Cardiology Flashcards
roles of ACEi?
HTN (in young, non afrocaribean)
diabetic nephropathy
secondary prevention for ischaemic heart disease
mechanism of action for ACEi?
activated by liver in phase 1 metabolism
prevent conversion of angiotensin 1 to 2
What are the side effects of ACEi?
cough - can occur up to a year after starting
hyperkalaemia
Hypotension
angioedema - may occur up to a year after
what is though to be the cause of the cough with ACEi?
increased levels of bradykinin?
What cautions should be taken with ACEi? What are the contraindications?
pregnancy /breast feeding - avoid
renal artery stenosis - avoid
aortic stenosis - could result in hypotension , caution
hereditary idiopathic angioedema
starting ACEi when potassium is >5 - seek specialist advice
How are the use of ACEi monitored?
UEs before and after starting
should accept a creatine rise up to 30% increase
Accept a potassium of up to 5.5
Outline the medical management of HTN?
<55 or T2DM
- ACEi
- ACEI + Ca channel blockers/ Thiazide diuretics
- all 3
- if K+ > 4.5 - add spironolactone. If >4.5 add B blocker or alpha blocker
> 55 or afrocaribean
- Calcium channel blockers
- ACEI + Ca channel blockers/ Thiazide diuretics
- all 3
- if K+ > 4.5 - add spironolactone. If >4.5 add B blocker or alpha blocker
Which drugs enhance the effects of adenosine and which block the effects?
theophyllines inhibit
dipyridamole enhances
Which condition should adenosine be avoided in?
asthma due to bronchospasm
What is the mechanism of action of adenosine?
a1 receptor agonist - blocks adenyl cyclase. less cAMP. K+ leaves cell. hyperpolerisation.
thus blocks AVN transiently (short half life)
used to treat SVTs
what are the adverse effects of adenosine?
chest pain
bronchospasm
flushing
can promote use of accessory pathways e.g. WPW
give examples of ADP (adenosine diphosphate) receptor blockers
clopidogrel
ticagrelor
prasugrel
Ticlopidine
how do ADP receptor inhibitors work?
bind ADP receptors which are P2Y1 and P2Y12. Mostly target P2Y12. this inhibits platelet aggregation and stabilisation.
ADP is one of the main platelet aggregation factors
Inhibits a different pathway to aspirin and thus can be used synergistically together.
In the current NICE guidelines, what is suggested as antiplatelet therapy for ACS?
In patients with ACS: aspirin + ticagrelor for 12 months as secondary prevention
In patients with ACS and undergoing PCI : aspirin + Ticagrelor/clopidogrel/prasugrel for 12 months and then aspirin alone there after
what are the adverse effects of ticagrelor ?
dyspnoea due to impaired clearance of adenosine.
what DDI exist for ADP receptor inhibitors?
clopidogrel use with PPIs - reduced antiplatelet effect of clopidogrel
TIA, stroke, high risk of bleeding or prasugrel hypersenstivity - absolute contraindications to prasugrel
high risk bleeding, intracranial haemorrhage or hepatic dysfunction - contraindication to ticagrelor. Also should avoid ticagrelor in asthma /copd due to dyspnoea effects
what is the chest compression ratio given to adults?
30:1
which rhythms are shockable? non shockable?
pulseless VT and VF = shockable
pulseless electrical activity and asystole = non shockable
How often and how much adrenaline is given in an arrest?
1mg ASAP for the non-shockables
after 3rd shock in shockables. rhythms
how can the shocks be given if a cardiac arrest is witnessed/ happens at the time you are ready?
3 consecutive shocks can be given
how is asystole/ pulseless electrical activity managed?
1mg adrenaline ASAP
no shocks just CPR
what are the 4Hs and 4Ts of a cardiac arrest?
Hs: hypoxia, hypotension, hyperkalaemia, hypothermia
T: thrombus, tamponade, tension pneumothorax, toxins
what is the class and action of amiodarone?
class III inhibits K+ channels - increases time taken to repolarise so prolongs next action potential. Also has some class I affects - inhibits Na VG channels
what type of arrhythmias is amiodarone used in?
atrial, nodal and ventricular tachycardia
why is a loading dose of amiodarone often used?
very long half like (days)
how is amiodarone given?
IV through central vein - causes thrombophlebitis
what are the DDIs of amiodarone?
Can interact with Cytochrome 450
decreases metabolism of warfarin
what monitoring is needed for amiodarone?
TFTs UEs LFTs CXR prior to starting
TFTs and LFTS every 6 months
what are adverse effects of amiodarone?
corneal deposits thyroid - hypo/hyperthyroid bradycardia/long QT pulmonary fibrosis/ pneumonitis hepatic fibrosis/ hepatitis peripheral neuropathy photosensitivity slate grey appearance thrombophlebitis at place its given
what class drug are the following…
candesartan
losartan
irbesartan
Angiotensin receptor 2 inhibitors
what are the side effects or ARBs?
hypotension
hyperkalaemia
What is the first and second line antiplatelet in ACS?
1st line : aspirin (lifelong) and ticagrelor (12 month)
2nd line: clopidogrel lifelong if aspirin is contraindicated
What is the first and second line antiplatelet in PCI?
1st line : aspirin (lifelong) and ticagrelor/prasugrel (12 month)
2nd line: clopidogrel lifelong if aspirin is contraindicated
What is the first and second line antiplatelet in TIA/ischaemic stroke?
1st line: life long clopidogrel
2nd line: aspirin + dipyrimadole lifelong
What is the first and second line antiplatelet in peripheral arterial disease?
1st line: clopidogrel life long
2nd line: aspirin life long
What is the pathophysiology of aortic dissection?
tunia intima tears
high pressure blood pools between layers of intima and media
separates layers and increases outside diameter of vessel.
what is type A and B aortic dissection?
A: tear near the heart or the section of aorta travelling upwards
B: tear in lower/descending aorta
both A and B can extend into abdomen
what are the causes of aortic dissection ?
causes: chronic high blood pressure aortic coarctation connective tissue disorders - ehlers danlos/marfarns aneurysms trauma bicuspid aortic valve turners and noonans pregnancy syphillis
What issues arise from aortic dissections?
blood pool between intima and media can continue to extend…
- aortic regurgitation - cause tamponade if it reaches the heart - can rupture through the tunica externa and leak into mediastinum - can expand and put pressure on other arteries e.g. renal artery
other complication MI - usually involving RCA
what are the symptoms of aortic dissection?
sharp pain in chest that radiate to back, tearing in nature
weak pulses at peripheries
difference in blood pressure - between L and R arm
aortic regurgitation
How can a aortic dissection be managed?
type A - surgery (blood pressure needs to be managed to 100-120mmHg whilst awaiting)
Type B - B blockers and nitroprusside, conservative/ IV labetolol
which type of aortic dissection is most common?
type A
what are the two classifications for aortic dissection?
stanford - type A and B
DeBakey - Type 1 to 3
what is the debakey classification for aortic dissection?
type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally
type II - originates in and is confined to the ascending aorta
type III - originates in descending aorta, rarely extends proximally but will extend distally
How can an aortic dissection be investigated?
CXR - widening of mediastinum
CT angiography of the chest, abdomen and pelvis is the investigation of choice
suitable for stable patients and for planning surgery
a false lumen is a key finding in diagnosing aortic dissection
Transoesophageal echocardiography (TOE) more suitable for unstable patients who are too risky to take to CT scanner
What are the risk factors / causes of aortic stenosis?
bicuspid valve
chronic rheumatic fever
stress overtime - older adults
williams syndrome - supravalvular aortic stenosis
HOCM - subvalvular
what are the complications of aortic stenosis?
left ventricular hypertrophy and HF
reduction in blood flow
- syncope, angina etc
Microangiopathic haemolytic anaemia - damage to RBC as they are forced through stenosis
what are the causes of aortic regurgitation?
idiopathic valve damage - rheumatic fever , Infective endocarditis aortic dissection sphyllis aneuryms RA/ SLE bicuspid valve
what murmur is heard in aortic stenosis/ regurgitation?
A.S: ejection systolic murmur, radiates to carotids
A.R: early diastolic murmur
what are the symptoms/signs of aortic regurgitation?
bounding pulse - increased pulse pressure - Quincke's sign (nailbed pulsation) - De Musset's sign (head bobbing) collapsing pulse - mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams
Heart failure - due to dilation of ventricles
what are the symptoms of aortic stenosis?
Classic triad:
chest pain
syncope
angina
what are the features of severe 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
how is aortic stenosis managed?
if asymptomatic then observe the patient is 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
cardiovascular disease may coexist. For this reason an angiogram is often done prior to surgery so that the procedures can be combined
balloon valvuloplasty is limited to patients with critical aortic stenosis who are not fit for valve replacement
What will the NEWS score be for an MI?
often normal
maybe tachycardic
unless complications of MI
What leads represent antior/ inferior/lateral MIs and which arteries do these correspond to?
Anterior MI : V1-V4 = LAD
Inferior MI – II, III, aVF = RCA
Lateral MI = I, V5-6 = left circumflex
Most heart attacks involve left ventricle – above 3 vessels supply left ventricles in different ways. The right ventricle and atria don’t often get affected.
what is the difference between subendocardial and transmural infarcts?
Subendocardial infarct – NSTEMI – only inner part of myocardium is necrosed.
Transmural infarct = STEMI = whole myocardium necrosed.
how is an MI diagnosed?
- ECG
- Troponin I and T , CK-MB = enzymes released
when are the cardiac enzymes most elevated during an MI? Which cardiac enzyme is best at distinguishing between two MIs that have occurred?
Troponin I and T elevated after 2 -4 hours and peak at 48hours
o CK-MB elevated after 2-4 hours but then returns to normal at 48 hours. Thus because it returns to normal more quickly it can be used to detect a second MI.
How are MIs treated - basic first steps of management?
MONA
morphine IV, O2 titrated, nitrates sublingual/IV (caution if hypotensive), aspirin 300mg
How are STEMIs managed?
MONA
Further antiplatelet prior to PCI –
if the patient is not taking an oral anticoagulant: prasugrel or ticagrelor
if taking an oral anticoagulant: clopidogrel
Once STEMI confirmed need to decide if coronary reperfusion therapy is necessary (PCI or fibrinolysis)
How quickly should PCI be performed?
within 12 hours of symptoms. Can be after if still evidence of ongoing ischaemia
How is PCI performed?
Now drug eluting stents are used – less likely to restenose.
Give prasugrel for PCI
PCI – balloon angioplasty followed by stent insertion. via radial artery – give unfractionated heparin + glycoprotein IIb/IIIa inhibitor
patients undergoing PCI with femoral access: bivalirudin with bailout GPI
when is fibrinolysis offered?
if PCI cant be offered
if no contraindication
How is fibrinolysis performed?
fibrinolytic agent
Also give antithrombin drug e.g fondaparinux
Repeat ecg after 60-90 mins and if resolved if still ischaemic – PCI considered
what scoring system is used to decide on management of NSTEMI?
What does this scoring system use and what does it show.
GRACE
Age, HR, BP, renal function, cardiac (Killip class) , cardiac arrest on presentation, ECG findings, troponin levels
Over 9% is highest mortality risk, 6-9 % still considered high. Below 3% is considered low
Which NSTEMI patients will have PCI during admission?
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 is the secondary prevention for MIs?
o Aspirin o Second antiplatelet – clopidogrel o B blocker o ACE inhibitor o Statin
what is the criteria for NSTEMI?
Clinical: symptoms consistent with ACS (>20mins of persistent chest pain)
ECG changes in 2 or more consecutive leads of:
o >2.5 small squares ST elevation in lead V2-3 in men <40yrs or >2 small squares in these leads in men >40yrs
o 1.5 small squares elevation in leads V2-3 in women.
o 1 small square ST elevation in other leads.
o New LBBB
what are the complications of an MI?
- Shock and acute heart failure
- Pericarditis
- Rupture of myocardium/ septum
- Embolus
- Arrhtyhmia
- Dresslers syndrome
What are the poor prognostic factors post MI?
- age
- development (or history) of heart failure
- peripheral vascular disease
- reduced systolic blood pressure
- Killip class*
- initial serum creatinine concentration
- elevated initial cardiac markers
- cardiac arrest on admission
- ST segment deviation
What is the Kilip class system?
system used to risk stratify post MI
- no clinical signs of heart failure - 6% 30 day mortality
- lung crackles, S3 - 17% 30 day mortality
- frank pulmonary oedema - 38% 30 day mortality
- cardiogenic shock - 81% 30 day mortality
what is pericarditis?
what are the complications?
inflammation of pericardium - made up of outer fibrous and inner serous layer. fluid can accumulate between these and lead to pericardial effusion which can lead to tamponade.
Chronic inflammation can result in constrictive pericarditis
what are the causes of pericarditis?
idiopathic viral - coksackie malignancy connective tissue disorders dresslers uraemic pericarditis (bread and butter appearance) radiation drugs hypothyroid
what are the symptoms of pericarditis?
chest pain
worse on inspiration
better leaning forward
fever/ flu like
friction rub
no productive cough
tachycardia/ tachypnoea
what are the ECG changes seen in pericarditis?
wide spread saddle shaped ST elevation
PR depression - most specific
T flattens eventually and ST flattens later too.
how can pericarditis be investigated?
ECG
CXR - widened mediastinum
ECHO - shows effusion
how is pericarditis managed?
NSAIDs and Colchicine
pericardiocentesis if effusion
pericardectomy for constrictive pericarditis
how is angina managed?
aspirin and statin for all patients unless contraindicated
sublinguial GTN
Bblockers/ CaB - based on comorbidities etc
Can give both Bblockers and CaCB if still symptomatic and on max dose of one.
If cant tolerate both - use long acting nitrate
name 3 long acting nitrate…
ranolazine
nicorandil
ivabradine
What is the problem with using nitrates for angina etc? How can this be overcome?
tolerance can develop
this can be overcome by using modified release or having smaller doses more often.
which particularly cause of pericarditis can cause constrictive pericarditis?
TB
what are the signs/symptoms of constrictive pericarditis?
dyspnoea pericardial knock - loud S3 Right sided HF signs - hepatomegaly, raised JVP, ascites kussmaul sign JVP shows prominent X and Y descent
what might be seen on CXR for constrictive pericarditis?
cardiac calcifications
what are the differences between cardiac tamponade and constrictive pericarditis?
Tamponade:
- kussmaul sign absent
- Absent Y descent
- pulsus paradox - present
constrictive pericarditis
- kussmaul sign positive
- X and Y on JVP are present
- pulsus paradox - absent
What is Becks Triad seen in Cardiac tamponade?
raised JVP
low BP
muffled heart sounds.
What ECG sign is seen in cardiac tamponade?
Alternating QRS complex heights.
What change is seen in JVP waveform in Cardiac tamponade?
absent Y descent - limited right ventricle filling.
What is arrhythmogenic right ventricular cardiomyopathy?
ARVC - inherited cardiovascular disease
presents as palpitations, syncope or sudden cardiac death
what is the most common and second most common cause of sudden cardiac death in young?
- HOCM
2. ARVC
what is the pathophysiology behind ARVC?
Autosomal dominant (variable expression pattern)
right ventricular myocardium is replaced by fatty and fibrofatty tissue
50% have a mutation of one of the several genes which encodes components of desmosome
What ECG findings are found in ARVC?
V1 -3 - T wave inversion
Epsilon wave found in 50% of patients - this is a terminal notch in QRS
what are the ECHO findings for ARVC?
enlarged hypokinetic right ventricle with thin free wall
what Ix can be used for ARVC?
ECG
ECHO
MRI - shows fibrofatty tissue
how is ARVC managed?
sotalol
catheter ablation to prevent VT
implantable cardioverter defib
what is Naxos disease?
an autosomal recessive variant of ARVC
a triad of ARVC, palmoplantar keratosis, and woolly hair
What are the causes / risk factors of AF?
M - mitral valve disease (stretches atrial and damages myocytes) I - ischaemic heart disease T - thyroid R A - alcohol L - lung pathology (pneumonia)
where does AF originate?
In pulmonary veins
what are the types of AF?
First episode
paroxysmal / reccurent - 2 or more episodes. episode lasts <7days
persistent AF - >7 days
permanent - clinician decides not to take any action to revert.
what are the uses of radiofrequency catheter ablation in AF?
Can ablate AV note to prevent SVTs + implantable pacemaker
Can do a maze proceedure - by making ablation you can create a path for electrical signals to travel in a more predictable way
How is the arrhythmia element of AF controlled?
rate control - Beta blocker/ CaB (diltiazam). If one of these doesnt work instead can combine them OR add in digoxin.
rhythm control (cardioversion) - electrical (DC cardioversion) or pharmacological. - must have had only a short duration of symptoms (<48hours) OR be anticoagulated for a 3 weeks prior
What is the CHADSVASC score?
C - congestive heart failure H - hypertension A 2 - age >75 (2 points), 65-74 (1 point) D - diabetes S2 - previous stroke/TIA - 1 point V- vascular disease (IHD, PVD) S - female sex
when is anticoag used using CHAD VASc?
0 - no treatment
1 - males consider anticoag
2 - offer anticoag
What is the HASBLED score?
H - hypertension
A - abnormal renal function (creatinine >200/ dialysis )
- abnormal LFTs (cirrhosis, billirubin 2x , ALT/AST/ALP >3x normal) - 1 point for renal and 1 point for liver
S - stroke history
B - bleeding history / tendancy
L - labile INR
E - elderly >65
D - drugs predisposing to bleed (antiplatelets, NSAIDS, alcohol) - 1 for drugs, 1 for alcohol.
> /= 3 is a high risk
When is electrocardioversion used in AF?
Electrical cardioversion as an emergency if the patient is haemodynamically unstable
electrical or pharmacological cardioversion as an elective procedure where a rhythm control strategy is preferred.
How does electrical DC cardioversion work?
synchronised to R wave - to prevent VF
what pharmacological agents are used for cardioversion and when?
flecanide - if no structural heart disease
amiodarone - if there is structural heart disease
for patients who have had AF for >48 hours that cannot be anticoagulated for 3 weeks prior to cardioversion, what other option is there?
TOE to check for thrombus in left atrial appendage.
if excluded - patients can be heparinised and cardioverted immediately.
NICE recommends electrical cardioversion in this scenario.
should anticoagulation be given post cardioversion?
for those who had AF <48 hours - no
for those who had AF >48 - yes continue for further 4 weeks.
how are patients with a Stroke + AF managed in terms of future clotting risk?
warfarin / DOAC
rather than antiplatelets
why is digoxin not first line for AF but when is it prefered?
Not good at controlling rate during exercise
prefered in those with coexistent HF.
what agents can be used for rhythm control in AF?
sotalol
amiodarone
flecanide
what factors favour rate control or rhythm control in AF?
rate:
- >65yrs
- history of IHD
rhythm:
- <65yrs
- symptomatic
- first presentation
- lone AF/ AF secondary to precipitant
- congestive heart failure
when is catheter ablation for AF offered?
in those who dont respond or want to avoid anti-arrhythmics
when is catheter ablation for AF offered?
in those who dont respond or want to avoid anti-arrhythmic
When is anticoagulation needed for catheter ablation in AF?
4 weeks before the preceedure.
afterwards still use CHADsVAS to decide if anticoag is needed ( still have a stroke risk even if in sinus rhythm)
what are the complications of catheter ablation in AF?
cardiac tamponade
stroke
pulmonary valve stenosis
what is a atrial myxoma?
most common primary cardiac tumour
where do atrial myxomas mainly occur?
left atrium - mainly attached to fossa ovalis
who are atrial myxomas most common in?
females
what are the symptoms/features of atrial myxomas?
systemic - dyspnoea, fatigue, clubbing, weight loss, fever
AF
mid diastolic murmur - ‘tumour plop’
emboli
what is seen on echo for atrial myxomas?
pedunculated heterogeneous mass typically attached to the fossa ovalis region of the interatrial septum
What are the uses of atropine and what type of drug is this?
Antagonist of the mAChR
used to treat organophosphate poisoning
and symptomatic bradycardias
no longer used for cardiac arrest
What are the effects of atropine?
tachycardia
Mydriasis
Where is B type natiuretic peptide produced?
primarily by myocytes of left ventricle
what can raise levels of BNP?
HF mainly
other cardiac dysfunction - valvular disease, ischaemia
CKD
what can reduce BNP levels?
ARBs, ACEi, diuretics
what are the effects of BNP?
vasodilation
inhibits RAAS pathway
diuresis and natriuresis
How is BNP used in the diagnosis of HF?
if low (<100) then HF unlikely so used to rule out HF. If high can indicate the need for ECHO to confirm HF
Can be used to monitor treatment of HF
Also used in prognosis - the higher the worse
what are the indications for B blockers?
angina secondary prevention for ACS anxiety long QT AF (and other arrhythmias) HF HTN thyrotoxicosis migraine prophylaxis
what are the side effects of B blockers?
bronchospasm bradycardia fatigue cold peripheries erectile dysfunction sleep disturbance inc nightmares
when are B blockers contraindicated?
uncontrolled HF
asthma
sick sinus syndrome
concurrent verapamil use - can induce severe bradycardia
what are the complications of a bicuspid aortic valve?
higher risk of…
aortic regurg
aortic stenosis
aortic dissection and aneurysm formation from ascending aorta
what is a left dominant coronary circulation?
the posterior descending coronary artery arises from the circumflex artery rather than the RCA
what conditions is bicuspid aortic valves associated with?
Turners
left dominant coronary artery circulation
around 5 % also have a coarctation of aorta
what is Bivalirudin?
reversible direct thrombin inhibitor
used in ACS
if a blood pressure cuff is too small - will the measurement be an overestimate OR underestimate?
overestimate
if too large - underestimate
if the arm is below the level of the heart, will a blood pressure reading be over or under estimate?
Over estimate if below level
underestimate if arm is raised above heart
if each arm gives a different BP reading, which should be taken?
the highest reading
What are the causes of broad complex tachycardias?
VT - until proven otherwise
SVT with aberrant conduction
What features on an ECG suggest VT rather than SVT with aberrant conduction?
AV dissociation positive QRS concordance in chest leads marked left axis deviation fusion/capture beats Hx of IHD lack of response to adenosine/ carotid sinus massage ventricular rate >160
what is Brugada syndrome?
inherited cardiovascular disease that may present with sudden cardiac death
inherited in autosomal dominant pattern
number of variants but most common gene is SCN5A which encodes a sodium channel protein of myocardium
who is brugada syndrome most common in?
asians
what are the ECG changes found in brugada syndrome?
convex ST elevation >2mm (or >1mm in V1-3) followed by negative T wave
partial RBBB
how is brugada syndrome investigated?
ECG changes
can give flecanide/ ajmaline and ECG changes become more prominant
how is brugada managed?
Implantable cardioverter defibrilator
What is Buerger’s disease?
small/medium vessel vasculitis strongly associated with smoking
a.k.a. thromboangiitis obliterans
what are the features of Buerger’s disease?
extremity ischaemia - intermittent claudication, ulcers
Raynauds
superficial thrombophlebitis
what is the oxygen saturation of blood returning to right atrium? left atrium
right heart - 70%
left heart - 98-100%
If there is an ASD or VSD what happens to oxygenation saturations of blood in different chambers of the heart?
normally - right side is 70%, left is 100%
ASD - the right side 85%, legt 100%
VSD - right atrium 70% (as normal), the rest of right heart 85%, left heart 100%
If there is an ASD or VSD what happens to oxygenation saturations of blood in different chambers of the heart?
normally - right side is 70%, left is 100%
ASD - the right side 85%, legt 100%
VSD - right atrium 70% (as normal), the rest of right heart 85%, left heart 100%
If there is a PDA what happens to oxygenation saturations of blood in different chambers of the heart?
right atrium and ventricle - 70% (as normal)
pulmonary artery = 85% (due to mixing)
left heart = 100%
what happens to O2 saturations of the heart if there is eisenmengers?
O2 saturations drop on left side of heart ..
E.g. Eisenmengers with VSD… the left ventricle and aorta drop to 85% O2 sats.
which cardiac enzyme is the first to rise in MI?
myoglobin
how long for CKMB and troponins to return to normal following MI?
troponins 10 days
CKMB - 2-3 days
myoglobin 1-2 days
what markers are raised in MI?
Troponin I , T CK MB CK LDH AST
what is a SPECT scan?
Single Photon Emission Computed Tomography (SPECT) scans
uses technetium radioisotope to assess myocardial perfusion and viability.
compares myocardium in rest and stress to identify areas of ischaemia.
what is a MUGA?
Multi Gated Acquisition Scan, also known as radionuclide angiography
radionuclide (technetium-99m) is injected intravenously
the patient is placed under a gamma camera
may be performed as a stress test
can accurately measure left ventricular ejection fraction. Typically used before and after cardiotoxic drugs are used
what are the two types of cardiac CT?
calcium score: to look at atherosclerotic plaque calcium to give a calcium score (predicts risk of ischameia)
contrast enhanced CT - visualises coronary arteries
what are the uses of cardiac MRI?
view structure of heart - gold standard
assess myocardial perfusion using gadolinium
what are the different types of genetic cardiomyopathy?
genetic
- HOCM
- Arrhythmogenic right ventricular dysplasia
mixed:
- dilated cardiomyopathy
- restrictive cardiomyopathy
acquired:
- peripartum cardiomyopathy
- takotsubo cardiomyopathy
secondary: infective infiltrative (amyloidosis) storage(haemachromatosis) toxicity (alcohol, doxorubicin) inflammatory (sarcoidosis) endocrine neuromuscular nutritional deficiency autoimmune (SLE)
what gene is mutated in HOCM?
B myosin heavy chain
What are the ECHO findings of HOCM?
Mitral regurgitation
systolic anterior motion (SAM)
anterior mitral valve
asymmetric septal hypertrophy
what pattern of inheritance is HOCM ?
autosomal dominant
What are the causes of dilated and restrictive cardiomyopathy?
dilated: alcohol, coxsackie, wet beri beri, doxorubicin
restrictive - amyloidosis, post radiotherapy, loefflers endocarditis
when does peripartum cardiomyopathy develop, who is it most common in?
last month of preg and 5 months after
more common in older women , greater parity and multiple gestations
What is Takotsubo cardiomyopathy?
stress induced cardiomyopathy
transient apical ballooning of the myocardium
what are the infective causes of cardiomyopathies?
coxsackie B
Chagas disease
What endocrine conditions can cause cardiomyopathies?
Diabetes
thyrotoxicosis
Acromegaly
what neuromuscular conditions can lead to cardiomyopathy?
Duchennes/Becks
Friedreich’s ataxia
myotonic dystrophy
which nutritional deficiency can cause cardiomyopathy?
thiamine = beri beri
What is Catecholaminergic polymorphic ventricular tachycardia?
form of inherited cardiac disease
associated with sudden cardiac death
autosomal dominant
what gene is mutated in catecholamine polymorphic ventricular tachycardia?
Ryanodine receptor (RYR2) gene mutation - found in myocardial sarcoplasmic reticulum
what are the features/symptoms of catecholamine polymorphic ventricular tachycardia?
exercise or emotion induced polymorphic ventricular tachycardia resulting in syncope
sudden cardiac death
symptoms generally develop before the age of 20 years
how is catecholamine polymorphic ventricular tachycardia managed?
B blockers
implantable defib
Which antihypertensive are centrally acting?
methyldopa
clonidine
moxonidine - alpha 2 receptor stimulation
what is the main cause of cholesterol emboli ?
vascular surgery
angiography
(but also atherosclerosis)
what are the features of a cholesterol emboli?
eosinophilia
purpura
renal failure
livedo reticularis
what are the DDI with clopidogrel?
PPI - make clopidogrel less effective
lansoprazole is okay to use
what is the mechanism of action of clopidogrel?
antagonist of the P2Y12 adenosine diphosphate (ADP) receptor, inhibiting the activation of platelets
class of drug = thienopyridines
What rate do atria contract in atrial flutter?
300 bpm
What is the pathophysiology behind atrial flutter?
Normally SAN –> AVN
In atrial flutter there are re-entry rhythms in atria so atria contract again and again
what are the different types of atrial flutter?
type 1 - single re-entry circuit that moves around the tricuspid valve isthmus in counter clockwise
type 2 - re-entry circuit in L or R atrium. less defined location
what are the causes of atrial flutter?
IHD - damage to myocytes
similar causes to AF
what are the ECG changes for atrial flutter?
saw tooth pattern - multiple contractions - flutter wave, no p.
1:2/3/4 ratio with QRS
what are the symptoms of atrial flutter?
If there is SVT - can lead to tachycardia, dyspnoea, fatigue, HF
Clots
what is the management of atrial flutter?
Like AF
Anticoag B blocker Rhtyhm control DC cardioversion ablation - of tricuspid valve isthmus = curative in most.
How can flutter be identified as a cause of an SVT?
carotid sinus massage/ adenosine - blocks AVN
What is the ostium primum, secundum and foramen ovale?
ostium primum - first gap between atria and ventricles.
This is closed by septum primum
The Septum primum then develops a gap further up called ostium secundum which remain.
A septum secundum then forms alongside the septum primum and a gap is left at the bottom of this septum = foramen ovale.
after birth the gaps can close. and foramen ovale is shut
What are the main causes of Atrial septal defects?
Ostium secundum = most common congenital heart defect in adults. The Ostium secundum doesnt grow enough during development and thus cant reach to shut with ostium primum
Other ASD cases are due to ostium primum
what are ASDs associated with?
fetal alcohol syndrome
ostium primum - down syndrome
ostium secundum - associated with Holt-Oram syndrome (tri-phalangeal thumbs)
what is the management of ASD?
children are monitored in the hope it will close
otherwise can close surgically
what are the features of ASD?
ejection systolic murmur, fixed splitting of S2
embolism may pass from venous system to left side of heart causing a stroke - paradoxical embolus
which ASD presents earliest?
Ostium primum
what other heart abnormality is ostium primum associated with?
abnormal AV valves
What ECG may be seen with ostium primum ?
RBBB with LAD
prolonged PR interval
what is LEV’s disease?
lenegre lev syndrome
describes the idiopathic causes of heart block
fibrosis progressive overtime over AVN.
what are the causes of heart block?
LEVs disease (idiopathic) IHD cardiomyopathy myocarditis electrolytes
what are the different types of heart block?
first degree - long PR, signals get to ventricle but delayed. often no symptoms.
second degree - type 1: PR increases progressively each time, misses one and restarts. assymptomatic or maybe light headed
second degree type 2 - PR fixed but misses conduction in a 2:1, 3:1 etc mannor. syptomatic - fatigue, syncpe, chest pain
3rd degree - no communication, P wave and QRS not related.
How is heart block managed?
for type 2 mobitz and 3rd degree - pace maker
otherwise can investigate and correct cause.
if first degree - no Mx
What is the PR interval measrued as in 1st degree heart block?
> 0.2s
How do you decide if someone with an episode of chest pain should go to hospital?
current chest pain or chest pain in the last 12 hours with an abnormal ECG: emergency admission
chest pain 12-72 hours ago: refer to hospital the same-day for assessment
chest pain > 72 hours ago: perform full assessment with ECG and troponin measurement before deciding upon further action
how is anginal chest pain defined by NICE?
- constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
- precipitated by physical exertion
- relieved by rest or GTN in about 5 minutes
patients with all 3 features have typical angina
patients with 2 of the above features have atypical angina
patients with 1 or none of the above features have non-anginal chest pain
what is the first line investigation for patients with chest pain who cant e diagnosed with angina by clinical symptoms alone?
CT coronary angiogram = 1st line
2nd line - non invasive cardiac imaging e.g. SPEC, stress ECHO, MRI
How is HF investigated (NICE guidance)?
NT-proBNP = 1st line Ix
if high - specialist in 2 weeks
if raised - specialist in 6 weeks
what can increase BNP?
Left ventricular hypertrophy Ischaemia Tachycardia Right ventricular overload Hypoxaemia (including pulmonary embolism) GFR < 60 ml/min Sepsis COPD Diabetes Age > 70 Liver cirrhosis
what can decrease BNP?
Obesity Diuretics ACE inhibitors Beta-blockers Angiotensin 2 receptor blockers Aldosterone antagonists
what is coarctation of the aorta?
congenital narrowing of the descending aorta
who is coarctation most common in?
males
What are the clinical features of coarctation of the aorta?
infants: HF
Adults: HTN
radiofemoral delay
mid systolic murmur (loudest over the back)
notching of inferior border of ribs (due to collateral vessels)
apical click from aortic valve
what conditions is coarctation of the aorta associated with?
Turners
bicuspid aortic valves
berry aneurysm
neurofibromatosis
How are patients with previous ACS and need for antiplatelets AND Atrial fibrilation with need for anticoagulation managed?
if an indication for anticoagulant exists (for example atrial fibrillation) it is indicated that anticoagulant monotherapy is given without the addition of antiplatelets
due to high risk of bleeding
How are patients post acute ACS/PCI and need for antiplatelets AND Atrial fibrilation with need for anticoagulation managed?
in these patients, there is a much stronger indication for antiplatelet therapy
generally patients are given triple therapy (2 antiplatelets + 1 anticoagulant) for 4 weeks-6 months after the event and dual therapy (1 antiplatelet + 1 anticoagulant) to complete 12 months
What are the 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 the examples of acyanotic CHDs?
ASD VSD - most common PDA coarctation of aorta aortic valve stenosis
What are the examples of cyanotic CHD?
Tetralogy of fallot
transposition of great vessels
tricuspid atresia
What is the most common cyanotic CHD?
Tetralogy of fallot
however only presents after 1-2 months and thus at birth the transposition of great vessles is seen more
what does the Left coronary artery divide into and what do these supply?
left anterior descending:
- travels down anterior AV sulcus
- anterior 2/3 of AV septum, anterolateral papillary muscle, anterior surface of left ventricle
left circumflex artery:
- travels around left side of heart
- supplies left atrium and posterior side of left ventricle
what does the Right coronary artery supply? what does it split into?
Right coronary artery supplies SAN
Then splits into right marginal artery and posterior descending artery
what does the branches of RCA supply?
right marginal artery - right ventricle (travels down the right side of the heart along the margin)
posterior descending artery - travels down posterior AV sulcus towards apex. supplies posterior 1/3 of AV septum, posterior 2/3 of ventricular walls and part of papillary muscle.
How does the LAD and posterior descending artery meet?
make anastomoses at the apex of the heart
where does the posterior descending artery branch from?
mostly RCA (right dominant circulation)
but sometimes LCA (left dominant circulation) or sometimes both (co-dominant circulation - very rare)
when is blood flow through coronary vessels maximal?
diastole
during systole they are compressed
how are the cardiac veins arranged?
great cardiac vein - in anterior intraventricular sulcus
middle cardiac vein - posterior intraventricular sulcus
small cardiac vein - inferior margin of right heart
all drain in the coronary sulcus into right atrium
what class of drug is dabigatran?
direct thrombin inhibitor
what are the indications for dabigatran use?
VTE prophylaxis post hip/knee surgery
stroke prevention in those with non-valvular AF who have one or more of the following:
- > 75yrs
- > 65yrs + Diabetes /Coronary artery disease/ HTN
- previous stroke, TIA or systemic emboli - left ejection fraction <40%
- NYHA classification 2 or more
what are the contraindications/ cautions of dabigatran?
reduce dose in renal failure
cant prescribe if creatinine clearance <30
what medication can be used to reverse dabigatrans effects?
Ibarucizumab
what is the blood pressure target for diabetics?
<140/90 mmHg for type 2
for type 1 <135/85 unless albuminuria or 2 or more featurs of metabolic syndrome in which case -<130/80mmHg
what is the first line antihypertensive in diabetics?
which medications should be avoided?
ACEi (renoprotective effect)
Africocaribeans - offered ACEi + thiazide/CaCB
use of B blockers should be avoided esp with thiazides as it can lead to insulin resistance/ alter autonomic response to hypoglycaemia.
what is the frank starling relationship?
increase in preload - increase in contraction (up to a point)
increase in end diastolic volume increases SV
what is dilated cardiomyopathy?
most common form of cardiomyopathy
heart is dilated so
reduced stroke volume due to impaired contraction (systolic dysfunction)
eccentric hypertrophy seen (sarcomeres added in series)
what are the symptoms/features of cardiomyopathy?
S3 gallop dyspnoea orthopnoea PND balloon appearance of heart on Xray systolic murmur - tricuspid / mitral regurg may occur from stretching.
what are the causes of dilated cardiomyopathy?
idiopathic
myocarditis - Coxsackie B, HIV, diphtheria, Chagas disease
IHD
peripartum
HTN
drugs - alcohol, cocaine, doxorubicin
inherited - duchennes, genetic predisposition
infiltrative - haemachromatosis, sarcoidosis
what is the mechanism of action of dipyrimadole?
inhibits phosphodiesterase elevating platelet cAMP levels which reduces intracellular Ca
reduce cellular uptake of adenosine
inhibit thromboxane
overall platelet inhibition.
what are the DVLA rules with HTN?
no need to form DVLA
for HGV cant drive if resting BP >180/100
What are the rules behind angioplasty, CABG and ACS with driving?
angioplasty - 1 week off
CABG - 4 weeks off
ACS - 4 weeks off (1 week if successfully treated with angio)
what are the rules behind driving and angina?
must stop if getting symptoms at rest/ behind the wheel.
what are the rules behind driving and…
pacemaker insertion
ICD
catheter ablation
?
pacemaker insertion - 1 week off
ICD: if implanted for sustained ventricular arrhythmias - 6 months off. if implanted prophylactically - cease for 1 month. if HGV cant drive with ICD
catheter ablation - 2 days off
what are the rules behind driving and aortic aneurysm?
6cm or more - inform DVLA
liscencing permitted with annual review
if 6.5 or more - no driving
what are the rules behind driving and heart transplant?
no driving for 6 weeks after
no need to inform DVLA
what is ebstein anomaly?
CHD with low insertion of tricuspid valve
results in large atria and small ventricle
(atrialisation of right ventricle)
what is Ebstein anomaly caused by?
exposure to lithium in utero
what is Ebstein anomaly assocaited with?
PFO or ASD
Wolff parkinson white
what are the clinical features of ebstein anomaly?
cyanosis
prominent ‘a’ wave in the distended jugular venous pulse,
hepatomegaly
tricuspid regurgitation
pansystolic murmur, worse on inspiration
right bundle branch block → widely split S1 and S2
what are the causes of left axis deviation on ECG?
left anterior hemiblock
LBBB
inferior myocardial infarction
Wolff-Parkinson-White syndrome* - right-sided accessory pathway
hyperkalaemia
congenital: ostium primum ASD, tricuspid atresia
minor LAD in obese people
what are the causes of right axis deviation on ECG?
right ventricular hypertrophy
left posterior hemiblock
lateral myocardial infarction
chronic lung disease → cor pulmonale
pulmonary embolism
ostium secundum ASD
Wolff-Parkinson-White syndrome* - left-sided accessory pathway
normal in infant < 1 years old
minor RAD in tall people
what leads on an ECG corresponds to anterolateral region?
V4-6 , I and aVL
What are the ECG features for digoxin?
Down sloping ST depression (reverse tick)
flattened / inverted T
short QT interval
arrhythmias - AV block, bradycardia.
What are the ECG features of hypokalaemia?
U waves small/ absent T waves prolonged PR ST depression long QT
U have no Pot (K+) and no T but a long PR and a long QT
what are the ECG changes for hypothermia?
bradycardia Long QT J wave - small hump at end of QRS first degree heart block atrial and ventricular arrhythmias
How can you identify LBBB and RBBB?
WiLLaM - M in V6 for L
MaRRoW - M in V1 for R
what are the causes of LBBB?
IHD HTN aortic stenosis cardiomyopathy idiopathic fibrosis , digoxin, hyperkalaemia - all rare
what are normal ECG variants in athletes?
sinus bradycardia
junctional rhythm
first degree heart block
Wenckebach phenomenon
what is a cause of increased p wave amplitude?
cor pulmonale
what is a cause of broad, notched (bifid P wave)?
often most prominent in lead 2
caused by atrial enlargement e.g. atrial stenosis
what are the causes of prolonged PR?
heart block hypokalaemia IHD digoxin rheumatic fever aortic root pathology (abscess secondary to I.E) lyme disease sarcoidosis myotonic dystrophy.
what condition causes a short PR?
WPW
what are the causes of RBBB?
normal variant - with age Right ventricular hypertrophy chronically increased right ventricular pressure pulmonary embolism MI ASD cardiomyopathy/ myocarditis
what are the causes of ST depression?
ischaemia digoxin hypokalaemia secondary to abnormal QRS - LBBB, RBBB, LVH syndrome X
what are the causes of ST elevation?
myocardial infarction pericarditis/myocarditis normal variant - 'high take-off' left ventricular aneurysm Prinzmetal's angina (coronary artery spasm) Takotsubo cardiomyopathy rare: subarachnoid haemorrhage
what are the causes of peaked T waves?
hyperkalaemia
Myocardial ischaemia
what are the causes of inverted T waves?
myocardial ischaemia
digoxin toxicity
subarachnoid haemorrhage
arrhythmogenic right ventricular cardiomyopathy
pulmonary embolism ('S1Q3T3')
Brugada syndromehow is pre-eclampsia defined?
> 20 weeks gestation
pregnancy induced HTN
proteinuria
what medication is used to prevent seizures in pre-eclampsia?
what monitoring is needed during this infusion?
MgSO4
given once decided on delivery.
Urine output, reflexes, resp rate, O2 sats
treatment continues 24 hours after last seizure/delivery.
MgSO4 can cause respiratory depression. What treatment is used in this situation?
gluconate
What is eisenmengers syndrome?
reversal of left to right shunt due to pulmonary HTN
what are the features of eisenmengers syndrome?
original murmur may disappear
cyanosis
clubbing
RV failure
Haemoptysis
embolism
what is an individuals maximum predicted HR?
220-age
in an exercise stress test what is the target heart rate?
85% of maximum predicted.
what are the contraindications to an exercise stress test?
myocardial infarction less than 7 days ago
unstable angina
uncontrolled hypertension (systolic BP > 180 mmHg) or hypotension (systolic BP < 90 mmHg)
aortic stenosis
left bundle branch block: this would make the ECG very difficult to interpret
when should an exercise stress test be stopped?
exhaustion / patient request
‘severe’, ‘limiting’ chest pain
> 3mm ST depression
2mm ST elevation.Stop if rapid ST elevation and pain
systolic blood pressure > 230 mmHg
systolic blood pressure falling > 20 mmHg
attainment of maximum predicted heart rate
heart rate falling > 20% of starting rate
arrhythmia develops
name 3 glycoprotein IIb/IIIa receptor antagonists…
abciximab
eptifibatide
tirofiban
How is heart failure managed (NICE)?
ACEi and Bblockers are first liune for all patients
- start one of these at a time
second line - aldosterone antagonist e.g. eplerenone or spironolactone. (monitor K+ especially if on ACEi too.)
third line:
- initiated by specialist.
- ivabradine
- sacubitril-valsartan
- hydralazine + nitrate/digoxin
- cardiac resynchronisation.
Furosemide good for fluid balance and symptom management - no effct on mortality.
For HF with a preserved ejection fraction which commonly used drugs have no effect on mortality?
ACEi and B blockers
which HF medications affect overall mortality?
ACEi
B blockers
NOT furosemide
NOT digoxin
what is the criteria for initiating the following drugs in HF…
Ivabradine
Sacubitril-valsartan
ivabradine:
◦criteria: sinus rhythm > 75/min and a left ventricular fraction < 35%
Sacubitril valsartan:
◦criteria: left ventricular fraction < 35%
◦is considered in heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs
when is digoxin strongly indicated in HF?
when there is co-existent AF
when is hydralazine + nitrates mainly indicated in HF?
◦this may be particularly indicated in Afro-Caribbean patients
when is cardiac resynchronisation therapy indicated in HF?
◦indications include a widened QRS (e.g. left bundle branch block) complex on ECG
Which vaccinations should HF patients recieve?
annual influenza
one off pneumococcal (unless asplenic or CKD then require 5yrly booster)
what is cardiac resynchronisation therapy?
biventricular pacing,. improves symptoms and reduced hospitalisation in NYHA class III patients.
How does exercise training help patients with HF?
improves symptoms but not hospitalisation/ mortality
what is the NYHA classification for HF?
class 1: - no symptoms , no limitation on ordinatry physical activity
class 2: - mild symptoms. slight limitation of physical activity - comfortable at rest but ordinary activity causes fatigue, dyspnoea, palpitations
class 3:
- moderate symptoms.
- marked limitation of physical activity. comfortable at rest but less than ordinary activity causes symptoms
class 4:
- severe symptoms
- unable to carry out any physical activity without discomfort.
- symptoms at rest
what does the S1 heart sound correspond to? when is this loud/ soft?
mitral and tricuspid valve closure
loud - mitral stenosis , left to right shunts, short PR, hyperdynamic state
soft - mitral regurg or long PR
what is the S2 heart sound correspond to? when is this soft? when does it split?
aortic and pulmonary valve closure.
soft in aortic stenosis
loud - HTN, hyperdynamic state, ASD without pulmonary HTN
normally splits with inspiration.
fixed split - ASD
wide splitting - RBBB, deep inspiration, pulmonary stenosis, severe mitral regurgiation
what is the S3 heart sound? when is this heard?
caused by diastolic filling of ventricles.
normal if <30yrs
heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (pericardial knock) and mitral regurgitation.
what is the S4 heart sound?
caused by atria contracting against stiff ventricle.
can be heard in HTN, HOCM, Aortic stenosis
what position on the chest can heart valves be heard best?
aortic - 2nd intercostal space, right sternal border
pulmonary - 2nd intercostal space, left sternal border
mitral - 5th intercostal space, mid clavicular line. left
tricuspid - 4th intercostal space - left sternal edge
what are the causes of reversal of S2 split?
severe AS LBBB right ventricular pacing WPW type B patent ductus arteriosus
what is the mechanism of hydralazine?
increases cGMP leading to smooth muscle relaxation
for HTN but not commonly used
what are the contraindications of hydralazine?
systemic lupus erythematous
•ischaemic heart disease/cerebrovascular disease
what are the adverse effects of hydralazine?
tachycardia •palpitations •flushing •fluid retention •headache •drug-induced lupus
what are the symptoms of hypercalcaemia?
bones, stones, groan and psychotic moans
- bone pain
- renal stones - polydipsia/ polyuria
- GI disturbances - N, V, constipation, abdo pain
- neuro: hypotonia, drowsiness, fatigue, depression, anxiety, psychosis
CVS: HTN, short QT
corneal calcification
what is an eruptive xanthoma most commonly due to?
high triglycerides e.g. familial hypertriglyceridaemia, lipoprotein lipase deficiency.
presents as multiple red/yellow xanthomas on extensor surfaces.
how can xanthelesma be managed?
surgically
topical treatment
laser
what treatment are women at high risk of eclampsia given?
aspirin 75mg from 12 weeks till birth
which women are at high risk of developing eclampsia?
- hypertensive disease during previous pregnancies
- chronic kidney disease
- autoimmune disorders such as SLE or antiphospholipid syndrome
- type 1 or 2 diabetes mellitus
what are the 3 types of HTN during pregnancy?
pre-existing HTN Pregnancy induced HTN - HTN occurring in second half of pregnancy - resolves following birth. Pre-eclampsia - pregnancy induced HTN + proteinuria - may be oedema too.
how is HTN classified? when is each class treated?
need to do Ambulatory or home blood pressure to confirm the following..
>/= 135/80 - stage 1
- Treat if <80 AND evidence of:
- target organ damage
- Cardiovascular disease
- renal disease
- diabetes
- Q risk 10 or more
- consider in <60yrs and Q risk <10
>/= 150/95 - stage 2
- treat regardless of age
clinically stage 1 correlates to 140/90 and stage 2 160/100 (we assume the BP will go up with white coat HTN) lowest reading is used
how is severe HTN classified?
> 180/120
what is ambulatory BP recording?
use average of at least 14 measurements throughout the day
How is HTN managed?
lower salt <6g/day
reduce caffeine
stop smoking, drinking, alcohol , exercise, weight loss
<55yrs or diabetes - A
>/=55yr or afrocaribean - C
2nd step A/C + A/C/D
3rd step A + C + D
A= ACEi, C = CaCB, D= thiazide diuretic
step 4: if K+ <4.5 - spironolacton, if K+>4.5 - B blocker/ alph blocker.
what are the BP targets?
<80 - 140/90 (ABPM - 135/85)
>80 - 150/90 (ABPM - 145/85)
what is aliskiren?
Direct renin inhibitor
blocks RAS activation
new HF drug
what are the secondary causes of HTN?
most common - primary hyperaldosteronism (including Conn’s)
Renal disease e.g. polycystic kidneys, renal artery stenosis
endocrine - pheochromocytoma, cushings, acromegaly, CAH, liddle syndrome
drugs - steroids, Monoamine oxidase inhibitros, COCP, NSAIDs
what is HOCM? (pathophysiology)
autosomal dominant
genes coding contractile protein - B myosin heavy chain protein OR myosin binding protien C
diastolic dysfunction
- left ventricular hypertrophy and thus decreased compliance and decreased cardiac output.
how does HOCM appear on biopsy?
myofibrillar hypertrophy
choatically organised myocytes
fibrosis
what are the features of HOCM?
often assymptomatic
dyspnoea
angina
syncope - typically following exercise
sudden death - mainly due to ventricular arrhythmias
jerky pulse
ejection systolic murmur - increases with valsava and decreases with squatting.
what other conditions can HOCM be associated with?
friedrichs ataxia
WPW
what are the ECHO findings in HOCM?
mitral regurgitation
assymetric hypertrophy
systolic anterior motion of anterior mitral valve
what are the ecg changes seen in HOCM?
eft ventricular hypertrophy
non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen
deep Q waves
How is HOCM managed?
ABCDE Amiodarone Bblockers Cardioverter defib Dual chamber pacemaker Endocarditis prophylaxis
which drugs should be avoided in HOCM?
nitrates
ACEi
Inotropes
what are the poor prognostic factors of HOCM?
syncope family hx of sudden death young age at presentation non-sustained VT on 24 hour/48 hour tape abnormal BP changes with exercise increased septal wall thickness
what are the indications for an implantable cardiac defib?
long QT HOCM previous cardiac arrest due to VT/VF previous MI with nonsustained VT on 24 hour tape / inducible VT brugada syndrome?
what is the biggest risk to developing infective endocarditis?
previous infective endocarditis
what is the commonest cause of infective endocarditis?
s.aureus - especially acute and IVDU
streptococcus viridans - in developing countries
which organism is most likely to cause infective endocarditis from indwelling lines and prosthetic valve surgery?
s. epidermidis
what are the culture negative causes of infective endocarditis?
prior antibiotic therapy Coxiella burnetii Bartonella Brucella HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
which organism is resposible for infective endocarditis secondary to poor dental hygiene?
streptococcus viridans
which organism is linked to causing infective endocarditis in those with colorectal Ca?
S.bovis - particularly a subtype called… Streptococcus gallolyticus
what is mirantic endocarditis?
subtype of endocarditis caused by malignancy
what is the modified dukes criteria for infective endocarditis?
2 major or 3 minor 1 major or 5 minor
major:
- 2x blood cultures of typical organism
- typical ECHO changes - endocardial invovlement/ new valve
minor:
- fever
- positive blood culture - atypical
- vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
- immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots
- predisposing factor
what are the poor prognostic factors of infective endocarditis?
S.aureus
culture negative
prosthetic valve
low complement levels
what is the initial therapy for infective endocarditis when the organism is unknown?
Native valve
amoxicillin, consider adding low-dose gentamicin
If penicillin allergic, MRSA or severe sepsis
vancomycin + low-dose gentamicin
If prosthetic valve
vancomycin + rifampicin + low-dose gentamicin
what is the initial therapy for infective endocarditis when the organism is s. aureus?
native valve:
- Flucloxacillin
- If penicillin allergic or MRSA: vancomycin + rifampicin
prosthetic:
Flucloxacillin + rifampicin + low-dose gentamicin
If penicillin allergic or MRSA
vancomycin + rifampicin + low-dose gentamicin
what is the initial therapy for infective endocarditis when the organism is s.viridans?
Benzylpenicillin
If penicillin allergic
vancomycin + low-dose gentamicin
what are the indications for surgery in infective endocarditis?
Severe valvular incompetence
aortic abscess (often indicated by a lengthening PR interval)
infections resistant to antibiotics/fungal infections
cardiac failure refractory to standard medical treatment
recurrent emboli after antibiotic therapy
how should isolated systolic HTN be treated?
same way as normal HTN
what is the function of ivabradine?
acts of If (funny current) ion channel to reduce SAN pacemaker activity
used in angina
what are the side effects of ivabradine?
headaches
visual changes
bradycardia
when is a non-pulsatile JVP seen?
SVC obstruction
what is the kussmaul sign?
paradoxical rise in JVP in inspiration
constrictive pericarditis
what do different parts of JVP waveform present?
a wave - atrial contraction c wave - tricuspid closure x descent - ventricular systole v wave - filling of heart against closed tricuspid y descent - tricuspid opens
when would the a wave of JVP be large?
large atrial pressure - tricuspid/ pulmonary stenosis, pulmonary HTN
when is the a wave of JVP absent?
AF
what are cannon a waves on JVP waveform? regular vs irregular
atria contracting against closed tricuspid
seen in heart block, arrhythmias, single chamber pacing
regular - VT, AVNRT
irregular - Heart block
when are giant v waves seen?
seen in tricuspid regurgitation.
what is Kawasaki disease?
vasculitis
children
can cause serious complications - coronary aneurysms
what are the features of kawasaki disease?
fever - 5 days, resistant to paracetamol strawberry tongue red cracked lips red palms/ soles of feet - later peel cervical lymphadenopathy conjunctivitis
how can you test for kawasaki?
no test
clinical diagnosis
how is kawasaki disease managed?
high-dose aspirin
intravenous immunoglobulin
echocardiogram (rather than angiography) is used as the initial screening test for coronary artery aneurysms
why is aspirin contraindicated in children? what is an exception?
Kawasaki disease is one of the few indications for the use of aspirin in children. Due to the risk of Reye’s syndrome aspirin is normally contraindicated in children
what are the congenital causes of long QT?
Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel)
Romano-Ward syndrome (no deafness)
what drugs can cause long QT?
Amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram)
methadone
chloroquine
terfenadine
erythromycin
haloperidol
ondanestron
what are non drug and non congential causes of long QT?
low Ca, low Mg, low K
hypothermia
SAH
myocarditis
MI
what are the different types of Long QT?
LQT1 - syncope after exertion e.g swimming
LQT2 - syncope after emotional stress, auditory stimulus
LQT3 - night or rest
how is long QT managed?
B blockers,
ICD in high risk
what are the side effects of loop diuretics?
hypotension
hyponatraemia
hypokalaemia, hypomagnesaemia
hypochloraemic alkalosis
hypocalcaemia
ototoxicity renal impairment (from dehydration + direct toxic effect)
hyperglycaemia (less common than with thiazides)
gout
what BP occurs in malignant HTN?
> 200/130
How is malignant HTN managed?
reduce diastolic no lower than 100mmHg within 12-24 hrs
bed rest
most patients: oral therapy e.g. atenolol
if severe/encephalopathic: IV sodium nitroprusside/labetolol
what are the most common valve disorders of the heart?
Aortic stenosis - no. 1
mitral regurg - no.2
what are the risk factors for mitral regurgitation?
Female sex Lower body mass Age Renal dysfunction Prior myocardial infarction - damage to papillary muscles/ chordae tendinae Prior mitral stenosis or valve prolapse Collagen disorders e.g. Marfan's Syndrome and Ehlers-Danlos syndrome infective endocarditis rheumatic disease
what murmur is heard in mitral regurgitation?
pansystolic
heart best at apex
radiates to axilla
S1 may be quiet (due to poor closure of mitral valve)
S2 may be widely split in severe MR
what may be seen on CXR and ECG in mitral regurg?
ECG - wide/large p wave due to enlarged atria
CXR - cardiomegaly
what causes mitral stenosis?
Rheumatic fever - main cause
others: mucopolysaccharidoses, carcinoid and endocardial fibroelastosis - seen in exams
what mumur/ sounds are heard in mitral stenosis?
mid- late diastolic murmur
loud S1 - opening snap
with severe Mitral stenosis - murmur becomes longer and opening snap becomes closer to S2
what are the features/ symptoms of mitral stenosis?
murmur
malar flush
low pulse volume
AF
what can be seen on CXR in mitral stenosis?
large atria
what is the mitral valve opening normally and what will it be in mitral stenosis?
the normal cross sectional area of the mitral valve is 4-6 sq cm. A ‘tight’ mitral stenosis implies a cross sectional area of < 1 sq cm
what conditions are associated with mitral valve prolapse?
congenital heart disease: PDA, ASD
cardiomyopathy
Turner’s syndrome
Fragile X
Marfan’s syndrome
Ehlers-Danlos Syndrome
osteogenesis imperfecta
pseudoxanthoma elasticum
Wolff-Parkinson White syndrome
long-QT syndrome
polycystic kidney disease
what are features of mitral valve prolapse?
mid-systolic click (occurs later if patient squatting)
late systolic murmur (longer if patient standing)
what is a multifocal atrial tachycardia?
irregular cardiac rhythm caused by at least three different sites in the atria, which may be demonstrated by morphologically distinctive P waves. It is more common in elderly patients with chronic lung disease, for example COPD
how is multifocal atrial tachy managed?
correct hypoxia
correct electrolytes
rate limiting CaB
which ejection systolic mumurs are louder on inspiration/expiration?
louder on expiration
aortic stenosis
hypertrophic obstructive cardiomyopathy
louder on inspiration
pulmonary stenosis
atrial septal defect
tetralogy of fallot is another ejection systolic murmur
name two pansystolic mumurs?
mitral/ tricuspid regurg
VSD
Give examples of a late systolic mumur?
mitral valve prolapse
coarctation of aorta
Give examples of early diastolic murmur?
aortic regurg
Graham-Steel murmur (pulmonary regurgitation)
both are high-pitched and ‘blowing’ in character
give examples of mid-late diastolic murmurs?
mitral stenosis
Austin-Flint murmur (severe aortic regurgitation)
both ‘rumbling’ in character)
what murmur does PDA give?
continuous machine like
what are the complications of an MI?
SPREAD:
Sudden death/ shock
- VF is most common cause of death post MI
- cardiogenic shock - ventricular damage
Pericarditis
- in first 48 hours following a transmural MI
Rupture
- rupture of septum
-left ventricle free wall rupture: tamponade and shock
- papillary muscles - mitral regurg
Embolus
- Thrombus can form within an aneurysm
- arrhythmia can lead to thrombus formation
Arrhythmias/ aneurysm
- VT/ VF
- brady cardia - damage to SAN/ AVN (heart block)
- left ventricular aneurysm
Dresslers
- two -six weeks following MI
- autoimmune reaction
Chronic:
- heart failure
what type of MI is most likely to cause AVN damage?
inferior
what are the symptoms/ features of dresslers syndrome?
fever
pleuritic pain
pericardial effusion
raised ESR
How is Dresslers treated?
NSAIDs
which type of MI is most likely to damage papillary muscles?
infero-posterior
what is the secondary prevention post MI?
b blockers
ACEi
statin
dual antiplatelet inc aspirin (usually with ticagrelor) - the ticagrelor is stopped after 12 months)
when can sexual activity ressume after an MI?
4 weeks
when are ARBs preffered to ACEi in MI?
ACEi side effects
patients who have had an acute MI and who have symptoms and/or signs of heart failure and left ventricular systolic dysfunction - start ARB within 3-14 days
How is an MI managed?
aspirin
clopidogrel/ticagrelor/prasugrel
if undergoing PCI - also unfractionated heparin/LMWH
PCI/thrombolysis
how long after thrombolysis in MI patients, is an ECG performed and why?
90 mins
if <50% resolution in ST elevation can offer PCI
what are the causes of myocarditis?
viral: coxsackie B, HIV
bacteria: diphtheria, clostridia
spirochaetes: Lyme disease
protozoa: Chagas’ disease, toxoplasmosis
autoimmune
drugs: doxorubicin
what are the symptoms of myocarditis?
chst pain
dyspnoea
arrhythmia
(fever)
what are the investigation findings for myocardiits?
increased cardiac enzymes, increased BNP, increassed inflammatory markers
ECG -tachyarrhythmias, ST / T changes inc ST elevation, T inversion
what is nicorandil?
vasodilatory drug for angina
It is a potassium-channel activator with vasodilation is through activation of guanylyl cyclase which results in increase cGMP.
what are the side effects of nicorandil?
headache
flushing
skin, mucosal and eye ulceration
gastrointestinal ulcers including anal ulceration
when is nicorandil contraindicated?
LV failure
what does nicotinic acid do?
Lowers cholesterol and triglyceride concentrations
it also raises HDL levels.
what are the complications/side effects of nicotinic acid?
Adverse effects
flushing: mediated by prostaglandins
impaired glucose tolerance
myositis
what is the function of nitrates?
nitrates cause the release of nitric oxide in smooth muscle, activating guanylate cyclase which then converts GTP to cGMP, which in turn leads to a fall in intracellular calcium levels
in angina they both dilate the coronary arteries and also reduce venous return which in turn reduces left ventricular work, reducing myocardial oxygen demand
what are the problems/side effects of nitrates?
headaches, flushing, hypotension, tachycardia
develop tolerance - not seen if modified release is taken.
what are the indications for a temporary pacemaker?
symptomatic/ haemodynamically unstable bradycardia
post anterior MI with type 2 or complete heart block
trifasicular block prior to surgery
what are the complications of PCI?
stent thrombosis - usually in 1 month, presents as MI
restenosis - due to proliferation around the stent. in first 3-6 months. angina symptoms
how have stents used in PCI developed to reduce stenosis risk? whats the limitation of these?
drug eluting stents - drugs that inhibit tissue growth
thrombosis rate increased
How is a bradycardia managed?
Atropine IV (can use up to 3mg , start with 500mcg)
need for treatment: haemodynamic compromise , very low HR
what is the next step if a bradyarrhythmia doesnt respond to atropine?
transcutaneous pacing
adrenaline/isoprenaline
When is transcutaneous pacing considered for brady-arrhythmias?
complete heart block with broad complex QRS
recent asystole
Mobitz type II AV block
ventricular pause > 3 seconds
how does fonduparinux work?
Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa. It is given subcutaneously.
what keeps a PDA open?
prostaglandins
who is a PDA most common in?
premature
born at high altitude
maternal rubella in 1st trimester
what are the features of PDA?
left subclavicular thrill continuous 'machinery' murmur large volume, bounding, collapsing pulse wide pulse pressure heaving apex beat
how is PDA managed?
indomethacin or ibuprofen
- given to the neonate
- inhibits prostaglandin synthesis
- closes the connection in the majority of cases
if associated with another congenital heart defect amenable to surgery then prostaglandin E1 is useful to keep the duct open until after surgical repair
How are regular narrow complex tachyarrythmias managed?
A-C
If unstable i.e. shock, syncope, MI, HF.. then DC cardiovert (up to 3 shocks)
Then..
vagal manoeuvres followed by IV adenosine
if above unsuccessful consider diagnosis of atrial flutter and control rate (e.g. beta-blockers)
How are irregular narrow complex tachyarrythmias managed?
A-C
If unstable i.e. shock, syncope, MI, HF.. then DC cardiovert (up to 3 shocks)
Then..
probably AF
if onset < 48 hr consider electrical or chemical cardioversion
rate control: beta-blockers are usually first-line unless there is a contraindication
How are irregular broad complex tachyarrythmias managed?
A-C
If unstable i.e. shock, syncope, MI, HF.. then DC cardiovert (up to 3 shocks)
then seek expert advice
what may cause an irregular broad complex tachyarrythmias ?
atrial fibrillation with bundle branch block - the most likely cause in a stable patient
atrial fibrillation with ventricular pre-excitation
torsade de pointes
how is a regular broad complex tachyarrhythmia managed?
A-C
If unstable i.e. shock, syncope, MI, HF.. then DC cardiovert (up to 3 shocks)
then
assume ventricular tachycardia (unless previously confirmed SVT with bundle branch block)
loading dose of amiodarone followed by 24 hour infusion
how is peripheral arterial disease managed?
lifestyle
statin - atorvastatin 80mg
clopidogrel rather than aspirin
exercise training
angioplasty, stenting, bypass graft surgery
what drugs can be used in peripheral arterial disease?
naftidrofuryl oxalate: vasodilator, sometimes used for patients with a poor quality of life
cilostazol: phosphodiesterase III inhibitor with both antiplatelet and vasodilator effects - not recommended by NICE
what is pre-eclampsia?
HTN (>140/90) with proteinuria after 20 weeks.
+ oedema
may have other end organ involvment… renal, liver, neuro, placental
what are the consequences of pre-eclampsia?
eclampsia
other neurological complications include altered mental status, blindness, stroke, clonus, severe headaches or persistent visual scotomata
fetal complications
intrauterine growth retardation
prematurity
liver involvement (elevated transaminases)
haemorrhage: placental abruption, intra-abdominal, intra-cerebral
cardiac failure
what are the features of severe pre-eclampsia?
hypertension: typically > 160/110 mmHg
proteinuria: dipstick ++/+++
headache
visual disturbance
papilloedema
RUQ/epigastric pain
hyperreflexia
platelet count < 100 * 106/l, abnormal liver enzymes or HELLP syndrome
what are the risk factors for pre-eclampsia?
high risk factors:
- hypertensive disease in a previous pregnancy
- chronic kidney disease
- autoimmune disease, such as systemic lupus erythematosus or antiphospholipid syndrome
- type 1 or type 2 diabetes
- chronic hypertension
medium risk factors:
- first pregnancy - age 40 years or older - pregnancy interval of more than 10 years - body mass index (BMI) of 35 kg/m² or more a - family history of pre-eclampsia - multiple pregnancy
how is pre-eclampsia prevented in those at risk?
women who have 1 high risk factor or 2 moderate should take 75-150mg aspirin from 12 weeks until birth
how is pre-eclampsia managed?
oral labetolol
nifedipine if asthmatic
how is a P.E investigated in pregnancy?
ECG and CXR in all
USS of legs - if DVT present, start treatment
otherwise decide on CTPA/VQ scan
what are the problems of CTPA/ VQ scan in pregnancy?
CTPA - increases risk of maternal breast cancer, (pregnancy makes breast more sensitive to the radiation)
VQ scan - increased risk of childhood cancer
what are the pros and cons of biological valve?
pros - no needs for long term anticoag (low dose aspirin still given long term)
cons - long term calcification and deterioration
what is the most common type of valve used in valve surgery now?
mechanical bileaflet valve
what are the advantages and disad of mechanical valves?
low failure rate
long term anticoag needed
what long term anticoag is used for mechanical valves?
warfarin (not doac)
what are the target INR ranges for mechanical valves?
aortic 3
mitral 3.5
how is pulmonary arterial hypertension defined?
resting pulmonary arterial pressure >25mmHg
who is pulmonary arterial hypertension most common in?
women , mainly 30-50yrs
what are the causes of pulmonary arteial HTN?
secondary to COPD etc
Can be primary - risk increased by HIV, cocaine
around 10% inherited in autosomal dominant fashion
what are the features of pulmonary artery HTN?
progressive exertional dyspnoea is the classical presentation
other possible features include exertional syncope, exertional chest pain and peripheral oedema
cyanosis
right ventricular heave, loud P2, raised JVP with prominent ‘a’ waves, tricuspid regurgitation
what test is essential to managing pulmonary artery HTN?
acute vasodilator testing is central to deciding on the appropriate management strategy
Acute vasodilator testing aims to decide which patients show a significant fall in pulmonary arterial pressure following the administration of vasodilators such as intravenous epoprostenol or inhaled nitric oxide.
how is pulmonary artery HTN managed?
If there is a positive response to acute vasodilator testing (a minority of patients)
oral calcium channel blockers
If there is a negative response to acute vasodilator testing (the vast majority of patients)
prostacyclin analogues: treprostinil, iloprost
endothelin receptor antagonists: bosentan, ambrisentan
phosphodiesterase inhibitors: sildenafil
progressive symptoms - heart lung transplant
how is pulmonary capillary wedge pressure managed?
balloon tipped Swan-Ganz catheter which is inserted into the pulmonary artery.
What is the PERC criteria?
pulmonary embolism rule out criteria
used to rule out P.E in those with a low probability ..
age >/= 50 Tachycardia >100 O2 sats =94% previous DVT/P.E Recent surgery in last 4 week haemoptysis unilateral leg swelling Oestrogen use
if all above are absent, the pre-test probability is <2%
to rule out P.E all of above must be absent
What is the 2 level PE wells score?
Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) 3
An alternative diagnosis is less likely than PE 3
Heart rate > 100 beats per minute 1.5
Immobilisation for more than 3 days or surgery in the previous 4 weeks 1.5
Previous DVT/PE 1.5
Haemoptysis 1
Malignancy (on treatment, treated in the last 6 months, or palliative) 1
more than 4 - P.E likely
How is P.E managed if the 2 level PE wells score is positive?
give DOAC whilst awaiting urgent CTPA
DOAC can be continued if PE confirmed
what can be done if 2 level PE wells score is unlikely?
d.dimer
if positive do a CTPA
whats the difference between sensitivity and specificity?
high sensitivity - unlikely to give false positive
high specificity - unlikely to give false neg
what ecg changes are seen in a P.E?
S1Q3T3
large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III
tachycardia
RBBB
what is the first line treatment for P.E? what are the exceptions?
DOAC - apixaban/ rivaroxaban
if neither apixaban or rivaroxaban are suitable then either LMWH followed by dabigatran or edoxaban OR LMWH followed by a vitamin K antagonist (VKA, i.e. warfarin)
if renal impairment is severe (e.g. < 15/min) then LMWH, unfractionated heparin or LMWH followed by a VKA
if the patient has antiphospholipid syndrome (specifically ‘triple positive’ in the guidance) then LMWH followed by a VKA should be used
how long should patients have anticoagulation for a P.E
atleast 3 months
provoked - 3 months only
unprovoked - up to 6 months
what is the management for massive P.E with haemodynamic instability?
thrombolysis
what are the causes of a collapsing pulse?
aortic regurgitation
PDA
what is pulsus paradox? what are the causes ?
fall in BP >10 (normal fall) with inspiration
severe asthma, cardiac tamponade
what is the cause of a slow rising pulse?
aortic stenosis
what is the causes of Bisferiens pulse?
‘double pulse’ - two systolic peaks
mixed aortic valve disease
what are the causes of constrictive pericarditis?
amyloidosis (e.g. secondary to myeloma) - most common cause in UK
haemochromatosis
post-radiation fibrosis
Loffler’s syndrome: endomyocardial fibrosis with a prominent eosinophilic infiltrate
endocardial fibroelastosis: thick fibroelastic tissue forms in the endocardium; most commonly seen in young children
sarcoidosis
scleroderma
what ECG is found in restrcitve cardiomyopathy?
low voltage QRS
what features suggest restrictive cardiomyopathy rather than constrictive pericarditis?
prominent apical pulse
absence of pericardial calcification on CXR
the heart may be enlarged
ECG abnormalities e.g. bundle branch block, Q waves
what is the pathogenesis behind rheumatic fever?
Streptococcus pyogenes infection
sets up immune response to produce antibodies
There is a cross reaction between antibodies for the M protein and myosin and smooth muscle of arteries
What are Ashcoff bodies?
Aschoff bodies describes the granulomatous nodules found in rheumatic heart fever
what is the diagnostic criteria for rheumatic fever?
evidence of recent strept infection +
2 major OR
1 major and 2 minor needed
Evidence of recent streptococcal infection:
raised or rising streptococci antibodies,
positive throat swab
positive rapid group A streptococcal antigen test
Major criteria:
- erythema marginatum
- Sydenham’s chorea (late feature)
- subcutaneous nodules
- polyarthritis- carditis and valvulitis (eg, pancarditis) -must be evidence of endocarditis
Minor criteria
- raised ESR or CRP
- pyrexia
- arthralgia (not if arthritis a major criteria)
- prolonged PR interval
how is rheumatic fever managed?
Antibiotics: oral penicillin V
anti-inflammatories: NSAIDs are first-line
treatment of any complications that develop e.g. heart failure
what is the ABCD2 score?
prognostic score post TIA
what is the DAS28 score?
measure of disease activity in rheumatoid arthritis
what is child pugh score?
A scoring system used to assess the severity of liver cirrhosis
what is the PHQ9 score
Patient Health Questionnaire - assesses severity of depression symptoms
Name 3 alcohol screening tools?
AUDIT, CAGE, FAST
what is the SCOFF score?
Questionnaire used to detect eating disorders and aid treatment
Whats the IPSS score? which other scoring system is used for these patients?
International prostate symptom score
Gleason score - indicates prognosis for prostate Ca
whats the bishop and apgar score
bishop - used to help assess the whether induction of labour will be required
apgar - assess health of new born immediately post birth
whats the waterlow score?
risk of developing pressure sore
whats the ranson criteria for?
acute pancreatitis
how do statins work?
inhibit HMG-CoA reductase to reduce cholesterol synthesis
what are the side effects of statins?
myopathy: includes myalgia, myositis, rhabdomyolysis and asymptomatic raised creatine kinase.
liver impairment
there is some evidence that statins may increase the risk of intracerebral haemorrhage in patients who’ve previously had a stroke. This effect is not seen in primary prevention. For this reason the Royal College of Physicians recommend avoiding statins in patients with a history of intracerebral haemorrhage
what are the risk factors for statin induced myopathy?
advanced age,
female sex,
low body mass index
presence of multisystem disease such as diabetes mellitus.
Myopathy is more common simvastatin, atorvastatin than rosuvastatin, pravastatin, fluvastatin
How are LFTs monitored during statin therapy?
checking LFTs at baseline, 3 months and 12 months. Treatment should be discontinued if serum transaminase concentrations rise to and persist at 3 times the upper limit of the reference range
what are the contraindications for statin use?
pregnancy
use of macrolides (erythromycin, clarithromycin) - stop statins while course is being completed
Who should be put on statins?
all people with established cardiovascular disease (stroke, TIA, ischaemic heart disease, peripheral arterial disease)
anyone with a 10-year cardiovascular risk >= 10%
patients with type 2 diabetes mellitus should now be assessed using QRISK2 like other patients are, to determine whether they should be started on statins
patients with type 1 diabetes mellitus who were diagnosed more than 10 years ago OR are aged over 40 OR have established nephropathy
what statin dose is used for primary /secondary prevention?
primary - atorvastatin 20mg
secondary - atorvastatin 80mg
what is the acute management of SVT if haemodynamically stable?
vagal manoeuvres: e.g. Valsalva manoeuvre, carotid sinus massage
intravenous adenosine 6mg → 12mg → 12mg: contraindicated in asthmatics - verapamil is a preferable option
electrical cardioversion
how can SVT episodes be prevented?
beta-blockers
radio-frequency ablation
what is syndrome X?
Chest pain on exercise
ST depression on exercise stress
normal coronary arteries
what drug can be good for syndrome x?
nitrates
what is takayasu’s arteritis?
large arteries such as aorta affected
question usually involved an absent limb pulse
most common in females and asians.
what are the symptoms of takayasu’s arteritis?
systemic features of a vasculitis e.g. malaise, headache
unequal blood pressure in the upper limbs
carotid bruit
intermittent claudication
aortic regurgitation (around 20%)
how is takayasu’s arteritis managed?
steroids
what is Takotsubo cardiomyopathy?
non ischaemic cardiomyopathy
apical balooning of myocardium - due to apex not contracting so instead balloons out
,ay be triggered by stress
how does Takotsubo cardiomyopathy present?
chest pain
HF symptoms
st elevation
normal coronary arteries
how is Takotsubo cardiomyopathy managed?
supportive treatment only
most patients improve
what is the most common cyanotic CHD and when does it present?
ToF
presents 1-2 months
what are the 4 features of ToF
pulmonary stenosis
right ventricular hypertrophy
VSD
over-riding aorta
degreee of severity determined by degree of pulmonary stenosis
what are the clinical features of ToF?
cyanosis
causes a right-to-left shunt
ejection systolic murmur due to pulmonary stenosis (the VSD doesn’t usually cause a murmur)
a right-sided aortic arch is seen in 25% of patients
chest x-ray shows a ‘boot-shaped’ heart, ECG shows right ventricular hypertrophy
how is ToF managed?
surgical repair is often undertaken in two parts
cyanotic episodes may be helped by beta-blockers to reduce infundibular spasm
what is the mechanism of a thiazide diuretic?
block Na CL symporter in DCT to block sodium reuptake
Potassium is lost as a result of more sodium reaching the collecting ducts.
what are the side effects of thiazides?
dehydration postural hypotension hyponatraemia, hypokalaemia, hypercalcaemia* gout impaired glucose tolerance impotence
Rare adverse effects thrombocytopaenia agranulocytosis photosensitivity rash pancreatitis
what are the contraindications of thrombolysis?
active internal bleeding recent haemorrhage, trauma or surgery (including dental extraction) coagulation and bleeding disorders intracranial neoplasm stroke < 3 months aortic dissection recent head injury severe hypertension
what are the side effects of thrombolysis?
haemorrhage
allergy and hypotension - espwith streptokinase
what is torsades de point?
type of VT where the QRS is variable height
associated with long QT
can deteriorate into VF
What are the causes of long QT?
congenital: Jervell-Lange-Nielsen syndrome, Romano-Ward syndrome
antiarrhythmics: amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants
antipsychotics
chloroquine
terfenadine
erythromycin
electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia
myocarditis
hypothermia
subarachnoid haemorrhage
What is the managedment of torsades de point?
IV magnesium sulphate
who is at increased risk of transposition of great vessels?
babies of diabetic mums
what are the clinical features of transposition of great vessels?
cyanosis tachypnoea loud single S2 prominent right ventricular impulse 'egg-on-side' appearance on chest x-ray
how is transposition of great vessels managed?
maintenance of the ductus arteriosus with prostaglandins
surgical correction is the definite treatment.
what are the signs of tricuspid regurg?
pan-systolic murmur
prominent/giant V waves in JVP
pulsatile hepatomegaly
left parasternal heave
what are the causes of tricuspid regurg?
right ventricular infarction pulmonary hypertension e.g. COPD rheumatic heart disease infective endocarditis (especially intravenous drug users) Ebstein's anomaly carcinoid syndrome
what are VSD associated with?
ongenital VSDs are often association with chromosomal disorders
Down's syndrome
Edward's syndrome
Patau syndrome
cri-du-chat syndrome
congenital infections
acquired causes
post-myocardial infarction
when can a VSD be detected?
20 weeks on USS
how does VSD present post natally?
failure to thrive features of heart failure hepatomegaly tachypnoea tachycardia pallor classically a pan-systolic murmur which is louder in smaller defects
how is a VSD managed?
small VSDs which are asymptomatic often close spontaneously are simply require monitoring
moderate to large VSDs usually result in a degree of heart failure in the first few months
nutritional support
medication for heart failure e.g. diuretics
surgical closure of the defect
what are the complications of a VSD?
aortic regurgitation
infective endocarditis
Eisenmenger's complex
- this is turn results in cyanosis and clubbing
right heart failure
pulmonary hypertensionwhat are the different types of VT?
monomorphic - associated with MI
Polymorphic - torsades - associated with long QT
how is VT managed?
haemodynamic instability - DC cardiovert
otherwise..
amiodarone, lidocaine or procainamide.
Do not use verapamil
if drug therapy fails - ICD
what is the mechanism of warfarin?
inhibits epoxide reductase -
prevents reduction of vitamin K
vit K cant act as a cofactor for carboxylation of clotting factors - II, VII, IX and X (1972) and protein C
what is the target INR for AF, mechanical valve, VTE?
AF - 2.5
VTE 2.5 unless recurrent then 3.5
valve depends on type
what is INR?
ratio of prothrombin time compared to normal.
what factors can potentiate warfarin effects?
liver disease
P450 enzyme inhibitors - amiodarone, ciprofloxacin
cranberry juice
NSAIDs (displace warfarin from plasma albumin and inhibit platelets too)
how is a patient on warfarin managed with major bleeding?
Stop warfarin
Give intravenous vitamin K 5mg
Prothrombin complex concentrate - if not available then FFP*
how is a patient on warfarin managed with minor bleeding and INR>8?
Stop warfarin
Give intravenous vitamin K 1-3mg
Repeat dose of vitamin K if INR still too high after 24 hours
Restart warfarin when INR < 5.0
how is a patient on warfarin managed with no bleeding and INR>8?
Stop warfarin
Give vitamin K 1-5mg by mouth, using the intravenous preparation orally
Repeat dose of vitamin K if INR still too high after 24 hours
Restart when INR < 5.0
how is a INR of 5 to 8 managed for patients on warfarin with minor bleeding and no bleeding?
minor bleeding INR 5-8:
Stop warfarin
Give intravenous vitamin K 1-3mg
Restart when INR < 5.0
no bleeding, INR 5-8:
withold 1 or 2 doses of warfarin. reduce subsequent maintainance dose.
what are the features of wolff parkinson white on ECG?
- short PR interval
- wide QRS complexes with a slurred upstroke - ‘delta wave’
- left axis deviation if right-sided accessory pathway*
- right axis deviation if left-sided accessory pathway*
what are the two types of WPW?
type A - left sided pathway - dominant R wave in V1
Type B - right sided pathway - no dominant R in V1
what is WPW associated with ?
- HOCM
- mitral valve prolapse
- Ebstein’s anomaly
- thyrotoxicosis
- secundum ASD
how is WPW managed?
- definitive treatment: radiofrequency ablation of the accessory pathway
- medical therapy: sotalol (avoid if AF coexists) amiodarone, flecainide
