Cardiac Exam Flashcards
TR Exam Findings
Some of these findings may be present and may vary depending on the severity of the condition:
Tricuspid regurgitation is most readily clinically diagnosed on the basis of peripheral signs, i.e. elevated JVP with prominent V wave & rapid Y descent, pulsatile liver and often the presence of a right ventricular heave and pulmonary hypertension.
A pansystolic murmur is best heard at the left lower sternal edge and as with all right sided murmurs is louder on inspiration.
Patients with chronic tricuspid regurgitation may develop portal hypertension and ascites (cardiac cirrhosis).
Peripheral oedema may also be present.
Tricuspid regurgitation commonly accompanies mitral regurgitation and pulmonary hypertension.
Causes of TR
Tricuspid regurgitation is commonly secondary to right ventricular dilatation. Rheumatic - rare alone Infective endocarditis Congenital - ebstein's anomoly TV prolapse RV papillary muscle infarction Trauma
It may also result as a complication of pacemaker insertion and of frequent trans-jugular cardiac biopsies.
Valsalva (decreases preload)
HOCM louder
Mitral prolapse longer + clock earlier
Squatting (increases preload)
AS and MR louder
Hand grip (increases afterload)
MR louder (all murmurs of regurg) + MS
AS causes
The most likely aetiology underlying aortic stenosis is degeneration of a bicuspid (& unicuspid) congenital valve. The risk factors involved are the same as those for ischaemic heart disease (hence these are very relevant in this case).
Calcific disease of a trileaflet valve.
Other causes include rheumatic heart disease.
AS exam findings
In the absence of other conditions, the patient is usually in sinus rhythm (atrial fibrillation is unusual).
It is unusual for the blood pressure to be very high in severe aortic stenosis.
In moderate-severe aortic stenosis the carotid pulse is often of small volume with a slow rise and a plateau pulse may be present.
The apex beat may be pressure loaded.
There may be a palpable thrill at the base of heart and/or in the aortic area.
On auscultation an ejection systolic murmur is heard, loudest in the aortic area and radiating to the neck.
The murmur is usually graded as 3 OR 4/6 (unless stroke volume is low when the murmur may then be soft).
Louder on exp + squatting
AS Signs of severity
A small volume, slow rising, plateau carotid pulse.
The presence of an aortic thrill.
A long late peaking ejection systolic murmur.
The presence of an S4, indicating reduced compliance of the left ventricle.
Paradoxical splitting of S2.
The presence of left ventricular failure.
Gallavardin phenomenon.
In this phenomenon, the harsh murmur of aortic valvular stenosis may change in quality and become musical at the apex ((i.e. ejection systolic in aortic stenosis versus pansystolic in mitral regurgitation).
Pansystolic
MR
TR
VSD
Aorto-pulmonary shunts
Midsystolic
Aortic stenosis
PS
HOCM
Late systolic
MV prolapse, papillary muscle dysfunction
Early diastolic
AR, PR
Mid-diastolic
MS, TS, atrial myxoma
Continuous
PDA
AV fistula
Aortopulmonary connection
Venous hum
AR pathologies
Valve pathologies include:
Rheumatic heart disease (although unlikely in isolated aortic regurgitation).
Congenital with or without ventricular septal defect (VSD).
As a complication of infective endocarditis.
Aortic root pathologies include:
Aortic root dissection.
In association with ankylosing spondylitis.
As a result of syphilitic aortitis.
As a complication of Marfan’s syndrome.
Manouevres
R) sided louder with insp, L) sided louder with exp
Most murmurs - valvsala (decreased preload - reduced)
Most - Hangrip - MS increased, murmurs of regurg increase
Squating - most increase (increased preload) + standing most decrease (decreased preload)
MR Auscultation
Auscultation in significant mitral regurgitation
Pansystolic murmur.
A soft S1.
A loud S2 suggests the presence of pulmonary hypertension.
An S3 generated by turbulent left ventricular blood flow.
MR summary of findings
The patient may be in atrial fibrillation.
A displaced, dyskinetic apex beat.
Soft S1.
Presence of an S3.
An apical thrill.
A pansystolic murmur that radiates to the axilla.
Evidence of heart failure.
Evidence of pulmonary hypertension and tricuspid regurgitation –> presence of parasternal impulse, S4 present in severe acute MR
Indicators of severity in MR
Left ventricular dilatation.
A soft S1.
The presence of pulmonary hypertension.
A split S2.
The presence of an S3.
Complication of left ventricular failure.
Small pulse volume (very severe mitral regurgitation).
Causes of MR
Primary mitral valve disease: (CHRONIC)
Mitral valve degeneration (e.g. myxomatous mitral valve disease).
Rheumatic mitral valve disease.
Involvement in infective endocarditis.
Congenital heart disease.
Ruptured chordae tendineae - from LVH or ischaemia
Infarcted papillary muscles.
Secondary mitral regurgitation:
Left ventricular dilatation e.g. dilated cardiomyopathy or IHD (post infarct MR, papillary muscle rupture/infarct)
(ACUTE)
- IE
- Myocardial infarction
- Surgery
- Trauma
Causes of MS
Normal - 4-6cm, severe < 1cm
Rheumatic heart disease is the most common cause, other causes being much less common.
E.g. of less common causes include radiation induced and congenital mitral stenosis.
Summary of findings in MS
The patient may be in atrial fibrillation.
Malar flush may be present.
The JVP may demonstrate a prominent a-wave (in the presence of sinus rhythm).
The apex beat is often only mildly displaced and the may be described as tapping (palpable S1).
A parasternal heave/lift may be present indicating right ventricular hypertrophy.
The 2nd heart sound may be palpable in the pulmonary area indicating pulmonary hypertension.
On auscultation the following may be noted at the apex:
A loud S1 when the leaflets are stiff but still mobile.
An opening snap.
A mid-diastolic rumbling murmur, there may be pre-systolic accentuation (provided the patient is in sinus rhythm).
Signs of severity in MS
A small pulse pressure.
A short distance between the opening snap and S2 (due to raised left atrial pressure)
A long mid-diastolic murmur (present as long as there is a gradient between LA & LV).
The presence of pulmonary hypertension.
An apical diastolic thrill.
