Tag Archives: nursing

“But doctor, he’s vomiting blood!!!” – The NEJM GI Bleed article by Villanueva: Yup, time to reassess transfusion in GI bleed! @FOAMed, @FOAMcc

thinking critical care

Screen Shot 2014-01-08 at 3.13.37 PM

Last january a highly anticipated paper came out in the NEJM (http://www.nejm.org/doi/pdf/10.1056/NEJMoa1211801), which should be a game changer, given a few provisos.  Villanueva et al reported on their large (almost 1,000 patients) randomized study on liberal (<90 mg/dl) vs restrictive (<70 mg/dl) strategy.  Interestingly but no longer surprisingly, the patients in the restrictive strategy did better.

Hmmm…sound familiar?  By now everyone  accepts the TRICC trial threshold of 70 in ICU patients, but when it first came out, there were a fair bit of disbelievers and concerned health care workers.  At the time, they excluded GI bleeds and acute coronary syndromes, understandably,

So what do the numbers say?  First lets see if there was any difference in the actual treatment. Definitely. In the restrictive group, 51% of patients required transfusion, vs 86% in the liberal group.  Sizeable difference. Now in terms of outcomes:

a. rebleeding decreased: 10% vs 16%

b. 6 week…

View original post 1,030 more words

Hash Tags

Hash Tags

A Hashtag is a word or a phrase prefixed with the symbol #. It is a form of metadata tag. Short messages on microblogging and social networking services such as Twitter, Tout, identi.ca,Tumblr, Instagram, Flickr, Google+ or Facebook may be tagged by putting “#” before important words, either as they appear in a sentence, (eg. “New artists announced for #SXSW 2012 Music Festival!”) or appended to it.

Hashtags provide a means of grouping such messages, since one can search for the Hashtag and get the set of messages that contain it. When another user uses Hashtags to find a particular word, they will see all posts containing that Hashtagged word. It’s a really handy skill to learn, as social media becomes the primary way we communicate.

The social media universe is vast and can be a little confusing to navigate. Hashtags are one of the most important and efficient ways of organizing information on various platforms like Twitter, Facebook, Google+, etc.

Anyone can make a Hashtag at any time, simply by typing a phrase of the form “#topic” in a tweet. The form for doing this is exactly the same as for including an already existing Hashtag. Simply type a phrase of the form “#topic.” Do not put any spaces in the phrase that you want to turn into a Hashtag, because the Hashtag begins with the “#” and ends with the first space. When you click “Tweet”, your new tweet will appear in your list of tweets, and the Hashtag you created will appear in blue. Scroll over it and click on it to be redirected to the page for the Hashtag. If you have really created a brand new Hashtag, your tweet should be the only one on the page. Now, every time someone includes your Hashtag in a tweet, it will be added to the page.However, a lot of Hashtags have already been created and in main stream use.

(If your new to Twitter and looking for a good introductory guide try Mashable’s – The Beginners Guide to Twitter)

The following is in no way an exhaustive list, and each category listed below is also far from complete, but it’s simply meant as a good starting point to jump into learning and familiarizing yourself with available Healthcare Hashtags.

What are your favorite Hashtags that you like that I have not listed?

Introductory Resources

  1. HashTags.org
  2. Using hashtags on Twitter
  3. The Healthcare Hashtag Project
    1. The goal of the Healthcare Hashtag Project is to make the use of Twitter more accessible for providers and the healthcare community as a whole. By lowering the learning curve of Twitter with a database of relevant Hashtags to follow, we hope to help new and existing users alike to find the conversations that are of interest and importance…Read More!
  4. How to use Hashtags with Twitter
  5. Introducing #EMConf Twitter Hashtag
  6. Twitter Teaches You How to Hashtag
  7. What Do #FF, #TBT, #GFF, FOH, RLRT And Other Twitter & Instagram Hashtags & Terms Mean?
  8. 14 Twitter Hashtags for Nursing Students to Monitor

General

I have linked the following examples to Twitter, but these examples are also used on a variety of other platforms listed above, think Facebook, Google+, etc.

  1. #Antibiotics – Antibiotics
  2. #CochraneEvidence – Cochrane Evidence
  3. #CritCareEP – Critical Care Emergency Physicians
  4. #DigitalHealth  – Digital Health
  5. #FF – Follow Friday –  It’s a Twitter trend created back in 2009 by Twitter users that has since become a customary Friday activity. An #FF is a shout out, a show of appreciation, a nice thing to do. Each Friday you recommend Twitter profiles that you appreciate and enjoy to all of your followers. The idea being that your #FF recommendation will encourage others to check out that profile, generating more followers for them. See? A nice thing to do. This is usually done in list form, with users tweeting a list of usernames along with #FF, so that people who trust their judgment can add a bunch of interesting accounts to their feeds.
  6. #HealthApps – Health Apps
  7. #HealthIT – Health Information Technology
  8. #HIT – Health Information Technology
  9. #MedDevice – Medical Devices
  10. #MentalHealthMatters – Mental Health Matters
  11. #Mentalillness – Mental Illness
  12. #PtSafety – Patient Safety
  13. #SuperBugs – Super Bugs
  14. #TBT – (Throwback Thursday) This is another “holiday” Twitter and Instagram hashtag, which shows up every Thursday on both sites. The impetus behind this one is that it is an opportunity for people to share photos and info that is a “throwback” to an earlier time. For instance, on Instagram, posting a picture of yourself as a child or when you were in school, or on Twitter telling a short quip about something in your past. This is a fun way for people to learn a little bit more about each other, and to see the funny or interesting past that each of us have, but many of our followers and friends don’t know about.

Health & Social Media

  1. #AusMed – Australia Medicine
  2. #GeneralPractice – General Practice
  3. #hcsmanz – health care social media Australia & New Zealand
  4. #hcsm – healthcare communications and social media
  5. #hcsmca = healthcare communications and social media Canada
  6. #hcsmeu = healthcare communications and social media EU
  7. #MHealth – mobile health, telecommunications 
  8. #PCEHR – personally controlled electronic health record
  9. #SoMeGP (SocialMediaGP)

Generalized Areas

  1. #BioTech – Biotech
  2. #Pharma – Pharmacology

Chat

  • discuss collaborative and other important ways of improving health care
  1. #CancerChat – Cancer Chat
  2. #ElderCareChat – Elder Care Chat
  3. #MDChat – MD Chat
  4. #NurChat – Nurse Chat
  5. #RNChat – RN Chat

Conferences

Healthcare Conferences – for a list of upcoming conferences and related information

  1. #EMConf – sharing pearls from the academic sessions (variably called “Conference” “Academic half-day” “Didactics” etc depending on the state/country/continent) of EM residency programs with the world.
    1. Introducing #EMConf Twitter Hashtag
  2. #IMConf – the purpose of this hashtag is to unite IM education through the use of social media. We can all learn from each other, and ask questions allowing all of us to contribute to the learning process of medicine.
    1. Introducing #IMConf Twitter Hashtag
  3. #SMACC – Social Media and Critical Care
    1. LITFL – SMACC
    2. The upcoming SMACC Gold conference
  4. #ICRE – International Conference of Residency Education

Diseases

    1. #Alzheimer – AlzHeimers
  1. #Diabetes – Diabetes
  2. #PanCan – Pancreatic Cancer Action Network

FOAM Clinical Resources

  1. #FOAM4GP – General Practitioners
  2. #FOAMcc – Critical Care
  3. #FOAMed – Emergency Department
  4. #FOAMped – Pediatrics
  5. #FOAMrn – Nursing

Governmental and Related Organization

  1. #CDC – Center for Disease Control
  2. #CMS – Center for Medicare and Medicaid Services
  3. #FDA – Federal Drug Administration
  4. #HHS – Health and Human Services
  5. #NHS – National Health Services
  6. #NIH – National Institutes Of Health
  7. #WHO – World Health Organization

Groups

  1. #AIRWAY – Airway
  2. #CATHLab – Cath Lab
  3. #EMBoardReview – Emergency Board Review
  4. #EssentialsEM – Essentials of Emergency Medicine
  5. #MedStudents  – Medical Students
  6. #Resus  – Resuscitation
  7. #RNChat – Nurse Chat
  8. #NursingStudentProblems – Nursing Student Problems
  9. #TipsForNewDocs – Tips For New Doctors

Journal and Book Clubs

  1. #AliemBookAliem Book Club
  2. #TwitJC – Twitter Journal Club

Legislation

  1. #ACA – Affordable Care Act
  2. #ObamaCare – Obama Care

Medical Education

  1. #APMEC – Asia Pacific Medical Education
  2. #EMTOT – emergency medicine trick of the trade
  3. #GMEP – Graduate Medical Education Project
  4. #GPexams13 – General Practitioner Exams
  5. #MedEd – Medical Education
  6. #PHARM – Pharmacology
  7. #USMLE – United States Medical License Exam

Organizations

  • These are tags that people use when posting something related to a particular organization. Using these tags does not indicate that the organization supports the post in anyway.
  1. #AACN – American Association of Critical Care Nurses
  2. #ABIM – American Board of Internal Medicine
  3. #ACEP – American College of Emergency Physicians
  4. #APHA – American Public Health Association

Places

  1. #ClevelandClinic – Cleveland Clinic
  2. #MayoClinic – Mayo Clinic

Trauma Fast Exam

Focused Abdominal Sonography for Trauma (FAST)

Introduction (Trauma.org)

The use of focused ultrasonography has now become an extension of the physical examination of the trauma patient. Performed in the trauma room by properly trained and credentialed staff, it allows the timely diagnosis of potentially life-threatening hemorrhage and is a decision-making tool to help determine the need for transfer to the operating room, CT scanner or angiography suite.

“The most important preoperative objective in the management of the patient with abdominal trauma is to ascertain whether or not a laparotomy is needed, and
not the diagnosis of specific injury” – Polk 1983

Blunt Abdominal Trauma

Blunt abdominal trauma is a leading cause of morbidity and mortality among all age groups. Identification of serious intra-abdominal pathology is often challenging; many injuries may not manifest during the initial assessment and treatment period.

Ultrasound in Trauma (Focused assessment with sonography for trauma (FAST))

The aim is to identify life-threatening intra-abdominal bleeding or cardiac tamponade with a view to expediting definitive surgical management. It does not aim to exclude abdominal or thoracic injury.

  1. It helps to detect haemoperitoneum and haemopericardium.
  2. The primary benefit is to rapidly direct appropriate operative interventions in unstable
    patients.
  3. It is useful in both blunt and penetrating abdominal trauma.
  4. A high specificity means a positive FAST indicates an intra-abdominal injury.
  5. Moderate sensitivity means a negative FAST (apparent absence of free fluid) does not exclude significant injury.
  6. FAST alters the management of trauma patients, such that
    1. there is more rapid disposition to the operating theatre,
    2. it indicates a more rapid search for other causes of hypotension when negative,
    3. it reduces the number of computed tomography (CT) scans and diagnostic peritoneal lavage examinations (DPLs) performed and
    4. it is associated with shorter hospitalizations, less complications and lower charges.
  7. At this stage, however, there is little conclusive evidence that its use improves patient
    survival.
  8. Extended FAST (EFAST) includes assessment of the thorax for haemothorax and pneumothorax.

Anatomical References

  1. The first is the intrathoracic abdomen, which is the portion of the upper abdomen that lies beneath the rib cage. Its contents include the diaphragm, liver, spleen, and stomach. The rib cage makes this area inaccessible for palpation and complete examination.
  2. The second is the pelvic abdomen, which is defined by the bony pelvis. Its contents include the urinary bladder, urethra, rectum, small intestine, and in females, the ovaries, fallopian tubes, and uterus.
  3. The third is the retroperitoneal abdomen, which contains the kidneys, ureters, pancreas, abdominal aorta, and inferior vena cava.
  4. The fourth is the true abdomen, which contains the small and large intestines, the uterus (if gravid), and the bladder (when distended).

FAST Anatomy

Peritoneal and Retroperitoneal Anatomy

Anatomical Description of main pelvic arteries and veinsmalebladder

Fast Exam Anatomical Reference

Ultrasound in Trauma (Focused assessment with sonography for trauma (FAST) – Indications and role of FAST in penetrating trauma)

The aim of FAST in penetrating trauma is to determine whether one or more of the abdominal, pericardial or pleural cavities has blood in it. This indicates breach in the integrity of the cavity and potentially significant injury. Lack of free fluid in the abdomen does not exclude significant injury, as penetrating bowel injury is frequently not associated with free abdominal fluid.

  1. Unstable patient with multiple wounds
    1. It helps to locate and quantify bleeding and direct initial therapeutic measures.
  2. Unstable patients with a single penetrating thoraco-abdominal wound of uncertain trajectory
    1. To locate and quantify bleeding and direct initial therapeutic measures.
  3. Stable patient with one or more penetrating wounds
    1. When it is not certain whether immediate surgery is required
    2. To locate and quantify bleeding and direct therapeutic measures.

Other imaging and/or surgical exploration is generally required to exclude significant injury.

Mount Sinai Emergency Medicine Ultrasound

Focused Questions:

  1. Is there fluid in the peritoneal cavity?
  2. Is there a pericardial effusion?
  3. Is there fluid in the thorax (ie. hemoperitoneum)?
  4. Is there a pneumothorax? (see separate pneumothorax tutorial)

UCSF-East Bay Trauma Service – FAST Exam

Rational

Focused Abdominal Sonography for Trauma (FAST) allows rapid and noninvasive determination of the presence of free intra-abdominal fluid.  In patients sustaining blunt truncal trauma who are in shock, this information will allow the clinician to forego other diagnostic tests and quickly transfer the patient to the operating room for emergency celiotomy and control of intra-abdominal hemorrhage.  The use of FAST has all but supplanted the diagnostic peritoneal lavage (DPL) in the evaluation of unstable patients after blunt truncal trauma.

Technique The FAST exam is performed as part of the initial evaluation of the trauma patient in the emergency center.  It consists of four separate views of four anatomic areas (see diagrams below):

  1. The right upper abdomen (Morison’s space between liver and right kidney)
  2. The left upper abdomen (perisplenic and left perirenal areas)
  3. Suprapubic region (perivesical area)
  4. Subxyphoid region (pericardium)

above: diagram of the RUQ and Morison’s space

Excerpts From Dr. Geoffrey Hayden Notes (Trauma Ultrasound and the FAST exam):

Pericardial view:

Description:

  1. Look at the interface between the right ventricle and the liver to identify pericardial fluid
  2. Cardiac tamponade identification is the immediate aim of this study
  3. A little fluid (non-circumferential) may be completely normal
  4. Circumferential pericardial fluid +/- RV or RA collapse is concerning

Sono technique:

  1. Probe in the subxiphoid area and angled toward the patient’s left shoulder, with the pointer at 9 o’clock
  2. Transducer is almost parallel to the skin of the torso
  3. Press firmly just inferior to the xiphoid
  4. May need to move the transducer further to the patient’s right in order to use the liver as an acoustic window
  5. Normal pericardium is seen as a hyperechoic (white) line surrounding the heart

Pitfalls:

  1. A pericardial fat pad can be hypoechoic or contain gray-level echoes; almost always located anterior to the right ventricle and is not present posterior to the left ventricle
  2. Small pericardial fluid (non-circumferential) may be normal; do not immediately ascribe hypotension to a small amount of pericardial fluid
  3. Scan may be limited by obesity, protuberant abdomen, abdominal tenderness, gas, as well as pneumoperitoneum/pneumothoraces
  4. Sometimes hard to differentiate pleural fluid versus pericardial fluid

Pearls:

  1. Transducer should be flat to the skin (overhand technique with probe)
  2. Have the patient take a breath in and “hold it”
  3. If the subxiphoid window is not available, may substitute with the parasternal long or short axis; know your alternatives

Perihepatic view (RUQ):

Description:

  1. Evaluating Morison’s pouch=potential space between the liver and the right kidney
  2. 4 areas to evaluate for “free fluid”:
    1. Pleural space
    2. Sub-diaphragmatic space
    3. Morison’s pouch
    4. Inferior pole of the kidney/paracolic gutter

Sono technique:

  1. Probe indicator in the subcostal window points cranially (stay midclavicular, fluid is dependent)
  2. Probe indicator in the intercostal window should point toward the right posterior axilla along the angle of the ribs (oblique angle)
  3. Right intercostal oblique and right coronal views: evaluate for right pleural effusion, free fluid in Morison’s pouch, and free fluid in the right paracolic gutter
  4. The paracolic gutter may be visualized by obtained by placing the transducer in either the upper quadrant in a coronal plane and then sliding it caudally from the inferior pole of the kidney
  5. The liver appears homogenous, with medium-level echogenicity; Glissen’s capsule is echogenic
  6. The kidneys have a brightly echogenic surface (Gerota’s fascia)

Pitfalls:

  1. Perinephric fat is a mimic for hematoma
  2. Duodenal fluid, the gallbladder, and the IVC are all mimics for free fluid (follow these carefully)

Pearls:

  1. Perinephric fat has even thickness (not pointy), and is symmetric with the opposite kidney
  2. Pleural fluid will present as an anechoic strip superior to the diaphragm, instead of the usual “mirror artifact”

Perisplenic view (LUQ):

Description:

  1. 4 areas to evaluate for “free fluid”:
    1. Pleural space
    2. Sub-diaphragmatic space
    3. Splenorenal recess
    4. Inferior pole of the kidney/paracolic gutter

Sono technique:

  1. Reach across the patient
  2. Probe indicator should point toward the left posterior axilla along the angle of the ribs (oblique angle, pointer toward 2 o’clock)
  3. Think more posterior and more cephalad than would be expected
  4. The left intercostal oblique and left coronal views may be used to examine for left pleural effusion, free fluid in the subphrenic space and splenorenal recess, and free fluid in the left paracolic gutter
  5. The spleen has a homogenous cortex and echogenic capsule and hilum

Pitfalls:

  1. Fluid-filled stomach can mimic fluid, as can loops of bowel and perinephric fat (see above)

Pearls:

  1. Posterior posterior posterior
  2. Angle probe with ribs

Pelvic view:

Description:

  1. Evaluating for free fluid around the bladder
  2. Most dependent part of the abdomen (though RUQ is still the most sensitive for FF)

Sono technique:

  1. Probe should be placed 2cm superior to the symphysis pubis along the midline of the abdomen
  2. Both transverse and longitudinal images should be obtained
  3. Angle probe down until the prostate or vaginal stripe is identified (any lower and you will be inferior to the peritoneal reflection)
  4. Sweep all planes of the bladder
  5. In the longitudinal plane, scan side to side to identify pockets of free fluid between bowel loops

Pitfalls:

  1. Fluid within a collapsed bladder or an ovarian cyst may appear as free intraperitoneal fluid
  2. Seminal vesicles may also be incorrectly identified as free fluid
  3. Premenopausal females may normally have a small amount of free fluid in the pouch of Douglas
  4. Watch out for gain artifact; turn your gain down for this exam
  5. The iliopsoas muscles can mimic free fluid (they look like kidneys)

Pearls:

  1. A full bladder is essential for an adequate scan (can’t do much about this with sick trauma patients)

Pneumothorax study:

Description:

  1. Evaluating for a pneumothorax
  2. Absence of a “sliding sign” and comet tail artifact supports the diagnosis

Sono technique:

  1. The pleural space is just deep to the posterior aspect of the ribs
  2. There is a notable echogenic line with a “sliding appearance” composed of the visceral and parietal pleura
  3. This is considered the normal “sliding sign” and is considered negative for pneumothorax
  4. May use a high-frequency, linear transducer or your abdominal probe
  5. The transducer is placed longitudinally (pointed cranially) in the midclavicular line over the third or fourth intercostal space
  6. The transducer is then moved inferiorly in a systematic fashion, ensuring an appropriate “sliding sign”

Pitfalls:

  1. Bilateral pneumothoraces may limit your comparison of sides
  2. Any movement of the probe may give you a false negative study (see pleural sliding when there isn’t…..)

Pearls:

  1. The abdominal probe is a reasonable alternative to the linear probe for the pneumothorax study; it may make the “sliding sign” easier to visualize
  2. Systematic scanning from cranial to caudal

Keys to the FAST exam:

  1. Complete exam in every view
  2. Identify pathology, not VIEWS
  3. All abnormalities should be imaged in 2 orthogonal planes
  4. Note incidental findings

Limitations to the FAST exam:

  1. Though the quantity of free intraperitoneal fluid that can be accurately detected on ultrasound has been reported as little as 100mL, the typical cut-off is around 500-600mL; smaller amounts of free fluid may be missed (one reason why a repeated exam can be helpful)
  2. Can’t detect a viscus perforation
  3. Can’t detect a bowel wall contusion
  4. Can’t detect pancreatic trauma
  5. Can’t detect renal pedicle injuries

Points to Consider

  1. Pelvis – most dependent
  2. Hepatorenal fossa – most dependent area in the supramesocolic region
  3. Pelvis and Supramesocolic Areas communicate – Phrenicolic ligament prevents flow
  4. Liver/Spleen Injuries – represents about 2/3 of cases of blunt abdominal trauma
  5. Intraperitoneal Fluid may consist of
    1. Blood
      1. Fresh Blood
        1. Anechoic (black)
      2. Coagulated Blood
        1. Hypoechoic
    2. Preexisting ascites
    3. Urine
    4. Intestinal contents
  6. Mimics of fluid in RUQ
    1. Perinephric fat
      1. May be hypoechoic like blood
      2. Usually evenly layered along kidney
      3. If in doubt, compare it to the left kidney
    2. Abdominal Inflamation
      1. Widened extra-renal space
      2. Echogenicity of kidney becomes more like the liver parenchyma
  7. LUQ (near ribs 9 and 10)
    1. Acoustic window (spleen) is smaller than the liver
    2. Mild inspiration will optimize image
    3. Bowel interference is common
  8. Pelvis (suprapubic)
    1. Helpful to image before placement of a Foley catheter
    2. If bladder is empty or Foley already placed
      1. Place an IV bag on the abdomen and scan through the bag
    3. A very large bladder can displace fluid from the pouch of Douglas
      (cul-de-sac) in females and cause a false-negative study
  9. Increased sensitivity with
    1. increased number of views
    2. Trendelenberg
    3. Serial Examinations
  10. Normal echo does not definitively rule out major pericardial injury
  11. Epicardial fat pad may easily be misinterpreted as a clot

SonoSite (Videos)

FAST RUQ Exam: Normal Exam (Hepatorenal)

FAST RUQ Exam: Hemorrhage (Hepatorenal)

FAST LUQ Exam: Normal and Abnormal (Splenorenal or Perisplenic)

FAST Suprapubic Exam: Normal (Bladder or Pelvic)

HQMedEd

Mike Stone

  1. FAST Bonus – RUQ Exam Technique
  2. FAST Bonus – LUQ Exam Technique
  3. FAST Bonus – Subcostal Exam Technique
  4. FAST Bonus – Pelvis Technique

Series

  1. FAST Part 2 – Getting the Right Upper Quadrant Right…
  2. FAST Part 3 – Heidi Kimberly Does the Left Upper Quadrant
  3. FAST Part 4 – The Pelvic View
  4. FAST Part 5 – Pneumothorax (E-FAST)
  5. FAST Part 6 – Josh Rempell covers hemothorax and reviews pneumothorax

Flow Diagrams

Schwartz’s Principles of Surgery

Fast Exam Chart

Wikipedia – Interpretation

File:FAST Algorithm.svg

Other

Penetrating Thoracoabdominal Trauma

Blunt Abdominal Trauma

Summary of FAST vs. CT vs. DPL (Diagnostic Peritoneal Lavage)

  1. Speed – FAST>DPL>CT
  2. Sensitivity – DPL>CT and FAST
  3. Specificity – CT>FAST>DPL
  4. Localization – CT>FAST>DPL
  5. Ease/portability – FAST>DPL>CT
  6. Safety – FAST>CT>DPL
  7. Cost – DPL<FAST<CT

References

  1. Anechoic Stripe Size Influences Accuracy of FAST Examination Interpretation
  2. Deep Impact of Ultrasound in the Intensive Care Unit – The “ICU-sound” Protocol
  3. Diagnostic accuracy of surgeon-performed focused abdominal sonography (FAST) in blunt paediatric trauma
  4. Emergency ultrasound-based algorithms for diagnosing blunt abdominal trauma
  5. EAST – Evaluation of Blunt Abdominal Trauma
  6. eMedicine
    1. Bedside Ultrasonography for Pneumothorax
    2. Focused Assessment With Sonography for Trauma (FAST): Slideshow
    3. Focused Assessment with Sonography in Trauma (FAST)
    4. Imaging in Kidney Trauma
    5. Pneumothorax
    6. Intra-abdominal injuries in polytrauma
  7. FAST scan – Is it worth doing in hemodynamically stable blunt trauma patients
  8. Focused abdominal sonogram for trauma – the learning curve of nonradiologist clinicians in detecting hemoperitoneum
  9. Focused Assessment with Sonography for Trauma (FAST): results from an international consensus conference
  10. Pediatric Abdominal Trauma Imaging
  11. Penetrating stab wounds to the abdomen: use of serial US and contrast-enhanced CT in stable patients
  12. Prospective analysis of the effect of physician experience with the FAST examination in reducing the use of CT scans
  13. Role of ultrasonography in penetrating abdominal trauma: a prospective clinical study
  14. The technical errors of physicians learning to perform focused assessment with sonography in trauma
  15. Test Characteristics of Focused Assessment of Sonography for Trauma for Clinically Significant Abdominal Free Fluid in Pediatric Blunt Abdominal Trauma
  16. The ultrasound screen for penetrating truncal trauma
  17. Ultrasound detection of blunt urological trauma: a 6-year study
  18. Ultrasound in Abdominal Trauma
  19. Ultrasound in Trauma
  20. Use of focused abdominal sonography for trauma at pediatric and adult trauma centers – a survey
  21. Validation of nurse-performed FAST ultrasound
  22. What is the utility of the Focused Assessment with Sonography in Trauma (FAST) exam in penetrating torso trauma

Capnography

Capnography

Capnography (end-tidal CO2 monitoring) is a non-invasive measurement of carbon dioxide in exhaled air to assess a patients’ ventilatory status. It may also be referred to as partial pressure end tidal carbon dioxide monitoring (PETCO2). The end-tidal CO2 (EtCO2) level is a reflection of global CO2 production in the body. Cardiac function, pulmonary function, and metabolic rate all influence the amounts of CO2 produced. The end-tidal CO2 provides information on systemic CO2 production (from exhaled alveolar gas), pathologic dead space, pulmonary blood flow, and confirmation of endotracheal tube placement. Capnography allows trending of CO2 levels using fewer arterial blood gas analyses, but does not completely replace arterial blood gas analysis. Age, smoking, general anesthesia, and systemic diseases can increase the difference between the CO2 value obtained from non-invasive monitoring and arterial blood gas monitoring. Note that capnography measures ventilation, not oxygenation.

Comparison of Capnography and Pulse Oximetry
Capnography Pulse Oximetry
Measures CO2 Measures oxygen saturation
Reflects ventilation Reflects oxygenation
Hypoventilation / apnea detected immediately Changes lag with hypoventilation / apnea
Should be used with pulse oximeter Should be used with capnography

CLINICAL APPLICATION
Maintenance of a patient’s airway is always a primary patient care objective. If the airway
patency is lost, no other treatment modalities can prevent death.

Definitions:

  1. Alveolar Dead Space: When gas exchange doesn’t occur because air is present, but no blood is available to exchange gas. Or there is blood but no air. It could also be because the exchange surface is compromised by pulmonary edema, pulmonary effusion, or swollen membranes
  2. Alveolar volume (Va) – Air that is available for gas exchange, which is typically about 350 cc (Vt – Vd = Va); Anything that affects the tidal volume only affects the alveolar volume.
  3. Anatomical Dead Space (Vd) – Air not available for gas Exchange, which is typically about 150 cc
  4. Bradypnea – slower than normal rate (<10 breaths/min), with normal depth and regular rhythm. Associated with ICP, brain injury, and drug overdose.
  5. Capnogram – the wave form.
  6. Capnography – the measurement of carbon dioxide (CO2) in exhaled breath.
  7. Capnometer – the numeric measurement of CO2.
  8. Dyspnea – air hunger, difficult or labored breathing, shortness of breath
  9. End Tidal CO2 (ETCO2 or PetCO2) – the level of (partial pressure of) carbon dioxide released at end of expiration. Normal values range between 35 and 45 mmHg
  10. Hyperventilation – Increased rate and depth of breathing that results in decreased PaCO2 level. Fast breathing (tachypnea) doesn’t necessarily increase tidal volume, which can be caused by anxiety, head injuries, diabetic emergencies, PE, AMI, and others
  11. Hypoventilation – Shallow, irregular breathing. Slow breathing (bradypnea) does not necessarily decrease tidal volume. Causes include CNS disorders, narcotic use and others.
  12. PACO2 – Partial pressure of CO2 in the alveoli.
  13. PaCO2 – Partial pressure of CO2 in arterial blood.
  14. PCO2 – Partial pressure of CO2 in the blood
  15. PETCO2 – Partial pressure of CO2 at the end of expiration. ~ 38 mm Hg (usually 1 – 6 mm Hg less than PaCO2)
  16. (a-ET)PCO2 – Arterial to end-tidal CO2 tension/pressure difference or gradient.
  17. PvCO2 – Partial pressure of CO2 in mixed venous blood.
  18. Physiologic Dead Space – is the alveolar gas that does not equilibrate fully with capillary blood. In normal subjects, dead space ventilation (VD) accounts for 20 to 30% of the total ventilation (VT), so VD/VT = 0.2 to 0.3
  19. Respiration (or diffusion) is measured by the amount of oxygen in the blood.
  20. Tachypnea – rapid, shallow breathing (>24 breaths/min). Associated with pneumonia, pulmonary edema, metabolic acidosis, septicemia, severe pain, or rib fracture.
  21. Tidal Volume (Vt) – The amount of air moved in one breath, which is typically around 500 cc in an adult at rest
  22. Ventilation is measured by the amount of carbon dioxide in the blood.

Anatomy

Upper and Lower Airways

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The Lungs

The lungs are cone-shaped organs that hold between 4 – 8 liters of volume. The top portion is known as the apex, and the bottom is known as the base. The apex of each lung rises above the clavicles a few centimeters and the base rests against the diaphragm. The right lung has 3 lobes: upper, middle, and lower. The left has two lobes: upper and lower.

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CLINICAL APPLICATION

Aspiration pneumonias are often located in the right middle lobe due to the shorter, straighter right mainstem bronchus.

The Diaphragm

The diaphragm is the major muscle of ventilation. It is a dome-shaped musculofibrous partition located between the thoracic and abdominal cavities. It is composed of two muscles: the right and left hemidiaphragms. The diaphragm allows the esophagus, the aorta, several nerves, and the inferior vena cava to exit through it. The phrenic nerve exits the central nervous system between cervical vertebrae 3 – 5 and extends down to innervate the diaphragm assisting in controlling ventilation.

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CLINICAL APPLICATION

Patients with cervical spine injuries of C3, C4 and C5 are often dependent on mechanical ventilation. This is due to interruption of nerve transmission to the diaphragm and other ventilatory muscles.

Accessory muscles of ventilation

During vigorous exercise and the advanced stages of pulmonary disease processes (e.g. COPD) the accessory muscles of inspiration and expiration are activated to assist the diaphragm.

Muscles of Inspiration (I)

Muscles of Expiration (E)

Scalene muscles

Rectus abdominis muscles

Sternocleidomastoid muscles

External abdominal obliquus muscles

Pectoralis major muscles

Internal abdominis obliquus muscles

Trapezius muscles

Transversus abdominis muscles

External intercostal muscles

Internal intercostal muscles

PaCO2 Equation – PaCO2 reflects ratio of metabolic CO2 production to alveolar ventilation

The PCO2 equation puts into physiologic perspective one of the most common of all clinical observations: a patient’s respiratory rate and breathing effort. The equation states that alveolar PCO2 (PACO2) is directly proportional to the amount of CO2 produced by metabolism and delivered to the lungs (VCO2) and inversely proportional to the alveolar ventilation (VA). While the derivation of the equation is for alveolar PCO2, its great clinical utility stems from the fact that alveolar and arterial PCO2 can be assumed to be equal. Thus,

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PaCO2

Condition in Blood

State of Alveolar Ventilation

> 45 mm Hg

Hypercapnia

Hypoventilation

35 – 45 mm Hg

Eucapnia

Normal ventilation

< 35 mm Hg

Hypocapnia

Hyperventilation

The constant 0.863 is necessary to equate dissimilar units for VCO2 (ml/min) and VA (L/min) to PACO2 pressure units (mm Hg). Alveolar ventilation is the total amount of air breathed per minute (VE; minute ventilation) minus that air which goes to dead space per minute (VD). Dead space includes all airways larger than alveoli plus air entering alveoli in excess of that which can take part in gas exchange.

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In the clinical setting we don’t need to know the actual amount of CO2 production or alveolar ventilation. We just need to know if VA is adequate for VCO2; if it is, then PaCO2 will be in the normal range (35-45 mm Hg). Conversely, a normal PaCO2 means only that alveolar ventilation is adequate for the patient’s level of CO2 production at the moment PaCO2 was measured.  From the PCO2 equation it is evident that a level of alveolar ventilation inadequate for CO2 production will result in an elevated PaCO2 (> 45 mm Hg; hypercapnia). Thus patients with hypercapnia are hypoventilating (the term hypoalveolar ventilating would be more appropriate but hypoventilating is the conventional term). Conversely, alveolar ventilation in excess of that needed for CO2 production will result in a low PaCO2 (< 35 mm Hg; hypocapnia) and the patient will be hyperventilating. (Confusion sometimes arises because the prefix (hyper-, hypo-) differs for the same condition depending on whether one is describing a blood value or the state of alveolar ventilation.) For reasons that will be discussed below, the terms hypo- and hyper- ventilation refer only to high or low PaCO2, respectively, and should not be used to characterize any patient’s respiratory rate, depth, or breathing effort.

From the PCO2 equation it follows that the only physiologic reason for elevated PaCO2 is a level of alveolar ventilation inadequate for the amount of CO2 produced and delivered to the lungs. Thus arterial hypercapnia can always be explained by:

  1. Not enough total ventilation (as may occur from central nervous system depression or respiratory muscle weakness); or
  2. Too much of the total ventilation ending up as dead space ventilation (as may occur in severe chronic obstructive pulmonary disease, or from rapid, shallow breathing); or
  3. Some combination of 1) and 2).

Excess CO2 production is omitted as a specific cause of hypercapnia because it is never a problem for the normal respiratory system unimpeded by a resistive load. During submaximal exercise, for example, where CO2 production is increased, PaCO2 stays in the normal range because VA rises proportional to the rise in VCO2. With extremes of exercise (beyond anaerobic threshold) PaCO2 falls as compensation for the developing lactic acidosis. In a healthy patient PaCO2 may be reduced but is never elevated.

An important clinical corollary of the PaCO2 equation is that we cannot reliably assess the adequacy of alveolar ventilation – and hence PaCO2 – at the bedside. Although VE can be easily measured with a handheld spirometer (as tidal volume times respiratory rate), there is no way to know the amount of VE going to dead space or the patient’s rate of CO2 production. Other clinical factors include respiratory effort, mental status, body habitus, temperature, etc.

A common mistake is to assume that because a patient is breathing fast, hard and/or deep he or she must be “hyperventilating.” Not so, of course.

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PCO2 vs. Alveolar Ventilation

The relationship is shown for metabolic carbon dioxide production rates of 200 ml/min and 300 ml/min (curved lines). A fixed decrease in alveolar ventilation (x-axis) in the hypercapnic patient will result in a greater rise in PaCO2 (y-axis) than the same VA change when PaCO2 is low or normal.
This graph also shows that if alveolar ventilation is fixed, an increase in carbon dioxide production will result in an increase in PaCO2.

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Effect of Increasing Arterial PCO2 or Reducing pH on Ventilation

Guyton & Hall, Textbook of Medical Physiology, 10th ed., 2000, Saunders p. 477.

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The effect of PCO2 on ventilation is primarily due to a region of the ventral medulla referred to as the chemosensitive area. In this area, there are sensor neurons that are excited by hydrogen ions. As arterial PCO2 rises, CO2 easily and rapidly diffuses through the blood brain barrier where it combines with water to form carbonic acid which releases a hydrogen ion. So, the net effect of increased arterial PCO2 is increased cerebrospinal fluid (CSF) and brain interstitial acidity. This strongly stimulates these sensor neurons which stimulate the respiratory centers to increase ventilation (this will tend to reduce the arterial PCO2 back to baseline).

Hydrogen ions themselves do not diffuse as easily across the blood brain barrier making the direct effect of pH less. The effect of PCO2 on ventilation is strongest in the acute phase. If the person has a high PCO2 for a prolonged period (days or longer, perhaps due to a lung or neurological problem), the pH of the CSF tends to return toward normal because of adaptive effects related to bicarbonate. The person becomes accustomed to the higher PCO2 and it causes less stimulus to hyperventilate.

Ventilation Increases as PaO2 Decreases at Constant PaCO2

Guyton & Hall, Textbook of Medical Physiology, 10th ed., 2000, Saunders p. 479.

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Integrated Effects of PCO2, PO2 & pH on Alveolar Ventilation

Guyton & Hall, Textbook of Medical Physiology, 10th ed., 2000, Saunders p. 479.

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Equipment

Currently, there are 2 basic types of CO2 detectors: quantitative and qualitative.

  1. Qualitative CO2 detectors are colorimetric detectors that contain material that reversibly reacts with CO2. This reaction causes the color to change, most commonly, from purple to yellow. Qualitative capnography units can be broken down into mainstream and sidestream configurations.
    1. Mainstream units, or in-line units, are used for ventilated patients who are intubated endotracheally. The sensor is placed directly on an adapter attached to the endotracheal tube. From there, EtCO2 can be directly measured.
    2. Sidestream units have a sensor that is located on the main unit itself. These systems aspirate the gas sample from the patient’s airway, which then measures the EtCO2. In turn, sidestream units can be used in awake or intubated patients.
  2. Quantitative CO2 detectors give a measured value of EtCO2. This numeric value is referred to as capnometry. Quantitative detectors can also be displayed as a waveform called a capnogram. This waveform of inspiratory/expiratory CO2 can be displayed over time or volume and is referred to as a capnograph.

How medical equipment works – Capnography

Levels or Phases

Information from Capnography can be broken down into levels, each with increasing degrees of information

1. Level 1

  1. Breathing or not, i.e. apnoea monitor
  2. Respiratory rate

2. Level 2

  1. Expired CO2 levels (4.5% or 35mmHg)
  2. Inspired CO2 levels (0%)
  3. From these parameters we can now begin to deduce the state of the patient with regard to respiration i.e. normocapnic, hypocapnic or hypercapnic

3. Level 3

  1. Waveform profile
  2. There are 4 recognised parts to a typical capnogram, each one having characteristics that impart specific information
  3. A typical capnogram obtained during controlled mechanical ventilation showing:
    1. i. Inspiratory baseline (A to B)
    2. ii. Expiratory upstroke (B to C)
    3. iii. Expiratory plateau (C to D)
    4. iv. Inspiratory down stroke (D to E)

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Advanced Emergency Nursing Journal Vol. 28, No. 4, pp. 301–313

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Angles

  1. “α” (Alpha) angle – Used to assess the Ventilation/ Perfusion (V/Q) status of lung. During mismatches, the alpha angle is > ~ 90 degrees. The more damaged and less uniform the alveoli, the larger the angle. Bronchospasm (sharkfin), COPD, etc.
  2. “β” (Beta) angle – Used to assess rebreathing. During rebreathing, the beta angle is > 90 degrees. May see in infants who are breathing faster than capnograph can account for.

A normal capnogram look like the following.

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Its analysis should include the following:

  1. Verify presence of exhaled CO2
    1. Is a waveform present?
  2. Inspiratory baseline
    1. Is there rebreathing?
  3. Expiratory upstroke
    1. Is it steep, sloping, or prolonged?
  4. Expiratory plateau
    1. Is it flat, prolonged, notched, or sloping?
  5. Inspiratory down stroke
    1. Is it steep, sloping, or prolonged?
  6. Check PICO2 min and PECO2max
  7. Estimate or measure PaCO2 – PECO2 max
  8. Search for causes of hypercapnia or hypocapnia, if either is present

Clinical Application Examples of Capnography

Slap the Cap – The Role of Capnography in EMS

  1. One of two sure signs of endotracheal intubation.

    1. This is probably the most common use of capnography, yet limiting oneself to this use only is a huge waste. In the beginning, color change devices would detect CO2 levels. This is widely believed to be able to accurately predict when the endotracheal tube is misplaced in the esophagus. Theoretically, there should be no CO2 exhaled from the esophagus, on the trachea. However, in low perfusion states, this is not a very accurate reading and the manufacturer even suggests using another confirming device besides this one. Therefore, waveform capnography is the gold standard for endotracheal tube confirmation. Tube confirmation is confirmed with a SQUARE waveform. With a square waveform, the tube cannot be in the esophagus, or the hypopharynx. It must be in the trachea, regardless of the value of the return of CO2.

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    2. Right mainstem intubation. A square waveform can occur with a right mainstem intubation because the tube is still in the main airway.Therefore, auscultation in the fifth intercostal space midaxillary, bilaterally, is necessary to rule out right mainstem intubation.
  2. Detection of untoward events e.g… Disconnections or inadvertent extubation.
  3. Maintenance of normocapnia
  4. Cardiopulmonary resuscitation
    1. As an assessment tool during CPR, capnography is a direct measurement of ventilation in the lungs, and it also indirectly measures metabolism and circulation. For example, a decrease in perfusion (cardiac output) will lower the delivery of carbon dioxide to the lungs. This will cause a decrease in the ETCO2 (end-tidal CO2), and this will be observable on the waveform as well as with the numerical measurement.
    2. Two very practical uses of waveform capnography in CPR are: 1.) evaluating the effectiveness of chest compressions; and 2.) identification of ROSC. Evaluating effectiveness of chest compressions is accomplished in the following manner: Measurement of a low ETCO2 value (< 10 mmHg) during CPR in an intubated patient would indicate that the quality of chest compressions needs improvement.
    3. An abrupt increase in PETCO2 may indicate return of spontaneous circulation (ROSC), Increase in pulmonary circulation brings more CO2 into lungs for elimination.  In most cases that have ROSC the ETCO2 goes into the 70-90’s!
  5. Weaning from mechanical ventilation
  6. Monitoring the seizure patient
    1. Generalized seizure, such as a tonic/clonic, can affects both hemispheres of the brain and the medulla. When the medulla is involved, the patient may not breath during seizure activity. Following the post-ictal state capnography can determine the need for further ventilation.
  7. Metabolic Uses: DKA
    1. Since CO2 is carried in the blood stream and bicarbonate Ion, it has a
      direct clinical relationship to serum bicarb levels. Therefore, if the patient
      has a high Blood glucose, measure their ETCO2. If it is less than 29, then
      the patient has DKA. The blood gas bicarb will show a very low level as
      well, indication metabolic acidosis.
  8. Pulmonary Embolism: This is easy. The combination of ETCO2 and an ABG CO2 can easily call a V/Q mismatch. All you need then is a CT scan to figure out where it is and
    they are on their way. A high blood gas CO2 and a low ETCO2 tells us the
    CO2 is not getting to the lungs to be exhaled.
  9. Trauma?
    1. In Tension Pneumothorax, pressure in the chest collapses a lung and then
      presses on the right side of the heart making it hard to fill with blood. It
      only takes about 7mm/hg pressure to stop the blood flow into the right
      atria. The first and must reliable sign of a TENSION pneumothorax is the
      sudden drop in perfusion that is picked up immediately on a capnogram.
      By the same token, when the chest is successfully decompressed, it is not
      a rush of air but a sudden increase in ETCO2 that confirms decompression
      success. Furthermore, the capnogram can be used to keep watch in case
      it develops again.
    2. The same is true for Pericardial Tamponade and cardiocentesis. In each
      of these obstructive forms of hypoperfusion, the capnogram will remain
      square because it is a perfusion problem, not an airway problem, but you
      knew that, right?
  10. Closed Head Injury. ITLS and the Brain Trauma Foundation have taken the
    lead in recommending capnography as the way titrate CO2 ventilations in
    the patient with a closed head injury. If the patient has a GCS of less than
    9 and they are posturing, have unequal pupils, or dropped two in front of
    you, then they should be selectively ventilated to an ETCO2 between 30-
    35mm/hg. If the patient does not the signs (above) of deterioration, then
    ventilate the patient to levels, 35-45. Never ever bag them to lower than
    25mm/hg. It causes cerebral vasoconstriction and creates an alkalosis not
    allowing O2 to dissociate from hemoglobin, make the brain injury worse.
  11. Monitoring the non-intubated patient
    1. Capnography helps conscious patients too

Specific Waveforms to Know

There are a few specific waveforms that you need to know.

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Capnography Outside the Operating Rooms

Kodali, Bhavani Shankar Anesthesiology. 118(1):192-201, January 2013. doi: 10.1097/ALN.0b013e318278c8b6

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A, Prolonged phase II, increased α angle, and steeper phase III suggest bronchospasm or airway obstruction.

B, Expiratory valve malfunction resulting in elevation of the baseline, and the angle between the alveolar plateau and the downstroke of inspiration is increased from 90°. This is due to rebreathing of expiratory gases from the expiratory limb during inspiration.

C, Inspiratory valve malfunction resulting in rebreathing of expired gases from inspiratory limb during inspiration (reference 5 for details).

D, Capnogram with normal phase II but with increased slope of phase III. This capnogram is observed in pregnant subjects under general anesthesia (normal physiologic variant and details in reference 9).

E, Curare cleft: Patient is attempting to breathe during partial muscle paralysis. Surgical movements on the chest and abdomen can also result in the curare cleft. (You have maybe 3 minutes to sedate the patient before they begin to waken or start to fight the tube.)

F, Baseline is elevated as a result of carbon dioxide rebreathing.

G, Esophageal intubation resulting in the gastric washout of residual carbon dioxide and subsequent carbon dioxide will be zero.

H, Spontaneously breathing carbon dioxide waveforms where phase III is not well delineated.

I, Dual capnogram in one lung transplantation patient. The first peak in phase III is from the transplanted normal lung, whereas the second peak is from the native disease lung. A variation of dual capnogram (steeple sign capnogram – dotted line) is seen if there is a leak around the sidestream sensor port at the monitor. This is because of the dilution of expired PCO2 with atmospheric air.

J, Malignant hyperpyrexia where carbon dioxide is raising gradually with zero baseline suggesting increased carbon dioxide production with carbon dioxide absorption by the soda lime.

K, Classic ripple effect during the expiratory pause showing cardiogenic oscillations. These occur as a result of to-and-for movement of expired gases at the sensor due to motion of the heartbeat during expiratory pause when respiratory frequency of mechanical ventilation is low. Ripple effect like wave forms also occur when forward flow of fresh gases from a source during expiratory pause intermingles with expiratory gases at the sensor.

L, Sudden raise of baseline and the end-tidal PCO2 (PETCO2) due to contamination of the sensor with secretions or water vapor. Gradual rise of baseline and PETCO2 occurs when soda lime is exhausted.

M, Intermittent mechanical ventilation (IMV) breaths in the midst of spontaneously breathing patient. A comparison of the height of spontaneous breaths compared to the mechanical breaths is useful to assess spontaneous ventilation during weaning process.

N, Cardiopulmonary resuscitation: capnogram showing positive waveforms during each compression suggesting effective cardiac compression generating pulmonary blood.

O, Capnogram showing rebreathing during inspiration. This is normal in rebreathing circuits such as Mapleson D or Bain circuit.

Resources

  1. AHRQ Guideline – Capnography/capnometry during mechanical ventilation: 2011 
  2. BCEMS
    1. Capnography Part I
    2. Capnography Part II
  3. Capnography
  4. Capnography Outside the Operating Rooms
  5. Capnography/Capnometry During Mechanical Ventilation: 2011 (pdf)
  6. Cecil medicine – Chapter 104 – Respiratory Monitoring in Critical Care
  7. Council of the Intensive Care Society – Capnography Guidelines
  8. Difficult Airway Society – Capnography the Future
  9. Emergency Nurses Association – Wave Form Capnography The 12 Lead of the Lungs!
  10. Interpreting your capnogram
  11. Life in the Fast Lane
    1. Capnography
    2. Respiratory Monitoring in the ED
  12. NIAA – National Audit Project 4
  13. Noninvasive Monitoring of End-Tidal Carbon Dioxide in the Emergency Department
  14. Phillips – Clinical Measurements – A Quick Guide to Capnography 
  15. Physiology of Oxygenation and Ventilation
  16. Slap the Cap – The Role of Capnography in EMS
  17. Rapid Results – Capnography: A Key Patient Assessment Tool
  18. Riding the Waves (pdf)
  19. The Alveolar Gas Equation (pdf)

Efficacy of Nimodipine Administration on Vasospasm after Subarachnoid Hemorrhage

I reviewed three articles on the efficacy of Nimodipine administration on vasospasm after subarachnoid hemorrhage in order to produce improved clinical outcomes.

Efficacy of Nimodipine Administration on Vasospasm after Subarachnoid Hemorrhage

Although the outcomes for these patients continues to remain poor, the current evidence suggests that calcium antagonist like Nimodipine can play an integral part of providing the best possible care for this populuation subset. The authors demonstrate that continuous local intra-arterial nimodipine administration (CLINA) is both safe and effective in helping reverse vasospasm and prevent delayed ischemic neurological deficit commonly associated with subarachnoid hemorrhage. They show that intra-arterial nimodipine administration shows good vessel widening effects against vasospasm. Additionally, the authors observed a positive correlation between the degree of blood vessel expansion and the improvement in clinical symptoms.

Here are the three main articles referenced in the paper. Unfortunately, only the first article is available without a fee.

  1. Angiographic Features and Clinical Outcomes of Intra-Arterial Nimodipine Injection in Patients with Subarachnoid Hemorrhage-Induced Vasospasm
  2. Continuous intra-arterial infusion of nimodipine at the onset of resistant vasospasm in aneurysmal subarachnoidal hemorrhage – A technical resport ($)
  3. Continuous Local Intra-arterial Nimodipine Administration in Severe Symptomatic Vasospasm after Subarachnoid Hemorrhage ($)

Here are the supporting related references, and fortunately most of them are available without a fee.

  1. American Association of Neurological Surgeons – Cerebral Aneurysm
  2. American Association of Neuroscience Nurses – Care of the Patient with Aneurysmal Subarachnoid Hemorrhage
  3. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association
  4. The Chocrane Library – Calcium Antagonists in Aneurysmal Subarachnoid Hemorrhage ($)
  5. Intra-Arterial Nimodipine for Severe Cerebral Vasospasm after Aneurysmal Subarachnoid Hemorrhage: Influence on Clinical Course and Cerebral Perfusion
  6. The role of transcranial Doppler ultrasonography in the diagnosis and management of vasospasm after aneurysmal subarachnoid hemorrhage ($)
  7. Inflammation and cerebral vasospasm after subarachnoid hemorrhage ($)
  8. Angiographic Features and Clinical Outcomes of Intra-Arterial Nimodipine Injection in Patients with Subarachnoid Hemorrhage-Induced Vasospasm

ARDS

Acute respiratory distress syndrome (ARDS) is a life-threatening lung condition that prevents enough oxygen from getting to the lungs and into the blood. It is the failure of the pulmonary system to provide sufficient exchange of oxygen to supply the body’s demands. There are around 200,000 cases each year in the US alone, and unfortunately around half of all those who develop ARDS do not survive.

There is a lot of great information on this topic available on ARDSNetMedscapePubMedPubMedHealth, and Wikipedia – ARDS, and UpToDate – ARDS. Here is a great mind map resource for understanding ARDS.

Additionally, I have a page on ARDS, where I have compiled a lot of this information into one source. Here are some of the key points to review.

Berlin Definition

Acute Respiratory Distress Definition

ARDS Pathophysiology

  • —Immune and inflammatory responses damage the alveolar capillary membrane
  • Hypoxemia
  • Increased elastance and decreased compliance
  • Increased minute volume requirement
  • Increased work of breathing
  • Pulmonary hypertension
  • —Exudative phase: capillary membrane begins to leak.  Fluid fills the alveoli causing profound impaired gas exchange
  • —Acute phase:  movement of fluid multiplies.  This lasts about 4 days with leakage of fluid continuing for about 7 days
  • —Appears on chest x-ray as bilateral infiltrates

ARDS

  • —Does not affect LV function, and initially PAWP remains below 18.
  • —Proliferative phase:  7 to 10 days after onset, and may last up to a month.  Lungs attempt to resolve the inflammation, surfactant production decreased, which causes further damage
  • —There is a Ventilation perfusion mismatch and hypoxemia
  • —Fibrotic phase:  development of fibrotic tissue in the alveoli, leads to further decreased lung compliance and worsening pulmonary hypertension

ARDS Early Clinical Symptoms

  • —Early signs are tachypnea, tachycardia,
  • —Dyspnea
  • —Rapid shallow respirations
  • —Use of accessory muscles
  • —Mottling, or cyanosis
  • —Breath sounds abnormal
  • —Dry Cough
  • —Altered loc
  • —Confusion
  • —Restlessness
  • —Retrosternal pain
  • —Fever

Diagnostic

  • —ABGS ( early hypoxemia, respiratory alkaloses)
  • —Chest x-ray
  • —CT chest

Management of ARDS

  • —Focus on resolving symptoms
  • —Anticipate intubation and mechanical ventilation
  • —Refractory Hypoxemia:  PaO2 does not respond to increases in FIO2

Ventilation

  • —Challenge in ARDS patients is to adequately ventilate while preventing injury to lungs from the high pressures required to inflate noncompliant lungs.
  • —Research is ongoing; prevention of ventilator induced lung injury is a major focus currently.
  • —Lower tidal volume and permissive hypercapnia results in alveolar hypoventilation
  • —Inverse Inspiratory/Expiratory ratio:  Normal ratio is that the inspiratory phase is < expiratory phase.  IVR reverses this so that inspiration takes longer than expiration, protecting the lungs.

Pharmacological Support in ARDS

  • —Corticosteroids:  decrease inflammation
  • —Vasodilators: Nitric Oxide:  relaxes pulmonary vascular smooth muscle.  Not supported in adults
  • —Surfactant:  Not supported in adults
  • —Manage fluids conservatively

Here is a great YouTube video synopsis.

Sepsis

INTRODUCTION

First, sepsis is a syndrome and not an individual disease. It is the 11th leading cause of death in the US. According to the Global Sepsis Alliance (GSA), “Sepsis is one of the most pressing healthcare challenges faced by the world today.”  The CDC shows sepsis hospital admissions “have grown from around 200 per 1000 inhabitants in 2000, to 340 in 2008. Also, in 2008 the costs for hospital treatment were US $14.8 billion, but these have increased by an annual rate of 11 percent.” According to Dr. Reinhardt “the main way it can be prevented is if it is recognized early and the patient receives adequate measures of treatment. Treatments, like antimicrobials and intravenous fluids must be initiated when the first signs of organ dysfunction appear. If they are given in the first few hours the survival rate may be up to 80 percent, but studies suggest with each hour of delay the mortality rate increases by five to eight percent.” (GSA – Stop Sepsis, Save Lives)

DEFINITION

Sepsis is a potentially deadly medical condition characterized by a whole-body inflammatory state (called a systemic inflammatory response syndrome or SIRS) that is triggered by an infection. The body may develop this inflammatory response by the immune system to microbes in the blood, urine, lungs, skin, or other tissues. A popular term for sepsis is blood poisoning. Severe sepsis is the systemic inflammatory response, infection and the presence of organ dysfunction. Septic Shock is the combination of sepsis with abnormally decreased blood pressure.

(Also, here is another great video about SIRS from the same source.)

PATHOPHYSIOLOGY

At this point in time, the literature richly illustrates that no single mediator / system / pathway / pathogen drives the pathophysiology of sepsis (Am J Pathol. 2007 May; 170(5): 1435–1444. doi:10.2353/ajpath.2007.060872Pathophysiology of Sepsis)

    • The basic pathophysiology of sepsis, severe sepsis, and septic shock includes:
      • Vasodilation
      • Third spacing due to capillary leak
      • Myocardial dysfunction.
    • Vascular endothelium is both a source and target of injury in SIRS / sepsis. Injury may be due to toxins such as LPS (endotoxin) or from ischemia itself. Tissue factor release leads to amplification of the inflammatory response and to DIC via the thrombin pathway. Thrombin not only catalyzes fibrin formation but also causes leukocyte adhesion which leads to further endothelial damage. As DIC progresses, clotting factors are consumed and bleeding occurs.
    • Clotting factors, pro-fibrinolytic, and anti-thrombin factors are consumed leading to loss of fibrinolysis & normal down-regulation of thrombin pathway. This phenomenon is both pro-inflammatory and pro-thrombotic.
    • Protein C depletion has been associated with increased mortality. This has led to a series of clinical trials utilizing protein C, activated protein C (APC), antithrombin III (AT-III), and tissue factor pathway inhibitor to try and disrupt this cycle. Activated protein C has in fact been shown to reduce mortality in severe sepsis in adults. Bleeding problems seems to outweigh the benefits in children.
    • Usually gram negative and usually originating in the urinary or respiratory systems
    • Frequent microbial causes of sepsis

 

IDENTIFYING SEPSIS

(Balk RA. Crit Care Clin 2000;16:337-52Surviving Sepsis Campaign 2008 SSC Guidelines)

Differentials

TREATMENT

DESPERATE MEASURES

These measures can help improve immunohomeostasis (pro/antiinflamatory mediators), improve coagulation response with decreased organ thrombosis, and provide mechanical support for organ perfusion during an acute episode, and may buy some time, but may or may not reduce mortality.

NOVEL THERAPIES

QUALITY

REVIEWS

CLINICAL TRIALS

DR. RIVERS TALK

Dr. Emmanuel Rivers gave a talk on Severe Sepsis Management via the EMCrit Blog. The talk is broken down into the three links to each of the episodes provided below.

ADDITIONAL RESOURCES

In addition, here are some more great resources related to sepsis.

  1. Advances in Sepsis
  2. Crashing Patient Severe Sepsis
  3. Development and Implementation of a Multidisciplinary Sepsis Protocol
  4. EMCrit – Severe Sepsis Resources*
  5. EM Guidlines – Sepsis
  6. Global Sepsis Alliance
  7. International Sepsis Forum
  8. MedicineNet – Sepsis
  9. Medline Sepsis
  10. Sepsis Alliance
  11. Sepsis know from day 1
  12. Stanford SOM – Septris
  13. Surviving Sepsis
    1. The Surviving Sepsis Campaign (SSC) was developed by the European Society of Critical Care Medicinethe International Sepsis Forum,and the Society of Critical Care Medicine, to help meet the challenges of sepsis and to improve its management, diagnosis, and treatment. The agreement between the three founding organizations and funding for the campaign was concluded December 31, 2008. A generous grant has been received to continue the important work of the campaign. The grant funding extends through 2013. Assistance for US hospitals interested in implementing the bundles can be obtained through the Society of Critical Care Medicine’s Paragon program.
    2. Surviving Sepsis Protocol Checklist

Additional References

  1. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis De?nitions Conference
  2. Cleveland Clinic – Sepsis
  3. Genetic Polymorphisms in Sepsis and Septic Shock:Role in Prognosis and Potential for Therapy
  4. New Approaches to Sepsis: Molecular Diagnostics and Biomarkers
  5. Role of oxygen debt in the development of organ failure sepsis, and death in high-risk surgical patients
  6. Oxidative stress as a novel target in pediatric sepsis management
  7. The Pathogenesis of Sepsis
  8. Rapid Treatment of Severe Sepsis
  9. Sepsis in cirrhosis: report on the 7th meeting of the International Ascites Club
  10. Thermo Scientific biomarker procalcitonin
  11. Time is tissue: Why emerging evidence on sepsis urges physicians to watch the clock
    Early volume resuscitation can help avoid organ dysfunction—if you act quickly after making a diagnosis

CONCLUSION

Sepsis poses a significant burden upon the US healthcare system, resulting in an estimated 750,000 hospital admissions, 570,000 Emergency Department visits, 200,000 deaths and $16.7 billion in medical expenditures annually, according to, the online journal article in PLOS ONE, Chronic Medical Conditions and Risk of Sepsis. Mortality rates remain high in severe sepsis, and despite recent therapeutic breakthroughs much remains to be done to advance our understanding and treatment of sepsis. Currently, anti-sepsis initiatives focus on acute care, with ED staff employing the “sepsis bundles,” a series of steps that includes aggressive administration of antibiotics, IV fluids and blood pressure-boosting medications, and management. Additionally, the  Surviving Sepsis Campaign 2012 guidelines will further suggest that in patients with elevated lactate levels as a marker of hypoperfusion, resuscitation should be targeted at normalizing lactate as rapidly as possible (grade 2C). Having said that, however, a normal lactate doesn’t indicate absence of shock. Other factors, such as the patient’s central venous oxygen saturation level, need to be considered as well. The Surviving Sepsis Campaign guidelines are sponsored by 27 medical organizations. Among them are the Society of Critical Care Medicine, ACEP, the Society of Hospital Medicine, the American College of Chest Physicians, the American Thoracic Society, the Infectious Diseases Society of America, the Surgical Infection Society, the Pediatric Acute Lung Injury and Sepsis Investigators, and a host of international groups. Hopefully, strategies will be developed to continue to improve and maximize our efforts towards ameliorating sepsis throughout the world.