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ADVANCED MEDICAL-SURGICAL NURSING ICASE SCENARIO

NURSING CARE OF CLIENTS WITH RESPIRATORY PROBLEMSPrepared by: John Henry O. Valencia, RN, RM

Master of Arts in Nursing Student

M.C. a 65-year-old man is admitted to your medical unit for exacerbation of his emphysema (COPD). He has a history of atopic asthma during his childhood and hypertension which has been well controlled by Enalopril for the last six years. He presents as a poorly nourished man who is experiencing difficulty breathing. He complains of coughing spells productive of thick yellow sputum. M.C. seems irritable and anxious when he tells you that he has been a two-pack-a-day smoker for 38 years. He tells you he has been sleeping poorly and lately feels very tired most of the time even when he has not done any physical activity. His VS are 162/84, 124, 36, 102 F, SaO2 88%. His admitting diagnosis is chronic emphysema with an acute exacerbation.

His admitting orders are as follows: Diet as tolerated Out of bed with assistance O2 at 2L/nc IV Plain NSSS 1L at 50 ml/hr Sputum C & S ABGs in AM CBC with WBC differential CXR followed by Pulmonary Function test in AM ECG

1. What are the significant data that you have gathered? What other relevant questions do you need to ask M.C.?

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2. What physical assessment findings do you expect to find? What specific changes in the respiratory system do you expect to find indicative of emphysema?

3. What is the most common cause of emphysema? Based on this information, what question will you ask about his health behaviors? What do you believe are the major cause/s of M.C’s emphysema?

4. Are M.C.’s VS and SaO2 appropriate? If not, explain why.5. Is your patient with chronic hypoxia? Is he compensating for his chronic hypoxia?6. Why is the O2 inhalation at 2LPM inspite of the SaO2 at 88%? How do we explain the “hypoxic

drive” in a pt. with emphysema? What important considerations do you have to remember regarding O2 administration in a pt. with COPD like M.C.?

7. Make an integrated pathophysiologic flowchart of MC’s disease condition.8. Given M.C.’s history and your knowledge of pathophysiologic processes, explain the

pathophysiologic basis of the assessment findings in M.C?9. What are the possible complications of Emphysema and their manifestations?10. Make a tabular comparison of the pathogenesis and pathophysiologic changes of Emphysema,

Bronchitis and asthma.11. Based on the assessment findings, identify five priority problems that M.C. may be

experiencing.

The laboratory sends the ff. report several hours after admission: RBC – 3.8thou/cmm, WBC- 13,000 thou/cmm, Hgb 12g/dL, ABGs: pH- 7.28, pO2 – 80 mmHg, pCO2 – 65 mmHg, HCO3 – 22.

12. Interpret the above results. How do the results relate to the pathophysiologic changes of emphysema?

13. With the ABG result, can you say that M.C. is in respiratory failure or respiratory insufficiency? Explain the scientific basis of your answer.

14. What are the major hallmarks of respiratory failure? What do you believe are the principal causes of this problem in M.C.?Explain your answer.

Five days after admission, M.C.’s condition has remarkably improved. The MD wants all medications continued and has shifted the antibiotics to oral preparations.

15. What made the MD say MC’s condition has improved? Give the assessment findings that supports the MD’s observation.

16. Summary of journal readings (3) related to the case. Use the table below.

Directions:1. This scenario is to be accomplished individually and to be submitted on Tuesday,Sept 16,

2014 This must be typewritten in A4 bond paper using Arial Narrow font 11. Late submission will have demerit rating. Please comply!

2. Discussion of the case will be done on Tuesday. Please come prepared for the discussion

3. Grading rubric is attached. Kindly attach a copy of this on the paper you will submit

ISTIONKO/USTGS/2014

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Answers:

1. What are the significant data that you have gathered? What other relevant questions do you need to ask M.C.?

Patient has a significant History of Chronic smoking (two-pack-a-day smoker for 38 years). Patient also has a history of atopic asthma and hypertension but well controlled by Enalopril. Patient was poorly nourished and experiencing DOB. Cough producing yellow-thick sputum.

Relevant Questions that we may asked:

Shortness of breath:

When were you first short of breath (at exercise or at rest)?

How often are you short of breath?

How long have you been short of breath? Is it getting worse?

How far can you walk, and how many steps can you climb before having to stop

because of shortness of breath?

Coughing:

How often and when do you cough?

How long have you been coughing? Is it getting worse?

Do you cough up mucus (sputum)? What color is it?

Have you ever coughed up blood?

Social History:

Childhood respiratory illnesses.

Family history of respiratory disease.

Other medical conditions you may have and their treatment.

How your condition is affecting your quality of life: missed work, disrupted routines,

and depression, for example.

The name and dose of all of the medicines you take, including any inhalers you use.

What type of family and social support you have. How long have you had cough, shortness of breath, or wheeze? Have you seen many doctors for it? What are you now doing to treat it? How many days did you miss from work last year because of the lung problem? Were you in the hospital for it? How long and how many times last year? Describe your usual good day. Do you have more good days than bad days in a week? What are you able to do when

you are feeling you’re very best? Who do you live with?

What recreation do you prefer? What have you learned to do that helps you to live with it? Does it ever embarrass you to have lung trouble?

Health history: Does the patient have a family history of COPD or other chronic respiratory diseases?

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How long has the patient had respiratory difficulty? What is the pattern of symptom development? Does exertion increase dyspnea? What type of exertion? What are the limits of the patient’s tolerance for exercise? At what times during the day does the patient complain most of fatigue and shortness of

breath? Which eating and sleeping habits have been affected? What is the impact of respiratory disease on quality of life? What does the patient know about his disease? Does patient has exacerbations or previous hospitalizations for respiratory problems? Are comorbidities present? How appropriate are current medical treatment?

2. What physical assessment findings do you expect to find? What specific changes in the respiratory system do you expect to find indicative of emphysema?

Assessment findings include:

INSPECTION

increased anterior-posterior diameter, or "barrel chest" use of accessory muscles to assist breathing tripod position shortness of breath common, especially on exertion tachypnea

PALPATION tactile fremitus decreased Chest expansion decreased.

PERCUSSION hyperresonant

AUSCULTATION

decreased vesicular breath sounds may have prolonged expiration muffled heart sounds from over distention of lungs usually no adventitious sounds; occasional wheeze

3. What is the most common cause of emphysema? Based on this information, what question will you ask about his health behaviors? What do you believe are the major cause/s of M.C’s emphysema?

SMOKING IS A MAJOR CAUSE OF EMPHYSEMA

In the vast majority of people, smoking is the cause of emphysema.Exactly how smoking destroys the air sac linings in the lungs isn'tknown. However, population studies show that smokers are about sixtimes more likely to develop emphysema than nonsmokers.

Estimates vary, but more than 24 million people in the U.S. likely have emphysema or another form of COPD, and probably many of them don't know it. Emphysema and chronic bronchitis are the third-leading cause of death in the U.S.

Interestingly, most heavy smokers do not develop emphysema. Why some smokers get emphysema and others do not is unknown. All heavy smokers experience other negative health effects of smoking, though.

ALPHA-1 ANTITRYPSIN DEFICIENCY

Besides smoking, the other major known cause of emphysema is alpha-1 antitrypsin deficiency. However, this is a minor cause compared to smoking.

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Alpha-1 antitrypsin (AAT) is a natural protein circulating in human blood. Its main function is to keep white blood cells from damaging normal tissues. White blood cells contain destructive substances they use to fight infections.

Some people -- perhaps 100,000 in the U.S. -- have a genetic condition that makes them deficient in alpha-1 antitrypsin. Deficient levels of the AAT protein in the blood allow normal white blood cells to continuously damage lung tissue. If people with AAT deficiency smoke, the damage is even worse.

Over years, most people with severe AAT deficiency develop emphysema. It's not known how many people have emphysema caused by AAT deficiency. Experts estimate that about 2% to 3% of people with emphysema have AAT deficiency.

Emphysema in AAT-deficient patients has the same symptoms as emphysema caused by smoking. However, people with AAT deficiency often develop emphysema at a younger age. Liver problems may also occur in people with emphysema from AAT deficiency.

SECONDHAND SMOKE AND OTHER POTENTIAL CAUSES

Secondhand smoke may contribute to emphysema. Exposure to environmental cigarette smoke is known to damage the lungs. Several studies suggest that people exposed to high amounts of secondhand smoke are probably at higher risk for emphysema.

Air pollution is also believed to contribute to emphysema, although how much is unknown. Most people are exposed to pollution, and emphysema takes years to develop, making this effect hard to study.

In the ABOVE scenario, MC’s condition was caused by his long exposure to cigarette.

4. Are M.C.’s VS and SaO2 appropriate? If not, explain why.

Patients Vital signs are: 162/84mmHg, 124bpm, 36pm, 102 F, SaO2 88%.

Patients VS are all abnormal indicating that the patient was in exacerbation of his condition, while his SaO2 is somewhat high this is due to body’s compensatory mechanism.

5. Is your patient with chronic hypoxia? Is he compensating for his chronic hypoxia?

Patient is evidently experiencing chronic hypoxia. Yes, patient is compensating as evidenced by increased HR and increased RR.

TOBACCO SMOKE

Inflammation of the airway epithelium

Infiltration of inflammatory cells and cytokines(neutrophils, macrophages, lymphocytes, leukotrienes and interleukins)

Increased protease activity with breakdown of elastin in connective tissues of the lungs(Elastases, Cathepsins, etc.)

Destruction of alveolar septa and loss of elastic recoil of bronchial walls

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“EMPHYSEMA”

6. Why is the O2 inhalation at 2LPM in spite of the SaO2 at 88%? How do we explain the “hypoxic drive” in a pt. with emphysema? What important considerations do you have to remember regarding O2 administration in a pt. with COPD like M.C.?

First things first. It is important to understand that Hypoxic Drive does exist, it is not a myth, but the Hypoxic Drive Theory is a myth. So let me differentiate the two:

o Hypoxic Drive: This is when a person’s body relies on low levels of O2 to signal them to breathe faster. A person without COPD normally relies on high levels of CO2 to signal them to increase their breathing rate.

o Hypoxic Drive Theory: When you give a person with COPD high concentrations of O2, say 100% O2, it will cause their hypoxic drive (their need to breathe) to shut off and they may stop breathing, go into respiratory failure, and die because of too much oxygen.

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Air Trapping Loss of surface area for gas exchange

Over Distended Lungs Total Lung Capacity and Residual Volume

Insufficient alveolar ventilation

Hypercapnia and Hypoxemia

Alveolocapillary distribution abnormality

Hyperexpansion of chest

Barrel Chest

CHRONIC HYPOXIA

Central Chemoreceptors(Ventrolateral Medullary Surface)

Increased Rate and Depth of

Breathing

Peripheral Chemoreceptor(Carotid and Aortic Bodies)

Chemoreceptor Relflexes

Use of Accessory muscles

Hyperpnea

Release of Epinephrine and Norepinephrine

Splenic Contraction

Release of stored RBC in blood from

the spleen

Erythrocytosis

Cardiac Stroke Volume

Vasoconstriction

Physical Activity

Erythropoiesis

Heart Rate(124 bpm)

Blood Pressure(162 / 84 mmHg)

Basal Metabolic Rate

Temperature(38.9oC / 102oF)

Respiratory Rate(36 bpm)

“ALL OF THESE changes in the Vital Signs are result of bodies COMPENSATORY MECHANISM to hypoxia”

According to Dr. John Hoyt in his article Debunking Myths of Chronic Obstructive Lung Disease:

“It is true that administration of oxygen to a patient with an exacerbated chronic obstructive lung

disease and acute respiratory failure may lead to an increased CO2. It is true that

the hypercarbia may become severe and be associated with cardiorespiratory arrest. The

problem is with interpreting the cause of the events…”

Both emphysema and chronic bronchitis patients may develop a hypoxic drive to breathe. Healthy people get their drive to breathe from the amount of carbon dioxide in the blood. Patients who have emphysema or chronic bronchitis build up consistently high levels of carbon dioxide. Because of this, the body looks to the levels of oxygen, rather than carbon dioxide, to determine the need to breathe. If oxygen levels are low, they breathe faster to get more oxygen.

Giving oxygen to a patient with hypoxic drive can be a problem. After oxygen is administered, its level in the blood increases. In the patient with a true hypoxic drive, increased levels of oxygen may signal the body to slow down or even stop breathing.

When you give a COPD patient O2, there are several ways in which it can increase CO2 according to Jeff Whitnack’s The Death of Hypoxic Drive Theory:

Haldane Effect: Describes the property of Hbg. The idea to this is that if Hbg is carrying a lot of O2 (oxygenated blood) then it has a lower capacity to carry CO2. It works in reverse too: if Hbg is carrying very few O2 (deoxygenated blood) then it can take on more CO2.

Hypoxic Pulmonary Vasoconstriction (HPV): This occurs when the alveoli in the lungs are poorly ventilated and causes the pulmonary arteries to constrict in order to divert more blood to the oxygen starved alveoli to better ventilate it. However, if we give 100% O2 to the pt, it fools our body, and this constriction does not happen, and CO2 will continue to build and be trapped in the alveoli. This causes a V/Q mismatch and increase physiological dead space in some patients (New, 2006).

The Most Important MechanismSo we now know that Haldane Effect and HPV, which leads to V/Q mismatch and increase in physiological dead space, plays a role in increasing CO2 within a COPD pt. But how big of a role does it play? Well, according to Irven H Young:

“…worsening ventilation-perfusion mismatching and an accompanying increase in dead space ventilation contribute about 50% of the increase in carbon dioxide levels.”

Understanding these effects are important because it shifts our focus of the possible exacerbation of respiratory failure in COPD patients from giving oxygen to CO2 being trapped. We all know that if we don’t get O2, we become hypoxic and we die. However, hypercapnia develops at a slower rate than hypoxaemia (New. 2006). As Dr. Busko wonderfully summarizes,

“Hypoxia kills, hypercapnia happens”.

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So what does this all mean? It means we should give COPD pts high concentrations of O2 because they need it, but we should do something about the CO2 build up. We need to help them blow off the CO2. We can do this by mechanical ventilation (Busko).

TOBACCO SMOKE

Inflammation of the airway epithelium

Infiltration of inflammatory cells and cytokines(neutrophils, macrophages, lymphocytes, leukotrienes and interleukins)

Increased protease activity with breakdown of elastin in connective tissues of the lungs(Elastases, Cathepsins, etc.)

Destruction of alveolar septa and loss of elastic recoil of bronchial walls

EMPHYSEMA

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Loss of surface area for gas exchange

Alveolocapillary distribution abnormality

Co2 in the blood

Chemoreceptor Reflex(Central and Peripheral)

Activation of Hypoxic Drive

Hypoxia / Hypercapnia

HALDANE EFFECT

HYPOXIC PULMONARY VASOCONSTRICTION

General points about oxygen therapy in chronic obstructive pulmonary disease:

The respiratory drive is normally largely initiated by PaCO2 but in chronic obstructive pulmonary disease (COPD) hypoxia can be a strong driving force and so if the hypoxia is corrected then the respiratory drive will be reduced. There will also be a loss of physiological hypoxic vasoconstriction which is partly protecting the patient from the effects of areas of gross alveolar hypoventilation.

Therefore, oxygen therapy in COPD must be used with care in the acute setting but it can have distinct benefits in the long-term.

Chronic hypoxaemia causes slowly progressive pulmonary with the development of right ventricular hypertrophy and possible cor pulmonale with secondary polycythaemia.

Secondary polycythaemia increases blood viscosity and hence resistance to flow. There is also sludging and a tendency to thrombosis.

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CO2 Diffuses to RBC

Carbonic acidCarbonic

Anhydrase

Carbinohaemoglobin

Diffusion rate of CO2

from the tissue

Deoxyhaemoglobin

Uptake of CO2 by the RBC

Acidity

Release of H+

H+ binds to HCO3+

Creating Carbonic Water

Respiratory center trigered

CONTINOUS BREATHING

Sympathetic Nervous system stimulation

Release of Epinephrine and Norepinephrine

Pulmonary Artery vasoconstriction

Blood goes to the O2 rich alveoli

Improved V/Q Ratio

ARTERIAL OXYGENATION(SaO2 of 88 %)

“Patient should be on a low level of O2 support to continuously trigger this HYPOXIC DRIVES to

maintain oxygenation”

“Haldane Effect and Hypoxic Pulmonary Vasoconstriction are both part of the Hypoxic

Drive”

7. Make an integrated pathophysiologic flowchart of MC’s disease condition.8. Given M.C.’s history and your knowledge of pathophysiologic processes, explain the pathophysiologic basis of the assessment findings in M.C?

Note: Numbers seven and eight will be discussed together by the below schematic diagram of the pathophysiologic basis of Emphysema and its manifestations.

TOBACCO SMOKING

Oxidative Toxins

Initiates immune and inflammatory response

Release of inflammatory Mediators from ALVEOLAR Macrophages(IL-6, IL-1, IL-8 and TNF-α; Metaloproteases)

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Interleukins and TNF-α

Recruit Neutrophils to the site(CHEMOTAXIS)

Secretes PROTEASES(Elastases and Cathepsins)

Metaloprotease

Damage to the surrounding tissue

Damage to the elastic fibres surrounding the alveoli and terminal bronchioles

Recruits T-Lymphocytes

T-Cell Mediated Apoptosis

Cells will have an unprogrammed cell death

Collagen deposition

Fibrosis formation

Irreversible enlargement of the air spaces distal to the terminal bronchiole

Destruction of alveolar walls and septa and loss of elastic recoil of bronchial walls

(EMPHYSEMA)

Legend:BOLD words: Present signs and symptomsBLUE words: Laboratory and diagnostic testsGreen Words: TreatmentRed Words: Potential complications

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Loss of fibrous and muscle tissue

Breakdown of Alveolar Elasticity

Large spaces within lung parenchyma (Bullae)

Air space adjacent to pleurae(Blebs)

Reduced pulmonary elastic recoil

End-expiratory (Residual) lung volume

Dynamic Hyperinflation

Over Inflated Lungs

Reconfiguration of the Rib cage

Dyspnea on Exertion

Barrel Chest(AP / Transverse ratio:

>1:2)

Horizontal Ribcage

Widened retrospinal clear space

Low Flat Diaphragm(<7 anteriorly and <10

posteriorly)

Pulmonary Function Test

Ventilation Perfusion Mismatch(V/Q Ratio of < 0.8 or <4/5)

Air Trapping

Hyperexpansion of chest

Work of breathing

Use of accessory muscles

Labored Breathing

Chest X-Ray

Persistent inflammatory response

Hyperactivity of bronchi

Hyperactivity of epithelial

cells

Bronchoconstriction Thick yellow sputum

production

Cough Reflex triggered

Coughing Spells

Bronchodilators

Airflow LimitationLoss of Respiratory Membrane

Ratio of Air to Lung Tissue

Diffusion Defects

Number of Pulmonary capillaries

Pulmonary resistance

Inability of the alveoli to recoil normally after expanding

Tactile fremetus on Palpation

Alveolar collapse on expiration

Crackles WheezingPulmonary

hypertension

Right Ventricular Hypertrophy(Cor Pulmonale)

Chest X-Ray

Electrocardiography

Expectorants

Hyper resonance on Chest Percussion

Hypercapnia / Hypoxemia

Ruptured Bullae

Spontaneous Pneumothorax

Hypoxia

Pursed lip Breathing

Impaired Glucose delivery and use

Release of cathecolamines and cortisol

Glycogenesis Gluconeogenesis

Energy Stores

Fatigue

Muscle Wasting

Diaphragmatic function

Hyperinflation of alveoli

Respiratory Acidosis

ABG Analysis

Appetite

Weight Loss

CTT

Chemoreceptor reflexes

Increased rate and depth of breathing

Hyperpnea

Increased respiratory Rate

Sputum C&S

9. What are the possible complications of Emphysema and their manifestations?

I. ACUTE EXACERBATIONS

Acute exacerbations are episodes that occur when airways suddenly become obstructed and symptoms worsen. Such events are associated with inflammation in the airways and are generally triggered by an infection in the airway or throughout the body.

Other factors that can trigger serious lung events:

Certain medications

Exposure to irritants in the air

Seasonal changes

Acute exacerbations include the following symptoms:

Increased volume of sputum Sputum that is thicker and darker Worsened shortness of breath that causes the patient to breathe faster and

harder. This is the most common and distressing acute symptom.Acute exacerbations occur, on average, between two and three times a year in

patients with moderate-to-severe Emphysema. In about 80% of the cases, they are triggered by infections. Smokers have more episodes than nonsmokers.

II. REDUCED QUALITY OF LIFE AND MOOD

Nearly half of patients with Emphysema report a limitation in daily activities. They have trouble walking up stairs or carrying even small packages. Breathing becomes hard work. More than half of patients with Emphysema have insomnia. Such impairment in quality of life can negatively affect mood.

Almost half of patients with Emphysema have anxiety, depression, or another psychiatric disorder, compared with 31% of people in the general population. Women with COPD are more susceptible to psychological problems than men. If patients with Emphysema become anxious or depressed, they may have a poorer outlook than those without these emotional problems. COPD patients with moderate-to-severe depression face a greater 3-year mortality rate than those who experience less depression. Low oxygen levels also can impair mental function and short-term memory. Psychological interventions may be particularly helpful for people with COPD.

III. MALNOURISHMENT

People with Emphysema often lack good nutrition. Patients with chronic bronchitis tend to be obese. Patients with emphysema tend to be underweight. Loss of weight and

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Splenic Contraction

Release of Epinephrine and Norepinephrine

Release of RBC from spleen into the bloodstream

Erythropoeisis

ErythrocytosisCBC

Cardiac Stroke Volume

Heart Rate

Vasoconstriction

Blood Pressure

Basal Metabolic Rate

Temperature

muscle mass is associated with a poor outcome in Emphysema. Good nutrition improves the ability to exercise, which in turn builds muscle strength and lung function. Obese patients with Emphysema who lose weight sleep better.

IV. HEART DISEASE

Over time, Emphysema causes low levels of oxygen (hypoxia) and high levels of carbon dioxide (hypercapnia) in the body. In order to boost oxygen delivery, the body compensates in a number of ways:

Blood vessels in the lung constrict to force blood and oxygen through the circulatory system. This leads to high blood pressure in the lungs (pulmonary hypertension).

More red blood cells are produced to increase the blood's oxygen-carrying capacity.

The heart rate increases to pump more blood. The rate of breathing increases.Eventually these activities can lead to very serious and even life-threatening

conditions:

Abnormally high blood pressure in the lungs can cause a complication called cor pulmonale, in which the right ventricle of the heart enlarges, eventually leading to heart failure.

Patients with prolonged and severe hypoxia and hypercapnia are at risk for acute respiratory failure, which can cause heart rhythm abnormalities or other life-threatening conditions.

V. OTHER SERIOUS MEDICAL PROBLEMS ASSOCIATED WITH COPD

The smoking that causes COPD is associated with high risks of pneumonia, lung cancer, stroke, and heart attack. Tobacco smoke contains more than 400 substances, many of which are oxidants, metals (such as lead, cadmium, and aluminum), and carcinogens. Nicotine itself may not damage tissues, but it is the chemical that addicts the smoker to tobacco.

Sleep Disturbance. About half of all people with severe COPD experience sleep disorders such as sleep-related hypoxia or insomnia. Nocturnal hypoxia, a lack of oxygen during sleep, occurs when breathing is shallowest during rapid-eye-movement (REM) sleep. It may be due to suppression of the cough reflex and a build-up of mucus. Nocturnal hypoxia is treated with overnight oxygen therapy. As COPD worsens, many patients have trouble falling or staying asleep. COPD patients should not use sleep medications. Nighttime oxygen or a change in COPD medications from beta-agonists to anticholinergics can sometimes help restore restful sleep.

Osteoporosis. Osteoporosis is a significant problem in patients with COPD. Many conditions associated with COPD, including smoking, vitamin D deficiency, sedentary lifestyle, and the use of corticosteroid medications put people at risk for bone density loss and osteoporosis.

Gastroesophageal Reflux (GERD). More than half of patients with severe COPD have GERD, a condition in which stomach acids back up from the stomach into the esophagus. However, many COPD patients don't report experiencing GERD symptoms such as heartburn.

10. Make a tabular comparison of the pathogenesis and pathophysiologic changes of Emphysema, Bronchitis and asthma.

ASTHMA COPD

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CHRONIC BRONCHITIS EMPHYSEMA

Age at onset At Any Age (usually <40 years) Usually >40 Years

Smoking history Possible Usually >10 packs per yearCough at Exacerbation Usually between 2 to 6am Gradual IncreaseSputum production Infrequent Common PossibleAllergy Common InfrequentAirway InflammationMain portion Large Airways Small Airways (Bronchi) Small Airways (Alveoli)

Pathophysiology Basement membrane Thickening Fibrosis of Bronchi Destruction of alveolar

wall

Bronchial Biopsies Th-2 dominant T Cells Th-1 dominant T Cells Neutrophils and Proteases

Reversibility (Peak Flow Results) Normalize with time May improve but not

normalize Non Reversible

Family History common Uncommon Possible (Alpha1 Antitrypsin deficiency)

Clinical ManifestationsTactile Fremitus Normal Normal Decreased

Percussion Resonant to hyper resonant Resonant Hyper Resonant

Auscultation Wheezes Normal to decreased breath sound; wheezes

Decreased intensity of breath sounds, usually

with prolonged expirationProductive Cough None Classic sign Late in course with

infectionDyspnea Common Late in course CommonWheezing Continuous Intermittent MinimalBarrel Chest None Occasionally ClassicProlonged Expiration Not Present Always present Always presentCyanosis Common Common UncommonChronic Hypoventilation Hyperventilation Common Late in CoursePolycythemia Uncommon Common Late in CourseCor Pulmonale Uncommon Common Late in Course

11. Based on the assessment findings, identify five priority problems that M.C. may be experiencing.

Priorities are:a. Achieving Airway Clearanceb. Improving Breathing Patternsc. Improving Activity Toleranced. Monitoring and Managing potential complicationse. Continuous assessment of the patient

Nursing Care Priorities:

f. Impaired Gas exchange and airway clearance due to chronic inhalation of toxinsGOAL: Improvement in gas exchange

g. Impaired gas Exchange related to ventilation-perfusion inequalityGOAL: Improvement in gas exchange

h. Ineffective airway clearance related to bronchoconstriction, increased mucous production ineffective cough, bronchopulmonary infections and other complicationsGOAL: Achievement of airway clearance

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Release of Epinephrine and Norepinephrine

i. Ineffective breathing pattern related to shortness of breath, mucus, bronchoconstriction and airway irritantsGOAL: Improvement in breathing pattern

j. Activity intolerance due to fatigue, hypoxemia and ineffective breathing patternsGOAL: Improvement in activity tolerance

The laboratory sends the ff. report several hours after admission: RBC – 3.8thou/cmm, WBC- 13,000 thou/cmm, Hgb 12g/dL, ABGs: pH- 7.28, pO2 – 80 mmHg, pCO2 – 65 mmHg, HCO3 – 22.

12. Interpret the above results. How do the results relate to the pathophysiologic changes of emphysema?

RBC: 3, 800, 000 cells/μL (Normal Value: 4.7 to 6.1 million/ μL) Hgb: 12 g/dL (Normal Value: 13.5 – 17.5 g/dL)

Anemia of chronic illness is typically a normocytic anemia and is most commonly observed in patients with concurrent infectious, and inflammatory or neoplastic diseases. COPD fulfills the criteria of a chronic, inflammatory, multisystemic disease leading to the expectation of anemia.

Anemia in COPD is an immune disorder that has been reported in numerous diseases with an inflammatory component. Inflammatory cytokines have various effects that play a key role in the pathogenesis of this form of anemia and ultimately interfere with the normal mechanisms of erythropoiesis. The following possible mechanisms have been proposed:

1. Dysregulation of iron homeostasis caused by the accumulation and retention of iron within cells of the reticuloendothelial system giving rise to a consequent decrease in available iron for use by progenitor cells. The administration of IL-1 and TNF-α has been shown to lead to the development of hypoferremia in experimental animals.

2. Impaired proliferation of erythroid precursors. The most potent inhibitor is interferon-γ , although the free radicals generated by oxidative stress also have this effect. This phenomenon can result in an increase in the apoptosis of these cells or a decrease in the expression of EPO in their receptors.

3. Impaired bone marrow response to EPO caused directly by cytokines. IL-1 and TNF-α inhibit the expression of this hormone in vitro. Finally, the activation of these mediators may stimulate the production of hepcidin, a recently discovered polypeptide synthesized in the liver that participates in the process of iron absorption and is thought to play a key role in the development of anemia of chronic disease.

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COPD INFLAMMATION

Cytokine release Acute-Phase Reactants(CRP,LDH, Fibrinogen)

TNF-α, IL-6, IL-8 Hepcidin

Inhibition of Erythroid precursors

Inteference with the action of EPO

Macrophage Iron Sequestration

Inhibition of Iron Absorption

ABGs: pH- 7.28, pO2 – 80 mmHg, pCO2 – 65 mmHg, HCO3 – 22.

Patient is experiencing Uncompensated Respiratory Acidosis a classic sign found in patients with emphysema (see schematic diagram of the clinical manifestations).

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Inhibition of Erythropoiesis

RBC production(3, 800, 000 cells/μL)

ANEMIA(Hgb: 12 g/dL)

Reference:1. Agusti AG, Noguera A, Sauleda J, et al. Systemic effects of chronic

obstructive pulmonary disease. Eur Respir J 2003; 21:347–360

AUTHOR; SOURCE

TITLE PROBLEM SUMMARY OF FINDINGSSIGNIFICANCE TO

NURSINGMatthias John, MD, PhD, Soeren Hoernig, MD

Anemia and Inflammation in COPD

Although chronic obstructive pulmonary disease (COPD) is traditionally associated with polycythemia, its systemic inflammatory components can interfere with erythropoietin and result in anemia of chronic disease. Researchers assessed the frequency of anemia and its relation to serum erythropoietin (EPO) levels and severity of the disease in a group of COPD patients.

This study documents

that anemia occurs relatively

frequently in COPD patients

and is related to the presence

of inflammation. Anemia is an

understudied issue in COPD

but may be of great importance

in this disease. In our cohort,

anemia (with hemoglobin

concentrations < 12.0 g/dL in

women and < 13.5 g/dL in

men) was present in as many

as 13% of all COPD patients.

This may be an

underestimation of the anemia

prevalence, as we have

excluded patients with anemia

related to bleeding and known

folate or vitamin B12 deficiency.

Furthermore, anemic COPD

patients showed increased

levels of erythropoietin

compared to nonanemic

patients and normal control

subjects.

Anemia of chronic illness is

typically a normocytic anemia

and is most commonly

observed in patients with

concurrent infectious, and

inflammatory or neoplastic

diseases. COPD fulfills the

criteria of a chronic,

inflammatory, multisystemic

The present study is

limited by a relative small

number of patients. For

future investigations,

larger study populations

are needed. This would

allow investigating

whether anemia is related

to the primary disease

process per se or to

secondary systemic

manifestations such as

weight loss, loss of lean

tissue mass, hypoxia, or

systemic inflammation.

Anemia in COPD is

understudied. There are

no previous reports on

anemia frequency and

pathophysiology in

COPD. More detailed

investigations on

hematologic and clinical

parameters ( ie ,

prevalence of anemia in

COPD and its gender

relatedness, exercise

capacity, 6-min walk test)

and prognosis are

required to provide

indications whether

anemia is merely a

marker or a mediator of

pathophysiologic

Page 17 of 20

disease leading to the

expectation of anemia. While

anemia in chronic heart failure

or renal insufficiency has been

frequently investigated, it is

understudied in COPD.

The mechanism of anemia

development in COPD might

be similar to that in other

chronic diseases. It has been

shown that mediators of the

immune and inflammatory

response, such as tumor

necrosis factor-α, IL-6, and

interferon-γ are potentially

involved in the development of

anemia in chronic illness. The

increased levels of

inflammatory cytokines lead to

a shortened RBC survival, with

a demand for a slight increase

in RBC production. The bone

marrow cannot adequately

respond to the increased

demand for RBCs. This is

caused by a relative

erythropoietin resistance due

to an impaired ability of RBC

progenitors to respond to

erythropoietin. An impaired

mobilization of

reticuloendothelial iron stores

is an additional

pathophysiologic factor.

processes that may

impair physical

functioning in COPD.

Interventions with

erythropoietin and iron

supplementation would

then seem very promising

in order to improve the

poor health status and

prognosis of patients with

COPD.

Monica J Fletcher, Birthe H Dahl

Expanding nurse practice in COPD: is it key

The prevalence of chronic obstructive pulmonary disease (COPD), a common and preventable

The nursing role in COPD – and essentially in all chronic diseases – is becoming increasingly important and is characterised by continuity of care. Nurses are involved in the

Nurses represent an appropriate resource to deliver care and support to individuals with COPD throughout the entire course of the disease.

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to providing high quality, effective and safe patient care?

chronic disease, is on the increase, and so are the financial and social burdens associated with it. The management of COPD is particularly challenging, as patients have complex health and social needs requiring life-long monitoring and treatment. In order to address these issues and reduce the burden imposed by COPD, the development of innovative disease management models is vital. Nurses are in a key position to assume a leading role in the management of COPD since they frequently represent the first point of contact for patients and are involved in all stages of care. Although evidence is still limited, an increasing number of studies have suggested that nurse-led consultations and interventions for the management of COPD have the potential to impact positively on the health and quality of life of patients. The role of nurses in the management

management of COPD at all stages, from prevention to provision of end-of-life care within a variety of settings, both in the community (including patients’ own homes and family practice) and hospitals. Nurses often play a key role in new care models based on different types of telemedicine support.5,6Nurse-led consultations and disease management interventions are important interventions which enable nurses to provide, complement, or extend the care delivered by doctors. Nurse-led consultations carried out by experienced nurses frequently include tasks that traditionally belong to physicians, such as physical examination of patients, diagnosis and, in countries such as the UK, prescription of medicines. Nurse-led management interventions are aimed at helping patients cope with their condition and improve their quality of life. They include patient education, guided self-management, smoking cessation, and pulmonary rehabilitation programmes.

Even though more research is needed to establish the effectiveness of nurse-led interventions and consultations, there is some growing evidence to demonstrate the benefits provided by these interventions, particularly in relation to the hospital-at-home and early discharge schemes, smoking cessation, and pulmonary rehabilitation programmes as well as interventions aimed at improving self-management behaviour. Studies have also shown that nurses are able to deliver care that is as effective as that provided by doctors. However, a paucity of standardised competencies and specified training requirements – coupled with a lack of clinical supervision, appropriate funding, and workload pressures among nurses delivering COPD care – highlight specific areas for improvement. Nurses need to strengthen their role to plan and deliver more strategies to improve the quality of life of patients with COPD and reduce the burden of this disease in the future. In doing so, nurses cannot assume an increased responsibility in isolation. More coordinated efforts and better mentorship and support from colleagues, along with a formal recognition of their new role, is needed to allow nurses to provide high-quality, safe, and cost-effective care and, in that way, to optimise the use of limited healthcare resources worldwide.

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of COPD around the world could be significantly expanded and strengthened. Providing adequate educational opportunities and support to nurses, as well as addressing funding issues and system barriers and recognising the importance of the expanding roles of nurses, is vital to the well-being of patients with long-term medical conditions such as COPD and to society as a whole, in order to reduce the burden of this disease.

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