Zuniga, Florentino Jr Orbe

Introduction

Respiratory failure is a physiologically devastating condition which can have life-threatening

consequences. Health professionals, especially nurses, must be equipped with the
understanding of the condition to promptly institute interventions and prevent further
deterioration of a patient’s condition. By definition, respiratory failure is a group of
interrelated symptoms that indicate the inability of the respiratory system to facilitate
oxygenation and/or expel carbon dioxide (Aitken, Marshall & Chaboyer 2015). This
academic writing will revolve around the in-depth analysis of the condition in the context of
an actual case study. The case study in focus will also highlight one of the conditions that
potentiates to acute respiratory failure, Acute Respiratory Distress Syndrome. Evidence based
literature will be utilised to draw understanding into the pathophysiology and the
interventions that tackle them as it connects to the case study.

The Case

The case study will revolve around a 68-year-old male patient which will be referred to by his
pseudonym, Patient XL. Initially, Patient XL was brought by his partner into an Emergency
Department of a major tertiary hospital. The main health complaints that were communicated
were worsening shortness of breath, low-grade fever, green tinged productive cough and a
new onset of altered mental status. His wife stated that a day prior to presentation, the patient
appeared confused and saying inappropriate things. The history of the present health concern
revealed that the patient developed flu-like symptoms five days ago and started to have a
gradual increase in difficulty of breathing two days after the start of the illness. The difficulty
of breathing was accompanied by an increase in yellow-green tinged sputum and worsening
cough.

The primary assessment in the Emergency Department reveals the following vital signs:
Temperature of 37.8 degrees Celsius, Heart Rate of 110 beats per minute, Respiratory rate of
30 breaths per minute, Blood Pressure of 100/60 mmHg and an Oxygen Saturation of 81 per
cent on room air concentration. In addition, Patient XL’s respiratory effort was laboured with
evident use of accessory muscles and a tracheal tug. The patient was also confused and
disorientated when conversing. A point-of-care viral test revealed a positive Influenza
infection with a consequent positive Immunofluorescence assay for Influenza A provided a
specific infective agent. With regards to the initial Arterial Blood Gas results, Partial Pressure
of Oxygen was at 55 mmHg, Partial Pressure of Carbon Dioxide was 30 mmHg, pH was

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7.45. The patient was immediately given 100 per cent oxygen via a Non-Rebreather Mask but
his respiratory status continued to deteriorate as evidenced by a non-improving Oxygen
Saturation and Partial Pressure of Oxygen reading and an above normal reading of 50 mmHg
of Partial Pressure of Carbon Dioxide. Moreover, the patient’s hemodynamic parameters
have also deteriorated as highlighted with a Blood Pressure of 80/50 mmHg. Patient XL was
then intubated and mechanically ventilated in consideration of persisting hypoxemia,
respiratory distress and hemodynamic instability. He was eventually transferred to the
Intensive Care Unit for rigorous monitoring and management. Patient XL’s ventilatory
support was configured to provide High Positive End Expiratory Pressure. A later Chest X-
Ray reveals bilateral diffuse lung infiltrates and perihilar air space opacity. The
pharmacologic management of the patient involved a Norepinephrine drip for hemodynamic
support, Antibiotics and an Antiviral to address the infective nature of the patient’s condition.
Consequently, the medical diagnosis for the patient was Acute Respiratory Failure secondary
to Acute Respiratory Distress Syndrome.

On day two of the patient’s admission in the Intensive Care Unit, he exhibited the following
Vital signs: Temperature of 37.5 degrees Celsius, Heart Rate of 93 beats per minute,
Respirations of 16 breaths per minute on Positive End Expiratory Pressure ventilation, Blood
Pressure of 90/50 mmHg and an Oxygen Saturation of 88-90 per cent.

Background Literature

Respiratory failure, as mentioned beforehand, is a condition wherein the respiratory system is

unable to either facilitate oxygenation or eliminate carbon dioxide or both (Aitken, Marshall
& Chaboyer 2015). This definition suggests that there are two types of respiratory failure.
The first type or Type I is described by the failure the respiratory system to facilitate the
exchange of oxygen and it is clinically defined as a Partial Pressure of Oxygen less than 60
mmHg or 8 kPa with a low or normal Partial Pressure of Carbon Dioxide (Gibson & Waters
2016). As the name implies, Type I Respiratory Failure occurs in conditions where there is a
lack of oxygen availability or when there is a mismatch between the air flow and blood
perfusion in the lungs (Aitken, Marshall & Chaboyer 2015). Type II Respiratory Failure, on
the other hand, is also referred to as Ventilation Failure (Marini & Roussos 2012). This type
is also characterised by a Partial Pressure of Oxygen less than 60 mmHg but has an
accompanying Hypercarbia or greater than 50 mmHg of Partial Pressure of Carbon Dioxide

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(Marini & Roussos 2012). It is present in conditions where ventilation to the alveolar space is
not sufficient to achieve normal oxygen and carbon dioxide levels (Marini & Roussos 2012).

In this case study, the condition that caused the Respiratory Failure was Acute Respiratory
Distress Syndrome. This condition, by definition, is a suddenly occurring widespread
inflammation of the lung parenchyma which causes an increased permeability of the
alveolacapillary membrane (Villar, Blanco & Kacmarek 2016). This, then, causes interstitial
fluid to flood the alveolar spaces and other adjacent structures which impacts the capability of
oxygen to freely diffuse from the airways towards the pulmonary capillaries impacting
oxygen levels in the blood (Matthay, Michael A & Zemans, Rachel L 2011). Acute
Respiratory Distress Syndrome is not a disease itself but a sequelae of another pathologic
condition (Matthay, Michael A & Zemans, Rachel L 2011). Patient XL initially had flu-like
symptoms then progressed to a concoction of respiratory-related concerns. Consequently, the
case information above mentioned that the patient was positive for Influenza A on the viral
screen which is the primary cause of respiratory insult.

Client-Specific Pathophysiology

The Influenza A virus primarily affects the structural cell integrity of the lining of the alveoli
(Short et al. 2014). To be specific, the virus causes pathological changes in the cellular
function of epithelial cells and the endothelial cells (Short et al. 2014). Upon entry to the
alveolus chamber, the virus initially encounters the epithelial cells which are further
subdivided into Type One (I) and Type Two (II) pneumocytes (Ramsey & Kumar 2011).
These cells perform vital functions within the alveoli so extensive damage to these can lead
to a diffuse respiratory episode (Aitken, Marshall & Chaboyer 2015). In context, Type One
pneumocytes are flat cells that facilitate the fluid diffusion of gases between the alveolar
space and the pulmonary capillaries whilst Type Two pneumocytes secrete surfactant which
is vital to reduce surface tension (Aitken, Marshall & Chaboyer 2015). These cells also
maintain the reduced permeability of the alveolar epithelial layer through structural, ion-gated
and protein transport mechanisms hence, the risk of fluid leakage into the alveolar space is
significantly reduced (Short et al. 2014). In the advent of an early Influenza A infection, the
virus causes fluid accumulation in the alveolar space by inhibiting the action of cellular ion-
channels and protein transport on cellular permeability (Ramsey & Kumar 2011). The
structural tight junctions are also compromised because of epithelial cell death due to viral
replication that further adds insult into the permeability of the alveoli (Töpfer et al. 2014).

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Moreover, the epithelial cells produce inflammatory mediators in the form of Cytokines
because of the viral infection (Töpfer et al. 2014). These Cytokines, then, further increases
cellular permeability in preparation to the recruitment of leucocytes to fight the virus (Töpfer
et al. 2014). Leucocytes, although pivotal in pathogen neutralization, damages the epithelial-
endothelial barrier in the alveolus (Töpfer et al. 2014).

The next line of cells that the Influenza A virus encounters are the endothelial cells. These
cells are immediately adjacent to the epithelial cells which line the alveoli (Aitken, Marshall
& Chaboyer 2015). These cells, on the other hand, line the capillaries that encapsulates the
alveoli and perform a vital function in facilitating the diffusion of oxygen and carbon dioxide
(Short et al. 2014). The effect of the virus on the endothelial cells is somewhat similar to that
of epithelial cells. Activation of cytokine production in these cells further increases the
inflammatory cascade in the epithelial-endothelial membrane with an accompanying
leucocyte recruitment (Töpfer et al. 2014). The virus, then, potentiates endothelial cell death
which mediates the development of pulmonary oedema (Töpfer et al. 2014).

The diffuse impaired capillary permeability occurring in the cellular level of the alveoli has a
collective physiological effect on the lung parenchyma and this trait is also the hallmark of
Acute Respiratory Distress Syndrome (Pierrakos et al. 2012). It is recognised that this causes
a widening difference between the alveolar ventilation and pulmonary capillary perfusion. As
fluid accumulates in the alveolar space, diffusion of gases vital to homeostasis are impaired
(Pierrakos et al. 2012). Effective diffusion of gases is dependent on the structural integrity of
the alveoli and the capillaries that encapsulates them (Aitken, Marshall & Chaboyer 2015).
Excess fluid in the alveolar space restricts the normal diffusion of oxygen from the alveoli to
the capillaries because oxygen has a lower liquid solubility (Matthay, Michael A. & Zemans,
Rachel L. 2011). Carbon dioxide, however, has a greater solubility which permits it to be
easily diffused through the membrane even in the presence of excess fluid (Belda, Soro &
Ferrando 2013). Therefore, there is a lower amount of oxygen moving from the alveoli to the
pulmonary capillaries despite a normal respiratory rate, drive and pulmonary blood flow. This
is reflected in the initial Arterial Blood Gas of Patient XL where he had a below than normal
Partial Pressure of Oxygen and a low tissue oxygen saturation of 81 percent indicative of
hypoxemia. The result of this pathological insult is a decrease in the amount of oxygen
carried in blood which triggers a number of compensatory mechanisms. One of which is the
increase in respiratory rate and drive as chemoreceptors detect a drop in arterial oxygen
(Pierrakos et al. 2012). If pulmonary oedema persist, this compensatory mechanism may only

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be effective in the short term (Pierrakos et al. 2012). An increase in the respiratory rate and
drive can also affect the level of carbon dioxide. Since the solubility of carbon dioxide is
greater than oxygen, its diffusion from the pulmonary capillaries to the alveolar space is not
affected by the presence of pulmonary oedema (Matthay, Michael A. & Zemans, Rachel L.
2011). Thus, the level of arterial carbon dioxide tends to be normal or below than normal
during the initial stage of ARDS (Matthay, Michael A. & Zemans, Rachel L. 2011). Patient
XL depicted this clinical feature on his initial ABG results with a PaCO2 of 30 mmHg.

In an attempt to correct the mismatch between alveolar hypoventilation and pulmonary

capillary perfusion, the pulmonary vasculature, particularly the arterioles, vasoconstricts
(Pierrakos et al. 2012). This phenomenon, which is known as Hypoxic Pulmonary
Vasoconstriction, tries to shift blood flow from areas of low ventilation to well-ventilated
lung areas thereby normalising gas exchange (Zochios et al. 2017). But in this clinical case,
the compensatory mechanism is not effective because of the widespread nature of alveolar
injury which resulted to little or no well-ventilated lung areas creating a shunt. The ongoing
hypoxemia further taxes this mechanism which then goes on a positive feedback loop until
there is very restricted perfusion (Price et al. 2012). Apart from this mechanism, the
cardiovascular system also compensates to the prevailing hypoxia through heart rate increase,
peripheral vasoconstriction and central vasodilation in an attempt to efficiently deliver
oxygen to the different organs of the body (Pierrakos et al. 2012). However, certain
physiological cascades develop if the reversal of the original insult is not achieved.

One of those that develops in ARDS is pulmonary hypertension which can be associated with
the original insult from the virus. As aforementioned, the injury in the capillary endothelium
led to inflammation and concomitant intravascular coagulation (Price et al. 2012). The
infiltration of inflammatory cells and coagulation components in the pulmonary capillaries
contribute to the occlusion of these vessels and to the larger distal vessels (Price et al. 2012).
In addition to this, Hypoxic Pulmonary Vasoconstriction further complicates the vascular
occlusion thereby increasing the pressure in the pulmonary vasculature (Price et al. 2012).
Pulmonary hypertension consequently increases the afterload in the right ventricle of the
heart which then increases its risk of having Right Sided Ventricular Failure (Price et al.
2012).

The failure of the respiratory system and its compensatory mechanisms to supply oxygen in
the different parts of the body have damaging effects. Firstly, lack of oxygen delivered to the

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Central Nervous System causes it to decrease in function which is evident in the level of
consciousness changes with Patient XL (Morton et al. 2017). Cardiac failure or arrest can
also ensue since oxygen is very much needed in the functioning of the heart and also the
positive feedback loop may overtax the organ and this was evident in the falling
haemodynamic parameters of Patient XL (Morton et al. 2017). Other vital organs
concurrently fail to function because of the low oxygen supply which then can result to
ischemia or even cell death (Morton et al. 2017).

Management

In this case study, the major interventions that have addressed the condition focused on
facilitating effective oxygenation and optimising cardiac output. Mechanical Ventilation was
instituted to ensure that there is optimal fraction of inspire oxygen (FiO2) delivered through a
positive pressure setting which pushes adequate oxygen into the airways (Pierrakos et al.
2012). This, in turn, facilitates oxygenation of the pulmonary capillaries which then decreases
the cardiac workload (Pierrakos et al. 2012). Aside from mechanical ventilation, vasoactive
medication are pivotal in supporting return to homeostasis by improving cardiac output and
function (Pierrakos et al. 2012). Other supportive interventions include facilitation of airway
suctioning, protection from aspiration and obstruction, close monitoring and reduction of
activity to reduce metabolic demand (Pierrakos et al. 2012).

Summary

In summary, respiratory failure results from the inability of the intact compensatory
mechanisms to facilitate effective function of the respiratory system. It may arise from a host
of different conditions. In this case study, Patient XL contracted a respiratory organism which
became the root cause of respiratory failure. The Influenza virus altered the integrity of the
epithelial-endothelial membrane in the alveoli which caused a diffuse extravasation of
interstitial fluid. This, then, caused problems in the ability of oxygen to freely diffuse from
the alveolar space to the capillary membrane. Compensatory mechanisms attempted to
normalise the prevailing hypoxemia but were ineffective. Further deterioration followed that
resulted into notable changes in the function of vital organs most notably central nervous
system and haemodynamic function. The interventions to address the patient’s clinical
presentation revolved around increasing oxygen availability to the tissues and optimising
cardiac function.

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References

Aitken, L, Marshall, A & Chaboyer, W 2015, ACCCN's Critical Care Nursing - E-Book,
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Belda, FJ, Soro, M & Ferrando, C 2013, 'Pathophysiology of respiratory failure', Trends in
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Gibson, V & Waters, D 2016, Respiratory Care, Taylor & Francis.

Marini, JJ & Roussos, C 2012, Ventilatory Failure, Springer Berlin Heidelberg.

Matthay, MA & Zemans, RL 2011, 'The acute respiratory distress syndrome: pathogenesis
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Matthay, MA & Zemans, RL 2011, 'The Acute Respiratory Distress Syndrome: Pathogenesis
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