CVS 10.1 - Ischaemic Heart Disease Flashcards Preview

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Flashcards in CVS 10.1 - Ischaemic Heart Disease Deck (45):

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)



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

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