Apex Respiratory

Airway Anatomy
Laryngeal muscles

  • Intrinsic (innervated by Recurrent Laryngeal muscle)

    • Control tension and position of the vocal cords and contribute to phonation

    • CricroThyroid: Cords Tense= elongate innervated by External branch of SLN

    • ThyroaRytenoid: They Relax= shorten

      • ADDucts and closes glottis

    • Posterior CricoArytenoid: Please come apart= aBduct Take away

      • Solely responsible for opening the vocal cords

    • Lateral CricoArytenoid: Let’s Close Airway= aDDuct LCAD

      • ADDucts and closes glottis

  • Extrinsic

    • Support the larynx inside the neck and assist with swallowing

    • all extrinsic end in -hyoid except digastric

Airway innervation

Sensory innervation (4) of the upper airway:

1.Trigeminal CN5: face and head
V1 (ophthalmic) = Nares anterior 1/3 of septum
V2 (maxillary)= Turbinates & nasal septum
V3 ( mandibular)= Anterior 2/3 of tongue (somatic)

2.Glossopharyngeal CN9: oropharynx to anterior side of epiglottis
Posterior 1/3 of tongue
Soft palate
oropharynx
Vallecula
Anterior side of epiglottis

3.Vagus nerve CN10: gives rise to SLN and RLN

Superior laryngeal:
Internal branch= posterior side of the epiglottis-> to level of the vocal cords
External branch= 0 sensory function (motor innervation to cricrothyroid muscle)

Recurrent laryngeal:
Below vocal cords-> trachea (innervates posterior cricoarytenoid muscle, tensing stops when paralyzed)

Risk factors for RLN injury:

  • overinflation of ETT or LMA cuff

  • tumor

  • excessive neck stretching and surgery (thyroidectomy)

  • Left side RLN injury

    • PDA ligation

    • L atrial enlargement (mitral stenosis, aortic arch aneurysm, thoracic tumor)

Effect of recurrent laryngeal nerve injury:
Bilateral:
Acute: Respiratory distress (unopposed action of cricothyroid muscle) Stridor, dyspnea aphonia PRESENTS similar to laryngospasm
Chronic: No respiratory distress
Unilateral:
Hoarseness
No respiratory distress

Effect of superior laryngeal nerve injury:

Bilateral:  Hoarseness/ No respiratory distress
Unilateral: No respiratory distress

Anesthetizing airway Block 3 nerves (Glossopharyngeal, SLN, RLN)

  • Base of tongue

  • oropharynx

  • hypopharynx

  • larynx

Benzocaine is commonly used; risk for methemoglobinemia and treatment is methylene blue
Cocaine can provide topical; avoid in PChE deficiency on MAOI drugs and SNS tone (CAD)

Land marks for 3 Airway blocks:

Glossopharyngeal nerve block: Palatoglossal arch at the anterior tonsillar pillar; carries 5% risk of seizure (intracarotid injection); needle is too deep if aspirate air, aspirate blood redirect needle medial
Super laryngeal nerve block: Greater cornu of hyoid, needle is too deep if aspirate air
RLN Transtracheal nerve block: Cricothyroid membrane (caudal direction) have patient breathe

Laryngeal Anatomy

Adult Larynx C3-C6-shaped like cylinder and narrowest part is glottic opening
Pediatric is shaped like a funnel < 5yrs
narrowest fixed region= cricoid ring
narrowest dynamic region= vocal cords

  • Components:

    • Bone: Hyoid

    • Ligaments: thyrohyoid, cricothyroid

    • Unpaired cartilages: epiglottis, thyroid. cricoid

    • Paired cartilages: corniculate, arytenoid, cuneiform

Needle is placed through cricothyroid membrane during cricothyroidotomy to emergently secure airway and for transtracheal block to anesthetize RLN

Cartilages:
Unpaired: Epiglottis, Thyroid, Cricoid
Paired: Corniculate, Arytenoid (ball joint can be impaired by rheumatoid arthritis and SLE), Cuneiform

Laryngospasm:
Signs:
Inspiratory stridor
Suprasternal and supraclavicular retraction during inspiration
“Rocking horse” appearance of the chest wall (paradoxical movement)
Increased diaphragmatic excursion
lower rib flaring
Absent or altered EtCO2 waveform
Risk factors:
second had smoke
reactive airway disease
GERD
Causes:
Light anesthesia
airway secretions
surgery in airway
active or recent respiratory tract infection (<2 weeks)
Age < 1 yr
Treatment:
100% Fio2
Remove noxious stimulation
Deepen anesthesia
CPAP 15-20 cm H20
Open the airway (head extension, chin lift)
Succinylcholine:
Submental administration is fasted onset
Neonate/infant= 2mg/kg
Adult or child: 1mg/kg
Dose of 0.1mg/kg preserves ventilation
Infants and small children should receive atropine 0.02mg/kg with succinylcholine
If no IV access, submental administration will produce the fastest onset
If no IV access and patient can receive Succinylcholine, then Rocuronium is the only other NMB that can be given IM

Upper Airway Anatomy
Extends from mouth and nares to cricoid cartilage
Resistance is 2x higher in nasal passage than mouth
Reduce trauma during airway instrumentation in nares: direct device between inferior turbinate and floor of nasal cavity and orient bevel towards the turbinates.

Lower Airway Anatomy
Begins at the trachea and ends at alveoli
Trachea begins at inferior border of cricoid cartilage and ends at carina T4-T5
Lower airway begins as single tube (trachea) and bifurcates along 23 generations
Tube goes where nose goes
L Bronchus is 5cm and takes off 45 degrees from long axis of trachea
R Bronchus is 2.5 cm in length and projects 25 degrees
Children up to 3- B Bronchi take off 55 degrees from long axis of trachea
Type 1 pneumocytes provide surface for gas exchange and Type 2 produce surfactant and Type 1

Respiratory Physiology
Diaphragm and external intercostals contract during tidal breathing (inspiration)
Exhalation is passive
Accessory muscles for inspiration include sternocleidomastoid and scalene muscles
Accessory muscles for active expiration include rectus abdominus, transverse abdominis internal oblique and external oblique.
Vital capacity of 15ml/kg is required for effective cough

3 Zones of airway exchange:

  1. Conducting zone= 0 gas exchange, anatomic dead space, begins in nares and mouth and ends in terminal bronchioles

  2. Transitional zone=air conduit and gas exchange, respiratory bronchioles

  3. Respiratory zone= gas exchange, begins at alveolar ducts and extends to alveolar sacs

Transpulmonary pressure is the difference between alveolar pressure (inside airway) and pleural pressure (outside airway)
TPP= Positive (airway stays open)
TPP= Negative (airway collapses)

Contraction of inspiratory muscles reduces thoracic pressure and increases thoracic volume= ex of Boyles law

Increase PaCo2 to EtCO2 gradient = Increase dead space:
PPV, HypoTN, Atropine
Dead spaces:
Anatomic Vd-Air confined to the conducting airway, Nose/mouth-> terminal bronchioles
Alveolar Vd-Alveoli that are ventilated but not perfused, Reduced pulmonary blood flow (decreased CO)
Physiologic Vd: Anatomic Vd: + Alveolar Vd
Apparatus Vd: Vd added by equipment Facemask. HME. Limb of circle system if incompetent valve present

Spontaneously ventilating patient Vd/Vt=0.33 (2mL/kg or 150mL in 70 kg patient)
Mechanically ventilated patient Vd/Vt=0.50

Factors that increase ratio of Vd to Vt= Facemask, atropine, neck extension
Factors that decrease ratio = ETT LMA and neck flexion

Physiological dead spec can be calculated with Bohr equation. Compares partial pressure of CO2 in the blood vs partial pressure of CO2 in exhaled gas

Most common cause of increased Vd/Vt under GA is HypoTN. Acute EtCO2 decrease first rule out HypoTN

Increases in Vd:
Facemask
HME
PPV
Anticholinergics
Old age
Extension
Decreased CO
COPD
PE (thrombus, air, amniotic fluid)
Sitting position
Decreases in Vd:
Endotracheal tube
LMA
Tracheostomy

In a circle system dead space begins at the y-piece. Anything proximal to the y-pieces does not influence dad space nor does increasing length of circuit. Except when there is incompetent valve in circle system.

Alveolar compliance curve:

Alveolar ventilation is a function of alveolar size and its position on the alveolar compliance curve.
The best ventilated alveoli are the most compliant (which is the steep slope of the curve)
The poorest ventilated alveoli are the least compliant (flat portion of the curve).
Ventilation is greatest at the lung base due to higher alveolar compliance.
Perfusion is greatest at the lung base due to gravity

Ventilation/Perfusion Mismatch
V/Q ratio

The V/Q ratio is the ratio of ventilation to perfusion (Ve/CO):
Normal Ve= 4L
Normal CO= 5L
Normal V/Q ratio= 0.8
Dead space and shunt are absolutes:
Dead space: V/Q=infinity (10/0=infinity)
Shunt: V/Q=0 (0/10=0)
V/Q mismatch occurs when the ratio is disturbed
If the number is larger than 0.8, then this moves towards dead space
If the number is smaller than 0.8 than this moves towards shunt
Atelectasis is most common cause of hypoxemia in the PACU. Leads to R-L shunt, V/Q mismatch, and hypoxemia

Patients with V/Q mismatch have more trouble with oxygenation than CO2 elimination. CO2 retention suggest severe V/Q mismatch

To combat dead space in Zone 1= bronchioles constrict to minimize ventilation of poorly perfusion alveoli
To combat shunt Zone 3- hypoxic pulmonary vasoconstriction reduces pulmonary blood flow to poorly ventilated alveoli

Law of Laplace- As the radius of a sphere or cylinder becomes larger, the wall tension increases as well. (Tension Pressure Radius)

Surfactant keeps alveolar pressure constant and prevents small alveoli from collapsing and emptying in to larger alveoli
Type 2 pneumocytes produce surfactant 22-26 wks with peak production 35-36 wks. Fetal lung maturity can be hastened by corticosteroids (betamethasone)

Zone 1:
PA> Pa>Pv
Dead space
Ventilation without perfusion

Zone 2:
Pa>PA> Pv
Waterfall
Normal physiology

Zone 3:
Pa> Pv>PA
Shunt
Perfusion without ventilation

Zone 4:
Pa>Pist>Pv>PA
Pressure in the interstitial space impairs ventilation and perfusion

Alveolar gas equation:
Hypoventilation can cause hypercarbia and hypoxemia. Supplemental oxygen reverses hypoxemia but does not reverse hypercarbia. Hypercarbia can go undetected.
Alveolar Oxygen= FiO2 x (Pb-PH2O)- (PaCO2/RQ)

Pb= Barometric/Atmospheric pressure (760 normal)
PH2O= 47mmHg
RQ= Respiratory quotient=0.8

RQ= (CO2 elimination/O2 consumption)= (200mL/250mL)

Hypoxemia & A-a Gradient
A-a gradient is the difference between alveolar oxygen (PAO2) and arterial oxygen (PaO2)
Calculating the A-a gradient diagnose the cause of hypoxemia by indicating the amount of venous admixture. Utilizes alveolar gas equation and obtain an ABG (PaO2).
Hypoxemia with normal A-a gradient <15mmHg:
low Fio2
hypoventilation
Hypoxemia with increased A-a gradient:
diffusion limitation
V/Q mismatch
shunt (NOT improved with supplemental oxygen)

Factors that increase A-a gradient:
Aging (closing capacity increases relative to FRC)
Vasodilators (decreased hypoxic pulmonary vasoconstriction)
R-L Shunt (atelectasis, pneumonia, bronchial intubation, intracardiac defect)
Diffusion limitation (alveolocapillary thickening hinders O2 diffusion)

Shunt increases 1% for every 20mmHg of Aa gradient

Lung Volumes & Capacities
Spirometry cannot measure residual volume therefore it cannot measure total lung capacity, functional residual capacity or closing volume.

Oxygen Content
VO2=3.5mL/kg
VO2 ~ 250mL/min


Oxyhemoglobin Dissociation Curve
Oxyhemoglobin dissociation curve tells the tendency of hemoglobin to bind oxygen

Right shift curve =hemoglobin has a lower affinity for oxygen (right=release) During normal physiology this occurs at the tissue level.
Left shift curve= hemoglobin has higher affinity for oxygen (left=love) During normal physiology this occurs int he lungs


P50 is the PaO2 where hemoglobin is 50% saturated with oxygen

Decreased P50= Left shift
Hgb has a stronger hold on oxygen
Examples: Hgb F, hypocarbia, methemoglobin and carboxyhemoglobin, alkalosis, decreased temperature, decreased 2,3 DPG

Increased P50= Right shift
Hgb is more willing to release oxygen
Examples: acidosis, hyperthermia, and increased 2, 3 DPG and temperature

A PaO2>100mmHg will increase O2 dissolved in blood but will not cause more to bind to hemoglobin.

The Bohr effect says that an increased partial pressure of CO2 and a decreased pH cause hemoglobin to release O2

2,3 DPG is produced during RBC glycolysis.
Maintains the curve in a slightly R shifted position
Hypoxia increases 2,3 DPG production= facilitates O2 offloading
Important compensation mechanism for chronic anemia
Banked blood the concentration of 2,3 DPG falls which causes curve to left shift and reduce O2 available to tissue.
HgbF doesn’t respond to 2,3 DPG= L shift P50-19mmHg

CO2 Transport
CO2 is primary by product of aerobic metabolism
CO2 is transported in 3 ways:
As bicarbonate 70%
Bound to Hgb 23%
Dissolved in plasma 7%

Carbonic acid is enzyme that facilitates formation of carbonic H2CO3 from H2O and CO2
To maintain electroneutrality, for every HCO3 that leaves the erythrocyte one Cl ion is transported in. This is known as the chloride or Hamburger shift.

An acidic environment of metabolically active tissue enhances O2 offloading from hemoglobin (Bohr effect) and increases CO2 loading in tot the blood (Haldane effect)
CO2 is 20x more soluble in blood than O2

Solubility is function of Henry’s Law

The Haldane effects describes CO2 carriage (oxygen causes erythrocyte to release CO2). Opposite of Bohr effect. Deoxygenated blood can carry more CO2

CO2 Dissociation curve
Oxygenated Hemoglobin shifts CO2 dissociation curve to the Right
Deoxygenated Hemoglobin shifts CO2 dissociation curve to the Left

Hypercapnia
Causes: sepsis, MH, Thyroid, storm, burns and shivering
Decreased CO2 elimination: airway obstruction, ARDS, COPD, opioid overdose
Causes of Rebreathing: exhausted soda lime, a faulty unidirectional valve in circle system and inadequate FGF in a Mapleson circuit.
Consequences of hypercarbia: hypoxemia, acidosis, cardiac depression, SNS stimulation and increased ICP.

CO2 Ventilatory Response Curve
Describes the relationship between PaCO2 and min ventilation
The central chemoreceptor in the medulla is the primary monitor of PaCO2
The peripheral chemoreceptor in the carotid bodied and transverse aortic arch play a secondary role in monitoring PaCO2

Conditions that shift CO2 curve down and to the right:
Volatile anesthetics
Opioids
NMBs
Metabolic alkalosis
Carotid enterectomy
Right shift= apneic threshold has increased

Conditions that shift CO2 curve to the left:
hypoxemia
metabolic acidosis
surgical stimulation
intracranial hypertension
Drugs: Salicylates, Aminophylline, Doxapram, norepinephrine
Left shift= apneic threshold has decreased

Neural Control of Ventilation
Reticular activating system in Medulla and Pons regulates speed and depth of breath (regulating PO2 and CO2)
Receives afferent input from the central and peripheral chemoreceptors as well as the stretch receptors in the lungs
Integrates signals with intrinsic resp pattern an sends response to diaphragm intercostals and accessory muscles.
Cerebral cortex modify these responses

Medullary respiratory center:
Dorsal: Active during inspiration
Ventral: Active during expiration

Pontine respiratory center:
Pneumotaxic center upper pons: Inhibits the DRG
Apneustic center lower pons: Stimulates the DRG

Resp rate and Pattern determined by:
Medulla:
Neural control in resp center
Chemical control in central chemoreceptors
Carotid Bodies and aortic arch:
Chemical control in peripheral chemoreceptors
Lungs:
Baroreceptors

Central chemoreceptors
Responds indirectly to PaCO2
BBB separates blood from CSF
CO2 free diffuse across BBB (H and HCO3 do NOT)
CO2 dissolves into H and HCO3 after reaching CSF
As rate of H rises in CSF, rate and depth of Resp increase until minute ventilation stabilizes (occurs in mins and control blood gas tension)
Non-Volatile acids (lactic acid)do not pass BBB
Central chemoreceptor is stimulated by hypercarbia and hypoxemia but is depressed by profound hypercarbia and hypoxemia.

Peripheral chemoreceptors
Reside in carotid bodies at bifurcation of common carotid artery and present in transverse aortic arch
Monitor hypoxemia PaO2 < 60mmHg
Carotid Enterectomy severs the afferent limb of the hypoxic ventilatory response. Don’t do B CEA
Sub anesthetic doses of inhalation and intravenous anesthetics (0.1 MAC) depress hypoxic ventilatory drive cause risk of hypoxemia in PACU.

Anemia and Carbon Monoxide poisoning affect tissue oxygenation but do not impair hypoxic ventilatory response.

The Hering-Breuer inflation reflex prevent alveolar over distention by stopping inhalation when lung volume is too large.
Hering-Breuer deflation reflex activates resp drive when lung vol is too small to prevent atelectasis.
J receptors or pulm C fiber receptors increase the resp rate in setting of pulmonary embolism or CHF. Causes tachypnea
Paradoxical reflex of head cause a newborn to take first breath

Hypoxic Pulmonary vasoconstriction
HPV is local reaction that occurs in response to a reduction in alveolar oxygen tension not arterial PO2
Goal is to improve matching of ventilation and perfusion to minimize shunt during atelectasis or one lung ventilation
The pulmonary vascular bed is the only region in the body that responds to hypoxia with vasoconstriction
Inhibited by volatile anesthetics >1.5 MAC, PDE, Dobutamine, hypervolemia, excessive PEEP and large tidal volumes
NOT inhibited by IV anesthetics: ketamine, propofol, and opioids

Excessive PEEP or high tidal volumes increase dead space and reduce V/Q matching

Respiratory acidosis activates H/K pump buffer CO2 acids in exchange cause K to be released in Plasma

Respiratory PathoPhysiology
Control of Airway diameter
Radius of the airway has most significant contribution to airflow resistant (radius 4)

PNS Vagus nerve= bronchoconstriction
Mast cells and non cholinergic PNS= bronchoconstriction
Non cholinergic PNS (nitric oxide)=bronchodilation
SNS (circulating catecholamines)= bronchodilation

Vagus nerve CN 10 supplies parasympathetic innervation to airway smooth muscle
Stimulation of the (Ache to) M3 receptor produces bronchoconstriction from Ca release
Beta 2 receptors= airway smooth muscle
Pulmonary Function testing
Normal FEV1 value is > 80% of predicted value
Normal FVC 4.8 Males & 3.7 Females
Normal FEV1/FVC ratio is > 75-80% of predicted value- useful in diagnosing obstructive (70%) vs restrictive
Lung vols and capacities are measured with spirometry
Forced expiratory flow at 25-75% vital capacity (mid maximal expiratory flow rate) is the most sensitive indicator of small airway disease reduced with obstructive

Postoperative Pulm Complications

Independent risk factors for PPC:
Old age, COPD, CHF and smoking
Surgery >2hrs, GA, abdominal or aortic thoracic
albumin <3.5g/dL

NON increased risk factors:
Asthma
ABG
PFT

Short term benefits of smoking cessation include reduction in carboxyhemoglobin improved P50 with in 12 hrs, Carbon monoxide- 4-6hrs , short term doesn’t reduce pulmonary complications

Intermediate effects of stopping smoking:
Return of pulm function test 6 wks:
airway function
mucociliary clearance
Sputum production
pulm immune function
hepatic enzyme induction also subside after 6 weeks

Risk reduction strategies:
Quit smoking > 6 wks
Employ alveolar recruitment + PEEP
Treat expiratory flow obstruction with bronchodilator and corticosteroids
Treat active infections (prophylaxis for pulm infection is not indicated)
Consider other anesthetic options beside GA
Teach pulm recruitment maneuver to patient

Obstructive vs restrictive

Obstructive have normal or decreased FEV1 and FVC and FEV1/FVC ratio is always decreased
Restrictive disease have decreased FEV1/and FVC but FEV1/FVC ratio is normal

Alpha-1 antitrypsin deficiency is most common metabolic disease in affecting the liver and causes a relative increase in alveolar protease activity. Degrades pulm connective tissue and leads to panlobular emphysema. Only treatment is live transplantation

Anesthetic management of COPD

  • Consider regional for procedures involving extremities and lower abdomen

  • No to neuraxial if patient requires blockade > T6

  • Interscalene causes paralysis of the ipsilateral hemidiaphragm

  • Caution with excessive sedation and ventilatory response

  • Select Volatile with low blood: gas solubility

  • All halogenated anesthetics are bronchodilators Sevo and Iso are better than Des

  • Volatile impair HPV > 1.5 MAC and increase shunt. Unless shunt is sever it can be overcome by increasing FiO2

  • NO is associated with rupture of pulm blebs→ pneumothorax

  • Use tidal volume 6-8mL/kg IBW

  • Use longer expiratory time

  • Add PEEP stay alert for dynamic hyperinflation

Anesthetic management of Restrictive lung disease

  • Minimize risk of barotrauma

  • smaller tidal volume 6ml/kg/IBW rr 14-16

  • Peak insp pressure <30cm H20

  • Prolong inspiratory time 1:1

Aspiration Pneumonitis and Ventilator-Associated Pneumonia

  • Lead to airway obstruction bronchospasm impaired gas exchange and bacterial respiratory infection

  • Risk factors:

    • pregnancy

    • trauma

    • emergency surgery

    • GI obstruction

    • peptic ulcer dx

    • hiatal hernia

    • ascites

    • cricoid pressure

    • seizures

  • Mendelson’s syndrome:

    • chemical aspiration first described in OB patients with roisl factors:

      • Gastric pH< 205

      • Gastric volume > 25mL (0.4mL/kg)

  • Phar Prophylaxis:

    • antacids

    • H2 antagonist

    • GI stimulants

    • proton pump inhibitors

    • antiemetics

  • s/s

    • hypoxemia ** hallmark

    • dyspnea

    • tachypnea

    • cyanosis

  • Treatment

    • tilting head downward or to the side

    • suctioning airway

    • securing airway

    • applying PEEP to reduce shunt

    • bronchodilators reduce wheeze

    • IV lidocaine to reduce neutrophil response

  • Patient who aspirate must be observed in PACU at least for 2hrs with out:

    • New cough or wheeze

    • Radiograph evidence of pulmonary injury

    • SpO2 decrease > 10% of preoperative values on room air

    • A-a gradient > 300mmHg

Pneumothorax and Flail Chest

  • Closed, communicating and tension

  • Tension:

    • hyposemia

    • increaased airway rpessure

    • tachcardia

    • hyPoTN

    • elevated CVP

    • ultrasound lack of sliding lung and absence of comet tails

    • mediastinal shift

  • DC NO immediately

  • Emergency treatment insertion of 14g angiocath into 2nd intercostal space at midclavicular line or the 4th or 5th intercostal space at the anterior axillary line

  • Flail chest = blunt trauma with multiple rib fractures= paradoxical movement of chest wall a the site of the fractures

    • alveolar collapse

    • hypoventilation

    • hypercarbia

    • and hypoxia

    • Tx= reduce pain= epidural or intercostal nerve block or mechanical ventilation and surgical fixation

Venous Air Embolism

  • Risk due to position: sitting>supine>prone> lateral

  • TEE most sensitive diagnostic tool

  • s/s:

    • observed on TEE

    • millwheel murmur on precordial

    • decreased EtCO2

    • increased EtN2

    • hypotension

    • dysrhythmias

    • hypoxemia cyanosis

    • cardiovascular collapse

  • tx:

    • 100% O2

    • flooding surgical field

    • dc insufflation

    • Durant method- Left lateral decubitus position

    • support with vasopressors, inotropes and IV fluids

Air trapped in the pulmonary circulation decreases left ventricular preload/cardiac output and leads to asystole and cardiovascular collapse

Pulmonary HTN

  • Defined as PaP> 25mmHg

  • avoid increases in PVR:

    • hypoxemia

    • hypercarbia

    • acidosis

    • hypothermia

    • pain

    • SNS stim

    • hypothermia

    • PEEP

    • atelectasis

    • Nitrous oxide

    • ketamine

    • Desflurane

    • mechanical ventilation

  • Decreases PVR

    • increased PaO2

    • hypocarbia

    • Alkalosis hyperventilation

    • spontaneous ventilation

    • prevent coughing straining

    • Inhaled nitric oxide

    • Nitroglycerin

    • PDE inhibitors

    • Prostaglandins PGE1 & PGI2

    • CCB

    • ACE inhibitors

  • Anesthetic considerations:

    • Do not hold prop op meds that reduce PVR

    • CO is fixed pts are sensitive to inadequate preload

    • Treat hypotension aggressively

    • Epidural anesthesia is better tolerated than spinal anesthesia

    • Inhaled nitric oxide

    • High frequency jet ventilation

Elevated RA pressure can open Foramen Ovale causing R-L shunt

Epidural is better than spinal for Pulm HTN

Too much preload can be bad. Uterine contraction push sig amt of blood toward heart and worsen PAH and RV function =Use Nitroglycerin*

Equation PVR= PaP-PAOP * 80/ CO

Carboxyhemoglobin

  • binds on hemoglobin 200x than Oxygen

  • shifts oxyhemoglobin curve to Left starving tissues of oxygen causes metabolic acidosis

  • at risk patients: burn victims, smoker, pts exposed to desiccated soda lime

  • pulse ox cannot measure and give falsely elevated result, need coximeter to diagnose

  • Oxygen administration 100% (until CoHgb <5%) and Hyperbaric oxygen therapy is treatment (if CoHgb >25% of total hgb)

  • Desiccated soda lime risk is greatest with DES>ISO>SEVO

  • Soda lime hydrated 13-15%

  • Desiccated soda lime with Sevo forms compound A and increases risk of fire

Indications for Mechanical Ventilation

  • Strong:

    • Vital capacity <15mL/kg

    • Inspiratory force < 25cm/H2O

    • Pa O2<200mmHg on 100% Fio2

    • A-s gradient> 450mmHg on 100% fiO2

    • PaCO2> 60mmHg

    • Respiratory rate > 40 or <6 bpm

Drug ETT administered NAVEL= narcan, atropine, vasopressin, epinephrine, lidocaine

One lung Ventilation

  • Best predictors for pul complications having pulm surgery

    • FEV1< 40% predicted

    • DLCO < 40% predicted

    • VO2max< 15mL/kg/min

  • Absolute indications for one-lung ventilation:

    • Infection

    • massive hemorrhage

    • bronchopleural fistula

  • Relative indications for one-lung ventilation:

    • Improved surgical exposure

    • pulm edema

    • severe hypoxemia due to lung disease

Left sided tuba is preferred.
Right sided tube used when Left main bronchus has distorted anatomy (tumor TAA) and surgical procedures : left pneumonectomy, left transplant or left sleeve resection
NO DLT for 8< use bronchial blocker or single lumen tube in to the main bronchus
Age 8-9 size 26
Age 10 +28 or 32
Female-35-37
Male- 39-41

Initiating OLV:

  • Fio2 100%

  • Tidal vol 6-8ml/kg/IBW

  • RR 12-15

  • Alveolar recruitment before OLV

  • PEEP 5-10 cm H2O

  • Adjust I:E if exp flow limitation

  • Consider TIVA vs Volatile

Addressing Hypoxemia in OLV

  • Verify 100% oxygen

  • Check position of tube/bronchial blocker via fiberoptic

  • Rule out causes: reduced CO, bronchospasm, mucus plug, pneumothorax of dependent lung

  • Apply CPAP to non-dependent lung or use suction catheter to insufflate oxygen

  • Apply PEEP 5-10 to dependent lung

  • Alt options:

    • Intermittently reinflate the non-depended lung

    • Ligate the pulm art

    • Eliminate drugs the inhibit HPV (Volatiles )

Placement complications:

DLT too far in of correct side= upper lobe not ventilated
DLT not deep enough in trachea= no lung separation
DLT is in wrong bronchus=wrong lung collapses

Bronchial blocker

  • Slow to collapse lung

  • Can contaminate or block ventilation if it slips

  • Can be used in children <8 yrs

  • can insufflate oxygen into non ventilated lung

  • Can be used to suction air from the non ventilated lung

  • Cannot suction blood, pus, or secretions from non ventilated lung

  • Can use with nasotracheal intubation

  • can use with tracheostomy

  • can use with existing ETT

Mediastinoscopy & trachea resection

  • Diagnose lung cancer

  • Most serious complications: 1. hemorrhage & 2. pneumothorax

  • Absolute contraindication = previous mediastinoscopy

  • Relative= Tracheal deviation, Thoracic aortic aneurysm, Superior vena cava obstruction

  • Compression of the innominate artery can impair cerebral perfusion R side of circle of Willis
    The innominate artery is also known as the brachiocephalic artery or brachiocephalic trunk (BCT). It's the first branch of the aortic arch and supplies blood to the head, neck, and upper extremities

  • Place pulse ox or art line on right upper extremity. If the scope compresses the innominate the waveform will dampen or disappear.

  • Place NIBP on LUE to measure BP

  • Large bore IV access PRBC available

  • Associate with Oat cell carcinoma and Eaton Lambert syndrome

    • sensitive to succinylcholine and non depolarizers

  • Indications for tracheal resection include tracheal stenosis, tracheomalacia, tumor and vascular lesions and congenital malformations

  • Reduce tension on the tracheal anastomosis, maintain flexed position for several days after surgery. Use flexible fiber optic if reintubation is needed.

  • Preop trachea resection:

    • asses for airflow limitations

    • Eval CT scan and flow-vol loop

    • If at risk for airway obstruction, preserve spon ventilation (sevo)

    • ETT, jet ventilation, ECMO

    ARDS

  • Non cardiogenic pulm edema

  • Pneumonia most common etiology and sepsis most common extra pulm etiology

  • Caused by inflammation injury mediated by neutrophils and platelets leading to diffuse alveolar destruction

  • Pathology:

    • protein rich pulm edema

    • loss of surfactant

    • hyaline membrane formation

    • possible long term lung injury

CXR reveal B opacities not explained by effusions, lobar/lung collapse or nodules. Diffuse patchy alveolar infiltrates appear peripherally about 12 hrs after initial insult which can lead to alveolar consolidation.
Prone position may improve V/Q matching used in patients with severe ARDS

Strategy for mechanical ventilation:

  • Pressure control

  • low tidal vol 4-6ml

  • PEEP titrate with fio2 below 50% if possible

  • Plateau pressure <30cmH2O

  • RR 6-35 per min ok for permissive hypercapnia

  • I:E ratio 1:1-1:3

  • Target Oxygen goals=PaO2 55-80 or SpO2 88-95%

Conditions associated with difficult airway

Ludwig’s angina-bacterial infection characterized by rapid progressing cellulitis in the floor of mouth. Most significant concern is posterior displacement of the tongue resulting in complete supraglottic airway obstruction.

Best method of securing airway=awake nasal intubation or awake tracheostomy