Cardiology Flashcards

(258 cards)

1
Q

Pulsus paradoxus

A

greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or absent pulse in inspiration
severe asthma, cardiac tamponade

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2
Q

Slow-rising/plateau pulse

A

aortic stenosis

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3
Q

Collapsing pulse

A

aortic regurgitation
patent ductus arteriosus
hyperkinetic states (anaemia, thyrotoxic, fever, exercise/pregnancy)

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4
Q

Pulsus alternans

A

regular alternation of the force of the arterial pulse

severe LVF

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5
Q

Bisferiens pulse

A

‘double pulse’ - two systolic peaks

mixed aortic valve disease

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6
Q

Jerky’ pulse

A

Hypertrophic obstructive cardiomyopathy- may also be associated with bisferiens pulse

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7
Q

ECG signs: Digoxin toxicity

A
ECG features
down-sloping ST depression ('reverse tick', 'scooped out')
flattened/inverted T waves
short QT interval
arrhythmias e.g. AV block, bradycardia
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8
Q

Ejection systolic murmur

A
louder on expiration
aortic stenosis
hypertrophic obstructive cardiomyopathy
louder on inspiration
pulmonary stenosis
atrial septal defect
also: tetralogy of Fallot
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9
Q

Holo/pan systolic murmur

A

mitral/tricuspid regurgitation (high-pitched and ‘blowing’ in character)
tricuspid regurgitation becomes louder during inspiration, unlike mitral stenosis
during inspiration, the venous blood flow into the right atrium and ventricle are increased → increases the stroke volume of the right ventricle during systole
ventricular septal defect (‘harsh’ in character)

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10
Q

Late systolic

A

mitral valve prolapse

coarctation of aorta

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11
Q

Early diastolic murmur

A
aortic regurgitation (high-pitched and 'blowing' in character)
Graham-Steel murmur (pulmonary regurgitation, again high-pitched and 'blowing' in character)
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12
Q

Mid-late diastolic murmur

A
mitral stenosis ('rumbling' in character)
Austin-Flint murmur (severe aortic regurgitation, again is 'rumbling' in character)
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13
Q

Continuous machine-like murmur

A

patent ductus arteriosus

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14
Q

Causes of prolonged QT

Congenital

A

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

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15
Q

Causes of prolonged QT

drugs

A
amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram)
methadone
chloroquine
terfenadine**
erythromycin
haloperidol
ondanestron
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16
Q

Causes of prolonged QT

other

A
electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia
acute myocardial infarction
myocarditis
hypothermia
subarachnoid haemorrhage
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17
Q

heart sounds

S1

A

closure of mitral and tricuspid valves
soft if long PR or mitral regurgitation
loud in mitral stenosis

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18
Q

heart sounds

s2

A

closure of aortic and pulmonary valves
soft in aortic stenosis
splitting during inspiration is normal

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19
Q

heart sounds s3

A

aused by diastolic filling of the ventricle
considered normal if < 30 years old (may persist in women up to 50 years old)
heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock) and mitral regurgitation

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20
Q

heart sounds S4

A

may be heard in aortic stenosis, HOCM, hypertension
caused by atrial contraction against a stiff ventricle
therefore coincides with the P wave on ECG
in HOCM a double apical impulse may be felt as a result of a palpable S4

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21
Q

Causes of left axis deviation (LAD)

ECG

A

left anterior hemiblock
left bundle branch block
inferior myocardial infarction
Wolff-Parkinson-White syndrome* - right-sided accessory pathway
hyperkalaemia
congenital: ostium primum ASD, tricuspid atresia
minor LAD in obese people

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22
Q

Causes of Right axis deviation (RAD)

A
right ventricular hypertrophy
left posterior hemiblock
lateral myocardial infarction
chronic lung disease → cor pulmonale
pulmonary embolism
ostium secundum ASD
Wolff-Parkinson-White syndrome* - left-sided accessory pathway
normal in infant < 1 years old
minor RAD in tall people
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23
Q

Adenosine

A

Adenosine is most commonly used to terminate supraventricular tachycardias. The effects of adenosine are enhanced by dipyridamole (antiplatelet agent) and blocked by theophyllines. It should be avoided in asthmatics due to possible bronchospasm.

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24
Q

Adenosine Mechanism of Action

A

causes transient heart block in the AV node
agonist of the A1 receptor in the atrioventricular node, which inhibits adenylyl cyclase thus reducing cAMP and causing hyperpolarization by increasing outward potassium flux
adenosine has a very short half-life of about 8-10 seconds

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25
Adverse effects of Adenosine
chest pain bronchospasm transient flushing can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)
26
what is an a wave?
large if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis, pulmonary hypertension absent if in atrial fibrillation
27
What are cannon 'a' waves?
caused by atrial contractions against a closed tricuspid valve are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm, single chamber ventricular pacing
28
what are 'c' waves?
closure of tricuspid valve | not normally visible
29
what are 'v' waves?
due to passive filling of blood into the atrium against a closed tricuspid valve giant v waves in tricuspid regurgitation
30
What is 'X' descent?
fall in atrial pressure during ventricular systole
31
What is 'Y' descent?
opening of tricuspid valve
32
Pathophysiology of Hypertrophic obstructive cardiomyopathy
the most common defects involve a mutation in the gene encoding β-myosin heavy chain protein or myosin-binding protein C results in predominantly diastolic dysfunction left ventricle hypertrophy → decreased compliance → decreased cardiac output characterized by myofibrillar hypertrophy with chaotic and disorganized fashion myocytes ('disarray') and fibrosis on biopsy
33
Features of hypertrophic obstructive cardiomyopathy
often asymptomatic exertional dyspnoea angina syncope typically following exercise due to subaortic hypertrophy of the ventricular septum, resulting in functional aortic stenosis sudden death (most commonly due to ventricular arrhythmias), arrhythmias, heart failure jerky pulse, large 'a' waves, double apex beat ejection systolic murmur increases with Valsalva manoeuvre and decreases on squatting hypertrophic cardiomyopathy may impair mitral valve closure, thus causing regurgitation
34
Conditions associated with hypertrophic obstructive cardiomyopathy
Freidreich's ataxia | Wolf-Parkinson's White
35
ECHO findings in hypertrophic obstructive cardiomyopathy
mnemonic - MR SAM ASH mitral regurgitation (MR) systolic anterior motion (SAM) of the anterior mitral valve leaflet asymmetric hypertrophy (ASH)
36
Mitral stenosis features
``` mid-late diastolic murmur (best heard in expiration) loud S1, opening snap low volume pulse malar flush atrial fibrillation ```
37
Features of severe mitral stenosis
lengthening of murmur | opening snap becomes closer to S2
38
CXR findings of mitral stenosis
left atrial enlargement may be seen
39
Third heart sounds (S3)
caused by diastolic filling of the ventricle considered normal if < 30 years old (may persist in women up to 50 years old) heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock) and mitral regurgitation
40
Fourth heart sounds (S4)
may be heard in aortic stenosis, HOCM, hypertension caused by atrial contraction against a stiff ventricle therefore coincides with the P wave on ECG in HOCM a double apical impulse may be felt as a result of a palpable S4
41
Anteroseptal MI | Leads and arteries
V1-V4 | Left anterior descending
42
Inferior MI | Leads and arteries
II, III, aVF, | Right coronary artery
43
Anterolateral MI | Leads and arteries
V4-6, I, aVL, | Left anterior descending or left circumflex
44
Lateral MI | Leads and arteries
I, aVL, V5-6 | Left circumflex
45
Posterior MI | Leads and arteries
Tall R Waves in V1-2 | Left circumflex and right coronary
46
Causes of left axis deviation
left anterior hemiblock left bundle branch block inferior myocardial infarction Wolff-Parkinson-White syndrome* - right-sided accessory pathway hyperkalaemia congenital: ostium primum ASD, tricuspid atresia minor LAD in obese people
47
causes of right axis deviation
``` right ventricular hypertrophy left posterior hemiblock lateral myocardial infarction chronic lung disease → cor pulmonale pulmonary embolism ostium secundum ASD Wolff-Parkinson-White syndrome* - left-sided accessory pathway normal in infant < 1 years old minor RAD in tall people ```
48
What is BNP
produced mainly by left ventricle in response to strain
49
effects of BNP
vasodilator diuretic and natriuretic suppresses both sympathetic tone and the renin-angiotensin-aldosterone system
50
What reduces BNP?
ACE-i ARBs diuretics
51
Patients at risk of infective endocarditis
- previously normal mitral valve - rheumativ heart disease - congenital defects - IVDU - recent piercings
52
Causes of infective endocarditis
- used to be staph epidermidis - up to 2 months post valve replacement- strep viridans - 2+ post valve replacement/ generally most common - staph aureus - SLE
53
Culture negative causes of infective endocarditis
``` prior antibiotic therapy Coxiella burnetii Bartonella Brucella HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella) ```
54
Causes of constrictive pericarditis
- TB | - any cause of pericarditis
55
Features of constrictive pericarditis
dyspnoea right heart failrue - raised JVP, ascites, oedema, hepatomegaly. JVP - prominent X & Y descent pericardial knock - loud S3 Kussmaul positive (paradoxical rise in JVP on inspiration
56
CXR findings - constrictive pericarditis
calcified pericardium
57
Features of cardiac tamponade
JVP - absent Y descent pulsus paradoxus Kussmaul - rare
58
Mechanism of action of Amiodarone
class III antiarrhythmic agent used in the treatment of atrial, nodal and ventricular tachycardias. The main mechanism of action is by blocking potassium channels which inhibits repolarisation and hence prolongs the action potential. Amiodarone also has other actions such as blocking sodium channels (a class I effect)
59
Amiodarone monitoring
TFT, LFT, U&E, CXR prior to treatment | TFT, LFT every 6 months
60
Adverse reactions to amiodarone
``` thyroid dysfunction: both hypothyroidism and hyper-thyroidism corneal deposits pulmonary fibrosis/pneumonitis liver fibrosis/hepatitis peripheral neuropathy, myopathy photosensitivity 'slate-grey' appearance thrombophlebitis and injection site reactions bradycardia lengths QT interval ```
61
Causes of prolonged PR interval
``` idiopathic ischaemic heart disease digoxin toxicity hypokalaemia* rheumatic fever aortic root pathology e.g. abscess secondary to endocarditis Lyme disease sarcoidosis myotonic dystrophy ```
62
History of cardiac tamponade
a 60-year-old man with a history of lung cancer presents with dyspnoea. On examination he is tachycardic, hypotensive, has a raised JVP with an absent Y descent and has pulsus paradoxus
63
History of constrictive pericardititis
a 60-year-old man with a history of tuberculosis presents with dyspnoea and fatigue. On examination the JVP is elevated, there is a loud S3 and Kussmaul's sign is positive. Hepatomegaly is also noted
64
Causes of constrictive pericarditis
TB | any other cause of pericarditis
65
Features of constrictive pericarditis
``` dyspnoea right heart failure: elevated JVP, ascites, oedema, hepatomegaly JVP shows prominent x and y descent pericardial knock - loud S3 Kussmaul's sign is positive ```
66
Mechanism of action of thiazide diuretics
inhibiting sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Cl− symporter. Potassium is lost as a result of more sodium reaching the collecting ducts.
67
Common adverse effects of thiazide diuretics
``` dehydration postural hypotension hyponatraemia, hypokalaemia, hypercalcaemia* gout impaired glucose tolerance impotence ```
68
Rare adverse effects of thiazide diuretics
thrombocytopaenia agranulocytosis photosensitivity rash pancreatitis
69
What is Takayasu's arteritis
Takayasu's arteritis is a large vessel vasculitis. It typically causes occlusion of the aorta and questions commonly refer to an absent limb pulse. It is more common in females and Asian people Associated with renal artery stenosis Managed with steroids
70
Features of Takayasu's arteritis
systemic features of a vasculitis e.g. malaise, headache unequal blood pressure in the upper limbs carotid bruit intermittent claudication aortic regurgitation (around 20%)
71
Causes of PR prolongation
``` idiopathic ischaemic heart disease digoxin toxicity hypokalaemia* rheumatic fever aortic root pathology e.g. abscess secondary to endocarditis Lyme disease sarcoidosis myotonic dystrophy ```
72
History of left ventrivcular wall rupture
a patient develops acute heart failure 10 days following a myocardial infarction. On examination he has a raised JVP, pulsus paradoxus and diminished heart sounds
73
History of post MI VSD
a patient develops acute heart failure 5 days after a myocardial infarction. A new pan-systolic murmur is noted on examination
74
Causes of LBBB
``` ischaemic heart disease hypertension aortic stenosis cardiomyopathy rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia ```
75
Causes of dilated cardiomyopathy
idiopathic: the most common cause myocarditis: e.g. Coxsackie B, HIV, diphtheria, Chagas disease ischaemic heart disease peripartum hypertension iatrogenic: e.g. doxorubicin substance abuse: e.g. alcohol, cocaine inherited: Duchenne's infiltrative e.g. haemochromatosis, sarcoidosis + these causes may also lead to restrictive cardiomyopathy nutritional e.g. wet beriberi (thiamine deficiency)
76
Pathophysiology of Dilated Cardiomyopathy
``` dilated heart leading to predominately systolic dysfunction all 4 chambers are dilated, but the left ventricle more so than right ventricle eccentric hypertrophy (sarcomeres added in series) is seen ```
77
Features of Dilated Cardiomyopathy
classic findings of heart failure systolic murmur: stretching of the valves may result in mitral and tricuspid regurgitation S3 'balloon' appearance of the heart on the chest x-ray
78
Risk factors for Mitral Regurgiation
``` Female sex Lower body mass Age Renal dysfunction Prior myocardial infarction Prior mitral stenosis or valve prolapse Collagen disorders e.g. Marfan's Syndrome and Ehlers-Danlos syndrome ```
79
Causes of Mitral Regurgitation
``` Following coronary artery disease or post-MI Mitral valve prolapse Infective endocarditis Rheumatic fever. Congenital ```
80
Symptoms of Mitral Regurgitation
Symptoms tend to be due to failure of the left ventricle, arrhythmias or pulmonary hypertension.
81
Signs of Mitral Regurgitation
The murmur heard on auscultation of the chest is typically a pansystolic murmur described as “blowing”. It is heard best at the apex and radiating into the axilla. S1 may be quiet as a result of incomplete closure of the valve. Severe MR may cause a widely split S2
82
Investigations of Mitral Regurgitation
ECG may show a broad P wave, indicative of atrial enlargement Cardiomegaly may be seen on chest x-ray, with an enlarged left atrium and ventricle Echocardiography is crucial to diagnosis and to assess severity
83
Treatment options of Mitral Regurgitation
Medical management in acute cases involves nitrates, diuretics, positive inotropes and an intra-aortic balloon pump to increase cardiac output If patients are in heart failure, ACE inhibitors may be considered along with beta-blockers and spironolactone In acute, severe regurgitation, surgery is indicated The evidence for repair over replacement is strong in degenerative regurgitation, and is demonstrated through lower mortality and higher survival rates When this is not possible, valve replacement with either an artificial valve or a pig valve is considered
84
Other processes during PCI Primary coronary intervention for patients with STEMI
thrombus aspiration, but not mechanical thrombus extraction, should be considered complete revascularisation should be considered for patients with multivessel coronary artery disease without cardiogenic shock
85
Drug therapy during PCI Primary coronary intervention for patients with STEMI
patients undergoing PCI with radial access: unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) - this is the action of using a GPI during the procedure when it was not intended from the outset, e.g. because of worsening or persistent thrombus patients undergoing PCI with femoral access: bivalirudin with bailout GPI
86
Antiplatelet therapy during PCI Primary coronary intervention for patients with STEMI
this is termed 'dual antiplatelet therapy', i.e. aspirin + another drug if the patient is not taking an oral anticoagulant: prasugrel if taking an oral anticoagulant: clopidogrel
87
Fibrinolysis for patients with STEMI
Fibrinolysis used to be the only form of coronary reperfusion therapy available. However, it is used much less commonly now given the widespread availability of PCI. Patients undergoing fibrinolysis should also be given an antithrombin drug. An ECG should be repeated after 60-90 minutes to see if the ECG changes have resolved. If patients have persistent myocardial ischaemia following fibrinolysis then PCI should be considered.
88
Management of unstable angina/NSTEMI
antithrombin treatment fondaparinux should be offered to patients who are not at a high risk of bleeding and who are not having angiography immediately if immediate angiography is planned or a patients creatinine is > 265 µmol/L then unfractionated heparin should be given
89
What does GRACE stand for?
``` Global Registry of Acute Coronary Events age heart rate, blood pressure cardiac (Killip class) and renal function (serum creatinine) cardiac arrest on presentation ECG findings troponin levels ```
90
Which patients with NSTEMI/unstable angina should have coronary angiography (with follow-on PCI if necessary)?
immediate: patient who are clinically unstable (e.g. hypotensive) within 72 hours: patients with a GRACE score > 3% i.e. those at intermediate, high or highest risk coronary angiography should also be considered for patients if ischaemia is subsequently experienced after admission
91
Primary coronary intervention for patients with NSTEMI/unstable angina Further drug therapy
unfractionated heparin should be given regardless of whether the patient has had fondaparinux or not further antiplatelet ('dual antiplatelet therapy', i.e. aspirin + another drug) prior to PCI if the patient is not taking an oral anticoagulant: prasugrel or ticagrelor if taking an oral anticoagulant: clopidogrel
92
Conservative management for patients with NSTEMI/unstable angina Further drug therapy
``` further antiplatelet ('dual antiplatelet therapy', i.e. aspirin + another drug) if the patient is not at a high risk of bleeding: ticagrelor if the patient is at a high risk of bleeding: clopidogrel ```
93
ECG P wave changes increased P Wave amplitude
cor pulmonale
94
ECG P wave changes Broad, notched (bifid) P waves
often most pronounced in lead II | a sign of left atrial enlargement, classically due to mitral stenosis
95
Tricuspid stenosis JVP
Large A waves
96
Causes of RBBB
normal variant - more common with increasing age right ventricular hypertrophy chronically increased right ventricular pressure - e.g. cor pulmonale pulmonary embolism myocardial infarction atrial septal defect (ostium secundum) cardiomyopathy or myocarditis
97
Thrombolysis
Thrombolytic drugs activate plasminogen to form plasmin. This in turn degrades fibrin and help breaks up thrombi. They in primarily used in patients who present with a ST elevation myocardial infarction. Other indications include acute ischaemic stroke and pulmonary embolism, although strict inclusion criteria apply. Examples alteplase tenecteplase streptokinase
98
Contra-indications to thrombolysis
``` active internal bleeding recent haemorrhage, trauma or surgery (including dental extraction) coagulation and bleeding disorders intracranial neoplasm stroke < 3 months aortic dissection recent head injury severe hypertension ```
99
Features of patent ductus arteriosus
``` left subclavicular thrill continuous 'machinery' murmur large volume, bounding, collapsing pulse wide pulse pressure heaving apex beat ```
100
Management of patent ductus arteriosus
indomethacin or ibuprofen given to the neonate inhibits prostaglandin synthesis closes the connection in the majority of cases if associated with another congenital heart defect amenable to surgery then prostaglandin E1 is useful to keep the duct open until after surgical repa
101
Patent Ductus Arteriosus
a form of congenital heart defect generally classed as 'acyanotic'. However, uncorrected can eventually result in late cyanosis in the lower extremities, termed differential cyanosis connection between the pulmonary trunk and descending aorta usually, the ductus arteriosus closes with the first breaths due to increased pulmonary flow which enhances prostaglandins clearance more common in premature babies, born at high altitude or maternal rubella infection in the first trimester
102
Features of Aortic regurgitation
early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre collapsing pulse wide pulse pressure Quincke's sign (nailbed pulsation) De Musset's sign (head bobbing) mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams
103
Valvular Causes of aortic regurgitation
rheumatic fever infective endocarditis connective tissue diseases e.g. RA/SLE bicuspid aortic valve
104
Aortic causes of aortic regurgitation
``` aortic dissection spondylarthropathies (e.g. ankylosing spondylitis) hypertension syphilis Marfan's, Ehler-Danlos syndrome ```
105
Stage 1 hypertension
Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg
106
Stage 2 hypertension
Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg
107
Stage 3 Hy[erension
Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 110 mmHg
108
Step 1 Hypertension Management
patients < 55-years-old or a background of type 2 diabetes mellitus: ACE inhibitor or a Angiotensin receptor blocker (ACE-i or ARB): (A) angiotensin receptor blockers should be used where ACE inhibitors are not tolerated (e.g. due to a cough) patients >= 55-years-old or of black African or African–Caribbean origin: Calcium channel blocker (C) ACE inhibitors have reduced efficacy in patients of black African or African–Caribbean origin are therefore not used first-line
109
Step 2 Hypertension Management
if already taking an ACE-i or ARB add a Calcium channel blocker or a thiazide-like Diuretic if already taking a Calcium channel blocker add an ACE-i or ARB or a thiazide-like Diuretic for patients of black African or African–Caribbean origin taking a calcium channel blocker for hypertension, if they require a second agent consider an angiotensin receptor blocker in preference to an ACE inhibitor (A + C) or (A + D) or (C + A) or (C + D)
110
Step 3 Hypertension Management
add a third drug to make, i.e.: if already taking an (A + C) then add a D if already (A + D) then add a C (A + C + D)
111
Step 4 Hypertension management
NICE define step 4 as resistant hypertension and suggest either adding a 4th drug (as below) or seeking specialist advice first, check for: confirm elevated clinic BP with ABPM or HBPM assess for postural hypotension. discuss adherence if potassium < 4.5 mmol/l add low-dose spironolactone if potassium > 4.5 mmol/l add an alpha- or beta-blocker
112
New hypertension drugs Direct renin inhibitors
e.g. Aliskiren (branded as Rasilez) by inhibiting renin blocks the conversion of angiotensinogen to angiotensin I no trials have looked at mortality data yet. Trials have only investigated fall in blood pressure. Initial trials suggest aliskiren reduces blood pressure to a similar extent as angiotensin converting enzyme (ACE) inhibitors or angiotensin-II receptor antagonists adverse effects were uncommon in trials although diarrhoea was occasionally seen only current role would seem to be in patients who are intolerant of more established antihypertensive drugs
113
Ischaemia of the papillary muscle History
a patient is noted to have a new early-to-mid systolic murmur 10 days after being admitted for a myocardial infarction
114
Post-myocardial infarction ventricular septal defect History
a patient develops acute heart failure 5 days after a myocardial infarction. A new pan-systolic murmur is noted on examination
115
What is bivalirudin?
Bivalirudin is a reversible direct thrombin inhibitor used as an anticoagulant in the management of acute coronary syndrome.
116
Nitrate side effects
hypotension tachycardia headaches flushing
117
Mechanism of action - nitrates
nitrates cause the release of nitric oxide in smooth muscle, activating guanylate cyclase which then converts GTP to cGMP, which in turn leads to a fall in intracellular calcium levels in angina they both dilate the coronary arteries and also reduce venous return which in turn reduces left ventricular work, reducing myocardial oxygen demand
118
Nitrate tolerance
many patients who take nitrates develop tolerance and experience reduced efficacy the BNF advises that patients who develop tolerance should take the second dose of isosorbide mononitrate after 8 hours, rather than after 12 hours. This allows blood-nitrate levels to fall for 4 hours and maintains effectiveness this effect is not seen in patients who take modified release isosorbide mononitrate
119
Mechanism of action of ACE-i
inhibit the conversion angiotensin I to angiotensin II | ACE inhibitors are activated by phase 1 metabolism in the liver
120
Side effects of ACE-i
cough occurs in around 15% of patients and may occur up to a year after starting treatment thought to be due to increased bradykinin levels angioedema: may occur up to a year after starting treatment hyperkalaemia first-dose hypotension: more common in patients taking diuretics
121
Cautions and contraindications of ACE-i
pregnancy and breastfeeding - avoid renovascular disease - may result in renal impairment aortic stenosis - may result in hypotension hereditary of idiopathic angioedema specialist advice should be sought before starting ACE inhibitors in patients with a potassium >= 5.0 mmol/L
122
Interactions with ACE-i
patients receiving high-dose diuretic therapy (more than 80 mg of furosemide a day) significantly increases the risk of hypotension
123
Monitoring ACE-i
urea and electrolytes should be checked before treatment is initiated and after increasing the dose a rise in the creatinine and potassium may be expected after starting ACE inhibitors acceptable changes are an increase in serum creatinine, up to 30% from baseline and an increase in potassium up to 5.5 mmol/l. significant renal impairment may occur in patients who have undiagnosed bilateral renal artery stenosis
124
Arrythmogenic right ventricular cardiomyopathy What is it?
Arrhythmogenic right ventricular cardiomyopathy (ARVC, also known as arrhythmogenic right ventricular dysplasia or ARVD) is a form of inherited cardiovascular disease which may present with syncope or sudden cardiac death. It is generally regarded as the second most common cause of sudden cardiac death in the young after hypertrophic cardiomyopathy.
125
Pathophysiology of arrhythmogenic right cardiomyopathy
inherited in an autosomal dominant pattern with variable expression the right ventricular myocardium is replaced by fatty and fibrofatty tissue around 50% of patients have a mutation of one of the several genes which encode components of desmosome
126
Presentation of arrhythmogenic right ventricular cardiomyopathy
palpitations syncope sudden cardiac death
127
Investigation of arrhythmogenic right ventricular cardiomyopathy
ECG abnormalities in V1-3, typically T wave inversion. An epsilon wave is found in about 50% of those with ARV - this is best described as a terminal notch in the QRS complex echo changes are often subtle in the early stages but may show an enlarged, hypokinetic right ventricle with a thin free wall magnetic resonance imaging is useful to show fibrofatty tissue
128
Management of arrhythmogenic right ventricular cardiomyopathy
drugs: sotalol is the most widely used antiarrhythmic catheter ablation to prevent ventricular tachycardia implantable cardioverter-defibrillator
129
What is Naxos disease
an autosomal recessive variant of ARVC | a triad of ARVC, palmoplantar keratosis, and woolly hair
130
What is Buerger's disease?
(also known as thromboangiitis obliterans) is a small and medium vessel vasculitis that is strongly associated with smoking.
131
Features of Buerger's disease
``` extremity ischaemia intermittent claudication ischaemic ulcers superficial thrombophlebitis Raynaud's phenomenon ```
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Contraindications to beta blockers
uncontrolled heart failure asthma sick sinus syndrome concurrent verapamil use: may precipitate severe bradycardia
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Side Effects of beta blockers
``` bronchospasm cold peripheries fatigue sleep disturbances, including nightmares erectile dysfunction ```
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Uses of adenosine
Adenosine is most commonly used to terminate supraventricular tachycardias. The effects of adenosine are enhanced by dipyridamole (antiplatelet agent) and blocked by theophyllines. It should be avoided in asthmatics due to possible bronchospasm.
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Mechanism of action of adenosine
causes transient heart block in the AV node agonist of the A1 receptor in the atrioventricular node, which inhibits adenylyl cyclase thus reducing cAMP and causing hyperpolarization by increasing outward potassium flux adenosine has a very short half-life of about 8-10 seconds
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Adverse effects of adenosine
Chest pain bronchospasm transient flushing can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)
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What is nicorandil?
vasodilatory drug used to treat angina. It is a potassium-channel activator with vasodilation is through activation of guanylyl cyclase which results in increase cGMP.
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Side effects of nicorandil
flushing headache kin, mucosal and eye ulceration gastrointestinal ulcers including anal ulceration Cntra indicated in LVF
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ECG changes in hypothermia
``` bradycardia 'J' wave - small hump at the end of the QRS complex first degree heart block long QT interval atrial and ventricular arrhythmias ```
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Anti-platelets ACS 1st line
Aspirin (lifelong) & ticagrelor (12 months)
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Anti-platelets ACS 2nd Line
If aspirin contraindicated, clopidogrel (lifelong
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Anti-platelets PCI 1st Line
Aspirin (lifelong) & prasurgrel or ticagrelor (12 months)
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Anti-platelets PCI 2nd Line
If aspirin contraindicated, clopidogrel (lifelong)
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Anti-platelets TIA 1st Line
Clopidogrel (lifelong)
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Anti-platelets TIA 1st Line
Aspirin (lifelong) & dipyridamole (lifelong)
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Anti-platelets Ischaemic stroke 1st line
Clopidogrel (lifelong)
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Anti-platelets Ischaemic stroke 2nd Line
Aspirin (lifelong) & dipyridamole (lifelong)
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Anti-platelets Peripheral arterial disease 1st Line
Clopidogrel (lifelong)
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Anti-platelets Peripheral arterial disease 2nd Line
Asprin (lifelong)
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Poor prognostic factors in infective endocarditits
Staphylococcus aureus infection (see below) prosthetic valve (especially 'early', acquired during surgery) culture negative endocarditis low complement levels
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DVLA rules Hypertension
can drive unless treatment causes unacceptable side effects, no need to notify DVLA if Group 2 Entitlement the disqualifies from driving if resting BP consistently 180 mmHg systolic or more and/or 100 mm Hg diastolic or more
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DVLA rules elective angioplasty
1 week off driving
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DVLA rules CABG
4 weeks off driving
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DVLA rules ACS
4 weeks off driving | 1 week if successfully treated by angioplasty
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DVLA rules Angina
driving must cease if symptoms occur at rest/at the wheel
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DVLA rules Pacemaker insertion
1 week off driving
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DVLA rules ICD insertion
if implanted for sustained ventricular arrhythmia: cease driving for 6 months if implanted prophylactically then cease driving for 1 month. Having an ICD results in a permanent bar for Group 2 drivers
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DVLA rules successful catheter ablation for an arrhythmia
2 days off driving
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DVLA rules aortic aneurysm >6cm or more
notify DVLA. Licensing will be permitted subject to annual review. an aortic diameter of 6.5 cm or more disqualifies patients from driving
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DVLA heart transplant
do not drive for 6 weeks, no need to notify DVLA
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Ranson criteria
Acute pancreatitis
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Waterlow score
Assesses the risk of a patient developing a pressure sore
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Alcohol screening tool
FAST CAGE Audit
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CHA2DS2-VASc
Used to determine the need to anticoagulate a patient in atrial fibrillation
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ABCD2
Prognostic score for risk stratifying patients who've had a suspected TIA
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What is Brugada syndrome
Brugada syndrome is a form of inherited cardiovascular disease with may present with sudden cardiac death. It is inherited in an autosomal dominant fashion and has an estimated prevalence of 1:5,000-10,000. Brugada syndrome is more common in Asians.
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Pathophysiology of Brugada
a large number of variants exist around 20-40% of cases are caused by a mutation in the SCN5A gene which encodes the myocardial sodium ion channel protein
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ECG changes in Brugada
convex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wave partial right bundle branch block the ECG changes may be more apparent following the administration of flecainide or ajmaline - this is the investigation of choice in suspected cases of Brugada syndrome
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Managment of Brugada
implantable cardioverter-defibrillator
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What is BNP
B-type natriuretic peptide (BNP) is a hormone produced mainly by the left ventricular myocardium in response to strain. Whilst heart failure is the most obvious cause of raised BNP levels any cause of left ventricular dysfunction such as myocardial ischaemia or valvular disease may raise levels. Raised levels may also be seen due to reduced excretion in patients with chronic kidney disease. Factors which reduce BNP levels include treatment with ACE inhibitors, angiotensin-2 receptor blockers and diuretics.
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Effects of Dyspnoea
vasodilator diuretic and natriuretic suppresses both sympathetic tone and the renin-angiotensin-aldosterone system
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Pathogenesis of Rheumatic Fever
Streptococcus pyogenes infection → activation of the innate immune system leading to antigen presentation to T cells B and T cells produce IgG and IgM antibodies and CD4+ T cells are activated there is then a cross-reactive immune response (a form of type II hypersensitivity) thought to be mediated by molecular mimicry the cell wall of Streptococcus pyogenes includes M protein, a virulence factor that is highly antigenic. It is thought that the antibodies against M protein cross-react with myosin and the smooth muscle of arteries this response leads to the clinical features of rheumatic fever Aschoff bodies describes the granulomatous nodules found in rheumatic heart fever
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Major criteria for Rheumatic Fever
treptococcus pyogenes infection → activation of the innate immune system leading to antigen presentation to T cells B and T cells produce IgG and IgM antibodies and CD4+ T cells are activated there is then a cross-reactive immune response (a form of type II hypersensitivity) thought to be mediated by molecular mimicry the cell wall of Streptococcus pyogenes includes M protein, a virulence factor that is highly antigenic. It is thought that the antibodies against M protein cross-react with myosin and the smooth muscle of arteries this response leads to the clinical features of rheumatic fever Aschoff bodies describes the granulomatous nodules found in rheumatic heart fever
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congenital heart conditions - acyanotic
``` ventricular septal defects (VSD) - most common, accounts for 30% atrial septal defect (ASD) patent ductus arteriosus (PDA) coarctation of the aorta aortic valve stenosis ```
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congenital heart conditions - cyanotic
tetralogy of Fallot transposition of the great arteries (TGA) tricuspid atresia
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features of cardiac tamponade
Hypotension Raised JVP Muffled heart sounds
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other features of cardiac tamponade
dyspnoea tachycardia an absent Y descent on the JVP - this is due to the limited right ventricular filling pulsus paradoxus - an abnormally large drop in BP during inspiration Kussmaul's sign - much debate about this ECG: electrical alternans
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features of Patent ductus arteriosus
``` left subclavicular thrill continuous 'machinery' murmur large volume, bounding, collapsing pulse wide pulse pressure heaving apex beat collapsing pulse ```
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management of patent ductus arteriosus
indomethacin or ibuprofen given to the neonate inhibits prostaglandin synthesis closes the connection in the majority of cases if associated with another congenital heart defect amenable to surgery then prostaglandin E1 is useful to keep the duct open until after surgical repair
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Hypercalcaemia features
'bones, stones, groans and psychic moans' corneal calcification shortened QT interval on ECG hypertension
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Mitral/tricuspid regurgitation murmur
Holosystolic murmur, high-pitched and 'blowing' in character
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ECG changes: arrhythmogenic right ventricular cardiomyopathy
inverted T waves
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JVP in SVC obstruction
a non-pulsatile raised JVP
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JVP in complete heart block
cannon A wave pulse
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Mechanism of action- hydralazine
increases cGMP leading to smooth muscle relaxation | Contra-indicated in SLE, IHD, CVD
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Adverse effects of hydralazine
``` tachycardia palpitations flushing fluid retention headache drug-induced lupus ```
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Pulse in patent ductus arteriosus (also aortic regurg)
Collapsing pulse
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pulse in aortic stenosis
slow rising pulse
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What is the most appropriate long-term antiplatelet choice for percutaneous coronary intervention (no drug allergies)?
Aspirin (lifelong) & prasugral or ticagrelor (12 months), no other antiplatelets
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ACS anti-platelets: Indications for Clopidogrel (lifelong), no other anti-platelets)
peripheral arterial disease (no drug allergies) ischaemic stroke (no drug allergies) TIA (no drug allergies)
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ACS anti-platelets: which conditions managed with: | Aspirin (lifelong) & dipyridamole (lifelong), no other antiplatelets
``` TIA (cannot take clopidogrel) ischaemic stroke (cannot take clopidogrel) ```
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Management of prosthetic valve endocarditis caused by staphylococci?
Flucloxacillin + rifampicin + low-dose gentamicin
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Management of native valve endocarditis caused by staphylococci
Flucloxacillin
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Adverse effects of adenosine
chest pain bronchospasm transient flushing can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)
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Hypertrophic obstructive cardiomyopathy is associated with which genetic condition
Freidreich's ataxia
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blood pressure target (> 80 years, clinic reading) is:
150/90
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What is Buerger's disease
Buerger's disease (also known as thromboangiitis obliterans) is a small and medium vessel vasculitis that is strongly associated with smoking. ``` Features extremity ischaemia intermittent claudication ischaemic ulcers superficial thrombophlebitis Raynaud's phenomenon ```
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Initial blind therapy of infective endocarditis (prosthetic valve)
Vancomycin + rifampicin + low-dose gentamicin
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Patent ductus arteriosus -murmur
Continuous 'machinery' murmur
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Opening snap
Mitral stenosis
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Split S2
mitral regurgitation
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JVP pulse: absent Y descent
cardiac tamponade
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NSTEMI identified, aspirin given, 6-month mortality intermediate/high(>3%) -
PCI within 72hrs
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What is ivabradine
Ivabradine is a class of anti-anginal drug which works by reducing the heart rate. It acts on the If ('funny') ion current which is highly expressed in the sinoatrial node, reducing cardiac pacemaker activity
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Adverse effects of ivabradine
visual effects, particular luminous phenomena, are common headache bradycardia, heart block
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Genetics of hypertrophic obstructive cardiomyopathy
Usually due to a mutation in the gene encoding beta-myosin heavy chain protein
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Side effects of ARBs
Hyperkalaemia | Hypotension
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ECG changes: Hypokalaemia
ST depression a long QT interval a prolonged PR interval U waves
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ECG Changes Brugarda syndrome
Elevated ST | inverted T wave
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mechanism of action: isosorbide mononitrate
Increases cGMP leading to smooth muscle relaxation
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Stereotypical history: aortic regurgitation
a 50-year-old man with Marfan syndrome presents with palpitations and dyspnoea. On examination he has a collapsing pulse, the blood pressure is 160/60 mmHg and a high-pitched diastolic murmur is heard
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Stereotypical history mitral regurgitaion
a 70-year-old woman is found to have a pan-systolic murmur after presenting with dyspnoea. A soft S1 and split S2 is also noted
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Causes of pulsus paradoxus
severe asthma, cardiac tamponade
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Mechanism of action of thienopyridines (clopidogrel, prasugrel, ticagrelor, ticlopidine)
antagonist of the P2Y12 adenosine diphosphate (ADP) receptor, inhibiting the activation of platelets
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indications of ticagrelor
Everyone who has a MI - NSTEMI or STEMI
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Contraindications for bisoprolol
Concurrent verapamil - can cause complete heart block | Use nicorandil instead
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Mechanism of action: dipyrimadole
Dipyridamole increases the levels adenosine and inhibits the phosphodiesterase enzymes that normally break down cAMP. Exogenous use of adenosine (e.g. treatment of supraventricular tachycardia) is contraindicated in patients on dipyridamole for this reason.
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Mechanism of action: nicorandil
relaxes coronary vascular smooth muscle by stimulating guanylyl cyclase and increasing cyclic GMP (cGMP) levels (as shown first in our laboratory) as well as by a second mechanism resulting in activation of K+ channels and hyperpolarization
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Ebstein's abnormality
tricuspid regurgitation → pansystolic murmur, worse on inspiration associated with benzos and lithium in pregnancy
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Indications for surgery in infective endocarditis
severe valvular incompetence aortic abscess (often indicated by a lengthening PR interval) infections resistant to antibiotics/fungal infections cardiac failure refractory to standard medical treatment recurrent emboli after antibiotic therapy
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what reduces the impact of adenosine
Aminophylline | Dipyramidole enhances the impact of adenosine
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Causes of ST depression
``` secondary to abnormal QRS (LVH, LBBB, RBBB) ischaemia digoxin hypokalaemia syndrome X ```
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What is syndrome X
Microvascular angina Relieved by rest or nitroglycerin Normal coronary arteriograms the cause of ischemia seems to be reflex intramyocardial coronary constriction and reduced coronary flow reserve. Other patients have microvascular dysfunction within the myocardium: The abnormal vessels do not dilate in response to exercise or other cardiovascular stressors; sensitivity to cardiac pain may also be increased.
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Treatment of pulmonary hypertension: vasodilator negative
much more common than a positive response, can be treated with prostacyclin analogues, endothelin receptor antagonists or phosphodiesterase inhibitors. Patients often require combination therapy. Bosentan is the correct answer and is an endothelin receptor antagonist. Treprostinil and iloprost are prostacyclin analogue
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Congential heart disease
cyanotic: TGA most common at birth, Fallot's most common overall acyanotic: VSD most common cause
226
Overview of cholesterol embolism
cholesterol emboli may break off causing renal disease the majority of cases are secondary to vascular surgery or angiography. Other causes include severe atherosclerosis, particularly in large arteries such as the aorta
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Features of cholesterol embolism
eosinophilia purpura renal failure livedo reticularis
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Pulmonary arterial hypertension
esting mean pulmonary artery pressure of >= 25 mmHg. Endothelin thought to play a key role in pathogenesis of PAH. It is more common in females and typically presents between the ages of 30-50 years. Pulmonary hypertension may of course develop secondary to chronic lung diseases such as COPD. 10% Autosomal dominant inheritance
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Features of pulmonary arterial hypertension
progressive exertional dyspnoea is the classical presentation other possible features include exertional syncope, exertional chest pain and peripheral oedema cyanosis right ventricular heave, loud P2, raised JVP with prominent 'a' waves, tricuspid regurgitation
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negative response to acute vasodilator testing (majority of patients) pulmonary artery hypertension
prostacyclin analogues: treprostinil, iloprost endothelin receptor antagonists: bosentan, ambrisentan phosphodiesterase inhibitors: sildenafil
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positive response to cute vasodilator testing (a minority of patients) pulmonary arterial hypertension
oral calcium channel blockers
232
Most important investigation in pulmonary artery hypertension
cardiac catheterisation to measure right heart pressures
233
ECG features of Wolf-Parkinson White
short PR interval wide QRS complexes with a slurred upstroke - 'delta wave' left axis deviation if right-sided accessory pathway* right axis deviation if left-sided accessory pathway*
234
Types of Wolf Parkinson White
``` type A (left-sided pathway): dominant R wave in V1 type B (right-sided pathway): no dominant R wave in V ```
235
Management of Wolf Parkinson White
definitive treatment: radiofrequency ablation of the accessory pathway medical therapy: sotalol***, amiodarone, flecainide **sotalol should be avoided if there is coexistent atrial fibrillation as prolonging the refractory period at the AV node may increase the rate of transmission
236
Conditions associated with Wolf Parkinson White
``` HOCM mitral valve prolapse Ebstein's anomaly thyrotoxicosis secundum ASD ```
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Mechanism of action: amiodarone
blocking potassium channels which inhibits repolarisation and hence prolongs the action potential. Amiodarone also has other actions such as blocking sodium channels (a class I effect)
238
Why should you check U+Es before giving amiodarone
to detect underlying hypokalaemia- dramatically increases the risk of arrhythmias
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Conditions associated with aortic dissection
hypertension: the most important risk factor trauma bicuspid aortic valve collagens: Marfan's syndrome, Ehlers-Danlos syndrome Turner's and Noonan's syndrome pregnancy syphilis
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DeBakey Classification of aortic dissection
type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally type II - originates in and is confined to the ascending aorta type III - originates in descending aorta, rarely extends proximally but will extend distally
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Stanford classification of aortic dissection
type A - ascending aorta, 2/3 of cases | type B - descending aorta, distal to left subclavian origin, 1/3 of cases
242
Features of aortic dissection
chest pain: typically severe, radiates through to the back and 'tearing' in nature pulse deficit weak or absent carotid, brachial, or femoral pulse variation (>20 mmHg) in systolic blood pressure between the arms aortic regurgitation hypertension other features may result from the involvement of specific arteries. For example coronary arteries → angina, spinal arteries → paraplegia, distal aorta → limb ischaemia the majority of patients have no or non-specific ECG changes. In a minority of patients, ST-segment elevation may be seen in the inferior leads
243
Warfarin guidelines in dentistry
check INR 72 hours before procedure, proceed if INR < 4.0
244
ECG changes in hypothermia
``` bradycardia 'J' wave - small hump at the end of the QRS complex first degree heart block long QT interval atrial and ventricular arrhythmias ```
245
Normal ECG variation in young athletes
sinus bradycardia junctional rhythm first degree heart block Wenckebach phenomenon
246
Poor prognostic factors in infective endocarditis
Staphylococcus aureus infection prosthetic valve (especially 'early', acquired during surgery) culture negative endocarditis low complement levels
247
Definitive investigation for Streptococcus gallolyticus
Colonoscopy. | Streptococcus gallolyticus is the subtype of Streptococcus bovis most linked with colorectal cancer
248
Drug causes of prolonged QT
``` amiodarone, sotalol, class 1a antiarrhythmic drugs tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram) methadone chloroquine terfenadine** erythromycin haloperidol ondanestron ```
249
Management of broad complex tachycardia
amiodarone: ideally administered through a central line lidocaine: use with caution in severe left ventricular impairment procainamide Verapamil should NOT be used in VT.
250
ECG changes in Hypercalcaemia
shortening of the QT interval. Other findings include prolonged PR, widened QRS and ST elevation Hypercalcaemia causes certain calcium ion channels to be opened for shorter amounts of time which in turn reduce phase 2 (the plateau phase) of the cardiomyocyte. This shortens the QT interval.
251
Causes of aortic stenosis
younger patients < 65 years: bicuspid aortic valve | older patients > 65 years: calcification
252
Clinical features (symptomatic disease) in aortic stenosis
chest pain dyspnoea syncope murmur an ejection systolic murmur (ESM) is classically seen in aortic stenosis classically radiates to the carotids this is decreased following the Valsalva manoeuvre
253
Features of aortic stenosis
``` narrow pulse pressure slow rising pulse delayed ESM soft/absent S2 S4 thrill duration of murmur left ventricular hypertrophy or failure ```
254
Causes of aortic stenosis
degenerative calcification (most common cause in older patients > 65 years) bicuspid aortic valve (most common cause in younger patients < 65 years) William's syndrome (supravalvular aortic stenosis) post-rheumatic disease subvalvular: HOCM
255
Management of aortic stenosis
if asymptomatic then observe the patient is general rule if symptomatic then valve replacement if asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction then consider surgery cardiovascular disease may coexist. For this reason an angiogram is often done prior to surgery so that the procedures can be combined balloon valvuloplasty is limited to patients with critical aortic stenosis who are not fit for valve replacement
256
Indications for warfarin
venous thromboembolism: target INR = 2.5, if recurrent 3.5 atrial fibrillation, target INR = 2.5 mechanical heart valves, target INR depends on the valve type and location. Mitral valves generally require a higher INR than aortic valves.
257
Factors that potentiate warfarin
liver disease P450 enzyme inhibitors, e.g.: amiodarone, ciprofloxacin cranberry juice drugs which displace warfarin from plasma albumin, e.g. NSAIDs inhibit platelet function: NSAIDs
258
Side effects of Warfarin
haemorrhage teratogenic, although can be used in breastfeeding mothers skin necrosis: when warfarin is first started biosynthesis of protein C is reduced. This results in a temporary procoagulant state after initially starting warfarin, normally avoided by concurrent heparin administration. Thrombosis may occur in venules leading to skin necrosis purple toes