Cardiology Flashcards
Aetiology of Aortic Stenosis
The most likely aetiology underlying aortic stenosis is degeneration of a bicuspid (or unicuspid) congenital valve. The risk factors involved are the same as those for ischaemic heart disease.
Calcific disease of a trileaflet valve.
Other causes include rheumatic heart disease.
Summary of Finding in Aortic Stenosis
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 and NOT markedly displaced.
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).
Indicator of Severity in Aortic Stenosis
- A small volume, slow rising, plateau carotid pulse.
- Narrow pulse pressure
- The presence of an aortic thrill.
- A long late peaking ejection systolic murmur.
- A loud murmur (grade 4 or greater) has a high specificity for severe AS
○ However, most patients with severe stenosis have a grade 3 murmur, and many have only a grade 1 or 2 murmur. - The presence of an S4, indicating reduced compliance of the left ventricle.
- Paradoxical splitting of S2.
- The presence of left ventricular failure.
- Pressure loaded apex beat.
- Soft/absent aortic component of the second heart sound
- Signs of pulmonary hypertension
What is Gallavardin Phenomenon?
The murmur of aortic stenosis may be heard at the apex
This is known as Gallavardin phenomenon.
In this phenomenon, the harsh murmur of aortic valvular stenosis may change in quality and become musical at the apex.
This can cause confusion in differentiating the murmur from that of mitral regurgitation, however they can be differentiated by the murmur quality (i.e. ejection systolic in aortic stenosis versus pansystolic in mitral regurgitation).
Severe Aortic Stenosis Murmur
The murmur is ejection systolic.
It is heard throughout systole, indicating that a pressure gradient is present throughout. The murmur peaks late in systole.
These are all indicators of the severity of aortic stenosis.
Mild Aortic Stenosis Murmur
In mild aortic stenosis, the carotid pulse is normal and the ejection systolic murmur is short with an early peak.
Aetiology of Mitral Regurgitation
Mitral regurgitation aetiology can be primary due to mitral valve disease or secondary due to left ventricular pathology
Primary Mitral Valve Disease
Mitral valve degeneration (e.g. myxomatous mitral valve disease). Rheumatic mitral valve disease. Involvement in infective endocarditis. Congenital heart disease. Ruptured chordae tendineae. Infarcted papillary muscles.
Secondary Mitral Regurgitation
Left ventricular dilatation e.g. dilated cardiomyopathy
Mitral Regurgitation Physical Finding (Summary)
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.
Indicator of Mitral Regurgitation Severity
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).
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.
CXR Findings for Mitral Regurgitation
- Left atrial enlargement (double heart border, splayed carina, straightening/convexity of the left heart border indicating enlarged left atrial appendage)
- Pulmonary hypertension (enlarged pulmonary trunks, especially on the left)
- Enlarged left ventricle (increased cardiothoracic ratio)
- Right ventricular enlargement (filling of the retrosternal space >1/3rd)
Common aetiologies of Tricuspid Regurgitation
Tricuspid regurgitation is commonly secondary to right ventricular dilatation.
It may also result as a complication of tricuspid valve infective endocarditis. [Right sided infective endocarditis may be a complication of intravenous cannulation and/or intravenous drug use.]
It may also result as a complication of pacemaker insertion and of frequent trans-jugular cardiac biopsies, as may occur post heart transplant.
Summary of findings in Tricuspid Regurgitation
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 earlobe), 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.
JVP in Tricuspid Regurgitation
large v-wave with a rapid y-descent causing earlobe pulsation
What is the finding of apex beat in TR without mitral valve disease?
Normal character and location
Parasternal lift/heave is usually indicates …?
right ventricular hypertrophy (rarely gross left atrial hypertrophy)
Common aetiology of Aortic Regurgitation
These can be divided into valve and aortic root pathologies
Valve pathology in Aortic Regurgitation
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 pathology in Aortic Regurgitation
Aortic root dissection.
In association with ankylosing spondylitis.
As a result of syphilitic aortitis.
As a complication of Marfan’s syndrome.
Peripheral signs of Aortic Regurgitation
Signs of a wide pulse pressure (note that severe aortic regurgitation may not be accompanied by a wide pulse pressure as left ventricular end-diastolic pressure rises).
Blood pressure measurement (wide systolic-diastolic difference).
A collapsing/water-hammer pulse.
Quincke’s sign (nail bed pulsation).
Head bobbing.
Pistol shot femoral artery sounds (systolic and diastolic sounds).
A displaced apex beat.
A diastolic thrill at the left lower sternal edge.
Auscultation findings of Aortic Regurgitation
A S3 maybe present.
An early decrescendo diastolic murmur loudest at the left lower sternal edge and best heard at end of expiration, with the patient leaning forward.
An Austin Flint mid-diastolic murmur may be heard at the apex in severe aortic regurgitation.
There may be evidence of left ventricular failure.
An ejection systolic murmur may be heard, caused by the large stroke volume and does not necessarily indicate co-existing aortic stenosis.
Indicators of Aortic Regurgitations Severity
A wide pulse pressure with associated collapsing pulse.
The presence of a long decrescendo diastolic murmur (in very severe aortic regurgitation with left ventricular decompensation, the murmur may become soft or absent with equalisation of aortic and ventricular diastolic pressures).
The presence of an S3.
The presence of a soft A2.
The presence of an Austin-Flint murmur.
The presence of left ventricular enlargement.
Apex beat in Aortic Regurgitation
In addition to “volume loaded” other descriptive terms include diffuse and hyperdynamic. These descriptions are in keeping with ventricular dilatation caused by the regurgitant blood and a hyperdynamic left ventricle.
Aetiology of Mitral Stenosis
Rheumatic heart disease is the most common cause, other causes being much less common.
Examples of less common causes include radiation induced and congenital mitral stenosis.
Summary of Physical Findings in Mitral Stenosis
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 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).
Murmur increases with isometric hand exercise.
Indicator of Mitral Stenosis Severity
A small pulse pressure –> signifies a low cardiac output state
A short distance between the opening snap and S2.
A long diastolic murmur (present as long as there is a gradient between LA & LV).
The presence of pulmonary hypertension.
Signs of pulmonary congestion
An apical diastolic thrill.
Graham-Steell murmur (pulmonary regurgitation) –> a short early diastolic murmur in the pulmonary area, radiating down the left sternal edge, louder in inspiration
CXR in Mitral Stenosis
- Signs of left atrial enlargement (double heart border, prominent left atrial appendage leading to straightening or convexity of the left heart border, splaying of the carina)
- Cardiac enlargement (enlarged cardiothoracic ratio)
- Boot-shaped cardiac silhouette suggestive of right ventricular hypertrophy
Common aetiology of Mixed Aortic Valve Disease
Rheumatic heart disease.
Degeneration of a congenital bicuspid aortic valve.
Endocarditis superimposed upon a stenotic aortic valve.
PE findings in Mixed Aortic Valve disease
In addition to recognising the murmurs, the physical examination should aim to determine the dominant haemodynamic lesion, i.e. aortic stenosis or regurgitation based on peripheral findings e.g. collapsing pulse if regurgitation dominant lesion, small volume carotid pulse if stenosis dominant.
Pulsus bisferiens (biphasic pulse) may be noted in carotid pulse.
The character and location of the apex beat, depends on the dominant lesion, e.g. often displaced and volume loaded if regurgitation is predominant.
Common causes of Pulsus Bisferiens
Common causes include moderate - severe aortic regurgitation, mixed aortic regurgitation and stenosis (predominant lesion aortic regurgitation). It may also be seen in hypertrophic obstructive cardiomyopathy.
Auscultation findings in Mixed Aortic Valve disease
An ejection systolic and an early decrescendo diastolic murmur are present.
An ejection systolic murmur may be present in patients with aortic regurgitation and often indicates a large stroke volume rather than coexistent aortic stenosis
Common Aetiology of Mitral Valve Prolapse
Commonly myxomatous degeneration of the valve in the absence of a connective tissue disorder.
Myxomatous degeneration associated with connective tissue disorders e.g. Marfan syndrome, Ehlers–Danlos syndrome.
PE in Mitral Valve Prolapse
The most common findings are a mid-systolic click with a mid or late systolic murmur of mitral regurgitation.
The click is thought to be caused by snapping of the mitral chordae during systole when the valve bows into the atrium.
Auscultation findings of Mitral Valve Prolapse
There is a midsystolic click followed by a late systolic murmur
What is the aetiology of HOCM?
Hypertrophic obstructive cardiomyopathy is a hereditary condition with autosomal dominant inheritance with variable penetrance.
Asymmetric septal hypertrophy can be acquired in long standing hypertension.
Hypertrophic cardiomyopathy maybe obstructive or non-obstructive.
Summary of clinical findings in HOCM?
Carotid pulse may be jerky, differentiating it from aortic stenosis.
The JVP may have a prominent a-wave.
The apex beat is typically described as possessing a double impulse.
A systolic thrill may be present at the left lower sternal edge
Auscultation at the left lower sternal edge typically reveals an ejection systolic murmur.
A pansystolic murmur of mitral regurgitation may be heard at the apex indicating mitral regurgitation secondary to systolic anterior motion.
An S4 may be heard (in sinus rhythm).
The ejection systolic murmur is louder on Valsalva and softer with hand grip. It does not radiate to the neck.
Describe the HOCM murmur on auscultation of left lower sternal edge
A harsh ejection systolic murmur at the left lower sternal edge which does not radiate to the neck (another feature differentiating it from aortic stenosis).
The murmur is louder on valsalva and softer on isometric exercise (hand grip).
Describe the auscultation of the apex in HOCM
There is a pan-systolic murmur at the apex which radiates to the axilla and represents mitral regurgitation caused by systolic anterior motion of the distal portion of the anterior leaflet of the mitral valve toward the left ventricular outflow area.
PE findings of ASD
Atrial Septal Defect (ASD)
Lesson 14 of 17
Overview of normal development of the atrial septum and pathology of secondum and primum ASD
Summary of physical findings
More common in females.
A parasternal heave may be present and is in keeping with right ventricular dilatation caused by increased blood flow in the right chambers due to the left to right shunt.
A midsystolic pulmonary ejection murmur that increases with inspiration.
Fixed splitting of S2.
Findings of pulmonary hypertension.
A mid-diastolic rumbling murmur at LSE may indicate increased flow through the tricuspid valve.
With reduction in L to R shunting:
Diminution of pulmonary & tricuspid murmurs.
P2 accentuated.
Diastolic murmur of pulmonary regurgitation may appear.
Auscultation findings
The classical findings in ASD with a large left-to-right shunts and normal pulmonary artery pressure are fixed splitting of the 2nd heart sound and an ejection systolic murmur, best heard in the pulmonary area.
Fixed splitting of the 2nd hear sound is caused by increase pulmonary blood flow. The increased flow also explains the ejection systolic pulmonary murmur.
Complications of ASD
Patients with a significant ASD are often asymptomatic until the mid forties.
Atrial arrhythmia, in particular atrial fibrillation are common.
Pulmonary hypertension may develop and reversal of the shunt to a right to left shunt when right sided pressures exceed those on the left (Eisenmenger syndrome). This may be associated with cyanosis, signs of pulmonary hypertension. However in this situation there is no fixed splitting of the 2nd heart sound. This is an uncommon complication and only seen in ASDs that are not repaired.
Stroke due to paradoxical embolisation may occur. In this situation a venous clot migrates to the right atrium and in the presence of a right to left shunt may migrate to the left side and embolise to the brain and other systemic locations.
Auscultation findings in ASD
The classical findings in ASD with a large left-to-right shunts and normal pulmonary artery pressure are fixed splitting of the 2nd heart sound and an ejection systolic murmur, best heard in the pulmonary area.
Fixed splitting of the 2nd hear sound is caused by increase pulmonary blood flow. The increased flow also explains the ejection systolic pulmonary murmur.
Complications of ASD
Atrial arrhythmia, in particular atrial fibrillation are common.
Pulmonary hypertension may develop and reversal of the shunt to a right to left shunt when right sided pressures exceed those on the left (Eisenmenger syndrome). This may be associated with cyanosis, signs of pulmonary hypertension. However in this situation there is no fixed splitting of the 2nd heart sound. This is an uncommon complication and only seen in ASDs that are not repaired.
Stroke due to paradoxical embolisation may occur. In this situation a venous clot migrates to the right atrium and in the presence of a right to left shunt may migrate to the left side and embolise to the brain and other systemic locations.
Aetiology of VSD
Usually congenital.
Ruptured myocardial infarct.
PE findings in VSD
Thrill, usually lower sternal edge.
Holosystolic/pansystolic murmur maximal at lower sternal edge (often louder with smaller defects).
S3/S4.
Softer with Valsalva.
Associated with mitral regurgitation, Down’s syndrome, Tetralogy.
Auscultation findings in VSD
A murmur was audible and maximal at the left lower sternal edge
The loudness of the murmur is inversely proportional to the size of the VSD.
Small VSDs cause a loud high-frequency systolic murmur, often accompanied by a palpable thrill in the third or fourth left intercostal space.
Large VSDs are often associated with softer murmurs.
The VSD murmur is typically holosystolic and maximal at the left lower sternal edge.
Complication of VSD
Small VSDs are usually asymptomatic.
Pulmonary hypertension and Eisenmenger syndrome may develop in large VSDs.
Once Eisenmenger syndrome develops, the patient may be cyanosed and develop signs of tricuspid regurgitation. There may also be a midsystolic pulmonary ejection murmur associated with severe pulmonary hypertension and often a diastolic decrescendo murmur from pulmonary valve regurgitation (Graham Steele murmur).
Common cause of Pulmonary Regurgitation
Pulmonary hypertension (Graham Steel).
Residual post Tetralogy of Fallot repair.
Absent pulmonary valve.
Common PE in pulmonary regurgitation
Decrescendo diastolic best heard in pulmonary area & increases with inspiration.
In pulmonary hypertension murmur often loud, high pitched, blowing.
In repaired Tetralogy maybe low pitched & soft.
P2 loud in presence of pulmonary hypertension.
What are the other causes of reversed splitting of the second heart sound?
Left bundle branch block
Hypertrophic obstructive cardiomyopathy
Patent ductus arteriosus
Wolf-Parkinson-White Syndrome (type B)
What other conditions could give a mid-diastolic rumbling murmur?
Left atrial mass (typically myxomas)
Left atrial thrombus
Cor triatriatum (3 atria)
Severe mitral regurgitation (increased forward flow across the mitral valve)
Complications of Mitral Stenosis
Left atrial enlargement Atrial fibrillation Left atrial thrombus formation Pulmonary hypertension Pulmonary oedema Right heart failure
What is the pathology underlying the malar flush in Mitral Stenosis?
Development of severe pulmonary hypertension, leading to a low cardiac output state
DD of malar flush?
Mitral stenosis Hypothyroidism Cold weather Carcinoid syndrome SLE Systemic sclerosis Irradiation Polycythaemia
Indication for surgery in Mitral Stenosis?
Pulmonary congestion
Pulmonary hypertension
Haemoptysis
Recurrent thromboembolic events despite therapeutic anticoagulation with warfarin (MS patients were excluded in DOAC trials, so no evidence with DOAC)
Complication of prosthetic valve
Thromboembolism
Complications of anticoagulation ie bleeding
Vlave dysfunction ie leakage, dehiscence and obstruction due to thrombosis, fibrosis and clogging
Endocarditis
Haemolysis
Indications for mitral valve replacement in Mitral Regurgitation?
Signs of left ventricular dysfunction
Ejection fraction <=60% (even in the absence of symptoms)
Left ventricular end-systolic diameter >=45mm (even in the absence of symptoms)
Auscultation findings of Prosthetic Mitral Valve?
Prosthetic clicks
Prosthetic (closing) click at the first heart sound
Flow murmur can be heard (short low-frequency mid-diastolic murmur at the apex, best heard in expiration in the left lateral position using the bell)
If with mitral regurgitation: pansystolic murmur at the lower left sternal edge, louder in expiration
Auscultation findings of Prosthetic Aortic Valve
Prosthetic click
Normal first heart sound, an ejection systolic murmur and a prosthetic (closing) click at the second heart sound
Causes of clubbing
COMMON:
CV: cyanotic congenital heart disease, infective endocarditis
Resp: lung ca (NOT small cell ca), chronic pulmonary suppuration (bronchiectasis, lung abscess, empyema), idiopathic pulmonary fibrosis
UNCOMMON:
Resp: cystic fibrosis, asbestosis, pleural mesothelioma/pleural fibroma
GI: cirrhosis (esp billiary cirrhosis), inflammatory bowel disease, coeliac disease
Thyrotoxicosis: familial/idiopathic
RARE:
neurogenic diaphragmatic tumours
pregnancy
secondary parathyroidism
UNILATERAL CLUBBING:
bronchial arteriovenous aneurysm
axillary artery aneurysm
Characteristic of apex beat and clinical findings
Pressure loaded: aortic stenosis/hypertension
Volume loaded: advanced MR or dilated cardiomyopathy
Dyskinetic: left ventricular dysfunction
Double impulse: hypertrophic cardiomyopathy
Tapping: mitral or (rarely) tricuspid stenosis
Causes of Left ventricular S3 louder at the apex than at left sternal edge, louder on expiration
Pregnancy Thyrotoxicosis Left ventricular failure and dilatation Aortic regurgitation Mitral regurgitation Ventricular septal defect Patent ductus arteriosus
Causes of right ventricular S3 lauder at left sternal edge and with inspiration
Right ventricular failure
Constrictive pericarditis
Causes of left ventricular S4
Aortic stenosis Acute mitral regurgitation Systemic hypertension Ischaemic heart disease Advanced age
Causes of right ventricular S4
Pulmonary hypertension
Pulmonary stenosis
