UNIT 8

Alterations in Respiratory Function

Originally developed by:

Marlene Reimer RN, PhD, CCN(C)

Associate Professor

Faculty of Nursing, University of Calgary

Associate in Nursing, Calgary Health Region

Revised (2000) by:

Karen Then RN, PhD

Associate Professor

Faculty of Nursing, University of Calgary

Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary

Unit 8 Alterations in Respiratory Function1

Unit 8 Table of Contents

Overview

Aim

Objectives

Resources

Orientation to the Unit

Web Links

Section 1: Alterations in Respiratory Function

Review of Normal Ventilation and Respiration

Clinical Manifestations of Pulmonary Alterations

Learning Activity #1—Quiz

Obstructive and Restrictive Pulmonary Disease

Learning Activity #2—Case Study: A Patient with COPD

References

Glossary

Acronym List

Answers to Learning Activities

Learning Activity # 1—Quiz

Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary

Unit 8 Alterations in Respiratory Function1

Rankin, Reimer & Then. © 2000 revised edition. NURS 461 Pathophysiology, University of Calgary

Unit 8 Alterations in Respiratory Function1

UNIT8
Alterations in Respiratory Function

As in other units you will find that a good understanding of normal structure and function will be helpful as you build your knowledge base regarding alterations in function and system failure. That is why the first activities involve review of the anatomy and physiology of the respiratory system. Rather quickly you will realize that “respiratory system” is a bit of a misnomer as respiration technically refers to the actual exchange of oxygen and carbon dioxide, whereas ventilation refers to the act of breathing.

As you go through this unit you will find yourself drawing on knowledge from the unit on: Alterations in Fluid and Electrolytes especially with relation to blood gases. In the case study at the end of this unit you will have some opportunities to test your application of that knowledge.

Overview

Aim

The emphasis in this unit is on acquiring a basic understanding of obstructive and restrictive pulmonary disease. To a lesser extent you will be assisted to examine developmental differences in vulnerability to alterations in respiratory function and the consequences of respiratory failure.

Objectives

On completion of this unit you should be able to:

  1. Differentiate between obstructive and restrictive respiratory diseases.
  2. Describe the etiology, pathophysiology and clinical manifestations of obstructive and restrictive diseases.
  3. Describe the management of chronic obstructive pulmonary disease.
  4. Describe the etiology and clinical manifestations of respiratory failure.
  5. Compare alteration of pulmonary function in children with adults in relation to effects of structural differences and types of conditions.

Resources

Requirements

Print Companion: Alterations in Respiratory Function

Most of the information that you require for this unit will come from Porth (7th ed.)Chapters 29 and 31. You should also plan to access a current pharmacology textbook.

Supplemental Reading

If you are interested in more information on any of the topics in this unit, check out the following references:

Brandstetter, R. (1986). The adult respiratory distress syndrome -- 1986. Heart and Lung, 15(2), 155-163.

Burrows, B. (1990). Differential diagnosis of chronic obstructive pulmonary disease. Chest (supplemental), 97(2), 165-185.

Carroll, P. (1986, July). What you can learn from pulmonary function tests. RN, 24-27.

Gross, N.J. (1990). Chronic obstructive pulmonary disease: current concepts and therapeutic approaches. Chest (supplemental), 97(2), 195 – 235.

Hahn, K. (1987). Slow-teaching the C.O.P.D. patient. Nursing 87, 17(4), 34-42.

Konishi, M., Fujiwara, T., Naito, T., Takeuchi, U., Ogawa, Y., Inukai, K., Fujimura, M., Nakamura, H., & Hashimoto, T. (1988). Surfactant replacement therapy in neonatal respiratory distress syndrome. European Journal of Pediatrics, 147, 20-25.

Owen, C.L. (1999). New directions in asthma management. AJN, 99(3), 26-33.

Stobart, M.J. (1999). Prevention and management of COPD. Professional Nurse, 14(4), 241-244.

Orientation to the Unit

Before you get started on the serious work of the unit try the following exercise:

Take a piece of paper and draw 3 columns on it. Now in the centre column list all of the diseases and conditions of the respiratory system that you can think of.

In the first column list the etiology and risk factorsfor conditions and diseases of the respiratory system. (Don’t worry about matches initially although looking at the centre column may help you think of different ones.)

Now draw lines matching up the first and second columns to the best of your knowledge.

What things from your first column seem to be the most common risk factors?

If your list was like mine you probably found that environmental irritants such as smoking and allergens linked with many of the respiratory conditions. Did you also consider infectious agents? trauma? developmental differences? conditions originating in other body systems (e.g., cardiovascular) which then impact the respiratory system?

The last column can be labelled pathogenesis. As you recall, pathogenesis refers to the development or evolution of the disease, for example, what does the pneumococcus actually do that results in the disease that we know as pneumonia? In this unit we certainly will not be able to address all of the conditions you listed in the centre column. However you will find that the basic mechanisms are not that varied (e.g., inflammation, obstruction) so that you should gradually be able to fill in most of the third column as you work through the unit.

Web Links

All web links in this unit can be accessed through the Web CT system.

Section 1: Alterations in Respiratory Function

Review of Normal Ventilation and Respiration

  • Skim Chapter 29 : Control of Respiratory Function in Porth (7th ed).

Clinical Manifestations of Pulmonary Alterations

Answer the following questions to reinforce your understanding of key points (see the end of this unit if you are unsure of the answers).

Learning Activity #1—Quiz

  1. Dyspnea is usually a manifestation of ______(localized, diffuse) pulmonary disease whereas haemoptysis indicates a ______(localized, diffuse) abnormality.
  1. Cyanosis is a reliable indicator of hypoxemia (true or false). In which patient would cyanosis be a more serious sign: a 50-year-old man with chronic bronchitis or a 29-year-old woman with postpartum haemorrhage?
  1. The differences between hypoxemia and hypoxia are
  1. Ventilation is ______.
  1. Respiration is ______.
  1. Low ventilation/perfusion ratio (V/Q) describes the state of ______(good, poor) ventilation of a ______(well perfused, poorly perfused) segment of the lung. An example of a condition which it is seen is ______.
  1. High V/Q describes the state of ______(good, poor) ventilation of a______(well perfused, poorly perfused) segment of the lung. An example of a condition where it is seen is ______.
  1. Administration of high levels of oxygen is not effective in adult respiratory distress syndrome and respiratory distress syndrome of the newborn because

Obstructive and Restrictive Pulmonary Disease – Porth, Chapter 31.

One way to simplify comprehension of the disorders of ventilation is to classify them as obstructed breathing or restricted breathing.

Obstructive pulmonary disease, as the name implies, refers to conditions that affect the movement of air in and out of the lungs. The most common obstructive lung diseases in adults are chronic bronchitis, emphysema, and asthma. Each disease has some distinct features (as outlined in Table 8.1) but they often coexist to varying degrees in the same individual so together are called chronic obstructive pulmonary disease (COPD). The pulmonary effects of cystic fibrosis can also be classified as obstructive. All of the obstructive pulmonary diseases are characterized by:

  • reduced vital capacity
  • difficult expiration
  • increased residual capacity (see Figure 8.1)

Restricted breathing results from conditions in which the lungs or chest wall are stiffened and compliance is reduced. Examples of restrictive pulmonary disease include:

Condition / Mechanism
pulmonary fibrosis / "stiff lungs” from scar tissue and loss of compliance
adult respiratory distress syndrome (ARDS) / “stiff lungs” from inactivated surfactant and progressive fibrosis
respiratory distress syndrome of the newborn (RDS) / “stiff lungs” from insufficient surfactant and atelectasis
kyphoscoliosis / stiff or distorted chest wall
neuromuscular diseases / impaired respiratory muscle function

All of the restrictive pulmonary diseases are characterized by reduced vital and residual capacity (see Figure 8.1).

Figure 8.1 Comparison of Vital and Residual capacity in three situations

Note:
Vital Capacity (VC) is: the largest volume of air that may be forcefully expired (after a maximum inspiration).
Residual Volume (RV) is: the amount or volume of air that remains in the lungs following a maximum expiration.
See glossary at the end of this unit for more definitions.

A chart summarizing the changes in selected restrictive, obstructive and pulmonary vascular conditions can be found in Table 8.1. You will probably want to add your own notes to the chart to further enhance your understanding.

Table 8.1 Disorders of Ventilation and Respiration

Type of Condition / Etiology / Pathogenesis
Restrictive
Interstitial Lung Disease /
  • inhaled agents (e.g. asbestos), silicosis  inflammation initially phagocytes? then fibroblasts take over
/
  • lay down abnormal amounts of fibrin collagen coating the outside of the alveoli making them stiff “stiff lung”

ARDS (Shock Lung) /
  • any major body disorder, i.e., “catastrophic event”
/
  •  permeability of capilliary membrane pulmonary edema & inactivation of surfactant  “stiff lung”

Newborn RDS (Hyaline membrane disease) /
  • immaturity -- not mature enough to produce surfactant
/
  • atelectasis, weak chest wall and lack of surfactant  “stiff lung”

Obstructive
Emphysema /
  • smoking  antibacterial activity of alveolar macrophages (normally part of surfactant film) 
  • deficiency of alpha/anti-trypsin (McCance & Heuther, 1994, pp. 1169-1172
/
  1. lose septa between alveolar sacs become floppy  rupture, over-inflate, collapse, air trapping
  1. 2. as septa  the bed of capillaries  (because walls of septa full of capillaries  right heart failure  cor pulmonale)

Bronchitis /
  • smoking and other inhaled irritants  hyperplasia goblet cells
  •  in ciliated cells
  •  mucociliary escalator
/
  • inflammation of the tracheo-bronchial tree  number of goblet cells, producing an excessive amount of mucus,  thickening,  hyper-secretion,  in diameter in small airways

Asthma
Obstructive but some unique features /
  • hypersensitivity of the bronchial walls and spasms of muscles surrounding bronchi
  • intrinsic vs. extrinsic (allergen) or mixed
/
  • disease of airways immunological component. Mast cells and other inflammatory cells release mediators  swelling
  • reflex component - inhaled antigen sets of protective response  bronchoconstriction & inflammation

Cystic Fibrosis /
  • genetic
/
  • bronchiolar obstruction with thick mucus, hyperplasia of goblet cells  bronchitis, etc.

Pulmonary Vascular
Pulmonary embolus
Fat emboli /
  • mainly secondary to other problems, e.g., immobility  deep vein thrombosis  pulmonary embolus trauma - # long bones  fat emboli
/
  • regional - part of the lungs and embolus occludes a portion of pulmonary circulation
  • general - dissemination throughout lung field
  • pulmonary hypertension

Other conditions and effects:
Pneumonia
  • may have  PO2 and  PCO2
  • infection in lungs interferes more with oxygen exchange than with CO2 exchange  hypoxia hyperventilation in an attempt to compensate
Respiratory Depression(e.g. due to general anaesthesia)
  • PO2 cannot stimulate respiration so PCO2 rises respiratory acidosis
Tuberculosis
  • microorganisms get lodged in lung and cause nonspecific pneumonitis
  • collagenous scar tissue forms
  • common clinical manifestations include fatigue, night sweats, weight loss, low-grade fever, cough and purulent sputum

Figure 8.2 Volumes with Normal Inspiration and Expiration, Maximum Inspiration, and Maximum Expiration in Three Situations

Figure 8.3 Forced Expiratory Volume in Three Situations

Your emphasis in this section should be on comprehension of the definition and essential mechanism(s) involved in each condition described. It is not necessary to try to memorize the details of clinical manifestations or treatments as comprehension of the basic mechanisms should make the rest fairly easy to predict. You may find it helpful to add to the previous chart and/or develop a table of definitions to summarize this segment of your reading.

Now that you have worked through the chart and the readings you are ready to apply your knowledge in a case study. To do the case study you will need to access a pharmacology textbook. You may want to have your notes from the unit on: Alterations in Fluids and Electrolytes handy.

Equally important however is the confidence to try to figure out the answers for yourself. It is not intended that you spend hours looking them up in assorted references. In fact you might not find all the answers in the depth you would like even if you did look for them. Our understanding is limited (even at the beginning of the 21st Century!) and sometimes treatments are used because we know they work, not because we understand exactly how they work. Likewise we cannot always explain some of the clinical manifestations that, from experience, we know typically occur.

Learning Activity #2—Case Study: A Patient with COPD

(Adapted from Unit IV: A Patient with COPD, Pulmonary System Series, Clinical Simulations for Critical Care Nurses, a computer assisted instructional program produced by the American Association of Critical Care Nurses and Medi-Sim.)

Context

You are a nurse working in an 8-bed Intensive Care Unit on the day shift. You are assigned to Mr. Smith, a 69-year-old white male with chronic obstructive lung disease (COPD) who has just been transferred from the Emergency Department in respiratory distress.

Admission Data

Jim Smith, a retired telephone lineman, has been treated over the past 10 days by his family physician for flu-like symptoms of fever, pulmonary congestion and cough productive of green purulent sputum. He became quite dyspneic this morning.

Mr. Smith has had COPD for the past 15 years with progressive dyspnea, fatigue and activity intolerance. He has no known allergies or environmental exposure to irritants. He has smoked 2 packs/day for the past 50 years. He has a long history of recurrent pulmonary infections.

  1. Vital signs and blood gases on admission at 0800 were as indicated in the chart below. Briefly explain the mechanism(s) contributing to each value that is abnormal.

Measurement/Lab Value / Mechanism(s) Contributing to Abnormal Values
Temp 38.6° C
Pulse 104
Resp 30
BP 143/86 mmHg
Blood gases
PO2 60
pH 7.35
pCO2 57
HCO3 31
O2 Sat 89%
  1. Explain the rationale for treatment initiated in the Emergency Department:

Ventolin nebulizer/Ventolin infusion
O2 @ 2 1itres per nasal cannulae
Steroid infusion
  1. As the nurse admitting him to ICU your initial assessment includes the following findings. Briefly discuss the significance and mechanisms accounting for each.

Assessment / Significance/mechanisms
Dusky, wide-eyed, restless, diaphoretic, fatigued
Respirations irregular, noisy, laboured
Nailbeds slightly cyanosed, clubbing of digits
Barrel-chested
Lung sounds –- fine crackles posteriorly, diminished breath sounds throughout, scattered rhonchi anteriorly
Heart sounds distant with S3 at the apex
Jugular veins distended, enlarged liver
Presence of increased fremitus to the midline of the posterior chest on palpation of the thorax
Hyperresonance in all lung fields with dullness and bronchial breath sounds elicited at the bases on percussion posteriorly
Pale and dusky at times with central cyanosis seen on the undersurface of the tongue
  1. What risk factor(s) for COPD are evident in Mr. Smith’s history? What is thought to be the mechanism(s) by which the risk factor(s) contribute to obstructive lung disease?
  1. Initial management for Mr. Smith is outlined below. Indicate the rationale for each intervention in the chart below.

Intervention / Rationale
Prescribed Medical Tx
Steroids
Antibiotics
Bronchodilators
Continuous 02 therapy
Chest physiotherapy
Nursing Tx
Encourage Diaphragmatic
breathing
Surveillance of vital signs,
breath sounds & neuro
status
Monitor ECG rhythm
Position in High Fowler’s
  1. At this point in his hospitalization what would be the most appropriate goal regarding his total fluid intake? Why?
  2. 1000-2000 ml/day
  3. 2000-3000 ml/day
  4. 3000-4000 ml/day
  1. At 1230 Mr. Smith’s ABG’s are as follows:

PO2 35 pH 7.28 pCO2 65 HCO3 29 O2 Sat 70% (on 2L of O2)

Which of the following terms is the most accurate interpretation of these results?

  1. severe uncompensated respiratory acidosis
  2. severe compensated respiratory acidosis
  3. severe uncompensated respiratory alkalosis

Mr. Smith is intubated and placed on a ventilator. He is discharged from hospital after 10 days in ICU and 3 days on a medical unit. The remaining questions apply to the long-term management of his condition.

  1. He is given instruction on pursed lip breathing prior to his discharge. Explain why this method is effective for COPD patients.
  1. Mr. Smith has been unable to sleep for more than 2-3 hours at a time. Why is such sleep pattern disturbance common with COPD patients?

  1. Mr. Smith is 190 cm tall and weighs 68 kg suggesting nutritional deficiency. Discuss the possible physiological bases for this deficiency and its significance with his condition.

References

Brandstetter, R. (1986). The adult respiratory distress syndrome -- 1986. Heart and Lung, 15(2), 155-163.

Burrows, B. (1990). Differential diagnosis of chronic obstructive pulmonary disease. Chest (supplemental), 97(2), 165-185.

Carroll, P. (1986). What you can learn from pulmonary function tests. RN, 24-27.

Gross, N.J. (1990). Chronic obstructive pulmonary disease: current concepts and therapeutic approaches. Chest (supplemental), 97(2), 195 – 235.

Hahn, K. (1987). Slow-teaching the C.O.P.D. patient. Nursing 87, 17(4), 34-42.

Kersten, L.D. (1989). Comprehensive respiratory nursing: A decision-making approach. Philadelphia: Saunders.

Konishi, M., Fujiwara, T., Naito, T., Takeuchi, U., Ogawa, Y., Inukai, K., Fujimura, M., Nakamura, H., & Hashimoto, T. (1988). Surfactant replacement therapy in neonatal respiratory distress syndrome. European Journal of Pediatrics, 147, 20-25.

Mahler, D., Rosiello, R., & Loke, J. (1986). The aging lung. Geriatric Clinics of North America, 2(2), 215-225.

Porth, C. M. (2005). Pathophysiology-Concepts of Altered HealthStates (7th ed). Philadelphia: Lippincott.

Glossary

apnea: Temporary cessation of breathing.

compliance: A measure of how easily a tissue is stretched. With respect to lung tissue it refers to the quality of yielding to pressure.

dyspnea: A subjective sensation of difficulty breathing.

elasticity: The ability of lung tissue to return to normal resting position and shape. It is the reciprocal of compliance.

elastance: The elastic forces of lung tissue that prevent over expansion or over distention of the thorax.

expiratory reserve volume (ERV): The maximum volume of air that can be expired forcibly following a normal expiration.

forced expiratory volume (FEV): The maximum volume of air forcefully expired (after a maximum inspiration) in one second.

functional residual capacity (FRC): At the completion of a normal expiration FRC represents the volume of air remaining in the lungs.

hypoxia: Refers to a reduction in tissue or cell oxygenation.

inspiratory capacity (IC): The maximum volume of air that can be breathed in after a normal breath out.

obstructive pulmonary disease: Refers to those conditions that affect the movement of air in and out of the lungs (e.g.,, chronic bronchitis, emphysema, asthma).