Cardiology IV Flashcards
Desribe the pathophysiology of AS
A pressure gradient develops across the valve
Initially, this leads to systolic dysfunction, the heart can not pump out a normal proportion of its end-diastolic volume and causes increased resistance to ejection and increases the systolic pressure gradient.
Compensatory mechanisms result in left ventricular (concentric) hypertrophy - hence, a sustained apex.
This then causes diastolic dysfunction by reducing ventricular filling during diastole
This reduces the compliance of the left ventricle and reduces overall myocardial contractility.
This causes left heart failure
ALSO: the back-pressure from the left ventricle also increases pulmonary artery pressure and can lead to pulmonary hypertension. This eventually progresses to right heart failure.
Describe the symptoms of AS
Patients with aortic stenosis (AS) may be asymptomatic for a prolonged period of 10-20 years.
-
Exertional dysopnea
Most common complaint -
Exertional angina
Increased o2 demand due to more LV mass and decreased perfusion pressure gradient due to elevated LV end diastolic pressure -
Exertional syncope or presyncope
Due to exercise induced vasodilation and inability to increase CO - Atrial fibrillation
- Epistaxis or bruising
Classical triad of ‘SAD’ is often described.
Syncope; Angina; Dysopnea
Describe the signs of AS [4]
Murmur:
* Loud mid-to-late peaking systolic ejection murmur
* Radiates to the carotids and becomes more prominent with sitting forward and in expiration
* Murmur becomes softer the more severe the stenosis
* Murmur radiates to carotids
Sustained apex
Slow rising pulse
Narrow pulse pressure
Soft S2
S4 - caused by the atria contracting against stiff, hypertrophied ventricles.
What ECG changes would you expect in AS? [1]
Left ventricular hypertrophy:
- deep S-waves in V1 and V2
- tall R-waves in V5 and V6).
How can you tell from a murmur in AS if it is mild-moderate c.f severe murmur? [2]
Early peaking is more consistent with mild or moderate AS and late peaking is consistent with severe AS
Murmur becomes softer the more severe the stenosis
When is dobutamine stress echo indicated in AS patients? [1]
By what mmHg does AS gr
Dobutamine stress echocardiogram:
- useful for patients who have low-gradient AS
- patients may be symptomatic but have seemingly low pressures due to a low ejection fraction
- gradient will increase > 40 mmHg after administration of low dose dobutamine
Describe the work conducted prior to a surgical aortic valve replacement {SAVR) or transcatheter aortic valve implantation (TAVI) [3]
-
Coronary angiogram:
to ID CAD and concomitant coronary revascularization if possible -
Trans-oesophageal echocardiogram (TOE):
assess for endocarditis and mitral valve abnormalities as well as monitoring the TAVI procedure -
MSCT:
assess the anatomy and dimensions of the aortic root, shape of the aortic valve annulus and the number of aortic valve cusps
How do you classify AS as being severe? [3]
Severe AS classified as:
- aortic jet velocity ≥4 m/s (direct measurement of the highest antegrade systolic velocity signal across the aortic valve)
- mean trans-valvular pressure gradient ≥ 40 mmHg
- aortic valve area ≤1 cm2.
What indicates surgery for AS? [3]
If symptomatic
If asymptomatic but have:
- LVEF < 50%
- Undergoing other cardiac surgery
- low surgical risk factors
Which treatment option is used for palliative measures / not suitable for surgery / young children with congenital AS? [1]
Percutaneous balloon valvotomy
What is Heyde’ syndrome? [1]
Triad of
- AS
- Recurrent bleeding due to angiodysplasia causing anaemia
- Acquired coagulopathy - VWDS
Describe the valve leaflet causes of AR [3]
-
rheumatic infection
Inflammation is a result of molecular mimicry to streptococcal infection: immune system produces antibodies that confuse foreign and self-antigens. -
infective endocarditis
Infective causes include Strep. viridans, Staph. aureus, Enterococci. -
congenital & degenerative disease
Congenital (e.g. bicuspid, quadcuspid valve).
Degenerative (e.g. calcification).
Describe the aortic root causes of AR
Connective tissue disorders
- Aortic regurgitation may feature in a number of connective tissue disorders. Aortic root diameter should be monitored in these individuals.
- Marfan’s syndrome - caused by a defect in the FBN1 gene.
Ehlers-Danlos syndrome - caused by collagen defects.
Aortitis
- inflammation of the aortic root.
- May be associated with chronic inflammatory conditions such as rheumatoid arthritis (RA) and ankylosing spondylitis (AS).
Aortic dissection
- Aortic regurgitation may complicate in Stanford A dissections, secondary to impaired leaflet coaptation or prolapse. Causes acute disease regurgitation and is a medical emergency.
Describe the pathophysiology of acute AR
MEDICAL EMERGENCY:
- Causes an acute rise in left atrial pressure
- Causes pulmonary oedema and cardiogenic shock
- Also get reduced coronary flow - the coronaries fill predominantly during diastole, regurgitant flow at this time reduces filling. Results in angina or in severe cases myocardial ischaemia.
Describe the pathophysiology of chronic AR [4]
Regurgitation of blood during diastole causes an increase in the left ventricular end-diastolic volume (essentially the preload).
Leads to systolic and diastolic dysfunction
LV dilatation occurs with eccentric hypertrophy
The dilation allows for an increased stroke volume compensating for regurgitant flow supported by the ventricular hypertrophy
These changes maintain ejection fraction, with a greater preload leading to greater contractility
Describe the following signs of AR [5]
de Musset’s
Quincke’s
Traube’s
Duroziez’s
Müllers’
de Musset’s - head nodding with the heart beat.
Quincke’s - pulsation of nail beds.
Traube’s - pistol shot femorals.
Duroziez’s - to and fro murmur heard when stethoscope compresses femoral vessels.
Müllers’ - pulsation of uvula.
Describe the managment of acute AR
Acute AR is a surgical emergency: Aortic valve replacement or repair should be performed as soon as possible. It primarily occurs secondary to infective endocarditis or aortic dissection, both of which carry very high morbidity and mortality:
Aortic dissection (Stanford type A):
- management depends on the patients pre-morbid state and severity of presentation. If not already there, patients are transferred to the local on-call dissection centre. Emergency open surgery is typically required, management depends on the exact pattern of findings but may consist of root replacement and valve repair or replacement.
Infective endocarditis:
- management depends upon pattern of valvular involvement (multiple valves may be affected) and complications (e.g. annular/aortic abscess, septic emboli). Coronary angiogram may be performed in selected stable patients prior to operative management. AR is generally an indication for early surgery.
-
The normal size of the aortic valve area is more than [] cm2, in mild AS it is more than [] cm2, in moderate AS it is from [] to []cm2, and in severe AS < [] cm2.
The normal size of the aortic valve area is more than 2 cm2, in mild AS it is more than 1.5 cm2, in moderate AS it is from 1.0 to 1.5 cm2, and in severe AS < 1 cm2.
What is an austin flint murmur? [1]
Early diastolic murmur heard in AR; the blood flows out of of atrial valve on onto mitral valve; heard on apex beat
VSDs are associated with
Aortic regurgitation
Aortic stenosis
Mitral stenosis
Mitral regurgitation
VSDs are associated with
Aortic regurgitation
Aortic stenosis
Mitral stenosis
Mitral regurgitation
Why are VSDs associated with aortic regurgitation? [1]
poorly supported right coronary cusp resulting in cusp prolapse
Which drug class are CI in AS? [1]
Why? [1]
GTN are CI in AS due to the fact that they are potent vasodilators, meaning that they would reduce BP, and the heart would have to work even harder (and likely cause blood back into the Pulmonary Circulation and Right Ventricle)
What are the symptoms of MR? [4]
SOB & dysopnoea (to increase in left atrial pressure)
Fatigue
Signs of RHF (ankle swelling; distended abdomen)
Palpitations due to afib
Describe the signs of MR [6]
- Pan systolic, high pitched whistling murmur (due to high velocity of blood flow through the leaky valve)
- Murmur radiates to left axilla
- Soft S1: due to incomplete closure.
- 3rd heart sound may be present due to rapid filling of a dilated ventricle.
- Thrill on palpitation
- Signs of HF
- Signs of pulmonary oedema
- Afib
What is a tell tale sign of left atrial enlargement on CXR? [1]
double-density sign, also known as the double right heart border
Normally the left atrium is located posteriorly and only the atrial appendage component is visible. But left atria becomes englarged enlarged, the right aspect may become visible as an extra shadow next to the right atria
If the double density sign is present on a CXR, what measurement can be taken to confirm left atrial enlargement? [1]
Olbique left atrial measurement: outer edge of atrium to midpoint of left main bronchus: > 7 cm = LA enlargement
Acute MR is characterised by which two features? [2]
Patients with acute MR are normally profoundly unwell. Condition characterised by shock and flash pulmonary oedema
Describe the pathophysiology of mitral stenosis [3]
Mitral stenosis results in raised left atrial pressures and atrial hypertrophy.
This predisposes to atrial fibrillation
Elevated left atrial pressure also causes pulmonary venous hypertension and subsequent pulmonary arterial hypertension resulting in right ventricular hypertrophy and dilation, ultimately progressing to right-sided heart failure
Decompensated heart failure accounts for most cases of AHF.
What are the most common precipitating causes of acute AHF? [4]
- Acute coronary syndrome
- Hypertensive crisis: e.g. bilateral renal artery stenosis
- Acute arrhythmia
- Valvular disease
There is generally a history of pre-existing cardiomyopathy. It usually presents with signs of fluid congestion, weight gain, orthopnoea and breathlessness.
CHAMP
Acute coronary syndrome (ACS)
Hypertensive crisis
Arrhythmias, e.g. atrial fibrillation, ventricular tachycardia, bradyarrhythmia
Mechanical problems, e.g. myocardial rupture as a complication of ACS, valve dysfunction
Pulmonary embolism
Explain how the heart tries to compensate for a failing heart [4]
Increasing preload (increasing venous pressures):
* Increases end-diastolic volume (EDV) compensating for the reduced ejection fraction, thus maintaining cardiac output.
* In severe disease, large increases result in pulmonary oedema, ascites and peripheral oedema.
Increasing heart rate (a sinus tachycardia)
Activation of the renin-angiotensin-aldosterone system (RAAS)
* due to renal hypoperfusion from the reduced cardiac output.
* contributes to increased venous pressures through vasoconstriction and there is retention of water and sodium that contributes to oedema.
Sympathetic nervous system activation
* via baroreceptors; increasing myocardial contractility and heart rate
What are you looking for to that might indicate HF in an ECHO [3] or CXR [5]
Echocardiogram:
* Evidence of previous MI
* Left ventricular strain / hypertrophy
* Conduction abnormalities / AF
CXR:
* Cardiomegaly (Cardiothoracic ratio > 50% on PA film)
* Alveolar shadowing oedema
* Kerley B lines (fluid in septae of secondary lobules)
* Pleural effusion
* Upper lobe diversion
What are normal, raised and high levels of BNP and NTproBNP? [9]
Explan your answer [1]
Left ventricular aneurysm
The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation. This is typically associated with persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.
A patient has chronic heart failure. You trial and ACEI but the patient is intolerant.
You then trial an ARB, but the patient is still intolerant.
What treatment should you consider nexr? [1]
Hydralazine and nitrate
A patient has chronic heart failure.
You iniate an ACEin and a BB as first line treatment. This does not resolve their EF.
You next trial and aldosterone antagonist. This does also not help.
They are Afro-Carribean.
What is the appropriate third line treatment?
- Ivabradine
- sacubitril-valsartan
- digoxin
- hydralazine in combination with nitrate
- cardiac resynchronisation therapy
- hydralazine in combination with nitrate
