What is Chronic Obstructive Pulmonary Disease?

Nurses care for patients with COPD across the spectrum of care, from outpatient
to home care to emergency department, critical care, and hospice settings.

 Chronic Obstructive Pulmonary Disease (COPD) is a condition of

chronic dyspnea with expiratory airflow limitation that does not
significantly fluctuate.
 Chronic Obstructive Pulmonary Disease has been defined by The
Global Initiative for Chronic Obstructive Lung Disease as
“a preventable and treatable disease with some significant
extrapulmonary effects that may contribute to the severity in
individual patients.”
 This updated definition is a broad description of COPD and its signs
and symptoms.
Classification
There are two classifications of COPD: chronic bronchitis and emphysema. These
two types of COPD can be sometimes confusing because there are patients who
have overlapping signs and symptoms of these two distinct disease processes.

Image source: [Link]

Chronic Bronchitis
 Chronic bronchitis is a disease of the airways and is defined as the
presence of cough and sputum production for at least 3
months in each of 2 consecutive years.
 Chronic bronchitis is also termed as “blue bloaters”.
 Pollutants or allergens irritate the airways and leads to the
production of sputum by the mucus-secreting glands and goblet
cells.
 A wide range of viral, bacterial, and mycoplasmal infections can
produce acute episodes of bronchitis.
Emphysema

 Pulmonary Emphysema is a pathologic term that describes

an abnormal distention of airspaces beyond the
terminal bronchioles and destruction of the walls of the alveoli.
 People with emphysema are also called “pink puffers”.
 There is impaired carbon dioxide and oxygen exchange, and the
exchange results from the destruction of the walls of overdistended
alveoli.
 There are two main types of emphysema: panlobular and
centrilobular.
 In panlobular, there is destruction of the respiratory
bronchiole, alveolar duct, and alveolus.
 All spaces in the lobule are enlarged.
 In centrilobular, pathologic changes occur mainly in the
center of the secondary lobule.
Pathophysiology
In COPD, the airflow limitation is both progressive and associated with an
abnormal inflammatory response of the lungs to noxious gases or particles.
Image source: [Link]
  An inflammatory response occurs throughout the proximal and
peripheral airways, lung parenchyma, and pulmonary vasculature.
 Due to the chronic inflammation, changes and narrowing occur in
the airways.
 There is an increase in the number of goblet cells and enlarged
submucosal glands leading to hypersecretion of mucus.
 Scar formation. This can cause scar formation in the long term and
narrowing of the airway lumen.
 Wall destruction. Alveolar wall destruction leads to loss of alveolar
attachments and a decrease in elastic recoil.
 The chronic inflammatory process affects the pulmonary vasculature
and causes thickening of the vessel lining and hypertrophy of
smooth muscle.
Epidemiology
Mortality for COPD has been increasing ever since while other diseases have
decreasing mortalities.

 COPD is the fourth leading cause of death in the United States.

 COPD also account for the death of 125, 000 Americans every year.
 Mortality from COPD among women has increased, and in 2005,
more women than men died of COPD.
 Approximately 12 million Americans live with a diagnosis of COPD.
 An additional 2 million may have COPD but remain undiagnosed.
 The annual cost of COPD is approximately $42.6 billion with overall
healthcare expenditures of $26.7 billion.
Causes
Causes of COPD includes environmental factors and host factors. These includes:

 Smoking depresses the activity of scavenger cells and affects the

respiratory tract’s ciliary cleansing mechanism.
 Occupational exposure. Prolonged and intense exposure to
occupational dust and chemicals, indoor air pollution, and outdoor
air pollution all contribute to the development of COPD.
  Genetic abnormalities. The well-documented genetic risk factor is a
deficiency of alpha1- antitrypsin, an enzyme inhibitor that protects
the lung parenchyma from injury.
Clinical Manifestations
The natural history of COPD is variable but is a generally progressive disease.

 Chronic cough. Chronic cough is one of the primary symptoms of

COPD.
 Sputum production. There is a hyperstimulation of the goblet cells
and the mucus-secreting gland leading to overproduction of
sputum.
 Dyspnea on exertion. Dyspnea is usually progressive, persistent,
and worsens with exercise.
 Dyspnea at rest. As COPD progress, dyspnea at rest may occur.
 Weight loss. Dyspnea interferes with eating and the work of
breathing is energy depleting.
 Barrel chest. In patients with emphysema, barrel chest thorax
configuration results from a more fixed position of the ribs in the
inspiratory position and from loss of elasticity.
Prevention
Prevention of COPD is never impossible. Discipline and consistency are the keys
to achieving freedom from chronic pulmonary diseases.

 Smoking cessation. This is the single most cost-

effective intervention to reduce the risk of developing COPD and to
stop its progression.
 Healthcare providers should promote cessation by explaining the
risks of smoking and personalizing the “at-risk” message to the
patient.
Complications
There are two major life-threatening complications of COPD: respiratory
insufficiency and failure.
  Respiratory failure. The acuity and the onset of respiratory failure
depend on baseline pulmonary function, pulse oximetry or
arterial blood gas values, comorbid conditions, and the severity of
other complications of COPD.
 Respiratory insufficiency. This can be acute or chronic, and may
necessitate ventilator support until other acute complications can be
treated.
Assessment and Diagnostic Findings
Diagnosis and assessment of COPD must be done carefully since the three main
symptoms are common among chronic pulmonary disorders.

 Health history. The nurse should obtain a thorough health history

from patients with known or potential COPD.
 Pulmonary function studies. Pulmonary function studies are used
to help confirm the diagnosis of COPD, determine disease severity,
and monitor disease progression.
 Spirometry. Spirometry is used to evaluate airway obstruction,
which is determined by the ratio of FEV1 to forced vital capacity.
 ABG. Arterial blood gas measurement is used to assess baseline
oxygenation and gas exchange and is especially important in
advanced COPD.
 Chest x-ray. A chest x-ray may be obtained to exclude alternative
diagnoses.
 CT scan. Computed tomography chest scan may help in the
differential diagnosis.
 Screening for alpha1-antitrypsin deficiency. Screening can be
performed for patients younger than 45 years old and for those with
a strong family history of COPD.
 Chest x-ray: May reveal hyperinflation of lungs, flattened
diaphragm, increased retrosternal air space, decreased vascular
markings/bullae (emphysema), increased bronchovascular markings
(bronchitis), normal findings during periods of remission (asthma).
 Pulmonary function tests: Done to determine cause of dyspnea,
whether functional abnormality is obstructive or restrictive, to
estimate degree of dysfunction and to evaluate effects of therapy,
e.g., bronchodilators. Exercise pulmonary function studies may also
 be done to evaluate activity tolerance in those with known
pulmonary impairment/progression of disease.
 The forced expiratory volume over 1 second (FEV1): Reduced FEV1 not
only is the standard way of assessing the clinical course and degree
of reversibility in response to therapy, but also is an important
predictor of prognosis.
 Total lung capacity (TLC), functional residual capacity (FRC), and
residual volume (RV): May be increased, indicating air-trapping. In
obstructive lung disease, the RV will make up the greater portion of
the TLC.
 Arterial blood gases (ABGs): Determines degree and severity of
disease process, e.g., most often Pao 2is decreased, and Paco2 is
normal or increased in chronic bronchitis and emphysema, but is
often decreased in asthma; pH normal or acidotic, mild respiratory
alkalosis secondary to hyperventilation
(moderate emphysema or asthma).
 DL CO test: Assesses diffusion in lungs. Carbon monoxide is used to
measure gas diffusion across the alveocapillary membrane. Because
carbon monoxide combines with hemoglobin 200 times more easily
than oxygen, it easily affects the alveoli and small airways where gas
exchange occurs. Emphysema is the only obstructive disease that
causes diffusion dysfunction.
 Bronchogram: Can show cylindrical dilation of bronchi on
inspiration; bronchial collapse on forced expiration (emphysema);
enlarged mucous ducts (bronchitis).
 Lung scan: Perfusion/ventilation studies may be done to
differentiate between the various pulmonary diseases. COPD is
characterized by a mismatch of perfusion and ventilation (i.e., areas
of abnormal ventilation in area of perfusion defect).
 Complete blood count (CBC) and differential: Increased
hemoglobin (advanced emphysema), increased eosinophils (asthma).
 Blood chemistry: alpha1-antitrypsin is measured to verify deficiency
and diagnosis of primary emphysema.
 Sputum culture: Determines presence of infection, identifies
pathogen.
 Cytologic examination: Rules out underlying malignancy or allergic
disorder.
  Electrocardiogram (ECG): Right axis deviation, peaked P
waves (severe asthma); atrial dysrhythmias (bronchitis), tall, peaked P
waves in leads II, III, AVF (bronchitis, emphysema); vertical QRS axis
(emphysema).
 Exercise ECG, stress test: Helps in assessing degree of pulmonary
dysfunction, evaluating effectiveness of bronchodilator therapy,
planning/evaluating exercise program.
Medical Management
Healthcare providers perform medical management by considering the
assessment data first and matching the appropriate intervention to the existing
manifestation.

Pharmacologic Therapy

Bronchodilators.
 Bronchodilators relieve bronchospasm by
altering the smooth muscle tone and reduce airway obstruction by
allowing increased oxygen distribution throughout the lungs and
improving alveolar ventilation.
 Corticosteroids. A short trial course of oral corticosteroids may be
prescribed for patients to determine whether pulmonary function
improves and symptoms decrease.
 Other medications. Other pharmacologic treatments that may be
used in COPD include alpha1-antitrypsin augmentation therapy,
antibiotic agents, mucolytic agents, antitussive agents, vasodilators,
and narcotics.
Management of Exacerbations

 Optimization of bronchodilator medications is first-line therapy and

involves identifying the best medications or combinations of
medications taken on a regular schedule for a specific patient.
 Hospitalization. Indications for hospitalization for acute
exacerbation of COPD include severe dyspnea that does not respond
to initial therapy, confusion or lethargy, respiratory muscle fatigue,
paradoxical chest wall movement, and peripheral edema.
  Oxygen therapy. Upon arrival of the patient in the emergency room,
supplemental oxygen therapy is administered and rapid assessment
is performed to determine if the exacerbation is life-threatening.
 Antibiotics. Antibiotics have been shown to be of some benefit to
patients with increased dyspnea, increased sputum production, and
increased sputum purulence.
Surgical Management
Patients with COPD also have options for surgery to improve their condition.

 Bullectomy. Bullectomy is a surgical option for select patients

with bullous emphysema and can help reduce dyspnea and
improve lung function.
 Lung Volume Reduction Surgery. Lung volume reduction surgery is
a palliative surgery in patients with homogenous disease or disease
that is focused in one area and not widespread throughout the
lungs.
 Lung Transplantation. Lung transplantation is a viable option for
definitive surgical treatment of end-stage emphysema.
Nursing Management
Management of patients with COPD should be incorporated with teaching and
improving the respiratory status of the patient. Learn about the nursing care
management of patients with Chronic Obstructive Pulmonary Disease using
the nursing process in this guide.
What is arterial blood gas?
Collection of arterial blood for arterial blood gas (ABG) test.

An arterial blood gas is a laboratory test to monitor the patient’s acid-base

balance. It is used to determine the extent of the compensation by the buffer
system and includes the measurements of the acidity (pH), levels of oxygen, and
carbon dioxide in arterial blood. Unlike other blood samples obtained through a
vein, a blood sample from an arterial blood gas (ABG) is taken from an artery
(commonly on radial or brachial artery).

What are the components of arterial blood gas?

There are six components of arterial blood gas (ABGs):

pH

The pH is the concentration of hydrogen ions and determines the acidity or

alkalinity of body fluids. A pH of 7.35 indicates acidosis and a pH greater than
7.45 indicates alkalosis. The normal ABG level for pH is 7.35 to 7.45.

PaCO2 (Partial Pressure of Carbon Dioxide)

PaCO2 or partial pressure of carbon dioxide shows the adequacy of the gas
exchange between the alveoli and the external environment (alveolar ventilation).
Carbon dioxide (CO2) cannot escape when there is damage in the alveoli, excess
CO2 combines with water to form carbonic acid (H2CO3) causing an acidotic
state. When there is hypoventilation in the alveolar level (for example, in COPD),
the PaCO2 is elevated, and respiratory acidosis results. On the other hand, when
there is alveolar hyperventilation (e.g., hyperventilation), the PaCO 2 is decreased
causing respiratory alkalosis. For PaCO2, the normal range is 35 to 45 mmHg
(respiratory determinant).
PaO2 (Partial Pressure of Oxygen)

PaO2 or partial pressure of oxygen or PAO2 indicates the amount of oxygen

available to bind with hemoglobin. The pH plays a role in the combining power of
oxygen with hemoglobin: a low pH means there is less oxygen in the
hemoglobin. For PaO2, the normal range is 75 to 100 mmHg

SO2 (Oxygen Saturation)

SO2 or oxygen saturation, measured in percentage, is the amount of oxygen in

the blood that combines with hemoglobin. It can be measured indirectly by
calculating the PAO2 and pH Or measured directly by co-oximetry. Oxygen
saturation, the normal range is 94–100%

HCO3 (Bicarbonate)

HCO3 or bicarbonate ion is an alkaline substance that comprises over half of the
total buffer base in the blood. A deficit of bicarbonate and other bases indicates
metabolic acidosis. Alternatively, when there is an increase in bicarbonates
present, then metabolic alkalosis results.

BE (Base Excess)

BE. Base excess or BE value is routinely checked with HCO 3 value. A base excess of
less than –2 is acidosis and greater than +2 is alkalosis. Base excess, the normal
range is –2 to +2 mmol/L

Normal Values in Arterial Blood Gas

To determine acid-base imbalance, you need to know and memorize these values
to recognize what deviates from normal. The normal range for ABGs is used as a
guide, and the determination of disorders is often based on blood pH. If the
blood is basic, the HCO 3 level is considered because the kidneys regulate
bicarbonate ion levels. If the blood is acidic, the PaCO 2 or partial pressure of
carbon dioxide in arterial blood is assessed because the lungs regulate the
majority of acid. The normal ABG values are the following:

 For pH, the normal range is 7.35 to 7.45

 For PaCO2, the normal range is 35 to 45 mmHg (respiratory
determinant)
 For PaO2, the normal range is 75 to 100 mmHg
 For HCO3, the normal range is 22 to 26 mEq/L (metabolic
determinant)
 Oxygen saturation, the normal range is 94–100%
 Base excess, the normal range is –2 to +2 mmol/L
Interpreting Arterial Blood Gas Imbalances
Interpreting arterial blood gases is used to detect respiratory acidosis or alkalosis,
or metabolic acidosis or alkalosis during an acute illness. To determine the type
of arterial blood gas the key components are checked. The best (and fun) way of
interpreting arterial blood gas is by using the tic-tac-toe method below:

Goals of Arterial Blood Gas analysis

To simplify this technique even further, keep these goals in mind.

For the purpose of this guide, we have set three (3) goals that we need to
accomplish when interpreting arterial blood gases. The goals are as follows:

1. Based on the given ABG values, determine if values interpret

ACIDOSIS or ALKALOSIS.
2. Second, we need to determine if values define METABOLIC or
RESPIRATORY.
3. Lastly, we need to determine the compensation if it is: FULLY
COMPENSATED, PARTIALLY COMPENSATED, or UNCOMPENSATED.
We need to keep these goals in mind as they’ll come up later in the steps for the
ABG interpretation technique.
Steps in ABG analysis using the tic-tac-toe method

There are eight (8) steps simple steps you need to know if you want to interpret
arterial blood gases (ABGs) results using the tic-tac-toe technique.

1. Memorize the normal values.

The first step is you need to familiarize yourself with the normal and abnormal
ABG values when you review the lab results. They are easy to remember:

 For pH, the normal range is 7.35 to 7.45

 For PaCO2, the normal range is 35 to 45
 For HCO3, the normal range is 22 to 26
Normal Blood pH Scale Diagram for the Tic-Tac-Toe Method for ABG Analysis

The recommended way of memorizing it is by drawing the diagram of normal

values above. Write it down together with the arrows indicating ACIDOSIS or
ALKALOSIS. Note that PaCO2 is intentionally inverted for the purpose of the Tic-
Tac-Toe method.
2. Create your tic-tac-toe grid.

Make a 3×3 grid and label it as follows.

Once you’ve memorized the normal values and the diagram, create a blank your
tic-tac-toe grid and label the top row as ACIDOSIS, NORMAL, and ALKALOSIS.
Based on their values, we need to determine in which column we’ll place pH,
PaCO2, and HCO3 in the grid.
3. Determine if pH is under NORMAL, ACIDOSIS, or ALKALOSIS.

The third step of this technique is to determine the acidity or alkalinity of the
blood with the given value of the pH as our determining factor. Remember in
step #1 that the normal pH range is from 7.35 to 7.45.

 If the blood pH is between 7.35 to 7.39, the interpretation is

NORMAL but SLIGHTLY ACIDOSIS, place it under the NORMAL
column.
 If the blood pH is between 7.41 to 7.45, interpretation is NORMAL
but SLIGHTLY ALKALOSIS, place it under the NORMAL column.
 Any blood pH below 7.35 (7.34, 7.33, 7.32, and so on…) is ACIDOSIS,
place it under the ACIDOSIS column.
 Any blood pH above 7.45 (7.46, 7.47, 7.48, and so on…) is ALKALOSIS,
place it under the ALKALOSIS column.
Please use the diagram below to help you visualize whether the normal value is
ACIDOSIS or ALKALOSIS.
Now we need to determine where we’ll plot pH in the tic-tac-toe grid.

Once you’ve determined whether the pH is under the ACIDOSIS or ALKALOSIS,

plot it on your tic-tac-toe grid under the appropriate column.
4. Determine if PaCO2 is under NORMAL, ACIDOSIS, or ALKALOSIS.

Do the same for the PaCO . (Click to enlarge)

2

For this step, we need to interpret if the value of PaCO 2 is within the NORMAL
range, ACIDIC, or BASIC and plot it on the grid under the appropriate column.
Remember that the normal range for PaCO 2 is from 35 to 45:

 If PaCO2 is below 35, place it under the ALKALOSIS column.

 If PaCO2 is above 45, place it under the ACIDOSIS column.
  If PaCO2 is within its normal range, place it under the NORMAL
column.
5. Determine if HCO3 is under NORMAL, ACIDOSIS, or ALKALOSIS.

In the fifth step, we need to know where HCO3 is placed in the ABG tic-tac-toe
3

grid.

Next, we need to interpret if the value of HCO 3 is within the NORMAL range,
ACIDIC, or BASIC and plot it under the appropriate column in the tic-tac-toe grid.
Remember that the normal range for HCO 3 is from 22 to 26:
  If HCO3 is below 22, place it under the ACIDOSIS column.
 If HCO3 is above 26, place it under the ALKALOSIS column.
 If HCO3 is within its normal range, place it under the NORMAL
column.
6. Solve for goal #1: ACIDOSIS or ALKALOSIS.

Solving for goal #1. Determining if the set of ABG values interpret as ACIDOSIS or
ALKALOSIS.
Now, we will start solving for our goals. Looking at the tic-tac-toe grid, determine
whether in what column the pH is placed and interpret the results:

 If pH is under the ACIDOSIS column, it is ACIDOSIS.

 If pH is under the ALKALOSIS column, it is ALKALOSIS.
 If pH is under the NORMAL column, determine whether the value is
leaning towards ACIDOSIS or ALKALOSIS and interpret accordingly.
In this step, we can accomplish goal #1 of determining ACIDOSIS or ALKALOSIS.
7. Solve for goal #2: METABOLIC or RESPIRATORY.

Solving for goal #2, we analyze where pH lines up with. If it lines up with PaCO ,
2

it’s RESPIRATORY. If it lines up with HCO , it’s METABOLIC.

3

Looking back again on the tic-tac-toe grid, determine if pH is under the same
column as PaCO2 or HCO3 so we can accomplish our goal #2 of determining if the
ABG is RESPIRATORY or METABOLIC. Interpret the results as follows:

 If pH is under the same column as PaCO2, it is RESPIRATORY.

  If pH is under the same column as HCO3, it is METABOLIC.
 If pH is under the NORMAL column, determine whether the value is
leaning towards ACIDOSIS or ALKALOSIS and interpret accordingly.
8. Solve for goal #3: COMPENSATION.

Solving for goal #3 where we determine the compensation of the ABG result.

Lastly, we need to determine the compensation to accomplish our goal #3.

Interpret the results as follows:

 It is FULLY COMPENSATED if pH is normal.

  It is PARTIALLY COMPENSATED if all three (3) values are abnormal.
 It is UNCOMPENSATED if PaCO 2 or HCO3 is normal and the other is
abnormal.
Application and Examples

Let’s solve for the ABG interpretation with the examples below:

Practice Problem #1:

pH=7.26 | PaCO2=32 | HCO3=18

1. Remember the normal values.

2. Make your tic-tac-toe grid.
3. pH of 7.26 ABNORMAL and under ACIDOSIS, so we place pH under
ACIDOSIS.
4. PaCO2 of 32 is ABNORMAL and under ALKALOSIS, so we place
PaCO2 under ALKALOSIS.
5. HCO3 of 18 is ABNORMAL and under ACIDOSIS, so we place
HCO3 under ACIDOSIS.
6. pH is under ACIDOSIS, therefore solving for goal #1, we have
ACIDOSIS.
7. pH is on the same column as HCO 3, therefore solving for goal #2, we
have METABOLIC.
8. All three values are ABNORMAL, therefore solving for goal #3, we
have a PARTIALLY COMPENSATED ABG.
The answer to Practice Problem #1:
Metabolic Acidosis, Partially Compensated

Practice Problem #2:

pH=7.44 | PaCO2=30 | HCO3=21

1. Remember the normal values.

2. Make your tic-tac-toe grid.
3. pH of 7.44 is NORMAL but slightly leaning towards ALKALOSIS, so
we place pH under the NORMAL column with an arrow pointing
towards the ALKALOSIS column.
4. PaCO2 of 30 is ABNORMAL and ALKALOSIS, so we place PaCO 2 under
the ALKALOSIS column.
 5. HCO3 of 21 is ABNORMAL and ACIDOSIS, so we place HCO 3 under
the ACIDOSIS column.
6. pH of 7.44 is NORMAL but leaning towards ALKALOSIS, therefore
solving for goal #1, we have ALKALOSIS.
7. pH is NORMAL but is leaning towards ALKALOSIS, therefore under
the same column as PaCO2. Solving for goal #2, we have
RESPIRATORY.
8. pH is NORMAL, therefore solving for goal #3, we have a FULLY
COMPENSATED ABG.
The answer to Practice Problem #2:
Respiratory Alkalosis, Fully Compensated

Practice Problem #3:

pH=7.1 | PaCO2=40 | HCO3=18

1. Remember the normal values.

2. Make your tic-tac-toe grid.
3. pH of 7.1 is ABNORMAL and ACIDOSIS, therefore, we place pH under
the ACIDOSIS column in the tic-tac-toe grid.
4. PaCO2 of 40 is NORMAL, therefore, place it under the NORMAL
column.
5. HCO3 of 18 is ABNORMAL and ACIDOSIS, so we place HCO 3 under
the ACIDOSIS column.
6. pH of 7.1 is ACIDOSIS, therefore, solving for goal #1, we have
ACIDOSIS.
7. pH is under the same column as HCO 3, therefore, solving for goal #2,
we have determined that it is METABOLIC.
8. pH is ABNORMAL so as HCO3, but PaCO3 is under the NORMAL
column. Solving for goal #3, we can interpret it as
UNCOMPENSATED.
The answer to Practice Problem #3:
Metabolic Acidosis, Uncompensated

How to draw Arterial Blood Gas?

Arterial blood is usually drawn via the brachial or radial artery.
 1. Inform the client about the procedure and that there is no food or
fluid restriction imposed.
2. Note if the client is taking anticoagulant therapy or aspirin as this
may affect results.
3. Note if the client is receiving oxygen therapy (flow rate, type of
administration device), and the client’s current temperature.
4. Using a heparinized needle and syringe, collect 1 to 5 mL of arterial
blood. Common sites for drawing arterial blood are the radial and
brachial artery.
5. Put the syringe with arterial blood in an ice-water bag to minimize
the metabolic activity of the sample.
6. Deliver the blood sample immediately to the laboratory.
7. Apply pressure to the puncture site for 5 minutes or longer.
Acid-Base Balance and Imbalances
Acid-base imbalances develop when a person’s normal homeostatic mechanisms
are dysfunctional or overwhelmed. One type of acid-base imbalance
is acidosis wherein the blood is relatively too acidic (low pH). The body produces
two types of acid, therefore, there are two types of acidosis: respiratory acidosis
and metabolic acidosis. On the contrary, alkalosis is a condition wherein the
blood is relatively too basic (high pH), there are also two types of alkalosis:
respiratory alkalosis and metabolic alkalosis.

When acid-base imbalances occur, the body activates its compensatory

mechanisms (the lungs and kidneys) to help normalize the blood pH. The kidneys
compensate for respiratory acid-base imbalances while the respiratory
system compensates for metabolic acid-base imbalances. This does not correct
the root cause of the problem, if the underlying condition is not corrected, these
systems will fail.

Respiratory Acidosis

Respiratory acidosis occurs when breathing is inadequate (alveolar

hypoventilation) and the lungs are unable to excrete enough CO2 causing
PaCO2 or respiratory acid builds up. The extra CO2 combines with water to form
carbonic acid, causing a state of acidosis — a common occurrence in
emphysema. The kidneys activate its compensatory process (albeit slow, often 24
hours or more) by increasing the excretion of metabolic acids through urination,
which increases blood bicarbonate.

Types of Respiratory Acidosis

There are two forms of respiratory acidosis: Acute and Chronic.

 Acute respiratory acidosis. This form of respiratory acidosis occurs

immediately. Left untreated, symptoms will get progressively worse.
It’s a medical emergency and can become life-threatening.
 Chronic respiratory acidosis. This form of respiratory acidosis
develops over time. It doesn’t cause symptoms. Instead, the body
adapts to the increased acidity. For example, the kidneys produce
more bicarbonate to help maintain balance. Chronic respiratory
acidosis may not cause symptoms. Developing another illness may
cause chronic respiratory acidosis to worsen and become acute
respiratory acidosis.
Risk Factors

Respiratory acidosis is typically caused by an underlying disease or condition. This

is also called respiratory failure or ventilatory failure.

 Hypoventilation. A decrease in ventilation increases the

concentration of carbon dioxide in the blood and decreases the
blood’s pH (brain trauma, coma, hypothyroidism: myxedema).
 Chronic Obstructive Pulmonary Disease (COPD). In chronic
respiratory acidosis in COPD patients, the body tries to compensate
by retaining more bicarbonate to overcome acidosis.
 Respiratory Conditions. The lungs are not able to eliminate enough
of the carbon dioxide produced by the body. Excess carbon dioxide
causes the pH of the blood and other bodily fluids to decrease,
making them too acidic. (pneumothorax, pneumonia, status
asthmaticus)
  Drug Intake. Overdose of an opiate or opioid, such as morphine,
tramadol, heroin, fentanyl, or magnesium sulfate (MgSO4) can cause
respiratory acidosis.
Signs and Symptoms

Signs and symptoms of respiratory acidosis are as follows:

 Altered level of consciousness. Respiratory acidosis may be the

result of an altered level of consciousness caused by encephalopathy
or cerebral edema.
 Confusion. Acute respiratory acidosis may also cause symptoms
involving the brain, including confusion, stupor, drowsiness,
and muscle jerks.
 Disorientation. Respiratory acidosis may result in disorientation,
headache, or even focal neurologic signs.
 Coma. When the lungs can’t remove all of the carbon dioxide
produced by the body through normal metabolism, the blood
becomes acidified, leading to increasingly serious symptoms, from
sleepiness to coma.
 Tremors. Manifest as shaking or jerking muscle movements.
 Asterixis. An inability to maintain the posture of part of the body.

Management of Respiratory Acidosis

Medical and nursing management of an arterial blood gas of respiratory acidosis

includes the following:

 Treat underlying conditions.

 Medications. Bronchodilator medicines and corticosteroids
may be used to reverse some types of airway obstruction,
like those linked to asthma and COPD.
 Weight loss. In the case of obesity hypoventilation
syndrome, significant weight loss may be necessary to
reduce abnormal compression of the lungs.
  Provide mechanical ventilation through oxygen
supplementation. Additional oxygen may be provided to alleviate
the low oxygen level in the blood.
 Manage hyperkalemia through the use of Kayexalate. Acidosis
causes potassium to move from cells to extracellular fluid (plasma) in
exchange for hydrogen ions, and alkalosis causes the
reverse movement of potassium and hydrogen ions. Kayexalate
increases fecal potassium excretion through the binding of
potassium in the lumen of the gastrointestinal tract.
 Maintain adequate hydration. Provide intravenous
fluids and electrolytes as ordered.
Respiratory Alkalosis

Respiratory alkalosis can result from hyperventilation since the lungs excrete too
much carbonic acid which increases pH. Since respiratory alkalosis occurs quickly,
the kidneys do not have time to compensate. Neurological symptoms such as
confusion, paresthesias, and cell membrane excitability occur when the blood pH,
CSF, and ICF increases acutely.

Risk Factors

Causes of hyperventilation include:

 Panic. Panic attacks and anxiety are the most common causes of
hyperventilation.
 Hyperthermia. Fever may manifest as hyperventilation. The exact
mechanism is not known but is thought to be due to carotid body or
hypothalamic stimulation by the increased temperature.
 Brainstem damage. Central neurogenic hyperventilation (CNH) is
the human body’s response to reduced carbon dioxide levels in the
blood. This reduction in carbon dioxide is caused by the contraction
of cranial arteries from damage caused by lesions in the brain stem.
 Metabolic acidosis. Hyperventilation occurs most often as a
response to hypoxia, metabolic acidosis, increased metabolic
demands, pain, or anxiety.
  Diabetic ketoacidosis (DKA). The only known compensatory
response to metabolic acidosis in DKA is hyperventilation with
consecutive respiratory alkalosis.
 Pregnancy. Progesterone levels are increased during pregnancy.
Progesterone causes stimulation of the respiratory center, which can
lead to respiratory alkalosis.
 Salicylate toxicity. Salicylate toxicity causes respiratory alkalosis
and, by an independent mechanism, metabolic acidosis.
Signs and Symptoms

Hyperventilation is a sign that respiratory alkalosis is most likely to occur.

However, low carbon dioxide levels in the blood also have a number of physical
effects, including:

Numbness. Increased neuromuscular irritability in which a person


loses feeling in a particular part of their body.
 Tingling sensation. Prickling sensation that is usually felt in the
hands, arms, legs, or feet, but can also occur in other parts of the
body.
 Palpitations. Palpitations are the perceived abnormality of the
heartbeat characterized by awareness of cardiac muscle contractions
in the chest.
 Tetany. Tetany or tetanic seizure is a medical sign consisting of the
involuntary contraction of muscles.
 Convulsions. A medical condition where body muscles contract and
relax rapidly and repeatedly, resulting in uncontrolled actions of the
body.
 Signs and symptoms of hypokalemia
and hypocalcemia. Persistent respiratory alkalosis can induce
secondary hypocalcemia and hypokalemia that may cause cardiac
arrhythmias, conduction abnormalities, and various somatic
symptoms such as paresthesia, hyperreflexia, convulsive disorders,
muscle spasm, muscle twitching, positive Chvostek’s sign, and tetany.
Management of Respiratory Alkalosis

The treatment for respiratory alkalosis depends on the underlying cause. Treating
the condition is a matter of rising carbon dioxide levels in the blood. The
following strategies and tips are useful for respiratory alkalosis caused by over-
breathing due to panic and anxiety.

 Breathe into a paper bag. Breathing through a paper bag fills it

with carbon dioxide helping in inhaling exhaled air back into the
lungs.
 Treat underlying condition:
 Medications. Administering an opioid pain reliever or anti-
anxiety medication to reduce hyperventilation.
 Relaxation techniques. Breathing exercises that help relax
and breathe from the diaphragm and abdomen, rather than
chest wall.
 Safety. Stay with the patient.
 Lavage. After massive aspirin ingestions, aggressive gut
decontamination is advisable, including gastric lavage.
 Correction of hypokalemia and hypocalcemia.
 Oxygenation as indicated. Providing oxygen to help keep a person
from hyperventilating.
Metabolic Acidosis

Metabolic acidosis is when there is a decrease in bicarbonates and a buildup of

lactic acid occurs. This happens in diarrhea, ketosis, and kidney disorders. It has
three main root causes: increased acid production, loss of bicarbonate, and a
reduced ability of the kidneys to excrete excess acids.

Risk Factors

 Diabetic Ketoacidosis (DKA). DKA develops when substances called

ketone bodies (which are acidic) build up during
uncontrolled diabetes. DKA occurs mostly in Type 1 Diabetes
Mellitus (DM).
 Chronic Renal Failure (CRF). This is due to reduced tubular
bicarbonate reabsorption and insufficient renal bicarbonate
production in relation to the number of acids synthesized by the
body and ingested with food.
  Chronic Hypoxia. With chronic hypoxia, metabolic and hypercapnic
acidosis develop along with considerable lactate formation and pH
falling to below 6.8.
 Obesity. Obesity, especially in conjunction with insulin resistance,
can increase metabolic acidosis and thus result in a reduction of
urinary citrate excretion.
 Diarrhea. Loss of bicarbonate stores through diarrhea or renal
tubular wasting leads to a metabolic acidosis state characterized by
increased plasma chloride concentration and decreased plasma
bicarbonate concentration.
 Dehydration. Electrolyte disturbances caused by
prolonged vomiting or severe dehydration can cause metabolic
acidosis.
 Aspirin Toxicity. Aspirin overdose causes the body to not produce
ATP, leading to anaerobic metabolism with consequent raised lactate
and ketone bodies. Acute aspirin or salicylates overdose or poisoning
can cause initial respiratory alkalosis through metabolic acidosis
ensues thereafter.
 Methanol Poisoning. Significant methanol ingestion leads to
metabolic acidosis, which is manifested by a low serum bicarbonate
level. The anion gap is increased secondary to high lactate and
ketone levels. This is probably due to formic acid accumulation.
Signs and Symptoms

Altered level of consciousness


 Confusion
 Disorientation
 Lack of appetite
 Coma
 Jaundice
Management of Metabolic Acidosis

Patients with arterial blood gas indicating metabolic acidosis are managed and
treated by:

 Sodium bicarbonate. Indicated in the treatment of metabolic

acidosis which may occur in severe renal disease, uncontrolled
 diabetes, circulatory insufficiency due to shock or
severe dehydration, extracorporeal circulation of blood, cardiac
arrest, and severe primary lactic acidosis.
 Treat the underlying condition.
 Hydration for diabetic ketoacidosis. The major treatment of this
condition is the initial rehydration.
 Dialysis for chronic renal failure. The control of metabolic acidosis in
hemodialysis is mainly focused on the supply of bicarbonate during
the dialysis sessions.
 Use of diuretics.
 Initiate safety measures.
 Kayexalate. Acidosis causes potassium to move from cells to
extracellular fluid (plasma) in exchange for hydrogen ions, and
alkalosis causes the reverse movement of potassium and hydrogen
ions. Kayexalate increases fecal potassium excretion through the
binding of potassium in the lumen of the gastrointestinal tract.
Metabolic Alkalosis

Metabolic alkalosis occurs when bicarbonate ion concentration increases, causing

an elevation in blood pH. This can occur in excessive vomiting, dehydration, or
endocrine disorders.

Risk Factors

 Vomiting. Vomiting causes metabolic alkalosis by the loss of gastric

secretions, which are rich in hydrochloric acid (HCl). Whenever a
hydrogen ion is excreted, a bicarbonate ion is gained in the
extracellular space.
 Sodium bicarbonate overdose. Administration
of sodium bicarbonate in amounts that exceed the capacity of the
kidneys to excrete this excess bicarbonate may cause metabolic
alkalosis.
 Hypokalemia. Due to a low extracellular potassium concentration,
potassium shifts out of the cells. In order to maintain electrical
neutrality, hydrogen shifts into the cells, raising blood pH.
  Nasogastric suction. Just like in vomiting, nasogastric (NG) suction
also generates metabolic alkalosis by the loss of gastric secretions,
which are rich in hydrochloric acid (HCl).
Signs and Symptoms

Metabolic alkalosis may not show any symptoms. People with this type of
alkalosis more often complain of the underlying conditions that are causing it.
These can include:

 Numbness
 Vomiting
 Diarrhea
 Swelling in the lower legs (peripheral edema)
 Fatigue
 Tingling sensation
 Agitation
 Disorientation
 Seizures
 Coma

Management of Metabolic Alkalosis

 Antiemetic. In the case of vomiting, administer antiemetics, if

possible.
 Ammonium chloride. Ammonium chloride is a systemic and urinary
acidifying agent that is converted to ammonia and hydrochloric acid
through oxidation by the liver. Intravenous (IV) ammonium chloride
is a treatment option for severe cases of metabolic alkalosis.
 Acetazolamide (Diamox). Acetazolamide also appears to be safe
and effective in patients with metabolic alkalosis following treatment
of respiratory acidosis from exacerbations of chronic obstructive
pulmonary disease (COPD).