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Section 4 Exam > Respiratory Lecture Notes 2 > Flashcards

Respiratory Lecture Notes 2 Flashcards

1
Q

When is the best and poorest Lung function throughout the day?

A

best is about 4pm and poorest is about 4am

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2
Q

What is Asthma and what is the patho of it?

A

Asthma is a chronic inflammatory disease of the airway that causes recurring acute wheezing, SOB, chest tightness, and coughing. The patho is the airway membranes become inflamed and glands stiulate excessive mucus production

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3
Q

What are 6 triggers of acute asthma attacks?

A
  1. Allergens
  2. Upper respiratory infections(URI)
  3. Excercise induced asthma
  4. Drugs and food additives
  5. GERD(aspirated acid will cause inflammation)
  6. Emotional stress (exacerbated by panic and anxiety attacks)
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4
Q

What is the 2 phase response of the body to Asthma?

Early phase?

A 
Early phase peaks at 30-60min
- Bronchospasm
- increased mucus secretion
- Vascular leakage 
All results in obstruction of airway, air trapping, hypoxemia, resp acidosis
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5
Q

What is the 2 phase response of the body to Asthma?

Late Phase?

A

Late phase peaks at bout 5-6 hours
- Infiltration of eosinophils and neutrophils
- inflamation
- Bronchial hyperactivity
- Within 1-2days infiltration of monocytes and lymphocytes
This results in airway obstruction, air being trapped which causes airway resistance, resp acidosis, hypoxemia

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6
Q

What is bronchoconstriction and what does it cause?

A

its bronchospasm caused by a hyper responsiveness to a certain stimui that lowers the airway diameter and constricts the bronchial smooth muscles

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7
Q

What effect does inflammation and edema have on the resp system?

A

caused by histamine, leukotrienes, cytokines, prostoglandins, and nitric oxide. these will decrease airway diameter and increase airway resistance

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8
Q

What are the clinical manifestations of Asthma?

A

Wheezing(usually on expiration, progresses to inspiration as well), Cough caused by bronchospasm, dyspnea(a subjective experience), chest tightness, breathing cycle becomes longer and requires more effort.

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9
Q

What are early and late signs of Hypoxemia?

A

Early:
Apprehension, anxiety, restlessness, ^ pulse, ^ BP, ^ RR >30 diminished or absent lung sounds = low airflow.
Late:
Accessory muscle use and position, and cyanosis

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10
Q

What is the concern for status asthmaticus?

A

It does not respond to treatments if not reversed the pt may develop pnuemothorax, and cardiac/respirtory arrest.

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11
Q

What is the treatment of Status Asthmaticus?

A

IV fluids
Systemic bronchodilators- IV aminophylline
Systemic corticosteeroids- Methyleprednisolone
Epinephrine
O2 to correct hypoxia( May require intubation)

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12
Q

What is the most accurate test to see lung function in someone with asthma?

A

Spirometry, this test measures how much air can be exhaled after full inspiration and how fast air can be exhaled

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13
Q

What is forced vital capacity (FVC)?

A

vol of air exhaled from full inhalation to full exhalation

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14
Q

What is forced expiratory volume in 1 sec (FEV1)?

A

Vol of air blown out as hard and fast as possible during the 1st second of the most forceful exhalation after the greatest inhalation

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15
Q

What is the peak expiratory flow rate (PEFR)?

A

fastest airfow rate reached at any time during exhaation

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16
Q

During asthma what is the PEFR predicted levl?

A

< 60% and severe life threatening when < 50%

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17
Q

What will a mild asthma attack see in the ABG?

A

Respiratory alkalosis c PaO2 near normal

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18
Q

What will you find in the sputum of a pt c asthma?

A

Eosinophils

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19
Q

Wat is the CBC in a pt c asthma?

A

^ WBC’s and neutrophils = infection
^ Eosinophils = Allergen trigger
^ IgE (Immunoglobulin E) levels

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20
Q

What are 4 types of anti-inflammatory agents used to treat asthma?

A
  1. Corticosteroids-most potent and effective available
  2. Mast cell stabilizer (NSAID)
  3. Immunoglobulin E blocker
  4. Leukotriene modifiers
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21
Q

Tell me something about inhaled corticosteroids….

A

Well they are the most effective available anti-inflammatory. they lower mucus secretion and lower bronchoconstriction. The effects however are not seen for 2-3 days. They are good to prevent late phase asthma. *make sure you rinse mouth out after each use also use a spacer, and lowest dose possible, preventing dry hoarseness in mouth.

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22
Q

What about oral corticosteroid agents?

A

They are indicated for acute asthma with an onset of 3-6hrs Some names are Prednisolone, prednisone. Do not abruptly stop use. must wean off.

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23
Q

So let me know what I need to know about Mast cell stabilizers? or NSAIDs

A

AKA cromolyn & nedocromil. They stabilize mast cells and prevent the membrane from opening when an allergen binds to IgE. This med is good for exercise. should take 10-20min b4 excercise. but will give you bad taste in mouth and cough

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24
Q

All of this is good. Now can you tell me about Immunomodulators / Immunoglobulin E (IgE) blocker?

A

AKA Omalizumab (Xolair). So…Monoclonal antibodies block IgE receptor sites on mast cell and basophils. Both of these are a cause of allergic asthma symptoms. Used to treat asthma related to allergies. Its a subQ every 3-4wks. Dont use for acute attacks. Be sure to assess for anaphylaxis.

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25
Q

Ok so for the last of the 4 anti-inflammatory agents tell me about Leukotriene modifiers….

A

AKA zafirlukast (Accolate), and montelukast (Singulair). The drug will interfere with synthesis or block the action of leukotrienes; which are a potent bronchoconstrictor and may caus pulmonary edema, and inflammation. Not for use in acute attacks. And may cause H/A, nausea

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26
Q

What are 4 bronchodilators?

A
  1. Beta2-adrenergic agonist
  2. Anticholinergics
  3. Xanthine derivatives
  4. Phosphodiesterase inhibitors
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27
Q

What are two Beta2-adrenergic agonists?

A

Short acting are: Albuterol, Levalbuterol, pirbuterol these are used short acting relief of bronchoconstriction

Long acting are: Salmeterol and formoterol useful for nocturnal asthma. But DO NOT give with inhaled steroid like beclomethasone, triamcinolone, flunisolide.

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28
Q

Drop some knowledge on me about Anticholinergics…

A

They inhibit bronchoconstriction related to parasympathetic nervous system primarily in the large airway. They are less effective than beta-agonist. This drug is typically used in combination c beta2-agonist (combivent). onset in about an hr not good for acute. lasts about 4-6hrs

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29
Q

Okay and who should not get anticholinergics?

A

people c peanut allergy due to risk of anaphylaxis.

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30
Q

Tiotropium (spiriva) is a……..

A

once-daily inhaled bronchodilator medication to control the symptoms of asthma. That’s commercial ha

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31
Q

What does Xanthine derivative do? ad what is the main concern with the medication?

A

It is a long-acting bronchodilator that provides up to 24hrs of relief. But it has a lot of drug-drug intractions so a knowledge of ALL pt meds is required.

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32
Q

What drug is an alternative to Xanthine derivative (theophylline)?

A

Phosphodiesterase inhibitors. It will decrease the swelling in the lungs and is more selective than theophylline with fewer SE. used with severe COPD

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33
Q

COPD

Chronic Obstructive Respiratory Disease

A

~ 4th leading cause of death for women/ 5th for men
~ Non-reversible
~ Progressive and associated with abnormal inflammatory response of lungs to noxious particles or gases
~ May have asthma/ some asthma patients develop a form of COPD
~ Most common form; combo of emphysema and chronic bronchitis

34
Q

COPD Etiologies

A 
Cigarette Smoking
Occupational Exposure
Passive Smoking
Infection
Heredity
Aging
35
Q

COPD & Cigarette Smoking

A

~85 - 90% of ALL cases
~ 8 Pack year Hx usu has obstructive lung changes with no S&S of disease
~ 20 pack year Hx or longer often has early stage COPD- manifests as changes in PFT’s
~ Causes hyperplasia of goblet cells leading to:
-Incr Production of Mucus
-Decr Airway Diameter
-Incr Difficulty in Clearing –Secretions
Decreased Ciliary Action
-May cause loss of ciliated cells
-Stimulates excessive release of the enzyme elastase protease from lungs. This enzyme
-Breaks down elastin a major component in alveoli
-Produces abnormal dilation of distal air spaces with destruction of alveolar walls

36
Q

COPD & Heredity

A

Alpha1 Antitrypsin (ATT) Deficiency
~ About 5% caused by inherited deficieney of this protein which serves to protect the lungs.
~Leads to permature development of emphysema, often with chronic bronchitis
~AAT normally protects lung tissue from enzymes that are secreted by the alveolar macrophages and leukocytes; absence of AA allows the enzymes to attack the lung tissue
~Smoking exacerbates the process; it inactivates the AAT this is available and stimulates the release of elastase protease

37
Q

COPD & Aging

A

~ Some degree of emphysema is common, but aging alone does not cause clinically significant emphysema
~Gradual loss of elastic recoil of lungs
~Lungs become more rounded and smaller, have fewer functional alveoli
~O2 levels decrease
~Thoracic cage becomes stiff and rigid
~Shape of rib cage changes because of increased functional residual capacity
~ The result of these changes is increased work in breathing

38
Q

Emphysema

A

Occurs when air sacs deep in lungs have been damaged. Enlargement and destruction of air sacs causes the surrounding airways to collapse.

39
Q

Pathophysiology of Emphysema

A

~Small bronchioles become obstructed with mucus, smooth muscle spasm, inflammatory process, and collapse of bronchiolar walls
~Recurrent infections increase production of neutrophils and macrophages that release proteolytic enzymes that destroy alveolar tissues = more inflammation, more edema, and exudates formation
~Abnormal, permanent enlargement of the air spaces distal to the terminal bronchioles

40
Q

Structural Changes in Emphysema

A

Hyper-inflation of alveoli-trapped air
Destruction of alveolar walls
Destruction of capillary walls
Narrowed, tortuous, small airways
Loss of lung elasticity - supporting structures are destroyed
Air goes into the lungs easily, but is unable to come out on its own
Bronchioles tend tocollapse and air is trapped in the distal alveoli
Trapped air gives pt. the characteristic barrel-chest appearance
Decreased SA available for diffusion of O2 = decreased blood levels of O2
Patient compensates by increasing RR

41
Q

Emphysema Early Clinical Presentation

A 
Progressively more severe dyspnea
Initially:
▪	First DOE
▪	Minimal coughing
▪	No sputum, or small amounts 
▪	Hypoxemia during exercise
42
Q

Emphysema Clinical Presentation as Disease Progresses

A

▪ Dyspnea interferes with ADL’s then at rest (later sign)
▪ Barrel-chest – alveoli over distended, air is trapped, diaphragm flattens, A-P diameter of chest increases
▪ Increased reliance on intercostals and accessory muscles to breathe; ribs become fixed in an inspiratory position
▪ Hypercapnia develops
▪ Characteristically thin with weight loss, exact cause unknown. One theory is the patient is in a hyper-metabolic state with increased energy requirements due to increased work of breathing. Protein-calorie malnutrition with loss of lean muscle mass and subcutaneous tissue.

43
Q

Emphysema Later Clinical Presentation

A

▪ Secondary chronic bronchitis may develop

▪ Finger clubbing

44
Q

Chronic Bronchitis

A

Excessive production of mucus in the bronchi with a recurring cough that persists for at least 3 months/year during at least 2 consecutive years

45
Q

Chronic Bronchitis Pathophysiology

A

 Hyperplasia of mucus-secreting glands in the trachea and bronchi
 Increased Number of goblet cells = excess thick mucus
 Disappearance of cilia
 Airways in lungs become narrow and partly clogged with mucus = physical barrier to ventilation
 Chronic inflammatory changes and narrowing of small airways
 Altered function of alveolar macrophages leading to increased bronchial infections
 Eventually scarring of the bronchial walls may occur
 Greater resistance to airflow increase the work of breathing
 Alveolar structure and capillaries are normal

46
Q

Chronic Bronchitis Clinicial Presentation

A

History:
▪Cigarette smoking almost always present

 Earliest symptom – frequent, productive cough during winter months
▪ Coughing stimulated by retained mucus that can’t be adequately removed as result of decreased cilia and mucociliary activity. Cough ineffective because pt can’t inspire deeply enough to cause air flow distal to retained secretions
▪ Brochospasm at end of paroxysms of coughing
 Frequent respiratory infections
 DOE develops later
 Hypoxemia and hypercapnia develop more frequently because the constricted bronchioles are clogged with mucus/ there is a physical barrier to ventilation (increased airway resistance)
▪ Many areas of the lung are not ventilated and O2 diffusion can’t occur
▪ Diminished respiratory drive with tendency to hypoventilate and retain CO2
 Frequently pt requires O2 at rest and during activity
 Bluish-red skin color 2° cyanosis and polycythemia (increased production of RBCs 2° body’s attempt to compensate for chronic hypoxemia)
 Hgb may reach 20 g/dL (normal range male 14 – 18 g/dL; female 12 – 16 g/dL)
 Appearance – usually normal weight or heavyset, with robust appearance.

47
Q

Complications of COPD

A 
	Acute exacerbations of chronic bronchitis
	Cor pulmonale 
	Acute Respiratory Failure 
	Peptic Ulcer Disease (PUD) and GERD
	Pneumonia
48
Q

Cor pulmonale

A

▪ Hypertrophy of the right side of the heart, with or without heart failure
▪ Caused by pulmonary HTN 2° constriction of pulmonary vessels due to alveolar hypoxia
▪ S & S – distended neck veins, hepatomegaly with RUQ tenderness, ascites, epigastric distress, peripheral edema, and wt. gain

49
Q

Peptic Ulcer Disease (PUD) and GERD

A

~ Increased incidence in COPD

~ Assess gastric aspirates and feces for occult blood

50
Q

Pneumonia

A

▪ Frequent complication of COPD
▪ Common manifestation purulent sputum
▪ May not have systemic symptoms – fever, chills, leukocytosis

51
Q

Diagnostic Studies for Patients with COPD

A

PFTs

ABGs

52
Q

PFTs

A

▪ For accurate, reproducible results, the patient must be able to participate
▪ During test patient wears a nose clip so he breathes through his mouth only
▪ The mouthpiece and tubing are connected to a machine that displays the patient’s breathing effort on a graph
▪ Significant findings R/T increased resistance to expiratory airflow
 Decreased Forced Vital Capacity (FVC) volume of air that can be forcefully expelled from a maximally inflated lung
 Decreased Forced Expiratory Vol in 1 second (FEV1) – vol of air that can be forcefully expelled from a maximally inflated lung during the 1st second
 Decreased FEV1/FVC ratio (< 70% suggests presence obstructive disease)
 Decreased Vital Capacity (VC)
 Increased Residual Volume (RV)
 increased Total Lung Capacity (TLC)
 Increased Functional Residual Capacity (FRC)

53
Q

FVC

A

Forced Vital Capacity- volume of air that can be forcefully expelled from a maximally inflated lung

54
Q

FEV1

A

Forced Expiratory Vol in 1 second- vol of air that can be forcefully expelled from a maximally inflated lund during the 1st second

55
Q

ABGs

A

~Early- normal or slightly decreased PaO2 and normal PaCO2

~ Later- decreased PaO2, increased PaCO2, decreased pH, increased bicarbonate levels

56
Q

Goals for Patients with COPD

A

▪ Improve ventilation
▪ Promote removal of secretions
▪ Prevent complications and progression of symptoms
▪ Promote patient comfort and participation in care
▪ Maximize quality of life
▪ Treatment will be based on the patients COPD stage (Iggy Table 32-2 on p. 617)

57
Q

Pharmacological Therapy

A

▪ Bronchodilators – maintenance therapy
 Beta-adrenergic agonists routinely used–
MDI or nebulizer
 Anticholinergics – ipratropium (Atrovent)
–More effective in pt with emphysema
 Use of corticosteroid therapy and theophylline are controversial – have limited use in COPD may be indicated for patients who have asthma

58
Q

FiO2

A

Fraction of Inspired Oxygen:

room air is 21%

59
Q

Oxygenation of arterial blood

A
  1. Saturation of arterial hemoglogin (SaO2 or SpO2) by pulse oximetry.
    ( normal > 95%)
  2. Partial Pressure of dissolved oxygen in arterial blood - PaO2 (normal > 80 mm Hg)
60
Q

Primary Goal of O2 Therapy

A

To provide an FiO2 that will result in a stable SaO2

Supplemental O2 therapy is used to prevent or reverse hypoxemia

61
Q

O2 Toxicity

A 
Can develop when pt. breathes 100% O2 for > 12 hours
S & S: 
-increased dyspnea
-substernal chest pain that increases with deep breathing
- dry cough
- nasal stuffiness
- sore throat
- eye and ear discomfort
- restlessness
- paresthesia in extremities
- signs of pulmonary edema
- decreased breath sound
62
Q

O2 weaning

A

~ 1/2 to 1 liter at a time
~ Recheck the SpO2 with 15 minutes and prn
~ Do not change more frequently than q 1 hour unless oatherwise specified

63
Q

Humidification

A

Necessary wen oxygen therapy is > 4L/m

64
Q

COPD Respiratory Drive

A

▪ Pt with COPD has persistent high levels of CO2, the respiratory center no longer responds to high levels of CO2 by stimulating breathing. Hypoxemia becomes the primary respiratory stimulant. If too much oxygen is administered the patient’s respiratory drive will be blocked and the patient’s breathing will slow or stop

65
Q

O2 flow rate for patient with COPD

A

May need O2 flow of 2 - 4L/min via nc or up to 40% by Venturi mask.
A hypoxic pt. who has chronic hypercarbia requires lower levels of O2 delivery - usu 1 - 2L/min via nc

66
Q

Hypercarbia

A

the physical condition of having the presence of an abnormally high level of carbon dioxide in the circulating blood. hypercapnia.

67
Q

Hypoventilation

A

Serious concern, but untreated or inadequately treated hypoxemia is greater threat to life

68
Q

Manifestations of hypoventilation seen during first 30 minutes of O2 therapy

A

The pts. color improves because of anincrease in PaO2 level before the apnea or respiratory arrest occurs from loss of the hypoxic drive, therefore carefully monitor the LOC, respiratory pattern and rate, and pulse oximetry for patient’s at risk of oxygen-induced hypoventilation, apnea, and respiratory arrest

69
Q

Pursed lip breathing

A

Prolongs expiration and increases airway pressure; prevents bronchiolar collapse and reduces air trapping. Exhalation should be twice as long as inhalation.

70
Q

Diaphragmatic Breathing

A
  • To achieve maximum inhalations, slows RR

- Requires more energy so teach after the patient is stable

71
Q

Controlled coughing

A
  • Reduces fatigue
  • Conserves energy
  • Facilitates removal of secretions
72
Q

Chest PT

A

Percussion, vibration, and postural drainage

- Vibratory PEP (positive expiratory pressure) Therapy

73
Q

Flutter Mucus Clearance Device

A
  • Helps COPD pts cough up secretions
  • Works by transmitting vibrations to the airways when the patient exhales into the handheld device that is shaped like a small fat pipe, a steel ball moves, which causes vibrations in the lungs and loosens mucus
74
Q

ThAIRapy Vest

A

Compressor inflates and deflates the vest rhythmically at timed intervals and thus imposes high frequency chest wall oscillations that are transferred to the lungs. The oscillations thin thick airway mucus, facilitating its removal by coughing

75
Q

Aerosol Nebulization Therapy

A

 Nebulizer delivery system consists of a nebulizer (small plastic bowl with screw-top lid) and a source for compressed air
 The airflow to the nebulizer changes the medication solution to a mist
 It is like breathing in steam or mist that builds up in a bathroom when taking a shower
 Easier for some patients to use nebulizer than to use an inhaler
 Medication has better chance to reach small airways
 Rapid-acting, few side effects
 Cleaning very important

76
Q

Nutritional Therapy

A

 Emphysema – feelings of bloating and early satiety
▪ Eat 5 – 6 small, frequent meals; rest at least 30 minutes before eating; select foods that can be prepared in advance; avoid foods that require a lot of chewing
 Chronic bronchitis – if overweight, low fat diet

77
Q

Surgery

A

 Bullectomy – rarely performed; few % have large bullae
 Lung volume reduction surgery (LVRS)
▪ Removing damaged air sacs air trapping is reduced and the function of rest of lung is improved
▪ Lung function returns to pre-surgical condition by 2 years. Pneumonia is a significant complication.
 Lung Transplantation – exchange of one set of medical problems for another

78
Q

Nursing Diagnoses

A

▪ Ineffective Airway Clearance Impaired Gas Exchange
▪ Self-Care Deficit: Bathing Risk For Infection
▪ Disturbed Sleep Pattern Disturbed Body Image
▪ Imbalanced Nutrition: Less Than Body Requirements

79
Q

Health Maintnence

A

▪ Pulmonary Rehab Program – offers exercise training, nutritional counseling, disease education, and support
 Functional improvement is sustained only as long as the patient maintains a regular exercise program
▪ Relaxation and Coping Skills – to decrease anxiety and fear that accompanies SOB
 Breathing Techniques
 Tense muscles use more oxygen than relaxed muscles
 Support Groups – Better Breathers Club
▪ Correct Use of Medications – ongoing review correct use of inhalers
▪ Difference between prn and daily maintenance medications – when to take meds
▪ Avoid Risk Factors – What to do if symptoms occur – S & S worsening symptoms
▪ Activity – Prevent SOB – How to pace activities
▪ Recognize if symptoms worsen – how to manage SOB – Breathing Techniques
▪ Know when emergency help is needed and who to call

80
Q

Health Promotion

A

▪ Avoid/stop smoking – Ask pt at each visit if they smoke, Advise them importance of quitting, Assess readiness to quit, Assist them in coordinating a cessation plan that works for them; Arrange follow up visit with their provider
▪ Early detection of small-airway disease
▪ Early diagnosis and treatment of respiratory tract infections
▪ Vaccines – influenza and pneumococcal pneumonia

Section 4 Exam (10 decks)

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