Session 10: Ischaemic Heart Disease Flashcards
Common causes of chest pain
Lungs and pleura: pulmonary embolism (sudden onset, breathless, DVT/risks for DVT), pneumoniae (fever, yellow sputum), pneumothorax (sudden onset, breathless)
GI (epigastric pain, ie pain in the epigastrium - the area between the sternum and the umbilicus): Oesophagus- Barret’s (acid reflux) (burning pain radiating upwards, worse when lying down/bending down/after some food, better with some antacids), peptic ulcer disease, Gall bladder -> colecystitis, biliary colic (pain due to colecystitis)
Chest wall (often localised pain, inc.s with movement, history of trauma etc): ribs -> frxs & bone metastases, muscles, skin
CVS: myocardium -> angina & MI (both involve tightening and pain generally radiating to the left side of the chest and left arm), pericardium -> pericarditis (sharp pain that gets worse with breathing but better when leaning forward), aorta -> aortic dissection (a tear in aorta wall -> blood in wall -> forces the vessel wall layers apart, symptoms are tearing pain that radiates between the shoulder blades and down the back)
Lungs and pleura causes of chest pain
pulmonary embolism (sudden onset, breathless, DVT/risks for DVT), pneumoniae (fever, yellow sputum), pneumothorax (sudden onset, breathless)
GI causes of chest pain
(epigastric pain, ie pain in the epigastrium - the area between the sternum and the umbilicus)
Oesophagus- Barret’s (acid reflux) (burning pain radiating upwards, worse when lying down/bending down/after some food, better with some antacids), peptic ulcer disease, Gall bladder -> colecystitis, biliary colic (pain due to colecystitis)
Chest wall causes of chest pain
(often localised pain, inc.s with movement, history of trauma etc)
ribs -> frxs & bone metastases, muscles, skin
CVS causes of chest pain
myocardium -> angina & MI (both involve tightening and pain generally radiating to the left side of the chest and left arm), pericardium -> pericarditis (sharp pain that gets worse with breathing but better when leaning forward), aorta -> aortic dissection (a tear in aorta wall -> blood in wall -> forces the vessel wall layers apart, symptoms are tearing pain that radiates between the shoulder blades and down the back)
Common symptoms of IHD, and pathophysiology in stable, unstable angina and an MI
Pain: can be central, retrosternal or l/sided, may radiat to shoulders and arms (l/ more common that r/), progressivelyorse from stable angina -> unstable angina -> MI
- it can feel constricting, crushing, tightening, heavy, pressure, occasionally burning epigastric pain (particularly in an MI)
Stable angina: from atherosclerosis blocking >70% of a coronary artery’s lumen, necrotic centre an fibrous cap
- pain: typical IHD pain, brought on by exertion, emotion particularly after meals and in cold weather, mild -> moderate
- Treatment: for acute: sublingual nitrate spray/tablet
- >prevent episodes: beta blockers, calcium channel blockers, oral nitrates
- >prevent cardiac events: aspirin, statins, ACE-Is
- >long term: revascularisation
Unstable angina: inc. occlusion of the lume, classified as isch. chest pain that occurs at rest/ w/ minimal exercise, severe pain occuring w/ a crescendo pattern
MI: complete occlusion of a coronary vessel -> infarction of tissue it supplies
- fibrous cap can erode/fissure, exposing the blood to thrombogenic material in necrotic core -> platelet clot followed by a fibrin thrombus leading to an embolism or occlusion of entire vessel
- presentation: faint, SOB, feeling of impending doom, SyNS (pallor, vomiting, nausea, sweating), not relieved by rest/nitrate spray, typical isch. pain
- > however, the pain is V. severe, persistent, at rest, w/ no apparent cause
- NSTEMI/STEMI: Non/ST Elevated MI: infarct is not full thickness of myocardium/is full thickness of myocardium
pathophysiology of stable angina, symptoms, treatment
from atherosclerosis blocking >70% of a coronary artery’s lumen, necrotic centre an fibrous cap
- pain: typical IHD pain, brought on by exertion, emotion particularly after meals and in cold weather, mild -> moderate
- Treatment: for acute: sublingual nitrate spray/tablet
- >prevent episodes: beta blockers, calcium channel blockers, oral nitrates
- >prevent cardiac events: aspirin, statins, ACE-Is
- >long term: revascularisation
unstable angina pathophysiology, symptoms
inc. occlusion of the lume, classified as isch. chest pain that occurs at rest/ w/ minimal exercise, severe pain occuring w/ a crescendo pattern
pathophysiology of an MI, symptoms, types
complete occlusion of a coronary vessel -> infarction of tissue it supplies
- fibrous cap can erode/fissure, exposing the blood to thrombogenic material in necrotic core -> platelet clot followed by a fibrin thrombus leading to an embolism or occlusion of entire vessel
- presentation: faint, SOB, feeling of impending doom, SyNS (pallor, vomiting, nausea, sweating), not relieved by rest/nitrate spray, typical isch. pain
- > however, the pain is V. severe, persistent, at rest, w/ no apparent cause
- NSTEMI/STEMI: Non/ST Elevated MI: infarct is not full thickness of myocardium/is full thickness of myocardium
Investigation of angina
based usually on history, although there are clues - RFs (inc. BP, corneal arcus), LV dysfunction, evidence of atheroma elsewhere eg signs of peripheral vasc. disease, but resting ECG may be normal (although may have a pathological Q wave, a sign of an MI
To confirm, an exercise stress test may be necessary: graded exercise until: target HR is reached, chest pain, altered ECG, or others eg arrhythmias, dec. BP etc
-test is +ve if ECG shows ST depression of >1mm, strong +ve test may be a sign of critiical stenosis
acute coronary syndrome and differences between causes
a group of symptoms attributed to obstruction of coronary arteries as a result of unstable angina, N/STEMI
Unstable angina: part. occlusion of arteries by thrombus, no myocardial necrosis, might have depressed ST, inverted T wave (though latter may be normal)
NSTEMI: part. occlusion, some myocardial necrosis, ST depressed, Tn biomarkers
STEMI: complete occlusion, large MI, elevated ST, Tn biomarkers
describe, on an ECG, how to differentiate between an NSTEMI/UA and a STEMI
UA = unstable angina
exercise stress test may be needed w/ a UA
changes in an ECG of an MI over time
previous MIs can be identified by the deep pathological q wave
desc. how to find the area of an MI using an ECG
abnormalities will be seen due to the dead myocardial tiss
use of cardiac biomarkers
Troponins: cTnI and cTnT: these are prot.s important in actin/myosin interactions, released in myocyte death, rises 3-4 hrs after 1st onset of pain and peaking at 18-36 hrs, then declining slowly for up to 10-14 hrs
CK: 3 isoenzymes are present in the body, one in the brain, heart and skeletal muscle - CK-MB is the isoenz. present in the heart
- rises 3-8 hrs after onset, peaks at 24 hrs, levels return to normal after 48-72 hrs
Presence of these biomarkers -> myocardial death -> distinguishes between NSTEMI and UA
