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CVS System - Coggle Diagram
CVS System
CONGENITAL DEFECTS
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SAS
subvalvular (>95%), valvular (<5%), supravalvular (rare)
certain large breed dogs
hx:
- exercise intolerance, syncope, sudden death, LS heart failure
clin exam:
- slow-rising hypokinetic pulses
- harsh systolic heart base murmur, radiates widely
+/- low heart base thrill
pathophys
- severity varies
- subvalvular fibrous ring
- develops in first few months of life
>> narrowing of LV outflow tract due to SUBVALVULAR FIBROUS RING = LV pressure overload >>> concentric hypertrophy >>> inadequate coronary perfusion which further worsens the outflow obstruction
Dx
RADIOLOGY
ECG
- exercise precipitated arrhythmia
- signs of LS cardiomegaly
+/- ST segment depression (myocardial ischaemia)
ECHO
- confirms the dx and also determines severity of stenosis
Mx
- referral; balloon dilatation or open heart sx
- B1 blocker (atenolol)
- exercise restriction
50% with severe SAS die within 3yrs if left untreated
PS
common in small dogs (namely, english bulldogs)
location: valvular > subvalvular >> supravalvular
hx
asymptomatic.. normal until about 1yo
- exercise intolerance, syncope, RS heart failure
clinical findings
- high left base systolic ejection murmur +/- thrill; does not radiate
+/- jugular pulse, arrhythmias
dx
RADIOGRAPHY
- RV enlargement + pulmonary artery bulge
ECG
- exercise precipitated ventricular tacharrhythmias
- signs RS cardiac enlargement
ECHO
- confirms dx
- determines deverity
mx
- balloon dilatation
- exercise restriction +/- beta blocker
- treat CHF if present
VSD
hx
may be tolerated, or may develop pulmonary hypertension, LSCHF
clinical findings
- harsh holosystolic murmur, loudes on RHS
dx
RADIOGRAPHY
- LS enlargemenr
- pulmonary over-circulation
- RV enlargement
ECG
ECHO
ASD
-
clinical findings
AUSCULTATION
- split S2 (prolonged RV emptying; lup-dupup)
+/- systolic murmur L heart base
+/- diastolic murmur (rumble) on RHS
RADIOLOGY
- RS cardiomegaly
- dilatation of main pulmonary artery
- over-circulation of pulmonary vessels
ECG
ECH
tetralogy of fallot
classic cyanotic heart dz; embryonic consequence of conotruncal septal malformation
1. PS
2. secondary RV hpertrophy
3. VSD
4. overriding aorta
hx
- may be tolerated for years
- exercise intolerance, syncope
clinical exam
- cyanosis
- audible murmur (PS or VSD)
- erythrocytosis (high PCV)
dx
RADS
- normal size or cardiomegaly
- pulmonary under-circulation
ECG
- RS enlargement
- ventricular arrhythmias
ECHO
rx
- phlebotomy if PCV >65% (norm 35-55)
+/- hydroxyurea to lower PCV
- enforce rest
- avoid stress
Heart murmurs
turbulent blood flow within the heart, valve malfunctions, hole between chambers
-
-
what if we hear a murmur in a healthy dog?? offer MINIMUM: rads, measure ABP, basic bloods, UA. if norma no further rx and reasses in 6-12mo. if abnormal commence pimobendan treatment
DOG DISEASES
-
IE
most common organisms = staph, strep, escherichia, pseudomonas
uncommon/rare in dogs. very rare in cats. medium-large purebreds, middle aged male dogs. may be assoc with SAS and PDA
mitral and aortic valves most commonly affected
- ulceration of valvular endothelium > platelet adhere > fibrin deposition > vegetative lesions (flimsy + friable, then fibrotic)
- young lesions travel to kidney and brains
- lesions cause valvular insufficiency, sometimes stenosis
- LCHF develops rapidly
clinical features:
- fever
- NEW heart murmur
- stiffness/lameness/joint swelling
- lethargy, anorexia, weight loss, GI signs
- signs CHF, syncope
SIGNS OF A VERY UNHAPPY AND SICK DOG!!!!!!
DX:
diastolic murmur + unhappy systemically sick dog + fever = strong basis of suspicion for IE
- echocardiogram; flopping "vegetations"/valve destruction
- genuinely new heart murmur
- two or more POSITIVE blood cultures
- PM
Rx;
aggressive therapy with bacteriocidals that are capable of penetrating fibrin
beta lactams + aminoglycosides (NB: amino toxicity)
fluoquinolone
px is poor to guarded
CMO
-
pathophys
decreased ventricular contractility + systolic dysfunction + low CO = fibrillation and tachycardia as compensatory mechanisms to increase the HR
progressive worsening over time = chamber enlargement (concentric hypertrophy) and inability of valve leaflets to meet in the middle = turbulence = systolic murmur >>> R and L CHF
atrial fibrillation > suddent death
Clinical features
- prolonged preclinical (occult) phase; progressive failure of myocardium + reduced ventricular contractility + reduced systolic function + reduced CO - echocardio can detect
- exercise intolerance
- weakness and lethargy
- tachypnoea, dyspnoea, cough
- anorexia, abdominal swelling, syncope
- remarkable loss of muscle mass = cardiac cachexia
Dx; signalment and history
- systolic mitral and/or tricuspid murmur +/- gallop
+/- irregularly irregular arrhythmia, MM pallor + decreased CRT, cold extremities, weak femoral pulse, CHF signs
- Dx of heart failure = proNTBNP
Rx
OCCULT
- pimobendan (prolongs CHF onset)
- ACEI (benazepril, enalapril)
sprionolactone, b blockers, anti-arrhythmias (ESP DOBERMANS AND BOXERS)
OVERT
v similar to CVHD with addition of anti arrhythmias
- excercise restriction + furosemide + pimobendan + ACEI/ARB
sprionalacton, digoxin
-
Heart failure
effects on kidneys: reduction in blood pressure/fluid volume causes renin release (kidneys) and angiotensin (liver) > renin acts on angio to form angiotensin I > ACS from lungs converts to ATII. ATII then causes vasoconstriction or acts on pancrea to release alodesterone > stimulate resorption of NaCl and H2O in kidneys >>> increase in BP and volume
L vs R heart failure
Left sided: blood backs up in the lungs and pulmonary vessels forcing fluid out into the lung tissue = PULMONARY CONGESTION
Right sided: reduced blood flow to the lungs, backflow into the CVC >>> passive congestion of other organs >>> LYMPH IN THE PERITONEAL CAVITY
CAT DISEASES
CMO
dominant form of heart dz in cats, very common
characterised based on morphology:
- HYPERTROPHIC, dilated, restrictive, indeterminate/unclassified, secondary etc.
strong breed predispositions: main coons, persians, american shorthairs, ragdoll
pathophys
thickening of LV wall + septum = small lumen
stiff ventricular walls, diastolic dysfunction, poor filling, low SV, neurohormonal activation, tachycardia >>> further worsens LV filling
- progressively higher LV filling pressures, enlarged LA
+/- pulm congestion, thrombus formation (LA or LV), arterial thromboembolism
pathophys complications:
- LV outflow tract obstruction
- myocardial ischaemia
- mitral insufficiency
- atrial fibrillation
- biventricular failure with pleural effusion
Clinical features
- middle-aged male cats
- can be asymptomatic for years +/- murmur
- most present with respiratory signs and aortic thromboembolism
- tachypnoea, panting with mild exertion, dyspnoea
- coughing uncommon
acute development CHF +/- sudden death possible
+/- systolic murmur, gallop, arrhythmia
usually good pulse (except femoral)
may have pulmonary crackles, pulmonary oedema
muffling if pleural effusion
Dx
compatible Hx and PEx findings
- Rad: valetine shaped heart (inconsistent), elongation of cardiac silhouette, pulmonary vessels may be branching and wide
- echo: cardiomegaly (LV hypertrophy +/- LA enlargement (CHF))
- ECG
must rule out secondary causes: hyperthyroidism, systemic hypertension, taurine def.
Rx
ASYMPTOMATIC
- prevent CHF/saddle club/suddent death and reverse myocardial abnormalities
NEVER TREAT A MURMUR EMPERICALLY!!!!!!!
SYMPTOMATIC
- enhance ventricular filling
- relieve congestion
- control arrhythmias
- minimise tissue ischaemia
- prevent saddle club
at home treatment - depends on stage presented
- furosemide, ACEI/ARB, beta blockers, anti thrombotics (clopidogrel), exercise restriction, salt-restricted diet
Px
good = asymptomatic/mild-moderate heart changes
poor = saddle club
LA size/age/presence of a fib/RCHF all have negative correlations with the px
median survival 1-2yrs
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