Cardiovascular 2 Flashcards
what is the pathophysiology of aortic dissection?
- aortic dissection begins with a tear in the intimal lining of the aorta
- the tear allows a column of blood under pressure to enter the aortic wall, forming a haemotoma which separates the intima from the adventitia and creates a false lumen
- the false lumen extends for a variable distance in either direction; anterograde (towards bifurcations) and retrograde (towards the aortic root)
what is the clinical presentation of aortic dissection?
- sudden onset of severe, tearing and central chest pain that radiates to the back and down the arms
- pain described as tearing in nature and may be migratory
- hypertension
- unequal BP in the arms
- pain is maximal from the time of onset, unlike in MI where the pain gains in intensity
- patients may be shocked and may have neurological symptoms secondary to loss of blood supply to the spinal cord
- peripheral pulses may be absent
what can aortic dissection develop into?
- may develop aortic regurgitation, coronary ischaemia and cardiac tamponade
- distal extension may produce acute kidney failure, acute lower limb ischaemia or visceral ischaemia
what are differential diagnoses of aortic dissection?
- acute coronary syndrome
- MI
- aortic regurgitation without dissection
- MSK pain
- pericarditis
- cholecystitis
- atherosclerotic embolism
how is aortic dissection diagnosed?
CXR:
• widened mediastinum
urgent CT scan, transoesophageal echocardiography or MRI will confirm diagnosis
what is the treatment of aortic dissection?
- at least 50% are hypertensive and may require urgent antihypertensive medication to reduce blood pressure to less than 120mmHg - give IV beta-blockers or vasodilators
- adequate analgesia
- surgery to replace aortic arch
- endovascular intervention with stents
- patients require long term follow-up with CT or MRI
what is peripheral vascular disease? what is its epidemiology?
- partial blockage of leg or peripheral vessels by an atherosclerotic plaque/resulting thrombus resulting in insufficient perfusion of the lower limb resulting in lower limb ischaemia
- commonly caused by atherosclerosis and usually affects the aorta-iliac and infra-inguinal arteries
- more common in men than women
what are risk factors for peripheral vascular disease?
- smoking
- diabetes
- hypercholesterolaemia
- hypertension
- physical inactivity
- obesity
what are features of intermittent claudication?
- this is a cramping pain that is induced by exercise and relieved by rest
- pain is distal to site of atheroma
- occurs when anaerobic metabolism comes into effect when O2 demand outstrips supply
- pain is the result of lactic acid production
- caused by inadequate blood supply to the affected muscles resulting in moderate ischaemia
- most commonly seen in the calf and leg muscles as a result of atheroma of the leg arteries
- leg pulses are often absent and the feet may be cold
what are features of critical limb ischaemia in moderate ischaemia/PVD?
• blood supply is barely adequate to allow basal
metabolism
• no reserve available for increased demand
• rest pain that is typically nocturnal
• risk of gangrene and/or infection
• chronic condition and the most severe clinical manifestation of peripheral vascular disease
what are general symptoms of chronic lower limb ischaemia?
- absent femoral, popliteal or foot pulses
* cold, white legs
what are differential diagnoses of chronic lower limb ischaemia?
- osteoarthritis of hip/knee due to knee pain at rest
* peripheral neuropathy
how is chronic lower limb ischaemia diagnosed?
- exclude arteritis by looking at ESR/CRP; they would be raised in arteritis
- FBC: looking particularly at haemoglobin to exclude anaemia or polycthaemia
- ECG to look for cardiac ischaemia
- severity of disease is indicated by the ankle/brachial pressure index (ABPI)
- colour duplex ultrasound; first line test
- MR/CT angiography to assess extent and location of stenoses and quality of distal vessels if considering intervention
what is the ankle/brachial pressure index (ABPI)? what are the values of intermittend claudication and critical leg ischaemia?
- measurement of the cuff pressure at which blood flow is detectable by Doppler in the posterior tibial or anterior tibial arteries compared to the brachial artery
- intermittent claudication associated with an ABPI of 0.5-0.9
- values less than 0.5 are associated with critical leg ischaemia
what are the symptoms of acute lower limb ischaemia?
- Pain
- Pallor
- Perishing cold
- Pulseless
- Paralysis
- Paraesthesia - abnormal tingling or prickling
- the more P’s present the more sudden and the more complete
what is done for risk factor modification for peripheral vascular disease?
- smoking cessation - since every time you smoke, small vessels in the muscles near to ischaemia that provide ‘back up supply’ contract in response to nicotine and tobacco resulting in a reduction in blood flow
- treat hypertension, hyperlipidaemia and diabetes
- antiplatelet agent such as P2Y12 inhibitor to prevent progression and minimise risk
- exercise and weight loss
how is revascularisation done for peripheral vascular disease?
- percutaneous transluminal angioplasty: essentially squash plaque and thus increase perfusion and reduce ischaemia
- bypass procedure
- amputation if severe
what is the treatment of acute ischaemia in peripheral vascular disease?
- surgical emergency requiring revascularisation within 4-6hrs to save limb
- this is an emergency and requires urgent surgery and angioplasty
- intra-arterial thrombolysis
- surgical removal of embolus if present
what are clinical symptoms and sings linked to diagnosis of critical/acute ischaemia?
- severe nocturnal pain in all toes of the left foot only relieved by hanging foot over the edge of bed (using gravity to perfuse) = critical ischaemia
- acute MI = acute ischaemia
- loss of the use of right side of body and fast irregular pulse = acute ischaemia
- non-healing painful ulcer on big toe with no trauma = critical ischaemia
what is the definition of shock?
term used to describe acute circulatory failure with inadequate or inappropriately distributed tissue perfusion (inadequate substrate for aerobic cellular respiration), resulting in generalised hypoxia and/or an inability of the cells to utilise oxygen
what is clinical presentation of shock?
- skin is pale, cold, sweaty and vasoconstricted
- pulse is weak and rapid
- pulse pressure reduced
- mean arterial pressure may be maintained
- arterial BP is not a good indicator of shock since it will be maintained until a very large amount of blood loss occurs
- reduced urine output
- confusion, weakness, collapse and coma
what is the earliest and most accurate sign of shock?
capillary refill time taking more than 3 seconds to turn pink after 5 seconds of compression
what are causes of shock?
- hypovolaemic shock
- cardiogenic shock
- distributive shock:
• septic shock
• anaphylactic shock
• neurogenic shock - anaemic shock
- cytotoxic shock
what are types of distributive shock?
septic, anaphylactic and neurogenic shock
what can cause loss of blood in hypovolaemic shock?
- acute GI bleeding
- trauma
- peri/post-operative
- splenic rupture
what can cause loss of fluid in hypovolaemic shock?
- dehydration - diarrhoea and vomiting
- burns - heat damage increases the permeability of capillaries so plasma leaks
- pancreatitis
what are causes of cardiogenic shock?
heart doesn’t pump
• cardiac tamponade - blood in pericardial sack placing pressure on heart thereby limiting cardiac output
• pulmonary embolism - flow of blood to lungs is blocked
• acute MI
• fluid overload
• myocarditis
what are causes of septic shock?
shock when an infection becomes out of control
• referred to as a distributive shock
• sepsis exists when a systemic inflammatory response is associated with an infection
• septic shock exists when sepsis is complicated by persistent hypotension that is unresponsive to fluid resuscitation
what are causes of anaphylactic shock?
release of IgE due to allergic response
• intense allergic reaction
• massive release of histamine and other vasoactive mediators causing haemodynamic collapse
• accompanied by breathlessness and wheeze (due to bronchospasm)
what is used to classify haemorrhagic shock?
Tennis score
what are features of class I haemorrhagic shock (Tennis score)?
- 15% blood loss
- pulse below 100 bpm
- BP normal
- pulse pressure normal
- resp rate; 14-20
- urine output greater than 30ml/hr
- slightly anxious
what are features of class II haemorrhagic shock (Tennis score)?
- 15-30% blood loss
- tachycardia
- BP normal due to autonomic response (increased sympathetic activity)
- pulse pressure decreased
- resp rate; 20-30
- urine output: 20-30ml/hr
- mental status: mildly anxious
what are features of class III haemorrhagic shock (Tennis score)?
- 30-40% blood loss
- pulse above 120 bpm
- BP decreased
- pulse pressure decreased
- resp rate; 30-40
- urine output: 5-15ml/hr
- mental status: confused
what is the pathophysiology of haemorrhagic shock?
- reduction in ventricular filling -> fall in BP and SV -> hypotension
- leads to reduced stimulation of baroreceptors -> increased sympathetic activity with release of noradrenaline and adrenaline
- vasoconstriction and increased contractility and heart rate helps restore BP and CO
- reduced capillary BP -> greater level of net movement of fluid into vascular compartment
- renin release -> Na and water retention
- angiotensin II causes thirst
- ADH release
- release of cortisol causes fluid retention
- release of glucagon raises blood sugar levels
what is the clinical presentation of hypovolaemic shock?
• inadequate tissue perfusion: - skin: cold, pale, clammy, slate-grey, - brain: drowsiness and confusion • increased sympathetic tone • tachycardia - narrow pulse pressure and weak pulse • sweating • BP may be maintained initially but later hypotension • bradycardia
what is the clinical presentation of cardiogenic shock?
- signs of myocardial failure
- raised jugular venous pressure (JVP)
- gallop rhythm
- basal crackles and pulmonary oedema
what is the clinical presentation of septic shock?
- pyrexia and rigors
- nausea and vomiting
- vasodilation with warm peripheries
- bounding pulse
what is the clinical presentation of anaphylactic shock?
- signs of profound vasodilation
- warm peripheries
- low BP
- tachycardia
- bronchospasm
- pulmonary oedema
what are organ systems at risk of shock? how are they affected?
- kidneys; acute tubular necrosis
- lung; Acute Respiratory Distress Syndrome (ARDs)
- heart; myocardial ischaemia and infarction
- brain; confusion, irritability and coma
what is treatment of shock?
A: airway (ensure patency)
B: breathing (give 100% O2) and correct immediately life threatening problems such as:
- congestive cardiac failure
- bronchospasm
- tension pneumothorax
C: circulation
- establish secure IV access
- give fluid quickly and blood if acute blood loss
- ensure haemostasis i.e. stop bleeding
what is acute respiratory distress syndrome?
- Impaired oxygenation
- bilateral pulmonary infiltrates
- no cardiac failure
- normal pulmonary arterial pressure (PAOP)
what are extrapulmonary causes of acute respiratory distress syndrome?
- shock of any cause
- head injury
- drug reaction
- sepsis
what are pulmonary causes of acute respiratory distress syndrome?
- pneumonia
- chemical pneumonitis
- smoke inhalation
- near drowning
what is the pathophysiology of acute respiratory distress syndrome?
- alveolar capillary membrane injury results in leakage of fluid into the alveolar spaces
- there is resulting neutrophil invasion which attracts more neutrophils (exudative phase)
- eventually fibroblasts come in and initiate healing (proliferative phase)
- and make scar tissue (fibrotic phase)
- results in severely stiff lungs and thus severe difficulty in ventilation and thus reduced O2 blood perfusion
what is the clinical presentation of acute respiratory distress syndrome?
- cyanosis
- tachypnoea
- tachycardia
- peripheral vasodilation
what is mitral stenosis?
- obstruction and narrowing of left ventricle inflow that prevents proper filling during diastole
- mitral valve has 2 cusps
what are the causes/epidemiology of mitral valve stenosis?
- normal mitral valve area is 4-6cm2, symptoms begin at areas less than 2cm2
- most common cause of mitral stenosis is rheumatic heart disease secondary to rheumatic fever
- the condition is more common in men than women
- prevalence and incidence is decreasing due to a reduction of rheumatic heart disease
what is the most common cause of mitral valve stenosis?
most common cause of mitral stenosis is rheumatic heart disease secondary to rheumatic fever due to infection with group A beta-haemolytic streptococcus e.g. Streptococcus pyogenes
how does rheumatic fever cause mitral valve stenosis? how does the condition progress?
- inflammation due to rheumatic fever leads to commissural fusion and a reduction in mitral valve orifice area, causing the characteristic doming
pattern seen on echocardiography - over many years, the condition progresses to valve thickening, cusp fusion, calcium deposition, a severely narrowed (stenotic) valve orifice and progressive immobility of the valve cusps
what are causes of mitral valve stenosis other than rheumatic fever/disease?
- infective endocarditis (3.3%)
- mitral annular calcification (2.7%) - rarely leads to mitral stenosis if extensive, particularly in elderly patients and those with end-stage renal disease
what are risk factors for mitral valve stenosis?
- history of rheumatic fever
- untreated streptococcus infections
what is the pathophysiology of mitral valve stenosis?
- thickening and immobility of the valve leads to obstruction of blood flow from the left atrium to the left ventricle
- for cardiac output to be maintained, the left atrial pressure increases and left atrial hypertrophy and dilatation occur
- pulmonary venous, pulmonary arterial and right heart pressures increase
- the increase in pulmonary capillary pressure leads to development of pulmonary oedema; seen particularly when atrial fibrillation occurs, due to the elevation of left atrial pressure and dilatation, with tachycardia and loss of coordinated atrial contraction
- partially countered by alveolar and capillary thickening and pulmonary arterial vasoconstriction
- pulmonary vasoconstriction leads to pulmonary hypertension and eventually right ventricular hypertrophy, dilatation and failure with subsequent tricuspid regurgitation
what is the clinical presentation of mitral valve stenosis?
- no symptoms until the valve orifice is moderately stenosed i.e. area is less than 2cm2
- usually doesn’t occur until several decades after the first attack of rheumatic fever
- progressive exertional dyspnoea
- haemoptysis
- atrial fibrillation leading to PE and abrupt deterioration
- pulmonary hypertension leading to right heart failure with fatigue and lower limb oedema
- systemic emboli
- prominent “a” wave in jugular venous pulsations
- mitral facies/malar flush
why does progressive dyspnoea occur in mitral valve stenosis?
due to left atrial dilation resulting in pulmonary
congestion (reduced emptying), which is worse with exercise, fever, tachycardia and pregnancy
why does haemoptysis occur in mitral valve stenosis?
due to rupture of bronchial vessels due to the elevated
pulmonary pressure
why does right heart failure occur in mitral valve stenosis?
due to the development of pulmonary hypertension with symptoms of weakness, fatigue and abdominal or lower limb swelling
why does atrial fibrillation occur in mitral valve stenosis?
due to left atrium dilation giving rise to palpitations
why do systemic emboli occur in mitral valve stenosis?
due to atrial fibrillation, most commonly in the cerebral
vessels
why does the prominent a wave in jugular venous pulsations occur in mitral valve stenosis?
due to pulmonary hypertension and right ventricular hypertrophy
why does mitral facies/malar flush occur in mitral valve stenosis?
bilateral, cyanotic or dusky pink discolouration over the upper cheeks; pinkish-purple patches on the cheeks due to vasoconstriction in response to diminished cardiac output
what heart sounds are heard in mitral valve stenosis on auscultation?
- diastolic murmur
- loud opening S1 snap
- the apex beat is ‘tapping’ in quality due to combination of a palpable first heart sound and left ventricular backward displacement produced by an enlarging right ventricle.
- auscultation at the apex reveals a loud first heart sound, an opening snap (when the mitral valve opens) in early diastole, followed by a rumbling mid-diastolic murmur. If the patient is in sinus rhythm the murmur becomes louder when atrial systole occurs (presystolic accentuation), as a result of increased flow across the narrowed valve.
when is the mitral valve stenosis murmur heard?
- heard when blood flows over a valve
- low-pitched diastolic rumble most prominent at the apex
- heard best with patient lying on the left side in held expiration
when is a loud opening S1 snap heard in mitral valve stenosis?
- heard at apex when leaflets are still mobile
- due to the abrupt halt in leaflet motion in early diastole, after a rapid initial opening, due to fusion at the leaflet tips
- as the valve cusps become more immobile, the loud first heart sound softens and the opening snap disappears
how is mitral valve stenosis diagnosed by CXR, ECG and echocardiogram?
CXR: • left atrial enlargement • pulmonary venous hypertension • pulmonary oedema/congestion in severe disease • occasionally calcified mitral valve
ECG:
• atrial fibrillation
• left atrial hypertrophy -> bifid P wave (P mitrale)
• features of right ventricular hypertrophy in progressive disease
Echocardiogram:
• gold standard for diagnosis, assesses severity
• assess mitral valve mobility, gradient and mitral valve area
• valve area of <2cm2 indicates moderate stenosis, <1cm2 severe
what is the treatment of mitral valve stenosis?
- mitral stenosis is a mechanical problem and medical therapy does not prevent progression
- beta-blockers and digoxin which control heart rate (for AF) and thus prolong diastole for improved diastolic filling
- diuretics for fluid overload
- anticoagulation in patients with AF to prevent clot formation and embolisation
- percutaneous mitral balloon valvotomy
- mitral valve replacement
what is done in percutaneous mitral balloon valvotomy as treatment for mitral valve stenosis?
- catheter is inserted into the right atrium via the femoral vein under local anaesthesia
- the interatrial septum is punctured and the catheter advanced into the left atrium and across the mitral valve
- the balloon is inflated and puts pressure on valve thereby separating the leaflets and increasing the size of the mitral valve opening, enabling more blood to flow from left atrium into left ventricle
what is mitral regurgitation? why does it occur?
• backflow of blood from the left ventricle to the left atrium during systole
• mild physiological mitral regurgitation (MR) is seen in 80% of normal individuals
- occurs due to abnormalities of the valve leaflets, chordae tendinae, papillary muscles or left ventricle
what is the most frequent cause of mitral regurgitation?
most frequent cause is myxomatous degeneration (MVP) (weakening of the chordae tendinae) resulting in a floppy mitral valve that prolapses
what are other causes of mitral regurgitation?
- ischaemic mitral valve
- rheumatic heart disease
- infective endocarditis
- papillary muscle dysfunction/rupture
- dilated cardiomyopathy
- ruptured chordae tendineae
- dilating left ventricle disease causing functional mitral regurgitation
- hypertrophic cardiomyopathy
- rarely: systemic lupus erythematosus, Marfan’s syndrome
- Ehlers-Danlos syndrome
what are risk factors for mitral regurgitation?
- associated with females
- lower BMI
- advanced age
- renal dysfunction
- prior MI
what is the pathophysiology of mitral regurgitation?
- regurgitation into the left atrium produces left atrial dilatation but little increase in left atrial pressure if the regurgitation is longstanding, since the regurgitant flow is compensated for by the large left atrium
- pure volume overload due to leakage of blood into left atrium during systole
- circulatory changes depend on the speed of onset and severity of regurgitation
- with acute mitral regurgitation there is a rise in left atrial pressure, resulting in an increase in pulmonary venous pressure and pulmonary oedema
- left ventricle dilates, but more so with chronic regurgitation
what are compensatory mechanisms for mitral valve regurgitation? what do they lead to?
left arterial enlargement, left ventricle hypertrophy (since left ventricle must put in same effort to pump less blood due to regurgitation so needs to pump harder to maintain cardiac output and thus hypertrophy occurs to increase stroke volume) and increases contractility:
- progressive left atrial dilatation and right ventricular dysfunction due to pulmonary hypertension
- progressive left ventricular volume overload leads to dilatation and progressive heart failure
what is the clinical presentation of mitral valve regurgitation on auscultation?
- soft S1 and a pansystolic murmur (palpated as a thrill) loudest at the apex radiating over the precordium and into the axilla
- prominent third extra heart sound (S3) in congestive heart failure/left atrium overload, caused by rapid filling of the dilated left ventricle in early diastole
- in chronic mitral regurgitation, the intensity of the murmur does not correlate with the severity
what is the clinical presentation of mitral valve regurgitation?
- exertion dysponea i.e. exercise intolerant
- dysponea develops because of pulmonary venous hypertension that arises as a direct result of the mitral regurgitation and secondarily as a consequence of left ventricular failure
- fatigue and lethargy due to reduced cardiac output
- increased stroke volume is felt as a palpitation
- symptoms of right heart failure and eventually lead to congestive cardiac failure
- heart failure may coincide with increased haemodynamic burden e.g in pregnancy, infection or atrial fibrillation
what is the prognosis of mitral valve regurgitation?
- compensatory phase: 10-15 years
- once patients ejection fraction becomes less than 60% and/or becomes symptomatic then mortality rises sharply
- severe mitral regurgitation has a 5%/year mortality rate
how is mitral valve regurgitation diagnosed?
ECG
• may show left atrial enlargement, atrial fibrillation and left ventricle hypertrophy in severe MR (seen late in course of disease)
• but not diagnostic
CXR:
• left atrial enlargement and central pulmonary artery enlargement
Echocardiogram:
• estimation of left atrium and left ventricle size and function
• also gives valve structure assessment
• transoesophageal is very helpful
• can establish the aetiology and haemodynamic consequences of mitral regurgitation
what medication is given for mitral valve regurgitation?
- vasodilators such as ACE-inhibitors
- heart rate control for atrial fibrillation with beta blockers, calcium channel blockers and digoxin
- anticoagulation in atrial fibrillation and flutter
- diuretics for fluid overload
what are indications for surgery for mitral valve regurgitation?
• symptomatic severe mitral regurgitation
- left ventricular fraction >30% and end-diastolic dimension of under 55mm
• asymptomatic:
- if ejection fraction is less than 60%
- left ventricular dysfunction (end systolic dimension >45mm and/or ejection fraction of under 60%)
- if new onset, atrial fibrillation, pulmonary hypertension
what is aortic stenosis?
narrowing of the aortic valve resulting in obstruction to the left ventricular stroke volume, leading to symptoms of chest pain, breathlessness, syncope and fatigue
what is the epidemiology of aortic stenosis?
- normal aortic valve area is 3-4cm2
- symptoms occur when valve area is 1/4th of normal area
- primarily a disease of ageing
- congenital is the second most common cause
- the most common type of valvular disease in the western world
what are the types of aortic stenosis?
- supravalvular e.g congenital fibrous diaphragm above the aortic valve
- subvalvular e.g congenital condition in which a fibrous ridge or diaphragm is situated immediately below the aortic valve
- valvular; most common
what are the 3 main causes of aortic stenosis?
- calcific aortic valvular disease (CAVD) - essentially calcification and degeneration of the aortic valve resulting in stenosis, most commonly seen in elderly
- calcification of a congenital bicuspid aortic valve (BAV) (valve has 2 leaflets instead of 3 due to genetic disease; this is the most common congenital heart disease) resulting in stenosis
- rheumatic heart disease; rare now due to eradication
what are risk factors for aortic stenosis?
- congenital bicuspid aortic valve (BAV) predisposes to stenosis and regurgitation
- congenital BAV is predominant in males
what is the pathophysiology of aortic stenosis?
- due to narrowing there is obstructed left ventricular emptying and a pressure gradient develops between the left ventricle and the aorta resulting in increased afterload
- results in increased left ventricular pressure and compensatory left ventricular hypertrophy
- this results in relative ischaemia of the left ventricular myocardium (since hypertrophy results in increased blood demand), and consequent angina, arrhythmias and left ventricular failure
- left ventricular systolic function is typically preserved in aortic stenosis
- the obstruction to left ventricular emptying is relatively more severe on exercise; since exercise causes a many-fold increase in cardiac output, however due to severe narrowing of the aortic valve, the cardiac output can hardly increase; thus, the blood pressure falls, coronary ischaemia worsens, the myocardium fails and cardiac arrhythmias develop
- when this compensatory mechanism is exhausted left ventricular function declines rapidly
what is the clinical presentation of aortic stenosis?
- think aortic stenosis in any elderly person with chest pain, exertional dysponea or syncope
- classic triad
- sudden death
- slow rising carotid pulse (pulsus tardus) and decreased pulse amplitude (pulsus parvus)
- heart sounds
what is the classic triad of aortic stenosis?
- syncope - usually exertional
- angina (increases myocardial oxygen demand; with resulting demand/supply mismatch)
- heart failure (usually after 60)
- dysponea on exertion due to heart failure
what heart sounds are heard in aortic stenosis?
- soft or absent second heart sound when the valve becomes immobile
- carotid pulse is slow rising (plateau pulse) and the apex beat thrusting
- harsh systolic ejection murmur (palpated as a thrill) at the right upper sternal border and radiating to the carotids
- prominent 4th (S4) heart sound due to left ventricular hypertrophy
- ejection systolic murmur crescendo-decrescendo character
- loudness does not tell you anything about severity
what are differential diagnoses are there for aortic stenosis?
- aortic regurgitation
- subacute bacterial endocarditis
how is aortic stenosis diagnosed through echocardiogram, ECG and CXR?
Echocardiogram:
• two measurements obtained are:
- left ventricular size and function; left ventricular hypertrophy, dilation and ejection fraction
- doppler derived gradient and valve area (AVA), allows for the assessment of the pressure gradient across the valve during systole
ECG:
• left ventricular hypertrophy
• left atrial delay
• left ventricular ‘strain’ pattern due to ‘pressure overload’ - depressed ST segments and T-wave inversion in leads orientated towards left ventricle i.e. I, AVL, V5 and 6 when disease is severe
CXR:
• left ventricular hypertrophy
• calcified aortic valve
• normal heart size, prominence of the ascending aorta
what is treatment of aortic stenosis?
- rigorous dental hygiene/care due to the increased risk of infective endocarditis (IE) in anyone with valvular heart disease; consider IE prophylaxis in dental procedures
- limited role for medication due to the fact that aortic stenosis is a mechanical problem
- vasodilators are contraindicated in severe aortic stenosis because they may trigger hypotension and thus syncope
- surgical aortic valve replacement (definitive treatment)
- TAVI
what is the definitive treatment for aortic stenosis?
surgical aortic valve replacement
what are indications for surgical aortic valve replacement for aortic stenosis?
- any symptomatic patients with severe aortic stenosis
- any patient with decreasing ejection fraction
- any patent undergoing CABG with moderate or severe aortic stenosis
what is involved in TAVI for aortic stenosis?
Transcutaneous Aortic Valve Implantation
• minimally invasive
• pass catheter up the aorta then inflate balloon across the narrowed valve which will crack the calcification
• then pass another catheter which leaves a stent with a valve = new aortic valve
what is aortic regurgitation?
- leakage of blood into the left ventricle from the aorta during diastole due to ineffective coaptation (bringing together) of the aortic cusps
- reflux of blood from the aorta through the aortic valve into the left ventricle during diastole
what is the epidemiology of aortic regurgitation? what are the main causes of it?
- can be associated with aortic stenosis
- main causes:
• congenital bicuspid aortic valve (BAV)
• rheumatic fever
• infective endocarditis
what are risk factors for aortic regurgitation?
- SLE
- Marfan’s and Ehlers-Danlos syndrome; connective tissue disorders
- aortic dilatation
- infective endocarditis or aortic dissection
what is the pathophysiology of aortic regurgitation?
- if net cardiac output is to be maintained, the total volume of blood pumped into the aorta must increase and the left ventricular size must enlarge -> left ventricle dilatation and hypertrophy
- progressive dilation leads to heart failure
- the remaining blood in the root of the aorta supplies the coronary arteries via the coronary sinus during diastole; regurgitation causes diastolic blood pressure to fall and thus coronary perfusion decreases
- the large left ventricular size is mechanically less efficient, so demand for oxygen is greater and cardiac ischaemia develops
- stroke volume increases, leading to increased pulse pressure
- contraction of the ventricle deteriorates -> left ventricular failure
- adaptation to volume load entering left ventricle don’t occur with acute regurgitation, leading to pulmonary oedema and reduced stroke volume
what is the clinical presentation of aortic regurgitation?
- in chronic regurgitation, patients remain asymptomatic for many years before symptoms develop
- exertional dysponea
- palpitations
- angina
- syncope
- wide pulse pressure
- apex beat displaced laterally
- collapsing water hammer pulse (bounding and forceful, rapidly increasing and subsequently collapsing)
- Quincke’s sign - capillary pulsation in the nail beds
- de Musset’s sign - head nodding with each heart beat
- pistol shot femoral - a sharp bang heard on auscultation
what heart sounds are heard in aortic regurgitation?
- early diastolic blowing murmur at the left sternal border in the 4th intercostal space; accentuated when patient sits forward with breath held in expiration
- ejection systolic murmur; due to increased stoke volume leading to turbulent flow across the aortic valve
- Austin Flint murmur: mid-diastolic murmur over the cardiac apex produced due to aortic jet impinging on the mitral valve, producing premature closure of the valve and physiological stenosis
what is collapsing water hammer pulse?
- bounding and forceful pulse rapidly increasing and subsequently collapsing
- seen in aortic regurgitation
what is Quincke’s sign?
- capillary perfusion in the nail beds
- seen in aortic regurgitation
what is de Musset’s sign?
- head nodding with each heart beat
- seen in aortic regurgitation
what is pistol shot femoral?
- a sharp bang heard on auscultation
- seen in aortic regurgitation
what are differential diagnoeses of aortic regurgitation?
- heart failure
- infective endocarditis
- mitral regurgitation
how is aortic regurgitation diagnosed with CXR, echocardiogram and ECG?
echocardiogram:
• evaluation of the aortic valve and aortic root
• measurement of left ventricle dimensions and function
• cornerstone for decision making and follow up evaluation
CXR:
• enlarged cardiac silhouette and aortic root enlargement
• left ventricular enlargement
ECG:
• signs of left ventricular hypertrophy due to ‘volume overload’ - tall R waves and deeply inverted T waves in left-sided chest leads, and deep S waves in right-sided leads
what is treatment of aortic regurgitation?
- in general consider infective endocarditis prophylaxis
- vasodilators and diuretics e.g ACE-inhibitors e.g. Ramipril will improve stroke volume and reduce afterload and regurgitation but only if patient is symptomatic or has hypertension
- serial echocardiograms to monitor progression
- surgery for valve replacement:
• if symptoms are increasing, enlarging heart on CXR/ECHO, ECG
deterioration (T wave inversion in lateral leads)
what is infective endocarditis?
- an infection of the endocardium or vascular endothelium of the heart
- known as subacute bacterial endocarditis (SBE)
- may occur as a fulminating or acute infection
where in the heart does infection of endocarditis occur on?
- valves with congenital or acquired defects (usually on the left side of the heart)
- right sided endocarditis more common in IV drug addicts
- normal valves with virulent organisms
- prosthetic valves and pacemakers
- in association with a ventricular septal defect or persistent ductus arteriosus
what is the epidemiology of infective endocarditis?
- more common in developing countries
- disease of:
• the elderly or those with prosthetic valves
• the young IV drug user
• the young with congenital heart disease - more common in males
what organisms cause infective endocarditis?
- Staphylococcus aureus (IVDU, diabetes and surgery); most common cause
- Pseudomonas aeruginosa
- Streptococcus viridans (dental problems); gram positive, alpha haemolytic and optochin resistant (Strep. mutans, strep, sanguis, strep. milleri and strep. oralis)
- enterococci
- Coxiella burnetii, Chlamydia spp., Bartonella spp. and Legionella
what are risk factors for infective endocarditis?
- IV drug use
- poor dental hygiene
- skin and soft tissue infection
- dental treatment
- IV cannula
- cardiac surgery
- pacemaker
what is the pathophysiology of infective endocaditis?
- a mass of fibrin, platelets and infectious organisms form vegetations along the edges of the valve
- damaged endocardium promotes platelet and fibrin deposition, which allows organisms to adhere and grow, leading to an infected vegetation
- aortic and mitral valves are most commonly involved; IV drug users are the exception since right-sided lesions are more common in them
- virulent organisms destroy the valve they are on, leading to regurgitation and worsening heart failure
what are things that would raise high clinical suspicion of infective endocarditis?
• new valve lesion/regurgitant murmur
• embolic events of unknown origin
• sepsis of unknown origin
• haematuria, glomerulonephritis and suspected renal infarction
• fever plus:
- prosthetic material inside the heart
- risk factor for infective endocarditis e.g. IV drug user
- newly developed ventricular arrhythmias or conduction disturbances
what are clinical presentations of infective endocarditis?
- headache, fever, malaise, confusion, and night sweats
- finger clubbing
- if Staphylococcus aureus, then will develop very quickly; high fever and feel ill rapidly, with the other virulent ones you don’t feel as ill
- embolisation of vegetations e.g. stroke, pulmonary embolus, bone infections, kidney dysfunction and myocardial infarction
- valve dysfunction results in in arrhythmia and heart failure
- endocarditis should be excluded in any patient with a heart murmur and fever
what are clinical manifestations of infective endocarditis?
- splinter haemorrhages on nail beds of fingers
- embolic skin lesions; black spots on skin (infarcts caused by bits of infective vegetation blocking small capillaries)
- Osler nodes; tender nodules in the digits
- Janeway lesions; haemorrhages and nodules in the fingers
- Roth spots; retinal haemorrhages with white or clear centres seen on fundoscopy
- Petechiae; small red/purple spots caused by bleeds in the skin
what are embolic skin lesions?
black spots on skin (infarcts caused by bits of infective vegetation blocking small capillaries)
- seen in infective endocarditis
what are Osler nodes?
painful, red, raised lesions found on the hands and feet
- seen in infective endocarditis
what are Janeway lesions?
rare, non-tender, small erythematous or haemorrhagic macular, papular or nodular lesions on the palms or soles only a few millimeters in diameter
- seen in infective endocarditis
what are Roth spots?
retinal haemorrhages with white or clear centres seen on fundoscopy
- seen in infective endocarditis
what are petechiae?
small red/purple spots caused by bleeds in the skin
- seen in infective endocarditis
how is infective endocarditis diagnosed?
- use Dukes criteria
- blood cultures and tests
- urinalysis (look for haematuria)
- CXR: cardiomegaly, heart failure or septic emboli in right-sided endocarditis
- ECG: long PR interval at regular intervals (may show MI or conduction defects)
- echocardiogram
- serum immunoglobulins are increased and complement levels are decreased due to immune complex formation
what is looked for in blood cultures when diagnosing infective endocarditis?
- 3 sets from different sites over 24 hours
- take before starting antibiotics
- identifies in 75% of cases
what is looked for in blood tests when diagnosing infective endocarditis?
- CRP and ESR raised
- normochromic, normocytic anaemia
- neutrophilia
what types of echocardiogram are used in diagnosing infective endocarditis?
- transthoracic echo (TTE)
- tranoesophageal echo (TOE)
how is transthorachic echo used to diagnose infective endocarditis?
- safe, non invasive, no discomfort but often poor images so low sensitivity but can identify vegetations
(if greater than 2mm); a negative TTE does not exclude the diagnosis of infective endocarditis - identifies vegetations and underlying valvular dysfunction
- smaller vegetations may be missed
how is transoesophageal echo used to diagnose infective endocarditis?
- more sensitive but very uncomfortable, is useful for visualising mitral lesions and possible development of aortic root abscess; better at diagnosing than TTE
- used in cases of suspected prosthetic valve endocarditis
what is the treatment of infective endocarditis?
- antibiotic treatment for 4-6 weeks
- if not staphylococcus then use penicillin, benzylpenicillin and gentamycin
- if staphylococcus then use vancomycin and rifampicin (if MRSA)
- treat complications
- surgery
- recommend good oral health and inform patients of symptoms
what are the complications of infective endocarditis?
arrhythmia, heart failure, heart block, embolisation, stroke rehab and abscess
how is surgery used to treat infective endocarditis?
- operate if the infection cannot be cured with antibiotics
- operate to remove infected devices
- operate to remove large vegetations before they embolise
what is the most common form of congenital heart disease?
bicuspid aortic valve (1-2% of live births)
what is the epidemiology of bicuspid aortic valve?
- most common form of congenital heart disease, occurring in 1-2% of live births
- more common in males than females
what occurs in bicuspid aortic valve?
- bicuspid aortic valve only has 2 cusps
- these can work well at birth and go undetected but can be severely stenotic in infancy or childhood
- degenerate quicker than normal valves
- become regurgitant earlier than normal valves
- are associated with coarctation and dilation of the ascending aorta
- may eventually develop aortic stenosis (requiring valve replacement) with or without aortic regurgitation thereby predisposing to infective endocarditis
- intense exercise may accelerate complications so do yearly echocardiograms on affected athletes
what is the epidemiology of atrial septal defects?
• often first diagnosed in adulthood and represents
one third of congenital heart disease
• more common in women than men
what are features of atrial septal defects?
• abnormal connection between the two atria
• a probe can be passed through the layers of the
foramen ovale (called the primum and secundum)
so is sometimes known as “Probe patent foramen
ovale”
• slightly higher pressure in the left atrium than the
right atrium
• shunt is left-to-right
• thus not blue i.e. acyanotic
• increased flow into the right heart and lungs
what can happen to untreated atrial septal defects?
if left untreated develop right heart overload and dilatation; the right ventricle is compliant and easily dilates to accommodate the increased pulmonary flow. this can result in:
- right ventricular hypertrophy
- pulmonary hypertension - Eisenmenger’s reaction
- increased risk of infective endocarditis
what is the clinical presentation of atrial septal defects?
- dysponea
- exercise intolerance
- may develop atrial arrhythmias from right atrial dilatation
- pulmonary flow murmur
- fixed split second heart sound (delayed closure of the pulmonary valve because more blood has to get out)
how can atrial septal defects be diagnosed?
CXR:
• large pulmonary arteries
• large heart
ECG:
• right bundle branch block (RBBB) due to right ventricle dilatation
echocardiogram:
• hypertrophy and dilation of right side of heart and pulmonary arteries
what are features of ventricular septal defects?
- abnormal connection between the two ventricles
- many close spontaneously during childhood
- common - 20% of all congenital heart defects
- higher pressure in left ventricle than right ventricle
- thus left-to-right shunt
- thus does not go blue i.e. acyanotic
- increased blood flow through the lung
what are some large defects in ventricular septal defects?
- the large volumes of blood flowing through the pulmonary vasculature lead to pulmonary hypertension and eventual Eisenmenger’s complex, when right ventricular pressure becomes higher than the left, as a result blood starts to shunt right-to-left resulting in cyanosis
- small breathless skinny baby
- increased respiratory rate
- tachycardia
- CXR: big heart
- murmur varies in intensity
what are some small defects in ventricular septal defects?
- large systolic murmur
- thrill (buzzing sensation)
- well grown
- normal heart rate
- normal heart size
what is treatment for ventricular septal defects?
- medical initially since many will spontaneously close
- surgical closure
- if small then no intervention is required
- prophylactic antibiotics
- if moderately sized lesion; furosemide, ACE inhibitor and digoxin may suffice
what are features of atrio-ventricular septal defects?
• associated with Downs syndrome
• basically a hole in the very centre of the heart
• involves the ventricular septum, the atrial septum,
the mitral and tricuspid valves
• can be complete or partial
• instead of two separate atrio-ventricular valves
there is just one big malformed one which usually leaks
what is the clinical presentation of a complete atrio-ventricular septal defect?
- breathlessness as neonate
- poor weight gain and feeding
- torrential pulmonary flow which can result in Eisenmenger’s resulting in cyanosis over time
what is the clinical presentation of a partial atrio-ventricular septal defect?
- can present in late adulthood
* presents similar to ventricular/atrial septal defect e.g. dysponea, tachycardia, exercise intolerance etc.
what is the treatment of atrio-ventricular septal defects?
- pulmonary artery banding if large defect in infancy; band reduces blood flow to lungs thereby reducing pulmonary hypertension and Eisenmenger’s syndrome
- surgical repair is challenging
- a partial defect may be left alone if there is no right heart dilatation
what is the definition of patent ductus arteriosus? what is its epidemiology?
• affects girls more than boys
• ductus arteriosus is a persistent communication
between the proximal left pulmonary artery and the
descending aorta
what usually happens to the ductus arteriosus?
• in foetal life, pulmonary vascular resistance is high
(since bronchioles are filled with fluid and vessels are
vasoconstricted due to lack of O2) and the right heart
pressure exceeds that of left; consequently flow is
from right to left atrium through foramen ovale, and
from pulmonary artery to aorta via the ductus arteriosus
• normally, the ductus arteriosus closes within a few hours of birth in response to decreased pulmonary resistance; however in some cases e.g. in premature babies and in cases with maternal rubella, the ductus persists
why may a ductus arteriosus not close?
- premature babies
- maternal rubella
what happens if the ductus arteriosus remains open?
• if it remains open, there is an abnormal left-to-right shunt (from aorta to pulmonary artery) and
eventually means that the lung circulation is overloaded with pulmonary hypertension (leading
to Eisenmenger syndrome) and right side cardiac
failure (due to right ventricular hypertrophy in
response to increased afterload)
• also increases risk of infective endocarditis
what is the clinical presentation of a patent ductus arteriosus?
- continuous ‘machinery’ murmus
- bounding pulse
- if large then large heart and breathlessness
- Eisenmenger’s syndrome with differential cyanosis that is clubbed and blue toes but pink and not clubbed fingers
- tachycardia
how can a patent ductus arteriosus be diagnosed?
CXR: with large shunt the aorta and pulmonary arterial system may be prominent
ECG: may demonstrate left atrial abnormality and left ventricular hypertrophy
echocardiogram: may show dilated left atrium and left ventricle
what is the treatment of patent ductus arteriosus?
- can be closed surgically or percutaneously
- low risk of complications
- venous approach may require an AV loop
- Indometacin (prostaglandin inhibitor) can be given to stimulate duct closure
what is the definition of coarctation of the aorta?
• a narrowing of the aorta at, or just distal to, the
insertion of the ductus arteriosus (distal to the origin of the left subclavian artery)
• the net result is a narrowing of the aorta just after the arch, with excessive blood flow being diverted through the carotid and subclavian vessels into systemic vascular shunts to supply the rest of the body, thus stronger perfusion to upper body compared to lower
what are the consequences of coarctation of the aorta?
resultant decreased renal perfusion leads to systemic hypertension that persists even after surgical correction
what is the epidemiology of coarctation of the aorta?
- more common in men than women
- associated with Turner syndrome, berry aneurysms and patent ductus arteriosus
what is the clinical presentation of coarctation of the aorta?
- often asymptomatic for many years
- right arm hypertension
- bruits (buzzes) over the scapulae and back from collateral vessels
- murmur
- headaches and nose bleeds (due to hypertension)
- hypertension in the upper limbs
- discrepant blood pressure in the upper and lower body (will notice radial pulse before femoral pulse)
