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RACP > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Unstable ACS - pathophysiology

A

Lipid rich plaques that erode, rupture and thrombose with associated inflammation

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2
Q

Stable angina - pathophysiology

A

Plaques cap over and inflammation settles, leading to demand ischaemia.

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3
Q

How do you estimate the probability of significant CAD?

A

CVD risk calculator - age, gender, smoking status, diabetes, HTN, cholesterol, Māori/Indigenous

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4
Q

Define typical angina

A
  1. Constricting discomfort in front of chest, or neck, jaw, shoulder, arm.
  2. Precipitated by physical exertion
  3. Relieved by rest or nitrates within 5mins.
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5
Q

Define atypical angina

A

Meets 2 of the typical angina characteristics

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6
Q

Define non-angina chest pain

A

Meets 1 or none of typical angina characteristics

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7
Q

Describe grading for angina

A

I. Angina only with strenuous, rapid or prolonged exercise e.g. walking, climbing stairs
II. Angina with moderate exertion - slight limitation of ordinary activities if performed rapidly, after meals, in cold, under stress, walking uphill or >1 flight of stairs at normal pace.
III. Angina with mild exertion - having difficulties walking 1-2 blocks or climbing 1 flight of stairs.
IV. Angina at rest

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8
Q

What percentage of ischaemic presentats with pleuritic chest pain?

A

5-19% of ACS

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9
Q

What percentage of patients have tenderness on chest wall palpation with AMI?

A

~15%

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10
Q

Who are more likely to present with atypical angina presentations?

A

Elderly, females, or people with diabetes

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11
Q

What are modifiable risk factors in terms of CAD?

A

Diet, obesity, alcohol (<15g/day), smoking, hypertension (lifestyle modification first, then meds), dyslipidaemia (LDL <1.4mmol/L), diabetes (aim near normal HbA1c), physical activity, cardiac rehabiliation.

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12
Q

Describe pharmacotherapy of chronic angina

A

Aspirin (indefinitely; can use ticagrelor/clopidogrel if aspirin intolerance, add if high risk features), B-blocker, ACE/ARB, statin. GTN spray for immediate symptoms, long acting nitrates for symptoms.

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13
Q

Describe role of revascularisation in chronic CAD

A
  1. Clinical context is most important.
  2. Stents/PCI target culprit lesions
  3. CABG targets culprit + some non-culprit lesions proximal to the bypass
  4. Sicker patients have the most to gain from revascularisation.
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14
Q

Describe key points of COURAGE study

A
  1. In patients who don’t have significant angina or impaired LV function, optimal medical therapy has equivalent survival.
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15
Q

Describe key points of ISCHAEMIA trial

A

Only applicable to people with stable CAD not ACS or high risk subsets.
1. No benefit of conservative vs invasive approach in people with stable CAD up to 5yrs.
2. Angina relieved early on with invasive approach

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16
Q

Prognostic improvement with revascularisation in chronic angina is associated with:

A
  1. Evidence/extent of ischaemia - refractory angina or life limiting symptoms
    - Evidence of large area of ischaemia
  2. Evidence of impaired cardiac function
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17
Q

Definition of acute myocardial infarction:

A

Elevated troponin + ONE of: symptoms, ECG changes, imaging evidence, angiography or autopsy.

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18
Q

Define type 1 MI:

A

atherosclerotic plaque rupture, ulceration, fissure or erosion with resulting intraluminal thrombus in one or more coronary arteries leading to decreased myocardial blood flow and/or distal embolisation and subsequent myocardial necrosis

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19
Q

Define T2MI:

A

Myocardial necrosis in which a condition other than coronary plaque instability causes an imbalance between myocardial oxygen supply and demand.

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20
Q

Causes of T2MI:

A

Extremes of BP (hypotension/hypertension), tachyarrhythmias, bradycarrhythmias, anaemia, hypoxaemia, coronary artery spasm, spontaenous coronary artery dissection (SCAD), coronary embolism

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21
Q

Define Type 3-5 MI

A

Type 3: MI resulting in death when biomarkers are not available.
Type 4+5: related to PCI and CABG

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22
Q

List differentials for chest pain

A
  • Ischaemic cardiovascular causes: ACS, stable angina, severe aortic stenosis, tachyarrhythmia (atrial or ventricular).
  • Non-ischaemic cardiovascular causes: aortic dissection, PE, pericarditis, myocarditis.
  • Non-cardiovascular causes: GI, MSK (costochronditis, cervical radiculopathy); pulmonary (pneumonia, pleuritis, pneumothorax); other
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23
Q

What historial features increase risk of ACS?

A

Age, diabetes, HTN, smoking, elevated cholesterol, syncope, family hx

24
Q

What are examination findings that increase risk of ACS?

A

Hypotension, tachycardia, signs of HF

25
Q

What is a high predictive valve for troponin rise?

A

> 5-fold the upper reference range has >90% PPV for acute type 1 MI.

26
Q

What troponin elevation has limited PPV?

A

Up to 3-fold the upper reference limit (50-60% PPV) and are associated with a broad spectrum of conditions

27
Q

What are causes of non-type I MI troponin rises?

A

Cardiac contusion or other trauma
CHF (acute AND chronic)
Coronary vasculitis e.g. SLE, Kawasaki syndrome
Aortic valve disease
HOCM
Tachy/bradyarrhythmias or heart block
Rhabdomyolysis
PE
Severe PHTN
Renal failure
Acute neurological disease
Infiltrative disease e.g. amyloidosis, haemochromatosis, sarcoidosis, scleroderma
Inflammatory diseases e.g. myocarditis, myocardial extension of endo/pericarditis.
Drug toxicity
Critically ill patients
Hypoxia
Burns esp if >30% surface area
Extreme exertion

28
Q

Describe a rule out patient who can go home after chest pain presentation

A

People with no troponin elevation, resolution of symptoms and no high risk features.
Low risk patients: age <40, atypical symptoms, no further symptoms, absence of known CAD, normal trop + ECG.

29
Q

Describe cornerstone of NSTEMI management

A
  1. Anti-thrombotic
    a. Aspirin +
    b. P2Y12 - clopidogrel (2-6hr) OR ticagrelor (0.5-2hr; marginal early benefit)
    c. LMWH/heparin infusion until PCI or clinical stability
  2. Revascularisation

Needs telemetry for 24hrs OR until PCI.

30
Q

What factors increase bleeding risk when considering antithrombotic therapy?

A

Elderly, female
Hx of prior bleeding
Liver disease
Renal dysfunction
Anaemia
Diabetes
Already on anticoagulation
Low body weight

31
Q

Symptom management if ongoing CP?

A
  • IV nitrates if ongoing ischaemic symptoms
  • Beta-blockers if HFrEF, EF <40%, prior MI
  • Statins
  • ACE/ARB if HFrEF
  • Diabetic therapy BSL <10
32
Q

What are very high risk features in NSTEMI?

A

Haemodynamic instability
Cardiogenic shock
Recurrent/refractory CP
Life threatening arrhythmias e.g. VT
Mechanical complications
Acute CHF
‘Left main’ ECG

These indicate PCI within 2hrs

33
Q

What is the main treatment for STEMI?

A
  • Revascularisation where primary PCI is available in a timely manner (delays increase mortality.
  • Can give fibrinolysis where PCI not available OR when PCI is contraindicated.
34
Q

What should someone be pretreated with for STEMI prior to PCI OR fibrinolysis?

A

Loading ticagrelor OR clopidogrel and UFH

35
Q

What is MINOCA?

A

Myocardial Infarction with Non-Obstructive Coronary Artery disease (could be secondary to spasm, plaque erosion or embolus formation)

36
Q

What is LVH criteria on an ECG:

A

Solokolov: S in V1/V2 + R in V6 >35mm
Cornell: S in V3 + R in aVL >22

37
Q

What are the differences between ST changes in LVH and ischaemic T-waves?

A

ST-depression V5-6, T-wave inversion is asymmetric (initial inflection > second inflection) in ECG with large voltages

38
Q

Define intraventricular conduction delay

A

QRS > 120ms (>3 small squares)

39
Q

Describe classical findings on ECG for LBBB

A

qS pattern in V1, ‘M’ pattern in V6

40
Q

Describe classical findings on ECG for RBBB

A

RSR’ pattern V1, persisting S in V6.

41
Q

Classically, what do T-waves do in V1-V3 RBBB?

A

Invert, secondary to altered depolarisation and repolarisation

42
Q

What medications block the AV node?

A

B-blockers, digoxin, CCBs

43
Q

What should you think of if a patient with an inferior STEMI has >2mm STD in V2?

A

A posterior infarction

44
Q

In an inferior STEMI, you should assume….

A

There is right ventricular infarction - this alters haemodynamics and should be cautious with GTN, diuretics and BBs.
- You want to maintain preload as right ventricular infarctions are reliant on preload to maintain perfusion.

45
Q

What are associated with an inferior STEMI?

A

Conduction abnormalities - mainly transient 24-48hr.
- Sinus bradycardia
- Sino-atrial exit block
- 1st degree block
- 2nd degree type 1 and type 2
- Complete heart block

46
Q

What does the right coronary artery supply?

A

The AV node and SA node

47
Q

In young people, how do you calculate max HR?

A

220 - age

48
Q

What are the 2 most common types of SVT?

A

AVNRT and AVRT

49
Q

What medication can you use in pregnancy for SVT?

A

Flecainide

50
Q

How do you treat unstable VT?

A

Synchronised cardioversion

51
Q

What ECG pattern and background is suspicious for Brugada?

A

rSr in V2, STE in V3.
History of sudden cardiac death in symptomatic young person

52
Q

What makes you think heart block?

A

More Ps than QRS complexes

53
Q

What is electrical/pulsus alternans?

A

Alternation of QRS amplitude

54
Q

What can pulsus alternans indicate?

A

A pericardial effusion

55
Q
A

RACP (1 decks)

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