Ischaemic heart disease Flashcards

1
Q

What is ischaemic heart disease?

A

Spectrum of diseases characterised by decreased blood supply to myocardium resulting in chest pain (angina pectoris) which may manifest into ACS or stable angina.

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2
Q

How is ischaemia heart disease categorised?

A
  • Stable angina
  • ACS: which can be further subdivided into unstable angina (no cardiac injury), NSTEMI (subendothelial infarction), or STEMI (transmural infarction – meaning full thickness of myocardium)
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3
Q

What does MI refer to?

A

Cardiac muscle necrosis from ischaemia.

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4
Q

What is the aetiology of ischaemic heart disease? (x4)

A
  • Atherosclerosis
  • Coronary artery spasm, such as from cocaine
  • Arteritis
  • Emboli
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5
Q

What are the risk factors of IHD? (x6)

A

Male, diabetes mellitus, FHx, HTN, hyperlipidaemia, smoking.

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6
Q

What is the mechanism of atherosclerosis?

A

Endothelial injury is followed by migration of monocytes into subendothelial space and differentiation into macrophages. Macrophages accumulate LDL lipids insudated in the subendothelium and become foam cells. They release growth factors which stimulate smooth muscle proliferation, production of collagen and proteoglycans. This leads to formation of an atheromatous plaque.

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7
Q

What is the pathophysiology of ischaemic heart disease?

A
  • Angina pectoris occurs when myocardial oxygen demand exceeds oxygen supply
  • MI is sudden occlusion of a coronary artery due to rupture of an atheromatous plaque and thrombus formation
  • UNSTABLE ANGINA: absence of biochemical evidence of myocardial damage but prolonged angina pectoris at rest
  • NSTEMI: myocyte necrosis from partial occlusion of coronary artery leading to subendothelial infarction.
  • STEMI: complete occlusion of a coronary artery leading to transmural infarction
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8
Q

What is the epidemiology of IHD: Gender? Age?

A

Male, increasing incidence with age.

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9
Q

What are the signs and symptoms of IHD?

A
  • STABLE ANGINA: chest pain brought on by exertion or emotional stress. Normal examination
  • ACS: chest pain with acute onset, central, heavy, and tight that radiates to arms (usually left), neck, jaw, or epigastrium. Occurring at rest.
  • May be associated with breathlessness, sweating, N&V, pallor, low-grade pyrexia
  • ! Unlike unstable angina, MI may be also be associated with haemodynamic instability
  • May be new heart murmurs such as pansystolic murmur of mitral regurgitation from papillary muscle rupture or ventricular septal defect
  • May be silent in elderly or diabetics
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10
Q

Why is breathlessness associated with MI?

A

Pulmonary congestion from compromised left ventricular function.

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11
Q

Why is sweating and pallor associated with MI?

A

Increased SNS output. Pallor occurs from peripheral vasoconstriction

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12
Q

How may presentation of ACS differ between the sexes?

A

Male patients typically present with chest pressure/discomfort lasting at least several minutes, at times accompanied by sweating, dyspnoea, nausea, and/or anxiety. Women present more commonly with middle/upper back pain or dyspnoea and similar associated symptoms.

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13
Q

What are the first investigations for IHD?

A

ECG and bloods to confirm MI, but don’t wait for bloods to begin treatment.

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14
Q

What are the main investigations for IHD? (x5)

A
  • ECG
  • Creatinine Kinase-MB or TROPONIN: dynamic elevation above 99th percentile
  • FBC: screen for thrombocytopenia as MI treatment increases bleeding risk. Also screen for anaemia as it is associated with increased mortality
  • CXR: to rule out other diagnoses such as aortic dissection, or screen for ACS complications such as heart failure
  • OTHER BLOODS: U&Es, LFTs, HbA1c, CRP, amylase: baseline, diabetes aetiology, and CRP raised in infection and amylase for acute pancreatitis which may suggest alternative aetiology to chest pain
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15
Q

What do ECGs show in IHD?

A
  • UNSTABLE ANGINA: ST depression and T wave inversion. May also be normal
  • NSTEMI: ST depression, T wave changes or TRANSIENT ST elevation. May also be normal
  • !!! STEMI: persistent ST elevation in at least two anatomically contiguous leads of at least 1mm (apart from V2 and V3 which must have at least 2.5mm in men under 40, 2mm in men over 40, and 1.5mm in women regardless of age). Later: T wave inversion (hours) and Q waves (days)
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16
Q

How should LBBB be treated in an ECG in relation to STEMI?

A

LBBB can mask a STEMI on an ECG. As such, treat any patient with LBBB and ischaemia suspicion as having a STEMI, regardless of whether the LBBB was previously known.

17
Q

What additional investigations that can be carried out for IHD? (x3)

A
  • EXERCISE ECG TESTING: using treadmill, for patients with unstable angina, or stable angina with a high risk of ACS. Positive test is defined as at least 1mm ST depression at 80ms after the end of QRS complex. But patient must achieve at least 85% of their predicted maximal heart rate (220-age). Patients must also not be on beta-blockers as this reduces maximal heart rate.
  • RADIONUCLIDE MYOCARDIAL PERFUSION IMAGING (rMPI): can be performed under exercise or pharmacological stress (dobutamine or dipyridamole). Stress testing should show low uptake in ischaemic myocardium in stable angina. Rest testing should be used for unstable angina patients. Similar testing can also be done with echocardiography
  • ECHOCARDIOGRAM: to assess ventricular function in unstable angina, and heart failure in MI
18
Q

What is the management of stable angina? (x5)

A
  • Antiplatelet therapy with 75mg/day aspirin
  • Immediate symptom relief: GTN as a spray or sublingually
  • Then stepwise with beta blockers, calcium channel blockers, long-acting nitrates (isosorbide dinitrate)
  • PCI for localised area of stenosis if angina not controlled medically
  • Coronary artery bypass graft for more severe cases such as three-vessel disease
19
Q

What is the management of unstable angina? (x4 and x4)

A
  • Single loading dose of aspirin 300mg (chewed), then 75mg once daily thereafter, plus a second anti-platelet – a P2Y12 inhibitor such as clopidogrel (300mg loading dose, 75mg once daily thereafter)
  • Anticoagulant such as heparin recommended in all patients
  • Analgesia: GTN (note this can cause hypotension) and give IV if chest pain persistent, or morphine sulfate
  • Anti-emetic if giving morphine or patient develops N&V. Prevent vomiting dual antiplatelet therapy
  • POST-STABILISATION:
  • Continue dual antiplatelet therapy
  • Consider stepwise beta blockers, calcium channel blockers, long-acting nitrates (isosorbide dinitrate) if previous medical therapy not working
  • PCI for localised area of stenosis if angina not controlled medically
  • Coronary artery bypass graft for more severe cases such as three-vessel disease
20
Q

How is NSTEMI managed? (+2 and x5)

A
  • Same as unstable angina, but with addition of ACEi or Ang-II receptor antagonist.
  • If haemodynamic instable, then immediate PCI and revascularisation
  • POST-STABILISATION:
  • Continue dual anti-platelet therapy
  • Put patient on beta blocker
  • Put patient on statin
  • Continue ACEi or Ang-II receptor antagonist
  • PCI for patients refractory to medical management
21
Q

How is STEMI managed?

A
  • WITHIN 120 MINUTES: PCI and revascularisation
  • Loading dose of 300mg aspirin and daily intake thereafter (75mg) with P2Y12 inhibitor
  • Analgesia: morphine sulfate IV
  • Anti-emetic IV
  • Parenteral anticoagulation during PCI. Do NOT start before PCI.
  • Consider glycoprotein IIb/IIIa inhibitor (such as eptifibatide) during PCI to tackle high thrombus burden
  • IF PCI NOT AVAILABLE: Fibrinolysis WITHIN 12 HOURS with streptokinase or rtPA (e.g., alteplase), plus parenteral anticoagulant. Then dual anti-platelet therapy, analgesia, anti-emetic
  • POST-STEMI: continue dual antiplatelet therapy, beta-blocker, ACEi/Ang-II receptor antagonist, and statin.
22
Q

What are the complications of IHD?

A
  • Other vascular disease such as stroke, peripheral vascular disease
  • EARLY COMPLICATIONS: cardiogenic shock, heart failure, ventricular arrythmias, heart block, pericarditis, thromboembolism
  • LATE COMPLICATIONS: ventricular wall rupture, valvular regurgitation, tamponade, Dressler’s syndrome (pericarditis)
23
Q

What is a prognostic score for ACS?

A

TMI score used for risk stratification of likelihood of cardiac events within 30 days, scoring 1 point for each of: (1) over 65, (2), known CAD, (3) aspirin in last 7 days, (4) severe angina – more than 2 episodes in 24 hours, (5) ST deviation over 1mm, (6) elevated troponin, (7) more than 3 coronary artery disease risk factors such as HTN and FHx.

24
Q

What is Killip classification of acute MI?

A
  • Predictor of prognosis. Higher class predicts higher mortality
  • CLASS I: no evidence of heart failure
  • CLASS II: mild-moderate heart failure (S3, crepitations less than 1/2 of posterior lung fields, JVP raised)
  • CLASS III: overt pulmonary oedema
  • CLASS IV: cardiogenic shock
25
Q

How can you differentiate between NSTEMI and unstable angina on ECG?

A

You CANNOT - must be reported as ‘myocardial ischaemia with no ST elevation’. You would differentiate with troponin