CVS - chest pain and ischaemic heart disease Flashcards Preview

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Flashcards in CVS - chest pain and ischaemic heart disease Deck (41):

What are potential causes of chest pain?

1. Musculoskeletal pain (ribs and muscles)
2. Pneumonia
3. MI or angina
4. Cholecystitis (gallbladder inflammation)


Describe the differences in pain between MI, pericarditis and aortic dissection:

All central pain.
1. Ischaemia - tightening pain
2. Pericarditis - sharp pain
3. Dissection - tearing pain


What is the imbalance that leads to ischaemic heart disease?

An imbalance of myocardial oxygen supply and myocardial oxygen demand.


What is the direction of coronary blood flow?

Epicardium -> endocardium


Which muscle of the heart is most vulnerable to ischaemia?

Sub endocardial muscle


What is the most common cause of IHD?

Fixed narrowing of coronary arteries due to atherosclerosis.


Where are collateral arteries found in the heart?

There are none between major arteries (they are functional end arteries) but some are found between smaller arteries and arterioles.


What two main factors determine myocardial oxygen supply?

1. Coronary blood flow
2. Oxygen carrying capacity of blood


What two factors determine coronary blood flow?

1. Perfusion pressure (diastolic BP)
2. Coronary artery resistance


What are the three factors that myocardial oxygen demand depend on?

1. Heart rate
2. Wall tension
3. Contractility


What determines the wall tension of the heart?

Preload and afterload


List some non-modifiable risk factors for coronary artery disease:

1. Increasing age
2. Male gender (females catch-up after menopause)
3. Family history


List some modifiable risk factors for coronary artery disease:

1. Hyperlipidaemia
2. Smoking
3. Hypertension (high diastolic or systolic)
4. Diabetes (doubles IHD risk)
5. Lack of exercise
6. Obesity


Describe a stable atheromatous plaque:

It has a small necrotic core, thick fibrous cap and so is less likely to rupture.


Describe an vulnerable/unstable atheromatous plaque:

It has a large necrotic core, thin fibrous cap and therefore the cap is less likely to rupture.


Name three acute coronary syndromes:

Unstable angina, NSTEMI and STEMI.


What are typical features of chest pain?

1. Central (sometimes on left or right side)
2. Tightening/ constricting
3. Characteristic pattern of radiation.


What coronary pathology can stable plaques cause?

Stable angina


What coronary pathology can ruptured plaques cause?

Acute coronary syndromes: unstable angina, NSTEMI and STEMI.


What is the difference between stable angina and acute coronary syndromes?

Stable angina has no pain at rest but is precipitated by stress or exertion - which is relived within 5 minutes by nitrates or rest. ACSs have pain at rest or minimal exertion which is not relieved by nitrates and is of longer duration.


How does a plaque form a thrombus?

1. Fibrous cap undergoes rupture or fissuring
2. Exposes blood to the thrombogenic material in the necrotic core
3. Platelet 'clot' followed by fibrin thrombus.


How does sub-endocardial ischaemia present itself on the ECG?

ST segment depression of >1mm.


Why is aspirin given for IHD?

It reduces platelet aggregation and therefore reduces thrombus formation.


Why are statins given for IHD?

Decrease LDL cholesterl and therefore slow the progression of atherosclerosis and increase the plaque stability.


Why are long-lasting (transdermal or oral) nitrates given for IHD?

They cause venodilation and therefore reduce preload (decrease wall tension) and therefore myocardial oxygen demand.


Why are calcium channel blockers given for IHD?

They cause peripheral vasodilatation and therefore reduce afterload and therefore myocardial oxygen demand.


Why are beta-blockers given for IHD?

They reduce heart rate and contractility and therefore myocardial oxygen demand.


List two revascularisation techniques:

1. PCI: percutaneous coronary intervention (angioplasty and stenting)
2. CABG: coronary artery bypass grafting.


How is it determined which revascularisation technique is best for a patient?

They undergo coronary angiography which identifies the sites of occlusion. The choice of procedure is influenced by these findings.


Which blood vessels are used for graft for CABG?

1. Internal mammary artery (internal thoracic artery)
2. Radial artery
3. Saphenous vein (using reversed segment of vein)


What is the difference in blood flow between NSTEMI and STEMI?

NSTEMI blood flow obstruction is typically incomplete whereas STEMI is complete obstruction.


How does a STEMI cause ST elevation?

Total occlusion of an artery causes transmural (full-thickness) injury which extends to the sub-epicardial area. ECG leads that face that area


How do you localise ST depression?

You can't! Unlike ST elevation it cannot be localised.


What are the diagnostic criteria for ST elevation?

Elevation greater than 1 small square in limb leads or 2 small squares in chest leads above the baseline. Seen in two contiguous leads.


Why is it important to recognise a STEMI?

90% are due to total occlusion and there if proved benefit from EMERGENCY RE-OPENING of the artery.


How can NSTEMIs and unstable angina be differentiated?

No biomarkers (e.g. troponin I) of myocyte necrosis seen in blood test of unstable angina as no myocyte necrosis has occurred.


What ECG changes may be seen in unstable angina or NSTEMI?

ST depression in leads facing injured area and/or T wave inversion. ECG may be normal.


What clues in the history of a patient with unstable angina MAY enable you to diagnose unstable angina over acute MI?

1. Acute worsening of stable angina
2. Angina at rest
3. Recent onset of new, effort limiting angina.
4. Or the story may be the same as in acute MI.


List some examination finding in an acute myocardial infarction:

1. Patient anxious, distressed
2. Sweating, pallor
3. Cold, clammy skin
4. Tachycardia/ arrhythmias (+/-)
5. Low BP (+/-)
6. Signs of heart failure: S3/S4, crackles in lung bases (left ventricular failure).


When do troponin levels peak? How long does it take their levels to decline?

Peak: 18-36 hours
Decline: slowly, up to 10-14 days


When do CK-MB (creatine kinase cardiac isoform) levels peak? How long does it take them to decline? When is it useful to measure?

Peak: 24 hours
Decline: back to normal 48-72 hours
Uses: when new episode of chest pain occurs within 10 days (troponin levels will be high from previous episode still but CK-MB will have come back down).