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

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. 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

    STEMI & NSTEMI: A Nurse’s Comprehensive Guide

    A STEMI is an ST-Segment Elevation Myocardial Infarction – the worst type of heart attack. This type of heart attack shows up on the 12-lead EKG.

    An NSTEMI (or Non-STEMI) does not have any ST elevation on the ECG, but may have ST/T wave changes in contiguous leads.

    Patients with STEMI usually present with acute chest pain and need to be sent to the cath lab immediately for reperfusion therapy – usually in the form of a cardiac cath with angiography +/- stent(s).

    Ruling out a STEMI is the main reason 12-lead ECGs are obtained, and it is critical that you learn to identify them – even as nurses.

    While Physicians/APPs should be laying their eyes on ECGs relatively quickly, this isn’t always the case. The sooner a STEMI is identified, the better the chance for survival for the cardiac tissue as well as for your patient!


    The coronary arteries lie on the surface of the heart (the epicardium).

    These arteries deliver vital blood flow and oxygen to the myocardial tissue to keep the heart perfused and beating.

    The three main coronary arteries are the left anterior descending artery (LAD), the circumflex artery (Cx), and the right coronary artery (RCA).

    The Right Coronary Artery (RCA)

    The RCA travels down the right side of the heart in the groove between the right atrium and right ventricle. The RCA supplies blood to

    • Right atria
    • Right ventricle
    • Inferior and posterior surface of the left ventricle (85% of people)
    • SA node (60% of people)
    • AV bundle (85-90% of people)

    The Left Coronary Artery

    The Left coronary artery begins thicker and is called the left main coronary artery. This branches off into the LAD and the Cx.

    The Left Anterior Descending Artery

    The LAD lies on the surface of the heart between the right and left ventricles. It often extends to the inferior surface of the left ventricle in most patients. The LAD supplies blood to:

    • Anterior surface and part of the lateral surface of the left ventricle
    • The anterior 2/3 of the intraventricular septum

    The Circumflex Artery

    The Cx wraps around the left side of the heart in the groove between the left atrium and left ventricle in the back (the coronary sulcus). The Cx supplies blood to:

    • The left atrium
    • The other part of the lateral surface of the left ventricle
    • Rarely the inferior and/or posterior portions of the LV
    • SA node (40%)
    • AV bundle (10-15%)

    The Posterior Descending Artery

    The posterior descending artery usually branches off from the RCA, although less commonly from the Cx. Whichever one does form the posterior descending artery is considered the “dominant coronary artery”.


    Acute coronary syndrome (ACS) is an umbrella term referring to any condition which causes decreased blood flow to the heart – also known as ischemia. Prolonged ischemia can lead to infarction – which is cell death of the heart tissue.

    This cell death causes the release of troponin into the bloodstream, an enzyme that is not usually found in the systemic circulation.

    Cardiac ischemia is usually secondary to atherosclerosis which is a buildup of plaque within the coronary arteries. This is usually caused by unhealthy eating habits, obesity, sedentary lifestyle, hyperlipidemia, smoking, and genetics.

    This plaque can rupture, releasing contents into the bloodstream which causes a local inflammatory reaction as well as begins a coagulation cascade.

    This blood clot can completely occlude an artery – leading to infarction.

    A Non-ST segment elevation myocardial infarction (NSTEMI) refers to a complete occlusion of a coronary artery that does not cause ST-segment elevation on the ECG.

    While some heart tissue dies, this is usually less extensive than a STEMI. The infarction is usually limited to the inner layer of the myocardial wall.

    NSTEMIs will often have nonspecific changes on the EKG. These changes include T wave inversion or ST-segment depression with or without T wave inversion in anatomically contiguous leads. However, NSTEMIs could also present with a completely normal ECG.

    Troponin levels will be elevated indicating myocardial cell death. However, the ECG does not have ST-segment elevation.

    An ST-segment Elevation Myocardial Infarction (STEMI) refers to a complete occlusion of a coronary artery that causes more significant infarction that extends the entire thickness of the myocardium (termed transmural).

    A STEMI will have ST-segment elevation in at least 2 contiguous leads on the ECG.

    Where this elevation occurs will indicate which heart wall is infarcting, as well as within which coronary artery.

    You may also like: “Cardiac Lab Interpretation (Troponin, CK, CK-MB, and BNP)”


    The ST-segment is the segment on the ECG right after the QRS segment and before the T wave. This represents the initial phase of ventricular repolarization and should be at the isoelectric line.

    The TP-segment should be used as the isoelectric baseline, but you can use the PR segment if the TP is difficult to see.

    The J-point is the point on the ECG where the QRS complex meets the ST segment. This is important for recognizing ST segment elevation.


    ST-segment depression most commonly identifies cardiac ischemia, as well as reciprocal changes in an acute MI.

    It can also indicate heart strain, digitalis effect, hypokalemia, hypomagnesemia, or even be rate related. However, these changes are usually more diffuse as opposed to localized to at least 2 contiguous leads.

    ST-segment depression is defined as ≥0.5 mm depression (1/2 small box) below the isoelectric line 80 ms after the J-point (2 small boxes).

    Horizontal and Down-sloping ST-segment depression are more specific to cardiac ischemia, whereas up-sloping tends to be less serious although still could indicate ischemia.

    De Winter T waves can be seen in 2% of acute LAD occlusions without significant ST-segment elevation. Instead, there will be ST-segment depression at the J-point with upsloping and tall, symmetric T waves in the precordial leads (V1-V6).


    ST-segment elevation usually indicates myocardial infarction when appearing in at least 2 contiguous leads.

    Other possible causes of ST-segment elevation include coronary vasospasm, pericarditis, benign repolarization, left BBB, LV hypertrophy, ventricular aneurysm, Brugada syndrome, ventricular pacemaker, increased ICP, blunt chest trauma, and hypothermia.

    ST-segment elevation is defined as ≥1 mm elevation (1 small box) above the isoelectric line at the J-point. However, in leads V2 and V3, it needs to be > 1.5mm in women, > 2mm in men >40, and > 2.5mm in men < 40.

    Concave ST elevation is considered less ominous and sometimes can indicate benign variant called early repolarization, especially when diffuse.

    Convex upward ST elevation is almost always indicative of a large MI. This is termed “tombstoning”.


    Q waves are the initial positive deflection of the QRS complex indicating septal depolarization. These are normal in all leads except V1-V3.

    Pathologic Q waves are abnormal Q waves that indicate underlying pathology – usually a current or previous MI.

    Pathologic Q waves are defined as >40ms wide (1 small box) and >2 mm deep (2 small boxes).

    Any Q waves seen in V1-V3 are always pathologic.

    Pathologic Q wave

    Q waves can begin hours to days after an infarction begins, and can last for years, even forever.


    Recognizing ST-segment elevation or depression can be difficult in the case of a left bundle branch block (LBBB) or ventricular paced rhythm. This is because there is normally some associated ST-elevation and discordant T waves with these conduction abnormalities.

    To determine possible ischemia or infarction in a patient with these conduction abnormalities, one of the following should be present:

    • ST-segment Elevation > 1mm in a lead with a positive QRS complex (concordant ST elevation)
    • ST-segment depression >1mm in V1, V2, or V3

    These are not always present, but if they are – you should highly suspect ACS in a patient with a pre-existing LBBB morphology.

    This is why a new LBBB and acute chest pain or SOB is concerning for acute MI.

    You may also like: “How to Read a Rhythm Strip”


    STEMIs typically have a normal progression that will be seen on the ECG.

    Hyperacute T waves are first seen, which are tall, peaked, and symmetric in at least 2 contiguous leads. These usually last only minutes to an hour max.

    Then, ST-segment elevation occurs in at least 2 contiguous leads at the J-point, initially concave, and then becomes convex or rounded upwards.

    The ST-segment eventually merges with the T wave and the ST/T wave becomes indistinguishable. This is a “tombstone” pattern.

    Reciprocal ST depression may be seen in opposite leads.

    The ST segment then returns to baseline after a week or so.

    Q waves eventually develop within hours to days, followed by T wave inversion which could be temporary. Over time, the Q wave deepens.


    STEMIs are classified based on where they are located anatomically – so which leads are they are affecting on the ECG.

    Contiguous leads simply means leads that are pertaining to the same anatomical region of the heart.

    The following leads pertain to each region of the heart:

    • Anteroseptal: V1, V2
    • Anteroapical: V3, V4
    • Anterolateral: V5, V6
    • Lateral: I, aVL
    • Inferior: II, III, aVF

    The precordial and lateral leads are often affected together as the area of infarction is not always exact. 

    As an example, the EKG below is an inferior wall STEMI:

    Inferior wall MI with ST elevation in leads II, III, and aVF, with reciprocal changes in the lateral leads.


    STEMIs are true medical emergencies.

    The patient is at a high risk of significant conduction disturbances and arrhythmias including cardiac arrest.

    The longer you wait – the more heart cells will die, leading to worse cardiac outcomes as well as increasing the possibility of patient death.

    A 12-lead ECG should be obtained within 10 minutes of any patient with significant cardiac symptoms including chest pain or SOB.

    Women, older adults, and diabetics may have atypical presentations including a “silent” MI, where they don’t even have chest pain.

    There are many actions that need to be taken in a short amount of time, and many medications that will need to be administered before the cath team gets there.

    A code STEMI should be activated (or whatever your facility’s version of it is), so the interventional cardiologist and the cath team can be alerted ASAP.

    The patient should be hooked up to the monitor, vital signs obtained, IV access x 2 should be established (preferably an 18g), labs drawn and sent including troponin and PT/PTT, and the defibrillation pads should be applied.

    Any abnormal vital signs should be addressed, and any arrhythmias should be managed via ACLS guidelines.

    STEMI medications

    Oxygen should be administered to maintain O2 >90%.

    Aspirin 324mg should be chewed and swallowed. A rectal suppository of 300mg can be given if the patient cannot tolerate PO for some reason.

    Antiplatelet therapy with P2y12 receptor blockers such as Plavix or Brilinta should be given in addition to the aspirin.

    Nitroglycerin should be administered 0.4mg SL x 3 q5min if the patient has persistent chest discomfort, HTN, or signs of heart failure.

    However, do not give if they have used phosphodiesterase inhibitors like Viagra or Cialis within the last 24h.

    Don’t give Nitro if they have a low blood pressure, if they have severe aortic stenosis, or if there is a possibility of a right ventricular infarct (sometimes presents with inferior wall MIs). Nitro can cause severe hypotension in these patients.

    For persistent symptoms, an IV nitro drip can be used.

    Anticoagulants like an unfractionated heparin drip should be given. Other options include Lovenox.

    If the patient has signs of left heart failure, treat with nitro as above, loop diuretic like Lasix, +/- Bipap.

    Morphine 2-4mg slow IVP q5-15min can be given for persistent severe chest pain or anxiety. However, there is research indicating an increased risk of death when morphine is given in STEMI.

    It is possible that morphine may interfere with the antiplatelet effect of P2y 12 receptor blockers. So morphine should be avoided unless absolutely required for pain control.

    Atorvastatin 80mg PO should be given ASAP, preferably before PCI in those who are not already on a statin. If the patient on it already, their dose should be increased to 80mg.

    Primary percutaneous coronary intervention (PCI) is the preferred reperfusion method and should happen ASAP.

    This is when the interventional cardiologist will take the patient to the cardiac cath lab and perform angiography and stent placement to open up the occluded vessel.

    Fibrinolytics can alternatively be given, specifically if there is no access to a cath lab within a reasonable time frame (120 min), as long as symptoms < 12 hours and no contraindications (i.e. risk of bleeding).

    Beta-blockers are initiated within 24 hours, unless they are contraindicated such as with bradycardia, HF, or severe reactive airway disease. This can be started after PCI.

    You may also like: “Adverse Drug Reactions Nurses Need to Know”

    Non-ST Segment Elevation Myocardial Infarction (STEMI)

    As the name suggests, an NSTEMI does not have ST elevation seen on the ECG, but it is still a heart attack.

    An elevated and rising troponin level is associated with an NSTEMI.

    The ECG can be completely normal, or it can have nonspecific T wave changes or even ST depression in contiguous leads.

    Management of an NSTEMI is similar to a STEMI in terms of medications. However, they are not given fibrinolytic and are not emergently brought to the cath lab. They may or may not get a cardiac cath during their hospital stay.

    Instead, medication therapy is maximized like the ones described above. The patient is continued to be monitored, and troponin levels are trended usually every 6-8 hours.

    STEMIs and NSTEMIs are critical emergent events that nurses need to know well! You will be running into this at some point in your nursing career, and you want to know exactly what you’re doing when it happens! Being able to recognize a STEMI on the ECG is the first step!

    Want to learn more?

    If you want to learn more, I have a complete video course “ECG Rhythm Master”, made specifically for nurses which goes into so much more depth and detail.

    With this course you will be able to:

    • Identify all cardiac rhythms inside and out
    • Understand the pathophysiology of why and how arrhythmias occur
    • Learn how to manage arrhythmias like an expert nurse
    • Become proficient with emergency procedures like transcutaneous pacing, defibrillation, synchronized shock, and more!

    I also include some great free bonuses with the course, including:

    • ECG Rhythm Guide eBook (190 pages!)
    • Code Cart Med Guide (code cart medication guide)
    • Code STEMI (recognizing STEMI on an EKG)

    You can use the code “SPRING2021” for a limited time 15% discount, exclusive to my readers!

    Check out more about the course here!

    You may also like:

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    How to Read an EKG Rhythm Strip

    This post contains affiliate links, which means I get a commission if you decide to purchase through my links, at no cost to you. Please read affiliate disclosure for more information

    Learning how to read an EKG rhythm strip is an essential skill for nurses!

    This skill becomes especially handy for nurses on Med-Surg, Telemetry, the Emergency Department, or Critical Care units.

    If reading an EKG rhythm strip is new to you – this is the perfect place to start!

    How to read an EKG Rhythm Strip - FB Share

    What is a Rhythm Strip?

    An EKG or ECG stands for Electrocardiography, which is the electrical activity of the heart traced on paper (or a monitor).

    A rhythm strip is at least a 6-second tracing printed out on graph paper which shows activity from one or two leads.

    Leads are “views” of the heart. There are 12 leads that are traditionally obtained with a 12-lead EKG, but most portable and bedside monitors only monitor 3-5 leads at a time.

    Luckily – interpreting a single rhythm strip is much easier than a 12-lead EKG. Most rhythm strips are interpreted from Lead II as this gives a great view of the heart.

    The goal of reading an EKG rhythm strip is to determine the rate and rhythm of the patient. This is great for identifying baseline cardiac rhythm as well as any arrhythmias or ectopy that may occur (like a premature beat).

    A 12-lead EKG also looks at the rate and rhythm, but additionally gives nearly a complete 360° view of the heart.

    This means it can be used to assess for things like cardiac ischemia or infarction, conduction delays, and even enlarged chamber size.

    The ECG Rhythm Strip Tracing

    As I said earlier – an ECG Rhythm tracing is the electrical activity of the heart recorded on paper or a monitor.

    This is traditionally printed out on a 6-second strip. This can make it easy to determine the rate of an irregular rhythm if it is not given to you (count the complexes and multiply by 10).

    Thick black lines are printed every 3 seconds, so the distance between 3 black lines is equal to 6 seconds.

    As you can see, a printed ECG rhythm strip is comprised of boxes – both small boxes and large boxes. 5 small boxes make up one large box.

    Each small box is 1mm wide, signifying 0.04 seconds or 40 milliseconds (ms).

    Each large box is 5 small boxes, signifying 0.20 seconds or 200ms.

    This becomes important to remember when determining the rate of regular rhythms. The boxes and lines are also important in recognizing whether a rhythm is regular or irregular.

    The PQRST

    Okay so that covers the paper, but what about the actual tracings? That’s where the alphabet comes into play. By alphabet – I mean PQRST.

    An electrical tracing of the heart is made up of waves, lines, complexes, and intervals, and each of these represents specific conduction within the heart. This is the key to interpreting a rhythm strip.


    P waves represent atrial depolarization. This means that the electrical signal that starts in the SA node (the normal pacemaker of the heart) is traveling through both atria (top chambers of the heart) during the P wave.

    A P wave should look smooth and upright in most leads including lead II.

    The 3 things you’ll want to specifically look for in P waves in a rhythm strip are:

    • Are there P waves before each QRS complex?
    • Are there any P waves that do not have a QRS complex that follows?
    • Do all the P waves look the same / have the same shape?

    Keeping these 3 questions in mind will help you determine where the rhythm originates from (i.e. the sinus node), if there are any potential extra beats, or if there could be certain heart blocks present.

    An inverted P wave means there is anterograde conduction to the atria (backwards direction). This means the electrical impulse originates from near, at, or below the AV node. Examples of this include Junctional rhythm, certain PACs, and PJCs.


    The QRS complex represents ventricular depolarization. This means that the electrical signal is traveling through both ventricles (the bottom chambers of the heart). In a healthy heart – this should correlate with the pulse.

    The QRS complex is actually made up of 1-3 waves, the Q wave, the R wave, and the S wave. Depending on which lead you look at and the specific heart, any combination of these waves may be present.

    In lead II, usually all three waves are present. This includes an initial downward deflection (Q wave), an upward deflection (R wave), followed by a downward deflection (S wave).

    The presence of a QRS complex indicates that the ventricles are receiving the electrical signal. These should follow shortly after a P wave in a sinus rhythm.

    The main abnormality that can occur is a wide QRS complex. This either means that there is aberrant conduction (like a bundle branch block), or that the electrical signal starts in either the left or right ventricle (i.e. a PVC or Ventricular Tachycardia).

    A bundle branch block just means there is a delay in the conduction tissue transmitting the signal to either the right or left ventricle. If the widened QRS is preceded by a P wave, it is probably a sinus rhythm with a BBB.

    If there is no preceding P wave, you may have a PVC or even VTACH if it is sustained.


    The T wave represents ventricular repolarization. This means that the myocardial cells within the ventricles are recovering and “getting ready for the next beat”.

    This should be smooth and upright in most leads, including lead II.

    Sometimes, the T wave can be inverted or flipped. This is nonspecific but can indicate cardiac ischemia or infarction, especially if it is in at least 2 contiguous leads (pertaining to the same anatomical area of the heart).

    People may have flipped waves in certain leads at baseline after a heart attack, with a bundle branch block, or with a PVC, VTACH, or ventricular paced rhythms.

    Tall or tented T waves are those that are > 1 large box in lead II and may be particularly pointed. This could be normal for the patient, but can also indicate hyperkalemia (high potassium).


    The PR interval is from the beginning of the P wave to the beginning of the QRS complex. This represents the time it takes for the electrical signal to reach the ventricles from the SA node.

    This should be 3-5 small boxes or 120-200ms. If longer, this is considered a first degree AV block.

    A short PR interval could be from a a PAC, a junctional rhythm (associated with an inverted P wave), or Wolff-Parkinson-White syndrome.


    The QT interval is the time between the start of the QRS complex to the end of the T wave. This will change depending on the heart rate, so a QTc (QT corrected) is calculated.

    This should be 350-440ms in men, and 350-460ms in women. A QT interval >500ms predisposes the patient to deadly ventricular arrhythmias such as Torsades de Pointes.

    QT prolongation can be caused by ischemia, electrolyte abnormalities, or from medications such as psych medications, Zofran, Azithromycin, Cipro, etc.

    While you can calculate the QT interval from a single strip, a 12-lead EKG should be obtained and it will be listed on the EKG for you. Otherwise, there are online calculators which can be used to determine the corrected QT interval for the heart rate.

    Arrhythmias on the ECG Rhythm Strip

    An arrhythmia is any abnormal rhythm other than normal sinus rhythm – the baseline rhythm of the heart. This can be a benign variant (like sinus arrhythmia), or it could be deadly (like ventricular fibrillation).

    In order to know how to read an EKG rhythm strip, you need to first be able to understand what normal sinus rhythm (NSR) looks like.

    You should be comparing every rhythm strip to NSR. Recognizing where the rhythm differs from NSR will help you identify the rhythm.

    Normal Sinus Rhythm (NSR)

    Normal sinus rhythm is the gold standard. This is what a normal functioning heart beat should look like.

    The “sinus” in the name indicates that the electrical signal is coming from the Sinoatrial node (SA node), the “normal” pacemaker of the heart.

    The presence of sinus rhythm means the cardiac conduction system is functioning appropriately (although certain blocks may still be present).

    The rate of NSR is 60-100 bpm.  Slower is sinus bradycardia, and faster is sinus tachycardia. This just means that the heart is functioning at altered rates, possibly due to sleep, medications, infection, exercise, etc.

    All sinus rhythms should be regular, meaning each of the QRS complexes are mapping out.

    You can do this by measuring the R-R interval between any two beats, and then making sure the R-R interval stays constant throughout the strip. Some people use calipers, but I recommend a good old-fashioned alcohol pad or piece of paper and a pen.

    Additionally, a P wave should precede each QRS complex.

    The QRS complex should be narrow unless there is a bundle branch block present.

    The ECG Rhythm Strip Interpretation

    To read an EKG rhythm strip, you should do so in a systematic way, so that you don’t miss anything.

    1. Is the rhythm regular? Is every R-R interval equal?
    2. What’s the rate? This is usually printed for you
    3. P wave: Are there P waves before every QRS?
    4. PR interval: Is it wide >200ms?
    5. QRS: Is the QRS narrow or wide (>100-120ms)?
    6. T waves: Are the T waves upright and normal-appearing?

    Using this systematic approach should help you interpret what each rhythm is. But you need to be familiar with most of the arrhythmias out there.

    Systematic approach to reading a rhythm strip

    Other Sinus Rhythms

    Other sinus rhythms are rhythms that may still “normal”. I include paced rhythms in this section as this replaces NSR once a pacemaker is placed.

    Sinus Bradycardia (SB)

    Sinus bradycardia is the same as NSR, but the HR is <60bpm.

    This can be normal for well-conditioned individuals like athletes, can be normal if the patient is on a beta-blocker or similar medication, and can also be normal while sleeping.

    The most important thing when the patient has SB is

    1. Is it new or severe (<40bpm or so)
    2. Are they symptomatic? (dizziness, lightheadedness, syncope, SOB, chest pain, etc)

    Since this is often a normal variant – if the patient is asymptomatic there’s usually nothing that needs to be done.

    Make sure a slow HR is actually SB and not a heart block!

    Sinus Tachycardia (ST)

    Sinus tachycardia is the same as NSR, but the HR is >100bpm and usually <150bpm, at least while at rest.

    This can often be seen with exercise, but ST at rest often indicates anxiety, certain drugs, sepsis, dehydration, or volume loss. ST is usually a response to an underlying cause within the body.

    You never treat the ST, but rather treat the underlying issue (i.e. give fluids with volume depletion).

    Paced Rhythm

    Paced rhythms will look different depending on the location of the leads. If the lead is in the right atria, the rhythm will appear like NSR but with a pacer spike before the P wave.

    If the lead is in the right ventricle, it will look like a slow VTACH with a pacer spike before the QRS. There can also be both of these at the same time.

    Some monitors only show the pacer spike if you turn that function on – if you see a very slow VT – ask the patient if they have a pacemaker and adjust the monitors appropriately.

    Other Cardiac Arrhythmias

    Heart Blocks

    Heart blocks are when there is significant delay or blockage in transmitting the signal from the atria to the ventricles. This is usually associated with a junctional or ventricular escape rhythm.

    First degree AV block is generally “no big deal” and common in older age and with beta-blockers. The PR interval is consistently >200ms.

    Second degree type 1 AV block or Wenckebach, is when there is a progressive lengthening of the PR interval which eventually leads to a dropped QRS complex.

    Second degree type 2 AV block or Mobitz II is when there is a consistent PR interval but QRS complexes are randomly dropped.

    Third degree AV block or complete heart block is when there is complete dissociation of the atria and the ventricles.

    Atrial Fibrillation (AF)

    Atrial Fibrillation is a very common type of arrhythmia that you will definitely run into in the hospital. AF could be new-onset, RVR (rapid ventricular response), could be intermittent (paroxysmal), or chronic/persistent.

    AF is an irregularly irregular rhythm, meaning that there is no rhyme or reason for the regularity of each QRS complex.

    This is usually from a structurally diseased heart where both atria are quivering rapidly, termed fibrillation. This leads to fast ventricular rates (AF RVR), as well as poor blood flow through the atria – predisposing the patient to blood clots.

    This is why these patients are started on rate-control medications such as metoprolol or Cardizem, and usually anticoagulants like heparin, Eliquis, etc.

    AF will not have p waves but instead, have a fibrillatory baseline. The QRS complexes will usually be narrow, and will not map out with each other in any way.

    Rates >100bpm are considered AF RVR.

    Atrial Flutter

    Atrial Flutter (Aflutter) is similar to Atrial fibrillation and is treated largely the same.

    This is when the atria aren’t fibrillating but rather “fluttering”. This is usually from a reentrant loop near the AV node.

    This will usually lead to a conduction ratio of 2:1, and a HR around 150bpm. Conduction ratios can be 3:1 (100bpm), 4:1 (75bpm) and variable as well.

    You will see saw-tooth P waves termed “f waves”. Depending on the conduction ratio, you will see 2 (3 or 4) F waves per QRS complex. Aflutter is usually regular.

    Supraventricular Tachycardia (SVT)

    Supraventricular Tachycardia is an umbrella term referring to any fast tachycardia that originates above the ventricles. However, in clinical terms, this usually refers to AV Nodal Reentrant Tachycardia (AVNRT).

    This occurs when there is an abnormal pathway of conduction tissue near/within the AV node, termed a “reentrant loop”.

    If a PAC or PVC comes at the wrong time, this can send the electrical signal around and around this loop of conduction tissue, leading to very fast heart rates.

    SVT can be as “slow” as 140bpm to as fast as 220bpm. The faster the heart rate, the more symptomatic the patient usually is.

    In SVT, P waves are usually not present, there is usually ST depression, and the rhythm is regular with narrow QRS complexes.

    Treatment for this involves vagal maneuvers and often adenosine or Cardizem.

    Ventricular Tachycardia (VTACH or VT)

    Ventricular Tachycardia is a fast tachyarrhythmia originating within the ventricles. This leads to very fast heart rates with or without a perfusing rhythm.

    This means the patient may not have a pulse and may be a code blue. Either way, VT is a very serious arrhythmia.

    VT is usually caused by Coronary heart disease, like a previous or current MI.

    The rhythm is regular, and the rate is anywhere from 100-330bpm, and the QRS complex is wide (>140ms).

    P waves are usually absent or undetectable, but 60% of cases can have AV dissociation present.

    If there is no pulse, you use ACLS cardiac arrest algorithm.

    If there is a pulse, you utilize the ACLS Adult tachycardia with a pulse algorithm.

    Ventricular Fibrillation (VF or VFIB)

    Ventricular Fibrillation is a deadly ventricular arrhythmia. There will not be a pulse, and the patient will be coding.

    VF is a similar concept as AF, except the ventricles are the ones fibrillating. Coronary artery disease is again one of the main causes of VF. Severe electrolyte abnormalities can also cause VF.

    VF is irregular and has no pattern. There is either coarse or fine fibrillation, eventually degenerating into asystole if not shocked back into a normal rhythm.

    These patients need fast defibrillation, high-quality CPR, Epinephrine, antiarrhythmics, etc (Code blue algorithm).


    Asystole is the absence of cardiac activity. This is essentially a straight wavy line but may have occasional p waves initially. The patient is dead. Follow ACLS algorithms as above.

    Pulseless Electrical Activity (PEA)

    PEA appears like a normal rhythm (Usually NSR or SB), but there is no actual mechanical contraction (no pulse). The patient will be unresponsive, pulseless, and this is a code blue as well (follow ACLS).

    Want to learn more?

    Hopefully this gave you a good idea about how to read an EKG rhythm strip. Unfortunately, I couldn’t include every single arrhythmia or detail, but this definitely should give you a good understanding of the basics!

    If you want to learn more, I have a complete video course “ECG Rhythm Master”, made specifically for nurses which goes into so much more depth and detail.

    With this course you will be able to:

    • Identify all cardiac rhythms inside and out
    • Understand the pathophysiology of why and how arrhythmias occur
    • Learn how to manage arrhythmias like an expert nurse
    • Become proficient with emergency procedures like transcutaneous pacing, defibrillation, synchronized shock, and more!

    I also include some great free bonuses with the course, including:

    • ECG Rhythm Guide eBook (190 pages!)
    • Code Cart Med Guide (code cart medication guide)
    • Code STEMI (recognizing STEMI on an EKG)

    You can use the code “SPRING2021” for a limited time 15% discount, exclusive to my readers!

    Check out more about the course here!

    You may also like:

    Heart Blocks EKG Rhythm Infographic
    How to read an EKG Rhythm Strip - Pin Share

    How to Start an IV [Ultimate Beginner’s Guide]

    This post (how to start an IV) may contain affiliate links, which means I get a commission if you decide to purchase through my links, at no cost to you. Please read affiliate disclosure for more information

    Learning how to start an IV is a very important skill that every nurse needs to know. Inpatient and ER nurses deal with IVs every day – whether they are inserting them, removing them, or administering fluids or medications through them. If you are new to nursing, then you will need to learn how to insert an IV with confidence and knowledge!

    When to start an IV?

    The short answer to this is “when an IV is ordered”. However, it is important to critically think as a nurse, and anticipate what will need to be done. Especially as an ER nurse, you may see your patient before the Provider and can start placing an IV if indicated.

    If you work as an inpatient nurse, most patients should have at least an IV, midlines, PICC lines, or other central access. These IVs often go bad, and you will need to know how to start an IV in these settings as well.

    INDICATIONS to Start an IV:



    IV fluids or medications is the main reason an order will be placed to start an IV.



    CTs or MRIs often require an IV for IV contrast to help visualize the anatomy, vasculature, and any potential abnormality going on.



    Most facilities will require an IV be placed if the patient is being admitted. However, the patient can refuse this.

    When to NOT start an IV?

    Contraindications to starting an IV:

    There is no outright contraindication to placing an IV, but certain factors will exclude specific locations. These include extremities with:



    Dialysis patients may have AV fistulas or grafts. You should NOT start an IV in these limbs unless specifically allowed.



    Patients with a history of mastectomy or lymph node dissection should not have IVs placed on that side if possible. This can cause/worsen lymphedema.

    BLOOD CLOTS icon


    Patient’s with an Active DVT in their arm should not have IVs placed in the same arm – this can further cause irritation of the veins and worsen thrombi formation.



    Significant burns or edema should not have an IV placed if possible over the burnt or edematous area.

    INFECTION icon


    Do not place an IV overlying an infection like cellulitis. This can introduce bacteria into the blood and lead to sepsis.

    It may be best to avoid limbs with significant motor or sensory deficits, as there is unclear evidence that may suggest increased DVT in these extremities. If their arm is numb, they also may not feel when it is infiltrated.

    What IV Gauge should you use?

    The IV gauge will determine how big the actual needle and catheter are.

    The bigger the IV – the faster fluid can be administered. Unfortunately, bigger sizes are also more painful and usually more difficult to start an IV. Bigger IVs also come with an increased risk of phlebitis and can cause some serious irritation to the vein.


    These are typically used for babies and generally should be avoided in adults. They are very short, flimsy, and won’t last long.

    • Good for: Infants
    • Bad for: Most other scenarios


    This is used for many kids and adults, especially older adults with fragile “easily-blown” veins. These are usually OK for IV contrast dye as well, but not for CTA. These are also generally easier to place.

    • Good for: Peds, many Med-Surg adult patients, easily blown veins
    • OK for: IV contrast, blood return
    • Bad for: Massive trauma or fluid resuscitation needs, CT Angiography


    20g IVs are an ER nurse’s best friend when you have to start an IV. This is because a 20g IV is adequate for multiple fluid boluses, IV medication infusions, and most CTA requirements. They often give great blood return and labs can often be drawn without hemolysis.

    • Good for: Most adult patients, CT Angiography
    • OK for: Emergency situations (code blues, RRTs)
    • Bad for: Massive trauma or fluid resuscitation needs


    18g IVs are your standard “large bore” IV. These are great in critical situations as they provide for rapid administration of fluids or blood products, rapid infusion of critical medications. The down-side is they tend to be a little more difficult to place in the absence of large veins.

    • Good for: Critical or emergency situations, rapid fluid administration, CTA, severe sepsis, burns, acute MI, etc
    • Bad for: Small, fragile veins

    14-16G: THE MONSTERS

    The 16g and 14g IVs are very large, and unnecessary for most indications. However, in critical situations these may serve you well.

    Also Check out: “10 IV Insertion Tips for Nurses”

    Start an IV Clinical Note

    Some nurses may tell you to place the largest IV catheter that the vein can support. However, this is contrary to good nursing judgment. If you ask my friend Brian (@TheIVGuy), he will tell you that you should choose your size based on the appropriate ordered therapy and anticipated needs. This means that for most patients, a 20-22 gauge is likely the best and safest choice.

    What Equipment to Start an IV?

    Before learning how to start an IV, you need to first know which equipment you will need. This becomes like second nature, but when starting out as a new nurse, this is often important to memorize. For an IV insertion, you will need:

    IV INSERTION KIT icon when you start an iv


    These kits should include:

    • Chlorhexadine or alcohol swab
    • Tegaderm dressing
    • 2×2 gauze
    • Tourniquet
    • Tape

    IV CATHETER icon


    Your IV catheter of choice, usually 18-22g.

    VACUTAINER icon for start an IV


    A blood transfer device will be needed if you are planning on drawing blood directly you start an IV.



    You will need to place an IV cap or extension loop onto the IV after insertion.

    SALINE FLUSH icon after you start an IV to flush the line with


    Make sure you have one or two flushes on hand.

    Once you have your equipment, you are ready to know how to start an IV.

    How to Start an IV

    1. PREPARE THE PATIENT to Start an IV

      To start an IV, you will first want to wash your hands (always the right starting point). You will also want to use universal precautions, so put on a pair of clean gloves as you will be possibly interacting with the patient’s blood.

      You should already have an idea of where you are going to place the IV and which size IV catheter you are going to use.

      IVPlace the tourniquet on the patient’s arm proximal to the area of cannulation. Look for straight, large veins. Palpate them as veins may not always be visible but can still be felt. Strong veins will have a good amount of bounce to them.

      Once you are happy with your vein selection, you can start prepping your area. Use a chlorhexidine (CHG) or alcohol swab to gently clean the surrounding area for 30 seconds, and allow it to completely dry. Start with the center and move outward in a circular fashion with alcohol, while CHG requires a back and forth scrubbing action.

      With deeper non-visible veins, some nurses will also apply alcohol to a finger of their non-dominant hand to help palpate during the procedure without “contaminating” the site. Please note that this is not the best practice for infection control. You should never tear off the finger of your glove either, instead – learn to palpate with your gloves on.


      While your site is drying, open your 10cc flush and your extension loop and/or cap.

      If you are drawing blood, hook up the blood transfer device to the dry extension loop or cap. Otherwise, you can connect the flush and prime the loop or cap. Set this aside back into your kit to keep it clean.

      Open up your IV, take off the needle cap, and twist the end of the catheter to make sure it is loose and ready for cannulation.

    3. HOLD SKIN TAUT when you start an IV

      Hold the patient’s skin taut with your non-dominant hand to secure the vein underneath, stabilizing it from rolling, and smoothing the skin for insertion.


      Place the tip of the needle against the skin at a 10-30 degree angle when you start an IV. The deeper the vein, the more angular your approach will need to be.


      With the bevel up, puncture the skin and advance through to the vein.

      If done correctly, you should see a flashback of blood in the flash chamber and/or catheter. This location will depend on the brand and size of the specific IV catheter. Once a flashback is seen, lower the angle even more parallel with the skin, and advance the whole unit about 2-6mm.

    Clinical Note

    If you initially don’t see flash of blood, pull the needle and catheter both out almost completely (but do not leave the epidermis). Re-palpate the vein, adjust your angle and advance again. This is termed “digging” and some patients will not tolerate this well. However, oftentimes it may only take 2 or 3 “digs” until success.


      Now advance only the catheter forward, sliding it off of the needle and cannulating the vein. If done correctly, the catheter should easily slip into the vein without resistance. If there is dimpling of the skin, the IV is likely within the extravascular space.
      advancing catheter when you start an IV


      Before pressing the activation button to retract the needle – take off the tourniquet and apply digital pressure beyond the catheter tip.

      Some brands will have a septum or shield function with gauges 20-24, which prevents the backflow of blood and negates the need for venous compression.

      Press your activation button to retract the needle.

    3. DRAW BLOOD After you Start an IV

      If ordered, now is the point where you will draw your blood. Hook up your loop/cap with the blood transfer device to the IV hub.

      Draw your blood tubes, and flush with a 10cc pulse flush afterward.If blood is ordered, you can immediately draw this after placing a new IV. If you are not drawing blood, skip this step and instead just connect the primed cap or extension loop to the IV and flush.

      After flushing a few mLs, make sure you can pull back blood return. This is reassurance that the IV is in the correct place after you start an IV. Then pulse flush the remaining amount through.


      Secure the IV with a securement device or tape, and a dressing like Tegaderm. Make sure the insertion site is covered. If you used an extension loop, secure the loop with tape as this can easily get caught on something and pull out the IV.

      If the patient is confused or may try pulling the IV out, wrap the IV with Coban, only leaving the cap accessible.

      Administer any medications or fluids through the IV as ordered. and Viola – you can check “Start an IV” off your task list!

    How to REMOVE an IV

    Knowing how to start an IV is important, but you also need to know how to remove an IV! If the patient is discharged or if there is a compilation with the IV, it will need to be removed. Removing the IV is easier, and can be performed by a nurse or a patient care assistant.


    1. Collect 2×2 gauze and tape or bandaid
    2. Wash your hands and don clean gloves
    3. While holding the catheter in place, start peeling off the Tegaderm and/or tape. Use an alcohol pad if very sticky and painful.
    4. Once the dressing is no longer secured to the skin, place a 2×2 gauze over the insertion site, and pull out the IV in a smooth fashion.
    5. Hold pressure for 1-2 minutes until bleeding as stopped
    6. Dress with gauze and tape or bandaid


    If you want to learn more about cardiac arrhythmias, I have a complete video course “ECG Rhythm Master”, made specifically for nurses which goes into so much more depth and detail.

    With this course you will be able to:

    • Identify all cardiac rhythms inside and out
    • Understand the pathophysiology of why and how arrhythmias occur
    • Learn how to manage arrhythmias like an expert nurse
    • Become proficient with emergency procedures like transcutaneous pacing, defibrillation, synchronized shock, and more!

    I also include some great free bonuses with the course, including:

    • ECG Rhythm Guide eBook (190 pages!)
    • Code Cart Med Guide (code cart medication guide)
    • Code STEMI (recognizing STEMI on an EKG)

    Check out the course!

    10 ER Nursing Hacks You Need to Know

    ER nursing hacks can be just what you need to make your shift go from terrible to not-as-terrible. As nurses, we aren’t afraid to get our hands dirty. We take charge, do what needs to be done, and then find a way to laugh about it in the end.

    Working in the Emergency Department can be especially draining – physically, mentally, and emotionally. However, just because nursing is HARD doesn’t mean we can’t utilize tips and tricks to make that 12-hour shift a little bit more bearable. Use these “10 Nursing Hacks Every ER Nurse Should Know” to save time, save your senses, and save your sanity!

    Please keep in mind the following hacks are anecdotally based. You must use these within your own judgment and within your facility’s protocols. You can read more about this on my disclaimer page.

    ER Nursing Hacks: Featured 2

    1 ER Nursing Hacks: Double-Glovin’ in the Oven

    As you know, personal protection equipment including clean gloves and gowns are absolutely necessary in a hospital environment. For some procedures, clean gloves are “good enough”. However, for high-risk infection procedures, sterile gloves are necessary.

    Foley catheter insertion is one of those procedures, as catheter-associated infections are very common. While putting in a Foley catheter can become like second-nature rather quickly, there can be some difficulties with the sterile procedure.

    ER Nursing Hacks 1: Double Glove

    For one – those cheap sterile gloves that come with the foley kit are typically a size 5.0. So unless you have baby-hands, I’d recommend grabbing an appropriately sized package of latex-free rubber gloves. You might want to go a half-size above your normal for this method.

    After grabbing your foley kit and sterile gloves, position the patient, and then wash your hands (duh). Afterward, put on a pair of clean gloves FIRST, then proceed to open your kit and apply your sterile gloves, and continue the insertion per normal.

    Using this nursing hack, once you insert the foley and blow up the balloon, you can take off your previously sterile gloves which are now likely dripping with Betadine and other fluids. Luckily – you still have a pair of gloves underneath to secure the cath-secure, position the foley bag, and clean up your pile of trash! Once that’s done, slip off the gloves, wash your hands, and you’re done! Easy-peasy-Kegel-Squeezy.

    2 Burp that Bolus

    This concept is a little more confusing, but it can save time! In the ER, we hang A LOT of boluses and every ER nurse knows that pumps are harder to find than a rectal thermometer. So naturally, ER nurses are resourceful and use gravity. Patients often require multiple boluses, and Lord knows you are almost always sometimes just too busy to switch out bags before the bag runs out and half of the tubing is now air.

    In this predicament, you could flush out the rest of the line in a trash can, then unspike and re-spike your new bag, and THEN re-prime the line. Or you could get a whole new tubing set and just throw out the old bag/tubing. As you can see – this wastes either valuable time or equipment/money!

    But what if I told you there was an ER nursing hack to solve this? When you go to prime the original bolus, clamp your tubing and spike your bag. Do NOT squeeze fluid into the drip chamber yet. Now, turn the bag upside down. Unclamp the tubing, and “burp” out the excess air at the top of the upside-down bag.

    ER Nursing Hacks 2: Bolus Burp

    Once the air is gone and some fluid is forced into the drip chamber, turn the bag right-side-up. Now prime the tubing as normal and hook the patient up. You’ve essentially created a vacuum so that the fluid will stop flowing before it empties the drip chamber – ready for your second bolus when you are. 

    3 Juice cup? Change it up!

    ER Nursing Hacks 3: Juice cup

    Unless you work at an adult-only ER, you are likely seeing patients that span the clinical spectrum – this includes pediatric patients. One thing about pediatric patients is that they HATE taking their medications.

    One particularly difficult medication to give a child PO is Dexamethasone oral solution. Unfortunately, it’s usually made with a good portion of alcohol content, and it smells and tastes like…vodka?

    After forcing it down, kids often vomit it up – all your hard work for nothing. One ER nursing hack to avoid having to give an IM shot is swapping oral Dexamethasone for the IV solution.

    IV medications cannot always be used orally, but sometimes they can! IV Dexamethasone has successfully been administered mixed with cherry-syrup, juice, or followed by a popsicle – and children take the medicine MUCH easier! Don’t forget though, you must run this by the provider before trying it, as studies are somewhat mixed on the efficacy (pharmacokinetic info here).

    4 Septic Sock

    Now I KNOW you have smelt some SMELLS in the ER (or anywhere in the hospital for that matter). There is nothing stronger than a nurse’s nose. C-diff, fungi, and bodily secretions aside – sometimes the worst smell comes from down under (the feet – ya nasty).

    Unfortunately, working 12-hour shifts where you are constantly on your feet and running around, you might find yourself with some STANKY feet. The good news is, even if you don’t have stinky feet, this ER nursing hack can help you deal with a patient’s particularly putrid piggy-toes. But first, a quick science lesson.

    While sweat is the main cause of foot odor, sweat doesn’t actually smell. Instead, it creates a perfect medium for bacteria. These bacteria include Brevibacteria and S. epidermidis (known for their cheese-like smell), as well as propionibacteria (known for its vinegar-like smell).

    Regardless of which bacteria are causing the odor, they are all highly acidic. So here’s the hack: If you or one of your patients has particularly powerful foot odor – use an antacid! Lather Maalox or Mylanta on the feet, put surgical booties over top, and you won’t believe how fast it can help! Another option is to scrub the feet with Hibiclens or betadine for antibacterial action. Better yet – do both!

    Fair warning though, if there is any fungi growing – these methods might not work as well. To prevent foot odor, it’s recommended to wear breathable shoes, breathable socks (cotton or wool), and wash and exfoliate your feet frequently. A little dab of foot-powder in your shoes every few days never hurt anyone either (Gold Bond anyone? #NotSponsored)

    Related Article: Six Steps for Sepsis Management

    5 Thinking Outside the Vial

    Every nurse knows that lidocaine is extremely helpful as a topical anesthetic for suturing , regional blocks, and even intra-articular injections to numb pain. However, lidocaine is not limited to only these uses. While not quite a “nursing hack”, these alternative uses of lidocaine are important to know so you can offer suggestions to the attending when indicated.


    OK, you probably knew this one – viscous lidocaine is often mixed with an antacid and sometimes an antispasmodic to create a “GI cocktail” to help with the pain of gastric or esophageal etiology. This is always a good suggestion for those young chest pain when GI etiology is suspected.

    NG Tube Insertion

    They have done research to see if lidocaine gel, nebulized lidocaine, and anesthetic spray have been useful for NG tube insertion. Not too surprisingly, patients who get lidocaine gel or spray administered intranasally/orally had significantly less pain with insertion – but can have a more difficult NG experience. Additionally, nebulized lidocaine has proven to decrease pain and increase comfort during NG tube insertions, but can increase the chances of nosebleeds.


    Sometimes with persistent laryngospasm, nebulized lidocaine can be used effectively to help with a cough. However, there isn’t a significant amount of research on this, so you likely won’t see it ordered often and will depend on the Provider.

    Oral Pain

    Those experiencing pain in their mouth from a painful lesion such as an aphthous or herpetic ulcers can benefit from viscous lidocaine “swished” and either swallowed or spit afterward.

    Foley Insertion (males)

    This is also more common, but the provider may order 5-10ml viscous lidocaine to inject into the urethra before a difficult-anticipated foley insertion in males. Luckily, this usually comes pre-packaged in a syringe called a Uro-Jet. This should be injected directly into the urethra a few minutes before attempting the foley insertion. This can help reduce pain and be especially helpful in patients with a small meatus, anatomical abnormalities, or prostate enlargement.

    Renal Colic ER

    While meds like morphine and Dilaudid are used frequently in the ER and hospital, sometimes there are effective alternatives to opioids that actually work really well. Slow infusion of low-dose IV lidocaine can be used effectively for kidney pain. It’s recommended for use if NSAIDs and Opioids are contraindicated or risky. One study even indicates that IV lidocaine at appropriate doses safely lowered the patient’s pain more than morphine.

    Related Article: Opioid Alternative Analgesics in the ER

    6 Alcohol Swab Nursing Hacks

    There are a few things we nurses usually load up our pockets with. Usually, these consist of tape, band-aids, paper, pens, and alcohol pads. But did you know how versatile alcohol pads can truly be?

    Blood Cleanup

    This is more of a no-brainer, but when you accidentally make a mess with blood while putting in an IV, patients appreciate it if you help clean up your mess. Busting out an alcohol swab can easily clean up dried blood on their skin. If alcohol doesn’t do the trick, sometimes using KY jelly lube works even better. Alternatively, you could use hydrogen peroxide.

    Nausea Nursing Hack

    Did you know that a few whiffs of alcohol pad can relieve nausea almost immediately? Sure – Zofran is still our bread and butter, but this nursing hack works pretty quickly!

    When your patient is nauseous, break open an alcohol swab and place it right under their nose. Tell them to take 3-4 deep slow breaths. Before you know it – they should start feeling somewhat better. In fact, clinical research suggests that alcohol may even be more effective than oral zofran, or at least a useful adjuct.

    Scientists don’t exactly know why this works. Some think it’s purely due to “olfactory distraction” – distraction while following the instructions, taking deep breaths, and relaxing the body.

    Pseudoseizure Nursing Hack

    In the ER, the nurses frequently experience patients who have not-so-believable “seizures”. These “fake” seizures are termed pseudoseizures, and the patient might not even know that they are “faking”. Typically when this happens, we bust out an ammonia salt and place it underneath the patient’s nose. This tends to stop their “seizures” pretty much immediately. But what do you do if you don’t have an ammonia inhalant on hand?

    Not every ER utilizes ammonia salts, and sometimes they can be hard to find. If you experience a patient with what you believe to be a pseudoseizure, try opening an alcohol pad and placing it directly beneath their nose. This may distract them and bring them out of their “seizure”. Please note this is anecdotal and is not in the literature. 

    Save your Senses (ER Nursing Hack)

    Clostridium Difficile (C-Diff) is a common diarrheal infection which can make people pretty sick. We often see these patients in the ER and hospitals. Unfortunately, C-diff is very contagious and tends to run rampant in nursing homes and hospitals. As we all know, C-Diff has a pretty distinct and powerful smell which can be hard to erase from our noses!

    Before going into a C-diff patient’s room, add a mask to your PPE. Break open an alcohol swab and place it inside the mask. This way, the isopropyl alcohol overpowers the C-diff smell and you save your senses – or at least make it more tolerable.

    If alcohol swabs are too strong for you, you can try rubbing toothpaste or Vix rub inside a double-layered mask. This nursing hack works well for C-diff, but also for other smelly situations including I&Ds, rotting flesh, nasty wounds, and fungal infections.

    7 IV Stick Trick

    Putting in IVs is super common in hospitals, especially within the emergency department. If one thing is sure – patients hate getting stuck! Some tense up, others look away, and then there’s those who shake, cry, and even syncopize. Ironically, the latter is usually buffed up guys with tattoos all over their bodies! People don’t like needle sticks because the needles hurt. But what if I were to tell you that there’s a way you can decrease pain, without any medication or extra equipment?

    This ER nursing hack will help your IV insertions go more smoothly! After you clean the IV site, place the needle flush with the skin right where you are going to poke. Press the needle into the cleansed skin with the bevel up for 3-5 seconds before you puncture the skin. The longer you wait – the more desensitized their pain receptors will become – this should decrease the pain felt.

    ER Nursing Hack: IV desensitization

    With less perceived pain, the patient may tell you “is that it?!” or “I could barely feel it!”. It also takes away the “shock” factor, making the patient less likely to jump! For most patients, this technique will be effective, however, some patients still will have a high amount of perceived pain, especially if you dig.

    Related Article:

    8 BP not Enough? Use the Bedside Cuff

    Vital signs are an important aspect of nursing care and patient monitoring. Blood pressures have a tendency in the ER to be very high or very low. When very low, we give large amounts of fluids as fast as we can. While pressure-bags are a great option and ensure fast infusion, they are not always available.

    Many ER rooms have bedside manual blood pressure sphygmomanometers. In place of a pressure-bag, use the blood pressure cuff around the middle to top of the bolus and pump it up until it flows nicely. Like the pressure bag – you will have to occasionally pump in more air as the bag empties.

    Related Articles: “5 Vital Sign Errors to Avoid”

    9 Neb-wick Air Freshener

    After a particularly smelly patient leaves, sometimes the aroma sticks around in the air. Unfortunately, Lysol sprays don’t always cut it. Now I personally am not a huge believer in the essential oil craze, but this nursing hack requires someone on staff to have essential oils or strong smelling lotion.

    Take a used nebulizer adapter and squirt some water or saline in the medication chamber. Next, add a few drops of an essential oil of your choice. Turn the oxygen on high and viola. This nursing hack will have the room smelling Glade-scented fresh in no time. Talk about Oxy-Clean!

    ER Nursing Hacks 9: Neb-wick

    10 The Dependable Bedpan Nursing Hack

    Many patients cannot or should not ambulate while they are in the ED. This is fine until they have to use the bathroom. Bedpans can be successfully used for both #1 and #2, but unfortunately, they have a tendency to cause messes. Whether you are using a fracture pan or a regular bedpan, line the pan with an adult diaper or absorbable pad. Secure it with tape or rubber bands. You can also use a large pull-up inverted inside-out and secure it over the bedpan. Place the bedpan underneath the patient as normal.

    This way, any urine or liquid stools are absorbed in the material and do not splash, spill, or cause messes. It also allows for easy cleanup! If you need to collect a urine or liquid stool sample – this method should not be used.

    Related Articles: “Comprehensive Urinalysis Interpretation”

    Hopefully, you found these 10 ER nursing hacks to be useful. Implementing them in our everyday shifts should help save our senses and our sanity, not to mention our time! As a nurse, we are pulled in so many different directions at once and expected to always be on top of our patient care. Utilizing these hacks will hopefully help.

    What are your personal nursing hacks which help save you time and make you a more efficient nurse? Let me know in the comments below, and share this article with your nursing friends!

    Check out more general nursing hacks over at FRESHRN here!

    ER Nursing Hacks: Pin 2