Cardiology

Question 1

CLUES IN CARDIAC HISTORY

what is the likely dx if:

i) sudden onset and pleuritic in nature
ii) cardiac chest pain - if exertional
iii) what type of pathology gives pain on exertion?
iv) if pain is positional

Answer 1

i) PE
ii) stable angina
iii) ischaemia
iv) pericarditis/myocarditis

Question 2

ON EXAMINATION

i) if there is a central sternotomy scar with scars on wrists or legs for harvesting - what operation may they have had?
ii) if there is a central sternotomy scar with no scars on wrists or legs for harvesting - what operation may they have had?
iii) if someone has a catheter in and is on furosemide infusion - what are they being treated for?
iv) what valve pathology causes a slow rising pulse or a collapsing pulse?
v) if apex is displaced and heaving
vi) what are you feeling for when feeling for thrills?

Answer 2

i) bypass
ii) valve operation
iii) heart failure

iv) slow rising - aortic stenosis
collapsing - aortic regurgitation

v) volume overload/LV hypertrophy
vi) feeling for a murmur

Question 3

MURMURS O/E

i) what can you ask the patient to do if you are listening for left sided murmurs and want to make them louder?
ii) what can you ask the patient to do if you are listening for right sided murmurs and want to make them louder?
iii) which type of murmurs get louder if you sit the pt forward? which get louder if you lay the pt on LHS?
iv) which murmurs radiate to the carotid? which radiate to apex?

Answer 3

i) ask pt to take a deep breath in and out and hold on the way out - increases flow through left heart transiently so murmur gets louder
ii) ask pt to take deep breath in and hold on inspiration - inc flow through right heart

iii) sit forward - aortic murmurs get louder
lie on LHS - mitral murmurs get louder

iv) aortic stenosis radiate to carotid
mitral regurg radiates to apex

Question 4

CARDIAC INVESTIGATIONS

i) which bedside test is useful for looking at arrhythmias, struc abnorms and ischaemia?
ii) give two signs of heart failure on CXR
iii) which imaging modality is good to look at heart struc and func espec valves?
iv) what is cardiac CT especially good for? what disease is it good at looking at? what condition is it the imaging of choice for?
v) what is cardiac MRI most useful for?
vi) what is used to detect long term rhythm disturbance?

Answer 4

i) ECG
ii) cardiomegaly/pulmonary oedema
iii) ECHO is good for struc and func

iv) cardiac CT - good for looking at cardiac structure
- good for coronary artery disease
- imaging of choice for aortic dissection

v) cardiac MRI - good at looking whether troponin rise is due to ischaemia or inflammation eg myocarditis
vi) cardiac monitor

Question 5

NORMAL ECG

i) what does the P wave represent?
ii) in which leads can the T wave be inverted and still be a normal variant?
iii) how can rate be calculated?
iv) if there are no P waves and rate is regularly irreg - what is dx?
v) how many small squares should QRS be?

Answer 5

i) atrial contraction
ii) V1, V3 and. AVf
iii) calculate number of big squares between R waves and then 300 / answer
iv) AF
v) 3 or less

Question 6

BRADYARRHYTHMIAS / HEART BLOCK

i) how many bpm is a BA?
ii) if PR interval is normal - which node is implicated? which people is this common in but not pathological?
iii) if PR interval is prolonged - which node is the problem in? what is the pathology here?
iv) what degree of heart block occurs (prolonged PR interval) when - all P waves are followed by QRS, some are followed by QRS and none are followed by QRS?

Answer 6

i)

ii) normal PR but BA = SA node = sinus bradycardia
- common in endurance atheletes

iii) prolonged PR = AV node problem = 1-3rd degree heart block

iv) all P > QRS = first degree
some P > QRS = second degree
no P > QRS = third degree

Question 7

whats the diagnosis

Answer 7

sinus bradycardia

Question 8

whats the diagnosis? why?

Answer 8

1st degree heart block

• long PR interval (heart block) but every P is followed by Q (1st degree)

Question 9

whats the diagnosis? why?

Answer 9

second degree heart block
- PR gets progressively longer then drop beat, then starts again = wenkebach (mobitz type I)

wenkebach is low risk

Question 10

what is the diagnosis? why? what is it aka?

is this a high risk rhythm?

Answer 10

i) 2nd degree heart block
- mobitz type II
- alternate P waves followed by QRS, PR interval remains constant
- only every other second atrial contrac is conducted so aka 2:1 heart block

• high risk rhythm

Question 11

SECOND DEGREE HEART BLOCK

i) which type is when the PR interval gets progressively longer then drops a QRS?
ii) which type looks regular but each second P wave doesnt have a QRS

Answer 11

i) mobitz type I (wenkebach)
ii) mobitz type II

Question 12

what kind of beat is circled?
- why does it look abnormal/wider?

Answer 12

ventricular ectopic
- looks abnormal because it starts in the ventricles - wider QRS because its slower

Question 13

BUNDLE BRANCH BLOCK

i) what does it mean if the QRS is broad?
ii) which two leads do you look at for deflections to determine if its right or left BBB?
iii) if there is negative deflection in ? lead - what bundle is blocked?
iv) if there is positive deflection in ? lead, what bundle is blocked?

Answer 13

i) conduction is slower - one of the bundles is blocked
ii) look at leads V1 and V6
iii) neg deflection in V1 = LBBB (turn left, indicator down)
iv) positive deflection = RBBB (turn right, indicator up)

Question 14

what side bundle branch block is shown here? (look at V1)

Answer 14

LBBB (negative deflection)

Question 15

what is circled?

in what situation is it normal to get LBBB?

Answer 15

pacing spike

• get LBBB after pacemaker has been put in (always look at whether there is pacing spikes if you see new onset LBBB)

Question 16

which sided heart block is shown? (look at V1)

Answer 16

RBBB
- positive deflections (turn right, indicator up)

Question 17

ISCHAEMIA ON ECG

i) what is the first thing to look for that needs urgent intervention?
ii) when may a deepening Q wave be seen on ECG? what may happen to the T wave?
iii) what ECG sign shows that the whole artery has been completely occluded?
iv) what could mask ischaemia on ECG?

Answer 17

i) ST elevation

ii) if someone is having an MI that has not been treated (hours/days later = full thickness infarct)
- T wave inversion

iii) ST elevation
iv) LBBB can mask STEMIs

Question 18

CORONARY ARTERY TERRITORIES

i) Which leads are implicated (ST elevation/depression/T wave change) in an anterior MI? (4) which artery does this correspond with?
ii) which two leads are implicated in lateral MI?
iii) which two leads are implicated in high lateral?
iv) which artery does an inferior STEMI correspond to? which three leads is abnormality seen in?
v) if there is ST elevation in one territory but depression in a different territory what does this fit with?

Answer 18

i) ST elevation in V1-V4
- corresponds with LAD

ii) V5-6 (left circumflex or diagonal LAD)
iii) I and aVL (left circumflex or diagonal LAD)

iv) inferior STEMI = right coronary artery
- II, III and aVF

v) fits with ischaemia - recprocal change
- if not ischaemia eg ST elevation in all leads - may be inflammation

Question 19

TESTING IN ISCHAEMIA

i) what do ischaemia stress tests look for?
ii) give three examples of ISTs
iii) what is the most common outpatient test used?
iv) what is invasive angiography?

Answer 19

i) check if there is evidence under stress that one of the arteries isnt properly perfused
ii) myocardial perfusion scan, stress ECHO, stress MRI
iii) CT angiography - slow heart rate down and look for filling of arteries
iv) pass wires through femoral artery to heart > pass a plastic tube and put dye down right and left systems > take pictures to see if blockages present

Question 20

MEDICATION

i) what would be started if someone has had an MI and a stent was going to be put in straight away?
ii) name two preventative medications
iii) what drug classes would be given to relieve pain? (2)
iv) what is ranolazine used for?
v) are stents or medications first line?

Answer 20

i) anti plat - clopidogrel
ii) statin and ACE inhibitor
iii) beta blocker and nitrates
iv) anti anginal (pain)
v) medication first line and if that fails then go for a stent

Question 21

REVASCULARISATION

i) when may a percutaneous coronary intervention (PCI) be one? is this high or low risk?
ii) when may coronary artery bypass grafting be done? (2)
iii) what is the worst thing for stents?
iv) what is given alongside aspirin before primary angioplasty for a stemi? (3)

Answer 21

i) partial occlusion of a blood vessel
ii) when multiple vessels are affected or if diabetic
iii) smoking
iv) clopidogrel or prasugrel or ticagrelor

Question 22

CLINICAL SPECTRUM ACS

i) what will most acute coronary events be?
ii) what is characterised by pain at rest but no troponin rise?
iii) what is charac by >1mm elevation in limb leads, >2mm elevation in V leads or new LBBB?

Answer 22

i) MI - stemi/nstemi
ii) unstable angina
iii) NSTEMI

Question 23

COMPLICATIONS OF STEMIS

i) give two ischaemic complications
ii) three mechanical complications
iii) two rhythm complications
iv) one inflammatory complication

Answer 23

i) angina or reinfarction
ii) heart failure, cardiogenic shock, aneurysm, acute mitral regurg
iii) atrial/ventric arrhythmias or heart block
iv) pericarditis

Question 24

in which area of the heart is the ischaemia?

Answer 24

antero-lateral STEMI

• ST elevation in anterior and lateral leads
• ST depression in inferior leads (reciprocal change)

Question 25

TROPONINS

i) name three other cardiac causes of a raised troponin
ii) respiratory cause
iii) infective cause
iv) neuro cause
v) renal cause
vi) MSK cause

Answer 25

i) aortic dissection, fast arrhythmia
ii) PE
iii) sepsis
iv) stroke/head trauma
v) CKD
vi) rhabdomyolysis / endurance exercise

Question 26

VALVULAR HEART DISEASE

i) what is a murmur?
ii) what is the most common type of valve disease in the UK? which valuve is most commonly affected
iii) what is a common cause of valve disease in young people?
iv) what type of valves does infective valve disease most commonly affect? who is most at risk of this?
v) which side of the heart is most commonly impacted in IVDU?

Answer 26

i) turbulent flow across a valve where the stethoscope is

ii) degenerative
- most commonly affects aortic then mitral

iii) rheumatic valve disease (post strep rheumatic fever)
- mitral > aortic

iv) abnormal valves
- most commom in immunocompromised

v) inject into vein > right heart > most commonly affects tricuspid valve

Question 27

AETIOLOGY

i) what happens in degenerative disease?
ii) what happens in rheumatic valvular disease
iii) what happens in stenosis? how does this affect SV and speed of ejection
iv) what happens in regurg? how does this affect the volume in the heart

Answer 27

i) calcification
ii) fibrosis and fusion of the leaflets
iii) stenosis = valve doesnt open all the way therefore not enough blood passes through > back pressure and loss of SV with fast ejection

iv) regurg = valvue doesnt close all the way so blood leaks backwards
- increases volume in heart and SV drops

Question 28

AORTIC STENOSIS

i) what chemical process is seen?
ii) which chamber of the heart is there increased pressure in? what does this eventually lead to?
iii) what is the most common cause >60yrs? name three things that can cause it <60yrs
iv) what are the three most common symptoms?
v) which symptom has the longest and shortest survival
vi) what type of murmur is heard? what is the best indicator of severity?

Answer 28

i) calcification of the valve

ii) high left ventricular systolic pressure to force blood through the valve
- leads to LV hypertrophy then decompen and dilatation

iii) degenerative
<60 = bicuspid valves, congenital, post rheum fever

iv) chest pain, breathlessness, dizziness/syncope
v) angina = longest and heart failure = shortest

vi) systolic crescendo decrescendo
- lack of second heart sound - more severe

Question 29

what is indicated by the arrow?

what type of valvular disease is this seen in?

Answer 29

shows thickened leaflets of the aortic valve

aortic stenosis

Question 30

VALVULAR DISEASE MANAGEMENT

i) is medical management curative?
ii) what are the two types of surgical intervention?
iii) why may someone be given percutaneous intervention? give two examples

Answer 30

i) no it is palliative
ii) valve repair or replace
iii) elderly

BAVI, TAVI

Question 31

VALVE REPLACEMENT

i) what must be given to a patient if they are given a mechanical valve?
ii) which valve is normally given to a younger patient?
iii) which type of valves do not need anti coagulation?
iv) what is a TAVI? are outcomes good? what is the highest risk of? how long must they be monitored for post procedure

Answer 31

i) patient needs to be on anti coagulants eg warfarin (not NOACs)
ii) mechanical valve
iii) biological valve - probably wont need a replacement

iv) trans catheter valve replacement > go through femoral > break old aortic valve with a balloon then replace with new valve
- good outcomes
- higher risk of strokes
- monitor for 24-48hrs

Question 32

ENDOCARDITIS

i) what is it?
ii) what is the characteristic lesion?
iii) what procdure can increase risk?
iv) what may be seen in the hands/feet (3)

Answer 32

i) microbial infection of the endothelial surface of the heart (valves)
ii) vegetation
iii) dental procedures - give prophylactic abx

iv) splinter haemm
- osler nodes - painful lesions on fingers
- janeway lesion - painless lesions on hands/feet

Question 33

what is seen in A,B,C? what are these signs of?

Answer 33

A - splinter haemmorhages

B - oslers nodes

C - janeway lesions

all signs of endocarditis

Question 34

what is indicated by the arrow? what is this a sign of?

Answer 34

vegetation

sign of endocarditis

Question 35

DIAGNOSIS OF ENDOCARDITIS

i) which criteria is used?
ii) what must be taken? (from three sites)

Answer 35

i) DUKE criteria
- major = positive blood culture from two diff cultures and endocardial involvement (vegetation, abscess)
- minor = predis, fever, single pos blood culture, vasc phenomena

ii) take blood cultures

Question 36

MANAGEMENT OF ENDOCARDITIS

i) what duration of treatment is required?
ii) give four reasons surgery may be indicated

Answer 36

i) 2-6 weeks
ii) surgery if ongoing sepsis, worsening valve regurg or HF, recurrent emboli eg strokes, vegetation >1.5cm, need removal of intra cardiac device

Question 37

CARDIOMYOPATHY

i) what are CMs? name four RF? which part of the cardiac cycle does it most commonly affect?
ii) name four symptoms? what is the gold standard investigation?
iii) name two things that need to be managed? what may a patient also need to be given?

Answer 37

i) CM is a group of disorder that aff the heart muscle (often mech or elec dysfunc)
- 50% are idiopathic but RF are excess ETOH ( can be reversed) , genetic, viral infection, hypothyroid, peripartum, chemo, cocaine
- causes predom systolic dysfunction

ii) symptoms of heart failure, dyspnoea and thromboembolism (may be asymp)
- Echocardiography is the gold standard
* determine underlying cause

iii) Manage HF symptoms /anti-coagulate
- may need an intra cardiac device or cardiac resynchronisation therapy

Question 38

HYPERTROPHIC CARDIOMYOPATHY

i) what is it? what is the most common defect that causes it? what is the inheritance pattern?
ii) what type accounts for 25% of cases and name three symptoms of this?
iii) what is it the most common cause of? how can the murmur intensity be increased?
iv) name three things that make it more likely that the dx is HCM? name three symptoms?

Answer 38

i) genetic disorder characterised by left ventricular hypertrophy (LVH) without an identifiable cause
- beta myosin heavy chain defects are most common)

ii) Auto dominant (50% cases are sporadic)
- Inc prev in males and afrocarrib/asian
- Obstructive form (HOCM - exertional dyspnoea & sudden cardiac death) is seen in 25% of cases - rest of cases are non obstructive

iii) Most common cause of sudden death under 35
* Valsalva manoeuvre will bring the hypertrophy septum closer to mitral valve and inc obstruction in blood flow so increase murmur intensity

iv) family history of HCM, history of pre-syncope or syncope, systolic ejection murmur
- symptoms = dyspnoea, angina, palpitations

Question 39

MX OF HYPERTROPHIC CARDIOMYOPATHY

iv) what is gold standard investigation? who should also be offered scrreening? what may be seen on imaging? (2)
v) what drugs are given first line? (2) what can be done if unresponsive to medical therapy? (2) how can sudden death be prevented?
vi) what is the the main complication? what causes this? (2)

Answer 39

iv) Echo is gold standard
- Offer screening for first degree relatives (ECG and echo)
- Don’t see dilatation on echo but most patients have a thickened IV septum

v) Give beta blockers and CCB first line
* Surgical myectomy if unresponsive to medical therapy
* Alcohol septal ablation (inject into coronary artery causing small MI to reduce septal thickness)
* Prev sudden death by implanting a ICD

vi) Sudden death usually caused by arrhythmias or severe LV outflow tract obstruction

Question 40

RESTRICTIVE CARDIOMYOPATHY

i) what causes it? which countries is it most prev in? what is the most common cuse? name three diseases that can predispose?
ii) how do the ventricles appear? how may the patient present?
iii) what is first line investigation? what is gold standard? what may be seen on imaging
iv) how is it treated? (3) what is there a high risk of?

Answer 40

i) Contrac of atria against stiff non dilated ventricles with near normal systolic function
* fibrosis or accum of protein in the myocardium
*least common cardiomyopathy
* dev countries - most common cause is amyloidosis
* systemic diseases such as saroid, haemochomratosis and malig can predispose

ii) Stiff ventricles > impaired diastolic filling
* may px with congestive HF with reduced CO

iii) Echo is first line
* Endomyocardial biopsy is gold standard
- See white speckles on echo if amyloid infiltration

iv) * Treat underlying cause
* anti coagulation
* treat heart failure
- High risk of arrhythmia and death

Question 41

AORTIC STENOSIS

i) what is stenosis? what is the preclinical phase? what are the SAD symptoms? how may pulse be affected? (2) why doees the LV fail over time?
ii) what investigation is done first? what is dx on this imaaging? name ttwo things that may be seen on ECG?
iii) how is asymp disease managed? name two procedures that improve survival and QOL?
iv) what type of valves are younger pts given? why? which are given to older pts? why?

Answer 41

i) Stenosis = opening is narrowed and may cause pressure overload in the preceeding chamber > hypertrophy
* Narrowing of aortic valve orifice
* Aortic sclerosis is preclinical phase = calcification/thickening of valve without signif obstruction
- SAD = Syncope (hypotension/transient arrhy), Angina, Dyspnoea (most common symp)
- slow rising / delayed pulse, narrow pulse pressure
* Narrowed orifice = inc afterload and therefore LV hypertrophy > LV fail over time

ii) do an echo firstt > Echo - narrow valve area is diagnostic
- ECG - LV hypertrophy/BBB

iii) If asymptomatic - routine follow up
- sx or percutaneous intervention eg aortic valve relacement or transcatheter aortic valve implant (TAVI) - improves survival and QOL
- Mech valve in younger pts (need anti coag)
- biol valves in elderly patients (dont last as long but dont need anti coag)

Question 42

MITRAL REGURG

i) what is regurgitation? what happens in MR? what causes acute MR? (4) what causes chronic MR? (3)
ii) why is LV systolic function reduced? name three ways it can px acutely? name two aspects of an emergency px? how is apex beat affected? what type of murmur is heard?
iii) what investigation is done first? what is it used for? what is ECG used for? what may be seen on CXR? (3)
iv) in which two cases do you anti coag? name three medical mx? what can be done for surgical mx? give two indications for sx?
v) what is there a risk of developing?

Answer 42

i) Regurgitation = back flow of blood through valve > vol overload, chamber dilat and failure
* backflow of blood from LV to LA due to leaky mitral valve
* acute MR - due to pap musc infarct, rupture chord tend, infec endocard, trauma
* chronic MR - MV prolapse (most common), ischaemic, rheumatic

ii) reduces CO and leads to vol overload in LA and LV > dilate over time > reduces systolic func of LV
- Acute - presents as emergency (sudden onset severe SOB & progressive pulm oedema)
- emergency = hypotension and cardiogenic shock
- blowing pan systolic murmur radiating to axilla

iii) DO an echo first - diagnostic (looks at ventric size, func and severity of regurg)
* ECG - detect AF
* CXR - look for cardiomegaly, signs of HF or pulm oedema

iv) Anticoagulate - if AF or severe LV dilat
* medical mx - diuretics, BB, ACEi for symp relief
* surgical mx - if severe/pulm hypertension/new onset AF/LV dysfunc (valve repair or replace)

v) risk of AF due to LV dilation

Question 43

HEART FAILURE

i) what is it? name three common causes? what happens as CO falls?
ii) how do frank starling mechanisms come into play? what happens as neurohumoral compensation?
iii) name four symptoms? name three signs of RHF?
iv) name three signs of LHF? why may BNP levels be raised? over what level is assoc with poor prognosis?

Answer 43

i) Inability of heart to produce a CO sufficient to meet body metab demands
* Most common causes are IHD, VHD, cardiomyop and HTM
* As CO falls - compen mechs activare to sustain tissue perfusion (initially beneficial but worsen HF over time)

ii) mech compen = frank starling = stretch myocardial fibres increases SV
* neurohumoral compen = inc SNS stim and activ of RAAS

ii) Dyspnoea
* orthopnea and PND
*nocturnal cough, chest discomfort, periph oedema and fatigue
* RHF - inc JVP, hepatomeg, ascites, periph oedema

iv) LHF - displaced apex beat, S3 heart sound, pulm congestion (usually R/L occ together > congestive)
- BNP level - rel in response to myocard stretch (>400 = poor prognosis)

Question 44

STABLE ANGINA

i) what causes it? name three things symptoms can be associated with?how do symptoms appear? does it affect men or women more?
ii) name three mod RF? what are the three features? what is someone has all three symp? what is two? what if none?
iii) what investigation should be done first? what two drugs are first prescribed?
iv) what is first line tx? (2) whaat is second line? (2) what is given if these drugs are contraindicated?
v) when is coronary artery bypass done? (3)

Answer 44

i) Fixed narrowing of CAs > symps assoc with exertion, emotion, eating and cold weather
* symptom onset is predictable and relieves once stim is removed
* affects 2x men compared to women

ii) Mod RFs - DM, HTN, hyperlipid, smoking, obesity
* Narrowing of CA > reduc in blood flow and o2 delivery to myocardium
* atheroma can cause endothelial dysfunc > vasodilator rel eg NO and prostacyc
* cant meet demand when increased demand for myocard 02 eg walking up hill
* Ischaemia > acidosis, reduc ATP prod and lactate rel > stim nerves in myoctes to cause pain
- three features are central chest pain - heavy/pressure/squeezing, Precipitated by exertion. Relieved by rest or nitrates (usually within 5 mins)
* if all 3 = typical angina, if 2 = atypical
* patient with non of these = non anginal pain

iii) do ECG first
- Prescribe aspirin and statins
- Pharma therapy - GTN

iv) First line - beta blocker or CCB
* Second line - BB and CCB
* if BB or CCB contraindic use ivabrad (HCN chan blocker that slows HR), ranolazine, nicorandil (vasodilator)
* Lipid mod therapy

v) Coronary artery bypass if signif left main disease, three vessel disease or two vessel disease in diabetics

Question 45

ACS - UNSTABLE ANGINA AND MI

i) what are acute coronary syndromes? what are they classified by? (2) what is the most common cause? what does it usually result from?
ii) what happens if a thrombus completely occludes a vessel? what happens in absence of total thrombotic occlusion? (2) what two things maay be seen onn ECG?
iii) what type of chest pain is felt? (3) naame three other symptoms? name two groups it may px atypically in?
iv) at what two time points should an ECG be done? name four things to look for on CXR? how many troponin bloods should be done? what score is used for UA/STEMI to predict 6 month mort?
v) name three reccomendations for dx of UA/MI

Answer 45

i) ACS = group of conds that result from sudden interrup of CA blood flow
* Classified acc to changes in ECG and biochemical markers
* Athero is the most common cause
* usually results from athero plaque rupture > thrombus > luminal blockage

ii) if thrombus occludes vessel completely = STEMI
* absence of total thrombotic occlusion = NSTEMI or unstable angina - ECG may shows ST depression or T wave inversion

iii) Chest pain is acute, central, crushing, retrosternal with or without rad to jaw and neck
* SOB, sweating, nausea and vom
* may present atypically in diabetics/elderly - may have a silent MI (not chest pain) or may pres ith delerium, hypotension or epigastric pain

iv) Do an ECG - 15-30 mins apart
* CXR - look at contours, lung fields and exclude non cardiac causes of chest pain eg pthx
* Bloods - troponin T or I (serial, 6h apart), FBC, UE, LFT
* GRACE score for UA/NSTEMI to predict 6 month mortality

v) dx > rise/fall of troponin with at least one value above 99th%
*with symps of ischaemia, ECG change indic of new isch eg LBBB, pathol Q waves, imaging evidence of loss of myocard
* ident intracoronary thrombus on angio

Question 46

MI/UA TREATMENT AND COMPLICATIONS

i) what tx should be started with? (2) what needs to be done in a STEMI? when is 02 given? when is GTN given?
ii) what can be given for pain? name an anti emetic that can be given? what is needed lifelong? what may be given for 12 months?
iii) name three drugs that can lower mortality?
iv) name five complications

Answer 46

i) Start anti plat treatment (aspirin plus clopid/prasu/ticagrelor)
* Re perfuse myocardium in a STEMI (PCI)
* prevent progression in US or NSTEMI
*O2 if sats <94%
* GTN if BP >90

ii) IV morphine for pain
* metoclopramide - anti emetic
later management
* lifelong aspirin / P2Y12 inhibs for 12 months (clopid etc)

iii) statins, ACEi and beta blockers lower mortality

iv) recurrent MI or re-occlusion
* acute pulm oedema
* cardiogenic shock
* arrhythmia - VT/VF > sudden death in 1/5 of patients
* ventric septum rupture (rare but occ within a week of MI)
* pap muscle rupture
* RV fail

Question 47

SYNCOPE

i) what is it? what is the most common type? name three causes? name three other causes of syncope
ii) name four things that can cause cardiac syncope?
iii) how do dysrhytmias cause syncope? name five
iv) name three pro-arrhythmic drugs that can cause syncope? name three structural causes

Answer 47

i) transient loss of conc caused by global cerebral hypoperfusion
* rapid onset, short duration and spontaneous complete recovery
* May be reflex syncope eg vasovagal or syncope due to orthostation hypotension, cardiac

ii) bradycardia, tachycardia, or hypotension due to low cardiac index, blood flow obstruction, vasodilatation, or acute vascular dissection

iii) Dysrhythmias produce syncope by decreasing ventricular filling and stroke volume, resulting in hypotension and diminished cerebral blood flow
- Ventricular arrhythmias, Sinus node dysfunction: including bradycardia/tachycardia syndrome, Atrioventricular conduction system blocks, Paroxysmal supraventricular tachycardia, Inherited syndromes: long QT syndromes, Brugada syndrome, Implanted device malfunction:

iv) sotalol, flecainide, quinidine, procainamide
- struc causes - cardiac valvular diseases. aortic or mitral stenosis (severe mitral stenosis is most commonly associated with syncope during periods of atrial fibrillation), acute aortic, mitral, or tricuspid insufficiency. prosthetic valve dysfunction, Hypertrophic obstructive cardiomyopathy

Question 48

SYNCOPE

i) what must first be done? name three differentials
ii) name four red flag symptoms? what do palpitations before LOC predict?
iii) what may cause syncope when turning head/shaving face? name four drugs that may be implicated in syncopal episodes?
iv) name five ways syncope can be differentiated from epileptic seizure?

Answer 48

i) differentiate syncope from non-syncopal conditions, such as seizures, falls, psychogenic pseudosyncope, drop attacks, and transient ischaemic attacks, and to try to identify the cause (mechanism) so that appropriate treatment may be offered

ii) red flag > chest pain, palpitations, back pain, haematemesis, melena before the syncopal episode, and syncope with exercise
- Palpitations before loss of consciousness are a significant predictor of a cardiac cause of syncope

iii) carotid sinus hypersens
- diuretics, vasodilators, venodilators, negative chronotropes, and sedatives

iv) Seizures are typically associated with longer duration of loss of consciousness, loss of bowel and bladder control, rhythmic clonic movements, and disorientation after the episode.
- Tongue biting can occur in patients with syncope, it greatly increases the chance that the patient has had an epileptic seizure
- Twitching and jerking are often seen with vasovagal or cardiac syncope, but these can be differentiated from rhythmic jerking of all the limbs in tonic-clonic seizures

Question 49

HF TX

i) what is first line tx? which drugs are given for symptom relief but dont reeduce mortality?
ii) which two drug types improve morbid/mortality?
iii) which drug class may be used post STEMI? what is given if patient does not have AF?

Answer 49

iii) Lifestyle mod (smoking, fluid/salt restriction/ETOH/diet/exercise)
*Diuretics - furosemide (loop), don’t reduce mort

ii) ACEi - improve morbid/mortal, improve vent function
* beta blocker - improve mort (bisop, carvedil) - start slow (first line if pt also has AF)

iii) Mineralocort receptor antag - improve mort (used post STEMI)
- Ivabradine if no AF