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Acute Respiratory distress syndrome (ARDS) is a result of either pulmonary or
extrapulmonary causes. Pulmonary causes are a result of damage to the alveolar
mem
anes causing an initiation of the inflammatory response (Bullock, XXXXXXXXXXThis diffuse
endothelial damage can be due to extreme systemic inflammatory response, initially
esulting in the alteration of pulmonary vascular endothelium followed by an increase in
capillary permeability (Bullock, 2013; Thompson, Chambers, & Liu, XXXXXXXXXXExtrapulmonary
causes are injuries which occur elsewhere in the body and inflammatory mediators are
transfe
ed via the bloodstream to the lungs (Thompson et al., XXXXXXXXXXDespite the cause the
end result is respiratory failure, comprising of three phases exudative in which the
inflammatory response initiates increased capillary mem
ane permeability causing
interstitial oedema and microvascular thrombi, impacting surfactant production (Thompson
et al., XXXXXXXXXXThis causes alveolar cell destruction, further increasing the inflammatory
esponse. Atelectasis results due to this decreased lung compliance and ventilation
perfusion mismatch (Bullock, XXXXXXXXXXThe proliferative stage occu
ing weeks later is when
cellular regeneration occurs, cellular granulation and collagen deposition ensues. Alveoli
ecome enlarged and i
egularly shaped, pulmonary capillaries become sca
ed and
obliterated (Urden, XXXXXXXXXXLastly, the fi
otic stage coagulation fi
inolysis imbalance is
developed, interstitial fi
in becomes deposited and causes chronic fi
osis and decreased
lung compliance (Bullock, XXXXXXXXXXThe Berlin definition criteria for ARDS as summarised
in Fan, 2018 is; timing of presentation within 7 days of known risk factors.
Bilateral opacities, exclusive of effusions, nodules, lobar or lung collapse present from chest
imaging. Origin of non-cardiogenic oedema from assessment by echocardiogram and lastly,
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hypoxaemia, mild moderate or severe determined by the value of PaO2/Fio2 (P/F) ratio,
considered only with a CPAP or PEEP of >5cmH2o (Fan, 2018).
Normal ABG parameters as per Larkin & Zimmanck, 2015
PH (The concentration of hydrogen irons in the blood): XXXXXXXXXX  
Pa02 (Partial pressure of O2 in arterial blood):  80mmHg – 100 mmHg 
PaC02 (Partial pressure of ca
on dioxide in arterial blood): 35mmHg – 45mmHg 
HCO3 (Concentration of bica
onate in blood): 22 mEq/L -26mEq/L. 
Sao2 (The percent of haemoglobin saturated with oxygen) >94%
Billy’s arterial blood gas was; PH 7.21, PaCo2 68 mmHg, PaO2 90mmHg, HcO3 26mEq/L,
SaO2 94%. The interpretation of Billy’s ABG is uncompromised respiratory acidosis. Billy had
a Spo2 92%, SAO2 at 94% and PaO2 91mmHg with an Fio2 requirement of 100% suggestive
of hypoxaemia. Additionally, the P/F ratio can be utilised to determine Billy’s level of
hypoxaemia. Billy’s P/F ratio is 90 (Pao2 90 / Fio2 100% = 90) according to Bilan, Dastranji, &
Ghalehgolab Behbahani, 2015 this is indicative of severe ARDS. His PH 7.21 and hypercapnia
with a Co2 of 68mmHg, which typically increases in patients who are beginning to fatigue,
indicates acidosis (Urden, XXXXXXXXXXAs his bica
onate is within normal limits it indicates that
his acidosis is uncompromised, indicating the body is not attempting to compensate.
According to Larkin & Zimmanck, 2015 if patients are incapable of compensating mechanical
interventions may be required. Thus, according to Billy’s ABG he was illustrative of signs of
espiratory distress.
In assessment of Billy’s condition Invasive ventilation would be most appropriate due to his
altering conscious level. Those with an altered level of consciousness increases the risk of
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patients being unable to protect their own airway, as was the case with Billy (Hess 2014).
The ventilation mode that can be proposed is a lung protective ventilation strategy,
synchronised intermittent mandatory ventilation, volume control (SIMV) (Hess, XXXXXXXXXXLung
protective strategies considered to be standard practice in caring for patients with ARDS,
lung protective modes are volume or pressure limitations during inspiratory phase and
during the expiratory phase to maintain alveolar recruitment (Hess, XXXXXXXXXXThis ventilation
mode delivers a set tidal volume and rate whilst allowing the patient to initiate
eaths,
synchronising ventilator
eaths with the patients-initiated
eaths (Urden, XXXXXXXXXXThe
suggested ventilation parameters for Billy are, tidal volume of 407 ml, PEEP 10, Rate 20, Fio2
100%. Tidal volume is calculated according to Billy’s ideal body weight, XXXXXXXXXXx [172 –
152.4]) = 67.83Kg, 6ml/kg means Billy’s set Tidal volume is 407 ml. It is vital to set the tidal
volume to the lowest possible, according to Hess, 2014 high flow rates can be injurious
ather than protective for patients with ARDS. Studies show more positive outcomes from
those who are treated with lower tidal volumes, with high tidal volumes respiratory support
ecomes removed. Studies suggest that a PEEP of >8 cmH20 is appropriate for ARDS
patients, in conjunction with Urden, 2018 that indicates a PEEP 10-15cmH20 is appropriate.
Both texts indicate that PEEP should be titrated according to oxygen requirements
determined when analysing the arterial blood gas, thus PEEP should initially be set to
10cmH2o and titrated accordingly (Hess, 2014; Urden, XXXXXXXXXXRespiratory rate should be set
to 20 to allow for adequate ca
on dioxide elimination to lower Billy’s raised PC02,
constantly re-evaluated and titrated according to the arterial blood gas and monitoring PH
levels (Urden, XXXXXXXXXXLastly, Fio2 initially should be set to 100% as that is what Billy is
equiring via the bag valve mask, similarly it should be titrated according to Pao2 when
analysing the arterial blood gas and aiming for Spo2 of 88% - 95%, it is vital to administer
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the lowest levels of oxygen to avoid oxygen toxicity that can perpetuate the entire process
(Urden, XXXXXXXXXXIt is essential that all parameters are constantly re-evaluated according to
Billy’s condition.
Peak End Expiratory Pressure (PEEP) keeps lungs open at the end of expiration of previously
collapsed areas of the lung (Chiumello et al., XXXXXXXXXXThe purpose of keeping the lungs open
at the end of expiration is to improve oxygenation whilst being able to titrate Fio2 to less
toxic levels (Urden, XXXXXXXXXXPEEP has the ability to recruit regions of the lung that were
previously atelactic, this allows for more of the lung to be available for inflation during
inspiration (Sahetya & Brower, XXXXXXXXXXPEEP has multiple positive effects on the lungs;
stabilizing flooded alveoli, increasing functional residual capacity and opening collapsed
alveoli (Urden, XXXXXXXXXXHowever, PEEP also has negative effects including decreasing cardiac
output, this is due to the decreased venous return secondary to increased intrathoracic
pressure. Increased thoracic pressure can cause barotrauma, the ruptured alveoli causing
gas to escape into su
ounding spaces (Urden, XXXXXXXXXXThe amount of PEEP that a patient
equires is determined by assessing PAO2, oxygen saturations and cardiac output, most
cases requiring PEEP 10-15 cmH20 (Urden, XXXXXXXXXXMany studies indicate that PEEP can
educe or prevent ventilator induced lung injury due to low volumes and pressures (Sahetya
& Brower, XXXXXXXXXXContrastingly, PEEP can increase the risk of barotrauma and ventilator
induced lung injury, due to the effect PEEP has on causing higher inspiratory pressures and
volumes (Sahetya & Brower, XXXXXXXXXXThus, it is imperative that patients’ pressures and tidal
volumes be closely monitored, it is largely accepted that the amount of PEEP a patient
should receive be a level that best compromises between the beneficial and adverse effects.
Therefore, it is recommended that higher levels of PEEP are utilised in order to minimize low
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pressures and volumes and improve patient outcomes (Sahetya & Brower, XXXXXXXXXXSahetya &
Brower, 2017 & Chiumello et al., 2014 suggested that higher PEEP levels only reduce
mortality in patients with severe hypoxaemia, a P/F ratio <200, and that those with not as
severe hypoxaemia who received high PEEP settings did not demonstrate a notable
eduction in patient mortality. Hence lower PEEP should be administered to those with
lower lung recruitability such as mild ARDS and higher levels of PEEP to those with
greater recruitibility like severe ARDS (Chiumello et al., XXXXXXXXXXAdditionally, it should be
noted that PEEP has cardiac effects. This includes raising intracardiac pressures involving
ight atrial pressure, impeding venous return and thus cardiac output. Furthermore, the
increase of right ventricular afterload as a result of compressed alveolar septal capillaries,
increases pulmonary vascular resistance due to PEEP (Sahetya & Brower, 2017).
Twenty-Four hours after admission to ICU Billy’s condition worsened, his symptoms were
indicative of severe sepsis. Sepsis can be described as a potentially life-threatening response
to the immune system due to a severe infection, it is a dynamic process requiring
continuous reassessment (Bonanno, XXXXXXXXXXSepsis is a form of distributive shock as a result
of infectious endotoxins that stimulate the immune system, triggering a release or
activation of inflammatory mediators, resulting in myocardial depression, altered
microvascular flow and diffuse endothelial injury. Organ dysfunction and fluid shifts follow
(Urden, XXXXXXXXXXEndothelial damage causes a loss of vascular smooth muscle sensitivity, thus
as blood pressure drops vascular tone cannot be maintained (Bullock, 2013) Initially the
ody compensates to this vasodilation by increasing heart rate and cardiac output in order
to maintain blood pressure, however damage to endothelial cells continue, resulting in
capillary leakiness and with a dwindling intravascular volume and tissue oedema that affects
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cardiac output. Severe sepsis becomes evident when the body is no longer able to
compensate and the patient becomes hypotensive and hypoxemic (Urden, XXXXXXXXXXAs was be
observed in the case of Billy twenty-four hours post admission. Billy’s Heart rate was still
tachycardic and however he became hypotensive with a blood pressure of 85/55 mmHg, a
marked sign of sepsis. This decrease in circulating blood volume is no longer enough for