General Cardiology Flashcards

1
Q

What is the mechanism of action of Statins?

A

Statins inhibit the action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis

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2
Q

What are adverse effects of Statins?

A
  • Myopathy
  • Liver impairment
  • Increased risk of Intracereberal haemorrhage
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3
Q

What are the myopathies caused by Statins?

A
  • Types
    • Myalgia
    • Myosistis
    • Rhabdomyolysis
    • Asymptomatic Raised Creatine Kinase
  • Myopathy is more common in lipophilic statins (simvastatin, atorvastatin) than relatively hydrophilic statins (rosuvastatin, pravastatin, fluvastatin)
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4
Q

How is liver impairment managed in statins?

A
  • Check 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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5
Q

Who should receive statins?

A
  • All people with established cardiovascular disease (stroke, TIA, ischaemic heart disease, peripheral arterial disease)
  • Following the 2014 update, NICE recommend anyone with a 10-year cardiovascular risk >= 10%
  • Patients with type 2 diabetes mellitus should now be assessed using QRISK2 like other patients are, to determine whether they should be started on statins
  • Patients with type 1 diabetes mellitus who were diagnosed more than 10 years ago OR are aged over 40 OR have established nephropathy
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6
Q

What is the statin used as Primary Prevention?

A

Atorvastatin 20mg OD

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7
Q

When should statins be taken?

A
  • Statins should be taken at night as this is when the majority of cholesterol synthesis takes place.
  • This is especially true for simvastatin which has a shorter half-life than other statins
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8
Q

How are statins used as Secondary Prevention?

A

Atorvastatin 80mg OD

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9
Q

What are nitrates?

A
  • Nitrates are a group of drugs which have vasodilating effects
  • Work on Veins
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10
Q

What is the mechanism of action of Nitrates?

A
  • Causes release of nitric oxide in smooth muscle, increasing cGMP which leads to a fall in intracellular calcium levels in angina which both work to dilate the coronary arteries
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11
Q

What are side effects of Nitrates?

A
  • Hypotension
  • Tachycardia
  • Headaches
  • Flushing
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12
Q

How should Nitrate tolerance be managed?

A

Patient develop tolerances and experience reduced efficacy

  • Patients who develop tolerance should take the second dose of isosorbide mononitrate after 8 hours, rather than after 12 hours.
  • Allows blood-nitrate levels to fall for 4 hours and maintains effectiveness
  • Effect is not seen in patients who take modified release isosorbide mononitrate
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13
Q

What is adenosine used for?

A

Used to terminate supraventricular tachycardias

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14
Q

What can enhance and block effects of adenosine?

A
  • Adenosine are enhanced by Dipyridamole (antiplatelet agent)
  • Blocked by Theophyllines
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15
Q

When should adenosine be avoided?

A

Avoided in asthmatics due to possible bronchospasm.

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16
Q

What is the mechanism of action of Adenosine?

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
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17
Q

What is the half life of adenosine?

A

8-10 seconds

  • Ideally be infused via a large-calibre cannula due to it’s short half-life,
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18
Q

What are some side effects of Adenosine?

A
  • Chest pain
  • Bronchospasm
  • Transient flushing can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)
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19
Q

What is a Syncope?

A
  • Defined as a transient loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery.
20
Q

What are the types of Syncope?

A
  • Reflex syncope (neurally mediated)
  • Orthostatic syncope
  • Cardiac syncope
21
Q

What causes Reflex Syncope?

A
  • Vasovagal: triggered by emotion, pain or stress. Often referred to as ‘fainting’
  • Situational: cough, micturition, gastrointestinal
  • Carotid sinus syncope
    • Most common cause
22
Q

What causes Orthostatic Syncope?

A
  • Primary Autonomic Failure: Parkinson’s disease, Lewy body dementia
  • Secondary Autonomic Failure: e.g. Diabetic neuropathy, amyloidosis, uraemia
  • Drug-induced: diuretics, alcohol, vasodilators
  • Volume Depletion: haemorrhage, diarrhoea
23
Q

What causes Cardiac Syncope?

A
  • Arrhythmias:
    • Bradycardias (sinus node dysfunction, AV conduction disorders)
    • Tachycardias (supraventricular, ventricular)
  • Structural:
    • Valvular
    • Myocardial infarction
    • Hypertrophic obstructive cardiomyopathy
  • Others:
    • Pulmonary Embolism
24
Q

How do you assess syncope?

A
  • Cardiovascular examination
  • Postural blood pressure readings
    • Symptomatic fall in systolic BP > 20 mmHg or diastolic BP > 10 mmHg or decrease in systolic BP < 90 mmHg is considered diagnostic
    • ECG
    • Carotid sinus massage
  • Tilt table test
    • 24 hour ECG
25
What is Pulsus Paradoxus?
Greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration
26
What causes Pulsus Paradoxus?
* Severe asthma * Cardiac tamponade
27
What causes a Slow-rising pulse?
**Aortic Stenosis**
28
What causes a collapsing pulse?
* **Aortic Regurgitation** * **Patent ductus arteriosus** * **Hyperkinetic States** (anaemia, thyrotoxic, fever, exercise/pregnancy)
29
What causes Pulsus Alterans?
* Regular alternation of the force of the arterial pulse * Severe LVF
30
What causes Bisferiens Pulse?
* 'double pulse' * Two systolic peaks * Mixed Aortic Valve Disease
31
What are pulses for HOCM?
* Jerky Pulse * Bisferiens pulse
32
What causes Ejection systolic mumurs?
* Aortic Stenosis * Pulmonary Stenosis * Hypertrophic obstructive cardiomyopathy atrial septal defect, tetralogy of Fallot
33
What causes late systolic?
* Mitral valve prolapse * Coarctation of aorta
34
What causes early diastolic murmurs?
* **Aortic Regurgitation** * high-pitched and 'blowing' in character * **Graham-Steel murmur** * pulmonary regurgitation, again high-pitched and 'blowing' in character
35
What causes mid-late diastolic murmurs?
* **Mitral stenosis** * 'rumbling' in character * **Austin-Flint murmur** * severe aortic regurgitation, again is 'rumbling' in character
36
What causes continuous machine-like murmur?
**Patent ductus arteriosus**
37
What gives an S1 heart sound?
* **Closure of mitral and tricuspid valves** * Soft in Long PR or Mitral Regurgitation * Loud in mitral stenosis
38
What gives an S2 heart sound?
* Closure of **Aortic** and **Pulmonary** valves * Soft in aortic stenosis * Splitting during inspiration is normal
39
What gives an S3 heart sound?
* 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
What gives an S4 heart sound?
* May be heard in Aortic stenosis, HOCM, hypertension * Caused by atrial contraction against a stiff ventricle in HOCM a double apical impulse may be felt as a result of a palpable S4
41
What are some abnormal waves on ECG?
* Q waves are associated with a previous myocardial infarction * Delta waves are associated with Wolff-Parkinson-White Syndrome * Saddle ST elevation is associated with pericarditis
42
What are normal variants on the ECG?
* Sinus arrhythmia * Right axis deviation (tall and thin individuals) * Left axis deviation (short, obese individuals) * Partial right bundle branch block
43
What are additional normal variants seems in athletes?
* Sinus bradycardia * 1st degree atrioventricular block * Wenckebach phenomenon (2nd degree atrioventricular block Mobitz type 1) * Junctional escape rhythm
44
What are risk factors for myopathy in Statins?
**Risks factors for myopathy include:** * Advanced age * Female sex * Low body mass index * Presence of multisystem disease such as diabetes mellitus.
45
What are the effects of Nitrates on the heart?
* Causes **Venous Dilation** * **Reduces Venous return** which in turn * **Reduces left ventricular work so** reduced preload * Reducing myocardial oxygen demand