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Flashcards in cardiac lab eval Deck (29)
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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
Q

relation b/t CRP and LDL?

A
  • 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
Q

What is homocystine?

A
  • 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
Q

Link b/t elevated levels of homocystine and CVD?

A
  • 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
Q

What is BNP?

A
  • 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
Q

Causes of elevated BNP other than CHF?

A
  • elderly
  • women
  • renal failure
  • cirrhosis
  • ACS
  • myocarditis
  • PE
  • primary pulm HTN