Clinical Topics Conference: Chapter 7, Hemodynamic Disorders
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  1. Congestive heart failure
  2. Pulmonary thrombo-embolism
  3. Gram-negative sepsis with DIC
  4. Caisson disease

Case 1: Congestive heart failure

Clinical vignette

The patient was a 44 year old man with a past medical history of longstanding essential hypertension and hypercholesterolemia. He had greater than a 60 pack year history of smoking cigarettes. Following several episodes of angina pectoris, he underwent cardiac catheterization in 1991, three years prior to his death. At that time he had evidence of atherosclerosis involving all three coronary arteries. In January of 1993 the patient suffered from an acute myocardial infarct. Since that time, during the subsequent 15 months, he had noted frequent episodes of shortness of breath (SOB), easy fatigability, dyspnea on exertion (DOE) and paroxysmal nocturnal dyspnea. In March, 1994, four months prior to his death, he was hospitalized at KUMC following another myocardial infarct. At that time he was noted to be in severe heart failure and was admitted for evaluation for cardiac transplantation.

Cardiac catheterization studies revealed the following: severely dilated left ventricle with mitral regurgitation. Cardiac output of 2.2 liters/minute. Left ventricular ejection fraction of 11%. Coronary artery atherosclerosis with 50% stenosis of the left main, 75-100% stenosis of the LAD, 75% stenosis of the left circumflex and 75-95% stenosis of the RCA. Blood pressure was 104/74 mm Hg. Serum cholesterol was 140 mg/dl (Normal 140-250). HDL was 17 mg/dl (Normal 37-60); LDL 74 (Normal 80-175).

On 4/17/94 he was readmitted in cardiac arrest and was resuscitated successfully. Plans were in process for heart transplant. Three weeks later he again developed a cardiac arrest. At that time he could not be resuscitated, and he was pronounced dead.

Discussion topics

  1. What factors did this man have that could have predisposed him to this condition? Which ones do you think are treatable?

  2. Explain the Starling forces one might expect within the pulmonary parenchyma.

  3. What organs are primarily affected by congestive heart failure? What pathologic changes would you expect to see at autopsy?

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    Case 2: Pulmonary thrombo-embolism

    Clinical vignette

    The patient was a 43 year old male who was well until 4 weeks prior to admission, when he developed acute posterior ankle pain while playing tennis. Upon examination, he was found to have suffered a ruptured Achilles tendon. The tendon was repaired surgically, and he was placed in lower leg cast. The past medical history was remarkable only for asthma, for which he used an inhaler, and occasionally systemic steroids. He did not smoke.

    The patient did well until 4 weeks after surgery, when he noticed shortness of breath. He attributed this to worsening asthma, for which he started himself on prednisone. He was unable to sleep, and could not lie flat in bed. His was also experiencing significant pain and swelling of the lower calf under his cast, which had previously been discounted by his orthopedic surgeon. He went to the emergency room, where a tentative diagnosis of pulmonary embolus was made.

    The patient was evaluated with a pulmonary arteriogram, which showed a large thrombus occluding a major pulmonary artery. The patient was heparinized, and a Greenfield filter was inserted in his inferior vena cava (a plastic screen designed to catch thrombi-emboli before they reach the lung).

    After a 3 week hospitalization, which included a complication of pneumothorax, treated with chest tube insertion, the patient was discharged in good condition. He was given warfarin (an oral anti-coagulant) to take indefinitely.

    Discussion topics

    1. What risk factor(s) does this patient have for pulmonary embolus?

    2. What are the hemodynamic consequences of massive pulmonary embolism?

    3. Is deep venous thrombosis a common disorder? Can anything be done to prevent it?

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    Case 3: Gram-negative sepsis with DIC

    Clinical vignette

    The patient was an 18 year old woman who complained of headache, fever, and malaise in the morning. About 8 PM of the same day, she developed widespread purpura, and a fever of 105 oF. She was taken to a local ER, where a spinal fluid specimen was obtained for culture. She was given 20 million units of IV penicillin. By 10 PM, her condition had worsened, and she was transferred to KUMC with vital signs of: BP 80/60 mm Hg, Temp 104.4 oF, Pulse 180/min, Respirations 32/min. Her hemoglobin was 12.9 g/dl, WBC 15,000/cubic mm, platelets 18,000 per cubic mm, prothrombin time(PT) 51 sec (normal 12), activated partial thromboplastin time (aPTT) 71 sec (normal 33). The plasma fibrinogen was 66 mg/dl (normal ~200). The spinal fluid was cloudy and contained 5000 WBC, predominantly PMNs, with a glucose of 20 mg/dl (serum was 94 - normal) and an elevated protein. Despite treatment with penicillin and vasopressors, she expired 7 hours after admission.

    At autopsy, the brain was edematous and showed bilateral tonsillar herniation. The meninges were cloudy and contained numerous PMNs microscopically. The adrenals were grossly hemorrhagic. A blood culture and spinal fluid culture from the outside hospital was reported positive for Neisseria meningitidis after the autopsy was begun.

    Discussion topics

    1. What is the Waterhouse-Friderichsen syndrome? Is N. meningitidis the only organism that can cause it?

    2. Review the signs, symptoms, and laboratory abnormalities associated with DIC. Can other things besides infection cause it? How is it treated?

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    Case 4: Caisson disease

    Clinical vignette

    The patient was a 42 year old lawyer who had been on vacation with his girlfriend in the Channel Islands off North Carolina just prior to admission. He had been in excellent health. He made two scuba dives on the last day of his trip. After surfacing from the last dive, he felt fine after diving to a depth of 120 feet. He and his girlfriend then boarded a turboprop charter to return to Charlotte, NC.

    Shortly after takeoff, the lawyer developed a severe headache, became dizzy and could not walk to the lavatory, and felt a tingling sensation over his abdomen. His vision began to "close in" and he became nauseated. A rash was noticed on his abdomen. Soon, he could not recognize his girlfriend, and became very sleepy. The pilot diverted to Raleigh-Durham, and the patient was life-flighted to Duke University Medical Center. He was met by physicians associated with the Divers Alert Network (DAN) at Duke, and was treated in a hyperbaric chamber. He recovered uneventfully.

    Discussion topics

    1. What caused the rash and tingling sensation on the patient's abdomen. What caused his neurologic symptoms?

    2. Why were the patient's symptoms delayed several hours until his return flight? Did the flight have anything to do with it?

    3. Why is this illness sometimes called "caisson disease"? What are some of the things that are being tried to prevent it?

    References

    1. The physiology of decompression illness. R.E. Moon, R.D. Vann, and P.B. Bennett. Scientific American, August, 1995.

    2. The Official WWW Scuba Sites List
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