Unrein Flashcards
Various etiologies of IHD
o Atherosclerosis: western diets and lack of exercise
o Hyperthyroidism
o Anemia: decreased oxygen carry capacity
o Emotional stress: catecholamines and increased HR
o Variant angina: Prinzmetal’s - vasospasm in etiology, associated with other vasospastic phenomena, usually more common in females
RFs for IHD.
Which is the best to stop to improve overall health?
What is the most powerful modifiable risk factor for IHD?
- Increasing age
- Male
- Smoking ** best thing to stop to improve health
- Hypertension
- Diabetes
- High cholesterol/Dyslipidemia ***the most powerful modifiable risk factor for iIHD
- Family history
- Male
What is hsCRP useful for? What risk score does it influence?
Useful in assessing patients with intermediate Framingham risk scores, reclassifies up to 30% into either low or high risk
Reynolds Risk Score 2 → Sex specific tool that accounts for family history and high sensitivity C-reactive protein → he recommends this one
What is tako-tsubo CM caused by? Is it reversible?
Depression, anxiety, anger
Is reversible
What is the CIRT trial
a trial that started about a year ago to see whether the common anti-inflammatory drug low-dose methotrexate (LDM, target dose of 15 to 20 mg po weekly) will reduce rates of recurrent myocardial infarction, stroke, or cardiovascular death among patients with established coronary artery disease and either type 2 diabetes or metabolic syndrome
• Determine whether LDM will reduce the rate of new onset type 2 diabetes among those with metabolic syndrome at study entry
***not sure if this is important, but he said RVU is participating…
Serum markers for IHD. Which is “too” sensitive?
o CPK – MM, MB, BB
o Troponin → can leak with angina, but will not have CPK MB fraction, troponin might be too sensitive
o LDH (1-5)
3 kinds of stress tests? When do you do each?
- Exercise stress test → Patients need to be stable as these are provocative tests.
- Pharmacological → Induce stress on heart via drugs. Do this if a patient just cannot do normal
- Imaging augmentation w/ nuclear and/or echo (do this when EKG is un-interpretable)
Gold standard for Dx’ing IHD?
• Angiography → gold standard → low dose radiation, squirt into left main and into right coronary
How is a CT determined coronary artery Ca score useful?
Maybe useful for patient with an intermediate risk for CAD, calcium helps if you see it to test more things, but does not give functional data and is not that useful.
Stable vs Unstable Angina vs MI
Unstable Angina –> Non-ST-elevation
- New onset
- At rest
- Crescendo
MI – ST-elevation MI
Stratified based upon ECG and serum biomarkers (troponin and creatine kinase – CPK)
Come back to this ???
Typical Features of CP. What does this determine?
o Central substernal pain/discomfort – usually retrosternal +/- radiation to shoulder, arms, jaw or back. May be Visceral, which is assx w/ nausea, vomiting, diaphoresis and/or shortness of breath
o Exertional – Brought on or increased with activity/emotional stress
o Relieved by nitrates or rest
What is Baye’s Theorem? What do you do for the different risk classes?
A chart that tells you based on # of typical Sxs vs age & genger, how high their risk is, and how much of a workup you need to do
- Low probability – no further work up
- Intermediate + Normal EKG – stress test
- Intermediate + Abnormal EKG – stress test w/ possible imaging augmentation, treatment based upon findings
- High probability – medical therapy and coronary angiography, treatment based upon findings
When might you see atypical (silent) IHD (does not present with any of the classic clinical features)?
Woman, diabetics, elderly
atypical Sxs = Shortness of breath, palpitations, dizziness, and syncope
TIMI trial risk scores
Similar idea - it’s for risk stratification - but he calls these “narrow”
What are some mimickers of acute coronary syndromes? What are some key findings for each?
Recent med use may mimik
Aortic dissection - Widened mediastinum on CXR
PE - New onset of Atrial fibrillation
CHF – SOB, orthopnea
MGMT of ST-elevation MI
Early reperfusion is indicated – time is muscle!
Needto get to cath lab w/in 90 minutes. If can’t meet that timeline, give t-PA (Thrombolytic therapy)
• Most significant determining factor is “Door to Balloon” time (
Absolute C-I’s to thrombolytic therapy
- Intracranial Hemorrhage
- Ischemic CVA in the last 3 months
- Facial trauma in the last 3 months
- Bleeding diathesis
- History of closed head trauma 2 months ago (CIS example)
MGMT of IWMI?
always think about RV infarct with inferior wall MI, and RV infarcts are volume dependent *** → treat volume
MGMT of AWMI?
Intra-aortic balloon pump synchronous counterpulsation → very invasive device, deflates during systole and allows heart to pump with very little resistance, in diastole, it inflates and helps push the blood distally and increase perfusion. Some backflow into coronary arteries as well. Used in times of desperation
EARLY complications of MIs that you may see post thrombolytics?
o Bleeding (2-3 times higher incidence of hemorrhagic CVA in women) o Reperfusion arrhythmias → rapid tachycardic idoventricular rhythms common, it will calm down
LATE complications of MIs (24-48 hrs)
• Cardiogenic shock → Pump function loss and thought to have an inflammatory component
• VSD → New systolic murmur and thrill on left sternal border
• Papillary muscle rupture and MR → New systolic murmur, pulmonary edema, thrill and cardiogenic shock → important to have a baseline before this happens so you can recognize something new
• Free wall rupture → usually not compatible with life
o Electromechanical dissociation → Electrical activity still working but not pumping b/c pericardium full of fluid that creates pressure against heart
o First infarction, anterior infarctions, females, elderly
• Left ventricular thrombus → strokes
o Blood stasis, endocardial injury and possible inflammation leading to a hypercoagulable state
o Most often located in the left ventricular apex
Indications for Angiography (revascularization in cath lab) for high-risk patients
o 3 vessel disease and left main disease
o
o EF
What has been shown to decrease mortality in post acute coronary artery syndrome (ACS) Pts?
• Beta-blockers 20%
• Anti-Plt drugs (ASA or clopidogrel) 33%
• Angiotensin-Converting Enzyme Inhibitors (ACE-Is)
• HMG-CoA Reductase Inhibitors 25-30% (Statins)
o Proportional to the reduction in LDL levels
o LDL goal
Why do we worry about IHD in diabetics?
Might not have ANY CP b/c of neuropathy (silent ischemia)!
• 2-8x more likely to suffer from and die from CVD
• Patients typically have more advanced and higher grade disease and less collateralization at presentation
• Need Glycemic control & BP control to reduce risk
• Fatigue, dyspnea, nausea and vomiting may predominate the presentation
• Some care with angiography, but not an absolute contraindication – contrast nephropathy → can hurt kidneys if not monitored
