Cardiology

Question 1

roles of ACEi?

Answer 1

HTN (in young, non afrocaribean)
diabetic nephropathy
secondary prevention for ischaemic heart disease

Question 2

mechanism of action for ACEi?

Answer 2

activated by liver in phase 1 metabolism

prevent conversion of angiotensin 1 to 2

Question 3

What are the side effects of ACEi?

Answer 3

cough - can occur up to a year after starting
hyperkalaemia
Hypotension
angioedema - may occur up to a year after

Question 4

what is though to be the cause of the cough with ACEi?

Answer 4

increased levels of bradykinin?

Question 5

What cautions should be taken with ACEi? What are the contraindications?

Answer 5

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

Question 6

How are the use of ACEi monitored?

Answer 6

UEs before and after starting
should accept a creatine rise up to 30% increase
Accept a potassium of up to 5.5

Question 7

Outline the medical management of HTN?

Answer 7

<55 or T2DM

1. ACEi
2. ACEI + Ca channel blockers/ Thiazide diuretics
3. all 3
4. if K+ > 4.5 - add spironolactone. If >4.5 add B blocker or alpha blocker

> 55 or afrocaribean

1. Calcium channel blockers
2. ACEI + Ca channel blockers/ Thiazide diuretics
3. all 3
4. if K+ > 4.5 - add spironolactone. If >4.5 add B blocker or alpha blocker

Question 8

Which drugs enhance the effects of adenosine and which block the effects?

Answer 8

theophyllines inhibit

dipyridamole enhances

Question 9

Which condition should adenosine be avoided in?

Answer 9

asthma due to bronchospasm

Question 10

What is the mechanism of action of adenosine?

Answer 10

a1 receptor agonist - blocks adenyl cyclase. less cAMP. K+ leaves cell. hyperpolerisation.

thus blocks AVN transiently (short half life)
used to treat SVTs

Question 11

what are the adverse effects of adenosine?

Answer 11

chest pain
bronchospasm
flushing
can promote use of accessory pathways e.g. WPW

Question 12

give examples of ADP (adenosine diphosphate) receptor blockers

Answer 12

clopidogrel
ticagrelor
prasugrel
Ticlopidine

Question 13

how do ADP receptor inhibitors work?

Answer 13

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.

Question 14

In the current NICE guidelines, what is suggested as antiplatelet therapy for ACS?

Answer 14

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

Question 15

what are the adverse effects of ticagrelor ?

Answer 15

dyspnoea due to impaired clearance of adenosine.

Question 16

what DDI exist for ADP receptor inhibitors?

Answer 16

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

Question 17

what is the chest compression ratio given to adults?

Answer 17

30:1

Question 18

which rhythms are shockable? non shockable?

Answer 18

pulseless VT and VF = shockable

pulseless electrical activity and asystole = non shockable

Question 19

How often and how much adrenaline is given in an arrest?

Answer 19

1mg ASAP for the non-shockables

after 3rd shock in shockables. rhythms

Question 20

how can the shocks be given if a cardiac arrest is witnessed/ happens at the time you are ready?

Answer 20

3 consecutive shocks can be given

Question 21

how is asystole/ pulseless electrical activity managed?

Answer 21

1mg adrenaline ASAP

no shocks just CPR

Question 22

what are the 4Hs and 4Ts of a cardiac arrest?

Answer 22

Hs: hypoxia, hypotension, hyperkalaemia, hypothermia

T: thrombus, tamponade, tension pneumothorax, toxins

Question 23

what is the class and action of amiodarone?

Answer 23

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

Question 24

what type of arrhythmias is amiodarone used in?

Answer 24

atrial, nodal and ventricular tachycardia

Question 25

why is a loading dose of amiodarone often used?

Answer 25

very long half like (days)

Question 26

how is amiodarone given?

Answer 26

IV through central vein - causes thrombophlebitis

Question 27

what are the DDIs of amiodarone?

Answer 27

Can interact with Cytochrome 450 | decreases metabolism of warfarin

Question 28

what monitoring is needed for amiodarone?

Answer 28

TFTs UEs LFTs CXR prior to starting | TFTs and LFTS every 6 months

Question 29

what are adverse effects of amiodarone?

Answer 29

``` 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 ```

Question 30

what class drug are the following... candesartan losartan irbesartan

Answer 30

Angiotensin receptor 2 inhibitors

Question 31

what are the side effects or ARBs?

Answer 31

hypotension | hyperkalaemia

Question 32

What is the first and second line antiplatelet in ACS?

Answer 32

1st line : aspirin (lifelong) and ticagrelor (12 month) | 2nd line: clopidogrel lifelong if aspirin is contraindicated

Question 33

What is the first and second line antiplatelet in PCI?

Answer 33

1st line : aspirin (lifelong) and ticagrelor/prasugrel (12 month) 2nd line: clopidogrel lifelong if aspirin is contraindicated

Question 34

What is the first and second line antiplatelet in TIA/ischaemic stroke?

Answer 34

1st line: life long clopidogrel | 2nd line: aspirin + dipyrimadole lifelong

Question 35

What is the first and second line antiplatelet in peripheral arterial disease?

Answer 35

1st line: clopidogrel life long | 2nd line: aspirin life long

Question 36

What is the pathophysiology of aortic dissection?

Answer 36

tunia intima tears high pressure blood pools between layers of intima and media separates layers and increases outside diameter of vessel.

Question 37

what is type A and B aortic dissection?

Answer 37

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

Question 38

what are the causes of aortic dissection ?

Answer 38

``` causes: chronic high blood pressure aortic coarctation connective tissue disorders - ehlers danlos/marfarns aneurysms trauma bicuspid aortic valve turners and noonans pregnancy syphillis ```

Question 39

What issues arise from aortic dissections?

Answer 39

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

Question 40

what are the symptoms of aortic dissection?

Answer 40

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

Question 41

How can a aortic dissection be managed?

Answer 41

type A - surgery (blood pressure needs to be managed to 100-120mmHg whilst awaiting) Type B - B blockers and nitroprusside, conservative/ IV labetolol

Question 42

which type of aortic dissection is most common?

Answer 42

type A

Question 43

what are the two classifications for aortic dissection?

Answer 43

stanford - type A and B | DeBakey - Type 1 to 3

Question 44

what is the debakey classification for aortic dissection?

Answer 44

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

Question 45

How can an aortic dissection be investigated?

Answer 45

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 ```

Question 46

What are the risk factors / causes of aortic stenosis?

Answer 46

bicuspid valve chronic rheumatic fever stress overtime - older adults williams syndrome - supravalvular aortic stenosis HOCM - subvalvular

Question 47

what are the complications of aortic stenosis?

Answer 47

left ventricular hypertrophy and HF reduction in blood flow - syncope, angina etc Microangiopathic haemolytic anaemia - damage to RBC as they are forced through stenosis

Question 48

what are the causes of aortic regurgitation?

Answer 48

``` idiopathic valve damage - rheumatic fever , Infective endocarditis aortic dissection sphyllis aneuryms RA/ SLE bicuspid valve ```

Question 49

what murmur is heard in aortic stenosis/ regurgitation?

Answer 49

A.S: ejection systolic murmur, radiates to carotids | A.R: early diastolic murmur

Question 50

what are the symptoms/signs of aortic regurgitation?

Answer 50

``` 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

Question 51

what are the symptoms of aortic stenosis?

Answer 51

Classic triad: chest pain syncope angina

Question 52

what are the features of severe aortic stenosis?

Answer 52

``` 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 ```

Question 53

how is aortic stenosis managed?

Answer 53

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

Question 54

What will the NEWS score be for an MI?

Answer 54

often normal maybe tachycardic unless complications of MI

Question 55

What leads represent antior/ inferior/lateral MIs and which arteries do these correspond to?

Answer 55

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.

Question 56

what is the difference between subendocardial and transmural infarcts?

Answer 56

Subendocardial infarct – NSTEMI – only inner part of myocardium is necrosed. Transmural infarct = STEMI = whole myocardium necrosed.

Question 57

how is an MI diagnosed?

Answer 57

- ECG | - Troponin I and T , CK-MB = enzymes released

Question 58

when are the cardiac enzymes most elevated during an MI? Which cardiac enzyme is best at distinguishing between two MIs that have occurred?

Answer 58

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.

Question 59

How are MIs treated - basic first steps of management?

Answer 59

MONA | morphine IV, O2 titrated, nitrates sublingual/IV (caution if hypotensive), aspirin 300mg

Question 60

How are STEMIs managed?

Answer 60

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)

Question 61

How quickly should PCI be performed?

Answer 61

within 12 hours of symptoms. Can be after if still evidence of ongoing ischaemia

Question 62

How is PCI performed?

Answer 62

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

Question 63

when is fibrinolysis offered?

Answer 63

if PCI cant be offered | if no contraindication

Question 64

How is fibrinolysis performed?

Answer 64

fibrinolytic agent Also give antithrombin drug e.g fondaparinux Repeat ecg after 60-90 mins and if resolved if still ischaemic – PCI considered

Question 65

what scoring system is used to decide on management of NSTEMI? What does this scoring system use and what does it show.

Answer 65

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

Question 66

Which NSTEMI patients will have PCI during admission?

Answer 66

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

Question 67

what is the secondary prevention for MIs?

Answer 67

``` o Aspirin o Second antiplatelet – clopidogrel o B blocker o ACE inhibitor o Statin ```

Question 68

what is the criteria for NSTEMI?

Answer 68

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

Question 69

what are the complications of an MI?

Answer 69

- Shock and acute heart failure - Pericarditis - Rupture of myocardium/ septum - Embolus - Arrhtyhmia - Dresslers syndrome

Question 70

What are the poor prognostic factors post MI?

Answer 70

* 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

Question 71

What is the Kilip class system?

Answer 71

system used to risk stratify post MI 1. no clinical signs of heart failure - 6% 30 day mortality 2. lung crackles, S3 - 17% 30 day mortality 3. frank pulmonary oedema - 38% 30 day mortality 4. cardiogenic shock - 81% 30 day mortality

Question 72

what is pericarditis? | what are the complications?

Answer 72

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

Question 73

what are the causes of pericarditis?

Answer 73

``` idiopathic viral - coksackie malignancy connective tissue disorders dresslers uraemic pericarditis (bread and butter appearance) radiation drugs hypothyroid ```

Question 74

what are the symptoms of pericarditis?

Answer 74

chest pain worse on inspiration better leaning forward fever/ flu like friction rub no productive cough tachycardia/ tachypnoea

Question 75

what are the ECG changes seen in pericarditis?

Answer 75

wide spread saddle shaped ST elevation PR depression - most specific T flattens eventually and ST flattens later too.

Question 76

how can pericarditis be investigated?

Answer 76

ECG CXR - widened mediastinum ECHO - shows effusion

Question 77

how is pericarditis managed?

Answer 77

NSAIDs and Colchicine pericardiocentesis if effusion pericardectomy for constrictive pericarditis

Question 78

how is angina managed?

Answer 78

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

Question 79

name 3 long acting nitrate...

Answer 79

ranolazine nicorandil ivabradine

Question 80

What is the problem with using nitrates for angina etc? How can this be overcome?

Answer 80

tolerance can develop | this can be overcome by using modified release or having smaller doses more often.

Question 81

which particularly cause of pericarditis can cause constrictive pericarditis?

Answer 81

TB

Question 82

what are the signs/symptoms of constrictive pericarditis?

Answer 82

``` dyspnoea pericardial knock - loud S3 Right sided HF signs - hepatomegaly, raised JVP, ascites kussmaul sign JVP shows prominent X and Y descent ```

Question 83

what might be seen on CXR for constrictive pericarditis?

Answer 83

cardiac calcifications

Question 84

what are the differences between cardiac tamponade and constrictive pericarditis?

Answer 84

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

Question 85

What is Becks Triad seen in Cardiac tamponade?

Answer 85

raised JVP low BP muffled heart sounds.

Question 86

What ECG sign is seen in cardiac tamponade?

Answer 86

Alternating QRS complex heights.

Question 87

What change is seen in JVP waveform in Cardiac tamponade?

Answer 87

absent Y descent - limited right ventricle filling.

Question 88

What is arrhythmogenic right ventricular cardiomyopathy?

Answer 88

ARVC - inherited cardiovascular disease presents as palpitations, syncope or sudden cardiac death

Question 89

what is the most common and second most common cause of sudden cardiac death in young?

Answer 89

1. HOCM | 2. ARVC

Question 90

what is the pathophysiology behind ARVC?

Answer 90

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

Question 91

What ECG findings are found in ARVC?

Answer 91

V1 -3 - T wave inversion | Epsilon wave found in 50% of patients - this is a terminal notch in QRS

Question 92

what are the ECHO findings for ARVC?

Answer 92

enlarged hypokinetic right ventricle with thin free wall

Question 93

what Ix can be used for ARVC?

Answer 93

ECG ECHO MRI - shows fibrofatty tissue

Question 94

how is ARVC managed?

Answer 94

sotalol catheter ablation to prevent VT implantable cardioverter defib

Question 95

what is Naxos disease?

Answer 95

an autosomal recessive variant of ARVC | a triad of ARVC, palmoplantar keratosis, and woolly hair

Question 96

What are the causes / risk factors of AF?

Answer 96

``` M - mitral valve disease (stretches atrial and damages myocytes) I - ischaemic heart disease T - thyroid R A - alcohol L - lung pathology (pneumonia) ```

Question 97

where does AF originate?

Answer 97

In pulmonary veins

Question 98

what are the types of AF?

Answer 98

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.

Question 99

what are the uses of radiofrequency catheter ablation in AF?

Answer 99

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

Question 100

How is the arrhythmia element of AF controlled?

Answer 100

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

Question 101

What is the CHADSVASC score?

Answer 101

``` 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 ```

Question 102

when is anticoag used using CHAD VASc?

Answer 102

0 - no treatment 1 - males consider anticoag 2 - offer anticoag

Question 103

What is the HASBLED score?

Answer 103

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

Question 104

When is electrocardioversion used in AF?

Answer 104

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.

Question 105

How does electrical DC cardioversion work?

Answer 105

synchronised to R wave - to prevent VF

Question 106

what pharmacological agents are used for cardioversion and when?

Answer 106

flecanide - if no structural heart disease | amiodarone - if there is structural heart disease

Question 107

for patients who have had AF for >48 hours that cannot be anticoagulated for 3 weeks prior to cardioversion, what other option is there?

Answer 107

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.

Question 108

should anticoagulation be given post cardioversion?

Answer 108

for those who had AF <48 hours - no for those who had AF >48 - yes continue for further 4 weeks.

Question 109

how are patients with a Stroke + AF managed in terms of future clotting risk?

Answer 109

warfarin / DOAC | rather than antiplatelets

Question 110

why is digoxin not first line for AF but when is it prefered?

Answer 110

Not good at controlling rate during exercise prefered in those with coexistent HF.

Question 111

what agents can be used for rhythm control in AF?

Answer 111

sotalol amiodarone flecanide

Question 112

what factors favour rate control or rhythm control in AF?

Answer 112

rate: - >65yrs - history of IHD rhythm: - <65yrs - symptomatic - first presentation - lone AF/ AF secondary to precipitant - congestive heart failure

Question 113

when is catheter ablation for AF offered?

Answer 113

in those who dont respond or want to avoid anti-arrhythmics

Question 114

when is catheter ablation for AF offered?

Answer 114

in those who dont respond or want to avoid anti-arrhythmic

Question 115

When is anticoagulation needed for catheter ablation in AF?

Answer 115

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)

Question 116

what are the complications of catheter ablation in AF?

Answer 116

cardiac tamponade stroke pulmonary valve stenosis

Question 117

what is a atrial myxoma?

Answer 117

most common primary cardiac tumour

Question 118

where do atrial myxomas mainly occur?

Answer 118

left atrium - mainly attached to fossa ovalis

Question 119

who are atrial myxomas most common in?

Answer 119

females

Question 120

what are the symptoms/features of atrial myxomas?

Answer 120

systemic - dyspnoea, fatigue, clubbing, weight loss, fever AF mid diastolic murmur - 'tumour plop' emboli

Question 121

what is seen on echo for atrial myxomas?

Answer 121

pedunculated heterogeneous mass typically attached to the fossa ovalis region of the interatrial septum

Question 122

What are the uses of atropine and what type of drug is this?

Answer 122

Antagonist of the mAChR used to treat organophosphate poisoning and symptomatic bradycardias no longer used for cardiac arrest

Question 123

What are the effects of atropine?

Answer 123

tachycardia | Mydriasis

Question 124

Where is B type natiuretic peptide produced?

Answer 124

primarily by myocytes of left ventricle

Question 125

what can raise levels of BNP?

Answer 125

HF mainly other cardiac dysfunction - valvular disease, ischaemia CKD

Question 126

what can reduce BNP levels?

Answer 126

ARBs, ACEi, diuretics

Question 127

what are the effects of BNP?

Answer 127

vasodilation inhibits RAAS pathway diuresis and natriuresis

Question 128

How is BNP used in the diagnosis of HF?

Answer 128

``` 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

Question 129

what are the indications for B blockers?

Answer 129

``` angina secondary prevention for ACS anxiety long QT AF (and other arrhythmias) HF HTN thyrotoxicosis migraine prophylaxis ```

Question 130

what are the side effects of B blockers?

Answer 130

``` bronchospasm bradycardia fatigue cold peripheries erectile dysfunction sleep disturbance inc nightmares ```

Question 131

when are B blockers contraindicated?

Answer 131

uncontrolled HF asthma sick sinus syndrome concurrent verapamil use - can induce severe bradycardia

Question 132

what are the complications of a bicuspid aortic valve?

Answer 132

higher risk of... aortic regurg aortic stenosis aortic dissection and aneurysm formation from ascending aorta

Question 133

what is a left dominant coronary circulation?

Answer 133

the posterior descending coronary artery arises from the circumflex artery rather than the RCA

Question 134

what conditions is bicuspid aortic valves associated with?

Answer 134

Turners left dominant coronary artery circulation around 5 % also have a coarctation of aorta

Question 135

what is Bivalirudin?

Answer 135

reversible direct thrombin inhibitor | used in ACS

Question 136

if a blood pressure cuff is too small - will the measurement be an overestimate OR underestimate?

Answer 136

overestimate | if too large - underestimate

Question 137

if the arm is below the level of the heart, will a blood pressure reading be over or under estimate?

Answer 137

Over estimate if below level underestimate if arm is raised above heart

Question 138

if each arm gives a different BP reading, which should be taken?

Answer 138

the highest reading

Question 139

What are the causes of broad complex tachycardias?

Answer 139

VT - until proven otherwise | SVT with aberrant conduction

Question 140

What features on an ECG suggest VT rather than SVT with aberrant conduction?

Answer 140

``` 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 ```

Question 141

what is Brugada syndrome?

Answer 141

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

Question 142

who is brugada syndrome most common in?

Answer 142

asians

Question 143

what are the ECG changes found in brugada syndrome?

Answer 143

convex ST elevation >2mm (or >1mm in V1-3) followed by negative T wave partial RBBB

Question 144

how is brugada syndrome investigated?

Answer 144

ECG changes | can give flecanide/ ajmaline and ECG changes become more prominant

Question 145

how is brugada managed?

Answer 145

Implantable cardioverter defibrilator

Question 146

What is Buerger's disease?

Answer 146

small/medium vessel vasculitis strongly associated with smoking a.k.a. thromboangiitis obliterans

Question 147

what are the features of Buerger's disease?

Answer 147

extremity ischaemia - intermittent claudication, ulcers Raynauds superficial thrombophlebitis

Question 148

what is the oxygen saturation of blood returning to right atrium? left atrium

Answer 148

right heart - 70% left heart - 98-100%

Question 149

If there is an ASD or VSD what happens to oxygenation saturations of blood in different chambers of the heart?

Answer 149

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%

Question 150

If there is an ASD or VSD what happens to oxygenation saturations of blood in different chambers of the heart?

Answer 150

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%

Question 151

If there is a PDA what happens to oxygenation saturations of blood in different chambers of the heart?

Answer 151

right atrium and ventricle - 70% (as normal) pulmonary artery = 85% (due to mixing) left heart = 100%

Question 152

what happens to O2 saturations of the heart if there is eisenmengers?

Answer 152

O2 saturations drop on left side of heart .. | E.g. Eisenmengers with VSD... the left ventricle and aorta drop to 85% O2 sats.

Question 153

which cardiac enzyme is the first to rise in MI?

Answer 153

myoglobin

Question 154

how long for CKMB and troponins to return to normal following MI?

Answer 154

troponins 10 days CKMB - 2-3 days myoglobin 1-2 days

Question 155

what markers are raised in MI?

Answer 155

``` Troponin I , T CK MB CK LDH AST ```

Question 156

what is a SPECT scan?

Answer 156

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.

Question 157

what is a MUGA?

Answer 157

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

Question 158

what are the two types of cardiac CT?

Answer 158

calcium score: to look at atherosclerotic plaque calcium to give a calcium score (predicts risk of ischameia) contrast enhanced CT - visualises coronary arteries

Question 159

what are the uses of cardiac MRI?

Answer 159

view structure of heart - gold standard assess myocardial perfusion using gadolinium

Question 160

what are the different types of genetic cardiomyopathy?

Answer 160

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) ```

Question 161

what gene is mutated in HOCM?

Answer 161

B myosin heavy chain

Question 162

What are the ECHO findings of HOCM?

Answer 162

Mitral regurgitation systolic anterior motion (SAM) anterior mitral valve asymmetric septal hypertrophy

Question 163

what pattern of inheritance is HOCM ?

Answer 163

autosomal dominant

Question 164

What are the causes of dilated and restrictive cardiomyopathy?

Answer 164

dilated: alcohol, coxsackie, wet beri beri, doxorubicin restrictive - amyloidosis, post radiotherapy, loefflers endocarditis

Question 165

when does peripartum cardiomyopathy develop, who is it most common in?

Answer 165

last month of preg and 5 months after more common in older women , greater parity and multiple gestations

Question 166

What is Takotsubo cardiomyopathy?

Answer 166

stress induced cardiomyopathy transient apical ballooning of the myocardium

Question 167

what are the infective causes of cardiomyopathies?

Answer 167

coxsackie B | Chagas disease

Question 168

What endocrine conditions can cause cardiomyopathies?

Answer 168

Diabetes thyrotoxicosis Acromegaly

Question 169

what neuromuscular conditions can lead to cardiomyopathy?

Answer 169

Duchennes/Becks Friedreich's ataxia myotonic dystrophy

Question 170

which nutritional deficiency can cause cardiomyopathy?

Answer 170

thiamine = beri beri

Question 171

What is Catecholaminergic polymorphic ventricular tachycardia?

Answer 171

form of inherited cardiac disease associated with sudden cardiac death autosomal dominant

Question 172

what gene is mutated in catecholamine polymorphic ventricular tachycardia?

Answer 172

Ryanodine receptor (RYR2) gene mutation - found in myocardial sarcoplasmic reticulum

Question 173

what are the features/symptoms of catecholamine polymorphic ventricular tachycardia?

Answer 173

exercise or emotion induced polymorphic ventricular tachycardia resulting in syncope sudden cardiac death symptoms generally develop before the age of 20 years

Question 174

how is catecholamine polymorphic ventricular tachycardia managed?

Answer 174

B blockers | implantable defib

Question 175

Which antihypertensive are centrally acting?

Answer 175

methyldopa clonidine moxonidine - alpha 2 receptor stimulation

Question 176

what is the main cause of cholesterol emboli ?

Answer 176

vascular surgery angiography (but also atherosclerosis)

Question 177

what are the features of a cholesterol emboli?

Answer 177

eosinophilia purpura renal failure livedo reticularis

Question 178

what are the DDI with clopidogrel?

Answer 178

PPI - make clopidogrel less effective | lansoprazole is okay to use

Question 179

what is the mechanism of action of clopidogrel?

Answer 179

antagonist of the P2Y12 adenosine diphosphate (ADP) receptor, inhibiting the activation of platelets class of drug = thienopyridines

Question 180

What rate do atria contract in atrial flutter?

Answer 180

300 bpm

Question 181

What is the pathophysiology behind atrial flutter?

Answer 181

Normally SAN --> AVN | In atrial flutter there are re-entry rhythms in atria so atria contract again and again

Question 182

what are the different types of atrial flutter?

Answer 182

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

Question 183

what are the causes of atrial flutter?

Answer 183

IHD - damage to myocytes | similar causes to AF

Question 184

what are the ECG changes for atrial flutter?

Answer 184

saw tooth pattern - multiple contractions - flutter wave, no p. 1:2/3/4 ratio with QRS

Question 185

what are the symptoms of atrial flutter?

Answer 185

If there is SVT - can lead to tachycardia, dyspnoea, fatigue, HF Clots

Question 186

what is the management of atrial flutter?

Answer 186

Like AF ``` Anticoag B blocker Rhtyhm control DC cardioversion ablation - of tricuspid valve isthmus = curative in most. ```

Question 187

How can flutter be identified as a cause of an SVT?

Answer 187

carotid sinus massage/ adenosine - blocks AVN

Question 188

What is the ostium primum, secundum and foramen ovale?

Answer 188

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

Question 189

What are the main causes of Atrial septal defects?

Answer 189

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

Question 190

what are ASDs associated with?

Answer 190

fetal alcohol syndrome ostium primum - down syndrome ostium secundum - associated with Holt-Oram syndrome (tri-phalangeal thumbs)

Question 191

what is the management of ASD?

Answer 191

children are monitored in the hope it will close | otherwise can close surgically

Question 192

what are the features of ASD?

Answer 192

ejection systolic murmur, fixed splitting of S2 embolism may pass from venous system to left side of heart causing a stroke - paradoxical embolus

Question 193

which ASD presents earliest?

Answer 193

Ostium primum

Question 194

what other heart abnormality is ostium primum associated with?

Answer 194

abnormal AV valves

Question 195

What ECG may be seen with ostium primum ?

Answer 195

RBBB with LAD | prolonged PR interval

Question 196

what is LEV's disease?

Answer 196

lenegre lev syndrome describes the idiopathic causes of heart block fibrosis progressive overtime over AVN.

Question 197

what are the causes of heart block?

Answer 197

``` LEVs disease (idiopathic) IHD cardiomyopathy myocarditis electrolytes ```

Question 198

what are the different types of heart block?

Answer 198

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.

Question 199

How is heart block managed?

Answer 199

for type 2 mobitz and 3rd degree - pace maker otherwise can investigate and correct cause. if first degree - no Mx

Question 200

What is the PR interval measrued as in 1st degree heart block?

Answer 200

>0.2s

Question 201

How do you decide if someone with an episode of chest pain should go to hospital?

Answer 201

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

Question 202

how is anginal chest pain defined by NICE?

Answer 202

1. constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms 2. precipitated by physical exertion 3. 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

Question 203

what is the first line investigation for patients with chest pain who cant e diagnosed with angina by clinical symptoms alone?

Answer 203

CT coronary angiogram = 1st line 2nd line - non invasive cardiac imaging e.g. SPEC, stress ECHO, MRI

Question 204

How is HF investigated (NICE guidance)?

Answer 204

NT-proBNP = 1st line Ix if high - specialist in 2 weeks if raised - specialist in 6 weeks

Question 205

what can increase BNP?

Answer 205

``` Left ventricular hypertrophy Ischaemia Tachycardia Right ventricular overload Hypoxaemia (including pulmonary embolism) GFR < 60 ml/min Sepsis COPD Diabetes Age > 70 Liver cirrhosis ```

Question 206

what can decrease BNP?

Answer 206

``` Obesity Diuretics ACE inhibitors Beta-blockers Angiotensin 2 receptor blockers Aldosterone antagonists ```

Question 207

what is coarctation of the aorta?

Answer 207

congenital narrowing of the descending aorta

Question 208

who is coarctation most common in?

Answer 208

males

Question 209

What are the clinical features of coarctation of the aorta?

Answer 209

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

Question 210

what conditions is coarctation of the aorta associated with?

Answer 210

Turners bicuspid aortic valves berry aneurysm neurofibromatosis

Question 211

How are patients with previous ACS and need for antiplatelets AND Atrial fibrilation with need for anticoagulation managed?

Answer 211

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

Question 212

How are patients post acute ACS/PCI and need for antiplatelets AND Atrial fibrilation with need for anticoagulation managed?

Answer 212

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

Question 213

What are the features of complete heart block?

Answer 213

``` syncope heart failure regular bradycardia (30-50 bpm) wide pulse pressure JVP: cannon waves in neck variable intensity of S1 ```

Question 214

What the examples of acyanotic CHDs?

Answer 214

``` ASD VSD - most common PDA coarctation of aorta aortic valve stenosis ```

Question 215

What are the examples of cyanotic CHD?

Answer 215

Tetralogy of fallot transposition of great vessels tricuspid atresia

Question 216

What is the most common cyanotic CHD?

Answer 216

Tetralogy of fallot however only presents after 1-2 months and thus at birth the transposition of great vessles is seen more

Question 217

what does the Left coronary artery divide into and what do these supply?

Answer 217

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

Question 218

what does the Right coronary artery supply? what does it split into?

Answer 218

Right coronary artery supplies SAN Then splits into right marginal artery and posterior descending artery

Question 219

what does the branches of RCA supply?

Answer 219

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.

Question 220

How does the LAD and posterior descending artery meet?

Answer 220

make anastomoses at the apex of the heart

Question 221

where does the posterior descending artery branch from?

Answer 221

mostly RCA (right dominant circulation) but sometimes LCA (left dominant circulation) or sometimes both (co-dominant circulation - very rare)

Question 222

when is blood flow through coronary vessels maximal?

Answer 222

diastole | during systole they are compressed

Question 223

how are the cardiac veins arranged?

Answer 223

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

Question 224

what class of drug is dabigatran?

Answer 224

direct thrombin inhibitor

Question 225

what are the indications for dabigatran use?

Answer 225

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

Question 226

what are the contraindications/ cautions of dabigatran?

Answer 226

reduce dose in renal failure | cant prescribe if creatinine clearance <30

Question 227

what medication can be used to reverse dabigatrans effects?

Answer 227

Ibarucizumab

Question 228

what is the blood pressure target for diabetics?

Answer 228

<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

Question 229

what is the first line antihypertensive in diabetics? which medications should be avoided?

Answer 229

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.

Question 230

what is the frank starling relationship?

Answer 230

increase in preload - increase in contraction (up to a point) increase in end diastolic volume increases SV

Question 231

what is dilated cardiomyopathy?

Answer 231

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)

Question 232

what are the symptoms/features of cardiomyopathy?

Answer 232

``` S3 gallop dyspnoea orthopnoea PND balloon appearance of heart on Xray systolic murmur - tricuspid / mitral regurg may occur from stretching. ```

Question 233

what are the causes of dilated cardiomyopathy?

Answer 233

idiopathic myocarditis - Coxsackie B, HIV, diphtheria, Chagas disease IHD peripartum HTN drugs - alcohol, cocaine, doxorubicin inherited - duchennes, genetic predisposition infiltrative - haemachromatosis, sarcoidosis

Question 234

what is the mechanism of action of dipyrimadole?

Answer 234

inhibits phosphodiesterase elevating platelet cAMP levels which reduces intracellular Ca reduce cellular uptake of adenosine inhibit thromboxane overall platelet inhibition.

Question 235

what are the DVLA rules with HTN?

Answer 235

no need to form DVLA for HGV cant drive if resting BP >180/100

Question 236

What are the rules behind angioplasty, CABG and ACS with driving?

Answer 236

angioplasty - 1 week off CABG - 4 weeks off ACS - 4 weeks off (1 week if successfully treated with angio)

Question 237

what are the rules behind driving and angina?

Answer 237

must stop if getting symptoms at rest/ behind the wheel.

Question 238

what are the rules behind driving and... pacemaker insertion ICD catheter ablation ?

Answer 238

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

Question 239

what are the rules behind driving and aortic aneurysm?

Answer 239

6cm or more - inform DVLA liscencing permitted with annual review if 6.5 or more - no driving

Question 240

what are the rules behind driving and heart transplant?

Answer 240

no driving for 6 weeks after | no need to inform DVLA

Question 241

what is ebstein anomaly?

Answer 241

CHD with low insertion of tricuspid valve results in large atria and small ventricle (atrialisation of right ventricle)

Question 242

what is Ebstein anomaly caused by?

Answer 242

exposure to lithium in utero

Question 243

what is Ebstein anomaly assocaited with?

Answer 243

PFO or ASD | Wolff parkinson white

Question 244

what are the clinical features of ebstein anomaly?

Answer 244

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

Question 245

what are the causes of left axis deviation on ECG?

Answer 245

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

Question 246

what are the causes of right axis deviation on ECG?

Answer 246

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

Question 247

what leads on an ECG corresponds to anterolateral region?

Answer 247

V4-6 , I and aVL

Question 248

What are the ECG features for digoxin?

Answer 248

Down sloping ST depression (reverse tick) flattened / inverted T short QT interval arrhythmias - AV block, bradycardia.

Question 249

What are the ECG features of hypokalaemia?

Answer 249

``` 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

Question 250

what are the ECG changes for hypothermia?

Answer 250

``` bradycardia Long QT J wave - small hump at end of QRS first degree heart block atrial and ventricular arrhythmias ```

Question 251

How can you identify LBBB and RBBB?

Answer 251

WiLLaM - M in V6 for L | MaRRoW - M in V1 for R

Question 252

what are the causes of LBBB?

Answer 252

``` IHD HTN aortic stenosis cardiomyopathy idiopathic fibrosis , digoxin, hyperkalaemia - all rare ```

Question 253

what are normal ECG variants in athletes?

Answer 253

sinus bradycardia junctional rhythm first degree heart block Wenckebach phenomenon

Question 254

what is a cause of increased p wave amplitude?

Answer 254

cor pulmonale

Question 255

what is a cause of broad, notched (bifid P wave)?

Answer 255

often most prominent in lead 2 | caused by atrial enlargement e.g. atrial stenosis

Question 256

what are the causes of prolonged PR?

Answer 256

``` heart block hypokalaemia IHD digoxin rheumatic fever aortic root pathology (abscess secondary to I.E) lyme disease sarcoidosis myotonic dystrophy. ```

Question 257

what condition causes a short PR?

Answer 257

WPW

Question 258

what are the causes of RBBB?

Answer 258

``` normal variant - with age Right ventricular hypertrophy chronically increased right ventricular pressure pulmonary embolism MI ASD cardiomyopathy/ myocarditis ```

Question 259

what are the causes of ST depression?

Answer 259

``` ischaemia digoxin hypokalaemia secondary to abnormal QRS - LBBB, RBBB, LVH syndrome X ```

Question 260

what are the causes of ST elevation?

Answer 260

``` myocardial infarction pericarditis/myocarditis normal variant - 'high take-off' left ventricular aneurysm Prinzmetal's angina (coronary artery spasm) Takotsubo cardiomyopathy rare: subarachnoid haemorrhage ```

Question 261

what are the causes of peaked T waves?

Answer 261

hyperkalaemia | Myocardial ischaemia

Question 262

what are the causes of inverted T waves?

Answer 262

``` myocardial ischaemia digoxin toxicity subarachnoid haemorrhage arrhythmogenic right ventricular cardiomyopathy pulmonary embolism ('S1Q3T3') Brugada syndrome ```

Question 263

how is pre-eclampsia defined?

Answer 263

>20 weeks gestation pregnancy induced HTN proteinuria

Question 264

what medication is used to prevent seizures in pre-eclampsia? what monitoring is needed during this infusion?

Answer 264

MgSO4 given once decided on delivery. Urine output, reflexes, resp rate, O2 sats treatment continues 24 hours after last seizure/delivery.

Question 265

MgSO4 can cause respiratory depression. What treatment is used in this situation?

Answer 265

gluconate

Question 266

What is eisenmengers syndrome?

Answer 266

reversal of left to right shunt due to pulmonary HTN

Question 267

what are the features of eisenmengers syndrome?

Answer 267

original murmur may disappear cyanosis clubbing RV failure Haemoptysis embolism

Question 268

what is an individuals maximum predicted HR?

Answer 268

220-age

Question 269

in an exercise stress test what is the target heart rate?

Answer 269

85% of maximum predicted.

Question 270

what are the contraindications to an exercise stress test?

Answer 270

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

Question 271

when should an exercise stress test be stopped?

Answer 271

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

Question 272

name 3 glycoprotein IIb/IIIa receptor antagonists...

Answer 272

abciximab eptifibatide tirofiban

Question 273

How is heart failure managed (NICE)?

Answer 273

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.

Question 274

For HF with a preserved ejection fraction which commonly used drugs have no effect on mortality?

Answer 274

ACEi and B blockers

Question 275

which HF medications affect overall mortality?

Answer 275

ACEi B blockers NOT furosemide NOT digoxin

Question 276

what is the criteria for initiating the following drugs in HF... Ivabradine Sacubitril-valsartan

Answer 276

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

Question 277

when is digoxin strongly indicated in HF?

Answer 277

when there is co-existent AF

Question 278

when is hydralazine + nitrates mainly indicated in HF?

Answer 278

◦this may be particularly indicated in Afro-Caribbean patients

Question 279

when is cardiac resynchronisation therapy indicated in HF?

Answer 279

◦indications include a widened QRS (e.g. left bundle branch block) complex on ECG

Question 280

Which vaccinations should HF patients recieve?

Answer 280

annual influenza | one off pneumococcal (unless asplenic or CKD then require 5yrly booster)

Question 281

what is cardiac resynchronisation therapy?

Answer 281

``` biventricular pacing,. improves symptoms and reduced hospitalisation in NYHA class III patients. ```

Question 282

How does exercise training help patients with HF?

Answer 282

improves symptoms but not hospitalisation/ mortality

Question 283

what is the NYHA classification for HF?

Answer 283

``` 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

Question 284

what does the S1 heart sound correspond to? when is this loud/ soft?

Answer 284

mitral and tricuspid valve closure loud - mitral stenosis , left to right shunts, short PR, hyperdynamic state soft - mitral regurg or long PR

Question 285

what is the S2 heart sound correspond to? when is this soft? when does it split?

Answer 285

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

Question 286

what is the S3 heart sound? when is this heard?

Answer 286

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.

Question 287

what is the S4 heart sound?

Answer 287

caused by atria contracting against stiff ventricle. | can be heard in HTN, HOCM, Aortic stenosis

Question 288

what position on the chest can heart valves be heard best?

Answer 288

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

Question 289

what are the causes of reversal of S2 split?

Answer 289

``` severe AS LBBB right ventricular pacing WPW type B patent ductus arteriosus ```

Question 290

what is the mechanism of hydralazine?

Answer 290

increases cGMP leading to smooth muscle relaxation for HTN but not commonly used

Question 291

what are the contraindications of hydralazine?

Answer 291

systemic lupus erythematous | •ischaemic heart disease/cerebrovascular disease

Question 292

what are the adverse effects of hydralazine?

Answer 292

``` tachycardia •palpitations •flushing •fluid retention •headache •drug-induced lupus ```

Question 293

what are the symptoms of hypercalcaemia?

Answer 293

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

Question 294

what is an eruptive xanthoma most commonly due to?

Answer 294

high triglycerides e.g. familial hypertriglyceridaemia, lipoprotein lipase deficiency. presents as multiple red/yellow xanthomas on extensor surfaces.

Question 295

how can xanthelesma be managed?

Answer 295

surgically topical treatment laser

Question 296

what treatment are women at high risk of eclampsia given?

Answer 296

aspirin 75mg from 12 weeks till birth

Question 297

which women are at high risk of developing eclampsia?

Answer 297

* hypertensive disease during previous pregnancies * chronic kidney disease * autoimmune disorders such as SLE or antiphospholipid syndrome * type 1 or 2 diabetes mellitus

Question 298

what are the 3 types of HTN during pregnancy?

Answer 298

``` 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. ```

Question 299

``` how is HTN classified? when is each class treated? ```

Answer 299

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

Question 300

how is severe HTN classified?

Answer 300

>180/120

Question 301

what is ambulatory BP recording?

Answer 301

use average of at least 14 measurements throughout the day

Question 302

How is HTN managed?

Answer 302

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.

Question 303

what are the BP targets?

Answer 303

<80 - 140/90 (ABPM - 135/85) | >80 - 150/90 (ABPM - 145/85)

Question 304

what is aliskiren?

Answer 304

Direct renin inhibitor blocks RAS activation new HF drug

Question 305

what are the secondary causes of HTN?

Answer 305

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

Question 306

what is HOCM? (pathophysiology)

Answer 306

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.

Question 307

how does HOCM appear on biopsy?

Answer 307

myofibrillar hypertrophy choatically organised myocytes fibrosis

Question 308

what are the features of HOCM?

Answer 308

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.

Question 309

what other conditions can HOCM be associated with?

Answer 309

friedrichs ataxia | WPW

Question 310

what are the ECHO findings in HOCM?

Answer 310

mitral regurgitation assymetric hypertrophy systolic anterior motion of anterior mitral valve

Question 311

what are the ecg changes seen in HOCM?

Answer 311

eft ventricular hypertrophy non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen deep Q waves

Question 312

How is HOCM managed?

Answer 312

``` ABCDE Amiodarone Bblockers Cardioverter defib Dual chamber pacemaker Endocarditis prophylaxis ```

Question 313

which drugs should be avoided in HOCM?

Answer 313

nitrates ACEi Inotropes

Question 314

what are the poor prognostic factors of HOCM?

Answer 314

``` 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 ```

Question 315

what are the indications for an implantable cardiac defib?

Answer 315

``` long QT HOCM previous cardiac arrest due to VT/VF previous MI with nonsustained VT on 24 hour tape / inducible VT brugada syndrome? ```

Question 316

what is the biggest risk to developing infective endocarditis?

Answer 316

previous infective endocarditis

Question 317

what is the commonest cause of infective endocarditis?

Answer 317

s.aureus - especially acute and IVDU | streptococcus viridans - in developing countries

Question 318

which organism is most likely to cause infective endocarditis from indwelling lines and prosthetic valve surgery?

Answer 318

s. epidermidis

Question 319

what are the culture negative causes of infective endocarditis?

Answer 319

``` prior antibiotic therapy Coxiella burnetii Bartonella Brucella HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella) ```

Question 320

which organism is resposible for infective endocarditis secondary to poor dental hygiene?

Answer 320

streptococcus viridans

Question 321

which organism is linked to causing infective endocarditis in those with colorectal Ca?

Answer 321

S.bovis - particularly a subtype called... Streptococcus gallolyticus

Question 322

what is mirantic endocarditis?

Answer 322

subtype of endocarditis caused by malignancy

Question 323

what is the modified dukes criteria for infective endocarditis?

Answer 323

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

Question 324

what are the poor prognostic factors of infective endocarditis?

Answer 324

S.aureus culture negative prosthetic valve low complement levels

Question 325

what is the initial therapy for infective endocarditis when the organism is unknown?

Answer 325

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

Question 326

what is the initial therapy for infective endocarditis when the organism is s. aureus?

Answer 326

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

Question 327

what is the initial therapy for infective endocarditis when the organism is s.viridans?

Answer 327

Benzylpenicillin If penicillin allergic vancomycin + low-dose gentamicin

Question 328

what are the indications for surgery in infective endocarditis?

Answer 328

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

Question 329

how should isolated systolic HTN be treated?

Answer 329

same way as normal HTN

Question 330

what is the function of ivabradine?

Answer 330

acts of If (funny current) ion channel to reduce SAN pacemaker activity used in angina

Question 331

what are the side effects of ivabradine?

Answer 331

headaches visual changes bradycardia

Question 332

when is a non-pulsatile JVP seen?

Answer 332

SVC obstruction

Question 333

what is the kussmaul sign?

Answer 333

paradoxical rise in JVP in inspiration | constrictive pericarditis

Question 334

what do different parts of JVP waveform present?

Answer 334

``` a wave - atrial contraction c wave - tricuspid closure x descent - ventricular systole v wave - filling of heart against closed tricuspid y descent - tricuspid opens ```

Question 335

when would the a wave of JVP be large?

Answer 335

large atrial pressure - tricuspid/ pulmonary stenosis, pulmonary HTN

Question 336

when is the a wave of JVP absent?

Answer 336

AF

Question 337

what are cannon a waves on JVP waveform? regular vs irregular

Answer 337

atria contracting against closed tricuspid seen in heart block, arrhythmias, single chamber pacing regular - VT, AVNRT irregular - Heart block

Question 338

when are giant v waves seen?

Answer 338

seen in tricuspid regurgitation.

Question 339

what is Kawasaki disease?

Answer 339

vasculitis children can cause serious complications - coronary aneurysms

Question 340

what are the features of kawasaki disease?

Answer 340

``` fever - 5 days, resistant to paracetamol strawberry tongue red cracked lips red palms/ soles of feet - later peel cervical lymphadenopathy conjunctivitis ```

Question 341

how can you test for kawasaki?

Answer 341

no test | clinical diagnosis

Question 342

how is kawasaki disease managed?

Answer 342

high-dose aspirin intravenous immunoglobulin echocardiogram (rather than angiography) is used as the initial screening test for coronary artery aneurysms

Question 343

why is aspirin contraindicated in children? what is an exception?

Answer 343

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

Question 344

what are the congenital causes of long QT?

Answer 344

Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel) Romano-Ward syndrome (no deafness)

Question 345

what drugs can cause long QT?

Answer 345

Amiodarone, sotalol, class 1a antiarrhythmic drugs tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram) methadone chloroquine terfenadine erythromycin haloperidol ondanestron

Question 346

what are non drug and non congential causes of long QT?

Answer 346

low Ca, low Mg, low K hypothermia SAH myocarditis MI

Question 347

what are the different types of Long QT?

Answer 347

LQT1 - syncope after exertion e.g swimming LQT2 - syncope after emotional stress, auditory stimulus LQT3 - night or rest

Question 348

how is long QT managed?

Answer 348

B blockers, | ICD in high risk

Question 349

what are the side effects of loop diuretics?

Answer 349

hypotension hyponatraemia hypokalaemia, hypomagnesaemia hypochloraemic alkalosis hypocalcaemia ``` ototoxicity renal impairment (from dehydration + direct toxic effect) ``` hyperglycaemia (less common than with thiazides) gout

Question 350

what BP occurs in malignant HTN?

Answer 350

>200/130

Question 351

How is malignant HTN managed?

Answer 351

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

Question 352

what are the most common valve disorders of the heart?

Answer 352

Aortic stenosis - no. 1 | mitral regurg - no.2

Question 353

what are the risk factors for mitral regurgitation?

Answer 353

``` 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 ```

Question 354

what murmur is heard in mitral regurgitation?

Answer 354

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

Question 355

what may be seen on CXR and ECG in mitral regurg?

Answer 355

ECG - wide/large p wave due to enlarged atria CXR - cardiomegaly

Question 356

what causes mitral stenosis?

Answer 356

Rheumatic fever - main cause others: mucopolysaccharidoses, carcinoid and endocardial fibroelastosis - seen in exams

Question 357

what mumur/ sounds are heard in mitral stenosis?

Answer 357

mid- late diastolic murmur loud S1 - opening snap with severe Mitral stenosis - murmur becomes longer and opening snap becomes closer to S2

Question 358

what are the features/ symptoms of mitral stenosis?

Answer 358

murmur malar flush low pulse volume AF

Question 359

what can be seen on CXR in mitral stenosis?

Answer 359

large atria

Question 360

what is the mitral valve opening normally and what will it be in mitral stenosis?

Answer 360

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

Question 361

what conditions are associated with mitral valve prolapse?

Answer 361

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

Question 362

what are features of mitral valve prolapse?

Answer 362

mid-systolic click (occurs later if patient squatting) late systolic murmur (longer if patient standing)

Question 363

what is a multifocal atrial tachycardia?

Answer 363

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

Question 364

how is multifocal atrial tachy managed?

Answer 364

correct hypoxia correct electrolytes rate limiting CaB

Question 365

which ejection systolic mumurs are louder on inspiration/expiration?

Answer 365

louder on expiration aortic stenosis hypertrophic obstructive cardiomyopathy louder on inspiration pulmonary stenosis atrial septal defect tetralogy of fallot is another ejection systolic murmur

Question 366

name two pansystolic mumurs?

Answer 366

mitral/ tricuspid regurg | VSD

Question 367

Give examples of a late systolic mumur?

Answer 367

mitral valve prolapse | coarctation of aorta

Question 368

Give examples of early diastolic murmur?

Answer 368

aortic regurg Graham-Steel murmur (pulmonary regurgitation) both are high-pitched and 'blowing' in character

Question 369

give examples of mid-late diastolic murmurs?

Answer 369

mitral stenosis Austin-Flint murmur (severe aortic regurgitation) both 'rumbling' in character)

Question 370

what murmur does PDA give?

Answer 370

continuous machine like

Question 371

what are the complications of an MI?

Answer 371

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

Question 372

what type of MI is most likely to cause AVN damage?

Answer 372

inferior

Question 373

what are the symptoms/ features of dresslers syndrome?

Answer 373

fever pleuritic pain pericardial effusion raised ESR

Question 374

How is Dresslers treated?

Answer 374

NSAIDs

Question 375

which type of MI is most likely to damage papillary muscles?

Answer 375

infero-posterior

Question 376

what is the secondary prevention post MI?

Answer 376

b blockers ACEi statin dual antiplatelet inc aspirin (usually with ticagrelor) - the ticagrelor is stopped after 12 months)

Question 377

when can sexual activity ressume after an MI?

Answer 377

4 weeks

Question 378

when are ARBs preffered to ACEi in MI?

Answer 378

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

Question 379

How is an MI managed?

Answer 379

aspirin clopidogrel/ticagrelor/prasugrel if undergoing PCI - also unfractionated heparin/LMWH PCI/thrombolysis

Question 380

how long after thrombolysis in MI patients, is an ECG performed and why?

Answer 380

90 mins | if <50% resolution in ST elevation can offer PCI

Question 381

what are the causes of myocarditis?

Answer 381

viral: coxsackie B, HIV bacteria: diphtheria, clostridia spirochaetes: Lyme disease protozoa: Chagas' disease, toxoplasmosis autoimmune drugs: doxorubicin

Question 382

what are the symptoms of myocarditis?

Answer 382

chst pain dyspnoea arrhythmia (fever)

Question 383

what are the investigation findings for myocardiits?

Answer 383

increased cardiac enzymes, increased BNP, increassed inflammatory markers ECG -tachyarrhythmias, ST / T changes inc ST elevation, T inversion

Question 384

what is nicorandil?

Answer 384

vasodilatory drug for angina It is a potassium-channel activator with vasodilation is through activation of guanylyl cyclase which results in increase cGMP.

Question 385

what are the side effects of nicorandil?

Answer 385

headache flushing skin, mucosal and eye ulceration gastrointestinal ulcers including anal ulceration

Question 386

when is nicorandil contraindicated?

Answer 386

LV failure

Question 387

what does nicotinic acid do?

Answer 387

Lowers cholesterol and triglyceride concentrations | it also raises HDL levels.

Question 388

what are the complications/side effects of nicotinic acid?

Answer 388

Adverse effects flushing: mediated by prostaglandins impaired glucose tolerance myositis

Question 389

what is the function of nitrates?

Answer 389

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

Question 390

what are the problems/side effects of nitrates?

Answer 390

headaches, flushing, hypotension, tachycardia develop tolerance - not seen if modified release is taken.

Question 391

what are the indications for a temporary pacemaker?

Answer 391

symptomatic/ haemodynamically unstable bradycardia post anterior MI with type 2 or complete heart block trifasicular block prior to surgery

Question 392

what are the complications of PCI?

Answer 392

stent thrombosis - usually in 1 month, presents as MI restenosis - due to proliferation around the stent. in first 3-6 months. angina symptoms

Question 393

how have stents used in PCI developed to reduce stenosis risk? whats the limitation of these?

Answer 393

drug eluting stents - drugs that inhibit tissue growth thrombosis rate increased

Question 394

How is a bradycardia managed?

Answer 394

Atropine IV (can use up to 3mg , start with 500mcg) need for treatment: haemodynamic compromise , very low HR

Question 395

what is the next step if a bradyarrhythmia doesnt respond to atropine?

Answer 395

transcutaneous pacing | adrenaline/isoprenaline

Question 396

When is transcutaneous pacing considered for brady-arrhythmias?

Answer 396

complete heart block with broad complex QRS recent asystole Mobitz type II AV block ventricular pause > 3 seconds

Question 397

how does fonduparinux work?

Answer 397

Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa. It is given subcutaneously.

Question 398

what keeps a PDA open?

Answer 398

prostaglandins

Question 399

who is a PDA most common in?

Answer 399

premature born at high altitude maternal rubella in 1st trimester

Question 400

what are the features of PDA?

Answer 400

``` left subclavicular thrill continuous 'machinery' murmur large volume, bounding, collapsing pulse wide pulse pressure heaving apex beat ```

Question 401

how is PDA managed?

Answer 401

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

Question 402

How are regular narrow complex tachyarrythmias managed?

Answer 402

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)

Question 403

How are irregular narrow complex tachyarrythmias managed?

Answer 403

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

Question 404

How are irregular broad complex tachyarrythmias managed?

Answer 404

A-C If unstable i.e. shock, syncope, MI, HF.. then DC cardiovert (up to 3 shocks) then seek expert advice

Question 405

what may cause an irregular broad complex tachyarrythmias ?

Answer 405

atrial fibrillation with bundle branch block - the most likely cause in a stable patient atrial fibrillation with ventricular pre-excitation torsade de pointes

Question 406

how is a regular broad complex tachyarrhythmia managed?

Answer 406

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

Question 407

how is peripheral arterial disease managed?

Answer 407

lifestyle statin - atorvastatin 80mg clopidogrel rather than aspirin exercise training angioplasty, stenting, bypass graft surgery

Question 408

what drugs can be used in peripheral arterial disease?

Answer 408

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

Question 409

what is pre-eclampsia?

Answer 409

HTN (>140/90) with proteinuria after 20 weeks. + oedema may have other end organ involvment... renal, liver, neuro, placental

Question 410

what are the consequences of pre-eclampsia?

Answer 410

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

Question 411

what are the features of severe pre-eclampsia?

Answer 411

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

Question 412

what are the risk factors for pre-eclampsia?

Answer 412

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

Question 413

how is pre-eclampsia prevented in those at risk?

Answer 413

women who have 1 high risk factor or 2 moderate should take 75-150mg aspirin from 12 weeks until birth

Question 414

how is pre-eclampsia managed?

Answer 414

oral labetolol | nifedipine if asthmatic

Question 415

how is a P.E investigated in pregnancy?

Answer 415

ECG and CXR in all USS of legs - if DVT present, start treatment otherwise decide on CTPA/VQ scan

Question 416

what are the problems of CTPA/ VQ scan in pregnancy?

Answer 416

CTPA - increases risk of maternal breast cancer, (pregnancy makes breast more sensitive to the radiation) VQ scan - increased risk of childhood cancer

Question 417

what are the pros and cons of biological valve?

Answer 417

pros - no needs for long term anticoag (low dose aspirin still given long term) cons - long term calcification and deterioration

Question 418

what is the most common type of valve used in valve surgery now?

Answer 418

mechanical bileaflet valve

Question 419

what are the advantages and disad of mechanical valves?

Answer 419

low failure rate long term anticoag needed

Question 420

what long term anticoag is used for mechanical valves?

Answer 420

warfarin (not doac)

Question 421

what are the target INR ranges for mechanical valves?

Answer 421

aortic 3 | mitral 3.5

Question 422

how is pulmonary arterial hypertension defined?

Answer 422

resting pulmonary arterial pressure >25mmHg

Question 423

who is pulmonary arterial hypertension most common in?

Answer 423

women , mainly 30-50yrs

Question 424

what are the causes of pulmonary arteial HTN?

Answer 424

secondary to COPD etc Can be primary - risk increased by HIV, cocaine around 10% inherited in autosomal dominant fashion

Question 425

what are the features of pulmonary artery HTN?

Answer 425

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

Question 426

what test is essential to managing pulmonary artery HTN?

Answer 426

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.

Question 427

how is pulmonary artery HTN managed?

Answer 427

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

Question 428

how is pulmonary capillary wedge pressure managed?

Answer 428

balloon tipped Swan-Ganz catheter which is inserted into the pulmonary artery.

Question 429

What is the PERC criteria?

Answer 429

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

Question 430

What is the 2 level PE wells score?

Answer 430

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

Question 431

How is P.E managed if the 2 level PE wells score is positive?

Answer 431

give DOAC whilst awaiting urgent CTPA | DOAC can be continued if PE confirmed

Question 432

what can be done if 2 level PE wells score is unlikely?

Answer 432

d.dimer | if positive do a CTPA

Question 433

whats the difference between sensitivity and specificity?

Answer 433

high sensitivity - unlikely to give false positive | high specificity - unlikely to give false neg

Question 434

what ecg changes are seen in a P.E?

Answer 434

S1Q3T3 large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III tachycardia RBBB

Question 435

what is the first line treatment for P.E? what are the exceptions?

Answer 435

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

Question 436

how long should patients have anticoagulation for a P.E

Answer 436

atleast 3 months provoked - 3 months only unprovoked - up to 6 months

Question 437

what is the management for massive P.E with haemodynamic instability?

Answer 437

thrombolysis

Question 438

what are the causes of a collapsing pulse?

Answer 438

aortic regurgitation | PDA

Question 439

what is pulsus paradox? what are the causes ?

Answer 439

fall in BP >10 (normal fall) with inspiration | severe asthma, cardiac tamponade

Question 440

what is the cause of a slow rising pulse?

Answer 440

aortic stenosis

Question 441

what is the causes of Bisferiens pulse?

Answer 441

'double pulse' - two systolic peaks | mixed aortic valve disease

Question 442

what are the causes of constrictive pericarditis?

Answer 442

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

Question 443

what ECG is found in restrcitve cardiomyopathy?

Answer 443

low voltage QRS

Question 444

what features suggest restrictive cardiomyopathy rather than constrictive pericarditis?

Answer 444

prominent apical pulse absence of pericardial calcification on CXR the heart may be enlarged ECG abnormalities e.g. bundle branch block, Q waves

Question 445

what is the pathogenesis behind rheumatic fever?

Answer 445

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

Question 446

What are Ashcoff bodies?

Answer 446

Aschoff bodies describes the granulomatous nodules found in rheumatic heart fever

Question 447

what is the diagnostic criteria for rheumatic fever?

Answer 447

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

Question 448

how is rheumatic fever managed?

Answer 448

Antibiotics: oral penicillin V anti-inflammatories: NSAIDs are first-line treatment of any complications that develop e.g. heart failure

Question 449

what is the ABCD2 score?

Answer 449

prognostic score post TIA

Question 450

what is the DAS28 score?

Answer 450

measure of disease activity in rheumatoid arthritis

Question 451

what is child pugh score?

Answer 451

A scoring system used to assess the severity of liver cirrhosis

Question 452

what is the PHQ9 score

Answer 452

Patient Health Questionnaire - assesses severity of depression symptoms

Question 453

Name 3 alcohol screening tools?

Answer 453

AUDIT, CAGE, FAST

Question 454

what is the SCOFF score?

Answer 454

Questionnaire used to detect eating disorders and aid treatment

Question 455

Whats the IPSS score? which other scoring system is used for these patients?

Answer 455

International prostate symptom score Gleason score - indicates prognosis for prostate Ca

Question 456

whats the bishop and apgar score

Answer 456

bishop - used to help assess the whether induction of labour will be required apgar - assess health of new born immediately post birth

Question 457

whats the waterlow score?

Answer 457

risk of developing pressure sore

Question 458

whats the ranson criteria for?

Answer 458

acute pancreatitis

Question 459

how do statins work?

Answer 459

inhibit HMG-CoA reductase to reduce cholesterol synthesis

Question 460

what are the side effects of statins?

Answer 460

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

Question 461

what are the risk factors for statin induced myopathy?

Answer 461

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

Question 462

How are LFTs monitored during statin therapy?

Answer 462

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

Question 463

what are the contraindications for statin use?

Answer 463

pregnancy | use of macrolides (erythromycin, clarithromycin) - stop statins while course is being completed

Question 464

Who should be put on statins?

Answer 464

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

Question 465

what statin dose is used for primary /secondary prevention?

Answer 465

primary - atorvastatin 20mg | secondary - atorvastatin 80mg

Question 466

what is the acute management of SVT if haemodynamically stable?

Answer 466

vagal manoeuvres: e.g. Valsalva manoeuvre, carotid sinus massage intravenous adenosine 6mg → 12mg → 12mg: contraindicated in asthmatics - verapamil is a preferable option electrical cardioversion

Question 467

how can SVT episodes be prevented?

Answer 467

beta-blockers | radio-frequency ablation

Question 468

what is syndrome X?

Answer 468

Chest pain on exercise ST depression on exercise stress normal coronary arteries

Question 469

what drug can be good for syndrome x?

Answer 469

nitrates

Question 470

what is takayasu's arteritis?

Answer 470

large arteries such as aorta affected question usually involved an absent limb pulse most common in females and asians.

Question 471

what are the symptoms of takayasu's arteritis?

Answer 471

systemic features of a vasculitis e.g. malaise, headache unequal blood pressure in the upper limbs carotid bruit intermittent claudication aortic regurgitation (around 20%)

Question 472

how is takayasu's arteritis managed?

Answer 472

steroids

Question 473

what is Takotsubo cardiomyopathy?

Answer 473

non ischaemic cardiomyopathy apical balooning of myocardium - due to apex not contracting so instead balloons out ,ay be triggered by stress

Question 474

how does Takotsubo cardiomyopathy present?

Answer 474

chest pain HF symptoms st elevation normal coronary arteries

Question 475

how is Takotsubo cardiomyopathy managed?

Answer 475

supportive treatment only | most patients improve

Question 476

what is the most common cyanotic CHD and when does it present?

Answer 476

ToF | presents 1-2 months

Question 477

what are the 4 features of ToF

Answer 477

pulmonary stenosis right ventricular hypertrophy VSD over-riding aorta degreee of severity determined by degree of pulmonary stenosis

Question 478

what are the clinical features of ToF?

Answer 478

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

Question 479

how is ToF managed?

Answer 479

surgical repair is often undertaken in two parts | cyanotic episodes may be helped by beta-blockers to reduce infundibular spasm

Question 480

what is the mechanism of a thiazide diuretic?

Answer 480

block Na CL symporter in DCT to block sodium reuptake | Potassium is lost as a result of more sodium reaching the collecting ducts.

Question 481

what are the side effects of thiazides?

Answer 481

``` dehydration postural hypotension hyponatraemia, hypokalaemia, hypercalcaemia* gout impaired glucose tolerance impotence ``` ``` Rare adverse effects thrombocytopaenia agranulocytosis photosensitivity rash pancreatitis ```

Question 482

what are the contraindications of thrombolysis?

Answer 482

``` 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 ```

Question 483

what are the side effects of thrombolysis?

Answer 483

haemorrhage | allergy and hypotension - espwith streptokinase

Question 484

what is torsades de point?

Answer 484

type of VT where the QRS is variable height associated with long QT can deteriorate into VF

Question 485

What are the causes of long QT?

Answer 485

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

Question 486

What is the managedment of torsades de point?

Answer 486

IV magnesium sulphate

Question 487

who is at increased risk of transposition of great vessels?

Answer 487

babies of diabetic mums

Question 488

what are the clinical features of transposition of great vessels?

Answer 488

``` cyanosis tachypnoea loud single S2 prominent right ventricular impulse 'egg-on-side' appearance on chest x-ray ```

Question 489

how is transposition of great vessels managed?

Answer 489

maintenance of the ductus arteriosus with prostaglandins | surgical correction is the definite treatment.

Question 490

what are the signs of tricuspid regurg?

Answer 490

pan-systolic murmur prominent/giant V waves in JVP pulsatile hepatomegaly left parasternal heave

Question 491

what are the causes of tricuspid regurg?

Answer 491

``` right ventricular infarction pulmonary hypertension e.g. COPD rheumatic heart disease infective endocarditis (especially intravenous drug users) Ebstein's anomaly carcinoid syndrome ```

Question 492

what are VSD associated with?

Answer 492

``` 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

Question 493

when can a VSD be detected?

Answer 493

20 weeks on USS

Question 494

how does VSD present post natally?

Answer 494

``` failure to thrive features of heart failure hepatomegaly tachypnoea tachycardia pallor classically a pan-systolic murmur which is louder in smaller defects ```

Question 495

how is a VSD managed?

Answer 495

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

Question 496

what are the complications of a VSD?

Answer 496

``` aortic regurgitation infective endocarditis Eisenmenger's complex - this is turn results in cyanosis and clubbing right heart failure pulmonary hypertension ```

Question 497

what are the different types of VT?

Answer 497

monomorphic - associated with MI | Polymorphic - torsades - associated with long QT

Question 498

how is VT managed?

Answer 498

haemodynamic instability - DC cardiovert otherwise.. amiodarone, lidocaine or procainamide. Do not use verapamil if drug therapy fails - ICD

Question 499

what is the mechanism of warfarin?

Answer 499

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

Question 500

what is the target INR for AF, mechanical valve, VTE?

Answer 500

AF - 2.5 VTE 2.5 unless recurrent then 3.5 valve depends on type

Question 501

what is INR?

Answer 501

ratio of prothrombin time compared to normal.

Question 502

what factors can potentiate warfarin effects?

Answer 502

liver disease P450 enzyme inhibitors - amiodarone, ciprofloxacin cranberry juice NSAIDs (displace warfarin from plasma albumin and inhibit platelets too)

Question 503

how is a patient on warfarin managed with major bleeding?

Answer 503

Stop warfarin Give intravenous vitamin K 5mg Prothrombin complex concentrate - if not available then FFP*

Question 504

how is a patient on warfarin managed with minor bleeding and INR>8?

Answer 504

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

Question 505

how is a patient on warfarin managed with no bleeding and INR>8?

Answer 505

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

Question 506

how is a INR of 5 to 8 managed for patients on warfarin with minor bleeding and no bleeding?

Answer 506

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.

Question 507

what are the features of wolff parkinson white on ECG?

Answer 507

* 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*

Question 508

what are the two types of WPW?

Answer 508

type A - left sided pathway - dominant R wave in V1 | Type B - right sided pathway - no dominant R in V1

Question 509

what is WPW associated with ?

Answer 509

* HOCM * mitral valve prolapse * Ebstein's anomaly * thyrotoxicosis * secundum ASD

Question 510

how is WPW managed?

Answer 510

* definitive treatment: radiofrequency ablation of the accessory pathway * medical therapy: sotalol (avoid if AF coexists) amiodarone, flecainide