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Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is infective endocarditis?

A

infection of endovascular structures of the heart

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2
Q

What is aortic regurgitation?

A

the reverse flow of blood across the aortic valve in diastole due to the incompetence of the valve

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3
Q

Acute cause of aortic regurgitation

A

Infective endocarditis
Aortic dissection
Traumatic rupture of the valve leaflets (blunt chest trauma or deceleration injury)
Iatrogenic causes (balloon valvotomy or TAVI)

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4
Q

Chronic causes of aortic regurgitation

A

Calcific aortic valve disease (age related)
Myxomatous degeneration
Congenital disease e.g. bicuspid aortic valve
Rheumatic heart disease
IE
Rheumatic causes (e.g. rheumatoid arthritis)
Marfan’s Syndrome

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5
Q

Presentation of aortic regurgitation

A

Early diastolic murmur heard best over left sternal border

collapsing pulse
wide pulse pressure

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6
Q

Management of Unstable Angina

A

MONA
Morphine IV
Oxygen
Nitrates GTN
Aspirin 300mg STAT

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7
Q

Management of STEMI

A

Presenting within 2 hrs
- PCI + antiplatelet (e.g. aspirin, ticagrelor)

After 2hrs
- Thrombolysis (e.g. alteplase, streptokinase, tenecteplase)

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8
Q

Management of NSTEMI

A

BATMAN
Beta-blocker
Aspirin 300mg stat
Ticagrelor
Morphine
Anticoagulation (e.g. LMWH)
Nitrates (e.g. GTN)

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9
Q

What is a J-Wave/Osborne wave

A

positive deflection at the J point between the end of the QRS and beginning of the ST segment

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10
Q

ECG features of hypothermia

A

Bradyarrhythmias
Osborne waves/J waves
Prolonged PR, QRS and QT intervals
Shivering artefact
Ventricular ectopics
Cardiac arrest (VT, VF or asystole)

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11
Q

ACE inhibitor mechanism

A

Inhibits angiotensin converting enzyme (ACE), thus reduces the generation of angiotensin-II and consequently aldosterone.
–> reducing sodium and water retention

Reduced tissue concentration of angiotensin-II also leads to arterial and venous dilation.

Drugs also inhibit bradykinin (a vasodilator) breakdown by ACE

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12
Q

Cautions for ACE inhibitors

A

Careful when used in combination drugs that can increase potassium, as ^ risk of hyperkalaemia (e.g. thiazide-like diuretics, potassium sparing diuretics)

Triple whammy: ACEi (or ARB) + Thiazide diuretics + NSAID
—> famous cause of renal failure
—> do not prescribe

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13
Q

Side effects of ACE inhibitors

A

Persistent dry cough

Postural hypotension - rare unless there is salt and water depletion (e.g. person taking diuretics)/

Renal impairment

Disturbance of taste, N&V, dyspepsia, bowel disturbance
Rashes
Angioedema

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14
Q

Indications for Amiodarone

A

Anti-arrhythmic drug, used in atrial fibrillation and atrial flutter.

Also indicated in:
- Paroxysmal Supraventricular Tachycardia (PSVT)
- Nodal + ventricular tachycardia
- AF + Flutter
- Ventricular fibrillation
- Tachycardias associated w/ Wolf-Parkinson-White syndrome

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15
Q

Mechanism of action of Amiodarone

A
  • Blocks K+ channels, therefore prolonging the refractory period.
  • Also effective at blocking Na+, having a high affinity for inactivated channels.
  • Anti-adrenergic effects by competitively blocking alpha and beta receptors
  • Also has weak Ca2+ blocking effect
  • Slows down the sinus rate and AV conduction, slightly prolongs the QT interval
  • Can also cause peripheral vasodilation
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16
Q

Side effects of Amiodarone

A

Corneal microdeposits
Thyroid function: contains iodine so can cause disorders of thyroid function
Hepatotoxicity
Pulmonary toxicity
Peripheral neuropathy

Pregnancy: possible risk of neonatal goitre, only use if no other alternative.
Breast feeding: avoid due to drug present in breast milk, theoretical risk of neonatal hypothyroidism

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17
Q

Monitoring tests for Amiodarone

A

TFT: before treatment & every 6 months
LFT: before treatment & every 6 months
Serum K+ before treatment
Chest X-Ray before treatment

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18
Q

Complications of coronary angiography

A

Mortality ~1%
Bruising at entry site
May have a false aneurysm at the femoral artery if this was used as the entry site
May get angina-type pain during the procedure
Infection at entry site
May have warm flushing when the dye is injected
Stroke and MI are possible but rare
Rarely, the coronary artery may be damaged and emergency bypass may need to be performed

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19
Q

Mechanism of Angiotensin II Receptor Blockers (ARBs)

A

Selectively inhibit angiotensin II at the AT1 receptor site.
Binding of angiotensin II at the AT1 receptor causes: vasoconstriction, release of aldosterone, sympathetic activation and other potentially harmful effects in the CV system. Therefore, by antagonising angiotensin II at the AT1 receptor it will prevent these effects.

Therefore, causes VASODILATION and blockage of aldosterone release.

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20
Q

Monitoring with ARBs

A

Monitor plasma K+ concentration, especially in elderly & in patient w/ renal impairment.
Can lead to hyperkalaemia

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21
Q

Side effects of ARBs

A

Dry cough

Headaches
N&V + D
Postural hypotension (most common w/ volume depletion e.g. taking diuretics)
Renal impairment
Hyperkalaemia

Avoid in pregnancy: teratogenic
Breastfeeding: generally not recommended

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22
Q

What is aortic stenosis?

A

The narrowing of the three cusps that form the aortic valve.

–> The left coronary cusp (LCC)
–> The right coronary cusp (RCC)
–> The non-coronary cusp (NCC)

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23
Q

Causes of aortic stenosis

A

Senile Calcification (THE most common cause)
–> calcium deposits form on the aortic valve causing narrowing
–> look for corneal arcus (white, blue or grey crescent shape that curves around outer edges of the cornea of the eye)

Congenital
–> Bicuspid Valve
–> Williams syndrome

24
Q

Symptoms and Signs of aortic stenosis

A

Symptoms
–> Angina
–> Syncope
–> Dyspnoea
–> Fatigue

Signs
–> Ejection Systolic murmur best heard in aortic area (R 2nd intercostal space at border of sternum), radiating to carotids
–> Slow-rising pulse, with narrow pulse pressure
–> Heave - but apex beat not displaced
–> Possible signs of:
- Heart failure/pulmonary hypertension: crackles at lung bases, pink forthy sputum, oedema, etc.
- AF - irregularly irregular pulse

25
Q

What does narrow and wide pulse pressure mean?

A

Narrow pulse pressure: difference between systolic and diastolic pressures is small
Wide pulse pressure: difference between systolic and diastolic pressures is large

26
Q

Murmur heard in aortic stenosis

A

Ejection Systolic murmur best heard in aortic area (R 2nd intercostal space at border of sternum), radiating to carotids

27
Q

Investigations for Aortic Stenosis

A

ECG
- L: LBBB (widened and downwardly deflected QRS in V1)
- L: Left Axis Deviation
- L: Left Ventricular Hypertrophy (large R waves in left-sided leads [V5, V6, aVL and I] and deep S waves in right sided leads [V1, V2])
- P: Poor R wave progression (depolarisation of ventricles is slow)

Doppler Echo
–> Used to estimate pressure across the valve
[0 mmHg – normal valve
<30 mmHg – mild aortic stenosis
30-50 mmHg – moderate aortic stenosis
>50 mmHg – severe aortic stenosis]

Cardiac catherisation
–> can assess the actual gradient across the valve as well as check for co-existing CAD

28
Q

Prognosis Aortic Stenosis

A

If untreated
- Angina present: 2 years
- Syncope present: 1 year
- Dyspnoea present: 6 months

29
Q

Management of Aortic stenosis

A

Surgical Valve Replacement if:
- symptomatic (prompt)
- patient has ECG signs
- moderate to severe disease on doppler/cardiac catheterisation

Prosthetic valve: lasts ~10yrs, may require replacement. No need for long term anticoagulant therapy.
Metal valve: lasts a lifetime, BUT require anticoagulation therapy for life. Also noisy.
–> 3 types: tilting disc, double tilting disc. ball in a cage

30
Q

What is Atrial Septal Defect (ASD)?

A

A congenital heart defect that causes a shunting of blood from the left to the right atria.
(i.e. hole in wall between left atria and right atria)

31
Q

Types of Atrial Septal Defect (ASD)

A

Secundum ASD
- 80% of ASD’s
- basically, a patent foramen ovale

Partial AVSD
- minority of cases
- usually involves a defect around the bottom of the atrial septum, and typically involves the tricuspid valve

32
Q

Clinical features of Atrial septal defect

A

Commonly asymptomatic
Recurrent chest infections/wheeze
Heart failure
Arrhythmias - not until >4th decade of life

O/E:
- Split second heart sound
- Ejection systolic murmur: best heard at left sternal edge

33
Q

Investigations for atrial septal defect

A

CXR: may show cardiomegaly and increased pulmonary markings

ECG
- Secundum:
—> RBBB (common in many children anyway)
—> Right axis deviation
- Partial AVSD
—> Left axis deviation
—> Superior QRS axis (AVSD is typically in the region of the AV node, thus conduction is altered)

34
Q

Management of atrial septal defect

A

Secundum ASD
- usually cardiac catheterisation: a device can be inserted to close off the defect

Partial AVSD
- surgery usually required
- usually performed at age 3-5 to prevent RHF and arrhythmias in later life

35
Q

Beck’s Triad and what does it show?

A
  1. Hypotension
  2. Muffled/Quiet heart sounds
  3. Raised JVP

Signs of cardiac tamponade

36
Q

What is the normal length of the PR interval?

A

120ms to 200ms

37
Q

ST elevation in leads II, III, aVF
a) area of myocardium
b) coronary artery

A

a) Inferior
b) RCA

38
Q

ST elevation in V1, V2
a) area of myocardium
b) coronary artery

A

a) Septal
b) Proximal LAD

39
Q

ST elevation in V3 V4
a) area of myocardium
b) coronary artery

A

a) anterior
b) LAD

40
Q

ST elevation in V5 V6
a) area of myocardium
b) coronary artery

A

a) apex
b) distal LAD/LCx/RCA

41
Q

ST elevation in I, aVL
a) area of myocardium
b) coronary artery

A

a) lateral
b) LCx

42
Q

ST elevation in V7 V9
a) area of myocardium
b) coronary artery
c) where would you see ST depression

A

a) posterolateral
b) RCA/LCx
c) you would see ST depression in leads V1-V3

43
Q

Management of Supraventricular Tachycardia

A

Stable SVT = Vagal manoeuvres –> 6mg adenosine –> 12mg adenosine
Unstable SVT = Synchronised DC cardioversion

44
Q

Management of Ventricular Tachycardia

A

Stable patient + pulse = Amiodarone/Procainamide

Unstable + pulse = Synchronised DC cardioversion

Unstable + Pulseless = Unsynchronised cardioversion 360J + CPR

45
Q

What is cardiac tamponade?

A

When fluid build up between the heart tissue and pericardial sac

46
Q

Mitral Valve Prolapse clinical findings

A

A non-ejection click (mid systolic click)
Followed by a pansystolic murmur (mitral regurgitation murmur)

47
Q

First line treatment for hypertension w/ diabetes

A

ACEi regardless of age

48
Q

Mobitz Type 1 Definition

A

Progressive lengthening of the PR interval resulting in a P wave that fails to conduct a QRS

49
Q

Mobitz Type 2 Definition

A

Second degree Av block where there are intermittent non-conducted P waves.
PR interval is constant

50
Q

Causes of Mobitz type 1

A

MI (mainly inferior)
Drugs such as beta/calcium channel blockers, digoxin
Professional athletes due to high vagal tone
Myocarditis
Cardiac surgery

51
Q

Causes of Mobitz type 2

A

Infarction (particularly anterior MI which damages the bundle branches)
Surgery: mitral valve repair or septal ablation
Inflammatory/autoimmune: rheumatic heart disease, SLE, systemic sclerosis, myocarditis
Fibrosis: Lenegre’s disease
Infiltration: sarcoidosis, haemochromatosis, amyloidosis
Medication: beta-blockers, calcium channel blockers, digoxin, amiodarone

52
Q

Management of Mobitz type II

A

Definitive management is with a permanent pacemaker as these patients are at risk of complete heart block and becoming haemodynamically unstable

53
Q

What is complete heart block (third degree)? (+ECG findings)

A

occurs when atrial impulses fail to be conducted to the ventricles
ECG shows severe bradycardia and dissociation between the P waves and QRS complexes

54
Q

Causes of Third degree/complete heart block

A

Myocardial infarction (especially inferior)
Drugs acting at the AV node (beta blockers, calcium channel blockers)
Idiopathic fibrosis

55
Q

Management of complete heart block

A

Permanent pacemaker due to risk of sudden death

Medicine (13 decks)

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