cardiac lab eval Flashcards
1
Q
What are the cardiac biomarkers?
A
- troponin (main one)
- CK-MB
- myoglobin
2
Q
Lab tests for CV risk assessment?
A
- hs-CRP
- homocystine
3
Q
When do you use BNP?
A
- in HF management
4
Q
When are cardiac biomarkers used?
A
- in dx and risk stratification of pts with cardiac sxs
- not necessary for dx of pts who present with ischemic chest pain and EKGs with ST elevation
- follow the trend to peak
- useful to assess myocardial injury
- proteins that leak from myocardium secondary to ischemia
- differences b/t various biomarkers: time from ischemic injury to elevation of the lab values, and variable degrees of specificity for myocardial injury
5
Q
What is troponin a high specific marker for?
A
- cardiac muscle cell death
- it is a protein that is integral to muscle contraction
- found in skeletal and cardiac muscle
- Troponin I and T are isolated proteins specific for cardiac muscle
- released into systemic circulation when there is myocyte necrosis that leads to cell membrane disruption
6
Q
Troponin can ID pts at increased risk for what?
A
- adverse cardiac events
- several trials have demonstrated direct correlation b/t level of troponin in regards to mortality rate and adverse cardiac event rate in ACS
- higher the troponin the worse the outcome - large MI will have very high elevation of troponin -
7
Q
Different troponins?
A
- check either I or T (depends on facility)
- mult different assays so reference ranges may vary
- POC troponin used in the ER for rapid dx may be useful
8
Q
When do troponin levels rise and when do they peak?
A
- rises within 2-3 hours after cardiac insult and may stay elevated for 10 days to 2 weeks after event
- peak at 12-16 hrs
- wash out after thrombolytics will cause sig rise in troponins (won’t be true elevated marker)
9
Q
Troponin and CK-MB levels with and without reperfusion?
A
- with reperfusion - very elevated over 100, peaks and falls off quickly
- without: up to 75, not as high as with reperfusion but peaks longer
- CK-MB: with reperfusion preaks quickly, higher than with no reperfusion
- CK-MB: with reperfusion peaks longer, not as elevated
10
Q
What cardiac causes other than ACS will result in elevated plasma cardiac troponin?
A
- cardiac contusion
- cardiac surgery
- cardioversion
- endomyocardial biopsy
- CHF
- aortic dissection
- post PCI
- rhabdomyolysis
- myocarditis
- aortic valve disease
- hypertrophic cardiomyopathy
- tachyarrhythmia
- bradyarrhythmia, heart block
- apical ballooing syndrome
- pericarditis
- endocarditis
11
Q
What are noncardiac causes of elevated plasma troponin?
A
- PE
- severe pulm HTN
- renal failure
- stroke
- subarachnoid hemorrhage
- infilt disease: ex - amyloidosis
- cardiotoxic drugs
- sepsis
- critical illness
- extensive burns
- extreme exertion
12
Q
How is troponin used to dx MI?
A
- measure at presentation to ED
- repeat in 3-6 hrs post sx onset, may take up to 6 hrs post sxs/MI for lab test to rise
- highly sensitive assays have high negative predictive value for NSTEMI in setting of CP 2 hrs post onset of sxs (if neg after 2 hours, most likely they don’t have MI)
- may repeat beyond 6 hrs if:
initial troponin normal, EKG changes present, pt has many high risk features
(if pt has renal failure - troponin will stay stable, won’t increase like it would in an MI)
13
Q
What biomarker should you use for dx MI?
A
- troponin
- other cardiac biomarkers are not as sensitive or specific
14
Q
What is creatine kinase?
A
- enzyme found in muscle cells
- elevations suggest muscle damage and can be indicative of injury, rhabdomyolysis, MI, myositis, and myocarditis
- elevated in 1% of pts on statins
- may increase in hypothyroidism: when T3 is low, CK becomes elevated
15
Q
What are the 3 isoenzymes of creatine kinase?
A
- CK-MM: skeletal muscle and heart: elev in muscle damage to heart or skeletal muscle, crush injury, seizures
- CK-MB: heart - elevated in MI, inflammation of heart muscle, RV and LV strain
- CK-BB: elevated in brain injury, meningitis, severe shock, stroke, hypothermia, restricted blood flow to bowel
16
Q
CK-MB peak levels?
A
- also found in skeletal muscle to lesser degree
- noted at 4-6 hrs after onset of sxs
- peaks at 24 hrs
- normalizes in 48-72 hrs
17
Q
Use of CK-MB in dx ACS?
A
- crusade registry: up to 28% of pts had discordant troponin and CK-MB results
- pts with neg troponin but CK-MB + their mortality = to pts who had neg troponin and CK-MB
Grace registry (in hosp mortality): both troponin and CK-MB positive = high, troponin + and CK-MB neg = intermediate, and both markers negative = lowest - shows that troponin is better inidcator for acute MI and mortality
18
Q
What is the CK-MB/CK relative index?
A
- helps to determine cardiac vs skeletal muscle injury
- clac by ratio of CK-MB to total CK
- ratio of less than 3 = skeletal muscle source, ratio is greater than 5 = cardiac source
19
Q
What is myoglobin?
A
- protein found in skeletal and cardiac muscle
- typically rises 2-4 hrs after onset of infarction
- peaks at 6-12 hrs
- normalizes in 24-36 hrs
- low sensitivity for AMI due to lack of cardioselectivity
20
Q
What is go to test for ruling out or in acute MI vs unstable angina?
A
- troponin is go to test
- some facilities still print out CK-Mb and myoglobin
- with sxs or an abnorm EKG a person may be having an MI with neg troponin if the lab is drawn prior to 2 hrs of onset of sxs, don’t tx the labs, tx your pt
21
Q
Lab tests of CV risk assessment?
A
- lipid profile
- hs-CRP
- homocystine
22
Q
What does CRP tell you?
A
- measure general levels of inflammation in the body, elevated in infections, chronic disease, and surgery
- nonspecific
23
Q
What is hs-CRP?
A
- high sensitivity
- an elevated hs-CRP: 2-3x the risk of MI, stroke, sudden cardiac death and PAD
- stronger predictor of heart disease and stroke than LDL
- major use is in primary prevention!!!!
- secondary prevention: may predict recurrent coronary events
24
Q
How can a pt lower the hs-CRP?
A
- cardiac diet
- exercise
- BP control
- smoking cessation
- statins
- do hs-CRP so pt will be motivated to lower it
25
relation b/t CRP and LDL?
- if low CRP/low LDL very good chance of staying CV event free
- if low CRP/high LDL increases chance of event
- if high CRP and low LDL increases it even more
- if both high CRP/High LDL: sig increase of vascular risk
26
What is homocystine?
- amino acid
- acquired mostly from meat protein
- elevated levels of homocystine are related to genetics and low levels of B6, B12, and folate
(veggie diet: naturally low homocystine) - green leafy veggies - low homocystine
27
Link b/t elevated levels of homocystine and CVD?
- elevated levels of homocystine linked to CVD
- decreasing homocystine levels with B vitamins may not improve outcomes
- hyperhomocystinemia: prone to endothelial injury, blood clots, heart attack, stroke, miscarriage, pre-eclampsia
- decreasing levels don't really improve CVD risk
28
What is BNP?
- brain naturetic peptide
- produced by ventricles and atria in response to an increase in volume and pressure
- stim the release of ANP: body rids itself of Na in an attempt to decrease total body volume
- may be helpful in diff b/t CHF and lung disease
- don't use routinely to follow stable CHF
29
Causes of elevated BNP other than CHF?
- elderly
- women
- renal failure
- cirrhosis
- ACS
- myocarditis
- PE
- primary pulm HTN
