Cardiolovascular Flashcards
(42 cards)
Define aortic dissection.
Tear in the tunica intima of the aorta
What are the RFs for aortic dissection?
- HTN
- Smoking
- Raised cholesterol
- Pre-existing aortic disease or AV disease
- FH of aortic disease
- History of cardiac surgery, cigarette smoking, direct blunt chest trauma
- IV drug use
- Marfan’s syndrome. Ehlers-Danlos syndrome and familial thoracic aneurysm type 1 and 2
- Congenital bicuspid valve
How do we classify aortic dissections?
The Stanford Classification in common use classifies the dissections into type A and type B:
- Type A involves ascending aorta (DeBakey types I and II).
- Type B does not involve the ascending aorta (DeBakey type III).
The DeBakey Classification classifies the dissections into:
- Type I: originates in the ascending aorta, then aortic arch, and maybe descending aorta.
- Type II: ascending aorta only.
- Type III: descending aorta distal to left subclavian.
How do aortic dissections present? How should we investigate them?
- Classical: tearing chest pain, radiates to the back, >20mmHg difference BP between arms
- Weak distal pulses
- Aortic regurgitation
- Myocardial Ischaemia
- Neurological complaints (i.e. hemiplegia, frontal headache, neck pain), incl. Horner’s syndrome
Investigations
-
Definitive:
- Stable (most commonly) → CTA CAP
- Unstable (cannot be taken to CT) → TOE/TTE
- Organ hypoperfusion → FTs (liver), U&Es (renal), lactate (GIT)
- ECG (ischaemia)
- CXR (widened mediastinum)
- FBC (haemoglobin)
- X-match/G&S
How do we manage aortic dissections?
- Type A (ascending) → surgery, IV beta blockade
- Type B (descending) → bed rest, IV beta blockade
General
- Intravenous access.
- Adequate analgesia - eg, morphine.
- Transfer to an intensive care unit or high dependency unit.
- Hypertension must be managed aggressively in all cases to reduce further damage. The aim is a systolic pressure of between 100 and 120 mm Hg.
What are the clinical features of aortic stenosis?
Features of severe aortic stenosis
- narrow pulse pressure
- slow rising pulse
- delayed ESM
- soft/absent S2
- S4
- thrill
- duration of murmur
- left ventricular hypertrophy or failure
What are the causes of aortic stenosis?
Causes of aortic stenosis
- degenerative calcification (most common cause in older patients > 65 years)
- bicuspid aortic valve (most common cause in younger patients < 65 years)
- William’s syndrome (supravalvular aortic stenosis)
- post-rheumatic disease
- subvalvular: HOCM
How do we investigate aortic stenosis?
- ECG (LVH, arrhythmias)
- Bloods (FBC, U&E, BNP, lipids, glucose)
- CXR (calcified valves, LVH, pul. oedema)
- Echo ± doppler (severity, cause, LV function); severe AS…
- Valve area <1cm2
- Pressure gradient >40mmHg
- Jet velocity >4m/s
- Coronary angiography
How do we manage Aortic stenosis?
- if asymptomatic then observe the patient is a general rule
- if symptomatic then valve replacement
- if asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction then consider surgery
- General Management
- MDT (cardiologist, GP, specialist nurses, cardiothoracic surgeon, dietician, OT/physiotherapist)
- RF modification (QRISK : statin, anti-platelet; manage HTN, angina, etc.)
- Regular f/u
- Valve replacement
- Surgical AVR - usually for young patients
-
Artificial:
-
Starr-Edwards / ball-in-cage [3 artificial sounds]
- Quiet click as valve opens
- Rumbling as ball rolls in the cage
- Loud thud as valve closes
-
Tilting disc / bileaflet [1 artificial sound]
- High-pitched click as valve closes
-
Starr-Edwards / ball-in-cage [3 artificial sounds]
-
Biological:
- Biological valve [normal heart sounds]
-
Artificial:
- Transcatheter AVR (TAVR) is used for patients with a high operative risk
- Balloon valvuloplasty
- may be used in children with no aortic valve calcification
- in adults limited to patients with critical aortic stenosis who are not fit for valve replacement
- Surgical AVR - usually for young patients
How does aortic regurgitation present?
Features
- early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre
- collapsing pulse
- wide pulse pressure
- Quincke’s sign (nailbed pulsation)
- De Musset’s sign (head bobbing)
- mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams
What causes aortic regurgitation?
How do we investigate Aortic regurgitation?
- ECG (LVH, LV strain – lateral lead TWI)
- Bloods (FBC, U&E, NT-proBNP, lipids, glucose, ESR, HLA-B27, ANA)
- CXR (cardiomegaly, LVH, pul. oedema)
- Echo ± doppler (severity, cause, LV function); severe AR…
- Jet width (>65% outflow tract)
- Regurgitant jet volume
- Premature closing of mitral valve
- Coronary angiography
How should we manage aortic regurgitation
- medical management of any associated heart failure
- surgery: aortic valve indications include
- symptomatic patients with severe AR
- asymptomatic patients with severe AR who have LV systolic dysfunction
What is mitral stenosis? What are the consequences of it?
Mitral stenosis describes the obstruction of blood flow across the mitral valve from the left atrium to the left ventricle.
This leads to increases in pressure within the left atrium, pulmonary vasculature and right side of the heart.
What causes MS?
It is said that the causes of mitral stenosis are rheumatic fever, rheumatic fever and rheumatic fever.
Rarer causes that may be seen in the exam include mucopolysaccharidoses, carcinoid and endocardial fibroelastosis
How do patients with MS present?
Features
- dyspnoea
- ↑ left atrial pressure → pulmonary venous hypertension
- haemoptysis
- due to pulmonary pressures and vascular congestion
- may range from pink frothy sputum to sudden haemorrhage secondary to rupture of thin walled and dilated bronchial veins
- mid-late diastolic murmur (best heard in expiration)
- loud S1, opening snap
- low volume pulse
- malar flush
- atrial fibrillation
- secondary to ↑ left atrial pressure → left atrial enlargement
Features of severe MS
- length of murmur increases
- opening snap becomes closer to S2
What are examples of evidence of Pulmonary hypertension?
- Malar flush
- JVP with large V-waves
- Right ventricular heave
- Loud S2 (P2)
How do we investigate MS?
- ECG (P-mitrale, AF)
- Bloods (FBC, U&E, NT-proBNP, lipids, glucose)
- CXR (LA hypertrophy (splaying of carina), calcified mitral valve, pul. oedema)
- Echo ± doppler (severity, cusp calcification, LV function, ? TOE); severe MS…
- Valve orifice <1cm2
- Pressure gradient >10mmHg
- Pul. artery SBP >50mmHg
- Coronary angiography
How do we manage MS?
- patients with associated atrial fibrillation require anticoagulation
- currently warfarin is still recommended
- asymptomatic patients
- monitored with regular echocardiograms
- percutaneous/surgical management is generally not recommended
- symptomatic patients
- percutaneous mitral balloon valvotomy
- mitral valve surgery (commissurotomy, or valve replacement)
This patient has had a sternotomy and a prosthetic mitral valve. There is splaying of the carina with elevation of the left main bronchus, a double right heart border and cardiomegaly. The features are those of left atrial enlargement. Although the entire heart is enlarged, a double contour is seen through the right side of the heart. The more medial line is the enlarged left atrium (white dotted line) and the heart heart border is more lateral (blue dotted line).
What is Mitral regurgitation?
Also known as mitral insufficiency, mitral regurgitation (MR) occurs when blood leaks back through the mitral valve on systole
How does MR present and progress?
MR is common in otherwise healthy patients to a trivial degree and does not need treatment.
As the degree of regurgitation becomes more severe, the body’s oxygen demands may exceed what the heart can supply and as a result, the myocardium can thicken over time. While this may be benign initially, patients may find themselves increasingly fatigued as a thicker myometrium becomes less efficient, and eventually go into irreversible heart failure.
Symptoms
- Most patients with MR are asymptomatic, and patients suffering from mild to moderate MR may stay largely asymptomatic indefinitely. Symptoms tend to be due to failure of the left ventricle, arrhythmias or pulmonary hypertension. This may present as fatigue, shortness of breath and oedema.
Signs
- The murmur heard on auscultation of the chest is typically a pansystolic murmur described as “blowing”. It is heard best at the apex and radiating into the axilla. S1 may be quiet as a result of incomplete closure of the valve. Severe MR may cause a widely split S2
What are the RFs for MR?
- Female sex
- Lower body mass
- Age
- Renal dysfunction
- Prior myocardial infarction
- Prior mitral stenosis or valve prolapse
- Collagen disorders e.g. Marfan’s Syndrome and Ehlers-Danlos syndrome
What are the causes of MR?
- Following coronary artery disease or post-MI: if the papillary muscles or chordae tendinae are affected by a cardiac insult, mitral valve disease may ensue as a result of damage to its supporting structures.
- Mitral valve prolapse: Occurs when the leaflets of the mitral valve is deformed so the valve does not close properly and allows for backflow. Most patients with this have a trivial degree of mitral regurgitation.
- Infective endocarditis: When vegetations from the organisms colonising the heart grow on the mitral valve, it is prevented from closing properly. Patients with abnormal valves are more likely to develop endocarditis as opposed to their peers.
- Rheumatic fever: While this is uncommon in developed countries, rheumatic fever can cause inflammation of the valves and therefore result in mitral regurgitation.
- Congenital