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| Question | Answer |
| CAS and ACS can both be categorized as problem in the ___________. | Coronary arterial circulation. |
| Stable CAD is usually caused by ________. It is the building up of plaque containing _________, __________, __________, and ________ in a damaged ________. | Stable CAD is usually caused by atherosclerosis. It is the building up of plaque containing fibrous cap, lipids, calcium, cellular debris, foam cells from macrophage, and smooth muscle cells in a damaged endothelium. |
| T/F: the fibrous cap may be calcified. | T. |
| Angina is a result of ________ or ______ or both. | Decreased oxygen supply. Or Increased oxygen consumption of the myocardium. |
| Which factors may affect decreased oxygen supply to the heart? | 1. Decreased O2 content 2. Decreased coronary blood flow |
| Which factors may cause decreased coronary blood flow? | 1. coronary perfusion pressure 2. intrinsic regulation 3. obstruction |
| Which factors may cause obstruction of coronary blood flow? | 1. spasm 2. stenosis (including plaque formation) 3. thrombus |
| Which factors may result in increased oxygen consumption of the heart? | 1. increased wall stress 2. increased heart rate 3. increased contractility |
| Make a tree diagram of the mechanisms of myocardial ischemia due to coronary dysfunction. | See slide 2. |
| What is the oxygen extraction rate of myocardium? | 75%. |
| Formula of MVO2? | MVO2 = coronary blood flow (CBF) x (CaO2 - CvO2) |
| How can we assess the myocardial oxygen consumption indirectly? | Use the rate pressure product (HR x SBP) - It is highly correlated with MVO2. |
| T/F: The higher the RPP, the harder the heart is working. | T. |
| When the patient experiences angina/ischemia at the same RPP, he/she is likely having _________ angina. | Stable. |
| The cut off for each level of RPP: | low: 10000 - 14999 low intermediate: 15000 - 19999 Intermediate: 20000 - 24999 high intermediate: 25000 - 29999 High: >30000 |
| T/F: Females are more prone to coronary heart disease as compared to males. | F. Males are more at risk, especially past 40 y.o. |
| T/F: lesion in coronary artery does not happen until the 3rd decade of lide. | F. Lesion can happen as early as 1st decade. |
| 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 ______. | Initial plaque growth is mainly due to lipid addition. It becomes mainly due to smooth muscle and collagen increase in the 3rd decade and may result in complicated lesion such as thrombosis and/or hematoma. |
| Atheroma is the _________ with __________ layers. Once atheroma is reached, the patient may have clinical symptoms. | 1. intracellular lipid accumulation 2. core of extracellular lipid |
| Pain is usually not a descriptor for CAD, which descriptions are common? | Pressure Discomfort Tightness Burning Heaviness |
| T/F: CAD symptoms vary significantly with inspiration or movement. | F. |
| T/F: Steady discomfort from CAD can last from a few second to 10 min. | F. Usually 5-10 min. Always longer than a few seconds. |
| What is 'Levine's sign'? | A clenched fist held over the chest to describe angina. |
| Is the discomfort diffuse or localized? | Diffuse. Anywhere below the nose and above the diaphragm. Most commonly felt on the left side. |
| 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 __________. | 1. the same embryonic segment 2. the same dermatome 3. same spinal nerve root |
| Describe the common 'anginal equivalents'. | 1. tachycardia 2. diaphoresis 3. nausea 4. SOB 5. paleness 6. transient fatigue and weakness |
| Which conditions are the 4 'E's that increase myocardial oxygen demand? | 1. Exertion 2. Emotion 3. Environment (such as cold) 4. Eating (post-prandial) |
| T/F: The 4 Es typically resolves if altered. | T. Also resolves by sublingual NTG. |
| List the risk factors of CAD. | 1. smoking 2. dyslipidemia 3. hypertension 4. diabetes 5. family history of premature CAD 6. personality/ stress etc. |
| Why may the patient have increased HR and BP during an ischemic attack? | Increased sympathetic activity. |
| Why may a patient have murmur of mitral regurgitation during an ischemic attack? | The papillary muscles may also become ischemic, unable to close the valves properly. |
| What is PMI and why might it shift during ischemic attack? | 1. PMI is the point of maximal impulse. 2. It may be shifted due to ventricular wall abnormalities |
| Why might an S4 heart sound be present during ischemic coronary disease? | The ventricular wall may stiffen. |
| If a patient is not having an attack when we are assessing them, how may we assess their presence of atherosclerosis? | Listen to peripheral pulses and pay attention to carotid bruits/ femoral bruits. |
| What is the gold standard to confirm an ischemic heart attack?? | 12-lead ECG (with or without cardiovascular stress test) |
| Which segments are primary indicators of CAD? | ST segment and T wave abnormalities. |
| Familiarize with abnormalities in T wave and ST segment. | See slide 23 |
| Which test can see the perfusion of heart? | Nuclear imaging with stress test. |
| Which test can allow visualization of exercise induced myocardial hypokinesis, dyskinesis, or akinesis? | Exercise Echocardiography. |
| Which imaging allows us to see the actual blockage of coronary artery? Is it invasive? | Coronary artery catheterization/ coronary angiography. It is invasive. |
| Components of conservative medical management of CAD. | 1. Therapeutic lifestyle change (diet, exercise, weight management) 2. Medications (beta-blockers, calcium channel blockers, ACE inhibitors, ARBs, nitrates, low-dose ASA/clopidogrel), statins. |
| What are the options for invasive procedures treating CAD? | 1. medication (heparin, thrombolytics) 2. Percutaneous coronary intervention (PCI) 3. Coronary artery bypass graft. |
| What are some good vascular candidates for CABG? | 1. Saphenous vein. 2. LIMA/RIMA. (L or R internal mammary artery) |
| Which factors might affect the prognosis of CAD? | 1. early detection can improve prognosis 2. low anginal threshold can result in poor prognosis 3. Better management of risk factors and improved cardiorespiratory fitness can improve prognosis 4. Good medication regimen is important too! |
| An ACS is a (stable/unstable) scenario requiring emergent care. | Unstable. |
| 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. | UA, or unstable angina, is when the atherosclerotic plaque become disrupted with platelet aggregation. Once thrombus is formed, a NSTEMI may occur. If the thrombus is so large that it completely blocks off the artery, a STEMI may occur, which will result in permanent tissue damage. |
| Compare and contrast the clinical presentations of UA from STEMI/NSTEMI | 1. UA usually has a cresendo pattern (with increased intensity/frequency, duration) in the patient with previous stable Sx. STEMI/NSTEMI also has crescendo pattern but has a 'sense of doom' 2. Episodes of UA may occur unexpectedly, while STEMI/NSTEMI has resting symptoms that may not respond to NTG. 3. Patient without previous h/o CAD may have new onset of angina (UA). While STEMI/NSTEMI lasts very long, is very severe, and radiates very wide. |
| T/F: STEMI/NSTEMI always respond to NTG. | F. |
| What are some common symptoms of ACS is men and women? | 1. Chest pressure, 2. shortness of breath, 3.pain 4. Pain in one or both arms. Pain in neck, back, jaw, or stomach |
| What are some unique ACS symptoms in women? | 1. lightheadedness/ dizziness 2. upper back pressure 3. fainting or extreme fatigue 4. described as 'flu like' |
| Which abnormal heart sound is normal in ACS? S3 or S4? | S4. (S3 may also be present) |
| Why may heart murmur also be heard in patients with ACS? | Papillary muscles ruptured/ ventricular septal defect. |
| What are the causes for dysrhythmias in ACS? | 1. blood flow is interrupted in the conduction pathway 2. accumulation of toxic metabolites and abnormal ion concentration due to membrane leaking 3. abnormal autonomic stimulation 4. certain drugs (arrhythmogenic drugs) |
| Which arrhythmias may be present in acute MI? | 1. PVC 2. PSVT 3. A-fib 4. Atrial flutter with viable AV conduction 5. atrial flutter with 1:1 conduction 6. monomorphic v-tach 7. v-fib 8. Torsades de pointes? |
| What are the 2 most important diagnostic tests for ACS? | 1. 12-lead EKC (look for ST segment changes) 2. Cardiac biomarkers (troponin) |
| If the person has ST elevation with troponin (+), he/she had: | STEMI (total occlusion with thrombus) |
| If the person had No ST elevation but (+) troponin, he/she likely had: | NSTEMI (sub-total occlusion with thrombus) |
| If the patient has no ST elevation and (-) troponin, he/she likely had: | Unstable angina (partial occlusion with platelet aggregation) |
| ST segment depression and/or T wave inversion only happens in NSTEMI, not in UA. | F. May happen in both. Hence must look at troponin level. If troponin +, NSTEMI; if troponin -, UA. |
| Why is (+) troponin level a marker for tissue damage? | Troponin is intracellular in healthy myocardial muscle. If troponin + in surrounding tissue, it suggests lesion. |
| What should be initiated after Dx of UA or STEMI? | 1. ASA treatment (acetylsalicylic acid, or aspirin) treatment. 2. Consider the need for oxygen, NTG, morphin. |
| What is the invasive procedure that can accompany ASA treatment? | PCI (percutaneous coronary intervention) |
| What are some medication available for long term treatment for UA. NSTEMI? | ASA, beta-blocker, ACE inhibitors, statins |
| The first line of treatment in STEMI is also | ASA treatment and considering need for oxygen, NTG, and morphin. |
| If the patient is admitted to ED <90 min of onset and PCI is available, then their options are: | 1. no intervention 2. PCI 3. CABG |
| If the patient is admitted to ER > 120 min of STEMI onset, or there is no access to PCI, then the options are | 1. lytic kinase and drugs (clot busters) 2. anti-ischemic and analgesic medication |
| T/F: Patients admitted with STEMI have a higher survival rate than NSTEMI. | F. (mortality rate for STEMI is 2.5 - 10%, for NSTEMI is 2%). |
| Chest pain of pt. is elicited by palpation. Is he/she likely to have angina? | No. (angina is exertion-related, not mechanically elicited) |
| What are the differences between unstable ACS from stable CAD? | Unstable ACS is usually: 1. onset at a lower workload 2. resting symptoms 3. longer persistence into recovery 4. greater intensity of discomfort 5. increased frequency |
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