The Ultimate ABGs Blood Gas Guide you Need to Calm Your Nerves

The Ultimate ABGs Blood Gas Guide you Need to Calm Your Nerves

Published: June 14, 2022

Last Updated: December 24, 2022

William Kelly, MSN, FNP-C

Author | Nurse Practitioner

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This ultimate ABGs Blood gas guide is exactly what you’ve been looking for to understand Arterial Blood Gases! ABGs are used frequently in the ER and ICU settings, and many critical patients will need their blood gases monitored frequently.

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What Are ABGs or a Blood Gas?

ABGs, or an Arterial Blood Gas, is a blood sample that is taken from an artery in the wrist. This is different than normal blood work, which is taken from the veins of the arms. The arterial blood sample is obtained by a respiratory therapist or a critical care nurse.

Arterial samples provide better indicators of oxygen and carbon dioxide levels, but ABGs also look at acidity and bicarbonate levels within the blood.

A blood gas is used to look at acid-base disturbances and/or to evaluate the adequacy of oxygenation/ventilation. When an ABG blood gas is ordered, 4 contents of the arterial blood are tested:

  • Oxygen Levels: This measures PaO2 as well as SaO2
  • Carbon Dioxide levels: PaCO2 levels
  • pH: the acidity of the blood
  • Bicarbonate: The amount of bicarb, which is a buffer

Oxygen (O2) and carbon dioxide (CO2) are the main gases within the blood, and these are measured in blood gas. However, ABGs also provide levels of blood pH and Bicarb.

Of all of the measurements, the most important levels to look at are the CO2, the Bicarb, and the pH in determining acid-base balance.

When are ABGs ordered?

ABGs are very useful in evaluating acid-base disturbances, as well as ventilation/oxygenation disturbances. The patients who are ordered ABGs are often sick – usually ICU bound. The most common patients who might have a blood draw include:

Things to keep in Mind with ABGs

There are some important factors to keep in mind when thinking about ABGs and interpreting them.

Things Aren't Always Simple

Patients can have mixed acid-base disturbances, which can make it confusing. That’s why the interpretation is ultimately best left up to the critical care physicians and other Providers within their care.


Remember the body is always trying to maintain homeostasis. The respiratory system will attempt to compensate for the metabolic system and vice versa.

Underlying Cause

Always focus on treating the underlying cause.

THE ABGs: Blood Gas Measurements

Okay, so lets dive a little deeper into what each measurement is on the ABG results, and what their levels mean.

The pH

pH is the “potential of Hydrogen”, which measures how acidic a solution is. The more hydrogen ions present in a solution, the more acidic it is. 

  • Normal pH of blood: 7.35-7.45
  • Low pH (<7.35): Indicates acidosis, and is termed acidemia
  • High pH (>7.45): Indicates alkalosis (metabolic or respiratory), and is termed alkalemia

pH may be normal or near-normal in chronic acid-base disturbances from compensation, or the patient can have multiple different acid-base disturbances going on at once.

The PaCO2

The PaCO2 is the partial pressure of Carbon Dioxide within the arterial blood. Essentially this is just a measure of the amount of carbon dioxide gas within the blood.

Remember that the lungs breathe in oxygen, deliver the oxygen to the cells, and the cells use that oxygen to create energy. To create energy (ATP), the cells utilize the Kreb’s Cycle, and a byproduct of that cycle is carbon dioxide. That CO2 is then breathed out when you exhale.

CO2 isn’t acidic by itself, but in the blood forms something called carbonic acid, which is acidic. Breathing out less CO2 will cause acidosis, and breathing out too much CO2 can cause alkalosis.

IF THE PaCO2 AND the pH are both high, think RESPIRATORY ACIDOSIS.

  • Normal: 35-45 mmHg
  • Elevated: >45 mmHg, termed hypercapnia
  • Decreased: <35 mmHg, termed hypocapnia

My Blood is BOILING

When you hold your breath, eventually you need to breathe again because it feels like your blood is boiling. This always helped me remember that when you aren’t breathing enough, the CO2 makes it boil – aka acidosis!

The HCO3 (Bicarb)

HCO3 on an ABG blood gas is the serum bicarb levels within the arterial blood. Bicarb acts as a buffer to make acidity less acidic. Think of it as the opposite of hydrogen ions. The less bicarb there is, the more acidic the blood is. To get technical, Bicarb reacts with H+ to form carbonic acid, which the body breaks down into CO2 and water – which it breaths out.

  • Normal: Between 22-26 mEq/L
  • Elevated: >26 mEq/L, associated with metabolic alkalosis
  • Decreased: <22 mEq/L (associated with metabolic acidosis)

The PaO2

PaO2 is the partial pressure of oxygen within arterial blood. This basically measures the actual oxygen blood gas content.

  • Normal: > 80 mmHg
  • Elevated: > 100 mmHg, usually due to over-oxygenation
  • Decreased: <80 mmHg, associated with respiratory failure, although could be from severe anemia as well

Oxygen Toxicity

Don’t forget that too much oxygen can be bad too. Oxygen toxicity can produce reactive oxygen species and cause cellular injury, inflammation, and cell death. It can also worsen hypercapnia like in patients with COPD.

The SaO2

The SaO2 is the peripheral oxygenation, which is equivalent to the Pulse Ox reading.

  • Normal: Above 94-96%
  • Decreased: <90-92%


When interpreting ABGs and blood gases, there are 4 general categories we use:

  • Respiratory Acidosis
  • Respiratory Alkalosis
  • Metabolic Acidosis
  • Metabolic Alkalosis

Using these categories, we can better understand what the possible underlying cause of the acid-base disturbance is!

Don’t forget someone can have multiple acid-base disturbances going on at one time, and this makes clinical interpretation difficult – everything is not black and white in medicine, but this should give you a pretty good idea of what may be causing your patient’s acid-base disturbance.


Respiratory acidosis is due to alveolar hypoventilation. The lungs are NOT able to remove enough carbon dioxide quickly enough, so CO2 and Hydrogen build up in the blood.

High CO2 tends to occur late in the lung disease or when respiratory muscles are fatigued – this is usually seen in severe respiratory failure. The acidosis can be acute or chronic.

This classically can happen to patients with COPD because they are less responsive to hypoxia and hypocapnia. There is also increased dead-space ventilation and decreased diaphragmatic function due to fatigue and hyperinflation.

Acute Respiratory Acidosis

Acute respiratory acidosis could be from multiple different reasons including:

  • Respiratory Failure & Airway Obstruction: Severe asthma, COPD, CHF
  • CNS disease: Stroke, Traumatic brain injury
  • Drug-induced: Opioid or benzodiazepine overdose
  • Neuromuscular Disease: Myasthenia Gravis, ALS, Guillan Barre

Chronic Respiratory Acidosis

Chronic respiratory acidosis may occur when the PaCO2 is elevated, but the pH remains normal or near-normal because the body adjusts (metabolic compensation). Causes of chronic respiratory acidosis include: be Obesity-Hypoventilation syndrome (Pickwickian syndrome), ALS, interstitial fibrosis, and thoracic skeletal deformities.

  • COPD with Chronic CO2 retention
  • Obesity-hypoventilation Syndrome: Also called Pickwickian syndrome
  • Others: ALS, Interstitial fibrosis, thoracic skeletal deformities

COPD & Oxygen

When your patient with COPD is on a lot of oxygen, there is always a risk of hypoventilation and CO2 retention. This is the classic patient you should be thinking about with respiratory acidosis.

The treatment for respiratory acidosis is treating the underlying cause (i.e. giving Narcan to someone who overdosed on opioids), but more often than not the treatment is BIPAP or Intubation.


This acid-base disturbance is due to alveolar hyperventilation. The lungs remove too much carbon dioxide too quickly, so hypocapnia (low PaCO2) and alkalosis occur.

It is commonly found in those who are critically ill, but can be found in various other conditions such as:

Ventilated Patients

The settings on the ventilator could be incorrect, and the patient may have a rate that is too fast


Patients experiencing panic attacks, severe anxiety, or psychosis can experience respiratory alkalosis. However, the patient’s with panic attacks almost never have ABGs ordered (it’s unnecessary)

Early-Intermediate Lung Disease

Pneumonia, pneumothorax, pulmonary embolism, asthma, bronchitis. This is more the increased respiratory rate compensating for the disease, but eventually, these issues can cause respiratory acidosis instead

Numbness & Tingling with Hyperventilation

Acute low CO2 levels lead to potassium and phosphorus shifting into the cells and cause calcium to increase its binding to albumin. This can cause temporary symptoms such as numbness/tingling in extremities that many patients may experience with acute panic attacks!

The treatment for respiratory alkalosis is treating the underlying cause, such as adjusting ventilator settings, administering anxiolytics, etc. 

Metabolic Acidosis

A bicarb level <22 mEq/L in addition to a pH <7.35 is metabolic acidosis. This acid-base disturbance is due to increased plasma acidity. Metabolic Acidosis is further broken down into whether or not the Anion Gap is normal or elevated.

Severe HCO3 levels <12 are almost always caused by some degree of metabolic acidosis, instead of just compensation for respiratory alkalosis.

Normal Gap Metabolic Acidosis

This type of metabolic acidosis usually has high chloride. This is when Bicarbonate is lost within the GI tract or kidneys (is peed or pooped out). This can be caused by:


Diarrhea can cause loss of Bicarb within the stool but tends to save chloride, which does not increase the anion gap.

Chronic Renal Failure

Typically when GFR is between 20-50ml/min

Renal Tubular Acidosis

In RTA, the kidneys do not remove acid from the blood like they should

Large-Volume Fluid Replacement

Replacing large volumes of Normal Saline can cause a modest metabolic acidosis that is termed dilutional acidosis. This can worsen kidney injury. Using Lactated Ringers is a possible benefit to this, as the lactate is used as a buffer.

Elevated Gap Metabolic Acidosis

The anion gap is the difference between the positive ions in the blood (sodium), and the negative ions in the blood (chloride, bicarb, lactic acid, ketones, etc). Common causes of elevated gap metabolic acidosis include:

    Diabetic Ketoacidosis

    DKA causes a massive increase of ketone bodies which are acidic, in addition to severe dehydration

    Lactic Acidosis

    Lactic acidosis, especially in setting of sepsis, can cause metabolic acidosis

    Acute Kidney Injury

    Injury to the kidneys can cause a decreased ability to excrete hydrogen ions as well as the ability to increase bicarb levels to help buffer the acidosis

    Ingestion of certain Poisons

    Certain substances are toxic and can cause metabolic acidosis including alcohols, salicylates, cyanide, and carbon monoxide

    The treatment of metabolic acidosis is to correct the underlying issue causing the acidosis in the first place. Bicarb drips can be used in severe cases of acidosis (pH < 7.1 or 7.2).  


    This acid-base disturbance is caused by increased serum bicarb and decreased acidity. Bicarb levels >35 mEq/L are almost always caused by some degree of metabolic alkalosis as opposed to just compensation.

    For metabolic alkalosis, the acidity or hydrogen ions (H+) are usually lost in some manner, either through the GI tract or the kidneys:

    Excessive Vomiting

    Gastric secretion has a high content of hydrogen ions, so excessive vomiting can reduce overall acidity within the body

    NG Tube

    Over time, NG tubes remove a lot of gastric fluid, similar to excessive vomiting, this can cause a decrease in hydrogen ions

    Alkalotic overdose

    Rare, but if you consume massive amounts of milk products or antacids this can cause metabolic alkalosis

    Renal Losses

    The use of certain diuretics or mineralocorticoid excess, and some other rare disorders can cause the kidneys to pee out too many hydrogen ions.


    It always helps to have a systematic approach when interpreting ABGs, as blood gasses can be somewhat confusing if you miss a step!

    Determine the pH

    First, see whether or not the patient is acidic (pH <7.35), or alkalotic (pH >7.45). This will tell you if there is an acute acid-base disturbance going on.

    PCO2 + HCO3 Abnormalities

    See which levels are abnormal. Are they leaning acidic or alkalotic?  

    Correlate with pH

    See which one (CO2 or HCO3) correlates with pH. For example, if the pH is 7.2 (acidic), which abnormality is also leaning towards acidity? If CO2 was 56 and HCO3 was 30, the CO2 correlates with the pH because both are acidic.

    Determine Compensation

    Now check the level that doesn’t correlate with the pH. Is this also abnormal but in the opposite direction? If so this is termed compensation. If the pH is abnormal, it is only partial compensation. 

    Check the Anion Gap

    This step is optional and done if there is metabolic acidosis. This will help give you a better idea of which type of acidosis it is. If it is high, think of kidney failure, sepsis, or DKA. If it is low, think severe diarrhea. 

    Hopefully, this gave a good idea of how to interpret ABGs, as well as the treatment involved with abnormal results.


    Emmett, M., & Szerlip, H. (2022). Approach to the adult with metabolic acidosis. In T. W. Post (Ed.), Uptodate.

    Emmett, M., & Szerlip, H. (2022). Causes of metabolic alkalosis. In T. W. Post (Ed.), Uptodate.

    Hopkins, E., Sanvictores, T., & Sharma, S. (2020, September 14). Physiology, Acid Base Balance. National Library of Medicine.

    Sood, P., Paul, G., & Puri, S. (2010). Interpretation of arterial blood gas. Indian J Crit Care Med, 14(2), 57-64.

    Theodore, A. C. (2022). Arterial blood gases. In Uptodate.

    Cardiac Lab Interpretation and Troponin

    Cardiac Lab Interpretation and Troponin

    William J. Kelly, MSN, FNP-C
    William J. Kelly, MSN, FNP-C

    Author | Nurse Practitioner

    If you work in the hospital – it is essential that you know and understand cardiac labs like troponin.

    Cardiac labs are life and death, and knowing these labs inside and out will help you in the clinical setting.

    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!

    Cardiac Labs FB


    Troponin is the most important cardiac lab that you will see, and it is also the most common.

    But what exactly is Troponin?

    Troponin is a family of enzymes or proteins found within muscle cells. Two members of this family, Troponin-I and Troponin-T, are found pretty much exclusive to cardiac tissue.

    When heart damage occurs, the cells of the heart lyse or split apart, releasing this troponin. 

    Since the heart is really the only tissue to have this type of troponin, the presence of troponin the bloodstream 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.

    Troponin is the preferred blood test in evaluating patients for a myocardial infarction (heart attack).

    Normal Troponin Levels

    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 that levels should be:

    Troponin-I = < 0.04 ng/mL

    Troponin-T = ≤ 0.01 ng/mL

    Pattern of Troponin

    Both types of Troponin 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.

    Significance of Troponin

    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, chest trauma.
    • 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.  


    It doesn’t matter what the Troponin level is during a STEMI – if it’s new-onset – expect the troponin to be negative. Remember – it can take time for the troponin to become positive.

    If the EKG reads STEMI – you need to hook your patient up to the defibrillator, establish 2 large-bore IVs, give aspirin, possibly another antiplatelet medication like Brlinta, pain relief, nitro, and get that pt to the Cath lab ASAP.


    This is really where troponin shine. NSTEMIs are a type of myocardial infarction that don’t have ST elevation on the EKG (Non-ST-Elevation-MI).

    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).

    This doesn’t mean that the patient does not have a high-grade blockage of their coronary arteries.  Stress tests and cardiac caths are needed to definitively detect significant cardiac blockages.

    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 an 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.

    Related Content:


    So you’re on your unit and your patient’s troponin level comes back elevated.

    What do you do?

    It will depend on the patient’s symptoms and what unit you are on, but in general, you should:

    1. Remain calm.
    2. Communicate it to the Provider (Physician or APP).
    3. Make sure the patient is connected to the heart monitor and is getting frequent vital signs. Apply oxygen if SPO2 < 94%.
    4. Obtain an EKG if they have not had one recently – worry about the order later.
    5. Monitor your patient and follow the orders given by the Provider.

    Cardiac Biomarkers | Learn about troponin, CK, CK-MB, and BNP (and NT-ProBNP)

    CK / CK-MB

    CK and CK-MB are cardiac labs that are somewhat outdated and have been replaced – for the most part – by troponin.

    But there are still some important clinical situations in which using these labs may be beneficial.

    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.

    Current Indications

    CK and CK-MB have mostly been replaced by troponin, but they can be used in certain instances.

    These include:

    • Suspected heart attack after heart instrumentation (CABG or PCI)
    • 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 that 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 to be elevated from the irritation within the heart.

    If it has been >48 hrs, an elevated CK-MB could indicate further myocardial injury.

    Normal Levels

    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.

    Also check out:


    BNP stands for Brain Natriuretic Peptide – however, it is primarily released by the ventricles of the heart.

    This hormone impacts how the kidneys manage fluid and sodium. 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 quickly go down if ventricular pressures improve.

    BNP levels infographic | BNP heart failure exacerbation

    Regular BNP

    Baseline BNP levels – no matter which kind – are affected by genetic variation. However, people with Heart Failure will have baseline elevations along with increases during exacerbations.

    Baseline levels tend to increase in age and are higher in women over men, and lower 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? These symptoms include:

    • Dyspnea
    • Pulmonary crackles
    • Peripheral edema
    • JVD

    Never rely only 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 they are not in a heart failure 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 for 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.

    Check out some of my other articles:

    Cardiac Labs Pin

    Urinalysis (UA) Interpretation

    Urinalysis Interpretation

    Everything you need to analyze the UA

    A specific cup half filled with yellow urine

    William Kelly, MSN, FNP-C

    Author | Nurse Practitioner

    Last Updated: August 29, 2022

    Urinalysis or UA is a lab test frequently ordered in all types of medical settings: hospitals (ER, ICU, Inpatient floors), urgent cares, and outpatient offices. In many cases, the correct evaluation of the urinalysis is imperative to making an accurate diagnosis. To provide additional data, many labs perform urine microscopy, giving you exact details on the contents within the urine and quantifying the results. Read all about how to interpret the Urinalysis dipstick, as well as the urine microscopy in this article!

    Initial Urine Assessment

    Before you even run the urinalysis, you can tell quite a bit about the patient just by using your God-given senses.


    The color of the urine is the easiest way to determine someone’s hydration status. Surprisingly, it can indicate other aspects of health as well.


    Normal urine varies from very clear yellow to a darker amber color. Generally speaking, the less hydrated you are – the more concentrated your urine. The more hydrated you are, the more diluted the urine, leading to clear yellow urine.

    The first void of the morning is typically darker and more concentrated – this is normal. 

    Red or Pink

    When we see red urine – we typically think of blood. Medical conditions such as kidney stones (nephrolithiasis), UTIs, glomerular damage, or even malignancy. As little as 1mL of blood can cause a color-change, and the presence of red urine does not automatically mean large amounts of blood. There are a few different causes of red urine:

    • Bloody causes: Cystitis, kidney stones, malignancy, trauma, menstrual contamination
    • Non-bloody Conditions: Rhabdo (from myoglobin)
    • Foods: Beets, Blackberries, and Rhubarb
    • Meds: Propfolol, Chlorpromazine, Ex-Lax


    Causes or orange urine include:

    • Rifampin (Antibiotic for TB)
    • Pyridium or over-the-counter AZO

    Blue or Green

    Also very rare, blue or green urine may be caused by:

    • Conditions: Familial benign hypercalcemia, Pseudomonas infection
    • Medications: Propofol, Amitriptyline, Indomethacin,
    • Foods: Strong Food dyes


    Termed “Purple Urine Syndrome” Or “Purple Urine Bag Syndrome”, this is very rare but can occur due to:

    • Conditions: UTIs with certain gram-negative bacteria with alkaline urine
    • Meds: Amitriptyline, Methylene Blue dye
    • Foods: Diet high in Tryptophan


    Urine turbidity is how cloudy urine is. When we see cloudy urine, our first thought should be an infection which may be accurate. However, other causes of cloudy urine are cell casts or cellular debris from kidney damage.


    Stronger-smelling urine tends to mean dehydration, but foul-smelling urine usually indicates infection. This odor is caused by the bacteria that split urea to form ammonia. 

    Sweet-smelling urine may mean the patient is spilling glucose into the urine from hyperglycemia.

    Lastly, If the urine smells like feces, a fistula might have formed somewhere between the GI tract and the Urinary tract.


    Nah I’m just kidding – but did you know they used to taste urine to detect glucose in the urine?…. GROSS!

    Urinalysis dipstick

    Once you’ve assessed the urine with your own senses, it’s time to assess the actual urinalysis. This can be done in the following ways:

    1. Dipping a dipstick in urine and assessing the colors next to a test strip color chart (usually printed on the dipstick bottle).
    2. Sticking the dipstick in an Automated Urine Analyzer. This will give you. a printout of the results.
    3. Send the urine off to the lab, where they will perform a urinalysis and upload the results to your electronic medical record. They will often perform microscopy if indicated, which can be used to help interpret the urine.


    Test Levels

    When serum glucose spills into the urine – this is termed glucosuria. Typically, glucose in urine does not occur until the kidney glucose threshold is reached – which is around 180mg/dL. As you can tell, this can be useful for evaluating hyperglycemia in the setting of diabetes. However, periods of stress or fever have been known to cause small amounts of glucose within the urine as well, so glucose in urine does not automatically mean diabetes

    Clinical Significance

    • Glucosuria can indicate hyperglycemia in undiagnosed diabetics when blood work is not obtained.
    • Fever or stress could cause mild glucosuria in non-diabetics
    • SGLT2 inhibitors like Farxiga can increase glucose in urine even without elevated glucose levels

    Testing Considerations


    • Ascorbic Acid (vitamin C) has been known to cause false-negatives


      Test Levels

      Urinary bilirubin may be present in low amounts in the urine normally, but increased levels are due to abnormalities of bilirubin metabolism or liver function.

      Clinical Significance

      • The presence of bilirubin may indicate elevated LFTs, but overall does not seem to add significant information toward diagnosis.

      Testing Considerations

      • Must be sent immediately as bilirubin is unstable when exposed to light


        Test Levels

        Normal Levels: None ( 0.3 mg/dL or  0.05 mmol/L)

        Clinical Significance

        The presence of ketones in the urine (ketonuria) indicates ketosis. This is usually caused by uncontrolled diabetes or DKA. However, acute illness, stress on the body, strenuous exercise, nausea/vomiting, and keto or other low-carb diets can cause ketonuria to occur. 

        Testing Considerations

        • Parkinson’s medications (Levodopa) can cause a false positive

          Ascorbic Acid

          Test Levels

          Normally ascorbic acid is not seen in the urine dipstick.

          Clinical Significance

          Ascorbid acid is Vitamin C. The presence of this in the urine can lead to false negatives for both Heme, glucose, leukocyte esterase, and protein.

          Testing Considerations

          Some dipsticks do add a chemical to neutralize the effect of ascorbic acid on the other tests.

          Specific Gravity

          Clinical Significance

          The specific gravity indicates how dilute or concentrated the urine is. This can give the interpreter a pretty good idea of hydration status when looking at the urinalysis.

          Test Levels

          Normal Levels: 1.005 – 1.030

          Low (<1.005): May indicate diabetes insipidus, renal failure, pyelonephritis, glomerulonephritis, psychogenic polydipsia, or malignant hypertension

          High (>1.030): May indicate severe dehydration, hepatorenal syndrome, heart failure, renal artery stenosis, shock, or SIADH.

          Testing Considerations

          • Protein, ketones, and glucose, as well as recent IV contrast dye, can falsely elevate the specific gravity.
          • Medications like diuretics can also impact this (like lasix).


          Clinical Significance

          Heme detects blood in the urine.

          There are many potential causes of hematuria including UTIs, kidney/glomerular damage, trauma, kidney stones, malignancy, vaginal contamination, or coagulopathies.

          In a patient over 50 years old who has persistent hematuria, malignancy should be ruled out. 

            Test Levels

            Normal Levels: Negative

            The test for heme is very sensitive and can detect down to 1-2 RBCs per High-powered field (HPF). So a negative dipstick excludes blood.

            Testing Considerations

            False Negative: Unlikely, but Ascorbic acid can lead to this

            False-Positives: Myoglobin (as during rhabdomyolysis), semen (recent ejaculation), alkaline urine >9.0, contamination from hemorrhoids, vaginal blood, or oxidizing compounds used to clean the perineum can all cause false-positive heme to occur in the urinalysis.

            A positive Heme requires urine microscopy for confirmation.



            Clinical Significance

            The pH of urine stands for the potential of hydrogen. The more hydrogen ions there are, the more acidic something is.

            The pH scale runs of 0-14, with lower numbers being more acidic, and higher numbers being more basic.

            Because the kidneys regulate your acid/base balance, any change within the body should show up in your urine. However, various different disease processes can interfere with your kidney’s ability to do this effectively.

              Test Levels

              Normal Levels: 6, but can range from 4.6 – 8

              Acidic urine <7.0 is associated with metabolic or respiratory acidosis or an E Coli UTI.

              Basic urine >7.0 is associated with most types of kidney stones, urea-splitting bacteria (proteus or klebsiella), renal tubular acidosis, or potassium depletion.

              Testing Considerations

              Diet: Cranberries and high-protein diets can cause acidic urine, whereas citrus fruits and low-carb diets can cause alkaline urine

              Medications: Sodium bicarbonate and thiazide diuretics can cause more basic urine


              Clinical Significance

              The urine protein dipstick is specific for albumin, which is a type of protein. Any damage to the glomerular basement membrane will let albumin and other larger particles pass through the membrane and into the urine.

              Protein in urine is typically used to evaluate kidney damage in diabetics, people with Congestive Heart Failure (CHF), or other causes of kidney damage.

              Benign causes of high protein in urine include dehydration, emotional stress, fever, heat injury, inflammation, intense activity, acute illness, or an orthostatic disorder.

              All other causes of proteinuria involve the kidney – specifically the glomerulus or the renal tubules. Some common causes of glomerular proteinuria include Diabetic nephropathy, lupus nephritis, preeclampsia, various infections (HIV, hepatitis B, post-streptococcal glomerulonephritis), certain cancers, and certain drugs like Heroin, NSAIDs, and Lithium. Some causes of tubular proteinuria include interstitial cystitis, Sickle-cell, and nephrotoxicity from NSAIDs or antibiotics like aminoglycosides.

                Test Levels

                Normal Levels: Undetectable

                The urine normally has <150mg/day of protein and should be undetectable on a dipstick, but when this level exceeds 300mg/day, high protein in urine will show up on a dipstick.

                Testing Considerations

                Urinary concentration will impact the results, so correlate with the Specific Gravity. Very dilute urine can lead to underestimation of protein, and very concentrated urine can lead to overestimation.

                In general, the dipstick is a crude estimate, and evaluation by 24-hr urine specimen is the standard of care for ongoing proteinuria. If renal cause is found, a Nephrology consult is warranted.

                In the acute setting, the dipstick for protein isn’t too informative as acute illness, inflammation, stress, and dehydration are common presentations and can cause a temporary elevation in urinary protein. 


                Clinical Significance

                Urobilinogen is a byproduct of bilirubin production, but unlike bilirubin is colorless.

                Elevated levels can indicate malaria, hemolytic anemia, liver disease, or internal bleeding.

                An increased urobilinogen level is one of the earliest signs of liver disease and hemolytic disorders.

                  Test Levels

                  Normal Levels: 0.1–1 Ehrlich U/dL or 1 mg/dL

                  Testing Considerations



                  Clinical Significance

                  Nitrates are present in the urine at baseline. Some species of bacteria, specifically the Enterobacteriaceae species (E. coli, Klebsiella, Proteus, Enterobacter, Citrobacter, and Pseudomonas), release an enzyme called nitrate reductase which converts urinary nitrate to nitrite, causing nitrites in urine.

                  If negative, it really doesn’t mean much. If positive, then it is highly likely an infection is present.

                    Test Levels

                    Normal Levels: Negative

                    Testing Considerations

                    This reaction requires dwelling time within the bladder to occur. Urinary frequency or the presence of a Foley catheter can make this impossible. It can take up to 4 hours of dwelling before nitrites are detected.

                    A person might not intake a sufficient amount of nitrates in their diet.

                    False-Positives: Azo dye metabolites and bilirubin, as well as letting the urine sit for too long can produce false positives. Higher specific gravity reduces the sensitivity.

                    False-Negatives: Ascorbic acid can produce false-negative.

                    Leukocyte Esterase

                    Clinical Significance

                    Leukocyte esterase is a component of WBCs that is released when these white blood cells are lysed (split open).

                    The presence of leukocyte esterase supports the diagnosis of a Urinary Tract Infection (UTI). However, the presence can also indicate various autoimmune disorders, STDs, kidney stones, or intra-abdominal infections.

                    If there is no leukocyte esterase, infection is pretty much ruled out.

                      Test Levels

                      Normal Levels: Negative

                      Testing Considerations

                      False-Negatives: Proteinuria, glycosuria, excessively concentrated urine, or tetracycline.

                      False-Positives: Contamination with vaginal discharge, certain medications (ampicillin), salicylate toxicity, and strenuous exercise.

                      Urine Microscopy

                      Urine microscopy is when they look at the patient’s urine under a microscope and further characterize the presence of certain cells. 


                      Crystals, as the name implies, are crystallizations within the urine. Crystals in urine can be normal as long as they are composed of substances normally found within the urine.

                      Crystallization can occur for a variety of reasons, and the type and quantity of these will depend on the urine’s pH and underlying cause. 

                      Amorphous Crystals

                      Amorphous crystals form naturally when urine cools, and are more often found in acidic urine. This is usually just some precipitation of electrolyte salts, and there is no clinical significance.

                      Uric Acid Crystal

                      Uric acid crystals are generally associated with gout. They can also be caused by kidney stones, tumor lysis syndrome, or chemotherapy

                      Calcium Oxalate

                      Calcium Oxalate crystals are usually found in acidic urine and associated with kidney stones. Dehydration and/or increased oxalate intake can cause this. Ingestion of antifreeze can also cause these.

                      Calcium Carbonate

                      Calcium carbonate crystals may be caused by too calcium supplementation, and is also associated with kidney stones.

                      Calcium Phosphate

                      Calcium phosphate crystals are more likely to precipitate in alkaline urine. This could rarely be caused by hypoparathyroidism. 

                      Triple Phosphate

                      Triple phosphate crystals, also called Struvite crystals, are made up of magnesium ammonium phosphate. These are typically found in alkaline urine and associated with kidney stones as well as UTIs with bacteria that split urea, like Proteus mirabilis and Pseudomonas aeruginosa.

                      Hippuric Acid

                      Hippuric acid crystals are rare but can be found in normal or acidic urine.


                      Cystine crystals are found in acidic urine in patients with a genetic condition called cystinuria.


                      Bacteria are NOT normally found in the urine as it should be a sterile environment. If found, it usually indicates infection or contamination.

                      A bunch of E coli bacteria swimming around


                      Bacteria multiply rapidly if the urine specimen is left standing for too long at room temperature.

                      If there are leukocyte esterase +/- nitrites present with <15-20 epithelial cells/HPF, then infection is highly likely.

                      Consider starting empiric antibiotics if symptomatic and obtain a culture and sensitivity for confirmation.


                      A bunch of E coli bacteria swimming around

                      Red Blood Cells

                      Normally there are less than 2 RBCs/HPF.

                      Microscopic hematuria is defined as the presence of at least 3 RBCs/HPF.

                      Microscopic hematuria confirms a heme+ dipstick.

                      A bunch of E coli bacteria swimming around

                      White Blood Cells

                      Normally there are less than 2-5 WBCs/HPF within the urine.

                      If >5 WBCS, this indicates possible infection, inflammation, or contamination.

                      Most of the WBCs found in the case of infection are neutrophils.

                      A bunch of E coli bacteria swimming around

                      Epithelial Cells

                      Squamous epithelial cells are the skin cell of the external urethra.

                      >15-20 epithelial cells/HPF indicates contamination and another urine sample should be obtained to rule out infection.


                      Casts are tube-like protein structures made of various cells. Low urine pH, low urine flow rate, and high urinary salt concentration promote cast formation by favoring protein denaturation and precipitation. The presence of casts, other than hyaline casts, represents pathology within the kidney itself.


                      A bunch of E coli bacteria swimming around

                      Hyaline Casts

                      Hyaline casts can be present in normal healthy adults and are nonspecific.

                      They can be found after strenuous exercise or dehydration, as well as with diuretic use.

                      A bunch of E coli bacteria swimming around

                      RBC casts

                      RBC casts usually indicate glomerulonephritis or vasculitis.

                      A bunch of E coli bacteria swimming around

                      WBC casts

                      Uncommon, but when present is usually seen with tubulointerstitial nephritis and acute pyelonephritis but also seen with renal tuberculosis and vaginal infections.

                      A bunch of E coli bacteria swimming around

                      Muddy-Brown Casts

                      Muddy-Brown Granular casts are diagnostic of acute tubular necrosis, the leading cause of Acute Kidney Injury.

                      A bunch of E coli bacteria swimming around

                      Waxy Casts

                      Waxy casts are consistent with acute or chronic renal failure.

                      A bunch of E coli bacteria swimming around

                      Broad Casts

                      Broad casts are consistenet with advanced renal failure.

                      A bunch of E coli bacteria swimming around

                      Fatty Casts

                      Fatty casts indicate nephrotic syndrome.

                      A bunch of E coli bacteria swimming around

                      Renal Tubular Epithelial Casts

                      Renal tubular epithelial cells are seen in acute tubular necrosis, interstitial nephritis, and proliferative glomerulonephritis.

                      Urinalysis UA interpretation Infographic