Critical Care

PAINE #PANCE Pearl – Critical Care

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Question

A large part of critical care and ICU management revolves around hemodynamic monitoring and support. But…..we typically don’t use traditional blood pressure (systolic and diastolic) numbers directly.

We use MAP!!!

  1. What is MAP?
  2. How do you calculate it?
  3. Why is it a better variable to monitor when it comes to blood pressure and critical care?

Answer

  1. Mean Arterial Pressure (MAP)
  2. It is calculated using the following formula:
    1. MAP = 1/3(SBP) + 2/3(DBP)
  3. MAP has the greatest influence on blood flow autoregulation within the organs, as well as whole body hemodynamic homeostasis. It is superior to systolic pressure because it is the true driving pressure for peripherial blood flow and it does not change as the pressure waveform moves more distally.
    1. Bonus Pearl – MAP > 65 is a general ICU mantra as the minimum pressure pressure to maintain organ perfusion

References

  • Marino, PL. Arterial Pressure Monitoring. In: The ICU Book. 4th ed. 2014.
  • The relevance of the mean arterial pressure. From: Deranged Physiology – Monitoring of Arterial Pressure. [Link]
  • Mean Arterial Pressure. From: Cardiovascular Physiology Concepts. [Link]

Ep-PAINE-nym

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Swan-Ganz Catheter

Other Known Aliases – pulmonary artery catheter

Definition – intravenous catheter that is maneuvered through the right side of the heart into the pulmonary artery.

Clinical Significance – This catheter can directly measure several important hemodynamic variables in critical illness:

  • right atrial pressures
  • right ventricular pressures
  • pulmonary artery pressures
  • left atrial filling pressures (wedge pressure)
  • cardiac output/cardiac index
  • systemic vascular resistance
  • pulmonary vascular resistance

It is “floated” through the right side of the heart using the flow of the blood to carry it into the pulmonary artery. This migration has a very characteristic pressure pattern to know where the catheter is in the vascular system.

History – Named after two physicians from Cedars-Sinai Medical Center, Jeremy Swan (1922-2005), an Irish American cardiologist, and William Ganz (1919-2009), a Slovak American cardiologist. Dr. Swan received his medical doctorate from Castleknock College and went on to become faculty at the Mayo Clinic before joining the faculty at Cedars-Sinai Hospital in Los Angeles. Dr. Ganz attended Charles University School of Medicine in Prague in 1938, but was closed in 1940 after the Nazi occupation of Czechoslovakia. Being jewish, he was then sent to a Hungarian Nazi labor camp and was actually scheduled to be sent to Auschwitz in 19944 before his escape. After hiding and waiting out the war, Dr. Ganz returned and graduated from Charles University in 1947 at the top of his class. He practiced in communist Czechslovakia until 1966 when he secretly defected to the US with his wife and sons. His first and only position as a physician in the US was at Cedars-Sinai Hospital, where he met Dr. Swan who got the idea of the catheter from watching the wind play with the sails of boats in the marina. Dr. Ganz had already published research on the use of thermodilution as a way to measure cardiac output and in 1970, they published their landmark article in the NEJM. It should be noted that German surgeon Werner Forssmann first demonstrated the safety of this type of catheter, by doing it on himself in 1929.

References

  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. Up To Date. www.uptodate.com
  6. Swan HJ, Ganz W, Forrester J, Marcus H, Diamond G, Chonette D. Catheterization of the heart in man with use of a flow-directed balloon-tipped catheter. The New England journal of medicine. 1970; 283(9):447-51. [pubmed]
  7. FRONEK A, GANZ V. [Local thermodilution method of measuring minute volume and circulation rate in the peripheral vessels]. Ceskoslovenska fysiologie. 1959; 8(3):189. [pubmed]
  8. W. Forssmann. Die Sondierung des Rechten Herzens. Klinische Wochenschrift, Berlin, 1929, 8: 2085.

Ep-PAINE-nym

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Osborn Wave

Other Known Aliases – J-wave, camel-hump, hypothermic hump

Definition – positive deflection occurring at the junction between the QRS complex and ST segment, commonly referred to as the J point

Clinical Significance – Osborn waves are classically seen in hypothermia with a core body temperature < 32°C (90°F), but also can be present in severe hypercalcemia, traumatic brain injury, and pericarditis. It is usually most prominent in the precordial leads.

NEJM. 2015

History – Named after John J. Osborn (1917-2014), who was an American intensivist, and received his medical doctorate from Johns Hopkins University in 1943. He completed a nine-month residency in pediatrics before serving as an Army medical officer in World War II in the Pacific Theatre. He first published his preliminary animal research on hypothermia in 1943 before his military service, and picked it back up after returning stateside. He practiced from New York University to Stanford University and was a founding member of the Society of Critical Care Medicine. His research fostered the initial golden age of intensive care medicine and he worked on heart-lung machine designs, as well as hemodynamic monitoring devices. His eponymous paper was published in 1953 entitled “Experimental hypothermia; respiratory and blood pH changes in relation to cardiac function”

References

  1. Firkin BG and Whitwirth JA.  Dictionary of Medical Eponyms. 2nd ed.  New York, NY; Parthenon Publishing Group. 1996.
  2. Bartolucci S, Forbis P.  Stedman’s Medical Eponyms.  2nd ed.  Baltimore, MD; LWW.  2005.
  3. Yee AJ, Pfiffner P. (2012).  Medical Eponyms (Version 1.4.2) [Mobile Application Software].  Retrieved http://itunes.apple.com.
  4. Whonamedit – dictionary of medical eponyms. http://www.whonamedit.com
  5. Up To Date. www.uptodate.com
  6. OSBORN JJ. Experimental hypothermia; respiratory and blood pH changes in relation to cardiac function. The American journal of physiology. 1953; 175(3):389-98. [pubmed]
  7. Partin C. Profiles in Cardiology: John J Osborn. Clin Cardiol. 1998;21;66-68 [link]

#36 – Basics of the Ventilator with Wes Johnson, PA-C

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***LISTEN TO THE PODCAST HERE***

 

Guest Information

 

Wes Johnson, MSPAS, PA-C, (soon to be), DHSc was a former student of mine at UAB and was a respiratory therapist prior to PA school.  He is the Regional Director of Clinical Education for Island Medical Management Emergency group in North Alabama.  He won the Preceptor of The Year award from UAB in 2016 and currently finishing up his doctorate degree from A.T. Still University.

Twitter – @wesj2288

Disclaimer

 

For the purposes of this podcast and post, we will be using the Puritan Bennett 840 ventilator (pictured below).  All the term we use are synonymous with all vents, but the screens will be different.

Puritan Bennett 840

Big Concepts of The Ventilator

 

  1. Mode
    1. Assist Control (AC)
      1. Every breath is either a machine driven (set by rate) or fully assisted (initiated by the patient)
        1. Uses either pressure (ACPC) or volume (ACVC)
    2. Synchronized Intermittent Mechanical Ventilation (SIMV)
      1. Set number of machine driven breaths, and patient intitated breaths are partially assisted
    3. Pressure Support (PS)
      1. No machine driven breaths and all breaths are initiated by the patient and partially assisted
  2. Delivery
    1. Pressure
      1. Static Controls
        1. Pressure
        2. Time (inspiratory)
        3. Peak flow
      2. Variable Factors
        1. Volume
        2. Total flow
    2. Volume
      1. Static Controls
        1. Tidal volume (cc)
        2. Flow (L/min)
      2. Variable Factors
        1. Pressure
  3. Positive End Expiratory Pressure (PEEP)
    1. The pressure left in the circuit at the end of expiration
    2. Prevents alveolar collapse and improves oxygenation
    3. Can cause barotrauma and affect hemodynamics

Static Controls

 

(For this section, refer back to the vent picture above)

  1. Fraction of Inspired Oxygen (FiO2)
    1. Start at 100% and titrate down to 21%
  2. f (machine breath rate)
  3. Control
    1. Pressure Control (PC)
      1. Inspiratory pressure (Pi)
        1. Peak pressure in circuit
        2. Initial setting = < 20 cm H20
      2. Inspiratory time (I-time)
        1. Initial setting = 1.25 seconds
    2. Volume Control (VC)
      1. Vt (tidal volume of each breath)
        1. Initial setting = 6-8 cc/kg IBW
      2. Vmax (flow rate)
  4. Spontaneous Support
    1. Trigger for spontaneous support
      1. Volume = V-trig
      3. Pressure = P-trig
    2. Pressure Support (PS)
      1. I was always taught at least 5 cm H20 to overcome circuit resistance

Real-Time Controls

 

  1. Flashing “C” and “S”
    1. Lets you know what breaths are controlled (machine) or spontaneous (patient)
  2. Airway Pressure
    1. Ppeak (max airway pressure)
      1. A marker of resistance
    2. Pmean (average airway pressure)
      1. A measure of alveolar pressure
    3. Pplat (small airway and alveoli pressure)
      1. A measure of compliance
  3. fTotal (machine + spontaneous breaths)
  4. I:E (inspiratory:expiratory ratio)
    1. Normal = 1:2 (at rest)
    2. Inverse ratio (2:1) can improve oxygen due to intention auto-PEEP

Wes Johnson’s Approach to Setting Up a Ventilator (after RSI)

 

Mode: AC

Vt: 6-8 mL/kg based on pt’s IBW

Rate: 12-16 bpm

FiO2: 100%

PEEP: 5.0

At the 5-minute mark:

  • Check an ABG
    • Titrate FiO2 off of PaO2 and pulse oximeter
    • Adjust minute ventilation off of PaCO2 and/or ETCO2

References

  1. Respiratory Review YouTube Channel https://www.youtube.com/channel/UCtaRF58UDVthvH36YYCttng
  2. Deranged Physiology.  Mechanical Ventilation. http://www.derangedphysiology.com/main/core-topics-intensive-care/mechanical-ventilation-0
  3. Weingart SD – “Spinning Dials – How to Dominate the Ventilator” – https://emcrit.org/wp-content/uploads/vent-handout.pdf
  4. Weingart SD. Managing Initial Mechanical Ventilation in the Emergency Department. Annals of emergency medicine. 2016; 68(5):614-617. [pubmed]
  5. Air Link Regional West – “Initial Adult Ventilator Settings” – https://www.rwhs.org/sites/default/files/airlink-factsheet-ventsettings.pdf
  6. Open Anesthesia. Modes of Mechanical Ventilation. https://www.openanesthesia.org/modes_of_mechanical_ventilation/
  7. Modern Medicine Network.  A Quick Guide to Vent Essentials. http://www.modernmedicine.com/modern-medicine/content/tags/copd/quick-guide-vent-essentials
  8. Tobin MJ. Extubation and the myth of “minimal ventilator settings”. American journal of respiratory and critical care medicine. 2012; 185(4):349-50. [pubmed]

Answer to Critical Care Question

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This patient is ready for extubation.  Everyone has their own magic numbers they want to see on the vent before they think about extubating a patient, but mine are:

  • Pressure support mode
    • every breath is initiated by the patient and only supported by the vent
  • Pressure support ≤ 8 cmH2O
    • This will be enough support to overcome the resistance in the circuit.
  • PEEP ≤ 7 cmH2O
    • Physiologic PEEP of the epiglottis is 5 cmH2O
  • FiO2 ≤ 40%
    • No more supplemental oxygen than what would be given via nasal cannula or open face mask
  • Stable ABG on these settings for at least 2 hours
  • A&Ox3 and following commands
    • Patients need to be able to participate in pulmonary toilet after the tube comes out

These are basic principles and there are many variables that go into deciding to extubate a patient.  LITFL does a great review here and goes through a very systematic approach.

Once this is all good, then you can perform a few bedside tests or measurements that can help predict success of extubation.

  1. Rapid Shallow Breathing Index (RSBI)
    • Respiratory Rate / Vt (L)
    • < 105 predicts successful extubation
  2. Negative Inspiratory Force (NIF)
    • Measurement of the maximal inspiratory pressure
    • This is a great measurement of a patient’s ability to generate an adequate tidal volume once extubated.
    • > -20 cmH2O predicts successful extubation

Prediction of Successful Extubation. The ICU Book.

Prediction of Successful Extubation. The ICU Book.

Great post from Intensive Blog on “The Art and Science of Extubation”

References

  1. http://lifeinthefastlane.com/ccc/spontaneous-breathing-trial/
  2. http://lifeinthefastlane.com/ccc/extubation-assessment/
  3. Fadaii, A.  Assessment of rapid shallow breathing index as predictor for weaning in a respiratory care unit.  Tanaffos.  2012;11(3):28-31.
  4. Yang KL, Tobin MJ. A prospective study of indexes predicting the outcome of trials of weaning from mechanical ventilation. N Engl J Med. 1991;324(21):1445–50. [PubMed]

#17 – Shock

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***LISTEN TO THE PODCAST HERE***

Definition and Cellular Physiology of Shock

The definition of shock is a clinical state of cellular and tissue hypoxia/perfusion due to:

  1. Reduced oxygen delivery
  2. Increased oxygen consumption
  3. Inadequate oxygen utilization

It basically comes down to the ratio between oxygen delivery (DO2) and oxygen extraction (VO2).

Extraction Ratio (ER)

Extraction Ratio (ER)

Deranged Physiology

Deranged Physiology

Components of Oxygen Delivery

At the cellular level, shock hypoxemia causes cell membrane dysfunction leading to intracellular edema and leakage, as well inability to regulate cellular pH.  This causes progressive acidemia, which in turn, have severe systemic effects on multiple organ systems.

Kherallah M.

Kherallah M.

Pathophysiology of Shock

BP = (HR x SV) x SVR

Factors effecting HR:

  • Autonomic regulation
  • Hormones
  • Fitness levels
  • Age
  • Medications

Factors effecting SV:

  • Preload
  • Contractility
  • Afterload

Factors effecting SVR:

  • Vessel length
  • Vessel diameter
  • Blood viscosity

Signs and Symptoms of Shock

As perfusion decreases and hypoxia starts, the body begins to compensate and the signs and symptoms of shock are generally a result of this compensation.

Picture1

Classifications and Causes of Shock

UpToDate

UpToDate

How to Diagnose Shock

Laboratory studies should be performed very early in the screening process for a patient with suspected shock as it will help you determine the degree of end organ perfusion.  These include:

  • Lactate (> 2 mmol/L)
  • Creatinine
  • LFTs
  • ABG or VBG

There has been a tremendous amount of advancement in the diagnosis and management of patients in acute shock.  For years, the pulmonary artery catheter was the gold standard for critically ill patients admitted to the ICU.  It allowed for serial “measurements” of almost all the hemodynamic parameters you needed (PACWP, CO, CI, SVR, PAP, SvO2), but it was not without serious complications.  It still has it’s place for certain disease management, but it is no longer indicated for diagnosing the different types of shock.  I bring this up only because these parameters can be helpful when learning the different shock states as you can focus on 3 main variables: PACWP, CO/CI, and SVR.

Picture1

Point-of-Care ultrasonography (POCUS) has really become the test of choice for an undifferentiated shock patient, as it provides fast, vital information of the different causes of shock and allows for rapid rule-out of life-threatening conditions.  There are several different types of POCUS algorithms used depending on the history and clinical context of the patient.

Screen Shot 2016-08-15 at 8.10.13 AM

Rapid Ultrasound in Shock (RUSH) is used for undifferentiated patients. Scott Weingart does a great podcast on this technique here and Sinae EM Ultrasound did a step-by-step review here.

Picture1

Another approach to undifferentiated shock is the Abdominal and Cardiac Evaluation with Sonography (ACES) protocol.  It is used primarily in the UK and a good review can be found here.

ACES Exam

ACES Exam

Focus Assessed Transthoracic Echo (FATE) is a more detailed look at the heart to identify specific cardiac abnormalities.

Picture1

If you have a trauma patient, you would use the Focused Assessment with Sonography for Trauma (FAST) exam to rapidly identify traumatic causes for hemorrhage and need for operative intervention.

FAST Exam

FAST Exam

Really good paper in Critical Care that reviews echocardiography in shock management

http://ccforum.biomedcentral.com/articles/10.1186/s13054-016-1401-7

Management of Shock

Once you diagnose a patient with a specific type of shock, the management is pretty straight forward.  If the patient is in hypovolemic, distributive, or obstructive shock, IV fluids should be used to improve perfusion and hemodynamics.  The amount depends on the conditions, but usually starting with 1-2L of crystalloids is a good bet and then you can re-evaluate and repeat your ultrasound to look at the effects.  If you have a trauma patient, then blood products should be started early on in the course until definitive control can be performed.

If adequate fluid resuscitation has not improved the hemodynamics or clinical picture, then pharmacologic agents are needed to improve perfusion.  These can be broken down into vasopressors (increase vasomotor tone) and inotropes (increase contractility).

Picture1

UpToDate

Picture1

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Screen Shot 2016-08-15 at 8.10.01 AM

References

  1. Vincent JL, De Backer D. Circulatory shock. NEJM. 369(18):1726-34. 2013. [pubmed]
  2. Barber AE, Shires GT. Cell damage after shock. New horizons (Baltimore, Md.). 4(2):161-7. 1996. [pubmed]
  3. Deranged Physiology. The Relationship of Venous Oxygenation and Cellular Metabolism. Accessed 08/16/16. http://www.derangedphysiology.com/main/core-topics-intensive-care/arterial-blood-gas-interpretation/Chapter%208.0.1/relationship-venous-oxygenation-and-cellular-metabolism
  4. Kherallah M. Approach and Hemodynamic Evaluation of Shocks.  Accessed 08/16/16. http://slideplayer.com/slide/3900131/
  5. Gaieski DF, Mikkelsen ME. Definition, classification, etiology, and pathophysiology of shcok in adults.  In: UpToDate, Parsons PE (ed), UpToDate, Waltham, MA.  Accesed 08/17/2016. http://www.uptodate.com/contents/definition-classification-etiology-and-pathophysiology-of-shock-in-adults?source=search_result&search=shock&selectedTitle=1%7E150#H18097167
  6. Shah MR, Hasselblad V, Stevenson LW. Impact of the pulmonary artery catheter in critically ill patients: meta-analysis of randomized clinical trials. JAMA. 294(13):1664-70. 2005. [pubmed]
  7. Perera P, Mailhot T, Riley D, Mandavia D. The RUSH exam: Rapid Ultrasound in Shock in the evaluation of the critically lll. Emergency medicine clinics of North America. 28(1):29-56, vii. 2010. [pubmed]
  8. Weingart SD, Duque D, Nelson B. EmCrit Blog.  Rapid Ultrasound for Shock and Hypotension – the RUSH Exam.  Accessed 08/17/16.  http://emcrit.org/rush-exam/
  9. Labovitz AJ, Noble VE, Bierig M. Focused cardiac ultrasound in the emergent setting: a consensus statement of the American Society of Echocardiography and American College of Emergency Physicians. Journal of the American Society of Echocardiography. 23(12):1225-30. 2010. [pubmed]
  10. Atkinson PR, McAuley DJ, Kendall RJ. Abdominal and Cardiac Evaluation with Sonography in Shock (ACES): an approach by emergency physicians for the use of ultrasound in patients with undifferentiated hypotension. Emergency medicine journal : EMJ. 26(2):87-91. 2009. [pubmed]
  11. AIUM practice guideline for the performance of the focused assessment with sonography for trauma (FAST) examination. Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine. 33(11):2047-56. 2014. [pubmed]
  12. Gaieski DF, Mikkelsen ME. Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock.  In: UpToDate, Parsons PE (ed), Waltham, MA.  Accessed on 08/17/16.  http://www.uptodate.com/contents/evaluation-of-and-initial-approach-to-the-adult-patient-with-undifferentiated-hypotension-and-shock?source=see_link#H87905481

Critical Care Question

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You are rounding on a ICU patient who has been on the ventilator for the past 4 days due to respiratory failure from community acquired pneumonia.  She has been gradually weaned down to the following settings:

 

Pressure Support Mode

PEEP – 6 cmH2O

Pressure Support – 8 cmH2O

Oxygen – 0.40

 

She is A&Ox3 and follows commands. Vital signs show BP – 122/72 mmHg, HR – 78, RR – 15, O2 – 100%, Temp – 99.8.

 

  1. What is your next step?
  2. What bedside measurements or tests can you do to help with your decision?