Advanced 1: RESPIRATORY

ANESTHETIC MANAGEMENT IN PULMONARY DISEASE

OBSTRUCTIVE DISEASE

• abnormal respiratory flow that does not change markedly over months of observation
• characterized by abnormal permenant enlargement of air spaces accompanied by disruption over walls without obvious fibrosis
• destroyed alveoli cannot regenerate leading to irreversible changes in lungs
• emphysema in the presence of chronic bronchitis is termed chronic obstructive pulmonary disease or chronic obstructive lung disease
• The inflammatory process in COPD is different from asthma, with different inflammatory cells, mediators, inflammatory effects, and response to therapy
• airway inflammation in asthma - characterized by eosinophilic inflammation affecting all airways but not lung parenchyma - linked to airway hyper-responsiveness
• in COPD - neutrophilic inflammation if airways.  Parenchymal destruction in an important irreversible feature and leads to airflow obstruction through dynamic compression
• eosinophilic inflammation in asthma is suppressed by corticosteroids but these have no affect on inflammation in COPD.  Long term corticosteroids fail to alter the progression of COPD

Causes:
Decrease in size of bronchial lumen
increase in collapsibility of bronchial walls
decrease in elastic recoil of lungs

COPD = COLD
terms used interchangeably describing combination of chronic bronchitis and emphysema (although these disease are capable of standing on their own)

Circulatory changes in COPD:

• exhalation requires incr positive pressure --> reduces right-sided return --> produces variation in arterial blood pressure or pulses paradoxis, found in 2/3 of pts
• increase in lung volume further impedes venous return
• HR increases
• CO increases d/t incr catecholamine levels
• renal function impaired with reduced GFR and renal plasma flow

PFTs in COPD:

• decrease in FEV1:FVC on spirometry is characteristic
• this measurement is < 70-80% in COPD
• may also indicate restrictive lung disease
• obstructivedisease also has increase in reserve volume and increase in FRC
• increased work of breathing is common with higher lung volumes

ABG analysis in COPD:

• PINK PUFFERS: PaO2 > 60 mmHg, PaCO2 is normal --> emphysematous
• BLUE BLOATERS: PaO2 < 60 mmHg, PaCO2 > 45 mmHg; presence of cor pulmonale --> bronchitic
• Cyanosis will be present if arterial blood contains more than 5 gm of deoxygenated Hgb per dL
• pulmonary vasoconstriction is a late sign as arterial hypoxemia represents a very advanced stage of the disease

X-ray findings in COPD:

• Hyperinflation
• flattening of diaphragm
• Bullae
• hyperlucency (decreased tissue density) of the lungs caused by arterial deficiency in the lung periphery
• *chronic bronchitis is best detected on CXR

PREOPERATIVE EVALUATION:

1. Determine severity of disease
2. identify treatments for reducing inflammation
3. clear secretions
4. treat infection
5. dilating airway caliber
6. supplemental oxygen if PaO2 < 60 mmHg, Hct is > 55% or there is evidence of cor pulmonale
7. ABG for pts with FEV1 < 1.5 L
8. repeat PFT after bronchodilator or steroid tx to evaluate airway constriction reversibility
9. pts with diminished FEV1 have successfully experienced general anesthesia - but can be reflective of CAD and incr total postop mortality

COMMON PULMONARY PARAMETERS:

FVC: Forced Vital Capacity
The total amount of air you can forcibly blow out after full inspiration, measured in L

FEV1: Forced Expiratory Volume in 1 Second
The amount of air you can forcibly blow out in 1 second, measured in L

FEV1/FVC Ratio:
measures the amount of the FVC that can be expelled in 1 second.  In healthy adults this should be approx 80%.

PEF: Peak Expiratory Flow:
speed of air moving out of your lungs at the beginning of expiration ; measured in L/sec

PFTs:
Assesses the functional status of the lungs as it relates to:

• how much?
• how fast?
• how stiff or compliant?
• how does the system respond to bronchodilator therapy?
• how well does gas diffuse?

Who gets them?

• unexplained dyspnea
• pulmonary disease suspected
• obesity
• age?
• smoking hx
• abdominal or thoracic procedure

Closing Capacity = Closing Volume + Residual Volume

Closing Volume
The point at which dynamic compression of the airway begins
Factors that affect CV:
-increasing age/smoking/lung disease
-body position: supine, erect

Residual Volume
air remaining in lungs following a VC breath

PREOPERATIVE EVALUATION:

• nutritional and fluid intake optimized
• skeletal strength optimized
• bronchodilators used if there is bronchoconstriction
• hypercarbia cannot be corrected too quickly
• sudden decrease in PaCO2 may result in alkalosis as the kidneys need time to adjust in order to excrete the excess bicarbonate

ANESTHESIA MANAGEMENT OF COPD:

• no specific drugs or techniques indicated
• COPD are most susceptible for developing respiratory failure postop
• postop intubation after chest or abdominal surgery may be needed
• regional anesthesia may be an option
• any block above T6 is not recommended

GENERAL ANESTHESIA IN COPD:

• VAAs faciliate bronchial dilation
• VAAs diminish ciliary function
• providing less than 100% O2 reduces absorptive atelectasis
• provide intermittent VC maneuvers
• if bullae are present, N2O is CI
• PEEPe may be used with caution up to 5 cmH2O
• expiration cycle should be prolonged in order to decrease pts own intrinsic PEEPi

PATHOPHYSIOLOGY OF COPD

• lung connective tissue usually provides elastic pull on the outside of the respiratory unit maintaining their patency
• in COPD, destruction of lung connective tissue leads to premature collapse of the airway
• exchange of CO2 and O2 between blood and alveoli is impeded
• inflammation of bronchial tubes and alveoli continue to progress
• airways narrow
• lungs become more compliant
• shorter quicker breaths are necessary
• hyperinflation of lungs results
• inspiratory muscles operate from a shorter initial length and produce less force
• diaphragm is widened and contracts ineffectively
• d/t incr demands on respiratory muscles greather proportion of CO is supplied to these muscles
• pts begin to assume comfortable postures to enable them to breath
• inflammation of the airway increases allowing foreign substances to gain access to the blood vessels, macrophases, mast cells, and nerves in lungs - this further initiates asthamatic component of airway reactivity

COPD VS ASTHMA:

• in COPD there is not a significant reversible component like there is in asthma
• measurement of ABG is desireable for longer cases esp chest and abdomen
• CO2 measurements help guide ventilation bc increased dead space widens the normal arterial venous ETCO2 gradient
• objective: maintain normal metabolics (pH)

INTRAOPERATIVE MANAGEMENT:

• hemodynamic monitoring depending upon the case
• COPD patients generally have underlying cardiac dysfunction
• in pts with pulm HTN, CVP measurements reflect R ventricular function rather than intravascular volume
• Extubation: pts with FEV1 below 50% most likely will require postop ventilatory support

EMPHYSEMA:
Progressive airflow obstruction reflected by decrease forced expiratory volume in one second (FEV1)

Causes:

• Imbalance between protease and antiprotease activity in lungs
• enhanced oxidant burden from cigarette smoke damages compounds of all chemical classes including amino acids, lipoproteins and CHO
• hyperplasia of mucus glands play a role in excessive mucus production

PFTs:

1. non-reversible obstruction
2. elevated lung volumes
3. low diffusing capacity
4. smoking history

BULLAE:
A form of emphysema
Are air containing spaces > 1 cm and result from lung tissue destruction
Located in deep elastic layer of the visceral pleural
Avoid N2O in bullae and pulm HTN

BLEBS:
are NOT  form of emphysema
A collection of air within the pleura
Do not involve the asinus (alveoli)
patients with blebs may be a candidate for pleurodesis which involves gluing together of 2 pleura - done to prevent recurrence of pneumothorax or pleural effusion.  Can be done chemically or surgically
Chemically: bleomycin, tetracyclin, povidone iodine, talc through chest drain; premedicate or instill LA into space
surgically: mechanically irritating parietal pleura with rough pad; thoracotomy or thoracoscopy

CHRONIC BRONCHITIS:
Condition with chronic excess mucus secretion into bronchial tree
Occurs for 3+ months of the year for 2 successive years
airway obstruction limits expiratory airflow

AIRWAY REACTIVITY:

• 25% of COPD pts have enhanced airway reactivity
• muscular aspect of airway actually thickens contributing to airway narrowing
• excessive mucus production present; mucociliary transport system paralyzed

MECHANICS OF VENTILATION:

• Laminar flow generally occurs only distal to small bronchioles
• Renolds Number:
• predicts turbulence
• < 1000 = laminar flow
• > 1500 = turbulent flow
• RN = (linear velocity x diameter x gas density) / gas viscosity
• Pathology of Airway Resistence:
• bronchospasm
• airway secretions
• mucosal edema
• volume-related diseases
• flow-related diseases
• Flow-related respiratory disease: Obstructive lung disease
• COPD
• asthma
• emphysema
• chronic bronchitis
• Volume-related respiratory diseases: Restrictive Lung diseases
• sarcoidosis
• extra-pulmonary restrictive lung disease
• interstitial lung disease
• scoliosis
• PEEP
• PEEPi = auto PEEP
• PEEPe = PEEP that we give the pt; 2.5-5 cmH2O
• PEEPi may result in breath stacking

ASTHMA

• Chronic inflammatory disease of airway
• involves many cells and cellular elements: mast cells, neutrophils, eosinophils, T-lymphocytes
• serotonin can be a potent vasocontrictor and active in response
• Disease of bronchoconstriction, airway inflammation and airway hyperirritability
• PANS maintains normal bronchial tone
• vagal afferents are sensitive to histamine, noxious stimuli, cold air, and irritants
• reflex vagal activation results in bronchoconstriction caused by incr in intracellular cGMP (cyclic guanosine monophosphate)
 
• extrinsic asthma: allergic asthma - children & young adults
• IgE mediated - infectious, psychological, environmental or physical factors
• Most common chronic disease of childhood
• intrinsic asthma: idiosyncratic asthma - middle age adults without specific asthma attack provoking stimuli

• Exposure to minute amts of offending agent cause activation of lymphocytes, histamine release from degranulated mast cells and cytokine release
• active inflammatory process demonstrated on biopsy
• potent chemical mediators promote vasoconstriction, incr smooth muscle tone, enchange mucus production, airway edema, enhance vascular permeability, and inflammatory cell chemotaxis

ASA and ASTHMA:

• cyclooxygenase inhibition promotes an incr in leukotriene levels via arachidonic acid pathway
• when prostaglandin production is blocked by NSAIDs like ASA, the cascade shunts entirely to leukotrienes causing overproduction of LT-4 and producing the severe allergy-like effects
• ETOH may induce the same rxn
• this triggers an asthma attack
• may also occur with NSAIDs
• not an IgE mediated event or allergic
• asthma ASA sensitivity is clinically associated with nasal polyps

ASTHMA ATTACKS:

• can send pt into acute distress
• tachypnea stimulated by bronchial receptors producing hypocapnia
• normal or high PaCO2 indicates pt can no longer maintain WOB
• may develop respiratory failure

S&S of advanced pulmonary disease and airway obstruction:

• pulses paradoxus
• EKG changes of right ventricular strain
• ST segment changes
• R-axis deviation
• R BBB

Treatment

• B2 adrenergic agonists
• albuterol; terbutaline
• sympathomimetic agents
• B2 stim activates adenylate cyclase resulting in formation of cAMP
• results in bronchial dilation
• methylxanthines
• theophylline
• produced bronchodilation by inhibiting phosphodiesterase
• phosphodiesterase breaks down cAMP
• results in the blockade of histamine, diaphragmatic stim, catecholamine stim
• narrow therapeutic range: 10-20 mcg/ml
• glucocorticoids
• anticholinergics

Asthmatic findings:

• Asthmatics must be optimized for surgery, even emergency surgery.
• FEV1 > 2-3 L
• FEV1/FVC > 70%
• PEF 200-500 ml should be utilized to confirm clinical impressions
• CXR - air trapping, flattened diaphragm, hyperlucent lung fields

Regional in Asthma:
It is possible that high regional anesthesia (T1-T4) may block the sympathetic innervation to the lower airway allowing unopposed PANS.

Anesthetic management in asthma:

• avoid histamine release Rx
• atracurium, miva, demerol and morphine
• thiopental - cause exaggerated histamine release
• ketamine promotes bronchodilation but when used in pts with high theophylline levels --> sz
• VAAs are effective bronchodilators
• atropine and glyco may blunt bronchoconstriction if given in larger doses but may produce tachycardia
• Succs may cause small histamine release but generally safe
• patient must be sufficiently deep before instrumentation of airway

• maintain Vt < 10 ml/kg
• prolong expiratory time 1:2.5 or 1:3
• prevent air trapping, breath stacking
• live with modest hypercapnia during acute bronchospasm unless there are CV or neuro CI
• tx intraop bronchospasm with B-adrenergic agonsts
• d/c gas sampling line when admin aerosolized agent as the carrier agent interferes with gas analysis

• admin hydrocortisone 1-2 mg/kg
• reversal of NMBs does not precipitate bronchoconstriction if preceded by anticholinergic
• consider deep extubation before airway reflexes return to prevent acute bronchospasm on emergence
• consider dose of lidocaine of possibly a lidocaine gtt in severe cases

RESTRICTIVE PULMONARY DISEASE



Any condition that interferes with normal lung expansion during inspiration
increase the inward elastic recoil of the lungs or chest wall

2 types: Intrinsic & Extrinsic

• results in decreased lung compliance
• decreased lung volumes
• FEV1 and FVC are reduced and reduction in TLV
• FEV1/FVC ratio is normal
• V/Q mismatching of diffusion abnormalities

Acute Intrinsic Pulmonary Disorders:

1. Pulmonary edema
2. ARDS
3. Infectious PNA
4. Aspiration pneumonitis
5. Reduced lung compliance d/t incr extravascular lung water

Chronic Intrinsic Pulmonary Disorders (Interstitial Lung Disease):
Characterized by pulmonary fibrosis
Onset insidious, chronic inflammation of the alveoli walls results in progressive pulmonary fibrosis
Eventually interfering with gas exchange and ventilatory function

Causes:

1. occupational and environmental pollutants
2. drug toxicity
3. autoimmune disease or "connective tissue disorders"
4. oxygen toxicity
5. chronic pulmonary aspiration
6. idiopathic pulmonary fibrosis (IPF)
7. radiation injury
8. sarcoidosis: intense interaction of lymphocytes and macrophages that result in tissue injury involving lungs, skin, eyes, myocardium

Interstitial Lung Disease, cont.

• disease of lung parenchyma and connective tissue
• lung parenchyma is damaged and inflammation occurs
• changes in parenchyma and connective tissue happen when the inflammation is chronic
• once significant amt of damage to air sacs develop, the disease is not reversible
• in advanced disease, air sac dilation occurs resulting in impaired blood flow in lungs
• this reduced blood flow can reduce amt of O2 available for the body to use and increase SOB

SARCOIDOSIS

• One type of interstitial lung disease
• multi-system d/o commonly affects lungs, skin and eyes
• during chronic inflammation, normally elastic tissue stiffens decreasing the flexibility of the lung tissue
• affected tissue in the lung looks like a honeycomb
• cause unknown

Chronic Extrinsic Lung Disease:
Disorders that inhibit the normal lung excursion such as:

1. flail chest
2. pneumothorax
3. atelectasis
4. pleural effusions
5. ascites
6. obesity
7. skeletal and neuromuscular d/o: scoliosis
8. pregnancy

ACID-BASE BALANCE

• Normal metabolism results in primarily acidic metabolic waste products
• these volatile acids are converted to carbonic acid gases exhaled at rate of 24,000 mEq per day
• Fixed acids (non-volatile) are also produced at rate of 50 mEq/day and excreted by kidneys

ABG Interpretation

• pH 7.35-7.45
• PaCO2 35-45 mmHg
• HCO3 25 mEq/L

Treatment of blood gas abnormalities:

• Correction with mechanical ventilation
• do not tx resp acidosis with bicarb as HCO3 dissociates into more CO2 worsening acidosis
• total body bicarb deficit = base deficit
• correction of 1/2 of deficit is indicated, not total correction
• acidemia in renal failure pts is best tx with dialysis
• hypoxemia involves incr FiO2, PEEP and correction of respiratory issues present
• suctioning, correcting atelectasis, etc.