Supporting Excellence in Nurse Anesthesia

• Human Physiology and Pathophysiology

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4

Pathophysiology and their

Anesthesia Management

Instructor: Paul Bennetts, PhD, CRNA

• I have no conflicts of interest.

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6

• Recognize / describe physiological and pathophysiological

respiratory events related to

• Obstructive lung diseases,

• Restrictive lung diseases,

• Pulmonary embolisms,

• Mediastinal masses,

• Acute respiratory distress syndrome (ARDS),

• Bronchospasm and

• Tension pneumothorax

• Manage anesthetics for patients with these disorders in

accordance with evidence-based practices.

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8

Emphysema, Chronic Bronchitis,

Asthma and Bronchospasm

• Pulmonary dysfunction marked by persistent airflow limitation

(outflow) in conducting airways

• 100,000 deaths per year in U.S.

• Not fully reversible

• Progressive in course

• Inflammatory response

• Types of COPD

• Emphysema

• Chronic Bronchitis

• Asthma

9

2

1

• Emphysema is characterized by an abnormal

permanent enlargement of air spaces distal to the

non-respiratory bronchioles

• Destruction of alveolar walls without obvious fibrosis

• Epidemiology

• Prevalence: 10% of the U.S. population

10

2, 3

• Etiology

• Principal causal factor is smoking

• May be result of α1- protease inhibitor deficiency

• Other environmental factors

• Exposure to chronic dust or chemical fumes

• Pathogenesis

• Destruction of lung elastic tissue

• Loss of surrounding supporting structures

• Small airway collapse resulting in obstruction to flow of air out of

the alveoli during exhalation

11

2, 3

2, 3

• Pathogenesis

• Protease (enzymes) secreted by alveolar macrophages and

neutrophils sequestered in pulmonary capillaries destroy

elastic fibers in the alveoli

• Inflammation results in ↑’d release of proteases &

recruitment of more neutrophils and macrophages

• α1- antitrypsin is an anti-protease (inhibits)

• Oxidative stress from smoking or other irritants

results in injury that inhibits α1-AT activity

12

13

• Higher levels of protease relative to α1-AT results

in elastic connective tissue destruction

• Outcomes:

• Increased compliance / diminished recoil

• Premature collapse of airways during expiration

• Destruction of alveolar septa with loss of septal walls

• Enlarged alveoli/airspaces

• Destruction of alveolar capillary walls

• Reduction in gas exchange surface area

14

• Centriacinar (Centrilobular):

• Commonly found in smokers

• Respiratory bronchioles are affected

• Distal Acinar (Paraseptal):

• Distal alveolar sacs are affected

• Emphysematous bullae

• Panacinar (Panlobular):

• Genetic (α1-antitrypsin deficiency)

• Both alveoli &respiratory bronchioles

15

2, 3

• “Barrel chest” appearance due to remodeling of the thorax from increased compliance and loss of recoil

• Chest x-ray – hyperinflation, with flattened diaphragm

• Dyspnea, little sputum production

• Individuals with genetic α1-AT develop emphysema at a younger age and particularly if they smoke

• At risk for development of pulmonary hypertension

• Probably due to vascular remodeling and not hypoxic vasoconstriction

16

17

Normal Emphysema

18McPhee & Hammer, p. 232, Fig. 9-20

Outflow obstruction

3

• Chronic bronchitis: chronic cough associated with

sputum production for more than 3 months of the

year for 2 or more consecutive years.

• Epidemiology: approximately 5.5% of U.S. adults

• 20-25% of men 40- to 65-years-old

• More common among smokers and urban-dwelling

adults

19

• Etiology: Tobacco smoke is a major factor

• Air pollutants

• Occupational exposures

• Previous infections

• Pathogenesis: Irritation results in inflammatory process

in the larger airways with mucosal thickening from

hypertrophy and hyperplasia of mucus glands &

goblet cells in the bronchi

• Mucus gland hypersecretion, resulting in airway narrowing

(obstruction) and secondary infection

20

• Lumen narrowing

• Further infiltration of the mucosa with inflammatory cells

→ more inflammation & narrowing

• Impaired clearance of airway secretions

• mucus plugging & infections

• Results in further bronchiolar inflammation:

wheezes, cough, thick sputum

21

• Pulmonary function testing

• Decreased expiratory flow (narrowed airways)

• Reduced FEV1 and FEV1/FVC (FEV1% ratio)

• Air trapping with increased RV

22

• Complications of chronic bronchitis

• Can be complicated by pulmonary hypertension and

cardiac failure

• Risk for the disorder to progress to the small airways

(bronchiolitis)

• Ongoing inflammation & fibrosis leads to obliteration of

bronchioles

23

• Exercise tolerance usually correlates well with

pulmonary function testing (PFT)

• PFTs do not reliably predict PPC

• Principals of medical management (mild to

moderate disease):

• Prevention, vaccination, pulmonary rehabilitation, long-

acting bronchodilators

• Severe disease → the patient may be on

corticosteroids and supplemental oxygen

24

1, 7

• Chest x-rays and CT chest only useful to rule out active infection or other disease (carcinoma)

• Not useful for routine screening

• ECG to detect right heart strain

• Patients with poor exercise tolerance should be evaluated for presence of coronary disease

• Routine labs of limited benefit

• Hypoxemia / hypercarbia (ABGs)

• Malnutrition (↓ albumin)

• Polycythemia (↑ Hgb /Hct)

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1

• Goal in anesthesia management: prevent PPC

• Pneumonia, COPD exacerbation, bronchospasm, or

respiratory failure

• Smoking is well-defined risk factor for post-op

pulmonary complications (PPC)

• Smoking cessation has been shown to ↓ PPC

• No improvement in risk in patients who quit 2 to 4 weeks

before surgery

• Best benefit to reduce PPCs was quitting 8 weeks prior

26

• If possible, consider neuraxial techniques,

peripheral blockade or general anesthesia without

endotracheal intubation (i.e. LMA) as first-line

choices

• Review of over 100 randomized clinical trials suggests

decreased incidence of mortality, PPC & post-op cardiac

complications with regional anesthesia (RA) techniques

• A few studies did fail to show significant support for

epidural anesthesia/analgesia over GA

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9

• Hausman et al. evaluated 2,644 matched pairs to determine benefits of RA for COPD

•Overall, GA patients had higher overall morbidity, including PPC

•Non-pulmonary complication rates were similar

• Epidural did not provide significant protection over GA, however spinal and peripheral anesthesia techniques did

• Improved outcomes not extended to patients with dyspnea at rest

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9

• Presence of residual neuromuscular

blocking agents is a predictor of PPCs in

patients with COPD

• NMBDs should be used judiciously

• Short acting agents preferred

• Careful neuromuscular monitoring

• (Quantitative versus qualitative monitors)

• Full reversal of neuromuscular blockade prior

to extubation

• Sugammadex?

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8

• Oxygen management in the COPD patient

• Higher FiO2 (100%) associated with reabsorption

atelectasis and increased O2 radical production

• FiO2 of 80%: less atelectasis (nitrogen splint)

• FiO2 of 60%: absorption atelectasis limited

30

• Fast-track tracheal extubation

• Avoidance of prolonged intubation / ventilation

• Effective pain relief critical for rapid recovery

• Concern with central effects of opioids as the sole

intervention for pain relief

• Use of regional techniques, catheters and long-acting

drug preparations such as liposomal local anesthetics

(Exparel)

• Multimodal analgesia: NSAIDS, IV acetaminophen

31

• Reactive airway disease (RAD) is highly relevant to

anesthesia providers because it may lead to

perioperative bronchospasm

• Commonly associated with asthma

• Frequently a lifelong condition

• Most common chronic respiratory disease

• Incidence of asthma up to 20% in westernized populations

(4 – 11% in the U.S.)

• Male > females

32

• Common cause of airway reactivity especially in

industrialized countries

• Asthmatics demonstrate variable degrees of airway

inflammation and remodeling

• Characterized by infiltration of eosinophils, mast cells and T-

helper lymphocytes into the peripheral airways

• Airway remodeling related to:

• Thickening of epithelial basal membrane

• Smooth muscle hypertrophy

• Hypertrophy of mucous-secreting goblet cells

33

2, 3

• Atopic (70%) – due to allergen sensitization

• Genetic predisposition to type I hypersensitivity

• Usually begins in childhood

• Often a positive history of asthma in the family

• Non atopic (30%)

• Pulmonary infection/viruses

• Environmental pollutants

• Stress, exercise

34

• Atopic individual

• Inflammatory response to allergen → type 2 helper T

cells (Th2) secretes

• IL-4 → stimulated B cells to produce IgE

• IL-5 → stimulates eosinophilic activity

• IL-13 → stimulates mucous production and promotes B cell

production of IgE

35

• Non-atopic individual

• Initial sensitization → Pulmonary infection/virus,

environmental pollutants, stress or exercise

inflammation of respiratory mucosa → lowers threshold

of response to irritants

36

• Immediate Phase Reaction (minutes)

• Antigen induced cross-linking of IgE activation of

mast cells on the respiratory mucosa

• Release of histamine and other substances which produce

prostaglandins and leukotrienes

• Opens mucosal intercellular junctions allowing

penetration of antigen to mucosal mast cells

37

• Vasodilation and increased vascular permeability

• Activation of more mast cells along the vascular walls

• Stimulates autonomic/other receptors resulting in

bronchoconstriction

• Edema (furthering airway narrowing)

• Smooth muscle contraction

• From activation of vagal nerve receptors and release of

leukotrienes

38

• Recruitment of additional inflammatory cells including

neutrophils, monocytes, lymphocytes, basophils and

particularly eosinophils to airway mucosa

• Mucus production → narrowing/airway occlusion

39

• Late phase reaction (2 – 24 hours)

• Inflammation and continued recruitment of eosinophils

• Results in injury to bronchiolar epithelium, increased penetration

of antigens to submucosal mast cells

• Secretion of cytokines:

• Growth and activation of mast cells & eosinophils

• Perpetuated inflammatory response

• Promotes IgE production in B cells

• Smooth muscle proliferation

40

• Long standing inflammation leads to:

• Damaged bronchial epithelium

• Diffuse luminal obstruction

• Hypersecretion of mucous

• Mucosal edema

• Thickened basal membrane

• Smooth muscle hypertrophy, remodeling

• Increase in interstitial collagen, submucosal fibrosis

41

• Reduced gas exchange leads to V/Q mismatch

• Outflow obstruction leads to air trapping, dynamic

hyperinflation and hypercarbia

• Expiratory wheezing

• Children are at increased risk of morbidity and

mortality from asthmatic obstruction due to smaller

airway diameters

42

• Surgery produces pro-inflammatory cytokines

• Higher levels in asthmatics may predispose them to

adverse events

• Reduction in ability to cough and mucociliary action

predisposes the asthmatic to problems

• Surgery site: closer to diaphragm = increased

respiratory complications

• Duration of intubation correlates with respiratory

complications

43

• Other Pharmacologic Adjuncts:• IV lidocaine before induction: not been demonstrated in

studies to be of benefit, however lidocaine 5 min. after induction did reduce airway resistance in patients with asthma

• Ketamine (bronchodilator) has been used to treat acute asthma, but data are insufficient

• Magnesium sulfate 1.2 - 2 Gm IV over 20 minutes has been reported in emergency treatment of bronchospasm

• Magnesium may promote bronchial smooth muscle relaxation

• Studies recommended

44

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12

• Patients undergoing general anesthesia may develop

bronchospasm for multiple reasons

• History of respiratory disease

• Reaction to medications or contrast dye

• Spontaneous, possibly due to airway stimulation by

instrumentation secretions or aspiration

• Inadvertent esophageal or endobronchial intubation

• Inadequate depth of anesthesia

45

• Severe perioperative bronchospasm in asthmatics

reported in 0.17 - 4.2% of all general anesthetics

• Some estimates as high as 20%

• Asthmatic children can be especially prone to bronchospastic

events

• Also a common symptom of anaphylaxis (present in

19% of events)

• Especially related to the administration of water soluble

radiographic contrast media

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13

• Mechanical: Tracheal and laryngeal sensory afferent

stimulation with efferent activation of vagal fibers

(parasympathetic)

• Anaphylactoid: Nonimmune-mediated medication

reaction

• Mast cell degranulation & histamine release

• Anaphylactic: Immune-mediated (IgE) reaction

• Also mast cell degranulation

47

• Idiopathic (airway manipulation) (55%)

• Especially laryngoscopy

• Allergy / anaphylaxis (21%)

• Esophageal intubation (12%)

• Aspiration (12%)

• Endobronchial intubation (2.5%)

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14

• Induction of anesthesia

• Airway irritation (oral airway, laryngoscopy, misplacement of

ET tube)

• Anaphylaxis

• Aspiration

• Maintenance of anesthesia

• Anaphylaxis

• Migration of ET tube

• No defined reasons

• Aspiration associated with the use of LMA

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14

• Emergence from anesthesia and recovery

• No defined causes

• Pulmonary edema

• Extubation

• Anaphylaxis

50

• Induction

• Increased ventilation pressures

• “Bronchospasm” with wheezing

• Low oxygen saturation

• Changes in capnography ( ↑ EtCO2, prolonged expiration)

• Maintenance

• Increased ventilation pressures

• Low oxygen saturation

• “Bronchospasm” with wheezing

• Reduction in tidal volumes

51

• Emergence and Recovery

• Low oxygen saturation

• “Bronchospasm” with wheezing

52

• Anaphylaxis/allergic reaction

• Latex, blood or fluid replacements

• IV administration of beta-blockers

• Irritation or secretions

• Pneumothorax

• Inadequate depth of anesthesia / failure of anesthetic

delivery system

• Bronchial obstruction

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• Increase FiO2 to 100% until spasm abates

• Cease stimulation or surgery

• Request assistance

• Deepen anesthesia (Propofol)

• Check tube position

• If LMA in place, consider possibility of aspiration

• Treat with beta-2 agonist

• Epinephrine (IV) 1 mcg/kg bolus

• Albuterol (salbutamol)

• Chest x-ray if not resolving

54

• Epinephrine 1 mcg/kg IV bolus

• 0.7 to 1 ml of 1:10,000 solution for 70-100 kg patient

• Albuterol (salbutamol)

• Metered dose inhaler 2 puffs (can be repeated)

• Nebulized in-line 0.5% solution, 1 ml in 3-5 ml NS

• 0.5% 0.1ml in 1 ml NS via ET tube

• Ipratropium bromide via inhaler (2 puffs) or nebulizer

(0.25 – 0.5 mg)

• Repeat twice, 20 minutes apart

55

• IV Corticosteroids (hydrocortisone 2-4 mg/kg)

• IV albuterol for adults and children > 12

• Bolus 3.5 mcg/kg over 5 - 10 minutes, infusion rate 0.04 -

0.29 mcg/kg/min

• IV Aminophylline – in severe asthma may improve lung

function over inhalers and steroids alone, but increases

risk of PONV

• Loading dose 4.6 - 6mg/kg over 20-30 minutes

• Maintenance 0.4 - 0.9 mg/kg/hr based on serum levels

• No differences between Aminophylline and IV beta-2s

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15

• Magnesium Sulfate either nebulized or intravenous

may also be of benefit

• Magnesium deficiency a risk factor in asthma

• MgSO4 has smooth muscle-relaxant effects, probably via

inhibition of calcium influx into muscle cells similar to calcium

channel blockers

• Other possible mechanisms include mast cell stabilization and

increased beta-receptor affinity

• Nebulized magnesium less effective for children

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Chronic Interstitial Parenchymal Diseases,

ARDS and Tension Pneumothorax

• Definition: Conditions that interfere with normal

lung expansion during inspiration

• Increased elastic recoil of lungs or chest wall

• Decreased compliance

• Decreased lung volume

• Total lung capacity below 5th percentile

• Other ventilation abnormalities

• Impaired diffusion

• V/Q mismatch

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• Classification of restrictive diseases

• Acute intrinsic

• Pneumonia

• ARDS

• Chronic intrinsic (Diffuse parenchymal disease)

• Idiopathic interstitial pneumonias

• Granulomatous diseases (including sarcoidosis)

• Environmental or toxin-induced, autoimmune

• Chronic extrinsic (conditions that inhibit normal excursion of the lungs)

• Traumatic injury (tension pneumothorax)

60

• Definition: ARDS is a clinical syndrome caused by

diffuse capillary and epithelial damage resulting

in increased permeability followed by interstitial

and alveolar edema

61

• Direct lung injury

• Pneumonia

• Aspiration

• Pulmonary contusion

• Fat embolism

• Near drowning

• Inhalational injury (burn victim)

• Reperfusion injury after lung transplantation

62

• Indirect lung injury (associated with a systemic

process)

• Sepsis

• Severe trauma with shock

• Cardiopulmonary bypass

• Acute pancreatitis

• Drug overdose

• Transfusion reaction

• Uremia

63

• Dyspnea

• Increasing Hypoxemia - Low V/Q

• Late hypercapnia

• Decreased compliance

• Development of infiltrates

• Increasing CXR opacity

• At least 30% to 40% mortality rate

64

• Direct or indirect lung injury

• Severe injury to alveolar epithelium

• Increased vascular permeability – fluids & proteins leak

from the pulmonary interstitium into the alveoli

• Alveolar flooding / loss of gas diffusion capacity

65

• Both pathways lead to:

• Activation of neutrophils and macrophages

• Capillary inflammatory response

• Release of cytokines and phospholipids from endothelium

• Reactive oxygen species, proteases

• Prostaglandin metabolites promote constriction of both airways and pulmonary vasculature

• Thromboplastin-triggered coagulopathy

• Microemboli → alveolar hypoxia, hypercapnia

• Damage to type II pneumocytes → surfactant abnormalities

66

• Increased pulmonary vascular resistance +

decreased compliance requires aggressive positive

pressure ventilation

• Increased workload on the right ventricle

• Right ventricular dysfunction → cor pulmonale

• 25% of cases

• Right to left shunt if patent foramen ovale is present

67

• Blum et al. reviewed 50,367 patient admissions

and identified specific preoperative risk factors

(decreasing order)

• ASA ≥ 3 (strongest risk factor)

• Emergent surgery

• Renal failure

• COPD

• Male gender

• Multiple anesthetics during the admission

68

• Intraoperative risk factors:

• PRBC transfusions

• Crystalloid administration

• Ventilator drive pressures

• Tidal volume not significant

• Large tidal volumes (pressure) should be avoided

• FiO2 (small effect)

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18

• Intraoperative fluid therapy

• Fluid-induced lung injury

• Surgery patients with respiratory failure who received > 20

mL/kg/h were 3.8 times more likely to develop ARDS than

patients who received < 10 mL/kg/hr

• Goal directed fluid therapy with NICOM or PPV

70

• Supportive

• Correct hypoxemia (FiO2 and PEEP)

• Inotropic support

• Afterload reduction

• Corticosteroids

• Inhaled nitric oxide to control PA pressures

• Exogenous surfactant

• Extracorporeal membrane oxygenation (ECMO)

71

• Careful evaluation of cardiac, pulmonary & renal

status

• Judicious fluid replacement (avoid overload)

• Prevent IV entrainment of air (PFO)

• Risk of right to left shunt

• Monitoring should include invasive arterial and cardiac

output if available

• Transesophageal echo to evaluate RV function

• Protective lung ventilation (PLV) strategies

72

• Close attention to peak inspiratory pressures and

use of PEEP

• Objective: reduce atelectasis, promote alveolar

recruitment & avoid right ventricular overload

• “Permissive hypercapnia” to limit airway pressures

• Goal-directed strategy: Maintain target pH or PaCO2

while providing optimal lung protection

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• Maintain target pH or PaCO2

• Use of higher PEEP to keep alveoli open and ensure

oxygenation at lower FiO2

• Lung protection

• Avoid barotrauma by using smaller volumes

• (VT ≤ 6 ml/kg)

• Limit plateau pressure to ≤ 30 cm H2O

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19

• Lung protective ventilation is insufficient – so what

now?

• Recruitment maneuvers: transiently increasing trans-

pulmonary pressures to recruit collapsed alveoli

• Airway Pressure Release Ventilation (APRV)

• High frequency oscillatory ventilation (HFOV)

• Inhaled pulmonary vasodilators

• Extracorporeal membrane oxygenation (ECMO)

• Prone positioning

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• Sigh: VT or PEEP increased to a pre-specified plateau

pressure for one or several breaths per minute

• Sustained pressure: Airways pressurized and

maintained for a specific duration

• i.e. 40 cm H2O for 5 - 40 seconds or progressive increases in

PEEP

• Watch for hemodynamic instability

• Benefits of RMs limited to short term improvement in

oxygenation

• Survival rates unaffected

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21

20

• Blood diverted from the patient and oxygenated

externally

• Controlled trial results were favorable but suffered from lack

of standard methods of ventilation in the control group

• “Last resort” in the management of ARDS

• Complications of ECMO:

• Bleeding,

• Thromboembolism,

• Vascular damage from cannulation

• Heparin-induced thrombocytopenia

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• Heterogeneous group of pulmonary disorders characterized mainly by bilateral involvement of the lung connective tissues

• Categories

• Fibrosis

• Idiopathic interstitial pneumonias

• Environmental (exposure to asbestos, silica, coal dust)

• Collagen-vascular disease (scleroderma)

• Granulomatous

• Sarcoidosis

• Hypersensitivity pneumonitis (exposure to mold, dust)

78

• Primary characteristics: infiltration of inflammatory

cells & production of fibrous tissue leading to

decreased compliance & hypoxia

• Initial injury → activation of leukocytes

• Eosinophils, macrophages, neutrophils, immune cells accumulate

in alveolar walls & spaces

• Release of pro-inflammatory cytokines

• Leukocytes secrete proteases

• Damage to alveolar epithelia and connective tissues

• Macrophages activate fibroblast proliferation

• Connective tissue cells – collagen deposits

79

• Injury to Type I alveolar epithelial cells (removed by apoptosis)

• Type I cells replaced by abnormal type II cells

• Decreased production & turnover of surfactant

• Recruitment of inflammatory cells

• Production of more fibroblasts, deposition of collagen and elastin

• Alveolar destruction/distortion with widespread fibrosis

• Destroyed pulmonary vasculature / pulmonary hypertension

• Disrupted capacity for gas exchange

• Increased lung elastic recoil and decreased compliance80

• Intermittent, irritating non-productive cough

• Dyspnea, tachypnea, inspiratory crackles

• Clubbing of the digits

• Increased work of breathing

• Decrease VT offset by increased rate

• Abnormal blood gas values

• Lowered PaO2 due to thickened alveolar wall = ↓ diffusion

capacity

• Initially lower PaCO2 due to tachypnea (increased in later stages

due to increased work of breathing and hypoventilation)

81

• Chest radiography: Small volume, increased density,

honeycombed appearance

• Alteration in pulmonary function

82

• Meticulous pre-op evaluation

• 90% of GA patients will develop atelectasis

• 10 to 30% will experience PPC

• RLD prevalent in older patients

• Most important is a quality of life evaluation

• Focus on activity levels

• Ability to climb 2 flights without dyspnea is associated with

lower risk

83

• PFTs may be useful but have less of a role in

predicting PPC

• FEV1 > 40% associated with fewer PPC

• ABGs useful as baseline for patients with respiratory

disease

• Limited value for risk stratification

• Radiography useful in diagnosis of causes of

dyspnea

84

1

• Patients with RLD at risk for exaggerated

pulmonary dysfunction post-op

• Few EBP perioperative recommendations for

patients with RLD

85

• Honma et al. (2007) published a single case report

about perioperative management of a 68 year old

patient having low anterior resection of rectal CA

• H/O chronic interstitial pneumonia, FVC = 44% pred

• Anesthesia with combined spinal/epidural

• Spinal at L3-4; epidural catheter placed at T 10-11

• Combination of lidocaine and fentanyl

• Propofol IV for sedation (total 550 mg in 4 hours)

86

23

• Honma continued:

• Patient did well initially following resection

• Day 10: re-operation for anastomotic leak

• GA/endotracheal tube with minimal FiO2 (30%)

• No anesthesia-related problems with this surgery

• Recommendations:

• Neuraxial / regional anesthesia when possible

• Low FiO2 if GA required

• High FIO2 may exacerbate chronic interstitial pneumonia

87

88

• Spontaneous pneumothorax – may be

• Primary (no history of respiratory disease)

• Secondary (due to pre-existing disease)

• Traumatic pneumothorax

• Penetrating (stab or gunshot wounds)

• Blunt (often due to rib fractures)

• Surgical or procedural complication

89

• Frequently due to pulmonary bullae

especially at the apex of the lung

• Greater negative pleural pressures at

the lung apex in tall individuals result in

larger gradient in pleural pressures

within the thorax

• May stimulate development of sub-

pleural blebs

90

• Patient with pre-existing lung disease

• Most commonly COPD (70% of cases)

• Necrotizing pneumonia

• Lung cancers

• Tuberculosis (in endemic areas) is common cause

• Age > 55

• More severe symptoms than primary

• Great co-morbidities

• Higher mortality

91

• Pneumothorax occurs when lung is pierced

• May be caused by to surgical or procedural

interventions

92

• Laparoscopic cholecystectomy

• Colonoscopy with polypectomy

• Carotid endarterectomy

• Transthoracic needle biopsy

• Interscalene block for shoulder surgery

• Thoracic epidural placement

• Placement of central lines (subclavian approach)

• Local anesthesia injection into the chest wall (intercostal block)

93

• Have been reported during both intra- and extra-

peritoneal laparoscopic procedures

• Veress needle insertion, trocar insertion, CO2 insufflation

or gallbladder dissection

• Tracking of insufflated CO2 around the aortic and

esophageal hiatuses of the diaphragm into the

mediastinum with rupture into intra-pleural space

• Congenital diaphragmatic defect?

94

• Associated with substantial rate of mortality

• Diagnosis may be delayed or missed

• Failure to diagnose and treat tension pneumothorax

markedly increases likelihood of a fatal outcome

• Presentation differs between spontaneously

breathing individuals and those receiving positive

pressure ventilation

95

96

Mechanically ventilated patients have increased intra-pleural pressures

throughout the respiratory cycle, leading to hypotension and cardiac arrest

97

Pneumothorax

Tracheal and

Mediastinal

Shift

98

Right Lung

Re-expanded

• Symptoms: chest pain, dyspnea

• Physical signs: respiratory distress, tachypnea

• Decreased breath sounds (58%)

• Hyperresonance to percussion (26.7%)

• Contralateral tracheal deviation (17.9%)

• Subcutaneous emphysema (10.5%)

• Jugular venous distension (4.7%)

• Elevated CVP

99

• Cardiovascular signs:

• Tachycardia (HR > 100) (43%)

• Hypotension (MAP ≤ 60 mmHg) (16.3%)

• Bradycardia (HR < 60) (5.8%)

• Cardiac arrest (2.3%)

• Conclusion: Key signs of tension pneumothorax (awake

patient) appear to be chest pain, dyspnea,

tachycardia and decreased breath sounds

• tracheal deviation and hypotension less common

100

• Initial Signs:

• Need for increased FiO2 (86.6%)

• Decreased breath sounds (45.4%)

• Subcutaneous emphysema (30.9%)

• Hyperresonance (8.3%)

• Cardiovascular

• Hypotension (66%)

• Tachycardia (30.9%)

• Cardiac arrest (28.9%)

• Most common dysrhythmia was PEA (75%)

101

• Emergent CXR in a monitored setting is desirable but may not be feasible in the OR setting• Sensitivity of chest x-ray is as low as 36-48%

• Upright A&P chest x-ray seldom possible

• CT scan best but not possible in most ORs

• Ultrasonography a superior choice for OR• Readily available

• 80 to 90% sensitivity (supine chest x-ray only 50%)

• Can be done at bedside or in operating room

• Recommend Wilkerson & Stone, (2009) or Kline et al., (2013)

102

25, 26

• Ventilated patients with tension pneumothorax can

progress to symptoms of hypotension or cardiac

arrest often within minutes of first clinical

presentation

• Early recognition and intervention is important

• Confirmation with either chest x-ray or ultrasound if

readily available and patient is stable, but treatment

should not be delayed in the absence of diagnostic

reassurance

103

• If radiography or ultrasonography not available, or if

patient is deteriorating:

• Decompression as soon as tension pneumothorax is suspected

is the mainstay of treatment

• Chest tube thoracostomy if trained personnel present

• Alternative # 1: large bore (14 ga.) sheathed catheter over

a needle is acceptable temporary intervention

• Alternative # 2: Trans-diaphragmatic use of laparoscopic

trocars for chest decompression has been reported by Hatch

in 2014

104

27

• Traditionally, placement recommended at 2nd

intercostal interspace (ICS), midclavicular line

105

• Laan et al. (2015) suggest alternate locations at either

the 4th or 5th ICS, anterior or mid axillary lines

106

26

107

• Problems with needle decompression

• Higher failure rate than tube decompression

• Does not relieve tension pneumothorax physiology

• Subject to kinking and obstruction

• Prone to dislodgement

• 14 gauge catheters are sometimes ineffective due to

insufficient length (5 cm.)

• Needle length of at least 7-8cm has been recommended

108

29, 30

109

• Readily available in laparoscopy trays

• Rigid catheter with blunt trocar

• Overcomes kinking problems of plastic catheters or

lack of sufficient length

110

29

111

Pulmonary Embolism and Anterior

Mediastinal Masses

• Definition: Blockage in the one or more branches of

the pulmonary arteries by a substance that has

migrated from elsewhere in the circulation.

• Types of Embolism

• 95% Are venous thrombi from lower extremities

• Air, fat, amniotic fluid, septic emboli

112

Pulmonary

emboli

• Hereditary: Deficiencies of antithrombin, Protein C, Protein S and Factor V Leiden

• Acquired: older age, cancer, ↓ mobility, acute illness (CHF), IBD, nephrotic syndrome, trauma, SCI, obesity

• Virchow’s Triad: venous stasis, endothelial dysfunction, hypercoagulability

• Medications: heparins, HRT, oral contraceptives, chemotherapy and antipsychotics

• Surgery: “major,” trauma, joint arthroplasty, general anesthesia (in contrast with neuraxial)

113

32, 33

• PE responsible for between 150K and 200K

deaths per year in the U.S.

• In fatal PE, death usually occurs within one hour

• Higher risk of PE in hip fracture repairs

• Probably R/T distortion of the femoral vein during the

procedure

• Mortality can be as high as 12.9%

• Much lower if patient receives anticoagulant prophylaxis

• Increase in reports of PE probably due to

greater detection with spiral CT

114

32, 34

• If underlying cause still present, a patient with PE has

a 30% chance of a second embolus

• There is a 5-fold increase in the incidence of PE during

and after surgery

• 0.3 to 1.6% of the general surgical population

• Acute inflammatory reaction R/T tissue trauma

• Activation of clotting cascade

• Immobilization and venous stasis

115

33

• Impaired gas exchange → Hypoxemia

• Ischemia of down-stream lung tissue = increased dead

space (V/Q mismatch)

• Impaired CO2 removal → hyperventilation

• Over-perfusion of tissue still receiving circulation

• Decreased surfactant production by type II alveolar cells

→ alveolar edema & atelectasis

• Hypoxia worse if patent foramen ovale present

116

32

33

• Increased pulmonary vascular resistance (PVR)

caused by vascular obstruction , vasoconstriction

• Right ventricle sensitive to pressure ↑

• Decreased CO → catecholamine-induced tachycardia

• Limits LV filling, decreases CO

• Acute cor pulmonale

• Catechols may sustain B/P temporarily but as the RV fails,

CO falls further and systemic hypotension results

117

34

• Clinical Manifestations

• Dyspnea, pleuritic chest pain, hypoxemia, rales

• Non-productive cough with hemoptysis

• Possible hypotension

• Co-existing deep venous thrombosis (DVT)

• Diagnostics

• Abnormal chest x-ray.

• A segmental or larger perfusion defect on V/Q scan

• Positive spiral CT scan

• Elevated D-dimer level

118

32

• May be masked in patients under GA

• Hypotension and tachycardia are classic findings

• Significant hemodynamic instability including hypotension

requiring vasopressors, shock and CV arrest

• Elevated jugular venous pressure, ↑ CVP

• Wheezing is a frequent finding

• Decrease in EtCO2 (R/T ↑ physiologic dead space)

• Earliest means of PE detection under anesthesia

119

32, 33

120

• Sinus tachy and atrial dysrhythmias common

• 83% of patients

• ST segment and T abnormalities (50%)

• RBBB & pre-cordial T-wave inversion correlates with PE

• Right heart strain (S1Q3T3 pattern)

• S-wave in lead 1, Q-wave in lead 3, T-wave ↓ in lead 3

• A-fib/flutter, heart block less common

S1Q3T3 Pattern in Pulmonary Embolism121

33

• Arterial blood gases

• Hypoxemia: reduction in PaO2 may be the only indicator of

PE with obstruction less than 25%

• Hypocarbia: Varies with the amount of physiologic dead

space created by the PE

• D-Dimer level: protein fibrin degradation product

• Elevated value during excessive clotting,

• Greater amount of product from fibrinolysis

• Elevated D-dimer is sensitive to PE but not specific

• A negative D-dimer rules out PE

• Positive D- dimer test requires alternative confirmation

122

33

• Changes in other lab values

• Serum troponin-I and troponin-T may be elevated in less than 50% of cases

• Brain natriuretic peptide (BNP) may be elevated due to RV dilation

• Also elevated in other conditions i.e. CHF

• Chest radiograph

• Not very helpful, may confirm cardiomegaly

• Good for ruling out other causes such as pneumothorax, effusion, pneumonia, & atelectasis

123

33

• Confirmatory diagnostic tests

• V/Q scans commonly used in non-surgical settings

• Limited value: often non-diagnostic / indeterminate

• Angiography is the gold standard for PE diagnosis

• Expensive, invasive, may not be available, potential for major complications

• Spiral CT scan: sensitivity 85%

• Even greater sensitivity in the presence of RV overload

• Transesophageal echocardiogram (TEE)

• May be available in the OR, but limited sensitivity in milder cases. More helpful in conditions of RV strain

• Evidence of tricuspid regurgitation

124

• Initial therapy can be started before definitive

diagnosis is made (treat the symptoms)

• Vasopressors (maintain BP & coronary perfusion

pressures)

• Avoid excess treatment with fluids if PE suspected

• Norepinephrine (α1 vasoconstriction and β1 for contractility)

• Alternates: dopamine, epinephrine, dobutamine

• Caution with dobutamine due to β2 peripheral vasodilation

125

32, 33

• Anticoagulation (has been used since 1960s)

• In surgery or PACU, the potential risks of life threatening

bleeding must be considered

• Subcutaneous LMWH (100 IU/BID) recommended for

non-massive PE

• Extensive PE: unfractionated IV heparin may be better

choice if concern about subq absorption or if

thrombolytic therapy is being considered

• Bolus 80U/kg with maintenance dose of 18 U/kg/hr

126

32, 33

• Pulmonary vasodilators

• Milrinone

• Benefit of pulmonary vasodilation and increased myocardial

contractility

• May lower systemic B/P

• Inhaled nitric oxide

• May be used to ↓ PA pressures and increase RV function

• Improve gas exchange and cardiac output with little effect on

systemic B/P

127

33

• Further treatment which may or may not involve the

CRNA may include:

• Thrombolytic therapy

• Placement of vena cava filter

• Catheter-directed embolectomy

• Surgical embolectomy

• Mortality rates reported 6 to 27%

128

• 80 to 85% survival rate for acute PE

• Especially if adequate anticoagulant therapy is initiated

• Two main sequelae:

• Development of thromboembolic pulmonary hypertension

• Post-thrombotic syndrome (varicosities)

• Both due to chronic vascular changes

129

• May be benign or malignant

• Clinical signs & symptoms relate to compression of

vital structures of breathing and circulation

• Tracheal/bronchial compression:

• Cough, dyspnea

130

Thymoma (red area)

Spatially defined by: • The sternum (anterior) and

• The middle mediastinum (heart and great vessels) posteriorly, and diaphragm inferiorly

• MM = middle mediastinum

• PM = posterior mediastinum

131

35

• Thymic mass: thymoma, cyst, hyperplasia or

carcinoma

• Thyroid tumor

• Cystic hygroma (congenital lymphatic lesion)

• Seminoma (germ cell tumor)

• Lymphoma

132

36

• Superior vena cava (SVC) compression

• SVC syndrome – cardiac tamponade, syncope

• Facial / neck swelling with nosebleeds & cyanosis

• Orthopnea

• Esophageal compression

• Dysphagia

• Recurrent laryngeal nerve compression

• Hoarseness

133

• Chest x-ray and CT scan evaluation of the mass

and affected structures

• PFTs have been recommended for risk eval

• Mixed restrictive-obstructive pattern suggests

increased risk for post-op respiratory complications

• Restrictive: parenchymal compression

• Obstructive: tracheal/bronchial compression

134

• Symptomatic or radiographic evidence of tracheal

compression is of concern

• Risk of severe, even fatal airway compromise

• Patients with > 50% reduction in tracheal cross-sectional

area (CSA) are more likely to be symptomatic and have

complications

135

• Low Risk

• Asymptomatic or mildly symptomatic

• No postural symptoms or evidence of compression

• Intermediate Risk

• Mild to moderate postural symptoms

• Tracheal compression < 50%

• High risk

• Severe postural symptoms, stridor, cyanosis

• Tracheal compression > 50% with associated bronchial compression, pericardial effusion or SVC syndrome

136

35

• Consequences due to competition for space with

heart, vessels, lungs and air pathways

• Anesthesia with neuromuscular block (NMB) will affect

the balance

• Decreased FRC under GA

• Decreased trans-pleural pressure gradient under GA

promotes airway collapse

• Positive pressure ventilation increases intrathoracic

pressure

137

• Tracheal compression or deviation may complicate

airway management

• Posterior masses of concern due to absence of tracheal

cartilage posteriorly → obstruction

• Myocardial compression may result in tamponade

syndrome

• Anterior compression will affect the RV

• Posterior compression will affect the LV

138

• Individualized plan based on patient needs

• Multidisciplinary: CRNA, surgeon, intensivist, perhaps

even the oncologist

• Initial plan may involve biopsy procedure

• Evaluation to determine if steroids, chemotherapy or

radiation could be used to reduce the tumor size to lower

the risk and enhance patient safety

139

35 - 37

• Patients with low risk profile probably not at

significant risk of complications

• Standard general anesthesia and monitoring are

acceptable

• Patients at intermediate or high level of risk need

detailed case plan

• Based on symptoms and diagnostic imaging

140

• Most cases of severe complications occur in the

absence of spontaneous ventilation (SV)

• General agreement that SV should be maintained in

these patients

• Based on:

• Numerous case reports in which compromise followed NMB

and/or PPV, or….

• Reports / series of high risk patients where SV was

maintained and complications were avoided

141

• Pre-op considerations

• Have enough staff available

• Plan ahead for ICU admission

• IV access in a lower extremity

• Pulse oximeter on right hand

• No sedative premedication

• Consider invasive monitoring

• Alternative (backup) airway options

142

35 - 37

143

• Airway management

• Awake fiberoptic intubation with local/sedation or

• Inhalation induction, SV maintained, standard DL for intubation

• If tracheal obstruction: the surgeon may try rigid bronchoscopy (airway stent?)

• Then establish surgical anesthesia with patient ventilating spontaneously

• Consider use of dexmedetomidine or ketamine for minimal respiratory depression + analgesia

• Prepare for emergency airway maneuvers if

obstruction occurs prior to resection of the mass

• Options:

• Rapidly reawaken the patient

• Shifting patient to preplanned “rescue” position

• Rigid bronchoscopy

• Rescue position: should be selected pre-op based

on anatomy / location of the mass and anticipated

area(s) of compression

• Upright seated / lateral decubitus / prone

144

• If rigid bronchoscopy becomes necessary:

• Maintain anesthesia with IV infusions

• Jet ventilation

• Severe hypotension

• May respond to placement of patient in the rescue position

• Decreases in cardiac output

• Lighten depth of anesthesia

• Principals of tamponade management: plasma volume expansion, vasopressors, inotropes

145

• Use of heliox

• Decreased gas flow may be R/T increased turbulence in narrow airways

• Helium/oxygen mix may improve flow

• Required helium concentration will limit FiO2

• If all else fails….

• Emergency sternotomy to elevate the mass from compromised structures

• Final option is cardiopulmonary bypass (CBP).

• In high risk patients, CPB should be anticipated and cannulations of femoral vessels done in advance

146

147

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