Cardio Flashcards
What is angina?
constricting chest pain caused by reduced blood flow (and hence oxygen supply) to the myocardium due to atherosclerosis narrowing the lumen of coronary arteries
What is stable angina?
symptoms only come on with exertion
relieved by rest or glyceryl trinitrate (GTN)
What is unstable angina?
symptoms appear randomly whilst at rest
type of acute coronary syndrome (ACS)
requires immediate management
What are the main signs and symptoms of aortic stenosis?
chest pain
SoB
syncope
exertional dizziness
ejection systolic murmur radiating to the carotids
What kind of murmur is associated with aortic stenosis?
ejection systolic murmur
radiating to the carotids
decreased during Valsalva maneuvre
What features are associated with severe aortic stenosis?
narrow pulse pressure
thrill
LV hypertrophy
What are the main causes of aortic stenosis?
degenerative calcification - most common cause in >65y.o.
bicuspid aortic valve - most common cause in < 65y.o.
William’s syndrome - supravalvular
post-rheumatic disease
subvalvular - hypertrophic cardiomyopathy
What is the management of aortic stenosis in asymptomatic patients?
conservative - observation
What is the management of aortic stenosis in symptomatic patients?
valve replacement
When do you consider surgery in asymptomatic patients with aortic stenosis?
if the valvular gradient is > 40mmHg and has features of left ventricular systolic dysfunction
What are the options for aortic valve replacement (AVR) in aortic stenosis?
surgical AVR
transcatheter AVR
What patients are suitable for surgical AVR?
young
low-medium operative risk
may have cardiovascular disease (combined surgery)
When should mechanical vs bioprosthetic valve be used?
mechanical
- younger patients (< 65 in aortic, <70 in mitral)
bioprosthetic
- older patients
- tend to last shorter
What patients are suitable for transcatheter AVR?
high operative risk
What patients are suitable for aortic balloon valvuloplasty?
children with aortic stenosis with no calcification
adults with critical aortic stenosis who are not fit for valve replacement
What is aortic regurgitation?
leaking of the aortic valve
What are the main causes of aortic regurgitation?
valve disease
aortic root disease
What are some causes of aortic regurgitation due to valve disease with chronic presentation?
rheumatic fever - most common cause in the developing world
calcific valve disease
connective tissue disease - SLE, rheumatoid arthritis
bicuspid aortic valve
What is the most common cause of aortic regurgitation in the developing world?
rheumatic fever
What are some causes of aortic regurgitation due to aortic root disease with chronic presentation?
bicuspid aortic valve
spondyloarthropathies - e.g. ankylosing spondylitis
HTN
syphilis
Marfan’s
EDS
What are some causes of aortic regurgitation due to valve disease with acute presentation?
infective endocarditis
What are some causes of aortic regurgitation due to aortic root disease with chronic presentation?
aortic dissection
What are some features of aortic regurgitation?
early diastolic murmur - loudest at left sternal edge
wide pulse pressure
collapsing pulse
Quincke’s sign - nailbed pulsation
Austin flint murmur - low pitched rumbling mid-diastolic murmur heard best at the apex (in severe AR)
How is aortic regurgitation assessed?
echocardiography
How is aortic regurgitation managed?
medical management of heart failure (if associated)
surgery if
- symptomatic with severe AR
- asymptomatic with severe AR and LV systolic dysfunction
What is mitral stenosis?
obstruction of blood flow across the mitral valve from LA to LV
leads to increases in pressure within the left atrium, pulmonary vasculature and right side of the heart
What is the most common cause of mitral stenosis?
rheumatic fever
What are the features of mitral stenosis?
SoB - due to pulmonary hypertension
haemoptysis - due to pulmonary hypertension
mid-late diastolic murmur - best heard in expiration over the apex
loud S1
malar flush
AF
opening snap - indicates mobility of mitral valve leaflets
What features can be seen in CXR in mitral stenosis?
LA enlargement
How is mitral stenosis managed?
if associated AF - anticoagulation
if asymptomatic - monitoring (conservative), regular echo
if symptomatic - percutaneous mitral balloon valvotomy OR mitral valve surgery
What are the two most common valve diseases?
aortic stenosis
mitral regurgitation
What are the risk factors for mitral regurgitation?
female
lower BMI
age
renal dysfunction
prior MI
prior mitral stenosis/prolapse
collagen disorders - Marfan’s, EDS
What murmur is associated with mitral regurgitation?
pansystolic murmur
loudest over mitral area
radiating to axilla
What are the causes of mitral regurgitation?
post MI / coronary artery disease - due to damage to papillary muscles
mitral valve prolapse
infective endocarditis - vegetations prevent closure of valve leaflets
rheumatic fever
congenital
What are the features of mitral regurgitation?
mostly asymptomatic
symptoms usually from LV failure - fatigue, SoB, oedema
What investigations are useful in suspected mitral regurgitation? What will they show?
ECG - broad P waves - atrial enlargement
CXR - cardiomegaly (enlarged LA and LV)
echocardiography
How is mitral regurgitation managed?
medical - in acute cases - nitrates, diuretics, intra-aortic balloon pump
if heart failure - ACE inhibitors, beta blockers, spironolactone
surgery - in acute and severe MR
surgical repair over replacement preferred in degenerative causes
What murmur does tricuspid regurgitation cause?
pansystolic
What are some features of tricuspid regurgitation?
thrill in tricuspid area
raised JVP with big C-V waves
pulsatile liver (regurgitation into the venous system)
peripheral oedema
ascites
What are the possible causes of tricuspid regurgitation?
“functional” - due to L-sided heart failure or pulmonary hypertension
infective endocarditis
carcinoid syndrome
Ebstein’s anomaly
connective tissue disorders (e.g. Marfan’s)
What murmur does pulmonary stenosis cause?
ejection systolic murmur
loudest in pulmonary area in deep inspiration
What are some features of pulmonary stenosis?
thrill on palpation
raised JVP with big A waves (RA contracting against hypertrophic RV)
peripheral oedema
ascites
What are the most common causes of pulmonary stenosis?
congenital
-> Noonan syndrome
-> tetralogy of Fallot
What is tetralogy of Fallot?
congenital pathology; four coexisting pathologies:
- ventricular septal defect
- overriding aorta
- pulmonary valve stenosis
- RV hypertrophy
What is infective endocarditis?
infection of the inner surface of the heart (endothelium)
mostly affects the valves
What are the risk factors for infective endocarditis?
IVDU
structural heart pathology
CKD (esp. dialysis)
immunocompromised
Hx of infective endocarditis
What structural heart pathologies can increase the risk of infective endocarditis?
valvular disease
congenital heart disease
hypertrophic cardiomyopathy
prosthetic valves
implanted cardiac devices
What organisms can cause infective endocarditis? And what is the most common one?
Staphylococcus aureus - most common
streptococcus
enterococcus
How does infective endocarditis present?
non-specific infective symptoms (fever, night sweats, fatigue)
new / changing murmur
splinter haemorrhages
Osler’s nodes / Janeway lesions
Roth spots
splenomegaly
finger clubbing (if chronic)
How is infective endocarditis investigated?
blood cultures - before ATB
echocardiography (transoesophageal is more sensitive - can see vegetations)
if prosthetic valves - special imaging:
- SPECT CT
- 18F-FDG CT/PET
What is the name of the tool used to diagnose infective endocarditis?
Duke Criteria
What score (from the Duke Criteria) is required to diagnose infective endocarditis?
1 major + 3 minor criteria
OR
5 minor criteria
What are the major criteria in Duke Criteria?
persistently positive blood cultures
specific imaging findings (e.g. vegetations on echo)
What are the minor criteria in Duke Criteria?
predisposition (e.g. valve pathology, IVDU)
fever above 38
vascular phenomena (e.g. intracranial haemorrhage, Janeway lesions, splenic infarction)
immunological phenomena (e.g. Osler’s nodes, Roth spots, glomerulonephritis)
microbiological phenomena (e.g. positive cultures not qualifying as major criteria)
How is infective endocarditis managed?
hospital admission
IV broad-spectrum ATB (e.g. amoxicillin) for 4 weeks (6 weeks if prosthetic valve)
surgery - if HF related to valve pathology / large vegetations / not responding to ATB
What are the key complications of infective endocarditis?
high mortality rate
heart valve damage -> regurgitation
HF
infective and non-infective emboli (-> stroke, splenic infarction)
glomerulonephritis -> renal impairment
What is pericarditis?
inflammation of pericardium - membrane surrounding the heart
What are the most common causes of pericarditis?
idiopathic
viral
other causes:
autoimmune
uraemia
medications - e.g. methotrexate
How does pericarditis present?
low-grade fever
chest pain
- pleuritic
- sharp
- central / anterior
- worse when lying down, better when sitting forward
What examination finding is typical for pericarditis?
pericardial friction rub - rubbing sound occuring alongside heart sounds
What is the potential space between the two layers of pericardium called? How is it relevant to pericarditis? What complications can arise from it?
pericardial cavity
in pericarditis - can fill up with fluid -> pericardial effusion
if pericardial effusion big enough to raise the intra-pericardial pressure -> cardiac tamponade
What is the function of the pericardial cavity?
contains small amount of fluid -> provides space to allow heart to beat without friction
What is cardiac tamponade? Why is it a problem?
large pericardial effusion that raised intra-pericardial pressure - > affects the heart’s ability to function
reduced heart filling during diastole -> decreases cardiac output during systole
emergency - requires quick drainage
How is pericarditis investigated?
blood tests - raised inflammatory markers
ECG changes
- saddle-shaped (concave) ST elevation
- PR depression
echocardiogram - to diagnose pericardial effusion
How is pericarditis managed? What are the first and second line treatment options?
first line:
NSAIDs
colchicine - longer-term treatment, prevents recurrence
second line:
steroids - if recurrent / associated with inflammatory condition
pericardiocentesis - removal of pericardial fluid if effusion/tamponade
treatment of underlying causes
What is the prognosis of pericarditis?
resolves within a month
may be recurrent
may become chronic
What is ejection fraction? What is the normal value?
% of blood in LV squeezed out with each ventricular contraction
normal is above 50%
What is systolic dysfunction?
problem with ventricle contracting during systole
What is diastolic dysfunction?
issue with ventricle relaxing and filling with blood during diastole
What are the main types of chronic heart failure? (2 answers correct)
preserved LVEF (LVEF > 50%)
reduced LVEF (LVEF < 50%)
OR
systolic HF (typically reduced LVEF)
diastolic HF (typically preserved LVEF)
What are some common causes of systolic dysfunction HF?
ischaemic heart disease
dilated cardiomyopathy
myocarditis
arrhythmias
What are some common causes of diastolic dysfunction HF?
hypertrophic obstructive cardiomyopathy
restrictive cardiomyopathy
cardiac tamponade
constrictive pericarditis
What are the potential causes of left-sided heart failure?
increased LV afterload - e.g. due to arterial HTN, aortic stenosis
increased LV preload - e.g. aortic regurgitation
What are the potential causes of right-sided heart failure?
increased RV afterload - e.g. pulmonary HTN
increased RV preload - e.g. tricuspid regurgitation
What does LV failure typically result in?
pulmonary oedema -> leads to signs and symptoms:
- dyspnoea
- orthopnoea
- paroxysmal nocturnal dyspnoea
- bibasal fine crackles
- wheeze
What does RV failure typically result in?
peripheral oedema
raised JVP
hepatomegaly - due to backflow
weight gain - due to fluid retention
anorexia - cardiac cachexia
What is “high-output heart failure”? What are some examples?
when a normal, healthy heart is unable to pump enough blood to meet the metabolic demands of the body
e.g. in
- anaemia
- arteriovenous malformation
- Paget’s disease
- pregnancy
- thyrotoxicosis
What are some examination signs in heart failure?
tachycardia
tachypnoea
HTN
murmurs
3rd heart sound
bilateral basal crackles
raised JVP
peripheral oedema
What are some symptoms of chronic heart failure?
SoB, worse on exertion
cough - can produce white/pink frothy sputum
cardiac wheeze (due to pulmonary oedema)
orthopnoea
paroxysmal nocturnal dyspnoea
peripheral oedema
fatigue
How is heart failure diagnosed?
clinical assessment - Hx, examination
NT-proBNP blood test
ECG
echocardiogram
+bloods - to check for anaemia, U&Es, LFTs, TFTs, lipids, diabetes
+CXR + lung function tests (spirometry)
How is severity of HF symptoms graded? What are the grades?
NYHA - New York Heart Association Classification
Class 1: no limitation on activity
Class 2: comfortable at rest, symptomatic with ordinary activities
Class 3: Comfortable at rest, symptomatic with any activity
Class 4: Symptomatic at rest
How is chronic heart failure managed? What are the main principles?
RAMPS:
R: Refer to cardiology
A: Advise about condition
M: Medical treatment
P: Procedural and surgical management
S: Specialist heart failure MDT input
How urgently are patients with HF refered to echocardiography?
NT-proBNP between 400-2000 - within 6 weeks
NT-proBNP > 2000 - within 2 weeks
What is the first-line medical treatment for chronic heart failure?
ABAL
A: ACE inhibitor - e.g. ramipril - up to 10mg
B: Beta blocker - e.g. bisoprolol - up to 10mg
A: Aldosterone antagonist (if symptoms still persist) - e.g. spironolactone, eplerenone
L: Loop diuretics - e.g. furosemide, bumetanide
Give some examples of ACE inhibitors
ramipril
lisinopril
…-pril
Briefly explain the mechanism of action of ACE inhibitors
- low BP - kidneys release renin
- renin converts angiotensinogen into angiotensin I
- ACE converts angiotensin I into angiotensin II in the lungs - inhibited by ACE inhibitors
- angiotensin II constricts blood vessels and stimulates release of aldosterone (to retain salt and water in kidneys) -> both increase BP
Give some examples of aldosterone antagonists
eplerenone
spironolactone
…-one
Briefly explain the mechanism of action of aldosterone antagonists
aldosterone - produced by adrenal glands
- regulates salt and water balance
- retention of Na (and water)
- excretion of potassium
aldosterone antagonists block this action:
- lower BP
- prevent loss of K
Briefly explain the mechanism of action of loop diuretics
they block the reabsorption of Na and Cl in the thick ascending limb of loop of Henle
more Na and water is excreted in urine -> lowers BP and blood volume
increases loss of K
Give some examples of loop diuretics
furosemide
bumetanide
What medications can be used instead of ACE inhibitors if poorly tolerated in HF?
angiotensin receptor blockers - e.g. candesartan
Which patients with HF should not be given ACE inhibitors?
if they have valvular disease
When are aldosterone antagonists used in HF?
reduced ejection fraction
symptoms not controlled with ACE inhibitors and beta blockers
Why blood test should be done regularly for patients on HF medications? Why?
U&Es, renal function - ACEi, aldosterone antagonists and diuretics can cause electrolyte disturbances
ACEi and aldosterone antagonists can cause hyperkalaemia
What specialist treatments can be used in patients with HF? When are they typically used?
used in LV fraction < 35%
SGLT2 inhibitors - e.g. dapagliflozin
sacubitril + valsartan
ivabradine
hydralazine + nitrate
digoxin
What additional management is recommended in patients with HF?
vaccinations
stop smoking
optimise treatment of co-morbidities
written care plan
cardiac rehabilitation - personalised exercise programme
What surgical interventions can be used in patients with HF?
valve replacement - if valve disease
inplantable cardioverter defibrillator - if previous VT / VF
cardiac resynchronisation therapy - if ejection fraction < 35%, BBB
heart transplant
What is cardiac resynchronisation therapy (CRT)? When is it used?
biventricular (triple chamber) pacemakers
leads in RA, RV, LV
objective - to synchronise the contractions to optimise heart function
used in severe HF, with ejection fraction < 35% and widened QRS (e.g. in LBBB)
When is sacubitril-valsartan used in HF?
heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs
LV fraction < 35%
initiated after ACEi / ARB wash-out period
What is acute heart failure?
life-threatening emergency
sudden onset or worsening of symptoms of HF
decompensated AHF is more common
caused by reduced cardiac output due to functional/structural abnormality
What are some causes of de-novo AHF?
increased cardiac filling pressures and myocardial dysfunction usually as a result of ischaemia
viral myopathy
toxins
valve dysfunction
What are some causes of decompensated HF?
acute coronary syndrome
hypertensive crisis
acute arrhythmia
valvular disease
What are the signs and symptoms of AHF?
SoB
reduced exercise tolerance
oedema
fatigue
cyanosis
tachycardia
elevated JVP
displaced apex beat
bibasal crackles, wheeze
S3
How is AHF diagnosed?
bloods - anaemia, electrolyte abnormalities, infection
CXR - pulmonary venous congestion, interstitial oedema, cardiomegaly
echocardiogram - new onset HF, suspected post-MI or valvular problems, cardiogenic shock
BNP - >100mg/L
How is HF acutely managed?
IV loop diuretics - furosemide, bumetanide
O2 - if hypoxic (<94%)
vasodilators - e.g. nitrites - only if hypertension, myocardial ischaemia or valve regurgitation
- NOT in hypotension!
CPAP - if respiratory failure
What sign is typical for cardiac tamponade?
pulsus paradoxus - abnormally large drop in BP during inspiration
electrical alternans - alteration of QRS complex amplitudes on ECG
absent Y descent in JVP (only X - TAMpaX)
What are the classical features of cardiac tamponade?
Beck’s triad:
hypotension
raised JVP
muffled heart sounds
How do patients with typical angina present?
all 3 of the following:
- precipitated by physical exertion
- constricting pain in anterior chest, neck, shoulder, jaw, or arms
- relieved by GTN or rest in 5 minutes
How do patients with atypical angina present?
2 of the following:
- precipitated by physical exertion
- constricting pain in anterior chest, neck, shoulder, jaw, or arms
- relieved by GTN or rest in 5 minutes
and atypical symptoms:
- GI discomfort / nausea / SoB
What factors make diagnosis of stable angina more likely?
- higher age
- male
- CV risk factors
- history of coronary artery disease
What factors make diagnosis of stable angina less likely?
- continuous/prolonged pain
- pain unrelated to activity
- pleuritic pain
- pain associated with dizziness, tingling, palpitations, difficulty swallowing
What bedside tests are used to investigate angina?
- physical exam
- ECG (can have signs of past MI, but can be normal)
- FBC (anaemia)
- U&E (before starting ACEi or other meds)
- LFTs (before starting statins)
- lipid profile
- TFTs
- HbA1C, fasting glucose
What are modifiable cardiovascular risk factors?
smoking
high LDL levels
lack of physical activity
unhealthy diet
high alcohol intake
overweight / obesity
What are non-modifiable cardiovascular risk factors?
higher age
male
FH of CVD
ethnic background (e.g. south Asian)
What ECG changes could indicate ischaemia / previous MI?
pathological Q waves
LBBB (always abnormal)
ST and T abnormalities
What is cardiac stress testing?
assessment of heart function during exertion
- exercise (treadmill)
- medication (dobutamine)
assessment of heart function by
- ECG
- echocardiogram
- MRI
- myocardial perfusion scan
How can suspected angina be investigated?
cardiac stress testing
CT coronary angiography
invasive coronary angiography - catheter into femoral artery -> into coronary arteries under XR guidance -> injection of cotrast
What is gold standard investigation for coronary artery disease?
invasive coronary angiography
How is suspected angina managed?
RAMPS
Referral to cardiology (rapid access chest pain clinic)
Advise about diagnosis, management, safety netting
Medications
Procedural interventions
Secondary prevention
What are the main aims of medical management options of angina?
immediate symptomatic relief
long-term symptomatic relief
secondary prevention
What are the medications for immediate symptomatic relief in angina?
sublingual GTN
How is GTN used in stable angina?
ake the GTN when the symptoms start
Take a second dose after 5 minutes if the symptoms remain
Take a third dose after a further 5 minutes if the symptoms remain
Call an ambulance after a further 5 minutes if the symptoms remain
What are the main side effects of GTN?
hypotension
tachycardia
headaches
flushing
How is long-term symptomatic relief achieved in angina?
either one or combination of
- beta blocker (e.g. bisoprolol)
- calcium channel blocker (diltiazem, verapamil) - AVOID in HFrEF
if symptomatic still on monotherapy - increase to max dose
if still symptomatic - add the second drug class
What calcium channel blockers are used in angina management and when? (monotherapy / combination therapy)
monotherapy - rate-limiting Ca blocker - verapamil, diltiazem
combination with beta blockers - longer-acting dihydropyridine Ca blocker - amlodipine, modified release nifedipine
Why shouldn’t verapamil be administered with beta blockers?
risk of complete heart block
What specialist treatments are available for long-term symptomatic relief in angina? When are they offered?
offered when on monotherapy, still symptomatic, and cannot tolerate addition of beta blocker / ca channel blocker
- long-acting nitrates - isosorbide mononitrate
- ivabradine
- nicorandil
- ranolazine
Iva a Nico randili, Rano boli Lazy
What medications are used for secondary prevention in angina?
4A
Aspirin - 75mg OD
Atorvastatin 80mg OD
ACEi - if HTN, DM, CKD, HF also present
Already on beta blocker for symptomatic relief
What surgical options are available for angina management?
PCI - percutaneous coronary intervention
CABG - coronary artery bypass grafting
What is PCI?
percutaneous coronary intervention
- insertion of catheter into patients brachial / femoral artery
- catheter passes into coronary arteries
- injection of contrast
- if areas of stenosis - balloon dilatation and stent insertion -> coronary angioplasty and stenting
What is CABG?
Coronary artery bypass graft
offered in severe coronary artery stenosis
midline sternotomy incision
harvest of graft vessel:
- saphenous vein
- internal thoracic artery
- radial artery
What are the advantages and disadvantages of PCI over CABG?
advantages:
- faster recovery rate
- lower rate of strokes
disadvantages:
- higher rate of requiring repeat revascularisation
What is ACS?
acute coronary syndrome
umbrella term covering a number of acute presentations of ischaemic heart disease
- ST elevation myocardial infarction (STEMI) - ST elevation + elevated biomarkers
- non-ST elevation myocardial infarction (NSTEMI) - ECG changes, no ST elevation + elevated biomarkers
- unstable angina - ischaemic symptoms suggestive of an ACS and no elevation in troponins, with or without electrocardiogram changes indicative of ischaemia
What is the typical presentation of ACS?
CHEST PAIN
- central/left sided
- radiating to jaw / left arm
- heavy, constricting
- may be abnormal / not be present in certain groups (e.g. diabetics, elderly)
SoB
sweating
N+V
observations might be normal or only slightly altered (e.g. tachycardia)
What are the most important investigations in ACS?
ECG
cardiac markers - e.g. troponins
Which leads will be affected on ECG in anterior MI? What artery is involved?
V1-V4
LAD artery
Which leads will be affected on ECG in inferior MI? What artery is involved?
II, III, aVF
right coronary artery
Which leads will be affected on ECG in lateral MI? What artery is involved?
I, V5-V6
left circumflex artery
What are the main aims of ACS treatment?
prevent further deterioration (further occlusion)
revascularise the occluded vessel
treat pain
How is ACS treated?
MONA
Morphine - if severe pain
Oxygen if required (sats <94%)
Nitrates - caution if hypotensive
Aspirin
What is secondary prevention therapy in ACS?
aspirin
second antiplatelet (e.g. clopidogrel)
beta blocker
ACEi
statin
What are the diagnostic criteria for STEMI?
clinical symptoms consistent with ACS (lasting > 20 mins) with persistent (>20 mins) ECG changes in 2 or more contiguous leads:
- ST elevation
- new LBBB
In addition to the general ACS treatment, how is STEMI managed?
goal is to revascularise
second antiplatelet - clopidogrel (if on oral anticoag), prasugrel (if not on oral anticoag), ticagrelor
PCI
- should be offered within 12 hrs of symptom onset
- radial artery preferred
- drug-eluting stents used
fibrinolysis
- within 12 hrs of symptom onset if significant delay in PCI provision
- antithrombin drugs should also be given
In addition to the general ACS treatment, how is NSTEMI managed?
aspirin 300mg / fondaparinux (if no immediate PCI)
use risk stratification tool (e.g. GRACE)
- low risk -> conservative management: ticagrol (not high bleeding risk) or clopidogrel (high bleeding risk)
- intermediate/high risk -> PCI (immediate if unstable, within 72 hrs if stable) + prasugrel/ticagrol + unfractioned heparin
What complications can arise as a result of MI?
cardiac arrest
cardiogenic shock
chronic HF
tachyarrhythmias
bradyarrhythmias
pericarditis
LV aneurysm
acute mitral regurgitation - due to rupture of papillary muscles
What changes would you expect on a 12 lead ECG in posterior MI?
ST depression
What is aortic dissection?
tear in tunica intima of aortic wall
What other conditions is aortic dissection associated with? (risk factors)
cardiovascular RFs
HTN
trauma (including heavy lifting)
bicuspid aortic valve (and other conditions affecting aorta - valve replacement, coarctation)
collagen disorders - Marfan’s, EDS
pregnancy
How does aortic dissection typically present?
sudden onset ripping/tearing chest pain
pulse deficit - weak or absent carotid / brachial / femoral pulse
variation of 20+mmHg in systolic BP between arms
aortic regurgitation
HTN
focal neuro deficit
How is aortic dissection classified based on the Stanford classification?
type A - ascending aorta (2/3 of cases)
type B - descending aorta, distal to left subclavian origin
How is aortic dissection classified based on the DeBakey system?
type 1 - begins in the ascending aorta and involves at least the aortic arch, if not the whole aorta
type 2 - isolated to the ascending aorta
type 3a - begins in the descending aorta and involves only the section above the diaphragm
type 3b - begins in the descending aorta and involves the aorta below the diaphragm
How is aortic dissection investigated?
CXR - widened mediastinum
CT TAP angiography - false lumen (more suitable for stable patients)
TOE (TransOesophageal Echocardiography) - for unstable patients
ECG - to exclude other causes
How is aortic dissection managed?
analgesia - morphine
beta blockers - to manage BP and HR
intervention:
ASS and BooBs
Type A - systolic management and surgery
Type B - beta blockers and bed rest
- type A - open surgery (midline sternotomy) - synthetic graft to replace the damaged part of aorta
- type B - TEVAR (Thoracic EndoVAascular Repair) - catheter via femoral artery with a stent graft
(or conservative)
What are the possible complications of aortic dissection?
backward tear:
- aortic regurgitation
- MI
- cardiac tamponade
forward tear:
- unequal arm pulses and BP
- stroke
- renal failure
What are some common causes of atrial fibrillation?
SMITH
Sepsis
Mitral valve pathology
Ischaemic heart disease
Thyrotoxicosis
Hypertension
How does AF typically present?
palpitations
SoB
dizziness / syncope
irregularly irregular pulse
How is AF investigated?
ECG
- absent P waves
- narrow QRS tachycardia
- irregularly irregular ventricular rhythm
echocardiogram - used if signs of:
- valvular heart disease
- heart failure
- or if cardioversion is planned
What is paroxysmal AF?
episodes of atrial fibrillation that reoccur and spontaneously resolve back to sinus rhythm
episodes can last between 30 seconds and 48 hours
How can paroxysmal AF be investigated?
24 hrs Holter monitoring
cardiac event recorder (1-2 weeks)
What is valvular AF?
AF with significant mitral stenosis or a mechanical heart valve
What are the principles of AF management?
rate control - HR < 100
rhythm control
anticoagulation
What treatment - rate or rhythm control - should be offered in patients with AF as first line? When is it different?
all patients should be offered rate control as first line
except:
- reversible cause of AF
- new onset AF (last 48hrs)
- HF caused by AF
- symptoms despite effective rate control
What are the options for rate control in AF?
- beta blocker - atenolol, bisoprolol
- Ca channel blocker - diltiazem, verapamil
- digoxin
can do a combination of 2 if one drug is not providing adequate rate control
What patients should be offered rhythm control first in AF?
R - eversible cause
A - atrial flutter thought to be treatable with ablation
N - ew onset < 48 hours
C - linician thinks rhythm control is more suitable
H - eart failure thought to be primarily due to AF
What options exist for rhythm control in AF?
cardioversion
long-term pharmacological rhythm control
What main categories of cardioversion can be used in AF?
immediate - if either:
- AF present for < 48hrs
- life-threatening haemodynamic instability
delayed - anticoag for 3 weeks prior
What are the two main types of immediate cardioversion?
pharmacological
- flecainide
- amiodarone
electrical - under sedation/GA
What factors favour rhythm control as first line in AF?
Age <65 years
First presentation of AF
Symptomatic.
What is paroxysmal SVT?
episodes of sudden onset narrow complex tachycardia
typically AVNRT (but can be AVRT or junctional as well)
What are the acute management options for SVT?
- vagal manoeuvres - Valsalva, carotid sinus massage
- IV adenosine - rapid bolus of 6mg - >12 if unsuccessful -> 18 if unsuccessful
- electrical cardioversion
What are the options for prevention of SVT episodes?
beta blockers
radio frequency ablation
What are the ECG features of hypokalaemia?
U waves
small / absent T waves (can be inverted)
prolonged PR interval
ST depression
long QT
What medication should be given to a patient with AF post stroke?
warfarin or NOAC
What conditions is S3 (3rd heart sound) associated with?
caused by diastolic filling of the ventricle
normal in < 30 y.o.
present in
- LV failure - dilated cardiomyopathy
- constrictive pericarditis
- mitral regurgitation
How is delayed cardioversion in AF performed?
patient anticoagulated for at least 3 weeks
usually electrical cardioversion
What are the options for long-term pharmacological rhythm control in AF?
- beta blockers
- dronedarone - used for maintenance of normal rhythm post-cardioversion
- amiodarone - for patients in HF / LV dysfunction
When is catheter ablation performed in AF?
if antiarrhythmics not effective / tolerated / patient wants to avoid them
What are the options for catheter ablation in AF?
LA ablation - ablation of region between pulmonary veins and LA
AV node ablation - permanent pacemaker required
How should patients suitable for catheter ablation for AF anticoagulated?
4 weeks prior to procedure + during the procedure
What are the risks associated with catheter ablation for AF?
cardiac tamponade
stroke
pulmonary vein stenosis
What is CHA2DS2-VASc?
tool for assessing the need of anticoagulation in patients with AF
the higher the score, the higher the risk of TIA/stroke
Congestive HF
Hypertension
Age > 75 (2 points)
Diabetes
Stroke / previous TIA (2 points)
Vascular disease
Age 65-74
Sex - female
When is anticoagulation recommended, based on the CHA2DS2-VASc score?
0 - not needed
1 - consider anticoagulation in men
2 - offer anticoagulation
What score is used to assess the need for anticoagulation in AF patients?
CHA2DS2-VASc
What score is used to assess the risk of major bleeding in patients with AF on anticoagulation?
ORBIT
What factors does the ORBIT score consist of?
Older age (75+)
Renal impairment (eGFR < 60)
Bleeding previously (Hx of GI / intracranial bleed)
Iron (low Hb or haematocrit)
Taking antiplatelet medication
What is LA appendage occlusion?
option for patients with contraindications to anticoagulation and a high stroke risk
LA appendage is a common site for thrombus formation
LA appendage occlusion - insertion of catheter via femoral vein -> RA -> LA
insertion of plug into LA appendage
How is HTN managed in patients < 55y.o. or T2DM?
- ACE inhibitor (-pril)
or angiotensin receptor blocker (-sartan) - add Calcium channel blocker (-dipine; verapamil, diltiazem)
or thiazide-like diuretic (indapamide) - add either Ca channel blocker
or thiazide-like diuretic
How us HTN managed in patients > 55y.o. or African-Caribbean?
- Ca channel blocker (-dipine; verapamil, diltiadem)
- add angiotensin receptor blocker (African-Caribbean) (-sartan)
or ACE inhibitor (-pril)
or thiazide-like diuretic (indapamide) - add Ca channel blocker
or thiazide-like diuretic
What ECG variations are considered normal in athletes?
sinus bradycardia
junctional rhythm
first degree heart block
Mobitz type 1
How is hypertrophic obstructive cardiomyopathy managed?
Amiodarone
Beta blockers / verapamil
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis
Which drugs should be avoided in hypertrophic obstructive cardiomyopathy?
nitrates
ACE inhibitors
inotropes
What are the echo signs of hypertrophic obstructive cardiomyopathy?
MR SAM ASH
MR - mitral regurgitation
SAM - systolic anterior motion of anterior mitral valve leaflet
ASH - asymmetric hypertrophy
When should you offer ambulatory BPM or home BPM?
if BP > 140/90
What are the next steps if BP is > 180/120?
- admit for specialist assessment if
- signs of retinal haemorrhage or papilloedema or
- life-threatening symptoms ( new onset confusion, chest pain, HF signs, AKI)
- suspect phaeochromocytoma - urgent investigations for end-organ damage (ECG, bloods, urine dip)
- if organ damage -> immediate antihypertensives
- if no organ damage - > repeat readings within 7 days
Which patients with NSTEMI/unstable angina should have coronary angiography (with follow-on PCI if necessary)?
immediate: patient who are clinically unstable (e.g. hypotensive)
within 72 hours: patients with a GRACE score > 3% i.e. those at intermediate, high or highest risk
coronary angiography should also be considered for patients if ischaemia is subsequently experienced after admission
What are some poor prognostic factors in ACS?
age
HF (new or Hx)
peripheral vascular disease
reduced systolic BP
elevated initial cardio markers
cardiac arrest on admission
What anticoagulants are preferred in patients with mechanical valves?
warfarin
What are the two most common causative organisms of endocarditis?
staphylococcus aureus
staphylococcus epidermis - if < 2 months post valve surgery
What valve is most commonly affected in endocarditis in IVDU?
tricuspid valve (don’t TRI drugs)
Which drugs reduce mortality in LV failure?
ACE-inhibitors
Beta-blockers
Angiotensin receptor blockers
Aldosterone antagonists
Hydralazine and nitrates
How is chronic HF managed?
BASHeD
Beta blockers
ACEi / ARB
Spironolactone
Hydralazine + nitrates
Digoxin
What complication (blood) can arise from prosthetic valves?
haemolytic anaemia
What patients can receive nitrates in acute HF?
NOT hypotensive
hypertension
myocardial ischaemia
valve regurg
How are patients with acute HF and hypotension / cardiogenic shock managed?
inotropic agents - e.g. dobutamine
vasopressors - e.g. norepinephrine
mechanical circulatory assistance - e.g. intra-aortic balloon counterpulsation, ventricular assist devices
Should regular HF medications be stopped or continued in acute HF?
continued
beta blockers - stopped if HR < 50
If acute HF is not responding to treatment, what should you do?
CPAP
What cardiomarker is used to look for re-infarction?
CK-MB - returns to normal after 2-3 days
while troponin remains elevated for up to 10 days
When do you give ivabradine in HF?
patient has sinus rhythm > 75/min and a LVEF < 35% and have not responded to to ACE-inhibitor, beta-blocker and aldosterone antagonist therapy
What, other than HF, can cause raised BNP?
myocardial ischaemia
valvular disease
CKD
