Respiratory Keywords

CA-0 and CA-1 Split Curriculum

Laryngospasm MechanismMechanism

• Afferent: Vagus Nerve– Superior Internal Laryngeal N

= above cords

– Recurrent Laryngeal N = below cords

• Efferent: Vagus Nerve– Superior Internal Laryngeal N

• lateral cricoarytenoid, thyroarytenoids

– Recurrent Laryngeal N.

• crycrothyroid

Causes

• Light Anesthesia

• Hypocalcaemia

• Vagal Hypertonicity

• Foreign Body

• Secretions

• PPV

• Jaw Thrust

• Lido/Prop

• Sux

• Cricothyroidotomy

Management

Dead Space• Volume of breath that does not participate in gas exchange• Ventilation without perfusion• Physiologic or total dead space = Anatomic dead space + Alveolar dead space• Alveolar dead space = volume of gas within unperfused alveoli

– negligible in healthy, awake patient

• Ratio of physiologic dead space to tidal volume is usually about 1/3

Factors that increase dead space:• GA = multifactorial, including loss of skeletal muscle tone and bronchoconstrictor tone• Anesthesia apparatus/circuit• Artificial airway• Neck extension and jaw protrusion • Positive pressure ventilation (i.e. increased airway pressure)• Upright as opposed to supine (decreased perfusion to uppermost alveoli)• PE, PA thrombosis, hemorrhage, hypotension, surgical manipulation of PA tree• Emphysema (blebs, loss of alveolar septa and vasculature)• Age• Anticholinergic drugs

Anatomic and Alveolar Dead Space

Anatomic Dead Space:

• Volume of gas within the conducting zone

• Oronasopharynx terminal & resp. bronchioles

• Trachea, Bronchus, Bronchioles, and Terminal Bronchioles

• Volume = 2ml/kg of Ideal body weight– 70kg person has ~ 150 ml dead space

Alveolar dead space:

• Volume of gas within unperfused alveoli

• Negligible in healthy, awake patient

• Ratio of physiologic dead space:tidal volume = about 1/3

Obstructive vs. Restrictive physiology on PFTs

Obstructive: low Fev1, low FEV1/FVC ratio, increased RV & normal to increased TLCRestrictive: Low Fev1, low FVC, normal to high Fev1/FVC ratio, low RV & low TLC

Goldman-Cecil Medicine 25th edition, chapter 85 “Respiratory Function: Mechanisms and Testing”by Paul D Scanlon Pages 539-545.

Recurrent Laryngeal Nerve Injury

Causes:• Thyroid and parathyroid surgeries

– 2-5 % during thyroid surgery per Faust. Usually transient, can be permanent– Surgeons can monitor nerve function with Nerve Integrity Monitor (NIM)

tracheal tube positioned at level of the larynx – Usually unilateral more often than bilateral

• Acromegaly – Stretching of the nerve leads to dysfunction• Trauma• Tumor compression• Ortner’s syndrome – cardiovascular disease leading to compression of L

recurrent laryngeal nerveDamage leads to:• Ipsilateral sensation loss• Paralysis of all intrinsic muscles except the cricothyroid muscle. • Can manifests as stridor or dysphonia after extubation

Atelectasis: Intraoperative predictor

• Hypoxemia / hypoxia with reduction in pulmonary elastic recoil – Pressure-volume curve shows static reduction in

elastic recoil & development of a lower inflexion point

• CXR: linear densities in the lung bases, displacement of the fissures toward the area of atelectasis, volume loss

• Lung-US: static air bronchograms

• Be vigilant of risk factors: obesity, duration, lung disease, neuromuscular disease, type of surgery

Ventilator Disconnection Detection

Lost EtCO2? Smelling Vapor? Low pressure alarm?

1. Survey circuit – Y connector, elbow, inflow/outflow hoses, ETT connector

- 70% disconnections occur at Y piece1

- Adding elements (HME) increases likelihood for disconnection2

2. Check distal ventilator - O2 sensor, scavenger tubing, etc.

3. Check CO2 absorbent for cracks

Note: Low pressure alarm only detects frank disconnections with positive pressure ventilation. It may not alarm with misconnections or obstructions.

1. Understanding Anesthesia Equipment. Dorsch, Jerry A, Dorsch, Susan E. 5E p.226.

2. Morgan & Mikhail’s Clinical Anesthesiology. Butterworth, John F. 5E. p.85.

DLTs & Bronchoscopic positioning

Blind DLT placement = 37-48% failure rate

• Entrance into opposite bronchus

• Too deep into bronchus

• Under-insertion

• RUL (w/ R-DLT) occlusion

• LUL (w/ L-DLT) occlusionFOB = increases success

Landmarks

• No herniated bronchial cuff

• 3 orifices in RUL

• LUL and RUL orifices

Pulmonary Vascular Resistance Calculation

• 𝑅𝑒𝑠𝑖𝑠𝑡𝑎𝑛𝑐𝑒 = 𝑃

𝑄

• 𝑃𝑉𝑅 =80(𝑃𝐴𝑃−𝑃𝐴𝑂𝑃)

𝐶𝑂

• PAP = Mean pulmonary artery pressure

• PAOP = Pulmonary artery occlusion pressure

• Units: dyn·s·cm−5

Mechanical Ventilation: Renal Effects

Hemodynamic Effects:- PPV -> decreased preload -> decreased CO -> hypotension -> decreased renal blood flow -> decreased GFR -> AKI- PPV -> compression of mediastinal structures and pulmonary vasculature -> increased RV afterload -> decreased CO -> … -> AKI

Neurohumoral Effects:- PPV -> increased sympathetic tone -> RAAS activation -> decreased renal plasma flow -> decreased GFR -> AKI, NA+ retention- PPV -> decreased preload -> decreased atrial stretch -> decreased ANP -> NA+

retention & oliguria- PPV -> relative intravascular volume depletion -> ADH secretion -> oliguria

Inflammatory Effects:- PPV -> pulmonary tissue trauma -> release of inflammatory mediators (IL-1β, IL-6, IL-8, IL-10, TNF-α) -> AKI

JW Kuiper, ABJ Groeneveld, AS Slutsky, FB Ploetz. Mechanical ventilation and acute renal failure. CritCare Med, 2005. 33:1408-15.JL Koyner, PT Murray. Mechanical Ventilation and the Kidney. Blood Purification, 2010. 29:52-68.

Respiratory Physiology: Aging - Increased stiffness of chest wall and decreased stiffness (increased compliance) of lung parenchyma

- Stiff chest (barrel-shaped 2/2 loss of height and calcification of vertebral column) + flattened diaphragm + loss of muscle mass More susceptible to respiratory fatigue/failure

- Increased compliance of lung parenchyma

- 2/2 loss of elastin

- Small airways lack inherent stiffness and depend on tethering by surrounding tissue to remain open

- Greater lung inflation needed to expand airways and prevent small airway collapse

- Increased closing capacity

- Exceeds FRC in mid-60s

- Exceeds tidal volume with later age

- Reduction in alveolar surface area

- Decline in resting PaO2

- Decrease in ventilatory response to hypercapnia and hypoxia

- Generalized low muscle tone – hypopharyngeal and genioglossal weakness and prediposition to upper airway obstruction

Hypoxic pulmonary vasoconstriction blunted (difficult one-lung ventilation)

- Increase in pulmonary vascular resistance and pulmonary arterial pressure 2/2 decreases in cross sectional area of the pulmonary capillary bed

- Volumes/capacities

- FRC and RV increase

- Vital capacity decreases

• Must be low velocity in smooth surface• Factors affecting: RADIUS OF TUBE, viscosity of

liquid/gas, pressure across tube, length of tube

• Anesthetic implications:– 16g IV (r = 0.6mm) flow rate 220mL/min – 20g IV (r = 0.4mm) flow rate 60mL/min– Old school move to increase flow is cut ETT close to

patient’s mouth

Laminar Flow

Q= flow, P= pressure, r = radius, n= viscosity, L = length

Pulmonary Compliance: Measurement• Compliance: quantification of elastic recoil

(technically, the inverse of elasticity) • CL= Change in Lung Volume / Change in

Transpulmonary Pressure• Where transpulmonary pressure is alveolar pressure

minus intrapleural pressure; the pressure required to keep the lung inflated given its tendency to collapse– Can calculate ΔV as PIP-PEEP (graph below)

• Compliance is decreased in restrictive/fibrotic dz and increased in obstructive dz

• Static (at equilibrium) vs Dynamic (with gas movement, also dependent on airway resistance)

• [Lower Right] S shape: At very high or low lung volumes, the transpulmonary pressure must increase to a higher degree for the same increase in volume

• [Top Right ] Pulm compl. differs from chest wall compl. (Change in chest volume / Change in transthoracic pressure)

Ventilation Monitoring

Continuous CO2 Monitoring• Goals:

– Verify ventilation– Estimate PaCO2

• ETCO2-PaCO2 gradient is ~6mmHg in healthy people who have 2-3% dead space

– Evaluate dead space• Shunting=no effect on ETCO2-PaCO2 gradient• Dead space decreases ETCO2 and increases gradient

• Capnography and capnometry to measure ETCO2• Respirometers to measure TV and minute ventilation

Standard ASA monitor to ensure adequate ventilation of patients during anesthetics…includes qualitative clinical signs (chest excursion, observing reservoir bag, breath sounds, patient color) and quantitative monitors (ETCO2, inspired anesthetic gases)

Inspired Anesthetic Gases• Infrared light used to detect anesthetic agent used and its concentration

Smoking Cessation

• Current smokers have increased odds of MI, stroke, respiratory events, and even death

• Surgery may represent a “teachable moment” for promotion of long-term smoking cessation

• ASA Recommendation: All patients should abstain from smoking for as long as possible both before and after surgery

• Preoperative smoking cessation can reduce postoperative complications, particularly wound and pulmonary

– Short-term (<4 weeks) does not appear to increase or reduce the risk of postoperative respiratory complications.

• 12 to 24 hours is enough to decrease carboxyhemoglobin levels and shift the dissociation curve rightward (increasing oxygen availability to tissues).

• 1 to 2 weeks may be enough to reduce sputum volume

– Long-term (>4 weeks) associated with 20-30% reduction in complications.

Pulmonary Aspiration Management

• Immediate head down and lateral if possible

• Suction oropharynx and trachea

• Intubate PEEP + Lung protective settings

• If unable to intubate must mask to avoid hypoxia, call for help, and further suctioning

• Generally bronchoscopy and lavage are unnecessary• Bronch may be required if there is known aspiration of

large particulate matter

• Prophylactic antibiotics and steroids are not required• If pneumonia develops penicillin and flagyl

• If necrotizing pneumonia Zosyn and getamycin

Subglottic Airway Obstruction

Definition: Blockage of breathing passage due to a disease, disorder, or condition of the area below the vocal cords

Causes:

• Tracheal Stenosis: may be congenital, idiopathic, or acquired– Grade 1: <50% obstruction

– Grade 2: 51-70% obstruction

– Grade 3: 71-99% obstruction

– Grade 4: 100% obstruction

• Tracheomalacia : – Type 1: Congenital, Type 2: Extrinsic, Type 3: Acquired

• Other: Trauma, Aspiration, Croup, Cyst, Abscess, Tracheitis

FRC: Disease-related Changes

INCREASED

• COPD

• Asthma

NO CHANGE

• Spinal/Epidural

DECREASED

• Restrictive lung dz– Sarcoid, IPF, pleural mass

– ALS, MG (decdiaphragmatic mvmt)

– Scoliosis

– Obesity (-> dec chest wall compliance)

• Pregnancy

• Post surgical

• Anesthesia!

• AtalectasisGCR 4/2017

Airway Nerve Blocks

Patrick Millan

Glossopharyngeal Nv• Innervates posterior 1/3 of

tongue, vallecula, anterior surface of epiglottis, walls of the pharynx, and the tonsils

• Can be blocked by topicalization, mucosal contact with soak pledgets, or infiltration

Superior Laryngeal Nv• Branch of CN X• Innervates base of tongue, posterior

epiglottis, aryepiglottic fold, and the arytenoids

• Direct infiltration – thyrohyoidmembrane inferior to the cornu of the hyoid bone bilaterally

Recurrent Laryngeal Nv• Innervates the trachea and

vocal folds• Translaryngeal block – at level

of cricothyroid membrane, needle advanced until air aspirated, then inject anesthetic

• Can also be blocked by topicalization via injection port of bronchoscope

Topicalization• Spray/swish anesthetic onto mucosa of

mouth, nose, pharynx, or tongue• Anesthetic-soaked pledgets/swabs placed on

mucosa and left for 5-15 mins• Local anesthetic added to nebulizer and

inhaled via mouthpiece or facemask for 15-30 mins

Reference

• http://www.nysora.com/techniques/nerve-stimulator-and-surface-based-ra-techniques/head-and-neck-blocka/3022-regional-topical-anesthesia-for-endotracheal-intubation.html

Causes of CO2 Rebreathing

• CO2 Rebreathing – if CO2 is not properly removed from the circular respiratory circuit, the patient will continue to inhale expired CO2, which can result in hypercapnia.

• Causes:

– Exhausted soda lime/Amsorb - Hydroxide salts in absorbent can no longer neutralize carbonic acid (end product of CO2 and H2O). Besides the color change (from changes in pH), a good sign of exhausted absorbent is the canister is no longer warm and no longer undergoing the exothermic neutralization reaction.

– Expired gas bypassing the absorber inadvertently

– Malfunctioning unidirectional valves

– Inadequate fresh gas flow

– Lengthening of the mechanical dead space – Space between the Y-piece and the patient

– Mapleson and Bain systems – Can occur during patient transport, especially when CO2 monitoring is not available. More likely to occur when fresh gas inflow is low

• Bain System – Rebreathing and hypercarbia will occur if the inner FGF tubing becomes kinked

Lung Volumes

Lung Volumes Lung Capacities

Inspiratory Reserve Vol.Inspiratory

CapacityVital Capacity Total Lung

Capacity

Tidal Vol.

Expiratory Reserve Vol. Functional Residual CapacityResidual Vol.

Alveolar vs Dead Space Ventilation

Dead Space

• Volume of a breath not participating in gas exchange– Anatomic – within conducting

zone (trachea, bronchus, bronchioles, terminal bronchioles)

– Alveolar – volume of gas within unperfused alveoli (negligible in healthy, awake patient)

– Physiologic (total) – sum of anatomic and alveolar. Ratio of total dead space to tidal volume is usually about 1/3

Factors that increase dead space:

Hypoxemia: Mechanisms and Diseases

• Hypoxemia vs hypoxia:– Low PaO2 (<80 mild; <60 mod; <40 severe) vs low PO2 of

tissue

• Mechanisms (Diseases)– Hypoventilation: (drugs, OSA, central apneas,

kyphoscoliosis, trauma, splinting, obesity…) – V/Q mismatch: (asthma, COPD, PE, pneumonia,

effusions…)– Shunt (RL) : (TOF, transposition of great vessels, TAPVR,

tricuspid atresia, Eisenmengers syndrome)– Impaired diffusion: (pHTN, pulmonary fibrosis,

emphysema)– Low FiO2: (altitude, Dan Smith as your anesthesiologist)

Factors Influencing Pulmonary Hypoxic Vasoconstriction

HPV = reflex contraction of vascular smooth muscle in the pulmonary circulation in response to low regional partial pressure of oxygen (Po2), and matches lung perfusion to ventilation in patients with lung disease and during one-lung ventilation

Influencing Factors:• Hypoxia (functions best when 30-70% of the lung is hypoxic)• Age (more intense in the fetal and neonatal circulations)• Temp (attenuated by hypothermia, elevated by hyperthermia in animal studies)• pH (alkalemia attenuates; acidemia improves but has no clinical effect)• CO2 (hypocarbia inhibits) • Drugs• IV anesthetic drugs have no effect on HPV• Volatile anesthetics attenuate HPV, however less-so with newer drugs• Other inhibitors: nitroglycerin, nitroprusside, infection, hypocarbia, and

alkalemia