PACU, Pain Management, MH Flashcards
How much does minute ventilation increase for every 1 mmHg increase in PC02?
Normally, minute ventilation increases by approximately 2 L/min for every 1–mm Hg increase in arterial PCO2.
Train of four percentage of block

Most appropriate/available monitors for transport
Pulse oximeter
- Hypoventilation may not be reliably detected by monitoring with pulse oximetry
- Time to desaturation may be longer than time to PACU
- Adequate ventilation must be confirmed by watching for the appropriate rise and fall of the chest wall with inspiration
◦Listening for breath sounds (precordial stethoscope)
◦Feeling for exhaled breath with the palm of one’s hand over the patient’s nose and mouth (roll glove down)
What is the alveolar oxygen pressure of a normocapnic patient breathing room air?
A rise in PaCO2 from 40-80mmHg results in what PaO2?
100mmHg is normal
PaO2 = 50mmHg when patient goes from PaCO2 of 40-80mmHg
“This demonstrates that even a patient with normal lungs will become hypoxic if allowed to significantly hypoventilate while breathing room air.”
Name at least three treatments for alveolar hypoventillation
Supplemental oxygen
Raise the head of the bed 30 degrees
Normalizing the PaCO2
External stimulation of the patient to wakefulness
Reversal of opioid or benzodiazepine
Mechanical ventilation
What is diffusion hypoxia and effects of it?
When using nitrous oxide, the gas diffuses into the alveoli towards the end of the case and dilutes alveolar gas thus decreasing PAO2and PACO2 producing arterial hypoxia and can persist for 5-10 minutes after the case on the way to the PACU.
Using supplemental oxygen on the way to PACU should erradicate the effects and decrease chances of PONV

Why is there a need for upper airway support in the postoperative period?
Loss of pharyngeal muscle tone in a sedated or obtunded patient
Residual depressant effects of inhaled and injected anesthetics
Common symptoms/observations:
Reflex compensatory increase in respiratory effort
Negative inspiratory pressure
Retraction of the sternal notch
Exaggerated abdominal muscle activity
Collapse of the chest wall
Protrusion of the abdomen with inspiratory effort (rocking horse motion)
Common treatment for airway support in PACU?
Jaw thrust
CPAP
LMA/Oral or nasal airway
ETT tube
If your patient is having an upper airway obstruction, what are the steps to take?
- Jaw thrust with CPAP (5 to 15 cm H2O)
- If ineffective, insert oral, nasal or LMA
- Can reverse opioids or benzos (naloxone (0.3 to 0.5 μg/kg IV) or flumazenil)
- NMB agents can also be reversed, although they already should be. Might have residual paralysis
_Main goa_l: Determine what is causing the obstruction quickly and effectively and treat it
Considerations for a patient with sleep apnea?
Redundant pharyngeal tissue
Prone to airway obstruction
Should not be extubated until they are fully awake and following commands
Subsequent intubation may be difficult or impossible!
Very sensitive to narcotics
Treatment:
CPAP immediately in PACU, have patient bring thiers or get respiratory therapy to bring one down
What has more of an effect on decreased pharyngeal muscle tone, benzos or narcotics?
Benzos
What is a TOF ratio?
TOF = T4/T1
3 twitches = TOF is zero
-Succinylcholine (Phase I) does not exhibit any fade
Phase II block you could exhibit fade
-Nondepolarizing MR do exhibit fade
Subjectively, a sustained head lift for 5 seconds is considered the GOLD STANDARD
Treatment for laryngospasm?
Jaw thrust with CPAP (up to 40 cm H2O)
If fails, succinylcholine (0.1 to 1.0 mg/kg IV or 4 mg/kg IM)
Don’t attempt to forcibly pass a tracheal tube through a glottis that is closed because of laryngospasm
Common causes of pulmonary edema, treatment options?

Causes:
Intravascular fluid volume overload
Congestive heart failure
Sepsis
Transfusion-related pulmonary edema
Post-obstructive pulmonary edema
Treatment:
Oxygen
Diuresis
Positive-pressure ventilation of the patient’s lungs
As a result of edema or hematoma after a thyroid or carotid surgery, your patient has an airway obstruction. What is the best course of action?
- Call surgeon
- May need to release the clips or sutures on the wound and evacuating the hematoma
- Get difficult airway equipment
- Surgical backup for performance of an emergency tracheostomy
- If spontaneous ventilation, an awake technique is preferred
- Visualization of the cords by direct laryngoscopy may not be possible
Name five causes of PACU hypertension
Postoperative pain
Hypoventilation and associated hypercapnia
Emergence excitement (sedation usually takes care of this)
Advanced age
Cigarette smoking
Preexisting renal disease
History of essential hypertension (greatest risk)
Intracranial operations seem to be at increased risk for postoperative hypertension
Postoperative nausea and vomiting (PONV) increases risk
Causes of hypotension in the PACU
Hypovolemia (decreased preload)
Cardiogenic (intrinsic pump failure)
Distributive (decreased afterload)
In as high as 65% (range, 5% to 65%) after general, and 33% after epidural and spinal anesthesia patients exhibit hypothermia and an increase of O2 consumption up to 400%, what class of patients are more at risk?
Greatest risk: male gender and propofol for induction of anesthesia
Treatment: warming patient and meperidine (12.5 to 25 mg IV)
Name five risk factors of PONV
Female gender
History of motion sickness
Previous PONV
Nonsmoking
Postoperative opioids
Treatment:
Decadron (up front) and Zofran (just before emergence) - Decreases risk by 26%
Propofol decreases by 19%
Suction gastric contents whenever you can, “Dan’s informal study 1976”
SBAR
SBAR (situation, background, assessment, recommendation)
Used for “hand-off” criteria in some hospitals
What items are most commonly missed in a handoff?
Preoperative Cognitive Function
Lines/catheters
Antiemetic’s
What are the 6 key elements on a handoff checklist?
Patient identification using the patient’s name band
Patient allergy information
Antibiotic information
Intake and output
Estimated blood loss
Pain management

What is “closed loop” communication?
ASA and the Joint Commission describe two-way communication as an integral part of any transition of care
The receiver repeats the message the sender states, thus closing the loop
Malignant Hyperthermia (MH)
Volatile agents and succinylcholine can induce a drastic and uncontrolled increase in oxidative metabolism in skeletal muscle
Autosomal dominant disorder
At least 6 genetic loci of interest
The ryanodine receptor gene (RYR1)
Susceptibility is phenotypically and genetically related to central core disease (CCD)
Usually revealed upon or shortly after exposure to certain general anesthetic agents
Typical signs of MH
Hyper catabolic state
Very high temperature
Tachycardia
Tachypnea
Hypercarbia
Hypoxia
Muscle rigidity
Mixed acidosis
Rhabdomyolysis
First signs of MH
Hypoxia
Hypercarbia
Sinus tachycardia
Masseter spasm
Treatment for MH
Declare MH Emergency
Discontinue Triggering Agents
Abandon machine (Ambu)
100% Oxygen at High Flow
Give Dantrolene
36 vials of dantrolene sodium for injection must be available wherever MH trigger agents are used
2.5 mg/kg IV push (Titrate to effect)
Relapse rate in MH victims
19% relapse rate
New clinical sign of MH>120 minutes after initial presentation
Including cardiac arrests and death
What is DIC?
Disseminated Intravascular Coagulopathy
(DIC) is characterized by systemic activation of blood coagulation, which results in generation and deposition of fibrin, leading to microvascular thrombi in various organs and contributing to multiple organ dysfunction syndrome (MODS).
Hence, a patient with DIC can present with a simultaneously occurring thrombotic and bleeding problem
For every 30 minute increase in the interval between 1st MH sign and 1st Dantrolene dose, the complication likelihood increased ___ times
1.6
For every 2°C increase in maximal temperature, the complication likelihood increased ___ times
2.9
To avoid MH complications, you need to give Dantrolene early andyou need to control temperature