Mrs. Fulcher is a 58-year-old married homemaker who was recently discharged from the hospital due to recurrent infective endocarditis. Her most recent episodes were a Staphylococcus aureus infection of the mitral valve 12 months ago and a Streptococcus mutans infection of the aortic valve 1 month ago. During her most recent hospitalization, an echocardiogram showed aortic stenosis, moderate aortic insufficiency, chronic valvular vegetation, and moderate atrial enlargement. In addition, Mrs. Fulcher has a history of chronic joint pain.

After being home for 1 week, Mrs. Fulcher was readmitted to your telemetry floor with endocarditis. She reports chills, fever, fatigue, joint pain, malaise, and a headache for the last 24 hours. Upon admission, IV infusion of normal saline at 125 mL/hr and vancomycin IV every 8 hours were ordered to be continued over the next 4 weeks. Other routine medications ordered included furosemide (Lasix), amlodipine (Norvasc), and metoprolol (Lopressor).

At admission, Mrs. Fulcher's blood pressure was 172/48 mmHg (supine) and 100/40 mmHg (sitting), her pulse was 116, respirations were 20, and her temperature was 101.9°F. Additional assessment findings included a murmur, 2+ pitting tibial edema, no peripheral cyanosis, clear lung sounds bilaterally, orientation to person, place, and time but drowsiness, hematuria, and multiple petechiae on the skin of her arms, legs, and chest.

1. What is the significance of the orthostatic hypotension, the wide pulse pressure, and tachycardia (relate these three to what is happening to her—don't just define the terms)?

2. What is the significance of hematuria, joint pain, and petechiae? (Be sure to read about infective endocarditis in the book)

3. For which complications of embolization should Mrs. Fulcher be assessed?

The significance of orthostatic hypotension, wide pulse pressure, and tachycardia in Mrs. Fulcher's case can be related to the hemodynamic changes and systemic response caused by infective endocarditis and her underlying condition of aortic stenosis.

Orthostatic hypotension refers to a drop in blood pressure upon assuming an upright position.

In Mrs. Fulcher's case, her blood pressure significantly decreased from supine (172/48 mmHg) to sitting (100/40 mmHg).

This suggests impaired compensatory mechanisms, such as decreased venous return and inadequate vascular tone regulation, which can be caused by the infective process and associated inflammation.

The wide pulse pressure (difference between systolic and diastolic pressure) is also notable, indicating increased stroke volume and impaired peripheral vascular resistance regulation.

This is likely due to the combination of aortic insufficiency, which allows blood to regurgitate back into the left ventricle during diastole, and aortic stenosis, which leads to a compensatory increase in stroke volume to maintain cardiac output.

Tachycardia (pulse rate of 116) is a compensatory response to maintain cardiac output in the presence of valvular dysfunction and inflammation.

Hematuria, joint pain, and petechiae are significant findings in the context of infective endocarditis.

Hematuria, or the presence of blood in the urine, can be an indication of renal complications associated with infective endocarditis.

The infection can lead to immune complex deposition, glomerulonephritis, or embolic events affecting the renal vasculature.

Joint pain, which Mrs. Fulcher has a history of, can be related to septic arthritis caused by the spread of infective organisms to the joints through the bloodstream.

The infection in the joint can result in pain, swelling, and limited range of motion.

Petechiae are small, pinpoint-sized red or purple spots on the skin caused by bleeding under the skin. In the context of infective endocarditis, petechiae can be a sign of septic emboli reaching the skin capillaries.

These emboli are composed of infected vegetations that can break off from the heart valves, leading to microinfarctions and subsequent petechiae formation.

Mrs. Fulcher should be assessed for various complications of embolization associated with infective endocarditis.

These can include:

Pulmonary embolism: Emboli can travel to the pulmonary circulation, leading to pulmonary infarction, chest pain, dyspnea, and hemoptysis.

Neurological complications: Emboli reaching the cerebral circulation can cause ischemic stroke, resulting in focal neurological deficits, confusion, or altered mental status.

Renal complications: Embolic events affecting the renal vasculature can lead to renal infarction, hematuria, or acute kidney injury.

Splenic complications: Emboli can lodge in the splenic circulation, causing splenic infarction and resulting in left upper quadrant abdominal pain.

Peripheral embolization: Emboli can occlude peripheral arteries, leading to ischemia in the extremities.

This can cause pain, pallor, diminished pulses, and potential tissue necrosis.

Given Mrs. Fulcher's presentation of symptoms, it is crucial to monitor her closely for these complications and promptly address any signs or symptoms that may arise.

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