RSI Intubation for Nurses: Rapid Sequence Intubation

RSI Intubation for nurses

Rapid Sequence Intubation

William Kelly, MSN, FNP-C

Author | Nurse Practitioner

RSI, or Rapid sequence intubation, is the process where we intubate people in the hospital, pre-hospital, and emergency department settings when the patient is awake.

It involves multiple different steps that need to occur to quick succession, to provide first sedation, then paralysis, then insertion of the endotracheal tube into the trachea. 

Learn all about RSI intubation, and specifically what the nurse’s role during an intubation is, and which compications and montioring parameters to watch out for!

RSI intubation: rapid sequence intubation for nurses Featured Image

Indications for RSI Intubation?

So when does a person need intubed? Well, this really depends, but emergent intubations often involve severe respiratory distress

Patients in acute respiratory failure will typically present with:

    Tachypnea

    Increased respiratory rate > 20 rpm

    Hypoxia

    SPO2 < 90%

    Increased WOB

    Increased work of breathing characterized by use of accessory muscles

    Adventitious Breath Sounds

    Presence of abnormal breath sounds including wheezing, crackles, rhonchi, or diminishment

    Other Abnormal Vital signs

    May be present including tachycardia, hypertension, hypotension, fever, or altered mental status

    Tripod position is when a patient is sitting over the bed leaning forward, supporting their upper body with their hands on the knees or another surface. This helps accessory muscles breath more easily, but can be an ominous sign to someone who is in respiratory distress. Think COPD!

    Indications for Rapid Sequence intubation (RSI intubation) includes:

    • Acute Respiratory Failure (from pneumonia, COPD, CHF, Covid, etc)
    • Anaphylactic reaction or Angioedema
    • When the patient cannot protect their airway (severe alcohol intoxication, drugs, etc.)
    • For surgery

    The Nurses Role during RSI

    So what is YOUR responsibility as the nurse?  Well don’t worry, you shouldn’t actually be the one to intubate the patient (although there are some exceptions such as NICU nurses and Flight nurses). 

    The person who placed the Endotracheal (ET) tube is usually a paramedic, physician, and sometimes an advanced practice provider (PA, NP, or CRNA). This is usually:

    • EM Physician but sometimes APP
    • IM Physician
    • Anesthesia

    The nurse’s role is not to physically intubate, but nurses are essential in making sure the intubation goes safely and smoothly. They are also on the front lines to notice and intervene when things go wrong!

    The nurse’s role is to prepare the patient and equipment,  administer the medications, help manage the airway (although this is usually the job of respiratory therapists), and monitor the patient.

    Afterwards, they are required to keep the patient sedated with titratable sedatives.

    It is still important for nurses to understand how the RSI intubation process goes, even if they are not the ones placing the ET tube. It takes a team of nurses, respiratory therapists, physicians, and more to have a successful intubation without any complications.

    Alternatives to RSI intubation

    Are there any alternatives to intubation? Yes and no. 

    There are certainly treatments we can try before jumping to intubation. These include nebulizers, certain IM/SQ meds, a non-rebreather, High-flow nasal cannula, and CPAP or BIPAP.

    However, usually when intubation is decided on, it is when the patient is in impending respiratory arrest, or when the other treatments already aren’t enough. 

    RSI intubation is kind of our last saving measure that we can do to save their life and stabilize their respiratory system. 

    RSI Medications

    Before diving into the steps of RSI, we need to review the important medications that are given during RSI.

    It is the nurses responsibility to draw these up, reconstitute them, and give them. Any medication that a nurse gives, they should know how the medication works, any side effects, and what to monitor for.

    Sedatives

    First we’re going to talk about sedatives. A sedative is a medication that acts as a CNS depressant – essentially putting the patient to sleep. Different sedatives work in different ways. Sometimes, it takes multiple different sedatives at the same time to effectively sedate a patient.

    Sedatives are also called induction agents – inducing sedation in the patient. They also decrease the sympathetic response, making the body better tolerate the overall intubation experience.

    In regards to RSI Intubation, SEDATIVES ARE ALWAYS GIVEN FIRST

    This is because you need to knock the patient out before you paralyze them, as this is a very frightening experience if not. It can also cause tachycardia, hypertension, and increased ICP if you don’t!

    Etomidate

    Etomidate is the most common sedative that will be ordered for RSI intubation. 

    Etomidate does not offer any analgesia, so sometimes fentanyl is added to minimize the SNS stimulation for patients with significant cardiovascular disease or increased ICP patients.

    Etomidate does not really affect blood pressure, but it can cause some mild increase in airway resistance.

    Side Effects & Monitoring

    Myoclonus

    Etomidate can cause myoclonus to occur, which is brief and harmless, but can be mistaken for a seizure.

    Adrenal Suppression

    Etomidate can cause adrenal suppression for 12-24 hours after the injection. This could potentially impact hemodynamic stability (blood pressure), mainly in patients who are at risk such as those with pre-existing adrenal insufficiency or severe sepsis.

    Patients with severe sepsis who are intubated with etomidate and become hypotensive despite fluids and a vasopressor should be given a 1x dose of hydrocortisone 100mg IV.

    Heart Failure Exacerbation

    Etomidate doesn’t cause HF, but patients with pre-existing HF may have exacerbated underlying myocardial dysfunction after administration.

    Versed

    Versed, also called Midazolam, is the most commonly used Benzodiazepine used for sedation for RSI intubation.

    Versed also does not cause analgesia, but is a good choice for patients in status epilepticus because it offers anticonvulsant properties.

    However, it can decrease the blood pressure, so this should be avoided in patients who are hemodynamically unstable.

    Side Effects & Monitoring

    Hypotension

    Versed can cause a decrease in Mean Arterial Pressure (MAP) by 10-25%. This means Versed should generally be avoided in hypotensive patients or those at risk for hypotension (severe sepsis, trauma, etc).

    Ketamine

    Ketamine is a newer sedative used for RSI intubation. It’s structurally similar to PCP, and can cause some interesting side effects. However, it can be a great sedative and analgesic to help with rapid sequence intubation.

    The good thing about Ketamine is it preserves the respiratory drive. This makes it excellent choice for minor procedural sedation where intubation is not needed.

    However, the increased catecholamine stimulation can cause tachycardia, hypertension, and possibly increased ICP, making it a poor choice for head traumas and hypertensive crises, and also those with cardiac ischemia or aortic dissections.

    However, this can be helpful in patients who are hypotensive to increase BP or in severe asthmatics to cause bronchodilation (in theory). 

    Side Effects & Monitoring

    Laryngospasm

    Ketamine increases the risk of laryngospasm, especially in those with history of upper respiratory disease or asthma. This is because ketamine does not suppress pharyngeal and laryngeal reflexes. In this case, it can be helpful to use fentanyl with it

    Ketofol

    Ketofol is the combination of ketamine and fentanyl. This can cause analgesia, sedation, and amnesia, and can be a good choice for patients with severe bronchospasm.

    Increased Cardiac Activity

    Ketamine causes increased stimulation of the sympathetic nervous system, releasing catecholamines leading to tachycardia, hypertension, increased myocardial demand, and even possible cardiac arrhythmias.

    This can be beneficial in patients who are hypotensive, but dangerous for those with active cardiac disease or aortic dissection.

    Emergence Reactions

    Ketamine can cause an “emergence phenomenon” primarily when used for procedural sedation. This is when the patient may experience vivid and/or disturbing dreams as they wake up. Hallucinations and frank delirium may occur postoperatively up to 24 hours. 

    This usually does not happen with patients who are intubated and sedated for over 24 hours.

    Propofol

    Propofol is a common sedative, and a frequent agent of choice for maintaining sedation with a slow titratable drip. It has a characteristic appearance of milk.

    Propofol is the drug that Michael Jackson was found to have overdosed on. It causes deep sedation and does diminish the patients respiratory drive.

    Propofol has the following actions on the body:

    • Decreases airway resistance: Good for bronchospasm
    • Neuro-Inhibition: Good for intracranial pathology
    • Suppresses SNS: Good for hypertension, bad for hypotension & conditions which decrease cerebral perfusion

    Propofol IV Push?

    Make sure your specific state and facility allow RNs to give IV boluses of propofol, and if so, make sure the provider is always at the bedside. Since propofol causes deep sedation, it may not be within your scope as a nurse to push it. Seems silly, but always protect your license!

    Side Effects & Monitoring

    Hypotension

    Propofol has a blood pressure lowering effect, which can decrease the MAP by 10%, but sometimes even ≥ 30%.

    Use caution if the patient has a borderline low pressure or baseline MAP of 60-70 mmHg.

    Patients at risk for hypotension include severe sepsis, trauma, severe aortic stenosis, etc.

    Bradyarrhythmias

    Propofol can cause bradyarrythmias to occur. This is more common with high doses, prolonged duration, and concurrent medications like beta-blockers, paralytics, and opioids. Patients with a history of cardiac disease are at increased risk.

    QT Prolongation

    QT prolongation can predispose your patient to dangerous ventricular arrhythmias like Torsades de Pointes and VFIB. This is more common with:

    • High propofol doses
    • Elderly patients
    • Structural heart disease
    • Congenital Long QT
    • QT prolonging medications
    • Electrolyte Disturbances

    Anaphylaxis

    Anaphylaxis is rare with Propofol but can occur, usually within 5-10 minutes after infusion. Those with a history of soybean or egg allergy are probably fine to take it.

    Soybean Allergy

    Allergy to soybeans or egg used to be a contraindication for receiving propofol, but newer formulations of the drug rarely produce a reaction and are likely safe

    Elevated Triglycerides & Lipase

    Propofol is a lipophilic fatty solution which contains triglycerides. Infusion can lead to elevations in triglycerides and lipase, which usually occurs 2-4 days after initiation. This can lead to pancreatitis, especially in those who are already at risk.

    PRIS

    PRIS stands for Propofol Infusion Syndrome. PRIS is rare but deadly. When occurs, the patient suffers from acute refractory bradycardia which may lead to asystole, and also may have:

    • severe metabolic acidosis,
    • cardiovascular collapse,
    • rhabdomyolysis
    • hyperlipidemia
    • renal failure
    • hepatomegaly

    This is more common with high doses (>4mg/kg/hr) and long duration of use (>48 hours).

    Choosing the Right Sedative

    There are some specific scenarios where one sedative may be more appropriate than others. Regardless, it is always the Providers preference and what they’re familiar with. 

    Head Injury or Stroke

    Etomidate

    Status Epilepticus

    Propofol or Etomidate

    Severe Bronchospasm

    Propofol or Ketamine (+/- fentanyl)

    Cardiovascular Disease

    Etomidate +/- Fentanyl

    Shock

    Etomidate 0.15mg/kg or ketamine 1mg/kg

    Paralytics

    Paralytics, also called neuromuscular blocking agents (NMBAs), are given immediately after the sedative kicks in, which produces a paralyzing effect on the body. This relaxes the patients muscles and makes the intubation easier for the Physician or APP, and minimizes complications.

    Succinylcholine

    Succinylcholine or Sux for short, is the classic paralyzing agent for RSI. It is termed a “depolarizing neuromuscular blocker” because they cause the muscle cells to “fire” or depolarize, but then don’t let the muscles repolarize, leading to paralysis.

    While used in most scenarios, this is contraindicated in conditions which may cause hyperkalemia or may lead to an exaggerated response. This is because even in normal patients, Sux can increase potassium levels by 0.5-1.0 mEq/L.

    These conditions include:

    • Malignant hyperthermia (personal or family history)
    • Neuromuscular disease with denervation (i.e. MS)
    • Muscular dystrophy
    • Stroke > 72h old (especially with significant motor denervation)
    • Rhabdho
    • Significant burn(s) over 72h old
    • Significant Hyperkalemia

    Myesthenia Gravis

    Patients with MG are resistant to Sux, so should be given 2mg/kg

    Side Effects & Monitoring

    Fasciculations

    Sux commonly causes fasciculations of the muscles prior to causing full paralysis.

    This may increase ICP and stimulate emesis leading to aspiration.

    Bradycardia

    A metabolite of Sux can stimulate muscarinic receptors to release acetylcholine, producing bradycardia of the sinus node. This can be treated with atropine.

    Rocuronium

    Rocuronium or “ROC” for short is a “non-depolarizing” NMBA used for sedation for RSI intubation. This is because it is an acetylcholine antagonist, blocking its effects and leading to paralysis.

    ROC is used when Sux is contraindicated as above.

    Some conditions which may decrease the efficacy of the paralysis include:

    • Respiratory alkalosis
    • Hypercalcemia
    • Demyelinating lesions (MS)
    • Peripheral neuropathies
    • Muscle trauma

    Side Effects & Monitoring

    Hypertension

    ROC can increase peripheral vascular resistant and cause a temporary increase in BP. It can also cause transient hypotension in some people. 

    Tachycardia

    ROC can cause temporary tachycardia for about 5 minutes.

    Right-sided HF

    ROC may worsen pulmonary HTN, leading to right-sided heart failure in those who are predisposed.

    Other Paralytics

    Other non-depolarizing paralytics include Vecuronium and Pancuronium, but these are not used as often.

    Vecuronium, shortened to “VEC”, is not used as frequently, as it has a longer onset of action – around 3 minutes. This can be reduced with a smaller “priming” dose.

    RSI INTUBATION PROCEDURE

    Prepare the Patient

    To prepare the patient for RSI intubation, make sure they are positioned in the “sniffing” position, supine with their neck flexed. Placing a towel between their head and neck can help.

    Make sure the patient is getting hyper-oxygenated at the same time, usually with a Non-rebreather or a Bag-valve mask at 100%.

    Respiratory therapists are often in charge of airway along with the Provider.

    Place the patient on the monitor including telemetry, continuous pulse ox, and end-tidal CO2 if possible.

    Explain the procedure to the patient and ensure informed consent is obtained, either written or verbal. Written is often not able to be obtained due to the emergent nature of many intubations.

    If the patient is altered, ensure there is no DNR or DNI order form or POLST. 

    Using a BVM

    If using a BVM hooked up to 100% oxygen, make sure you are squeezing the BVM with each spontaneous breath to ensure the valve opens and the oxygen is given to the patient!

    Prepare the Equipment

    Bring the code cart at the bedside. You don’t necessarily need to hook up the defibrillation pads, but always follow facility protocol.

    Most of the equipment needed will be found in the Airway drawer, usually one fo the last drawers.

    The equipment needed for the actual intubation will be:

    • Laryngoscope
    • ET tube
    • Stylet
    • 10cc syringe
    • Suction Tubing & Yankauer
    • ETCO2 or CO2 detector
    • Stethoscope
    • Bag-valve mask

    Ask the Provider which size ET tube they’ll want, which is often 7.0 for females, and 8.0 for males.

    The stylet will need to be placed inside the ET tube, which is usually cuffed. This will be removed once the Provider gets the tube in the right spot.

    Administer Medications

    The Provider will give you a verbal order for which sedative(s) and paralytic they want.

    Verbally clarify the name and dose, and begin to draw up the medications. You may need to grab these medications from an “RSI kit” in the Accudose, or they may be located in your code cart.

    Usually one of the nurses will assume the “medicine” responsibility while the others are preparing the patient and equipment.

    Some medications will require reconstitution. This means you may need to mix saline with powdered medication to make a solution. Verify the final doses/amounts with another nurse.

    Make sure to accurately label each, so you don’t mix up the sedative and the paralytic!

    Once everyone is ready for the intubation, wait for the Provider’s verbal “ok” to give the medications, and administer the medications as above. Most are given quickly over 5-10 seconds. 

    First the sedative, then once the patient has decreased LOC and you get the next verbal OK from the Provider, administer the paralytic.

    RT should be bagging the patient at this time until the Provider is ready for the intubation. This is usually within 30-60 seconds after administering the paralytic.

    The Intubation

    Your main job is now done, and now you just watch the intubation procedure and monitor the patient, following any verbal orders that are given.

    The Provider will place the ET tube between the vocal cords, typically 21cm deep in women and 23cm in men. This is measured at the teeth.

    Verify Placement

    Immediately after intubation, the tube needs to be verified. This is verified in multiple ways.

    First, a CO2 detector may be attached to the ET tube. Observing color change from purple to yellow indicates CO2.

    If the patient is hooked up to an ETCO2, with each BVM breath, you should see normal CO2 levels near 35-45 mmHg.

    Additionally, someone should listen to all breath sounds listening for equal breath sounds.

    Lastly, the patient should have a portable CXR ordered to verify the placement. The radiologist may recommend pulling out or pushing deeper x amount of cm.

    Maintain Vent + Sedation

    Now the patient is successfully intubated. Your main job now is keeping the patient sedated so that the Ventilator can do its job and breath for the patient.

    This usually involves a continuous titratable drip, often propofol. The patient may also require additional sedatives, analgesics, and sometimes further paralytics.

    Of course, make sure to chart everything and continue to monitor the patient’s vital signs.

    If in the ER or Med-Surg, your goal should be to get that patient admitted/transferred ASAP.

    RSI Intubation Complications

    Unfortunately, not all RSI intubations go smoothly. These are usually emergent procedures and are not done in a controlled environment. 

    As the nurse, you are the first one who is going to notice any complications while monitoring your patient.  It’s important to know what to look out for and how these complications are managed.

    Esophageal Intubation

    This is when the ET tube is in the esophagus instead of the trachea. This becomes obvious when verifying placement.

    When it occurs, the ET tube will be completely removed and the Provider will re-insert the tube with another attempt.

    Gastric Tube

    An OG or NG to suction should be placed in all patients after intubation to decompress the stomach to prevent emesis and to decrease intrathoracic pressure.

    A foley should also be placed.

    Right Mainstem Intubation

    If the ET tube is placed slightly too deep, it will often go into the Right Mainstem Bronchus of the right lung. This is because it is more vertical than the left.

    If left, the patient may have signs of hypoxemia and worsening respiratory status, and if not fixed can cause barotrauma, pneumothorax, and hemothorax.

    Breath sounds should be equal throughout the lobes, but a CXR will need to be done to verify this isn’t the case. 

    Treatment involves pulling out the ET tube per radiologists recommendations, which the Provider should do.

    Perforation

    A traumatic insertion can cause perforation of the esophagus or trachea. This is very rare, but severe.

    Signs include presence of subcutaneous emphysema in the mediastinum, and worsening respiratory status.

    A CXR may show pneumomediastinum, subcutaneous emphysema, and possible pneumothorax.

    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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    • Understand the pathophysiology of why and how arrhythmias occur
    • Learn how to manage arrhythmias like an expert nurse
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    Oxygen Delivery Devices and Flow Rates

    Oxygen Delivery Devices and Flow Rates

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

    Author | Nurse Practitioner

    Oxygen Delivery Devices and Flow Rates are important concepts to understand as a nurse. Oxygen is a life-saving therapy that nurses and respiratory therapists administer every day in the hospital.

    Whether your patient is on chronic oxygen, or whether they are in acute respiratory failure, your patients will commonly have oxygen ordered and it will be up to you as the nurse to administer it. 

    Knowing the oxygen delivery devices and flow rates will tremendously help you take care of your patients who requires oxygen.

    Oxygen delivery devices and flow rates FB

    The Role of Oxygen

    Oxygen is used every day in and out of the hospital. In order to understand oxygen delivery devices and flow rates, we need to first understand a few basic principles and definitions.

    Oxygen is the most important gas in our atmosphere that allows for humans and animals to live. Our cells use oxygen to create energy (Kreb’s cycle anyone?). Our ability to create energy without oxygen is very limited.

    Without oxygen, our cells will die within minutes.

    Oxygen occurs naturally in our atmosphere, at a concentration of 21%. Another term for oxygen concentration is FIO2, or fraction of inspired oxygen.

    When we breathe in air, the air (including oxygen) enters into our lungs and makes contact with all of the alveoli. Alveoli are small sac-like structures within the lungs.

    The oxygen diffuses across these alveoli into the bloodstream, where it attaches to hemoglobin on our red blood cells. Our blood carries this oxygen throughout the body where it is absorbed by the tissue to give life and energy to our cells.

    A healthy patient has a respiratory rate of 12-20 respirations per minute (rpm). Lower than 12 is usually from medications like opioids or benzos, and higher is usually from anxiety, asthma, COPD, CHF, a PE, pneumonia, or some other type of respiratory failure.

    The tidal volume is the amount of air breathed into the lungs with each breath. The tidal volume will depend on the patient’s physical size of their lungs and their respiratory effort, but is generally around 400-500ml in a healthy adult.

    The FIO2 or the fraction of inspired oxygen is the percentage or concentration of oxygen that a person inhales. Remember room air is always at 21% FIO2 on earth.

    Oxygen Delivery Devices and Flow Rates

    There are different oxygen delivery devices and flow rates to know, with each device allowing for certain flow rates of oxygen (L/min), as well as different concentrations of oxygen (FIO2).

    Blow-by Oxygen

    Blow-by oxygen is just that – it’s oxygen that blows by. This does not not apply oxygen directly, but rather indirectly by “blowing” on the patient’s face.

    This is usually only used in infants and young toddlers who become agitated when masks or tubing is applied.

    Less than 30% FIO2 can be provided with this, which is not much greater than room air of 21%.

    If used, the oxygen rate should be at least 10 L/min through a simple mask or even a tubing sticking through a styrofoam cup, which infants and toddlers may be less scared of.

    Nasal Cannula

    Nasal cannula is tubing that runs from the oxygen source to the patient’s bilateral nares or nostrils.

    This is the most common use of oxygen within the hospital, especially for non-critical patients and those who need chronic oxygen delivery like with COPD.

    Nasal Cannula is typically started at 2L/min and then titrated upwards to as high as 6L/min, although 2-4L/min is ideal. This delivers 25-40% FIO2, depending upon their respiratory rate, tidal volume, and amount of mouth breathing.

    The nasal cannula is good for most patient needs with lower levels of oxygen requirements.

    Nasal cannula can be very irritating and cause dry nares at rates >2L/min, so the oxygen should be heated and humidified if possible at higher flow rates.

    Simple Face Mask

    Simple face masks are a mask with tubing that is hooked up directly to an oxygen source. This is similar to Nasal Cannula, except it is delivered in a mask format over the mouth and the nose, instead of just the nose.

    Simple face masks allow for flow rates between 6-10L/min, with an FIO2 of 35-50%.

    Simple face masks tend to be a temporary solution, used when titrating your oxygen delivery devices and flow rates. 

    Ventimask

    Ventimask or a Venturi mask is a face mask that is connected to corrugated tubing with a venturi valve on the end.

    This piece connects to the oxygen tubing, which mixes oxygen with room air to provide a consistent high flow of oxygen even with irregular respiratory rates or tidal volumes.

    Depending on the oxygen flow rate, there are different colored venturi pieces that are used, with FIO2 of 24-60% FIO2 depending on which venturi valve is used. Levels >40% are generally not used and likely don’t offer more benefit.

    The oxygen flow rate will be indicated on the specific venturi valve used, but generally is from 3-10L/min.

    Some Ventimasks come in an all-in-one rotational setup, where the FIO2 can be adjusted on a single venturi valve.

    Ventimasks are usually used with COPD patients when they require high levels of oxygen, but there is concern for CO2 retention. It can also be helpful for asthma exacerbations and general respiratory distress.

    This is typically not used long-term.

    Non-Rebreather

    A Non-rebreather is typically what is initially used when the patient is requiring a high flow of oxygen and nasal cannula’s are not cutting it.

    A non-rebreather provides the highest concentration of oxygen that can be provided to a patient who is breathing on their own, up to 95% FIO2, without any additional machines.

    However, this is NOT a long-term solution, and unless they can be titrated down, patients will need to be transitioned to a BIPAP, HFNC, or intubation, unless they can be titrated down.

    In a non-rebreather, there is a reservoir bag attached to the mask, with a one-way valve separating the two. This prevents exhaled CO2 from entering the reservoir, and only allows oxygen.

    There are holes or “exhalation ports” in the sides of the mask that allow expired are out also do not allow room air back in (usually only one of these is “blocked” to prevent suffocation if the oxygen turns off).

    Oxygen flow rates of 10-15L/min can deliver FIO2 of up to 95% in these individuals. However, there is a small amount of room air which “gets in” the system, so the FIO2 is invariably lower, more like 80-90%.

    Remember over-oxygenation can also be dangerous termed “oxygen toxicity”. This can cause vasoconstriction, worsen outcomes, and even cause seizures.

    This means you want to keep the patient’s SPO2 at 94-99%, as a pulse ox does not measure above 100%.

    If a patient is still struggling to breathe with SPO2 of 88-94% or lower on a NRB, then they probably need intubated.

    High-Flow Nasal Cannula

    High-Flow Nasal Cannula (HFNC) is a newer method of delivering a high flow and FIO2 of oxygen in patients who have higher oxygen requirements. COVID patients tend to do well on these devices, but it can be used for all sorts of respiratory distress.

    High-flow Nasal cannula consists of a specific machine and tubing used to deliver a very high flow of oxygen that is heated and humidified.

    HFNC can be delivered from 8-60L/min (30-60 L/min in adults), and an FIO2 of 100%.

    HFNC is more comfortable and studies have shown that using HFNC may be a better alternative than using a face mask.

    HFNC also adds PEEP-like pressure equivalent to about 3-4 cm H2O, similar to a CPAP, helping to keep the alveoli open and increase ventilation (gas exchange).

    It is also an alternative to BIPAP other than those patients who are hypercarbic (high CO2 levels like in COPD).

    Knowing the difference between the oxygen delivery devices and flow rates, HFNC is not a good option for those who are CO2 retainers for very long .

    CPAP

    CPAP or Continuous Positive Airway Pressure is a method of non-invasive ventilation. This helps open up the alveoli allowing for better gas exchange.

    This can be useful in acute pulmonary edema like in CHF, because it reduces intrathoracic pressure and can reduce preload and increase cardiac output, as well as decrease alveolar congestion.

    It is also used for obstructive sleep apnea (OSA) to keep the airway open.

    Oxygen is not always added (especially if the patient is just using it for OSA). The pressure is set at 5-20 cm H2O, usually beginning at 5-8 cm H2O.

    Increased pressures will increase intrathoracic pressures.

    Oxygen is added to keep SPO2 >90%.

    BIPAP

    BIPAP or Bilevel Positive Airway Pressure is the “better” version of CPAP. This can often be used as an alternative to intubation, and is great for hypercapnic respiratory failure (think COPD).

    This uses a higher pressure during inspiration and a lower pressure during expiration.

    BIPAP uses 3 settings:

    • Rate: The respiratory rate is usually set to a backup or spontaneous rate, as these patients are awake and breathing spontaneously. This is usually 8-12 rpm. Most patients on a BIPAP will be breathing much faster than this.
    • IPAP: The inspiratory positive airway pressure is how much pressure is given during inspiration. This is anywhere from 5-30 cm H2O, but usually started at 8-12 cm H2O. A higher level will increase tidal volume.
    • EPAP: The expiratory positive airway pressure is the pressure during expiration, which is typically 3-5 cm H2O.

    Oxygen delivery is then used as well to ensure SPO2 >90%. FIO2 is started at 100% and titrated down.

    Clinical Note: Settings are usually given as IPAP/EPAP, Rate, and FIO2. This means you would relay the settings as 10/5, backup rate of 10, and an FIO2 of 30%. The RT should tell you the settings and they should be the ones to titrate the FIO2.

    This is used for Acute COPD exacerbations, and acute respiratory failures like in CHF or ARDS. It can work great for reducing CO2 retention in hypercarbia subsequent and respiratory acidosis.

    This is not good for those who are nauseous or have thick secretions, as this may be a risk for aspiration. This can be dangerous for those who are altered for the same reason, although is sometimes still used.

    Ventilator

    Mechanical Ventilation is the best way of controlling a patient’s oxygenation (oxygen delivery) and ventilation (gas exchange).

    Mechanical ventilation is used as a last resort when a patient is in severe respiratory distress and cannot tolerate non-invasive ventilation.

    These patients are in respiratory failure and may be altered, cannot protect their airways, are throwing up, or just continue to be hypoxic despite alternative oxygenation.

    To be put on a ventilator, a patient will need intubated, likely sedated, and hooked up to a ventilator.

    Ventilators have various settings which control the respiratory rate, the IPAP, the EPAP, the inspiratory flow rate, and the FIO2%.

    If ventilation can be avoided, it should be. Some patients are difficult to wean off the vent (like in severe COPD or ARDS).

    And that is an overview of oxygen delivery devices and flow rates. Hopefully you have a solid understanding of each device and when it is appropriate to use each one.

    References

    Hyzy, R. C., & McSparron, J. I. (2021). Noninvasive ventilation in adults with acute respiratory failure: Practical aspects of initiation. In T. W. Post (Ed.), UpToDate. https://www.uptodate.com/contents/noninvasive-ventilation-in-adults-with-acute-respiratory-failure-practical-aspects-of-initiation

    ICU Advantage. (2020, January 13). CPAP vs BiPAP – Non-Invasive Ventilation EXPLAINED [Video]. YouTube. https://www.youtube.com/watch?v=Te0WLR71HwA

    Nagler, J. (2021). Continuous oxygen delivery systems for the acute care of infants, children, and adults. In T. W. Post (Ed.), UpToDate. https://www.uptodate.com/contents/continuous-oxygen-delivery-systems-for-the-acute-care-of-infants-children-and-adults

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    With this course you will be able to:

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    • 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!

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    Oxygen delivery devices and flow rates Pin