Cardiac Lab Interpretation (Troponin, CK, CK-MB, and BNP)
If you work in the hospital – it is essential that you know and understand labs pertaining to the heart. Cardiac labs are life and death, and a good base knowledge of these will help you in the clinical setting – whether you work in the Emergency Department, Med-Surg, Critical Care, or really any other unit within the hospital. Cardiac labs are used to identify cardiac conditions and will often guide diagnostic and treatment courses for your patients – so buckle up because you’re about to become an expert!
I am starting with this lab because it is the most important cardiac lab that you will see, and it is also the most common. But what exactly is Troponin? Troponin is family of enzymes within muscle cells. Two members of this family, Troponin-I and Troponin-T, are found pretty much exclusive to cardiac tissue. When myocardial cell death occurs and the cell lyses or splits apart – the cell releases its contents including it’s troponin. Since the heart is really the only tissue to have this, the presence in the blood stream signifies myocardial necrosis or cell death. The higher the level of Troponin – the more cell death has occurred. As you can see – this can come in handy when diagnosing heart attacks. It is the preferred blood test in evaluating patients for a myocardial infarction.
Normal levels of Troponin (whether T or I) are zero, as or close to zero as you can get. Labs may utilize different assays which may have different specific cutoffs, but generally you will find:
Troponin-I = <0.04 ng/mL
Troponin-T = ≤0.01 ng/mL
Both Troponins will typically show up within 2-3 hours after cell death has begun – but they may not be detectable until 6-12 hours later. It will peak in 24 hours but can take up to 1-2 weeks for the troponin to return back to non-detectable levels.
As stated above – Troponin signifies myocardial cellular death. The prime example of this is during a Myocardial infarction (whether STEMI or NSTEMI… see below). However, there are other causes that can cause mild elevations in troponin, such as:
- Demand-ischemia: Sepsis, hypovolemia, shock, arrhythmias, CHF exacerbation.
- Other cardiac damage: Various forms of carditis, aortic dissection, post-cardiac surgery, post-cardiac cath, CPR, defibrillation.
- Kidneys: Renal damage, Acute Kidney injury, Chronic kidney disease (Especially if on dialysis).
- Vascular: Pulmonary embolism and Stroke.
This isn’t a complete list, but most of these may cause minor elevations in the Troponin. When cardiac damage is sustained, the Troponin level should rise significantly. Aside from cardiac surgery, CPR, or inflammation of the heart itself – this likely will not occur as dramatically otherwise.
It doesn’t matter what the Troponin level is during a STEMI – if its new onset – expect the Troponin to be negative. If the EKG reads STEMI – you need to hook your pt up to the defibrillator, establish 2-3 large-bore IVs, give that pt ASA, Fluids, pain relief, nitro, and get that pt to the Cath lab ASAP.
This is really where troponins shine. NSTEMIs are a type of myocardial infarction that don’t have ST elevation on the EKG, so serial checks of the Troponin can determine whether or not the pt is actually having a heart attack. It will vary based on the facility, but most facilities will check the troponin Q6-8hrs at least 2-3 times. 2-3 negative troponins in a row basically rule out any type of acute coronary syndrome (heart attack).
Is there a specific level that a troponin has to rise to be considered an nSTEMI? Not really, it just needs to be above the 99th percentile – which is any positive number. However, just because there is elevation in Troponin doesn’t mean it is an NSTEMI (See above for other causes of troponin elevation). These patients should be having some symptoms of an MI (chest pain, SOB, nausea), and/or EKG changes (ST-depressions or T-wave inversions).
Something important to remember is that NOT ALL PATIENTS EXPERIENCE CLASSIC SYMPTOMS of an MI. Diabetics are well-known to be at higher risk for “silent” MIs, and women can have atypical symptoms as well.
So you’re on your unit and your patient’s Troponin level comes back elevated. What do you do? It will vary depending on the patient’s symptoms and what unit you are on, but in general you should:
- Remain calm…
- Communicate it to the Provider (Physician, PA, or NP).
- Make sure the patient is connected to the heart monitor and is getting frequent vital signs. Apply oxygen if SPO2 < 94%.
- Obtain an EKG if they have not had one recently – worry about the order later.
- Monitor your patient and follow the orders given by the Provider.
CK / CK-MB
These labs tend to be somewhat outdated and have been replaced – for the most part – by Troponin. However – there are still some clinical implications for using these exams.
CK, or Creatine Kinase, is found within most muscle cells and is released into the bloodstream when muscular cellular necrosis or damage occurs. This includes the heart – so with the same principle as troponin – elevations in CK could indicate heart muscle damage. However – CK is NOT specific. This is why a more specific isoenzyme – CK-MB (Creatine Kinase Muscle/Brain), is used to help differentiate musculoskeletal muscle damage from heart damage. Ck-MB is found in higher concentrations within the heart.
With the implementation of Troponin, CK and CK-MB have minimal value, but they can be used in certain instances. These instances are typically after heart instrumentation (CABG or PCI), or to detect a second MI – since troponins have such a long half-life and do not return to baseline levels until 1-2 weeks after the initial incident.
The reason CK-MB can be useful is because while the onset is similar to Troponin (can take 4-12 hours to be detectable), the half-life is shorter and levels drop back down to undetectable levels in 36-48 hours. Troponin levels can take 10-14 DAYS to return to normal. This means that if a patient has a 2nd heart attack >2 days after the first, an elevated CK-MB level can indicate a 2nd MI. The same principle is related to myocardial instrumentation. If someone had a stent placed or especially a CABG, their Troponin will be expected be elevated from the irritation within the heart. If it has been >48 hrs, an elevated CK-MB could indicate further myocardial injury.
CK Male Normal: 39-308 U/L
CK Female Normal: 26-192 U/L
CK-MB Normal: 5-25 IU/L
Myocardial Infarction: Levels should be >2x the patient’s baseline.
Remember that CK and even CK-MB are not as specific as Troponin-I or T to the heart. In the presence of musculoskeletal injury – the usefulness of these tests diminishes greatly.
Any type of muscular damage or surgery can increase CK. Rarely, chronic muscle disease, hypothyroidism, and alcoholism can increase CK-MB.
BNP stands for Brain Natriuretic Peptide – however it is primarily released by the ventricles of the heart. This hormone impacts fluid and sodium handling in the kidneys. When the ventricles experience high-pressures, the cells release this enzyme.
BNP has a diuretic (fluid out) , natriuretic (salt out) , and hypotensive effect. BNP has actually been found to be somewhat protective in cardiac remodeling (cardiomyopathies).
What’s confusing about BNP is that some hospital labs utilize BNP, and some utilize NT-ProBNP – basically an inactive byproduct of the enzymatic reaction that occurs to produce BNP. It is important to know which kind of BNP your hospital utilizes in order to be able to understand and interpret the results.
While BNP levels can assist in the diagnosis of HF if it is uncertain, they are especially helpful in evaluating treatment response as the BNP half-life is only about 20 minutes. This means that BNP levels will should quickly go down if ventricular pressures improve.
Baseline BNP levels – no matter which kind – are affected by genetic variation. However, people with HF will have baseline elevations along with increases during exacerbations. Baseline levels tend to increase in age and are higher in women over men, and decrease in obesity.
Levels <100 pg/mL have a great negative predictive value – meaning they likely are NOT in an exacerbation. Levels >400 pg/mL have a high likelihood that they ARE in an acute HF exacerbation. Levels between these (100-400 pg/mL) is the gray zone – meaning they may or may not be in an acute exacerbation. It is ALWAYS important to take the clinical exam into account – Do they have clinical signs or symptoms of HF? (Think crackles, peripheral edema JVD, hepatomegaly). NEVER rely solely on labs – especially with BNP levels. BNP levels should be used as an adjunct to, and not a substitute for, clinical assessment.
NT-ProBNP levels rise much higher than regular BNP levels. They also have a longer half-life (25-70min), which means they do not fluctuate as quickly. It is also impacted by renal failure more so than regular BNP levels.
All ages: Levels <300 pg/mL – you can be almost completely sure that they do not in a HF exacerbation.
Age <50: Levels >450 pg/mL indicate acute exacerbation.
Age 50-75: Levels >900 pg/mL indicate acute exacerbation.
Age >75: Levels >1800 pg/mL indicate acute exacerbation.
With any BNP level, obesity can decrease the results, and age and renal failure can increase them.
Non-HF causes of elevated BNPs include renal failure, constrictive pericarditis, valvular disease, pulmonary hypertension, and sepsis.
And those are the main cardiac lab tests used to evaluate the heart. An EKG should always be performed at these patients above, and they should all be admitted with continuous cardiac monitoring as well. Whether you’re a nurse, nurse practitioner, or physician – it’s very important to understand these labs and be able to interpret them to provide the best care for your patients.