It is important to explore the chest pain and sudden shortness of breath (dyspnea) in details as they indicate serious blunt chest injury. I would ask for details about the accident in perspectives of time and scene setting. I would also question for existing pulmonary conditions and presence of peritoneal irritation. It is also advisable to explore a pulmonary embolism diagnosis since it manifests under similar symptoms of dyspnea and chest pain. having a previous leg trauma, is also a facilitating factor to clotting which may result to P.E. Considering his traumatic experience, it is important to consider critical pulmonary aspects in; trachea orientation (presence of deviation), respiration rate, breath sounds distance, resonance after percussion and paradoxical chest movement. A CT pulmonary angiogram would be efficient in discerning P.E. from blunt chest.
The man’s anxiety is facilitated by both traumatic experience and uncertainty for medical outcomes in relation to the sudden pulmonary status and past smoking behavior. Temperature increase to 99.7F relates to fever development while the heave (parasternal) is a sign of enlarged right ventricle in response to difficulties experienced in the lungs therefore being compromised. Late inspiration crackles are resulted by opening up of alveolar sacs due to insufficient aeration and alveolar secretion during inhalation. Respiration distress which can further be examined by functional tests can be used as diagnostic steps for hypoxemia. The patient’s respiration rate is 28 per minute, which is higher than the upper limit of 22, while his heart rate is 112 beats per minute, also above 110/minute upper limit. Both aspects are essential in characterizing presence of hypoxemia.
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ABG Interpretation
The man’s pH and hydrogen carbonate levels show that his blood is alkaline and carbon dioxide partial pressure is within the recommended range of 30-40 mmHg which indicates sufficient exchange and elimination of the context gas. Partial pressure of oxygen is 60 PaO2 which is less than the lowest recommended rate of 70 therefore explaining the insufficiency of pulmonary capacity to oxygenate blood. Base excess is normal showing little change in equilibrium deviations. At this time, the treatment plan is anticoagulation of blood clots usually by heparin and warfarin as the commonly used medications. The most crucial information to acquire is the ventilation efficiency in relation to perfusion.
V/Q Interpretation
After the V/Q scan, results obtained showed abnormal tissue development and concentration within the lungs’ alveoli. Extensive bright spaces are attributed to fluid and blood retention therefore developing dead spaces with limited oxygenation. Inadequacy of oxygen and nutrients in the brain, facilitated by compromised pulmonary functioning is the cause of the patient’s abnormal mental behavior. i.e., the patient exhibits reduced brain perfusion thus negatively affecting cognitive ability. Lack of enough oxygen in the brain causes the increased prevalence to confusion. In respect to the decreased blood pressure (hypotension), reduced cardiac output facilitated by blocked pulmonary activity as evident with skin changes.
The results necessitate anticoagulation intervention with heparin or warfarin. I would consider an in-patient setting as it would be efficient to reduce risks through extensive care, observation and monitoring, which would be difficult when using oral anticoagulants in an outpatient approach. Central venous pressure is higher than the normal range, lower diastolic pressure as exhibited by pulmonary artery wedge pressure and low cardiac index which indicated low cardiac output. Low cardiac output is facilitated by right ventricle reduced functioning therefore causing cardiogenic shock. prognosis is usually rated at approximately 30 %.ABG results indicate low partial pressure, alkaline pH, low oxygen saturation, low carbon dioxide partial pressure and a compromised gaseous exchange. a compromised pulmonary function, in addition to ventricular failure plus anticoagulant use is the cause for the metabolic alkalosis.
