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10 Clinical Calculators for Inpatient Providers

10 Clinical Calculators for Inpatient Providers

Working in a hospital as a provider can be unexpected and stressful. There are so many factors to consider when managing a patient’s acute and chronic diseases. Luckily, there has been a great amount of research involving management of patients within the hospital. There are many different systems and calculations which can help with risk stratification, prevention, diagnosis, and management. These inpatient clinical calculators are sure to be useful to you during your shift in the hospital!

1

Padua Predictive Score for Risk of VTE

Inpatient medicine constantly involves predicting, preventing, diagnosing, and treating blood clots. Venous Thromboembolism (VTE) is the general term used to describe blood clots (thrombi) in the body which may have moved (embolized) to the lungs (pulmonary embolism).

VTE are an important cause of morbidity and mortality – especially with patient’s who have many comorbidities. Approximately 900,000 patients in the US are affected by VTE each year, and 60,000-100,00 American’s die. The first symptom of a PE is sudden cardiac death in 25% of people! You can see why it is SO important to prevent this from occurring within the hospital. Those admitted to the hospital are at higher risk for developing health-care associated VTE due to decreased mobility and recent surgery and/or procedures.

The Padua Predictive Score is a useful tool which separates patients into high and low risk groups for developing VTE. Those who score < 4 points are considered low-risk, and those >/= 4 are considered high risk. This calculator takes into account 11 factors which increase risk for VTE including age, mobility, history of cancer, heart disease, or respiratory disease, obesity, among others. If scores less than 4, consider non-pharmacologic measures such as SCDs or early ambulation. With scores greater than 4, pharmacologic measures are indicated including unfractionated heparin (UFH) or Lovenox (Enoxaparin).

Check out the Calculator!

2

Wells’ Criteria for DVT

The Wells’ criteria score system is a method to quantify the diagnostic probability for a patient presenting with a DVT/PE, however the calculators are different depending on which you are assessing for.

The Wells’ score for DVT involves specific risk factors for developing a DVT including the presence of symptoms such as calf/leg edema, recent immobility or surgery, leg tenderness, etc. The modified Wells’ score factors in a previous history of DVT.

Low Probability

Scores of 0 or less have a low-probability of needing further workout to rule out a DVT.

Moderate Probability

Scores of 1-2 points have a moderate probability and should get a high-sensitive D-dimer result. If <500 ng/ml, this effectively rules out a DVT. However, since the D-dimer test is nonspecific, a score >500 ng/ml warrants further investigation (i.e. a venous duplex).

High Probability

Scores of 3-8 have a high probability of a DVT and should get a venous duplex to rule out a clot regardless.

https://www.mdcalc.com/wells-criteria-dvt

3

Wells’ Criteria for PE

Just like the Wells’ score for DVT, there is a calculator for the pretest probability of a PE. The calculator assesses for PE risk factors including s/s of DVT, clinical suspicion of PE, HR >100, immobility/recent surgery, previous VTE, the presence of hemoptysis, and malignancy.

Low Probability

Scores <2 indicate a low probability of a PE. However, if s/s of PE are present (pleuritic chest pain, SOB, tachycardia, etc) then clinicians are encourages to use the PERC rule. The PERC rule is a list of 8 criteria which effectively rule out a PE in those with low-probability of having a PE. The patient must meet all of the following criteria:

  • Age < 50 years
  • Heart rate < 100 bpm
  • Oxyhemoglobin saturation ≥ 95% on RA
  • No hymoptysis
  • No estrogen use
  • No prior DVT/PE
  • No unilateral leg swelling
  • No surgery/trauma requiring hospitalization within the prior 4 weeks

If the patient meets any of the above, a D-dimer should be performed. In those already admitted to the hospital or critically ill patients, a D-dimer should be obtained regardless. As above, levels < 500 ng/ml do not require further workup, but levels > 500 ng/ml need further workup (i.e. CT Pulmonary Angiography).

Moderate Probability

Scores 2-6 indicate moderate probability for having a PE. This is handled with a high-sensitivity D-dimer score as above – the PERC rule is not used. If less than the cut-off, PE is ruled out. Otherwise, further testing must be performed.

High Probability

Scores >6 indicate high probability for having a PE. Those with high-risk should NOT have a D-dimer level checked. Instead, they should have diagnostic imaging to rule out PE regardless. The preferred test is a CTPA, but if this cannot be obtained than a V/Q scan should be ordered.

https://www.mdcalc.com/wells-criteria-pulmonary-embolism

4

CHA₂DS₂-VASc Score for AFIB Stroke Risk

Some medical conditions predispose patients to blood clot formation. One of those conditions is Atrial fibrillation, which increases the chance of clot formation within the atria of the heart. Clots formed in the right atria may embolize to the lungs, and clots formed in the left atria may embolize to the brain and cause a embolic stroke.

The CHA₂DS₂-VASc Score is a scoring system which helps clinicians to determine the need for oral anticoagulation to prevent clot formation and subsequent embolization. The score includes their age, sex, and their medical history including CHF, HTN, CVA, VTE, Vascular dz, or Diabetes.

Low Risk

Scores of 0 indicate a low-risk for stroke in those with Afib. No oral anticoagulation is recommended. Sometimes these patients are placed on low-dose aspirin.

Low-Moderate Risk

Scores of 1 indicate a low-moderate risk of stroke in those with Afib. In this category, clinical judgement must be used. If you are a generalist, remember that cardiology will often be the one to make this decision. Many choose not to anticoagulate those who’s only score is that they are a woman.

Moderate-High Risk

Scores ≥ 2 points indicate a moderate-high risk of stroke in those with Afib. Anticoagulation in this group is highly recommended. All studies have shown the benefit of anticoagulation significantly exceeds the risk for almost all patients with afib and a score ≥ 2. Typically the cardiologists specialists will be determining which anticoagulation that will be used.

https://www.uptodate.com/contents/clinical-presentation-evaluation-and-diagnosis-of-the-nonpregnant-adult-with-suspected-acute-pulmonary-embolism

5

HAS-BLED Score for Major Bleeding Risk

HAS-BLED is a system which scores the risk for major bleeding for those with Afib who are on oral anticoagulation. The system is scored by the following:

  • Hypertension – 1 point
  • Abnormal renal and/or hepatic function – 1 point each
  • Stroke – 1 point
  • Bleeding tendency/predisposition – 1 point
  • Labile INR on warfarin – 1 point
  • Elderly (age >65) – 1 point
  • Drugs (asa or NSAIDs) and/or alcohol – 1 point each

https://www.mdcalc.com/has-bled-score-major-bleeding-risk

Results are not separated into probability categories. Instead, clinical judgement must weight the benefits vs risks. However, the following risk can be estimated:

  • 0 points – 1.13 bleeds per 100 patient-years
  • 1 point – 1.02 bleeds per 100 patient-years
  • 2 points – 1.88 bleeds per 100 patient-years
  • 3 points – 3.74 bleeds per 100 patient-years
  • 4 points – 8.70 bleeds per 100 patient-years
  • 5-9 points – insufficient data (but high risk)

Remember this decision should be made with specialty consultation to cardiology.

6

Serum Osmolality

Other than blood clots and anticoagulation, inpatient providers often have to manage electrolyte abnormalities. One important electrolyte which often is low is sodium – called hyponatremia. The treatment of hyponatremia depends on the etiology. In order to determine the cause, an important calculation is the serum osmolality.

The calculator uses the serum sodium, BUN, Glucose, and ETOH to estimate the osmolality.

HypoOsmolar

Calculated osmolality <275 mOsm/kg is considered hypoosmolar (and usually hypotonic). This is the most common type of hyponatremia and fluid status must then be considered to determine etiology:

Euvolemic

Often caused by SIADH (from many causes) or thiazide diuretics.

Hypovolemic

Often caused by decreased PO intake, diuretics, GI losses, 3rd spacing, or adrenal insufficiency. This is treated with careful fluid resuscitation as replacing sodium too quickly can lead to deleterious effects such as osmotic demyelination syndrome (previously referred to as central pontine myelinosis).

Hypervolemic

Often caused by heart failure, liver cirrhosis, nephrotic syndrome, and severe AKI/CKD. Treatment in this case involves restricting water, loop diuretics (i.e. IV Lasix), and sometimes medications.

IsoOsmolar

Calculated osmolality 275-290 mOsm/kg is considered IsoOsmolar (and usually isotonic). This used to be caused by lab errors secondary to high lipid or protein levels.  However, Ion-specific electrodes are now used in the lab, so this error does not really happen anymore.

HyperOsmolar

Calculated osmolality >290 mOsm/kg is considered hyperOsmolary (and usually hypertonic). This is usually caused from solutes which cause osmotoic shifts of water out of cells into the extracellular fluid (i.e. glucose, mannitol, sorbitol, etc).

https://www.mdcalc.com/serum-osmolality-osmolarity

7

Sodium Correction for Hyperglycemia

Due to the osmotic shifts caused by hyperglycemia, hyponatremia should be corrected when glucose levels are elevated. The serum sodium concentration will fall by ~2. mEq/L for every 100 mg/dL of glucose elevation. For example, if the blood sugar is 400 and the sodium level is 124, the corrected sodium level is ~130 mEq/L. But you don’t have to do math, just use the calculator! It’s recommended to base your treatment plan on the calculated sodium level, as once the glucose is corrected the osmotic shifts will resolve.

https://www.mdcalc.com/sodium-correction-hyperglycemia

8

Fractional Excretion of Sodium (FENa)

The Fractional Excretion of Sodium (FENa) is calculated to determine the cause of acute kidney injury (AKI), and is a useful tool that many nephrologists utilize. This can help determine the difference between prerenal AKI from Acute tubular necrosis (ATN). This is calculated from the serum sodium creatinine, and the urine sodium and creatinine.

FENa levels < 1% generally indicate prerenal disease (i.e. decreased bloodflow to kidneys). Levels >2% usually indicates ATN. Levels between 1-2% can indicate both.

Remember that the FENa will not be accurate if the patient is on a diuretic. In general FENa is utilized by Nephrology, but can be useful to calculate if the etiology is unclear.

https://www.mdcalc.com/fractional-excretion-sodium-fena

9

Fractional Excretion of Urea (FEUrea)

The Fractional Excretion of Urea (FEUrea) can be used to differentiate between prerenal AKI and ATN in patients who are on diuretics as FENa will not be accurate. Levels 50-65% generally indicate ATN , and levels <35% indicate prerenal disease.

Again, many factors can determine these tests and they should be interpreted with the consultation of specialists (nephrologists).

https://www.mdcalc.com/fractional-excretion-urea-feurea

10

    Calcium Correction for Hypoalbuminemia

Unrelated to sodium and fluid status, calcium levels can be falsely altered in the presence of hypoalbuminemia. Calcium ions have two forms – ionized and protein-bound. About 40% of calcium in the blood is bound to protein (i.e. albumin), and about 50% circulates as free ionized calcium. The ionized calcium is what is truly clinically significant because this is what is physiologically active. If a patient is symptomatic from hypocalcemia – their ionized calcium will be low.

Since almost half of the calcium in the bloodstream attached to albumin, abnormal albumin levels will affect serum calcium levels. To correct this, you need to know the patients serum calcium and their albumin level. The calculator will give you a good idea of what their corrected calcium level actually is. So if you see a malnourished patient with an Albumin of 2.0 and a serum calcium of 7.0, the corrected calcium is 8.6 mg/dl.

This is not an exact science and many factors (i.e. acid-base disturbance) will alter calcium binding to protein and may cause ionized calcium levels to fluctuate. This is why most clinicians will order an ionized calcium level when serum calcium levels are significantly low (even in the presence of low albumin).

https://www.mdcalc.com/calcium-correction-hypoalbuminemia

1

Padua Predictive Score for Risk of VTE

Inpatient medicine constantly involves predicting, preventing, diagnosing, and treating blood clots. Venous Thromboembolism (VTE) is the general term used to describe blood clots (thrombi) in the body which may have moved (embolized) to the lungs (pulmonary embolism).

VTE are an important cause of morbidity and mortality – especially with patient’s who have many comorbidities. Approximately 900,000 patients in the US are affected by VTE each year, and of those 60,000-100,00 die. The first symptom of a PE is sudden cardiac death in 25% of people! You can see why it is SO important to prevent this from occurring within the hospital. Those admitted to the hospital are at higher risk for developing health-care associated VTE due to decreased mobility and recent surgery and/or procedures.

The Padua Predictive Score is a useful tool which separates patients into high and low risk groups for developing VTE. Those who score < 4 points are considered low-risk, and those ≥ 4 are considered high risk. This calculator takes into account 11 factors which increase risk for VTE including age, mobility, history of cancer, heart disease, or respiratory disease, obesity, among others. If scores less than 4, consider non-pharmacologic measures such as SCDs or early ambulation. With scores 4 or greater, pharmacologic measures are indicated including unfractionated heparin (UFH) or Lovenox (Enoxaparin).

2

Wells’ Criteria for DVT

The Wells’ criteria score system is a method to quantify the diagnostic probability for a patient presenting with a DVT/PE, however the calculators are different depending on which you are assessing for.

The Wells’ score for DVT involves specific risk factors for developing a DVT including the presence of symptoms such as calf/leg edema, recent immobility or surgery, leg tenderness, etc. The modified Wells’ score factors in a previous history of DVT, as these patients are more likely to develop another one.

Low Probability

Scores of 0 or less have a low-probability of DVT, and thus usually do not warrant further workup to rule out a DVT.

Moderate Probability

Scores of 1-2 points have a moderate probability and should get a high-sensitive D-dimer. If <500 ng/ml, this effectively rules out a DVT. However, since the D-dimer test is nonspecific, a score >500 ng/ml warrants further investigation (i.e. a venous duplex).

High Probability

Scores of 3-8 have a high probability of a DVT and should get a venous duplex to rule out a clot regardless. This means that a D-dimer test is not indicated since a Venous Duplex will be obtained regardless.

3

Wells’ Criteria for PE

Just like the Wells’ score for DVT, there is a calculator for the pretest probability of a PE. This calculator assesses for PE risk factors including s/s of DVT, clinical suspicion of PE, HR >100, immobility/recent surgery, previous VTE, the presence of hemoptysis, or malignancy.

Low Probability

Scores <2 indicate a low probability of a PE. However, if s/s of PE are present (pleuritic chest pain, SOB, tachycardia, etc) then clinicians are encourages to use the PERC rule. The PERC rule is a list of 8 criteria which effectively rules out a PE in those with low-probability of having a PE. The patient must meet all of the following criteria:

  • Age < 50 years
  • Heart rate < 100 bpm
  • Oxyhemoglobin saturation ≥ 95% on RA
  • No hymoptysis
  • No estrogen use
  • No prior DVT/PE
  • No unilateral leg swelling
  • No surgery/trauma requiring hospitalization within the prior 4 weeks

If the patient meets any of the above, a D-dimer should be performed. In those already admitted to the hospital or critically ill patients, a D-dimer should be obtained regardless. As above, levels < 500 ng/ml do not require further workup, but levels > 500 ng/ml do (i.e. CT Pulmonary Angiography).

Moderate Probability

Scores 2-6 indicate moderate probability for having a PE. This is handled with a high-sensitivity D-dimer score as above – the PERC rule is not used. If less than the cut-off, PE is ruled out. Otherwise, further testing must be performed.

High Probability

Scores >6 indicate high probability for having a PE. Those with high-risk should NOT have a D-dimer level checked. Instead, they should have diagnostic imaging to rule out PE regardless. The preferred test is a CT Pulmonary Angiography (CTPA) – but if this cannot be obtained, a V/Q scan should be ordered.

4

CHA₂DS₂-VASc Score for AFIB Stroke Risk

Some medical conditions predispose patients to blood clot formation. One of those conditions is Atrial fibrillation, which increases the chance of clot formation within the atria of the heart. Clots formed in the right atria may embolize to the lungs and cause a pulmonary embolism, and clots formed in the left atria may embolize to the brain and cause an embolic stroke.

The CHA₂DS₂-VASc Score is a scoring system which helps clinicians to determine the need for oral anticoagulation to prevent clot formation and subsequent embolization. The score includes their age, sex, and their medical history including CHF, HTN, CVA, VTE, Vascular dz, or Diabetes.

Low Risk

Scores of 0 indicate a low-risk for stroke in those with Afib. No oral anticoagulation is recommended. Sometimes these patients are placed on low-dose aspirin.

Low-Moderate Risk

Scores of 1 indicate a low-moderate risk of stroke in those with Afib. In this category, clinical judgement must be used. If you are a generalist, remember that cardiology will often be the one to make this decision. Many choose not to anticoagulate those who’s only score is that they are a woman.

Moderate-High Risk

Scores ≥ 2 points indicate a moderate-high risk of stroke in those with Afib. Anticoagulation in this group is highly recommended. All studies have shown the benefit of anticoagulation significantly exceeds the risk for almost all patients with afib and a score ≥ 2. Typically the cardiologists specialists will be determining which anticoagulation that will be used.

Remember to always take into account the patient’s risk of major bleeding (see below!)

 

5

HAS-BLED Score for Major Bleeding Risk

HAS-BLED is a system which quantifies the risk for major bleeding for those with Afib who are on oral anticoagulation. The system is scored by the following:

  • Hypertension – 1 point
  • Abnormal renal and/or hepatic function – 1 point each
  • Stroke – 1 point
  • Bleeding tendency/predisposition – 1 point
  • Labile INR on warfarin – 1 point
  • Elderly (age >65) – 1 point
  • Drugs (asa or NSAIDs) and/or alcohol – 1 point each

Results are not separated into probability categories. Instead, clinical judgement must weight the benefits vs risks. However, the following risk can be estimated:

  • 0 points – 1.13 bleeds per 100 patient-years
  • 1 point – 1.02 bleeds per 100 patient-years
  • 2 points – 1.88 bleeds per 100 patient-years
  • 3 points – 3.74 bleeds per 100 patient-years
  • 4 points – 8.70 bleeds per 100 patient-years
  • 5-9 points – insufficient data (but high risk)

Remember the decision for a patient with Afib to not be on oral anticoagulation should be made with specialty consultation.

6

Serum Osmolality

Other than blood clots and anticoagulation, inpatient providers often have to manage electrolyte abnormalities. One important electrolyte which often is low is sodium – called hyponatremia. The management of hyponatremia depends on the etiology. In order to determine the cause, an important calculation is the serum osmolality.

The calculator uses the serum sodium, BUN, Glucose, and ETOH to estimate the osmolality.

HypoOsmolar

Calculated osmolality <275 mOsm/kg is considered hypoosmolar (and usually hypotonic). This is the most common type of hyponatremia and fluid status must then be considered to determine etiology:

Euvolemic

Often caused by SIADH (from many causes) or thiazide diuretics.

Hypovolemic

Often caused by decreased PO intake, diuretics, GI losses, 3rd spacing, or adrenal insufficiency. This is treated with careful fluid resuscitation as replacing sodium too quickly can lead to deleterious effects such as osmotic demyelination syndrome (previously referred to as central pontine myelinosis).

Hypervolemic

Often caused by heart failure, liver cirrhosis, nephrotic syndrome, or severe AKI/CKD. Treatment in this case involves restricting water, administering loop diuretics (i.e. IV Lasix), and sometimes other medications.

IsoOsmolar

Calculated osmolality 275-290 mOsm/kg is considered IsoOsmolar (and usually isotonic). This used to be caused by lab errors secondary to high lipid or protein levels.  However, ion-specific electrodes are now used in the lab, so this error does not really happen anymore.

HyperOsmolar

Calculated osmolality >290 mOsm/kg is considered hyperOsmolary (and usually hypertonic). This is usually caused from solutes which cause osmotoic shifts of water out of cells into the extracellular fluid (i.e. glucose, mannitol, sorbitol, etc).

 

7

Sodium Correction for Hyperglycemia

Due to the osmotic shifts caused by hyperglycemia, hyponatremia should be corrected when glucose levels are elevated. The serum sodium concentration will fall by ~2. mEq/L for every 100 mg/dL of glucose elevation. For example, if the blood sugar is 400 and the sodium level is 124, the corrected sodium level is ~130 mEq/L. But you don’t have to do math, just use the calculator! It’s recommended to base your treatment plan on the corrected sodium level, as once the glucose is corrected the osmotic shifts will resolve.

8

Maintenance Fluid Rate

As inpatient providers, we have to order IV fluids on many patients. Maintenance fluids may need ordered if the patient is NPO, or if they have fluid losses/dehydration. In order to determine the best rate at which to run the IV fluids, there is a simple calculation. Take their weight in Kg, subtract 20 Kg and add 60mL. Then for every over Kg left, add 1mL. So a 60Kg patient gets 100ml/hr. If this is confusing – you can just use the calculator below!

Keep in mind this rate is a general estimation, and the patient’s own medical history should be taken into account. If they are fluid overloaded (i.e. CHF, Liver cirrhosis, etc), then a slower rate may be more appropriate. Always use your physical examination to guide your management. If the patient is elderly, consider slowing the rate as well. If the patient is having continuous fluid losses (i.e. diarrhea), then consider increasing the rate to 1.5x the maintenance rate – or using your best judgement.

(The calculator also lists the 20ml/kg bolus amount for sepsis patients)

9

Calcium Correction for Hypoalbuminemia

Unrelated to sodium and fluid status, calcium levels can be falsely altered in the presence of hypoalbuminemia. Calcium ions have two forms – ionized and protein-bound. About 40% of calcium in the blood is bound to protein (i.e. albumin), and about 50% circulates as free ionized calcium. The ionized calcium is what is truly clinically significant because this is what is physiologically active. If a patient is symptomatic from hypocalcemia – their ionized calcium will be low.

Since almost half of the calcium in the bloodstream attached to albumin, abnormal albumin levels will affect serum calcium levels. To correct this, you need to know the patients serum calcium and their albumin level. The calculator will give you a good idea of what their corrected calcium level actually is. So if you see a malnourished patient with an Albumin of 2.0 and a serum calcium of 7.0, the corrected calcium is 8.6 mg/dl.

This is not an exact science and many factors (i.e. acid-base disturbance) will alter calcium binding to protein and may cause ionized calcium levels to fluctuate. This is why most clinicians will order an ionized calcium level when serum calcium levels are significantly low (even in the presence of low albumin).

10

   Arterial Blood Gas (ABG) Analyzer

Arterial Blood Gases (ABGs) are commonly ordered in patients with respiratory failure in the hospital. This helps clinicians determine etiology and guides management of many respiratory conditions. If you struggle with analyzing ABGs, this calculator can help. Simply input the pH, PaCO2, Bicarb, Sodium, Chloride, and Albumin. This will help you determine whether the ABG abnormality is respiratory, metabolic, and which type with compensation (if any).

It is important for clinicians to be able to analyze blood gases on their own as well. You can read more about ABG interpretation in my ABG guide!

 

If you’re a practicing NP or NP student and need access to my free NP Resource library – sign up here! It has both inpatient and outpatient SOAP note templates, History and physical sheets, death pronouncement notes, and more to come!

References:

Barbar, S., Noventa, F., Rossetto, V., Ferrari, A., Brandolin, B., Perlati, M., … Prandoni, P. (2010). A risk assessment model for the identification of hospitalized medical patients at risk for venous thromboembolism: the Padua Prediction Score. Journal of Thrombosis and Haemostasis, 8(11), 2450-2457. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/20738765

Bauer, K. A., & Lip, G. Y. (2019). Overview of the causes of venous thrombosis. In UpToDate. Retrieved from https://www.uptodate.com/contents/overview-of-the-causes-of-venous-thrombosis

Data and Statistics on Venous Thromboembolism. (2019, August 9). Retrieved August 11, 2019, from https://www.cdc.gov/ncbddd/dvt/data.html

Garcia, D. A., & Crowther, M. (2019). Risks and prevention of bleeding with oral anticoagulants. In UpToDate. Retrieved from https://www.uptodate.com/contents/risks-and-prevention-of-bleeding-with-oral-anticoagulants

Goltzman, D. (2019). Diagnostic approach to hypocalcemia. In UpToDate. Retrieved from https://www.uptodate.com/contents/diagnostic-approach-to-hypocalcemia

Higgins, C. (2007, July). Ionized calcium. Retrieved from https://acutecaretesting.org/en/articles/ionized-calcium

Hoorn, E. J., & Sterns, R. H. (2019). Causes of hyponatremia without hypotonicity (including pseudohyponatremia). In UpToDate. Retrieved from https://www.uptodate.com/contents/causes-of-hyponatremia-without-hypotonicity-including-pseudohyponatremia

Kearon, C., & Bauer, K. A. (2019). Clinical presentation and diagnosis of the nonpregnant adult with suspected deep vein thrombosis of the lower extremity. In UpToDate. Retrieved from https://www.uptodate.com/contents/clinical-presentation-and-diagnosis-of-the-nonpregnant-adult-with-suspected-deep-vein-thrombosis-of-the-lower-extremity

Lip, G. Y. (2011). Implications of the CHA2DS2-VASc and HAS-BLED Scores for Thromboprophylaxis in Atrial Fibrillation. The American Journal of Medicine, 124(2), 111-114. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/20887966

Manning, W. J., Singer, D. E., & Lip, G. Y. (2019). Atrial fibrillation: Anticoagulant therapy to prevent thromboembolism. In UpToDate. Retrieved from https://www.uptodate.com/contents/atrial-fibrillation-anticoagulant-therapy-to-prevent-thromboembolism

Sterns, R. H. (2019). Causes of hypotonic hyponatremia in adults. In UpToDate. Retrieved from https://www.uptodate.com/contents/causes-of-hypotonic-hyponatremia-in-adults

Sterns, R. H. (2019). Overview of the treatment of hyponatremia in adults. In UpToDate. Retrieved from https://www.uptodate.com/contents/overview-of-the-treatment-of-hyponatremia-in-adults

Sterns, R. H. (2019). General principles of disorders of water balance (hyponatremia and hypernatremia) and sodium balance (hypovolemia and edema). In UpToDate. Retrieved from https://www.uptodate.com/contents/general-principles-of-disorders-of-water-balance-hyponatremia-and-hypernatremia-and-sodium-balance-hypovolemia-and-edema

Sterns, R. H. (n.d.). Diagnostic evaluation of adults with hyponatremia. In UpToDate. Retrieved from https://www.uptodate.com/contents/diagnostic-evaluation-of-adults-with-hyponatremia

Thompson, B. T., Kabrhel, C., & Pena, C. (2019). Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism. In UpToDate. Retrieved from https://www.uptodate.com/contents/clinical-presentation-evaluation-and-diagnosis-of-the-nonpregnant-adult-with-suspected-acute-pulmonary-embolism

Wells, P. S., Anderson, D. R., Bormanis, J., Guy, F., Mitchell, M., Gray, L., … Lewandowski, B. (1997). Value of assessment of pretest probability of deep-vein thrombosis in clinical management. The Lancet, 350(9094), 1795-1798. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed?term=9428249

Yu, A. S., & Stubbs, J. R. (2019). Relation between total and ionized serum calcium concentrations. In UpToDate. Retrieved from https://www.uptodate.com/contents/relation-between-total-and-ionized-serum-calcium-concentrations

Six Steps for Sepsis Management

Six Steps for Sepsis Management

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

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

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

  1. Recognition and Early Intervention

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

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

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

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

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

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

  2. Fluid Resuscitation!

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

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

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

  3. Timely Antibiotic Administration

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

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

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

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

  4. Hemodynamic Management

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

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

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

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

  5. Monitoring

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

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

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

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

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

  6. Patient Disposition and Follow-Up

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

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

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

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

 

Welcome!

Will Kelly, MSN, FNP-C
Thank you for visiting my site! I help nurses and nurse practitioners improve their clinical knowledge by providing high-quality content to turn their nursing education into practical application!  Read More

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

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

It is essential that nurses be able to interpret cardiac labs – it could literally be the difference between life and death for your patients! Learn about cardiac labs including Troponin, CK, CK-MB, and BNP – and what these labs could mean for your patients!

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

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

If you work in the hospital – it is essential that you know and understand labs pertaining to the heart. Cardiac labs are life and death, and a good base knowledge of these will help you in the clinical setting – whether you work in the Emergency Department, Med-Surg, Critical Care, or really any other unit within the hospital. Cardiac labs are used to identify cardiac conditions and will often guide diagnostic and treatment courses for your patients – so buckle up because you’re about to become an expert!

Troponin

I am starting with this lab because it is the most important cardiac lab that you will see, and it is also the most common. But what exactly is Troponin? Troponin is family of enzymes within muscle cells. Two members of this family, Troponin-I and Troponin-T, are found pretty much exclusive to cardiac tissue. When myocardial cell death occurs and the cell lyses or splits apart – the cell releases its contents including it’s troponin. Since the heart is really the only tissue to have this, the presence in the blood stream signifies myocardial necrosis or cell death. The higher the level of Troponin – the more cell death has occurred. As you can see – this can come in handy when diagnosing heart attacks. It is the preferred blood test in evaluating patients for a myocardial infarction.

Cardiac Biomarkers | Learn about troponin, CK, CK-MB, and BNP (and NT-ProBNP)Normal Levels

 Normal levels of Troponin (whether T or I) are zero, as or close to zero as you can get. Labs may utilize different assays which may have different specific cutoffs, but generally you will find:

Troponin-I = <0.04 ng/mL

Troponin-T = ≤0.01 ng/mL

Pattern

Both Troponins will typically show up within 2-3 hours after cell death has begun – but they may not be detectable until 6-12 hours later. It will peak in 24 hours but can take up to 1-2 weeks for the troponin to return back to non-detectable levels.

Significance

As stated above – Troponin signifies myocardial cellular death. The prime example of this is during a Myocardial infarction (whether STEMI or NSTEMI… see below). However, there are other causes that can cause mild elevations in troponin, such as:

  • Demand-ischemia: Sepsis, hypovolemia, shock, arrhythmias, CHF exacerbation.
  • Other cardiac damage: Various forms of carditis, aortic dissection, post-cardiac surgery, post-cardiac cath, CPR, defibrillation.
  • Kidneys: Renal damage, Acute Kidney injury, Chronic kidney disease (Especially if on dialysis).
  • Vascular: Pulmonary embolism and Stroke.

This isn’t a complete list, but most of these may cause minor elevations in the Troponin. When cardiac damage is sustained, the Troponin level should rise significantly.  Aside from cardiac surgery, CPR, or inflammation of the heart itself – this likely will not occur as dramatically otherwise.


STEMI

It doesn’t matter what the Troponin level is during a STEMI – if its new onset – expect the Troponin to be negative. If the EKG reads STEMI – you need to hook your pt up to the defibrillator, establish 2-3 large-bore IVs, give that pt ASA, Fluids, pain relief, nitro, and get that pt to the Cath lab ASAP.

NSTEMI

This is really where troponins shine. NSTEMIs are a type of myocardial infarction that don’t have ST elevation on the EKG, so serial checks of the Troponin can determine whether or not the pt is actually having a heart attack. It will vary based on the facility, but most facilities will check the troponin Q6-8hrs at least 2-3 times. 2-3 negative troponins in a row basically rule out any type of acute coronary syndrome (heart attack).

Is there a specific level that a troponin has to rise to be considered an nSTEMI? Not really, it just needs to be above the 99th percentile – which is any positive number. However, just because there is elevation in Troponin doesn’t mean it is an NSTEMI (See above for other causes of troponin elevation). These patients should be having some symptoms of an MI (chest pain, SOB, nausea), and/or EKG changes (ST-depressions or T-wave inversions).

Something important to remember is that NOT ALL PATIENTS EXPERIENCE CLASSIC SYMPTOMS of an MI. Diabetics are well-known to be at higher risk for “silent” MIs, and women can have atypical symptoms as well.

NEXT STEPS

So you’re on your unit and your patient’s Troponin level comes back elevated. What do you do? It will vary depending on the patient’s symptoms and what unit you are on, but in general you should:

  1. Remain calm…
  2. Communicate it to the Provider (Physician, PA, or NP).
  3. Make sure the patient is connected to the heart monitor and is getting frequent vital signs. Apply oxygen if SPO2 < 94%.
  4. Obtain an EKG if they have not had one recently – worry about the order later.
  5. Monitor your patient and follow the orders given by the Provider.

CK / CK-MB

These labs tend to be somewhat outdated and have been replaced – for the most part – by Troponin. However – there are still some clinical implications for using these exams.

CK, or Creatine Kinase, is found within most muscle cells and is released into the bloodstream when muscular cellular necrosis or damage occurs. This includes the heart – so with the same principle as troponin – elevations in CK could indicate heart muscle damage. However – CK is NOT specific. This is why a more specific isoenzyme – CK-MB (Creatine Kinase Muscle/Brain), is used to help differentiate musculoskeletal muscle damage from heart damage. Ck-MB is found in higher concentrations within the heart.

Current Indications

With the implementation of Troponin, CK and CK-MB have minimal value, but they can be used in certain instances. These instances are typically after heart instrumentation (CABG or PCI), or to detect a second MI – since troponins have such a long half-life and do not return to baseline levels until 1-2 weeks after the initial incident.

Pattern

The reason CK-MB can be useful is because while the onset is similar to Troponin (can take 4-12 hours to be detectable), the half-life is shorter and levels drop back down to undetectable levels in 36-48 hours. Troponin levels can take 10-14 DAYS to return to normal. This means that if a patient has a 2nd heart attack >2 days after the first, an elevated CK-MB level can indicate a 2nd MI. The same principle is related to myocardial instrumentation. If someone had a stent placed or especially a CABG, their Troponin will be expected be elevated from the irritation within the heart. If it has been >48 hrs, an elevated CK-MB could indicate further myocardial injury.

Levels

CK Male Normal: 39-308 U/L
CK Female Normal: 26-192 U/L
CK-MB Normal: 5-25 IU/L

Myocardial Infarction: Levels should be >2x the patient’s baseline.

Remember that CK and even CK-MB are not as specific as Troponin-I or T to the heart. In the presence of musculoskeletal injury – the usefulness of these tests diminishes greatly.

Any type of muscular damage or surgery can increase CK. Rarely, chronic muscle disease, hypothyroidism, and alcoholism can increase CK-MB.

BNP

BNP stands for Brain Natriuretic Peptide – however it is primarily released by the ventricles of the heart. This hormone impacts fluid and sodium handling in the kidneys. When the ventricles experience high-pressures, the cells release this enzyme.

BNP has a diuretic (fluid out) , natriuretic (salt out) , and hypotensive effect. BNP has actually been found to be somewhat protective in cardiac remodeling (cardiomyopathies).

What’s confusing about BNP is that some hospital labs utilize BNP, and some utilize NT-ProBNP – basically an inactive byproduct of the enzymatic reaction that occurs to produce BNP. It is important to know which kind of BNP your hospital utilizes in order to be able to understand and interpret the results.

While BNP levels can assist in the diagnosis of HF if it is uncertain, they are especially helpful in evaluating treatment response as the BNP half-life is only about 20 minutes. This means that BNP levels will should quickly go down if ventricular pressures improve.

BNP levels infographic | BNP heart failure exacerbation

Regular BNP

Baseline BNP levels – no matter which kind – are affected by genetic variation. However, people with HF will have baseline elevations along with increases during exacerbations. Baseline levels tend to increase in age and are higher in women over men, and decrease in obesity.

Levels <100 pg/mL have a great negative predictive value – meaning they likely are NOT in an exacerbation. Levels >400 pg/mL have a high likelihood that they ARE in an acute HF exacerbation. Levels between these (100-400 pg/mL) is the gray zone – meaning they may or may not be in an acute exacerbation. It is ALWAYS important to take the clinical exam into account – Do they have clinical signs or symptoms of HF? (Think crackles, peripheral edema JVD, hepatomegaly). NEVER rely solely on labs – especially with BNP levels. BNP levels should be used as an adjunct to, and not a substitute for, clinical assessment.

NT-ProBNP

NT-ProBNP levels rise much higher than regular BNP levels. They also have a longer half-life (25-70min), which means they do not fluctuate as quickly. It is also impacted by renal failure more so than regular BNP levels.

All ages: Levels <300 pg/mL –  you can be almost completely sure that they do not in a HF exacerbation.
Age <50: Levels >450 pg/mL indicate acute exacerbation.
Age 50-75: Levels >900 pg/mL indicate acute exacerbation.
Age >75: Levels >1800 pg/mL indicate acute exacerbation.

With any BNP level, obesity can decrease the results, and age and renal failure can increase them.

Non-HF causes of elevated BNPs include renal failure, constrictive pericarditis, valvular disease, pulmonary hypertension, and sepsis.

 

And those are the main cardiac lab tests used to evaluate the heart. An EKG should always be performed at these patients above, and they should all be admitted with continuous cardiac monitoring as well. Whether you’re a nurse, nurse practitioner, or physician – it’s very important to understand these labs and be able to interpret them to provide the best care for your patients.

Arterial Blood Gas (ABG) Interpretation

Arterial Blood Gas (ABG) Interpretation

Arterial Blood Gases (ABGs) are obtained within the hospital setting by nurses or respiratory therapists, after a physician or advanced practice provider orders them. As the name implies, this arterial blood sample is sent to the lab to evaluate the “gases” within the arterial blood – looking at acid-base disturbances or evaluate adequacy of oxygenation/ventilation. Brace yourselves – this is going to be a long confusing topic but once you understand the concepts, it can really help you manage your patient’s acid-base disturbance like a pro. 

Oxygen (O2) and carbon dioxide (CO2) are the main gases within the blood, and these are two of the main components evaluated in an ABG. However, an ABG sample also provides levels of blood pH, as well as bicarbonate. Of all of the measurements, the most important levels to look at are the CO2, the Bicarb, and the pH in determining acid-base balance.

The ability to interpret an ABG is essential for advanced practice providers and physicians, but it is also important for the nurse to be able to have a good understanding of how to interpret ABGs, especially those working in critical care (ER, ICU, etc). This can give you valuable insights into your patient’s medical status and overall condition.

Unfortunately, ABGs can be difficult to understand. Acid-Base balances is exactly that – a balance. A rise in one level will affect other levels – and this can make it difficult to understand the underlying picture. The purpose of this article is to help you be able to master ABG interpretation in order to help you become a better nurse, clinician, or provider.

So… When Should an ABG be Obtained?

As stated above, ABGs are very useful in evaluating acid-base disturbances within a patient. This can come in handy for patients with Diabetic Ketoacidosis (DKA), other forms of metabolic acidosis (kidney failure, sepsis, etc), and CO2 retention (COPD). Patients with active respiratory failure, usually with underlying COPD or CHF, often have an ABG to evaluate their CO2 retention, their O2 saturation, and their acid-base balance – as all of these factors will affect each other.

The Measurements

pH

The pH is the first measurement which will give you the overall picture of the patient: are they acidotic or alkalotic? pH is simply the acidity of the blood. Normal values for arterial blood pH is 7.35-7.45, which is a narrow window where body homeostasis works best.
Low pH (<7.35): Indicates acidosis (metabolic or respiratory), and is termed acidemia.

High pH (>7.45): Indicates alkalosis (metabolic or respiratory), and is termed alkalemia.

pH may be normal or near normal in the presence of chronic acid-base disturbances from compensation, or the patient can have multiple different acid-base disturbances playing a factor.

Arterial Partial Pressure Carbon Dioxide (PaCO2)

The PaCO2 is the partial pressure of Carbon Dioxide within the arterial blood. Normal values for PaCO2 is 35-45 mmHg.

Did your parent or guardian ever tell you that holding your breath would cause your blood to boil, and that’s why you can’t hold it for long? This tidbit has helped me always remember that hypoventilation (not breathing enough) causes acidosis (boiling blood), and hyperventilation (breathing too much) causes the opposite.

High PaCO2: levels greater than 45mmHg are considered high and termed “hypercapnia”.

A high PaCO2 indicates a primary respiratory acidosis (blood boiling! pH<7.35), but can also indicate compensation for a metabolic alkalosis. You see, acid-base is regulating by two organs in your body – your kidneys (metabolic) and your lungs (respiratory). These always hang in balance, and when the scale tips one way (metabolic acidosis), the body will attempt to compensate by increasing production and retention of bicarbonate to act as a buffer to normalize pH (respiratory compensation). This means the compensation will always be in the opposite direction from the primary acid-base disturbance. If one becomes too acidi – the other becomes basic, and vice versa. This is another perfect example of the body performing homeostasis to maintain balance and health. Respiratory compensation tends to occur quickly, as the pt is able to change their ventilation pattern almost instantly.

Low PaCO2: levels less than 35mmHg are considered low and termed “hypocapnia”.

Low PaCO2 indicates a primary respiratory alkalosis, which means the pH must be alkylotic as well (>7.45). Or it could also mean respiratory compensation for metabolic acidosis. If a patient is breathing fast (tachypneic), but doesn’t have a respiratory complaint – you may want to investigate their acid-base to assess for respioratory compensation. This was something I did NOT catch as a new nurse on a telemetry floor. My patient was breathing fast all night and I didn’t know why – by morning her pH was 6.9! A better understanding of acid-base physiology would have helped me recognize the signs of respiratory compensation (Kussmaul respirations), and my patient would have been better off for it.

Arterial Bicarbonate Concentration (HCO3)

HCO3 is the serum bicarb within arterial blood. Bicarb acts as a buffer to make acidity less acidic. Think of it as the oposite of H+. The less bicarb there is, the more acidic the blood is. To get technical, Bicarb reacts with H+ to form carbonic acid, which the body breaks down into CO2 and water – which it breaths out. Normal levels vary, but typically are somehwere around 22-26 mEq/L.

High HCO3: Levels greater than 26mEq/L are considered high.

High HCO3 indicates a primary metabolic alkalosis (pH >7.45) – meaning for whatever reason the body is losing its acidity (See specific causes in next section). However, just as in the case of PaCO2, abnormal HCO3 levels could indicate compensation as well. A high HCO3 level could indicate metabolic compensation for respiratory acidosis – the body is trying to buffer more acid to normalize the pH. Compensation from the kidneys can take a few hours to kick in, but won’t typically reach their peak compensatory effect until a couple days into the acid-base disturbance.

Low HCO3: Levels less than 22mEq/L are considered low.

Low HCO3 levels indicate primary metabolic acidosis (pH <7.35). This is an acid-base disturbance you will see often – although they are all fairly common. Their is accumulation of acid within the body, and the kidneys are unable to get rid of it quick enough. Just as with the others, low HCO3 could indicate metabolic compensation for respiratory alkalosis.

Arterial Partial Pressure of Oxygen (PaO2)

PaO2 is the partial pressure of oxygen within arterial blood. This basically measures the actual oxygen content of the blood. Normal values for PaO2 is generally thought to be greater than 80 mmHg.

High PaO2: Usually due to over-oxygenation from supplemental O2 (Think non-rebreather or too high FIO2). This may be better than low PaO2, but don’t forget that too much oxygen can be deleterious as well. Oxygen toxcitiy can produce reactive oxygen species and cause cellular injury, inflammation, and cell death. It can also accentuate hypercapnia (i.e. COPD).

Low PaO2: Hypoexmia from respiratory dz or anemia

Peripheral Oxygenation (SaO2)

The SaO2 is the peripheral oxygenation, which is equivalent to the Pulse Ox reading.

Normal levels are >96%, whereas levels <92% indicate hypoxia.ABG Interpretation Infographic

The 4 Acid-Base Disturbances

The following 4 categories are the 4 acid-base disturbances that can occur in someone who is sick. The above information will tell you which acid-base disturbance you may be dealing with. The below information is for you to understand what could possibly be causing the underlying disturabce. Don’;t forget someone can have multiple acid-base disturbances going on at one time, and this makes clinical interpretation difficult – everything is not black and white in medicine, but this should give you a pretty good idea of what may be causing your patient’s acid-base disturbance.

Respiratory Acidosis

Respiratory acidosis is due to alveolar hypoventilation. The lungs are NOT able to remove enough carbon dioxide quick enough, so it builds up in the blood. It also decreases Bicarbonate levels, which decreases pH and causes acidosis.

Hypercapnia tends to occur late in the lung disease or when respiratory muscles are fatigued – this is usually seen in severe respiratory failure. The acidosis can be acute or chronic.

Acute: Could be from CNS disease (think stroke, traumatic brain injury), drug-induced respiratory depression (Opioid or Benzo overdose), Neuromuscular disease (Myesthenia Gravis, ALS, Guillan Barre), or most commonly airway obstruction (asthma/COPD).

Chronic: Chronic respiratory acidosis may occur when the PaCO2 is elevated, but the pH remains normal secondary to renal compensation and elevated serum Bicarb levels. Causes of chronic  respiratory acidosis may be Obesity-Hypoventilation syndrome (Pickwickian syndrome), ALS, interstitial fibrosis and thoracic skeletal deformities.

COPD: Person’s with COPD have less responsiveness to hypoxia and hypercapnia. There is also increased dead-space ventilation, and decreased diaphragmatic function due to fatigue and hyperinflation.

Respiratory Alkalosis

This acid-base disturbance is due to alveolar hyperventilation. The lungs remove too much carbon dioxide too quickly, so hypocapnia (low PaCO2) and alkalosis occurs.

It is commonly found in those who are critically ill including those who are mechanically ventilated, early-intermediate pulmonary disorders (PNA, PTX, aspiration, PE, Asthma, bronchitis), pain, panic/anxiety, psychosis, fevers, high-altitude, sepsis, severe anemia, hepatic failure, CHF

Electrolyte disturbances:

Acute hypocapnia causes reduction in serum K+ levels (intracellular shifts) and phosphorus, as well as ionized calcium (it increases binding to albumin so there is less calcium in it’s ionized active form). This explains the common symptoms of numbness/tingling that people having a panic attack may experience.

Metabolic Acidosis

This acid-base disturbance is due to increased plasma acidity. Metabolic Acidosis is further broken down into whether or not the Anion Gap is normal (termed hyperchloremic metabolic acidosis) or elevated (Elevated gap metabolic acidosis).

Severe HCO3 levels <12 are almost always caused by some degree of metabolic acidosis, instead of just compensation for respiratory alkalosis.

Normal Gap: characterized by hyperchloremia, Bicarb is lost via the GI tract or kidneys. This usually occurs from diarrhea, chronic renal failure, or renal tubular acidosis.

Elevated Gap: Can be from multiple underlying pathology, but usually caused by Lactic acidosis as in the case of sepsis, ketoacidosis in the case of DKA, acute kidney injury (acute renal failure), and ingestion of certain poisons.

Metabolic Alkalosis

This acid-base disturbance is caused by increased serum bicarb and decreased acidity. The acidity, or hydrogen ions (H+) are usually lost in some manner. You know when you throw up and you taste the acid in your throat? This is one way the body loses it’s acidity – through vomiting. This can also occur in the setting of prolonged NG tube suction. The kidneys can also lose bicarb with the use of diuretics. Sometimes too much alkylotic agents are given and the kidney’s aren’t able to excrete them fast enough – this can rarely occur from massive over-consuption of milk products or antacids.

Bicarb (HCO3) levels >35 almost always is caused by some degree of metabolic alkalosis instead of compensation for respiratory acidosis.

 

And That’s about it for Acid-Base Disturbances. I Know – it’s long and hard and I probably lost many of you along the way. Half the battle is remmebering which terms have which meanings. Once you establish that – it gets easier understanding the balance that is acid-base homeostasis.

If you have any questions, or notice an error (because let’s be real), drop a comment and I’ll be sure to respond/fix it! Otherwise, sign up below for free nursing organization sheets!

10 IV Insertion Tips for Nurses

10 IV Insertion Tips for Nurses

IV Insertion is a skill that most nurses will need to become familiar with. Nurses in the hospital use IVs every day to infuse fluids and medications. While IVs are very useful, sometimes IV insertion can be difficult,  especially for the new inexperienced nurse. With time and experience, your IV skills will improve. In the meantime, use these 10 IV insertion tips to help you start an IV and sink those IVs like a pro.

  1. IV Insertion: Location Location Location

    AC

    IV insertion - vein anatomyThe best location of your IV insertion really depends on which setting you are in, as well as the specific patient’s chief complaint. It is common for inpatient nurses to be upset with AC lines, but the fact of the matter is an AC line is likely an ER nurse’s best friend.

    If a patient presents with anything that can even possibly get a CTA – You’re better off choosing the AC. The LAST thing anybody wants to do is have to unnecessarily poke someone again. So – if the patient has a neurological complaint (stroke s/s), cardiac complaint, or pulmonary complaint – a CTA may possibly be ordered and most hospital facilities/radiology staff won’t inject the high-pressured dye unless there is at least an 18g or 20g in a large vein (aka AC and above). Additionally, patients who are hemodynamically unstable should receive a 16g – 18g in an AC for large fluid resuscitation.

    Forearm

    Forearms are the perfect location for continuous fluids because they don’t kink with arm bending. However, not everyone has great forearm options. Additionally, starting an IV in a forearm vein does not always reliably give great blood return for bloodwork, although this may mainly be a consideration in the ED where they typically draw blood work during IV insertions.

    Hand

    Hand IVs are sometimes the easiest veins to see, however, they are usually relatively small veins and can usually only fit 20g – 22g. They are great for short periods of time, but can easily become irritated. Additionally, they limit the use of the hand and are more likely to start hurting the patient – especially with vasocaustic infusions such as vancomycin or potassium.

  2. Small veins? Make them Larger

    Heat

    Heat is great because it causes vasodilation. When veins dilate, they become bigger. Applying a warm compress or hot pack can help you visualize the vein, palpate the vein, and can even make threading the IV easier when starting an IV. Just ensure the compress is not too hot to cause thermal burns.

    Gravity

    Putting the arm in a dependent position forces blood pooling in the distal veins, which will make them bigger and easier to see and palpate. This should make IV insertion easier with a higher chance of success.

    Also Read: “10 ER Nursing Hacks you Need to Know”

    Nitroglycerin Ointment 2%

    A small amount of 2% Nitroglycerin can be topically applied to a small area in order to dilate the peripheral veins. In a small study, those with 2% Nitro ointment applied to the dorsum of their hands required fewer needle sticks than the controlled group. Please note that this is a medication, so an order needs to be placed by the Physician/APP.

  3. IV Insertion with Fragile Veins

    Change your Selecton

    Sometimes, elderly patients tend to have crappy veins. Sure, you can see them alright, but once you stick them – they blow immediately (even with a 22g). This is definitely a good time to look for larger more proximal veins, as IV insertion in these veins tends to be more stable and not blow immediately.

    Forget the Tourniquet

    If you can visualize or palpate the vein without a tourniquet and it appears to be engorged enough to thread the catheter – try the IV insertion without the tourniquet. Tourniquets are great for engorging the vein and causing it to dilate, but they also add pressure to the vein. Already fragile veins will have an increased tendency to blow with the added pressure from the tourniquet. Never forget to remove the tourniquet before flushing the IV!

  4. Don’t Give Up during IV Insertion

    OK – some people HATE digging when starting an IV – and this is understandable. However, sometimes it is minimally painful and you can thread the catheter within a few seconds of “digging”. The trick is to not “dig” blindly – but instead use your fingers to palpate the accurate direction of the vein.

    After inserting the needle with the catheter, if you do not get a flash of blood, pull the needle back out to almost out of the skin, re-palpate the vein, and aim again in the direction of the vein. I can’t even count how many times I missed on the first pass, but immediately threaded the IV on the 2nd or 3rd advancement. The patient also experiences some desensitization of their pain receptors and it is usually less painful than being poked again. However, some patients really do NOT tolerate this, and you will know which patients you probably shouldn’t go digging.

    Related content: “How to Start an IV”

  5. Go Big or Go Home

    Smaller is not always easier. Sometimes 22g and below are too flimsy. When the veins are sclerosed, hardened, or there is scar tissue – choosing a 20G might be a better bet in order to thread the catheter without any issues. Besides – larger gauges are better in an emergency, are more durable, and tend to cause less irritation to the veins.

    Related content: “5 Vital Signs Error to Avoid”

  6. Arterial Stick

    When inserting an IV, you can accidentally hit an artery instead of a vein. First, if the IV is pulsating – take it out immediately. It’s possible the vein is just right next to the artery, but it is likely you are actually in the artery. This is usually accompanied by blood filling up the catheter VERY quickly – depending on the patient’s mean arterial pressure. Arterial blood tends to be a bright red, versus the darker red of venous blood.

    So what’s the harm? Access is access, right? Well, sure that makes sense on the surface. But peripheral IV’s inserted in arterial lines tend to have much higher complications – the worst of which being thrombophlebitis. You can literally cause a blood clot in the patient’s arm. This is even more of a risk if medications are infused through it. Remove the catheter and try again in an actual vein.

  7. Inserting the IV “Outside the Box”

    Or rather – think outside the lower arm. If you can, look at the upper arm as sometimes there are large veins close to the surface. Most facilities prefer you to stick an IV in an arm, but there are exceptions. If the patient is an extremely hard stick and needs access, you can look at lower extremities, but caution against as these are high risk for infection.

    No – don’t go for these strange areas initially, but in an emergency, any access is better than none. However, in a code situation, temporary placement of an Intraosseous catheter is preferred. If a better IV site still cannot be obtained, someone skilled with ultrasound-guided IV placement should try, or a PICC/Central line should be considered.

  8. Angle Danger

    I have watched MANY nurses and nursing students miss when inserting an IV purely because of their technique. They hold the skin taut, stabilize the vein, and insert – but they go right through the vein and can’t thread the catheter. I’ve found that this is often from having too much of an angle with the skin. You should really aim to be near parallel with the skin (10-30 degrees). Gliding the needle into the vein with this angle means once you get a flash, the needle is likely still within the vein and the catheter can be advanced. The exception is if by chance you are aiming for a deeper vein, you may need to increase the angle accordingly.

    If you find that you insert the needle and cannot float the catheter in, despite having a “good” flash of blood – try pulling the needle and catheter out just a millimeter or two, and try advancing just the plastic catheter again.

    Related content: “Top 5 Apps for ER Nurses”

  9. Rollie Pollie Ollie

    Sometimes patient’s veins just like to roll – and the patient will likely forewarn you about this. There are a few things you can do to minimize this.

    First, pick a larger more proximal vein. These veins tend to be more stable.

    Second, make sure you stabilize the vein by holding the skin taut with your non-dominant hand.

    Lastly, make sure the patient does not tense up their muscles during the insertion. Tensing of muscles will cause movement of the veins. To minimize muscular contractions – use the tip below!

  10.     Patient Comfort

    This IV insertion tip is really more for patient comfort than anything else. After you clean the IV site, place the needle flush with the skin right where you are going to poke. Press the needle with the bevel up into the cleansed skin for 3-5 seconds before you poke. The longer you wait – the more desensitized their skin receptors will become – this theoretically decreases pain.

    With less perceived pain, the patient is less likely to tense up and should lead to a smoother successful IV placement. When I was an ER nurse, I used this technique every time and seemed to have good results.

Well, there you have it – 10 IV insertion tips to improve your IV game! If you have any additional tips that I didn’t mention – leave a comment below letting everyone know!

5 Vital Sign Errors to Avoid

5 Vital Sign Errors to Avoid

Vital signs are essential in every aspect and setting of medicine – whether that be inpatient such as in the emergency department, the Intensive Care Unit (ICU), the medical/surgical floors,  or pediatrics – as well as virtually every outpatient office setting. Vital signs are objective measures of patient’s health, and can tell A LOT of information about the patient. This can give great indications of their health status and prognosis, as well as aid in the differential of many different medical conditions. When a patient can’t speak, sometimes all the medical team has to go on is their vital signs. Vital signs, matched with a thorough history and physical assessment, can mean the difference between life and death.

To sum it up – vital signs are SUPER important. While ignored by many, the slightest changes in vital signs can clue the nurses and Providers into acute changes in the patient’s status, and diligence with early correction can avoid prolonged hospitalizations and improve patient outcomes.

Vital signs are frequently obtained by nursing assistants, patient care technicians, medical assistants, nurses, and sometimes even physicians or advanced practice providers. All are important to the healthcare team. We ALL know how to take vital signs, but it is up to the Provider (often notified by the nurse) to interpret those vital signs and make patient interventions accordingly. It is because of this crucial importance that it is absolutely necessary that vital signs are taken correctly to give the most accurate readings.

There are many errors that novices and even some experts can make when taking vital signs, but these 5 errors will help any member of the medical team to provide accurate measurements.  

  1. Incorrect Cuff Size and Location

    Blood pressure is a key vital sign to obtain, and it seems everyone is worried about their blood pressure. This is because high and low blood pressure are indications of underlying diseases. A very high blood pressure could indicate uncontrolled hypertension, a stroke, a medication reaction, etc. Low blood pressure could indicate internal bleeding, systemic infection (sepsis), an adrenal crisis, etc. The lists go on. So many different diseases affecting various body systems can affect the blood pressure, and this is why it is so important to obtain the right measurement.

    Blood pressure cuffs should be sized appropriately to fit the patient’s arm. But what is appropriately? The correct answer is that the bladder (the part that inflates with air) should encompass 80% of the person’s arm circumference. That means it should just about fall short of wrapping around their entire arm. In reality though, you just kindof know if its too big or too small after some experience. Most adults with regular-sized arms will fit the regular adult size, and larger individuals or gym-rats will benefit from the larger size. It should fit nice and snug, but not too-snug. 

    Place the middle of the bladder (usually marked with some type of marking such as “Artery Here”) over their brachial artery. This is usually on the medial aspect of their antecubital fossa. Place the cuff 2-3cm above the crease, or about an inch.

    So why does it matter so much? Incorrect cuff sizes will lead to incorrect blood pressure measurements. If you place a cuff too small on an individual, the blood pressure will likely be falsely elevated. If you place a cuff to big on an individual – you guessed it – the reading could be falsely decreased. This becomes very important when blood pressures begin to push the boundaries of normal.Top 5 Vital Sign Errors from medical providers - Chalkboard Style

  2. Incorrect Positioning

    Patient positioning, which is also important in blood pressure, should not be overlooked. In the office-setting, patients should be seated with uncrossed legs for 5 minutes before getting their blood pressure checked. This usually does not lead to many issues due to the routine and setting of the office. However, in the hospital this error occurs very frequently.

    While patients do not need to be sitting in a chair for 5 minutes prior to a blood pressure reading within the hospital, it is important to maintain proper positioning. Patient’s are often going to be bed-bound, on bedrest, or perhaps sleeping when you go to take their vital signs. Semi or high-fowler’s positioning for at least 5 minutes before checking the blood pressure is ideal, but supine is often accepted as well. The MOST IMPORTANT thing to remember is that the blood pressure cuff is at the level of the heart (more specifically the right atrium) when the reading is taken.

    Patients who are on their sides will give you inaccurate readings. The arm above their heart will read falsely lowered readings, and the arm below may render falsely elevated readings. This is common, especially within the units that have constant blood pressure monitoring with frequent intervals (ER and ICUs).

  3. Incorrect Waveform

    Blood oxygen saturation is monitored with a pulse-oximetry sensor usually on a finger, and this is another important vital sign which we need correct measurements. While of great value, sometimes oxygen sensors read incorrectly low, and with a little practice it can be easy learn when a low reading is actually dangerous.

    The important thing to check with a pulse-ox reading is whether or not there is a good wave-form. This is usually within the hospital where a bedside monitor or dinamap displays the pleth – that is, the waveform that “beats” in congruence with the heartbeat. Peripheral pulse-ox’s can measure how much blood is passing with each beat through the device sensor. This should look equal, symmetric, and have adequate amplitude. If all you see is a straight line with occasional movements, this is NOT a good pleth, and likely an inaccurate reading.

    The waveform or pleth may look poor due to poor circulation (cold fingers, peripheral artery disease, hypotension, etc), or the patient may be shaking, or moving their finger too much. Try changing to a different finger or hand. With cold fingers with poor circulation, try using an earlobe (infant probes are often easy to use in this location). If the patient has nail polish on, you may be able to get a reading but it is possible that this is interfering with the spectrum of light for the sensor. If you are getting a bad reading – it may be wise to remove the nail polish on one finger and try again.

    Another important fact to remember is to ALWAYS CHECK THE HEART RATE from the pulse-ox. Does this match their HR on the heart monitor? If they are not hooked up to the heart monitor, does this match their peripheral pulses? If your heart monitor reads a HR of 82, and your Pulse-ox is reading 78% and a HR of 30 – this is likely not a good reading as the heart rates do not match up. The exception is arrhythmia, so make sure they are in a Sinus Rhythm before assuming it is an error. 

  4. Incorrect Temperature Method

    Infections often present with fevers, and severe infections can have either really high temperatures or really low temperatures. It is important to use the correct temperature method for the correct situation, as using the wrong method can lead you to not picking up on a fever.

    Oral Method

    In most settings and for most patients, the oral thermometer is adequate. As long as the patient can follow instructions and leave it under their tongue for 10 seconds or so, you will likely get an accurate reading. However, if the patient recently drank something, this can lead to a falsely lower reading. The colder and more recently they drank it, the more likely it is to interfere with the reading. Cold beverages can decrease the temperature for up to 30 minutes, and hot beverages can falsely elevate the temperature for up to 5 minutes or so. Interestingly enough, if the patient is chewing gum this can also slightly increase the temperature reading. Additionally, if the patient has a high respiration rate (greater than 20 breaths per minute), this can lead to falsely low readings. In these instances, it may be prudent to check the temperature with another method.

    Rectal Method

    The rectal thermometer is the “gold standard” because it is the closest to the core-body temperature, but it is not always practical. Studies have shown that a significant amount of fevers are missed in triage due to less invasive methods.

    Rectal temperatures should be obtained on anyone whom there is suspicion of fever when other methods are afebrile. A basic summary is that a rectal temperature should be performed on those suspected of serious infection or sepsis, those with hypothermia from the field, and those who are critical or unresponsive.

    Rectal temperatures are also frequently obtained in children under a certain age. It depends on facility protocol, but obtaining rectal temperatures in infants and young children (often under 2 years) is common, especially if they present with complaints of fever.

    Rectal temperatures tend to be 0.5-1.0°F HIGHER than the “normal” oral temperatures – 98.6°F.

    Temporal Method

    The temporal method is dependent on the facility and available equipment, but does offer quick and fairly accurate temperature readings. If the patient is not very acute, has no symptoms, and simply needs a quick screening temp – the temporal thermometer can be your best friend. However, the diagnostic accuracy of the temporal thermometer is iffy, and if there is concern for altered temperature, another method should likely be used. Forehead sweat is a common cause for false low readings. 

    Tympanic Method

    The tympanic method is commonly used in and out of the hospital setting, but often can yield lower-than-accurate readings. This is often due to the fact that the end of the probe needs to be pointed directly at the tympanic membrane. Improper technique can lead to inaccurately low readings. If done properly, tympanic readings actually tend to run hotter than oral readings, similar to rectal readings at 0.5-1.0°F higher than 98.6°F. The tympanic thermometer has shown to be useful, comfortable, and generally tolerable. It is generally appropriate to use 6 months and older, depending on the device.

    Axillary Method

    Axillary temperatures tend to be unreliable and are not often recommended in the hospital setting. They can be used for screening purposes in the office-setting if the patient is not complaining of fever. Additionally, they can be used for screening in an infant or young child, but some settings will accept an axillary temperature for children above 2 years old. This method often yields results about 0.5-1°F lower than 98.6°F. If there is any doubt, use another method. These readings will be inaccurate in very sick patients who have compensatory peripheral constriction or dilation, so this method should generally be avoided within the hospital.

    Long story short – do a rectal when the patient is severely sick or unresponsive, in those very young (generally under 2), and in various specific circumstances when asked or ordered by the provider. In all other scenarios, use the most appropriate, comfortable, least-invasive method which is likely to yield accurate results.

  5. Respiration Rate

    The respiration rate is crucial in evaluating those with respiratory complaints. It can clue the clinician into impending respiratory failure, indicate acid-base balance, and guide patient interventions. However, it seems as though most hospital workers (nurses, techs) don’t actually count respirations. It happen very often when someone just puts “16”, “18”, or “20” – without even thinking twice. I can’t even tell you how many times another medical professional put in a normal respiration rate and the patient actually had a rate greater than 30, sometimes above even 50. 

    I get it – do you REALLY want me to stand here and count their respirations for 30-60 seconds?! AINT NOBODY GOT TIME FOR THAT, and we are BUSY. However, accurate respirations can lead to quick and timely recognition of a change in patient status.

    All in all, you should be counting. But if the patient appears to be breathing fast, having respiratory difficulty, is an infant, or came in with a respiratory complaint – this becomes a necessity and there really is no excuse for “just putting 16”.

  1. Hopefully you found these errors illuminating and helpful. Remember to always try to obtain accurate results in the least-invasive, most respectful manner possible. When in doubt, consult with the nurse, physician, or advanced practice provider.

Let me know in the comments if you’ve seen these errors occur, and any other errors that might be helpful to other readers!