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Flashcards in ASHD/ACS Deck (43):
1

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

2

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*

3

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

4

Atherosclerotic plaques may remain stable or ?? or ??

progress only gradually

Plaques may rupture, often related to the inflammatory process and metalloproteinase activity

5

Increased plaque vulnerability

Higher lipid content
Higher concentration of macrophages
Very thin fibrous cap

6

Precipitants of plaque rupture include

exercise, eating, cold weather, and emotional stress

7

Myocardial ischemia are ?? others are ??

symptomatic, causing angina pectoris

completely silent

8

Myocardial hibernation

Areas of myocardium that are persistently underperfused but still viable may develop sustained contractile dysfunction

Reversible following coronary revascularization (cath)

9

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

10

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

11

change in exercise tolerance implies

switch from stable to unstable angina

12

Angina pectoris is usually due to ??

atherosclerotic heart disease

13

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)


14

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)

15

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)

16

takes about ??? hours for trop and CK-MB to rise

6 hrs

additional for acute phase: myoglobin >900

screen for risk factors

17

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)

18

how to read posterior MI

flip around, depression that's actually elevation

leads to acute decompensated CHF

19

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

20

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

21

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

22

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

23

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

24

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

25

when can't do ex. stress test


do Myocardial Stress Imaging

26

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

27

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

28

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)


29

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)

30

alternative stress test

-use low-dose adenosine: vasodilates coronary vessels (ragidenosine)

31

Positron emission tomography

Demonstrate either perfusion or metabolism of myocardium

Can accurately distinguish transiently dysfunctional (“stunned”) myocardium from scar tissue

32

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

33

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

34

*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

35

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

36

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

37

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)

38

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)

39

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!)

40

slide 35 EKG

anteriolateral MI
left main?

41

complications

Postinfarction ischemia
Arrhythmias
Acute LV failure
RV infarction
Mechanical defects (papillary muscles)
Myocardial rupture

42

if have anterior wall MI, have ST elevation in ??

have reciprocal changes in ??

V1-V4


II, III, aVF (inferior)

43

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