Monthly Archives: August 2019

Protected: Conscious Sedation Course (PDF FILE)

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Heparin Normogram (Stroke)

INITIAL DOSING:

a

 

 

TITRATION:

b

 

DARTMOUTH PROTOCOL FOR STROKE:

a.JPG

P-614_Heparin_Stroke_Protocol_11-9-09

 

METHODIST PROTOCOL: (click on link PDF file)

PT+Neuro+Heparin+Therapy+Protocol+Plan+23056+QM1018+PP+112018

 

MASS GEN PROTOCOL:

AntiThrombotic_Medications

 

REFERENCES:

https://www.dartmouth-hitchcock.org/dhmc-internet-upload/file_collection/P-614_Heparin_Stroke_Protocol_11-9-09.pdf

https://www.methodistmd.org/contentAsset/raw-data/059efe02-a88c-4993-a495-43af7b46e074/fileAsset

https://www.massgeneral.org/stopstroke/assets/protocols/AntiThrombotic_Medications.pdf

Oxygen Supplementation

METHODS OF OXYGEN DELIVERY

  1. Nasal Cannula
  • delivers O2 at rate of 2-6 L/min
  • concentration 24%-44%

1 L/min – 24%
2 L/min – 28%
4 L/min – 36%
6 L/min – 44%

2. oxygen mask

  • 3 basic styles:
    1. simple mask – small vents on each site, delivesr up to 50% O2, entrainment of room air makes actual FiO2 variable
    2. non-rebreathing mask – flutter valves on each, prevents etnrainment, reservoir bag holds supply of 100% O2, delivers maximum O2 conc of 90%
    3. venturi mask – delivers fixed amounts of supplemental O2 (24%-40%)

 

3. Bag-valve mask or “Ambu-Bag”

  • self-inflating resuscitation bag
  • manually delivers positive pressure ventilation
  • with flow rate of 10-15 L/min, FiO2 90% delivered
  • must fit snugly to prevent air leaks
  • may have one-way expiratory valves (prevent entry of room air) –> delivery of greater than 90% oxygen to ventilated and spontaneously breathing patients
  • without expiratory valves – delivers high concentration of oxygen during positive pressure ventilation but only 30% oxygen during spontaneous breaths
  • self-inflating bags have “pop-off” valves which must be closed tightly to achieve positive pressure ventilation

 

ETCO2 Capnography

Capnography – non-invasive, continuous measurement of inhaled and exhaled CO2

End-tidal CO2 (EtCO2) – maximum CO2 at end of exhalation.

 

NORMAL CAPNOGRAM

Normal Capnogram

During inspiration, CO2 is negligible and recorded at zero baseline.

 

  1. Phase 1 (A to B)
    1. exhalation indicated by the first
    2. represents gas exhaled from upper airways
  2. Phase 2 (B to C)
    1. rapid rise in CO2 concentration as anatomical dead space is replaced with alveolar gas
  3. Phase 3 (C to D )
    1. alveolar gas passes the CO2 sensor
    2. capnograph flattens out, “alveolar plateau”
    3. End-tidal CO2 = value taken at the end of exhalation
  4. Phase 4 (D to E)
    1. a rapid downward stroke
    2. fresh gas passing the sensor is essentially free of carbon dioxide

 

ABNORMAL CAPNOGRAPHS

  • Hyperventilation
  • high RR reduces amount of carbon dioxide in the exhaled air
  • waveform with regular shape but with a plateau below normal (CO2 deficiency)
  • check for hyperventilation, decreased pulmonary perfusion, hypothermia and decreased metabolism

 

2. Hypoventilation

  • regular shape with plateau above normal
  • indicates increased EtCO2 secondary to hypoventilation, respiratory depressant drugs, or increased metabolismHypoventilation

3. Bronchospasm

  • waveform develops a “shark fin” shapeBronchospasm

4, Shallow breathing

  • even though blood and alveolar CO2 are elevated, EtCO2 will appear to decrease
  • When the patient takes a deep breath, the carbon dioxide in the airway system is exhaled and the EtCO2 level is elevatedShallow breathing

STOP-BANG Screening Tool

Snoring Do you snore loudly (louder than talking or loud enough to be heard through closed doors)? Yes
No
Tiredness Do you often feel tired, fatigued, or sleepy during the daytime? Yes
No
Observed apnea Has anyone observed you stop breathing during your sleep? Yes
No
Pressure Do you have or are you being treated for high blood pressure? Yes
No
BMI BMI>35 kg/m2 Yes
No
Age >50 years Yes
No
Neck circumference Male 17 inches (43cm)
Female 16 inches  (41 cm)
Yes
No
Gender male Yes
No

0-2 “Yes” = low risk  
3-4 “Yes” = moderate risk
5-8 “Yes” = high risk

Continuum of Depth of Sedation: Definition of General Anesthesia and Levels of Sedation / Analgesia

Capture.JPG

 

 

Cortical Spreading Depolarizations

DEFINITION: profound disruptions of homeostasis that slowly propagate through gray matter, and induced suppression of cortical activity (termed “spreading depression”)

COSBID – Co-Operative Studies on Brain Injury Depolarizations), an international research consortium, first meeting 2003

⁃ focus on SDs in the setting of NCC, testing the idea that SDs contribute to injury

⁃ potential therapeutic improbable

⁃ Evolved into iCSD (International Conference on Spreading Depolarizations)

CHALLENGE QUESTIONS:

“Which SDs are deleterious to brain tissue?”

“Which factors render some SDs more injurious than others?”

Pathological changes in major tissue variables seen in SD: reduced CBF or intercellular Ca loading,

MAJOR Mechanisms SDs thought to cause cellular injury:

1. ATP depletion

2. Excitotoxicity

3. Spreading ischemia – SD-induced, local decrease in cbf seen in animals and patients, prolongs electrophysiologic depolarized state.

Energy Challenge presented by SD:

⁃ Membrane potential almost completely dissipated for tens of seconds to minutes, energy required to depolarize is extreme

⁃ Dramatic structural changes including cellular swelling, fragmentation of ER, disruption of dendritic spines, etc.

GLUCOSE

⁃ SD results in sharp decreases in local brain glucose levels

⁃ Moves Brian to a more metabolicallyi compromised state

⁃ Repetitive SDs progressively drive glucose to detrimental levels

*would be helpful to have methods to observe SDs over larger regions.

Potential Benefits of SD:

⁃ synaptic strengthening

⁃ Increase in neurotrophic factors

⁃ Neuroproctective preconditions

⁃ Neurogenesis

*limit expansion of ICH in the mouse

*hyperemic response to SD observed in healthy tissues could have positive effects

At present, there is little or no direct evidence that SD has meaningful beneficial effects, in contrast to strong evidence for injury. Any evidence for benefit would have to be dramatic to outweigh potential therapeutic gains of treating and preventing SDs.

Consider improving tissue perfusion rather than solely focusing on SD blockade.

Reference:

Shuttleworth, C., Andrew, R., Akbari, Y., Ayata, C., Balu, R., & Brennan, K. et al. (2019). Which Spreading Depolarizations Are Deleterious To Brain Tissue?. Neurocritical Care. doi: 10.1007/s12028-019-00776-7