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SRNA's responsibility for CQI
Post op rounds, makes notes of post op complications, follow up with the patient's CRNA, and report to department.
Importance of CQI in Anesthesia?
Errors effect more than 18% of all hospitalizations, trend patient safety and identify problems. Anesthesia is not therapeutic, so any M&M needs to be investigated. CQI is used as staff educational mechanism
process of continually evaluating anesthesia practice to identify systematic problems and implement strategies to prevent their occurance
events that cause or have the potential to cause patient injury if not noticed and corrected in a timely manner
Single, isolated events that may indicate a systemic problem. May or may not result in significant pt injury or death
Root Cause Analysis
Includes everyone involved in the are of the effected patient in reconstructing the events to identify system flaws that facilitated medical error.
Learning environment in which managers encourage reporting of errors by avoiding inappropriate punitive reactions to errors
Why focus on safety?
No error is acceptable, many are preventable, public knows about errors, Joint commission, and the financial implications of errors.
100,000 Lives Campaign
an initiative to engage US hospitals in a commitment to implement changes in care proven to improve patient care and prevent avoidable death. EBP, education, accountability, patient centered care
What is SEAT?
Stop, Engage, Audible, Timing. Keystone should be done after positioning but before draping.
When does the most human error occur?
During maintenance phase are the most preventable errors. We can prevent errors by reducing complexity and creating redundance.
Error reduction through CQI
Encourage documentation of all incidents, non-punitive environment, identify need for in-services or policy changes, protocols for "handling incidents" such as fire or equipment
What are other ways errors
Clinical event reviews, peer review process, making system wide changes when problems are found, M&M meetings
Serious Clinical event?
event that resulted in an adverse patient outcome or had the potential to lead to an adverse outcome. Can be related to anesthesia, surgery, or pre existing condition. If there is death, CNS event, MI, neurological deficit, fire...then a RCA must be done
Joint Comission Sentinel Events
Must report events are wrong side surgery, transfusion reactions, suicide, infant abduction, discharge error, rape
What are some methods to prevent events?
Site and sidedness, moment of silence, final verification, audits on blood verification
What are the clinical events that are serious?
Post op aspiration pneumonitis, periop respiratory arrest, peri op CNS complication, periop peripheral neurological deficit, cardiac arrest up to 24 hrs, periop acute MI, death, pulmonary edema, perioperative thermal injury
What are the most common causes of allergies?
Latex and muscle relaxants are most common cause of anaphylaxis and allergic reactions
What do you need prior to any induction?
Machine check, table top setup, suction on and at head of bed, patient prepared, patient assessment complete, consents completed.
What is the importance of checking the machine?
You want to make sure there are no leaks because if you need to give positive pressure for a laryngospasm and can't, you won't be able to treat it. occlude end of circuit with hand and occlude APL valve to make sure the bag blows up tight
Why do we preoxygenate?
denitrogenize the patient and buy CRNA time to safely complete induction. Normal FRC is 2500 ml. If you denitrogenate for 3 minutes you can meet the pt's metabolic demands for 8-10min.
What is the suggested time of preoxygenation?
Tidal breathing 100% O2 for 3-5 minutes. If the mask is lifted off face, then you need to start over!
What is Propofol?
GABA mimetic, less PONV but short lived effects, people wake up quickly with propofol, it reduces ICP and can be considered anticonvulsant, does not trigger MH, anti-itch
What is the dose of Propofol?
2mg/kg for induction. It is used for sedation and is a hypnotic. Maintenance does is 100-300mcg/kg/min, MAC is 25-75mcg/kg/min. Immediate onset and lasts 10minutes.
What are the disadvantages of Propofol?
1) Lowers BP because of negative inotropic effect,
2) Causes the largest decrease in SVR,
3) Burns on injection,
4) Expires in 6hrs,
5) Formulated from soybean, glycerol, and egg lecithin 6) Sulfite allergy to generic drug, Diprivan does not have preservsative.
7) Lactic acidosis risk
What are the respiratory effects of Propofol?
initial brief increases followed by a decrease in minute ventilation. The reduction in minute ventilation has to do with a reduction in tidal volume. Dose dependent ventilatory depression. Propofol also has a mild bronchodilation effect.
What is sodium pentothal?
Barbituate. Dose dependent decreases in CMRO2 and cerebral blood flow. Protection for circulatory arrest because you decrease metabolic rate of brain. Dose is 4mg/kg. Sedative properties are prolonged with accumulation. GABA mimetic
What are disadvantages of sodium penothal?
1) There is a decrease in venous capacitance vessels that results in venous pooling
2) Direct inotropic effect so there is low venous return and low CO, dose dependent reductions
3) Post op drowsiness with hangover effect
4) It will precipitate other drugs.
5) dose dependent resp depression and doesn't blunt reflexes unless at high doses
What is Etomidate?
GABA mimetic, short acting hypnotic. Dose is 0.2-0.4mg/kg for induction, lasts 4-10 minutes and has onset in 30-60 seconds.
What does Etomidate cause?
Produces EEG burst supression, decreases ICP, used in patients with decreased cardiac function because it doesn't drop blood pressures, sedation & hypnosis
What are advantages to Etomidate?
1) hemodynamic stability because it doesn't have drop in inotropoic effect
2) reduces ICP, cerebral blood flow, and oxygen use in the brain
What are the disadvantages of Etomidate?
1) produces myoclonus
2) pain on injection
3) adrenal suppression for 6hrs post op
4) Increases PONV
5) decreases seizure threshold
6) dose dependent respiratory effects- minute volume decreases, but RR increases. If given with opioids it is worse.
What is Ketamine?
It is usually as an adjunct to anesthesia. Dosed 1mg/kg. LSD derivative, produces dissociative state of anesthesia. Onset is relatively slow compared to other drugs 2-5 minutes.
What are the advantages Ketamine?
1) Circulatory stimulant causes increase in HR, BP, CO, and CVP
2) Positive inotrope
3) Increases in MVO2 so not good to use with heart patients
4) Potent bronchodliaotr will dilate airway for asthmatics
5) maintains airway and respiratory reflexes
6) good to use with older people
What are the disadvantages of Ketamine?
1) produces a dissociative state
2) Increased cerebral metabolic rate, increased cerebral blood flow, and increases ICP
3) Increases salivation and respirator secretions.
4) Associated with emergence delirium, nightmare, and hallucinations
5) don't use with heart patients, neuro patients and psych patients.
What is Versed?
Versed is dosed 2mg/IV. Onset is 60 seconds and it lasts 60 minutes, subject to first pass
What are the advantages to Versed?
1) It relieves anxiety, produces mild sedation, and also has amnestic properties.
2) Less respiratory depression except in the very young, very old, or debilitated
3) Decreases cerebral blood blow and CMRO2 so it decreases blood flow to the head and decreases O2 demand by the brain
When do you us an inhalation induction?
1) Slower onset than any IV agent
2) Dose dependent decrease in BP
3) Does causes airway irritability and Sevo is less irritating
What are anesthetic indications for cardiac patients?
want smooth induction, you want to keep them stable and not have any spikes or dips in blood pressure. You want to avoid significant change in vitals
What are anesthetic indications for neurosurgical patients?
stable hemodynamics and you don't want drugs that increases ICP or cerebral blood flow
What are the anesthetic indications for pediatric patients?
Volume distribution is different because kids have more body fluid. Pediatric patients take different doses of medications
What are anesthetic considerations for geriatric patients?
Longer circulation time so more time needed for drug's action. Slower induction process with the elderly. Want the pt's vital signs to not have any major spikes or dips.
What is the preparation for an LMA case?
Head straps in place, arm boards applied and arms secured prior to induction, all monitors on, precordial on suprasternal notch, induction drugs ready, oral airway at head of bed, preoxygenate for 3-5min at 5L/min, APL open until pt is no longer breathing, tell pt they will feel drowsy, ensure good mask fit and make sure there is no leaks. SUCTION AT HEAD OF BED! check lash reflex.
What are the steps of induction?
1) Run IV wide open
2) give calculated dose of induction agent at steady rate
3) Recheck IV, make sure drug has infused
4) watch patient and observe for long deep breaths
5) assess LOC
6) Once pt is asleep, tape eyes, and gently assist ventilation. Insert oral airway if you cannot ventilate
7) If using LMA, insert once asleep
8) turn on agent of choice and overpressure them to get them deep.
What is the positive pressure limit that you don't want to exceed?
20cm H2O. When assisting ventilation make sure the patient initiates the breath and then finish it.
Why do you need the patient deep at incision?
Because they can spasm on incision. You want vital signs in range, low RR, an okay blood pressure.
What are the essentials for an induction for general anesthesia with planned intubation?
Peripheral nerve stimulator, laryngoscope, ETT, OPA of correct size, and SUCTION!!
What are the first steps of induction in regards to prepration?
1) make sure machine is checked
2) Adjust height of OR table
3) preoxygenate 3-5 minutes
4) administer narcotic (this blunts the airway reflexes- 2cc of fentanyl usually)
5) if using propofol give Lidocaine 20-30mg to numb vein.
Once pt is preoxygenated, what are the next steps with induction?
1) give dose of induction agent
2) assess LOC, check lash reflex, and tape eyes
3) Assess airway patency, assist and control ventilation. Insert an OPA if necessary
4) If airway is manageable say airway is good and give muscle relaxant
5) Turn on agent of choice while waiting for muscle relaxant onset.
What are the onsets of the different muscle relaxants?
Rock takes 3-5 mintues and succ takes 30-60 seconds. Floppy head and slacked jaw are indications that the pt is ready for intubation.
Once the muscle relaxant is given, what do you do next?
1) place intubating equiptment near patient's head, ETT on pts chest and scope on LEFT side of head
2) Check onset of muscle relaxant with PNS
3) Preform laryngoscopy and insert ETT
4) Remove carefully
5) Inflate cuff
6) Check intubation
7) turn on agent, put pt on ventilator, and adjust flows
8) secure ETT
How do you check intubation?
visualization of tube passing through cords, chest expansion, ETCO2, breath sounds. Listen at 2ICS on Left side.
What is the most reliable site for nerve stimulation?
Ulnar, with positive red lead closest to heart
When do you remove the stylet?
Right before moving the tube through the cords. Make sure the stylet is above the eye of the tube
What are special indications for a RSI?
-When patient has a full stomach
-Known hiatal hernia with reflux
What is required during an RSI?
SUCTION at the head of bed, an assistant to hold cricoid pressure, and strict adherence to policy.
What happens if you have a NGT?
If you keep it in, make sure it is on suction the whole time. There is no evidence supporting leaving it in vs taking it out.
What are the steps for an RSI?
Suction at HOB and always on, preoxygenate, pretreat with subclinical dose of NDMR to avoid facculiations.
2) Give full dose of induction agent
3) Have assistant hold pressure as soon as drugs are injected
4) follow with FULL dose of succ
5) Do not ventilate
6) wait for succ to work then intubate
How do you apply cricoid pressure?
exert in an anteriorposterior direction occluding the esophagus. 5Kg of pressure.
When do you release cricoid presure?
once the ETT placement is confirmed with ETCO2 and breath sounds
What is maintenance?
Period from the end of induction to anesthetic emergence. Plans are adopted constantly and decisions are made continuously
What are the goals of intraop maintenance?
Provide protective functions of life, render the patient insensible to pain, provide optimal exposure and surgical conditions for surgeon
What are important factors of maintenance?
monitoring, oxygenation, ventilation, positioning, temperature, charting, fluids, blood loss, assuring depth, assuring amnesia, assuring analgesia, muscle relaxation, preparing for emergence, preparing for the next case
What factors determine types of monitors?
type of surgery, patient condition, length of surgery, access to extremities
What senses are used during intraop?
observation for the rise and fall of chest, nail beds,
lips are blue,
look at surgical field and also at canister, mucous membrane,
skeletal muscle tone
What are we listening for?
alarms, heart rate, SPO2, suction, listen for cues for the end of surgery
Non invasive monitors during intraop
pulse ox, ekg, BP, temp, BIS, salter cannula, PNS, precordial stethoscope, evoked potentials.
What are considerations for the evoked potentials?
not as much muscle relaxant because it could affect motor and not as much gas because it could affect sensory.
EKG during intraop
Lead II monitors arrythmias
Lead V monitos ischemia
Get strip before induction
Do a 5 lead on pts with heart history
You want set for every 3 minutes, standard is every 5 minutes, for regional you want every 1 minute. Put a regular sized cuff on forearm if they are obsese. Cuff width should equal 40% of arm circumference
What are considerations for temp?
Forehead is most widely used but least accurate, nasal temp will put pt at risk for nose bleeds
Why is controlling body temp such a big deal?
-heat loss and gain center is in the hypothalamus anterior and posterior respectively
-Redistribution of body heat and anesthetic interferes with hypothalamus 1-5 degrees during first hr
-After the first hr, the temp decreases at slower rate.
Do anesthetics inhibit central thermoregulation?
Yes, because they interfere with hypothalamic functions.
What happens when a patient is cold?
Left shift when pt is hypothermic!!
Platelet dysfunction when cold
Stress response and catabolism
Impaired renal function
Decreased drug metabolites
Poor wound healing
Increased incidence of infection
Why do patients with spinal anesthesia lose heat?
vasodilation and altered perception of temp in the blocked dermatones
What is the purpose of BIS?
to reduce patient awareness, there are a higher incidence of recall with hearts. titrate drugs, so less drug used and a faster wake up time. Sedation is 65-85 and general anesthesia is 40-65
Why use salter?
when pt is deep with anesthesia it can be a helpful monitor. You can move it to your mouth if pt is a mouth breather.
Why use a peripheral nerve stimulator?
All pts using long acting NMRB. When you have no twitch is when it is the best time to intubate. All patients getting NMRB should be tested with a tetnus and TOF
Where are nerve stimulator placed?
Adductor pollicis for ulnar and the orbicularis oculi for facial nerve.
What should be considered when you see twitches when using the orbicularis oculi?
The orbicularis oculi recovers from neuromuscular blockade before the adductor pollicis.
What could also happen with the orbicularis oculi?
Make sure you have the electrodes over the facial nerve because it can cause the muscles to twitch
What is special about a precordial stethoscope?
earliest detection of respiratory issue because you could hear a circuit disconnections. Make sure you have on left side of patient.
What can you see on the visual screen on the anesthesia machine?
TV, CO2, inspired and expired gases, FiO2, capnography, EKG, pulse Ox, Aline, CVP, Swan
This is the only reliable way of monitoring urinary output. Should maintain 0.5ml/kg/hr. Longer than 2hr cases and expected fluid shifts.
Table turning considerations
Think about tube connections and taping of the tube. Make sure the monitors will end up on the side the CRNA is on. CHECK BREATH SOUNDS everytime the table is turned.
What is the only continuous record of the intraop course?
Charting. It is not uniform from provider to provider but try as best you can to put down most vital information
What is the basic core information that must be documented?
patient identification, provider information, equiptment checks, minimal monitors, anesthesia techniques, medications, intake and output, procedural data, parameters measured
What fluid is required intro-operatively to replace?
basal requirements, preop deficits, third space loss, blood loss, transcellular fluid loss
How can we measure unconsciousness?
response to stimuli. If no stimulus is applied, nonresponsiveness can be induced by deep sleep, boring lecture, 2% iso.
What is the distinguishing factor for unconsciousness?
differential in stimulus that penetrates nonresponsiveness and rouses brain to conscious perception.
What is the order of loss of response?
2) Formation of implicit and explicit memories
3) Purposeful movement
4) Ventilation (loss of RR and apnea)
5) sudomotor (tearing and sweating)
What is associated with a BIS of less than 60?
the probability of awareness and responsiveness to surgery are very low. This is associated with general anesthesia
How do you assure amnesia?
1) premedicate patient with amnestic agent, particularly if clinical situation suggests light anesthesia might be required.
2) Measure and document ET concentration of volatile anesthetic minimally every 15 minutes.
3) ask surgeon if there has been change on their field if you see CO2 goes up.
Assuring analgesia with regional cases
1) patients typically awake enough at incision and are able to communicate pain
2) if relief is not adequate: block may need more time to work or the patient may need to be converted to deep sedation or general anesthetic
What are considerations for sedation cases?
1) keep track of local anesthetics
2) B3, Li5, R4
3) ask surgeon to give more local
What are considerations before the end of case?
have all drugs ready for emergence, have oral airway in before the patient wakes up so they don't bite tube, if they have a full stomach then do an awake extubation RSI,
for plastics do a deep extubation
When giving medication...
open the IV and then return to the maintenance rate. DO NOT INFUSE ENTIRE BAG!!
What is included in the break report?
Past medical history, anesthetic plan, surgical plan, important airway information, fluid/blood loss, complications, allergies, and ask if they need any more information
What are some intraop complications?
1) accidents during maintenance phase due to a lack of vigilance
2) human error causes most anesthesia related deaths
3) most adverse complications are respiratory
What are the common intra-op complications?
PVC's after surgical stimulation, patient moving, bronchospasm, tachycardia, bradycardia, hypotension, hypertension, bleeding, allergy, power outage.
Have a plan for every complication
1) use ambu bag if electricity goes out
2) have a plan for every complication possible
3) take care of the immediate problem
4) always label syringes
What are factors complications associated with human errors?
1) inadequate preparation
2) inadequate machine checkout
3) preop eval
4) haste in preparation
5) Inadequate experience and training
6) Environmental limitations
7) Poor communication with surgeon
8) physical and emotional factors fatigue and personal problems
Complications in the OR
1) unrecognized breathing circuit disconnection
2) mistaken drug administration
3) airway mismanagement
4) anesthesia machine misuse
5) fluid mismanagement
6) IV line disconnection
Low Flow system O2
if you are okay with pt having entrained air, it supplies less than the total inspired volume of O2 needed by the patient because it supplements it with room air
What does the FiO2 depend on?
1) reservoir for O2
2) the oxygen flow rate
3) the patient's ventilation pattern
4) O2 device must fit properly
A low flow system...
depends on effort and rate of the patient. Greater than normal tidal volume and/or more rapid respiratory rate reduces the inspired concentrations of fiO2.
You would use a low flow system if...
minute ventilation was 8-10ml/min, RR less than 20, 800cc or less, or if the patient is not in resp distress. For patients who are not profoundly
not as comfortable, does not have valve, 35-60% O2 with 5-8L/min flow
-Rate should always be at least 5 L/min to avoid re-breathing
-Not as comfortable as NC and may not be as tolerated
-Valveless system with a reservoir bag 50-60% at 10L/min
-Valves are off and air is entrained
Non rebreathing mask
-Includes unidirectional valve and reservoir bag
-Inhaled FiO2 is close to 100% when 10L/min is utilized
-Difficult to get a good enough mask fit to assure no room air.
-Increased flows can cause GI bloating and skin breakdown
-Passive flow of O2 could be a risk and start a fire
-flow rate 4-8L/min 30-55%
-Utilized in the eye room, post nasal plastic surgery
T piece/ Trach mask
1) Similar to regular masks but bypassing of the naso & oropharynx DOES NOT allow for air entrainment
2) This can cause a decrease in FiO2 unless a sufficient reservoir is utilized
Flow of O2 will override passive flow, these systems have a high flow rate and reservoir capacity adequate to provide the total inspired volume to the patient. Can give an exact FiO2 which can range from 24-50%. Venturi mask compare to a perfume bottle, force is high.
Why is giving high O2 to COPD patients a problem?
They breathe by hypoxic drive and should receive O2 at precise FiO2. PaO2 is 60-70 generally and SaO2 is 96%. ABG sat on blood vs sat on probe tend to make sure not getting too high on O2.
Giving O2 over period of time. The air we breathe has nitorgen which keeps our alveoli open. When you get rid of N, it causes alveoli to shink. This can happen quickly
Takes more time for this to affect patient. 10-20hr can cause toxicity if you are giving 100%. 50-60% can cause O2 toxicity at 20-40hrs. Free radicals and cellular breakdown. O2 mediated breakdown of alveolar capillary membrane which can lead to ARDS
ROP retinaopathy of prematurity
O2 promotes disorganized vascular proliferation and fibrosis. This can happen when O2 is given without justification. Retinal detachment and partial blindness. PaO2 50-80, don't strive for 100
common intraop and post op, secondary to atelectasis. Usually have hypoxemia, hypercarbia, and low pH
streamlines molecular flow in which there is little friction between the gas molecules themselves. Organized flow
gas molecules molecules in a random, chaotic, rapid pattern, interfering with each other and creating more resistance
set volume delivered, insp pressure set 10-15 higher, will alarm if the set volume cannot be given before inspiratory is reached. If it tries to give it but cannot, then it will alarm.
RR, TV, and I:E is set, used in brain dead patients and commonly used in anesthestized patients who are paralyzed. used for patients who cannot take their own breath
What if you see the bellows quivering on controlled ventilation?
It means the patient is trying to take their own breath and that they may need more muscle relaxant
TV, RR, I:E. Pt will initiate breath, but the machine will give the breath at the programmed settings
The pt can initiate their own breaths and the ventilator will not help them, but when the ventilator is set to take a breath, the pt will get that mandatory setting thus leading to stacking of breath.
Detects when they are taking a breath and then adjusts the breath to the settings on the machine...lets the patient initiate their own volume and breath...but does not stack breaths and times the next breath with the ventilator
Pressure is set and volume can vary. No set tidal volume. The inspiratory phase is fast so it can open up the alveoli to allow O2 exchange to take place. This setting limits shearing and prevents atelectasis
Variations of pressure control
Smaller TV and higher RR, works to overcome the critical opening pressure in the alveoli
Pressure control volume guarantee
protects against trauma, delivers consistent TV at the lowest pressure possible. The machine delivers a pressure control breath auto set to whatever pressure is necessary to deliver the tidal volume.
SIMV pressure support
Delivers mandatory tidal volume and respiration rate, however synchronizes with patient effort when detected, no stacking of breaths and pts own breath is supported
for spontaneously breathing patients, doesn't have TV or rate but gives patient support with each breath. Prevents CRNA from having to bag.
What are downfalls of PEEP?
1) decreased venous return
2) Barotrauma with PEEP greater than 10, mean airway pressure greater than 30, and PIP greater than 50
3) Increased intrathoracic pressure
4) Alterations in kidney function b/c venous return is impaired
Inspiratory pressure for spontaneously breathing patients. Indications are the same as those for PEEP, commonly used for those with sleep apnea and neonates.
What causes hypercapnia
Conditions that affect rate of breathing, high deadspace, low minute volume, failure of the resp center
How much higher is the PaCO2 than ETCO2?
3-5. COPD will have a more drastic difference, accentuated by the admixture of deadspace air.
Difference is due to the fact that some units are underventilated for the amount of blood perfusing them (some units have not enough air and they have a lot of blood)
due to the V/Q imbalance or diffusion impairment not a true oxygen gradient between alveolus and pumlonary capillary bed.
What is the O2 pressure?
PaO2 x 0.003. This is the free oxygen molecules those not bound to hemoglobin, they are free in plasma
What is the O2 saturation?
Hbg x 1.34 x SaO2. On the hemoglobin molecules, there are Fe+++, prophyrin binding site. When all these sites are occupied by oxygen molecules, it is said to be saturated.
What is hypoxia?
Impaired o2 delivery to the tissues, include cardiac output and tissue uptake. The problem getting O2 to the tissues
The oxygen content is the determinant of patient severity
If the O2 content is low, they are considered hypoxemic. Physical assessment of this is not always reliable.
in amounts greater than 10%, a person will start to experience symptoms and the curve will shift to the left
What is the significance of HCO3?
HCO3 has a lower pKa but is more available. Bicarb is in RBC and is also in the plasma. Not a higher capacity buffer, but more available.
What happens in regards to CO2, HCO3, and Cl during buffering?
CO2 enters cell, forms carbonic acid, the H binds with the hbg and the HCO3 goes outside of cell, the Cl comes back in to maintain neutrality
What happens in the lungs?
Cl comes out of the cell, HCO3 goes in, it makes carbonic acid with the H from the cell, then CO2 leaves to go into lungs.
Did the change in HCO3 result from a change in CO2 tension?
Determin this before the change in HCO3 caused by a metabolic state
What are causes of respiratory acidosis?
neuromuscular dysfunction, COPD, pickwickian disorder, CNS depression
What does body do when there is acidosis?
systemic depression: decreased myocardial contracitlity, decreased CO, blood vessels dilate thus less responsive to vasoactive drugs, ventricular irritability attenuates the effects of bronchodilating drugs.
With chronic respiratory acidosis, how long does it take the kidneys to compensate?
12hrs, peaks 3-5 days. Renal correction is slower. Each 10mmHG increase in PaCO2 means 4mEq increase in HCO3
How do you treat respiratory acidosis?
Increase mV, treat with bicarb if pH is less thatn 7.1 or HCO3 is less than 15, with chronic respiratory acidosis the goal is to return the patient to baseline
What happens in the body when there is resp alkalosis?
Hyperventilation lowers PacO2 resulting in lower HCO3, nonbicarb buggers respond by releasing H+, mild hypokalemia occurs, acute changes in PaCO2 will make cerebral blood flow decrease by half.
What causes respiratory alkalosis?
physiologic response to hypoxemia, emotional disturbance, CNS disorders, excessive mechanical ventilation
What are hazards to respiratory alkalosis?
decreased cerebral blood flow, hypokalemia, arrhythmias, constriction of bronchiolar smooth muscle, shifts the O2 curve to the left
What causes metabolic alkalosis?
aggressive diuretics or steroid therapy, cushing disease, NG suctioning, N/V/D, overaggressive bicarb administration, metabolism of citrate to HCO3, ingestion of antacids.
What is the primary stimulus for metabolic alkalosis?
decreased arterial volume. This stimulates the release of renin and aldosterone, which act on renal tubes to increase NaCl resorbtion and promotes H+ ion secreation.
the extent of ventilatory response should be proportional to the severity of metabolic acidosis
Lactic acidosis produces a greater degree of hyperventialtion and hypocarbia than ketoacidosis because lactic acidosis is produced by the brain. IF pt has lactic acidodic state, then the pt will be more prone for hyperventilation
What causes metabolic acidosis?
hypoperfusion, conditions that will affect where bicarb has gone, like increase anion gap means that higher lactate because bicarb is being used up to buffer the anion because it is being used as a buffer
If there is no anion gap?
you are losing bicarb to something that is going on....it is not being used to buffer because it is leaving the body itself
What causes an increased ion gap?
lactic acidosis, ketoacidosis, renal failure, toxin ingestion, ethylene glycol, methanol, salicylate
Normal anion gap
renal tubular acidosis, early renal failure, diarrhea,, drainage of pancreatic juice. normal is 12 +/- 4
Why can patients be more at risk for sedation and depression when acidodic?
because the opioids become nonionized and can penetrate the brain more.
Why is the circulatory depressant effect of anesthetic gases and IV meds be exaggerated in acidosis?
because they are depressants and make us have unopposed decreases in sympathetic tone by agents.
What can alkalosis cause?
respiratory alkaloids may prolong the duration of opioid induced respiratory depression
What is a negative effect of alkalosis?
when accompanied with hypokalemia, alkalosis can precipitate severe atrial and ventricular arrhythmia and it may also potentate NDMB
Citrate, phosphate, dextrose, adenine
Citrate- anticoagulant binds to calcium
Dextrose- energy source for RBCs
Adenine- precursor to ATP synthesis
rescue drug when standard therapy has failed. though to enhance thrombin generation on already activated platelets
What is special about hextend?
it can help cougalation up to 20ml/kg...then you can't clot effectively
Complex carb with different molecular weight and molar substitution than hespan. Max dose 50ml/kg/day. Can be given to cardiac patients. Give with large abdominal cases with fluid shifts because you can give more of it.
What is hapten?
Substance capable of combining with immunoglobuins not producing a reaction, give with dextran
When would you use dextran 40?
use during carotid case to make viscosity of blood lower....reduces cell aggregation.
What are storage lesions?
cellular debris, microaggregates, decreased in pH, increase in plasma potassium, decrease in plasma Ca, decrease in factors V and VIII, decrease in 2,3, DPG, increase in lactate and CO2, increased hemoglobin
Why is there metabolic acidosis r/t storage lesions?
perseratives, continued metabolic function of RBC's, mostly related to PCO2 levels of 150-220, but does not always lead to metabolic acidosis
How does hyperkalemia develop?
quickly administered blood, storage temps 1-6 deg will slow down the pump. This is very rare
What happens when there is a decreased in 2,3 DPG?
there is an increased of affinity of hemoglobin and there is less O2 available for tissues.
What are the signs and symptoms of citrate intoxication?
hypotension, narrow pulse pressure, increased intraventricular EDP, increased CVP
rate of blood transfusion is over 50ml/min, if the patient has hypothermia or liver disease, neonates
Why do patients get hypothermia?
because blood is stored at low temp and it can cause cardiac irritability and post op shivering bc it can increase O2 consumption
Complications of Blood Therapy?
impairs coagulation, impairs metabolism of citrate, lactate, and drugs, increases, increases blood viscosity, impairs RBC deformability, increases intracellular K, cause leftward shift of O@ curve.
there are increased protein C levels which is a cascade of coagulation abnormalities, when you give large amounts of blood
What are the most important causes of coagulopathy?
1) volume of blood given dilutional coagulopathy because that part of blood doesn't have coag factors
2) duration of hypotension and hypoperfusion.
Dilution of coagulation factors due to transfusion of large amounts of stored blood....
1) dilutional thrombocytopenia
2) low factors of 5 and 7
3) DIC like syndrome
S/Sx of dilutional coagulopathy
1) oozing into surgical field
3) gum bleeding
4) petechial bleeding
What is dilutional thrombocytopenia?
1) cause of hemorrhagic diathesis in patient with multiple blood transfusions
2) Few viable platelets in blood stored > 24 hrs
3) Plt count less than 50,000-75,000
What happens when there are low factor 5 and 8 levels?
1) these decrease in stored blood
2) unlikely to be the primary cause of bleeding during massive transfusions
3) may intensify bleeding from other causes
DIC like syndrome?
Deranged clotting system leading to disseminated fibrin deposition, unclottable blood, severely altered microcirculation leading to ischemic necrosis esp kidney.
What product has the highest incidence of viral infection B or C?
CRYO. These viruses are associated with viral hepatitis
What is TRI?
Transfusion related immuonodulation suppresses cell-mediated immunity. More plasma in product the higher risk and leukoreduction decreases TRI
#1 cause of transfusion related fatalities, within 6hrs, highest risk is FFP, characterized by dyspnea and hypoxemia non cardiogenic
How do you monitor for TRALI?
pulmonary edema in absence of L atrial HTN or circulatory overload and also the pulmonary fluid has high protein.
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