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Unit VI Promoting Health in Patients With Circulatory or Perfusion Disorders
To measure orthostatic hypotension, have the patient assume a supine position for at least 2 minutes and record the blood pressure and heart rate. Then have the patient assume an upright position and record the blood pressure and heart rate. Generally, a reduction of 20 mm Hg or more in the systolic reading and/or 15 mm Hg in the diastolic value denotes the presence of orthostatic hypotension, also known as postural hypotension . In the patient who is highly symptomatic or with a history of syncope, this procedure can be performed in three stages: supine, sitting, and standing. The patient with orthostatic hypotension should be cautioned to transition from the supine or sitting to the standing position slowly by sitting briefly before standing. Some antihypertensive medications should be given with caution, starting with a lower dose and evaluating the patient’s response, especially in older adults, to reduce the incidence of orthostatic hypotension. CASE STUDY: EPISODE 2 Mr. Thompson is admitted to the step-down unit for further man- agement. On physical examination, he is lying in bed with the head of the bed in a semi-Fowler’s position. He is afebrile, with a temper- ature of 97.7°F (36.6°C). His blood pressure is 185/102 mm Hg. His heart rate is 124 bpm and appears to be irregular on the monitor. His respirations are 40 per minute and labored. Auscultation of his lung fields reveals crackles throughout. At a 30° angle, his jugular vein is distended and measures at 5 cm above the sternal border. He is on oxygen at 4 L/min via nasal cannula with an oxygen satura- tion of 95%. He has significant pitting edema of the lower extrem- ities. Capillary refill is decreased to the fingers, and his extremities are cool to the touch…
z Metabolic syndrome z Obesity z Smoking z High sodium dietary intake z Sleep apnea
Other conditions that can cause HF include valvular dysfunction; cardiomyopathies; infectious and inflamma- tory heart disorders, such as pericarditis and endocarditis; dysrhythmias; anemia; thyroid disease; and cardiotoxic substance exposure, such as alcohol, chemotherapy, and illicit drugs. Less common causes of HF are respiratory conditions such as pulmonary artery hypertension, chronic obstructive pulmonary disease, interstitial lung diseases, and obstructive sleep apnea. With these problems, pulmo- nary vessels constrict and put an added strain on the right side of the heart. This is called cor pulmonale. Almost 7 million people have HF, but with advances in management the incidence of HF is flat or declining. Mortality rates remain high at about 42% to 75% 5 years after diagnosis. Heart failure is a leading cause of hospital- izations among persons older than 65 and hospitalizations from HF have increased 26% since 2012. The large num- ber of persons with HF and hospitalizations related to HF contribute to an estimated annual cost of $43.6 billion. Pathophysiology Heart failure is a progressive disease characterized by myocardial cell dysfunction, resulting in the inability of the heart to pump enough cardiac output to meet the demands of the body. The normal physiology of the heart is governed by the Frank–Starling law, which states that the contractility of the myocardial muscle is influenced by the amount of blood within the ventricle before sys- tole. In other words, high end-diastolic volume stretches the myocardium, increasing the force of each contraction. However, in people with risk factors for HF, such as hyper- tension, the constant demands on the myocardial muscles over time cause them to become weakened and unable to pump effectively. Compensatory mechanisms are activated in response to decreased stroke volume and cardiac output. These responses are actions that enable the body to maintain func- tion. The sympathetic nervous system releases epinephrine and norepinephrine, resulting in an increased heart rate, increased myocardial contractility, and increased vaso- constriction in an effort to increase cardiac output. This additional workload stimulates ventricular remodeling, which results in hypertrophy or stiffening of the ventricu- lar walls. Although sympathetic nervous system responses and ventricular remodeling may be successful in the short term, the long-term effects are damaging. They produce an increase in cardiac workload and cardiac oxygen con- sumption, worsening the failure. The neurohormonal compensatory response leads to the activation of the renin–angiotensin–aldosterone system (RAAS). This is done in reaction to decreased
HEART FAILURE Epidemiology
The prevalence of heart failure (HF) is estimated at 6.5 million people aged 20 years or older in the United States, with about a million new cases each year. The lifetime risk of developing HF at age 40 is at least one in five for both genders. The number of persons with HF is expected to continue rising. Heart failure is more common in people who are 65 years old or older, persons of African descent, persons who are overweight, and persons who have had a heart attack. Male individuals have a higher rate of heart failure than female individuals. The risk factors associated with the development of HF include the following: z CAD z Hypertension z Diabetes mellitus
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