MI Flashcards
What 2 conditions come under Acute Coronary Syndrome?
- Unstable angina
- MI
How can you clinically differentiate between MI and unstable angina?
MI causes a rise in troponin T due to myocardial cell death, unstable angina does not
What are the 2 types of MI?
STEMI
Non-STEMI
What are the clinical features of MI?
- Chest pain > 20 mins
- Nausea, sweating and palpitations
- Distress, anxiety
- Pallor
- Pansystolic murmor
- Low grade fever
- Signs of heart failure - (MI can render either the left or right ventricle non functional)
What is ACS without chest pain referred to as?
Silent MI
What are the clinical features of silent MI?
- Syncope
- Acute confusional state
- Vomiting
- Pulmonary oedema
- Epigastric pain
What is the differential diagnosis of MI?
- Unstable Angina
- Pericarditis
- Myocarditis
- Takusubo cardiomyopathy
- Aortic dissection
- PE
- Pneumothorax
What are the risk factors of MI?
- Smoking
- Cocaine use
- Hypertension
- Hyper-lipidemia
- Age
- Gender
- Family History
What is the pathophysiology of MI?
- Occurs as a result of fatty deposits and thrombus formation on top completely blocking the coronary vessels (coronary artery atherosclerosis)
- Lack of oxygen causes myocardial cell death
=> Arteries most likely affected by MI
- Left Anterior Descending (LAD) - supplies the anterior LV (V1, V2, V3, V4)
- Right coronary artery - supplies RA, RV and inferior LV (II, III, aVF)
- Left Circumflex artery - supplies lateral LV and LA (I, aVL, V5, V6)
What are the short term complications of MI?
=> Ventricular Fibrillation (most common cause of death):
- Presents clinically as a cardiac arrest
- Necrotic myocytes release K+ causes hyper-excitability of surrounding tissue
- Other arrhythmias include: bradycardia, tachycardia, VT, SVT
=> Muscle Ruptures:
- Rupture of free wall of ventricle - Cardiac tamponade
- Rupture of interventricular septum - Ventricular septal defect
- Rupture of papillary muscle of mitral valve - Mitral regurgitation
=> Pericarditis:
Transmural infarct spreads causing inflammatory response of pericardium
=> Mural thrombus
What are the long term complications of MI?
- Progression of Chronic Heart Failure
- Recurrent MI
- Ventricular Aneurysm
- Dresslers syndrome (self limiting autoimmune Pericarditis)
What are the investigations carried out in suspected MI?
=> Bloods
Rise in troponin
CK-MB is most useful for re-infarction
=> ECG
Pathological Q ways
STEMI
Non-STEMI
=> Echo
Regional wall abnormalities
=> CXR
Cardiomegaly, pulmonary oedema, widened mediastinum
What is the emergency management of STEMI?
- Attach ECG leads
- Establish IV access and take bloods
- History and Examination
- GTN spray, IV Diamorphine + metaclopramide
- Aspirin + 2nd anti-platelet (Ticagrelor, Clopidogrel, Prasugrel)
- Determine if PCI is available within 120 mins?
- Unfractionated heparin or LMWH given if patient going to have PCI
PCI AVAILABLE WITHIN 120 MINS:
- Do Primary PCI
PCI NOT AVAILABLE WITHIN 120 MINS:
- Thrombolysis. Do an ECG within 90 mins to see if there is an improvement
- Transfer for PCI if fibrinolysis not successful
IF MI CONTINUES POST PCI, CABG MUST BE PERFORMED
=> Oxygen therapy:
- For those with SaO2 < 94% and not at risk of hypercapnic failure
- For those with COPD who are at risk of hypercapnic failure
What is the emergency management of NSTEMI?
All patients should receive:
- Aspirin
- IV morphine or nitrates in cases of pain
Oxygen should only be given if the patient is hypoxic
=> Considering a second anti-platelet:
- Fondaparinux only given if patient not at high risk of bleeding and does not have angiography within the next 24 hours
- Ticagrelor and Prasugrel preferred as the second anti-platelet over clopidogrel. Continued after initial treatement for at least 12 months
- IV glycoprotein receptor antagonists (eptifibatide or tirofiban) given to patients with intermediate or higher risk of cardiovascular events and who will undergo angiography within 96 hours
=> Coronary angiography should be considered in patients within the first 96 hours of admission. And in patients who are clinially unstable
What are the main options for anti-platelets in a clinical setting?
=> Aspirin
Inhibits production of thromboxane A2
=> Clopidogrel
Inhibits ADP binding to its platelet receptor
=> Enoxaprain
Activates antithrombin III
=> Fondaparinux
Activates antithrombin III
=> Eptifibatide, Tirofiban
Glycoprotein receptor antagonists