solved

Question
Answered step-by-step
Asked by DukeTapirMaster322

Client Scenario: 

Sam Dukes, age 70 years, was admitted to the hospital after visiting his primary physician with 
complaints of having experienced general malaise for 3 to 4 days, shortness of breath, and abdominal 
pain. Initial assessment revealed bibasilar crackles, an audible S3, and tachycardia. Mr. Dukes also 
informed the nurse of occasional epigastric pain, which he attributed to his “ulcer acting up.” 

Mr. Dukes’s history includes hypertension and coronary artery disease (past examinations indicated 
an 80% blockage of the left anterior descending coronary artery and 60% blockage of the right 
coronary artery). He also has a history of a peptic ulcer. Following are his diagnostic data on 
admission: 

BP 
HR 
Respirations 
Temperature 
Height 
Weight 
Urine 
Na+ 
K+ 
Hgb 
Hct 
AST (SCOT) 
c1- 
BUN 
Glucose 
Creatinine 
LDH 
CK 

150/72mm Hg 
102-123 bpm 
irregular 24-32 breaths/min 
37.3° C (99.2° F) tympanic 
175 cm 
79 kg* 
yellow and cloudy 
135 mmol/L 
4.2mmol/L 
11.8 g/dl 
36.2% 
134 U/L 
102 mmol/L 
17 mg/dl 
120 mg/dl 
1.2 mg/dl 
705 U/L 
587 U/L

 

 

A chest x-ray film showed mild heart failure (HF) superimposed on chronic obstructive pulmonary 
disease (COPD) and chronic pulmonary parenchymal changes. 

An electrocardiogram (ECG) revealed atrial fibrillation with a ventricular response of 112, no Q 
waves or ST-segment or T-wave changes. 

*Mr. Dukes stated that his weight had increased approximately 3 kg (6.6 lb) during the past 3 
days. 
Shortly after admission Mr. Dukes’s skin became cool and clammy. Respirations were labored, and 
he complained of abdominal pain. Upon physical examination Mr. Dukes was found to be 
diaphoretic and gasping for air, with jugular venous distention and a positive hepatojugular 
reflux and diminished bowel sounds. Bilateral crackles were present with an expiratory wheeze. 
Audible crackles were also heard with respirations. Mr. Dukes was placed in a high Fowler’s 
position, and oxygen therapy of 4 L/min was initiated. It was noted that urinary output had been 
less than 30 ml/hr since admission. 

Within 30 minutes Mr. Dukes showed further decompensation as he developed pulmonary 
edema. He was immediately transferred to the cardiac care unit (CCU) for aggressive diuretic 
therapy. Creatinine kinase myocardial band (CK-MB), an isoenzyme of CK, was confirmed at 
this time to be 4%. 

Routine CCU orders were initiated, and the plan of care was briefly explained to Mr. Dukes. 
His heart monitor showed atrial fibrillation with a rapid ventricular response of 130. Furosemide 
(Lasix) 100 mg intravenously (IV) and digoxin 0.5 mg IV were administered. A Swan-Ganz 
catheter was inserted to monitor his hemodynamic parameters. His overall condition continued 
to deteriorate, and dobutamine (Dobutrex) 1 g in 250 ml of normal saline solution at 5 μg/kg/min 
was begun. Additional diagnostic data include the following: 

BP 
HR 
Respirations 
PAP 
PAOP 
PCWP) 
co 
Cl CVP 
SVR 
HC03- 
pH 
PaC02 
Pao2 
Sao2 

190/100 mm Hg 
130bpm 
42 breaths/min 
50/22 mm Hg 
24mm Hg 
4.64L/min 
2.34 L/min/m2 
19 cm H2O 
1810 dynes/sec/cm-5 
24 mmol/L 
7.46 
31 mm Hg 
80mm Hg 
96% (with 4 L of oxygen by nasal cannula)

 

 

At this point, Mr. Dukes’s dobutamine drip was increased to 10 μg/kg/min. Administration of 
nitroprusside (Nipride) was initiated and titrated at 0.3μg/kg/min. A dopamine drip was ordered 
to be on standby. An additional 200 mg of furosemide was administered IV, and a significant 
improvement in urinary output was obtained. 

Within a short time, Mr. Dukes said that he found it “easier to breathe.” Hemodynamic and 
laboratory results were as follows: 
BP 
HR 
Respirations 
PAP 
PAOP 
(PCWP) 
co 
Cl CVP SVR 
HC03- 
pH 
PaC02 
Pao2 
Sao2 
140/190mm Hg 
109 bpm 
24 breaths/min 
30/l0mm Hg 
12mm Hg 
5.5 L/min 
2.8 L/min/m2 8cm H2O 
1340 dynes/sec/cm-s 
25 mmol/L 
7.43 
36mm Hg 
89mm Hg 
98% (with 4 L of oxygen by nasal cannula)
Over the next 2 days, Mr. Dukes’s dobutamine and nitroprusside drips were dis- continued, and he 
was given furosemide 160 mg twice daily, captopril 25 mg every 6 hours, and digoxin 0.125 mg daily. 
The heart monitor showed normal sinus rhythm, and an echocardiogram indicated an ejection 
fraction (EF) of 30%. Once stabilized Mr. Dukes was started on a low dose of carvedilol. The patient 
was transferred to the medical-surgical floor, and discharge planning, including patient and family 
teaching, was begun. Mr. Dukes was discharged 2 days later and was scheduled to be followed in 
the cardiology clinic 1 week after discharge where his treatment regimen was reassessed, and his-
blocker was gradually increased.

 

 

2. Discuss the various classifications of HF.
3. Discuss Mr. Dukes’s signs and symptoms that were consistent with HF.
4. Describe Mr. Dukes’s predisposing risk factors for HF.
5. List the nursing diagnoses appropriate for Mr. Dukes’s care.
6. Briefly define the following terms: cardiac output (CO), cardiac index 
(Cl), central venous pressure (CVP), preload, afterload, pulmonary artery 
pressure (PAP), and pulmonary artery occlusive pressure (PAOP).
7. Describe the benefits of using a pulmonary artery catheter during HF.
8. Briefly describe the pathophysiology of pulmonary edema.

 

 

9. List the pharmacologic agents used in Mr. Dukes’s care and explain their 
importance to his treatment.
10. Discuss long term management of a patient with HF.
11. Discuss new drug therapies for HF that are on the horizon.

 

 

SCIENCE
HEALTH SCIENCE
NURSING
NURSING EXIT

******CLICK ORDER NOW BELOW AND OUR WRITERS WILL WRITE AN ANSWER TO THIS ASSIGNMENT OR ANY OTHER ASSIGNMENT, DISCUSSION, ESSAY, HOMEWORK OR QUESTION YOU MAY HAVE. OUR PAPERS ARE PLAGIARISM FREE*******."