ARDS, or the acute respiratory distress syndrome, reveals a complicated reaction to the lung injury. It is characterized by excessive alveolar-capillary permeability, diffuse alveolar damage, and pulmonary edema. The pathology is accompanied by impaired gas exchange and severe hypoxemia (Matthay 6). Because ARDS is a syndrome, but not a disease, it contains a variety of associated clinical indications. In particular, the same symptom can include different variations of pneumonia and diffuse alveolar damage, or DAD, which is the most evident.
It has been acknowledged that ARDS and acute lung injury can emerge in association with certain clinical conditions and common risk factors. In particular, recently reviewed indicators have revealed that sepsis is considered to be the most frequently occurred factor that causes ARDS. Other risk factors involve shock and SIRS, or systemic inflammatory response syndrome. Aspiration injury, new-drowning, trauma, and burns occur rarely as common risk factors for the syndrome (Parrillo and Dellinger 710).
It should be stressed that the above-enumerated clinical conditions are synergistic. Therefore, if more than one factor is present, the probability of ARDS increases and can lead to more negative outcomes. If the syndrome arises from a pulmonary insult, it can lead to positive end-expiratory pressure (PEEP) (Parrillo and Dellinger 710).
The pathophysiological changes in ARDS are caused by a serious trauma of the body or a physical insult of the entire body that is not related to the pulmonary system. ARDS also causes such pathologies as inflammation, mechanical ventilation, and respiratory acidosis, which is initiated by ventilation, and increased capillary pressure. Ventilation/perfusion mismatch in ARDS often results in uneven distribution of the lungs processes.
Shunting is reduced and ventilation is impaired in edematous areas and fluid presented in alveoli (Weinberger, Cockrill, and Mandel 351). About this, hypoxemia can be initiated by both true shunting (V/Q mismatch equals zero) and ventilation-perfusion mismatch (containing areas of low V/Q ratio). Because shunting directly influences the decline in PO2, SaO2 can hardly return to normal oxygenation (Weinberger et al. 351).
As has been mentioned earlier, ARDS syndrome causes impaired gas exchange that results in decreased static compliance. The static compliance shows the alveoli’s ability to expand its volume on inspiration. Therefore, if static compliance is below the normal level, it reveals an excessive stiffness of the lung and pulmonary edema. It also means that respiratory frequency or PaCO2 is below the accepted limit. Hence, if our patient’s PaCO2 equals 30, which is low, it means that it has hyperventilation because stiff lung requires more work to reach a normal volume of oxygen.
Hyperventilation and respiratory alkalosis are initiated by low PaCO2 that, in its turn, is caused by an insufficient flow of blood oxygen due to pulmonary edema. About the medical card, our patient has increased pH (7.48 and 7.50). This may be caused by a low level of PaCO2. Such a misbalance was triggered by the necessity of the organism to compensate and regulate the acid-balance.
PEEP is responsible for regulating mechanic ventilation and for calculating airway pressure to identify the expiratory cycle. It is aimed at reducing shear forces caused by the collapse of alveoli. To successfully establish a PEEP ideal level, it is necessary to apply to the pressure-volume curve of the pulmonary system or some arbitrary scales of PEEP (Williams and Wilkins 5). In the case under consideration, the application of PEEP is crucial because the patient suffers from oxygen deficiency, which can be deduced from high blood pressure and low hyperventilation. The intervention of PEEP can improve the gas exchange and decrease the fluid in the alveoli. As a result, the patient’s respiratory frequency decreases, which leads to the lessening the heart beat.
The admission of the patient to ICU is predetermined by several indications. Excessive heartbeat related to the low level of PaCO2 and evidenced by static compliance; bilaterally diminished breath and expiratory wheeze related to the serious injury of the lung resulted in inflammation of the lung alveoli and impaired gas exchange.
Abnormality of respiration (28/per minute) and the high heartbeat was evidenced by low-level PaCO2 and PaO2. In 24 hours, the patient’s ABGs continued to deteriorate. Perhaps, this is connected with increased input of the oxygen via venturi mask and increased level of PEEP leading to high rates of tidal volume (Matthay 195). The intubation and ICU admission, hence, was predetermined by extremely low indicators of respiratory frequency. Diffuse, bilateral infiltrates are evidenced by chest x-rays.
In this case, the following nursing interventions for the patient can improve the pulmonary status:
- To stabilize the tidal volume by regulating the level of PEEP that may decrease the cardiac output. For this, it is necessary to control hypotension, decreased urine output, and tachycardia. Also, the patient needs appropriate medication for decreasing alveoli inflammation and disinfecting the damaged alveoli. Also, it is necessary to control the fluid restrictions from the lungs.
- To regulate and monitor the respiratory frequency and supplementary oxygen to lessen tachypnea. Most damaged alveoli should be recruited to lessen the pulmonary edema.
- To normalize the acid-balance of patience. For this, it is necessary to normalize the heartbeat that is caused by respiratory complications. It is also to reposition the patient.
According to recent researchers, the survival of the rate of patients with ARDS counts about 70 %. The severity of the prognosis is predetermined by the fact that nearly 50 % of patients die from refractory hypoxemia, which is one of ARDS indications (Stoller, Michota, and Mandell 453). For instance, increased alveolar dead space caused by injury with obstruction due to inflammation is also closely associated with lethal outcomes.
Also, patients recovering from ARDS can have near-normal or even normal lung function. However, there are severe cases when patients are left with a certain degree of lung defect. Moreover, the patients who were discharged from ICU were not able to work for 1 year. Many patients have considerable functional restrictions due to decreased lung compliance and muscle weakness.
Analyzing the etiology of the syndrome, it should be stressed that there are direct and indirect reasons for morbidity increase. In particular, direct reasons include infections, aspiration, trauma, sepsis, and pancreatitis (Stoller, Michota, and Mandell 453). Another common cause of ARDS is a blood product transfusion that can lead to acute lung injury. Judging from the above, there are a lot of factors that contribute to the morbidity rate. Therefore, the elimination of the above factors is the only way to improve the situation.
Matthay, Michael A. Acute Respiratory Distress Syndrome. US: CRC Press, 2003.
Parrillo, Joseph E. and Dellinger, R. P. Critical Care Medicine. US: Elsevier Health Sciences , 2001.
Stoller, James. K., Michota, Franklin. A., and Mandell, Brian. F. The Cleveland Clinic Intensive Review of Internal Medicine, US: Lippincott Williams & Wilkins, 2009.
Weineberger, Steven E., Cockrill, Barbara. A., and Mandel, Jess. Principles of pulmonary medicine. US: Elsevier Health Sciences, 2008.
Williams, Lippincott, and Wilkins. Critical Care Nursing. US: Lippincott Williams & Wilkins, 2006.