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CVS > Acute MI > Flashcards

Acute MI Flashcards

1
Q

What is an atheroma?

A

Build up of a fatty, fibrous plaque in the endothelium of the artery, narrowing the lumen and restricting blood flow

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2
Q

What is chronic stable angina?

A

Chronic chest pain due to ischaemic cardiac tissue. Fixed stenosis (narrowing) Only occurs on demand. Predictable, safe

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3
Q

What does a patient do for chronic stable angina?

A
  • Stop activity - Sit - Use GTN spray
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4
Q

Where is central chest pain felt? Where can it radiate to?

A

Left sided usually. Rough area. Radiates to left arm Can radiate to the back Or up the neck into the jaw. Felt as “heavy weight”, “pressure, tightness”

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5
Q

What is acute coronary syndrome?

A

Acute presentation of any coronary artery disease. Umbrella term for - unstable angina - Acute Non STEMI - STEMI

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6
Q

What are the factors for ACS, compared to chronic stable angina?

A
  • Dynamic stenosis - Supply led ischaemia - Unpredictable, dangerous
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7
Q

What are the main steps underlying the pathogenesis of ACS?

A
  1. Endothelial injury 2. Platelet activation 3. Platelet aggregation 4. Thrombus formation 5. Vascular blockage (MI, Stroke, death)
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8
Q

How are platelets taken to the site of endothelial injury?

A
  • Endothelial injury exposes collagen - Collagen binds to Glycoprotein Ia/IIb on platelets. Von Willebrand factors also attract platelets. - Platelets recruited and adhere to site of injury. - Platelets join together= Forms a Monolayer
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9
Q

What key mediators cause platelet activation?

A

Platelet adhesion leads to activation Platelets release ADP and thromboxane A2, which are picked up by receptors of circulating Platelets. Process amplified, leading to platelet aggregation.

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10
Q

How does platelet aggregation lead to thrombus formation?

A
  • Platelets express receptors for leukocytes. - Leukocytes attach to the platelets - Other factors (II, V, X) involved - Thrombin converts fibrinogen to fibrin - Fibrin meshes activated platelets together. - Result is a Thrombus or a blood clot.
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11
Q

What is the result of an acute coronary occlusion?

A

Acute STEMI

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12
Q

What is the result of a person with an acute STEMI who survives?

A
  • Cardiac tissue beyond the occlusion is starved of blood. - Eventually dies and loss of muscle layer - Increased stretch of ventricles causes dilation. - End result= thin layer of scar tissue, dilated ventricle. Diagnosis- Heart failure (usually left)
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13
Q

What are some things in a patients history who have an STEMI?

A
  • Central, crushing chest pain - Often radiates to neck, jaw and left arm - Similar but more severe than angina, not relieved by GTN - Nausea, vomiting
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14
Q

Difference in symptoms between angina and STEMI?

A
  • More sever pain - Lasts longer - Not relieved by GTN - Associated with vomiting, nausea - Onset at rest, not exertion
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15
Q

What is a NON cardiac diagnosis for chest pain?

A

Pneumothorax

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16
Q

What are the key ECG changes in acute STEMI?

A
  1. ST elevation (1st few hours) 2. T wave inversion (after a day) 3. Q waves (after the MI)
17
Q

What ST changes are required to diagnose STEMI?

A

>1mm STE in 2 adjacent limb leads >2mm STE in 2 contiguous precordial leads new onset of Left bundle branch block

18
Q

What anatomical sites are linked with the ECG leads?

A
  1. Right Coronary artery- II,III,avF
  2. LAD- V1,V4
  3. Circumflex- I,avL, V5-6
19
Q

What cardiac proteins and enzymes are useful for MI diagnosis?

A
  1. enzyme- Creatinine Kinase 2. protein marker- Troponin: detects any myocardial necrosis. Will be elevated in MI. May not have time to have these checked in acute MI.
20
Q

What is the immediate treatment for acute STEMI?

A
  1. Aspirin (300mg) 2. Clopidogrel (300mg) Both stop platelet aggregation in the coagulation cascade
21
Q

What other medical interventions are used in early treatment of MI?

A
  1. Analgesia- dimorphine IV. Antiemitic 2. Oxygen if hypoxic 3. Aspirin + Clopidogrel 4. GTN 5. Angioplasty 6. Thrombolysis- if angioplasty unavailable after 90min
22
Q

Summarise the complications (4) that can arise from an MI?

A
  • Death - Arrhythmic complications - Structural “ - Functional “
23
Q

Main arrhythmic complication in MI? What is its treatment?

A

Ventricular fibrillation- disordered ventricular output. Loss of CO. Death v likely. Infarcted muscle is a substrate for VF. Treatment- Defibrilator

24
Q

Some structural complications of MI?

A
  • Ventricular septal defect (recurrent chest pain, shock, low CO) - Mitral valve regurgitation (presents as pulmonary oedema) - Cardiac rupture - Left ventricular aneurysm formation - Dresslers syndrome - Inflammation - Acute pericarditis - Mural thrombus
25
Q

Functional complications of MI?

A
  • Acute ventricular failure (left, right, both) - Chronic cardiac failure - Cardiogenic shock
26
Q

Routine things that need to be observed in these patients?

A
  • Cardiac monitor - Patients feelings - Pulse and BP - Heart sounds, specially Added - Any murmurs - Pulmonary crepitations - Fluid balance (urine output)
27
Q

Examples of fibrniolytics?

A

tissue plasminogen activator Streptokinase

28
Q

What is the difference of pathogenesis in STEMI compared to NSTEMI?

A

Thrombus or clots formed in the vessel and broken down by natural thrombolytics (Plasmin) which breaks down fibrin. Thus no vessel occlusion. NB- NSTEMI is a type of ACS.

29
Q

Three most important things in diagnosing NSTEMI?

A
  • History (detail of chest pain) - ECG, MAY BE NORMAL. could see ST depression or T wave inversion - Troponin investigations: highly specific to cardiac muscle. Can detect microscopic levels of myocyte necrosis. (can be a marker for other problems, CCF, Arrhythmia, pericarditis)
30
Q

Main treatment for NSTEMI?

A
  1. Aspirin 2. Clopidogrel for 3 months onwards. (often Ticagrelor used instead)
31
Q

What are some methods of achieving coronary revascularisation in these patients?

A
  • Putting a balloon in the artery to dilate it - If there is a ruptured plaque, a stent pushes it outwards allowing blood flow.

CVS (21 decks)

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