Anesthesia Principles and Practice I: Lecture 6 - Airway Complications Flashcards

Question

What is the effect of beta-blockers in asthmatic patients?

Answer 1

Non-selective beta blockers can cause bronchospasm.

Answer 2

Make sure patient is not light before surgical stimulation. Use caution with Beta-Blockers!!!! Use lowest amount of Beta1 agents (esmolol/metoprolol) Non-selective beta blockers can cause bronchospasm because of Beta2-blocking Inderal, Sotalol, Propranolol Controlled Ventilation during Anesthesia GOAL= Reduce air trapping = prolonged expiration. Reduce- Inspiratory time and RR 6-8 ml/kg TV and PEEP 6-8 cm H2O Gentle recruitment breathes Allow exhalation time before flipping to vent Albuterol to increase expiratory flow Esmolol and Metoprolol may have dose dependent effects on Beta2

Answer 3

Decreased compliance and Increased exhalation * High peak pressures and decreased tidal volume * Upsloping ETCO2 * Decreased/absent waveform if severe * Decreased O2 saturation * Wheezing on auscultation What does it mimic? How do I know? Endobronchial intubation- ↓ breath sounds (usually left side) and deep ETT Pneumothorax- ↓breath sounds, asymmetric chest rise Def consider if high peak pressures are used or in trauma Pulmonary Edema- frothy secretions, crackles on auscultation Kinked/obstructed ETT- Inability to pass suction catheter or remove secretions

Answer 4

* 100% O2 and hand ventilate * Deepen anesthetic Prop and Ketamine bolus or turn up vaporizer * Give 8-10 puffs of Albuterol * Anticholinergics (Glycopyrrolate 0.2 mg) Onset is 20-30 mins Glycopyrrolate gives longer bronchodilation than atropine by inhibiting acetylcholine’s muscarinic effects in airway smooth muscle * Epinephrine (10-50 mcg for refractory bronchospasm) * Magnesium Sulfate (2 g) Magnesium blocks calcium channels in airway smooth muscle, scavenges free radicals, stabilizes T-cells and mast cells, even facilitates endogenous Nitric Oxide release * High-dose glucocorticoids 4-6 hour onset hydrocortisone 100 mg IV or methylprednisolone 60-80 mg IV

Answer 5

Postoperative ventilation may allow for adequate neuromuscular blockade recovery without reversal.

Answer 6

Bronchospasm- can occur when anesthetic level is decreased and NMB is reversed. Airway obstruction, laryngospasm, decreased ventilation and hypoxia can occur Neostigmine- can increase bronchial secretions and lead to broncho, but rare Sugammadex- 2.6% chance of broncho, use with caution in asthma Consider 8-10 puffs albuterol during emergence Lidocaine 1 mg/kg- can decrease reactivity Can also spray lidocaine down et tube, some studies show lidocaine in et cuff prevent cough and throat pain on emergence. Tubes sitting right above carina can hit it as patient raises/flexes head. Super stimulating. Head up position- to prevent atelectasis from decreased FRC

Answer 7

A disease state characterized by airflow limitation that is not fully reversible.

Answer 8

Pros (May Reduce) Coughing Straining Laryngospasm Hemodynamic Stress Cons (An option but not without risk) Patient emerges with unprotected airway- stomach contents and secretions may still be present Bronchospasm can still occur Aspiration can cause bronchospasm Obstruction is very common Never perform in patient anticipated to be difficult mask/reintubation. ***SUCTION IS A GREAT WAY TO SEE HOW DEEP THEY ARE... GOOD MEDICINE IS TO DEFLATE CUFF, OBSERVE VITALS

Answer 9

If nothing bad happened post op course is the same as a regular patient If bronchospasm occurred- post op ventilation may allow for adequate NMB recovery without reversal and return of pulmonary function Post op CPAP may be of use if extubated Incentive Spirometry, bronchodilators, good pain control and early mobilization are key. Epidural anesthesia- should be considered for thoracic, upper GI Sx Prevent splinting, atelectasis, maintain respiratory muscle function Ketorolac- blocks COX-1/2 can cause bronchoconstriction in asthmatics

Answer 10

* Small and large airway disease (Chronic Bronchitis/Bronchiolitis) * Parenchymal destruction (Emphysema)

Answer 11

Most common pulmonary disorder encountered in anesthesia practice Strongly associated with cigarette smoking and has a male predominance. Defined as- disease state characterized by airflow limitation that is not fully reversible.

Answer 12

Presence of productive cough on most days for 3 consecutive months. Defined by- Presence of productive cough on most days of 3 consecutive months. Caused by- cigarette smoking, exposure to air pollutants, occupational dust exposure, recurrent pulmonary infection In COPD disease processes chronic hypoxemia leads to erythrocytosis, pulm HTN, and eventually Right heart failure (Cor Pulmonale) Erythrocytosis- too many RBCs produced to deliver adequate oxygen.

Answer 13

Irreversible enlargement of airways distal to terminal bronchioles, destruction of alveolar septa. Loss of elastic recoil structure results increased closing capacity meaning they close earlier, at higher lung volumes. This is d/t increased muscularity and mucus content making them narrow. Result is hyperinflation and air-trapping Result? Decreased diffusion lung capacity. V/Q mismatch, and impairment of gas exchange. Potential for Chronic CO2 retention and respiratory acidosis. Treatment?- Mostly supportive. Smoking cessation. Inhaled B2 Agonists, glucocorticoids, and ipratropium. Initiate preop incentive muscle training Deep breathing and Incentive spirometry

Answer 14

* Supportive care * Smoking cessation * Inhaled beta2 agonists * Glucocorticoids * Ipratropium

Answer 15

Preoxygenation is key Bronchodilators only improve the reversible bit of airflow obstruction Dynamic hyperinflation (AKA auto PEEP or Breath Stacking)- Can cause volutrauma, hemodynamic instability, hypercapnia, and acidosis. GIVE THESE FOLKS TIME TO EXHALE! DECREASE RR AND I:E RATIO Allowing moderate permissive hypercapnia may help: rightward shift of O2 dissociation curve delivers more O2 to tissues. But not too much! The alveolar gas equation PAO2 = (FiO2 x [Patm-PH2O)-(PaCO2/R) ↑PaCO2 will decrease PAO2 Imagine a patient on room air (0.21 FiO2) at sea level. If their PaCO2 ↑from 40 mmHg-80 mmHg the PAO2 decreases from 100 mmHg to 60 mmHg. A PaO260 mmHg is generally held as the definition of hypoxemia Increased intrathoracic pressures from breath stacking will increasingly worsen hemodynamics as it makes it more difficult for the ventricles to fill and therefore ↓stroke volume O2 titration to sats less than 100% is recommended. Why? O2 Toxicity and a Little bit of Nitrogen helps. 80% FiO2 is where it switches from good to bad with results... Hypoxic Pulmonary Vasoconstriction- Is the most efficient way to alter V/Q ratio to improve gas exchange. High FiO2 delivery counteracts this phenomenon Shunts blood back to poorly ventilated areas, increasing shunt fraction. V/Q mismatch results in hypercapnia from increased deadspace (less perfusion) at well ventilated alveoli Consider Arterial access to assess oxygenation and pCO2. ## Footnote Imagine a patient on room air (0.21 FiO2) at sea level. If their PaCO2 ↑from 40 mmHg-80 mmHg the PAO2 decreases from 100 mmHg to 60 mmHg. A PaO260 mmHg is generally held as the definition of hypoxemia Increased intrathoracic pressures from breath stacking will increasingly worsen hemodynamics as it makes it more difficult for the ventricles to fill and therefore ↓stroke volume

Answer 16

Remember respiratory drive in COPD patients may be more tied to PaO2. A Higher FiO2 will therefore decrease ventilatory drive, ↓Minute Ventilation This impairs hypoxic pulmonary vasoconstriction which make elimination of CO2 less efficient. Blood flow going to poorly ventilated areas, where less CO2 can be offloaded Haldane effect When hemoglobin isn’t carrying oxygen (deoxygenated) it has an ↑ability to carry CO2 Oxygenated hemoglobin has a reduced capacity for carbon dioxide

Answer 17

Can cause volutrauma, hemodynamic instability, hypercapnia, and acidosis.

Answer 18

When deoxygenated hemoglobin has an increased ability to carry CO2. Haldane effect is more related to deoxygenated hemoglobin binding the H+ when carbonic acid (H2CO3) dissociates. CO2 + H20 ⇔ H2CO3 ⇔ H+ + HCO3- Oxygenated hemoglobin frees up protons (H+) to push the above equilibrium towards making more CO2

Answer 19

1:2 ## Footnote This means there are 1 part inspiration to 2 parts expiration.

Answer 20

Divide total time per breath by the sum of the I:E ratio parts ## Footnote For an I:E ratio of 1:2 and 6 seconds per breath, the calculation is 6 seconds / 3 = 2 seconds per unit.

Answer 21

* 2 seconds for inspiration * 4 seconds for expiration

Answer 22

To allow more time for exhalation ## Footnote Patients with obstructive lung disease require extended expiration time.

Answer 23

* 2.5 seconds for inspiration * 7.5 seconds for expiration

Answer 24

It can lead to hypercarbia ## Footnote Reducing minute ventilation too much can result in elevated CO2 levels.

Answer 25

Let’s imagine a patient on a ventilator in the OR with a respiratory rate of 10 breathes/min and I:E ratio of 1:2 (1 𝑚𝑖𝑛)/(10 𝑏𝑟𝑒𝑎𝑡ℎ𝑒𝑠 ) (60 𝑠𝑒𝑐)/(1 𝑚𝑖𝑛) = 6 seconds/ breathe (combined inspiratory & expiratory time) We add together the inspiratory and expiratory ratio parts (1+2=3) and divide them into 6 sec/breathe to figure out how much time to allow for each unit in the ratio. (6/3= 2 sec for each unit of the ratio) Multiplying back out by each term in the ratio gives us 2 seconds in inspiration and 4 seconds in expiration for a RR of 10 and an I:E of 1:2 Folks with obstructive lung disease need more time to exhale, so we could change our I:E to 1:3 With the same RR of 10 we have 6 seconds/4 units in the ratio (1+3) = 1.5 sec for each unit in the ratio Multiplying back out we get 1.5 sec/inspiration and 4.5 sec for exhalation The patient has half a second longer to exhale, without adjusting RR

Answer 26

Let’s assume we changed our I:E to 1:3 but are still seeing breathe stacking on our end tidal CO2 at a respiratory rate of 10. We know from the previous slide that a RR of 10 and an I:E of 1:3 gives a patient 1.5 sec for inspiration and 4.5 sec for expiration on each breathe. What happens if we reduce the RR to 6? (1 𝑚𝑖𝑛𝑢𝑡𝑒 )/(6 𝑏𝑟𝑒𝑎𝑡ℎ𝑒𝑠) 𝑥 (60 𝑠𝑒𝑐𝑜𝑛𝑑𝑠)/(1 𝑚𝑖𝑛𝑢𝑡𝑒)= 10 seconds/breathe ((10 𝑠𝑒𝑐)/𝑏𝑟𝑒𝑎𝑡ℎ𝑒)/(4 𝑟𝑎𝑡𝑖𝑜 𝑢𝑛𝑖𝑡𝑠)= 2.5 sec/unit 2.5 sec for inspiration, a whopping 7.5 sec for expiration So why not just have a super low RR for obstructive patients? At some point reducing minute ventilation will result in hypercarbia

Answer 27

6-8 weeks to decrease secretions and pulmonary complications 12-24 hours- may be enough to decrease carboxyhemoglobin and shift O2 dissociation curve to the right (increasing availability of O2 to tissues.) 1-2 weeks- may be enough to decrease sputum production Smoking decreases wound healing time

Answer 28

* Dyspnea * Morning headaches

Answer 29

Decreased lung compliance with preserved expiratory flow rates Decreased Lung Volumes with preserved expiratory flow rates. ↓Lung Compliance increases work of breathing, so shallow rapid breathing is seen. Preop considerations- no elective surgery with acute disease. Treat fluid overload with diuretics Large pleural effusions may need drained before anesthesia. Abdominal decompression with NG suction, paracentesis of Ascites (will drop their BP, will want to replace with a protein filed fluid, Colloids - in particular Albumin)

Answer 30

* Interstitial lung disease (affects parenchyma) * Causes Scarring and inflammation

Answer 31

Abnormalities of Chest Wall Kyphosis, Pectus Excavatum Pleural Defects Effusion, Trapped lung (restrictive pleural layer) Abdominal Defects Ascites, Obesity, Masses

Answer 32

Myasthenia Gravis Guillain-Barre Amyotrophic lateral sclerosis (AML) Muscular Dystrophy Multiple Sclerosis

Answer 33

High Rate of peri-operative M&M Assess for signs of hypoxemia, hypercapnia, increased work of breathing, difficulty clearing secretions What position worsens symptoms? Supine- diaphragmatic dysfunction RLD- significant Right-sided pleural disease V/Q mismatch strikes again What is the patient’s need for oxygen therapy? Hypoxemia signs- dyspnea, morning headaches Hypercapnia signs- muscle twitching, lethargy, confusion, headache Presence of cardiopulmonary conditions- Pulmonary hypertension, Right heart failure History of Tobacco Use Record from previous hospitalizations Especially ones requiring intubation History of Bleomycin treatment Chemo known for causing pulmonary fibrosis When do I order PFTs? Hypoxemia on RA Serum Bicarb level >33 mEq/L or PaCO2>50 mmHg Hs of respiratory failure Suspected pulmonary hypertension Need to see response to multiple bronchodilators Need to predict function after lung resection ## Footnote These Patients do not do well typically, a pulmonary function test is typically ordred, especially if having a lung surgery.

Answer 34

Supine position ## Footnote This position can impair diaphragmatic function.

Answer 35

* Muscle twitching * Lethargy * Confusion * Headache

Answer 36

If there are signs of hypoxemia on room air or elevated serum bicarbonate levels

Answer 37

Consider careful MAC Dexmedetomidine may preserve respiration and airway patency Neuraxial Effects on respiratory mechanics dependent on motor blockade Peripheral Nerve Blocks Spare phrenic if possible Beware pneumothorax with interscalene and supraclavicular General Anesthesia Head up to preserve FRC IV lidocaine 1-1.5 mg/kg

Answer 38

Sudden hypoxemia due to atelectasis

Answer 39

V/Q mismatch Sudden hypoxemia usually d/t atelectasis Atelectasis =collapsed alveoli This means V=0 , Q likely unchanged This is an example of Pulmonary Shunt Increasing FiO2 to 100% is unlikely to ↑PaO2 in a patient with intrapulmonary shunt Why? The alveoli that are being ventilated are already filled with oxygen The blood from the non-ventilated alveoli won’t aren’t going to pick up anymore oxygen Treatment 5-10 cm H2O of PEEP (High PEEP can decrease Venous Return as well as OTHER THINGS??? LOOK UP) Recruitment breathes Is a mucus plug at fault? -> Tracheal Suction Impaired diffusion Avoid tachycardia- decreased perfusion time and ↓PaO2 Arrythmia More at risk d/t hypoxemia/hypercapnia, acid/base disturbances, increased sympathetic nervous system activity B2 Agonist- tachycardia Correct ASAP Worsening Pulmonary HTN Avoid triggers like hypoxemia, hypercapnia, acidosis, hyperthermia, nitrous oxide, and hyperinflation of lung Be mindful of PEEP and avoid large TV Nitric oxide can help (ITS COUSIN IS NOT GOOD???)

Answer 40

Obstruction of the pulmonary artery or its branches Has many presentations making diagnosis difficult Life-threatening Prompt diagnosis and treatment dramatically reduces M&M Accounts for nearly 100,000 deaths/yr in the US alone. 1/3 or patients that survive initial insult die of a future embolic disease process As the right ventricle gets bigger to try and beat the PE, the left ventricle doesnt have the space to do its job, BP drops

Answer 41

Virchow’s triad- venous stasis, endothelial injury, hypercoagulable state. Most emboli come from lower extremity source Microthrombi that are usually broken down can propagate Who Gets Them? Immobilized patients ICU level patients Pregnant Hx of DVT Hx of CHF or MI Obesity Long bone fracture or surgery Major trauma

Answer 42

Pulmonary Infarct- Dead lung tissue Hemoptysis, Pleuritic pain (pain on inhalation/exhalation) Abnormal gas exchange- alters V/Q ratio Dead Space- impairs perfusion to conducting alveoli, reduces ability to off CO2 CV compromise/collapse with Massive PE- diminished SV and CO Increased PVR leads to impedes R Ventricle outflow causing dilation leads to decreased LV preload RV dilation impinges upon LV which worsens filling, ↓LV Stroke Volume leads to ↓coronary perfusion The RV literally pushes on the LV

Answer 43

CONSCIOUS PATIENT Most Common Dyspnea preceding chest pain, COUGH, symptoms of DVT Patients with large PE may be asymptomatic Patients can have massive CV collapse Hypoxemia CXR: pleural effusion/atelectasis Rales and wheeze on auscultation Tachypnea Calf or thigh swelling Tachycardia UNDER GA Intraop you may see End tidal CO2 decrease precipitously in half (if it is changes slowly, could be other factors???) Tachypnea- in the unparalyzed patient Hypotension and tachycardia Increased PA pressures ECG: ST, bradycardia, asystole, and PEA

Answer 44

* Venous stasis * Endothelial injury * Hypercoagulable state

Answer 45

If suspected check a D-Dimer level Protein fragment made when a clot dissolves CT with Pulmonary Angiography if available. Consider TEE if hemodynamically unstable

Answer 46

1st- Focus on oxygenation and stabilization Supplemental O2 all the way up to ventilatory support and pressors Do not over fluid resuscitate as this can further distend a dilated RV 2nd- Don’t intubate/PPV Can decrease preload and compress RV Thrombolytic therapy may be necessary Streptokinase, urokinase, or Alteplase (t-PA) Anticoagulation- prevents more clots and allows body to resorb active clots faster IV heparin first, then oral warfarin SubQ Low molecular weight heparin may be substituted

Answer 47

PE left untreated can lead to death in as many as 30% of patients Often a complication in a patient with multiple comorbidities

Answer 48

May require IVC filter (Pulmonary Embolism) Less M&M than surgical interventions Used if patient cannot be anticoagulated or if they have ongoing PE despite anticoagulation Percutaneous Insertion under LA through jugular or femoral access. 5% Risk of recurrent emboli, leg swelling may occur

Answer 49

For sub-massive PE (when less than 50% of the pulmonary arterial tree is obstructed) Usually performed in IR

Answer 50

What keeps the pulmonary interstitium and alveoli dry? Plasma oncotic pressure (25 mmHg) higher than pulmonary capillary pressure (7-12 mmHg) Connective tissue and cellular barriers generally do not allow plasma proteins to pass through Lymph System Often caused by Congestive Heart Failure (CHF) Need to be careful about fluid management, typically try to avoid too much crystalloid The pulmonary interstitium is a lace-like support network for the alveoli, like a scaffold, of sorts

Answer 51

Stage 1- Increased fluid transfer into lung interstitium Lymphatic flow usually increases commensurately = no net increase in interstitial volume Stage 2- Lymphatic drainage capacity is exceeded and liquid begins to fill the interstitial spaces around bronchioles and lung vasculature Stage 3- Fluid build-up = ↑ pressure forcing fluid around alveoli. Eventually disrupts tight junction membranes of alveolar membranes

Answer 52

This is a general application of the oncotic (protein) pressure and hydrostatic (water) pressure. Why things move across membranes is important to visualize when we are talking bout such things.

Answer 53

Major causes are ARDS, less often altitude and neurogenic pulmonary edema Can also be from opioid overdose and even over reversal of narcotics with Narcan causing flash pulmonary edema. Narcotic based edema mechanism thought to be related to hypoventilation/cerebral edema. Abrupt naloxone reversal can release a catecholamine surge. ARDS causes permeability of water and protein from intravascular to interstitial space TURP-excessive absorption of electro-lyte free and hypotonic washing solution. TURP- transurethral resection of prostate, this is a side effect of TURP syndrome addressed later in life. Somewhere. PE, eclampsia, TRALI, and acute kidney injury are less likely causes TRALI is Transfusion related acute lung injury, neutrophil (WBC) activation leads to leaky membranes. High altitude Pulmonary Edema- high degree of hypoxic pulmonary vasoconstriction is underlying cause Neurogenic Pulmonary Edema- Sympathetic over-reactivity d/t catecholamine surges shifts blood to pulmonary circulation (TBI, Hemorhage, Grand Mal Seizure)

Answer 54

Potentially fatal cause of acute respiratory failure. Generally seen in acute decompensated heart failure, ie systolic or diastolic impairment Systolic dysfunction- CAD, HTN, Valvular disease, hypothyroidism, toxins, viral myocarditis Diastolic dysfunction- Reduced compliance in diastole d/t LV hypertrophy, acute hypertensive crisis. Hypothyroidism can change cardiac contractility, myocardial oxygen consumption, CO, BP, and SVR

Answer 55

Can result from laryngospasm or other airway obstruction post-extubation. Classic presentation- Young, athletic male presenting with acute upper airway obstruction Upon relief of obstruction- dyspnea, and pink frothy sputum, bilateral infiltrates on Chest X-ray. 0.05-0.1% of all GA with ETT Extubation in Stage 2 is a risk factor 1) Negative intrathoracic pressures, essentially a revere Valsalva. 2) Right heart blood flow increases 3) Pulmonary Vascular bed dilates 4)Interstitial pressure around the capillaries becomes more negative 5) Intravascular fluid is drawn into interstitial space Bronchodilators, CPAP, and Diuretics are treatment. ## Footnote Typically young, athletic male, who gets light, bites down on tube, and takes big deep breath (has the muscle mass to create that pressure)

Answer 56

* Assess respiratory effort * Administer oxygen * Reduce preload with diuretics * Use anti-inflammatories - glucocorticoids, statins, prostaglandin E1 * Vasodilators- Nitric Oxide, prostacyclin * CPAP- may limit decrease in FRC, improve respiratory mechanics, and decrease afterload

Answer 57

Can lead to death in as many as 30% of patients

Answer 58

Focus on oxygenation and stabilization

Answer 59

5% risk of recurrent emboli and leg swelling

Answer 60

Young athletic male with acute upper airway obstruction

Answer 61

* Stage 1: Increased fluid transfer into lung interstitium * Stage 2: Lymphatic drainage capacity exceeded * Stage 3: Fluid build-up disrupts alveolar membranes

Answer 62

Catheter-Assisted Pulmonary Embolectomy

Answer 63

Cardiogenic Pulmonary Edema

Answer 64

Noncardiogenic Pulmonary Edema

Answer 65

Anesthesia for patients with interstitial lung disease

Answer 66

Diagnosis of the nonpregnant adult

Anesthesia Principles and Practice I: Lecture 6 - Airway Complications Flashcards

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