Question

Case Study 1 Introduction Bob, a 53-year-old caucasian man, arrives at the emergency department accompanied by his friend, complaining of increasing difficulty breathing and productive cough with green sputum. His friend says he dropped in to visit Bob, who lives alone, and found him sitting up on the edge of his bed, unable to breathe and seemed quite confused. When he last saw Bob 4 days ago, he says he had a cough and a temperature for which he has been taking paracetamol. Bob has been a smoker for 27 years but quit about a year ago when he was diagnosed with stage II (moderate) chronic obstructive pulmonary disease (COPD). Since being diagnosed, Bob has been taking salbutamol PRN and tiotropium bromide (Spiriva) daily. He has no other medical conditions, and no known allergies. A brief triage assessment reveals the following: Unwell looking male, drowsy but rousable, confused regarding time and place. His Glasgow Coma Score is 14/15 (E3 V4 M6), with pupils equal and reactive to light. He is speaking words only and breathing with obvious accessory muscle use and has a prolonged expiratory phase. His initial respiratory rate is 28 breaths/min and auscultation reveals widespread inspiratory and expiratory wheezes, with crackles at the right base. His SpO2 on room air is 74% and he is peripherally cyanosed. His pulse is 124 beats/min and regular, and his blood pressure is 176/93 mmHg. He is sweaty and hot to touch with a tympanic temperature of 38.200 Bob is immediately triaged ATS category 2 to the resuscitation cubicles and commenced on 8L/min Oxygen therapy via a nebuliser mask with 5mg Salbutamol and 500mcg ipratroprium. Within minutes he has an Spo2 of 89%. On ECG he has a sinus tachycardia of 124 beats/min with but no evidence of ischaemic changes. In the resuscitation area “Primary survey " AIRWAY Clear Speaking in words only Lips and tongue and peripheries noted to have bluish tinge

Answer 1

Chronic obstructive pulmonary disease(COPD)

                           Chronic obstructive pulmonary disease (COPD) is a common lung disease. Having COPD makes it hard to breathe.

There are two main forms of COPD:

1. Chronic bronchitis, which involves a long-term cough with mucus.
2. Emphysema, which involves damage to the lungs over time.

Pathophysiology of COPD

                   COPD reduces lung function by damaging the airways and air sacs in the lungs.When a person with healthy lungs inhales air, it travels down their windpipe and into the airways of the lungs, known as bronchial tubes.Inside the lungs, the bronchial tubes branch into thousands of smaller, thinner channels called bronchioles.At the end of these tubes are bunches of tiny round air sacs called alveoli. There are more than 300 million alveoli in the lungs. Larger lungs have more alveoli.

             Capillaries are small blood vessels that surround the walls of the air sacs. Once air makes its way to the air sacs, oxygen passes through the walls of the air sac into the capillaries that transport blood.At the same time, carbon dioxide moves from the capillaries into the air sacs. These events happen at the same time, and scientists refer to this as gas exchange.

                   Healthy air sacs are elastic and very stretchy. As a person breathes in, the air sacs fill up with air like a balloon. As they breathe out, the air sacs deflate due to the air moving out. The body uses energy to blow the air sacs up but does not use any energy to empty them as they return to their original size.

                   People with COPD have less air flowing in and out of the airways. Several physical problems in the lungs can contribute to this:

• the airways and air sacs have lost their stretchiness
• the walls between the air sacs are partially or completely damaged
• the walls of the airways become inflamed and thickened
• the airways produce more mucus, causing them to clog

Top of Form

COPD exacerbation Increased ventilatory drive of Paoz Tachypnoea (e.g. anxiety) pH Worsening expiratory flow limitation Dynamic hyperinflation (IEELV, HIC) onoea Mechanical Gas Neuromechanical disadvantage exchange uncoupling PEEPI • IVDNI due to constraint of VT CDYN Elastic/threshold loading of inspiratory muscles Inspiratory muscle dysfunction Cardiovascular effects . Pulmonary arterial pressure • HRV preload • LV afterload

Arterial Blood Gas changes in a COPD patient

The main measurements from the arterial blood gas test include:

• The level of hydrogen ions (H⁺) in the blood. Normal values are between 7.38 and 7.42. The acidity or alkalinity of the blood is linked with the amount of carbon dioxide in the blood. Acidic blood (pH less than 7.38) has high carbon dioxide levels in the blood. Alkaline blood (pH greater than 7.42) has low carbon dioxide levels in the blood.
• Partial pressure of oxygen (PaO₂). This is the amount of oxygen gas dissolved in the test. Values below 75 to 100 mm Hg (blood pressure is measured in millimeters of mercury) show that carbon dioxide levels in the blood are high and pH is acidic (less than 7.38).
• Partial pressure of carbon dioxide (PaCO₂). This is the amount of carbon dioxide in the blood. If PaCO₂ levels are above normal values (38 to 42 mm Hg), blood is more acidic (pH less than 7.38). PaCO₂ levels below normal values mean that the blood is alkaline.

In COPD, the blood is more acidic, as the pH levels are low and the PaCO₂ levels are above normal.

Oxygenation and Ventilation status of a COPD patient

COPD occurs when obstructions block the flow of air through the lungs. The lung damage that occurs with COPD can cause hypoxia if it becomes too severe.COPD can have harmful effects on the body when it interferes with oxygen levels. If hypoxia progresses too far, it can lead to disability and death.

Oxygen passes into the blood from lung tissue through the alveoli, or air sacs. Oxygenated blood then leaves the lungs and travels around the body to other tissues. Vital organs and systems, especially the brain and heart, need enough oxygen to survive.

A person’s body can adapt to cope with lower oxygen levels than are usual. However, in people with COPD, hypoxia in the lungs means oxygen levels become extremely low.

Individuals with acute exacerbations of COPD have a greater degree of ventilation defect (causing hypercapnia) than chronic patients who mainly develop perfusion defect (causing hypoxia). Nonetheless, hypoxic vasoconstriction and collateral ventilation in chronic patients decrease the expected V/Q mismatch.

HEMODYNAMIC PARAMETERS

COPD patients with varying degrees of airflow

limitation severity by means of right-heart catheterization

shows that PH at rest is uncommon in patients with moder-

ate airflow limitation but has a similar prevalence to patients

with severe and very-severe airflow obstruction from other

studies, highlighting that airflow limitation is a poor predic-

tor of PH occurrence. In advanced COPD, the coexistence

of pulmonary gas exchange impairment is of great influence

on the development of PH. In contrast, an abnormal vascular

response to exercise was observed in the majority of patients,

even in those with mild airflow limitation, highlighting the

notion that pulmonary vascular derangement is an early event

in the natural history of COPD. Progression of these abnor-

malities may lead to the development of PH that restrains

the increase of CO during exercise, which might contribute

to limiting exercise tolerance.

Acknowledgments

COPD patients with varying degrees of airflow

limitation severity by means of right-heart catheterization

shows that PH at rest is uncommon in patients with moder-

ate airflow limitation but has a similar prevalence to patients

with severe and very-severe airflow obstruction from other

studies, highlighting that airflow limitation is a poor predic-

tor of PH occurrence. In advanced COPD, the coexistence

of pulmonary gas exchange impairment is of great influence

on the development of PH. In contrast, an abnormal vascular

response to exercise was observed in the majority of patients,

even in those with mild airflow limitation, highlighting the

notion that pulmonary vascular derangement is an early event

in the natural history of COPD. Progression of these abnor-

malities may lead to the development of PH that restrains

the increase of CO during exercise, which might contribute

to limiting exercise tolerance.

Acknowledgments

COPD patients with varying degrees of airflow

limitation severity by means of right-heart catheterization

shows that PH at rest is uncommon in patients with moder-

ate airflow limitation but has a similar prevalence to patients

with severe and very-severe airflow obstruction from other

studies, highlighting that airflow limitation is a poor predic-

tor of PH occurrence. In advanced COPD, the coexistence

of pulmonary gas exchange impairment is of great influence

on the development of PH. In contrast, an abnormal vascular

response to exercise was observed in the majority of patients,

even in those with mild airflow limitation, highlighting the

notion that pulmonary vascular derangement is an early event

in the natural history of COPD. Progression of these abnor-

malities may lead to the development of PH that restrains

the increase of CO during exercise, which might contribute

to limiting exercise tolerance.

Acknowledgments

COPD patients with varying degrees of airflow

limitation severity by means of right-heart catheterization

shows that PH at rest is uncommon in patients with moder-

ate airflow limitation but has a similar prevalence to patients

with severe and very-severe airflow obstruction from other

studies, highlighting that airflow limitation is a poor predic-

tor of PH occurrence. In advanced COPD, the coexistence

of pulmonary gas exchange impairment is of great influence

on the development of PH. In contrast, an abnormal vascular

response to exercise was observed in the majority of patients,

even in those with mild airflow limitation, highlighting the

notion that pulmonary vascular derangement is an early event

in the natural history of COPD. Progression of these abnor-

malities may lead to the development of PH that restrains

the increase of CO during exercise, which might contribute

to limiting exercise tolerance.

Acknowledgments

COPD patients with varying degrees of airflow limitation severity by means of right-heart catheterization shows that PH at rest is uncommon in patients with moder-ate airflow limitation but has a similar prevalence to patients with severe and very-severe airflow obstruction from other studies, highlighting that airflow limitation is a poor predic-tor of PH occurrence. In advanced COPD, the coexistence of pulmonary gas exchange impairment is of great influence on the development of PH. In contrast, an abnormal vascular response to exercise was observed in the majority of patients, even in those with mild airflow limitation, highlighting the notion that pulmonary vascular derangement is an early event in the natural history of COPD. Progression of these abnor-malities may lead to the development of PH that restrains the increase of CO during exercise, which might contribute to limiting exercise tolerance.

NEUROLOGICAL OBSERVATION FOR COPD

LVRS Medication Zadherence Length of 4 hospital stay Pulmonary rehabilitation Mortality Oxygenation and ventilation Cognitive impairment SDischargez Z destination Cognitive training Treating comorbidities Health status 3 ADL 3 n

NON-INVASIVE VENTILATION

Non-invasive ventilation is used in acute respiratory failure caused by a number of medical conditions, most prominently chronic obstructive pulmonary disease (COPD)

The most common indication for acute non-invasive ventilation is for acute exacerbation of chronic obstructive pulmonary disease. The decision to commence NIV, usually in the emergency department, depends on the initial response to medication (bronchodilators given by nebulizer) and the results of arterial blood gas tests. If after medical therapy the lungs remain unable to clear carbon dioxide from the bloodstream (respiratory acidosis), NIV may be indicated. Many people with COPD have chronically elevated CO₂ levels with metabolic compensation, but NIV is only indicated if the CO₂ is acutely increased to the point that the acidity levels of the blood are increased (pH<7.35).^[5] There is no level of acidity above which NIV cannot be started, but more severe acidosis carries a higher risk that NIV alone is not effective and that mechanical ventilation will be required instead.^[5]

BENEFITS OF BIPAP

• BiPAP is a better treatment for those with breathing restrictions. People with breathing restrictions may have trouble getting enough oxygen and expelling enough CO2. BiPAP can improve gas exchange, which helps the body function more efficiently. Clearing the body of CO2 can also prevent a dangerous and sometimes deadly condition called hypoxia.

• BiPAP makes exhaling easier—which is good for those with a need for a higher inspiratory pressure. Working to exhale is no fun, and it may actually lead to a higher blood CO2 level.

• BiPAP includes an optional breath timing feature. This setting can measure sleep respiration rate and set an “ideal rate” for how often patient should inhale and exhale over a set period of time. When the patient is asleep, if go too long without inhaling, the BiPAP will increase air pressure temporarily. This forces you to take a breath. Once you resume breathing at normal rate, the automatic setting returns to the previous air pressure level.
• CPAP intolerance. If patient cannot tolerate CPAP, BiPAP can be approved as an alternative..
• A need for increased ventilation. If patient have a pulmonary disease or other condition that requires assistance with both inhaling and exhaling, BiPAP may be a better choice for than CPAP; for example, if have an obstructive and restrictive component like central sleep apnea, obesity hypoventilation, COPD, or Overlap Syndrome.

NURSING MANAGEMENT PLAN FOR COPD

Objective Data : patient is having difficult to expel the sputum, dull, sweating. Nursing Diagnosis : Ineffective airway clearance related to secretions in the bronchi as evidenced by auscultation Expected outcome : client will expectorate secretions & maintain patent airway Planning Implementation Rationale Evaluation Assess ability to protect own Client is able to protect | To know baseline Through airway airway but coughing data. these entire effort is ineffective and measures Evaluate amount & type of unable to expel sputum. client secretions being produced To assess the maintained Secretions is excessive difficulty in clear Provide proper position & sticky maintaining airway as airway evidenced Semi fowler's position Give expectorant as prescribed provided using back Upright position diminished rest. facilities crackles on respiratory auscultatio Auscultate breath sounds after Administered function by use of n. administering expectorant expectorant corex syrup gravity 5ml oral as prescribed Teach about breathing Expectorants exercise, pursed lip breathing On auscultation, stimulate exercise. crackles reduced bronchial secretions Reassess breathing pattern Taught deep breathing To assess the & coughing exercise, effectiveness of pursed lip breathing expectorants by Crackle reduced on auscultation To reduce risk of pneumonia To identify