Flashcards in Cardiovascular Deck (81):
Name 8 risk factors for the development of IHD.
What is the WHO definition of an AMI?
At least 2 of the following 3 features:
-Symptoms of myocardial ischaemia
-Elevation of cardiac markers (troponin or CK)
-Typical ECG pattern involving the development of Q waves, ST segment changes or T wave changes
What are the reperfusion options in AMI and how soon should they be implimented?
Options: percutaneous intervention or fibrinolysis
Should be performed within 90 minutes of symptom onset
When is fibrinolysis preferred over PCI for treatment of AMI?
-Invasive strategy not an option
-There will be a delay to invasive option
What are the adjunctive therapies in AMI?
Oxygen, IV morphine, aspirin, IV heparin/clexane, IV GTN, additional antiplatelets if applicable
What are the benefits of starting a beta-blocker after AMI?
-Reduced rates of recurrent MI
-Improved LV function
What are contraindications to starting a beta blocker after AMI?
Hypotension, bradycardia, second- or third-degree heart block, severe asthma
In CCF following an AMI, what changes might you see on a chest X-ray?
Cardiomegaly, Kerley B lines, pleural effusions
What are cholesterol targets post-AMI?
What is the post-hospital management following a STEMI?
-Review at 1 month; then 6 monthly
-Repeat ECHO at 6 months
-Stress testing at 1 year
-Cholesterol profile, renal & liver function tests, CK, FBE 6 monthly
-Regular review of lifestyle changes
-Regular review of medication chart & compliance
What is the most common clinical presentation of a tachyarrhythmia?
What is the most common clinical presentation of a bradyarrhythmia?
Name 1 vital investigation in palpitations and 5 others you may consider.
Others: Holter monitor, Event recorder, Loop recorder, Echocardiogram, Electrophysiology study, Stress testing
What is the usual management of premature ventricular/atrial complexes in an otherwise healthy patient?
2. Cut down caffeine
3. Occasionally requires beta blockers or calcium channel blockers if very frequent & symptomatic
What is the usual management of AF?
1. Rule out precipitant (eg/ hyperthyroidism, infection)
2. Look for a cause (eg/ cardiomyopathy)
3. Decide whether to rate control or rhythm control
4. Evaluate the risk of stroke & how best to manage it (CHADS2)
Which 3 medications might be used in AF to maintain sinus rhythm (rhythm control)?
Sotalol, flecainide, amiodarone
Which 3 medications might be used to control rate in AF?
Beta blockers, calcium channel blockers, digoxin
What location does an ablation procedure target in AF?
Pulmonary veins (4)
A majority of SVTs involve which part of the cardiac conduction system?
What are 3 possible acute treatments of SVT?
1. Vagal manoeuvres
2. IV adenosine (induces transient AV block)
3. IV verapamil
What are the long-term options for treatment of SVT?
1. No treatment
2. Beta blockers or calcium channel blockers - 'pill in the pocket' approach
3. Catheter ablation (>95% success rate)
42 year-old male who has occasional palpitations - sudden onset, at rest, regular, last 5-10 minutes, resolve spontaneously & suddenly. Presents with a further episode of palpitations lasting >1 hour. What is the likely arrhythmia causing his palpitations?
What is the acute management for a patient presenting with VT?
If unstable -> DC cardioversion
If stable, can try amiodarone before DC cardioversion
Always investigate & treat the cause
What are the 'red flag' features of palpitations?
-Past history of cardiac disease
-Evidence of cardiac disease on baseline tests
-Family history of sudden cardiac death
-High risk work environment
-High level sporting activities
What is the definition of syncope?
Transient LOC that is self-limiting. Onset is relatively rapid, leads to a fall. Recovery is complete, rapid & spontaneous.
What are some indications for a PPM?
-Symptomatic sinus bradycardia
-Sinus pauses >2s (day) or 2.5s (night)
-Symptomatic 2nd or 3rd degree AV block
-Intermittent 3rd degree AV block
What is the usual management of sick sinus syndrome?
1. Insert PPM
2. Once PPM inserted, you can use AV nodal blocking agents to control tachycardias
What is a normal PR interval?
What does a bifid P wave suggest?
'P mitrale' - a sign of mitral stenosis
What does a peaked P wave suggest?
'P pulmonale' - a sign of lung disease
What is the Wenkebach phenomenon?
Progressive lengthening of the PR interval until a P wave is non-conducted (2nd degree heart block, Mobitz type I)
What is a normal QRS width?
What is a pathological Q wave?
A marker of electrical silence which implies established full thickness death of the myocardium (scar)
-must be >25% the height of the corresponding R wave
-must be present in more than 1 contiguous lead
What are some causes of left axis deviation?
Left anterior hemiblock, ischaemic heart disease, cardiomyopathy, hypertension, WPW syndrome
What are some causes of right axis deviation?
(normal in children & tall thin adults)
RV volume/pressure overload, COPD, PE, WPW syndrome
What are some causes of extreme right axis deviation?
Lead transposition, VT, emphysema, hyperkalaemia, paced rhythm
In which leads are the T waves normally inverted?
V1 (sometimes V2), III, aVR
What does a biphasic T wave represent?
Critical LAD stenosis
What does an inverted T wave represent?
From where to where is the QT interval measured?
From the start of the QRS complex to the end of the T wave
What are the common causes of long QT?
Drugs (amiodarone, sotalol, azithromycin, amitriptyline, clozapine), electrolyte imbalance (hypokalaemia, hypomagnesaemia), MI
What does echocardiography show?
-Chamber size & function (EF)
-Doppler -> flow velocities
What is rheumatic fever?
A type II hypersensitivity reaction to grp A beta haemolytic Strep
What are the clinical features of rheumatic fever?
-Rash (erythema marginatum)
How is rheumatic fever diagnosed?
Based on Jones criteria
What is the management of rheumatic fever?
Antibiotics + NSAIDs
In mitral regurgitation, when should you aim to operate?
BEFORE symptoms - on echo criteria (symptoms coincide with severe disease with irreversible changes in the LV)
In aortic stenosis, when should you aim to operate?
When the stenosis becomes symptomatic - the LVH will regress after surgery
Which 2 valve pathologies can result in pulmonary hypertension?
Mitral regurgitation & mitral stenosis
What are the 3 causes of aortic stenosis?
-Congenital (AS 0.33% or bicuspid aortic valve 1-2%)
-Calcific - COMMON
What is the pathophysiology of aortic stenosis?
Aortic stenosis creates a much greater pressure gradient across the valve that the LV must push to overcome, leading to left ventricular hypertrophy
What are the 3 main symptoms of aortic stenosis?
SOB on exertion, chest pain on exertion, syncope (only appear when stenosis is severe)
What are some physical signs of aortic stenosis (besides the murmur)?
-Slow upstroke carotid pulse with a plateau
-Heaving apex beat
-Thrill over upper R sternal edge
What murmur might be heard in aortic stenosis?
Ejection systolic 'crescendo-decrescendo' murmur best heard over the upper R sternal edge (with radiation to the carotids)
What echocardiography criteria signify severe aortic stenosis?
-Aortic valve area
What are the treatment options for severe aortic stenosis?
-Open aortic valve replacement
-Transcatheter aortic valve implant (TAVI)
What are some cases of aortic regurgitation?
-Aortic leaflet damage (endocarditis, rheumatic fever)
-Aortic root dilation (Marfan's syndrome, aortic dissection, collagen vascular disorders, syphilis)
What are the symptoms of aortic regurgitation?
NONE - until LV decompensates & person develops heart failure (SOB)
What are some signs of aortic regurgitation (besides the murmur)?
-Collapsing pulse - fast up & down stroke
-Wide pulse pressure
What is the murmur heard in aortic regurgitation?
Early diastolic murmur, best heard at the upper left sternal edge
What is the management for aortic regurgitation?
-Echo every 6-12 months for severe AS
-Aortic valve replacement (when LV decompensates)
What are the causes of mitral regurgitation?
-Ruptured chordae tendinae
-Myocardial infarct (ruptured papillary muscle)
-Collagen vascular disease
What are the symptoms of mitral regurgitation?
NONE - until the LV decompensates & symptoms of heart failure occur (SOB)
What is the murmur heard in mitral regurgitation?
Pansystolic murmur best heard over the apex beat during expiration
What is the management for mitral regurgitation?
-Follow-up echo 6-12 monthly for severe MR
-LV decompensation or pulmonary hypertension are triggers for valve replacement or repair
What is the commonest valve lesion caused by rheumatic fever?
What is the major cause of mitral stenosis?
Rheumatic fever (esp. in women)
What are the symptoms of mitral stenosis?
SOB, oedema, pulmonary disease
What are some signs of mitral stenosis (besides the murmur)?
-Mitral facies (flushing)
-Tapping apex beat - correlates with loud S1
What murmur is heard with mitral stenosis?
-Rumbling diastolic murmur with opening 'snap'
What are the heart changes observed over time in mitral stenosis?
-Pulmonary congestion & oedema
-Right heart failure
What are the principles of management for mitral stenosis?
-Anticoagulation if AF
-Mitral valve intervention
What are the interventions for mitral stenosis?
-Mitral valvotomy - open or closed
-Mitral valve replacement
What are the features of cardiogenic syncope?
-Complete & rapid recovery
-Sudden with acute onset
-May be exertion related
What are some features of a LOC that suggest epilepsy?
-Urine or faecal incontinence
In an otherwise healthy individual, at what level should you treat blood pressure?
SBP >160mmHg and DBP
When the individual has associated risk factors, at what level should you treat high blood pressure?
Or high CV risk
What constitutes critical limb ischaemia?
-Ischaemic rest pain
What is the white cell trapping hypothesis of chronic venous insufficiency?
-WBCs are larger & less deformable than RBCs
-When perfusion pressure is reduced by venous hypertension, WBC plug capillaries & RBC build up behind
-WBC activation occurs
-Endothelial adhesion by WBC releases proteolytic enzymes & ROS causing endothelial & tissue damage
What is the fibrin cuff hypothesis of chronic venous disease?
-Increased venous pressure if directly transmitted to capillaries resulting in capillary elongation & increased endothelial permeability
-Larger molecules such as fibrinogen become deposited into tissues -> fibrin
-Accumulation of fibrin acts as a barrier to oxygen -> tissue hypoxia -> ulceration