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Cardiology RACP > Topic summary Gems > Flashcards

Topic summary Gems Flashcards

1
Q

Three forms of atherosclerotic plaques

A

Ruptured atheromatous plaque: Large lipid pool, thin fibrous plaque that ruptures with adherent clot
Fibrous plaque: Calcium depoition and burried cap. More stable as has thick cap and small lipid pool
Superficial erosion: Acculuation of proteoglycan with focally denuded endothelium + adherant thrombus

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2
Q

Location of lesion by ECG changes: Septal

A

V1, V2 : LAD

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3
Q

Location of lesion by ECG changes: Anterior

A

V3, V4: LAD

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4
Q

Location of lesion by ECG changes: Anteroseptal

A

V1-4, LAD

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5
Q

Location of lesion by ECG changes: Anterolateral

A

V3,4,5,6 I aVL with reciprocal II, III, aVF Left anterior decendin, left circ or obtuse marginal

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6
Q

Location of lesion by ECG changes: Extensive anterior

A

V1-6 with I and aVL with reciprocal II, III, aVF

Left main CA

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7
Q

Location of lesion by ECG changes: inferior

A

II, III, aVF and reciprocal in I and aVL

Right coronary or R circ.

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8
Q

Location of lesion by ECG changes: lateral

A

I, aVL V5 V6 reciprocal in II, III, aVF

L Circumflex or obtuse marginal

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9
Q

Location of lesion by ECG changes: Posterior

A

V7-9 with reciprocal V1-4 Posterior descending (Branch of RCA or left circuflex)

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10
Q

Location of lesion by ECG changes: Right ventricular

A

II, III, aVF, V1, V3, V4 reciprocal in I and aVL

Right coronary

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11
Q

Framingham risk score: highest risk parameter

A

Age: 13 points as a maximum. With each decade of life the risk of vascular disease doubles.
Highest modifiable risk factor was total cholestrol specifically >280 in young people (20-39), smoker age 20-39 also risk of 8 points. Cholestrols importance decreases with age. E.g by 70-79 over 280 only worth 1 point

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12
Q

Smoking impact of MI

A

Incidence of MI increased x6 in F and x3 in M who smoke at least 20 cigs/day compared to non-smokers

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13
Q

Interheart study: highest modifiable risk factor (2004)

A

Abdominal obesity 61x risk increase, followed by smoker: 44 x

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14
Q

High Risk Patients (risk>15% in next 5 years) - treat with full preventative strategy!

A

• Patients with known coronary artery disease
• Patients with vascular disease (eg. Legs)
• Patients with other high risk conditions
o Age >60 with diabetes
o Diabetes and microalbuminuria
o Moderate or severe CKD
o Familial hypercholesterolaemia
o SBP >180, DBP >110
o Total cholesterol >7.5mmHg

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15
Q

Lipid Targets

A

o TC <4
o LDL <2 in high risk patients
o HDL >1
o TG<1.5

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16
Q

Lipid Targets

A

o TC <4
o LDL <2 in high risk patients
o HDL >1
o TG<1.5

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17
Q

Cardiac ladder of change in atherosclerosis

A

Normal –> perfusion abnormality on cardiac stress nuclear–> diastolic dysfunction on echo –> regional systolic dysfunction on ECHO –> ischemic ECG changes –> Angina pectoris

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18
Q

‘Good quality stress test’

A

adequate workload and 85% max heart rate reached

Contraindications: Recent ACS, uncontrolled arrythmia, severe AS, heart failure (decompensated), PE, dissection

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19
Q

Best predictor of outcome in exercise stress testing

A

<5METs (i.e. poor exercise capacity –> unable to exert to 5 or more metabolic equivalents)

20
Q

Invasive angiography: meaning of fractional flow reserve

A

Measures pressure drop across a lesion: FFR <0.8 needs stent or alteration, >0.8 normal

21
Q

Proven benefit of survival of CABGs in which 3 groups

A

left main disease
2 or 3 vessel CAD with prox. LAD
3 vessel CAD with impaired proximal LAD

22
Q

Medication with clear benefit in stable angina

A

aspirin

23
Q

Types of myocardial infarction

A

Type 1: spontaneous, likely related to atheroscleprosis
Typce 2: MI secondary to demand ischemia
Type 3: MI resulting in death without biomarkers available
Type 4a: MI related to PCI
Type 4 b: MI related to stent thrombosis
Tpe 5: MI related to CABG

24
Q

Cardiac biomarkers and peak times: first through last

A

Myoglobin, CK, Troponin, LDH

25
Q

NSTEMI management

A

• Aspirin to all
• DAPT if confirmed intermediate to high risk NSTEACS - continue for 12/12
• Don’t give P2Y12 inhibitor if possibility of emergency CABGs
• Anticoagulation
• Unfractionated heparin or Enoxaparin if confirmed intermediate to high risk NSTEACS
• Glycoprotein IIb/IIIa Inhibitors
• At time of PCI if high risk clinical and angiographic characteristics
Bivalirudin - alternative to glycoprotein IIb/IIIa inhibition and heparin (if likely high risk bleeding)

26
Q

Glycoprotein IIb/IIIa inhibitors

A

abciximab, eptifibatide, tirofibran last two have lower affinity to the glycoprotein than abciximab

27
Q

Abciximab MOA

A

By competing with fibrinogen and von Willebrand factor (vWF) for GP IIb/IIIa binding, GP IIb/IIIa antagonists interfere with platelet cross-linking and platelet-derived thrombus formation. Therefore agents blocking the GP IIb/IIIa receptor are very potent platelet inhibitors.

28
Q

Algorithm for statin therapy

A

Is the LDL >4.9 mmol ? yes no (FH or not)
If no to >4.9 then evaluate risk. If >10% risk-statin, if 5-10% assessment further with CAC or lipoprotein-a level, if <5%, no statin
If >10% and commenced - recheck at 6 weeks. Hi intesity statin for >20% risk + LDL remaining >2.5
Moderate if 10-20

29
Q

Statins are contraindicated in which patient group?

A

pregnant women

30
Q

Secondary prevention post NSTEMI

A

• Statin - initiate and continue indefinitely
• Beta Blocker - initiate in patients with reduced LV function <40%
ACEI/ARB - initiate in those with CCF, LV dysfunction, DM, anterior MI or co-existant hypertension

31
Q

STEMI: Patient presents within 60 minutes of pain

A

Access to cath within 60 mins: percutaneous cornoary intervention, if not Fibrinolysis

32
Q

STEMI with symptom onset 1-3 hours before presentation

A

within 90mins available: PCI if not Fibrinolysis

33
Q

STEMI with symptom onset 3-12 hours:

A

PCI avaialable withint 90 mins onsite or 2 hours offsite: PCI if yes, Lysis if no

34
Q

Inidcation for rescue PCI

A

Fibrinolysis and no reperfusion iwthin 90 mins –> PCI within 12 hours.

35
Q

STEMI >24 hours of symptoms

A

No benefit of intervention

36
Q

Best outcome PCI candidates

A

present within 3 hours and 1 year mortality RR increases by 7.5 % every 30 minute delay

37
Q

Contraindications to fibrinolysis

A

♣ active bleeding,
♣ significant closed head or facial trauma within 3/12,
♣ suspected aortic dissection, any prior ICH,
♣ ischaemic stroke w/in 3/12,
♣ known structural cerebral vascular lesion,
♣ known intracranial neoplasm
♣ Active bleeding or bleeding diathesis

38
Q

Indications for implantable cardiac device post STEMI

A

Use if:
• LVEF ≤ 30% at least 40d post MI
LVEF ≤ 35%, cardiomyopathy (ischaemic/non-ischaemic), NYHA II/III, at least 40d post MI

39
Q

Management of cardiogenic shock in STEMI

A

Most have extensive disease: L main or triple vessel. Treat as previously explained: however avoid bBlockers or any negative ionotrope. Arrythmia treated wtih amiodarone. Nor-adrenaline is useful as vasopressor support.

40
Q

Timing of in stent thrombus and risk of DAPT

A

o BMS - Highest risk of stent thrombosis within 6 weeks post stent insertion
DES - High risk of stent thrombosis ongoing for 1 year post stent insertion

41
Q

Causes of Pericarditis

A 
Infectious
Idiopathic
Malignancy
Autoimmune
Metabolic (Uraemia)

MIAMI

42
Q

Diagnostic criteria for pericarditis

A

Typical chest pain
Pericardial rub
ST changes on ECG
New pericardial effusion

2 criteria needed

43
Q

Management of pericarditis

A

Depends on the cause (malignancy, bacterial etc.)
High risk patients (Fever, tamponade, immunosuppression) - admit
Low risk–> home

Avoid strenuous exercise
Colchicine + NSAIDs
Colchicine can reduce recurrence

44
Q

Constrictive pericarditis: causes, physiology and presentation

A

Idiopathic, viral, post surgical, post radiation

Ventricular interdependance: negative intrathoracic pressure generated by inspiration doesn’t augment filling pressures to right heart
Early diastolic filling: Filling restricted due to pericardial fibrosis - fast filling first 1/3 of diastole, then slows

X and Y descent are prominent on JVP
Kussmal’s sign: paradoxical increase in JVP during inspiration
Pulsus paradoxus

Echo is diagnostic

45
Q

Cardiac Tamponade: Presentation, Physiology

A

Becks triad: hypotension, soft heart sounds and JVP distension
Increased ventricular interdependance: Shifting of interventricular septum toward L during inspiration and R in expiration due to changes in intrathoracic pressure
Progressive decrease in venous return: Cardiac volume reduced due to compressive effusion: therefor as the ventricle contracts and creates a potential space, diastolic filling occurs. Total venous return falls.

Prominant X descent and absent Y descent

Cardiology RACP (4 decks)

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