Approach to young animal with murmur Flashcards
What is your first step when you detect a murmur in a young animal?
Determine if it is an:
Innocent murmur?
Murmur indicative of disease?
Why do young animals have ‘innocent/flow murmurs’?
Due to the fact neonates have lower PCV (so blood is less viscous), lower protein concentration (blood less viscous) and increased CO (because growing rapidly). These features predispose to turbulent flow –> low grade murmur (usually 3 out of 6 or 7)
Steps for young animal with a murmur which is indicative of disease? 5
Refine your DDx list with careful PE
Perform/interpret diagnostic tests in light of knowing what different diseases will do to the heart and circulation
Reach definitive diagnosis where possible
Referral?
Explore Tx where appropriate
What are flow murmurs?
May occur in normal young individuals. Characteristics:
no associated CS
Low intensity ( type in characteristic - i.e. crescendo-decrescendo
What do significant murmurs in young animals signify?
presence of congenital heart disease
Incidence - congenital heart disease
Variable with species
Highest in dogs (0.5-1% of all live births) - breed selection pressure
Types of congenital abnormality
VALVULAR MALFORMATIONS (dysplasia) –> stenosis or insufficiency of any of the heart valves
PRESISTENCE OF FOETAL VESSEL - PDA
VASCULATURE MALFORMATION - vascular ring anomlay, PRRA or PSS
SPETAL DEFECTS - heart or great vessels affected, complex, classically ToF, common AV canal, PTA
What are examples of heart disease that can be acquired at a young age?
Paroviral myocarditis - puppies
HCM - young cats
Why are murmurs discovered in young animals?
Indcidental finding - vaccination PE
Murmur with CS of heart disease (cyanosis, syncope, stunted growth)
Overt CHF
Non-cardiac signs (HE for PSS, regurgitation for VRA)
What about foals and PDA?
The murmur of PDA is audible in the majority of new-born foals but the diastolic component should disappear within a few days.
How can congenital heart disease be investigated?
Signalment, history Clincial exam Narrow DDx list Echo Radiography (less useful in horse) \+/- ECG
IF AVAILABLE: Doppler Echo Cardiac catheterisation Angiography Blood-gas estimation
BEST TIME: before onset of CS of HF rather than wait and see approach.
How do you refine the pathophysiology? 4
Is it due to a volume load or a pressure load?
Is heart murmur present with CS or not?
Is there evidence of hypertrophy?
Which chambers are affected?
What are continuous murmurs likely to be due to?
PDA
What are left heart base murmurs likely to be due to?
Stenosis of OF valve
What are intense right sided murmurs likely to be caused by?
VSD
What are dynamic pulses associated with?
PDA (waterhammer pulse) - higher SV, lower aortic diastolic pressure
What are dampened/poor pulses associated with?
Aortic stenosis
What aspects need to be considered on PE? 5
Do the location, timing and audibility of the murmur gives clues as to which sort of defect is present?
Pulse quality
Evidence of cyanosis?
Animal well grown compared to littermates? BCS?
Evidence of HF?
What might cyanosis imply?
May imply ‘cyanotic’ heart disease where right to left shunting can occur
What might cause a systolic murmur on left side, apex?
Mitral insufficiency
What might cause a systolic murmur on left side, base? 2
Aortic or pulomary stenosis
What might cause a systolic murmur on right side, sternal border?
VSD
What might cause a systolic murmur on right side, cranially?
Tricuspid insufficiency
Aortic stenosis
What type of overload do left to right shunts cause?
volume loads (these occur along the ‘path of the shunting eryhtrocyte’)
What type of overload do stenoses of the outflow valves cause?
Pressure overloads (increased resistance to ejection from the ventricles)
Pathophysiology - VSD
Volume load –> enlargement - dilatation of LA, LV, murmur at pulmonic valve due to relative pulmonic stenosis (nothing wrong with valve per se but there is increased volume)
What is the most common congenital heart defect in all species except the dog?
VSD
Outline VSD: NATURE OF DEFECT: PATHOPHYSIOLOGY PE: DIAGNOSTICS: THERAPY: PROGNOSIS
NATURE OF DEFECT: failure of normal formation of interventricular septum
PATHOPHYSIOLOGY: left to right shunt unless there is a pulmonary hypertension
PE: intense systolic murmur usually loudest on the right, accompanied by a palpable thrill known as a ‘precordial thrill’
DIAGNOSTICS: volume overloaded left side and pulmonary circulation
THERAPY: definitive treatment not available
PROGNOSIS: fair if defect is small and pressure difference is maintained across the defect.
Why look at velocity of the shunt with a VSD?
High velocity –> indicates small VSD hole –> better prognosis (known as a restrictive or a resistive defect)
What if there is pulmonary hypertension or pulmonic stenosis with VSD? PATHOPHYSIOLOGY PE: DIAGNOSTICS: THERAPY:
PATHOPHYSIOLOGY: ‘cyanotic’ congenital heart disease, usually have severe compromise, right ventricular pressure overload and systemic hypoxia. The pressure difference between the right and left ventricles is less than is seen with the VSD. Body perfused with deoxygenated blood. Lungs are under-perfused.
PE: poorly grown, may be no murmur or only a quiet murmur
DIAGNOSTICS: RVH, may see shunting defect, may be polycythaemia
TREATMENT: no definitive therapy, some palliative therapy for certain defects, need to control PCV
Define polycythaemia
an abnormally high amount of Hb in the blood - either decreased plasma volume or increased RBC numbers
Outline PDA: Defect and nature PE Diagnostics Treatment Prognosis
DEFECT:persistence of foetal connection, left to right shunt (unless pulmonary hypertension develops)
PE: continuous left base murmur and bounding pulses
DIAGNOSTICS: volume loaded left side and pulmonary circulation, can see ductal flow (Doppler) - may see ‘three knuckles’ or radiography - Ao, PA, LA
TREATMENT: surgical ligation or interventional closure
PROGNOSIS: good if closed
What is meant by ‘3 knuckles’?
Seen on DV radiograph of the heart = distinct enlargement of Ao, PA and LA.
How can a PDA be closed surgically?
Ligation - competent surgeon in a 1st opinion practice if no alternative.
Interventional closure - referral only
Ductal occluder in PDA (i.e. transvascular technique)
Outline aortic stenosis: Nature Pathophysiology PE Diagnostics Management
NATURE: narrowing of LV OT
PATHOPHYSIOLOGY: pressure overload LV
PE: left base systolic murmur, poor pulse
DIAGNOSTICS: concentrically hypertrophied LV, increased aortic outflow velocity (Doppler)
MANAGEMENT: definitive cure not available, medical management currently best option although weak evidence, warn owners of the risk of sudden death
Outline pulmonic stenosis: Nature Pathophysiology PE Diagnostics Management
NATURE: narrowing of RVOT
PATHO: RV pressure overload
RE: left base systolic murmur (very like AS), pulse may be less affected (subjective), apex beat may be on RHS
DIAGNOSTICS: RVH, PA dilatation, increased pulmonary outflow velocity (doppler)
MANAGEMENT: balloon valvuloplasty and surgical patch grafting described.
What is balloon valvuloplasty?
Balloon catheter placed in CrVC- –>inflated in PA for a short time and then taken down asap –> resolves the pulmonic stenosis.
Important to take down asap as you are completely occluding the PA whilst it is in place.
Outline vascular ring anomaly: Defect Pathophysiology PE Diagnostics Managmeent
DEFECT: malformation of great vessels (e.g. PRAA)
PATHO: obstruction of thoracic oesophagus (impact is mainly on the GIT)
PE: no murmur, signs of regurgitation
DIAGNOSITCS: dilated oesophagus cranial to heart
MANAGEMENT: surgical relief of compression, even then prognosis is guarded.
Outline ASDs: Nature of defect Pathophysiology PE Diagnostics Treatment
NATURE: failure of formation of the atrial septum
PATHO: may have left to right shunt but often not significant
PE: may be normal, may have soft murmur over pulmonic valve, ‘relative pulmonic stenosis’
DIAGNOSTICS: often found incidentally (often missed)
TREATMENT: usually not required.
Outline mitral and tricuspid dysplasia
NATURE: malformation of one/both AV valve(s)
PATHO: stenosis and/or insufficiency of vlave leads to volume load of left (M) or right (T) side
PE: murmurs of MR or TR (stenosis murmurs less audible)
DIAGNOSTICS: enlargement of left/right side
TREATMENT: definitive repair attempted surgically but with limited success.
Define annulus
= a ring-shaped object, especially in a region bounded by 2 concentric circles.
What should be looking for with diagnostic imaging?
Enlargement of cardiac silhouette or pulmoary vessels (xray) or enlargement of specific chambers (echo)
Which chamber/vessel is enlarged?
Hypertrophy - concentric or eccentric
Evidence of HF - pulmonary congestion, pulmonary oedema or ascites
How are definitive diagnoses often made?
Specialist procedures - Doppler echo or cardiac catheterisation.
Is it possible to treat severe sub-aortic stenossi?
Currently impossible to treat successfully
What is ‘cyanotic’ heart disease?
Right to left (pulmonary to systemic) shunting disease. Requires shunt AND pressure greater on RHS.
EXAMPLES:
Right to left VSD - when there is a VSD in conjunction with pulmonic stenosis or pulmonary hypertension
Right to left ASD - occurs when there is an ASD in conjunction with increased RA pressures. The latter may occur secondary to pulmonary hypertension, pulmonic stenosis or tricuspid dysplasia.
Right to left PDA (a ‘reverse’ PDA) - when there is a PDA and pulmonary hypertension)
What is ‘Eisenmenger’s physiology’?
When there is a large left to right shunt (large VSDs or PDAs), pulmonary hypertension may develop in the early post-natal period due to large volume of blood shunting through the vasculature. Thus a defect starts out shunting left to right but may end up shunting right to left.
Effects of persistent delivery of deoxygenated blood to systemic circulation = ?
Stunted growth
Cyanosis - some/all MM
Severe exercise intolerance (exercise –> increased systemic vascular resistance –> increase in shunting blood)
Polycythaemia (due to persistent stimulus to erythropoiesis due to hypoxia). CS result from ‘sludging’ of blood due to exaggerated viscosity causing thrombossi or compromised cerebral oxygen delivery and seizures. this may require specific managment with drugs that suppress RBC production, intermittent phlebotomy or even leeches.
