Cardiology Flashcards

1
Q

Give 4 methods of secondary prevention of cardiovascular disease

A

4 A’s:
1. Aspirin (+12 months of clopidogrel)
2. Atorvastatin
3. Atenolol (or propranolol)
4. ACE inhibitor (commonly ramipril)

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2
Q

Give the pathophysiology of angina

A

Narrowing of coronary arteries reduces blood flow to myocardium.
In high demand there is insufficient flow.

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3
Q

What is the difference between stable and unstable angina?

A

Stable: relieved by rest/GTN

Unstable: occurs at rest

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4
Q

Give the recommended investigations for angina

A

CT angiography - GOLD STANDARD

ECG, FBC, U&Es, LFTs, Lipid profile, HbA1c

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5
Q

Give the management of angina

A
  1. GTN
  2. Beta-blocker OR CCB
  3. Secondary prevention (4 A’s)
  4. Percutaneous coronary intervention with coronary angioplasty
  5. Coronary artery bypass graft
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6
Q

Give the ECG changes seen in STEMI

A

ST elevation in arterial distribution

New left bundle branch block

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7
Q

What investigations should be undertaken when no ST elevation but strong suspicion of MI?

A
  1. Troponin
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8
Q

Which ECG leads demonstrate the inferior aspect of the heart, and which artery supplies this area?

A

II, III, aVF

Right coronary artery

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9
Q

Which ECG leads demonstrate the septal aspect of the heart and which artery supplies this area?

A

V1, V2

Left anterior descending

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10
Q

Which ECG leads demonstrate the anterior aspect of the heart and which artery supplies this area?

A

V3, V4

Left anterior descending

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11
Q

Which ECG leads demonstrate the lateral aspect of the heart and which artery supplies this area?

A

I, aVL, V5, V6

Circumflex artery

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12
Q

Give the presentation of MI

A
  1. Central crushing chest pain, radiating to L arm and jaw
  2. Nausea and vomiting
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13
Q

What are the differential diagnoses of raised troponin?

A
  1. ACS
  2. Renal failure
  3. Sepsis
  4. Myocarditis
  5. PE
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14
Q

Give the acute management of MI

A

MONA:

  1. Morphine
  2. Oxygen
  3. Nitrates
  4. Aspirin
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15
Q

Give the management of STEMI

A
  1. Primary percutaneous coronary intervention (within 12 hours)
  2. Thrombolysis if PCI not available - alteplase/streptokinase
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16
Q

Give the management of acute NSTEMI

A

BATMAN

  1. Beta blocker (bisoprolol)
  2. Aspirin
  3. Ticagrelor (P2Y12 inhibitor)
  4. Morphine
  5. Anticoagulant (fondaparinux)
  6. Nitrates

PCI if indicated

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17
Q

Give the complications of ACS

A
  1. Cardiogenic shock - presents with low BP
  2. Death
  3. Cardiac failure
  4. Arrhythmia
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18
Q

Which ECG leads demonstrate the posterior aspect of the heart?

A

V1-V3

Posterior MI causes ST depression in these leads

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19
Q

What is Dressler’s syndrome?

A

Autoimmune pericarditis provoked by MI

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20
Q

Give the presentation of Dressler’s syndrome

A
  1. Onset 1-3 weeks post MI
  2. Fever, pericardial effusion, anaemia, cardiomegaly
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21
Q

Give the management of Dressler’s syndrome

A

Self-limiting within a few days

NSAIDs and steroids

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22
Q

Give the triggers of left ventricular failure

A
  1. Iatrogenic
  2. Sepsis
  3. MI
  4. Arrhythmia
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23
Q

Give the presentation of acute left ventricular failure

A
  1. ACUTE BREATHLESSNESS (type 1 resp. failure) - worse when lying flat
  2. Cough
  3. Tachypnoea
  4. Decreased sats.
  5. Bilateral basal crepitations
  6. Hypotension - signifies cardiogenic shock
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24
Q

Give the presentation of right sided heart failure

A
  1. Raised JVP
  2. Peripheral oedema
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25
Give the investigations for left ventricular failure
1. ECG - assess for underlying cause 2. ABG 3. CXR 4. BNP
26
What does a raised BNP reflect?
BNP is a protein released by ventricles when excessively stretched. Indicates fluid overload of heart, tachycardia, sepsis, PE, renal impairment, COPD.
27
Give the management of acute left ventricular failure
1. Stop IV fluids 2. Stat dose of furosemide if necessary 3. Oxygen - if sats falling 4. Sit up - will relieve symptoms 5. Inotropes (rarely) - e.g. noradrenaline
28
What is the method of action of dabigatran
1. Anticoagulant 2. Direct thrombin inhibitor
29
What is the reversal method for dabigatran
Idarucizumab
30
Describe the 2 types of chronic heart failure
1. Systolic HF - impaired left ventricular function 2. Diastolic HF - left ventricular relaxation
31
Give the presentation of chronic heart failure
1. Breathlessness 2. Cough 3. Orthopnoea (SOB when lying flat) 4. Paroxysmal nocturnal dyspnoea (sudden waking at nights with attacks of SOB and cough) 5. Peripheral oedema
32
Describe the diagnosis of chronic heart failure
1. BNP 2. Echocardiogram 3. ECG
33
Give the causes of chronic heart failure
1. IHD 2. Valvular heart disease (aortic stenosis) 3. Hypertension 4. Arrhythmias
34
Give the management of chronic heart failure
First line - ABAL: 1. ACE inhibitor (ramipril) 2. Beta blocker (bisoprolol) 3. Aldosterone antagonist (spironolactone) - if Sx not controlled by 1. and 2. 4. Loop diuretic (furosemide) Second line - cardiac resynchronisation therapy
35
Give the side effects of furosemide
Hyponatraemia causing: 1. Confusion 2. Somnolence 3. Peripheral oedema
36
Give the role of digoxin in chronic heart failure
Does not reduce mortality. Provides symptomatic relief due to it's inotropic properties.
37
Give the mechanism of action of digoxin
Cardiac glycoside Positively inotropic, negatively chronotropic.
38
Give the indications for digoxin use
1. AF - not commonly used 2. Atrial flutter 3. Chronic heart failure
39
Give causes of digoxin toxicity
1. Overdose 2. Renal failure (digoxin excreted renally) 3. Hypokalaemia
40
Give the presentation of digoxin toxicity
1. Xanthopsia – a yellow ring / discolouration of the vision 2. Bradycardias 3. Ventricular ectopic beats 4. Heart block (various types) 5. VT/VF – rare
41
Define cor pulmonale
Right sided heart failure caused by respiratory disease
42
Give the causes of cor pulmonale
1. COPD - most common 2. PE 3. Cystic fibrosis
43
Give the presentation of cor pulmonale
1. Often asymptomatic 2. SOB 3. Peripheral oedema 4. Syncope 5. Hypoxia/cyanosis 6. Raised JVP 7. Hepatomegaly Back-log of blood through venous system leads to 3, 6, 7
44
Give the management of cor pulmonale
1. Treat underlying cause 2. Oxygen therapy
45
What values are considered hypertension?
Clinic: 140/90 Ambulatory: 135/85
46
Give the causes of hypertension
1. Essential HTN 2. Renal disease 3. Obesity 4. Pregnancy 5. Endocrine (hyperaldosteronism)
47
Give the complications of hypertension
1. IHD 2. CVA 3.Hypertensive retinopathy (diagnose with fundoscopy) 4. Hypertensive nephropathy (haematuria on dipstick) 5. Heart failure
48
Give the investigations for hypertension
24 hour ambulatory BP monitoring - indicated if clinic BP is high
49
Describe the first line management of hypertension
1. Age <55 and non-black: ACE inhibitor (ramipril) 2. Age >55 or black: CCB (amlodipine) 3. Diabetic: ACEi/ARB regardless of age
50
Describe the second line management of hypertension
1. Non-black: ACEi + CCB (ramipril + amlodipine) 2. Black: CCB + ARB (amlodipine + candesartan)
51
Describe the third line management of hypertension
ACEi + CCB + Thiazide Diuretic (indapamide)
52
Give the fourth line management of hypertension
ACEi + CCB + Thiazide Diuretic + Beta-Blocker/A-Blocker (bisoprolol/doxazosin)
53
Give 3 side effects of thiazide diuretics and their presentation
Erectile dysfunction Hypokalaemia ECG: 1. T wave depression 2. ST sagging 3. U wave prominence 4. Prolonged P-R interval Hypercalcaemia
54
When are aldosterone antagonists indicated in hypertension?
When thiazides cause hypokalaemia - spironolactone is potassium sparing. *ACEi and spironolactone both cause hyperkalaemia - monitor U&Es
55
Give the role of verapamil in hypertension
Verapamil is a CCB Contra-indicated as is rate-limiting. B-blocker + verapamil may cause asystole.
56
What action causes the S1 heart sound?
AV valves closing 'lub dub'
57
What action causes the S2 heart sound?
Semi-lunar valves closing 'lub dub'
58
What action causes the S3 heart sound?
Chordae-tendinae 'twang' - normal in young people. Indicates heart failure in older people due to stiffening of ventricles and chordae tendinae. 'lub de dub'
59
What action causes the S4 heart sound?
Stiff or hypertrophic ventricle - demonstrates turbulent flow from atria to non-compliant ventricle 'le lub dub'
60
Where can the pulmonary valve be auscultated?
2nd ICS - L sternal edge
61
Where can the aortic valve be auscultated?
2nd ICS - R sternal edge
62
Where can the tricuspid valve be auscultated?
5th ICS - L sternal edge
63
Where can the mitral valve be auscultated?
5th ICS - mid-clavicular line (apex space)
64
When is mitral stenosis most audible?
When lying on left hand side
65
When is aortic regurgitation most audible?
When sat up, leaning forward and holding exhalation
66
Which murmur radiates to the carotid arteries?
Aortic stenosis
67
How are murmurs described?
SCRIPT: 1. Site 2. Character 3. Radiation 4. Intensity 5. Pitch 6. Timing (systolic/diastolic)
68
How are murmurs graded?
1. Difficult to hear 2. Quiet 3. Easy to hear 4. Easy to hear with palpable thrill 5. Can be heard with stethoscope barely on chest 6. Can be heard with stethoscope off chest
69
Give the cause of mitral stenosis
1. Rheumatic heart disease 2. Infective endocarditis
70
Give the pathophysiology of mitral stenosis
Causes left atrial hypertrophy
71
Describe the murmur heard in mitral stenosis
Mid-diastolic, low-pitched rumbling
72
Give the cause of mitral regurgitation
1. Idiopathic 2. IHD 3. Infective endocarditis 4. Rheumatic heart disease 5. Ehler's Danlos/Marfan Syndrome
73
Give the pathophysiology of mitral regurgitation
Left atrial dilation Results in congestive cardiac failure
74
Describe the murmur heard in mitral regurgitation
Pan-systolic high-pitched whistling
75
Give cause of aortic stenosis
1. Idiopathic calcification 2. Rheumatic heart disease
76
Describe the pathophysiology of aortic stenosis
Causes left ventricular hypertrophy
77
Describe the murmur heard in aortic stenosis
Ejection-systolic crescendo-decrescendo high-pitched murmur radiating to the carotids
78
Give the cause of aortic regurgitation
1. Idiopathic age-related weakness 2. Ehler's Danlos/Marfan
79
Give the pathophysiology of aortic regurgitation
Causes left ventricular dilation
80
Describe the murmur heard in aortic regurgitation
Soft early diastolic murmur associated with collapsing pulse and head nodding (De Mussett's sign)
81
Give the lifespan of biosynthetic prosthetic valves
10 years
82
Give the lifespan of mechanical valves
20+ years Require life-long warfarin with target INR of 2.5-3.5
83
Give the clotting screen results seen on warfarin
Prolonged prothrombin time, with a normal activated partial prothrombin time (APTT).
84
Give the major complications of prosthetic heart valves
1. Infection endocarditis (staphylococcus, streptococcus, enterococcus) 2. Thrombus formation 3. Haemolysis
85
Which valvular disease is associated with polycystic kidney disease?
Mitral valve prolapse
86
Define atrial fibrillation
Uncoordinated, rapid, irregular contraction of the atria due to disorganised electrical activity.
87
Give the presentation of AF
1. Irregularly irregular pulse 2. Tachycardia 3. Heart failure 4. Palpitations 5. SOB 6. Syncope
88
Describe the ECG presentation of AF
1. Absent p waves 2. Narrow QRS 3. Irregularly irregular ventricular rhythm
89
Give the causes of AFM
"AF affects Mrs Smith" 1. Sepsis 2. Mitral valve pathology 3. IHD 4. Thyrotoxicosis 5. Hypertension
90
Define paroxysmal AF
Comes and goes, with attacks not lasting longer than 48 hours.
91
Give the management of paroxysmal AF
Flecanide "Pill-in-pocket" approach - carry medication, take when have attacks. Anti-coagulate based on CHADS-VASc
92
Give the first-line management of atrial fibrillation
Rate control: 1. Allows for adequate ventricular filling 2. B-blocker (atenolol)/CCB (diltiazem)/digoxin
93
Give the second-line management of atrial fibrillation
Rate control - if rhythm control not indicated, e.g. 1. Cause is reversible 2. New onset 3. AF causing heart failure Rate control: 1. Cardioversion - immediate if AF onset <48 hours or patient unstable 2. Cardioversion can be pharmacological (flecanide/amiodarone) or electrical (defibrillation under GA/sedation)
94
Describe anticoagulation therapy in AF
First-line: 1. NOAC - e.g. apixaban/rivaroxaban (Xa inhibitor) 2. Reverse using andexanet alfa Second-line: 1. Warfarin (vitamin K antagonist) 2. Target INR 2-3
95
Describe the CHADS-VASc score
Assesses risk of developing stroke or TIA in the presence of AF Score >1 indicates anticoagulant recommendation C - congestive heart failure H - hypertension A2 - age >75 D - diabetes S2 - stroke or TIA previously V - vascular disease A - age 65-74 S - sex (female)
96
What are the 4 cardiac arrest rhythms?
Shockable: 1. Ventricular fibrillation 2. Ventricular tachycardia Non-Shockable: 1. Pulseless electrical activity (PEA) 2. Asystole
97
Describe the presentation of atrial flutter on ECG
1. HR >150bpm 2. 'Saw tooth' appearance
98
Give the management of atrial flutter
1. Rate control: beta blocker 2. Rhythm control: cardioversion 3. Treat underlying cause (IHD, HTN, cardiomyopathy)
99
Give the pathophysiology of supra-ventricular tachycardia
Electrical signals re-enter the atria from the ventricles - then travel back through the AV node to cause an additional contraction.
100
Give the management of supra-ventricular tachycardia
1. Valsalva manoeuvre - blowing hard against resistance (e.g. sealed syringe) 2. Carotid sinus massage 3. Adenosine bolus 4. Direct current cardioversion - if systolic BP <90
101
Describe the mechanism of action of adenosine
1. Slows conduction through the AV node, to 'reset' back to sinus rhythm 2. Causes brief asystole/bradycardia - causes sense of impending doom/chest pain
102
Describe the pathophysiology of Wolff-Parkinson-White syndrome
1. Extra electrical pathway connecting the atria and ventricles 2. Causes SVT ECG: short PR, wide QRS
103
Describe the management of Wolff-Parkinson-White
Radiofrequency ablation of additional pathway Heat applied to burn areas of heart and convert to non-conducting scar tissue. Curative in AF, atrial flutter, WPW, SVT. Will need to continue lifelong clopidogrel for anticoagulation after ablation even if curative.
104
Describe the pathophysiology of Torsades de Pointes
Ventricular tachycardia in which the height of the QRS complex progressively gets smaller, then larger again, then smaller again etc.
105
Give the causes of Torsades de Pointes
1. Hypokalaemia/hypocalcaemia/hypomagnasaemia 2. Antipsychotics 3. Citalopram (also causes QT prolongation) 4. Amiodarone 5. Macrolides (e.g. clarithromycin)
106
Give the management of Torsades de Pointes
1. Correct underlying cause 2. Magnesium infusion 3. Defibrillation if necessary 4. Beta blocker 5. Pacemaker
107
Give the pathophysiology of ventricular ectopics
Premature ventricular beats, presenting with brief palpitations
108
Give the ECG presentation of ventricular ectopics
Random, abnormal brief broad QRS complexes on an otherwise normal ECG
109
Give the management of ventricular ectopics
Correct underlying electrolyte disturbance Reassurance - no treatment required in healthy individuals
110
Define 1st degree heart block
PR interval <0.2s with no beats dropped
111
Describe 2nd degree heart block
Mobitz I: progressive prolongation of PR interval until a beat is dropped Mobitz II: constant PR interval with occasional dropped beats
112
Describe third degree heart block
P waves and QRS complexes with no association Significant risk of asystole
113
Describe the ratio of chest compressions:ventilation:defibrillation in adult advanced life support
30 chest compressions:2 breaths Single shock delivered with 2 minutes of CPR between shocks
114
Describe the drug management in adult advanced life support
Adrenaline: 1mg ASAP if non-shockable rhythm. 1mg after 3rd shock in VT/VF, repeat every 3-5 minutes Amiodarone: 300mg after 3rd shock in VT/VF (used to treat arrhythmias - if patient has non-shockable rhythm then is not indicated) Thrombolysis: if PE suspected, then continue CPR for 60-90 minutes
115
Give the management of AV node block (heart block)
1. Atropine (IV bolus) - if no improvement then repeat up to 6x with increasing doses 2. Inotroped (e.g. noradrenaline) 3. Transcutaneous cardiac pacing 4. Pacemaker
116
Give the mechanism of action of atropine
Anti-muscarinic (anti-cholinergic) - acts to inhibit the parasympathetic nervous system and increase heart rate
117
Define cardiac tamponade
Condition where the heart becomes compressed by fluid in the pericardial space, limiting its expansion and reducing diastolic filling. May cause cardiac arrest.
118
Give the causes of cardiac tamponade
1. Trauma (particularly penetrating injury of the chest allowing blood to accumulate) 2. Pericarditis 3. Cancer
119
Give the presentation of cardiac tamponade
Beck's Triad: 1. Hypotension 2. Distended neck veins 3. Muffled heart sounds 4. Tachycardia 5. SOB 6. Chest pain 7. Pleural effusion
120
Give the management of cardiac tamponade
1. Pericardiocentesis - insertion of wide-bore cannula to drain fluid 2. Surgery 3. Conservative management
121
Give the pathophysiology of aortic dissection
Tear in the tunica intima of the aortic wall
122
Give the causes of aortic dissection
1. Hypertension 2. Trauma 3. Ehler's Danlos syndrome 4. Marfan syndrome 5. Turner syndrome 6. Noonan syndrome
123
Give the presentation of aortic dissection
1. Chest/back pain - tearing in nature. 2. Pulse deficit 3. Hypertension
124
Which classification of aortic dissection most commonly presents with chest pain?
Type A
125
Which classification of aortic dissection most commonly presents with back pain?
Type B
126
Describe the classification system used for aortic dissection
Stanford classification Type A: ascending aorta (2/3 of cases) Type B: descending aorta distal to L subclavian origin ## Footnote Type A = Ascending Aorta
127
Describe the pathophysiology of obstructive hypertrophic cardiomyopathy
An autosomal dominant disorder of muscle tissue caused by defects in the genes encoding contractile proteins.
128
Describe the management of obstructive hypertrophic cardiomyopathy
ABCDE: 1. Amiodarone 2. Beta blocker 3. Cardioverter defibrillator 4. Dual chamber pacemaker 5. Endocarditis prophylaxis
129
Give the presentation of obstructive hypertrophic cardiomyopathy
1. Often asymptomatic 2. Exertional dyspnoea 3. Angina 4. Syncope 5. Mitral regurgitation 6. Sudden cardiac death
130
Give the pathophysiology of infective endocarditis
Infection of the endocardium by bacteria, most commonly affecting the valves. Commonly caused by staphylococcus, streptococcus, enterococcus.
131
Which valve is commonly affected by infective endocarditis in IVDU?
Tricuspid valve - most commonly by Staph. aureus
132
Give the causes of infective endocarditis
1. IVDU 2. Poor dental hygiene 3. Cannulae 4. Surgery
133
Describe the presentation of infective endocarditis
New murmur PLUS fever is infective endocarditis until proven otherwise! 1. Petechiae 2. Cardiac/renal failure 3. Night sweats 4. Rigors/malaise/fatigue 5. Splinter haemorrhages 6. Roth spots 7. Janeway lesions 8. Osler nodes ECG: non-specific saddle shaped ST elevation
134
Define Roth spots
Retinal haemorrhages with a pale centre
135
Define Janeway lesion
Non-tender small lumps on palms or soles
136
Define Osler nodes
Painful red lesions on palms or soles
137
How is infective endocarditis diagnosed?
1. Blood culture (x3 in 24 hours) 2. Echocardiogram 3. ECG - non-specific ST elevation
138
Give the management of infective endocarditis
Gentamycin + fluclox OR benzylpenicillin If artificial valve: Gentamycin + vancomycin + rifampicin If penicillin allergy: Gentamycin + vancomycin If resistant to Abx: Surgery to replace or repair valve
139
Describe the pathophysiology of left ventricular aneurysm
The ischaemic damage sustained during MI may weaken the myocardium resulting in aneurysm formation.
140
Describe the presentation of left ventricular aneurysm
1. Left ventricular failure 2. Ankle oedema 3. Dull chest pain ECG: persistent ST elevation
141
Give the management of left ventricular aneurysm
Anticoagulation - thrombus may form within the aneurysm
142
Give the management of ventricular tachycardia
No adverse signs: 1. Amiodarone 2. Electrical cardioversion (if amiodarone fails) Adverse signs (e.g. low BP): 1. Immediate electrical cardioversion
143
Describe the presentation of left ventricular free wall rupture
Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). This is seen in around 3% of MIs and occurs around 1-2 weeks afterwards
144
Describe the management of left ventricular free wall rupture
Urgent pericardiocentesis and thoracotomy are required.
145
Give the adverse effects of loop diuretics
1. hypotension 2. hyponatraemia 3. hypokalaemia, hypomagnesaemia 4. hypochloraemic alkalosis 5. ototoxicity 6. hypocalcaemia 7. renal impairment (from dehydration + direct toxic effect) 8. hyperglycaemia (less common than with thiazides) 9. gout
146
Give the features of acute heart failure on chest xray
Bilateral fluffy opacification with Kerley-B lines
147
Give the mechanism of action of loop diuretcs
Furosemide and bumetanide are loop diuretics that act by inhibiting the Na-K-Cl cotransporter (NKCC) in the thick ascending limb of the loop of Henle, reducing the absorption of NaCl.
148
What is the most appropriate management of complete heart block following an inferior MI?
Atropine External pacing not indicated
149
What is the most appropriate management of wide complex tachyarrhythmias with hypotension?
DC cardioversion
150
Give the presentation of right axis deviation on ECG
Negative QRS complex in lead I and positive QRS complex in lead II and aVF
151
Give the presentation of Takotsubo cardiomyopathy
History of acute or subacute chest pain in a post-menopausal woman after an emotionally stressful experience or situation is typical of Takotsubo cardiomyopathy Shortness of breath, dizziness and syncope
152
What are xanthomata suggestive of?
Hypercholesterolaemia/hyperlipidaemia Xanthomata: yellowish papules and plaques commonly seen on eyelids
153
Give the first line management for stable angina
1. GTN 2. A beta-blocker or a calcium channel blocker is used first-line to prevent angina attacks
154
Give the ECG presentation of hypokalaemia
Hypokalaemia - U waves on ECG
155
Give the management of symptomatic aortic stenosis
Symptomatic aortic stenosis: 1. surgical AVR for low/medium operative risk patients 2. transcatheter AVR for high operative risk patients
156
Give the indications for PCI in acute STEMI
should be offered if the presentation is within 12 hours of the onset of symptoms AND PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given (i.e. consider fibrinolysis if there is a significant delay in being able to provide PCI)
157
Give the management of provoked PE
'Provoked' pulmonary embolisms are typically treated for 3 months with apixaban
158
Give 1 drug interaction for simvastatin
1. Clarithromycin
159
What tool should be used to assess bleeding risk in AF when considering anticoagulation?
ORBIT score
160
Give 1 medication which causes Torsades de Pointes
Macrolides can cause torsades de pointes (e.g. erythromycin)
161
Give 1 medication which causes hypocalcaemia
Hypocalcemia is a side effect of loop diuretics (e.g. furosemide)
162
Give the management of aortic dissection
Type A: IV labetalol + surgery Type B: IV labetalol
163
Give the ECG changes seen in hypokalaemia
presence of U waves (small upward deflections seen after the T waves), flattened T waves, and a borderline elongated PR interval.
164
When is cardiac resynchronisation therapy indicated in chronic heart failure?
heart failure not responding to ACE-inhibitor, beta-blocker and aldosterone antagonist therapy, a widened QRS complex favours cardiac resynchronisation therapy
165
Describe the New York Heart Association grading of chronic heart failure
NYHA Class I 1. no symptoms 2. no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations NYHA Class II 1. mild symptoms 2. slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea NYHA Class III 1. moderate symptoms 2. marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms NYHA Class IV 1. severe symptoms 2. unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity
166
What does PCI involve?
administration of prasugrel, unfractionated heparin and a bailout glycoprotein IIb/IIIa inhibitor.
167
Give 1 example of a long-acting nitrate
Ivabradine
168
Give the management of acute pericarditis
First line management of acute pericarditis involves combination of NSAID and colchicine
169
Give the mechanism of action of dabigatran
Direct thrombin inhibitor