Ischemic heart disease: ACS and CSA Flashcards Preview

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Flashcards in Ischemic heart disease: ACS and CSA Deck (36):

Acute coronary syndrome (ACS)

-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


Pathophysiology of ACS

-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


Consequence of coronary thrombosis

-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


Uncommon causes of ACS

-Severe coronary artery spasm
-Coronary emboli
-Coronary trauma
-increased blood viscosity
-Aortic stenosis/aortic regurg
-Vasculitis syndrome
-Congenital coronary arter anomalies



-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


Principal presentations of UA

-Previously Dx CSA that is now more frequent, lasts longer, or lower threshold to onset
-New onset angina within 2 months


Dx of ACS

-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


Risk factors for CAD

-Smoking, hyperlipidemia, hypertension, diabetes, family history
-Recent use of meth or coke
-Regular and recent meds use, including NTG (nitroglycerine)


ECG changes after STEMI

-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


Cardiac biomarkers and echocardiography

-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


Rx of STEMI and non-STEMI

-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


Necrosis wave front

-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)


Primary angioplasty vs fibrinolysis for STEMI

-1o angioplasty preferred if DTB 3hrs since Sx onset), cardiogenic shock
-Dx of STEMI in doubt


Non-STEMI and UA Rx

-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


Overlap in Rx for nSTEMI/UA and STEMI

-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


Stable angina

-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


Coronary arterial resistance

-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


Myocardial O2 demand

-Increased wall stress/tension leads to increased O2 consumption
-Heart rate
-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)


Pathophysiology of CSA

-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)


Coronary vasomotor tone at rest and at stress

-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


Consequences of ischemia

-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


Clinical consequences of ischemia-induced systolic dysfunction

-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


Various types of angina

-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


Chronic stable angina

-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


Silent ischemia

-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


Syndrome X

-Angina w/ ischemia inducible on stress test but no evidence of obstruction on angiogram
-Microvascular dysfunction in resistance vessels along with increased pain


Hx for angina pts

-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


Classes of angina

-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


PE of angina pt

-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)


Diagnostic ECG for angina

-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


Stress test

-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


Stress test + imaging

-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


Coronary angiography

-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


Rx goals for CSA

-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


Rx for CSA

-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


Coronary revascularization

-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