2025 Airway Management Exam 3 Flashcards

Question

Complications Arising Immediately after Intubation: Accidental Endobronchial Intubation

Answer 1

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"

Answer 2

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

Answer 3

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

Answer 4

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

Answer 5

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

Answer 6

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)

Answer 7

Endotracheal intubation provokes increases in ICP Dangerous in patients with: Intracranial aneurysm (big time problem, attending should be there) Intracranial bleeding Elevated ICP

Answer 8

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

Answer 9

Can occur immediately after a premature extubation Patients may not have recovered from: Anesthesia Narcotic and sedative drugs Neuromuscular blocking agents

Answer 10

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

Answer 11

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

Answer 12

Pay attention to details Be vigilant Avoid Hypoxemia (#1 Job) Never use force when placing an endotracheal tube Confirm placement of the endotracheal tube

Answer 13

Being on a ventilator does not mean they are asleep... can be awake and be ventilated

Answer 14

Two major types of ventilators: Negative pressure (essentially obsolete) Positive pressure Noninvasive (not tubed) CPAP BiPAP Invasive (tubed) Anesthesia ventilators ICU ventilators

Answer 15

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

Answer 16

Ventilators are used commonly in the operating room and in the ICU to deliver mechanical ventilation to the lungs.

Answer 17

Not under anesthesia

Answer 18

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

Answer 19

Damage at 60 cmH2O??? and above with Peak Pressure

Answer 20

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

Answer 21

Volume and Pressure Control are both the same as Assist Control Paralyzed pt needs help SLIDE WRONG - will not be on spontaneously breathing patient

Answer 22

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!!!!

Answer 23

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

Answer 24

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)

Answer 25

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

Answer 26

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)

Answer 27

Is how inspiration is initiated in association with patient breaths Ventilators may be triggered by changes in: Pressure Flow preset time interval having elapsed

Answer 28

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

Answer 29

Used to be Pressure and Volume Ventilators... now they are all the same and just dictated by machine settings

Answer 30

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

Answer 31

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

Answer 32

SIMV always a good option if this isn't working

Answer 33

KNOW HOW THE Hz works!!! Used when the pt can not tolerate pressures

Answer 34

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)

Answer 35

Increased intrathoracic pressure leads to the venous return issues *** KNOW This for test

Answer 36

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

Answer 37

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

Answer 38

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

Answer 39

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

Answer 40

Renal malfunction Pulmonary atelectasis Infection Oxygen toxicity Loss of respiratory muscle tone

Answer 41

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

Answer 42

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

Answer 43

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

Answer 44

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

Answer 45

1 Tidal Volume stay same PIP goes up 2 Tidal volume decrease PIP goes up 3 ACV 4 Tidal Volume

Answer 46

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+]

Answer 47

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

Answer 48

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

Answer 49

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

Answer 50

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)

Answer 51

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+)

Answer 52

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

Answer 53

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

Answer 54

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

Answer 55

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

Answer 56

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-]

Answer 57

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

Answer 58

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

Answer 59

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

Answer 60

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

Answer 61

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

Answer 62

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

Answer 63

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

Answer 64

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

Answer 65

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

Answer 66

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

Answer 67

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

Answer 68

Calculate amount of NaHCO3 necessary to correct base deficit NaHCO3 = BD * body weight in L

Answer 69

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+

Answer 70

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

Answer 71

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

Answer 72

Respiratory alkalosis can lead to cerebral ischemia Secondary to decreased CBF Severe atrial and ventricular arrhythmias can occur with combos of alkalemia and hypokalemia

Answer 73

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

Answer 74

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

2025 Airway Management Exam 3 Flashcards

Lectures 7-10: Airway Complications, Vents, BloodGas