Blood Pressure Crash Course for nurses

Blood Pressure Crash Course for nurses

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

Author | Nurse Practitioner

Blood pressure is one of the 5 vital signs, and it is so important to understand what normal and abnormal blood pressures are, and how we manage them (don’t get me started on the “6th” vital sign…).

Within the hospital, vital signs are typically checked every 4 hours, and you will frequently run into both high and low blood pressures.

Low blood pressure is often much more worrisome, and you may want to call an RRT if the BP is significantly low, especially when the patient is altered or has significant symptoms.

High blood pressure is common, but often is not considered a big deal unless VERY high. In these cases, we want to slowly decrease the blood pressure instead of too quickly.

What is Blood Pressure?

As you probably know, blood pressure is not the pressure of your blood, but rather the pressure within your vascular system.

The vascular system refers to your arteries and veins. When speaking of systemic blood pressure, we are specifically talking about the pressure in the arteries. 

This pressure temporarily increases with each heartbeat, and decreases in-between each heartbeat. 

The pressure in your arteries when your heart beats or contracts is called the systolic blood pressure. Systolic just means during the heartbeat. Systolic blood pressure can never be below the diastolic pressure.

When the heart is not beating, the pressure “rests” back to its normal baseline pressure. This is called the diastolic blood pressure. The diastolic blood pressure should never be 0. 

This pressure is measured in millimeters of mercury (mmHg).

“Normal” Blood Pressure

As we said above, systolic is the pressure during contraction of the heart, and diastolic is the pressure in-between beats. When looking at a blood pressure reading, there are two numbers: a numerator and a denominator. The numerator or top number is the systolic blood pressure. The denominator or the bottom number is the diastolic blood pressure.

Normal systolic blood pressures are between 100 – 120 mmHG. Normal diastolic pressures are between 60-80 mm Hg. Traditionally 120/80 mmHg was considered the “gold standard” for blood pressure, but now its recommended to be at most 120/80 mmHg. 

A "Good" Pressure

A “good pressure” is relative. In the ER, a pressure below 160/90 tends to be considered pretty good and usually won’t require any medications. However, a pressure of 160/90 is considered very high if that is the normal daily blood pressure at home, and should be started on medications.

How to Measure Blood Pressure

We check people’s blood pressures in the hospital, in the outpatient office setting, and pretty much every area of patient care. Nowadays, we have machines that do most of it for us. But machines aren’t perfect, and its an essential nursing skill to know how to check blood pressure.

In general, there are 3 main ways to check someone’s blood pressure:

Manual Blood Pressure

A manual blood pressure is checked using a sphygmomanometer and a stethoscope. The stethoscope if placed over the brachial artery, and the cuff is placed on the patient’s bicep.

The cuff is pumped up to about 160 or 180 (in most people unless BP is very high). Slowly release the cuff pressure while you auscultate the brachial artery. 

Systolic blood pressure is identified by the first Korotkoff clicking sound. The diastolic is noted when you can’t hear anything left.

Palpating BP?

You can palpate the patient’s radial artery when a machine or cuff is pumping up or down. When the radial artery disappears, this is your systolic pressure. There is no way to check diastolic with palpation

Automated Blood Pressure

An automated blood pressure is checked by a machine, often a portable Dinamap or a bedside monitor. These machines essentially perform a manual BP on their own.

They have a sensor which detects tiny oscillations from your pulse. So when the pulse goes away – this is your systolic pressure. When the pulse reappears, this is your diastolic pressure.

A-Line Blood Pressure

Arterial lines are commonly placed in the ICU for strict BP monitoring. This is the most accurate way to check a blood pressure because it is directly measured by a sensor within the arteries, instead of indirectly like with the methods above. This gives you real-time changes in blood pressure.

What’s the deal with the “MAP”?

If you’ve been working for a bit, or in clinicals, you may hear about the term “MAP”. While systolic blood pressure is often considered the most important part of the blood pressure, the actual important number is the MAP. 

The MAP stands for Mean Arterial Pressure. This is the average pressure in the arteries from one cardiac cycle (systolic + diastolic). This is measured by a calculation:

But don’t go busting out your calculators. The bedside monitors should automatically calculate this for you, or possibly your EMR. If you need to calculate it, there are plenty of good online calculators to quickly do it. 

MAP is a great indicator of tissue perfusion. If the MAP stays above 65 mmHg, then this should be enough pressure to provide essential tissue perfusion and prevent anoxic injury (injury from a lack of oxygen to the cells!).

Nurses and Providers in the ICU will care much more about MAP than systolic blood pressure, especially when looking at low blood pressures.

Hypertension

Hypertension, also known as high blood pressure, comes in many different forms. While often thought of as “not a big deal”, it really is the silent killer, and can put a lot of strain on the heart, vasculature, and kidneys.

Overtime, this organ damage becomes more pronounced, placing the patient at risk for heart disease, strokes, kidney failure, and more!

Another reason why it’s termed the silent killer is because it often is asymptomatic – meaning there are no symptoms. But just because there aren’t any symptoms doesn’t mean it isn’t dangerous, especially in the long run. 

In medicine, we use JNC8 guidelines to classify and manage hypertension. 

Blood pressure levels include:

Normal: < 120 / 80 mmHg
Stage 1 HTN: 130 – 140 / 80-89 mmHg
Stage 2 HTN: > 140 / 90 mmHg

Normal Blood Pressure Levels

Hypertension can be chronic or acute. Its also important to know if the patient is having any symptoms such as chest pain, SOB, headache, etc.

3 main types of hypertension that we’ll talk about include:

Primary Hypertension

Primary hypertension, previously referred to as essential hypertension, is a chronic hypertension that has no clear cause, but is thought to involve genetic, dietary, and lifestyle factors. This is what most people are diagnosed with when they have high blood pressure. Risk factors include:

  • Increased age
  • Obesity
  • Family History of HTN
  • Black race
  • High sodium diet
  • Excessive ETOH
  • Sedentary lifestyle

Hypertensive Urgency

Hypertensive urgency is a very high blood pressure > 180/110 mmHg. While there is no evidence of organ damage (i.e. lack of symptoms or lab abnormalities), the patient is at risk for organ damage or strokes to occur.

Hypertensive Emergency

Hypertensive emergency is a very high blood pressure > 180/110 mmHg when there IS evidence of organ damage. The patient should have at least one of the following signs or symptoms:

  • Chest Pain or SOB
  • Pulmonary Edema
  • Severe headache, Seizures, or confusion
  • Elevated Troponin
  • Acute Kidney Injury (elevation in creatinine levels)

Treatment of Hypertension:

Treatment of hypertension is often not aggressive, and is often made by slow gradual changes to outpatient medication regimens.

However, if the patient is symptomatic, blood pressure medications should be given. 

At home blood pressures should be checked, as patients BPs are often higher in emergency and urgent care settings, and “White coat hypertension” is common. 

Some oral medications used to lower BP include:

  • ACE Inhibitors like Lisinopril
  • ARBs like Losartan
  • Calcium channel blockers like Amlodipine
  • Beta-blockers like Labetalol
  • Diuretics like Hydrochlorothiazide
  • Alpha blockers like Clonidine

In hypertensive urgency and when in the hospital, sometimes IV medications may be required including:

  • IV Hydralazine
  • IV Cardizem or Nicardipine
  • IV Labetalol
  • IV Lopressor (metoprolol)

In general, blood pressure should never be lowered too fast. In severe cases, the goal should be to lower the MAP by 10-20% within the first hour, then another 5-15% over the next day. In many cases, this is less than 180/120 in the first hour, and less than 160/110 after 24 hours. 

Lowering the blood pressure too quickly can actually cause ischemic damage in patients who have had elevated blood pressure for a long time. Basically the body becomes used to that high pressure, and while it is dangerous to have high blood pressure in general, lowering it too quickly can cause damage as well.

BP & Symptoms

When it comes to blood pressure (and even heart rates while we’re at it), its always important to ask the patient if they have any symptoms. Ask about any CP, SOB, dizziness, palpitations, headache, numbness/tingling/ etc.

Hypotension

Hypotension is when the blood pressure is too low. Low blood pressure is defined as any pressure less than 100/60 mmHg. However, this is often not considered true hypotension until below 90/50 mmHg.

Patients who are small in stature and thin may have borderline low blood pressures at baseline.

Trend Alert

Worried about the patient’s BP? Trend what their BP has been this hospital visit, as well as previous hospital visits. If their BP is 92/48 but they always run around there and are asymptomatic otherwise – this is reassuring.

Remember if the MAP is less than 65 mmHg, this places the patient at risk for tissue ischemia and organ damage. 

Low blood pressure is often a serious sign, especially in the hospital setting. Common causes of hypotension include:

Sepsis

Septic shock is when there is a severe systemic response to infection. These patients will have persistent hypotension despite adequate fluid resuscitation (30ml/kg bolus). They usually require IV vasopressors, a central line, IV antibiotics, and ICU admission.

Anaphylaxis

Anaphylactic shock is a type of distributive shock that occurs with a severe allergy. Release of inflammatory mediators causes massive systemic vasodilation, swelling, and hypotension. This is treated with IV steroids and antihistamines, +/- epinephrine.

Hemorrhage

When the patient loses enough blood, they will become hypotensive. These patients need STAT blood, usually O negative blood that hasn’t been crossmatched. 

Cardiogenic Shock

Cardiogenic shock occurs when the heart can’t keep up with the body’s demand. This can occur in severe CHF or bradyarrhythmias.

Drugs / Medications

Maintenance medications given for blood pressure can cause low BP, especially if taken in wrong doses or if they become toxic. Some other medications have hypotension as a possible side effect such as amiodarone. 

Adrenal insufficiency

Patients with a history of adrenal insufficiency will often require stress-dosed steroids to maintain their blood pressure. 

Severe dehydration

Dehydration needs to be severe before the patient becomes hypotensive. This can occur in those with DKA or diabetes insipidus, or really anything that causes dehydration.

Treatment of Hypotension:

Treatment of hypotension will involve treating the underlying cause, but generally involves 2 steps:

  • IV Fluid boluses: to increase the volume of the blood
  • Vasopressors: To cause constriction of the blood vessels

If fluid boluses do not improve blood pressure, or if the BP drops back again once its done, then the patient may need vasopressors in the ICU.

Depending on the cause, the underlying cause should be addressed, including:

  • Blood for blood loss
  • Antibiotics and fluids for sepsis
  • Steroids for adrenal crisis
  • Steroids & Antihistamines for Anaphylaxis

Wrapping Up

You are going to run into TONS of patients who either have high blood pressure, or low blood pressure. Managing vital signs is a huge part of our jobs as nurses and doctors, and its so important to understand how to manage blood pressure!

Remember these important concepts when it comes to blood pressure:

Double Check the Pressure

Double check your blood pressures. If it doesn’t seem right – check a manual BP. The provider may ask you to do this anyway.

Always ask about Symptoms

If your patients BP is high or low, ask them if they have any symptoms. Focus on any headache, chest pain, shortness of breath, dizziness, lightheadedness, palpitations, syncope, etc.

Trend the Pressures

Remember high blood pressure shouldn’t be corrected too quickly. Look at previous trends. Don’t freak out about blood pressures that are high unless the patient has symptoms. Worry more about low blood pressures!

REFERENCES

Basil, J., & Bloch, M. J. (2022). Overview of hypertension in adults. In T. W. Post (Ed.), Uptodate. https://www.uptodate.com/contents/evaluation-of-and-initial-approach-to-the-adult-patient-with-undifferentiated-hypotension-and-shock

Calder, S. A. (2012). Shock. In B. B. Hammond & P. G. Zimmerman (Eds.), Sheey’s manual of emergency care (7th ed., pp. 213-221). Elsevier.

Gaieski, D. F., & Mikkelsen, M. E. (2022). Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock. In T. W. Post (Ed.), Uptodatehttps://www.uptodate.com/contents/overview-of-hypertension-in-adults

Roe, D. M. (2015). Cardiac emergencies. In B. A. Tscheschlog & A. Jauch (Eds.), Emergency nursing made incredibly easy! (2nd ed., pp. 97-197). Lippincott Williams & Wilkins.

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!

 

STEMI & NSTEMI: A Nurse’s Comprehensive Guide

STEMI & NSTEMI: A Nurse’s Comprehensive Guide

Understand the key differences in a STEMI & an NSTEMI including how to detect a STEMI on the EKG, the different kinds of STEMIs, and the acute management involved including which medications to give!

Pulmonary Embolism: Nurse’s Reference Guide

Pulmonary Embolism: Nurse’s Reference Guide

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

Author | Nurse Practitioner

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

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

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

What is a Pulmonary Embolism?

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

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

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

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

Pulmonary Embolism

Causes of a PE

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

Virchow’s Triad

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

Stasis of Blood

Anything that causes blood to “sit still”

Endothelial Injury

Damage to the vascular system (arteries & veins)

Hypercoagulable State

Something that increases likelihood for clotting

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

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

Stasis of Blood

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

Endothelial Injury

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

Hypercoagulable State

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

Nursing Assessment

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

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

Symptoms of a PE

Common symptoms of a PE include:

Dyspnea

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

Chest Pain

Usually pleuritic, aka worse with deep breaths or coughing

Cough

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

Syncope

Syncope with chest pain and SOB is suspicious for PE

Signs of DVT

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

Quick Note

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

The Physical Exam

Inspection

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

Vital Signs

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

Auscultation

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

Quick Tip

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

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

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

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

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

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

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

Nursing Interventions

Cardiac Monitoring

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

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

Patients with PEs can have all sorts of arrhythmias including:

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

STAT EKG

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

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

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

  • Right heart strain pattern
  • S1Q3T3
S1Q3T3 teaser

Oxygen Support

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

In these cases, BIPAP or Intubation may be needed.

IV Access

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

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

Diagnosis of a PE

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

Well's Criteria

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

This assigns points to each of the following:

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

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

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

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

D-Dimer

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

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

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

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

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

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

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

Other Lab Work

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

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

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

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

ABGs

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

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

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

CXR

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

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

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

CTA

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

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

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

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

Pulmonary Embolism

V/Q Scan

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

Quick Note

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

Treatment of PE

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

Patients who have significant hemodynamic compromise may require reperfusion therapy.

Parenteral Anticoagulation

Treatment for pulmonary embolisms primarily involve anticoagulation.

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

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

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

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

Quick Note

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

Oral Anticoagulation

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

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

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

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

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

IVC Filter

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

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

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

Thrombolytics

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

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

Procedural Removal

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

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

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

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

Saddle PE

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

Patient monitoring

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

Oxygen Support

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

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

A BIPAP or Intubation may be needed in severe cases.

Blood Pressure Support

Monitor their blood pressure per department protocol.

If hypertensive, treat with analgesics and antihypertensives.

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

Vasopressors may be required in severe cases.

Cardiac Monitoring

These patients should have telemetry ordered. 

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

Bleeding / Falls

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

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

Clinical Deterioration

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

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

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

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

REFERENCES

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

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

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

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

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

Want to learn more?

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

With this course you will be able to:

  • Identify all cardiac rhythms inside and out
  • Understand the pathophysiology of why and how arrhythmias occur
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Pulmonary Embolism: A nurses reference Guide

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!

 

STEMI & NSTEMI: A Nurse’s Comprehensive Guide

STEMI & NSTEMI: A Nurse’s Comprehensive Guide

Understand the key differences in a STEMI & an NSTEMI including how to detect a STEMI on the EKG, the different kinds of STEMIs, and the acute management involved including which medications to give!

Blood Transfusion Reactions: A Comprehensive Nursing Guide

Blood Transfusion Reactions: A Comprehensive Nursing Guide

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

Author | Nurse Practitioner

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

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

Acute Hemolytic Transfusion Reaction

What are blood products?

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

Packed Red Blood Cells (PRBCs)

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

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

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

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

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

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

Fresh Frozen Plasma (FFP)

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

Some reasons FFP may be ordered for your patient include:

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

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

Platelets

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

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

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

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

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

Why are Blood products Given?

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

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

Blood Transfusion Reactions

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

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

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

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

Acute Hemolytic Transfusion Reaction

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

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

Compatible blood is outlined below:

Acute Hemolytic Transfusion Reaction

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

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

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

If this reaction occurs, the nurse should:

Acute Hemolytic Reaction: Nursing Steps

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

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

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

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

Acute Hemolytic Blood Transfusion Reaction

Anaphylactic Transfusion Reaction

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

This reaction occurs seconds to minutes after starting the transfusion.

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

Signs of an anaphylatic reaction include:

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

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

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

More significant interventions may be needed, including:

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

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

Anaphylactic Blood Transfusion Reaction

Urticarial Transfusion Reaction

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

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

When an urticarial transfusion reaction occurs:

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

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

Urticarial Blood Transfusion Reaction

Febrile Non-Hemolytic Transfusion Reaction (FNHTR)

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

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

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

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

Signs/symptoms include:

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

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

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

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

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

Febrile Non-Hemolytic Blood Transfusion reaction

Transfusion-Associated Acute Lung Injury (TRALI)

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

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

Patients at risk for TRALI include patients with:

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

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

  • Hypoxia
  • Fever
  • Hypotension
  • Cyanosis

New bilateral infiltrates on CXR are often seen.

TRALI: Nursing Actions

When TRALI is suspected, the nurse should:

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

Sometimes steroids are given, although evidence is not great.

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

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

TRALI

Transfusion-Associated Sepsis

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

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

Signs/Symptoms of transfusion-associated sepsis includes:

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

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

SEPSIS: Nursing Actions

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

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

Transfusion-Associated Circulatory Overload (TACO)

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

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

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

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

Patients will develop symptoms of respiratory distress which include:

  • Dyspnea
  • Tachypnea
  • Hypoxia
  • Orthopnea

The patient will also usually develop hypertension.

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

TACO: Nursing Actions

When TACO is suspected, the nurse should:

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

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

  CLINICAL TIP

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

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

TACO blood transfusion Reaction

Primary Hypotensive Reactions

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

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

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

This is also more common with platelet administration.

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

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

REFERENCES

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

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

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

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

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

18 Acute Skin Rashes for Nurses to Know (with pictures)

18 Acute Skin Rashes for Nurses to Know (with pictures)

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

Author | Nurse Practitioner

Skin rashes are a common reason why patients and parents seek medical care. Skin rashes can look gross and are often uncomfortable – whether they itch, burn, or cause pain.

Many causes of skin rashes are temporary, but some are chronic and can be ongoing.

Understanding the most common types of skin rashes and their treatment will be important, as you will run into skin-related problems in any setting of healthcare.

Oxygen delivery devices and flow rates FB

Skin Rashes: Taking the History

In order to successfully diagnose a skin rash, you need to know which questions to ask.

Timing is an important factor to consider. How long has the rash been there, does it come and go? Did the rash look different when it first occurred, and how has it changed? If it occurred before, what was it and what treatment worked?

Associated symptoms can be key in making the right diagnosis. Does it itch, burn, or is it painful? Are there any fevers, chills, pain anywhere else in their body?

Related activities that may have caused or worsen the rash should be investigated. This includes things like sunlight exposure, being out in the woods, using a new skin product like shampoos or lotions, or new medications or foods.

Treatments that the patient has already tried should be evaluated, which usually includes OTC creams and sometimes prescribed medications from a previous diagnosis or from another recent healthcare visit. This may be Benadryl cream, steroid cream (like hydrocortisone), moisturizers, etc.

A detailed past medical history and current medications should be evaluated as well.

Meds that are more likely to cause a rash include:

  • Antibiotics
  • Anti-epilepsy medications
  • allopurinol

The Skin Rash Physical Exam

When looking at skin rashes, they are described using various describers which have different meanings and significance.

A lesion is a general umbrella term that essentially means any non-normal “spot” or region.

Macules are lesions that are flat, <1 cm in diameter, and have different pigmentation from the base skin color. These are called patches when they are >1cm.

  • Macules: Café au Lait, freckles
  • Patches: Vitiligo

Papules are like macules, except they are raised and palpable, also <1cm, and have different coloring from the base skin color. Lesions >1cm are termed plaques. Pustules are papules with purulent fluid inside.

  • Papules: Acne, moles, warts
  • Pustule: Cystic Acne, Folliculitis
  • Plaque: Psoriasis

Purpura are red-purple discolored lesions that do not blanch. Blanching is when you press on an area of skin and it turns white from capillary compression. Purpura occurs due to leakage of blood into the extra-capillary space.

Vesicles are small papules <1cm that contains clear or bloody fluid. Bullae are bigger than 1cm.

  • Vesicles: Shingles
  • Bullae: Bullous pemphigoid

Wheals are elevated irregular-shaped areas of edema that are pale or erythematous. An example of this is urticaria like with an allergic reaction.

These lesions and skin rashes can present in certain patterns and distributions, which can also help you successfully identify the rash.

Skin rashes can be clustered in small groups, grouped together in some fashion, linear (in a line), following the dermatome (termed zosteriform), and even coalescing together. Various rashes have certain patterns which can make the diagnosis easier.

IMPORTANT DISCLAIMER!

The following images are examples of how these rashes present on white and light-skinned individuals. For examples of how these rashes may present in darker-skinned individuals, please check out @brownskinmatters on Instagram.

20 COMMON SKIN RASHES

TABLE OF CONTENTS

Allergy-Related Rashes

CONTACT DERMATITIS

Contact dermatitis is when the skin has a reaction to something that it has come into contact with. 80% of cases are caused by an irritant, and 20% are caused by allergens. Contact dermatitis is the most common dermatologic diagnosis.

Irritant contact dermatitis is very common and often occurs from exposures to heavy metals, strong acids, rubbing alcohol, and certain ingredients in soaps and lotions. Patients often complain of pain or burning with some itching.

The skin will typically look erythematous, dry, and irritated. There may be pustules present as well.

In Allergic contact dermatitis, common causes include nickel, black hair dye, topical medications, latex, and various cosmetics and environmental exposures (like poison ivy or poison oak). Allergic dermatitis tends to be itchier with less pain or burning. There may be vesicles present as well.

Treatment for these includes steroids for the reaction, and benadryl for the itching. If the lesion is smaller, a topical steroid like Triamcinolone 0.5% once daily for 2-4 weeks can be effective. If the lesion is more widespread, systemic steroids can be used like prednisone.

ALLERGIC URTICARIA

Urticaria or hives are itchy raised wheals that are often erythematous or pale. They are often a response to an allergy such as in anaphylaxis, but many cases of urticaria are non-allergic and some are idiopathic (aka we don’t know why).

Allergic urticaria occur after contact with an allergen. These allergens can be in the environment (like dust or pollen), in food (like nuts or dyes), and in medications like with antibiotics. Urticaria can also occur after bug bites and stings.

Treatment for urticaria skin rashes depends on the underlying cause, but in cases of allergic cause includes anthistamines like benadryl, and sometimes steroids like prednisone.

ECZEMA

Eczema, also termed atopic dermatitis, is a chronic allergic-related chronic skin condition which is very itchy.

Ecezema involves very dry skin that is erythematous with oozing and crusting, excoriation from scratching, and eventual lichenification (when the skin becomes thick and leathery).

In adults, eczema skin rashes often occurs on skin flexures like the elbows and behind the knees, on the face, neck, and hands, but can occur anywhere.

All patients with eczema should liberally use a water-based emollient moisturizer like Cetaphil, Aquafor, or CeraVe.

Since eczema is a chronic condition, it cannot be taken away completely, but there are treatments that can help. Depending on the severity of the eczema, lower or higher strength steroid creams can be used once or twice daily for 2-4 weeks.

  • Low Potency: Hydrocortisone 2.5%
  • Mid Potency: Triamcinolone 0.1%
  • High Potency: Usually not prescribed for eczema

Clinical Note: Higher potency steroids on the face or thinner areas of skin have a higher risk for atrophy and permanent discoloration, so use cautiously and for limited amounts of time.

For more severe eczema, topical calcineurin inhibitors can be used as well or even monoclonal antibodies. A dermatologist should be the ones to prescribe these advanced medications.

AUTOIMMUNE-RELATED RASHES

PSORIASIS

Psoriasis is a type of chronic autoimmune skin rash condition. This is characterized by erythematous flaking thick patches of skin. They can be itchy and even burn.

Treatment for psoriasis depends on the severity of the disease, but can range from topical steroids, retinoids, tacrolimus, or at times systemic steroids and immunomodulators.

VIRAL-RELATED RASHES

SHINGLES

Shingles, also called Herpes zoster, occurs from reactivation of inactive varicella virus within the body (the chicken pox virus). Shingles almost always occurs in adults and usually >50 years old.

Shingles begins as an erythematous maculopapular rash that develops fluid-filled vesicles that scab over in 7-10 days and clear up by 2-4 weeks. The rash will follow 1-2 dermatomes (termed zosteriform), and should not cross the midline. Shingles is often very painful and can itch, which may even precede the rash.

Treatment involves pain control. Antivirals like acyclovir can be started within 72 hours that the lesion develops, otherwise they are unlikely to be beneficial.

Shingles is very contagious, especially if any vesicles pop open until the lesion scab over.

PITYRIASIS ROSEA

Pityriasis rosea is a self-limiting rash thought to be secondary to viral infections. Skin rashes and reactions secondary to viruses are termed viral exanthems. This is often preceded by a viral prodrome including headache, malaise, arthralgias, and/or chills.

Pityriasis rosea starts as a herald patch which is a single oval-shaped erythematous macule or patch on the trunk with central clearing. 1-2 weeks later, a christmas tree pattern will appear on trunk with similar smaller lesions.

There is no specific treatment for pityriasis rosea, and only time will cause the rash to resolve. Pityriasis can be itchy so benadryl can help. This is not contagious.

HAND-FOOT-MOUTH

Hand Foot and Mouth disease is a viral rash that occurs due to the Coxsackie Virus A16 and some other enteroviruses.

HFM typically occurs in outbreaks every few years in the summer months. 

While HFM usually affects children, it can easily spread to parents and family members via droplets. Adults and teenagers will often have systematic symptoms including fevers, body aches, and flu-like symptoms. HFM may be preceded by upper respiratory symptoms by a few days. 

The HFM rash appears on the palms, soles, buttock, and mouth of patients. The oral lesions have football shaped vesicles that are very painful and are on the soft palate, buccal mucosa, gums, and tongue. The posterior pharynx is unaffected. 

Skin lesions are red papules with a red halo, then become gray vesicles, then ulcers after the vesicles rupture, then heal 7-10 days later. 

Like all viruses, treatment is symptomatic. Antipyretics and NSAIDs for pain and fevers and topical lidocaine for painful oral lesions. Keeping the patient well-hydrated is very important. 

In severe cases, the patient can have altered mental status from encephalitis or myocarditis.

MEASLES

Measles, once nearly eradicated, has begun to make a comeback, largely due to the growing Anti-Vax movement. However, since COVID cases have dropped again. The measles, caused by the morbillivirus, causes 150,000 deaths per year worldwide, usually in those less than 5 years old.

The rash itself is an red-brown maculopapular rash that starts 3-5 days after systemic symptoms of severe cough, nasal congestion, red eyes, high fevers, and photophobia. 

The rash starts on the forehead and spreads to the face, neck, trunk, extremities. It spreads to the palms and soles in 50% of patients. 

Koplik spots are small white spots with red halos in the mouth on the inside of the cheeks that occur early in measles, which is very specific to measles.

Treatment is largely supportive with antipyretics, analgesics, vitamin A, and hydration. More severe cases will need hospitalization and sometimes the antiviral medication Ribavirin.

FUNGAL RASHES

INTERTRIGO

Intertrigo is inflammation and infection of the skin folds, usually in obese individuals with diabetes. This is often a fungal infection, but can have a bacterial component as well.

Candida is the most common fungus, with erythema, scaling, satellite lesions, and foul odor.

Common sites include the groin, axillae, underneath the breasts, and inbetween fat rolls.

These places will often be itchy, burning, and may smell bad.

When in the groin region, this is often called tinea cruris

Prevention and treatment includes measures to reduce friction, reduce moisture (talcom powder), use of barrier cream or ointment, and wearing breathable fabric.

The fungal infections can be treated with topical antifungals including clotrimazole cream or nystatin powder 2-3x per day.

TINEA CORPORIS

Tinea corporis, also known as ringworm, is a fungal infection of the trunk or extremities. This is spread via skin-to-skin contact with an infected individual or animal, but can also be picked up by fomites. This is also common in athletes like wrestlers and in warm-moist locker rooms where fungus likes to live.

Tinea corporis is a pruritic, round, erythematous or hyperpigmented, scaly patch or plaque with a raised border. They can coalesce together as well. Pustules can appear as well, although not as common.

Treatment inovlves the use of topical antifungals 1-2x/day for 1-3 weeks. An example includes Clotrimazole 1% BID. More severe infections may need oral antifungals.

BACTERIAL RASHES

CELLULITIS

Cellulitis is a local bacterial skin infection. This starts as some sort of breach to the skin barrier (small cut or puncture), and subsequent infection of the skin and surrounding soft tissue.

Cellulitis presents as localized erythema, edema, pain, and warmth to touch. This often presents in a unilateral leg, but can present anywhere on the body.

Cellulitis may be associated with systemic symptoms such as fevers, chills, and generalized malaise. Sometimes abscesses can form.

Cellulitis is treated with PO antibiotics, but if significant systemic symptoms, high risk, or severe disease – IV antibiotics may be necessary.

  • PO: keflex 500mg QID x 7 days
  • IV: Ancef 1gm q8h

MRSA is resistant to certain antibiotics such as those above. Risk factors for MRSA include a personal history of MRSA, recent hospitalization, surgery, or nursing home stay; recent antibiotic use, immunocompromised, open wounds, etc.

The following antbiotics should cover MRSA:

  • PO: Bactrim, Clindamycin, or Doxycycline
  • IV: Vancomycin, Linezolid, or Daptomycin

FOLLICULITIS

Folliculitis is a bacterial infection of the hair follicle, usually caused by staph aureus.

This causes a tender, red, elevated papule/pustule. These skin rashes can occur anywhere where hair follicles are. This is common after hot tub use in young healthy individuals.

If mild, folliculitis is self-limiting and may not need any specific treatment. A topical antibiotic like Mupirocin ointment TID x 7 days can be used.

More significant folliculitis can be treated with PO antibiotics like dicloxacillin, keflex, or another antibiotic with good gram positive coverage.

FURUNCLE & CARBUNCLE

A furuncle is a larger painful infection of a hair follicle which is deeper than folliculitis. Another term for furuncle is a boil.

A furuncle is a well-circumscribed painful erythematous lesion which is full of purulent fluid. This can extend into the dermis and soft tissue, leading to skin abscess. These often occur in areas of friction such as the buttock, axillae, extremities, breasts, etc.

Multiple furuncles can coalesce together to form a carbuncle.

Smaller lesions can be successfully treated with warm compresses, but larger more significant lesions will need treated with Incision & Drainage.

PO antibiotics are often given, however may not be necessary if I&D is performed. They should be given if there is cellulitis present, significant comorbidities like diabetes, with systemic symptoms, or unreliable follow-up. 

PO antibiotic choices are the same for cellulitis, except MRSA should probably be covered regardless.

Personal hygeine should be encouraged as this can help prevent skin abscesses from occurring.

 BITE-RELATED SKIN RASHES

There are plenty of bugs that can bite, sting, and infest our skin, leaving skin rashes behind.

BED BUGS

Bed bugs inhabit typically houses and beds that are somewhat unclean (very common in group homes and homeless shelters). They feed on blood which causes a local reaction in the skin.

While not everyone reacts the same to these bites, they will typically present as itchy papules or wheals, macules, or bullae. They have a habit of appearing in a linear pattern, indicating the bed bug’s trajectory. These can show up when the patient wakes up but can take a few days.

Treatment includes benadryl for itching, and if there is significant itching, a low to medium potency topical steroid can be used.

Maintaining good hygiene is essential, and a pest service will need to be used to clear out an infestation.

FLEA BITES

Flea bites occur when fleas are transmitted from animals to humans. This is usually due to infested domesticated cats or dogs who transmit the fleas to their owners.

When a flea bites, it will cause pruritic papules, most common on the ankles.

An antihistamine like benadryl or zyrtec can be given for itching. Ice packs and calamine lotion can also help with the itching. Topical steroids are usually not necessar but can help.

SPIDER BITES

Spider bites are actually pretty rare, as many spiders do not have fangs strong enough to pierce human skin. They also usually do not bite unless they are provoked or about to be squished.

Most cases of “spider bites” are something else (i.e. furuncle, abscess, MRSA, etc).

When there is a real spider bite – a papule, pustule, or wheal will appear. Two small central fang marks can often be visualized in the center. The most common areas are in the axillae, the waist, and the ankles/feet.

Most spider venoms are benign and only cause a local reaction. Black widows, funnel web, and phoneutria spiders are more poisonous and the patient may have systemic symptoms including body aches, hypertension, tachycardia, abdominal pain, etc.

Brown recluse spiders can cause systemic symptoms, but often causes a more significant local reaction with potential necrosis.

Treatment for simple spider bites involves cleaning the area, and they will spontaneously resolve in 7-10 days. If there is associated cellulitis, appropriate antibiotics should be given as above. More severe reactions may need more supportive care and hospitalization.

SCABIES

Scabies is more common in children but can happen in adults as well. It is also associated with poor hygiene and crowded living conditions similar to bed bugs.

Scabies is not exactly a bite, but rather an infestation of the scabies mite into the patient’s skin where they burrow and lay eggs, leaving behind nasty skin rashes.

Scabies rash appears initially as tiny to small erythematous papules, and will often form vesicles or pustules. They will often present in lines as the mites burrow through the epidermis. This can be easily noticeable in the web spaces of the fingers, wrists, and elbows.

Scabies is very itchy as well, and itching may persist 2-6 weeks after treatment.

Benadryl can help with the itching, but scabies will need treated with Permethrin 5% cream applied to the entire body, left on overnight (8-14 hours), and washed off in the morning. This should be reapplied in one week.

Everything else in the house that could be infested should be cleaned. Bedding and clothing within the last 48 hours should be washed in hot water and heat-dried. Non-washable items should be placed in plastic bags for at least 1 week (stuffed animals, etc).

ERYTHEMA MIGRANS

Erythema migrans is the “bulls eye rash” of early lymes disease.

This rash occurs in about 90% of lymes cases, and occurs 3-30 days after getting bit by a deer tick that carries lymes.

The initial rash will be a small red painless papule, which will expand over a few days and turn into a circular erythematous rash with central clearing and induration. This resolves in weeks if left untreated.

Treatment for this rash is treatment of the underlying Lymes disease. Lymes should be treated with doxycycline 100mg BID x 21 days.

Be sure to have your patient EAT with and directly after doxycycline, as it can cause significant GI upset and pill esophagitis.

STEMI & NSTEMI: A Nurse’s Comprehensive Guide

STEMI & NSTEMI: A Nurse’s Comprehensive Guide

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.

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!

Want to learn more?

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

With this course you will be able to:

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

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

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

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

Check out more about the course here!

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Vagal Maneuvers: How to Stop your Patient’s SVT

Vagal Maneuvers: How to Stop your Patient’s SVT

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

Author | Nurse Practitioner

Vagal maneuvers are used in the clinical setting to slow down fast heart rates – primarily for supraventricular tachycardia (SVT)  and sometimes rapid atrial fibrillation (AF RVR).

There are numerous physical maneuvers that can slow down the heart rate – and there is an important modified technique which can almost triple your chances of success!

Vagal maneuvers for SVT fbook image

Svt and Vagal Maneuvers

Supraventricular Tachycardia (SVT) is a very rapid regularly arrhythmia caused by a reentrant loop within the heart.

Essentially – the signal goes around and around in a circuit, producing very fast heart rates.

reentrant loop gif

While SVT is an umbrella term for any tachycardia originating above the ventricles of the heart, it usually is used in reference to AV Nodal Reentrant Tachycardia (AVNRT). This arrhythmia is due to a reentrant loop within/near the AV node itself.

Some patients have abnormal conduction tissue in this area, and if a premature beat comes at the wrong time – it can throw them into this very fast heart rhythm.

This condition occurs more often in younger patients, females, and can be secondary to certain triggers like exercise, stimulants, or even alcohol.

Patients will usually be symptomatic and feel palpitations, fatigue, or dizziness. They can also have chest pain, SOB, or syncope.

Remember when the heart is beating this fast, the cardiac chamber’s ability to fill is decreased, and cardiac output can suffer – leading to symptoms.

When a patient comes in with SVT, their heart rate is usually very fast, with rates often between 150-200 bpm.

AVNRT-svt

We want to stop or “break” this rhythm as soon as possible, so the patient does not decompensate.

If we look at the Adult tachycardia ACLS algorithm, we can see that the first thing we do to attempt to stop the SVT in a stable patient is vagal maneuvers.

The Vagus nerve and the Heart

In order to understand vagal maneuvers, you first need to understand how the vagus nerve works.

The vagus nerve is the primary method that the parasympathetic nervous system affects the body.

This is the 10th cranial nerve which travels from your brain throughout the body. This is how the brain controls certain automatic functions.

When the vagus nerve is activated, the following effects on the body occur:

  • Bronchial constriction
  • Pupillary constriction
  • Increased blood flow to the stomach’
  • Increased digestion

Remember – “rest and digest”

Regarding the heart, the vagus nerve also has important physiological effects on the cardiac system. These include:

  • Slowing of the heart rate
  • Slowing of the conduction velocity of the AV node
  • Decreases the strength of contractions

As you can see, stimulation of the vagal nerve can be utilized to slow the conduction and increase the refractory period of the AV node which hopefully breaks the SVT reentrant loop, leading to conversion back to normal sinus rhythm (NSR).

There are various physical maneuvers that can stimulate the vagus nerve – and many you may do without trying. These include:

  • Coughing
  • Vomiting
  • Cold water immersion

Then there are certain physical maneuvers termed “vagal maneuvers” that we can perform in the hospital to intentionally cause vagal response and hopefully slow down a tachyarrhythmia such as with SVT.

These maneuvers include the Valsalva maneuver and the carotid sinus massage.

But did you know that by modifying the Valsalva maneuver – you can almost triple your chances of success?

The Modified Valsalva Maneuver

The Valsalva maneuver is the classic vagal maneuver used to stimulate the vagus nerve and stop SVT.

This is used on patients who are stable (stable vital signs) and can follow commands.

To perform the Valsalva maneuver, the patient intentionally “bears down” or strains for 10-15 seconds.

This has a 17% success rate in converting SVT. However, by modifying the Valsalva maneuver we can almost triple this success rate!

The Modified valsalva or the positional valsalva maneuver has a significantly higher success rate of 43%!

That’s almost half of your patients with SVT who this can convert back to NSR without any additional medications or interventions.

To perform the modified Valsalva maneuver:

  1. Have a Physician or APP at the bedside
  2. Place the patient in a semi-recumbent position (45° Semi-fowlers)
  3. Have the patient take a normal breath in
  4. Have them forcefully exhale with a closed glottis (bearing down) for 15 seconds
  5. Immediately place them supine and raise their legs to 45 degrees for 15 seconds
  6. Return to semi-fowlers position and watch for up to 1 minute for resolution of the SVT

Clinical Tip: If the patient has trouble bearing down, you can place an empty 10-mL syringe in their mouth and have them blow hard enough to see the plunger move.

As you can see, this technique requires a few assistants, but it is clearly the better option when attempting to convert SVT with vagal maneuvers.

The modified valsalva maneuver infographic

The Carotid Sinus Massage

The carotid sinus massage is a vagal maneuver that you can perform on someone who cannot follow commands.

The carotid sinus is an area located just below the internal carotid artery at the level of the thyroid cartilage, near the pulse.

This area is very sensitive to mechanical pressure, and mechanical pressure to this area can stimulate the vagus nerve.

To perform the carotid sinus massage:

  1. Place the patient supine with their neck extended toward the opposite side
  2. Ensure there is no carotid bruit with your stethoscope
  3. Locate the carotid sinus. This is inferior to the angle of the mandible at the level of the thyroid cartilage near the pulse
  4. Apply firm pressure for 5-10 seconds
  5. You can repeat on the other side if needed

The carotid sinus should never be performed in the following circumstances:

  • Without a physician / APP at the bedside
  • On both sides simultaneously
  • In someone with TIA or stroke within the last 3 months
  • In someone with known carotid stenosis or active carotid bruit

Carotid sinus massage infographic

Complications of Vagal Maneuvers

Any side effects from vagal maneuvers are usually short-lived and an “over-exaggeration” of expected effects.

These include sinus pauses, brief asystole, bradycardia, AV blocks and hypotension.

These will usually fix themselves within seconds to minutes.

Strokes are a major concern with the carotid sinus massage and can happen in <1% of patients.

This is why those with potential carotid stenosis or recent history of strokes should not have the carotid sinus massage.

References:

Aehlert, B. J. (2017). ECGs made easy (6th ed.). Elsevier Health Sciences.

Burns, E. (2019). Supraventricular tachycardia. In ECG Library. Retrieved from https://litfl.com/supraventricular-tachycardia-svt-ecg-library/

Frisch, D. R., Zimetbaum, P. J. (2020). Vagal maneuvers. In UpToDate. Retrieved from https://www.uptodate.com/contents/vagal-maneuvers

Grauer, K., MD. (2014). ECG Pocket Brain: Expanded Version (6th ed., pp. 65-68). Gainesville, FL: KG/EKG Press.

Knight, B. P. (2020). Atrioventricular nodal reentrant tachycardia. In UpToDate. Retrieved from https://www.uptodate.com/contents/atrioventricular-nodal-reentrant-tachycardia

Tintinalli, J. E., Brady, W. J., Laughrey, T. S., & Ghaemmaghami, C. A. (2016). Cardiac Rhythm Disturbances. In Tintinalli’s emergency medicine: A comprehensive study guide (8th ed., pp. 126). McGraw-Hill Education.

Want to Learn More?

If you want to learn more about vagal maneuvers, SVT, and every other cardiac arrhythmia – check out my ECG Rhythm online video course out now!

It’s specifically designed for nurses, and not only teaches you how to identify each arrhythmia, but also why and how they occur, and what to do about it!

If you’re not ready to take that leap yet but still want to learn more about ECG rhythms – be sure to download my free ECG Cheat Sheet below!

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