Cardiology Flashcards

1
Q

what causes right sided heart failure?

A

left sided heart failure
chronic lung disease (hypoxia causes pulmonary capillary contraction - increases pressure in right heart) - cor pulmonale
atrial or ventricular shunt - blood moves down pressure gradient into the right side, increasing the pressure

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2
Q

What are the complications of an MI

A

Bradyarrythmias, tachyarrythmias, pericarditis (dresslers syndrome), cardiac tamponade, RVF, mitral regurgitation, systemic embolism, septal defect, cardiac arrest, cardiogenic shock

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3
Q

what are the signs and symptoms of malignant hypertension (aka a hypertensive emergency)?

A
papilloedema 
retinal bleeding 
headaches and nausea (due to raised intracranial pressure)
chest pain (due to an overactive heart)
haematuria (failing kidneys)
uncontrollable epistaxis (nosebleeds)
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4
Q

How do we manage low risk NSTEMI ACS patients? (After initial management)

A

Discharge on aspirin and clopidogrel/ticagrelor

Arrange outpatient echocardiogram appointment

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5
Q

how do me manage a patient with a PE Wells score above 4?

A

send for a CTPA or V/Q scan, but if this is delayed, treat as if it is a confirmed PE with a LMWH (e.g. tinzaparin)

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6
Q

what’s the target INR for patients with AF?

A

2.5

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7
Q

whats the first step in managing AF?

A

beta blocker

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8
Q

what is dresslers syndrome?

A

a complication following an MI.
it is pericarditis occurring 2-6 weeks after the MI, and is thought to be an autoimmune reaction against antigenic proteins produced as the myocardium recovers
its characterised by pleuritic pain, fever, pericardial effusion and raised ESR
treated with NSAIDs

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9
Q

what are symptoms of CHF?

A

when the left side of the heart fails, blood backs up into the lungs. this leads to fluid leaking out into the lungs causing pulmonary oedema. this causes dyspnoea, orthopnea and crackles.
capillaries can rupture, leaking blood into the lungs. this blood is taken up by alveolar macrophages creating haemosiderin laden macrophages (heart failure cells)

when the right side of the heart fails, blood backs up into the body, this causes hepatosplenomegaly, peripheral pitting oedema, ascites, raised JVP

general symptoms include exercise intolerance, fatigue, weight loss

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10
Q

What are the symptoms of ACS?

A

Acute central chest pain, lasting over 20 mins

With associated nausea, sweating, breathlessness, palpitations

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11
Q

what are the investigations for an acute exacerbation of HF?

A

immediate CXR (looking for pleural effusion and consolidation) and ECG - looking for ACS, will probably point towards aetiology

blood tests - ABGs, FBC, U&E, LFTs, BNP, troponins (has there been an MI?)

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12
Q

What is involved in fibrinolysis reperfusion therapy?

A

IV administered clot dissolving enzymes
Most suitable is tenecteplase (a tissue plasminogen activator)
Goal: administer within 30 mins of admission
Once administered, patients should be transferred to a PCI centre. If thrombolysis is unsuccessful (residual STEMI) they should receive PCI.
If successful, receive angiography only.

CI: previous haemorrhage, stroke, bleeding disorders

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13
Q

Definition of stable angina

A

Not a new symptom.

No Change in frequency/ severity of attacks.

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14
Q

what drugs do we use to chemically cardiovert a patient in A Fib? (who’s stable)

A
amiodarone 
or flecinide (only in patients without structural abnormalities)
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15
Q

what concerns are there if a diabetic patient has changes on his ECG?

A

he may have had a silent MI
this can occur if neuropathy prevents him from sensing chest pain
you should test the patients troponins

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16
Q

how do we manage a cardiac arrest in VF/pVT?

A

1 shock followed by 2 minutes of CPR

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17
Q

what are side effects of beta blockers?

A
bronchospasm
cold peripheries 
fatigue 
erectile dysfunction
sleep disturbances incl. nightmares
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18
Q

Soft s1 is seen in…

A

Mitral regurgitation

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19
Q

What is the long term management for STEMIs?

A

Modify RFs
Anticoagulate with Fondaparinux until discharge
Double anti-platelet therapy for 12 months - aspirin and clopidogrel
Beta blockers - begin early for best outcome. If CI then CCB (verapamil or diltiazem)
ACE-Inhibitors for patients with HTN, LVF, diabetes
High dose statins
Eplerenone (anti mineral-corticoid) for those with EF <40%

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20
Q

What are the first line investigations for suspected ACS?

A

ECG - repeat at 3, 6 and 24 hours. Look for signs of MI
CXR - look for cardiomegaly, pulmonary oedema, widened mediastinum
Bloods: U&Es, HbA1C, lipids, FBC, troponins (looking for a rise)

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21
Q

what is a patient with takayasus arteritis at a risk of developing?

A

renal artery stenosis

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22
Q

what do anti-streptolysin antibodies show?

A

rheumatic fever

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23
Q

when is electrical cardioversion for AF favoured over pharmalogical cardioversion?

A

if the patient has new onset AF which has lasted longer than 48 hours

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24
Q

what’s the most common cause of infective endocarditis?

A

staphylacoccus aureus

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25
Q

what is an atrial myxoma?

A

a benign tumour, most commonly occuring the left atria (75% cases)

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26
Q

how does Left ventricular aneurysm present?

A

persistent ST elevation in anterior leads
couple weeks after an MI
pulmonary oedema

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27
Q

How is HBPM carried out?

A

the patients takes 2 sets of readings twice of day for at least 4 days.
for each set - he must take his BP twice, 1 minute apart - whilst sitting.
the readings from the first day are discarded and an average is taken from the remainder of the measurements

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28
Q

how do we manage ventricular tachycardia?

A

amiodarone ideally through a central line
lidocaine - not in severe left ventricle impairment
procainamide

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29
Q

Unstable angina definition

A

Recent onset angina - within 24 hrs (new symptom)
Change in frequency or severity of attacks - deterioration of previously stable angina with symptoms occurring increasingly at rest

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30
Q

how is primary pulmonary hypertension inherited?

A

autosomal dominant

10% of cases are familial

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31
Q

how do you manage severe chocking?

A

5 back-blows
5 abdominal thrusts
continue this cycle if unsuccessful

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32
Q

what factors can falsely raise BNP levels?

A

myocardial ischaemia, valvular disease, kidney disease (poor excretion),

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33
Q

in what ECG leads would you expect to see changes if the LAD is infarcted?

A

V1-V4 - the anteroseptal leads

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34
Q

what presents in a young female with an absent limb pulse, malaise, headaches?

A

Takayasu’s arteritis

a lager artery vasculitis

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35
Q

what is a typical echo finding for an atrial myxoma?

A

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

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36
Q

persistent hypotension, tachycardia and raised JVP despite fluid resuscitation in a trauma patient - what do you suspect?

A

cardiac tamponade

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37
Q

which HTN med is important to stop if an AKI develops?

A

any ACE-i or ARBs

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38
Q

what’s the most common cause of aortic stenosis?

A

in elderly >65 = calcification

in the young <65 = bicuspid aortic valve

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39
Q

what medications should a post- MI patient be on after discharge?

A
aspirin
clopidogrel
statin
beta blocker 
ACE-I
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40
Q

which anti-anginal medication do patients often develop tolerance to?

A

standard release isosorbide mononitrate

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41
Q

whats the MoA of statins?

A

it inhibits HMG-CoA reductase - the rate limiting enzyme in hepatic cholesterol synthesis

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42
Q

what murmur would you expect in ehlers danlos or marfans syndrome?

A

mitral valve prolapse and mitral regurgitation are associated with these collagen disorders
this would be a pansystolic murmur

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43
Q

what does clopidogrel interact with?

A

PPIs make clopidogrel less effective

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44
Q

which 3 drugs are used in anyphalaxis?

A

adrenaline, hydrocortisone and chlorphenamine (anti histamine)

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45
Q

what should we offer a stage 2 hypertensive patient with a QRISK3 of >20%?

A

statins!!!

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46
Q

what medication when combined with a macrolide antibiotic (-rythromycin) can cause rhabdomyolosis?

A

statins

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47
Q

what are ECG signs for acute pericarditis?

A
PR depression  (most specific)
widespread 'saddle shaped' ST elevations
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48
Q

what are the steps for BP management?

A

1) ACE-I or CCB
2) ACE-I and CCB
3) ACE-I and CCB and Thiazide diuretic
4) if K+>4.5 then higher dose thiazide like diuretic
if K+<4.5 then spironolactone

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49
Q

who do we usually give mechanical valves to?

A

younger patients - last longer. we give biprosthetic valves to older patients

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50
Q

when do you offer statins to BP patients/?

A

if QRISK3 is over 10%

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51
Q

what are common examination findings associated with aortic stenosis?

A
narrow pulse pressure 
slow rising pulse 
thrill over apex
4th heart sound showing LV hypertrophy 
absent/soft S2
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52
Q

What further investigations are needed for typical and atypical angina?

A

1st line: CT angiography of heart, with contrast
2nd line: Functional tests e.g. stress echo, myocardial perfusion imaging/scintigraphy(aka nuclear stress test) with PET/ SPECT
3rd line: transcatheter angiography

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53
Q

What are the first line investigations for suspected Angina?

A

1) ECG. Usually normal but may show signs of previous MI

2) Blood tests: U&Es, Lipids, FBC, HbA1C, TFTs

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54
Q

what is Eisenmengers syndrome and its pathophysiology?

A

the reversal of a left to right shunt due to pulmonary HTN and damage.

a left to right shunt exists, this leads to increased blood flow through the pulmonary system. increased pressure causes microvascular damage and irreversible pulmonary resistance. the shunt reverses, to blood moves from right to left - causing hypoxia and erythrocytosis

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55
Q

Soft s2 is seen in…

A

Aortic stenosis

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56
Q

which diuretics are responsible for hypocalcaemia?

A

loop diuretics e.g. furosemide

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57
Q

what adverse signs in bradycardia indicate treatment?

A

shock
syncope
heart failure
myocardial ischaemia

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58
Q

what is first line treatment for a massive PE?

A

thrombolysis

with immediate unfractioned heparin

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59
Q

what is classed as stage 2 hypertension?

A

clinical BP readings of 160/100

or ABPM/HBPM of 150/95 or above

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60
Q

how do you treat ventricular tachycardia?

A

amiodarone

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61
Q

Statins + erythromycin/clarithromycin - an important and common interaction. true or false?

A

TRUE
causes myopathy
raised creatinine kinase

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62
Q

how do we treat bradycardia with adverse signs?

A

immediate atropine

if this fails or there is a risk of asystole - the transvenous pacing is indicated

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63
Q

what is trifascicular block?

A

features of bifascicular block with first degree block as well

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64
Q

Chest pain causes (%)

A

25% Cardiovascular (99.9% ischaemic causes)

75% non cardiac (MS, GI, Resp)

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65
Q

what causes a rise in BNP?

A

LV hypertrophy, ischaemia, sepsis, RV overload, tachycardia, COPD, diabetes, liver cirrhosis, low GFR

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66
Q

What are symptoms of a silent MI?

A

Syncope, pulmonary oedema, Epigastric pain, vomiting, oliguira, confusion

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67
Q

a hypertensive patient with higher BP in upper limb than lower limb raises the suspicion of…

A

coarctation of the aorta - distal to the left subclavian branching off

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68
Q

what are features of Eisenmengers syndrome?

A
origional murmur may dissapear 
cyanosis 
clubbing
RV failure 
haemoptysis, embolism
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69
Q

what are the DUKEs criteria for diagnosis of infective endocarditis?

A

2 major criteria
or 1 major and 3 minor
or 5 minor

Major criteria:

1) +ve blood culture for microorganisms assoc. with infective endocarditis (e.g. Staph A)
2) evidence of endocardal involvement e.g. new valvular regurgitation or +ve echo findings

minor criteria:

1) predisposition
2) temperature
3) vascular phenomena
4) microbiological phenomena
5) immunological phenomena

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70
Q

What is the MoA of adenosine ?

A

Agonist of the A1 receptor at the AV node

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71
Q

what does CHA2DS2 VASc score measure?

A

the risk of a stroke in patients with AF and therefore the need to anticoagulate them

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72
Q

how do we manage a cardiac arrest patient in asystole?

A

CPR, checking the rhythm every 2 minutes.

giving adrenaline

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73
Q

whats dipyridamole used for and what’s its MoA?

A

its an antiplatelet used in conjunction with aspirin after a stroke or TIA
its a phosphodiesterase inhibitor

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74
Q

What are the Indications for revascularisation?

A

If 2 anti anginals are tried and do not work

Aka medical therapy is inadequate

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75
Q

which beta blockers are used in heart failure?

A

bisoprolol

carvedilol

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76
Q

what does HASBLED measure?

A

the risk of a bleed in patients being anticoagulated because of AF

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77
Q

how does 100% occlusion of LAD present on ECG?

A

ST elevation in V1-V4

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78
Q

how do we treat Long QT syndrome?

A

avoid medications which lengthen the QT interval
Beta blockers
implantable cardioverter defibs in high risk cases

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79
Q

how does dilated cardiomyopathy present on echo?

A

reduction in LVEF <55%
dilated LV
no regional wall motion abnormalities

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80
Q

why do we measure BNP and what are the normal levels?

A

B type natriuretic peptide is a hormone produced mainly by the LV in response to strain.

normal levels <100
raised levels 100-400
high levels >400

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81
Q

what is the long term damage due to hypertension?

A

end organ damage:
eyes - hypertensive retinopathy, papiloedema, cotton wool spots, hard exudate, flame haemorrhages
kidneys - hypertensive nephropathy, shrunken kidneys, damaged glomeruli
brain - hypertensive cerebrovascular disease
heart - LV hypertrophy, HF, ischaemic heart disease

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82
Q

what signs are seen on ECG in digoxin toxicity?

A

short QT
elongated PR
inverted T waves
sloping ST depression (reverse tick)

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83
Q

what is torsades de pointes

A

a rare arrythmia associated with extended QT interval. it may lead to ventricular fibrillation and sudden death

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84
Q

what is the half life of adenosine?

A

10 seconds

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85
Q

what is rheumatic fever?

A

it develops after an immunological reaction to a recent (2-6 weeks) streptococcal infection
it requires evidence of a recent strep infection with 2 major features or 1 major and 2 minor features

major: sydnehams chorea, carditis, errythema magnimeta, polyarthritis, subcutaneous nodules
minor: raised CRP/ESR, polyarthralgia, pyrexia, prolonged PR

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86
Q

what is the most common presentation for pulmonary embolus?

A

normal clinical findings - with tachypnoea and tachycardia

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87
Q

How do patients with infective endocarditis present?

A
recent fever and breathlessness
raised HR, RR, temp
decreased oxygen sats 
fatigue, collapse
low grade fever, pansystolic murmur
clinical signs of heart failure
classic peripheral signs (osler nodes, janeway lesions, splinter haemorrhages, petechia, Roth spots (haemorrhages seen in retina)
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88
Q

what is the most common cause of mitral stenosis?

A

rheumatic fever

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89
Q

what are the 4 classes of HF? (new york associates)

A
Class 1 = no limitation on ordinary activity
class 2 = mild limitation on ordinary activity 
class 3 = marked limitation on less than ordinary activity e.g. walking a short distance 
class 4 = severe limitations at rest
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90
Q

what is subclavian steel syndrome?

A

it is an occlusive disease of the subclavian, proximal to where the vertebral artery branches off. this leads to posterior circulation symptoms (vertigo and dizziness) when exerting the arm.
treating with angioplasty and stenting

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91
Q

how do we treat symptomatic aortic stenosis?

A

valve replacement

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92
Q

what dosage of adrenaline should we give for an infant, child and adult?

A

<6 years = 150 micrograms
6-12 years = 300 micrograms
>12 year = 500 micrograms

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93
Q

which drugs interact with adenosine?

A

theophyllines block its effect

and dipyridamole enhances its effect

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94
Q

What are the initial/acute managements for a STEMI ?

A
  1. Do investigations
  2. Gain IV access
  3. Give aspirin 300mg P.O. (consider ticagrelor or prasugrel)
  4. Morphine 5-10mg IV and anti-emetic (metoclopramide)
  5. Oxygen if sats <95%
  6. Restore coronary perfusion for those presenting within 12 hours of symptom onset
  7. If PCI is available within 120 mins of presentation then PCI!
  8. If not - fibrinolysis/thrombolysis
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95
Q

when do we anti coagulate AF patients?

A

Males: CHADSVASC score 1 or more
Females: CHADSVASc score of 2 or more

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96
Q

what are the clinical features of aortic stenosis

A

chest pain
dyspnoea
syncope

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97
Q

which ECG leads are inferior leads and what artery is this area supplied by?

A

leads 2, 3 and aVF

supplied by right coronary

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98
Q

Which organism is most associated with infective endocarditis after the first 2 months following a prosthetic valve replacement ?

A

Staphylococcus Aureus

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99
Q

what medication is contraindicated if atenalol is already prescribed?

A

verapamil

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100
Q

when should statins be stopped?

A

if serum transaminase levels raise to 3 times the upper limit and persist there

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101
Q

in the jugular waveform, what do the waves A C X V and Y signify?

A
A = RA contraction
C = Carotid pulse transmitted
X = RA relaXation 
V = RA filling (Villing)
Y = RA emtpYing (RV filling)
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102
Q

what % of HTN cases are due to secondary HTN?

A

10%

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103
Q

what drugs can cause QT elongation??

A

antiarythmics: sotalol, amiodarone
psychiatric drugs: TCA, SSRIs and haloperidol
antibiotics: erythromycin, clarithromycin, ciprofloxacin

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104
Q

are alcoholics at a greater risk of dilated cardiomyopathy?

A

yes

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105
Q

what is the most common cause of death following an MI?

A

cardiac arrest due to ventricular fibrillation

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106
Q

how should we manage a MI patient on the coronary care unit with type 2 diabetes?

A

stop his metformin etc and start IV insulin - tight glycaemic control post MI is very important

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107
Q

whats the MoA of aspirin?

A

inhibits production of thromboxane A2

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108
Q

how do we manage a patient in sinus tachycardia without a palpable carotid pulse?

A

this is an unshockable rhythm - manage with CPR for 2 minutes and then reassess rhythm

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109
Q

how do we manage heart failure?

A

firstly - treat fluid overload with IV loop diuretics e.g. furosemide

first line = ACE-I and BB
Second line = add an aldosterone antagonist (spironelactone) OR ARBs (-sartan) OR hydralazine in combination with a nitrate (isosorbide dinitrate)
Third line = if symptoms persist - cardiac resynchronisation therapy or digoxin.
ivabradine can be used as an alternative

all patients should have yearly influenza vaccinations and a one-off pneumococcal vaccine

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110
Q

following a PCI, what is the law in regards to driving and the DVLA?

A

a private vehicle owner should wait 4 weeks before driving again but does not have to notify the DVLA
a group 2 vehicle driver (bus or lorry) must notify the DVLA and not drive for 6 weeks. he then must meet assessment criteria before having his license reinstated

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111
Q

what is a widened pulse pressure?

A

larger difference between the systolic and diastolic pressures
can be caused by exercise

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112
Q

what is the target INR for patients with VTE disease?

A

2.5 and 3.5 if recurrent

113
Q

when do we administer synchronised DC shocks for a patient in tachycardia?

A
if the patient is 'unstable'
meaning they have:
-symptoms of shock (systolic BP<90), sweaty, pallor
- heart failure 
- myocardial ischaemia
- syncope
114
Q

What further investigations are needed in a patient presenting with typical angina and a history of IHD?

A
  1. Treat as stable angina

2. If needed - use non invasive testing e.g. exercise testing

115
Q

in treating ventricular fibrillation, what is the correct initial dose of amiodarone?

116
Q

how is aortic dissection classified?

A

stanford A = in ascending aorta (2/3 cases)

stanford B = in descending aorta, distal to the left subclavian

117
Q

What are the key coronary artery branches

A
Right marginal 
Right posterior descending 
Left marginal
Left anterior descending
Left circumflex
118
Q

how is AF secondary to a chest infection treated?

A

if the cause is reversible then only rhythm control is indicated - whilst the underlying cause is treated

119
Q

what’s the first line of investigation in a patient with suspected heart failure?

A

in a patient without a previous MI: measure serum BNP, (B-type natriuretic peptide) if BNP is raised then Echo

in a patient with a previous MI: Echo within 2 weeks,

120
Q

a patient develops complete heart block post- MI. which coronary artery was likely to have been affected?

A

right coronary artery

the AV node is supplied in most people, by a branch of the RCA (posterior interventricular artery)

121
Q

How do we manage Angina?

A

1) address exacerbating factors (anaemia, thyrotoxicosis)
2) secondary prevention of CVD: smoking cessation, Aspirin 75mg OD, statin for hypercholesterolemia, consider ACE-I.
3) PRN relief : GTN spray/sublingual tabs
4) anti-anginal medication:
1st line: Beta blocker (bisoprolol) +/ Calcium channel blocker (amlodopine)
(Do NOT combine a BB with a non-dihydropyridine CCB e.g. verapamil/diltiazem)
2nd line: Isosorbide mononitrate, nicorandil, ivabradine, ranolazine
Last resort: Revascularisation (PCI or CABG)

122
Q

Causes of myocardial ischaemia

A
Coronary artery disease - atherosclerosis 
Aortic stenosis 
Hypertrophic cardiomegaly 
Anaemia 
Thyrotoxicosis 
Tachyarrythmias
Cocaine use
123
Q

what is an acute exacerbation of HF?

A

sudden onset of symptoms of HF, with or without previous CVD

showing clinical signs of decreased CO, tissue hypoperfusion, increased pulmonary pressure, fluid overload

124
Q

how do we manage a warfarin patient whos INR is 5-8?

A

if there is no bleeding - withhold 2 warfarin doses and continue at a lower dose
if there is minor bleeding, stop warfarin and give IV vitamin k (1-5mg). restart when INR<5

125
Q

how are tachycardias classified?

A

broad complex tachys (AKA arising in the ventricles)

  • ventricular tachycardia
  • ventricular fibrilation
  • torsades de pointes (polymorphic VT)
  • OR a Supraventricular tachy with a BBB

narrow complex tachy (Supraventricular tachycardia)

  • sinus tachycardia
  • atrial tachycardia
  • atrial fibrillation
  • atrial flutter
  • reentrant tachycardia
126
Q

how do we monitor statin use?

A

LFTS at baseline, 3,and 12 months

Statins may cause liver damage

127
Q

what are the indications for loop diuretics?

A

Heart failure

and resistant hypertension

128
Q

what is first line investigation for a patient with renal failure and suspected PE?

A

a ventilation/perfusion scan

we avoid CTPA because of the contrast (renal failure)

129
Q

what’s constrictive pericarditis commonly associated with?

130
Q

what would you suspect when a patient with CLL presents with burning lower chest pain?

131
Q

what can cause Left sided HF?

A
ANYTHING DECREASING STROKE VOLUME:
long term hypertension leading to hypertrophy 
dilated cardiomyopathy 
ischaemic heart disease
valvular disease 
ANYTHING DECREASING PRELOAD:
hypertrophic cardiomyopathy
restrictive cardiomyopathy
long term hypertension causing hypertrophy 
aortic stenosis causing hypertrophy
132
Q

what murmur would you expect to hear in an IV drug user?

A

a tricuspid regurgitation murmur
IV drug users are at a high risk of right sided cardiac valvular endocarditis
triccuspid regurg sounds like tricuspid valve endocarditis

133
Q

what is normal correct QT interval?

A

<430 in males

<450 in females

134
Q

what is Boerhaave syndrome?

A

transmural perforation of the oesophagus

135
Q

what is the mackler triad for boerhaave syndrome?

A

vomiting
thoracic pain
subcutaneous emphysema

136
Q

what are the criteria for ivabradine use in HF?

A
  • patient already on suitable medication (ACEI, BB and Aldosterone antagonist)
  • heart rate >75
  • ejection fraction <35%
137
Q

what ECG changes are present with RBBB?

A

wide QRS complex >120ms
rSR pattern in leads V1-3 (M)
slurred, wide S wave in lateral leads (aVL, V5, V6)

138
Q

what Is the most appropriate first-line anti-anginal for stable angina in a patient with known heart failure, if there are no contraindications

139
Q

what are the systemic effects of angiotensin 2?

A

increases SNS activity
causes aldosterone release from adrenal glands
causes increased ADH release from hypothalamus
arterial vasoconstriction
H2O retention, NaCl absorption, K excretion

140
Q

what BP is classified as a hypertensive emergency (malignant hypertension)?

A

systolic>210

diastolic>130

141
Q

when is only rhythm control used to treat AF?

A

if there is coexist heart failure
first onset AF
obvious reversible cause

142
Q

what are some causes for secondary HTN??

A

renovascular disease: diffuse atherosclerosis, unilateral small kidney
renal disease: diabetic nephropathy, glomerularnephritis, chronic nephritis, polycyistic kidney disease

primary aldosteronism 
cushings syndrome 
pheochromocytoma
NSAIDs
oral contraceptives
drugs/stimulants 
antidepressants
hypothyroidism 
primary hypoparathyroidism 
sleep apnoea
coarction of the aorta
143
Q

how do we treat isolated systolic HTN?

A

the same way as we treat standard HTN

144
Q

is there an association between marfans and pneumothorax?

145
Q

what are the contraindications for thrombolysis?

A

recent haemorrhage, bleeding disorder, stroke in past 3 months, intracranial neoplasm, severe hypertension, pregnancy, active internal bleeding, recent trauma

146
Q

how do we diagnose HF?

A

first line investigation is serum BNP. if this is raised we arrange for a transthoracic echo within 2-6 weeks (depending on the level)
if the patient has had a previous MI, we do not wait for BNP but book an echo within 2 weeks.

147
Q

what is coarction of the aorta?

A

it is a congenital narrowing of the descending aorta.
it is more common in males
it is associated with bicuspid aortic valves, turner syndrome, berry aneurysms and neurofibromitosis

148
Q

What are the 4 classes of Angina?

Canadian Cardiology Society

A

Class 1 - angina with strenuous/ prolonged exertion
Class 2 - slight limitation of ordinary daily activities. Able to walk 2 blocks/ climb 1 flight of stairs without angina.
Class 3 - marked limitation of ordinary daily activities - unable to walk 2 blocks/ climb 1 flight of stairs.
Class 4 - unable to do any physical activity without discomfort. Angina may be at rest.

149
Q

what 3rd agent should you had to a hypertensive patient who’s already on an ACE-I and CCB?

A

a thiazide-like diuretic

e.g. indapamide or chlortalidone

150
Q

what tests are important prior to starting oral amiodarone treatment?

A

CXR - because of the risk of pulmonary fibrosis

U and E - potassium levels may increase risk of arrhythmias

151
Q

what are causes for torsades de pointes?

A

a rare arrythmia associated with long QT - may deteriorate to ventricular fibrillation
causes of long QT include: subarachnoid haemorrhage, hypothermia, myocarditis, hypo-calcaemia/kalaemia/magnesium, TCAs, antipyschotics, erythromycin,

152
Q

what medication do we use to rate control AF in an asthmatic patient?

A

NOT a beta blocker! contraindicated

use a CCB = diltiazem

153
Q

how does aortic dissection present?

A

it presents very similarly to a myocardial infarction. sudden onset, severe, central chest ripping/tearing pain, that radiates into back and down arms

154
Q

how do we investigate suspected aortic stenosis

A

transthoracic echo followed by a more invasive transoesophageal echo in more severe cases.

155
Q

how do we treat a post-MI patient who now develops AF?

A

switch from antiplatelets (aspirin and clopidogrel) to an oral anticoagulant (e.g. warfarin or apixaban)

156
Q

what are the classic ECG changes in a pulmonary embolism?

A

S1Q3T3
big S wave in lead 1
large q wave in lead 3
inverted t wave in lead 3

157
Q

what CCB should be used in conjunction with a BB in management of stable angina?

A

a long acting dihydropyridine e.g. nifedipine

158
Q

which ECG changes point to myocardial ischaemia?

A

hyperacute T waves
ST elevation
pathological Q waves
T wave inversion

159
Q

explain the Frank-Starling Law

A

this law describes the relationship between the Stroke Volume and the End Diastolic Volume. the larger the EDV, the bigger the contraction and therefore the bigger the SV. Simply, the more you put in, the more that comes out. untill a certain point where no matter how much you increase the EDV, the heart is unable to contract with enough force to maintain the SV.

in a failing heart, there is decreased contractility. this means the curve shifts to the right - downwards. so to reach the same SV, you need a much higher end diastolic pressure and more powerful contractions

160
Q

how long do you have to wait before administering a second dose of adrenaline in an anaphylactic patient?

161
Q

what are the features of ostium secondum?

A

thrombi can pass through the atrial septal defect in the left heart and cause a stroke
ECG shows RBBB with RAD
50% mortality by age 50

162
Q

when can ivabradine not be used?

A

if the patient is NOT in sinus rhythm e.g. has AF

163
Q

whats doses of chlorphenamine should be given in anaphylaxis?

A

<6 months 25 micrograms
6 months - 6 years 2.5 mg
6-12 years 5 mg
>12 years 10 mg

164
Q

what factors can falsely lower BNP levels?

A

ACE-I, ARBs, BBs, diuretics

165
Q

what is HOCM?

A

hypertrophic obstructive cardiomyopathy
an autosomal dominant disease, 1:500
a genetic mutation causing problems with contractile proteins

166
Q

what are side effects of nitrates?

A

hypotension
headaches
tachycardia
flushing

167
Q

what dermatological side effects are associated with Warfarin?

A

skin necrosis

168
Q

what does of adrenaline should be given in a cardiac arrest?

169
Q

how do you differentiate between aortic stenosis and aortic sclerosis?

A

in aortic sclerosis there is no radiation to the carotids and the ECG is normal

170
Q

how do we treat AF, post stroke?

A

2 weeks 300 mg aspirin

lifelong anticoagulation - warfarin is preferred

171
Q

when should clopidogrel be stopped before an elective surgery?

A

7 days before

172
Q

what are the limitations to amiodarone?

A

long half life: 20-100 days
best given through a central vein: there’s a risk of thrombophlebitis
interacts with commonly used drugs e.g. warfarin
long list of long term adverse effects
lengthens the QT interval (proarrythmic effect)

173
Q

what is Wolff Parkinson White

A

a congenital accessory conduction pathway between atria and ventricle (can be right or left sided)
can cause AF which degenerates into VF

174
Q

what is the first line treatment for supraventricular tachy?

A

valsalva manouvre

175
Q

what are the ECG features of Wolff Parkinson White (WPW)

A

short PR duration
delta waves - slurred upstroke after QRS
wide QRS

176
Q

what are side effects of loop diuretics?

A

ototoxicity, hyponatraemia, hypokalaemia, hypotension, hypochloraemic alkalosis

177
Q

in AF treatment, when do we use amiodarone over flecanide?

A

if the patient has structural disease of the heart

178
Q

ATYPICAL ANGINA features

A

2 of the following 3 features present:

1) central constricting CP, radiating to shoulder, jaw, neck
2) precipitated by exertion
3) relieved by rest or GTN within 5 mins

179
Q

describe a mitral stenosis murmur

A

mid-late diastolic murmur, best heard on expiration

180
Q

what are complications of malignant hypertension?

A

target organ damage:
Brain - stroke, haemorrhage, encephalopathy
myocardium - damage, HF (common)
kidneys - renal insufficiency, failure

181
Q

what is an Austin-Flint murmur?

A

a Mid-end diastolic murmur, signifying severe aortic regurgitation

182
Q

what are side effects of Bendroflumethiazide?

A

hyponatraemia

hypokalaemia

183
Q

what ECG changes are an indication for urgent thrombolysis or PCI?

A

> 2mm ST elevation in 2 consecutive anterior leads (V1-V6)
OR
1mm ST elevation in 3 or more consecutive inferior leads (2,3 aVF or aVL)
OR
New LBBB

184
Q

what are causes for LBBB?

A
ischaemic heart disease
cardiomyopathy 
hypertension 
aortic stenosis
rarely: idopathic fibrosis, digoxin toxicity, hyperkalaemia
185
Q

what antihypertensive first line medication do we give to a diabetic patient who’s over 55?

A

an ACE-I

if he wasn’t diabetic, we would try a CCB

186
Q

Describe the procedure of Percutaneous coronary intervention (PCI)

A
  • a balloon is inflated in the stenosed vessel and usually a stent is left in place to prevent restenosis
  • accessed via brachial/radial/femoral artery
  • very cost effective
  • dual platelet therapy (aspirin and clopidegrol) is recommended for 12 months post PCI
  • best for young uncomplicated patients - CAD of 1 or 2 vessels, not involving the LAD and no diabetes
187
Q

what are the features of constrictive pericarditis

A

dyspnoea
right heart failure ( raised JVP, oedema, hepatomegaly, ascies)
positive kussmuls sign (paradoxical raising of JVP on inspiration)
pericardial knock - S3
prominent X and Y descents on JVP waveform

188
Q

how do we treat atrial fibrillation?

A

if onset is less than 48 hours, consider chemical or electrical cardioversion to return to normal sinus rythm
if cardioversion is NOT an emergency - ensure patient has been anticoagulated for 3 weeks prior to cardioversion. (with heparin)
OR just control the heart rate with beta blockers, CCBs and digoxen (and anticoagualation )

189
Q

what is a stokes adam attack?

A

sudden collapse into unconsciousness due to a heart arrhythmia

190
Q

what is the mechanism of action of loop diuretics?

A

act on the Na-K-Cl cotransporter in the thick ascending loop of Henle - to prevent the reabsorption of NaCl

191
Q

Musculoskeletal causes of CP

A

Costochondritis

Herpes zoster - shingles

192
Q

which murmur is a ventricular septal defect associated with?

A

pansystolic

193
Q

can warfarin be used when breast feeding?

194
Q

how does a patient with ventricular fibrillation present?

A

unconscious

v fib does not produce a cardiac output

195
Q

What are the differential diagnoses for suspected ACS?

A

Stable angina, pericarditis, myocarditis, aortic dissection, PE, pneumothorax, GORD, pancreatitis, musculoskeletal pain

196
Q

what drug is eptifibatide?

A

glycoprotein 2b/3a receptor antagonist

197
Q

what is the traid for atrial myxoma?

A
mitral valve obstruction 
systemic embolisation (stroke)
constitutional symptoms e.g. weightloss, breathlessness, fever
198
Q

how does a patient with acute pericarditis present?

A
pleuritic chest pain - relieved by sitting forward 
tachypnoea, tachycardia
flu-like symptoms 
non-productive cough, dyspnoea
pericardial rub
199
Q

What are the risk factors for developing CAD? (And IHD)

A
Age 
Male 
Hypertension 
Diabetes 
Hypercholesterolemia 
Obesity 
Smoking
200
Q

what condition is associated with a double systolic pulse beat (bisferiens beat)?

201
Q

what does the RAAS contribute in HF?

A

in left sided HF, decreased perfusion of the kidneys leads to activation of the RAA system, this leads to water retention (and low sodium) - leading to fluid overload.

202
Q

how do we test if a reaction was due to anaphylaxis?

A

measure serum tryptase levels

these can be elevated for 12 hours post reaction

203
Q

How do you initially manage suspected non- STEMI?

A

Assess and investigate

If sats low, oxygen 
Morphine and antiemetic 
Aspirin 300mg 
GTN spray 
Fondaparinux (or unfractioned heparin for those who may undergo PCI within 24 hours)

Use GRACE score to determine risk.

As soon as risk has been assessed, offer a loading dose of Ticagrelor/clopidogrel (in combo with aspirin) (recommended for 12 months for those with NSTEMI Or hospital admittance with unstable angina.)

204
Q

What are the signs of ACS?

A

Anxiety, distress, pallor, sweatiness
Raised or lowered pulse or BP
May be signs of HF or pan-systolic murmur
4th heart sound
Later there may be signs of pericardial rub or peripheral oedema

205
Q

which ACS patients do we give a glycoprotein receptor antagonist to?

A

those who have a high GRACE score (intermediate to high risk) and who are set to have an angiography within 96 hours of hospital admission

206
Q

what are side effects of ACE -inhibitors?

A

cough, angioedema (may begin during year after starting), first dose hypotension, hyperkalaemia

207
Q

What is the MoA of amiodarone

A

Blocks potassium channels

208
Q

what medication is bosentan ?

A

an endothelin-1 receptor antagonist. used to treat pulmonary hypertension

209
Q

what is a common side effect of ticagrelor?

A

breathlessness (described as air hunger) - sudden onset and episodic
present in 10-20%

210
Q

how do thiazide diuretics work?

A

they inhibit sodium reabsorption in the beginning (proximal part) of the distal convoluted tube (DCT)

211
Q

what is bifascicular block?

A

RBBB with left anterior or posterior hemiblock e.g. left axis deviation

212
Q

What does primary PCI involve?

A

Angiographic detection of the disease coronary artery and deployment of a metallic stent to reduce the narrowing.
Recommended for all patients who can be transferred to a primary PCI centre within 120 mins of first medical contact (who present within 12 hours of symptom onset and STEMI)

Anticoagulation must be used in all PCI. e.g. bivalirudin (direct thrombin inhibitor)

Patients who don’t receive PCI should be given fondaparinux or enoxaparin (heparin)

213
Q

what MoA is clopidogrel etc?

A

adenosine diphosphate inhibitor (ADP)

214
Q

which heart rythms are shockable rhythms in a situation of cardiac arrest?

A

ventricular fibrillation and ventricular tachycardia

215
Q

what are BP targets for diabetic patients?

A

<130/80 if renal disease
othewise
<140/80

216
Q

Describe Coronary artery bypass grafting CABG

A

Veins/ arteries are harvested and anastomosed to the ascending aorta and then to the coronary arteries, distal to the stenosed region.
Best outcome for complicated and multi vessel disease and less need for repeat revascularisation compared to PCI
But the very invasive surgery means more risky, slower recovery and patients left with 2 large scars: sternal and vein harvesting.

217
Q

in resuscitation, how do we manage shockable rhythms?

A

(Shockable rhythms include pulseless VT and VF)

immediate CPR and then defibrillate as soon as possible. continue CPR whilst defibrillator is charging

if pVT/VF persists, give 1mg IV adrenaline and 300mg amiodarone IV

218
Q

Respiratory Causes of CP

A

PE
Pneumothorax
Pleurisy
Pneumonia

219
Q

what is pulmonary hypertension?

A

when pulmonary pressure is >25 at rest or >30 when exercising.
it causes progressive SOB and cyanosis.
common in females, ages 20-40

220
Q

what ECG signs are seen in hypokalaemia?

A

U waves
absent T waves
long QT and PR

221
Q

do we give adenosine to asthmatics?

A

NO it is contraindicated

instead give verapamil

222
Q

what is the most common ECG finding in a patient with pulmonary embolism?

A

sinus tachycardia

223
Q

how many doses of adenosine do we give when treating supraventricular tachycardia?

A

6mg then 6mg then 12mg

224
Q

what is wellens syndrome?

A

ECG sign: deep arrowhead inversion of T waves in anterior leads
associated with myocardial ischaemia

225
Q

what are causes of a 3rd heart sound?

A

failure of LV e.g. dilated cardiomyopathy, mitral regurg and constrictive pericarditis

226
Q

What ECG changes indicate a STEMI?

A

> 1mm ST elevation in both leads 2 and 3

Or new LBBB

227
Q

what is the mechanism of action of thrombolytic drugs?

A

they activate plasminogen to form plasmin. plasmin then breaks down fibrin which breaks down the clot/thrombi

228
Q

when do we treat hypertension?

A

1) stage 1 hypertension in under 80 YO patient with one of the following:
- established target organ damage
- diabetes
- CVD
- renal disease
- 10 year CVD risk of 20%+
2) or stage 2 hypertension`

229
Q

How do we calculate a HAS BLED score?

A
Hypertension 
Abnormal liver/renal 
Stroke
Bleeding history/disorder
Labile INR (unstable)
Elderly >65
Drugs which increase risk of bleeding/alcohol 

a score of 3 means high risk.

230
Q

how do you identify a Graham Steell murmur and what does it indicate?

A

it is a high-pitched, early distolic murmur, best heard in the 2nd ICS at the Left sternal edge. during inspiration

it is associated with pulmonary regurgitation (which goes on to cause cor pulmonale)

231
Q

how does HOCM present?

A

in young
mostly asymptomatic
chest pain, breathlessness, syncope
sudden death (arrythmias, heart failure) - mostly due to ventricular arrythmias
jerky pulse, double apex beat
ejection systollic murmur
ECG changes (LV hypertrophy, deep Q waves, progressive T wave inversion)

232
Q

how do we manage a PE?

A

give LMWH or fondaparinux straight away (or unfractioned heparin if thrombolysis is being considered for a massive PE)
start warfarin within 24 hours
continue LMWH/fondaparinux for 5 days or until INR is 2 for 24 hours
warfarin should be continued for 3 months and then reassess for risk
cancer patients should be on 6 months
usually unprovoked PE patients will continue beyond 3 months

233
Q

what type of bacteria commonly cause endocarditis?

A

gram positive cocci

234
Q

what are common ECG findings for atrial flutter?

A

saw tooth appearnce
multiple atrial deplarisations with a ventricular depolarisation
depends on the amount of AV block, what atrial:ventricular ratio is

235
Q

if ACE inhibitors are not tolerated, what medication should you use?

A

angiotensin receptors blockers
‘sartans’
e.g. losartan

236
Q

what are the rules re- driving post- MI?

A

can’t drive for 4 weeks post-MI

237
Q

what are fusion and capture beats on ECG associated with and what are they?

A

ventricular tachycardia
fusion beats = a complex beat made from an atrial and ventricular signal occurring simultaneously and acting on the ventricles.
capture beats = a supra-ventricular signal seen amongst beats showing AV dissociation. an attempt of the atria to regain control of the ventricles.

238
Q

GI Causes of CP

A

GORD
gall stones
Peptic ulcers
Pancreatitis

239
Q

what is the most important cause of ventricular tachycardia clinically?

A

hypokalaemia

and hypopmagnesemia

240
Q

how are Ambulatory BP measurements carried out?

A

2 measurements are taken every hour during the patients waking hours
it is worn for 7 days
an average is taken of at least 14 measurements

241
Q

an inferior STEMI and aortic regurgitation raise suspicions of what?

A

ascending aortic dissection

242
Q

what will the pulse of a patient with heart failure be like?

A

pulsus alternans

the upstroke varies between strong and weak - signifying systolic dysfunction

243
Q

Prinzmetal Angina/ variant angina/ coronary vasospasm definition

A

Angina that occurs without provocation, at rest, due to coronary artery spasm
Occurs mainly in women
ST elevation seen on ECG during pai.

244
Q

how is malignant HTN managed?

A

in intensive care unit

with IV BP meds e.g. vasodilators, beta blockers, CCB

245
Q

Acute coronary syndrome is an umbrella term for…

A

Unstable angina
Non STEMI
STEMI

246
Q

Classic ischaemic CP symptoms

A
Gripping, heavy, tight pain
Central, retrosternal pain 
Ranging from mild to severe
Radiates to left shoulder, neck, jaw 
Associated with nausea, sweating, breathlessness, fear
247
Q

what are the symptoms of severe HTN? (>180 systolic or >110 diastolic)

A

headaches, nosebleed, SOB, severe anxiety

248
Q

what decreases the effects of warfarin?

A

anything which induces the P450 enzymes. e.g. phenobarbitone, St. Johns wort

249
Q

what are the stages of hypertension?

A

Stage 1 = clinical reading >140/90, ABPM >135/85
Stage 2 = clinical reading >160/100, ABPM >150/95
Severe HTN = stystolic >180, diastolic >110

250
Q

what is the QT region?

A

from start of Q wave to end of T wave

251
Q

3 features of TYPICAL ANGINA PECTORIS

A
  1. Constricting discomfort in centre of chest radiating to shoulder, neck, jaw
  2. Precipitated by physical activity, made worse after a meal, with cold weather or heightened emotions
  3. Relieved by rest or GTN spray- within 5 minutes
252
Q

what is the long term treatment for AF post-stroke?

A

anticoagulation with warfarin or another anticoagulant e.g. apixaban

253
Q

why do we measure CK-MB?

A

to test for reinfarction
troponins remain raised for 10 days
CK-MB returns to normal after 2 days

254
Q

what is the target BP for type 2 diabetics?

A

<130/80 if they have end organ damage e.g. retinopathy

<140/80 in other cases

255
Q

can you use ACEI or ARBs in pregnancy?

256
Q

how do we treat a regular narrow complex tachycardia?

A

vagal manouevers (e.g. carotid sinus massage) followed by IV adenosine - first 6 mg, followed by 12 mg if no response and a further 12mg.

257
Q

when do we send a patient with CP to hospital under emergency admission?

A

CP within past 12 hours with abnormal ECG

258
Q

what is QRISK3?

A

an assessment tool to calculate the risk of CVD over a 10 year period
(if it is 20% or more, treatment for stage 1 HTN is indicated)

259
Q

How do we manage high risk NSTEMI patients? (After initial management)

A

Consider glycoprotein inhibitors e.g. eptifibatide or tirofiban in combination with a heparin

Offer coronary angiography (with PCI if indicated) within 96 hours of admission if no contraindications and patient has moderate to severe risk of CV incidence.

Patients should be placed on cardio protective medication: statins, beta blockers/CCB, ACE-I etc. If needed

260
Q

In what situations do we offer Atorvastatin 20mg to Type 1 diabetic patients?

A
  • if they are over 40
  • had diabetes for >10 years
  • have established nephropathy
  • have other CVD risk factors (obesity or HTN)
261
Q

how do we treat torsades des pointes?

A

IV magnesium sulphate

262
Q

how are proximal aortic dissections generally managed?

A

aortic root replacement

263
Q

what are the preferred rate control drugs in AF patients?

A

Beta blockers
then maybe a CCB
digoxin (no longer first line)

264
Q

what are the symptoms of malignant hypertension?

A

SOB, CP, weakness, difficulty speaking, numbness, back pain, change in vision

265
Q

what is the first line investigation for suspected mitral stenosis?

A

echocardiography

266
Q

what kind of murmur does aortic regurgitation produce?

A

early diastolic murmur

267
Q

what is the target BP for treated hypertension ?

A

<140/90 in patients under 80

268
Q

why are troponins raised in sepsis?

A

inadequate perfusion leads to ischaemie of cardiac tissue and so release of troponins
this can be called type 2 MI
other causes include anaemia, heart failure, rate-releated ischaemia

269
Q

how do we manage a patient on warfarin with a major bleed?

A

stop warfarin
give IV vitamin K
give prothrombin complex concentrate (or FFP if unavailable)

270
Q

Which organism is most associated with infective endocarditis in the first 2 months following a prosthetic valve replacement ?

A

Staphylococcus epidermis

271
Q

what’s the mechanism of action of fondaparinux?

A

it activates prothrombin 3 which then potentiates the inactivation of clotting factor Xa
it acts the same as LMWH (enoxaparin)

272
Q

how do we manage a post- PE patient whos INR is <2?

A

increase warfarin dose and give rapid acting LWMH

273
Q

what are names of thrombolytic drugs

A

tenecteplase
alteplase
streptokinase

274
Q

in what respiratory conditions do we find a respiratory alkalosis patter in ABGs?

A

pulmonary embolism, asthma and pneumonia

due to hyperventilation

275
Q

when do we offer ABPM? (or HBPM)

A

if the clinical BP reading is over 140/90

276
Q

what does CHA2DS2 VASc measure and what does it stand for?

A

it measures the risk of a patient with AF having a stroke. do we need to anticoagulate?

congestive heart failure 1
hypertension 1
age >75 2
diabetes 1
stroke/TIA 2

Vascular disease 1
Age 65-75 1
Female 1

277
Q

What are the main types of cardiovascular disease

A

Coronary heart disease
Stroke
Peripheral arterial disease

278
Q

what drug is tirofiban?

A

glycoprotein 2b/3a receptor antagonist

279
Q

when can an anaphylactic patient by discharged?

A

after observation for 6-12 hours. a reaction can be biphasic