Case Study Ards Essay example

The higher her respiratory rate the more liters of oxygen needed to supply for the loss in her lungs. To get the minute ventilation you take the breaths per min times 500mL/breath and that gets your liters of oxygen per min.

Mr. Steward’s priority problems include impaired cardiac tissue perfusion, impaired gas exchange, and pain. We are concerned about impaired cardiac tissue perfusion because the pt. is exhibiting signs of myocardial ischemia including chest pain and shortness of breath (Gillespie, 2012). Although we acknowledge that impaired cardiac tissue perfusion can decrease the function of the heart and will have the potential to affect the perfusion and delivery of oxygen to other end organs, our primary focus will be a focused cardiovascular assessment (House-Kokan, 2012). At 1800, Mr. Steward was SOB, had shallow and rapid breathing (RR = 44), and a SaO2 of 72% on RA. Due to the fluid buildup in his lungs, Mr. Steward has impaired gas exchange, and requires supplemental oxygen to maintain his SaO2; this warrants a focused respiratory assessment.

The diffusion of oxygen across the lungs and into the blood is decreased. The oxygen levels will be lowered, triggering chemoreceptors to send an afferent message to the brain, creating the sensation of dyspnea.

The observation of both animal and humans has revealed that mechanical ventilation can cause severe lung injury if over-distention occurs (Roupie et al., 1995). To make the matter even worse, the very patients that need mechanical ventilation the most, patients with the acute respiratory distress syndrome for example, are especially susceptible to over-distention and therefore, lung injury (Stewart et al., 1998). The main reason that patients with acute respiratory distress syndrome or respiratory distress syndrome are in higher risk of lung injury is due to over-distention, caused by reduced numbers of alveoli as result of fluid buildup, consolidation, and atelectasis (Roupie et al., 1995).

ARDS is acute respiratory failure with persistent hypoxemia, decreased pulmonary compliance, dyspnea, noncardiac-associated pulmonary edema, and dense pulmonary infiltrates on the chest x-ray. The main site of injury within the lung is the alveolar-capillary membrane

Other times severe trauma can cause pulmonary edema such as blood in the lungs. Patients who are unresponsive for various reasons such as cardiac arrest, alcohol intoxication, or low blood sugar can aspirate stomach contents due to the loss of their ability to protect their own airway. Aspiration can severely impede the alveoli’s ability to exchange gases. The patient can suffocate if action is not taken promptly. The aspiration may also cause pneumonia or other types of infections that can be potentially deadly for the patient. This is one of the reasons why managing and controlling n unconscious patient’s airway is so crucial during pre-hospital care. Another critical respiratory emergency is a pulmonary embolism. A pulmonary embolism can be caused by a blood clot, by an air bubble, by a large foreign body in the circulatory system such as a catheter shear, or in rare cases by amniotic fluid in pregnant females. Whatever the cause of the embolism, the results can have the same deadly consequences. Most blood clots that become pulmonary embolisms originate in the legs of patients with poor circulation of some type of leg

This physical damage can result from _____________. Mechanical ventilation can also cause the development of AKI by alteration of systemic and renal hemodynamics through changes to cardiac output. Studies have shown that PPV, by increase intrathoracic pressure, can decrease cardiac output (CO), which has been correlated with a decrease in renal plasma flow (RPF), GFR and UO (25). This correlation is supported in a canine study done by Qvist et al., in which they found that when CO was not altered during PPV, there was no decrease in GFR or UO (26). In addition to the hemodynamic effects seen in PPV, there are also marked neurohormonal effects of mechanical ventilation resulting in AKI. These include the increase of antidiuretic hormone (ADH) secretion, suppression of atrial naturitic peptide release, as well as alteration of the renin-angiotensin-aldosterone-axis (RANA) through the increase in sympathetic flow, and the accompanying increase in renin activity. These changes result in decreased renal blood flow, GFR, and UO. There is also an increase in fluid retention, however, there is some evidence that this occurs as a result of the release of vasoactive substances, which shift intrarenal blood flow from the cortex to the medulla, resulting in greater fluid retention, regardless of the level of renal

This leads to oedema, coagulation in alveolar spaces causing deficit of anatomical structure & function. This injury can take up to 24 hours to develop eventually leading to poor perfusion, increased pulmonary vascular resistance and decreased lung compliance. “50-60% of patients with significant pulmonary contusions will develop bilateral Acute Respiratory Distress Syndrome (ARDS)...(trauma.org 2004)”

In those patients under anesthesia, reduced end-tidal CO2 may be noted as the earliest indicator of air embolus. Additionally, the anesthesiologist may also note reduced oxygen saturations. Importantly, reduced oxygen saturation on pulse oximetry is considered a late sign of vascular air embolism [7].Many radiologists may never see a case of symptomatic air embolus in their careers, and so understanding the pathophysiology and treatment is important.

Following a painful crisis, acute chest syndrome may start. The sickling in blood vessel deprives a person’s lungs of oxygen damaging lung tissue and the lungs are unable to exchange oxygen properly and at least one segment of the lung is damaged.

Depending on the cause, symptoms may appear suddenly or develop over time. Experiencing extreme shortness of breath or difficulty breathing that worsens when lying down is one of the most common symptoms. Among many different symptoms like feeling of suffocating, drowning, wheezing or gasping for breath, anxiety, restlessness, irregular heartbeat, fatigue, or swelling in your lower extremities. All off this symptoms are from the causes of Pulmonary Edema any of these symptoms require immediate medical attention or they can be life threating.

Atelectasis is causing reduced ventilation perfusion (V/Q) as oxygen is not getting into the mid and lower zone of the right lung to transfer into the blood stream, there is a pulmonary shunt here (Wyka 2002), consequently Mr. Wrens oxygen saturation and PaO2 have dropped despite his positive inspiratory pressure (PIP) being increased. This is leading to reduced oxygen in the blood returning to the heart to be pumped around the body, as the body tissues need oxygen to survive it is critical that Mr. Wrens blood oxygen levels be returned to normal (Hough 2001). Atelectasis is also preventing CO2 from perfusing from the capillaries into the alveoli to be excreted consequently Mr. Wrens high PaCO2 (Wyka 2002). His blood pH is also high, this combined with the increased

Name of Diagnosis – ARDS is essentially fluid in your alveoli which is the thick elastic that builds up in your lungs. It is typically what helps keeps your lungs from filling up when adequate amount of air is being expelled, which results in less oxygen entering your bloodstream. Likewise, ARDS normally occurs in incidents where a particular individual may shows signs of shortness of breath or individuals who may be severely sick. The patients who are more prone to ARDS are those who experience a fatal injury of some sort or an infection.

Acute respiratory distress syndrome is characterized by three main symptoms or signs. [1]This includes rapid shallow breathing, Low blood oxygen levels, the feeling of not being able to get enough air in your lungs, rapid heart rate, confusion, heart arrhythmias, and extreme lethargy/

Usually other diseases caused infect lung such as infection, injuries or smoke people that cause to enter a small amount of water in alveoli and lung blood vessels it cause obstructed the work of lung and the amount of oxygen that entering