Ischemic heart disease: ACS and CSA Flashcards
1
Q
Acute coronary syndrome (ACS)
A
- Clinical symptoms compatible with acute myocardial ischemia
- Includes sudden death, STEMI (w/ or w/o Q waves), non-STEMI (w/ or w/o Q waves) and unstable angina
2
Q
Pathophysiology of ACS
A
- Progressive buildup of atherosclerosis in coronary arteries
- Leads to rupturing of vulnerable plaques and thrombus-induced infarction/ischemia
- In most cases, the ruptured plaques occluded less than 50% of the vessel diameter (hemodynamically insignificant lesions)
- These plaques are more likely to rupture b/c they have thinner fibrous walls
3
Q
Consequence of coronary thrombosis
A
- After thrombus occlusion in coronary artery, there are 3 main possible outcomes
- If there is reperfusion of the vessel within 20 min, the lumen is narrowed and remains that way (causing unstable angina)
- However there is no myocardial damage, thus no increase in TnI (or TnT), STE, and no Q waves
- If there is reperfusion after 20 min but before 2 hrs there is some myocardial damage (subendocardial layers)
- There will be positive TnI, but no STE or Q wave
- If there is no reperfusion within 2 hrs there is massive heart damage (transmural damage)
- Thus there is elevated TnI, with STE and Q waves
4
Q
Uncommon causes of ACS
A
- Severe coronary artery spasm
- Coronary emboli
- Coronary trauma
- increased blood viscosity
- Aortic stenosis/aortic regurg
- Vasculitis syndrome
- Congenital coronary arter anomalies
5
Q
ACS vs CSA
A
- In ACS:
- Angina is more severe, lasts longer, and radiates more widely
- Rapid onset with crescendo to feeling of impending
- Associated symptoms: diaphoresis (sweating), cool/clammy skin, nausea, vomitting, weakness, dyspnea
- Little relief w/ rest in ACS, whereas CSA disappears with rest
6
Q
Principal presentations of UA
A
- Previously Dx CSA that is now more frequent, lasts longer, or lower threshold to onset
- New onset angina within 2 months
7
Q
Dx of ACS
A
- If symptoms are present, TnI test and ECG should be done and ECG should be interpreted in 10 min of presentation to ER
- Supportive medical Hx: prior Hx of CABG (coronary artery bypass grafting), PCI, angina, or MI
- Use STEMI vs non-STEMI to Dx which type of MI
- Use TnI test to see if its an MI or UA
8
Q
Risk factors for CAD
A
- Smoking, hyperlipidemia, hypertension, diabetes, family history
- Recent use of meth or coke
- Regular and recent meds use, including NTG (nitroglycerine)
9
Q
ECG changes after STEMI
A
- First ECG is normal, once STEMI occurs the first change is the STE (acute)
- After a number of hours there are deep Q waves (indicating massive necrosis) and smaller R waves
- 1-2 days after STEMI there is T wave inversion and deeper Q waves, along with the STE
- After 2 days the STE normalizes, but the T wave inversion, deep Q, and small R waves persist
- Weeks later the T wave normalizes but the small R and deep Q waves persist
10
Q
Cardiac biomarkers and echocardiography
A
- Cardiac troponins (TnT, TnI) are more sensitive than CK-mb
- Tns are first detected 3-6 hours after MI, thus negative value at time of presentation does not rule out MI
- Must do test 8-12 hrs after first assessment to ensure a dependable result
- Echocardiography: used only if uncertain after Tn tests, ECG, and Hx are taken into account
- Then do an echo to see wall motion abnormalities in the suspected region of ischemia/infarction
11
Q
Rx of STEMI and non-STEMI
A
- Lifestyle changes (!)
- Use dual antiplatelet Rx (aspirin and clopidogrel), along with BBs and/or nitrates/Ca channel blockers for both STEMI and non-STEMI
- Use heparin for both
- General measures (O2, morphine, statin, ACE inh) for both
- Main difference: for STEMI need to bust the clot (reperfuse), either thru PCI or fibrinolytic Rx (use GPIIb/IIIa inh w/ PCI)
- For non-STEMI, no PCI/finbrinolytic, but do use GPIIb/IIIa inh and then cardiac cath
12
Q
Necrosis wave front
A
- Necrosis starts 20-30 min after complete occlusion
- Begins in subendocardium and moves to full thickness of the heart wall over 3-12 hrs (endocardium-> epicardium)
- Reperfusion only good in first 12 hrs after initiation of MI, after 24 hrs more harm than good is done by reperfusion
- Goal is door to needle time (DTN) <90 min (door= first contact w/ medical care)
13
Q
Primary angioplasty vs fibrinolysis for STEMI
A
- 1o angioplasty preferred if DTB 3hrs since Sx onset), cardiogenic shock
- Dx of STEMI in doubt
14
Q
Non-STEMI and UA Rx
A
- Thrombolytics contraindicated in nSTEMI and UA
- Must classify pts into high, intermediate, and low risk categories
- Only pts in high risk get cardiac caths
- Other Rx must be done first, for all risk: relieve ischemia (BB, nitrates, Ca-blockers), prevention of thrombosis (2 antiplatelets and heparin)
- Plus bed rest, monitoring, O2, morphine if pain
15
Q
Overlap in Rx for nSTEMI/UA and STEMI
A
- Lifestyle changes (!)
- Anti-ischemic Rx: BB or NTG or Ca-blockers, and ACE inh (not in first 24 hr), statins
- Discontinue all NSAIDs except aspirin
- Need 2 anti platelets: aspirin, P2Y12 inh and/or GPIIb/IIIa inh
- Int/high risk: antiplatelets plus an antithrombotic (heparin, bivalirudin, fondaparinoux)
- Failure of Rx: add GP IIb/IIIa
- Main difference btwn this Rx and CSA: in CSA only use 1 anti platelet plus anti ischemic drugs
16
Q
Stable angina
A
- Occurs when there is partial ischemia of the heart, due to lack of perfusion of heart muscle and increased O2 demand
- Coronary perfusion pressure= Ao diastolic pressure - LV end diastolic pressure
- High intraventricular pressure during systole causes reduced subendocardial blood flow
17
Q
Coronary arterial resistance
A
- Controlled at the pre capillary arterioles, the most important determinant of myocardial perfusion
- Resistance controlled by: endothelial factors (NO, prostacyclin, EDHF, endothelin), local metabolic factors (adenosine increases during exercise-> vasodilation), neural factors
18
Q
Myocardial O2 demand
A
- Increased wall stress/tension leads to increased O2 consumption
- Heart rate
- Contractility
- Afterload and preload
- LaPlace’s principle: intraventricular pressure (Ao stenosis, HTN), increased LV size (Ao regurg, Mitrial regurg), and reduced LV wall thickness all increase tension and thus increase O2 consumption
- But overall, the most important contributors to increasing O2 consumption are: increasing HR, increasing Ao pressure (after load), and increasing force of contraction (inotropy)
19
Q
Pathophysiology of CSA
A
- Fixed obstruction due to atherosclerotic plaque w/ reduction in coronary perfusion pressure distal to stenosis
- Plus changes in coronary vasomotor tone due to endothelial dysfunction
- Length and radius of lesion are most important factors contributing to reduced coronary blood flow (CBF)
20
Q
Coronary vasomotor tone at rest and at stress
A
- Due to stenosis of a coronary artery, the arterioles must vasodilate in order to maintain normal CBF and perfusion
- But this means that upon stress, the arterioles are unable to vasodilate more and thus there is inadequate perfusion of the heart during exercise
- CBF is not affected at rest until stenosis is >80% (if angina is apparent at rest then stenosis is at least 80%)
- Maximum CBF (via exercise) is reduced starting at 50% stenosis
- The difference (coronary flow reserve) will thus be reduced starting at 50% stenosis
- The reduction in flow reserve usually manifests as CSA: chest pain during exercise
21
Q
Consequences of ischemia
A
- Not all ischemia results in pain, in fact pain is the last manifestation of ischemia
- At low ischemia elves there is metabolic alteration and diastolic dysfunction (DOE)
- At increasingly severe ischemia there are ECG changes, dyssyngergy
- Then there is chest pain (angina) upon exertion
- Angina due to stimulation of pain receptors by lactate, 5HT, adenosine
22
Q
Clinical consequences of ischemia-induced systolic dysfunction
A
- Stunned myocardium: acute systolic dysfunction after severe ischemia and reperfusion (due to Ca overload and free radicals)
- Proportional to degree of ischemia
- Hibernating myocardium: chronic systolic dysfunction in the presence of persistently reduced CBF
- Decreased function to conserve energy since CBF is chronically low
- Both of these are reversible (tissue still viable)
- MI: prolonged (>20 min) total occlusion leading to necrosis, irreversible
23
Q
Various types of angina
A
- Stable: stenosis due to place causes ischemia on exertion (demand ischemia)
- UA: plaque has ruptured and thrombus is present, can have chest pain w/o exercise (supply ischemia)
- Variant angina: due to intense vasospasm, no plaque present (supply ischemia), can happen at rest
24
Q
Chronic stable angina
A
- Recurrent brief period of predictable angina during exertion or emotional stress and relieved w/ rest
- No change in frequency, intensity of pain, or threshold of pain onset for >2 mo
- Differentiate from UA: in UA there is new onset angina in last 2 mo, rest angina, accelerating angina in pts w/ CSA, or post-MI angina
- Differentiate from variant: in variant angina there are early morning cluster of rest angina w/ spontaneous resolution
- Its due to coronary vasospasm on non-obstructive plaque due to endothelial dysfunction and increase symp activity
25
Q
Silent ischemia
A
- No angina but other ischemia manifestations: seen on ECG-monitored stress test
- Can present w/ hibernating LV myocardium or silent MI
- More common in diabetics
26
Q
Syndrome X
A
- Angina w/ ischemia inducible on stress test but no evidence of obstruction on angiogram
- Microvascular dysfunction in resistance vessels along with increased pain
27
Q
Hx for angina pts
A
- Quality of pain (tightness/squeezing/vise/burning, crescendo increase w/ relief)
- Location: diffuse retrosternal w/ radiation (arm, jaw, neck, epigastrium)
- Associated Sx: diaphoresis, nausea, SOB
- Precipitating factors: exercise, emotional stress, carb rich meal, cold temp (predictable)
- Risk factors for CAD
28
Q
Classes of angina
A
- Class I: only w/ strenuous or prolonged exertion
- Class II: early onset limiting ordinary activity
- Class III: drastically limiting normal activities
- Class IV: inability to carry out any physical activity, occurs during rest
29
Q
PE of angina pt
A
- Often normal, but look for signs of atherosclerosis (pulse differences, carotid bruit)
- Look for dyslipidemia syndromes (xanthelasma)
- Signs of HTN and diabetes: retinal vascular change, S4 gallop
- Useful labs: Hb, fasting glc, fasting lipid pannel, CRP, BNP (indicative of CHF)
30
Q
Diagnostic ECG for angina
A
- Resting ECG: resting ECG normal in 50% of pts, can also see non-specific ST depression or T inversion
- During anginal episode 50% of normal show abnormal ECGs
- Pathologic Q waves means previous MI
- After reviewing all of the data, must categorize the pt as low, intermediate, or high risk for CAD
- Stress test only for intermediate risk pts
31
Q
Stress test
A
- Increase myocardial O2 demand to precipitate ischemia
- Look at pt Sx, ECG, and possibly radionuclides or echo
- Positive test means chest pain or ST depression on ECG
- Goal is to identify the intermediate risk pts that need revascularization, from the intermediate risk pts who can have just medical Rx
- High risk pts always need revascularization
32
Q
Stress test + imaging
A
- Inject radionuclides and see what part of myocardium they are not delivered to (area of ischemia): seen as cold area
- If the cold area is filled at rest then the area was only ischemic
- If the cold area is not filled in the the area is infarcted
- With Echo: look at LV contractility at baseline and after stress to see decreased wall motion or impaired function
- Pharmacological stress test only in those who cannot exercise
33
Q
Coronary angiography
A
- Indicated in high-risk pts (clinical criteria), high-risk stress test, pts who failed to respond to medications, pts who survived sudden death
- Can only see anatomic definition of lumen, not plaque morphology
- Purpose is to determine which pts will have survival benefit w/ revascularization
- The requirements: left main, 3 vessel disease, or 2 vessel disease w/ proximal LAD and LV dysfunction
34
Q
Rx goals for CSA
A
- All pts need medical Rx, even those who receive revascularization
- Medical Rx for life, to improve quality of life
- Also to prevent future episodes of ACS and thus improving survival
35
Q
Rx for CSA
A
- Reduce angina/ischemia: use BBs (reduce MI in all secondary pts after MI and in primary pts w/ HTN, but do not reduce risk of ACS in other primary pts)
- Can use nitrates or Ca-blockers instead of BBs
- Lifestyle changes (!): smoking cessation, exercise, diet, Rx of chronic diseases
- Antiplatelet (usually ASA) for life, NO dual antiplatelet
- Reduce risk of ACS: statins and ACE inh
- In high-risk pts or those who fail meds: coronary revascularization
36
Q
Coronary revascularization
A
-Either percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG)
-Does not reduce risk of MI, but does reduce angina/ischemia and improves survival
-In CABG use LIMA for LAD, RIMA for R main/PDA
-Stent put in via PCI
CABG is most effect, but more invasive
-But even w/ these, medical Rx and lifestyle changes are most important
