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MSRA revision > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What are the uses of ACE inhibitors?

A

1st line <55 y/o and/or T2DM for hypertension
Used in diabetic nephropathy
2ndry prevention in IHD

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2
Q

What is the MOA of ACEi?

A

inhibit the conversion on Angiotensin 1 to Angiotensin 2
activated by Phase 1 metabolism in the liver

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3
Q

What are the side effects of ACEi?

A
  • cough (due to raised bradykinin levels)
  • angioedema
  • Hyperkalaemia
  • 1st dose hypotension (more common in patient’s taking diuretics)
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4
Q

What are the cautions/ C.I of ACEi?

A
  • breast feeding/ pregnancy - avoid
  • hereditary angioedema
  • renovascular disease (renal artery stenosis)
  • Aortic stenosis - can cause hypotension
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5
Q

What are the monitoring requirements for ACEi?

A

initial U+Es on initiation and on dose increase
up to 30% increase from baseline in creatinine
up to 25% fall in eGFR
K+ level up to 5..5 mol/l

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6
Q

What is Acute Pericarditis?

A

the inflammation of the pericardial sac,
lasts <4-6 weeks

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7
Q

list the possible causes of Acute Pericarditis?

A
  • Viral (Coxasckie)
  • post MI
    >early: fibrinous pericarditis
    > late (weeks/months): autoimmune (Dressler’s syndrome)
  • SLE/Rheumatoid arthritis
  • Hypothyroidism
  • Lung/ Breast cancer
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8
Q

list the symptoms of pericarditis?

A

Pleuritic chest pain
non productive cough
dyspnoea
flu-like symptoms
pericardial rub
symptoms improved on sitting forward (worse on lying flat)

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9
Q

What are the common ECG changes seen in Pericarditis?

A
  • global/widespread ST and PR segment changes
    > ST: saddle-shaped ST elevation
    > PR: PR depression
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10
Q

What is the most specific ECG changes for Pericarditis

A

widespread PR depression

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11
Q

What investigation is required for all patients suspected of pericarditis

A

ECG
transthroacic echo
bloods: infection markers + troponin

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12
Q

What is the management of acute pericarditis?

A

NSAIDS + colchicine (until symptom resolution and normalisation of inflammatory markers)

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13
Q

What is the main use of adenosine?

A

to terminate SVT

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14
Q

What drug enhances the affects of Adenosine?

A

Dipyridamole (Antiplatelet)

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15
Q

What drug blocks the effects of Adenosine?

A

Theophylline’s

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16
Q

In what patient group should Adenosine be AVOIDED in?

A

Asthmatics

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17
Q

What is the MOA of Adenosine

A

transient heart block in AV node (agonist of A1 receptor)

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18
Q

List the possible side effects of Adenosine

A
  • chest pain
  • bronchospasm
  • Transient flushing
  • enhances conduction down accessory pathways –> increases ventricular rate (WPW syndrome)
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19
Q

List the possible side effects of Adenosine

A
  • chest pain
  • bronchospasm
  • transient flushing
  • enhance conduction down accessory pathways - increase ventricular rate (WPW syndrome)
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20
Q

What type of drug is Amiodarone?

A

Class III anti-arrhythmic
used to repeat atrial, nodal and ventricular tachycardias

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21
Q

What type of drug is Amiodraone?

A

Class III anti-arrhythmic
used to repeat atrial, nodal and ventricular tachycardias

22
Q

What is the MOA of Amiodraone

A
  • blocks potassium channels inhibiting depolarisation (hence prolonged AP)
  • also blocks Na channels (class I effect)
23
Q

What effect does amiodarone have on the P450 system?

A

P450 inhibitor (reduces metabolism of warfarin)

24
Q

What is the initial monitoring of Amiodraone?

A
25
Q

What are the main monitoring parameters of Amiodarone?

A

TFTs, LFTs every 6 months

26
Q

List the possible side effects of Amiodarone?

A
  • Hypo/Hyperthyroidism
  • slate-grey appearance
  • corneal deposits
  • pulmonary fibrosis/ pneumonitis
  • liver fibrosis/ hepatitis
  • peripheral neuropathy (myopathy)
  • photosensitivity
  • thrombophlebitis - injection site reaction
  • Bradycardia
  • QT prolongation
27
Q

List the possible side effects of Amiodarone?

A
28
Q

What is the initial monitoring of Amiodraone?

A

TFTs, LFTs, U+E + CXR prior

29
Q

What is the MOA of Amiodarone?

A
  • blocks potassium channels inhibiting depolarisation (hence prolonged AP)
  • also blocks Na channels (class I effect)
30
Q

What is the MOA of Amiodarone?

A
  • blocks potassium channels inhibiting depolarisation (hence prolonged AP)
  • also blocks Na channels (class I effect)
31
Q

What is the initial monitoring of Amiodarone?

A

TFTs, LFTs, U+E + CXR prior

32
Q

Define Angina pectoris

A

clinical syndrome of chest pain on exertion, secondary to myocardial ischaemia. It is due to the narrowing of the arteries, secondary to coronary heart disease

NICE defines as:
1. constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
2. precipitated by physical exertion
3. relieved by rest or GTN in about 5 mins

33
Q

What are the features of stable angina

A
  • classically left sided chest pain, may radiate to the left arm/neck
  • dyspnoea
  • nausea, lightheadedness and fatigue
34
Q

what artery and ECG leads correlate to the anterolateral area of the heart?

A

artery: left coronary artery

ECG: I aVL, V3-6

35
Q

what artery and ECG leads correlate to the anterior area of the heart?

A

artery: left anterior descending

ECG: V1-4

36
Q

what artery and ECG leads correlate to the lateral area of the heart?

A

artery: circumflex

ECG: I, aVL, V5-6

37
Q

what artery and ECG leads correlate to the inferior area of the heart?

A

artery: inferior

ECGL II, III, aVF

38
Q

What can happen if you use verapamil and a beta-blocker together

A

risk of complete heart block

39
Q

What is the common management of all patients with ACS?

A
  • Aspirin 300mg
  • O2 if stats <94%
  • IV morphine + anti-emetic
  • Nitrates sublingually or IV - be cautious in hypotension
40
Q

How do you define a STEMI?

A
  • clinical symptoms consistent with ACS (generally of >20 minutes)
  • with persistent (>20 minutes) ECG features in 2 contiguous leads
41
Q

What are the ECG changes that define a STEMI?

A

ECG features in >2 contiguous leads of:
- 2.5 mm (i.e. >2.5 small squares) ST evolution in leads V2-3 in men <40 yrs
—> OR >2 mm (>2 small squares) ST elevation in leads V2-3 in men >40 yrs

  • 1.5 mm ST elevation in V2-3 in women
  • 1mm ST elevation in other leads
  • new LBBB (LBBB should be considered new unless there is evidence otherwise)
42
Q

When should primary percutaneous coronary intervention be offered to patient with confirmed STEMI?

A
  • if the presentation is within 12 hours of the onset of symptoms
  • PCI can be delivered within 120 minutes

NB: if patients present after 12 hours and still have evidence of ongoing ischaemia - then PCI should still be considered

43
Q

When should fibrinolysis be offered to patients with confirmed STEMI?

A

within 12 hours of the onset of symptoms if primary PCI cannot be delivered within 120 minutes

HOWEVER if an ECG taken 90 minutes after fibrinolysis shows no resolution of the ST elevation - the patient requires PCI

44
Q

What medications must be given prior to pPCI

A

dual anti platelet therapy i..e Aspirin + another drug

  • if the patient is NOT taking an oral anticoagulant: Prasugrel
  • if patient IS taking an oral anticoagulant: Clopidogrel
45
Q

What drug therapies are given during pPCI?

A

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

46
Q

following fibrinolysis what should be performed

A

an ECG after 60-90 minutes to see if the ECG changes have resolved. if the patient haves persistent myocardial ischaemia, then PCI should be considered

47
Q

What medication is given alongside fibrinolysis

A

antithrombin

48
Q

what medication is given after fibrinolysis

A

Ticagrelor

49
Q

What is the medical management of an STEMI?
HINT: BATMAN

A

B - Base the decision about angiography and PCI on the GRACE score

A- Aspirin 300mg stat dose

T - Ticagrelor 180 mg stat dose (clopidogrel if high bleeding risk, or prasugrel if having angiography)

M - Morphine titrated to control pain

A- Antithrombin therapy with fondaparinux (unless high bleeding risk of immediate angiography)

N-Nitrate (GTN)

Give oxygen only if their saturation drops

50
Q

What is the GRACE score

A

the GRACE score gives a 6-month probability of death after having an NSTEMI
- age
- heart rate, BP
- cardiac (Fillip class) and renal function (serum creatinine)
- cardiac arrest on presentation
- ECG findings
- troponin levels

3% or less is considered low risk
>3% is considered edict to high risk

51
Q

what medications are used as a secondary prevention for ACS?

HINT: 6 A’s

A

Aspirin 75mg OD indefinitely
Another Anti-platelet e.g. ticagrelor or clopidogrel0 for 12 months
Atorvastatin 80mg OD
ACEi
Atenolol (or another beta blocker - usually bisoprolol)
Aldosterone antagonist for those with clinical heart failure 9i.e. eplerenone tirade to 50mg OD)

52
Q

list some possible complications of myocardial infarction

A
  • cardiac arrest
  • cardiogenic shock (may require inotropic support and/or an intra-aortic balloon pump)
  • chronic heart failure (loop diuretics e.g. furosemide will decrease fluid overload, ACEi +BBB are shown to improve long-term prognosis)
    -VF/VT
    AV node block is more common following inferior MI

MSRA revision (3 decks)

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