ASHD/ACS Flashcards
ASHD: atherosclerotic heart disease is ??
the number one killer in the United States and worldwide
Every minute, an American dies of coronary heart disease
Death rates of coronary heart disease have declined every year since 1968, with about half of the decline from 1980 to 2000 due to treatments (med tech, stents, dx) and half due to improved risk factors
Coronary heart disease is still responsible for approximately one of five deaths and over 600,000 deaths per year in the United States
Coronary heart disease afflicts nearly 16 million Americans
risk factors ASHD
Positive family history (the *younger the onset in a first-degree relative, the greater the risk) Male sex DM HTN Physical inactivity Abdominal obesity Cigarette smoking Psychosocial factors Diet
**Hypercholesterolemia is an important modifiable risk factor for coronary heart disease **
Metabolic syndrome
metabolic syndrome**
constellation of 3+ the following:
abdominal obesity triglycerides: 150 mg/dL or higher HDL cholesterol: less than 40 mg/dL for men and less than 50 mg/dL for women fasting glucose 110 mg/dL or higher HTN
Atherosclerotic plaques may remain stable or ?? or ??
progress only gradually
Plaques may rupture, often related to the inflammatory process and metalloproteinase activity
Increased plaque vulnerability
Higher lipid content
Higher concentration of macrophages
Very thin fibrous cap
Precipitants of plaque rupture include
exercise, eating, cold weather, and emotional stress
Myocardial ischemia are ?? others are ??
symptomatic, causing angina pectoris
completely silent
Myocardial hibernation
Areas of myocardium that are persistently underperfused but still viable may develop sustained contractile dysfunction
Reversible following coronary revascularization (cath)
Myocardial stunning
Acute, Persistent contractile dysfunction following prolonged or repetitive episodes of myocardial ischemia
Often seen after reperfusion of acute MI and is defined with improvement following revascularization
Angina pectoris due to AHD-5 main history clues (symptoms)
Circumstances that precipitate and relieve angina (rest, nitro -stable)
Characteristics of the discomfort (crushing pain)
Location (substernal, epigastric (inferior/posterior wall)) and radiation
Duration of attacks: last btw 5-30 min
Effect of nitroglycerin
change in exercise tolerance implies
switch from stable to unstable angina
Angina pectoris is usually due to ??
atherosclerotic heart disease
ASHD signs: BP
Significant elevation in systolic and diastolic BP
may be hypotensive: may reflect more severe ischemia or inferior ischemia (especially with bradycardia) due to a Bezold-Jarisch reflex
- acute decompensated CHF (inf/post wall)
- don’t give nitro, B-blocker* (decrease pre-load)
ASHD signs: heart rhythms
Gallop rhythm and an apical systolic murmur due to transient mitral regurgitation from papillary muscle dysfunction are present during pain only
Supraventricular or ventricular arrhythmias may be present (CHF) -may be fatal (AEDs)
ASHD/ACS labs
Standard laboratory tests to evaluate for acute coronary syndrome (troponin and CK-MB)
*timeline issues
Factors contributing to ischemia
Screen for risk factors that may increase the probability of true coronary heart disease
(used to use LDH : non-sp. muscle breakdown, then CK, now CK-MB)
takes about ??? hours for trop and CK-MB to rise
6 hrs
additional for acute phase: myoglobin >900
screen for risk factors
EKG
Often normal in patients with angina
Old myocardial infarction, nonspecific ST–T changes, and changes of LVH
Horizontal or downsloping ST-segment depression that reverses after the ischemia disappears, T wave flattening or inversion (NSTEMI, not reciprocal depression)
Transient ST-segment elevation (STEMI)
how to read posterior MI
flip around, depression that’s actually elevation
leads to acute decompensated CHF
Pretest probability**
know likelihood of getting a + or - test
History/Physical
Laboratory and ECG
Age
Sex
- Pts with low to intermediate pretest probability for CAD should undergo noninvasive stress
- Pts with high pretest probability are generally referred for cardiac catheterization*** (don’t stress out high risk pt)
26 yo should get EKG, troponins, not stress test
slide 14
algorithm for stable CHD when to give ASA give nitro when anginal symptoms don't give nitro for post/inf wall don't get B-blocker for inf. wall or decompensated HF
ASA and clopidogrel
TIMI risk score **
slide 15
1: age >=65
1: >= 3 CAD risk factors (HTN, DM, smoking, fam hx, elev. cholesterol)
1: known CAD (sten. >50%)
1: ASA use in past 7 days (CP despite doing right thing! -concerning)
presentation:
1: recent severe angina(less than 24 hrs ago)
1: elevated cardiac markers
1: ST deviation more than/= 0.5 mm
total: 0-7 pts
Precautions and risks of Exercise Stress
Risk of exercise testing is about one infarction or death per 1000 tests
Individuals who have pain at rest or minimal activity are at higher risk and should NOT be tested
pt must be stable and ambulatory
Indications for Exercise Stress test
To confirm the diagnosis of angina
To determine the severity of limitation of activity due to angina
To assess prognosis in patients with known coronary disease
To evaluate responses to therapy (rarely)
- if can do ex. stress test, you should
- get to 85% max HR
Interpretation of ex. stress test
Positive test is 1 mm (0.1 mV) horizontal or downsloping ST-segment depression (beyond baseline) measured 80 msec after the J point
60–80% of patients with anatomically significant coronary disease will have a positive test
10–30% of those without significant disease will also be positive
False positives are uncommon when a 2-mm depression is present
Additional information is inferred from the time of onset and duration of the ECG changes, their magnitude and configuration, BP and heart rate changes, the duration of exercise, and the presence of associated symptoms
when can’t do ex. stress test
do Myocardial Stress Imaging
Myocardial Stress Imaging (MSI) indications
When the resting ECG makes an exercise ECG difficult to interpret
Confirmation of the results of the exercise ECG when they are contrary to the clinical impression
To localize the region of ischemia
To distinguish ischemic from infarcted myocardium
To assess the completeness of revascularization following bypass surgery or coronary angioplasty
Prognostic indicator in patients with known coronary disease
MSI: Myocardial perfusion scintigraphy (radionuclide imaging)
Provides images in which radionuclide uptake is proportionate to blood flow at the time of injection
Scintigraphic defects indicate a zone of hypoperfusion that may represent either ischemia or scar
If the myocardium is viable, as relative blood flow equalizes over time or during a scintigram performed under resting conditions, these defects tend to “fill in” or reverse, indicating reversible ischemia
many false +
compare rest and stress images, if same, normal (- test)
if at rest fills in, but during stress “chunks missing”, then + test
Brown does if higher risk
MSI: Radionuclide angiography (Multi Gated Acquisition Scan, or MUGA scan)
Uses radionuclide tracers to image the LV and measures its EF and wall motion
In coronary disease, resting abnormalities usually represent infarction, and those that occur only with exercise usually indicate stress-induced ischemia
used for monitoring patients exposed to cardiotoxic therapies (such as chemotherapeutic agents)
Stress echocardiography
Echocardiograms performed during supine exercise or immediately following upright exercise may demonstrate exercise-induced segmental wall motion abnormalities as an indicator of ischemia
High-dose dobutamine (20–40 mcg/kg/min) can be used as an alternative (inc. HR)
alternative stress test
-use low-dose adenosine: vasodilates coronary vessels (ragidenosine)
Positron emission tomography
Demonstrate either perfusion or metabolism of myocardium
Can accurately distinguish transiently dysfunctional (“stunned”) myocardium from scar tissue
CT scanning can image the heart and, with contrast medium and multislice technology, the coronary arteries
High sensitivity for excluding significant CAD
Electron beam CT (EBCT) can quantify coronary artery calcification
Cardiac MRI
Excellent assessment of pericardial disease, neoplastic disease of the heart, myocardial thickness, chamber size, and many congenital heart defects
rare, tertiary care centers
coronary angiogram(cath lab)
Life-limiting stable angina despite an adequate medical regimen
Clinical presentation (unstable angina, postinfarction angina, etc) or noninvasive testing suggests high-risk disease (see Indications for Revascularization)
Concomitant aortic valve disease and angina pectoris, to determine whether the angina is due to accompanying coronary disease
Asymptomatic older patients undergoing valve surgery so that concomitant bypass may be done if the anatomy is propitious
Recurrence of symptoms after coronary revascularization to determine whether bypass grafts or native vessels are occluded
(door to balloon time of 60-90 min)
acute event: go after offending vessel ONLY
coronary angiogram 2
Cardiac failure where a surgically correctable lesion, such as LV aneurysm, mitral regurgitation, or reversible ischemic dysfunction, is suspected
Survivors of sudden death, symptomatic, or life-threatening arrhythmias when CAD may be a correctable cause
Chest pain of uncertain cause or cardiomyopathy of unknown cause
Emergently performed cardiac catheterization with intention to perform primary PCI in patients with suspected acute myocardial infarction
Coronary vasospasm
Cocaine can induce myocardial ischemia and infarction by causing coronary artery vasoconstriction or by increasing myocardial energy requirements and contribute to accelerated atherosclerosis and thrombosis
Ischemia in Prinzmetal (variant) angina usually results from coronary vasoconstriction
Patients with chest pain associated with ST-segment elevation should undergo coronary arteriography
If significant lesions are not seen and spasm is suspected, avoid precipitants, such as cigarette smoking and cocaine
Treat with nitrates and calcium channel blockers (don’t use B-blockers w. cocaine use)
-unopposed alpha will cause problems
make sure not underlying STEMI
NSTEMI/UA
Unstable angina (UA):
Change in nature of pain
Change in response to meds
(no cardiac enzyme elevation)
NSTEMI:
Cardiac enzyme elevation (demand ischemia: sepsis, ESRD)
Can have EKG changes, however not ST segment elevation
*urgent not emergent cath (w.in 24-48 hrs)
STEMI
Sudden but not instantaneous development of prolonged (more than 30 minutes) anterior chest discomfort (sometimes felt as “gas” or pressure).
Sometimes painless, masquerading as acute heart failure, syncope, stroke, or shock.
ECG: ST-segment elevation or left bundle branch block. (NEW LBBB)
STEMI tx
Immediate reperfusion treatment is warranted.
Primary PCI within 90 minutes of first medical contact is the goal and is superior to fibrinolytic therapy.
Fibrinolytic therapy within 30 minutes of hospital presentation is the goal, and reduces mortality if given within 12 hours of onset of symptoms.
get tPA if outside 45 min drive of cath lab (but many complications!)
slide 35 EKG
anteriolateral MI
left main?
complications
Postinfarction ischemia Arrhythmias Acute LV failure RV infarction Mechanical defects (papillary muscles) Myocardial rupture
if have anterior wall MI, have ST elevation in ??
have reciprocal changes in ??
V1-V4
II, III, aVF (inferior)
if looking at inferior MI, also need to look at ??
posterior leads
depression that is actually elevation in V1 (flip EKG around) -may lead to CHF
