Lecture 1 CAD and ACS

CAS and ACS can both be categorized as problem in the ___________.

Stable CAD is usually caused by ________. It is the building up of plaque containing _________, __________, __________, and ________ in a damaged ________.

T/F: the fibrous cap may be calcified.

Angina is a result of ________ or ______ or both.

Which factors may affect decreased oxygen supply to the heart?

Which factors may cause decreased coronary blood flow?

Which factors may cause obstruction of coronary blood flow?

Which factors may result in increased oxygen consumption of the heart?

Make a tree diagram of the mechanisms of myocardial ischemia due to coronary dysfunction.

What is the oxygen extraction rate of myocardium?

Formula of MVO2?

How can we assess the myocardial oxygen consumption indirectly?

T/F: The higher the RPP, the harder the heart is working.

When the patient experiences angina/ischemia at the same RPP, he/she is likely having _________ angina.

The cut off for each level of RPP:

T/F: Females are more prone to coronary heart disease as compared to males.

T/F: lesion in coronary artery does not happen until the 3rd decade of lide.

Initial plaque growth is mainly due to ________. It becomes mainly due to ______ and _______ in the 3rd decade and may result in complicated lesion such as _____ and/or ______.

Atheroma is the _________ with __________ layers. Once atheroma is reached, the patient may have clinical symptoms.

Pain is usually not a descriptor for CAD, which descriptions are common?

T/F: CAD symptoms vary significantly with inspiration or movement.

T/F: Steady discomfort from CAD can last from a few second to 10 min.

What is 'Levine's sign'?

Is the discomfort diffuse or localized?

The dermatomal rule suggests that when pain is referred, it is usually to a structure that developed from the _______ or _______ as the pathological structure. The CNS misinterprets the origin of pain from somatic structure innervated by the same __________.

Describe the common 'anginal equivalents'.

Which conditions are the 4 'E's that increase myocardial oxygen demand?

T/F: The 4 Es typically resolves if altered.

List the risk factors of CAD.

Why may the patient have increased HR and BP during an ischemic attack?

Why may a patient have murmur of mitral regurgitation during an ischemic attack?

What is PMI and why might it shift during ischemic attack?

Why might an S4 heart sound be present during ischemic coronary disease?

If a patient is not having an attack when we are assessing them, how may we assess their presence of atherosclerosis?

What is the gold standard to confirm an ischemic heart attack??

Which segments are primary indicators of CAD?

Familiarize with abnormalities in T wave and ST segment.

Which test can see the perfusion of heart?

Which test can allow visualization of exercise induced myocardial hypokinesis, dyskinesis, or akinesis?

Which imaging allows us to see the actual blockage of coronary artery? Is it invasive?

Components of conservative medical management of CAD.

What are the options for invasive procedures treating CAD?

What are some good vascular candidates for CABG?

Which factors might affect the prognosis of CAD?

An ACS is a (stable/unstable) scenario requiring emergent care.

UA, or ______, is when the atherosclerotic plaque become disrupted with ______ aggregation. Once thrombus is formed, a ______MI may occur. If the thrombus is so large that it completely blocks off the artery, a ___MI may occur, which will result in permanent tissue damage.

Compare and contrast the clinical presentations of UA from STEMI/NSTEMI

T/F: STEMI/NSTEMI always respond to NTG.

What are some common symptoms of ACS is men and women?

What are some unique ACS symptoms in women?

Which abnormal heart sound is normal in ACS? S3 or S4?

Why may heart murmur also be heard in patients with ACS?

What are the causes for dysrhythmias in ACS?

Which arrhythmias may be present in acute MI?

What are the 2 most important diagnostic tests for ACS?

If the person has ST elevation with troponin (+), he/she had:

If the person had No ST elevation but (+) troponin, he/she likely had:

If the patient has no ST elevation and (-) troponin, he/she likely had:

ST segment depression and/or T wave inversion only happens in NSTEMI, not in UA.

Why is (+) troponin level a marker for tissue damage?

What should be initiated after Dx of UA or STEMI?

What is the invasive procedure that can accompany ASA treatment?

What are some medication available for long term treatment for UA. NSTEMI?

The first line of treatment in STEMI is also

If the patient is admitted to ED <90 min of onset and PCI is available, then their options are:

If the patient is admitted to ER > 120 min of STEMI onset, or there is no access to PCI, then the options are

T/F: Patients admitted with STEMI have a higher survival rate than NSTEMI.

Chest pain of pt. is elicited by palpation. Is he/she likely to have angina?

What are the differences between unstable ACS from stable CAD?