Nurs614 Exam 3 Anesthetic Implications Of Lung Disease

Front 1

Types of Lung Disease?

Back 1

Obstructive
Restrictive

Front 2

What is asthma?

Back 2

Chronic airway inflammation
Reversible expiratory airway obstruction
Airway/bronchial hyper-reactivity
Generally allergen-induced immunologic responses

Front 3

There is ANS regulation of airway function. How is this altered with asthma?

Back 3

There is an imbalance between excitatory bronchoconstriction and inhibitory bronchodilation neural input --> increased expiratory airflow obstruction.

Front 4

How does asthma differ from chronic bronchitis?

Back 4

The degree of reversibility;
In asthma there is increased airway hyper-reactivity;
In asthma, after administration of a bronchodilator thre will be a 12% or greater increase in FEV1 and a 200 ml increase in PEFR.

Front 5

When doing a preop eval on an asthmatic pt, what are pertinent questions to ask?

Back 5

What is your breathing baseline and how is your breathing now?
Exercise tolerance?
Latest exacerbations? infections?
Sputum baseline and what is it currently?
Last time presented to the ED and last time received systemic corticosteroids?

Front 6

What is the optimal time frame for a smoker to stop smoking pre-operatively?

Back 6

8 wks preop.
(But stopping the mn prior to surgery decreases the COhb).

Front 7

For smokers, how long pre-op should they stop smoking to decrease COHb?

Back 7

Midnight prior to surgery

Front 8

In the asthmatic pt, even slight hypercapnia is indicative of severe air trapping and may be a sign of impending resp failure.
What level FEV1 may be predictive of resp failure?

Back 8

An FEV1 of < 40%

Front 9

Anticholinergic agents are generally not given in asthmatics unless?

Back 9

Secretions are copious or if ketamine is used for induction. They may exacerbate the bronchoconstriction

Front 10

True/false
Benzos are unsatisfactory for pre-op sedation in asthmatic pts

Back 10

False.
Benzos are the satisfactory for pre-op sedation

Front 11

Why is the use of H2 blockers (cimethidine, ranitidine or famotidine) detrimental to asthmatics?

Back 11

H2 receptor activation normally produces bronchodilation and in the event of histamine release, unopposed H1 activity with H2 blockade may accentuate bronchoconstriction.

Front 12

What periop consideration should be given to pts taking longterm glucocorticoids?

Back 12

Pts taking longterm glucocorticoids should be given supplemental doses to compensate for adrenal suppression – hydrocortisone 50-100mg pre-op and 100mg Q8hrs for 1-3 post-op days, depending on the degree of surgical stress.

Front 13

Regarding pre-op labs/studies for the asthmatic pts - what is the purpose of the CXR?

Back 13

For baseline status, signs of infection & severity of disease. (Xray is normal in more than 75% of patients).

Front 14

In the asthmatic pts, what does the FEV1 or PEFR assess?

Back 14

The severity of the disease.

Front 15

What is PERF?

Back 15

PERF is the max rate of airflow that can be achieved during a sudden forced expiration following a full inspiration

Front 16

An approximate PEFR = ?

Back 16

[Ht (cm) – 80] X 5
Measured in (L/min).

Front 17

What does the FVC, FEV1, FEV1/FVC & PERF measure?

Back 17

Expiratory airflow

Front 18

Normal FEV1 =

Back 18

Men = 3L,
Women = 2L

Front 19

FEV1/FVC is normally _______?

Back 19

> 70%

Front 20

Normal PERF is ____?

Back 20

> 200 L/min.
(can be > 500 in young adult males)

Front 21

Less than 50% of any of these parameters - FVC, FEV1, FEV1/FVC & PERF is indicative of?

Back 21

Moderate to severe asthma

Front 22

For pts who routinely use inhalers and perhaps systemic corticosteroids, just prior to induction what should you do?

Back 22

Give an additional dose of ipratropium and beta agonist

Front 23

Why is STP not a desirable induction agent for the asthmatic pt?

Back 23

Thiopental (STP) releases histamine

Front 24

Why is Ketamine not a preferred induction agent for the asthmatic pt?

Back 24

Although Ketamine is a bronchodilator (via SNS Beta 2 stimulation), it also stimulates secretions.

Front 25

What are the preferred induction agents in the asthmatic pt?

Back 25

Etomidate & propofol.
Propofol is a bronchodilator & neither release histamine.
***Generic Propofol contains sulfites – consider avoiding in the asthmatic.

Front 26

What MRs should be avoided in the asthmatic pt?

Back 26

Neuromuscular relaxants
that trigger histamine release like succinylcholine, curare, mivacurium, atracurium.
Their release of histamine is dose and speed of administration dependent.

Front 27

When providing pain management to the asthmatic pt, what should be avoided and what is preferred?

Back 27

Avoid those that stimulate histamine release like morphine & ketorolic (toradol). Fentanyl and analogues are preferred.

Front 28

All VAs are potent bronchodilators. Which are the least preferred in the asthmatic & why?

Back 28

Isoflurane and desflurane MAY irritate the airways during induction and/or emergence.

Front 29

Volatile agents & asthma:
_____ is the classic volatile agent for the asthmatic but is being supplanted by _______.

Back 29

Halothane
Sevoflurane

Front 30

Why is giving neuromuscular blocking agent reversal to asthmatic not a problem?

Back 30

Anticholinesterase is always given with an anticholinergic, so it is not a problem.

Front 31

List 5 strategies to reduce bronchospasm in the asthmatic pt prior to induction?

Back 31

Administer ipratropium & beta2 agonist just before induction;
Give adequate dose of induction agent;
Lidocaine 1 – 1.5 mg/kg IV;
Ideally, choose fentanyl or one of its analogues for opioid;
Deepen anesthetic level with volatile agent via mask.

Front 32

List 10 differential diagnosis for wheezing

Back 32

Foreign body (like gastric tube in the lung);
Partially blocked/kinked ETT;
Too light anesthesia;
Aspiration;
Endobronchial intubation;
Tension Pneumothorax;
Pulmonary embolus;
Pulmonary edema;
Acute exacerbation of asthma;
Anaphylaxis.

Front 33

List 5 class of medications used as preop asthma management

Back 33

Histamine blockers
Corticosteroids
Leukotriene Inhibitors
Beta Adrenergic Agonists
Anticholinergic Drugs

Front 34

What is the MOA of Cromolyn?

Back 34

It is a histamine blocker that suppresses the secretory response of IgE-Antigen reaction.
It is effective only in Mast Cells (Not Basophils)

Front 35

How is Cromolyn delivered and when is it used?

Back 35

Delivered only by inhalation.
Prophylactic use only -
ineffective following histamine release

Front 36

How much do the inhaled corticosteroids Beclomethasone & Triamcinolone affect the hypothalmic-pituitary-adrenal suppression in the asthmatic pt?

Back 36

Minimally

Front 37

If the asthmatic pt has received corticosteroids (oral prednisone) in the past 6 months, how does it affect the adrenals?

Back 37

It causes hypothalamic-pituitary-adrenal suppression.
The pt must be given Solucortef 100 mg preop.

Front 38

How do corticosteroids treat asthma?

Back 38

They have anti-inflammatory effects on the bronchial mucosa which --> stabilization of mast cell membranes;
they decreases airway hyper-responsiveness;
they control chronic symptoms and prevents exacerbations.

Front 39

What is the MOA of leukotriene inhibitors like Zafirlukast, Montelukast & Pranlukast?

Back 39

They are cysteinyl-leukotriene1 (CysLT1) antagonist that
competitively blocks Leukotriene D4 from binding to the receptor.
They are used for asthma prophylaxis.

Front 40

What is the MOA of leukotriene inhibitors like Zileuton?

Back 40

They inhibits the conversion of arachidonic acid to leukotriene A4, inhibiting the generation of leukotrienes.
(Leukotrienes are potent vasodilators).

Front 41

What is the class of the asthma drug Terbutaline & Albuterol

Back 41

β-2 agonist

Front 42

What is the class of the asthma drug Theophylline?

Back 42

PDEI

Front 43

What is the class of the asthma drug Atrovent (ipatropium)?

Back 43

Anticholinergic

Front 44

What causes laryngospasm?

Back 44

Secretions & Blood

Front 45

List clinical manifestations of laryngospasm?

Back 45

Stridor
Hypoxemia
Tachypnea
Tachycardia
Retractions
No airflow despite ventilatory efforts
Inability to phonate

Front 46

List strategies to prevent laryngospasm

Back 46

Minimize airway manipulation during Stage 2 recovery;
Extubate either deeply anesthetized or fully awake;
Clear all secretions from the airway;
Consider Topical/IV Local Anesthetics.

Front 47

If laryngospasm does occur, list ways to resolve it

Back 47

Positive Pressure Ventilation
CPAP with bag/mask & 100% oxygen – ensure tight mask fit;
Use maximum efforts to open the airway - head tilt, jaw thrust;
Oral or nasal airway;
Administer Succinylcholine -
adult 20 mg or 4mg/kg IM,
pdiatric 0.1-0.3 mg/kg IV or 0.2-0.6 mg/kg IM;
Reintubate if unable to ventilate.

Front 48

What is negative pressure pulmonary edema?

Back 48

A pt trying to breathe against laryngospasm.
Occurs mostly in young black men.

Front 49

How does CPAP resolve laryngospasm?

Back 49

CPAP may break laryngospasm by lowering the pressure gradient across the obstructed segment and possibly by pneumatically resetting the pharyngeal and laryngeal muscles.

Front 50

List manifestation of bronchospasm

Back 50

Reversible narrowing of the medium and small airways d/t to smooth muscle contraction;
Audible wheezing during exhalation;
Decreased Pulmonary Compliance;
Decreased TV;
ETCO2 may be absent;
Increased PIP.

Front 51

How is mild bronchospasm resolved?

Back 51

Hand Ventilate with 100% Oxygen;
Increase anesthetic depth;
(VA - Sevo/Halothane;
Propofol/Ketamine);
Lidocaine - 1.5 mg/kg IV;
Administer Beta Agonist - MDI vs neb
(Albuterol, Atrovent via ETT (4-8 puffs).

Front 52

List possible causes of bronchospasm

Back 52

Kinked tube, ETT right main stemed or at the carina.

Front 53

What is the Epi (bronchodilator) dose to treat severe bronchospasm?

Back 53

Epinephrine (0.5-1 ug/kg IV or 0.1-0.5 ml of 1:1000 SQ);
Infusion - 1mg/250ml D5W @ 4-8 mcg/min (0.05-1.0 mcg/kg/min) titrate to desired effect.
Epi is rarely required unless bronchospasm is in conjunction with anaphylaxis.

Front 54

What is the terbutaline dose to treat severe bronchospasm?

Back 54

Terbutaline - 0.01 mg/kg or 0.25 mg SQ q 20 min

Front 55

What is the Ephedrine dose used to treat severe bronchospasm?

Back 55

Ephedrine 5 mg IV
It is readily available but not as effective as other drugs.

Front 56

What is the Aminophylline dose used to treat severe bronchospasm?

Back 56

Aminophylline 5-6 mg/kg over 20-30 min.
Infusion 0.4-0.9 mg/kg/hr

Front 57

What is the Isoproterenol dose used to treat severe bronchospasm?

Back 57

Isoproterenol 0.5-1.0 mcg/min infusion.
It is rarely used.

Front 58

What is the Diphenhydramine dose used to treat severe bronchospasm?

Back 58

Diphenhydramine, 1 mg/kg IV
It reduce H1 effects.

Front 59

What is the Cimetidine dose used to treat severe bronchospasm?

Back 59

Cimetidine 4 mg/kg
It reduces H2 effects in allergic reactions

Front 60

What is the Ranitidine dose used to treat severe bronchospasm?

Back 60

Ranitidine 1 mg/kg IV
It is a H2 antagonists

Front 61

What is the dose of Methylprednisolone used to treat severe bronchospam?

Back 61

Methylprednisolone (1-2 mg/kg)

Front 62

What is the dose of Hydrocortisone used to treat severe bronchospam?

Back 62

Hydrocortisone, 5-10 mg/kg IV (up to 1gm) for initial dose, then 2.5 mg/kg q 6 hr for 24 hr.

Front 63

What is COPD?

Back 63

Loss of elastic recoil of the lung due to destruction of lung parenchyma that --> collapse of airways during exhalation, leading in turn to an increase in airway resistance.

Front 64

What does the chronic obstruction of airway outflow in COPD lead to?

Back 64

Enlargement of air spaces (bullae) distal to terminal bronchioles.

Front 65

Define chronic bronchitis

Back 65

Productive cough on most days of 3 consecutive months for at least 2 yrs

Front 66

What causes chronic bronchitis?

Back 66

Prolonged exposure to environmental irritants (cigarette smoking, air pollutants, occupational exposure to dust), recurrent pulmonary infections & familial factors

Front 67

Clinical manifestation of chronic bronchitis?

Back 67

Secretions from hypertrophied bronchial mucus glands and mucosal edema from inflammation of the airway which produce airflow obstruction.

Front 68

What is asthmatic bronchitis?

Back 68

The term asthmatic bronchitis may be used when bronchospasm is a major feature. Recurrent bacterial and viral infections are common and associated with bronchospasm.

Front 69

In chronic bronchitis, RV is _____ (normal/increased) & TLC is _________ (normal/increased)?

Back 69

RV is increased but TLC is often normal

Front 70

Can chronic bronchitis cause intrapulmonary shunting?

Back 70

Yes. Intrapulmonary shunting is prominent, and hypoxemia is common.

Front 71

Why is there an increased H&H with chronic bronchitis?

Back 71

The body is trying to compensate by increasing hgb

Front 72

Explain the blue bloater syndrome seen in chronic bronchitis

Back 72

Chronic hypoxemia --> erythrocytosis (↑ H&H), PHTN & eventually cor pulmonale. 5% of COPDers fit this profile

Front 73

Explain how sensitivity to oxygen increases as COPD progresses

Back 73

As COPD progresses, pts become chronic CO2 retainers and become less sensitive to arterial CO2 tension & may be depressed by oxygen administration

Front 74

What is Emphysema?

Back 74

Irreversible enlargement of airway distal to terminal bronchioles (alveoli) & destruction of septa

Front 75

What causes early emphysema?

Back 75

Early emphysema is usually from a homozygous deficiency of alpha-1 antitrypsin. This is a protease inhibitor that prevents excessive activity of proteolytic enzymes (mainly elastase) in the lungs; these enzymes are produced by pulmonary neutrophils & macrophages in response to infection and pollutants.

Front 76

How are airflow parameters altered in the pt with emphysema?

Back 76

Pts characteristically have ↑ RV, TLC, FRC & RV/TLC ratios

Front 77

Compare dyspnea in chronic bronchitis vs pulmonary emphysema

Back 77

Chronic bronchitis - moderate
Pulmonary emphysema - severe

Front 78

Compare FEV1 in
chronic bronchitis vs pulmonary emphysema

Back 78

Chronic bronchitis - decreased
Pulmonary emphysema - decreased

Front 79

Compare PaO2 in
chronic bronchitis vs pulmonary emphysema

Back 79

Chronic bronchitis - marked decrease (blue bloated)
Pulmonary emphysema - modest decrease (pink puffer)

Front 80

Compare PaCO2 in chronic bronchitis vs pulmonary emphysema

Back 80

Chronic bronchitis - increased
Pulmonary emphysema - normal to decreased

Front 81

Compare the diffusing capacity
of chronic bronchitis vs pulmonary emphysema

Back 81

Chronic bronchitis - normal
Pulmonary emphysema - decreased

Front 82

Compare hct in chronic bronchitis vs pulmonary emphysema

Back 82

Chronic bronchitis -increased
Pulmonary emphysema - normal

Front 83

Compare cor pulmonale in chronic bronchitis vs pulmon. emphysema

Back 83

Chronic bronchitis - marked
Pulmon. emphysema - mild

Front 84

Compare prognosis in
chronic bronchitis vs pulmonary emphysema

Back 84

Chronic bronchitis - poor
Pulmonary emphysema - good

Front 85

Preoperative evaluation for bronchitis?

Back 85

Assessment of pt’s current symptoms: dyspnea, cough, and sputum production;
obtain history of respiratory infection and exercise tolerance;
thorough chest auscultation;
consider PFTs (to assess disease status - address reversible component, if present);
ABG, CXR & EKG.

Front 86

Preop bronchitis therapy

Back 86

Educate on the benefit of smoking cessation 8 wks preop however no smoking after MN prior to surgery (to decrease COHb – carbon monoxide hgb;
Give antibiotics for evidence of respiratory infection;
Give oxygen for hypoxemia and/or evidence of increased pulmonary vascular resistance;
bronchodilators to address reversible component, if present.

Front 87

Anesthetic management guidelines for the pt with chronic bronchitis?

Back 87

Minimize the risk of post-op respiratory failure;
Regional anesthesia may offer benefits for surgery of the extremities and lower abdomen (T10 level or below); VA +/- NO for GA;
Judicious use of opioids – prevent and/or treat post-op pain but avoid respiratory depression.

Front 88

Chronic bronchitis:
what are the advantages of N2O

Back 88

It decrease the needed dose of volatile anesthetic and has good kinetics (quick on, quick off).

Front 89

Chronic bronchitis:
what are the disadvantages of N2O

Back 89

There is the potential to diffuse into airspaces quicker than nitrogen can exit, potentially leading to bullae rupture and tension pneumothorax.
(***Nitrous concentrations between 50 and 70% limits the concentration of oxygen that can be administered)

Front 90

What is intrinsic PEEP?

Back 90

Intrinsic PEEP aka dynamic hyperinflation occurs due to air trapping.
Because the air cannot be exhaled, pressure builds in the lung, leading to positive end expiratory pressure.

Front 91

What causes increased A-a gradient in chronic bronchitis and asthma?

Back 91

Increased dead space due to airway obstruction.
All inspired air does not participate in gas exchange and exhaled gas may not contain a “normal” amount of CO2 measured by capnography

Front 92

What are the characteristics of restrictive lung disease?

Back 92

Decreased vital capacity;
Expiratory flow rates remain normal;
FEV1 & FVC (forced vital capacity) will be reduced;
FEV1/FVC is preserved at > 0.7

Front 93

What causes sarcoidosis?

Back 93

Sarcoidosis is an immune system disorder characterised by non-caseating granulomas (small inflammatory nodules).

Front 94

What part of the body is sarcoidosis most often found?

Back 94

Ninety percent of the cases of sarcoidosis are found in the lungs, but it can occur in almost any organ.

Front 95

What are the characteristics of sarcoidosis?

Back 95

It causes small lumps, or granulomas, which generally heal and disappear on their own. However, for those granulomas that do not heal, the tissue can remain inflamed and become scarred, or fibrotic.

Front 96

What can pulmonary sarcoidosis lead to ?

Back 96

Pulmonary fibrosis, which distorts the structure of the lungs and can interfere with breathing. Bronchiectasis, a lung disease in which pockets form in the air tubes of the lung and become sites for infection.

Front 97

List extrinsic causes of restrictive lung disease

Back 97

Obesity, kyphoscoliosis, ascites, pregnancy & opioid overdose

Front 98

List intrinsic causes of restrictive lung disease

Back 98

Idiopathic fibrosis, effusions, pulmonary edema.
May see an increased AaO2 gradient with intrinsic causes.

Front 99

Why is there increased WOB in restrictive lung disease?

Back 99

Increased work is needed to move air in and out of the lungs – less air (volume) is moved per decrease in intrapleural pressure (pressure).

Front 100

What does increased PaCO2 in restrictive lung disease indicate?

Back 100

Advanced disease.
(Early on, these patients may be hypocarbic. However late in the disease the patient will live with a higher PaCO2 in return for not working as hard to breathe).

Front 101

What is the longterm consequence of hypercarbia and arterial hypoxemia.

Back 101

Hypercarbia and arterial hypoxemia cause vasoconstrictive pulmonary hypertension and cor pulmonale

Front 102

When is regional anesthesia preferred over GA in restrictive lung disease?

Back 102

For a peripheral or lower abdominal procedure with the anesthesia level below T10 as pulmonary function is minimally affected.

Front 103

Why is regional anesthesia contraindicated above T10 for pts with restrictive lung disease?

Back 103

At levels above T10, breathing may be impaired as advanced disease patients rely on accessory muscles of respiration.

Front 104

What are intraop considerations using GA in the pts with restrictive lung disease?

Back 104

There are few intraop considerations.
PEEP and increased oxygen may be required;
Preop FVC less than 15 ml/kg and a preop PaCO2 higher than 50 torr are good predictors of postop problems.

Front 105

What does FVC measure?

Back 105

Exhalation that is as hard and as rapid as possible.
This provides information on airway resistance.

Front 106

Restrictive lung disease:
what are postop concerns?

Back 106

Surgery, especially of the abdomen or thorax, decrease lung volumes further.
With these reductions in lung volumes, patients with restrictive lung disease may find it difficult to clear secretions.

Front 107

Anesthetic Concerns - sarcoidosis

Back 107

Preop: CXR, EKG, ABG, PFTs, LFTs;
Preop Solucortef 100 mg IV;
Difficult airway due to obstruction or distortion by granulomas;
Epiglottic/Arytenoid involvement;
Nares polyps;
Hypoxia due to lung disease
Dec. VC & Diffusing capacity;
Listen for rales.