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

The Ultimate ABGs

Blood gas guide you need to calm your nerves

William Kelly, MSN, FNP-C

Author | Nurse Practitioner

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.

Compensation

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%

ACID-BASE DISTURBANCES

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

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.

RESPIRATORY ALKALOSIS

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

Hyperventilation

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

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).  

    METABOLIC ALKALOSIS

    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.

    STEPS TO INTERPRET ABGs

    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.

    REFERENCES

    Emmett, M., & Szerlip, H. (2022). Approach to the adult with metabolic acidosis. In T. W. Post (Ed.), Uptodate. https://www.uptodate.com/contents/approach-to-the-adult-with-metabolic-acidosis

    Emmett, M., & Szerlip, H. (2022). Causes of metabolic alkalosis. In T. W. Post (Ed.), Uptodate. https://www.uptodate.com/contents/causes-of-metabolic-alkalosis

    Hopkins, E., Sanvictores, T., & Sharma, S. (2020, September 14). Physiology, Acid Base Balance. National Library of Medicine. https://www.ncbi.nlm.nih.gov/books/NBK507807/

    Sood, P., Paul, G., & Puri, S. (2010). Interpretation of arterial blood gas. Indian J Crit Care Med, 14(2), 57-64. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2936733/

    Theodore, A. C. (2022). Arterial blood gases. In Uptodate. https://www.uptodate.com/contents/arterial-blood-gases

    Pulmonary Embolism: Nurse’s Reference Guide

    Pulmonary embolism

     A NURSE’S REFERNCE GUIDE

    William Kelly, MSN, FNP-C

    Author | Nurse Practitioner

    A pulmonary embolism, frequently abbreviated as a PE, is a blood clot that lodges into the pulmonary vasculature of the lungs. Sometimes this can be asymptomatic, often there are mild-moderate symptoms, and other times patients can go into cardiac or respiratory arrest.

    No matter the symptoms, pulmonary embolisms can be deadly, and it is important for nurses to understand this disease and how to treat and monitor your patients with pulmonary embolisms.

    This article is part of a new series where we outline various medical conditions and the nursing assessment and management involved with each condition.

    What is a Pulmonary Embolism?

    A pulmonary embolism is a blood clot that lodges within the lungs. These are more commonly abbreviated to PEs. These can be very large or very small; only one, or many at the same time.

    The larger and more PEs that there are, the more dangerous this can be on the body. This can put significant strain on the heart, and can even cause cardiac arrest.

    Remember that a Thombus is one of the Hs and Ts to think about when a patient is coding!

    Pulmonary embolism‘s are highly associated with Deep Vein Thrombosis (DVT). You might hear the term VTE, which is an umbrella term for any blood clot within the body including DVTs and PEs.

    Pulmonary Embolism

    Causes of a PE

    There are many different causes that can cause a PE to develop, but it all goes back to Virchow’s Triad.

    Virchow’s Triad

    Virchow states that in order for blood clots to form within the body, there needs to be at least one of three things:

    Stasis of Blood

    Anything that causes blood to “sit still”

    Endothelial Injury

    Damage to the vascular system (arteries & veins)

    Hypercoagulable State

    Something that increases likelihood for clotting

    The more they have – the higher their risk of a blood clot from forming. However, a small percentage of patients won’t have any of these risk factors and still get a blood clot.

    Breaking down Virchow’s Triad, common risk factors for blood clot formation includes:

    Stasis of Blood

    • Immobility
    • Hospitalization
    • Varicose Veins
    • Atrial Fibrillation
    • Heart Failure
    • Elderly Age (>65)

    Endothelial Injury

    • Recent Surgery (especially orthopedic surgeries)
    • Trauma
    • Chemotherapies
    • Implanted devices
    • Central Lines
    • Inflammation
    • Sepsis

    Hypercoagulable State

    • Malignancy
    • Estrogen use (i.e. birth control)
    • Pregnancy
    • Inherited genetic predisposition (i.e. Factor V Leidin mutation)
    • Severe liver disease
    • Smoking
    • Obesity
    Pulmonary Embolism

    Nursing Assessment

    Patients with pulmonary embolisms usually present to the hospital or emergency department with shortness of breath.

    This is because an area of their lungs are not able to exchange gas normally. They are able to breathe in adequate oxygen, however they are unable to exchange that oxygen with carbon dioxide wherever the PE is, leading to a ventilation perfusion mismatch.

    Symptoms of a PE

    Common symptoms of a PE include:

    Dyspnea

    Also referred to as shortness of breath, and may be with exertion or at rest

    Chest Pain

    Usually pleuritic, aka worse with deep breaths or coughing

    Cough

    Usually not productive, but may have pinky frothy or bloody sputum

    Syncope

    Syncope with chest pain and SOB is suspicious for PE

    Signs of DVT

    • Extremity Erythema
    • Extremity Edema
    • Extremity Pain
    Many patients may be asymptomatic or have mild nonspecific symptoms as well, or they could go right into cardiac arrest, especially with very large PEs.

    Quick Note

    Hemoptysis is not nearly as common of a symptom in a PE as your nursing textbook may have led you to think!

    The Physical Exam

    Inspection

    • Respiratory Distress
      • Tachypnea
      • Increased work of breathing
      • Use of accessory muscles
    • Cough
    • Pallor
    • Diaphoresis

    Vital Signs

    • Temp: May have low grade temps
    • BP: Normal, increased, or decreased (severe)
    • Pulse/HR: Tachycardic
    • Respirations: Increased
    • SPO2: May be normal or low

    Auscultation

    • Lungs
      • Usually Normal
      • May be diminished
      • May have crackles if pulmonary infarct or acute CHF
      • Pleural friction rub
    • Heart
      • Tachycardia

    Quick Tip

    If a patient has CP/SOB and just recently had surgery or is pregnant, always think PE!

    The first thing you’ll usually notice is an increased rate of respirations, also called tachypnea. Patients with PEs are often in some visible respiratory distress.

    Patients with PEs often have pleuritic chest pain as well, so they’re unable to take full breaths without significant pain. This can increase the respiratory rate as they compensate by taking more frequent, shallow breaths.

    Patient’s pulse ox will often be normal unless there is significant respiratory distress. Patients may have a low-grade fever as well.

    Patience with PEs will often have tachycardia – which is a heart rate greater than 100 bpm.

    Blood pressure is often normal, but may be high secondary to pain. However very large PEs can put significant strain on the heart, causing significant hemodynamic compromise including hypotension and shock.

    When auscultating the lungs, a lot of times you aren’t really going to hear any specific bad breath sounds. You may hear some diminishment in the lung with the PE. Sometimes you may hear crackles and rarely wheezing.

    Nursing Interventions

    Cardiac Monitoring

    Place all patients with chest pain or SOB on a cardiac monitor to detect any arrhythmia that may occur and monitor heart rate.

    Patients with PEs will often have sinus tachycardia that does not completely improve with fluid administration.

    Patients with PEs can have all sorts of arrhythmias including:

    • Atrial fibrillation
    • bradycardia
    • RBBB
    • PVCs
    • VTACH/VFIB

    STAT EKG

    All patients presenting with chest pain and/or SOB should have an EKG obtained within 10 minutes of arrival.

    This is primarily to rule out any STEMI or ischemia. However, large PEs can cause significant righ theart strain.

    While they occur in < 10% of patients, signs of right heart strain on an EKG include:

    • Right heart strain pattern
    • S1Q3T3
    S1Q3T3 teaser

    Oxygen Support

    If the patient is significantly hypoxic or tachypneic, apply 2-4 L/min NC. If this is not enough to titrate SPO2 > 90%, apply a non-rebreather.

    In these cases, BIPAP or Intubation may be needed.

    IV Access

    Start a peripheral IV at least 18-20g in an AC line, as there is a high likelihood that these patients will be needing a CTA. These large bore IVs are needed to inject high-pressure dye.

    While drawing blood, make sure to draw a blue top as D-dimer may be ordered, as well as a PT/INR.

    Diagnosis of a PE

    To diagnose a PE, you will usually need advanced lung imaging, but lab work is part of the workup as well.

    Well's Criteria

    The Wells’ Criteria for PE is a clinical tool that is able to be used to determine the risk of a PE.

    This assigns points to each of the following:

    • Signs of DVT: 3 points
    • PE #1 likely dx: 3 points
    • HR > 100 bpm: 1.5 points
    • Immobiilization x 3 days: 1.5 points
    • Surgery within 4 weeks: 1.5 points
    • Previous PE/DVT dx: 1.5 pnts
    • Hemoptysis: 1 point
    • Malignancy w/ tx in last 6mo or palliative: 1 point

    Once you calculate their score, you can stratify their risk into one of the following:

    • Low risk: 0-1 point
    • Moderate: 2-6 points
    • High risk: >6 points

    Scores of 4 or less with a negative D-dimer can effectively rule out a PE.

    D-Dimer

    Blue Top blood work - DdimerOne way to minimize radiation is to obtain a D-Dimer in a patient with low to moderate suspicion of a PE.

    A D-dimer is a byproduct of fibrin which is increased in the blood whenever there is a blood clot.

    While this is a great test to see if there is a possibility of blood clots within the body, it is not very specific. This means that a negative D dimer (less than the threshold) is a pretty good way to tell if someone doesn’t have a blood clot. However, a positive D-dimer doesn’t necessarily mean there IS a blood clot in the body.

    Any bruise or minor injury can cause elevations in D-dimer, as well as pregnancy, heart disease, infections, and more.

    This means that if a D-dimer is above the threshold (around 230 but depends on your lab), then the Provider is pretty much forced to get a CTA to see if their truly is a PE.

    If a D-dimer is less than the threshold, then a PE can usually be ruled out. However, this is only the case is clinical suspicion is low to moderate.

    In patients who have a high liklihood of a PE, a D-dimer can miss a PE up to 15% of the time!

    Other Lab Work

    A troponin should be ordered in patients with chest pain and/or SOB. This can sometimes be mildly elevated in PEs, or significantly elevated if a PE causes a STEMI or NSTEMI.

    A BNP may be ordered if there are s/s of heart failure.

    Renal function should be checked before a CTA can be done, to make sure their kidneys can handle the dye. A GFR > 30 is usually adequate to obtain a CTA.

    Coagulation studies may be performed inpatient to see if there are any genetic mutations predisposing the patient to forming thrombi.

    ABGs

    An ABG may be obtained if the patient is in significant respiratory distress or has altered mental status.

    With a PE causing significant distress, you’ll typically see the following results on an ABG:

    • PaO2: Low (<80 mmHG)
    • PCO2: Low (<35 mmHG)
    • pH: Alkalotic (> 7.45)
    • HCO3: May be low (<22 mEq)

    CXR

    A chest x-ray (CXR) will almost always be ordered on patients who are suspected of having a PE, because these can rule out some other causes of chest pain and SOB such as a pneumothorax or pneumonia.

    However, a CXR is not going to pick up a pulmonary embolism. A CXR may show nonspecific signs including atelectasis or effusions, but often will be completely normal.

    In order to actually see the pulmonary embolism, a CT pulmonary angiography (CTPA or just CTA) is required.

    CTA

    Angiography is when a radiopaque dye is injected into the patient’s vein in order to get a good look at the patient’s vasculature during a CT scan. This can be timed to look at specific areas of the heart.

    CT Pulmonary Angiography is when this is done to look at the pulmonary arteries and veins. This means the radiologist can directly visualize pulmonary embolisms.

    If the patient’s GFR is <30, we generally avoid contrast dye. However, this may be completely facility dependent.

    If a patient cannot be given the dye (GFR < 30 or anaphylactic reaction), the alternative test is to obtain a V/Q Scan.

    Pulmonary Embolism

    V/Q Scan

    A VQ scan is a nuclear medicine test where they use radioisotopes in conjunction with X-rays to see if there are any ventilation/perfusion mismatches. Well this is not as definitive as a CTA, it does give probabilities of their being a PE, such as a “very low probability”.

    Quick Note

    The patients CXR really should be a clear study, otherwise the VQ scan will be poor quality. So if the patient has significant consolidation or pleural effusions, the VQ scan is unlikely to be very sensitive to finding a PE.

    Treatment of PE

    Treatment of a patient with a PE who is hemodynamically stable will generally consist of admission to the hospital, parenteral anticoagulation, and then transition onto an oral anticoagulant.

    Patients who have significant hemodynamic compromise may require reperfusion therapy.

    Parenteral Anticoagulation

    Treatment for pulmonary embolisms primarily involve anticoagulation.

    In the hospital setting this is usually IV unfractionated heparin. This Heparin is given as a Heparin drip, which is titratable depending on PTT levels. Each facility should have their own heparin drip protocol.

    In general, a bolus dose is given IV (can push fast), and then a slow drip is started. The PTT levels are usually checked every 6 hours but will depend on the protocol.

    SQ Lovenox is an alternative to IV heparin, and is given in a dose of 1mg/kg BID.

    But how does anticoagulants really help if the blood clot is already there? The role of the anticoagulants are to prevent further clots from forming, as well as to stabilize the clot from moving. This can be especially helpful if there is a DVT or an atrial thrombus within the heart. These can embolize and cause further PEs or even strokes.

    Quick Note

    I’ve found that usually IV heparin is ordered because this is more easily titrated and can be stopped quicker in case there is any bleeding or procedure that need done while inpatient.

    Oral Anticoagulation

    Sometimes the patient can be started directly on an oral anticoagulant and discharged home if they are otherwise stable, but this will depend on the Provider and the facility standards.

    Eliquis for PEOnce the patient is stable enough for discharge, they are started on long-term oral anticoagulation, such as Eliquis or coumadin.

    Patients with very recent surgery, hemorrhagic stroke, or active bleeding are not started on anticoagulation.

    Patients will often need to stay on the anticoagulation for at least 3 months, but sometimes longer. The blood clot should be reabsorbed by the body in about 6 weeks, but will depend on the size of the thrombus.

    Some patients will require life-time anticoagulation if they are found to have any genetic predispositions to blood clots. This is also true for patients with atrial fibrillation.

    IVC Filter

    IVC Filter for PEAn inferior vena cava filter, commonly referred to as an IVC filter, is a device that is sometimes placed to “catch” clots before they enter the right atria.

    This is usually placed in for patients who cannot be on anticoagulation, or those who have gotten repeat PEs despite anticoagulation therapy.

    They can be temporary and need removed eventually, but some that are placed are permanent.

    Thrombolytics

    In patients who are hemodynamically unstable from their PE, thrombolytic therapy can be given to dissolve the clot. This is like TPA in a stroke, but given for a PE.

    However, there are many contraindications to thrombolytic therapy, and there is a risk of bleeding.

    Procedural Removal

    An Embolectomy can be performed if needed and if the facility is capable of doing so, particularly when thrombolytic therapy is unsuccessful or cannot be used due to contraindications.

    There are additional procedures that can be done to retrieve / break up the clot including:

    • Ultrasound-assisted thrombolysis
    • Rheolytic embolectomy
    • Rotational embolectomy
    • Suction embolectomy
    • Thrombus fragmentation
    • Surgical embolectomy

    Many facilities will not have these capabilities, but most should have thrombolytics.

    Saddle PE

    A Saddle pulmonary embolus is a very large PE located at the bifurcation of the main pulmonary artery. These PEs are rare but likely to cause significant hemodynamic compromise and cardiopulmonary respiratory arrest!

    Patient monitoring

    Monitoring the patient will mainly consist of monitoring their vital signs and supporting them however you can.

    Oxygen Support

    Monitor their oxygen status by respirations and pulse oximetry. Stable patients may only need q4h vitals.

    oxygen delivery devices and flow rates - simple maskIf their oxygen is low or if there is significant respiratory distress, titrate up their oxygen levels.

    A BIPAP or Intubation may be needed in severe cases.

    Blood Pressure Support

    Monitor their blood pressure per department protocol.

    If hypertensive, treat with analgesics and antihypertensives.

    If hypotensive, treat with fluid boluses, paying careful attention to respiratory and cardiac status. 

    Vasopressors may be required in severe cases.

    Cardiac Monitoring

    These patients should have telemetry ordered. 

    Monitor their cardiac rhythm per department protocol, and notify any changes to the Provider.

    Bleeding / Falls

    These patients are usually placed on anticoagulation as above. Be sure to place the patient on fall precautions, and monitor for any bleeding.

    Titrate the heparin drip according to protocol, and a high PTT may require that you stop the heparin drip for some time.

    Clinical Deterioration

    If the patient begins to deteriorate, be sure to notify the physician or APP and/or call an RRT.

    Remember that PEs put strain on the heart, so patients can go into flash pulmonary edema. Those with pre-existing CAD may have heart attacks.

    Overall Pulmonary Embolisms are a serious medical condition that can be deadly, so it is important to know how to treat these patients at the bedside.

    Do you have any crazy PE stories? Let us know in the comments below!

    REFERENCES

    Haag, A., et al (2022). Pulmonary embolism. In R. I. Donaldson (Ed.), WikEM, The Global Emergency Medicine Wikihttps://wikem.org/wiki/Pulmonary_embolism

    Sharma, R. (2022). Pulmonary embolism | Radiology reference article. Radiopaedia.org. Retrieved February 8, 2022, from https://radiopaedia.org/articles/pulmonary-embolism

    Tapson, V. F., & Weinberg, A. S. (2022). Treatment, prognosis, and follow-up of acute pulmonary embolism in adults. In T. W. Post (Ed.), Uptodatehttps://www.uptodate.com/contents/treatment-prognosis-and-follow-up-of-acute-pulmonary-embolism-in-adults

    Thompson, B. T., Kabrhel, C., & Pena, C. (2022). Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism. In T. W. Post (Ed.), Uptodatehttps://www.uptodate.com/contents/clinical-presentation-evaluation-and-diagnosis-of-the-nonpregnant-adult-with-suspected-acute-pulmonary-embolism

    Thompson, B. T., & Kabrhel, C. (2022). Overview of acute pulmonary embolism in adults. In T. W. Post (Ed.), Uptodatehttps://www.uptodate.com/contents/overview-of-acute-pulmonary-embolism-in-adults

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    Blood Transfusion Reactions: A Comprehensive Nursing Guide

    Blood Transfusion Reactions: A Comprehensive Nursing Guide

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

    Author | Nurse Practitioner

    Blood transfusion reactions are common within the hospital setting because so many blood products are given. Transfusing blood products that are lacking or actively being lost (i.e. GI bleed) is literally life-saving treatment.

    In this article, we will talk about the different blood products, why they are given, and then dive into each type of blood transfusion reaction, what causes them, their signs and symptoms, and how to manage them as the nurse.

    Acute Hemolytic Transfusion Reaction

    What are blood products?

    There are multiple different blood products that are transfused within the hospital, and each one can have adverse reactions called blood transfusion reactions.

    Packed Red Blood Cells (PRBCs)

    Packed Red Blood Cells or PRBCs are given to patients when their hemoglobin levels are low. This is called anemia. Some common causes of anemia that may need a transfusion include:

    • Acute and chronic blood loss (i.e. GI Bleed)
    • Untreated ongoing Anemia (Iron-deficiency anemia)
    • Destruction of blood cells
    • Decreased production of red blood cells (i.e. Chemotherapy, aplastic anemia)

    PRBCs are usually ordered when hemoglobin levels drop below 7g/dL, but it depends on the nature of the patient’s anemia as well as their medical history and their hemodynamic stability (are their vital signs normal?)

    1 to 2 units will be ordered of PRBCs depending on how low the patient’s hemoglobin level is, as well as if there is active blood loss. Each unit of PRBCs should increase the hemoglobin by about 1g/dL.

    Before blood products are given, a type and screen is done to verify the patient’s blood type and screen for any antibodies that may require special blood. The exception is if the patient has significant ongoing hemorrhage and the patient needs emergent blood. In this case, O Negative blood is given as they are the universal donor.

    Each unit of blood will take about 2 hours to transfuse, but the maximum amount of time is 4 hours when the blood will expire. In emergencies, blood can be run as fast as needed, often with pressure bags.

    Fresh Frozen Plasma (FFP)

    Fresh Frozen Plasma or just Plasma is the portion of whole blood that doesn’t include the red blood cells, which contains clotting factors.

    Some reasons FFP may be ordered for your patient include:

    • Massive blood transfusions
    • Severe liver disease or DIC
    • Coumadin with bleeding or surgery (in addition to Vitamin KL when Kcentra not available)
    • Factor deficiency with bleeding or surgery

    In massive transfusions, you replace 1 unit of FFP for every unit of PRBCs replaced (along with 1 unit of platelets).

    Platelets

    Platelets are a blood product that help the body form blood clots and prevent bleeding.

    These can often become low from various autoimmune disorders, cancers and chemotherapies, medication reactions, and liver disease.

    Platelets are replaced when platelet levels are low, termed thrombocytopenia. Platelets are usually ordered for:

    • Active bleeding with platelet count <50,000/microL
    • Thrombocytopenia in need of invasive procedure or surgery
    • To prevent spontaneous bleeding, usually when platelet levels <10,000/microL

    Most platelets that are given are obtained by “apheresis”. One apheresis unit is equal to 4-6 “pooled random donor units”. 1 unit of platelets by apheresis should increase the platelets by about 30K.

    Why are Blood products Given?

    Blood products are given whenever the blood levels are too low, or when there is acute bleeding. While this will depend on each specific patient and clinician, blood products are generally given when:

    • PRBCs are given when hemoglobin is below 7 or there is ongoing blood loss with hemodynamic compromise
    • Platelets are given when active bleeding with levels <50K, or when <10K.
    • FFP is given with massive blood transfusions, severe liver disease or DIC, or as a coumadin reversal option.

    Blood Transfusion Reactions

    As with any medication or fluid, there are possible adverse reactions that can occur and that you need to monitor for.

    Because we are infusing blood products from a donor, this adds an increased risk of adverse reactions to occur.

    Because of this, nurses must monitor their patients very closely during blood product transfusions. The nurse must stay with the patient the first 15 minutes of a blood transfusion (may change depending on specific facility protocol), and frequently check vital signs.

    There are common blood reactions, and then there are more rare and severe reactions that can occur.

    Acute Hemolytic Transfusion Reaction

    An acute hemolytic transfusion reaction is a rare life-threatening blood transfusion reaction to receiving blood, specifically PRBCs.

    This happens when incompatible blood is accidentally infused with the patient. This is why the patient’s blood type is checked in the first place so that an appropriate donor can be given.

    Compatible blood is outlined below:

    Acute Hemolytic Transfusion Reaction

    When having a true acute hemolytic reaction, the patient will quickly experience:

    • Fever and/or chills
    • Severe flank pain or back pain
    • Signs of DIC (like oozing form IV site)
    • Hypotension
    • Urine turning red or brown (hemoglobinuria)

    This is a severe reaction as the patient’s own immune system and the donor’s immune system attack each other, destroying blood products and causing damage in the process. The patient may experience hemodynamic instability including life-threatening hypotension.

    If this reaction occurs, the nurse should:

    Acute Hemolytic Reaction: Nursing Steps

    If an acute hemolytic reaction is suspected, the nurse should:

    1. Stop the blood immediately and check vitals
    2. Hang NS through a patent IV line. Pt should be ordered least 100-200ml/hr to prevent oliguria/renal failure, or boluses if hypotensive
    3. Notify the MD/APP and blood bank, or call an RRT if unstable
    4. Recheck identifying tags and numbers on blood
    5. Administer diuresis as ordered in those at risk for volume overload
    6. Additional testing may include DIC testing and additional blood compatibility and screenings.
    7. Transfer the patient if required

    The Provider should guide treatment, but these are serious reactions and would likely need monitoring in the ICU.

    Your facility should have a specific protocol in the event of significant blood transfusion reactions, which often involves re-testing the patient as well as re-testing the blood unit itself.

    Acute Hemolytic Blood Transfusion Reaction

    Anaphylactic Transfusion Reaction

    An anaphylactic transfusion reaction is a severe allergic reaction to something within the blood product. These are rare, with an estimated 1 in 20-50K transfusions.

    This reaction occurs seconds to minutes after starting the transfusion.

    The recipient is severely allergic to something within the donor blood, which they may have antibodies against, specifically those who are IgA deficient or haptoglobin deficient.

    Signs of an anaphylatic reaction include:

    • Urticaria
    • Wheezing and/or Respiratory Distress
    • Angioedema (facial swelling)
    • Hypotension with/without Shock

    Treatment involves immediately stopping the transfusion, and then treatment with standard anaphylactic medications. These medications include:

    • Solumedrol 125mg IV STAT
    • Benadryl 50mg IV STAT
    • PEPCID 20mg IV STAT
    • IV Fluids

    More significant interventions may be needed, including:

    • Epinephrine .3mg IM STAT +/- IV epinephrine drip with severe bronchospasm or airway edema
    • Vasopressors for hypotension
    • Oxygen and Intubation

    The blood cannot be restarted, and additional testing will need to be performed, and blood from another donor will have to be given.

    Anaphylactic Blood Transfusion Reaction

    Urticarial Transfusion Reaction

    An urticarial transfusion reaction is a less severe allergic reaction to a component within the blood products, but much more common, occurring in 1-3% of blood transfusions. This is an antigen-antibody interaction, usually with donor serum proteins.

    Patients with this blood transfusion reaction will develop urticaria (hives) with no other allergic signs/symptoms such as wheezing, angioedema, or hypotension.

    When an urticarial transfusion reaction occurs:

    1. Immediately stop the transfusion
    2. Check Vital signs and ask the patient for other symptoms (like trouble breathing or facial/throat swelling, dizziness, chest pain, etc)
    3. Notify the Provider
    4. Give IV antihistmine as ordered
    5. Restart blood if hives resolve and no other signs of allergic reaction develop

    When an urticarial transfusion reaction is diagnosed, stop the blood for 15-30 minutes, give IV antihistamine like Benadryl, and then restart the infusion once hives resolve but slowly and cautiously. Check your specific facility’s protocol.

    Urticarial Blood Transfusion Reaction

    Febrile Non-Hemolytic Transfusion Reaction (FNHTR)

    A febrile non-hemolytic transfusion reaction is exactly what it sounds like – the patient develops a fever after/during a transfusion, but they are not experiencing other signs of a hemolytic reaction.

    This is usually due to a systemic response to cytokines which developed during the process of storing the blood.

    These are very common, occurring in .1-1% of all transfusions.

    This fever will occur 1-6 hours after the transfusion begins.

    Signs/symptoms include:

    • Fever (38-39*+ C)
    • Chills
    • Severe Rigors
    • Mild dyspnea

    If the temperature is more than 39°C or 102.2°F, consider a hemolytic transfusion reaction.

    Whenever there is a fever present, the main thing to consider is if this could be the first sign of a more serious transfusion reaction such as a hemolytic reaction, TRALI (see below), or Sepsis.

    If there is just a fever and no other significant reaction is suspected, antipyretics should be be given, usually Acetaminophen 650-975mg PO. The transfusion can usually be continued but monitored closely.

    Future transfusions should be “leukocyte reduced”, which is a process that removes most of the white blood cells within the blood.

    Febrile Non-Hemolytic Blood Transfusion reaction

    Transfusion-Associated Acute Lung Injury (TRALI)

    Transfusion-Associated Acute Lung Injury, known as TRALI, is a rare but one of the severe blood transfusion reactions that can occur after transfusion of a blood product.

    This is when the transfused product activates the recipient’s neutrophils, causing acute lung damage.

    Patients at risk for TRALI include patients with:

    • Liver transplants
    • Chronic ETOH abuse
    • Smokers
    • Volume overload
    • Shock

    The patient will experience sudden and severe respiratory failure during or shortly after a transfusion, but up to 6 hours after the transfusion. This is often associated with:

    • Hypoxia
    • Fever
    • Hypotension
    • Cyanosis

    New bilateral infiltrates on CXR are often seen.

    TRALI: Nursing Actions

    When TRALI is suspected, the nurse should:

    1. Stop the transfusion immediately
    2. Check vitals and ask patient their symptoms
    3. Call an Rapid Response if the patient is in respiratory distress and/or hypoxic/hypotensive (or notify Provider in ED/ICU).
    4. Support oxygen status (oxygen, intubation if needed)
    5. Support blood pressure (fluid boluses, vasopressors if needed)
    6. Notify the Blood Bank
    7. Obtain a Stat portable CXR
    8. Follow any additional orders / administer any additional medications

    Sometimes steroids are given, although evidence is not great.

    These patients may need to be intubated and will likely need to be transferred to the ICU and closely monitored.

    They do not seem to be at increased risk for TRALI to occur again with a different transfusion in the future, however, donors who are implicated are banned from donating ever again.

    TRALI

    Transfusion-Associated Sepsis

    Transfusion-Associated Sepsis is a life-threatening blood transfusion reaction that can occur with the administration of contaminated blood products which are infected with bacteria.

    The patient will start developing signs or symptoms within 5 hours after the infusion, but usually around 30 minutes.

    Signs/Symptoms of transfusion-associated sepsis includes:

    • Fever >39ºC or 102.2ºF, sometimes hypothermia
    • Rigors
    • Tachycardia >120bpm or >40bpm above baseline
    • Rise or fall of systolic BP 30mmHg
    • Abdominal pain or back pain
    • Nausea and vomiting

    Remember that Transfusion-associated Sepsis, Acute Transfusion Hemolytic Reaction, and TRALI can all have similar symptoms.

    SEPSIS: Nursing Actions

    If transfusion-associated sepsis is suspected, the nurse should:

    1. Stop the transfusion immediately
    2. Check vitals and quickly assess the patient
    3. Notify the Provider (Call an RRT if patient unstable)
    4. Support oxygen and hemodynamic status with oxygen, fluids, etc
    5. Obtain blood work from opposite arm (blood cultures, Coombs test, plastma-free hgb, and repeat crossmatch
    6. Administer ordered antibiotics ASAP (Usually Vanco/Zosyn)
    7. Notify the Blood Bank
    8. Follow any additional orders / administer any additional medications
    Transfusion Associated Sepsis

    Transfusion-Associated Circulatory Overload (TACO)

    Transfusion-Associated circulatory overload, also known as TACO, is when the patient develops acute volume overload after administration of blood products.

    This blood transfusion reaction is fairly common, occurring in up to 1% or more of transfusions. This can occur up to 12 hours after the transfusion is given, and risk factors include patients with:

    • CHF
    • End-Stage Renal Failure (i.e. on dialysis)
    • Extremes of age
    • Small stature & low body weight

    The more units transfused and the quicker transfused, the higher risk of TACO (just like with IV fluids).

    Patients will develop symptoms of respiratory distress which include:

    • Dyspnea
    • Tachypnea
    • Hypoxia
    • Orthopnea

    The patient will also usually develop hypertension.

    Remember TRALI can have similar symptoms, as well as a pulmonary embolism.

    TACO: Nursing Actions

    When TACO is suspected, the nurse should:

    1. Stop the transfusion immediately
    2. Check vitals and quickly assess the patient (pay attention to respiratory status and breath sounds)
    3. Notify the Provider (Call an RRT if patient unstable)
    4. Support oxygen status with supplementary oxygen, BIPAP, or intubation if needed
    5. Make sure a STAT portable CXR is ordered/performed
    6. Administer diuretics as ordered (i.e. 40mg IV Lasix)
    7. Follow any additional orders / administer any additional medications

    In milder cases, the patient may just require diuretics and supplemental oxygen. More severe cases may require Bipap or intubation.

      CLINICAL TIP

    It is a smart idea for the Provider to order 20mg IV Lasix in-between units when multiple units of blood are ordered in someone with a history of CHF or who is very old. If it is not ordered and you feel it may benefit the patient, offer this suggestion to the Provider as it can prevent TACO from occurring.

    “Hey this is Jan calling from Med-surg, I just wanted to make sure you didn’t want any Lasix in-between blood units for Mark Smith in 147-2, as they have a history of CHF?”

    TACO blood transfusion Reaction

    Primary Hypotensive Reactions

    Primary hypotensive reactions are very rare, but occur when there is a sudden drop in systolic blood pressure >30 mmHg within minutes of starting a transfusion.

    The blood pressure normalizes once the transfusion is stopped. While rare, other severe blood transfusion reactions can also have hypotension, so the patient will need to be evaluated to rule those out as well.

    Patients who take an ACE inhibitor like lisinopril are at increased risk for this to occur.

    This is also more common with platelet administration.

    And those are the acute blood transfusion reactions that can occur when administering blood in the hospital.

    Keep in mind that there can also be transmission of infections such as HIV and hepatitis, although very rare and will not present itself during the transfusion or shortly after.

    REFERENCES

    Kleinman, S., & Kor, D. (2022). Transfusion-related acute lung injury (TRALI). In UpToDate. UpToDate. Retrieved from https://www.uptodate.com/contents/transfusion-related-acute-lung-injury-trali

    Silvergleid, A. (2022). Approach to the patient with a suspected acute transfusion reaction. In UpToDate. UpToDate. Retrieved from https://www.uptodate.com/contents/approach-to-the-patient-with-a-suspected-acute-transfusion-reaction

    Silvergleid, A. (2022). Immunologic transfusion reactions. In UpToDate. UpToDate. Retrieved from https://www.uptodate.com/contents/immunologic-transfusion-reactions

    Silvergleid, A. (2022). Transfusion-associated circulatory overload (TACO). In UpToDate. UpToDate. Retrieved from https://www.uptodate.com/contents/transfusion-associated-circulatory-overload-taco

    Spelman, D., & MacLaren,G. (2022). Transfusion-transmitted bacterial infection. In UpToDate. UpToDate. Retrieved from https://www.uptodate.com/contents/transfusion-transmitted-bacterial-infection