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STEMI & NSTEMI: A Nurse’s Comprehensive Guide

Jun 16, 2021 | 5 comments

STEMI & NSTEMI: A Nurse’s Comprehensive Guide

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

Author | Nurse Practitioner

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!

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CORONARY ARTERY ANATOMY

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

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)”

ISCHEMIA & INFARCTION (STEMI) ON THE ECG

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

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

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

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.

LBBB OR VENTRICULAR PACED

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”

STEMI PROGRESSION

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.

STEMI LOCATION

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.

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ACUTE MANAGEMENT OF STEMI

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!

References

Textbooks

ECGs Made Easy (6th ed.) <<< this is my favorite ECG PDF

Ekgs for the nurse practitioner and physician assistant

UpToDate

Overview of the acute management of ST-elevation myocardial infarction

ECG tutorial: Myocardial ischemia and infarction

Other

AHA ACLS Algorithms

Attributions

“Coronary Blood Vessels” by OpenStax College is licensed under CC BY 2.0, changes were made.

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.

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  • 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:

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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:

  • How to Read an EKG Rhythm Strip
  • Cardiac Lab Interpretation (Troponin, CK, CK-MB, and BNP)
  • Vagal Maneuvers: How to Stop your Patient’s SVT
  • 20 Tips for New Nurses In the Hospital
  • 10 Nursing Hacks Every ER Nurse Should Know
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21+ mRNA Vaccine Questions Answered for Nurses

Jan 27, 2021 | 2 comments

21+ mRNA Vaccine Questions Answered for Nurses

Last updated: January 27, 2021

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The new mRNA vaccines for COVID are being distributed, and as a nurse, it is important to know these vaccines, how they work, and their safety data!

Our patients respect our medical opinion, and we need to give accurate information so they can make an informed decision.

This article mainly focuses on the mRNA vaccines (Pfizer and Moderna), as they are currently the vaccines being distributed as they have obtained FDA emergency use authorization.

With these vaccines being so new – it leaves many wondering, “is it’s safe?”

I’m going to go over what the data tells us and hopefully give you enough insight into making an informed decision, and help your patients do the same!

Quick Note: I want to preface this article by first stating that I am a nurse practitioner and I see many COVID patients on the frontlines in the ED. I am not, however, an epidemiologist or scientist who works directly with COVID in a lab, so I am simply basing my own opinions on what the data says, as well as my understanding of the virus by seeing it firsthand.

mRNA Vaccines - Featured Image

1. How do mRNA Vaccines Work?

Vaccines generally work by introducing a dead or weakened virus, or part of a virus into your bloodstream via an Intramuscular or subcutaneous injection.

This creates an immune response that helps your body be able to attack the real virus whenever it comes into contact with it in the future. Typical vaccines include those with:

  • A live but weakened or “attenuated” virus, which leads to a better immune response, but can actually cause the disease in very few people – mainly those who are immunocompromised.
  • A dead or “inactivated” virus, in which the virus has been inactivated and is unable to replicate and cause disease. This doesn’t create as good of an immune response so it may need multiple doses or boosters. An example of this is the flu shot or hepatitis A.
  • Those that contain a piece of the virus, like part of its specific protein. This also cannot replicate or cause disease. Examples include hep B, meningitis, and HPV.
  • There’s also some vaccines that contain a toxoid that the virus creates, such as tetanus or diphtheria, like the Tdap vaccine.

The mRNA Vaccines (Pfizer and Moderna) actually do not inject the virus or any of it’s parts into you.

Instead, it contains mRNA which codes for the COVID spike protein – a protein specifically found on the COVID virus.

RNA is a single-stranded molecule that normally takes information from your DNA in the nucleus of the cell, and brings it to the ribosome of the cell to create proteins which basically keep the cell running and functioning appropriately.

So what scientists at Pfizer and Moderna have done is isolated the genome sequence of the mRNA which codes for the spike protein in the coronavirus, as this protein is not naturally found within your body. So what does the body do with this mRNA?

The mRNA is absorbed into your cells and carried to your ribosome where it is used as instructions to create the spike protein of COVID.

This protein cannot lead to disease, but it should lead to an immune response. Your body sees this foreign entity and creates antibodies to kill it and any future proteins it detects.

If the actual COVID virus now enters your body, your body should be able to detect it, and your immune system will target the cell and destroy it before it has a chance to replicate enough to cause disease and hopefully prevent you from spreading it.

mRNA Vaccines - DNA

2. Are mRNA Vaccines Safe?

This isn’t an easy question since it is so new, but so far it seems to be very safe and effective.

While mRNA vaccines have not actually been used in the US, researchers have been studying them for decades and have tested them on humans before for viruses like rabies, flu, CMV, and Zika.

In order to test the safety and efficacy of these new vaccines, clinical trials were conducted.

Pfizer and Moderna injected this vaccine into willing people and followed them for any adverse side effects, as well as those who ended up getting symptomatic COVID or severe disease.

Over 30,000 people were enrolled in the Moderna trial and over 40,000 people in the Pfizer trial.

Those who got the Pfizer vaccine get 2 injections, 21 days apart. Those who got the Moderna vaccine get 2 injections, 28 days apart.

Pfizer was tested on people 16 years and older, and Moderna was tested on adults 18 years and older.

Long story short – what they found was that most symptomatic covid cases were occurring in the placebo groups, which means those who did not receive the vaccine. Severe cases of COVID almost exclusively occurred in the placebo group!

The Pfizer vaccine boasts 95% efficacy beginning 1 week after the second dose, and Moderna boasts 94.1% efficacy 2 weeks after the second dose.

Both mRNA vaccines essentially use the same mRNA, basically the same ingredients, and both had very similar findings in their trials. This in and of itself is reassuring and offers an element of reproducibility.

The data from these trials are overall VERY reassuring. You can read more about the Pfizer or Moderna trials to get more information!

mRNA Vaccines - clinical trial

3. What Side Effects Can be Expected?

Common side effects include local injection site pain, headache, and fatigue. These vaccines should not cause COVID symptoms such as cough or SOB. It is impossible for these vaccines to cause actual COVID disease.

These vague side effects are common and expected when getting a vaccination, and are often an indication of the body’s immune response. They are short-lived and not severe.

Symptoms after the first injection tend to be less severe, and symptoms after the second injection were more significant – although both were very short lived (1-2 days).

Anecdotal Note: I have received both injections from the Moderna Vaccine. After the first shot, I had arm soreness which was worse than a typical vaccine, but resolved over 1-2 days. The day after my second injection, I had body aches and fatigue which resolved by the next day.

These symptoms seem common based on my colleagues experiences as well. Those who had symptomatic COVID anecdotally reported worsened symptoms after the first dose, although still short-lived.

Are all side effects mild and short-lived? We’ll dive more into that in future questions!

4. Can the mRNA Vaccines cause Anaphylaxis?

Just like any medication or vaccine, allergic reactions can occur.

Anaphylactic reactions have occurred after COVID vaccine administration, although not common, and seem to mainly occur in those with a history of severe allergies.

Overall it seems to be very rare – 11 people per million. Regardless, we know how to treat anaphylaxis and allergic reactions very well – Benadryl, Solumedrol, and Pepcid!

The CDC recommends those without a history of anaphylaxis to wait 15 minutes after their injection for monitoring, and those with a history of anaphylaxis to wait 30 minutes – just to be on the safe side.

Related Article: “Adverse Drug Reactions Nurses Need to Know”

5. Can the mRNA Vaccines cause Facial Paralysis?

Bell’s palsy is unilateral facial paralysis that can occur, which is usually temporary.

In the COVID vaccine trials, there were 7 reported cases of Bell’s palsy, in the over 70,000 participants in Pfizer/Moderna’s clinical trials.

While there were slightly more cases in the vaccine groups than the placebo groups, this rate is consistent with bell’s palsy rates in the general public, so likely not statistically significant.

However, some viruses and vaccines have been associated with bell’s palsy in the past, although rare.

Even if there is a small rare chance of the COVID vaccine causing Bell’s Palsy – it is usually temporary and treatable, and the benefits outweigh the risks.

Related Article: “The Cranial Nerve Assessment for Nurses”

6. Can the mRNA Vaccines cause COVID?

No – it is physiologically impossible for it to cause COVID disease.

Vaccines that contain live “weakened” viruses do have the capacity to cause disease in those who are immunocompromised – an example being the MMR vaccine.

However, those with only pieces of the virus or mRNA that code for pieces of the virus cannot cause COVID. So mRNA Vaccines cannot cause COVID illness.

7. Will these Vaccines cause False Positive Results on Testing?

No, the vaccine should not alter PCR or antigen testing. Test swabs collect viral particles and test for their genetic code. These swabs are collected from areas where you are expressing the virus, like the nasopharynx.

While the mRNA causes your cells to produce the COVID spike protein, they are not expressed or spread outside of your body.

The PCR and antigen tests check for active infection and do not check for antibodies. The vaccine should not alter these test results. 

8. Do the Vaccines Change your DNA?

No. Only specific viruses can alter your DNA. These viruses are called retroviruses and require a specific protein called reverse transcriptase.

The mRNA in the COVID vaccines do not alter your DNA in any way.

9. Do the Vaccines Contain a Microchip?

No – this is nonsense and I’m not really sure what else to say about it.

10. Do the mRNA Vaccines cause Infertility Issues?

There is no convincing evidence to suggest that the mRNA vaccines cause infertility.

This idea was picked up and used by anti-vax propaganda. This myth started when a German Epidemiologist and a former Pfizer employee asked the FDA to not grant authorization to use the vaccine.

They said that the COVID vaccine’s mRNA is similar to the syncytin-1 protein which is used in mammals to help create placenta during pregnancy.

While the proteins do share a minimal amount of similar code, the scientist and medical community at large reject the notion that it could cause infertility.

While it is still so new – it cannot be said with certainty because we don’t have the data. However, 23 women did conceive during these trials, and they are still being followed.

11. Can Pregnant Patients Get an mRNA Vaccine?

This is a decision that should be discussed with the patient’s OBGYN, and they can come to a decision together.

The clinical trials did not study vaccination in pregnant mothers, so we don’t have specific data regarding pregnant individuals. There were some animal studies that looked promising.

The American College of Obstetricians and Gynecologists (ACOG) recommends that COVID-19 vaccines should not be withheld from pregnant individuals who meet the criteria for vaccination based on priority groups. 

This means it is likely a good idea for pregnant mothers who are at an increased risk of getting COVID to get the mRNA vaccine.

What we do know is that pregnant mothers are at increased risk from side effects and complications if they get COVID.

They are more likely to be hospitalized, placed in the ICU, ventilated, and die than if they weren’t pregnant.

mRNA Vaccine - Pregnancy

12. Can Breastfeeding Mothers get the Vaccine?

Again – this decision should be made with the patient’s OBGYN and Pediatrician.

There is just not enough data studying this to make a sweeping recommendation.

It is unlikely that the vaccines would be unsafe for the baby, and there is a possibility of passing on some passive immunity obtained from the vaccine to a breastfeeding infant.

Passive IMMUNITY breast milk

13. Can those with Autoimmune Diseases get the Vaccine?

While there doesn’t appear to be any specific contraindications, this is something that should be discussed with the patient’s physician / Rheumatologist.

The risks of getting symptomatic COVID may be worse than the risks of getting the COVID vaccine.

14. Should Patients who had Symptomatic COVID get the Vaccine?

The idea is that if you had symptomatic COVID – you should have natural antibodies already for the virus – so why get the vaccine?

This is a decision you have to decide on with your Provider. It likely won’t hurt and could help, so the CDC is in favor or those who had COVID to also get vaccinated.

While it may be recommended to wait 90 days after symptomatic covid for the infection, this is not a rule and there is no specific timeline established.

This is more to allow those who have not built any immunity to receive the vaccine first.

You should get the vaccine after you recover from symptomatic COVID and when you feel it is appropriate.

Related Article: “These 8 COVID nursing tips could save your life”

15. What if you or your Patient doesn’t get the Vaccine?

As of today COVID has killed over 400,000 people in the US and 2.15 million people worldwide. This number is rising very quickly.

Even if COVID doesn’t kill you or your patients, it can cause many long-lasting side effects.

During an active COVID infection, it can cause multifocal pneumonia and respiratory failure leading to hospitalization, ventilation, and possibly death.

Severe COVID can also cause blood clots leading to pulmonary embolisms and embolic strokes.

It can cause inflammation of your brain and heart as well, leading to irreversible damage in some cases.

There have been observational studies done which show that up to one-third of patients who had symptomatic COVID had persistent symptoms after resolution of the virus. These include:

  • Fatigue
  • Dyspnea (Shortness of breath)
  • Chest Pain
  • Cough
  • Anosmia (loss of smell)
  • Ageusia (loss of taste)
  • More (joint pains, headaches, myalgias, etc)

There may still be other long-term side effects that we still don’t know about. 

So what’s riskier? Getting a vaccine that seems to be very safe and doesn’t seem to have any serious long-lasting side effects, or take your chances with getting COVID?

I can’t make that decision for you or your patients.

But if you do decide to get the vaccine, what can you expect?

16. If you get the Vaccine, What can you Expect?

You can expect to get 2 injections, 21 days apart with Pfizer or 28 days apart with Moderna.

The full efficacy seems to be established about 1-2 weeks after the second injection, depending on the vaccine (1 week after Pfizer, 2 weeks after Moderna).

These were the timelines studied in the clinical trials.

17. Can I Stop Wearing Masks and Social Distancing once I’m Vaccinated?

Well – no, not immediately.

Remember that even a 94-95% efficacy still leaves that 5-6% of people who will still get symptomatic COVID.

These people will likely be contagious, and they still could get severe COVID and have to be hospitalized or worse.

Secondly, both Pfizer and Moderna require 2 shots before full efficacy is expected. The body takes time to build up an antibody response. It can take 1-2 weeks after the second dose for full efficacy.

Additionally, it has not been proven by evidence that these vaccines prevent you from spreading COVID. The trials only prove that they are 94-95% effective at reducing symptomatic COVID.

That’s right. Even if you don’t get symptomatic COVID – you could possibly spread it.

mRNA vaccines - asymptomatic Spread

18. Could you get the COVID vaccine and be an Asymptomatic Spreader?

Theoretically, it is unlikely that you will be spreading the virus after vaccination.

Hopefully, your body has created an immune response and antibodies which will attack COVID before it can replicate and cause disease or be contagious.

HOWEVER – we don’t have the data to back this up, and there another important consideration – Mucosal Immunity.

We don’t know how well the antibodies penetrate the nasal mucosa. There is a possibility that the virus can still replicate in the mucosa of your nasopharynx.

While it may not cause symptomatic disease since you should have circulating antibodies – you might still spread it to others when coughing, sneezing, or even breathing.

This is something that we should have more data on soon.

This is why it is imperative to continue to wash our hands, wear our masks, and practice social distancing.

19. When will Herd Immunity be Established?

It is going to take some time for the majority of the US to become vaccinated.

This means we need about 70%+ of the population to be vaccinated or infected before some type of herd immunity can be expected and established.

Herd immunity occurs at different percentages of vaccinated/infected individuals based on each specific virus.

This number is unknown for COVID, but experts say at least 70% need to be vaccinated and/or infected for some type of herd immunity to protect us.

It is unlikely that mask mandates and social distancing will become a “thing of the past” until we get to this point.

20. Will the mRNA Vaccines Cover the New Strains?

Unfortunately, there are multiple mutated strains or variants popping up in the UK, Africa, and other places.

These strains are spreading fast as they are more contagious (30-70% more transmissible).

However, these don’t necessarily seem to be more deadly. However, with surges in COVID cases and hospitalizations, increased deaths could occur due to the burden put on the healthcare system.

As far as we know, these vaccines should be effective against these mutated variants.

However, preliminary data does suggest that the vaccines may not work as well against the South African variant! Just in case, Moderna has already begun production on a “booster shot” which would specifically target these variants.

21. How Long will Immunity Last from these mRNA Vaccines?

As mentioned above – complete immunity is not guaranteed.

However, if antibodies are created, it is unknown how long they will last.

What we do know is that immunity wanes over time. Those who get symptomatic illness tend to build a better immune response than those who get vaccinations.

Many patients who had symptomatic COVID in early 2020 still have antibodies – this is good news!

We don’t know how long immunity will last, and we don’t know how much further mutations will alter the effectiveness of the immunity.

22. Are there other Vaccines Available?

Pfizer and Moderna are mRNA vaccines which have already obtained emergency use authorization (EUA) from the FDA.

There are two other vaccines that may obtain approval as well. These are not mRNA vaccines. They include:

  • Johnson & Johnson, which uses adenovirus to carry genetic material for COVID
  • AstraZeneca, which uses a chimpanzee adenovirus to do this

These do not appear to be as effective as the mRNA vaccines, but may still prove helpful, and we must continue to follow the data.

Production and distribution of the mRNA vaccines will prove tough, and additional effective vaccines will be helpful!

So Should you or your Patient get the Vaccine?

That’s for you to decide, based on the data and taking into account what your physician or healthcare provider recommends.

Additionally, it is for your patients to decide based on informed consent.

It is not your job to judge them or tell them what to do. All you can do is offer evidence-based recommendations and up to date information, and allow them to make that decision for themselves.

You can also lead by example and get the vaccine for yourself, trusting the science and once again being that hero that we were once called in the beginning of this pandemic.

I think frontline workers and those with a high risk should seriously consider getting vaccinated.

As far as everyone else – that’ a decision you (or they) have to make, but the data looks promising and this could be our chance at returning to a state of semi-normalcy.

Note: If you want more information – you should follow Dr. Kat the Epidemiologist on TikTok! She creates great content backed in science on all things COVID and mRNA Vaccines!

Nurse - Vaccinated

I got my vaccine! Did you? Why or why not? Let us know in the comments below!

You might like: “These 8 COVID nursing tips could save your life”

References:

Pfizer / Moderna Studies:

Moderna Announces Primary Efficacy Analysis in Phase 3 COVE Study for Its COVID-19 Vaccine Candidate and Filing Today with U.S. FDA for Emergency Use Authorization

PFIZER AND BIONTECH CONCLUDE PHASE 3 STUDY OF COVID-19 VACCINE CANDIDATE, MEETING ALL PRIMARY EFFICACY ENDPOINTS

Safety and Efficacy of the BNT162b2 mRNA Covid-19 Vaccine (Pfizer)

Safety and Immunogenicity of SARS-CoV-2 mRNA-1273 Vaccine in Older Adults (Moderna)

Vaccine Info:

Coronavirus disease 2019 (COVID-19): Vaccines to prevent SARS-CoV-2 infection (UTD)

Facts about COVID-19 Vaccines (CDC)

Understanding mRNA COVID-19 Vaccines (CDC)

Vaccine Types

Anaphylaxis:

Allergic Reactions Including Anaphylaxis After Receipt of the First Dose of Pfizer-BioNTech COVID-19 Vaccine

Interim Considerations: Preparing for the Potential Management of Anaphylaxis After COVID-19 Vaccination

Bell’s Palsy:

FDA: Track Vaccine Recipients for Facial Paralysis

Pregnancy & Breastfeeding:

COVID-19 Vaccines and Pregnancy: Conversation Guide for Clinicians (ACOG)

Vaccination Considerations for People who are Pregnant or Breastfeeding (CDC)

Why COVID Vaccines are Falsely Linked to Infertility

Persistent COVID:

Coronavirus disease 2019 (COVID-19): Evaluation and management of adults following acute viral illness (UTD)

COVID-19 (coronavirus): Long-term effects (Mayoclinic)

Herd Immunity / Still Wear Masks:

Coronavirus disease (COVID-19): Herd immunity, lockdowns and COVID-19 (WHO)

Here’s Why Vaccinated People Still Need to Wear a Mask

How Long Does Immunity Last After COVID-19? What We Know

New Strains of COVID:

A New Strain of Coronavirus: What You Should Know

How Dangerous Are New COVID-19 Strains?

    COVID Cheat Sheet

    Everything you need to know about treating COVID pneumonia in the ER and Inpatient setting!

    COVID cheat sheet promotional image

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    13 Nursing Myths You Probably Fell For

    Dec 21, 2020 | 0 comments

    13 Nursing Myths You Probably Fell For

    [social_warfare]

    Not everything you learn on the job is factual, and there are many nursing myths that are still commonly believed and “passed on” today. While some myths are rooted in truth, other nursing myths don’t seem to have any evidence of substance to back them up. 

    There is nothing more embarrassing than learning something, teaching that to others, and then realizing that it’s not actually accurate!

    You might be aware of some of these, but there are other common nursing myths that you may not be aware of, so make sure you read all 13!

    Nursing Myths -Featured Image

    1. Hemolysis of blood

    One common nursing myth is that “leaving blood tubes sit for too long can cause hemolysis of the blood”, which is not true.

    When blood hemolyzes, the red blood cells “lyse” or split open. This lysis releases their intracellular contents and disrupts normal lab values.

    Remember that intracellular potassium is much higher than extracellular potassium. This means that hemolysis will cause false elevations in potassium. It also can falsely elevate magnesium, phosphorus, liver enzymes, ammonia, and the anion gap. It can falsely lower RBCs, hematocrit, PTT, and more!

    So obviously we don’t want the blood to hemolyze, and this common nursing myth assumes that by leaving the blood sit for too long at the bedside, this can cause or worsen this hemolysis.

    Hemolysis actually occurs when there is damage to the red blood cells, usually when being drawn into the tube due to collection technique. True causes of hemolysis include:

    • Drawing from an IV with poor blood return
    • Drawing from an old IV
    • Having the tourniquet on for an excessive amount of time or excessive clenching of fists
    • Vigorous shaking or mixing of the tubes. Tubes should be gently turned 5-10 times to mix the anticoagulant.
    • Needle or catheter partially occluding the vein wall (you may feel vibration)
    • Tubes that aren’t filled completely

    Blood drawn from IVs are much more likely to hemolyze, but finding a site with great blood return and large veins should help. That is one more reason why the AC is a great choice for the ER to place new IVs – they’re great for blood return!

    As it turns out, while leaving blood sit too long shouldn’t cause hemolysis, leaving blood to sit too long CAN alter results, and this all depends on each type of tube and the actual lab test. But regardless – this doesn’t cause hemolysis.

    Sometimes blood tubes are drawn and left at the bedside, mainly within the ED. However, these tubes need to be run within a certain amount of time. The following blood tubes for common blood tests can be kept at room temperature with accurate results for:

    • CBC: up to 24 hours
    • CMP: should be centrifuged within 2 hours for accurate glucose and potassium results
    • PT/PTT: up to 2 hours if on heparin, otherwise up to 4 hours
    • D-dimer: up to 8 hours

    Nursing Myths - hemolysis

    2. The MONA Nursing Myth

    As nurses, we encounter those with chest pain all the time. In school we are taught the acronym MONA – Morphine, Oxygen, Nitroglycerin, and Aspirin. These are our “treatment” for those with chest pain when it is suspected to be cardiac.

    While this isn’t completely wrong, its oversimplification, and sometimes these treatments can actually harm the patient!

    The Nursing Myth: Oxygen

    When a patient comes in with chest pain, we traditionally throw them on the monitor, apply oxygen, and anticipate to give nitro and aspirin once ordered.

    Don’t fall into the trap of applying oxygen to every patient with chest pain, even if you suspect a true heart attack! First, check their pulse ox and apply oxygen only if their SPO2 is <94% (some sources even recommend 90%).

    This is because too much oxygen can be bad for the patient. Hyperoxia has been shown to cause direct vasoconstriction of the coronary arteries.

    If the patient is significantly short of breath or has CHF, it probably isn’t a bad idea to apply some oxygen, but just make sure it stays between the 94-99% range.

    Will this kill the patient? Probably not – but no benefit has been found when applying oxygen to a normoxic patient, and it could potentially harm them. So only apply oxygen if absolutely necessary.

    Morphine

    In addition to nitro, morphine can be given for chest pain and was traditionally taught as a mainstay of treatment. However – morphine given to patients with heart attacks has been shown to potentially cause harm!

    In fact, patients with NSTEMI who were treated with morphine were found to have an overall increased chance of dying. Scientists aren’t really sure why – but they think it may interfere with the antiplatelet effect of Plavix, Brlinta, etc.

    Can morphine still be given? Of course! But should probably be limited to those with severe pain after the other measures have already been implemented.

    Nursing Myth - MONA

    Related Content: Cardiac Lab Interpretation (Troponin, CK, CK-MB, and BNP)

    3. The Bigger IV the Better

    Nurses love to place large IV catheters, especially in the ED. And oftentimes an 18 gauge is great peripheral access to obtain in those with trauma or who may need large volumes of fluid or blood.

    However, an 18g should not be the standard IV size that you place in every patient. Most fluids and medications can be given through 20g and even 22g. But what’s the harm of placing a 16 or an 18g just because you are confident that you can?

    First off, it may be more difficult to place and lead to failure. Second, it will be more painful for the patient. Lastly and probably most importantly – bigger IV catheters have higher rates of mechanical phlebitis and thrombophlebitis.

    Nursing Myth - Mechanical phlebitisInstead of placing the largest IV catheter that you are able to, you should instead place the size that you think will be needed for the anticipated therapy. As a general rule of thumb:

    • 18g: If suspecting large volumes of fluids may be needed (codes, hypotension, critical patients)
    • 20g: If you need IV access for boluses, maintenance fluid, IV pushes, CT angiography (in an AC line), or blood transfusion
    • 22g: If you need IV access for boluses, maintenance fluids, IV pushes, or other IV medications

    You can never go wrong with a 20g, and true emergencies will benefit from an 18g.

    Related Articles:

    • How to Start an IV
    • 10 IV Insertion Tips for Nurses

    4. A Nurses Nose Knows CDIFF

    Clostridium Difficile is a bacterial infection of the intestines which can cause severe diarrhea, hospitalization, severe inflammation of the colon, and even death in older at-risk patients.

    If you have ever worked in the hospital – you have had experience with CDIFF. The profuse diarrhea, the putrid smell, the patients who just seem to get it over and over again. CDIFF can be very difficult to completely get rid of.

    Nursing Myths - CDIFOne thing my preceptor on my first nursing unit taught me was that “CDIFF has that smell”. And while I agree that it often does have a smell, are nurse’s noses sensitive enough to tell regular diarrhea from CDIFF diarrhea?

    There were previous studies that seemed to suggest that a nurse could tell the difference. However, when conducted in a blinded controlled laboratory setting, nurses were unable to tell the difference between CDIFF stool and regular diarrhea. They did not perform better than chance.

    The nurse’s individual experience or confidence in detecting the smell played no impact on their results.

    So what does this mean? Well – you May be able to smell CDIFF, but you should always notify the physician/APP and obtain a sample to send to the lab to be safe. If the patient has liquid diarrhea and no stool sample has been sent, don’t assume it isn’t CDIFF just because “it doesn’t smell like it”.

    5. If a Patient Leaves Insurance Won’t Cover Their Visit

    When I was a new nurse, I was taught that “If a patient leaves AMA – insurance may not cover their visit”. This was something I would pass onto my patients – not to try and manipulate them to stay, but instead to make sure they understood there might be financial consequences of leaving AMA.

    What I didn’t know was that this just isn’t true. There is simply no basis for this claim. Leaving AMA does not impact insurance coverage.

    Over half of medical residents and almost half of attending physicians commonly believed this myth, and nurses are no exception.

    We should be intentional about explaining the consequences of leaving AMA. This includes the patient getting sicker or potentially dying as a result of refusing medical treatment. However, we should not mention insurance coverage since this is not true and can manipulate the patient into staying when that is against their wishes.

    6. High Fevers Cause Seizures

    Many nurses, especially those who work in the ED, have probably witnessed febrile seizures. These are common in children and often associated with high fevers.

    Many nurses and medical professionals correlate high fevers with seizures. But what if I were to tell you that the high fever does not actually cause the seizure, or at least, not alone?

    The true “trigger” of the seizures seems to a rapid rise in temperature, with high fevers lowering the seizure threshold. Yes, the higher the fever the more likely the seizure will occur, but the trigger seems to be the rapid rise in temperature instead of the fever itself.

    Fevers can also lead to insensible water losses, dehydration, and hyponatremia, which all contribute to lowering the seizure threshold as well.

    Often febrile seizures accompany viral infections and can even occur after certain vaccinations. The good thing is these febrile seizures are brief and usually have no long-lasting effects.

    And speaking of fevers – you don’t always need to treat them! Sure – high fevers can be treated to alleviate symptoms and prevent dehydration. Treating high fevers >102 may even help prevent febrile seizures in young children.

    But remember, there is some utility in not treating fevers, especially low-grade as this is a natural defense mechanism that your body uses to fight the infection. So if the patient can stay hydrated – an antipyretic is not always absolutely necessary.

    7. Pseudoseizures are Faking It!

    Speaking of seizures – sometimes patients have a “seizure” and.. well.. we don’t believe them. These are termed pseudoseizures – because they aren’t real seizures.

    Now – not all seizures are the classic tonic-clonic Grand Mal seizure, but sometimes people really do have “fake seizures”. But does that mean they are faking it?

    Nursing Myth -PseudoseizureMaybe not! Those with a significant history of psychological disorders, a history of trauma, and poor coping mechanisms can have what’s called “Psychogenic nonepileptic seizures”. These are often psychosomatic and the patient may not realize that they are indeed not true seizures.

    Now, do some people actually fake it? Sure – they might do it for attention or to get out of a DUI (yeah… it happens).

    But just because someone is having a “fake seizure” doesn’t mean that it’s fake for them. Although it may seem difficult at times – try to maintain compassion and understanding, even when it might seem like they’re wasting your time.

    Related Content: 10 Nursing Hacks Every ER Nurse Should Know

    8. Flu Shots Cause the Flu

    While this one seems pretty basic – I’m a little dismayed by how many RNs that I know personally and professionally seem to perpetuate this nursing myth.

    There is no possible way that the flu shot can cause the flu. Let me repeat that – there is NO possible way that the flu shot can cause the flu.

    The IM Flu vaccinations contain inactivated virus or a viral protein, both of which cannot replicate or cause disease. It is physically impossible for them to cause influenza.

    However, common side effects after the injection include local site reaction, body aches, low-grade fevers, nausea, and fatigue. These are short-lived and probably represent your immune system creating antibodies.

    If you do actually get full-blown flu shortly after the vaccination, there are multiple explanations:

    • You were exposed before the shot
    • You were exposed before you created significant antibodies, which takes about 2 weeks from the date of vaccination
    • You were infected with a strain that the vaccination didn’t cover
    • You were infected with a strain that the vaccine did cover, but you still developed illness. This illness was likely less severe than it would have been without the vaccination.

    While not nearly as common, a live-attenuated flu vaccination can be given, but this is intranasal and not via intramuscular injection. This technically can cause the flu, although unlikely to call full-blown illness.

    The flu vaccination is always recommended for healthcare providers, as the flu kills between 12-60K people in the US per year (meanwhile COVID has claimed over 300K within the last 6 months… but it’s “just the flu” I guess).

    Nursing Myth - Flu Vaccines

    9. Vancomycin Broad-spectrum?

    Vancomycin is a “heavy-hitter” antibiotic that we commonly give within the hospitals for MRSA infections. Because of this, it is commonly considered broad-spectrum. However, Vancomycin is actually pretty narrow-spectrum.

    The term “broad-spectrum” indicates that the antibiotic has a wide range of bacteria that it can kill. This includes gram-positive organisms, gram-negative organisms, aerobes, and/or anaerobes.

    Vancomycin works wonders for gram-positive organisms, but that’s really it. Yes, this includes MRSA, but it doesn’t really have any activity against gram-negative organisms. Because of this, it is actually a narrow-spectrum antibiotic. This is why you will usually see this ordered with another antibiotic at the same time. But why does this even matter?

    In sepsis, it is important to give antibiotics STAT, and it’s recommended that you give the broad-spectrum antibiotic first. This ensures that antibiotics that are more likely to cover the bacteria are given in a timely manner.

    Vancomycin can take a while to infuse (1-2 hours), and a broad-spectrum antibiotic like Zosyn or Cefepime should have been given first and infuses quickly (over about 30 minutes).

    Related Content: 6 Steps for Sepsis Management

    10. Toradol Works Better than Ibuprofen

    Toradol is an IV or IM medication that we commonly give within the ED and inpatient settings. It’s an injection form of an NSAID, and due to this I tell my patients “it’s like IV ibuprofen”.

    Since it is an NSAID, it does decrease inflammation, help with pain, as well as reduce fever. Toradol tends to work great for migraines, kidney pain, arthritic/orthopedic pain, etc.

    Since given via IM injection or via IV, most people automatically assume it will work better than a pill. This isn’t poor logic either as many medications work better when given intravascularly as they essentially have 100% bioavailability and do not undergo the “first-pass effect” through the liver.

    Interestingly enough, studies do not show that IV/IM Toradol is any more effective at reducing pain than PO ibuprofen.

    There also appears to be a ceiling dose of Toradol for pain, which is about 10mg IV. This means that a 30mg IV Toradol injection is no more effective at alleviating pain than a 15mg injection.

    Don’t forget that NSAIDs inhibit prostaglandin synthesis. These prostaglandins are important in protecting your stomach as well as maintaining perfusion to your kidneys. This is why too much NSAID, whether PO or IV, should be avoided in those with a history of PUD, upper GI bleed, or kidney disease.

    Nursing Myth -Toradol better than ibuprofen

    Related Content: Opioid Alternative Analgesics in the ER

    11. Normal Saline Always Helps Hyponatremia

    When a patient’s sodium level is low (<135 mEq/L), called hyponatremia – this is often due to dehydration. A simple treatment is to give them Normal Saline which usually does improve their sodium levels. And this is the most common cause of mild hyponatremia = dehydration.

    But it’s not always that simple. Sodium is a complicated electrolyte that can be influenced by many different factors. To simplify the treatment of hyponatremia, it depends on fluid status:

    • Hypovolemic: Give Fluids (NS)
    • Hypervolemic: Restrict Fluids and give diuretic like lasix
    • Euvolemic: Do not give fluids and consider SIADH as a cause

    Serum osmolality is often taken into account, and urine electrolytes/osmolarity can also help. It is not always this easy, and a nephrologist can help determine the cause and treatment.

    In general, if you see mild decreases in sodium with elevations in renal function and a history that is consistent with decreased PO intake or possible dehydration – you won’t go wrong administering a 500-1000mL bolus followed by a slower maintenance rate and following the labwork.

    Remember that sodium levels should always be corrected SLOWLY, with a goal correction of about 4-6mEq/day, and no more than 8 mEq/day. If corrected too quickly, this can cause irreversible brain damage called Osmotic Demyelination Syndrome.

    Don’t forget that high glucose elevations will falsely lower the sodium level! You can use a calculator to make the correction here!

    Related Content: Intravenous Fluids Breakdown

    12. Respiratory Rate Isn’t Important

    One of the 5 vital signs is the respiratory rate (don’t get me started on the 6th vital sign). For some reason, it has become commonplace to not count respirations and simply chart “16-18”.

    Why is this done? Well first off, nurses and nurse’s aides are busy, and sitting and counting for 30-60 minutes just seems like a waste of time. This is reinforced when the patient appears well, is non-toxic appearing, and has nothing respiratory going on.

    Honestly – I get it. When I was a floor nurse I did the same thing. But sometimes it is especially important to count respirations, even when you might not realize it.

    When I was a new nurse on a Med-Surg floor, I had a patient who I took over at 11 pm. I knew something didn’t look right with her, but I wasn’t quite sure what. She had a flushed face and was breathing about 30 rpm, but she denied any symptoms and her vital signs were fine – at least the ones we actually checked.

    Long story short – in the morning she was found to have been in severe metabolic acidosis secondary to renal failure, with a pH of 7.1. Her increased respiratory rate was actually respiratory compensation to try and breathe off some CO2 to compensate for her acidosis. So even though she had “nothing respiratory” going on, it was still an important vital sign that I should not have overlooked.

    Please be mindful to count accurate respiratory rates on people who are breathing fast or have any type of respiratory complaint, especially with COVID.

    Best practice is to count respirations for a full minute since respiration patterns tend to fairly irregular. However, any counting is better than none. You can count for 10 seconds and multiply by 6, count for 15 seconds and multiply by 4, count for 20 seconds and multiply by 3, or count for 30 seconds and multiply by 2. The longer you count, the more accurate the rate will be.

    Nursing Myth - Respirations

    Related Content: 5 Vital Sign Errors to Avoid

    13. Don’t Let Concussions Sleep

    After mild-to-moderate trauma to the head, many people develop concussions. This is a common presentation to the ED. There is a running myth that those with concussions should not be allowed to sleep as “they may never wake up”.

    When my brother was in high school he was a baseball pitcher, and he got hit in the head and suffered a pretty significant head injury. I vividly remember trying to keep him awake in the backseat for fear of him “not waking back up”. Now, this might not be a great example because he did end up having a subdural hematoma… but regardless – keeping someone awake won’t really help them.

    The worry is thought someone who falls asleep and actually has a brain bleed will die in their sleep if no one checks on them. Since they are sleeping, no one will recognize their decreased neurologic status.

    While this could happen, it is unlikely to occur from a concussion. However – it is important that patients be evaluated by medical professionals and have a neurological exam and possibly a CT of the head.

    Those who should get a CT of the head include:

    • Nursing Myth - ConcussionGlasgow Coma Scale <15 or any neuro deficit
    • Suspected skull fracture
    • >1 episode of vomiting or seizures
    • >65 years old or anticoagulant use
    • Amnesia
    • Dangerous mechanisms (like a pedestrian hit by a car)

    If you are discharging a patient who had a CT of the head which did not show any bleed, there is no indication for them to “stay awake” or be checked on throughout the night, as you’ve essentially ruled out a head bleed.

    Yes, delayed bleeds can occur but this is not likely to happen in those at low-risk with concussions. If they are cleared for discharge, they should be encouraged to rest as this will help them to heal.

    Related Content: The Cranial Nerve Assessment for Nurses

    And those are the 13 nursing myths that you probably fell for, or at least maybe you fell for one or two! Don’t let these nursing myths be perpetuated, as we should always strive for accurate and excellent education of nursing professionals!

    Are there any other nursing myths I didn’t mention? Leave them below in the comments!

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    References:

    Hemolysis

    Geisinger Medical Lab Specimen Collection Manual and Test Catalog

    Hemolysis: What is it and how to prevent it

    How Long can we Store Blood Samples: A Systematic Review and Meta-Analysis (2017)

    Morphine and Oxygen in Heart Attacks

    Overview of the acute management of ST-elevation myocardial infarction (UTD)

    Oxygen therapy in acute coronary syndrome: are the benefits worth the risk? (2013)

    Air Versus Oxygen in ST-Segment-Elevation Myocardial Infarction (2015)

    CDIFF

    The Nose Knows Not: Poor Predictive Value of Stool Sample Odor for Detection of Clostridium difficile (2013)

    AMA Insurance Coverage

    Know Your Rights: Understanding Hospital Discharge Against Medical Advice

    Financial Responsibility of Hospitalized Patients Who Left Against Medical Advice: Medical Urban Legend? (2012)

    Febrile Seizures

    Clinical features and evaluation of febrile seizures (UTD)

    Febrile Seizures Fact Sheet

    Pseudoseizures

    Psychogenic nonepileptic seizures (UTD)

    Psychogenic nonepileptic seizure (Wikem)

    Influenza Vaccine

    Misconceptions about Seasonal Flu and Flu Vaccines (CDC).

    Seasonal Flu Shot (CDC)

    Seasonal influenza vaccination in adults (UTD)

    Toradol vs Ibuprofen

    Intramuscular ketorolac vs oral ibuprofen in emergency department patients with acute pain (1998)

    Myth: Parenteral ketorolac provides more effective analgesia than oral ibuprofen (2007)

    Hyponatremia

    Overview of the treatment of hyponatremia in adults

    Concussions

    MYTH: SLEEPING SAFE AFTER SUFFERING A CONCUSSION

    https://www.concussion.org/news/concussion-myths-debunked/

     

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    Intravenous Fluids: Types of IV fluids

    Nov 25, 2020 | 28 comments

    Intravenous Fluids: Types of IV fluids

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

    Author | Nurse Practitioner

    Intravenous fluids are commonly used in hospitals and emergency departments. There are many different types of IV fluids, which are used both as IV boluses as well as maintenance fluids. Understanding the difference between the types of IV fluids can be challenging, but as a nurse, it is important to understand.

    Intravenous fluids featured image

    Indications for Intravenous Fluids

    Intravenous fluids are very commonly used in healthcare settings. Most frequently, IV fluids are used to hydrate those with dehydration. Additionally, they can be used to support blood pressure in those with hypotension or sepsis.

    IV fluids can also be used as maintenance fluids for those who are not able to intake enough hydration throughout the day.

    In the ER, I commonly order Intravenous fluid to those with nausea and vomiting, diarrhea, dehydration, acute kidney injury, abdominal pain, headaches, bleeding, or infections.

    Maintenance Fluids vs IV Bolus

    Maintenance fluids are intravenous fluids that are run at a slower rate, usually to account for decreased PO intake or expected fluid losses. Patients who are NPO (nothing by mouth) are commonly ordered maintenance fluids, as well as those with ongoing fluid losses.

    Maintenance Fluids

    Ongoing fluid losses commonly occur with various medical conditions. Fevers commonly require increased maintenance fluid, as they cause “insensible water losses” from sweating and overall increased metabolism.

    Those experiencing frequent vomiting or diarrhea require increased fluid to account for their ongoing water losses in their vomit or stool. The same goes for those with drains experiencing significant drainage.

    Those with burns or pancreatitis often require a large volume of fluids.

    Those admitted with dehydration, mild hyponatremia, or acute renal failure will usually require maintenance fluids in order to slowly correct their hydration, sodium levels, and renal function.

    When a patient is NPO, maintenance fluids keep the patient hydrated. To calculate maintenance fluids when a patient is NPO, you can take the patient’s body weight in Kilograms, and use the following equation: (Kg – 20) + 60 = mL/hr. (Ref).

    Please note that this is not a hard rule. Those with ongoing fluid losses and various medical conditions may require a faster rate, and those who are older or with CHF may require slower rates.

    Clinical Note: Just because a patient is NPO after midnight does not mean that they need maintenance fluids ordered. Do you usually drink water in the middle of the night while you sleep?

    IV Bolus

    IV boluses are intravenous fluids given rapidly over a short amount of time. This is most frequently used within acute care settings such as the ER or the ICU in those who are unstable with low blood pressure. Giving an IV bolus helps support blood pressure and correct hypotension.

    It is common for a 1 liter IV bolus to be ordered on patients initially presenting to the ER, as fluids can help many different conditions. You will commonly see between 1-3 Liters of IV boluses, for conditions such as dehydration, sepsis, shock, migraines, abdominal pain, and n/v/d.

    In sepsis, 30ml/kg boluses are commonly ordered. If a bolus is ordered, hang the bolus (usually 1L bags) by gravity and open the clamp wide open. Make sure the patient keeps their arm straight if the IV is in the AC, otherwise the bolus won’t flow.

    Clinical Note: If using a pump, run the fluid at 999ml/hr. Please note that in true emergencies this may not be fast enough, and using gravity and/or a pressure bag will infuse the fluid more quickly.

    Important Fluid Concepts to Understand

    Before diving into the different types of IV fluids, there are a few important underlying concepts we need to understand.

    Tonicity, Osmolarity, and Osmosis

    Tonicity refers to a fluid’s ability to move fluid into or out of cells and is related to osmolarity – which is the total concentration of solutes within a solution. The more solutes, the higher the osmolarity.

    In the body, water shifts into or out of our cell through a semi-permeable membrane – the cell wall. This means water freely flows through it, but larger solutes do not such as our electrolytes (sodium, chloride, potassium, etc).

    Osmosis occurs, which is when water flows from a higher osmolarity to a lower osmolarity to “balance” out the concentrations of each side, in this case inside and outside of the cell.

    Isotonic, Hypotonic, and Hypertonic Fluids

    Isotonic fluids are IV fluids that have nearly the same osmolarity as intracellular fluid. This means that this IV fluid should not cause any significant net fluid shifts into or out of cells.

    Hypotonic fluids are IV fluids that have a lower osmolarity than inside the cells, which causes net fluid shifts into the cells. This leads to cellular swelling, which can be deadly in certain conditions like severe head injuries and increased Intracranial Pressure (ICP).

    Hypertonic fluids are IV fluids that have a higher osmolarity than inside the cells, which causes net fluid to shift out of the cells. This leads to cellular dehydration and shrinking.

    Types of IV Fluids

    There are many different types of IV fluids that can be ordered, and knowing the difference between them is important. Certain intravenous fluids are useful for certain situations, and others can be harmful.

    As a nurse, it is important to know the basics. As a nurse practitioner, you will be responsible for ordering these fluids so this becomes even more necessary to understand.

    Normal Saline (0.9% NS)

    Normal Saline, NS, or NSS is the standard fluid given in both boluses and as maintenance fluids. Normal saline contains sodium chloride (NaCl) and is isotonic. This means when given through the IV, there should be no net movement of fluid or electrolyte into or out of the cells.

    This ensures that there is no unnecessary swelling or shrinking of the cells when infused. Normal saline is the cornerstone intravenous fluid because it can be given for most situations, including:

    • Hydration
    • Maintenance Fluids
    • Hyponatremia
    • Hypotension or Shock
    • Sepsis
    • with Blood transfusions

    Normal saline is cheap and does not result in allergic reactions, and almost all medications are compatible.

    Use caution with heart failure or end-stage renal disease, and those on dialysis or in acute fluid overload should probably not receive IV fluids.

    A large amount of Normal Saline (3-5+ liters) can cause significant hyperchloremic non-anion gap metabolic acidosis, especially if the patient has renal failure. This can worsen their outcomes within the hospital.

    As with any IV fluid, continually monitor fluid status by making sure the patient is not having worsened lower extremity edema or new rales/crackles in the lungs.

    If the patient develops sudden shortness of breath during IV fluid administration, consider fluid overload and flash pulmonary edema as a potential cause, especially with a history of heart failure.

    You should always be assessing for IV infiltration as well. If there is significant swelling, blanching, and coolness near the IV site – you probably need to remove it and start a new IV.

    Related articles:

    • “Arterial Blood Gas (ABG) Interpretation”
    • “Cardiac Lab Interpretation (Troponin, CK, CK-MB, and BNP)”

    Lactated Ringers (LR)

    Lactated Ringers (LR) is another isotonic fluid that is commonly given. LR is the fluid of choice by surgeons, and some consider LR to be slightly better than NS, but the general consensus is that ‘One is not better than the other’.

    Lactated Ringers differ from NS in that it not only has sodium chloride, but also has sodium lactate, potassium chloride, and calcium chloride.

    So why choose LR over NS? LR is buffered and won’t cause the hyperchloremic metabolic acidosis that large volumes of NS can. Some studies showed improvement in renal function in critically ill patients who were on LR as opposed to NS, but the evidence is mixed.

    LR can be given for all of the indications that NS can be given, including:

    • Dehydration
    • Maintenance Fluids when NPO
    • Ongoing fluid losses
    • Sepsis
    • Allergic Reactions

    LR is preferred over NS in certain situations, including:

    • Pancreatitis
    • Burns
    • Surgical patients (surgeon preference)
    • Sepsis

    LR should be avoided in:

    • Severe liver or renal failure
    • Metabolic alkalosis > 7.5
    • Hyperkalemia or Hypercalcemia
    • Blood transfusions (If run in the same line can cause precipitation)

    As with any fluid administration, be on the lookout for fluid overload as well as local site reactions including infiltration or phlebitis.

    Side Note: LR contains sodium lactate, not lactic acid. However, giving LR during sepsis can mildly influence the lactic acid level (about .9 mmol/dL), but this does not actually worsen the sepsis, and has actually giving LR has been shown to indicate lower mortality overall. Interestingly enough, NS also seems to elevate Lactic levels within in the blood. 

    Intravenous Fluids IVF - Isotonic fluids

    Half Normal Saline (0.45% NS)

    Half normal saline (.45% NS) has half the tonicity of Normal saline. This means Half-NS is hypotonic, so the IV fluid has a lower osmolarity than the fluid inside the cells.

    This means that half normal saline will cause fluid to shift inside the cells, causing the cells to swell. This can be good in certain situations, and very bad in others.

    Half-Normal Saline is rarely given alone, but usually in combination with Potassium or dextrose. However, you may see slower rates given in conditions which cause significant cellular dehydration, such as with:

    • Hypernatremia
    • Severe DKA

    Half-Normal saline, when run alone, is typically the wrong choice for most other scenarios as it can deplete intravascular volume and cause cellular edema. Hypotonic fluids are especially bad when it comes to:

    • Head injuries or increased ICP
    • Trauma
    • Burns
    • Liver disease

    When given, make sure the patient’s sodium levels are monitored daily, as this can cause hyponatremia.

    Intravenous Fluids IVF - Hypotonic fluids

    Hypertonic Saline (3% NS)

    Hypertonic saline is given with severe hyponatremia or with increased intracranial pressures.

    Hypertonic saline is carefully and selectively given, as correcting sodium too quickly can lead to osmotic demyelination syndrome, causing irreversible neural damage.

    If a patient has severe hyponatremia and symptoms consistent with cerebral edema, then hypertonic saline should be administered. These symptoms include:

    • Seizures
    • Severe headaches
    • Decreased LOC
    • Tremors

    The dose is usually a 100mL bolus given over 10 minutes (a rate of 600ml/hr), which can be repeated twice if needed.

    Additionally, hypertonic saline can be given in the setting of severe head injury to reduce intracranial pressure.

    If your patient is ordered hypertonic saline, this needs to be on a pump, and the patient needs to be hooked up to the monitor and have frequent neuro checks. Seizure precautions should also be taken if severe hyponatremia is present.

    Related article: “The Cranial Nerve Assessment for Nurses”

    Hypertonic Fluids

    Dextrose-Containing Solutions

    Dextrose can be added to any of the fluids mentioned above, as well as to water. Dextrose solution is usually ordered for:

    • Hypoglycemia
    • Maintenance fluids

    Dextrose is osmotically active, meaning it does cause the fluid to increase its tonicity, and will lead to net fluid shifts out of the cells. However, dextrose is rapidly metabolized, so the effective osmolarity tends to be higher than the base fluid, but lower than the calculated osmolarity.

    Common dextrose solutions include:

    • D5W: Dextrose 5% in Water
    • D10W: Dextrose 10% in Water
    • D5NS: Dextrose 5% in NS
    • D5 1/2 NS: Dextrose 5% in 1/2 NS
    • D5LR: Dextrose 5% in LR

    Overall, there is little evidence that dextrose with NS has any benefit or harm when compared to saline alone. However, dextrose should probably be added in:

    • Hypoglycemia
    • Alcohol intoxication
    • Starvation ketosis

    Dextrose should not be used in:

    • Hyperglycemia
    • Hypokalemia

    An amp (25gm) of 50% Dextrose (D50) is often given as an IV push medication to treat profound hypoglycemia or in conjunction with IV insulin to lower potassium levels.

    D5W and D10W are often used for slow correction of chronic hypernatremia, or when hyponatremia has been too-rapidly corrected. It is often commonly found mixed with certain medications.

    A patient on dextrose-solution should have their blood sugar monitored, as well as their electrolytes as with any IV fluid. Dextrose-containing solutions should not be given in boluses unless as described above with D50.

    Potassium-containing Solutions

    Sometimes potassium may be added to each liter bag of fluids. Potassium may be added to maintenance fluid in:

    • Hypokalemia
    • Ongoing potassium losses
    • DKA or severe hyperglycemia

    Potassium is as osmotically active as sodium, so this will increase the osmolarity and cause the fluid to be more hypertonic.

    This means that adding potassium to an isotonic fluid will make it hypertonic, so may not be a good choice in those with cellular dehydration like in DKA.

    In these instances, adding potassium to a hypotonic base fluid such as D5NS with potassium is a great alternative option.

    Remember that potassium should NEVER be used as a bolus. IV administration should not exceed 10mEq/hour in most situations, or 20mEq/hour in critical situations with cardiac monitoring and preferably a central line.

    Related Article: “9 Nursing Medication Errors that KILL”

    Bicarbonate-containing Solutions

    Sometimes Bicarb can be added to IV fluids, in order to assist with significant metabolic acidosis. This is not super common outside of the ICU.


    And that sums up IV fluids! Hopefully you found this article helpful. If you have any unanswered questions, please comment down below!

    References:

    Rochwerg, B. et al (2014). Fluid resuscitation in sepsis: a systematic review and network meta-analysis. Annals of internal medicine, 161(5), 347–355. https://pubmed.ncbi.nlm.nih.gov/25047428/

    Sterns, R. H. (2020). Maintenance and replacement fluid therapy in adults. In T. W. Post (Ed.), UpToDate. https://www.uptodate.com/contents/maintenance-and-replacement-fluid-therapy-in-adults

    Wilkins, L. W. (2005). Fluids and electrolytes made incredibly easy. Lippincott Williams & Wilkins.

    Zitek, T., Skaggs, Z. D., Rahbar, A., Patel, J., & Khan, M. (2018). Does Intravenous Lactated Ringer’s Solution Raise Serum Lactate?. The Journal of emergency medicine, 55(3), 313–318. https://pubmed.ncbi.nlm.nih.gov/25047428/

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    The Cranial Nerve Assessment for Nurses

    Oct 31, 2019 | 4 comments

    The Cranial Nerve Assessment for Nurses

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    The cranial nerve assessment is an important part of the neurologic exam, as cranial nerves can often correlate with serious neurologic pathology. This is important for nurses, nurse practitioners, and other medical professionals to know how to test cranial nerves and what cranial nerve assessment abnormalities may indicate. This becomes especially important when evaluating potential new strokes.

    In school, cranial nerves tend to be something you memorize and then forget the day after the test. But they are important in testing a patient’s neurologic status, as an abnormality in a cranial nerve can indicate a central lesion (stroke, tumor, bleed, etc).

    Every nurse should at the least know how to do a basic cranial nerve assessment, specifically the visual acuity and pupillary light reflex. When evaluating a stroke, The NIH scale is a method to evaluate the severity of a stroke. This scale walks you through evaluating many of the cranial nerves, but not all of them. If you want to feel confident when you chart “Cranial nerves II-XII grossly intact”, then keep reading!

    Table of Contents

    CN 1: Olfactory Nerve
    CN2: Optic Nerve
    CN3: Oculomotor Nerve
    CN4: Trochlear Nerve
    CN5: Trigeminal Nerve
    CN6: Abducens Nerve
    CN7: Facial Nerve
    CN8: Vestibulocochlear Nerve
    CN9: Glossopharyngeal Nerve
    CN10: Vagus Nerve
    CN11: Accessory Nerve
    CN12: Hypoglossal Nerve

    1. The Olfactory Nerve (CNI)

    The olfactory nerve is responsible for the sense of smell. Although rarely tested in practice, alterations in smell can be caused by serious intracranial pathology (brain tumors, strokes, TBI), neurodegenerative diseases like Alzheimer’s, Parkinson’s, or MS, or benign and transient causes such as the common cold.

    If both branches of the olfactory nerve are damaged, this can lead to permanent anosmia (loss of smell) and can lead to food tasting bland and decreased appetite. In most individuals, the sense of smell decreases over time, with up to 75% of individuals older than 80 have some degree of anosmia.

     How to test the Olfactory Nerve

    The olfactory nerve is almost never tested within an acute care setting such as in the hospital. However, this is sometimes tested in outpatient neurology offices. To test the olfactory nerve, blindfold the patient and have them smell and identify common scents such as vanilla, cinnamon, coffee, or peppermint while covering up one nostril at a time. Do not use ammonia or alcohol as these can trigger intranasal trigeminal nerve receptors and bypass the olfactory nerve.

    2. The Optic Nerve (CNII)

    The optic nerve is the second of the cranial nerves and is responsible for vision. This nerve transmits signals perceived in the retina and cones of the retina to the occipital lobe. This is commonly tested within the clinical setting and for a variety of presentations.

    Partial or complete loss of vision can be caused by conditions such as:

    • Diabetes
    • Intracranial pathology (ischemia, stroke, tumors)
    • Inflammation or infection of the eye
    • Toxicity

    How to test the Optic Nerve

    When testing the optic nerve, you need to examine the visual fields, the visual acuity, and the pupillary light reflex. All three are an important part of the cranial nerve assessment, although the pupillary light reflex involves cranial nerve 3 as well.

    Testing the Visual Fields (II)

    If the patient loses part of their vision on one side, it is termed partial hemianopia, and if they lose complete vision on one side it is complete hemianopia. There are a few different ways to test visual fields, but here is an easy way. Stand one arm length away from the patient and ask them to cover up one eye or do it for them if they are unable. Close your own eye on the same side. Now hold up numbers with your fingers at each of the four corners of their vision. Once satisfied, test the other eye.

    Testing the Visual Acuity (II)

    Nurses often assess visual acuity, and most emergency departments will have a Snellen eye chart to use. The distance the patient stands depends on the visual acuity chart (it should say). If you do not have easy access to this, there is an app you can get on your phone which is super helpful!

    Have the patient stand the appropriate distance away and have them cover up one eye. Do not have them forcibly close the eye as this can somewhat inhibit their ability to see out of their open eye. Ask the patient to read the 20/20 line on the chart. On a standard Snellen eye chart, this would be 20 feet away. If the patient gets more than half wrong, move onto the line above. Stop once the patient gets over 50% right. Mark this down and test the other eye. If they wear glasses – have them wear their glasses for this as well!

    Pupillary Light Reflex (II, III)

    The pupillary light reflex tests both cranial nerves II and III. First, inspect both pupils and make sure they are equal in size and shape. Then dim the lights if possible and shine a penlight directly into the right eye. Both pupils should constrict and maintain symmetry. Note if they are brisk or sluggish and if they are symmetric. Remove the light source and watch both eyes dilate equally as well. Do the same for the left eye.

    3. The Oculomotor Nerve (CNIII)

    The oculomotor nerve controls the majority of the extraocular muscles. It is primarily responsible for eye movement, eyelid movement, and pupillary constriction. If there is any oculomotor nerve impairment, there will be a pupillary dilation, ptosis (drooping eyelid), and outward deviation of the eye – termed abduction. When a patient has diplopia (double vision), it is often due to a unilateral lesion on this cranial nerve. In most cases, third nerve palsy resolves over weeks to months.

    Causes of oculomotor nerve palsy include:

    • Intracranial aneurysm
    • Microvascular ischemia (in diabetics especially)
    • Trauma: Severe blows to head with skull fracture

    Testing Extraocular Muscles (III, IV, VI)

    To test the oculomotor nerve, you need to assess the EOMs. Testing the EOMs also tests cranial nerves IV and VI, as all three nerves are responsible for eye movement.

    Hold your finger or a pen 2 feet in front of the patient’s eyes midline and have the patient focus on it with both eyes. Ask the patient to follow your finger or pen with only their eyes, moving the pen to the right, back to the midline, and then to the left and back again. Do this again for up and down. Lastly, do this again to the down-left diagonal angle, and then the down-right diagonal angle. You should have tested a total of 6 different directions – termed the “6 cardinal directions”.

    Eye movement should be symmetric, smooth, and moving in all directions. At each extremity of vision, you should be observing excessive nystagmus. Nystagmus is repetitive uncontrolled eye movement.

    Conjugate nerve palsy is when both eyes are unable to look in a specific direction during your testing. This most commonly occurs in the horizontal directions. This is usually due to a stroke within or near the brain stem.

    The pupillary light reflex listed above is also used to assess the oculomotor nerve.

    4. CN IV: The Trochlear Nerve

    The fourth cranial nerve, the trochlear nerve, innervates the superior oblique muscle of the eyes. This means it controls the downward movement of the eyeball and prevents it from rolling upward. When there is a fourth nerve palsy, patients will often complain of vertical diplopia and/or tilting of objects. This may be most noticeable when in a downward gaze such as when going down the stairs. They may also have a head tilt, as the visual changes improve with tilting of the head. On exam, the eye will with deviated upward and rotated outward.

    Testing the trochlear nerve involves evaluating the patient’s extra-ocular movements as described above.

    5. CN V: The Trigeminal Nerve

    The Trigeminal nerve is the 5th cranial nerve and responsible for facial sensation, as well as moving the muscles involved with biting and chewing. This has three branches including the ophthalmic V1, maxillary V2, and Mandibular V3. Compression of this nerve root can cause trigeminal neuralgia – a rare but painful condition.

    How to test the Trigeminal Nerve

    To test the trigeminal nerve, you are testing their facial sensation. Lightly touch both sides of the forehead and ask if they felt the same. Do this on the cheek, and then the chin. If the patient is uncooperative, you can test their corneal reflex. Do this by having the patient look right, then touch their left cornea with a whisp of cotton. They should blink. Do this on both sides.

    6. CN VI: The Abducens Nerve

    The sixth cranial nerve, the abducents nerve innervates the lateral rectus muscle of the eye. This means its responsible for outward movement of the eyes. Patients with dysfunction of this nerve will be unable to outwardly move their eyes. This causes horizontal diplopia, where the double images are side-by-side, which is worse at far distances.

    This nerve is often the first nerve compressed when there is any increased intracranial pressure (ICP). However, more common causes include vascular disease (diabetes, hypertension, atherosclerosis) or trauma.

    To test the abducents nerve, test the EOMs as described above.

    7. CN VII: The Facial Nerve

    Cranial nerve VII is the facial nerve, which controls the muscles of facial expression, as well as the sensation of taste of the front of the tongue. Facial nerve palsy can occur for various reasons, the most common being Bell’s palsy. Some other common causes include stroke, Lymes disease, trauma, or even diabetes.

    How to test the Facial Nerve

    To test the facial nerve, you must assess the patient’s facial expressions. Have the patient close their eyes tightly, then have them open their eyes. Ask them to frown, looking for symmetry in the forehead muscles. Have them smile and look for any drooping or asymmetry.

    Clinical Tip: To differentiate Bell’s palsy from stroke, assess the patient’s use of their forehead muscles. Peripheral nerve lesions (such as with Bell’s palsy) cause paresis of the entire side of the face. Central lesions tend to only effect the lower portion of the face. This is not always the case though, so you must use clinical judgement. Bell’s palsy should have no other associated neuro deficits. Check out my Infographic for more information!

    8. CN VIII: The Vestibulocochlear Nerve

    The vestibulocochlear nerve, also called the auditory vestibular nerve, is responsible for hearing and balance. Vestibular neuritis is when the nerve becomes inflamed and can cause vertigo, dizziness, and balancing difficulties – most likely from a viral infection.

    How to test the Vestibulocochlear Nerve

    While not routinely tested within the hospital, the vestibulocochlear nerve involves testing both hearing and balance. Hearing is tested by holding your fingers a few inches away from their ears and rubbing them together. If they can hear, then that is a pass. Test their balance by assessing their gait while walking. The presence of nystagmus can also indicate vestibular dysfunction.

    9. CN IX: The Glossopharyngeal Nerve

    The glossopharyngeal nerve is partially responsible for the sensation of taste, pharyngeal sensation, as well as for the gag reflex. A damaged glossopharyngeal nerve can cause a loss of taste in part of the tongue and cause trouble swallowing.

    How to test the Glossopharyngeal Nerve

    Palatal Movement (IX, X)

    Instead of doing the gag reflex which can be very uncomfortable for patients, you can instead assess palatal movement. Do this by having the patient yawn or say “ahh”, and observe their palate movement for symmetry. If this is abnormal, consider testing the gag reflex.

    Gag Reflex (IX, X)

    When performing the cranial nerve assessment, the easiest way to test the glossopharyngeal nerve is to test their gag reflex, however, this is usually not necessary in the clinical setting. Remember that approximately 20% of people will not have a gag reflex at baseline. Check both sides of the pharyngeal wall by gently poking the pharynx with a cotton swab.

    Dysarthria (IX, X, XII)

    There is no specific test for this but listen to the patient’s speech. Assess for any slurred speech or abnormality of the voice. Ask the patient or the family if it sounds different than normal.

    10. CN X: The Vagus Nerve

    The Vagus nerve innervates the hearts, lungs, and digestive tract, along with a few muscles. Most noticeably, it controls the heart rate, GI motility, sweating, and speech. It is also partially responsible for the gag reflex (along with cranial nerve IX).

    Overstimulation of the vagal nerve can drop the heart rate and cause syncope, termed vasovagal syncope. Activities that stimulate the vagal nerve include bearing down, holding breath, carotid massage, or extreme fear or stress.

    There are even implantable vagus nerve stimulators that can help slow down the firing of neurons within the brain and thus help manage seizures.

    How to test the Vagus Nerve

    The only real way to test the vagus nerve is via the gag reflex as described above.

    11. CN XI: The Accessory Nerve

    The accessory nerve innervates the sternocleidomastoid and trapezius muscles. This means it is responsible for tilting/rotating the head as well as shrugging the shoulders. This nerve can be damaged after neck surgery or blunt force trauma.

    How to test the Accessory Nerve

    To test the trapezius muscle, ask the patient to shrug both of their shoulders at the same time. Then apply some downward pressure with both hands and ask them to shrug both shoulders against the resistance.

    To test the sternocleidomastoid, place a hand against their cheek and ask them to rotate their head against resistance in each direction. If you notice weakness, this indicates the opposite side is the weaker muscle.

    12. CN XII: The Hypoglossal Nerve

    The hypoglossal nerve controls most of the movement of the tongue. This means it is highly responsible for speech and swallowing. Damage to the hypoglossal nerve is rare, but if so are likely to be caused by tumors or gunshot wounds. Other causes include stroke or neurodegenerative disease.

    How to test the Hypoglossal Nerve

    To test the hypoglossal nerve, ask the patient to stick out their tongue. If the tongue deviates to one side, this indicates hypoglossal nerve dysfunction on the side of deviation. Then ask them to move their tongue from side to side rapidly. Additionally, listen for dysarthria when the patient is speaking as described above.

    Cranial Nerve Assessment Cheat sheetCranial Nerve Assessment Cheat Sheet

    How’s that for a refresher?  Although we may have forgotten some of the in’s and out’s of the cranial nerve assessment, this should serve as a reminder for how to examine cranial nerves. Hopefully, after reading this, you can feel more confident in your neurologic assessment!

    If you need an easy cranial nerve assessment handout, you can download my handout here! This is the perfect cheat-sheet that you can refer to in practice when assessing cranial nerves!

    References:

    Gelb, D. (2019). The detailed neurologic examination in adults. In UpToDate. Retrieved from https://www.uptodate.com/contents/the-detailed-neurologic-examination-in-adults

    Lee, A. G. (2019). Third cranial nerve (oculomotor nerve) palsy in adults. In UpToDate. Retrieved from https://www.uptodate.com/contents/third-cranial-nerve-oculomotor-nerve-palsy-in-adults

    Lee, A. G. (2019). Fourth cranial nerve (trochlear nerve) palsy. In UpToDate. Retrieved from https://www.uptodate.com/contents/fourth-cranial-nerve-trochlear-nerve-palsy

    Mullen, M. T. (2014). Differentiating Facial Weakness Caused by Bell’s Palsy vs. Acute Stroke. Journal of Emergency Medical Services, 39(5). Retrieved from https://www.jems.com/2014/05/07/differentiating-facial-weakness-caused-b

    Oculomotor Nerve. (n.d.). Retrieved from https://www.sciencedirect.com/topics/neuroscience/oculomotor-nerve

    Olfactory Nerve. (n.d.). Retrieved from https://www.sciencedirect.com/topics/neuroscience/olfactory-nerve

    Rea, P. (2014). Clinical Anatomy of the Cranial Nerves. Cambridge, MA: Academic Press.

    Trigeminal Nerve. (n.d.). Retrieved from https://www.sciencedirect.com/topics/medicine-and-dentistry/trigeminal-nerve

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    Six Steps for Sepsis Management

    Nov 26, 2018

    Six Steps for Sepsis Management

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    Sepsis is not a specific disease but rather a clinical syndromewhich represents the body’s response to severe bacterial infection. Sepsis is very common. In fact, within the hospital, you will take care of patients with sepsis in any department. Sepsis is a very serious condition with a poor prognosis. As the medical team suspecting and treating sepsis – there are important management steps that need to be taken in order to maximize patient outcomes and save lives!

    Early sepsis– while not clearly defined – is the presence of infection and bacteremia – which can and likely will progress to sepsis without intervention. Sepsis used to be identified using SIRS criteria– Systemic Inflammatory Response syndrome. This syndrome is defined as the presence of at least 2 of the following 4 clinical indicators: Fever >38C or <36C, HR >90bpm, RR > 22/min or PaCO2 <32 mmHg, or WBC >12,000/mm3, <4,000/mm3, OR 10% BANDS. Once SIRS is identified with suspected source of infection – sepsis diagnosis was met. However, the definition of sepsis has changed with 2016. Sepsis is now is defined as life-threatening organ dysfunction in response to infection. Organ dysfunction, usually from hypoperfusion, can be evidenced by hypotension, altered mental status, tachypnea, or increased sofa score by 2 points (see below).  Septic shockis defined as those patients who have received fluid resuscitation and still have a MAP <65 mmHg and a lactic >2.0 mmol/L. These patients require vasopressors and should be monitored in the ICU.

    Sepsis can be very serious and even fatal. Because of this – it is important to kn ow the steps to take in sepsis management. Performing these correct steps can literally mean the difference between life and death.

    1. Recognition and Early Intervention

    The most important aspect of sepsis management is recognizing it’s presence and acting quickly. Common symptoms of sepsis include fever, chills, sweats, and confusion. Common signs include altered mental status, elevated temperature, tachypnea, tachycardia, and hypotension.

    Initial management should include investigating the extensiveness of their infection, and applying initial measures to help them. After vital signs are taken an IV should be established and lab work drawn. If the patient’s blood pressure is low – consider starting 2 large-bore IVs. Be sure to draw at least 1 set of blood cultures per IV site (up to 2) as this will need ordered in all sepsis patients. Make sure the blood cultures get drawn before antibiotics are started.

    Diagnostics should investigate the source of the infection – sometimes it is not obvious. If unsure – it is a good idea to obtain a urinalysis with culture to r/o UTI and a Chest x-ray to r/o pneumonia should be ordered. A wound culture, sputum culture, or abdominal imaging may be ordered if clinically indicated. Blood work will usually include blood cultures x 2, CBC with differential, CMP, and a lactic acid level. Sometimes in severe cases, an ABG can be ordered to evaluate acid-base status.

    Lactic acid levels are very important in sepsis. Lactate is released from cells when they are forced to utilize glycolysis instead of the Kreb’s cycle (throwback to Cell Biology!). This means that there is decreased tissue perfusion due to decreased volume, increased oxygen demand, and decreased oxygen delivery. Lactic levels correlate with severity of sepsis.

    Apply oxygen at 2 L/min unless contraindicated – titrate if SPO2 <92%. During sepsis, oxygen demand increases and delivery diminishes. Supplemental oxygen will help put less stress on the body and may help diminish lactic acidosis.

    The qSOFA (Quick Sequential Organ Failure Assessment) score is now starting to be used as a clinical tool for sepsis. This is usually used within the hospital to stratify the mortality of patients with sepsis (see infographic for more details).

    2. Fluid Resuscitation!

    Fluid resuscitation during sepsis is the staple of sepsis management. Evidence shows early fluid intervention decreases mortality. There is such a massive need for fluid because during sepsis there is poor tissue perfusion and often hypovolemia. To correct this – large amounts of fluids are needed.

    Typically, 0.9% normal saline is used 9 times out of 10. The recommended standard volume is a 30 ml/kg bolus. So if a patient was 70 Kg, they would receive 2100 ml total. This should be given as quickly as possible – as tolerated. This amount is typically given to anybody recognized as possibly having sepsis, but is especially indicated in those with sever sepsis, fast heart rate, or low blood pressure. Traditionally even larger amounts of fluids were given (5-6 Liters), but several randomized control trials showed no difference in mortality compared with the now-recommended 2-3 Liters.

    Exceptions to receiving this bolus includes those with active pulmonary edema. Those with a history of Heart Failure, end-stage renal disease, or severe liver disease should still receive fluids. However – it is recommended to give fluids in 500mL bolus increments and to reassess lung sounds and breathing status after each bolus. If pulmonary edema ensues – the bolus should be stopped and the patient may need diuretics.

    3. Timely Antibiotic Administration

    Another very important aspect of sepsis management is early antibiotics. The term empiric simply means antibiotics based on the best “clinical guess”.

    The choice of empiric antibiotics will be selected based off of the patient’s signs or symptoms and where the likely source – since certain organisms are more likely from one source as opposed to another. This means the antibiotic regimen should be geared towards covering all likely gram-positive and gram-negative organisms. For sepsis – usually a broad spectrum antibiotic like Zosyn or a Carbapenem is combined with another antibiotic of a different lass – such as Vancomycin. Vanco is often added when the patient has risk factors for MRSA.

    Correct regimen of antibiotics are important – however timely administration of those antibiotics are just as important. Antibiotics should be initiated within the first hour after suspecting sepsis – especially during severe sepsis or septic shock. This is because several observational studies have shown poorer outcomes with delayed antibiotic initiation. Once again, try to be sure you obtain both sets of blood cultures before you start the antibiotics!

    As nurses, it is often up to you to choose which antibiotic to start first as both are often ordered concurrently. If you have both Zosyn and Vancomycin ordered – start with the broad-spectrum antibiotic first. But what exactly is broad-spectrum? This means heavy-hitter antibiotics that cover most pathogens – both gram positive and negative. Contrary to popular belief – vancomycin is NOT broad-spectrum. In fact, it has a very narrow spectrum specific for gram positive organisms such as Staph or Strep. Most cases of sepsis are from gram negative sources. This means starting the Zosyn first should be your priority. Additionally – Zosyn runs much quicker as a loading dose (4.5 grams over 30 minutes) – whereas vancomycin usually runs over 1.5 hours.

    4. Hemodynamic Management

    Sometimes when sepsis becomes severe – distributive shock can occur. This is termed septic shock. When this occurs – hemodynamic compromise is present.  If blood pressure remains low, the patient’s tissue perfusion continues to suffer and steps need to be taken to improve outcomes.

    The patient may require more fluid if they are still hypovolemic after the initial bolus and can tolerate more fluids. However, the mainstay of treatment of septic shock is intravenous Vasopressors. For the most part – Norepinephrine (Levophed) is the go-to pressor for sepsis. However, other choices can be chosen based on clinician discretion (i.e. If very tachycardic consider Vasopressin which has no beta stimulation). Sometimes, multiple vasopressors may need to run concurrently to manage septic shock.

    When a patient is in septic shock with hemodynamic compromise – they should have a central venous catheter inserted and/or an arterial line. Vasopressors can be started in a peripheral line, but a central line should be ordered as vasopressors can be caustic and damaging to the peripheral vasculature. Additionally, these catheters can monitor CVP and continuous blood pressures. If a patient is in cardiogenic shock and has inadequate cardiac output – cardiac inotropes can be added such as dobutamine or epinephrine.

    Sometimes during severe septic shock, IV glucocorticoids may or may not help. Usually this is ordered if fluid resuscitation and vasopressors have failed.

    5. Monitoring

    Monitoring is the essential last step to sepsis management. Patient’s with sepsis can respond well to the regimen – or they can decompensate unexpectedly. Sepsis has a high mortality and the patient’s should be monitored very closely.

    If the patient has any hemodynamic compromise and are on pressors – they should be monitored in the ICU for a few days until they become stable. Patient’s with mild to moderate sepsis should be closely monitored on a med-surg or telemetry floor. Continuous cardiac monitoring is essential during sepsis. The increased tissue demand for oxygen places the heart at a greater risk for having cardiac events secondary to the sepsis. It is not uncommon for someone with sepsis and cardiac comorbidities to have secondary myocardial ischemia and/or infarctions.

    Blood pressure should be monitored closely – especially initially. Normotensive blood pressure should be maintained (SBP >100). However – maybe even more importantly the MAP (mean arterial pressure) should be monitored closely. The goal of MAP should be >65mmHg – this ensures adequate tissue perfusion (i.e. brain). Heart rate is also an important metric to monitor. Tachycardia is usually present – often in the 120s-130s during fever and sepsis – sometimes higher. While giving fluids – heart rate should improve. This can be somewhat helpful in monitoring the response of fluid therapy. Fever should be monitored as well – as sometimes it can become very high and increases insensible water losses and further propitiates hypovolemia. Remember a rectal temperature is preferred in those with suspected sepsis – especially the elderly. Urine output is also often monitored during severe sepsis – as secondary hypoperfusion of the kidneys can cause acute kidney injury and decreased urine output.

    Nursing assessments should include skin color and perfusion, mucous membranes (i.e. dry vs moist), mental status, and heart/lung sounds. Nurses should be vigilant in recognizing flash pulmonary edema or cariogenic shock which may develop after rapid administration of fluids with underlying comorbidities (i.e heart failure, ESRD, etc). 

    If the initial lactic acid level is elevated > 2 mmol/L, then a repeat level should be drawn in 4 – 6 hours. The lactic acid level should respond quickly to changes in tissue perfusion. CBC should be trended each day to monitor for resolution of the leukocytosis, bandemia, and/or thrombocytopenia. Electrolytes and kidney/liver function should also be monitored closely dpeneding on which abnormalities are present.

    6. Patient Disposition and Follow-Up

    Last but certainly not least – the patient needs to be sent to the correct unit, needs the correct consults, and needs adequate follow-up. Almost all patients admitted to the hospital with sepsis will warrant an Infectious Disease consultation. Additionally, if they have any pre-existing comorbidities these consults should be made as well (i.e. cardiology for heart failure, nephrology for kidney disease).

    Patients should have frequent nursing assessments and daily physician assessments, with close follow-up of labs. Blood cultures can start showing growth at about 24 hours. The pathologist will gram-stain the growth and give a report of “gram positive cocci” a similar description. This tells the clinician if they are on the right track and can guess at the offending organism. At about 48 hours, most clinically significant bacteria will be identified and a sensitivity is done to detect the bacteria’s sensitivity vs resistance to various antibiotics. Urine, wound, and sputum cultures have similar timelines. Antibiotics may be changed depending on the results. Remember, Infectious Disease should likely be involved in this decision.

    And those are the six steps to sepsis management. Knowing the general steps to sepsis can help you as the nurse provide high quality care to your septic patients and help improve outcomes. As always, it is a collaborative team effort in offering you patients the best possible care.

    Do you have any other sepsis tips? leave them in the comments below!

     

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    William Kelly, MSN, FNP-C

    Will is a Nurse Practitioner who is the founder and author of Health and Willness, an online educational platform to build clinical knowledge and skills of nurses and nurse practitioners!

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