J.F. is a 50-year-old married homemaker with a genetic autoimmune defi ciency; she has suffered from recurrent bacterial endocarditis. The most recent episodes were a Staphylococcus aureus infection of the mitral valve 16 months ago and a Streptococcus mutans infection of the aortic valve 1 month ago. During this latter hospitalization, an ECG showed moderate aortic stenosis, moderate aortic insuffi - ciency, chronic valvular vegetations, and moderate left atrial enlargement. Two years ago J.F. received an 18-month course of parenteral nutrition (PN) for malnutrition caused by idiopathic, relentless nausea and vomiting (N/V). She has also had coronary artery disease (CAD) for several years, and 2 years ago suffered an acute anterior wall myocardial infarction (MI). In addition, she has a history of chronic joint pain.
Now, after being home for only a week, J.F. has been readmitted to your fl oor with endocarditis, N/V, and renal failure. Since yesterday she has been vomiting and retching constantly; she also has had chills, fever, fatigue, joint pain, and headache. As you go through the admission process with her, you note that she wears glasses and has a dental bridge. She is immediately started on PN at 85 ml/hr and on penicillin 2 million units IV piggyback (IVPB) q4h, to be continued for 4 weeks. Other medications are furosemide (Lasix) 80 mg/day PO, amlodipine 5 mg/day PO, potassium chloride (K-Dur) 40 mEq/day PO (dose adjusted according to lab results), metoprolol 25 mg PO bid, and prochlorperazine (Compazine) 2.5 to 5 mg IV push (IVP) prn for N/V. On admission vital signs (VS) are 152/48 (supine) and 100/40 (sitting), 116, 22, 100.2° F. When you assess her, you fi nd a grade II/VI holosystolic (throughout systole) murmur and a grade III/VI diastolic murmur; 2+ pitting tibial edema but no peripheral cyanosis; clear lungs; orientation \3 but drowsy; soft abdomen with slight left upper quadrant (LUQ) tenderness; hematuria; multiple petechiae on skin of arms, legs, and chest; and splinter hemorrhages under the fi ngernails.
1. What is the significance of the orthostatic hypotension, the wide pulse pressure, and the tachycardia? [1 point]
Orthostatic Hypotension: a sudden fall in blood pressure that occurs when a person in a supine position assumes a sitting or standing position. This can make you feel dizzy, lightheaded, blurred vision, and even feeling faint.
Orthostatic hypotension usually occurs when something interrupts or interferes with the body's process of counteracting low blood pressure. Many things can cause this to occur such as: heart problems, diabetes, dehydration, medications, acute/chronic disease or disorder, or even problems with the nervous system. Age is a big contributing factor as well. Geriatrics usually develop orthostatic hypotension from the aging process of the body.
In mild to moderate fluid volume deficit, compensatory mechanisms include sympathetic nervous system stimulation of the heart and peripheral vasoconstriction. Stimulation of the heart increases heart rate and, combined with vasoconstriction, maintains blood pressure within normal limits. A change in position from lying to sitting or standing may elicit a further increase in heart rate or a decrease in blood pressure (orthostatic hypotension). If vasoconstriction and tachycardia provide inadequate compensation, hypotension occurs when the patient is recumbent. Severe fluid volume deficit can cause a weak, thready pulse that is easily obliterated and flattened neck veins. Severe, untreated fluid deficit will result in shock (Lewis, 2007, pg 322). Wide pulse pressure: A widening of the pulse pressure may be a sign of aortic valve dehiscence. Pulse pressure is the difference between systolic and diastolic blood pressures. Normally, systolic pressure is about 40 mm Hg higher than diastolic pressure. Widened pulse pressure — a difference of more than 50 mm Hg — commonly...