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CVS > Ischemic heart disease: ACS and CSA > Flashcards

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
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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
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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
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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
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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
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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
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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
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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)
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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
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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
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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
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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)
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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
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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
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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
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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

CVS (27 decks)

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