Cardio Flashcards
What are the shockable rhythms
ventricular fibrillation/pulseless ventricular tachycardia (VF/pulseless VT)
What are the non shockable rhythms
asystole/pulseless-electrical activity (asystole/PEA)
what do you do when you defibrillate (how many shocks etc)
single shock for VF/pulseless VT followed by 2 minutes of CPR
or three successive shocks if the patient is a ‘monitored patient’
When do you give adrenaline in a cardiac arrest
1mg asap for non shockable rhythms
during VF/VT, 1mg given once chest compressions have restarted after third shock
repeat adrenaline every 3-5mins
when do you give amiodarone in cardiac arrest
300mg for patients in VF/pulseless VT after 3 shocks
further dose of 150g after 5 shocks
lidocaine can be used as an alternative
when do you use thrombolytic drugs in cardiac arrest
if PE is suspected
give alteplase
What are the reversible causes of cardiac arrest
The ‘Hs’
Hypoxia
Hypovolaemia
Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
Hypothermia
The ‘Ts’
Thrombosis (coronary or pulmonary)
Tension pneumothorax
Tamponade - cardiac
Toxins
Person has cardiac arrest with shockable rhythm, what do you do
CPR 30:2
attach defib
assess rhythm
1 shock
continue CPR for 2 mins
reassess rhythm
repeat
3 shocks -> 1mg adrenaline,300mg amiodarone
5 shocks -> 150mg amiodarone
Person has cardiac arrest with non-shockable rhythm, what do you do
1mg adrenaline
resume CPR for 2 mins
reassess rhythm
What does a raised troponin level in the context of chest pain suggest
MI
What is the difference between unstable angina and NSTEMI
no elevation of troponin
however, troponin may take a few hours to rise so treated the same until known
What are classic symptoms of ACS
chest pain (central/left sided)
radiates to jaw or left arm
described as heavy, ‘like an elephant on my chest’
dyspnoea
sweating
nausea and vomiting
What investigations do we do for chest pain
ECG
cardiac markers eg troponin
What ECG changes are linked to anterior STEMI and what artery
V1-V4 left anterior descending
What ECG changes are linked to inferior STEMI and what artery
II, III, aVF right coronary
What ECG changes are linked to lateral STEMI and what artery
I, V5-V6 left circumflex
how do you treat ACS generally
in general = MONA:
morphine, oxygen, nitrates, aspirin
If NSTEMI, use risk tool eg GRACE to determine management, if high risk/unstable, do coronary angiography
what is secondary prevention of ACS
aspirin
a second antiplatelet if appropriate (e.g. clopidogrel)
a beta-blocker
an ACE inhibitor
a statin
What are features of hypercalcaemia
‘bones, stones, groans and psychic moans’
corneal calcification
shortened QT interval on ECG
hypertension
what can cause a prolonged QT interval
Drugs
amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants, fluoxetine
chloroquine
terfenadine
erythromycin
Other
electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia
acute myocardial infarction
myocarditis
hypothermia
subarachnoid haemorrhage
How do you treat VT/TdP
(in TdP) IV mag sulph first line to stabilise cardiac membrane
amiodarone
If drug therapy fails
electrophysiological study (EPS)
implant able cardioverter-defibrillator (ICD) - this is particularly indicated in patients with significantly impaired LV function
Give shock if unstable
What ECG changes are linked to posterior STEMI and what artery
V1-V3
Reciprocal changes of STEMI are typically seen:
horizontal ST depression
tall, broad R waves
upright T waves
dominant R wave in V2
Posterior infarction is confirmed by ST elevation and Q waves in posterior leads (V7-9)
Usually left circumflex, also right coronary
‘widened QRS complexes and a notched morphology of the QRS complexes in the lateral leads’ what is it
left bundle branch block, prompts investigation for ACS
‘Delta waves and a short PR-interval’
Wolff-Parkinson-White syndrome
‘New widening QRS complexes and an RSR’ pattern in V1’
right bundle branch block
‘T-wave flattening and the appearance of U-waves’
hypokalaemia
what is acute management of heart failure
IV loop diuretics
e.g. furosemide or bumetanide
oxygen
can give nitrates if concomitant myocardial ischaemia, severe hypertension or regurgitant aortic or mitral valve disease
with resp failure -> CPAP
if hypotensive -> inotropic agents eg dobutamine
mechanical circulatory assistance
e.g. intra-aortic balloon counterpulsation or ventricular assist devices
when should you stop beta blockers for heart failure
heart rate less than 50 beats per minute, second or third degree atrioventricular block, or shock
how do you manage VTE/PE
massive PE + unstable -> alteplase
otherwise -> DOAC (apixaban or rivaroxaban)
if significant renal impairment -> LMWH, unfractionated heparin or LMWH followed by vitamin K antagonist eg warfarin
if antiphospholipid syndrome -> LMWH followed by VKA
how long do you stay on anticoagulation for VTE/PE
If provoked, stop after 3 months (3-6 months if cancer)
if unprovoked, go up to 6 months
how do you manage broad complex tachycardia
Regular
assume ventricular tachycardia (unless previously confirmed SVT with bundle branch block)
loading dose of amiodarone followed by 24 hour infusion
Irregular
seek expert help. Possibilities include:
atrial fibrillation with bundle branch block - the most likely cause in a stable patient
atrial fibrillation with ventricular pre-excitation
torsade de pointes
how do you manage narrow (<0.12s) complex tachycardia
Regular
vagal manoeuvres followed by IV adenosine
if the above is unsuccessful consider a diagnosis of atrial flutter and control rate (e.g. beta-blockers)
Irregular
probable atrial fibrillation
if onset < 48 hr consider electrical or chemical cardioversion
rate control: beta-blockers are usually first-line unless there is a contraindication
What are side effects of loop diuretics
hypotension
hyponatraemia
hypokalaemia, hypomagnesaemia
hypochloraemic alkalosis
ototoxicity
hypocalcaemia
renal impairment (from dehydration + direct toxic effect)
hyperglycaemia (less common than with thiazides)
gout
what is stage 1 hypertension defined as?
Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg
what is stage 2 hypertension defined as?
Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg
what is stage 3 hypertension defined as?
Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 120 mmHg
When do you treat hypertension
> =135/85 - only if they are <80 and have one of:
-target organ damage
-established cardiovascular disease
-renal disease
-diabetes
-10 year cardiovascular risk >=10%
> =150/95 - always treat
how do you manage hypertension
lifestyle advice:
-low salt diet <6g a day ideally 3g
-reduce caffeine intake
-stop smoking etc
If <55 or T2DM
start with ACEi or ARB
then add CCB or thiazide like diuretic
then add both
then if K+<4.5 add low dose spironolactone, if >4.5 add alpha or beta blocker
If >55 and no T2DM or african/afro caribbean
start with CCB
add ACEi/ARB or thiazide like diuretic
then add both
then if K+<4.5 add low dose spironolactone, if >4.5 add alpha or beta blocker
What are blood pressure targets
<80 clinic=140/90, ABPM/HBPM = 135/85
>80 clinic=150/90, ABPM/HBPM = 145/85
What is CHA2DS2-VASc scoring system
Used to determine the need to anticoagulate a patient in atrial fibrillation
What is NYHA scoring system
Heart failure severity scale
DAS28
Measure of disease activity in rheumatoid arthritis
Child-Pugh classification
A scoring system used to assess the severity of liver cirrhosis
Wells score
Helps estimate the risk of a patient having a deep vein thrombosis
MMSE
Mini-mental state examination - used to assess cognitive impairment
HAD
Hospital Anxiety and Depression (HAD) scale - assesses severity of anxiety and depression symptoms
PHQ-9
Patient Health Questionnaire - assesses severity of depression symptoms
GAD-7
Used as a screening tool and severity measure for generalised anxiety disorder
Edinburgh Postnatal Depression Score
Used to screen for postnatal depression
SCOFF
Questionnaire used to detect eating disorders and aid treatment
AUDIT, CAGE, FAST
Alcohol screening tool
CURB-65
Used to assess the prognosis of a patient with pneumonia
Epworth Sleepiness Scale
Used in the assessment of suspected obstructive sleep apnoea
IPSS
International prostate symptom score
Gleason score
Indicates prognosis in prostate cancer
APGAR
Assesses the health of a newborn immediately after birth
Bishop score
Used to help assess the whether induction of labour will be required
Waterlow score
Assesses the risk of a patient developing a pressure sore
FRAX
Risk assessment tool developed by WHO which calculates a patients 10-year risk of developing an osteoporosis related fracture
Ranson criteria
Acute pancreatitis scoring system
MUST
Malnutrition scoring system
What are features of complete heart block
syncope
heart failure
regular bradycardia (30-50 bpm)
wide pulse pressure
JVP: cannon waves in neck
variable intensity of S1
What is first degree heart block
PR interval > 0.2 seconds
What is second degree heart block
type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurs
type 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS complex
What is third (complete) degree heart block
there is no association between the P waves and QRS complexes
infarction of what vessel can cause complete heart block post MI
right coronary artery
How do you manage STEMI
If STEMI,
aspirin 300mg
percutaneous coronary intervention (PCI) if presenting <12 hours and can be given within 120 mins of the time that fibrinolysis can be given (basically you want to give PCI but would consider fibrinolysis if you cant give it in time. if fibrinolysis, also give antithrombin drug and do ECG after 60-90 mins to see if changes have resolved)
PCI is given with drug eluting stent through radial access preferred over femoral
During PCI, unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) is given
second antiplatelet should be given with aspirin eg clopidogrel (if taking oral anticoagulant), prasugrel (if not taking oral anticoagulant)
How do you manage NSTEMI
aspirin + fondaparinux (if no immediate PCI)
estimate 6 month mortality eg GRACE
low risk (<3%) - ticagrelor or clopidogrel (if high risk of bleeding)
higher risk (>3%) - Offer PCI (immediately if unstable otherwise within 72 hours)
give prasugrel or ticagrelor
give unfractionated heparin
how do you treat bradycardia
IV atropine 5oomcg
then use again up to 3mg
then transcutaneous pacing
then isoprenaline/adrenaline infusion
then transvenous pacing with specialist
what are side effects of ACEi
cough
angioedema
hyperkalaemia
first dose hypokalaemia
what are some cautions and contraindications for ACEi
pregnancy and breastfeeding - avoid
renovascular disease - may result in renal impairment
aortic stenosis - may result in hypotension
hereditary of idiopathic angioedema
what electrolytes change when using an ACEi
creatinine
potassium
what is an acceptable change for creatinine/potassium when using ACEi
acceptable changes are an increase in serum creatinine, up to 30% from baseline and an increase in potassium up to 5.5 mmol/l.
what condition can using an ACEi with result in significant renal impairment
bilateral renal artery stenosis
how would you manage angina pectoris
aspirin + statin for every patient
sublingual glyceryl trinitrate to abort angina attacks
beta blocker/CCB first line - if CCB used solely, a rate limiting one such as verapamil or diltiazem should be used - if used in combo, use a longer acting dihydropyridine CCB eg amlodipine, modified release nifedipine
if poor response, increase to max tolerated dose
if still symptomatic after monotherapy add the other thing (ie CCB/beta blocker) then if still symptomatic add one of
long acting nitrate
ivabradine
nicorandil
ranozaline
How do people using nitrates avoid nitrate tolerance
use an assymetric dosing interval if using standard release isosorbide mononitrate which allows a daily nitrate free time of 10-14 hours
what are features of acute pericarditis
chest pain: may be pleuritic. Is often relieved by sitting forwards
other symptoms include a non-productive cough, dyspnoea and flu-like symptoms
pericardial rub
what do you see on ECG for acute pericarditis
widespread changes
‘saddle shaped’ ST elevation
PR depression (most specific for acute pericarditis)
what investigations would you do for acute pericarditis
ECG
transthoracic echocardiography
bloods - inflam markers, troponin for possible myopericarditis
how do you manage acute pericarditis
mainly outpatients unless fever >38 or high troponin
treat underlying cause
avoid physical activity
combination of NSAID and colchicine used until symptoms go or inflam markers go down followed by tapering of dose
what is mitral stenosis
describes the obstruction of blood flow across the mitral valve from the left atrium to the left ventricle leading to increased pressure within the left atrium, pulmonary vasculature and right side of the heart
what causes mitral stenosis
rheumatic fever
what are features of mitral stenosis
dyspnoea - increased left atrial pressure -> pulmonary venous hypertension
haemoptysis
mid-late diastolic murmur (best heard on expiration)
loud S1
opening snap - indicates mitral valve leaflets are still mobile
low volume pulse
malar flush
atrial fib - secondary to increased left atrial pressure -> left atrial enlargement
when severe - length of murmur increases, opening snap becomes closer to S2
what do you see on xray of mitral stenosis
possible left atrial enlargement
how do you manage mitral stenosis
asymptomatic - monitor
symptomatic - percutaneous mitral balloon valvotomy, mitral valve surgery
associated aFib - require anticoagulation - usually warfarin
how do you deal with severe airway obstruction (emergency setting)
give up to 5 back blows
give up to 5 abdominal thrusts (pressing forcibly into the upper abdominal area with an upward moment)
keep continuing above cycle
What is the pulmonary embolism rule out criteria (PERC)
you do it when you have a low suspicion (<15% probability) of PE but just want reassurance.
All criteria must be negative to rule it out
negative test reduces probability to <2%
What is the 2 level Wells score and how do you manage the patient
you do it if PE is suspected
>4 points means its likely, <4 means unlikely
if likely
arrange immediate CTPA
if there is a delay in doing this then interim anticoagulation should be given (DOAC)
if positive result, PE confirmed
if negative, consider proximal leg vein US scan if DVT expected
If unlikely
arrange a D dimer test
if positive arrange immediate CTPA (give anticoag if delay)
If negative, PE is unlikely so stop anticoags and consider an alternative diagnosis
When would you do V/Q scan over CTPA
if there is renal impairment
What ecg changes could you see in PE
S1Q3T3 - large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III (RARE)
RBBB and right axis deviation
sinus tachycardia
What xray changes do you see in PE
usually normal but could see wedge shaped opacification
how do you investigate chronic heart failure
first line - N-terminal pro-B-type natriuretic peptide (NT-proBNP) blood test
if high (>2000pg/ml) - arrange specialist assessment including transthoracic echo within 2 weeks
if raised (400-2000 pg/ml) do the same within 6 weeks
if levels are ‘high’ arrange specialist assessment (including transthoracic echocardiography) within 2 weeks
if levels are ‘raised’ arrange specialist assessment (including transthoracic echocardiography) echocardiogram within 6 weeks
how do you decide whether to use anticoagulation for aFib
use CHA2DS2-VASc score
C Congestive heart failure 1
H Hypertension (or treated hypertension) 1
A2 Age >= 75 years 2
Age 65-74 years 1
D Diabetes 1
S2 Prior Stroke, TIA or thromboembolism 2
V Vascular disease (including ischaemic heart disease and peripheral arterial disease) 1
S Sex (female) 1
0 = no treatment
1 = males - consider treatment, females no
>=2 = offer anticoag
if no treatment, do transthoracic echo to exclude valvular heart disease
Use DOACs, warfarin second line
what is atrial flutter and what do you see
a succession of rapid atrial depolarisation waves.
‘sawtooth appearance’
how do you manage atrial flutter
radiofrequency ablation of the tricuspid valve isthmus is curative
what is the triad for cardiac tamponade + what are other features
Becks Triad:
hypotension
raised JVP
muffled heart sounds
dyspnoea
tachycardia
absent Y decent on JVP
pulsus paradoxus - abnormally large drop in BP during inspiration
electrical alternans on ECG
What are the differences between cardiac tamponade and constrictive pericarditis
1) JVP
CT = Absent Y descent
CP = X + Y present
2) Pulsus paradoxus
CT = Present
CP = Absent
3) Kussmaul’s sign
CT = Rare
CP = Present
4) Characteristic features
CP = Pericardial calcification on CXR
how do you manage cardiac tamponade
urgent pericardiocentesis (pericardial needle aspiration)
what are features of takayasu’s arteritis
systemic features of a vasculitis e.g. malaise, headache
unequal blood pressure in the upper limbs
carotid bruit and tenderness
absent or weak peripheral pulses
upper and lower limb claudication on exertion
aortic regurgitation (around 20%)
What other condition is takayasu’s arteritis associated with
renal artery stenosis
how do you investigate takayasu’s arteritis
magnetic resonance angiography (MRA) or CT angiography (CTA)
how do you manage takayasu’s arteritis
steroids
What ecg changes do we see with hypothermia
bradycardia
‘J’ wave (Osborne waves) - small hump at the end of the QRS complex
first degree heart block
long QT interval
atrial and ventricular arrhythmias
what are features of buergers disease
Young male smoker with symptoms similar to limb ischaemia - think Buerger’s disease
extremity ischaemia
intermittent claudication
ischaemic ulcers
superficial thrombophlebitis
Raynaud’s phenomenon
what are features of tension pneumothorax
Severe respiratory distress, tracheal deviation, unilateral absent breath sounds, and haemodynamic instability
what are features of hypokalaemia
U waves
small or absent T waves (occasionally inversion)
prolong PR interval
ST depression
long QT
what is aortic regurgitation
leaking of aortic valve causing blood flow in reverse direction during ventricular diastole
caused by aortic root disease or valve disease
what are acute valvular causes of aortic regurg
infective endocarditis
what are chronic valvular causes of aortic regurg
rheumatic fever: the most common cause in the developing world
calcific valve disease
connective tissue diseases e.g. rheumatoid arthritis/SLE
bicuspid aortic valve (affects both the valves and the aortic root)
what are chronic aortic root causes of aortic regurg
bicuspid aortic valve (affects both the valves and the aortic root)
spondylarthropathies (e.g. ankylosing spondylitis)
hypertension
syphilis
Marfan’s, Ehler-Danlos syndrome
what are acute aortic root causes of aortic regurg
aortic dissection
what are features of aortic regurg
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
how do you investigate aortic regurg
echocardiography
how do you manage aortic regurg
medical management of associated heart failure
surgery for symptomatic patients or asymptomatic with LV dysfunction
how do thiazide diuretics work
inhibiting sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Clˆ’ symporter
what are side effects of thiazide diuretics
dehydration
postural hypotension
hypokalaemia
due to increased delivery of sodium to the distal part of the distal convoluted tubule → increased sodium reabsorption in exchange for potassium and hydrogen ions
hyponatraemia
hypercalcaemia
the flip side of this is hypocalciuria, which may be useful in reducing the incidence of renal stones
gout
impaired glucose tolerance
impotence
thrombocytopaenia
agranulocytosis
photosensitivity rash
pancreatitis
when is cardioversion used for Afib
if patient is unstable
electrical or pharmacological cardioversion as an elective procedure where a rhythm control strategy is preferred.
how is cardioversion used when patient has Afib
synchronised to R wave to prevent delivery of a shock during the vulnerable period of cardiac repolarisation when ventricular fibrillation can be induced
how do you manage Afib
<48 hours - patient is heparinised, put on lifelong anticoagulants if they have risk factors
otherwise can be cardioverted using electrical ‘DC’ cardioversion or pharmacologically with amiodarone
> 48 hours - anticoags given for >3 weeks prior to cardioversion or do a transoesophageal echo to exclude left atrial appendage thrombus
then anticoags for >4 weeks
what are features of Hypertrophic obstructive cardiomyopathy (HOCM)
often asymptomatic
exertional dyspnoea
angina
syncope
typically following exercise
due to subaortic hypertrophy of the ventricular septum, resulting in functional aortic stenosis
sudden death (most commonly due to ventricular arrhythmias), arrhythmias, heart failure
jerky pulse, large ‘a’ waves, double apex beat
systolic murmurs
ejection systolic murmur: due to left ventricular outflow tract obstruction. Increases with Valsalva manoeuvre and decreases on squatting
pansystolic murmur: due to systolic anterior motion of the mitral valve → mitral regurgitation
What echo findings do you see in HOCM
MR SAM ASH
mitral regurgitation (MR)
systolic anterior motion (SAM) of the anterior mitral valve leaflet
asymmetric hypertrophy (ASH)
What ecg changes do you see in HOCM
left ventricular hypertrophy
non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen
deep Q waves
atrial fibrillation may occasionally be seen
what investigation do you do for cardiac tamponade
echo
which valve is most commonly affected in infective endocarditis
mitral valve (tricuspid in IVDU)
What is the most common cause of infective endocarditis for
1)all patients
2)dental patients
3)<2 months after prosthetic valve surgery
1 - staph aureus
2 - staph viridans
3 - staph epidermidis
how do you manage hypothermia
Removing the patient from the cold environment and removing any wet/cold clothing,
Warming the body with blankets
Securing the airway and monitoring breathing,
If the patient is not responding well to passive warming, you may consider maintaining circulation using warm IV fluids or applying forced warm air directly to the patient’s body
You warm a patient with hypothermia but they go into shock, what happened?
rapid rewarming
What are features of constrictive pericarditis
dyspnoea
right heart failure: elevated JVP, ascites, oedema, hepatomegaly
JVP shows prominent x and y descent
pericardial knock - loud S3
Kussmaul’s sign is positive
what do you see on xray of constrictive pericarditis
pericardial calcification
What are features of rheumatic fever
Recent sore throat, rash, arthritis, murmur → ?rheumatic fever
erythema marginatum
Sydenham’s chorea: this is often a late feature
polyarthritis
carditis and valvulitis (eg, pancarditis)
subcutaneous nodules
how do you manage rheumatic fever
oral penicillin V
NSAIDs
what other investigation should you always do with PE
xray to exclude pneumothorax, pleural effusion etc
how do you manage HOCM
Amiodarone
Beta-blockers or verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis*
what drugs do you avoid in HOCM
nitrates
ACE-inhibitors
inotropes
what are features of coarctation of the aorta
infancy: heart failure
adult: hypertension
radio-femoral delay
mid systolic murmur, maximal over the back
apical click from the aortic valve
notching of the inferior border of the ribs (due to collateral vessels) is not seen in young children
how do we investigate palpitations
12 lead ecg
tfts for thyrotoxicosis
u’s and e’s - potassium
FBC
then you want to capture episodic arrythmias using Holter monitoring
if no abnormality found, can do external loop recorder or implantable loop recorder
What is adenosine most commonly used for?
A: Adenosine is most commonly used to terminate supraventricular tachycardias.
Q: Which agents enhance the effects of adenosine?
A: The effects of adenosine are enhanced by dipyridamole (antiplatelet agent).
Q: Which agents block the effects of adenosine?
A: The effects of adenosine are blocked by theophyllines.
Q: Why should adenosine be avoided in asthmatics?
A: Adenosine should be avoided in asthmatics due to possible bronchospasm.
Q: What is the mechanism of action of adenosine?
A: Adenosine causes transient heart block in the AV node by acting as an agonist of the A1 receptor in the atrioventricular node, inhibiting adenylyl cyclase, reducing cAMP, and causing hyperpolarization by increasing outward potassium flux.
Q: How long is the half-life of adenosine?
A: The half-life of adenosine is about 8-10 seconds.
Q: How should adenosine be administered due to its short half-life?
A: Adenosine should ideally be infused via a large-calibre cannula due to its short half-life.
Q: What are some adverse effects of adenosine?
A: Adverse effects of adenosine include chest pain, bronchospasm, transient flushing, and enhanced conduction down accessory pathways, resulting in increased ventricular rate (e.g., WPW syndrome).
Q: What is the 1st line antiplatelet treatment for acute coronary syndrome (medically treated)?
A: Aspirin (lifelong) & ticagrelor (12 months).
Q: What is the 2nd line antiplatelet treatment for acute coronary syndrome if aspirin is contraindicated?
A: Clopidogrel (lifelong).
Q: What is the 1st line antiplatelet treatment for percutaneous coronary intervention?
A: Aspirin (lifelong) & prasugrel or ticagrelor (12 months).
Q: What is the 2nd line antiplatelet treatment for percutaneous coronary intervention if aspirin is contraindicated?
A: Clopidogrel (lifelong).
Q: What is the 1st line antiplatelet treatment for TIA?
A: Clopidogrel (lifelong).
Q: What is the 2nd line antiplatelet treatment for TIA if clopidogrel is contraindicated or not tolerated?
A: Aspirin (lifelong) & dipyridamole (lifelong).
Q: What is the 1st line antiplatelet treatment for ischaemic stroke?
A: Clopidogrel (lifelong).
Q: What is the 2nd line antiplatelet treatment for ischaemic stroke if clopidogrel is contraindicated or not tolerated?
A: Aspirin (lifelong) & dipyridamole (lifelong).
Q: What is the 1st line antiplatelet treatment for peripheral arterial disease?
A: Clopidogrel (lifelong).
Q: What is the 2nd line antiplatelet treatment for peripheral arterial disease if clopidogrel is contraindicated or not tolerated?
A: Aspirin (lifelong).
Q: What is aortic dissection?
A: Aortic dissection is a rare but serious cause of chest pain characterized by a tear in the tunica intima of the wall of the aorta.
Q: What is the most important risk factor for aortic dissection?
A: Hypertension.
Q: What are some conditions associated with aortic dissection?
A: Hypertension, trauma, bicuspid aortic valve, Marfan’s syndrome, Ehlers-Danlos syndrome, Turner’s syndrome, Noonan’s syndrome, pregnancy, and syphilis.
Q: How is the chest/back pain in aortic dissection typically described?
A: The pain is typically severe, sharp, and tearing in nature, and it is maximal at onset.
Q: What type of pain is more common in type A dissection versus type B dissection?
A: Chest pain is more common in type A dissection, while upper back pain is more common in type B dissection.
Q: What are some pulse-related features of aortic dissection?
A: Pulse deficit (weak or absent carotid, brachial, or femoral pulse) and variation in systolic blood pressure (>20 mmHg) between the arms.
Q: What are some complications of aortic dissection involving specific arteries?
A: Coronary arteries can lead to angina, spinal arteries can lead to paraplegia, and distal aorta can lead to limb ischemia.
Q: What are the typical ECG findings in aortic dissection?
A: The majority of patients have no or non-specific ECG changes, but a minority may show ST-segment elevation in the inferior leads.
Q: Describe the Stanford classification of aortic dissection.
A: Type A involves the ascending aorta (2/3 of cases) and Type B involves the descending aorta, distal to the left subclavian origin (1/3 of cases).
Q: Describe the DeBakey classification of aortic dissection.
A: Type I originates in the ascending aorta and propagates to at least the aortic arch and possibly beyond; Type II originates in and is confined to the ascending aorta; Type III originates in the descending aorta, rarely extends proximally but will extend distally.
Q: What chest X-ray finding is associated with aortic dissection?
A: Widened mediastinum.
Q: What is the investigation of choice for aortic dissection in stable patients?
A: CT angiography of the chest, abdomen, and pelvis.
Q: What key finding on CT angiography helps diagnose aortic dissection?
A: A false lumen.
Q: Which investigation is more suitable for unstable patients with aortic dissection?
A: Transoesophageal echocardiography (TOE).
Q: What is the management for type A aortic dissection?
A: Surgical management, with blood pressure controlled to a target systolic of 100-120 mmHg while awaiting intervention.
Q: What is the management for type B aortic dissection?
A: Conservative management, including bed rest and blood pressure reduction with IV labetalol.
Q: What are the complications of a backward tear in aortic dissection?
A: Aortic incompetence/regurgitation and myocardial infarction (often with an inferior pattern due to right coronary involvement).
Q: What are the complications of a forward tear in aortic dissection?
A: Unequal arm pulses and blood pressure, stroke, and renal failure.
Q: What are the clinical features of symptomatic aortic stenosis?
A: Chest pain, dyspnoea, syncope/presyncope (e.g., exertional dizziness), and murmur.
Q: What type of murmur is classically seen in aortic stenosis and how does it radiate?
A: An ejection systolic murmur (ESM) that classically radiates to the carotids and is decreased following the Valsalva manoeuvre.
Q: What are the features of severe aortic stenosis?
A: Narrow pulse pressure, slow rising pulse, delayed ESM, soft/absent S2, S4, thrill, duration of murmur, and left ventricular hypertrophy or failure.
Q: What is the most common cause of aortic stenosis in older patients (>65 years)?
A: Degenerative calcification.
Q: What is the most common cause of aortic stenosis in younger patients (<65 years)?
A: Bicuspid aortic valve.
Q: When should valve replacement be considered in aortic stenosis?
A: If symptomatic or if asymptomatic with a valvular gradient > 40 mmHg and features such as left ventricular systolic dysfunction.
Q: What are the options for aortic valve replacement (AVR)?
A: Surgical AVR, transcatheter AVR (TAVR), and balloon valvuloplasty.
Q: Which type of AVR is the treatment of choice for young, low/medium operative risk patients?
A: Surgical AVR.
Q: When is transcatheter AVR (TAVR) typically used?
A: For patients with a high operative risk.
Q: What is arrhythmogenic right ventricular cardiomyopathy (ARVC)?
A: ARVC, also known as arrhythmogenic right ventricular dysplasia (ARVD), is an inherited cardiovascular disease that may present with syncope or sudden cardiac death and is the second most common cause of sudden cardiac death in the young after hypertrophic cardiomyopathy.
Q: What is the inheritance pattern of ARVC?
A: Autosomal dominant with variable expression.
Q: What happens to the right ventricular myocardium in ARVC?
A: It is replaced by fatty and fibrofatty tissue.
Q: What are the common presentations of ARVC?
A: Palpitations, syncope, and sudden cardiac death.
Q: What are the typical ECG findings in ARVC?
A: T wave inversion in V1-3 and an epsilon wave, which is a terminal notch in the QRS complex, found in about 50% of those with ARVC.
Q: What echocardiographic changes might be seen in ARVC?
A: Subtle changes in the early stages, but may show an enlarged, hypokinetic right ventricle with a thin free wall.
Q: What are the management options for ARVC?
A: Drugs (sotalol), catheter ablation to prevent ventricular tachycardia, and implantable cardioverter-defibrillator (ICD).
Q: What is the most common sustained cardiac arrhythmia?
A: Atrial fibrillation (AF).
Q: What is the most important aspect of managing patients with AF?
A: Reducing the increased risk of stroke.
Q: How is AF classified?
A: First detected episode, paroxysmal, persistent, or permanent.
Q: What is paroxysmal AF?
A: AF that terminates spontaneously and lasts less than 7 days (typically < 24 hours).
Q: What is persistent AF?
A: AF that is not self-terminating and usually lasts greater than 7 days.
Q: What is permanent AF?
A: Continuous AF that cannot be cardioverted or when attempts to do so are deemed inappropriate.
Q: What are the symptoms of AF?
A: Palpitations, dyspnoea, and chest pain.
Q: What investigation is essential to diagnose AF?
A: ECG (electrocardiogram).
Q: What are the two key parts of managing AF?
A: Rate/rhythm control and reducing stroke risk.
Q: What is the aim of rate control in AF management?
A: To slow the rate down to avoid negative effects on cardiac function while accepting an irregular pulse.
Q: What is the aim of rhythm control in AF management?
A: To get the patient back into, and maintain, normal sinus rhythm through cardioversion.
Q: What is the first-line treatment for rate control in AF?
A: A beta-blocker or a rate-limiting calcium channel blocker (e.g., diltiazem).
Q: What combination therapy does NICE recommend if one drug does not adequately control the rate in AF?
A: Any 2 of the following: a beta-blocker, diltiazem, digoxin.
Q: When is rhythm control considered in AF management?
A: For specific situations such as coexistent heart failure, first onset AF, or if there is an obvious reversible cause, and if symptoms/heart rate fail to settle with rate control.
Q: Why is it important to anticoagulate patients before attempting cardioversion?
A: To reduce the risk of embolism leading to stroke when the patient switches from AF to sinus rhythm.
Q: What does a CHA2DS2-VASc score of 0 indicate for anticoagulation?
A: No treatment.
Q: What does a CHA2DS2-VASc score of 1 indicate for anticoagulation in males and females?
A: Males: Consider anticoagulation; Females: No treatment (score of 1 is due to gender).
Q: What does a CHA2DS2-VASc score of 2 or more indicate for anticoagulation?
A: Offer anticoagulation.
Q: What anticoagulation options does NICE recommend for AF patients?
A: Warfarin and novel oral anticoagulants (NOACs).
Question: What should be ensured if a CHA2DS2-VASc score suggests no need for anticoagulation?
Answer: A transthoracic echocardiogram should be done to exclude valvular heart disease, which is an absolute indication for anticoagulation.
Question: What is the ORBIT scoring system used for in AF?
Answer: The ORBIT scoring system is used to assess bleeding risk before starting anticoagulation.
