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Cardiology Flashcards

1
Q

roles of ACEi?

A

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

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2
Q

mechanism of action for ACEi?

A

activated by liver in phase 1 metabolism

prevent conversion of angiotensin 1 to 2

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3
Q

What are the side effects of ACEi?

A

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

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4
Q

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

A

increased levels of bradykinin?

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5
Q

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

A

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

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6
Q

How are the use of ACEi monitored?

A

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

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7
Q

Outline the medical management of HTN?

A

<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
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8
Q

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

A

theophyllines inhibit

dipyridamole enhances

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9
Q

Which condition should adenosine be avoided in?

A

asthma due to bronchospasm

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10
Q

What is the mechanism of action of adenosine?

A

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

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

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11
Q

what are the adverse effects of adenosine?

A

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

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12
Q

give examples of ADP (adenosine diphosphate) receptor blockers

A

clopidogrel
ticagrelor
prasugrel
Ticlopidine

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13
Q

how do ADP receptor inhibitors work?

A

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.

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14
Q

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

A

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

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15
Q

what are the adverse effects of ticagrelor ?

A

dyspnoea due to impaired clearance of adenosine.

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16
Q

what DDI exist for ADP receptor inhibitors?

A

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

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17
Q

what is the chest compression ratio given to adults?

A

30:1

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18
Q

which rhythms are shockable? non shockable?

A

pulseless VT and VF = shockable

pulseless electrical activity and asystole = non shockable

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19
Q

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

A

1mg ASAP for the non-shockables

after 3rd shock in shockables. rhythms

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20
Q

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

A

3 consecutive shocks can be given

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21
Q

how is asystole/ pulseless electrical activity managed?

A

1mg adrenaline ASAP

no shocks just CPR

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22
Q

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

A

Hs: hypoxia, hypotension, hyperkalaemia, hypothermia

T: thrombus, tamponade, tension pneumothorax, toxins

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23
Q

what is the class and action of amiodarone?

A 
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
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24
Q

what type of arrhythmias is amiodarone used in?

A

atrial, nodal and ventricular tachycardia

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25
Q

why is a loading dose of amiodarone often used?

A

very long half like (days)

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26
Q

how is amiodarone given?

A

IV through central vein - causes thrombophlebitis

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27
Q

what are the DDIs of amiodarone?

A

Can interact with Cytochrome 450

decreases metabolism of warfarin

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28
Q

what monitoring is needed for amiodarone?

A

TFTs UEs LFTs CXR prior to starting

TFTs and LFTS every 6 months

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29
Q

what are adverse effects of amiodarone?

A 
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
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30
Q

what class drug are the following…
candesartan
losartan
irbesartan

A

Angiotensin receptor 2 inhibitors

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31
Q

what are the side effects or ARBs?

A

hypotension

hyperkalaemia

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32
Q

What is the first and second line antiplatelet in ACS?

A

1st line : aspirin (lifelong) and ticagrelor (12 month)

2nd line: clopidogrel lifelong if aspirin is contraindicated

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33
Q

What is the first and second line antiplatelet in PCI?

A

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

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34
Q

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

A

1st line: life long clopidogrel

2nd line: aspirin + dipyrimadole lifelong

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35
Q

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

A

1st line: clopidogrel life long

2nd line: aspirin life long

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36
Q

What is the pathophysiology of aortic dissection?

A

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

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37
Q

what is type A and B aortic dissection?

A

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

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38
Q

what are the causes of aortic dissection ?

A 
causes:
chronic high blood pressure
aortic coarctation 
connective tissue disorders - ehlers danlos/marfarns
aneurysms 
trauma
bicuspid aortic valve
turners and noonans
pregnancy 
syphillis
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39
Q

What issues arise from aortic dissections?

A

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

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40
Q

what are the symptoms of aortic dissection?

A

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

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41
Q

How can a aortic dissection be managed?

A

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

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42
Q

which type of aortic dissection is most common?

A

type A

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43
Q

what are the two classifications for aortic dissection?

A

stanford - type A and B

DeBakey - Type 1 to 3

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44
Q

what is the debakey classification for aortic dissection?

A

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

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45
Q

How can an aortic dissection be investigated?

A

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
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46
Q

What are the risk factors / causes of aortic stenosis?

A

bicuspid valve
chronic rheumatic fever
stress overtime - older adults

williams syndrome - supravalvular aortic stenosis
HOCM - subvalvular

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47
Q

what are the complications of aortic stenosis?

A

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

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48
Q

what are the causes of aortic regurgitation?

A 
idiopathic 
valve damage - rheumatic fever , Infective endocarditis
aortic dissection
sphyllis
aneuryms
RA/ SLE
bicuspid valve
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49
Q

what murmur is heard in aortic stenosis/ regurgitation?

A

A.S: ejection systolic murmur, radiates to carotids

A.R: early diastolic murmur

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50
Q

what are the symptoms/signs of aortic regurgitation?

A 
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

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51
Q

what are the symptoms of aortic stenosis?

A

Classic triad:
chest pain
syncope
angina

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52
Q

what are the features of severe aortic stenosis?

A 
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
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53
Q

how is aortic stenosis managed?

A

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

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54
Q

What will the NEWS score be for an MI?

A

often normal
maybe tachycardic
unless complications of MI

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55
Q

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

A

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.

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56
Q

what is the difference between subendocardial and transmural infarcts?

A

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

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57
Q

how is an MI diagnosed?

A
  • ECG

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

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58
Q

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

A

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.

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59
Q

How are MIs treated - basic first steps of management?

A

MONA

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

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60
Q

How are STEMIs managed?

A

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)

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61
Q

How quickly should PCI be performed?

A

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

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62
Q

How is PCI performed?

A

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

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63
Q

when is fibrinolysis offered?

A

if PCI cant be offered

if no contraindication

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64
Q

How is fibrinolysis performed?

A

fibrinolytic agent

Also give antithrombin drug e.g fondaparinux

Repeat ecg after 60-90 mins and if resolved if still ischaemic – PCI considered

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65
Q

what scoring system is used to decide on management of NSTEMI?

What does this scoring system use and what does it show.

A

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

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66
Q

Which NSTEMI patients will have PCI during admission?

A

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

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67
Q

what is the secondary prevention for MIs?

A 
o	Aspirin 
o	Second antiplatelet – clopidogrel
o	B blocker
o	ACE inhibitor
o	Statin
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68
Q

what is the criteria for NSTEMI?

A

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

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69
Q

what are the complications of an MI?

A
  • Shock and acute heart failure
  • Pericarditis
  • Rupture of myocardium/ septum
  • Embolus
  • Arrhtyhmia
  • Dresslers syndrome
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70
Q

What are the poor prognostic factors post MI?

A
  • 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
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71
Q

What is the Kilip class system?

A

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
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72
Q

what is pericarditis?

what are the complications?

A

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

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73
Q

what are the causes of pericarditis?

A 
idiopathic 
viral - coksackie
malignancy
connective tissue disorders
dresslers 
uraemic pericarditis (bread and butter appearance) 
radiation 
drugs
hypothyroid
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74
Q

what are the symptoms of pericarditis?

A

chest pain
worse on inspiration
better leaning forward

fever/ flu like
friction rub
no productive cough
tachycardia/ tachypnoea

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75
Q

what are the ECG changes seen in pericarditis?

A

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

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76
Q

how can pericarditis be investigated?

A

ECG
CXR - widened mediastinum
ECHO - shows effusion

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77
Q

how is pericarditis managed?

A

NSAIDs and Colchicine

pericardiocentesis if effusion
pericardectomy for constrictive pericarditis

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78
Q

how is angina managed?

A

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

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79
Q

name 3 long acting nitrate…

A

ranolazine
nicorandil
ivabradine

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80
Q

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

A

tolerance can develop

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

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81
Q

which particularly cause of pericarditis can cause constrictive pericarditis?

A

TB

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82
Q

what are the signs/symptoms of constrictive pericarditis?

A 
dyspnoea
pericardial knock - loud S3
Right sided HF signs - hepatomegaly, raised JVP, ascites
kussmaul sign
JVP shows prominent X and Y descent
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83
Q

what might be seen on CXR for constrictive pericarditis?

A

cardiac calcifications

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84
Q

what are the differences between cardiac tamponade and constrictive pericarditis?

A

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
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85
Q

What is Becks Triad seen in Cardiac tamponade?

A

raised JVP
low BP
muffled heart sounds.

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86
Q

What ECG sign is seen in cardiac tamponade?

A

Alternating QRS complex heights.

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87
Q

What change is seen in JVP waveform in Cardiac tamponade?

A

absent Y descent - limited right ventricle filling.

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88
Q

What is arrhythmogenic right ventricular cardiomyopathy?

A

ARVC - inherited cardiovascular disease

presents as palpitations, syncope or sudden cardiac death

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89
Q

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

A
  1. HOCM

2. ARVC

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90
Q

what is the pathophysiology behind ARVC?

A

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

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91
Q

What ECG findings are found in ARVC?

A

V1 -3 - T wave inversion

Epsilon wave found in 50% of patients - this is a terminal notch in QRS

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92
Q

what are the ECHO findings for ARVC?

A

enlarged hypokinetic right ventricle with thin free wall

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93
Q

what Ix can be used for ARVC?

A

ECG
ECHO
MRI - shows fibrofatty tissue

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94
Q

how is ARVC managed?

A

sotalol
catheter ablation to prevent VT
implantable cardioverter defib

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95
Q

what is Naxos disease?

A

an autosomal recessive variant of ARVC

a triad of ARVC, palmoplantar keratosis, and woolly hair

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96
Q

What are the causes / risk factors of AF?

A 
M - mitral valve disease (stretches atrial and damages myocytes)
I - ischaemic heart disease
T - thyroid 
R
A - alcohol
L - lung pathology (pneumonia)
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97
Q

where does AF originate?

A

In pulmonary veins

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98
Q

what are the types of AF?

A

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.

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99
Q

what are the uses of radiofrequency catheter ablation in AF?

A

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

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100
Q

How is the arrhythmia element of AF controlled?

A

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

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101
Q

What is the CHADSVASC score?

A 
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
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102
Q

when is anticoag used using CHAD VASc?

A

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

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103
Q

What is the HASBLED score?

A

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

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104
Q

When is electrocardioversion used in AF?

A

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.

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105
Q

How does electrical DC cardioversion work?

A

synchronised to R wave - to prevent VF

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106
Q

what pharmacological agents are used for cardioversion and when?

A

flecanide - if no structural heart disease

amiodarone - if there is structural heart disease

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107
Q

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

A

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.

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108
Q

should anticoagulation be given post cardioversion?

A

for those who had AF <48 hours - no

for those who had AF >48 - yes continue for further 4 weeks.

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109
Q

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

A

warfarin / DOAC

rather than antiplatelets

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110
Q

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

A

Not good at controlling rate during exercise

prefered in those with coexistent HF.

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111
Q

what agents can be used for rhythm control in AF?

A

sotalol
amiodarone
flecanide

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112
Q

what factors favour rate control or rhythm control in AF?

A

rate:
- >65yrs
- history of IHD

rhythm:

  • <65yrs
  • symptomatic
  • first presentation
  • lone AF/ AF secondary to precipitant
  • congestive heart failure
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113
Q

when is catheter ablation for AF offered?

A

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

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114
Q

when is catheter ablation for AF offered?

A

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

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115
Q

When is anticoagulation needed for catheter ablation in AF?

A

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)

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116
Q

what are the complications of catheter ablation in AF?

A

cardiac tamponade
stroke
pulmonary valve stenosis

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117
Q

what is a atrial myxoma?

A

most common primary cardiac tumour

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118
Q

where do atrial myxomas mainly occur?

A

left atrium - mainly attached to fossa ovalis

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119
Q

who are atrial myxomas most common in?

A

females

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120
Q

what are the symptoms/features of atrial myxomas?

A

systemic - dyspnoea, fatigue, clubbing, weight loss, fever

AF
mid diastolic murmur - ‘tumour plop’
emboli

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121
Q

what is seen on echo for atrial myxomas?

A

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

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122
Q

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

A

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

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123
Q

What are the effects of atropine?

A

tachycardia

Mydriasis

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124
Q

Where is B type natiuretic peptide produced?

A

primarily by myocytes of left ventricle

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125
Q

what can raise levels of BNP?

A

HF mainly
other cardiac dysfunction - valvular disease, ischaemia

CKD

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126
Q

what can reduce BNP levels?

A

ARBs, ACEi, diuretics

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127
Q

what are the effects of BNP?

A

vasodilation
inhibits RAAS pathway
diuresis and natriuresis

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128
Q

How is BNP used in the diagnosis of HF?

A 
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

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129
Q

what are the indications for B blockers?

A 
angina 
secondary prevention for ACS
anxiety 
long QT
AF (and other arrhythmias) 
HF 
HTN 
thyrotoxicosis 
migraine prophylaxis
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130
Q

what are the side effects of B blockers?

A 
bronchospasm
bradycardia
fatigue
cold peripheries
erectile dysfunction
sleep disturbance inc nightmares
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131
Q

when are B blockers contraindicated?

A

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

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132
Q

what are the complications of a bicuspid aortic valve?

A

higher risk of…

aortic regurg
aortic stenosis
aortic dissection and aneurysm formation from ascending aorta

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133
Q

what is a left dominant coronary circulation?

A

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

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134
Q

what conditions is bicuspid aortic valves associated with?

A

Turners
left dominant coronary artery circulation

around 5 % also have a coarctation of aorta

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135
Q

what is Bivalirudin?

A

reversible direct thrombin inhibitor

used in ACS

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136
Q

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

A

overestimate

if too large - underestimate

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137
Q

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

A

Over estimate if below level

underestimate if arm is raised above heart

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138
Q

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

A

the highest reading

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139
Q

What are the causes of broad complex tachycardias?

A

VT - until proven otherwise

SVT with aberrant conduction

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140
Q

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

A 
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
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141
Q

what is Brugada syndrome?

A

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

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142
Q

who is brugada syndrome most common in?

A

asians

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143
Q

what are the ECG changes found in brugada syndrome?

A

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

partial RBBB

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144
Q

how is brugada syndrome investigated?

A

ECG changes

can give flecanide/ ajmaline and ECG changes become more prominant

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145
Q

how is brugada managed?

A

Implantable cardioverter defibrilator

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146
Q

What is Buerger’s disease?

A

small/medium vessel vasculitis strongly associated with smoking

a.k.a. thromboangiitis obliterans

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147
Q

what are the features of Buerger’s disease?

A

extremity ischaemia - intermittent claudication, ulcers

Raynauds

superficial thrombophlebitis

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148
Q

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

A

right heart - 70%

left heart - 98-100%

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149
Q

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

A

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%

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150
Q

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

A

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%

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151
Q

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

A

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

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152
Q

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

A

O2 saturations drop on left side of heart ..

E.g. Eisenmengers with VSD… the left ventricle and aorta drop to 85% O2 sats.

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153
Q

which cardiac enzyme is the first to rise in MI?

A

myoglobin

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154
Q

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

A

troponins 10 days

CKMB - 2-3 days

myoglobin 1-2 days

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155
Q

what markers are raised in MI?

A 
Troponin I , T
CK MB
CK
LDH
AST
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156
Q

what is a SPECT scan?

A

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.

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157
Q

what is a MUGA?

A

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

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158
Q

what are the two types of cardiac CT?

A

calcium score: to look at atherosclerotic plaque calcium to give a calcium score (predicts risk of ischameia)

contrast enhanced CT - visualises coronary arteries

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159
Q

what are the uses of cardiac MRI?

A

view structure of heart - gold standard

assess myocardial perfusion using gadolinium

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160
Q

what are the different types of genetic cardiomyopathy?

A

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)
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161
Q

what gene is mutated in HOCM?

A

B myosin heavy chain

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162
Q

What are the ECHO findings of HOCM?

A

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

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163
Q

what pattern of inheritance is HOCM ?

A

autosomal dominant

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164
Q

What are the causes of dilated and restrictive cardiomyopathy?

A

dilated: alcohol, coxsackie, wet beri beri, doxorubicin

restrictive - amyloidosis, post radiotherapy, loefflers endocarditis

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165
Q

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

A

last month of preg and 5 months after

more common in older women , greater parity and multiple gestations

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166
Q

What is Takotsubo cardiomyopathy?

A

stress induced cardiomyopathy

transient apical ballooning of the myocardium

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167
Q

what are the infective causes of cardiomyopathies?

A

coxsackie B

Chagas disease

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168
Q

What endocrine conditions can cause cardiomyopathies?

A

Diabetes
thyrotoxicosis
Acromegaly

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169
Q

what neuromuscular conditions can lead to cardiomyopathy?

A

Duchennes/Becks
Friedreich’s ataxia
myotonic dystrophy

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170
Q

which nutritional deficiency can cause cardiomyopathy?

A

thiamine = beri beri

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171
Q

What is Catecholaminergic polymorphic ventricular tachycardia?

A

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

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172
Q

what gene is mutated in catecholamine polymorphic ventricular tachycardia?

A

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

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173
Q

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

A

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

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174
Q

how is catecholamine polymorphic ventricular tachycardia managed?

A

B blockers

implantable defib

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175
Q

Which antihypertensive are centrally acting?

A

methyldopa
clonidine
moxonidine - alpha 2 receptor stimulation

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176
Q

what is the main cause of cholesterol emboli ?

A

vascular surgery
angiography

(but also atherosclerosis)

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177
Q

what are the features of a cholesterol emboli?

A

eosinophilia
purpura
renal failure
livedo reticularis

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178
Q

what are the DDI with clopidogrel?

A

PPI - make clopidogrel less effective

lansoprazole is okay to use

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179
Q

what is the mechanism of action of clopidogrel?

A

antagonist of the P2Y12 adenosine diphosphate (ADP) receptor, inhibiting the activation of platelets

class of drug = thienopyridines

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180
Q

What rate do atria contract in atrial flutter?

A

300 bpm

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181
Q

What is the pathophysiology behind atrial flutter?

A

Normally SAN –> AVN

In atrial flutter there are re-entry rhythms in atria so atria contract again and again

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182
Q

what are the different types of atrial flutter?

A

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

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183
Q

what are the causes of atrial flutter?

A

IHD - damage to myocytes

similar causes to AF

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184
Q

what are the ECG changes for atrial flutter?

A

saw tooth pattern - multiple contractions - flutter wave, no p.

1:2/3/4 ratio with QRS

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185
Q

what are the symptoms of atrial flutter?

A

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

Clots

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186
Q

what is the management of atrial flutter?

A

Like AF

Anticoag
B blocker
Rhtyhm control
DC cardioversion
ablation - of tricuspid valve isthmus = curative in most.
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187
Q

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

A

carotid sinus massage/ adenosine - blocks AVN

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188
Q

What is the ostium primum, secundum and foramen ovale?

A

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

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189
Q

What are the main causes of Atrial septal defects?

A

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

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190
Q

what are ASDs associated with?

A

fetal alcohol syndrome

ostium primum - down syndrome

ostium secundum - associated with Holt-Oram syndrome (tri-phalangeal thumbs)

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191
Q

what is the management of ASD?

A

children are monitored in the hope it will close

otherwise can close surgically

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192
Q

what are the features of ASD?

A

ejection systolic murmur, fixed splitting of S2

embolism may pass from venous system to left side of heart causing a stroke - paradoxical embolus

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193
Q

which ASD presents earliest?

A

Ostium primum

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194
Q

what other heart abnormality is ostium primum associated with?

A

abnormal AV valves

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195
Q

What ECG may be seen with ostium primum ?

A

RBBB with LAD

prolonged PR interval

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196
Q

what is LEV’s disease?

A

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

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197
Q

what are the causes of heart block?

A 
LEVs disease (idiopathic) 
IHD
cardiomyopathy
myocarditis 
electrolytes
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198
Q

what are the different types of heart block?

A

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.

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199
Q

How is heart block managed?

A

for type 2 mobitz and 3rd degree - pace maker

otherwise can investigate and correct cause.
if first degree - no Mx

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200
Q

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

A

> 0.2s

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201
Q

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

A

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

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202
Q

how is anginal chest pain defined by NICE?

A
  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
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203
Q

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

A

CT coronary angiogram = 1st line

2nd line - non invasive cardiac imaging e.g. SPEC, stress ECHO, MRI

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204
Q

How is HF investigated (NICE guidance)?

A

NT-proBNP = 1st line Ix

if high - specialist in 2 weeks
if raised - specialist in 6 weeks

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205
Q

what can increase BNP?

A 
Left ventricular hypertrophy
Ischaemia
Tachycardia
Right ventricular overload
Hypoxaemia (including pulmonary embolism)
GFR < 60 ml/min
Sepsis
COPD
Diabetes
Age > 70
Liver cirrhosis
206
Q

what can decrease BNP?

A 
Obesity
Diuretics
ACE inhibitors
Beta-blockers
Angiotensin 2 receptor blockers
Aldosterone antagonists
207
Q

what is coarctation of the aorta?

A

congenital narrowing of the descending aorta

208
Q

who is coarctation most common in?

A

males

209
Q

What are the clinical features of coarctation of the aorta?

A

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

210
Q

what conditions is coarctation of the aorta associated with?

A

Turners
bicuspid aortic valves
berry aneurysm
neurofibromatosis

211
Q

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

A

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

212
Q

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

A

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

213
Q

What are the features of complete heart block?

A 
syncope
heart failure
regular bradycardia (30-50 bpm)
wide pulse pressure
JVP: cannon waves in neck
variable intensity of S1
214
Q

What the examples of acyanotic CHDs?

A 
ASD
VSD - most common 
PDA
coarctation of aorta
aortic valve stenosis
215
Q

What are the examples of cyanotic CHD?

A

Tetralogy of fallot
transposition of great vessels
tricuspid atresia

216
Q

What is the most common cyanotic CHD?

A

Tetralogy of fallot

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

217
Q

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

A

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
218
Q

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

A

Right coronary artery supplies SAN

Then splits into right marginal artery and posterior descending artery

219
Q

what does the branches of RCA supply?

A

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.

220
Q

How does the LAD and posterior descending artery meet?

A

make anastomoses at the apex of the heart

221
Q

where does the posterior descending artery branch from?

A

mostly RCA (right dominant circulation)

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

222
Q

when is blood flow through coronary vessels maximal?

A

diastole

during systole they are compressed

223
Q

how are the cardiac veins arranged?

A

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

224
Q

what class of drug is dabigatran?

A

direct thrombin inhibitor

225
Q

what are the indications for dabigatran use?

A

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
226
Q

what are the contraindications/ cautions of dabigatran?

A

reduce dose in renal failure

cant prescribe if creatinine clearance <30

227
Q

what medication can be used to reverse dabigatrans effects?

A

Ibarucizumab

228
Q

what is the blood pressure target for diabetics?

A

<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

229
Q

what is the first line antihypertensive in diabetics?

which medications should be avoided?

A

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.

230
Q

what is the frank starling relationship?

A

increase in preload - increase in contraction (up to a point)

increase in end diastolic volume increases SV

231
Q

what is dilated cardiomyopathy?

A

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)

232
Q

what are the symptoms/features of cardiomyopathy?

A 
S3 gallop
dyspnoea
orthopnoea
PND
balloon appearance of heart on Xray 
systolic murmur - tricuspid / mitral regurg may occur from stretching.
233
Q

what are the causes of dilated cardiomyopathy?

A

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

234
Q

what is the mechanism of action of dipyrimadole?

A

inhibits phosphodiesterase elevating platelet cAMP levels which reduces intracellular Ca

reduce cellular uptake of adenosine

inhibit thromboxane

overall platelet inhibition.

235
Q

what are the DVLA rules with HTN?

A

no need to form DVLA

for HGV cant drive if resting BP >180/100

236
Q

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

A

angioplasty - 1 week off

CABG - 4 weeks off

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

237
Q

what are the rules behind driving and angina?

A

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

238
Q

what are the rules behind driving and…

pacemaker insertion
ICD
catheter ablation
?

A

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

239
Q

what are the rules behind driving and aortic aneurysm?

A

6cm or more - inform DVLA
liscencing permitted with annual review

if 6.5 or more - no driving

240
Q

what are the rules behind driving and heart transplant?

A

no driving for 6 weeks after

no need to inform DVLA

241
Q

what is ebstein anomaly?

A

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

242
Q

what is Ebstein anomaly caused by?

A

exposure to lithium in utero

243
Q

what is Ebstein anomaly assocaited with?

A

PFO or ASD

Wolff parkinson white

244
Q

what are the clinical features of ebstein anomaly?

A

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

245
Q

what are the causes of left axis deviation on ECG?

A

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

246
Q

what are the causes of right axis deviation on ECG?

A

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

247
Q

what leads on an ECG corresponds to anterolateral region?

A

V4-6 , I and aVL

248
Q

What are the ECG features for digoxin?

A

Down sloping ST depression (reverse tick)

flattened / inverted T

short QT interval

arrhythmias - AV block, bradycardia.

249
Q

What are the ECG features of hypokalaemia?

A 
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

250
Q

what are the ECG changes for hypothermia?

A 
bradycardia
Long QT
J wave - small hump at end of QRS
first degree heart block 
atrial and ventricular arrhythmias
251
Q

How can you identify LBBB and RBBB?

A

WiLLaM - M in V6 for L

MaRRoW - M in V1 for R

252
Q

what are the causes of LBBB?

A 
IHD
HTN
aortic stenosis
cardiomyopathy
idiopathic fibrosis , digoxin, hyperkalaemia - all rare
253
Q

what are normal ECG variants in athletes?

A

sinus bradycardia
junctional rhythm
first degree heart block
Wenckebach phenomenon

254
Q

what is a cause of increased p wave amplitude?

A

cor pulmonale

255
Q

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

A

often most prominent in lead 2

caused by atrial enlargement e.g. atrial stenosis

256
Q

what are the causes of prolonged PR?

A 
heart block 
hypokalaemia 
IHD
digoxin 
rheumatic fever 
aortic root pathology (abscess secondary to I.E)
lyme disease
sarcoidosis 
myotonic dystrophy.
257
Q

what condition causes a short PR?

A

WPW

258
Q

what are the causes of RBBB?

A 
normal variant - with age
Right ventricular hypertrophy 
chronically increased right ventricular pressure 
pulmonary embolism 
MI
ASD
cardiomyopathy/ myocarditis
259
Q

what are the causes of ST depression?

A 
ischaemia
digoxin
hypokalaemia 
secondary to abnormal QRS - LBBB, RBBB, LVH
syndrome X
260
Q

what are the causes of ST elevation?

A 
myocardial infarction
pericarditis/myocarditis
normal variant - 'high take-off'
left ventricular aneurysm
Prinzmetal's angina (coronary artery spasm)
Takotsubo cardiomyopathy
rare: subarachnoid haemorrhage
261
Q

what are the causes of peaked T waves?

A

hyperkalaemia

Myocardial ischaemia

262
Q

what are the causes of inverted T waves?

A 
myocardial ischaemia
digoxin toxicity
subarachnoid haemorrhage
arrhythmogenic right ventricular cardiomyopathy
pulmonary embolism ('S1Q3T3')
Brugada syndrome
263
Q

how is pre-eclampsia defined?

A

> 20 weeks gestation
pregnancy induced HTN
proteinuria

264
Q

what medication is used to prevent seizures in pre-eclampsia?

what monitoring is needed during this infusion?

A

MgSO4

given once decided on delivery.

Urine output, reflexes, resp rate, O2 sats

treatment continues 24 hours after last seizure/delivery.

265
Q

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

A

gluconate

266
Q

What is eisenmengers syndrome?

A

reversal of left to right shunt due to pulmonary HTN

267
Q

what are the features of eisenmengers syndrome?

A

original murmur may disappear

cyanosis

clubbing

RV failure

Haemoptysis

embolism

268
Q

what is an individuals maximum predicted HR?

A

220-age

269
Q

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

A

85% of maximum predicted.

270
Q

what are the contraindications to an exercise stress test?

A

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

271
Q

when should an exercise stress test be stopped?

A

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

272
Q

name 3 glycoprotein IIb/IIIa receptor antagonists…

A

abciximab
eptifibatide
tirofiban

273
Q

How is heart failure managed (NICE)?

A

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.

274
Q

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

A

ACEi and B blockers

275
Q

which HF medications affect overall mortality?

A

ACEi
B blockers

NOT furosemide
NOT digoxin

276
Q

what is the criteria for initiating the following drugs in HF…

Ivabradine
Sacubitril-valsartan

A

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

277
Q

when is digoxin strongly indicated in HF?

A

when there is co-existent AF

278
Q

when is hydralazine + nitrates mainly indicated in HF?

A

◦this may be particularly indicated in Afro-Caribbean patients

279
Q

when is cardiac resynchronisation therapy indicated in HF?

A

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

280
Q

Which vaccinations should HF patients recieve?

A

annual influenza

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

281
Q

what is cardiac resynchronisation therapy?

A 
biventricular pacing,.
improves symptoms and reduced hospitalisation in NYHA class III patients.
282
Q

How does exercise training help patients with HF?

A

improves symptoms but not hospitalisation/ mortality

283
Q

what is the NYHA classification for HF?

A 
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
284
Q

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

A

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

285
Q

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

A

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

286
Q

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

A

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.

287
Q

what is the S4 heart sound?

A

caused by atria contracting against stiff ventricle.

can be heard in HTN, HOCM, Aortic stenosis

288
Q

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

A

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

289
Q

what are the causes of reversal of S2 split?

A 
severe AS
LBBB
right ventricular pacing 
WPW type B 
patent ductus arteriosus
290
Q

what is the mechanism of hydralazine?

A

increases cGMP leading to smooth muscle relaxation

for HTN but not commonly used

291
Q

what are the contraindications of hydralazine?

A

systemic lupus erythematous

•ischaemic heart disease/cerebrovascular disease

292
Q

what are the adverse effects of hydralazine?

A 
tachycardia
•palpitations
•flushing
•fluid retention
•headache
•drug-induced lupus
293
Q

what are the symptoms of hypercalcaemia?

A

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

294
Q

what is an eruptive xanthoma most commonly due to?

A

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

295
Q

how can xanthelesma be managed?

A

surgically
topical treatment
laser

296
Q

what treatment are women at high risk of eclampsia given?

A

aspirin 75mg from 12 weeks till birth

297
Q

which women are at high risk of developing eclampsia?

A
  • hypertensive disease during previous pregnancies
  • chronic kidney disease
  • autoimmune disorders such as SLE or antiphospholipid syndrome
  • type 1 or 2 diabetes mellitus
298
Q

what are the 3 types of HTN during pregnancy?

A 
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.
299
Q 
how is HTN classified?
when is each class treated?
A

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

300
Q

how is severe HTN classified?

A

> 180/120

301
Q

what is ambulatory BP recording?

A

use average of at least 14 measurements throughout the day

302
Q

How is HTN managed?

A

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.

303
Q

what are the BP targets?

A

<80 - 140/90 (ABPM - 135/85)

>80 - 150/90 (ABPM - 145/85)

304
Q

what is aliskiren?

A

Direct renin inhibitor
blocks RAS activation
new HF drug

305
Q

what are the secondary causes of HTN?

A

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

306
Q

what is HOCM? (pathophysiology)

A

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.

307
Q

how does HOCM appear on biopsy?

A

myofibrillar hypertrophy
choatically organised myocytes
fibrosis

308
Q

what are the features of HOCM?

A

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.

309
Q

what other conditions can HOCM be associated with?

A

friedrichs ataxia

WPW

310
Q

what are the ECHO findings in HOCM?

A

mitral regurgitation
assymetric hypertrophy
systolic anterior motion of anterior mitral valve

311
Q

what are the ecg changes seen in HOCM?

A

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

312
Q

How is HOCM managed?

A 
ABCDE
Amiodarone
Bblockers
Cardioverter defib
Dual chamber pacemaker
Endocarditis prophylaxis
313
Q

which drugs should be avoided in HOCM?

A

nitrates
ACEi
Inotropes

314
Q

what are the poor prognostic factors of HOCM?

A 
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
315
Q

what are the indications for an implantable cardiac defib?

A 
long QT 
HOCM 
previous cardiac arrest due to VT/VF
previous MI with nonsustained VT on 24 hour tape / inducible VT
brugada syndrome?
316
Q

what is the biggest risk to developing infective endocarditis?

A

previous infective endocarditis

317
Q

what is the commonest cause of infective endocarditis?

A

s.aureus - especially acute and IVDU

streptococcus viridans - in developing countries

318
Q

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

A

s. epidermidis

319
Q

what are the culture negative causes of infective endocarditis?

A 
prior antibiotic therapy
Coxiella burnetii
Bartonella
Brucella
HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
320
Q

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

A

streptococcus viridans

321
Q

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

A

S.bovis - particularly a subtype called… Streptococcus gallolyticus

322
Q

what is mirantic endocarditis?

A

subtype of endocarditis caused by malignancy

323
Q

what is the modified dukes criteria for infective endocarditis?

A

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
324
Q

what are the poor prognostic factors of infective endocarditis?

A

S.aureus
culture negative
prosthetic valve
low complement levels

325
Q

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

A

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

326
Q

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

A

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

327
Q

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

A

Benzylpenicillin

If penicillin allergic
vancomycin + low-dose gentamicin

328
Q

what are the indications for surgery in infective endocarditis?

A

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

329
Q

how should isolated systolic HTN be treated?

A

same way as normal HTN

330
Q

what is the function of ivabradine?

A

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

used in angina

331
Q

what are the side effects of ivabradine?

A

headaches
visual changes
bradycardia

332
Q

when is a non-pulsatile JVP seen?

A

SVC obstruction

333
Q

what is the kussmaul sign?

A

paradoxical rise in JVP in inspiration

constrictive pericarditis

334
Q

what do different parts of JVP waveform present?

A 
a wave - atrial contraction
c wave - tricuspid closure
x descent - ventricular systole
v wave - filling of heart against closed tricuspid
y descent - tricuspid opens
335
Q

when would the a wave of JVP be large?

A

large atrial pressure - tricuspid/ pulmonary stenosis, pulmonary HTN

336
Q

when is the a wave of JVP absent?

A

AF

337
Q

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

A

atria contracting against closed tricuspid
seen in heart block, arrhythmias, single chamber pacing

regular - VT, AVNRT
irregular - Heart block

338
Q

when are giant v waves seen?

A

seen in tricuspid regurgitation.

339
Q

what is Kawasaki disease?

A

vasculitis
children
can cause serious complications - coronary aneurysms

340
Q

what are the features of kawasaki disease?

A 
fever - 5 days, resistant to paracetamol
strawberry tongue
red cracked lips
red palms/ soles of feet - later peel
cervical lymphadenopathy
conjunctivitis
341
Q

how can you test for kawasaki?

A

no test

clinical diagnosis

342
Q

how is kawasaki disease managed?

A

high-dose aspirin

intravenous immunoglobulin

echocardiogram (rather than angiography) is used as the initial screening test for coronary artery aneurysms

343
Q

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

A

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

344
Q

what are the congenital causes of long QT?

A

Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel)

Romano-Ward syndrome (no deafness)

345
Q

what drugs can cause long QT?

A

Amiodarone, sotalol, class 1a antiarrhythmic drugs

tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram)

methadone

chloroquine
terfenadine
erythromycin

haloperidol
ondanestron

346
Q

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

A

low Ca, low Mg, low K
hypothermia

SAH
myocarditis
MI

347
Q

what are the different types of Long QT?

A

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

348
Q

how is long QT managed?

A

B blockers,

ICD in high risk

349
Q

what are the side effects of loop diuretics?

A

hypotension

hyponatraemia
hypokalaemia, hypomagnesaemia
hypochloraemic alkalosis
hypocalcaemia

ototoxicity
renal impairment (from dehydration + direct toxic effect)

hyperglycaemia (less common than with thiazides)
gout

350
Q

what BP occurs in malignant HTN?

A

> 200/130

351
Q

How is malignant HTN managed?

A

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

352
Q

what are the most common valve disorders of the heart?

A

Aortic stenosis - no. 1

mitral regurg - no.2

353
Q

what are the risk factors for mitral regurgitation?

A 
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
354
Q

what murmur is heard in mitral regurgitation?

A

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

355
Q

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

A

ECG - wide/large p wave due to enlarged atria

CXR - cardiomegaly

356
Q

what causes mitral stenosis?

A

Rheumatic fever - main cause

others: mucopolysaccharidoses, carcinoid and endocardial fibroelastosis - seen in exams

357
Q

what mumur/ sounds are heard in mitral stenosis?

A

mid- late diastolic murmur
loud S1 - opening snap

with severe Mitral stenosis - murmur becomes longer and opening snap becomes closer to S2

358
Q

what are the features/ symptoms of mitral stenosis?

A

murmur
malar flush
low pulse volume
AF

359
Q

what can be seen on CXR in mitral stenosis?

A

large atria

360
Q

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

A

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

361
Q

what conditions are associated with mitral valve prolapse?

A

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

362
Q

what are features of mitral valve prolapse?

A

mid-systolic click (occurs later if patient squatting)

late systolic murmur (longer if patient standing)

363
Q

what is a multifocal atrial tachycardia?

A

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

364
Q

how is multifocal atrial tachy managed?

A

correct hypoxia
correct electrolytes
rate limiting CaB

365
Q

which ejection systolic mumurs are louder on inspiration/expiration?

A

louder on expiration
aortic stenosis
hypertrophic obstructive cardiomyopathy

louder on inspiration
pulmonary stenosis
atrial septal defect

tetralogy of fallot is another ejection systolic murmur

366
Q

name two pansystolic mumurs?

A

mitral/ tricuspid regurg

VSD

367
Q

Give examples of a late systolic mumur?

A

mitral valve prolapse

coarctation of aorta

368
Q

Give examples of early diastolic murmur?

A

aortic regurg
Graham-Steel murmur (pulmonary regurgitation)

both are high-pitched and ‘blowing’ in character

369
Q

give examples of mid-late diastolic murmurs?

A

mitral stenosis

Austin-Flint murmur (severe aortic regurgitation)

both ‘rumbling’ in character)

370
Q

what murmur does PDA give?

A

continuous machine like

371
Q

what are the complications of an MI?

A

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

372
Q

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

A

inferior

373
Q

what are the symptoms/ features of dresslers syndrome?

A

fever
pleuritic pain
pericardial effusion
raised ESR

374
Q

How is Dresslers treated?

A

NSAIDs

375
Q

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

A

infero-posterior

376
Q

what is the secondary prevention post MI?

A

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

377
Q

when can sexual activity ressume after an MI?

A

4 weeks

378
Q

when are ARBs preffered to ACEi in MI?

A

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

379
Q

How is an MI managed?

A

aspirin
clopidogrel/ticagrelor/prasugrel

if undergoing PCI - also unfractionated heparin/LMWH

PCI/thrombolysis

380
Q

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

A

90 mins

if <50% resolution in ST elevation can offer PCI

381
Q

what are the causes of myocarditis?

A

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

382
Q

what are the symptoms of myocarditis?

A

chst pain
dyspnoea
arrhythmia
(fever)

383
Q

what are the investigation findings for myocardiits?

A

increased cardiac enzymes, increased BNP, increassed inflammatory markers

ECG -tachyarrhythmias, ST / T changes inc ST elevation, T inversion

384
Q

what is nicorandil?

A

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

385
Q

what are the side effects of nicorandil?

A

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

386
Q

when is nicorandil contraindicated?

A

LV failure

387
Q

what does nicotinic acid do?

A

Lowers cholesterol and triglyceride concentrations

it also raises HDL levels.

388
Q

what are the complications/side effects of nicotinic acid?

A

Adverse effects
flushing: mediated by prostaglandins
impaired glucose tolerance
myositis

389
Q

what is the function of nitrates?

A

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

390
Q

what are the problems/side effects of nitrates?

A

headaches, flushing, hypotension, tachycardia

develop tolerance - not seen if modified release is taken.

391
Q

what are the indications for a temporary pacemaker?

A

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

392
Q

what are the complications of PCI?

A

stent thrombosis - usually in 1 month, presents as MI

restenosis - due to proliferation around the stent. in first 3-6 months. angina symptoms

393
Q

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

A

drug eluting stents - drugs that inhibit tissue growth

thrombosis rate increased

394
Q

How is a bradycardia managed?

A

Atropine IV (can use up to 3mg , start with 500mcg)

need for treatment: haemodynamic compromise , very low HR

395
Q

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

A

transcutaneous pacing

adrenaline/isoprenaline

396
Q

When is transcutaneous pacing considered for brady-arrhythmias?

A

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

397
Q

how does fonduparinux work?

A

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

398
Q

what keeps a PDA open?

A

prostaglandins

399
Q

who is a PDA most common in?

A

premature
born at high altitude
maternal rubella in 1st trimester

400
Q

what are the features of PDA?

A 
left subclavicular thrill
continuous 'machinery' murmur
large volume, bounding, collapsing pulse
wide pulse pressure
heaving apex beat
401
Q

how is PDA managed?

A

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

402
Q

How are regular narrow complex tachyarrythmias managed?

A

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)

403
Q

How are irregular narrow complex tachyarrythmias managed?

A

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

404
Q

How are irregular broad complex tachyarrythmias managed?

A

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

then seek expert advice

405
Q

what may cause an irregular broad complex tachyarrythmias ?

A

atrial fibrillation with bundle branch block - the most likely cause in a stable patient

atrial fibrillation with ventricular pre-excitation

torsade de pointes

406
Q

how is a regular broad complex tachyarrhythmia managed?

A

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

407
Q

how is peripheral arterial disease managed?

A

lifestyle
statin - atorvastatin 80mg
clopidogrel rather than aspirin
exercise training

angioplasty, stenting, bypass graft surgery

408
Q

what drugs can be used in peripheral arterial disease?

A

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

409
Q

what is pre-eclampsia?

A

HTN (>140/90) with proteinuria after 20 weeks.
+ oedema

may have other end organ involvment… renal, liver, neuro, placental

410
Q

what are the consequences of pre-eclampsia?

A

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

411
Q

what are the features of severe pre-eclampsia?

A

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

412
Q

what are the risk factors for pre-eclampsia?

A

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
413
Q

how is pre-eclampsia prevented in those at risk?

A

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

414
Q

how is pre-eclampsia managed?

A

oral labetolol

nifedipine if asthmatic

415
Q

how is a P.E investigated in pregnancy?

A

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

416
Q

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

A

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

VQ scan - increased risk of childhood cancer

417
Q

what are the pros and cons of biological valve?

A

pros - no needs for long term anticoag (low dose aspirin still given long term)

cons - long term calcification and deterioration

418
Q

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

A

mechanical bileaflet valve

419
Q

what are the advantages and disad of mechanical valves?

A

low failure rate

long term anticoag needed

420
Q

what long term anticoag is used for mechanical valves?

A

warfarin (not doac)

421
Q

what are the target INR ranges for mechanical valves?

A

aortic 3

mitral 3.5

422
Q

how is pulmonary arterial hypertension defined?

A

resting pulmonary arterial pressure >25mmHg

423
Q

who is pulmonary arterial hypertension most common in?

A

women , mainly 30-50yrs

424
Q

what are the causes of pulmonary arteial HTN?

A

secondary to COPD etc

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

425
Q

what are the features of pulmonary artery HTN?

A

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

426
Q

what test is essential to managing pulmonary artery HTN?

A

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.

427
Q

how is pulmonary artery HTN managed?

A

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

428
Q

how is pulmonary capillary wedge pressure managed?

A

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

429
Q

What is the PERC criteria?

A

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

430
Q

What is the 2 level PE wells score?

A

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

431
Q

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

A

give DOAC whilst awaiting urgent CTPA

DOAC can be continued if PE confirmed

432
Q

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

A

d.dimer

if positive do a CTPA

433
Q

whats the difference between sensitivity and specificity?

A

high sensitivity - unlikely to give false positive

high specificity - unlikely to give false neg

434
Q

what ecg changes are seen in a P.E?

A

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

tachycardia

RBBB

435
Q

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

A

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

436
Q

how long should patients have anticoagulation for a P.E

A

atleast 3 months

provoked - 3 months only
unprovoked - up to 6 months

437
Q

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

A

thrombolysis

438
Q

what are the causes of a collapsing pulse?

A

aortic regurgitation

PDA

439
Q

what is pulsus paradox? what are the causes ?

A

fall in BP >10 (normal fall) with inspiration

severe asthma, cardiac tamponade

440
Q

what is the cause of a slow rising pulse?

A

aortic stenosis

441
Q

what is the causes of Bisferiens pulse?

A

‘double pulse’ - two systolic peaks

mixed aortic valve disease

442
Q

what are the causes of constrictive pericarditis?

A

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

443
Q

what ECG is found in restrcitve cardiomyopathy?

A

low voltage QRS

444
Q

what features suggest restrictive cardiomyopathy rather than constrictive pericarditis?

A

prominent apical pulse

absence of pericardial calcification on CXR

the heart may be enlarged

ECG abnormalities e.g. bundle branch block, Q waves

445
Q

what is the pathogenesis behind rheumatic fever?

A

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

446
Q

What are Ashcoff bodies?

A

Aschoff bodies describes the granulomatous nodules found in rheumatic heart fever

447
Q

what is the diagnostic criteria for rheumatic fever?

A

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
448
Q

how is rheumatic fever managed?

A

Antibiotics: oral penicillin V

anti-inflammatories: NSAIDs are first-line

treatment of any complications that develop e.g. heart failure

449
Q

what is the ABCD2 score?

A

prognostic score post TIA

450
Q

what is the DAS28 score?

A

measure of disease activity in rheumatoid arthritis

451
Q

what is child pugh score?

A

A scoring system used to assess the severity of liver cirrhosis

452
Q

what is the PHQ9 score

A

Patient Health Questionnaire - assesses severity of depression symptoms

453
Q

Name 3 alcohol screening tools?

A

AUDIT, CAGE, FAST

454
Q

what is the SCOFF score?

A

Questionnaire used to detect eating disorders and aid treatment

455
Q

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

A

International prostate symptom score

Gleason score - indicates prognosis for prostate Ca

456
Q

whats the bishop and apgar score

A

bishop - used to help assess the whether induction of labour will be required

apgar - assess health of new born immediately post birth

457
Q

whats the waterlow score?

A

risk of developing pressure sore

458
Q

whats the ranson criteria for?

A

acute pancreatitis

459
Q

how do statins work?

A

inhibit HMG-CoA reductase to reduce cholesterol synthesis

460
Q

what are the side effects of statins?

A

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

461
Q

what are the risk factors for statin induced myopathy?

A

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

462
Q

How are LFTs monitored during statin therapy?

A

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

463
Q

what are the contraindications for statin use?

A

pregnancy

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

464
Q

Who should be put on statins?

A

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

465
Q

what statin dose is used for primary /secondary prevention?

A

primary - atorvastatin 20mg

secondary - atorvastatin 80mg

466
Q

what is the acute management of SVT if haemodynamically stable?

A

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

467
Q

how can SVT episodes be prevented?

A

beta-blockers

radio-frequency ablation

468
Q

what is syndrome X?

A

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

469
Q

what drug can be good for syndrome x?

A

nitrates

470
Q

what is takayasu’s arteritis?

A

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

471
Q

what are the symptoms of takayasu’s arteritis?

A

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

472
Q

how is takayasu’s arteritis managed?

A

steroids

473
Q

what is Takotsubo cardiomyopathy?

A

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

474
Q

how does Takotsubo cardiomyopathy present?

A

chest pain
HF symptoms
st elevation
normal coronary arteries

475
Q

how is Takotsubo cardiomyopathy managed?

A

supportive treatment only

most patients improve

476
Q

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

A

ToF

presents 1-2 months

477
Q

what are the 4 features of ToF

A

pulmonary stenosis
right ventricular hypertrophy
VSD
over-riding aorta

degreee of severity determined by degree of pulmonary stenosis

478
Q

what are the clinical features of ToF?

A

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

479
Q

how is ToF managed?

A

surgical repair is often undertaken in two parts

cyanotic episodes may be helped by beta-blockers to reduce infundibular spasm

480
Q

what is the mechanism of a thiazide diuretic?

A

block Na CL symporter in DCT to block sodium reuptake

Potassium is lost as a result of more sodium reaching the collecting ducts.

481
Q

what are the side effects of thiazides?

A 
dehydration
postural hypotension
hyponatraemia, hypokalaemia, hypercalcaemia*
gout
impaired glucose tolerance
impotence
Rare adverse effects
thrombocytopaenia
agranulocytosis
photosensitivity rash
pancreatitis
482
Q

what are the contraindications of thrombolysis?

A 
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
483
Q

what are the side effects of thrombolysis?

A

haemorrhage

allergy and hypotension - espwith streptokinase

484
Q

what is torsades de point?

A

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

485
Q

What are the causes of long QT?

A

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

486
Q

What is the managedment of torsades de point?

A

IV magnesium sulphate

487
Q

who is at increased risk of transposition of great vessels?

A

babies of diabetic mums

488
Q

what are the clinical features of transposition of great vessels?

A 
cyanosis
tachypnoea
loud single S2
prominent right ventricular impulse
'egg-on-side' appearance on chest x-ray
489
Q

how is transposition of great vessels managed?

A

maintenance of the ductus arteriosus with prostaglandins

surgical correction is the definite treatment.

490
Q

what are the signs of tricuspid regurg?

A

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

491
Q

what are the causes of tricuspid regurg?

A 
right ventricular infarction
pulmonary hypertension e.g. COPD
rheumatic heart disease
infective endocarditis (especially intravenous drug users)
Ebstein's anomaly
carcinoid syndrome
492
Q

what are VSD associated with?

A 
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

493
Q

when can a VSD be detected?

A

20 weeks on USS

494
Q

how does VSD present post natally?

A 
failure to thrive
features of heart failure
hepatomegaly
tachypnoea
tachycardia
pallor
classically a pan-systolic murmur which is louder in smaller defects
495
Q

how is a VSD managed?

A

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

496
Q

what are the complications of a VSD?

A 
aortic regurgitation
infective endocarditis
Eisenmenger's complex
     - this is turn results in cyanosis and clubbing
right heart failure
pulmonary hypertension
497
Q

what are the different types of VT?

A

monomorphic - associated with MI

Polymorphic - torsades - associated with long QT

498
Q

how is VT managed?

A

haemodynamic instability - DC cardiovert
otherwise..
amiodarone, lidocaine or procainamide.

Do not use verapamil

if drug therapy fails - ICD

499
Q

what is the mechanism of warfarin?

A

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

500
Q

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

A

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

501
Q

what is INR?

A

ratio of prothrombin time compared to normal.

502
Q

what factors can potentiate warfarin effects?

A

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

503
Q

how is a patient on warfarin managed with major bleeding?

A

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

504
Q

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

A

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

505
Q

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

A

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

506
Q

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

A

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.

507
Q

what are the features of wolff parkinson white on ECG?

A
  • 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*
508
Q

what are the two types of WPW?

A

type A - left sided pathway - dominant R wave in V1

Type B - right sided pathway - no dominant R in V1

509
Q

what is WPW associated with ?

A
  • HOCM
  • mitral valve prolapse
  • Ebstein’s anomaly
  • thyrotoxicosis
  • secundum ASD
510
Q

how is WPW managed?

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

MRCP (7 decks)

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