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Respiratory Presentation
Respiratory Presentation
Respiratory Presentation
Introduction
Breathlessness is common among patients
and can indicate a physiological problem in
any body system, not just the respiratory
system.
An increase in RR is a compensatory
mechanism in DKA. Conversely, a reduced
RR is often seen in CNS depression or
opiate drug overdose
Introduction
Deep sighing respirations are seen in an
attempt to increase the elimination of CO2.
A change in RR indicates either a physiological
or psychological problem.
The respiratory system is the first system in
the body to respond to altered homeostasis.
Changes in the rate and depth of respiration
occur within seconds of a problem that may
be remote from the respiratory system.
Introduction
The measurement of RR in clinical practice
continues to be omitted or, if recorded at all,
serial measurements are often absent.
Some patients with respiratory problems
require immediate resuscitative interventions.
Always undertake an ABCDE assessment.
This will identify those patients with actual or
impending airway obstruction and those with
absent or ineffective respirations
Nursing Assessment
History:
Clinical features to be obtained from history
include:
When the difficulty in breathing started
Breathlessness on exertion
Nocturnal dyspnea; orthopnoea; cough
Sputum - colour, amount and presence
of blood
Breathlessness or inability to take a deep
breath due to chest injuries and related pain
Nursing Assessment
History:
Chest pain - site and quality
Any trauma - elicit the clear mechanism of
injury
Fever, smoking
Exercise tolerance - how many stairs can be
climbed, or how far the patient can walk on
the flat without breathlessness
Treatment at home or on the way to hospital.
Nursing Assessment
History:
Patients with asthma or COPD may have
increased their own medications before
coming.
If there was no improvement after increasing
their own inhaled therapy, this is significant.
For patients with existing respiratory
diseases, ensure to document: medications;
recent admissions; any ICU admissions,
intubation, non-invasive ventilation; previous
pneumothoraces.
Nursing Assessment
Respiratory distress or difficulty among
patients with respiratory problems may
present acutely with shortness of breath.
They may also exhibit the following signs and
symptoms, which require immediate
intervention:
◦ Marked tachypnoea (RR >30 breaths/min);
altered level of consciousness, agitation,
confusion; marked accessory muscle use;
inability to speak due to breathlessness;
cyanosis and exhaustion
Nursing Assessment
Physical Examination:
Inspection:
Observe for pursed lip breathing.
Drooling indicates an upper airway problem
and cyanosis (central or peripheral) require
immediate intervention
Check the patient’s ability to talk and
complete sentences.
RR, respiratory depth and pattern.
Nursing Assessment
Physical Examination:
Note the patient’s posture. Patients with
partial or impending upper airway
obstruction will adopt a posture that
maximizes ventilation. Usually they lean
forward.
Observe chest rise and fall, noting any
asymmetry or paradoxical movement.
Inspect the chest wall for trauma e.g.
abrasions, bruises, wounds, FBs, and scars.
Observe for accessory muscle usage
Nursing Assessment
Physical Examination:
Observe and document the patient’s
conscious level and degree of agitation,
confusion, and restlessness.
Palpation:
Feel the position of the trachea to check that
it is in the midline.
Palpate the clavicles, sternum, and ribs in
patients with a chest injury. This may reveal
crepitus, surgical emphysema or tenderness.
Nursing Assessment
Palpation:
Patients with a lower chest injury may also
have sustained a significant upper abdominal
or retroperitoneal injury.
Auscultation and percussion:
Listen for breath sounds. Are they equal and
clear bilaterally? Are there any added sounds
such as wheeze or crepitations?
A silent chest in an asthmatic patient is life-
threatening and requires immediate action.
Nursing Assessment
Auscultation and percussion:
Is there any stridor or an audible wheeze?
Is the percussion note normal? Dullness
indicates fluid or consolidation, whereas
hyper-resonance indicates air in the pleural
cavity.
Vital signs: Record the RR; pulse; BP; Oxygen
saturations; temperature; peak flow (in
patients with asthma); GCS score.
Diagnostic Investigations
ABGs in patients with SpO2 of <93% on air.
Sputum for culture and susceptibility
FBC if there is a clinical indication (e.g. infection,
anaemia).
U&E if there are signs of dehydration (may be seen
in asthma through insensible losses).
Blood cultures, if indicated.
Pain score.
CXR.
ECG, if indicated.
Nursing interventions
Positioning – should be nursed in an upright
position.
Those with severe respiratory distress often
want to sit with their legs over the side
Venous access - some patients will require
administration of I.V bronchodilators.
Analgesia - pleuritic chest pain responds well
to NSAIDs.
Patients with severe pain may require opiate
analgesia.
Nursing interventions
Inhaled therapies – steroids /bronchodilators.
Psychological support - it can be extremely
distressing to be breathless.
A calm, reassuring manner will help to reduce
the patient’s anxiety.
Oxygen therapy - all patients who are unable
to maintain normal O2 saturations on air will
require O2 therapy.
Administer supplemental O2 by mask to all
patients with SpO2 of <95%.
Nursing interventions
In patients with known COPD, give a
controlled amount of O2 by mask, starting at
24 – 28% and gradually increase to achieve a
target saturation range of 88– 92%.
O2 concentrations should be reduced if the
patient becomes drowsy or saturations reach
≥93%.
Obtain an ABG values immediately as O2
therapy should be titrated to ABGs, not
saturations.
Airway obstruction
Upper airway obstruction is an
interruption in the flow of air through
the nose, mouth, pharynx or larynx.
Obstruction of the upper airway is
considered a life-threatening situation
that can progress to respiratory arrest.
Respiratory arrest will lead to cardiac
arrest, that requires cardiopulmonary
resuscitation (CPR).
Etiology
A patient’s airway can become obstructed by
vomitus; food; edema or his tongue, teeth or
saliva.
The commonest cause of upper airway
obstruction is the tongue.
Partial airway obstruction is commonly
caused by edema or a small foreign object
that doesn’t completely obstruct the airway.
Etiology
Edema of tongue (caused by trauma), laryngeal
edema and smoke inhalation edema—in anatomical
structures of the upper airway can lead to an
obstruction.
Other potential causes of airway obstruction
include: anaphylaxis; aspiration of a foreign object;
burns to the head, face or neck area; epiglottitis;
laryngospasms; peritonsillar or pharyngeal
abscesses; tenacious secretions in the airway;
trauma of the face, trachea or larynx; tumors of the
head or neck.
Mechanism of obstruction
Once an airway obstruction
occurs, the patient is partially able
or not able to take in oxygen
through inhalation.
This state leads to hypoxemia the
longer the obstruction remains.
Clinical Manifestations
Signs of a partial airway obstruction
include restlessness, agitation and
anxiety, diaphoresis, tachycardia,
coughing, stridor, respiratory distress
and elevated blood pressure.
Patients with a partial obstruction may
also experience no symptoms.
Clinical Manifestations
With a complete airway obstruction, the following
symptoms may be observed:
◦ universal choking sign—patient clutches throat
with hands
◦ inability to speak
◦ Sudden onset of choking or gagging
◦ Stridor
◦ Cyanosis
◦ Wheezing or any other unusual breath sound that
indicates breathing difficulty
◦ Diminished breath sounds (bilateral or unilateral)
◦ Sense of impending doom
◦ Progression to unconsciousness.
Diagnostic Evaluation
Physical examination may indicate
decreased breath sounds.
Tests to diagnose an upper airway
obstruction but may include X-rays,
bronchoscopy and laryngoscopy.
If there are persistent symptoms of an
upper airway obstruction, a chest X-ray,
neck X-rays, laryngoscopy or CT scan may
be ordered to rule out the presence of a
tumor or foreign body.
Management
Rapidly assess the airway patency, breathing,
and circulation.
Assess the patient’s breath sounds bilaterally.
Quickly assess the obstruction’s cause.
When an obstruction relates to the tongue
or an accumulation of tenacious secretions,
place the head in a slightly extended position
and insert an oropharyngeal airway.
Head tilt, chin lift method; Jaw thrust to be
considered if neck trauma is suspected
Oropharyngeal Airways
Management
Sizing the
Oropharyngeal
Airway
Measure from
corner of mouth
to angle of jaw
Indications/cont
raindications
Management
Quickly remove objects visible in the mouth
with suction, fingers or Magill forceps.
If the patient can breathe (partial obstruction),
encourage them to sit forward and cough to
relieve the obstruction.
Note that coughing might worsen the
obstruction and may totally occlude the airway.
ET intubation and removal of the foreign object
during insertion of the laryngoscope enables
visualization of the obstruction.
If an oral or ET airway doesn’t provide
ventilation, patient is prepared for emergency
cricothyroidotomy.
Management
Monitor oxygen saturation (using pulse
oximetry) and cardiac rhythm continuously.
Continually assess for stridor, cyanosis and
changes in LOC and notify the doctor.
Monitor chest X-ray and ABG results after
the obstruction is relieved.
Anticipate cardiac arrest if the obstruction
isn’t cleared promptly.
Oxygen therapy
It is the administration of oxygen at concentrations
greater than that in ambient air to treat or prevent
symptoms and manifestations of hypoxia.
The aim is to provide adequate transport of oxygen
in the blood; decreasing the work of breathing and
reducing stress on the myocardium.
A change in the patient’s respiratory rate or pattern
is the earliest indicator of the need for oxygen
therapy.
These changes may result from hypoxemia or
hypoxia.
Hypoxemia, a decrease in the arterial oxygen
tension in the blood. Hypoxemia usually leads to
hypoxia, a decrease in oxygen supply to the tissues
Oxygen therapy
Indications: respiratory failure; acute
myocardial infarction; cardiac failure; shock;
anaemia; during anaesthesia; post-operatively;
sleep apnoea; severe pain; asthma; pulmonary
embolus; conditions that affect the
neuromuscular control of breathing e.g.
muscular dystrophy, Guillain–Barré; severe
trauma to diaphragm, ribs, lungs or trachea;
tension pneumothorax; pleural effusion
Oxygen delivery
Any oxygen delivery system will include these basic
components:
Oxygen supply, from either a piped supply or a
portable cylinder
A reduction gauge: to reduce the pressure to
atmospheric pressure
Flow-meter: a device that controls the flow of oxygen
in litres per minute
Tubing: disposable tubing of varying diameter and
length
Mechanism for delivery : a mask or nasal cannulas
Humidifier: to warm and moisten the oxygen before
administration
Water trap if humidifier in use
Oxygen delivery
Nasal cannulas consist of two plastic prongs that
are inserted inside the anterior nares and
supported on a light frame.
Nasal cannulas can be used only where the
patient requires a low percentage of oxygen and
are used with flow rates of 1–4 litres of oxygen
per minute and provide 28–35% oxygen
They are well tolerated and are useful post-
operatively or where the patient requires
minimal support.
They are also used in chronic settings where a
patient at home requires long-term oxygen
therapy
Oxygen delivery
Simple semi-rigid plastic masks are low-flow (5–
10 L/ min) masks which entrain the air from the
atmosphere and therefore are able to deliver a
variable oxygen percentage (from 40% to 60%).
Oxygen concentrations vary depending on the
flow rate and the patient’s rate and depth of
breathing
Useful for patients who need a higher
percentage of oxygen temporarily as the cause of
their hypoxia is treated.
This type of mask may be worn for hours or
several days, but with a humidifier if used for
more than 12 hours.
Simple oxygen face mask
Oxygen delivery
Non-rebreathing masks are similar to the simple
semi-rigid plastic masks with the addition of a
reservoir bag.
This allows the oxygen to be delivered at higher
concentrations (60% - 90%) when used at flow
rates of 10–15 L/min
Oxygen flows into the bag and mask during
inhalation and the valve prevents expired air
from flowing back into the bag.
This device should only be used in the presence
of expert nursing and medical support and
during emergency intervention or before more
invasive ventilatory therapy is instituted
Non-rebreathing masks
Management
Venturi-type oxygen masks deliver high-flow
oxygen via a Venturi adaptor.
The adaptors are colour coded according to
the percentage of oxygen they deliver with
different oxygen flow rates.
Venturi masks are available in the following
concentrations: 24%, 28%, 35%, 40% and 60%.
Venturi masks with 24% and 28% are suited
to those at risk of CO2 retention
Management
Tracheostomy masks perform in a similar way to
the simple semi-rigid plastic facemask
The mask is placed over the tracheostomy tube
or stoma.
T-piece circuit is a simple, large-bore, non-
rebreathing circuit which is attached directly to an
endotracheal or tracheostomy tube.
Humidified oxygen is delivered through one part
of the T and expired gases leave through the
other part.
Used as part of the weaning process when a
patient has been ventilated previously by a
mechanical ventilator
ASTHMA
Definition: it
is a chronic inflammatory
disease of the airways that is associated
with airway hyper responsiveness,
mucosal edema and mucus production.
Asthma literally means ‘panting’ and is
characterized by acute exacerbations
interspersed by symptom- free periods.
The airways become inflamed, narrow,
and hyper-responsive.
Introduction
Airway hyper responsiveness implies that the
airways will narrow easily and too much in response
to various stimuli.
The chronic airway inflammation is associated
with airway hyper responsiveness that leads to
recurrent episodes of wheezing, breathlessness,
chest tightness and coughing particularly at night
or in the early morning.
These symptoms are variable, intermittent and
often reversible either spontaneously or with
treatment.
Introduction
Estimated that 10% of Kenyan
population have asthma.
The prevalence of asthma in older
children between ages of 12-14 years
may be increasing
Asthma is more prevalent in urban as
opposed to rural areas in Kenya
Introduction
Intrinsicasthma has no known allergic
cause and tends to occur later in life.
Extrinsic asthma has allergic triggers
such as pollen, animal hair, certain foods,
or certain drugs. Emotion and exercise
can also trigger an exacerbation.
Risk factors to development of
asthma
They include:
Genetic predisposition
Atopy
Airway hyperresponsiveness
Early in life common in boys than
girls
Obesity
Exposure to tobacco smoke
Trigger factors for asthma attacks
They include:
Exposure to allergens
URT viral infections
Tobacco smoke
Irritants like paint fumes and household sprays
Air pollution
Cold air
Excessive exercise
Stress/intense emotional reactions
Drugs e.g. beta blockers, aspirin
Menses
Pathophysiology
Chronic inflammation of the airways which is
present even when patients are symptom free.
A wide array of inflammatory cells are involved
in asthma inflammation including mast cells,
eosinophils, T lymphocytes, dendritic cells,
macrophages and neutrophils
These cells further produce chemical mediators
like chemokines, leukotrienes, cytokines etc and
their involvement leads to the damage of the
airways causing structural changes e.g. basement
membrane thickening
Pathophysiology
The airway inflammation causes airway hyper
responsiveness, airway narrowing due to
airway smooth muscle contraction,
overproduction of airway mucus, airway
edema and airway remodeling from
deposition of collagen in the basement
membrane.
The resultant effect is airway limitation that
leads to wheezing, cough, dyspnea and chest
tightness
Clinical manifestations
3 main symptoms occur,
Cough -with or without mucus production
Dyspnoea-breathlessness
Wheezing-airflow through narrow airways
Chest tightness
Diaphoresis
Tachycardia
Hypoxemia
Central cyanosis
Assessment of the asthmatic
patient
Initial assessment- History of episodic symptoms
include severe breathlessness (including too
breathless to complete sentences in one breath),
tachypnoea, tachycardia, silent chest, cyanosis or
collapse.
None of these symptoms singly or together is
specific and their absence does not exclude a
severe attack
Positive family history and environmental factors
Presence of other comorbidities associated with
asthma e.g. GERD, drug induced asthma, allergic
reactions e.g. eczema
Assessment of the asthmatic
patient
The following observations are important and they
help to establish the severity of asthma and also
enable the success of treatment interventions to be
evaluated:
Pulse oximetry-Oxygen saturation (SpO2)
determines the adequacy of oxygen therapy and the
need for arterial blood gas measurement (ABG).
Arterial blood gases-Patients with SpO2 <92% or
other features of life-threatening asthma require
ABG measurement
Assessment of the asthmatic
patient
RR; pulse; temperature; BP; pain score; GCS score.
Elevated serum IgE levels in cases of allergy
Chest X-ray is not routinely recommended in
patients in the absence of:
Suspected pneumothorax or consolidation
Life-threatening asthma or failure to respond to
treatment;
Requirement for mechanical ventilation
Assessment of the asthmatic
patient
Forced Expiratory Volume in 1 second and Peak
Expiratory Flow (PEF/FEV) are useful and valid
measures of airway calibre. PEF expressed as a % of
the patient’s previous best value is most useful
clinically.
PEFR must be measured on arrival in the hospital
and documented.
Assessment to determine the severity of the asthma
will guide treatment and the need for admission.
Presence of any features of severe or life-
threatening asthma requires calling for help
immediately.
Levels of severity of acute asthma
exacerbations
Moderate asthma:
Increased symptoms
PEF >50–75% best or predicted
No features of acute severe asthma
Acute severe asthma:
Any one of the following:
PEF 33–50% best or predicted
RR ≥25/min
HR ≥110/min
Inability to complete sentences in one
breath
Levels of severity of acute asthma
exacerbations
Life- threatening asthma:
Any one of the following in a patient with severe asthma:
PEF <33% best or predicted
SpO2 <92%
PaO2 <8 kPa
‘Normal’ PaCO2 (4.6–6.0 kPa)
Silent chest
Cyanosis
Poor respiratory effort
Arrhythmia
Exhaustion
Altered level of consciousness
Hypotension
Complications
Statusasthmaticus
Respiratory failure
Pneumonia
Atelectasis
Hypoxemia
Treatment
Goals:
Prevent chronic and troublesome symptoms
Maintain near normal pulmonary function
Maintain normal activities
Prevent recurrent episodes and emergency
hospitalisation
Provide optimal pharmacotherapy
Medical management
Two classes of asthma medications exist:
Quick relief meds and long acting meds to
achieve and maintain control of persistent
asthma
Quick relief meds include Short-acting
beta2-adrenergic agonists (SABA) are used
for acute symptoms a they relax airway
smooth muscles e.g. albuterol, ventolin,
levalbuterol; Anticholinergics e.g.
ipratropium bromide can also be used
Medical management
Long acting control meds are mainly anti-
inflammatory drugs. Corticosteroids are
initially used by inhalation e.g.
Beclomethasone Dipropionate, budesonide,
fluticasone; systemic forms e.g. prednisolone
are used to rapidly control asthma and
manage severe, persistent asthma.
Long-Acting Beta2-Agonists (LABAs) –
inhaled: salmeterol, formoterol; orals:
albuterol are used with AIDs to control
asthma
Medical management
Cromolyn sodium and nedocromil are
alternative anti-inflammatory drugs
Methylxanthines e.g. aminophylline a
bronchodilator are used with inhaled
corticosteroid (ICS) for nighttime symptom
relief
Leukotriene inhibitors e.g. montelucast can
also be used
Nursing Diagnoses
Impaired gaseous exchange related to airway
obstruction as evidenced by difficulty in
breathing
Ineffective airway clearance related to
increased mucus production as evidenced by
productive cough
Ineffective tissue perfusion related to
hypoxemia as evidenced by cyanosis
Nursing interventions
Management priorities will depend on the severity
of the asthma.
Nurse the patient in high fowlers position to ease
breathing
Continuous SpO2 and HR monitoring.
RR should be recorded every 30min at the very
minimum, until it is stable.
Administer supplemental high-flow oxygen to all
hypoxaemic patients with acute severe asthma to
maintain an SpO2 level of 94–98%.
Lack of pulse oximetry should not prevent the use
of oxygen.
ABG analysis and monitoring
Nursing interventions
Administer high-dose inhaled beta-2 agonists as
first line agents in patients with acute asthma and
administer as early as possible.
In patients with acute asthma with life-threatening
features the nebulization (oxygen-driven) with
ventolin 2mls:3mls N/saline is recommended.
In severe asthma that is poorly responsive to an
initial bolus dose of beta-2 agonist, consider
continuous nebulization with an appropriate
nebulizer.
Nursing interventions
Add nebulised ipratropium bromide (0.5 mg 4–6
hourly) to beta-2 agonist treatment for patients with
acute severe or life-threatening asthma or those
with a poor initial response to beta-2 agonist
therapy.
Steroid therapy-administer steroids in adequate
doses in all cases of acute asthma attack. Continue
prednisolone 40–50 mg daily for at least five days or
until recovery.
Consider giving a single dose of IV magnesium
sulfate to patients with acute severe asthma (PEF
<50% best or predicted) who have not had a good
initial response to inhaled bronchodilator therapy.
Nursing interventions
Monitor PEFR 30minutes post-nebulization.
Administer prescribed analgesics to manage pain.
Administer intravenous fluids in cases of
dehydration
Teach the patient on self care with emphasis on
adherence to prescribed therapy; preventive
measures and need to keep follow up appointments
with health care providers
Self care includes inhaler use, reduced exposure to
allergens, ability to recognize signs of asthma attack,
performance of coughing and deep breathing
exercises
How to use an inhaler
Nursing interventions
Refer any patient:
◦ Requiring ventilatory support
◦ With acute severe or life-threatening asthma,
who is failing to respond to therapy, as evidenced
by:
- Deteriorating PEF
- Persisting or worsening hypoxia; hypercapnia
- ABG analysis showing decreasing pH or
increasing H+
- Exhaustion, feeble respiration; drowsiness,
confusion, altered conscious state
- Respiratory arrest.
Status asthmaticus
It is a severe and persistent form of asthma that is
unresponsive to conventional therapy.
The attacks occur without warning and rapidly
progress to asphyxiation
Possible causes include: Anxiety, nebulizer abuse,
dehydration, increased adrenergic blockage, irritants,
drug hypersensitivity.
It is associated with severe bronchospasms and
mucus plugging leading to asphyxia
The ventilation-perfusion mismatch causes
hypoxemia. Initially the patients have respiratory
alkalosis but later progresses to respiratory acidosis
Status asthmaticus
Signs and symptoms include labored breathing,
prolonged exhalation, engorged neck veins and
wheezing.
Hospitalization may be required and pulmonary
function studies are accurate in assessing acute
airway obstruction
Patient is initially treated with inhaled SABA with
systemic corticosteroids (to decrease intense
airway inflammation and swelling). Nebulization
of the medications is required.
Magnesium sulfate a calcium antagonist may be
administered to induce smooth muscle
relaxation hence bronchodilation
Status asthmaticus
High flow supplemental oxygen using non-rebreather
mask to treat dyspnea, hypoxemia and central
cyanosis
Intravenous fluids are also administered to hydrate
the patient
If there is no response to repeated treatments,
mechanical ventilation may be required
The nurse is expected to constantly monitor the
patient for the first 12-24 hours until control is
achieved
Blood pressure and cardiac rhythm are also closely
monitored
Patient should be nursed in a quiet room, free of
respiratory irritants.
PNEUMONIA
Introduction
Pneumonia is an inflammation of the lung
parenchyma (respiratory bronchioles and
alveoli) caused by various microorganisms.
It is the leading cause of death among
infectious diseases.
Accounts for about 10% of hospital
admissions.
Pneumonia may be infectious when it is
caused by bacteria, viruses, fungi and
protozoa or non-infectious when it is caused
by aspiration of gastric content and irritating
gases.
Risk factors
Lung cancer
Cigarette smoking
Chronic obstructive pulmonary disease
Depressed cough reflex
Immunosuppression
Prolonged immobility
Unconsciousness
Drugs – anaesthetic, sedatives, opioids
Advanced age
Classification of infectious Pneumonia
Community acquired pneumonia (CAP)
Hospital acquired pneumonia (nosocomial )
Pneumonia in the immunocompromised host
(Opportunistic)
Aspiration
Another categorization
Primary-occuring in previously healthy person living
in the community, usually lobar pneumonia due to
pneumococci.
Secondary-develops in association with prior
respiratory, immunocompromised patient,
Community acquired pneumonia
Occurs in the community or within 48 hours after
hospitalization. The common causative agents
include
Streptococcus pneumonia-causes 66% of infections
• Haemophylus influenza
• Psedomonas Aeruginosa
• Legionnella pneumophila
• Mycoplasma pneumoniae
• Viruses – cytomegalovirus, adenovirus, herpes simplex
virus and respiratory syncytial virus
Hospital acquired pneumonia
Also called nosocomial pneumonia. It is the onset of
pneumonia symptoms more than 48 hours after
admission for patients with no evidence of infection
on admission.
HAP is usually contracted by patients who are
already vulnerable to infection (e.g.
immunocompromised, critically ill, intubated or
ventilated).
Common organisms causing HAP include:
Staphylococcus aureus
Pneumonia in Immunocompromised
host