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Medicine and Surgery Mushkies > Passmed Cardiology Mushkies > Flashcards

Passmed Cardiology Mushkies Flashcards

1
Q

How can you classify management of VT?

A
  1. Haemodynamically stable –> amiodarone through a central line (2nd line = lidocaine (use with caution in severe LV impairment)/procainamide)
  2. Haemodynamically unstable –> Synchronised DC cardioversion
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2
Q

What are some causes of orthostatic hypotension?

A
  1. Exercise-induced
  2. Postprandial
  3. Prolonged bed rest (decondiitoning)
  4. Primary autonomic failure
  5. Secondary autonomic failure
  6. Drug induced = diuretics, alcohol, vasodilators
  7. Volume depletion = haemorrhage, diarrhoea
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3
Q

What are some causes of primary autonomic failure?

A
  1. Parkinsons

2. LBD

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4
Q

What are some causes of secondary autonomic failure?

A
  1. Diabetic neuropathy
  2. Amyloidosis
  3. Uraemia
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5
Q

How can syncope be defined?

A

Transient loss of consciousness due to global cerebral hypoperfusion with rapid onset

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6
Q

How can you classify the causes of syncope?

A
  1. Reflex (neurally mediated)
  2. Orthostatic
  3. Cardiac
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7
Q

What are come causes of reflex syncope?

A
  1. Vasovagal (emotion/pain/stress)
  2. Situational (cough, micturition, GI)
  3. Carotid sinus
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8
Q

What are some causes of cardiac syncope?

A
  1. Arrhythmias (bradycardias/tachycardias)
  2. Structural = valvular, MI, HOCM
  3. Other = PE
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9
Q

How does one diagnose a postural drop?

A
  1. A symptomatic fall in systolic BP >20mmHg or diastolic BP >10mmHg
  2. Decrease in systolic Bp to <90mmHg
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10
Q

What are some investigations for syncope?

A
  1. Examination
  2. BP lying and standing
  3. ECG (+/- 24hrs)
  4. Echo
  5. Tilt table test
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11
Q

What is the management for VF/pulseless VT?

A
  1. Defib 150J ASAP
  2. Compressions 30:2 for 2 minutes
  3. Defib 150J ASAP
  4. Compressions 30:2 for 2 minutes
  5. Defib 150J ASAP + 1mg adrenaline + 300mg amiodarone
  6. Afterwards, adrenlaine should be given after every other shock and 2nd dose of amiodarone considered after a total of 5 defib attempts
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12
Q

What is the management of VF/pVT in a CCU/cathlab?

A

3 successive shocks, if 3rd is unsuccessful then CPR should be initiated

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13
Q

What has to be given ASAP after diagnosis of asystole/PEA (non-shockable rhythms)?

A

Adrenaline 1mg

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14
Q

What should resus oxygen be after successful resuscitation and why?

A

Titrated to sats 94-98% to address potential harm caused by hyperoxaemia

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15
Q

What are the 4Hs of reversible causes of cardiac arrest?

A
  1. Hypoxia
  2. Hypovolaemia
  3. Hypothermia
  4. Hypo/hyperkalaemia, hypoglycaemia, hypocalcaemia, acidaemia
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16
Q

What are the 4Ts of reversible causes of cardiac arrest?

A
  1. Thrombosis (coronary/pulmonary)
  2. Tension pneumothorax
  3. Tamponade
  4. Toxins
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17
Q

What is a definition for VT?

A

A broad-complex tachycardia originating fro a ventricular ectopic focus

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18
Q

What are the 2 main types of VT?

A
  1. Monomorphic = most commonly causes by MI

2. Polymorphic VT = e.g. torsades de pointes

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19
Q

What are 4 normal ECG variants in an athlete?

A
  1. Sinus bradycardia
  2. Junctional rhythm
  3. 1st degree heart block
  4. Wenckebach phenomenon
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20
Q

What does a posterior MI show on ECG?

A

Tall R waves in V1-V2

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21
Q

What is an ECG feature of cardiac tamponade?

A

Electric alternans

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22
Q

When should a pt who has had an acute ischaemic stroke have anticoagulation therapy started?

A

2 weeks after the event, due to the risk of haemorrhagic transformation

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23
Q

What is Eisenmenger’s syndrome?

A

The reversal of a left-to-right shunt

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24
Q

What is the management of a sinus bradycardia in a pt who is showing adverse signs (shock/syncope/MI/HF)?

A
  1. 500mg IV atropine
  2. If above fails –> atropine up to 3mg
    a. Transcutaneous pacing
    b. isoprenaline/adrenaline infusion titrated to response
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25
Q

What are 2 indications for loop diuretics?

A
  1. HF (acute and chronic)

2. Resistant HTN

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26
Q

What medication used to treat HF can cause hearing loss?

A

Loop diuretics e.g. furosemide can cause ototoxicity

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27
Q

What is an example of Glycoprotein IIa/IIIb receptor antagonists used for the tx of NSTEMI?

A

Tirofiban

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28
Q

When should fondaparinux be offered in NSTEMI?

A

Patients who are not at a high risk of bleeding and who are not having angiography within the next 24 hours

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29
Q

When should unfractionated heparin be offered in NSTEMI?

A

If angiography is likely within 24 hours or a patients creatinine is > 265 µmol/l unfractionated heparin should be given

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30
Q

What antiplatelet is now preferred instead of clopidogrel in NSTEMI?

A

Ticagrelor

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31
Q

When should IV glycoprotein IIb/IIIa receptor antagonists be given in NSTEMI?

A

Patients who have an intermediate or higher risk of adverse cardiovascular events (predicted 6-month mortality above 3.0%), and who are scheduled to undergo angiography within 96 hours of hospital admission.

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32
Q

What is the investigation of choice for PE in a pt with renal impairment?

A

V/Q scan due to nephrotoxicity of contrast media

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33
Q

What is the management for a PE depending on the Wells’ score?

A
  1. If a PE is ‘likely’ (more than 4 points) arrange an immediate computed tomography pulmonary angiogram (CTPA). If there is a delay in getting the CTPA then give low-molecular-weight heparin until the scan is performed.
  2. If a PE is ‘unlikely’ (4 points or less) arranged a D-dimer test. If this is positive arrange an immediate computed tomography pulmonary angiogram (CTPA). If there is a delay in getting the CTPA then give low-molecular-weight heparin until the scan is performed.
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34
Q

What are the ECG changes typically seen with PE?

A
  1. S1Q3T3
  2. RBBB and RAD
  3. Sinus tachycardia
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35
Q

What is the gold standard investigation for PE?

A

Pulmonary angiography

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36
Q

What is the MOA of furosemide?

A

Inhibits the Na-K-Cl cotransporter in the thick ascending limb of the loop of Henle

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37
Q

What are some causes of S3?

A
  1. Normal < 30y/o
  2. DCM
  3. Constrictive pericarditis
  4. Mitral regurgitation
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38
Q

What are some causes of S4?

A
  1. AS
  2. HOCM
  3. HTN
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39
Q

How does one manage T2DM in the immediate period following an MI?

A

IV insulin infusion

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40
Q

Rogue mushkie boi

A

Myocardial infarction: STEMI management

A number of studies over the past 10 years have provided an evidence for the management of ST-elevation myocardial infarction (STEMI)

In the absence of contraindications, all patients should be given
aspirin
P2Y12-receptor antagonist. Clopidogrel was the first P2Y12-receptor antagonist to be widely used but now ticagrelor is often favoured as studies have shown improved outcomes compared to clopidogrel, but at the expense of slightly higher rates of bleeding. This approached is supported in SIGN’s 2016 guidelines. They also recommend that prasugrel (another P2Y12-receptor antagonist) could be considered if the patient is going to have a percutaneous coronary intervention
unfractionated heparin is usually given for patients who’re are going to have a PCI. Alternatives include low-molecular weight heparin

NICE suggest the following in terms of oxygen therapy:
do not routinely administer oxygen, but monitor oxygen saturation using pulse oximetry as soon as possible, ideally before hospital admission. Only offer supplemental oxygen to:
people with oxygen saturation (SpO2) of less than 94% who are not at risk of hypercapnic respiratory failure, aiming for SpO2 of 94-98%
people with chronic obstructive pulmonary disease who are at risk of hypercapnic respiratory failure, to achieve a target SpO2 of 88-92% until blood gas analysis is available.

Primary percutaneous coronary intervention (PCI) has emerged as the gold-standard treatment for STEMI but is not available in all centres. Thrombolysis should be performed in patients without access to primary PCI

With regards to thrombolysis:
tissue plasminogen activator (tPA) has been shown to offer clear mortality benefits over streptokinase
tenecteplase is easier to administer and has been shown to have non-inferior efficacy to alteplase with a similar adverse effect profile

An ECG should be performed 90 minutes following thrombolysis to assess whether there has been a greater than 50% resolution in the ST elevation
if there has not been adequate resolution then rescue PCI is superior to repeat thrombolysis
for patients successfully treated with thrombolysis PCI has been shown to be beneficial. The optimal timing of this is still under investigation

Glycaemic control in patients with diabetes mellitus
in 2011 NICE issued guidance on the management of hyperglycaemia in acute coronary syndromes
it recommends using a dose-adjusted insulin infusion with regular monitoring of blood glucose levels to glucose below 11.0 mmol/l
intensive insulin therapy (an intravenous infusion of insulin and glucose with or without potassium, sometimes referred to as ‘DIGAMI’) regimes are not recommended routinely

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41
Q

What is the treatment for torsades de pointes?

A

IV magnesium sulphate

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42
Q

What is torsades de pointes?

A

A form of polymorphic Vt associated with a long QT interval

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43
Q

What is the pharmacological cardioversion management for new-onset A?

A

1, Fleicanide/amiodarone if there is no evidence of structural/IHD
2. Amiodarone if there is evidence of structural heart disease

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44
Q

What ECG changes are associated with hypothermia?

A
  1. Bradycardia
  2. J wave (small hump at the end of the QRS complex)
  3. 1st degree HB
  4. Prolongation of all intervals
  5. Atrial and ventricular arrhythmias
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45
Q

What is a J wave?

A

A small hump at the end of the QRS complex

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46
Q

What is the most common cause of infective endocarditis?

A

Staphylococcus aureus

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47
Q

What is the most common cause of infective endocarditis in a prosthetic valve?

A

CoNS e.g. S. epidermidis

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48
Q

What do you call SLE-associated endocarditis?

A

Libman-Sacks endocarditis

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49
Q

What do you call malignancy associated endocarditis?

A

Marantic endocarditis

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50
Q

What are the HACEK organisms that cause a culture negative infective endocarditis?

A 
Haemophilus
Aggregatibacter
Cardiobacterium
Eikenella
Kingella
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51
Q

What are the two most important causes of VT?

A

Hypokalaemia and hypomagnesaemia

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52
Q

What is the triad of aortic stenosis presentation?

A

Syncope
Angina
Dyspnoea

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53
Q

What is the management for aortic stenosis?

A
  1. Asymptomatic = observe
  2. Symptomatic = valve replacement
  3. Symptomatic and valvular gradient >40mmHg with features e.g. LV systolic dysfunction = surgery
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54
Q

What should never be prescribed alongside CCBs and why?

A

BBs, due to risk of heart block and fatal arrest

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55
Q

What are indications for beta blockers?

A
  1. Angina
  2. Post-MI
  3. HF
  4. Arrhythmia
  5. HTN
  6. Thyrotoxicosis
  7. Migraine
  8. Anxiety
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56
Q

What are 5 s/es of BBs?

A
  1. Bronchospasm
  2. Cold peripheries
  3. Fatigue
  4. Sleep disturbance
  5. Erectile dysfunction
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57
Q

What are C/Is for BBs?

A
  1. Uncontrolled HF
  2. Asthma
  3. SSS
  4. Verapamil
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58
Q

What are options for tx of angina if a pt doesnt tolerate BBs or CCBs?

A

Monotherapy with

  1. A long acting nitrate
  2. Ivabridine
  3. Nicorandil
  4. Ranolazine
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59
Q

What is the management of stable angina?

A
  1. Aspirin and statin
  2. Sublingual GTN to abort attacks
  3. Either a BB or CCB
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60
Q

What are some s/es of ivabridine?

A

Visual disturbance: Phosphenes and green luminescence

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61
Q

What is the MOA of ivabridine?

A

It acts on the If (‘funny’) ion current which is highly expressed in the sinoatrial node, reducing cardiac pacemaker activity.

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62
Q

What is ivabridine used for?

A

Symptomatic relief of angina in patients with a heart rate >70, as an alternative to first line therapies

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63
Q

What are 4 s/es of warfarin?

A
  1. Haemorrhage
  2. Skin necrosis
  3. Purple toes
  4. Teratogenic
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64
Q

What are some factors that may potentiate warfarin?

A
  1. Liver disease
  2. PY450 enzyme inhibitors
  3. Cranberry juice
  4. NSAIDs (displace warfarin from plasma albumin and inhibit platelet function)
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65
Q

What is the dose of adrenaline in anaphylaxis in a child aged 6-11 y/o?

A

300 micrograms

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66
Q

What are some ECG findings of hypokalaemia?

A
  1. Prominent u waves
  2. T wave is sine wave
  3. Prolonged QTc
  4. Borderline PR interval
    In hypokalaemia, U have no Pot and no T, but a long PR and a long QT
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67
Q

What are some associations of coarctation of the aorta?

A
  1. Turner’s syndrome
  2. Bicuspid aortic valve
  3. Berry aneurysms
  4. NF
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68
Q

What cardiac medication is c/i in aortic stenosis?

A

Nitrates

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69
Q

What can thiazides do to calcium levels?

A

Cause hypercalcaemia

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70
Q

What is the MOA of dipyridamole?

A

Non-specific phosphodiesterase inhibitor

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71
Q

Haemorrhagic stroke in pt on warfarin - whats the management?

A
  1. Stop warfarin
  2. IV Vit K 5mg
  3. Prothrombin complex concentrate
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72
Q

What are some factors favouring rate control of pts with AF?

A
  1. > 65 y/o

2. IHD

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73
Q

What are some factors favouring rhythm control of pts with AF?

A
  1. <65 y/o
  2. Symptomatic
  3. First presentation
  4. Lone AF
  5. CCF
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74
Q

What medication must be stopped when a macrolide Abx is being started?

A

Statins (increased risk of rhabdo when combining these 2 drugs)

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75
Q

What are 2 C/Is to statins?

A
  1. Macrolides

2. Pregnancy

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76
Q

What is the atorvastatin dose for primary and secondary prevention?

A
  1. Primary = 20mg OD

2. Secondary = 80mg OD

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77
Q

What are 3 adverse effects of statins?

A
  1. Myopathy
  2. Liver impairment
  3. Increased risk of intracerebral haemorrhage
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78
Q

Discuss liver monitoring on statins

A

The 2014 NICE guidelines recommend 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

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79
Q

What does an inferior MI on ECG and an AR murmur suggest?

A

Proximal aortic dissection

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80
Q

What is the Mackler triad for Boerhaave syndrome?

A

Vomiting, thoracic pain, subcutaneous emphysema

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81
Q

How are Stanford type A and B aortic dissections usually treated?

A

Type A = surgically

Type B = non-operatively

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82
Q

What is the difference between Stanford type A and B aortic dissections?

A

Type A = commence proximally to left subclavian artery

Type B = commence distally to left subclavian artery

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83
Q

What is S1Q3T3 a sign of, and what is it?

A

PE

  1. S waves in lead I
  2. Q waves in lead III
  3. Inverted T waves in Lead III
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84
Q

What is Boerhaaves syndrome?

A

Spontaneous rupture of the oesophagus as a result of repeated episodes of vomiting

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85
Q

What is the management for Boerhaaves syndrome?

A

Thoracotomy and lavage

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86
Q

What are 4 associations of coarctation of the aorta?

A
  1. Turner’s
  2. Bicuspid aortic valve
  3. Berry aneurysms
  4. NF
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87
Q

What may you see in coarctation of the aorta on CXR?

A

Notching of the ribs due to collateral vessels

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88
Q

What are some possible ECG features of WPW?

A
  1. Short PR interval
  2. Wide QRS complexes with a slurred upstroke
  3. LAD if right-sided accessory pathway
  4. RAD if left-sided accessory pathway
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89
Q

What are 5 associations of WPW?

A
  1. HOCM
  2. Mitral valve prolapse
  3. Ebstein’s anomaly
  4. Thyrotoxicosis
  5. Secundum ASD
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90
Q

Which drugs have been shown to improve mortality in pts with chronic HF?

A
  1. ACEi (SAVE, SOLVD, CONSENSUs)
  2. Spironolactone (RALES)
  3. BBs (CIBIS)
  4. Hydralazine with nitrates (VHEFT-1)
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91
Q

What vaccinations should be offered in HF?

A
  1. Annual influenza vaccine

2. One-off pneumococcal vaccine

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92
Q

What 3 things can be offered if triple therapy for HF is not sufficient?

A
  1. CRT
  2. Digoxin
  3. Ivabridine
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93
Q

What medications have no effect on mortality in HFpEF?

A

ACEi and BBs

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94
Q

What medication is first line for treating HTN in diabetics?

A

ACEi

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95
Q

How long are ‘provoked’ PEs typically treated for?

A

3 months

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96
Q

How long are ‘unprovoked’ PEs typically treated for?

A

6 months

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97
Q

When is thrombolysis used for PE?

A

Massive PE where there is circulatory failure (e.g. hypotension)

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98
Q

What is bifascicular and trifasciscular block?

A
  1. Bifascicular block = RBBB w/ LAD or posterior hemiblock

1. Trifascicular block = features of bifascicular block + 1st degree heart block

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99
Q

What scoring system is used for hypermobility?

A

Beighton score

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100
Q

What can be used to treat dyspnoea and anxiety in acute exacerbation of HF?

A

Morphine

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101
Q

How does one define a pathological Q wave?

A

Q wave of >0.04s and an amplitude >25% of the R wave in that lead. present in at least 2 contiguous leads

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102
Q

In what kind of body habitus may one seed RAD?

A

Tall and thin individuals

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103
Q

In what kind of body habitus may one see LAD?

A

Short, obese individuals

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104
Q

What is pulsus paradoxus? What is it a sign of?

A
  1. Grater than the normal 10mmHg fall in SBP during inspiration
  2. Severe asthma, cardiac tamponade
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105
Q

What is a slow rising pulse a sign of?

A

Aortic stenosis

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106
Q

What is pulsus alternans and what is it a sign of?

A

Regular alternation of the force of the arterial force, a sign of LVF

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107
Q

What is a bisferiens pulse and what is it a sign of?

A

A ‘double pulse’ with two systolic peaks, it is a sign of mixed aortic valve disease/HOCM

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108
Q

What is a ‘jerky’ pulse a sign of?

A

HOCM

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109
Q

What is the management of a haemodynamically stable pt with a regular broad complex tachycardia?

A

Assume VT –> Loading dose of amiodarone followed by 24 hour infusion

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110
Q

What is the management of a haemodynamically stable pt with an irregular broad complex tachycardia?

A
  1. AF w/ BBB –> tx as for narrow complex tachycardia

2. Polymorphic VT –> IV magnesium

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111
Q

What is the management of a regular narrow complex tachycardia?

A
  1. Vagal manoeuvres followed by IV adenosine (6mg –> 12mg –> 12mg)
  2. Electrical cardioversion
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112
Q

What are 2 causes of a regular broad complex tachycardia?

A
  1. VT

2. SVT w/ BBB

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113
Q

What will P450 inducers do to INR?

A

INR will decrease

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114
Q

What will P450 inhibitors do to INR?

A

INR will increase (inhibit –> increase)

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115
Q

What is Kussmaul’s sign, and what may it indicate?

A

A paradoxical rise in JVP with inspiration, may indicate constrictive pericarditis

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116
Q

What may you see on CXR with constrictive pericarditis?

A

Pericardial calcification

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117
Q

What is the textbook triad of PE?

A
  1. Pleuritic chest pain
  2. Dyspnoea
  3. Haemoptysis
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118
Q

What is the most common clinical sign of PE?

A

Tachypnoea

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119
Q

If a pt with AF has a stroke/TIA, what is the anticoagulant of choice?

A

Warfarin or a directin thrombin/factor Xa inhibitor

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120
Q

When should anticoagulation therapy be started in acute stroke pts, in the absence of haemorrhage?

A

After 2 weeks

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121
Q

What is the commonest association for aortic dissection?

A

Hypertension

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122
Q

What proportion of aortic dissections are Type A and Type B?

A 
A = 2/3rd
B = 1/3rd
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123
Q

What could cause an irregular narrow complex bradycardia with no discernible P waves?

A

AF with a slow ventricular response

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124
Q

What are the ECG changes in a posterior STEMI?

A
  1. ST depression in leads V1-V3
  2. Tall, broad R waves
  3. Upright T waves
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125
Q

What do hyperacute T waves signify?

A

That an MI is imminent

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126
Q

Below what HR can ivabridine not be used in HF?

A

75

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127
Q

Where should an epipen be injected?

A

Anterolateral aspect of the middle third of the thigh

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128
Q

What is a valsalva manoeuvre?

A

Forced expiration against a closed glottis

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129
Q

What is the target INR if a pt has recurrent VTEs?

A

3.5

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130
Q

What is an important interaction to consider when a pt is receiving a statin?

A

Macrolides (can lead to statin-induced myopathy)

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131
Q

What is the investigation of choice for PE if the pt has renal impairment?

A

V/Q scan

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132
Q

How should one manage IE causing CCF?

A

Emergency valve replacement surgery

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133
Q

What is the most common site of mutation in HOCM?

A

B-myosin heavy chain or MYBP-C

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134
Q

What do you see on biopsy of HOCM?

A

Myocyte disarray

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135
Q

What are 2 associations of HOCM?

A

Friedrich’s ataxia and WPW

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136
Q

What are the echo findings of HOCM?

A

MR SAM ASH

  1. MR = mitral regurgitation
  2. SAM = systolic anterior motion of the anterior mitral valve leaflet
  3. ASH = asymmetric hypertrophy
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137
Q

If a pt has 1st degree heart block during/following an MI, which vessel has been affected and why?

A

RCA, as it supplies the AVN –> ECG changes in II, III, aVF

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138
Q

What is the main ECG abnormality seen with hypercalcaemia?

A

Shortening of the QT interval

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139
Q

What are bizarre, wide, inverted T waves in a pt who has presented with collapse associated with?

A

Stokes-Adams attacks

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140
Q

Which coronary artery can be involved in an aortic dissection, causing an MI?

A

RCA

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141
Q

What is the most useful blood test to confirm an anaphylactic reaction?

A

Serum tryptase

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142
Q

What should one add after ACEi and CCB for tx of HTN?

A

A Thiazide-like diuretic e.g. Indapamide

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143
Q

Why are venodilators used in the treatment of pulmonary oedema?

A

Because in cardiogenic shock, pulmonary pressures are often high

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144
Q

What is pulmonary artery occlusion pressure an indirect measure of?

A

Left atrial pressure

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145
Q

What is normal pulmonary artery occlusion pressure?

A

8-12 mmHg

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146
Q

What is a sign of hypokalaemia on ECG?

A

U waves

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147
Q

What are 3 words to describe an atrial myxoma on echo?

A

Pedunculated heterogeneous mass, attached to the fossa ovalis region of the interatrial septum

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148
Q

What is the triad of presentation of an atrial myxoma?

A
  1. Mitral valve obstruction
  2. Systemic embolisations
  3. Constitutional symptoms
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149
Q

What is the most common primary cardiac tumour?

A

Atrial myxoma

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150
Q

What are atrial myxomas typically attached to?

A

The fossa ovalis

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151
Q

Why are statins c/i in pregnancy?

A

They might disrupt cholesterol synthesis in the developing foetus

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152
Q

Can T wave inversion in Lead III be a normal variant?

A

Yes

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153
Q

What is the adult adrenaline dose and route for anaphylaxis?

A

IM 0.5mg 1:1000 (0.5ml of 1 in 1,000)

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154
Q

What ECG change might you see with an aortic dissection?

A

ST elevation in the inferior leads if it involves the RCA

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155
Q

What is the DeBakey classification system for aortic dissections?

A
  1. Type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally
  2. Type II - originates in and is confined to the ascending aorta
  3. Type III - originates in descending aorta, rarely extends proximally but will extend distally
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156
Q

What is the management for a Type A aortic dissection?

A

Surgical management, but blood pressure should be controlled to a target systolic of 100-120 mmHg whilst awaiting intervention

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157
Q

What is the management for a Type B aortic dissection?

A
  1. Conservative management
  2. Bed rest
  3. IV labetalol
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158
Q

What are the complications of a backwards aortic dissection tear?

A
  1. Aortic incompetence/regurgitation

2. Inferior MI due to RCA involvement

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159
Q

What are the complications of a forwards aortic dissection tear?

A
  1. Unequal arm pulses and BP
  2. Stroke
  3. Renal failure
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160
Q

What is the adrenaline dose for anaphylaxis in children 6m -6y/o?

A

IM adrenaline 150 mcg (0.15ml of 1 in 1,000)

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161
Q

What is the recommended dose of adrenaline to give during advanced ALS?

162
Q

What are Type A and Type B WPW?

A
  1. Type A = left sided pathway

2. Type B = right sided pathway

163
Q

How do you differentiate between Type A and Type B WPW?

A
  1. Type A = L sided pathway = dominant R wave in V1

2. Type B = R sided pathway = no dominant R wave in V1

164
Q

What is the management for WPW?

A
  1. Medical = Sotalol, amiodarone, fleicanide

2. Definitive = RFA of accessory pathway

165
Q

What is the inheritance pattern of HOCM?

A

Autosomal dominant

166
Q

in the absence of contraindications, what should all pts with MI be given in terms of medications?

A
  1. Aspirin
  2. P2Y12 receptor antagonist e.g. Ticagrelor/Clopidogrel
  3. UFH if having PCI
167
Q

What kind of anti-anginal medication do pts commonly develops tolerance to?

A

Standard release isosorbide mononitrate

168
Q

What should you do if pts develop a tolerance to their nitrate?

A

Take second dose of isosorbide mononitrate after 8 hours rather than after 12 hours

169
Q

What is the management of acute pericarditis?

A
  1. Treat the underlying cause

2. Combination of NSAIDs and Colchicine for acute idiopathic/viral pericarditis

170
Q

What is the more formal term for the ‘M’ seen in V1 in RBBB?

A

RSR pattern

171
Q

If a pt is in SVT and has asthma, what medication would you use in the acute phase?

A

Verapamil, as adenosine is c/i in asthmatics

172
Q

What is the prophylaxis for SVT?

A
  1. BBs

2. RFA

173
Q

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

174
Q

When does Dressler’s syndrome occur?

A

2-6 weeks following an MI

175
Q

What is the treatment for Dressler’s syndrome?

176
Q

What is the management for LV free wall rupture after an MI?

A

Urgent pericardiocentesis and thoracotomy

177
Q

What can be used to differentiate between Cardiac tamponade and constrictive pericarditis?

A

Kussmaul’s sign

178
Q

What is the most specific ECG marker for pericarditis?

A

PR depression

179
Q

What are 4 s/es of ACEi?

A
  1. Cough (15%)
  2. Angioedema
  3. Hyperkalaemia
  4. First dose hypotension
180
Q

What electrolyte changes are expected after starting ACEi?

A

Creatinine and potassium

181
Q

What are the acceptable changes in creatinine and potasssium after starting an ACEi?

A
  1. Creatinine up to 30% from baseline/ >310umol/l

2. Potassium up to 5.5 mmol/l

182
Q

What does p mitrale represent?

A

LA hypertrophy/strain e.g. in mitral stenosis

183
Q

What is the ECG finding of p mitrale?

A

Bifid p wave

184
Q

What is a cause of increased p wave amplitude?

A

Cor pulmonale

185
Q

What is the management of major bleeding in a pt on Warfarin?

A
  1. Stop warfarin
  2. IV Vitamin K 5mg
  3. Prothrombin complex concentrate, if not available then FFP
186
Q

When should an ICD be implanted in a pt with prolonged QT?

A
  1. QTC > 500ms

2. Previous episodes of cardiac arrest

187
Q

What is the normal QTc in males and females?

A
  1. Males = <430 ms

2. Females = <450 ms

188
Q

What is the management of long QT interval?

A
  1. Avoid QT prolonging drugs and precipitants e.g. strenuous exercise
  2. Beta blockers
  3. ICD in high risk cases
189
Q

Cause of pericardial calcification in a pt from South Africa?

190
Q

In the treatment of anaphylaxis, how frequently can adrenaline be repeated?

A

Every 5 minutes

191
Q

In the treatment of anaphylaxis, how frequently can salbutamol be repeated?

A

Back to back

192
Q

How long after anaphylaxis should pts be monitored and why?

A

6-12 hours from onset of symptoms, as biphasic reactions can occur in up to 20% of pts

193
Q

How long after a case of anaphylaxis do tryptase levels remain elevated?

A

Up to 12 hours

194
Q

What is the investigation of choice for pts presenting with non-cardiac chest pain but whose ECG shows signs of ischaemia?

A

Contrast-enhanced CT coronary angiography

195
Q

What heart scan can be done before and after cardiotoxic drugs are used?

A

MUGA scan (multi gated acquisition scan)

196
Q

What are the 2 main methods of Cardiac CT for assessing suspected IHD?

A
  1. Calcium score

2. Contrast enhanced CT

197
Q

Breathing problems with a clear chest is suggestive of?

A

Pulmonary Embolism

198
Q

What baseline tests are needed before starting a pt on amiodarone?

A
  1. TFT
  2. LFT
  3. U&E
  4. CXR
199
Q

What Vaughn-Williams class is amiodarone, and its MOA?

A

Class III, is mainly a potassium channel blocker. and thus inhibits repolarisation and hence prolongs the action potential. Also blocks sodium channels.

200
Q

Why is a loading dose needed for amiodarone?

A

It has a very long half life of 20-100 days

201
Q

Why should amiodarone ideally be given into central veins?

A

Causes thrombophlebitis

202
Q

What bloods need to be done whilst on amiodarone and how often?

A

TFT and LFT every 6 months

203
Q

What medication causes a slate-grey appearance?

A

Amiodarone

204
Q

What artery is affected in a lateral MI?

205
Q

What is bronchial breathing?

A

A generic breath sound associated with consolidation. They are louder and higher pitched than normal breathing, with an obvious gap between inspiration and expiration.

206
Q

What is required for the diagnosis of malignant HTN?

A
  1. Systolic BP >180 or diastolic BP >120

2. Evidence of acute organ damage

207
Q

What are some features of malignant HTN?

A
  1. Eyes = bilateral retinal haemorrhage, papilloedema
  2. Brain = raised ICP –> headache and nausea
  3. Heart = CP due to increased strain
  4. Kidneys = haematuria
  5. Nosebleeds difficult to stop
208
Q

What are 4 medications that should offered to all pts after an MI?

A
  1. DAPT
  2. ACEi
  3. BB
  4. Statin
209
Q

What antiplatelets are now more commonly used instead of clopidogrel?

A

Ticagrelor and prasugrel

210
Q

When should ticagrelor/prasugrel/clopidogrel be stopped after an MI?

211
Q

When should IV glycoprotein IIb/IIIa receptor antagonists be given to patients with MI?

A
  1. Pts with high risk of adverse cardiovascular events

2. Scheduled to undergo angio within 96 hours of hospital admission

212
Q

What are 3 examples of glycoprotein IIb/IIIa receptor antagonists?

A
  1. Abciximab
  2. Tirofiban
  3. Eptifibatide
213
Q

What do you call aortic stenosis if the murmur doesnt radiate to the carotids?

A

Aortic sclerosis

214
Q

Does PCI provide any prognostic benefit over optimal medical therapy for stable angina?

215
Q

What is the ABG finding for a PE and why?

A

Respiratory alkalosis due to hyperventilation

216
Q

What would you call an ECG with sawtooth waves that are irregular?

A

Atrial flutter with variable block

217
Q

What is Wellen’s syndrome?

A

Critical stenosis of the LAD, with deeply inverted or biphasic T waves in V2-V3 on ECG

218
Q

What is downsloping ST depression (‘tick sign’) indicative of?

A

Digoxin toxicity

219
Q

What are 2 pharmacological options for treatment of orthostatic hypotension?

A
  1. Fludrocortisone

2. Midodrine

220
Q

What is the MOA of midodrine?

A

An alpha-1 receptor agonist

221
Q

What are some ECG findings of HOCM?

A
  1. LVH
  2. T wave inversion
  3. Nonspecific ST segment and T wave abnormalities
222
Q

What is a saddle embolus?

A

A large embolus where the pulmonary trunk splits to form the right and left pulmonary arteries

223
Q

What do you do in stable cardiovascular disease with an indication for an anticoagulant?

A

Anticoagulant monotherapy should be given without the addition of antiplatelets

224
Q

What are 3 agents used to control rate in pts with AF?

A
  1. BB
  2. CCB
  3. Digoxin (also preferred choice if pt has HF)
225
Q

What are 3 agents used to control rhythm in pts with AF?

A
  1. Sotalol
  2. Amiodarone
  3. Fleicanide
226
Q

What is the HAS-BLED score?

A

Scoring system used to assess 1-year risk of major bleeding in pts taking anticoagulants with AF

227
Q

What are the components of the HAS BLED score?

A
  1. HTN
  2. Abnormal renal and liver function
  3. Stroke
  4. Bleeding
  5. Labile INR
  6. Elderly
  7. Drug/alcohol
228
Q

What is first line antiplatelet therapy after an ACS?

A

Aspirin lifelong and ticagrelor 12m

229
Q

What is first line antiplatelet therapy after a PCI?

A

Aspirin lifelong and prasugrel/ticagrelor 12m

230
Q

What is first line antiplatelet therapy after a TIA?

A

Lifelong clopidogrel

231
Q

What is first line antiplatelet therapy after a stroke?

A

Lifelong clopidogrel

232
Q

What is first line antiplatelet therapy for peripheral arterial disease?

A

Lifelong clopidogrel

233
Q

What is rheumatic fever?

A

An immunological reaction to a recent (2-6wks ago) Strep pyogenes infection

234
Q

What is the MOA of thiazides?

A

Inhibits sodium reabsorption by blocking the Na+-Cl− symporter at the beginning of the distal convoluted tubule

235
Q

What can sometimes present with a pericardial friction rub?

A

Acute pericarditis

236
Q

What antihypertensive causes both a hyponatraemia and a hypokalaemia?

A

Bendroflumethiazide

237
Q

What antihypertensive causes hypercalcaemia?

A

Bendroflumethiazide

238
Q

What is persistent ST elevation after a previous MI very suggestive of?

A

A LV aneurysm

239
Q

What is a compliction of a LV aneurysm?

A

Blood stagnates around a left ventricle aneurysm, thereby promoting platelet adherence and thrombus formation. Embolisation of left ventricular thrombi can lead to embolic stroke or other systemic embolisms.

240
Q

Beck’s triad for cardiac tamponade?

A
  1. Hypotension
  2. Raised JVP
  3. Muffled heart sounds
241
Q

What foods are high in Vit K?

A

Sprouts, spinach, kale and broccoli

242
Q

HOCM heart sound?

243
Q

Why S4 in HOCM?

A

Causes reduced compliance of the ventricular wall, reducing the rate of diastolic filling. As a consequence, there is a vigorous atrial contraction at the end of diastole to overcome the raised ventricular end-diastolic pressure. This creates a fourth heart sound.

244
Q

HOCM inheritance?

245
Q

HOCM prevalence?

246
Q

HOCM septum size?

247
Q

HOCM death cause?

A

Ventricular arrhythmia

248
Q

Mx of HOCM

A

ABCDE

  1. Amiodarone
  2. BB or verapamil for sx
  3. ICD
  4. Dual chamber pacemaker
  5. Endocarditis prophylaxis
249
Q

Statin for secondary prevention dose?

A

Atorvastatin 80mg

250
Q

Statin for primary prevention dose?

A

Atorvastatin 20mg

251
Q

3 myopathies caused by statins?

A
  1. Myalgia
  2. Myositis
  3. Rhabdomyolysis
252
Q

2 c/is of statins?

A
  1. Macrolides

2. Pregnancy

253
Q

Who should receive a statin?

A
  1. Established CVD
  2. QRISK2 > 10
  3. T1DM Dx >10yrs ago OR >40y/o OR established nephropathy
254
Q

Poorly controlled hypertension, already taking an ACE inhibitor, calcium channel blocker and a standard-dose thiazide diuretic. K+ > 4.5mmol/l, nextstep?

A

Add alpha or beta blocker

255
Q

Most common cause of IE?

256
Q

IE cause from an indwelling line?

A

S. epidermidis

257
Q

Strep viridans fuckery?

A

Technically Streptococcus viridans is a pseudotaxonomic term, referring to viridans streptococci, rather than a particular organism. The two most notable viridans streptococci are Streptococcus mitis and Streptococcus sanguinis. They are both commonly found in the mouth and in particular dental plaque so endocarditis caused by these organisms is linked with poor dental hygiene or following a dental procedure

258
Q

What strep is associated with colorectal cancer?

A

Strep. bovis

259
Q

Causes of long QT syndrome?

A
  1. Genetic
  2. Electrolytes
  3. Drugs
260
Q

Genetic causes of LQTS?

A
  1. LQT1/2/3
  2. Jervell and Lange-Neilsen syndrome (associated with deafness)
  3. Romano-Ward syndrome
261
Q

Electrolyte causes of LQTS?

A
  1. Hypocalcaemia
  2. Hypomagnesaemia
  3. Hypokalaemia
262
Q

Drug causes of LQTS?

A
  1. Antiarrythmics e.g. amiodarone, sotalol
  2. Abx e.g. erythromycin, clarithromcyin, ciprofloxacin
  3. Antidepressants e.g. SSRIs, TCA. neuroleptic agents
263
Q

How does HOCM lead to diastolic dysfunction?

A
  1. LVH –> decreased compliance –> decreased CO
264
Q

Complications of VSD?

A
  1. AR
  2. IE
  3. Eisenmenger’s complex
  4. RHF
  5. Pulmonary HTN
265
Q

Why AR with VSD?

A

A poorly supported right coronary cusp results in cusp prolapse

266
Q

What is c.i in women with pulmonary HTN?

A

Pregnancy due to 30-50% risk of mortality

267
Q

Elevated JVP, HTN, tachycardia despite fluid resus in a pt wit chest wall trauma?

A

Cardiac tamponade

268
Q

What is flail chest?

A

Detachment of rib cage from the chest wall due to trauma

269
Q

Triad of cardiac tamponade?

A

Beck’s triad

  1. Hypotension
  2. Raised JVP
  3. Muffled HS
270
Q

Max dose of amlodipine?

271
Q

Any need for DVT prophylaxis whilst travelling?

272
Q

BP targets for diabetics?

A
  1. If end-organ damage <130/80

2. Otherwise <140/80

273
Q

Young male smoker with sx similar to limb ischaemia?

A

Buerger’s disease

274
Q

Buerger’s disease?

A

Aka thrombangiitis obliterans is a small and medium vessel vasculitis strongly associated with smoking

275
Q

Features of Buerger’s disease?

A
  1. Extremity ischaemia
  2. Superficial thrombophlebitis
  3. Raynaud’s phenomenon
276
Q

Features of severe AS on examination?

A
  1. Narrow pulse pressure
  2. Slow rising pulse
  3. Thrill over apex
  4. S4 indicative of LVH
  5. Soft/absent S2
277
Q

What valve disease is associated with PCKD?

A

Mitral valve prolapse

278
Q

1st line mx of SVT?

A

Vagal manoeuvres e.g. Valsalva/carotid sinus massage

279
Q

Acute mx of SVT?

A
  1. Vagal manoeuvres
  2. IV adenosine 6mg –> 12mg –> 12m
  3. Electrical cardioversion
280
Q

Mx of atrial flutter?

A
  1. Similar to AF although meds may be less effective
  2. More sensitive to cardioversion than AF so lower energy levels may be used
  3. RFA of the tricuspid valve isthmus is curative for most pts
281
Q

5 drugs after MI?

A
  1. ACEi
  2. BB
  3. Statin
  4. Aspirin
  5. Clopidogrel
282
Q

When may sexual activity resume after an uncomplicated MI?

283
Q

Complete heart block after MI, which vessel affected?

A

RCA lesion

284
Q

What artery supplies the AVN?

A

Posterior interventricular artery, which in the majority of pts is a branch of the RCA, but can be supplied by the LCX in some

285
Q

4 most common clinical signs in PE?

A
  1. Tachypnoea (96%)
  2. Crackles (58%)
  3. Tachycardia (44%)
  4. Fever (43%)
286
Q

PE ix of choice if there is renal impairment?

287
Q

Gold standard ix for PE?

A

Pulmonary angiography

288
Q

C/Is for BBs?

A
  1. Uncontrolled HF
  2. Asthma
  3. SSS
  4. Concurrent verapamil use - may precipitate severe bradycardia
289
Q

5 s/es of BBs?

A
  1. Bronchospasm
  2. Cold peripheries
  3. Fatigue
  4. Sleep disturbance
  5. Erectile dysfunction
290
Q

ACEi, BB, Furosemide, statin, which causes osteoporosis?

A

Furosemide, due to increased urinary excretion of calcium

291
Q

Mechanism of carotid sinus hypersensitivity?

A

Carotid sinus pressure/massage –> stimulates the baroreceptors and the parasympathetic nervous system. This increases the vagal tone and affects the SA and AV node, leading to a decrease in BP and HR. If the baroreceptor is hypersensitive, this response is exaggerated.

292
Q

2 possible features of carotid sinus hypersensitivity?

A
  1. Cardioinhibitory = Ventricular pause of >3s

2. Vasodepressive = SBP fall >50mmHg

293
Q

What is the HASBLED scoring system/

A

To assess 1-year risk of major bleeding in patients taking anticoagulants with atrial fibrillation.

294
Q

What CM are alcoholics at risk of?

A

Dilated CM

295
Q

Most common cause of cardiomyopathy?

A

Dilated (accounts for 90% cases)

296
Q

2nd line antihypertensive for afrocaribbeans?

A

ARB NOT ACEi (2019 guideline change)

297
Q

Why are ACEi first line antihypertensive for diabetes?

A

Due to their renoprotective effect

298
Q

Why can flash pulmonary oedema happen after MI?

A

Due to acute mitral valve regurgitation, due to rupture of tendinous cords

299
Q

Persistent ST elevation and LV failure after MI?

A

LV aneurysm

300
Q

Definitive investigation for acute pericarditis?

301
Q

Mx of acute pericarditis?

A
  1. The cause

2. NSAIDs and colchicine if acute idiopathic or viral pericarditis

302
Q

Preferred anti-epileptic in pregnancy?

A

Lamotrigine

303
Q

4 drugs that improve mortality with chronic HF?

A
  1. ACEi (SAVE, SOLVD, CONSENSUS)
  2. Spironolactone (RALES)
  3. BB (CIBIS)
  4. Hydralazine with nitrates (VHEFT-1)
304
Q

Features of Takayasu’s arteritis?

A
  1. Systemic features
  2. Unequal BP in limbs
  3. Carotid bruit
  4. Intermittent claudication
  5. Aortic regurgitation (20%)
305
Q

Association of takayasu’s arteritis?

A

Renal Artery Stenosis

306
Q

Mx of Takayasu’s arteritis?

307
Q

Normal corrected QT interval?

A
  1. <430 ms in males

2. <450ms in females

308
Q

How do drugs prolong Qt interval?

A

Blockage of potassium channels

309
Q

What type of immune response is rheumatic fever?

A

Type II hypersensitivity reaction

310
Q

Notching of the inferior border of the ribs?

A

70% of adults with coarctation of the aorta

311
Q

Mechanism of rib notching in coarctation?

A

Aortic obstruction gives rise to the development of dilated intercostal collateral vessels to allow sufficient blood flow to reach the descending aorta. The pressure of these vessels erodes the inferior margin of the ribs

312
Q

MOA of nitrates?

A
  1. Cause the release of NO in smooth muscle, activating guanylate cyclase which then converts GTP to cGMP, which in turn leads to a fall in intracellular calcium levels
  2. In angina they both dilate the coronary arteries and also reduce venous return which in turn reduces left ventricular work, reducing myocardial oxygen demand
313
Q

4 s/es of nitrates?

A
  1. Hypotension
  2. Tachycardia
  3. Headaches
  4. Flushing
314
Q

When to electrically cardiovert acute AF?

A

If < 48 hours

315
Q

AF onset <48 hours mx?

A
  1. Pt heparinised
  2. Electrical DC cardioversion
  3. Pharm = amiodarone if structural heart disease, flecainide or amiodarone in those without structural heart disease
316
Q

AF onset >48 hours mx?

A
  1. Anticoagulation for at least 3 weeks prior to electrical cardioversion (alternative = TOE to exclude LAA thrombus, if absent then immediate heparin and cardioversion)
  2. BB
317
Q

AF < 48 hours, terminated by cardioversion, further anticoagulation necessary?

318
Q

AF > 48 hours, terminated by cardioversion, further anticoagulation necessary?

A

At least 4 weeks, then review

319
Q

Causes of postural hypotension?

A
  1. Hypovolaemia
  2. Autonomic dysfunction = diabetes, Parkinsons
  3. Drugs
  4. Alcohol
320
Q

Potassium > 6mmol/L in hypertensive pt with CKD mx?

A

Cessation of ACEi

321
Q

4 s/es pf ACEi?

A
  1. Cough (may occur up to a year after starting)
  2. Angioedema (may occur up to a year after starting)
  3. Hyperkalaemia
  4. First dose hypotension
322
Q

Acceptable changes after starting ACEI?

A
  1. Increase in serum creatinine up to 30% from baseline

2. Increase in K up to 5.5mmol/l

323
Q

Which beta blocker is known to cause QT prolongation?

324
Q

Ostium secundum or primum ASD more common?

A

Ostium secundum

325
Q

Tri-phalangeal thumbs and ostium secundum?

A

Holt-Oram syndrome

326
Q

AF pharmacological cardioversion agents?

A

Amiodarone and fleicanide (‘pill in pocket’)

327
Q

Main complication of Boerhaaves?

A

Severe sepsis secondary to mediastinitis

328
Q

Dx of boerhaaves?

A

CT contrast swallow

329
Q

Mx of boerhaaves?

A

Thoracotomy and lavage

330
Q

Mx of pt on warfarin undergoing emergency surgery?

A

Give four-factor prothrombin complex concentrate

331
Q

7 causes of ST elevation?

A
  1. MI
  2. Pericarditis/myocarditis
  3. Normal variant (high take-off)
  4. LV aneurysm
  5. Prinzmetal’s angina
  6. Takotsubo’s cardiomyopathy
  7. Subarachnoid haemorrhage
332
Q

Mx of native valve endocarditis (NVE)?

A

Amoxicillin + Gentamicin

333
Q

Mx of endocarditis with suspected MRSA?

A

Vancomycin + Gentamicin

334
Q

What is c/i in ACS in pts with hypotension (<90mmHg)?

335
Q

Eponym of murmur grading scale?

A

Levine scale

336
Q

What are the 6 Levine grades?

A
  1. Grade 1 - Very faint murmur, frequently overlooked
  2. Grade 2 - Slight murmur
  3. Grade 3 - Moderate murmur without palpable thrill
  4. Grade 4 - Loud murmur with palpable thrill
  5. Grade 5 - Very loud murmur with extremely palpable thrill. 6. Can be heard with stethoscope edge
    Grade 6 - Extremely loud murmur - can be heard without stethoscope touching the chest wall
337
Q

AF rate control drugs?

A
  1. BB
  2. CCBs
  3. Digoxin
338
Q

AF rhythm control drugs?

A
  1. Sotalol
  2. Amiodarone
  3. Fleicanide
339
Q

2 factors favouring rate control for AF?

A
  1. Older than 65 y/o

2. Hx of IHD

340
Q

Factors favouring rhythm control for AF?

A
  1. <65 y/o
  2. Symptomatic
  3. First presentation
  4. Lone AF/due to corrected precipitant e.g. alcohol
  5. Congestive HF
341
Q

Mx of peri-arrest bradycardia?

A
  1. Atropine 500mg IV
  2. Atropine up to max 3mg
  3. Transcutaneous pacing
  4. Isoprenaline/adrenaline infusion titrated to response
342
Q

How long before surgery is warfarin stopped?

A

5 days, and once INR is <1.5 surgery can go ahead

343
Q

Definitive mx of proximal aortic dissection?

A

Surgical aortic root replacement

344
Q

Biomarker for detection of re-infarction 4-10 days after MI?

A

CK-MB (only remains elevated for 3-4 days post infarction

345
Q

How long does troponin remain elevated after MI?

346
Q

What is the first cardiac enzyme that rises?

347
Q

Takotsubo on echo?

A

Apical ballooning of the myocardium, resembling an octopus pot

348
Q

Why does apical ballooning occur in Takotsubo?

A

Severe hypokinesis of the mid and apical segments with preservation of activity of the basal segments. In simple terms, the bottom of the heart (the apex) does not contract and therefore appears to balloon out.

349
Q

Features of Takotsubo’s cadiomyopathy?

A
  1. Chest pain
  2. Features of HF
  3. ST elevation on ECG
  4. Normal coronary angiogram
350
Q

Mx of Takotsubo’s?

A

Treatment is mainly supportive

351
Q

Most commonly used vein for venous cutdown?

A

Long saphenous vein

352
Q

Where does the long saphenous vein pass?

A

Anterior to medial malleolus

353
Q

Where does the short saphenous vein pass?

A

Posterior to the lateral malleolus

354
Q

Amiodarone dose in ALS?

355
Q

Mx of pt post-PCI for MI experiencing pain or haemodynamic instability post-PCI?

356
Q

When is unfractionated heparin given for MI?

A

For pts who are going to have MI

357
Q

2 main mx strategies for AF?

A
  1. Rate/rhythm control

2. Reducing stroke risk

358
Q

IPSS?

A

International prostate symptom score

359
Q

LAD and RBBB?

A

Bifascicular block

360
Q

LAD + RBBB + 1st degree HB?

A

Trifascicular block

361
Q

Ventricular escape rhythm in complete HB?

362
Q

Adenosine half life?

A

8-10 seconds

363
Q

Adenosine MOA?

A
  1. Causes transient heart block in the AVN
  2. Agonist of the A1 receptor in the atrioventricular node, which inhibits adenylyl cyclase thus reducing cAMP and causing hyperpolarization by increasing outward potassium flux
364
Q

AF post-stroke Mx?

A
  1. Warfarin or direct factor Xa inhibitor

2. Should only be commenced after 2 weeks

365
Q

IV amiodarone s/e?

A

Thrombophlebitis

366
Q

Amiodarone half life?

A

20-100 days

367
Q

Amiodarone monitoring?

A
  1. TFT, LFT, U&E, CXR prior to tx

2. TFT, LFT every 6m

368
Q

Slate grey appearance?

A

Amiodarone

369
Q

How should adenosine be infused and why?

A

Via a large calibre cannula e.g. 16G due to its short half life

370
Q

4 adverse effects of adenosine?

A
  1. Chest pain
  2. Bronchospasm
  3. Transient flushing
371
Q

Fondaparinux MOA?

A

Activates antithrombin III, just like LMWH

372
Q

Bisferiens pulse?

A

HOCM or mixed aortic valve disease

373
Q

Subclavian steal syndrome presentation?

A

Posterior circulation symptoms e.g. dizziness and vertigo, during exertion of an arm

374
Q

Pathophysiology of subclavian steal syndrome?

A

Subclavian artery steno-occlusive disease proximal to the origin of the vertebral artery and is associated with flow reversal in the vertebral artery

375
Q

Mx of subclavian steal syndrome?

A

Percutaneous trnasluminal angioplasty/stent

376
Q

5 branches of the subclavian artery?

A
  1. Vertebral artery
  2. Internal thoracic artery
  3. Thyrocervical trunk
  4. Costocervical trunk
  5. Dorsal scapular artery
377
Q

Why is a CXR essential when Ix PE?

A

To rule out any other pathologies causing CP

378
Q

DVLA advice post MI?

A

Cannot drive for 4 weeks

379
Q

Mx of HF is symptoms persist despite maximal management with triple therapy?

A
  1. CRT
    2, Digoxin
  2. Ivabridine
380
Q

Raised JVP with inspiration?

A

Kussmaul’s sign, typical of contrictive pericarditis

381
Q

Drop in BP and SV with inspiration?

A

Pulsus paradoxus, a sign of cardiac tamponade

382
Q

3 examples of thrombolytics?

A
  1. Alteplase
  2. Tenecteplase
  3. Streptokinase
383
Q

What antihypertensive is C/I in pregnancy?

A

ACEi, because they cause foetal abnormalities and renal failure

384
Q

How do thiazides cause gout?

A

Reduce uric acid secretion from the kidney

385
Q

Pulmonary HTN effect on heart sounds?

A

Loud S2 (due to a loud P2)

386
Q

U waves?

A

Hypokalaemia

387
Q

What 2 things is GFR dependent upon?

A
  1. Overall blood flow to kidney

2. Autoregulation of the afferent and efferent arterioles to fine tune the pressure

388
Q

What mediates afferent renal arteriole dilation?

A

PGE2, to increase flow

389
Q

What mediated efferent renal arteriole constriction?

A

Ang II, to increase pressure

390
Q

How do NSAIDs cause AKI?

A

Blog PGE2 and disrupt possible afferent arteriole dilation (oral aspirin however, does NOT do this)

391
Q

Atypical chest pain defn?

A

Meets 2/3 of criteria of stable angina

  1. Constricting CP
  2. Precipitated by physical exertion
  3. Relieved by GTN spray within 5 mins
392
Q

First line Ix for stable CP of suspected CAD aetiology?

A

Contrast-enhanced CT coronary angio

393
Q

QRISK threshold for statin?

394
Q

HTN in DM Mx?

A

ACEi, regardless of age

395
Q

Orthostatic HTN time measurement?

A

Within 3 mins of standing

396
Q

Which BBs are used for HF in UK?

A

Bisoprolol, carvedilol and nebivolol

397
Q

2 types of VT?

A
  1. Monomorphic = most commonly following MI

2. Polymorphic = subtype is Torsades

398
Q

What CVS drug can reduce hypoglycaemic awareness?

399
Q

MOA of BBs causing reduced hypoglycaemic awareness?

A

Can theoretically suppress all of the adrenergically mediated sx of hypoglycameia and can thus lead to unawareness

400
Q

Where are inhaled foreign objects most likely to be found?

A

Right main bronchus

Medicine and Surgery Mushkies (52 decks)

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