CVS 10.1 - Ischaemic Heart Disease Flashcards
What are some potential causes of chest pain?
- Rib/muscle pain (localised)
- Pneumonia
- MI/Angina
- Cholesystitis
- Gastroesophogeal Reflux Disease (burning pain)
Give some causes of central chest pain and the type of pain they produce
- Myocardial ischaemia = tightening pain
- Pericarditis = Sharp pain
- Aortic dissection = tearing pain
What is pericarditis?
Inflammation of the pericardium which causes swelling
How can pericarditis be tested for/diagnosis be confirmed?
- Friction rub heard when using a stethoscope
- Sounds like squeaky leather/ scratching
What is Beck’s Triad?
- Signs of pericarditis
- Low arterial blood pressure
- Distended neck veins (increased venous blood pressure)
- Muffled heart sounds (due to fluid)
Why is arterial blood pressure lowered due to pericarditis?
- Accumulation of pericardium = Increased pressure
- Limits pre-load and decreases end diastolic volume & stroke volume
What can pericarditis lead to?
- Cardiac tamponade
- Limits ability of the heart to adequately pump blood
What is aortic dissection?
- Tear in the tunica intima of the aorta
- Increases space between layers as blood can flow through
- Leads to a murmur
What can aortic dissection lead to?
- Decreased blood supply to other organs common with hypertension
- Can get pseudohypotension (false low measure due to brachiocephalic subclavian arteries)
Describe respiratory pain
- Lateral chest pain
- Pleuritic i.e. becomes worse with inspiration/coughing
In what direction is coronary blood flow? What does this result in?
- Epicardium to endocardium
- Leaves subendocardial surface as most vulnerable place to ischaemia
When does filling occur? How can ischaemia be caused by interrupted filling?
- Occurs during diastole
- ↑ heart rate = ↓ time of diastole
- ↓ filling = ↓ coronary blood flow
- Leads to ischaemia
What are the non-modifiable risk factors for coronary atheroma?
- Age
- Male sex (up to menopause)
- Family history
- Ethnicity
What are the modifiable risk factors for coronary atheroma?
- Hyperlipidaemia
- Cigarette smoking
- Hypertension
- Diabetes type 2
- Lifestyle i.e. obesity
What does coronary atheroma lead to?
- ↓ lumen diameter
- ↑ risk of thrombosis
- ↑ risk of MI
Descibe stable plaque
- Small necrotic core
- Thick fibrous cap
- Not likely to rupture
Describe vulnerable plaque
- Large necrotic core
- Thin fibrous cap
- More likely to rupture
What causes rupturing of vulnerable plaque?
What does this lead to?
- High sheering forces e.g. hypertension
- Erosion/fissuring (splits)
- Exposes blood to thrombogenic core causing formation of a clot
- Causes variable obstruction to flow in lumen and downstream ischaemic myocardial injury
- Complete obstruction = STEMI
- Incomplete obstruction = NSTEMI and/or unstable angina
What is stable angina?
- Chest pain/discomfort due to activity or emotional stress
- 70-80% occlusion = limited blood flow during exertion
- Has stable, fixed plaque
How can stable angina be tested for?
- Do an exercise stress test
- ECG on a treadmill with continuous monitoring whilst increasing difficulty
- ECG changes = positive result
- No pain at rest
What ECG changes would be seen during stable angina?
- Like a left bundle branch block
- Inverted S-T elevation (more than 1mm)
- DURING EXERTION
How can stable angina be treated?
- Sublingual nitrates (immediate effect)
- Lifestyle changes
- Revascularisation
What is acute coronary syndrome?
Conditions due to a decrease in blood flow to coronary arteries, usually caused by thrombus, plaque rupture or platelet aggregation
How do acute coronary syndromes present?
- Pain at rest
- Becomes more severe upon exertion
- No relief with nitrates
- Lasts a while
What is unstable angina?
Angina caused by the disruption of atheroslerotic plaque with partial thrombosis
What are the signs of unstable angina?
- Long lasting pain at rest/with minor exercise
- Pain is severe and new in onset
- Has a crescendo pattern of occurrence i.e. becomes longer, more frequent and more severe
- Has no biomarkers of necrosis
- ST depression/ T wave inversion/ normal ECG
How can unstable angina be treated?
- Antithrombin therapy
- Aspirin (↓ platelet clotting so ↓ thrombus)
- Coronary Angiography
- Revascularisation
What is revascularisation?
- Angioplasty and stenting
- Catheter is inserted and guided to blocked area via wrist/groin
- Small balloon is attached that then inflates so holds artery open
- Stent is inserted and balloon is removed so keeps artery open
What is bypass grafting?
- Anastamose internal mammary artery
- Sew it to LAD at a site that is distal to the occlusion
- Can use radial artery/ reversed saphenous vein (so valves are down)
What is a STEMI
- Myocardial death due to stoppage of blood flow
- ST segment elevation in leads facing the injured area
What are the different levels of occlusion in a STEMI?
- Total occlusion (>90%) = injury to full thickness of ventricular wall/is transmural
- Partial occlusion = subendocardial area is affected
How is an ECG changed during a STEMI?
- Acute T wave elevation
- ST elevation (0-12 hours after)
- Q wave develops over 1-12 hours
- ST elevation with T wave inversion = 2-5 days
What is an NSTEMI?
- Non ST segment elevation MI
- ST depression/ T inversion/ normal
- Troponins are released
- Pain like MI
What is a myocardial infarction?
- Irreversible damage to heart muscle due to a lack of blood flow (prolonged ischaemia and hypoxia)
Describe the pain felt during an MI
- Severe
- Crushing
- Persistent
- Central
- Radiating chest pain that isn’t relieved by rest/nitrates
Why would a patient become pale and sweaty during an MI?
- Increased sympathetic stimulation
- Increased by baroreceptor reflex due to ↓ blood pressure
- ↑ circulating catecholamines
Why would a patient suffer from nausea and vomiting during an MI?
Decreased parasympathetic stimulation
What are the most commonly used biochemical markers of myocyte damage? Why are they used?
- Cardiac troponin I or cardiac troponin T
- Released during myocyte death/damage = ↑ levels during STEMI/NSTEMI
- Are more sensitive and more specific
- Levels are raised for 7 days
Give another biomarker of myocyte damage, when would it be used?
- Creatinine kinase
- Specific as long as skeletal muscle isn’t damaged too
- Levels return to normal within 2-3 days
Which artery would be occluded if the area of infarction was inferior? Which leads would this show in?
- Right coronary artery
- Leads: 2, 3 and AvF
Which artery would be occluded if the area of infarction was antero-septal? Which leads would this show in?
- Left anterior descending artery
- V1 - V2
Which artery would be occluded if the area of infarction was antero-apical? Which leads would this show in?
- Left anterior descending artery (distal)
- V3 - V4
Which artery would be occluded if the area of infarction was anterolateral? Which leads would this show in?
- Circumflex artery
- 1, AvL, V5 - V6
Which artery would be occluded if the area of infarction was extensive anterior? Which leads would this show in?
- Proximal left coronary artery
- 1, AvL, V2 - V6
Which artery would be occluded if the area of infarction was true posterior? Which leads would this show in?
- Right coronary artery
- Tall R wave in V1
