Flashcards in CVS S10 - Ischaemic Heart Disease Deck (36)
What are the general common sources of chest pain?
Lungs & Pleura
CVS - heart & great vessels
Give examples of conditions originating in the lungs and pleura which can cause chest pain
Give examples of conditions originating in the GI system which can cause chest pain
Peptic ulcer disease
Gall bladder (cholecystitis, biliary colic)
Give examples of conditions originating in the chest wall which can cause chest pain
Give examples of conditions originating in the CVS which can cause chest pain
Myocardium - angina, MI
Pericardium - pericarditis
Aorta - aortic dissection
Give some non-modifiable risks for coronary atheroma (and by extension, IHD)
Genetics (family history)
Give some modifiable risks for coronary atheroma (and by extension, IHD)
Describe ischaemic chest pain
Central, retrosternal or left-sided
Described as crushing, tightening, heavy, constricting
Can radiate along jaw, arm, neck and back (particularly left side of all)
Is IHD-caused chest pain always the same?
Can be different in different people
Can have radiation or not, can be only referred pain, can vary in intensity, duration, precipitating and relieving factors
Describe stable angina
Mild to moderate IHD chest pain brought on by exertion or emotion, particularly after meals or in cold weather
Relieved by rest
Occurs when >70% of the lumen of a coronary artery is occluded by an atheromatous plaque
How is angina treated?
Acutely: sub-lingual GTN spray
Preventatively: beta blockers, Ca channel blockers, oral nitrates
Preventing cardiac events: aspirin, statins, ace inhibitors
Long term: consider revascularisation
Describe unstable angina
Ischaemic chest pain which occurs at rest or with minimal exertion. Described as severe and as having a crescendo pattern (becoming distinctly more severe, prolonged or frequent than before)
Caused by worsened stable angina as plaques grow and more coronary lumen is occluded
How would a patient with an MI present?
With very serious ischaemic chest pain at rest
Not alleviated by rest or GTN spray
May have no precipitant
Autonomic features eg sweating pallor nausea vomiting
Breathlessness and fainting due to LV dysfunction
How does a myocardial infarction occur?
Complete occlusion of a coronary artery leads to ischaemia and infarction of the myocardium it supplies
The fibrous cap of an atheromatous plaque can erode or fissure, allowing blood to the necrotic core & causing thrombus formation which can completely occlude a coronary artery
What are the two general categories of myocardial infarction?
Describe a STEMI
A myocardial infarction where the ST wave on an ECG is elevated, leading to the abbreviation (ST Elevated Myocardial Infarction)
Occurs when the infarct is the full thickness of the myocardium
Describe a NSTEMI
An MI where the ST wave of an ECG is not elevated
Occurs when the infarct is not the full thickness of the myocardium
Discuss the diagnosis of angina
ECG is usually normal so an exercise stress test is used
Diagnosis is based on history so these may contribute to diagnosis:
Evidence of atheroma elsewhere eg peripheral vascular disease
Describe an exercise stress test
Graded exercise whilst connected to an ECG until:
-Target heart rate reached
-Other problems (arrhythmia, low bp, ect)
What constitutes a positive exercise stress test result for diagnosis of angina?
ST depressions of >1mm
What is acute coronary syndrome?
A group of symptoms attributed to the obstruction of coronary arteries as a result of NSTEMI, STEMI or unstable angina
How can an unstable arrhythmia be differentiated from an NSTEMI?
UA has no myocardial necrosis whereas NSTEMI has some
So UA would have no bio markers like troponin in the blood but an NSTEMI would have a small amount
In an ECG, there may or may not be a difference
How can a STEMI be differentiated from an NSTEMI?
An NSTEMI has partially occluded coronary arteries whereas a STEMI would have complete occlusion
A STEMI would also have significantly more necrosis than an NSTEMI so significantly more troponin and CK bio marker release
On an ECG, a STEMI would show ST elevation but NSTEMI wouldn't
What does a deep or pathological q wave indicate?
A previous myocardial infarction which has since healed
What troponin isotopes are looked for in suspected MI? Discuss timescales of appearance
Cardiac troponin I (cTnI) and T (cTnT)
Rise 3-4h after onset of ischaemic chest pain
Peak 18-36h after
Slowly decline over the next 10-14 days
What creatine kinase isotopes are looked for in suspected MI? Discuss timescales of appearance
CK-MB is the cardiac iso-enzyme
Rises 3-8h after onset of ischaemic chest pain
Peaks after 24h
Returns to normal in 48-72h
Give examples of bio markers seen in the blood after an MI
Troponin (types I and T)
Creatine kinase (the MB isoenzyme)
What does presence of CK-MB, cTnI or cTnT in the blood indicate?
There has been death of myocardium
How may progression of thrombosis be achieved?
Anti platelet agents eg aspirin
Anticoagulants eg heparin