Complications of MI Flashcards

1
Q

How does cardiac arrest arise due to MI?

A
  • Most commonly occurs due to patients developing ventricular fibrillation
  • Most common cause of death following a MI
  • Patients are managed as per the ALS protocol with defibrillation.
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2
Q

How does cardiogenic shock arise due to MI?

A
  • If a large part of the ventricular myocardium is damaged the ejection fraction of the heart may decrease ==> cardiogenic shock
  • Difficult to treat.
  • Other causes of cardiogenic shock include the ‘mechanical’ complications such as left ventricular free wall rupture
  • Patients may require inotropic support and/or an intra-aortic balloon pump.
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3
Q

How does CHF arise from MI?

A
  • If the patient survives the acute phase their ventricular myocardium may be dysfunctional resulting in CHF
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4
Q

How do tachyarrhythmias arise due to MI?

A
  • Ventricular fibrillation is the most common cause of death following a MI
  • Other common arrhythmias including ventricular tachycardia
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5
Q

How do bradyarrhythmias arise due to MI?

A

Atrioventricular block is more common following inferior myocardial infarctions

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6
Q

How does pericarditis arise from MI?

A
  • Pericarditis in the first 48 hours following a transmural MI is common (c. 10% of patients).
  • Dressler’s syndrome tends to occur around 2-6 weeks following a MI:
    • Autoimmune reaction against antigenic proteins formed as the myocardium recovers
    • Combination of fever, pleuritic pain, pericardial effusion and a raised ESR.
    • Treated with NSAIDs.
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7
Q

How does a left ventricular aneurysm occur?

A
  • The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation
  • Associated with persistent ST elevation and left ventricular failure
  • Thrombus may form within the aneurysm increasing the risk of stroke
  • Patients are therefore anticoagulated.
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8
Q

How does left ventricular free wall rupture arise due to MI?

A
  • Seen in around 3% of MIs and occurs around 1-2 weeks afterwards
  • Patients present with AHF secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds)
  • Urgent pericardiocentesis and thoracotomy are required
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9
Q

How does ventricular septal defect occur due to MI?

A
  • Rupture of the interventricular septum usually occurs in the first week and is seen in around 1-2% of patients
  • Features: acute heart failure associated with a pan-systolic murmur
  • An ECHO is diagnostic and will exclude acute mitral regurgitation which presents in a similar fashio
  • Urgent surgical correction is needed.
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10
Q

How does acute mitral regurgitation occur due to MI?

A
  • More common with infero-posterior infarction and may be due to ischaemia or rupture of the papillary muscle
  • Features: Acute hypotension and pulmonary oedema
  • An early-to-mid systolic murmur is typically heard
  • Treated with vasodilator therapy but often require emergency surgical repair
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11
Q

What drugs should patients be offered after an MI?

A
  • Dual antiplatelet therapy (aspirin plus a second antiplatelet agent)
  • ACE inhibitor
  • Beta-blocker
  • Statin
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12
Q

What is the lifestyle advice given to patients following an MI?

A
  • Diet: advise a Mediterranean style diet, switch butter and cheese for plant oil based products. Do not recommend omega-3 supplements or eating oily fish
  • Exercise: advise 20-30 mins a day until patients are ‘slightly breathless’
  • Sexual activity may resume 4 weeks after an uncomplicated MI.
  • Reassure patients that sex does not increase their likelihood of a further MI. PDE5 inhibitors (e.g, sildenafil) may be used 6 months after a MI.
  • They should however be avoided in patient prescribed either nitrates or nicorandil
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13
Q

When are aldosterone antagonists used post-STEMI?

A
  • Patients who have had an acute MI and who have symptoms and/or signs of:
    • heart failure
    • Left ventricular systolic dysfunction
  • Treatment with an aldosterone antagonist licensed for post-MI treatment (e.g. eplerenone) should be initiated within 3-14 days of the MI, preferably after ACE inhibitor therapy
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14
Q

When are patients thrombolysed in STEMI?

A
  • Primary percutaneous coronary intervention (PCI) has emerged as the gold-standard treatment for STEMI but is not available in all centres
  • Thrombolysis should be performed in patients without access to primary PCI.
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15
Q

What thrombolytic agents should be used in STEMI patients?

A
  1. Tissue plasminogen activator (tPA) has been shown to offer clear mortality benefits over streptokinase
  2. Yenecteplase is easier to administer and has been shown to have non-inferior efficacy to alteplase with a similar adverse effect profile
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16
Q

What should be done post-thrombolysis after an STEMI?

A

An ECG should be performed 90 minutes following thrombolysis to assess whether there has been a greater than 50% resolution in the ST elevation:

  • NO adequate resolution = rescue PCI is superior to repeat thrombolysis
  • Adequate resolution = PCI has been shown to be beneficial. The optimal timing of this is still under investigation
17
Q

What is NICE’s guidelines for hyperglyceamic ACS?

A
  • Recommends using a dose-adjusted insulin infusion with regular monitoring of blood glucose levels to glucose below 11.0 mmol/l
  • Intensive insulin therapy (an intravenous infusion of insulin and glucose with or without potassium, sometimes referred to as ‘DIGAMI’) regimes are not recommended routinely