic arterial thromboembolism
thrombi usually form in left heart, usually in an enlarged LA or auricle, neoplastic and systemic inflammatory disease is usually associated with it
signs of cariogenic arterial thromboembolism
acute paresis/paralysis, extremely painful extremities, cyanosis of paw pads, cold extremities, pulselessness, poikilothermic, signs of poor systemic perfusion,
diagnosis of cariogenic arterial thromboembolism
heart murmur (gallop)
- combination of acute onset paraparesis and absent femoral pulse
- blood glucose values lower, lactate high in blood from limbs affected by ATE
- abdominal US – presence of thrombus in distal aorta
- Xray, Echo
- azotaemia, metabolic acidosis, DIC, electrolyte abnormalities (low Na, Ca, K and high P), stress hyperglycaemia
- elevation in CK, ALT and AST
- myoglobinuria
treatment of cariogenic arterial thromboembolism
external warming, opioids, antiplatelet therapy, acepromazine not recommended
- antiplatelet therapy (sodium heparin, enoxaparin, dalteparin sodium)
- thrombolytic therapy (rt-PA)
prognosis of cariogenic arterial thromboembolism
overall median long-term survival is approx. 6-9
predisposition of pericardial effusion
Older golden retrievers, GSD, St. Bernard dogs, no predisposition, 6-9years
types of pericardial effusion
Congenital (peritoneopericardial diaphragmatic hernia and pericardial cysts), acquired (pericardial effusion and constrictive pericarditis)
cause of pericardial effusion
neoplastic, idiopathic, cardiovascular (R HF, rupture of left atrium), infections (intrapericardial FB or fungal infections), metabolic (toxic): (uraemia, coagulopathies)
signs of pericardial effusion
weakness, lethargy, ascites, exercise intolerance, respiratory distress, collapse, cough, vomiting
muffled heart sound, depression, hepatomegaly, ascites/ distended jugular veins, hypodynamic pulse, pleural effusion, pale MM
diagnosis of pericardial effusion
physical exam ECG X-rays echo Lab
treatment of pericardial effusion
- Pericardiocentesis – initial therapy result in short-term recovery
o Left flank, ECG monitoring, right 4-6th IC space, +/- LA, 15-20cm long catheter, complete evacuation of the effusion - conversative therapy – periodic pericardiocentesis
- surgical (total/subtotal pericardiectomy, pericardiotomy, tumour removal)
- glucocorticoids, NSAIDs
prognosis of pericardial effusion
idiopathic effusion = good to excellent, hemangiosarcoma = very bad, heart base tumours – cautious, mesothelioma = extremely bad, infectious = not great
cause of heart murmur
many: structural abnormalities and considered pathologic, also some are nonpathological
- nonpathological murmurs are systolic in timing
o functional: anaemia or cardiac output is increased from fever/hyperthyroidism
o innocent: soft murmur, without evidence of structural cardiac disease/ physiological alteration (often in young puppies)
pathogenesis of heart murmur
occur due to a turbulence in blood flow
grades of heart murmur
- very soft, localised murmur; heard over listening intently in quiet surrounding
- soft murmur, yet heard easily
- moderate intensity murmur that radiates, equal in intensity to that of heart tones
- loud murmur, louder than normal heart tones
- loud murmur accompanied by a palpable precordial thrill
- very loud murmur accompanied by a palpable precordial thrill that can be heart with the stethoscope lifted away from the chest wall
diagnosis of heart murmur
- auscultation
- echo
echo: LA enlargement
mitral insufficiency, cardiomyopathies, PDA, subaortic stenosis, ventricular septal defect, mitral stenosis
echo: RA enlargement
tricuspid insufficiency, chronic respiratory disease, interatrial septal defect, pulmonic stenosis
echo: LV enlargement (hypertrophy)
HCM, subaortic stenosis
echo: LV enlargement (dilation)
mitral insufficiency, DCM, aortic insufficiency, PDA, ventricular septal defect, subaortic stenosis
echo: RV enlargement
pulmonic stenosis, tetralogy of fallot, tricuspid insufficiency, severe heartworm severe pulmonary hypertension
jugular veins
- persistent jugular vein distension – occurs with right sided CHF
- distension alone: pericardial effusion, right atrial mass, DCM, cranial mediastinal mass, jugular vein thrombosis
- pulsation +/- distension: tricuspid regurgitation, pulmonic stenosis, pulmonary hypertension, 3rd degree block, constrictive pericarditis, hypervolemia
arterial pulse
- weak pulse: DCM, subaortic stenosis, pulmonic stenosis, shock, dehydration
- strong pulse: excitement, hyperthyroidism, fever, HCM
- very strong: PDA, fever/sepsis, severe aortic regurgitation
differential for cyanosis
reverse PDA
