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Cardiology Flashcards

1
Q

Cardiology: What is the definition of syncope?

A

A transient loss of consciousness due to transient global cerebral hypoperfusion characterized by rapid onset, short duration and complete recovery.

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2
Q

Cardiology: What features would suggest vasovagal syncope?

A
  • Long-history of syncope
  • Prolonged standing
  • Noxious stimulus
  • Nausea and vomiting associated.
  • Absence of cardiac disease
  • After exertion
  • After head tilting / carotid pressure
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3
Q

Cardiology: What features would suggest cardiac syncope?

A
  • Known history of cardiac disease
  • Evidence of structural abnormality
  • Preceded by chest pain / palpitations
  • During exercise
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4
Q

Cardiology: What is the treatment for syncope? (In broad terms)

A

Treat the underlying condition.

E.g. Ischaemia, drug-induced.

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5
Q

Cardiology: What is the normal PR interval? (In squares and time)

A

120-200ms

3-5 small squares

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6
Q

Cardiology: What is the normal size of a QRS?

A

120ms

3 small squares

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7
Q

Cardiology: What is the first-line treatment for symptom relief in chronic stable angina?

A

Nitrates, e.g. GTN

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8
Q

Cardiology: What is the mechanism of action of nitrates?

A

Release of NO to activate and increase cyclic-GMP which causes smooth muscle relaxation and subsequent cardiac vasodilation.

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9
Q

Cardiology: What are the side-effects of nitrates?

A
  • Hypotension
  • Headache
  • Flushing
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10
Q

Cardiology: What are the contraindications of nitrates?

A
  • Hypotension
  • Aortic/ Mitral stenosis
  • Hypertrophic cardiomyopathy
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11
Q

Cardiology: What is the first-line treatment of chronic stable angina?

A

Beta-blockers

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12
Q

Cardiology: What is the mechanism of action for beta-blockers in the treatment of chronic stable angina?

A
  • Reduces sympathetic stimulation to the heart, causing a reduction in heart rate and myocardial contraction.
  • Reduces cardiac workload to increase exercise tolerance and reduce symptoms.
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13
Q

Cardiology: If a patient is contra-indicated for beta-clockers what is the first-line treatment for the management of chronic stable angina?

A
  • Non-dihydropyridine calcium channel blocker.

* E.g. Verapamil, Diltiazem

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14
Q

Cardiology: What are the side-effects of beta-blockers?

A

Bronchospasm, bradycardia, cold peripheries, sleep disturbance, sexual dysfunction, fatigue.

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15
Q

Cardiology: What are the contra-indications of beta-blockers?

A 
Asthma
Bradycardia
Uncontrolled heart failure
2/3rd degree heart block
Severe peripheral arterial disease
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16
Q

Cardiology: Which medications may be added for treatment of chronic stable angina if beta-blockers are not provided sufficient relief?

A
  • 2nd Line - Calcium-channel blockers (Amlodipine, Felodipine, Nifedipine)
  • Longer-acting nitrates
  • Potassium channel activators (Nicorandil)
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17
Q

Cardiology: What is the mechanism of action of calcium channel blockers in the treatment of chronic stable angina?

A
  • Smooth muscle relaxation due to inhibition of influx of calcium ions.
  • Relaxation of coronary and peripheral smooth muscle.
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18
Q

Cardiology: Non-dihydropyridine calcium channel blockers (Verapamil, Diltiazem) have an additional mechanism to other calcium channel blockers, what is it?

A

Slows conduction of AV node so has a rate limiting effect.

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19
Q

Cardiology: What are the side-effects of dihydropyridine calcium channel blockers? (amlodipine, felodipine, nifedipine)

A
  • Flushing
  • Dizziness
  • Ankle-swelling
  • Hypotension
  • Headache
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20
Q

Cardiology: What are the contraindications for the use of dihydropyridine calcium channel blockers? (Amlodipine, felodipine, nifedipine)

A
  • Uncontrolled heart failure
  • Within one month post-MI
  • Severe aortic stenosis
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21
Q

Cardiology: What are the side-effects of non-dihydropyridine calcium channel blockers? (Verapamil, diltiazem)

A
  • Bradycardia
  • AV/SA heart-block
  • Constipation (Verapamil)
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22
Q

Cardiology: What are the contraindications of non-dihydropyridine calcium channel blockers? (Verapamil, diltiazem)

A
  • Bradycardia
  • 2/3 degree heart block
  • Verapamil not to be used with beta-blocker
  • Heart failure
  • Acute porphyria
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23
Q

Cardiology: What is the mechanism of action of nicorandil in the treatment of chronic stable angina?

A
  • NO donor to acticate cyclic-GMP to act as a vasodilator to both venous and arteries.
  • Opens K channels resulting in efflux of K and reduction in Ca causing smooth muscle relaxation.
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24
Q

Cardiology: What are the side-effects of nicorandil?

A
  • Headache
  • GI irritation
  • Hypotension
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25
Q

Cardiology: What is the acronym for the initial management of a suspected ACS?

A 
MONA
• Morphine (5-10mg Given by slow I.V, an anti-emetic will also be needed)
• Oxygen
• Nitrates
• Aspirin (300mg stat)
26
Q

Cardiology: What is the MI-5? (Secondary prevention for an ACS)

A
  • Aspirin
  • ACE-I
  • Beta-blocker
  • Statin
  • Clopidogrel
27
Q

Cardiology: What is the mechanism of action of aspirin?

A
  • Irreversibly inhibits COX-1 and COX-2.
  • This inhibits the production of Thromboxane A2.
  • Which in turn inhibits platelet aggregation.
28
Q

Cardiology: What are the side-effects of aspirin?

A
  • GI irritation

* Bronchospasm

29
Q

Cardiology: What are the contra-indications and interactions of aspirin?

A
  • Active peptic ulceration, hypersensitivity, bleeding disorder.
  • Any other drugs that increase the risk of bleeding.
30
Q

Cardiology: What is the mechanism of action of clopidogrel?

A
  • A prodrug converted to active metabolite by CYP enzymes.

* Irreversibly blocks py12 receptor on platelet surface.

31
Q

Cardiology: What are the side-effects of clopidogrel?

A

• GI irritation

32
Q

Cardiology: What are the contra-indications and interactions of clopidogrel?

A
  • Active bleeding.
  • Any other drug which increases bleeding risk, Fluoxetine (reduces antiplatelet effect), Enzyme inducers (carbamazepine, fluconazole, PPIs)
33
Q

Cardiology: What is the mechanism of action of ACE-I?

A
  • Reduces formation of Angiotensin II from angiotensin I.

* Results in reduced vasoconstriction and reduced formation of Aldosterone (Which promotes sodium and water retention)

34
Q

Cardiology: What are the side-effects of ACE-I?

A
  • Cough
  • Hyperkalaemia
  • Renal impairment
  • Hypotension
  • Angioedema
  • Hepatic impairment
35
Q

Cardiology: What are the contra-indications and interactions of ACE-I?

A
  • Use with caution in renal impairment. Bilateral renal artery stenosis, severe aortic stenosis.
  • Diuretics, nephrotoxic drugs.
36
Q

Cardiology: What is the mechanism of action of ARBs (sartans)?

A

• Direct antagonist of Angiotensin II - blocks the vasoconstriction and aldosterone release.

37
Q

Cardiology: What are the side-effects of ARBs?

A
  • Hypotension
  • Angioedema
  • Renal impairment
  • Hyperkalaemia
38
Q

Cardiology: What are the contra-indications and interactions of ARBs?

A
  • Cautions - renal artery stenosis, renal impairment.

* Diuretics, use with ACE-I only under specialist supervision.

39
Q

Cardiology: What is the definition of hypoxia?

A

• A lack of oxygen resulting in a decrease in aerobic oxidative respiration resulting in cell injury.

40
Q

Cardiology: What is the definition of ischaemia?

A

A lack of blood supply to a tissue or drainage away from a tissue due to stenosis or obstruction of a vessel. This results in a loss of oxygen and a build up of toxic metabolites. Tissue injury is quicker from ischaemia than hypoxia.

41
Q

Cardiology: What is the definition of infarction?

A

Irreversible damage to a tissue due to ischaemia and hypoxia.

42
Q

Cardiology: What are the mechanisms of cell injury?

A
  • Decreased ATP production
  • Membrane damage
  • Increased intracellular calcium
  • Increased oxygen derived free radicals
43
Q

Cardiology: Give some differentials for chronic stable angina.

A
  • Reflux oesophagittis
  • PE
  • Pneumothorax
  • Aortic Dissection
  • Costochondral pain
  • Pleuritis
  • Varicella zoster
44
Q

Cardiology: What are the three indications for coronary bypass surgery (According to AHA)

A
  • 3 vessel disease
  • 2 vessel disease with LV impairment
  • LMS
45
Q

Cardiology: What are the four life-threatening causes of chest pain that you should never miss?

A
  • MI
  • PE
  • Tension pneumothorax
  • Dissecting thoracic aneurysm
46
Q

Cardiology: What are the three main causes of aortic stenosis?

A
  • Calcific degeneration
  • Bicuspid valve
  • Rheumatic
47
Q

Cardiology: What are the complications of aortic stenosis? (Cardiac)

A

Pressure build up in the left ventricle leading to left ventricular hypertrophy, LV dilation and LV failure.

48
Q

Cardiology: What pulse do you get with aortic stenosis?

A

Slow-rising

49
Q

Cardiology: What is the classification of severe aortic stenosis, in terms of mean gradient mmHg, Jet velocity and valve area.

A
  • Mean gradient >40mmHg
  • Jet velocity m/s >4.0
  • Valve area cm2
50
Q

Cardiology: In which four situations is AVR recommended for aortic stenosis?

A
  • Symptomatic severe AS.
  • Severe AS undergoing CABG
  • Severe AS undergoing surgery on aorta or other heart valves.
  • Severe AS and LV systolic dysfunction.
51
Q

Cardiology: What are the two structures that allow blood to bypass the lungs in the fetal circulation?

A
  • Ductus arteriosus

* Foramen Ovale

52
Q

Cardiology: What changes occur in the fetal lungs following birth?

A
  • Birth causes the infant to take first breaths.
  • Lungs fill with air and alveolar fluid is cleared.
  • Pulmonary capillaries absorb oxygen from the air, pulmonary arterioles dilate causing pulmonary vascular resistance to fall dramatically.
  • Blood flows into the pulmonary vascular system.
53
Q

Cardiology: What causes the ductus arteriosus to close following birth?

A
  • Due to decreased pulmonary vascular resistance, the pressure in the pulmonary artery falls.
  • This causes blood to flow from the aorta through the Ductus arteriosus into the pulmonary artery.
  • The ductus closes in response to oxygen by the contraction of smooth muscle.
54
Q

Cardiology: How does the foramen ovale close following birth?

A
  • Due to increased blood flow returning from the lungs, the pressure in the left atrium increases.
  • As blood flow returning from placaenta is decreased, the pressure in the right atrium decreases.
  • Both these changes close the foramen ovale by pressing the septum primum against the septum secundum.
55
Q

Cardiology: What structures do the ductus arteriosus, ductus venosus, umbilical arteries and umbilical vein become?

A
  • Ductus arteriosus - ligamentum arteriosum
  • Ductus venosus - ligamentum venosum
  • Umbilical arteries - Medial umbilical ligaments
  • Umbilical vein - ligamentum teres
56
Q

Cardiology: What are the symptoms of persistent pulmonary hypertension of the newborn?

A
  • Right to left shunting across PDA and PFO
  • Cyanosis
  • Acidosis
  • Lower limb sats
57
Q

Cardiology: What is the treatment for pulmonary hypertension of the newborn?

A
  • Oxygen, ventilation, nitric oxide.

* Extracorporeal membrane oxygenation.

58
Q

Cardiology: What is Starling’s law of the heart?

A

The ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return.

59
Q

Cardiology: The presence of a bicuspid aortic valve is associated with which conditions?

A
  • Aortic root dilation
  • Heyde’s syndrome
  • Coarctation
  • Williams syndrome
  • PDA
  • Turner’s syndrome
60
Q

Cardiology: What are the symptoms of aortic stenosis?

A 
SAD
- Syncope - Exertional
- Angina
- Dyspnoea
(May be asymptomatic in earlier stages)
61
Q

Cardiology: What are the initial investigations for suspected aortic stenosis?

A
  • FBC - ensure not anaemic
  • Renal function
  • ECG (Heart block, LBBB)
  • CXR (coarctation, heart failure, aneurysm.)
  • Echocardiogram
62
Q

Cardiology: What are the four types of mechanical heart valves?

A
  • Ball and cage
  • Tilting disk
  • Bi-leaflet
  • Tri-leaflet

Revision Cards (61 decks)

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