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Jugular vein distention is a sign of right-sided heart failure, not left-sided. It indicates increased pressure in the right atrium and vena cava.

Peripheral edema is also a sign of right-sided heart failure, not left-sided. It indicates fluid retention in the lower extremities and abdomen.

Decreased systemic vascular resistance is not a characteristic of left-sided heart failure. It is a compensatory mechanism that occurs in response to reduced cardiac output.

Decreased cardiac output would result in a decrease in blood pressure, not an increase. Cardiac output is the amount of blood pumped by the heart per minute.

Decreased vascular resistance would also result in a decrease in blood pressure, not an increase. Vascular resistance is the force that opposes the blood flow in the blood vessels.

Hypovolemia would also result in a decrease in blood pressure, not an increase. Hypovolemia is the condition of having low blood volume due to fluid loss or dehydration.

The cells of the myocardium become hypertrophic in response to increased workload or pressure, not as a result of myocardial infarction. Hypertrophy is an adaptive mechanism that can lead to impaired ventricular function over time.

There is a temporary alteration in electrolyte balance that can be corrected. This is not the primary cause of impaired ventricular function after a myocardial infarction. Electrolyte imbalance can occur due to fluid loss, renal impairment, or medication side effects, but it can be managed with appropriate interventions.

There is too much pressure on the heart and the ventricles begin to dysfunction. This is not the direct cause of impaired ventricular function after a myocardial infarction. Increased pressure on the heart can result from hypertension, valvular disease, or pulmonary embolism, but it is not related to myocardial ischemia or necrosis.

Lipid-laden mast cells are not foam cells. Mast cells are immune cells that release histamine and other inflammatory mediators. They do not accumulate lipids or have a soap-like texture.

Injured neutrophil clots are not foam cells. Neutrophils are immune cells that fight infection and form pus. They do not engulf LDLs or contribute to atherosclerosis.

Deposited adipose cells are not foam cells. Adipose cells are fat cells that store energy and secrete hormones. They do not phagocytose LDLs or form plaques in the blood vessels.

Abnormally dilated arteries and veins are not a result of atherosclerosis. They are a sign of aneurysms or varicose veins, which are caused by different factors.

Arterial wall thinning and weakening are not a result of atherosclerosis. They are a sign of arteriosclerosis, which is a general term for the loss of elasticity and flexibility of the arteries.

Autonomic nervous system imbalances are not a result of atherosclerosis. They are a sign of dysautonomia, which is a disorder of the nervous system that affects the regulation of vital functions.

Cardiac output has not fallen below normal levels. Cardiac output is the amount of blood pumped by the heart per minute. It is affected by the heart rate and the stroke volume. Angina pectoris does not directly affect the cardiac output, but it can reduce the stroke volume due to impaired ventricular filling.

The vagus nerve is not stimulated. The vagus nerve is a cranial nerve that innervates the heart and other organs. It is part of the parasympathetic nervous system, which slows down the heart rate and lowers the blood pressure. Angina pectoris does not activate the vagus nerve, but it can trigger the sympathetic nervous system, which increases the heart rate and blood pressure.

Myocardial stretch has not exceeded the upper limits. Myocardial stretch is the degree of tension or load on the cardiac muscle fibers. It is determined by the end-diastolic volume, which is the amount of blood in the ventricle at the end of relaxation. Angina pectoris does not cause excessive myocardial stretch, but it can impair the myocardial contractility due to ischemia.

Potassium is not restricted in the management of high blood pressure. In fact, potassium can help lower blood pressure by balancing the effects of sodium and relaxing the blood vessel walls.

Magnesium is not restricted in the management of high blood pressure. Magnesium can also help lower blood pressure by regulating the calcium channels and improving the endothelial function.

Calcium is not restricted in the management of high blood pressure. Calcium can also help lower blood pressure by inhibiting the renin-angiotensin system and reducing the vascular resistance.

An increase in antithrombotic substances is not a cause of atherosclerosis. Antithrombotic substances are agents that prevent or reduce the formation of blood clots. They can be used to treat or prevent atherosclerosis, not cause it.

Congenital heart disease is not a cause of atherosclerosis. Congenital heart disease is a condition that is present at birth and affects the structure or function of the heart. It can be caused by genetic or environmental factors, not by atherosclerosis.

High serum potassium levels are not a cause of atherosclerosis. High serum potassium levels are a condition that affects the balance of electrolytes in the blood. It can be caused by kidney disease, medication side effects, or excessive intake of potassium-rich foods. It can affect the heart rhythm and function, but it does not cause atherosclerosis.

Respiratory rate increased to 38 breaths/min does not indicate that albuterol was effective. It indicates that the patient is still experiencing respiratory distress and hypoxia. The normal respiratory rate for adults is 12 to 20 breaths/min. A high respiratory rate can also be a side effect of albuterol, as it can stimulate the sympathetic nervous system and increase the heart rate and blood pressure.

Sputum production is clear and watery does not indicate that albuterol was effective. It indicates that the patient has a productive cough and is expelling mucus from the lungs. Sputum production is not directly affected by albuterol, as it does not have anti-inflammatory or mucolytic properties.

Use of neck muscles does not indicate that albuterol was effective. It indicates that the patient is using accessory muscles to breathe and is exerting more effort to inhale. This is a sign of severe respiratory distress and airway obstruction. Albuterol should relieve the bronchospasm and reduce the need for accessory muscle use.