Assignment #2

1. A 34 year-old woman with diabetes mellitus is admitted in a stuporous state. Her skin is flushed and warm, her breath has a sweet smell, her pulse is rapid and weak, and her respirations are rapid and deep. Her laboratory tests indicate a blood glucose (sugar) of 320 mg/dL, serum bicarbonate (HCO3) of 16 mEq/L (normal is 22-26), and a blood pH of 7.1 (normal is 7.35 7.45).

1. What is the most likely cause of her lowered pH and bicarbonate levels? The most likely cause if the patients lowered pH and bicarbonate levels is diabetic ketoacidosis. In certain types diabetes the pancreas is unable to secrete sufficient amounts of insulin and the body begins to break down fatty acids for energy, which produces ketone bodies (Ernest, Mandel, Curhan, Hu, & Taylor, 2012). These ketone bodies produce acid byproducts. When the acid byproducts build up in the blood, the bodys pH level is lowered (Story, 2012). Sodium bicarbonate is a buffer that helps maintain normal pH levels in the body. Metabolic disorders, such as diabetes, can disrupt normal bicarbonate levels in the body (Ernest, Mandel, Curhan, Hu, & Taylor, 2012).

2. How would you account for her rapid and deep respirations? The patients respiratory system will try to compensate for the acidosis by adjusting her respiratory rate This adjustment will result in deep, rapid breathes to excrete more carbon dioxide (Story, 2012).

References:

Ernest I., Mandel, E.I., Curhan, G.C., Hu, F.B.,& Taylor, E.N. (2012). Plasma Bicarbonate and Risk of Type 2 Diabetes Mellitus. Retrieved from http://www.cmaj.ca/content/184/13/E719.long

Story, L. (2012). Pathophysiology: A Practical Approach. Sudbury, MA: Jones and Bartlett Learning, LLC.

2. A 41 year-old man is brought to the emergency department by ambulance with a suspected drug overdose. His vital signs are; respiratory rate 4 -6 breaths/minute, heart rate 126 beats/minute, BP 92/60, temperature 97.0 degrees F rectally. His arterial blood gasses (ABGs) are pH 7.30, PCo2 80 mm Hg, HCO3 24 mm HG, PO2 60 mm Hg. 1. What is the cause of his high PCO2 and low PO2 levels? The patient is suffering from respiratory acidosis. This is caused from a high level of carbonic acid in the system due to carbon dioxide retention. This will also decrease the pH level. A high level of carbon dioxide in the body is usually is the result of hypoventilation or decreased gas exchange in the lungs (Story, 2012).

2. Hypoventilation almost always causes an increase in PCO2 levels. Explain why. Hypoventilation, also called respiratory depression, occurs when the body cannot adequately perform the necessary gas exchange. This leads to an increased concentration of carbon dioxide in the body. 3. Even after he receives oxygen and his PO2 levels resume normal levels his PCO2 levels remain high. Why? The supplemental oxygen will increase the patients oxygen level, however, it does not aide in expelling the carbon dioxide from the body. Therefore, the patient will still have high PCO2 levels.

References: Chebbo, A., Tfaili, A., & Jones, S (2011). Hypoventilation Syndromes. Retrieved from http://www.mdconsult.com/das/article/body/366722248-386/ Story, L. (2012). Pathophysiology: A Practical Approach. Sudbury, MA: Jones and Bartlett Learning, LLC.

3. A 45 year-old man presents with substernal chest pain that radiates to his left shoulder. His pain is 8-9 on a scale of 0 10 (0 is no pain 10 the worst pain he has ever had). He states he feels short of breath (SOB), nauseated, and as if an elephant is sitting on my chest. His vital signs are heart rate 110 beats/minute and irregular, BP 148/90, respiratory rate 24 and shallow, temperature 98.0 degrees F orally. He is also diaphoretic. His ECG (EKG) shows an ST segment elevation. Blood tests reveal elevated troponin and CKMB levels. 1. What is the probable cause of his clinical manifestations? Based on the patients symptoms, labs, and the ECG, he is most likely suffering from a ST segment elevation myocardial infarction (STEMI) (Bolooki & Askari, 2010). During this type of infarction the coronary artery is completely blocked causing the area of the muscle to become infarcted.

2. Explain the origin of his left shoulder pain and nausea. The heart is located between the lungs and behind the sternum. The myocardium is the muscle of the heart. A myocardial infarction occurs when there is diminished blood supply to the heart (Story, 2012). This can cause pain in the sternum which will radiate to the left shoulder (Bolooki & Askari, 2010). Nausea from a myocardial infarction is related to the vaus nerve (Bolooki &Askari, 2010). The vaus nerve travels from the brain, down to the neck, along the esophagus and gives off nerve fibers to the heart (Bolooki & Askari, 2010). It then travels down to the abdomen and supplies nerves to the stomach (Bolooki &Askari, 2010).

References:

Bolooki, H.M., & Askari, A. (2010). Acute Myocardial Infarction. Retrieved from http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/acutemyocardial-infarction

Story, L. (2012). Pathophysiology: A Practical Approach. Sudbury, MA: Jones and Bartlett Learning, LLC.

4. An asthmatic 10 year-old boy has an acute asthma attack that does not respond to his emergency inhalers at home. His parents bring him to the emergency department. He is sitting up, leaning slightly forward, and appears to be struggling to breath. You see he is using his accessory muscles to breathe (intercostal, etc). His pulse is rapid, heart sounds are distant, breath sounds are virtually nonexistent. His parents tell you he developed a cold 2 days ago and his asthma has worsened since then. 1. Explain the changes in his physiological function since he developed the cold. In other word, why did his asthma worsen after he developed the cold?

Asthma is a chronic disorder of the airways that is characterized by acute airway inflammation (Story, 2012). The common cold also affects the upper airways. It can cause bronchospasms, which will trigger an asthma attack and cause the airways to narrow and become swollen. It can also cause excess mucous production, which can also exacerbate an asthma attack (Rosethal et al, 2011).

References:

Rosenthal, L.A., Avila, P.C., Heymann, P.W., Martin, R.J., Miller, K., Papadopoulos, N.G., Peebles, R.S., & Gern, J.E. (2011). Viral Respiratory Infections and Asthma: The Course Ahead. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2880817

Story, L. (2012). Pathophysiology: A Practical Approach. Sudbury, MA: Jones and Bartlett Learning, LLC.