Flashcards in Cardiology Cases Deck (40):
What are the key presenting symptoms of an acute myocardial infarction?
Chest pain; PSANS symptoms - nausea, feeling like they're going to die; SANS - sweating, palpitations.
What is a silent MI?
ACS without chest pain.
What is the presentation of a silent MI?
Syncope, pulmonary oedema, epigastric pain and vomiting, post-operative hypotension or oliguria, acute confusional state, stroke, diabetic hyperglycaemic states.
Who is more likely to have a silent MI?
Elderly and diabetic patients.
Why might a diabetic person have no chest pain with MI?
Peripheral neuropathy of the nerves supplying the heart so no pain is felt.
What is the typical pain in acute MI? (SQITARPS)
Site - central chest; quality - crushing; intensity - bad; timing - acute; secondary symptoms - radiating pain to left arm, jaw, back.
What are the risk factors of AMI?
Non-modifiable - age, male gender, family history of IHD (MI in 1st degree relative <55). Modifiable - smoking, hypertension, DM, hyperlipidaemia, obesity, sedentary lifestyle, cocaine use. Others (debatable) - stress, type A personality, LVH, increased fibrinogen, hyperinsulinaemia, increased homocysteine levels, ACE genotype.
What are the signs of a patient presenting with AMI?
Distress, anxiety, pallor, sweatiness, pulse change, BP change, 4th heart sound, signs of heart failure, pansystolic murmur, low-grade fever.
What are the ECG test results from AMI?
STEMI - tall T waves, ST elevation, new LBBB wwithin hours --> Q waves and T wave inversion after a few hours-days. NSTEMI/unstable angina - ST depression, T wave inversion, non-specific changes.
What are the CXR signs from AMI?
Cardiomegaly, pulmonary oedema, widened mediastinum.
What investigations should be ordered for AMI?
ECG, CXR, bloods (FBC, U&E, glucose, lipids, cardiac enzymes).
What are the cardiac enzyme results from AMI?
Troponin T and I are sensitive and specific markers of myocardial necrosis.
How is AMI diagnosed?
Increased biomarkers + symptoms of ischaemia or ECG changes of new ischaemia or Q waves or new loss of myocardium or regional wall motion abnormalities on imaging.
What are the differential diagnoses of AMI?
Stable angina, pericarditis, myocarditis, Takotsubo cardiomyopathy, aortic dissection, PE, oesophageal reflux/spasm, pneumothorax, musculoskeletal pain, pancreatitis.
Why can AMI be ST elevated or not?
In full thickness infarction due to full vessel occlusion, there is ST elevation. In NSTEMIs, there isn't full vessel occlusion so less infarction.
What is the brief pathophysiology of AMI?
Acute coronary syndrome has plaques in the arteries, these can fissure, releasing thrombogenic material. This blocks the artery so the heart tissue doesn't have enough O2, therefore infarcts.
What is acute coronary syndrome?
Build up of atheromatous plaques occluding arteries. Pathology: plaque rupture, thrombosis, inflammation.
What is the pneumonic for treatment of AMI?
MONA - morphine, oxygen, nitrates, and aspirin.
How should symptoms be controlled in AMI?
PRN GTN and opiates. If insufficient - GTN infusion.
How should risk factors be reduced to prevent future AMI?
Stop smoking; treat hypertension, diabetes mellitus, hyperlipidaemia; diet high in oily fish, fruit, vegetable, and fibre, and low in saturated fats; encourage daily exercise; mental health flag to GP.
What are the cardioprotective medications that should be optimised after AMI?
Antiplatelets - aspiring and clopidogrel for 12 months with PPI for gastric protection; anticoagulate with fondaparinux until discharge; B-blockers (or verapamil or diltiazem if contraindicated); ACE-i if LV dysfunction, hypertension, diabetes (ARB if not tolerated); high-dose statin; eplerenone if heart failure.
How should STEMI patients and very high-risk NSTEMI patients be managed surgically?
Immediate angiography ± PCI.
Who should be considered for CABG in AMI patients?
Patients with multivessel disease.
What are the complications of AMI?
Cardiac arrest, cardiogenic shock, LV failure, bradyarrhythmias, tachyarrhythmias, RV failure/infarction, pericarditis, systemic embolism, cardiac tamponade, mitral regurgitation, ventricular septal defect, late malignant ventricular arrhythmias, Dressler's syndrome, LV aneurysm.
What is the most common bradyarrhythmia seen in inferior MI patients?
First degree heart block.
What are the bradyarrhythmias seen after AMI?
Sinus bradycardia, 1st degree heart block, Wenckebach phenomenon (Mobitz I 2nd degree heart block), Mobitz type II block, complete AV block, bundle branch block.
What predisposes post AMI patients to tachyarrhythmias?
Hypokalaemia, hypoxia, and acidosis.
What are the tachyarrhythmias seen after AMI?
Sinus tachycardia, SVT, AF or atrial flutter, freqent PVCs (premature ventricular complexes), non-sustained VT, sustained VT, ventricular fibrillation.
How does RV failure/infarction post AMI present?
Low CO and increased JVP.
How is RV failure/infarction post AMI treated?
Avoid vasodilators and diuretics. Inotropes needed in some cases.
What is the presentation of pericarditis?
Central chest pain, relieved by sitting forwards.
What is the ECG of pericarditis?
Saddle shaped ST elevation in all leads.
How is pericarditis managed?
NSAIDs. Echo to check for effusion.
How does cardiac tamponade post AMI present?
Low CO, pulses paradoxus, Kussmaul's sign (JVP rises in inspiration), muffled heart sounds.
How is cardiac tamponade diagnosed post AMI?
How is cardiac tamponade treated post AMI?
Pericardial aspiration and surgery.
What is Dressler's syndrome (complication of AMI)?
Recurrent pericarditis, pleural effusions, fever, anaemia, increased ESR 1-3 weeks post AMI.
How is Dressler's syndrome treat post AMI?
NSAIDs or steroids if severe.
How does LV aneurysm post AMI present?
4-6 weeks post AMI, presents with - LVF, angina, recurrent VT, systemic embolism.