Choice A reason: 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.

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

Choice C reason: 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.

Choice D reason: Pulmonary congestion is a characteristic of left-sided heart failure. It indicates fluid accumulation in the lungs due to the inability of the left ventricle to pump blood effectively.

Choice A reason: 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.

Choice B reason: 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.

Choice C reason: 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.

Choice D reason: Vasoconstriction would result in an increase in blood pressure. Vasoconstriction is the narrowing of the blood vessels, which increases the vascular resistance and the blood pressure.

Choice A reason: 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.

Choice B reason: The resulting hypoxia leads to ischemic injury and myocardial cell death. This is the main cause of impaired ventricular function after a myocardial infarction. The loss of viable myocardial tissue reduces the contractility and pumping ability of the heart.

Choice C reason: 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.

Choice D reason: 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.

Choice A reason: Oliguria is not a forward effect of left ventricular heart failure. It is a backward effect that occurs due to reduced renal perfusion and activation of the renin-angiotensin-aldosterone system.

Choice B reason: Increased heart rate is a forward effect of left ventricular heart failure. It is a compensatory mechanism that occurs due to reduced cardiac output and sympathetic stimulation.

Choice C reason: Wet cough is a forward effect of left ventricular heart failure. It is a sign of pulmonary congestion and edema that result from increased pressure in the pulmonary veins and capillaries.

Choice D reason: Confusion is not a forward effect of left ventricular heart failure. It is a backward effect that occurs due to reduced cerebral perfusion and hypoxia.

Choice E reason: Jugular venous distention is not a forward effect of left ventricular heart failure. It is a backward effect that occurs due to increased pressure in the right atrium and vena cava.

Choice A reason: 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.

Choice B reason: Macrophages that engulf low-density lipoproteins (LDLs) are foam cells. They are part of the atherosclerotic process that leads to plaque formation in the blood vessels. They are called foam cells because they have a foamy appearance under the microscope.

Choice C reason: 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.

Choice D reason: 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.

Choice A reason: 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.

Choice B reason: 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.

Choice C reason: 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.

Choice D reason: Abnormal thickening and hardening of vessel walls are a result of atherosclerosis. They are caused by the accumulation of plaque, which is composed of cholesterol, fatty substances, calcium, and other materials.

Choice A reason: 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.

Choice B reason: 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.

Choice C reason: 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.

Choice D reason: The myocardial oxygen supply has fallen below demand. This is the main cause of angina pectoris. It occurs when the coronary arteries, which supply blood and oxygen to the heart muscle, are narrowed or blocked by atherosclerosis or spasm. This creates an imbalance between the oxygen demand of the heart, which increases during exertion, and the oxygen supply, which is reduced by the obstruction.

Choice A reason: 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.

Choice B reason: 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.

Choice C reason: 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.

Choice D reason: Sodium is restricted in the management of high blood pressure. Sodium can increase blood pressure by retaining water in the body and increasing the blood volume and pressure.

Choice A reason: 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.

Choice B reason: 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.

Choice C reason: Endothelial injury and inflammation are causes of atherosclerosis. Endothelial injury is the damage to the inner lining of the blood vessels, which can be caused by various factors such as high blood pressure, high cholesterol, smoking, or diabetes. Inflammation is the body's response to the injury, which involves the activation of immune cells and the release of cytokines and growth factors. These processes lead to the formation of plaque, which is composed of cholesterol, fatty substances, calcium, and other materials.

Choice D reason: 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.

Choice A reason: Decrease in wheezing present on auscultation indicates that albuterol was effective. Albuterol is a bronchodilator that relaxes the smooth muscles of the airways and reduces the airway resistance. This improves the airflow and reduces the wheezing sound that is caused by the turbulent flow of air through the narrowed airways.

Choice B reason: 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.

Choice C reason: 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.

Choice D reason: 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.

Choice A reason: Decrease in wheezing present on auscultation indicates that albuterol was effective. Albuterol is a bronchodilator that relaxes the smooth muscles of the airways and reduces the airway resistance. This improves the airflow and reduces the wheezing sound that is caused by the turbulent flow of air through the narrowed airways.

Choice B reason: 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.

Choice C reason: 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.

Choice D reason: 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.

Choice A reason: Exudative fluid is not the type of fluid drained from the patient. Exudative fluid is a high-protein fluid that results from inflammation or infection of the pleura. It is usually cloudy and contains white blood cells, bacteria, or blood.

Choice B reason: Purulent fluid is not the type of fluid drained from the patient. Purulent fluid is a thick, yellow-green fluid that results from a bacterial infection of the pleura. It is also known as empyema and contains pus and dead tissue.

Choice C reason: Transudative fluid is the type of fluid drained from the patient. Transudative fluid is a low-protein fluid that results from increased hydrostatic pressure or decreased oncotic pressure in the pleural space. It is usually clear and contains few cells or organisms. It can be caused by conditions such as heart failure, cirrhosis, or nephrotic syndrome.

Choice D reason: Infectious fluid is not the type of fluid drained from the patient. Infectious fluid is a general term that can refer to any fluid that contains microorganisms that cause disease. It can be exudative or purulent, depending on the type and severity of the infection.

Choice A reason: Infection in the blood is not empyema. It is sepsis, which is a life-threatening condition that occurs when the body's response to infection causes tissue damage, organ failure, or death.

Choice B reason: Infection in the pleural space is empyema. It is a collection of pus in the space between the lungs and the chest wall, usually caused by a bacterial infection that spreads from the lungs or the chest cavity.

Choice C reason: Exudative bronchitis is not empyema. It is a type of bronchitis that involves inflammation and excess mucus production in the bronchi, the airways that carry air to the lungs.

Choice D reason: Infection localized in the lung is not empyema. It is pneumonia, which is an inflammation of the lung tissue, usually caused by a viral or bacterial infection that affects the air sacs or the interstitial tissue.

Choice A reason: Hyperplasia and deformation of bronchial cartilage are not the causes of airway obstruction in COPD type B. Bronchial cartilage is the rigid structure that supports the bronchi, the large airways that branch from the trachea. Hyperplasia is an increase in the number of cells, and deformation is a change in the shape or structure of the cells. These processes can affect the bronchial cartilage, but they do not directly obstruct the airway.

Choice B reason: Loss of alveolar elastin is not the cause of airway obstruction in COPD type B. Alveolar elastin is the elastic fiber that allows the alveoli, the tiny air sacs at the end of the bronchioles, to expand and recoil during breathing. Loss of alveolar elastin is a characteristic of COPD type A (emphysema), which causes the alveoli to lose their shape and collapse. This reduces the surface area for gas exchange, but it does not obstruct the airway.

Choice C reason: Pulmonary edema is not the cause of airway obstruction in COPD type B. Pulmonary edema is the accumulation of fluid in the lungs, usually due to heart failure or lung injury. It causes shortness of breath, coughing, and crackles in the lungs. It can impair gas exchange and oxygenation, but it does not obstruct the airway.

Choice D reason: Thick mucus, fibrosis, and smooth muscle hypertrophy are the causes of airway obstruction in COPD type B. Thick mucus is the result of chronic inflammation and infection of the bronchi, which stimulates the mucus glands to produce more and thicker mucus. Fibrosis is the formation of scar tissue in the bronchial walls, which narrows the airway and reduces its elasticity. Smooth muscle hypertrophy is the enlargement of the smooth muscle cells that surround the bronchi, which increases the airway resistance and causes bronchospasm. These processes combine to obstruct the airway and cause chronic cough, wheezing, and dyspnea.

Choice A reason: Hereditary decrease in IgE responsiveness is not related to airway hyper-responsiveness in extrinsic asthma. IgE is an antibody that binds to allergens and triggers the release of histamine and other inflammatory mediators from mast cells. A decrease in IgE responsiveness would reduce the allergic reaction, not increase it.

Choice B reason: Increased sympathetic nervous system response is not related to airway hyper-responsiveness in extrinsic asthma. The sympathetic nervous system is the part of the autonomic nervous system that prepares the body for fight or flight. It stimulates the bronchodilation, or the widening of the airways, by activating the beta2 receptors on the smooth muscle cells. This would improve the airflow, not obstruct it.

Choice C reason: The release of stress hormones is not related to airway hyper-responsiveness in extrinsic asthma. Stress hormones, such as cortisol and adrenaline, are secreted by the adrenal glands in response to stress. They have anti-inflammatory and bronchodilator effects, which would reduce the symptoms of asthma, not worsen them.

Choice D reason: Exposure to an allergen causing mast cell degranulation is related to airway hyper-responsiveness in extrinsic asthma. Mast cell degranulation is the process of releasing histamine and other inflammatory mediators from the granules inside the mast cells. These substances cause bronchoconstriction, or the narrowing of the airways, by stimulating the smooth muscle contraction and mucus secretion. This leads to the symptoms of asthma, such as wheezing, coughing, and dyspnea.

Choice A reason: Respiratory acidosis does not cause no change in affinity of hemoglobin with oxygen. It causes a decrease in affinity of hemoglobin with oxygen, which means that hemoglobin releases more oxygen to the tissues. This is known as the Bohr effect, which is a physiological response to low pH and high CO2 levels.

Choice B reason: Respiratory acidosis causes a decrease in affinity of hemoglobin with oxygen, which means that hemoglobin releases more oxygen to the tissues. This is the correct statement that describes the expected finding in this patient. The decrease in affinity of hemoglobin with oxygen is a compensatory mechanism that tries to restore the oxygen balance in the body.

Choice C reason: Respiratory acidosis does not cause an increase in affinity of hemoglobin with oxygen. It causes a decrease in affinity of hemoglobin with oxygen, which means that hemoglobin releases more oxygen to the tissues. An increase in affinity of hemoglobin with oxygen would mean that hemoglobin holds on to oxygen more tightly, which would worsen the hypoxia in the patient.

Choice D reason: Respiratory acidosis does not cause a decrease in blood CO2. It causes an increase in blood CO2, which is the primary cause of the low pH. A decrease in blood CO2 would indicate respiratory alkalosis, which is a condition of high pH and low CO2 levels.

Choice A reason: Use of accessory breathing muscles is a sign of respiratory distress and increased work of breathing. Accessory muscles are the muscles of the neck, chest, and abdomen that assist the diaphragm and intercostal muscles in breathing. They are normally not used for breathing, but they are recruited when the airway is obstructed or the lung function is impaired.

Choice B reason: Foul-smelling sputum is not a sign of an acute asthma episode. It is a sign of a bacterial infection or a lung abscess. Sputum is the mucus that is coughed up from the lungs. It can have different colors, textures, and odors depending on the cause and severity of the condition.

Choice C reason: Feeling of chest tightness is a sign of an acute asthma episode. It is caused by the bronchoconstriction, or the narrowing of the airways, that occurs during an asthma attack. It can also be accompanied by pain or pressure in the chest.

Choice D reason: Coughing is a sign of an acute asthma episode. It is a reflex action that tries to clear the airways of mucus, irritants, or foreign particles. It can also be triggered by the inflammation and hypersensitivity of the airways that occur during an asthma attack.

Choice E reason: Expiratory wheezing is a sign of an acute asthma episode. It is a high-pitched whistling sound that is heard when the person exhales. It is caused by the turbulent flow of air through the narrowed airways. It can also be heard on inspiration, but it is more prominent on expiration.

Choice A reason: This is not the definition of ejection fraction. The percentage of blood that leaves the heart in a minute is related to the cardiac output, which is the product of the heart rate and the stroke volume.

Choice B reason: This is the correct definition of ejection fraction. It is the ratio of the stroke volume (the amount of blood pumped by the left ventricle) to the end-diastolic volume (the amount of blood in the left ventricle at the end of diastole). It is a measure of the efficiency of the heart and reflects the contractility of the cardiac muscle.

Choice C reason: This is not the definition of ejection fraction. The amount of blood that leaves the heart with each beat is the stroke volume, which is one of the factors that determine the ejection fraction.

Choice D reason: This is not the definition of ejection fraction. The amount of blood that leaves the heart in a minute is the cardiac output, which is influenced by the ejection fraction, but not equivalent to it.

Choice A reason: This is not the cause of airway obstruction in asthma. Collapse of the cartilaginous rings in the bronchi is a feature of tracheobronchomalacia, a condition in which the airways are weak and floppy.

Choice B reason: This is not the cause of airway obstruction in asthma. Type II alveolar cell injury and decreased surfactant are associated with acute respiratory distress syndrome (ARDS), a condition in which the alveoli are damaged and filled with fluid.

Choice C reason: This is not the cause of airway obstruction in asthma. Alveolar changes and pulmonary congestion are seen in chronic obstructive pulmonary disease (COPD), a condition in which the alveoli are enlarged and lose their elasticity.

Choice D reason: This is the correct cause of airway obstruction in asthma. Asthma is a chronic inflammatory disorder of the airways, characterized by mucus secretion, bronchoconstriction, and airway edema. These factors reduce the diameter of the airways and increase the resistance to airflow.

Choice A reason: This is not a sign of left-sided heart failure. Jugular vein distension is a sign of right-sided heart failure, which occurs when the right ventricle fails to pump blood effectively to the lungs.

Choice B reason: This is not a sign of left-sided heart failure. Increased blood pressure is a risk factor for developing heart failure, but it does not indicate the severity or location of the heart failure.

Choice C reason: This is not a sign of left-sided heart failure. Hepatomegaly is a sign of right-sided heart failure, which occurs when the right ventricle fails to pump blood effectively to the systemic circulation.

Choice D reason: This is a sign of left-sided heart failure. Decreased urine output is a result of reduced renal perfusion, which occurs when the left ventricle fails to pump blood effectively to the aorta and the rest of the body.

Choice A reason: This is the correct instruction by the nurse. Nausea and vomiting are signs of digoxin toxicity, which can be life-threatening. The patient should report these symptoms to their health care provider as soon as possible and have their digoxin level checked.

Choice B reason: This is not a correct instruction by the nurse. Auditory hallucinations are not common adverse effects of digoxin. They are more likely to occur with other drugs, such as antipsychotics or opioids.

Choice C reason: This is not a correct instruction by the nurse. Decreasing the amount of high-potassium foods can increase the risk of digoxin toxicity, as potassium competes with digoxin for binding sites on the cardiac cells. The patient should maintain a normal potassium intake and avoid sudden changes in their diet.

Choice D reason: This is not a correct instruction by the nurse. Omitting the dose of digoxin if the pulse is 70 can lead to underdosing and ineffective treatment of heart failure. The patient should only omit the dose of digoxin if their pulse is below 60, as this indicates bradycardia, which is another sign of digoxin toxicity.

Choice A reason: This is not the cause of pulmonary symptoms in left heart failure. Decreased cardiac output is a consequence of left heart failure, which affects the perfusion of vital organs and tissues.

Choice B reason: This is not the cause of pulmonary symptoms in left heart failure. Bronchoconstriction is a feature of asthma and chronic obstructive pulmonary disease (COPD), which affect the airways and cause wheezes and shortness of breath.

Choice C reason: This is not the cause of pulmonary symptoms in left heart failure. Inflammatory pulmonary edema is a type of non-cardiogenic pulmonary edema, which occurs when the alveolar-capillary membrane is damaged by an inflammatory process, such as pneumonia or sepsis.

Choice D reason: This is the correct cause of pulmonary symptoms in left heart failure. Pulmonary vascular congestion is a result of increased pressure in the pulmonary circulation, which occurs when the left ventricle fails to pump blood effectively to the aorta and the rest of the body. This causes fluid to leak into the alveoli and interstitial spaces, leading to cough, dyspnea, crackles, and pink frothy sputum.

Choice A reason: This is not a symptom of right heart failure. Hypertension is a risk factor for developing heart failure, but it does not indicate the severity or location of the heart failure.

Choice B reason: This is not a symptom of right heart failure. Dyspnea upon exertion is a symptom of left heart failure, which occurs when the left ventricle fails to pump blood effectively to the lungs.

Choice C reason: This is a symptom of right heart failure. Significant edema to both lower legs and feet is a result of increased pressure in the systemic circulation, which occurs when the right ventricle fails to pump blood effectively to the rest of the body. This causes fluid to accumulate in the dependent areas, such as the lower extremities.

Choice D reason: This is not a symptom of right heart failure. Decreased urine output is a symptom of left heart failure, which occurs when the left ventricle fails to pump blood effectively to the aorta and the rest of the body. This causes reduced renal perfusion and oliguria.

Choice A reason: This is not what will happen when a person is hypotensive. Baroreceptors are sensory receptors that detect changes in blood pressure. When a person is hypotensive, the baroreceptors are more active, not less, and they send signals to the brain to increase the blood pressure.

Choice B reason: This is what will happen when a person is hypotensive. SNS stands for sympathetic nervous system, which is the part of the autonomic nervous system that prepares the body for fight or flight response. When a person is hypotensive, the SNS is activated to increase the heart rate, contractility, and vasoconstriction, which all raise the blood pressure.

Choice C reason: This is not what will happen when a person is hypotensive. Person will be bradycardic means that the person will have a slow heart rate, usually below 60 beats per minute. When a person is hypotensive, the opposite will happen, as the heart rate will increase to compensate for the low blood pressure.

Choice D reason: This is not what will happen when a person is hypotensive. SNS is suppressed means that the sympathetic nervous system is inhibited or reduced in activity. When a person is hypotensive, the SNS is not suppressed, but rather stimulated, to increase the blood pressure.

Choice A reason: This is not a physiological response to hydralazine. Cool extremities are a sign of poor peripheral perfusion, which can be caused by vasoconstriction, not vasodilation.

Choice B reason: This is not a physiological response to hydralazine. Increased urinary output is a sign of diuresis, which can be caused by diuretic medications, not vasodilators.

Choice C reason: This is not a physiological response to hydralazine. Pale skin is a sign of reduced blood flow to the skin, which can be caused by vasoconstriction, not vasodilation.

Choice D reason: This is a physiological response to hydralazine. Reflex tachycardia is a compensatory mechanism that occurs when the blood pressure drops due to vasodilation. The heart rate increases to maintain the cardiac output and perfusion pressure.