Name : Deka Ade Yusmawan

No.Reg: 22020116410058

Chronic obstructive pulmonary disease (COPD) is a leading and increasingly major

cause of morbidity and mortality worldwide . COPD results in a substantial and increasing
burden in terms of prevalence, incidence and mortality, and is predicted to be the third leading
cause of global mortality by 2030 (WHO, 2013) [2]. Results of the Burden of Obstructive Lung
Disease (BOLD) study-a multinational investigation of the prevalence of COPD showed that
Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage II COPD range from 5.9%
in Hannover, Germany, to 19.1% in Cape Town, South Africa. The findings from the five sites in
the Latin American Project for the Investigation of Obstructive Lung Disease (PLATINO) study
indicated that adjusted prevalence of COPD ranged from 11.9% in Mexico City to 19.4% in
Montevideo.(Journal, 2016)
COPD poses a major health and socioeconomic burden in the Asia-Pacific region, as it
does worldwide [5]. The estimated prevalence of moderate to severe COPD among adults aged
30 years was 6.3% in the 12 Asia-Pacific countries, and the COPD prevalence in Taiwan was
5.4% [6]. Recent research of the impact of COPD in the AsiaPacific region: the Epidemiology
and Impact of COPD (EPIC) Asia population -based survey, indicated that the overall prevalence
of COPD was 6.2%, ranging from 4.5% (Indonesia) to 9.5% (Taiwan) in 2012 [7]. According to
a government report, chronic lower respiratory diseases was the 7th-leading cause of death in
Taiwan,
The main risk factor for COPD is smoking. It causes up to 90 percent of COPD deaths,
according to the American Lung Association (ALA). People who smoke are 13 times more likely
to die from COPD than those who never smoked. Long-term exposure to tobacco smoke is
dangerous. The longer you smoke and the more packs you smoke, the greater your risk is of
developing the disease. Pipe smokers and cigar smokers are also at risk. Exposure to secondhand
smoke also increases your risk. Secondhand smoke includes both the smoke from burning
tobacco and smoke exhaled by the person smoking.(Brashier & Kodgule, 2012)
Patient J.T to the emergency room with a three-day historyof progresif dyspnea, cough,
and increased production of clear sputum. He usually coughs up only a scant amount.
The patient J.T manifest clinic risk factor at her beef products worker and always 2 pack/day
camel smoker for 37 years, with emphysema(Brashier & Kodgule, 2012)

At stage 3 COPD, symptoms are far too debilitating to ignore any longer. Along with the
common COPD symptoms you may begin to experience more advanced symptoms that indicate
your COPD is more severe. And according to GOLD guidelines, stage 3 COPD patients have an
FEV1 of 30-49%. Stage 3 COPD treatment becomes a little more intense than with previous
stages. This is partly because your symptoms are more persistent and harder to manage. Your
treatment goal is to keep your symptoms at a manageable level and to prevent loss of quality of
life.

Stage 3 COPD is the stage where symptoms become more severe, difficult to manage,
and more persistent.Your treatment options have become more intense and you have to closely
monitor your symptoms. Your doctor may try switching treatment methods up to see if there's a
more effective way to manage your COPD.You might experience more advanced symptoms like
morning headaches and edema. Supplemental oxygen is more than likely being used at night and
possibly 24/7. Your goals at stage 3 should be to slow the progression of your disease through a
strict treatment regiment and healthy lifestyle changes.(Loftus & Bowden, 2016)

In copd disease there is a collection of blood gases that are very influential in the stage of
copd disease. When the parameters of preoperative, post-extubation and 3-6 h after extubation
arterial blood gas analysis were compared, no significant difference was found. Interestingly, the
number of patients with high preoperative PaCO was higher in Group 1 than in Group 2. The
number of patients with low preoperative PaO was close to each other between the groups.(Sami,
Gnay, zkan, Gven, & Yurtsever, 2016)

Chronic alcohol abuse or alcoholism cost $223 billion to US economy and 79,000
deaths each year (Bouchery et al., 2011). The worldwide death toll is estimated to be 30-fold
greater than that in the US (CDC, 2004; NIAAA, 2000). Approximately 1020 million people
meet the criteria of alcoholic dependence in the United Statesand >500 million worldwide (Grant
et al., 2004; Lieber, 1995). Alcohol over consumption damages almost every organ in the body
andpredisposes the host to a wide range of infectious diseases such as pneumonia, acute
respiratory distress syndrome (ARDS) and chronic obstructive pulmonary disease (COPD)
(Liang et al.,2012; Pabst et al., 2011; Zhang et al., 2002a). The majority of ingested ethanol is
metabolized in the liver by cytosolic alcohol dehydrogenase (ADH) to acetaldehyde, which is
further oxidized by mitochondrial aldehyde dehydrogenase (ALDH) to acetate (Lieber, 2004).
Mammalian lungs can metabolize ingested ethanol by ADH followed by ALDH at rates
dependent on its concentration (Bernstein, 1982; Jones, 1995; Qin and Meng, 2006; Vasiliou and
Marselos, 1989; Yin et al., 1992). Ethanol can also be metabolized by microsomal cytochrome
P450 2E1 (CYP2E1) and peroxisomal catalase to acetaldehyde in both the liver and in lungs
(Bernstein et al., 1990; Jones, 1995; Rikans and Gonzalez, 1990; Yin et al., 1992). CYP2E1 is
particularly induced during chronic alcohol abuse and is shown to be responsible for production
of reactive oxygen species.(Kaphalia & Calhoun, 2013)

The main nding of this study is the high prevalence of CRF (concealed and overt)
among patients with COPD. About half of the COPD patients have CRF and one of each four
COPD patients has CRF despite normal serum creatinine. The overall prevalence of CRF (GFR
< 60 mL/min/1.73 m2) was 46% in the COPD group (26% concealed CRF and 20% overt CRF)
and 22% in the control group (10% concealed CRF and 12% overt CRF) (P < 0.001). While
serum creatinine greater than 1.26 mg/dL for men and 1.04 mg/mL for women is a reliable
marker of CR [11], the GFR is frequently depressed in patients with COPD despite normal serum
creatinine [26% of COPD patients have low GFR despite normal serum creatinine (concealed
CRF) in comparison with 10% in the control group]. The association between COPD and CRF
may be explained by several factors. First; it was found that arteriolar renal resistances are
increased in COPD patients, perhaps because of local adrenergic discharge secondary to
hypercapnia. In the initial phase of COPD, renal perfusion is usually normal, but as the disease
worsens, particularly as CO retention develops,renal blood ow decreases. PaCO2 has been
found to correlate inversely with ERPF (effective renal plasma ow) and with the ability to
excrete sodium and water. Hypercapnia may cause renal vasoconstriction directly and indirectly
by stimulating sympathetic tone as detected by the increase in the circulating levels of
norepinephrine. (Elmahallawy & Qora, 2013).
 Long-term use of supplemental oxygen improves survival in patients with COPD and
severe resting hypoxemia. However, the role of oxygen in symptomatic patients with COPD and
more moderate hypoxemia at rest and desaturation with activity is unclear. The few long-term
reports of supplemental oxygen in this group have been of small size and insufcient to
demonstrate a survival benet. Short-term trials have suggested benecial effects other than
survival in patients with COPD and moderate hypoxemia at rest. In addition, supplemental
oxygen appeared to improve exercise performance in small short-term investigations of patients
with COPD and moderate hypoxemia at rest and desaturation with exercise, but long-term trials
evaluating patient-reported outcomes are lacking. This article reviews the evidence for long-term
use of supplemental oxygen therapy and provides a rationale for the National Heart, Lung, and
Blood Institute Longterm Oxygen Treatment Trial. The trial plans to enroll subjects with COPD
with moderate hypoxemia at rest or desaturation with exercise and compare tailored oxygen
therapy to no oxygen therapy. (Stoller, Panos, Krachman, Doherty, & Make, 2010)

Infection can cause a recurrence of chronic pulmonary infection, which is marked by a

symptom. Vaccines play a vital role in treating COPD at every stage of the disease. While they
aren't going to do anything to directly impact your lung function or your symptoms, for stage 1
COPD, vaccines will help protect you from viruses that could speed up the progression of your
COPD and possibly put you in the hospital.

The two most important vaccines for COPD are the:

Flu vaccine
Pneumonia vaccine
AAT (Apha-1 Antitripsin) deciency is a genetic disorder that affects an approximated 3.4
million individuals worldwide, when individuals with the ZZ, SZ or SS phenotype are included.
This condition is clinically characterised by early-onset emphysema and liver disease.(Kelly,
Greene, Carroll, McElvaney, & ONeill, 2010).

In this patient Mr. J.T experience complications of COPD disease due to a damaged
lifestyle. He was diagnosed COPD since 6 years ago. He also works as a social worker and that
worsens his diagnosis.
 Nursing Diagnosis for COPD

1. Ineffective breathing pattern

Releted to: shortness of breath, bronchoconstriction, mucus, airway irritants.
2. Ineffective Airway Clearance
related to: increased sputum production, bronchoconstriction, ineffective cough,
bronchopulmonary infection, fatigue / lack of energy.
3. Impaired Gas Exchange
related to: ventilation perfusion inequality.
4. Activity Intolerance related to generelazide weakness
Related: Weakness,
5. Knowledge Deficit
related to: lack of information, do not know the source of information.

Nursing Diagnosis NIC NOC

Nursing Intervention Clasification Nursing Outcomes
Clasification
Ineffectiveness of Airway Management Patency of airway
airways clerance o Suctioning Respiration Status
related to obstructive o Chest fisiotherapy Vital Sign
airway Cough Management Symptom Control
o Inhalation medication
o Oksigen Therapy
Respiration Monitoring
o Monitoring vital sign
o Monitoring Arterial
Blood Gas Analysis
o Fluid Monitoring

Ineffectiveness of Airway Management Respiration status

breath pattern related o Suction Status Gas Exchange
to hyperventilation o Management ansietas Weakness complaint
Cough Management Vital Sign
o Management
ventilation non-invasif
o Oksigen therapy
Respiration Monitoring
o Vital Sign Monitoring
o Monitoring Arterial
Blood Gas analysis
o Chest fisiotherapy
o Realaxation Muscle
Progressive
Activity Intolerance Therapy Activities Acitivity Tolerant
related to o Improvment of body Weakness
generelazide mechanics Rest Management
weakness Energy Management Vital sign
o Environment Quality Of Life Status
managamen
o Exercise
o Sleep Management
o Meditation
 Bibliography

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Pulmonary Disease ( COPD ), 60(February), 1721.
Elmahallawy, I. I., & Qora, M. a. (2013). Prevalence of chronic renal failure in COPD patients.
Egyptian Journal of Chest Diseases and Tuberculosis, 62(2), 221227.
http://doi.org/10.1016/j.ejcdt.2013.02.005
Journal, I. (2016). ClinMed, 3(3).
Kaphalia, L., & Calhoun, W. J. (2013). Alcoholic lung injury: Metabolic, biochemical and
immunological aspects. Toxicology Letters, 222(2), 171179.
http://doi.org/10.1016/j.toxlet.2013.07.016
Kelly, E., Greene, C. M., Carroll, T. P., McElvaney, N. G., & ONeill, S. J. (2010). Alpha-1
antitrypsin deficiency. Respiratory Medicine, 104(6), 763772.
http://doi.org/10.1016/j.rmed.2010.01.016
Loftus, N. W., & Bowden, T. (2016). Tension pneumothorax recurrence in COPD: a care study,
(October), 10581064.
Sami, ., Gnay, R., zkan, S., Gven, T. S., & Yurtsever, N. (2016). Arterial Blood Gas
Analysis in Chronic Obstructive Pulmonary Disease Patients Undergoing Coronary Artery
Bypass Surgery, 9399. http://doi.org/10.5578/ttj.30503
Stoller, J. K., Panos, R. J., Krachman, S., Doherty, D. E., & Make, B. (2010). Oxygen therapy
for patients with COPD: Current evidence and the long-term oxygen treatment trial. Chest,
138(1), 179187. http://doi.org/10.1378/chest.09-2555