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Y3 Medicine: Cardiovascular > Myocardial Infarction: STEMI > Flashcards

Myocardial Infarction: STEMI Flashcards

1
Q

What is a STEMI?

A

Acute myocardial infarction is myocardial cell death that occurs because of a prolonged mismatch between perfusion and demand. In the case of ST-elevation myocardial infarction (STEMI) this is caused predominantly by complete atherothrombotic occlusion of a coronary artery.

A STEMI is diagnosed clinically when there is new (or increased) and persistent ST-segment elevation.

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2
Q

What risk factors are asscociated with a STEMI?

A
  • Smoking
  • Hypertension
  • Diabetes
  • Obesity
  • Dyslipiademia
  • Metabolic syndrome
  • Established coronary artery disease
  • Family history of premature coronary artery disease
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3
Q

What is Acute Coronary Syndrome?

A

Historically ACS has been divided into three clinical categories according to the presence or absence of ST-segment elevation on a presenting ECG and on elevations of cardiac troponin T or I.

  • ST-elevation myocardial infarction (STEMI): ECG shows persistent ST-segment elevation in at least two anatomically contiguous leads.
  • Non-STEMI (NSTEMI): ECG does not show ST-segment elevation, but cardiac biomarkers are elevated. The ECG may show ischaemic changes such as ST-segment depression, T-wave inversion, or biphasic T waves.
  • Unstable angina pectoris: non-specific ischaemic ECG changes, but cardiac biomarkers are within the normal range.
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4
Q

Briefly differentiate the pathophysiology between a STEMI and NSTEMI

A

STEMI: transmural infarction

NSTEMI: subendocardial infarction

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5
Q

What are the symptoms of a STEMI?

A
  • Chest pain
  • Dyspnoea
  • Nausea and vomiting
  • Pallor
  • Diaphoresis
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6
Q

How does chest pain present in a STEMI?

A
  • Classically retrosternal, crushing, heavy, severe and diffuse in nature.
  • Might be described by the patient as ‘pressing or squeezing’.
  • May occur at rest or on activity.
  • May be constant or intermittent or wax and wane in intensity.
  • Sometimes radiating to the left arm, neck or jaw.
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7
Q

What are the signs of a STEMI?

A
  • Abnormal beath sounds (e.g. rales and crackles)
  • Additional heart sounds (e.g. muffled)
  • Signs of cardiogenic shock
  • Hypotension
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8
Q

What are the signs of cardiogenic shock?

A
  • Altered mental status/reduced consciousness
  • Tachypnoea
  • Severe dyspnoea
  • Tachycardia
  • Orthopnoea
  • Cool peripheries
  • Grey, ashen, pale appearance
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9
Q

Briefly describe the diagnosis of cardiogenic shock

A

Cardiogenic shock is primarily a clinical diagnosis supported by haemodynamic measures. It is defined as persistent hypotension (systolic blood pressure [SBP] <90 mmHg) together with signs of end-organ hypoperfusion.

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10
Q

What investigations should be ordered in a STEMI?

A
  • ECG
  • Cardiac troponin
  • Glucose
  • FBC
  • Electrolytes, urea, creatinine and eGFR
  • CRP
  • Serum lipids
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11
Q

Why investigate ECG? And what may this show?

A
  • Perform a 12-lead ECG within 10 minutes of first medical contact in any patient who presents with chest pain and/or other signs of possible STEMI.
  • A STEMI is diagnosed in the appropriate clinical context (a patient with chest pain or other symptoms consistent with myocardial ischaemia) when there is new (or increased) and persistent ST-segment elevation in at least two contiguous ECG.
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12
Q

Why investigate cardiac troponin? And what may this show?

A
  • Troponin I and T are the preferred biomarkers for definitive confirmation of an MI. Cardiac troponins are biological markers of cardiac muscle death (cardiomyocyte necrosis) that are released into the circulation when damage to cardiac muscle has occurred.
  • Acute MI is definitively confirmed by a rise and/or fall in cardiac troponin (with at least one value >99th percentile of the upper reference limit) in a patient who has symptoms or signs of ischaemia.
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13
Q

Why investigate glucose? And what may this show?

A
  • Hyperglycaemia is common in the setting of acute MI, with or without a history of diabetes.
  • Normal or elevated plasma glucose.
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14
Q

Why investigate FBC? And what may this show?

A
  • Look for anaemia, which may influence the duration of dual antiplatelet therapy prescribed.
  • Normal range but can be elevated or reduced.
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15
Q

Why investigate electrolytes, urea, creatinine and eGFR? And what may this show?

A
  • Potassium, calcium, and magnesium homeostasis is crucially important to prevent both bradyarrhythmias and tachyarrhythmias during the peri-infarct interval. Baseline renal function at the time of hospital admission will provide a benchmark.
  • Normal range but can be elevated or reduced
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16
Q

Why investigate CRP? And what may this show?

A
  • May be raised as a direct result of the acute-phase response to acute MI but may also point to a concomitant infection.
  • Normal range or elevated.
17
Q

Why investigate serum lipids? And what may this show?

A
  • Not useful in the acute period of STEMI management but will inform assessment of the patient’s risk factor profile for recurrent cardiovascular events. Cholesterol levels may be lowered by high catecholamine levels mediated by an acute MI in its early phases.
  • Normal range or elevated.
18
Q

What are the 5 steps in acute management of a STEMI?

A
  1. Morphine
  2. Oxygen
  3. Nitrates
  4. Aspirin
  5. Coronary reperfusion therapy
19
Q

What is the preferred reperfusion strategy to treat a STEMI?

A

Percutaneous coronary intervention (PCI)

20
Q

When is fibrinolysis appropriate in the treatment of STEMI?

A

If percutanous coronary intervention (PCI) is a lack of access to timely PCI. Idelly PCI should be performed within 120 minutes.

21
Q

What drugs are given in the dual anti-platelet treatment of a STEMI?

A

Aspirin plus a P2Y12 inhibitor (e.g. ticagrelor, prasugrel, or clopidogrel)

22
Q

What must not be given if the patient is eligible for percutanous coronary intervention?

A

Anticoagulation with unfractionated heparin, enoxaparin, or bivalirudin will be started by the interventional cardiology team in the catheterisation laboratory.

23
Q

What is the long term management following a STEMI?

A
  • Beta-blocker or non-dihydropyridine calcium-channel blocker
  • ACE-inhibitor or angiotensin-II receptor antagonist
  • Statin
  • Dual anti-platelet
24
Q

What differentials should be considered for a STEMI?

A
  1. Unstable angina
  2. NSTEMI
  3. Aortic dissection
  4. Pulomary embolism
  5. Pneumothorax
25
Q

How does STEMI and unstable angina differ?

A
  • Differentiating signs and symptoms: clinical presentation may not differentiate.
  • Differentiating investigations: ECG may show non-specific ST-segment and T-wave changes.

Cardiac biomarkers are normal.

26
Q

How does STEMI and NSTEMI differ?

A
  • Differentiating signs and symptoms: clinical presentation may not differentiate.
  • Differentiating investigations: ECG may show non-specific ST-segment and T-wave changes, but does not show ST-segment elevation. Cardiac biomarkers are elevated in both non-ST-elevation MI and STEMI.
27
Q

How does STEMI and aortic dissection differ?

A
  • Differentiating signs and symptoms: patients typically present with tearing chest pain, notably between the shoulder blades. They can be in considerable distress and haemodynamically unstable. Peripheral pulses may be unequal or absent distally.
  • Differentiating investigations: CXR may show a widened mediastinum. A CT of chest and abdomen with intravenous contrast showing the presence of a dissection flap and a true lumen and false lumen is diagnostic for aortic dissection.
28
Q

How does STEMI and pulmonary embolism differ?

A

Differentiating signs and symptoms: patients classically present with acute onset of sharp stabbing chest pain that is pleuritic in nature and associated with shortness of breath. A background of increased clotting tendency, such as known hereditary thrombophilia or connective tissue disease; known deep venous thrombosis; or previous PE increases the likelihood of the diagnosis.

Differentiating investigations: patients are hypoxic with an increased arterial-alveolar gradient on the arterial blood gas.ECG may show sinus tachycardia or right ventricular strain. CT pulmonary angiography (CTPA) is the most definitive diagnostic test of pulmonary embolism.

29
Q

How does STEMI and pneumothorax differ?

A
  • Differentiating signs and symptoms: patients present with sudden onset of pleuritic chest discomfort and shortness of breath. Known underlying medical conditions that predispose to pneumothorax, such as chronic obstructive pulmonary disease, connective tissue disease, or recent chest trauma, may support this diagnosis.
  • Differentiating investigations: CXR shows a visceral pleural line.

Y3 Medicine: Cardiovascular (31 decks)

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