Ischemic Heart Flashcards
Coronary artery disease
Pathologic process affecting coronary arteries (atherosclerosis)
Coronary heart disease
Includes angina pectoris, MI, silent myocardial ischemia and mortality from CAD
Cardiovascular disease
Pathologic process affecting entire arterial circulation
Myocardial infarct
Irreversible death of heart muscle due to prolonged lack of oxygen
What is the role of nitric oxide?
Inhibits plaque formation, anti-inflammation
Damage leads to development of atherosclerosis
Major risk factors of IHD
Diet, HTN, DM, dyslipidemia (high LDL, low HDL, high TAGs), cigarettes
Also can be male, older, FH, obesity, metabolic syndrome
When are atypical sxs of IHD more common?
Women, elderly and pts with DM
Transient vs prolonged ischemia
Transient may lead to angina pectoris and prolonged cal lead to MI
What is another name for stable angina?
Angina pectoris
What is the pain like in a stable angina?
Not pain (heaviness, pressure, squeezing, choking)
Substernal so Levine’s sign
Can radiate to arms, neck, jaw, epigastrium, mid-back
How long does the pain in a stable angina last?
2-10 min (crescendo-decrescendo)
Usually with rest of sublingual nitro
What are atypical sxs of angina?
Dyspnea (common in women), nausea, fatigue or faintness
What sxs are not likely to be ischemia or angina?
Sharp, fleeting stabs of chest pain
Prolonged, dull ache in left precordial area
What exactly is stable angina?
Exertional or stress-related chest or arm discomfort that resolves with rest or nitro
Diagnostic tests done for stable angina
12 lead EKG (may have ST and T wave changes that occur during episodes of chest pain)
What is the Bruce protocol?
For exercise stress tests where speed/incline adjusted every 3 min to get HR to 85% of maximum
What are we looking for in stress testing?
EKG changes, decreased myocardial perfusion in nuclear imaging, drop in SBP >10 or any other sxs
When can exercise stress testing be unreliable?
Women, elderly, obesity, debility, bundle branch block, pacemaker
What are the indications for a pharmacologic stress test?
Pt unable to exercise, not able to achieve target HR with exercise or high likelihood of false positive
Gold standard for diagnosisng CAD
Angiography
What is the focus of IHD tx?
Treat signs and sxs of established IHD, rather than preventing it
What is the optimal diet?
Plant based (grains, legumes, veggies, fruits, <15% calories from fat)
What types of meds are used for stable angina?
Meds to decrease O2 demand, meds that increase oxygen supply, antiplatelets, statins, revascularization
What are meds that decrease O2 demand?
Nitrates (preload reduction), betablockers (afterload reduction) and calcium channel blockers (afterload reduction)
First line tx for chronic angina
Beta blockers
Meds that increase O2 supply
Nitrates (.3-.6 mg sublingually or spray), CCBs
What are the antiplatelet meds?
Aspirin (every pt on this unless contra), clopidogrel or a combo
What do statins do?
Stabilize plaques to reduce clinical events, slow progression and induce regression of atherosclerosis
What are the acute coronary syndromes?
Unstable angina, non-st segment elevation MI or ST segment elevation MI
What is the presentation of ACS?
Ischemic pain, SOB, weakness, nausea, anxiety, sense of doom and may see those atypical sxs
Potentially fatal ddx of chest pain
Aortic dissection, PE, pneumothorax, perforated viscous in GI, cocaine abuse
Presentation of unstable angina
Ischemic discomfort and 1 of 3:
Occurs at rest, >10 min
Severe and of new onset (4-6 wks)
Occurs with crescendo pattern (gets worse)
What is Prinzmetal’s angina?
Ischemic sxs secondary to vasospasm
Usually younger pts
Chest pain at rest with transient ST segment elevation
Tx: nitrates and CCBs
Possible pathophysiologic processes of UA or NSTEMI
Plaque rupture or erosion with superimposed nonocclusive thrombus (most common)
Dynamic obstruction (coronary artery spasm)
Progressive mechanical obstruction
UA secondary to increased myocardial O2 demand/decreased supply
Stress testing in UA/NSTEMI
Only in situations where there is no evidence for infarction (normal enzymes) but diagnosis unclear
Clinical features of unstable angina
No elevation of CK-MB or troponin (no myocardial cell necrosis)
Clinical features of non-ST elevation MI
Definite elevation of CK-MB and/or troponin (no ST elevation)
Txs for UA/NSTEMI
Bedrest with monitoring, MONA, beta blockers, antiplatelets, anticoagulation with heparin, statins, PCI
(STEMI is very similar)
TIMI variables for risk stratification of UA/NSTEMI
Age > 65 >3 risk factors of CHD Prior coronary stenosis >50% ST segment deviation on admitted EKG >2 anginal episodes in 24 hrs Increaesd cardiac biomarkers Aspirin in last 7 days 1 pt for each
Interpretation of TIMI risk score
As it increases, it increases the number of events that occur over 14 days
Who is at an increased risk for STEMI?
Ppl with multiple risk factors or history of UA
Identifiable precipitating factors of STEMI
Vigorous exercise, extreme stress, medical/surgical illness
Common causes of STEMi
Rupture of vulnerable plaque (complete occlusion of coronary artery)
Slowly developing stenosis of coronary artery
Diagnostics for STEMI
12 lead EKG, CXR, biomarkers, CBC, lipid panel, cardiac imaging, angiogram
EKG changes and cardiac markers for UA, STEMI and NSTEMI
UA: negative biomarkers and either!
STEMI: positive markers and ST segment elevation
NSTEMI: positive markers and no ST elevation
What is MONA?
Management of IHD
Oxygen first
Then nitro or morphine if that doesn’t work
Antiplatelet therapy to limit size of infarct
When must you start thrombolytic therapy?
Within first 12 hrs of STEMI (so 30 min after dx)
Absolute contraindications of thrombolytic therapy
Hx of intracranial hemorrage, stroke in last year, poorly controlled HTN, suspected dissection, active internal bleeding
What is revascularization indicated for?
STEMI (can be more effective than thrombolytics if doc is good)
Complications post mI
Recurrent ischemia, pump failure, ventricular arrhythmias, pericarditis, mural thrombus, cardiac rupture, depression
Management post MI
Risk stratification, treat risk factors, beta blockers/aspirin or ACE/ARB is LV dysfunction
