Case 4

Seth Johnson is a 54 year old college physics professor with ahistory of coronary artery disease who was admitted to the hospitalfor increasing lower extremity edema, abdominal swelling, andshortness of breath. Professor Johnson noted a 30-pound weight gainover the past month, and during the past week he has hadthree-pillow orthopnea.

Professor Johnson is in moderate respiratory distress in thehospital. His skin is cool, pale, and clammy. His pulse is 95,irregular, and weak. His respirations are 28, regular, adequatevolume, labored, with bilateral rales. His blood pressure is140/80. His abdomen is enlarged, and lower extremities areremarkable for pitting edema. His physician orders laboratorytests, results are as follows:

Plasma Na+: 133 mEq/L (normal 136-140 mEq/L) Plasma K+: 6.0mEq/L (normal 3.5-5.3 mEq/L)
Plasma Cl-: 93 mEq/L (normal 98-108 mEq/L)
Plasma HCO3-: 16 mEq/L (normal 24 mEq/L)
Plasma Creatinine: 3.7 mg/dLL (normal 0.7-1.5 mg/dL) Plasma PO43-:6.8 mg/dL (normal 2.7-4.5 mg/dL)

pCO2: 36 mmHg (normal 40 mmHg)
Blood urea nitrogen: 101 mg/dL (normal 7-22 mg/dL) pH: 7.25
SpO2: 96%

Upon evaluation of the findings, Professor Johnson’s physiciandiagnoses him with both congestive heart failure and acute renalfailure.

Questions:

14.Discuss Professor Johnson’s signs and symptoms in the contextof his diagnoses (edema, weight gain, skin, pulse, respiration,shortness of breath, blood pressure).

15.Discuss Professor Johnson’s electrolyte levels in the contextof his diagnoses (Na+ K+ PO43-). Why are these findings common inacute renal failure? When a health care practitioner reads thesevalues, what might they expect in terms of his behavior or abilityto move? (Hint for PO43-: it binds with calcium, so the effects ofhigh phosphate are similar to those of low calcium)

16.Why are congestive heart failure and renal failure oftenfound together?

17.Which acid-base disorder does he have? What caused it? Whatis the compensation? (identify laboratory values)

Case 5

Daniel Purcel was diagnosed with type 1 diabetes mellitus whenhe was 12 years old. He is now a nursing student. He has managed tocontrol his diabetes throughout school. However, when he began hisclinicals, his regular schedule of meals and insulin injections wascompletely disrupted. One morning, Daniel completely forgot to takehis insulin. At 7am he drank orange juice and ate two doughnuts. At8am he drank more juice because he was very thirsty. He mentionedto a fellow student that he felt confused, weak, and that his heartwas racing. At 9:06 am, he fell unconscious. He was transferredimmediately to the emergency room, where the following informationwas obtained:

Blood pressure: 90/40
Pulse: 130, regular, strong
Respirations: 32, regular rhythm, deep, labored (“Kussmaul”) Plasmaglucose: 560 mg/dL (normal fasting 70-110 mg/dL) Plasma HCO3-: 8mEq/L (normal 24 mEq/L)
Plasma ketones: ++ (normal none)
Arterial PO2: 112 mmHg (normal 100 mmHg)
Arterial PCO2: 20 mmHg (normal 40 mmHg)
Arterial pH: 7.22

The physician determined that Daniel was in diabeticketoacidosis. He was given an intravenous infusion of isotonicsaline and insulin. Later, after his blood glucose had decreased to175 mg/dL, glucose was added to the infusion. Daniel stayed in thehospital overnight. By the next morning, his blood glucose,electrolytes, and blood gas values were normal.

Questions:

18.Which acid-base disorder did Daniel have? What caused it? Whydid he present with Kussmaul respirations? Explain these all in thecontext of the laboratory test results.

19.How did Daniel’s failure to take insulin cause this acid-basedisorder?

20.Explain Daniel’s thirst, low blood pressure, tachycardia,confusion, and weakness.

21.Explain the basis for the treatments provided (saline,insulin, and glucose).