2025 Airway Management Exam 3 Flashcards
Lectures 7-10: Airway Complications, Vents, BloodGas
What is a Claim
A financial demand made to an insurance company by a person alleging injury sustained from medical care
What is a Closed Claim
It is a claim that has been resolved
6% of all claims concerned airway injury
Difficult intubation 39%
87% of injuries were temporary
8% resulted in death
21% inappropriate standard of care
Closed Claims Summary
For your information – use it to your benefit
Many claims involve the most basic airway problems
Many difficult airways are not predicted
Anesthesia – because of the protocols, guidelines, and training in place, it has become one of the safest specialties of medical practice
Omission, Commission, & Communication
Errors of omission
Failure to:
Recognize the magnitude of a problem
Make appropriate observations
Act in a timely manner
Errors of commission
Include:
Trauma to lips, nose, or laryngotracheal mucosa
Forcing sharp instuments into areas in which they do not belong
Introducing air or secretions into regions of the body in which further complications will ensue
Most frequent cause of fatal errors d/t ignoring, inadequate experience & skills, and not calling for help
Complications Arising During Intubation
Eyes
Lips
Teeth
Larynx
Pharynx
Esophagus
Trachea
Bronchi
Complications Arising During Intubation: Eyes
Complications Arising During Intubation: Lip Trauma
Taping Lip
Biting on OPA
Complications Arising During Intubation: Pharyngeal Mucosal Damage
Pharyngeal Perforation
Death occurred in 81% and was caused by mediastinitis
Lacerations and contusions
Localized infection
Sore throat
- Associated with difficult intubation
Complications Arising During Intubation: Tooth Damage
Complications Arising During Intubation: Laryngeal Injuries
Complications Arising During Intubation: Esophageal Trauma
Complications Arising During Intubation: Tracheal/Bronchial Injuries
Let Syringe Rebound when filling bulb on Intubation
Can every couple of hours deflate all the way, then move the ETT every so slightly
Complications Arising During Intubation: Lung
Complications Arising During Intubation: Hypoxemia
Complications Arising During Intubation: Acute Hypoxic Encephalopathy
Complications Arising During Intubation: Failure of O2 at the Source
Complications Arising During Intubation: Failure of O2 at the Delivery Site
Big one is Ventilator Disconnect
Complication = Start at Patient and working back to Machine
Complications Arising During Intubation: Improper Procedure Leading to Hypoxemia
Complications Arising During Intubation: Inability to Intubate or Ventilate Due To…
Obesity
Age
Beard
Macroglossia
Mallampati grade III of IV
History of snoring
Short thyromental distance
Any reason at all
Complications Arising During Intubation: Vomiting and Aspiration
Cricoid Pressure - some believe it helps, some don’t
0.4 ml/kg for Peds
Complications Arising During Intubation: Vomiting and Aspiration (Pathophysiological Processes)
Complications Arising During Intubation: Preventative Measures After Aspiration and After Intubation
Change FiO2 to 100% immediately if not already at
Complications Arising Immediately after Intubation
High Fentanyl dosage (200-250 mcg) to really blunt the airway reaction to intubation if they have a Hx of hypertension, tachy, arrhythemia???
Hypoxemia - bag till you get them up over 90, then can go to ventilator
Complications Arising Immediately after Intubation: Accidental Esophageal Intubation
Accidental esophageal Intubation
** The most reliable method for tracheal intubation and continuously monitoring tracheal intubation is capnometry**
Wave Form
Numbers
Chest Rise
Misting in Tube
… all this together is what confirms proper ETT placement
DELAYED DIAGNOSIS
Preoxygenated patient with good respiratory function
… could of exceeded 20mmHg, which opens esophageal lower sphincter, so you were putting O2 into the stomach - which is what is showing on ETO2 for a while
An accidental extubation with movement of patient… be OCD about taping the tube
An endotracheal tube may slide up and down in the trachea
Accidentally extubated attempting to insert a nasogastric tube… if the airway is really dry
Complications Arising Immediately after Intubation: Ingestion of Laryngoscope Lightbulb
Complications Arising Immediately after Intubation: Accidental Endobronchial Intubation
Identified by:
Asymmetrical movement of chest wall
Increase in Peak Inspiratory Pressures (PIP)
CO2 waveform (decreased due to only one getting the reading)
Auscultation of chest
Called “Main stemming”
Complications Arising Immediately after Intubation: Bronchospasm
Complications Arising Immediately after Intubation: Difficulty with Ventilation
First deliver 100% O2 until problem solved
Maybe caused from:
Endobronchial tube placement (to include Main Stem)
Bronchospasm
Pneumothorax
Ask yourself these questions:
Is the problem related to disease process in the patient?
Is it related to tube placement?
Is it caused by the oxygen delivery system?
Is it due to obstruction of the tube?
Kinked or even Mucus in the tube
Complications Arising Immediately after Intubation: Obstruction of the Tube
Complications Arising Immediately after Intubation: Laryngeal Intubation
Complications Arising Immediately after Intubation: Accidental Extubation
Failure to secure tube properly
Want to tape as close to the corner of the mouth as possible… if tube has to be in middle of the mouth, tape as close to lips as possible
Tension on the tube
… do you need to hook up an extension?
Transportation/repositioning of patient
Complications Arising Immediately after Intubation: Tension Pneumothorax
Immediate Treatment is Necessary
Cardinal signs:
Marked cyanosis
Deteriorating vital signs
Diminished breath sounds
Decreased pulmonary compliance
How do you treat?
Insert a large bore needle into the affected side of the chest beneath the second rib or have a surgeon place a chest tube
Complications Arising Immediately after Intubation: Rupture of Trachea or Bronchus
Mainly associated with endobronchial tube usage
Predisposing factors:
Trauma
Age
Preexisting disease
Tissue Fragility
Anatomic difficulties
Blind, or rushed intubation
Inadequate positioning
Poor visualization
Inexperience
Complications Arising Immediately after Intubation: Hypertension, Tachycardia, Arrhythmias
Caused by laryngoscopy and intubation
(this is the high Fentanyl dosage idea…)
Increase in BP
Arrhythmias
Increase BP and HR due to vasomotor stimulation (adult)
Bradycardia during Intubation – vagally mediated
(Children)
Complications Arising Immediately after Intubation: Elevated ICP
Endotracheal intubation provokes increases in ICP
Dangerous in patients with:
Intracranial aneurysm (big time problem, attending should be there)
Intracranial bleeding
Elevated ICP
Complications Arising Immediately after Extubation: Laryngospasm
If patient is trying to take a deep breath with a closed glottis, they could be giving themselves negative pressure injury
Incidence
8.7 per 1,000 patients (all age groups)
17.4 per 1,000 (ages 0-9)
Highest range between 1 and 3 months, and children with upper respiratory tract infections – 95.8/1,000
5/1000 patients who develop laryngospasm develop cardiac arrest
Factors that influence its development:
Inadequate anesthesia
Premature extubation**
Semicomatose state
Aspiration
Presence of a nasogastric tube
Clinical Features:
Sudden onset
Absence of air movement in or out
(SaO2) saturation falls rapidly
Hypoxemia
Cardiac arrest
Treatment:
Positive pressure ventilation (may be ineffective)
Firm jaw thrust… Larsons Maneuver
Propofol (50-100 mg depending on patient, higher if big drinker and big marijuana smoker)
Small dose of neuromuscular blocking drugs:
Succinylcholine (10-20 mg)
Prevention
Timely extubation – deep
Patient bucking – allow them to wake up or enter Stage I before extubation
Lidocaine 2 mg/kg can be given for coughing 2-3 minutes prior to extubation
… better options
Complications Arising Immediately after Extubation: Airway Obstruction
Can occur immediately after a premature extubation
Patients may not have recovered from:
Anesthesia
Narcotic and sedative drugs
Neuromuscular blocking agents
Complications Arising Immediately after Extubation: Sore Throat
Most common complaint of patients
Abrasions to the oropharynx and nasopharynx
Doubled in those that are intubated vs. those who weren’t
Greater in patients with nasogastric tube
Greater in female than male
Proportional to the internal diameter of the endotracheal tube
In areas that are Dry (like Colorado), LMAs can cause a sore throat
Complications Arising Immediately after Extubation: Vocal Cord Damage
Postintubation Croup
Occurs with edema of the vocal cords – seen in children
Treatment: humidified O2, racemic epinephrine, dexamethasone (8-10 mg (increased dose))
Neural Injury: Recurrent Laryngeal Nerve Injury (RLN)
Unilateral or bilateral vocal cord paralysis
Possible causes include:
Possible cuff pressure on one or both of RLN’s
Anterior RLN compressed against lamina of thyroid cartilage by cuff
Nitrous oxide can diffuse into the cuff and increase pressure, applied to the tracheal mucosa
Normal capillary pressure 25-30mmHg
Complications of Endotracheal Intubation: Summary
Pay attention to details
Be vigilant
Avoid Hypoxemia (#1 Job)
Never use force when placing an endotracheal tube
Confirm placement of the endotracheal tube
Basic Aspects of Ventilatory and Respiratory Support
Being on a ventilator does not mean they are asleep… can be awake and be ventilated
Mechanical Ventilation and Respiratory Support
Two major types of ventilators:
Negative pressure (essentially obsolete)
Positive pressure
Noninvasive (not tubed)
CPAP
BiPAP
Invasive (tubed)
Anesthesia ventilators
ICU ventilators
Negative Pressure Ventilation
POSITIVE PRESSURE VENTILATION
Positive Pressure Ventilator
Uses pressures above atmospheric pressure to push air into lungs
Requires use of artificial airway*
(could use vent with a mask if need to free up a hand)
Types
Pressure cycled
Time cycled
Volume cycled
Mechanical Ventilation and Respiratory Support
Ventilators are used commonly in the operating room and in the ICU to deliver mechanical ventilation to the lungs.
Mechanical Ventilation and Respiratory Support: ICU
Not under anesthesia
Mechanical Ventilation and Respiratory Support: OR
In the operating room:
anesthetized
pharmacologically paralyzed
predominantly normal lungs (trauma or lung surgery changes this)
These ventilators are relatively simple and are designed to deliver, through an anesthesia circuit, varying concentrations of the following:
Oxygen
Air
Nitrous oxide
Volatile agents
Initiation of Mechanical Ventilation (1)
Damage at 60 cmH2O??? and above with Peak Pressure
Initiation of Mechanical Ventilation (2)
Trigger Sensitivity tells you how strong their breathing is getting (its what initiates a breath)
What to incrementally increase as they hit each Trigger Sensitivity to see/watch/know their breathing strength is returning
Basic Aspects of Ventilatory and Respiratory Support
Assist control (AC/CMV)
Volume and Pressure Control are both the same as Assist Control
Paralyzed pt needs help
SLIDE WRONG - will not be on spontaneously breathing patient
Synchronized Intermittent Mandatory Ventilation (SIMV)
Minimum RR and Volume (or Pressure)… allows the pt to start breathing on their own
Helps if pt’s breath falls on cycle, but will let them breath if they start on their own
RESEARCH MORE!!!!
Pressure Support Ventilation (PSV)
Patient is not Paralyzed… patient is determining the RR
No mandatory breath
10 cmH2O should get you up to 400 Tv… good test amount to see whether need to go up or down
Need to realize that more pressure means the body will be lazy to regain its breathing strength
Pressure Control Ventilation
Pt paralyzed
Machine breathing entirely for them.
Delivering pressure that will pop out a certain Vt
If deliver a certain pressure, that means your Vt is not fixed (depends on lots of factors, pt position, drugs onboard, etc.)
Good way to avoid barotrauma, because will set to avoid it (30 cmH20)
Inverse Ratio Ventilation
Inverse Ratio Ventilation
Goals:
↓ peak airway pressure
maintain oxygenation
Maintain alveolar ventilation
Usually used with PCV, very difficult to use with volume controlled modes
Contraindicated in COPD and asthma
Ventilation Modes
Ventilation Modes
The ventilator cycle is defined by three phase
variables:
Trigger
Allow the initiation of inspiration
(Time, pressure, or flow)
Limit
once the limit is reached, (flow, volume or pressure) it will shut it off (the breath)
Variable that cannot be exceeded during inspiration
Cycle
Variable that terminates the inspiratory phase
(pressure, volume, flow, or time)
Triggering (Initiation)
Is how inspiration is initiated in association with patient breaths
Ventilators may be triggered by changes in:
Pressure
Flow
preset time interval having elapsed
Cycling
Determines how the ventilator switches from inspiration to expiration
Time cycling
used in pressure-controlled ventilation
Flow cycling
used in pressure-support ventilation, where a reduction of the peak inspiratory flow cycles the ventilator into expiration
Volume cycling
used in volume-controlled ventilation where the ventilator cycles to expiration once a set tidal volume has been delivered
Control
Breath Types Defined by the Machine vs. Patient Control Phase Variable
Pressure ventilation:
Used to be Pressure and Volume Ventilators… now they are all the same and just dictated by machine settings
Positive Pressure Ventilators: Pressure
Positive Pressure Ventilators: Volume
Most widely used system
Terminates inspiration at preset volume
Delivers volume at whatever pressure is
required up to specified peak pressure
May produce dangerously high intrathoracic pressures
Pressure Ventilation: Pros
Pressure Ventilation: Cons
Variable tidal volume as lung compliance changes
Should lung compliance worsen Vt will drop (if the ETT plugs, Vt drops to zero, but the ventilator does not sense it)
Should compliance improve (following surfactant for
example) this may result in overdistention
Volume ventilation
Volume-Cycled Ventilator Modes
SIMV always a good option if this isn’t working
Volume ventilation: Pros and Cons
Pressure vs Volume Ventilation
Ventilator Response and Monitoring during Pressure and Volume Ventilation
High Frequency Ventilators
KNOW HOW THE Hz works!!!
Used when the pt can not tolerate pressures
Positive End Expiratory Pressure (PEEP)
Equivalent to function of CPAP in spontaneously breathing patients
(KNOW HOW CPAP WORKS FOR OSA!!!)
Increases lung compliance and oxygenation while
decreasing shunt fraction and work of breathing
May predispose to barotrauma and decreased CO due to increased
intrathoracic pressure (some pts may not tolerate)
PEEP (1)
Increased intrathoracic pressure leads to the venous return issues
*** KNOW This for test
PEEP (2)
Noninvasive Positive Pressure Ventilation
CPAP and BiPAP
Not a protected airway… know that is big for the contraindications
Useful for = issues in PACU potentially
… might want ready to go in PACU
CPAP : Continuous positive airway pressure
Respiratory therapy for individuals breathing with or without mechanical assistance in which airway pressure is maintained above atmospheric pressure throughout the respiratory cycle by pressurization of the ventilatory circuit
(CPAP) can be a machine that helps a person who has obstructive sleep apnea (OSA) breathe more easily during sleep
A CPAP machine increases air pressure in the throat/airway so that airway collapse does not occur on inspiration
Continuous positive airway pressure (CPAP) is treatment provided by a machine worn at night or during times of sleep to treat obstructive sleep apnea, a sleep disorder in which a person regularly stops breathing during sleep for 10 seconds or longer because of upper airway obstruction
Ventilator Basics - Anesthesia
Complications of Mechanical Ventilation
Equipment failure
Upper airway trauma and injury
Barotrauma
Volutrauma
Overdistention of the lung from large tidal volumes causing inflammatory changes in the lung
Ventilator associated pneumonia
Swallowing disorders
Ventilator Complications
Mechanical Malfunction:
Keep all alarms activated at all times
Bag Mask Ventilation must always be available
If malfunction occurs, disconnect ventilator and ventilate manually
Airway Malfunction:
Suction patient as needed
Auscultate chest
End tidal CO2 monitoring
Maintain desired end-tidal CO2
Assess tube placement
Ventilator Complications: Pulmonary Barotrauma
Ventilator Complications: Hemodynamic alterations
Ventilator Complications: Other organ systems
Renal malfunction
Pulmonary atelectasis
Infection
Oxygen toxicity
Loss of respiratory muscle tone
Troubleshooting Ventilator Problems
If you can’t find the problem immediately then:
Hand ventilate the patient w/ a self inflating bag and
100% oxygen
Call for help!
Then troubleshoot - don’t forget to ventilate the pt!
SUMMARY
If ventilators fail, the patient’s condition may deteriorate quickly – revert to the basics
Troubleshooting Ventilator Problems Summary
Check the endotracheal tube
Administer 100% oxygen w/ anesthesia machine bag or ambu bag
Auscultate the chest for breath sounds
Finger on the pulse if monitors not working
Call for help
Difficulty with Ventilation (intubation)
Hypoxia Algorithm
Extubation Criteria
Adequate oxygenation and ventilation can be maintained by the patient spontaneously
(some people might on PSV Pro? trigger probably really low)
(DEEP)
Negative Inspiratory Force (NIF) of -20 cmH2O (or more negative, i.e. -30 or -40)
(DEEP)
No airway obstruction after extubation is anticipated
(DEEP)
Muscle relaxant reversed
Sustained tetany for 5 seconds
Lifts head for 5 seconds
Patient follows commands
Squeezes hand
Opens eyes
How to Extubate
Breath in on pulling tube is good practice to make sure patient’s next phase is expiration to breath out any secretions, and might open up some alveoli
Questions
1
Tidal Volume stay same
PIP goes up
2
Tidal volume decrease
PIP goes up
3
ACV
4
Tidal Volume
Acid-Base Chemistry
The Basics
Acid
proton donor (Bronsted-Lowry)
compound containing H and reacts with H2O to form hydrogen ions (Arrhenius)
weak acid: reversibly donates H+
Base
proton acceptor
compound that produces hydroxide ions in water
weak base: reversibly binds H+
KW = the dissociation constant of water molecules (into H and OH)
SID = strong ion difference
Cations and anions from solutions in the body can affect Kw, thereby affecting [H+]
Acids & Bases in the Body
Anesthesia can significantly alter acid-base balance due to changes in ventilation, perfusion, and fluid administration/distribution
Strong ion difference (SID), PCO2, and [ATOT] are most important in understanding physiologic acid-base relationships
SID = sum of all strong, completely or almost completely dissociated cations minus strong anions
Strong cations: sodium, potassium, calcium, magnesium
Strong anions: chloride, lactate
Buffers
A solution that contains conjugate pairs (a weak acid and its conjugate base or a weak base and its conjugate acid)
Minimize [H+] changes by readily accepting or donating H+
Most efficient at minimizing changes in [H+] when pH = pKa
Acid-Base Clinical Disorders
Suffix –osis denotes pathological processes that alter arterial pH
acidosis vs alkalosis
Suffix –emia denotes the net effect of all primary processes and compensatory responses on arterial blood pH
Acidemia = pH <7.35
Alkalemia = pH >7.45
Clinical Acid-Base Disorders
Acidosis
Reduces pH to values below normal
Alkalosis
Increases pH to values above normal
Metabolic
Affects [HCO3-]
Respiratory
Affects PaCO2 (partial pressure of CO2 in arterial blood)
Compensatory Mechanisms
Body Buffers
Bicarbonate (H2CO3/HCO3-)
Hemoglobin (HbH/Hb-)
Intracellular proteins (prH/Pr-)
Phosphates (H2PO4-/HPO42-)
Urinary buffer until pH reaches 4.4 all phosphates are in H2PO4- form reaching distal tubule
No HPO42- ions available for eliminating H+
Ammonia (NH3/NH4+)
Buffers
Bicarbonate is the most important buffer in the extracellular fluid compartment
Effective against metabolic acid-base disturbances
Not effective against respiratory acid-base disturbances
Henderson-Hasselbalch for bicarbonate
pH = pK’ + {[HCO3-]/0.03 PaCO2}
pK’ = 6.1
Important to note that PaCO2 and plasma [HCO3-] are closely regulated by lungs and kidneys, so these organs have a strong influence on arterial pH by affecting the [HCO3-]/PaCO2 ratio
Buffers - Hemoglobin
Hemoglobin is an important buffer in blood, despite being restricted to RBCs.
Can buffer carbonic and noncarbonic acids (unlike bicarbonate)
Weak acid, HHb, and potassium salt, KHb exist in equilibrium
H+ + KHb HHb + K+
H2CO3 + KHb HHb + HCO3-
Histidine is abundant in Hb and a highly effective buffer between pH 5.7-7.7
Most important noncarbonic buffer
pKa = 6.8
Buffers - Phosphate and Ammonia
Phosphate and ammonia are important urinary buffers
Extracellular compartment buffering
Bone demineralization can occur due to the release of alkaline compounds in response to acid loads
CaCO3 (calcium carbonate) and CaHPO4 (calcium hydrogen phosphate)
Carbonate deposition in bone can increase due to alkaline loads
NaHCO3
Respiratory Compensation
Chemoreceptors in brainstem, carotid bodies, and aortic bodies mediate respiratory compensation of PaCO2 by making changes in alveolar ventilation
CSF: pH changes initiate the response
Minute ventilation increases 1-4 L/min for every acute 1 mmHg increase in PaCO2
Respiratory compensation is an important response during metabolic disturbances
Lungs can eliminate ~15 mEq CO2 per day
Metabolic Acidosis, Respiratory Compensation
Decrease in arterial blood pH stimulates medullary respiratory centers
Alveolar ventilation increases and PaCO2 decreases
Usually restores pH closer to normal, but it never restores completely to normal
Steady state in PaCO2 may not occur for 12-24 hrs
pH decreases 1-1.5 mmHg below 40 mmHg for every 1 mEq drop in plasma [HCO3-]
Less predictable than respiratory response to acidosis
Hypoxemia from hypoventilation triggers O2-sensitive chemoreceptors leads to ventilation stimulation and limits the compensatory respiratory response
Arterial blood pH increases will depress respiratory centers
Alveolar hypoventilation increases PaCO2, brings pH toward normal, but PaCO2 does not rise above 55 mmHg in response to metabolic alkalosis
PaCO2 can increase 0.25-1 mmHg for each 1 mEq/L increase in [HCO3-]
Renal Compensation
Kidneys can compensate for major pH changes during respiratory and metabolic acid-base disturbances
Eliminate ~1 mEq/kg/day of sulfuric acid, phosphoric acid, uric acid, and incompletely oxidized organic acids
Keto acids and lactic acid form from incomplete metabolism of fatty acids and glucose
Renal Compensation During Acidosis
Effects not seen for 12-24 hrs; max effect not seen for up to 5 days
Increased reabsorption of filtered HCO3-
Increased excretion of titratable acids
Increased ammonia production
Renal Compensation During Alkalosis
Usually only in pts with sodium deficiency or mineralocorticoid excess
Na+ deficiency lowers extracellular fluid volume leads to Na+ reabsorption in proximal tubule
Na+ transferred along with Cl-, and Cl- decrease leads to HCO3- (bicarb) reabsorption
Increased mineralocorticoid activity affects aldosterone-mediated Na+ reabsorption in distal tubules leads to can propagate metabolic alkalosis, even if Na+ deficiency/chloride deficiency not apparent
Base Excess
The amount of acid or base (mEq/L) that must be added for pH to return to 7.4 and PaCO2 to return to 40 mmHg @ 100% O2 sats & 37∘C
Adjusts for noncarbonic buffering in blood
BE represents the metabolic component of an acid-base disturbance
+ value = metabolic alkalosis
- value = metabolic acidosis
Acidosis
Severe acidosis (pH<7.20) directly depresses myocardial and smooth muscle
Decreased cardiac contractility
PVR decreases
Hypotension
Hemoglobin-dissociation curve: H+ create rightward shift, but in severe acidosis tissue hypoxia can still occur due to cardiac and vascular smooth muscle less responsive to endogenous/exogenous catecholamines
Lowers V-fib threshold
Circulation to tissues affected
Acidosis resulting in hyperkalemia can be lethal
Body exchanges extracellular H+ with intracellular K+
For each 0.1 decrease in pH, plasma K+ increases ~0.6 mEq/L
CO2 narcosis
CNS depression from respiratory acidosis more likely than metabolic acidosis
Unlike CO2, H+ do not readily penetrate blood-brain barrier
Respiratory Acidosis
H2O + CO2 H2CO3 H+ + HCO3-
Increase in PaCO2 drives rxn to the right
A primary increase in PaCO2 leads to a drop in arterial pH and increase in [H+]
Bicarbonate minimally affected
PaCO2 is the balance between CO2 production and elimination
PaCO2 = CO2 production/alveolar ventilation
Most common cause of respiratory acidosis = alveolar hypoventilation
Limited response to acute PaCO2 elevation (6-12 hrs)
Typically buffered by Hb and extracellular exchange of H+ for K+/Na+ from bone and intracellular fluid compartment
Plasma [HCO3-] increases only ~1mEq/L for each 10 mmHg PaCO2 increase above 40 mmHg
Chronic respiratory acidosis may have renal compensation after 12-24 hrs, but max compensation ~3-5 days
Chronic respiratory acidosis increase plasma [HCO3-] by ~4mEq/L for each 10 mmHg increase in PaCO2 above 40 mmHg
Respiratory Acidosis Treatment
Metabolic Acidosis
Primary decrease in [HCO3-]
Arterial pH decrease from a dip in plasma [HCO3-] without a proportional dip in PaCO2
3 mechanisms
Consumption of HCO3- by strong nonvolatile acid
Renal or GI wasting of bicarbonate
Rapid dilution of extracellular fluid compartment with bicarbonate-free fluid
Anion Gap (AG)
Difference between major measured cations and major measured anions
AG = ([Na+] – ([Cl-] + [HCO3-]))
AG decreases by 2.5 mEq/L for every 1 g/DL reduction in plasma [albumin]
Normal AG = 7-14 mEq/L
Anion Gap Metabolic Acidosis
High AG metabolic acidosis
Lactic acidosis
Normal lactate levels 0.3-1.3 mEq/L
Normal AG metabolic acidosis
Most commonly seen with hyperchloremia from GI or renal losses of HCO3- or excessive NS administration
Metabolic Acidosis Treatment
Correct respiratory components of acidemia
May need to drop PaCO2 to low 30s to partially return pH to normal
Alkali therapy may be necessary if pH <7.20 consistently
7.5% NaHCO3 solution
Dose using calculated bicarbonate space or BE
Bicarbonate Space
Volume to which HCO3- will distribute when administered IV
25-60% of body weight, depends on duration and severity of acidosis
Due to amount of intracellular and bone buffering that’s already taken place
Base Deficit
Calculate amount of NaHCO3 necessary to correct base deficit
NaHCO3 = BD * body weight in L
Acidotic Patients and Anesthesia
Acidemia can potentiate sedatives and anesthetic agents acting on CNS and circulatory system
Potentiates opioids by ↑ fraction of drug in nonionized form
Opioids are weak bases
Facilitates brain penetration and sedative effect
Avoid sux in these patients
Likely already have elevated K+
Alkalosis
Respiratory Alkalosis
Primary decrease in PaCO2
Caused by inappropriate increase in alveolar ventilation relative to CO2 production
Plasma [HCO3-] usually decreases by 2-5 mEq/L for each 10 mmHg decrease in PaCO2 below 40 mmHg
Treatment: treat underlying causes
Severe alkalemia (pH>7.60): IV HCl, arginine chloride, or ammonium chloride
Metabolic Alkalosis
Metabolic Alkalosis Treatment
Treat underlying disorder first
Normalize PaCO2 with controlled ventilation
Chloride-sensitive: treat w/ NS and K+ IV
If vomiting: H2-blocker therapy
If edematous pt: acetazolamide
Mineralocorticoid activity-mediated alkalosis: treat w/ aldosterone antagonists
spirinolactone
If arterial blood pH >7.60, treat w/ HCl, arginine hydrochloride, or hemodialysis
Alkalemia Anesthetic Considerations
Respiratory alkalosis can lead to cerebral ischemia
Secondary to decreased CBF
Severe atrial and ventricular arrhythmias can occur with combos of alkalemia and hypokalemia
Diagnosis of Acid-Base Disorders
Rapid Approach to ABG Interpretation
Every 1 mmHg change in CO2 corresponds to 0.08 U change in opposite direction of pH
Every 6 mEq ∆ in HCO3- changes pH by 0.1 in the same direction
If ∆pH is greater or less than predicted, mixed acid-base disorder present
Arterial vs. Venous Blood Gas Samples
Venous blood oxygen tension reflects tissue extraction, not pulmonary function
Normal ~40 mmHg
PvCO2 is usually 4-6 mmHg higher than PaCO2
Venous blood pH is usually 0.05 U lower than arterial blood pH
