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Cardiology > IHD > Flashcards

IHD Flashcards

1
Q

What is Angina?

A
  1. Angina is chest pain caused when heart muscle does not get enough blood (demand>supply)
  2. Usually due to narrowing of coronary arteries and pain occurs when heart has to do more work e.g. exercise or stress
  3. Stable angina = pain is precipitated by predictable factors - usually exercise.
  4. Unstable angina = angina occurs at any time and should be considered and managed as a form of ACS
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2
Q

Aetiology of Stable Angina (5)

A
  • Atherscelerosis + CAD
  • valve disease, especially aortic stenosis
  • hypertrophic obstructive cardiomyopathy
  • hypertensive heart disease
  • arrhythmias
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3
Q

RF of Stable Angina

A
  1. Age
  2. smoking
  3. Fx
  4. hyperlipidaemia, HTN, kidney disease
  5. obesity, physical inactivity

(Top 3 are the most important)

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4
Q

What is Stable Angina? Factors that influence oxygen demand and supply, exacerbating factors?

A

Imbalance between heart’s oxygen demand and supply.
Usually from an increase in demand (e.g. exercise) accompanied by limitation of supply.

Factors influencing oxygen demand:
- Inc HR, LVH, HTN, Valve disease

Factors influencing oxygen supply:

  • Duration of diastole
  • Coronary vasomotor tone
  • Oxygenation (hb, oxygen saturation)
  • Coronary perfusion pressure

Exacerbating factors
- Physical exertion, Cold weather, heavy meals, emotional stress

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5
Q

Signs and symptoms of Stable Angina. What would exacerbate the Sx?

A

(1.) Anginal pain is:
(a.) Constricting discomfort in chest, neck, shoulders, jaw, arms
(b.) Precipitated by physical exertion
(c.) Relieved by rest or GTN
All 3 features = typical angina, 2 features = atypical angina, 0-1 features = non-anginal chest pain.

(2. ) Other Sx: Dyspnoea, nausea, sweatiness, faintness
(3. ) Exacerbating factors = Pain with exertion? after meals? often when bending over? aggravated by cold weather?

(4. ) Unlikely to be angina if chest pain is:
- Continuous, unrelated to activity, brought on by breathing in, associated with fluid retention, palpitation, dizziness, tingling

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6
Q

Investigations of Stable Angina

A

Initial Investigation comprising of BLOODS + ECG

(1. ) Blood tests: FBC, Lipids, Troponin, LFTs before starting statins
(2. ) ECG: Usually normal but may show Q-wave, LBBB, ST depression, inverted T wave
(3. ) Additional ix if needed: CXR If lung tumour is suspected, ECHO.

(4. ) Further investigation required to confirm IHD diagnosis:
- If stable-angina suspected: Exercise ECG
- If normal exercise ECG but high clinical suspicion: myocarial perfusion scanning or stress echo
- if CAD present: CT coronary arteriography

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7
Q

Treatment and management of Stable Angina (1st, 2nd, 3rd line, prevention, failure of tx)

A

(1.) GTN = for acute atacks. Advise pt to repeat dose if not gone after 5mins + call ambulance if not gone after second dose. SE: headaches and dec BP.

(2. ) b-blockers (1st line) or CCB
- if fails switch, then combine

(3. ) monotherapy (2nd line, if 1st is not tolerated or CI):
- long acting nitrates
- OR Ivabradine (If channel antagonist)
- OR Ranolazine or Nicorandi (K-channel activator)

(4.) Combination of 2nd line with b-blocker, CCB (3rd line)

(5. ) Secondary CVD Prevention:
- Lifestyle: diet exercise, optimise HTN and DM control
- Aspirin (if CI: Clopidogrel), Statin, ACEi if DM

(6.) Revascularisation, PCI/ CABG: If combination of drugs fails

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8
Q

4 Special Test/Investigations for IHD

A
  1. Myocardial Perfusion MRI
    - Non-invasive
    - evaluate perfusion of cardiac muscle via the coronary arteries after stress and at rest
  2. Exercise ECG
    - Assess for ischaemic changes
  3. CT Coronary angiography
    - 1st line fo ruling out CAD
    - 3D image of heart and vessels
  4. Stress echo
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9
Q

Risk assessment CVD risk in IHD pts

A
  • QRISK and JBS3 can be used to assess 10-year risk of CVD
  • Factors that are taken into account include: Gender, Age, Ethnicity,Smoker status, Diabetes status, Hx of heart attack or angina in first degree relative, AF HTN, BMI etc
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10
Q

Whats the difference between infarction and ischaemia?

A
  1. Infarction = reduction in blood flow causing deaths of cells
  2. Ischaemia = reduction in blood flow (cells do not necessarily die)
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11
Q

What is troponin? And what do high levels of troponin indicate?

A
  1. Troponins are proteins involved in cardiac and skeletal muscle contractions
  2. Elevated troponin levels indicates myocardial damage.
  3. Elevated troponin levels can also be due to other causes of myocardial damages:
    a. Myocarditis
    b. Pericarditis
    c. Ventricular Strain
    d. Arrhythmias
    e. Iatrogenic - CPR, DC cardioversion, ablation therapy
    f. Non-cardiac aetiology - sepsis, cytotoxic drugs, pulmonary embolism
  4. Troponins I and T are specific to heart and can be used as a cardiac biomarker when ACS is suspected.
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12
Q

What cardiac biomarkers are raised after MI?

A
  1. Troponins (T or I)
  2. Creatine kinase (CK, specifically CK-MB)
  3. Myoglobin

These rise at diff time points post-MI

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13
Q

RF of acute coronary syndrome

A
  • Age
  • Male
  • Fx of IHD
  • HTN, DM, hyperlipidaemia
  • smoking, obesity, sedentary lifestyle
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14
Q

What is Acute Coronary Syndrome?

A
  • ACS is a term that encompassses both unstable angina and MI
  • These all share a common underlying pathology: atheroma plaque - rupture, thrombosis, inflammation.
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15
Q

Symptoms of ACS (6)

A
  1. Cardiac pain >20mins - chest, throat, arm, epigastrium, back
  2. New-onset chest pain or abrupt deterioration in stable angina, occurring with little or no exertion
  3. Associated with N+V, sweating, breathlessness, or haemodynamic instability
  4. Can be painless or ‘silent’ MI in older or diabetic patients.
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16
Q

Diagnosis of ACS

A

Troponin levels + either:

a. Symptoms of ischaemia
b. ECG changes of new ischaemia
c. Development of pathological Q waves
d. New loss of myocardium
e. Regional wall motion abnormalities or imagine

17
Q

Investigations of ACS

A
  1. ECG
    - STEMI = ST elevation, tall T waves or LBBB
    - NSTEMI/Unstable angina = ST depression or T-wave inversion
  2. Bloods
    - Troponin
    - Lipids: fall in cholesterol following infarction
    - BGL –> hyperglycaemia at the time of admission with ACS is a predictor of poorer survival and inc risk of complications while in hospital
  3. CXR: may show complications of ischaemia (eg, pulmonary oedema), or explore alternative diagnoses
  4. ECHO
    - Any wall motion abnormalities due to ischaemia.
    - May be useful in identifying precipitants for ischaemia - eg, ventricular hypertrophy and valvular disease.
  5. Coronary angiography
    - provides info on presence and severity of CAD
    - in pts considered for revascularisation
18
Q

Treatment and Management of ACS

A
  1. Admit urgently, MONA, ECG
  2. Revascularisation
    (a. ) ACS: US or NSTEMI
    - Troponin levels to differentiate
    - medium-high GRACE score: angiography +/- PCI

(b. ) STEMI onset <12hrs
- PCI within 2hrs + IV GP2b/3ai
- PCI not feasible within 2hrs –> thrombolysis + fondaparinux or LMW heparin

(c. ) STEMI onset >12hrs
- Fondaparinux or LMW heparin
- Use Grace score & Angiography +/- PCI

  1. Optimise cardioprotective mechanisms (5As)
    - Nitrates, B-blockers, Statin, ACEi, Antiplatelet and anticoagulant therapy
  2. Lifestyle/Minimise risk
    - Smoking cessation
    - Diet and exercise
    - Management of DM, HTN, hyperlipidemia, mental health
19
Q

Pathophysiology of Unstable Angina?

A
  1. Chest pain due to heart not receiving enough oxygen due to narrowed coronary artery.
  2. Reduced blood flow –> reduced myocardial perfusion.
  3. This can be due to plaque formation, thrombosis, vasospasm, elevated BP.
  4. Factors that provoke this and increase myocardial oxygen demand: Arrhythmias, Fever, HTN, Aortic stenosis etc
20
Q

Aetiology of Unstable Angina (2)

A
  • Coronary artery narrowing due to atherosclerosis plaque rupture and thrombus formation (common).
  • Vasospasm of coronary artery known as Prinzmetal angina (less common).
21
Q

Complications of Unstable Angina

A
  • Unstable Angina may indicate a forthcoming MI.
  • Stoke
  • Death
22
Q

RF of Unstable Angina

A
  • Non modifiable (Male, menopause, Fx)
  • Modifiable (obesity, smoking, diabetes, cholesterol)
  • Vasculitis, anaemia in the absence of history of diabetes/smoking/cholesterol
23
Q

Presentation of Unstable Angina

A

PAIN AT REST AND WORSENING SYMPTOMS

(1. ) Chest pain at rest
- Tight, burning, sharp
- Radiates to jaw, arm
- Pain may not resolve with relieving factors

(2. ) Other Sx: N+V, SoB, palpitations
(3. ) Hx of stable angina but acquires new-onset pain with limitation of activity

Examination

(1. ) Murmurs? Oedema? Cardiac findings?
(2. ) Haemodynamic instability? Tachypnoea, tachycardia, HTN, reduced saturation

24
Q

Investigations of Unstable Angina

A

Bloods

  • Troponins levels = No rise in unstable angina
  • Lipid profile
  • FBC to check for anaemia

ECG

  • Usually normal sinus rhythm
  • may show hyperacute T-wave, flattening of the T-waves, inverted T-waves, an ST depression
  • Look for signs of ischaemia, possible STEMI

Imaging
- Rule out other causes

25
Q

Treatment and Management for Unstable Angina

A
  1. Management of lifestyle and other Co-morbidities
  2. Managing Chest pain with GTN
  3. Optimise cardioprotective mechanisms:
    - Aspirin, Statins, B-blockers, Anticoagulants
  4. GRACE score to assess mortality risk within 6m
    (a. ) high = angiography w/GP2b/3bi
    (b. ) Angiography also indicated if angina refractory to pharmacological therapy
  5. Revascularisation: PCI or CABG
    - If pain not controlled or not responded well to treatment
  6. After Stent insertion
    - Aspirin + Clopidogrel can be continues for up to 12 months
26
Q

What is the rationale behind treatment and management in unstable angina

A

Mainstay of treatment focuses on:

  • improving perfusion of coronary arteries
  • prevent angina pains as much as possible and to ease pain quickly if it occurs.
  • limit further deposits of atheroma
  • Reduce risk of MI
27
Q

Antiplatelet and anticoagulant therapy in ACS

A

(1. ) Aspirin and ticagrelor
- Do not offer dual antiplatelet therapy in pts w/chest pain before diagnosis of unstable angina or NSTEMI is made.

(2. ) Clopidogrel monotherapy
- if aspirin tolerated or contraindicated

(3. ) Aspirin and clopidogrel up to 12m
- unstable angina or NSTEMI if have indication for ongoing oral anticoagulation.

(4. ) Aspirin and Prasugrel
- option for preventing atherothrombotic events in ACS having primary or delayed PCI

(5. ) Ticagrelor and low-dose aspirin up to 12m
- STEMI that intend to have primary PCI
- NSTEMI
- Admission to hospital with unstable angina.

(6. ) Glycoprotein IIb/IIIa inhibitors
- considered as adjunct to PCI for moderate-higher risk pts who are not receiving a glycoprotein inhibitor

(7. ) Antithrombin therapy:
- fondaparinx
- Pts without a high bleeding risk unless angiography is planned within 24 hours

28
Q

Pathophysiology of MI

A

(1. ) Heart attack - myocardial necrosis as a result of complete OR partial occlusion of coronary arteries
(2. ) Dec blood flow resulting in dec myocardial perfusion
(3. ) Cardiomyocytes send pain signals to the brain after lack of perfusion, often feels like indigestion
(4. ) Cardiomyocytes slow down and then die. Their membranes break down and leak troponin into the bloodstream

29
Q

Aetiology of MI

A

Restriction of blood supply due to:

  • Atherosclerosis
  • Coronary thrombosis
30
Q

RF of MI

A

Age, Smoking, HTN, Fx, Sedentary lifestyle, high cholesterol, diabetes

31
Q

What is STEMI?

A
  • Most serious type of MI
  • TOTAL OCCLUSION of coronary artery
  • Extensive necrosis and damage to large areas of the heart (transmural)
  • ECG = ST elevation and Q waves.
32
Q

What is NSTEMI?

A
  • Less serious than STEMI
  • Cardiac blood supply only partially blocked, causing ischameia
  • Necrosis to distal aspect of myocardial wall
  • It is still a medical treatment as w/o treatment it can progress to serious heart damage or STEMI
  • ECG = ST depression
33
Q

Investigations for MI

A
  1. Blood: troponins, lipids, elevated NT-proBNP level
  2. ECG
    - ST depression or elevation? [take note their reciprocal in other leads]
    - New LBBB?
    - Pathological Q wave?
    - Inverted T-wave?
  3. CXR: Cardiomegaly, pulmonary oedema, widening of mediastinum
34
Q

Acute MI Management?

A
  • Medical emergency - ‘MONA’ (morphine, oxygen, nitrates, aspirin)
  • ECG, but do not delay transfer to hospital
  • Revascularisation - PCI or CABG
35
Q

Treatment and Management of MI

A

(1. ) Patient Education and lifestyle
- Advise pt to call for emergency if chest pain >15mins and unresponsive to GTN
- Lifestyle/minimise RF = smoking, diet, exercise, alcohol

(2. ) Optimise Cardioprotective medications
- DUAL Antiplatelet therapy
- Anticoagulants
- Statins
- B-blockers (start low and inc slowly)
- ACEi = for LV dysfunction, HF, HTN, diabetes

(3. ) Revascularisation: PCI/CABG
- Depends on risk/GRACE score:
- STEMI = angiography +/- PCI + GP2b/3ai within 12hrs otherwise give pt LMW heparin
- NSTEMI = angiography within 24h (hi-risk) or 3d (moderate risk)

(4. ) Long-term dual antiplatelet therapy
- PY12i continued for >1 year in high risk aspirin-treated pts
- Must not have a risk of life-threatening bleeding

Cardiology (19 decks)

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