How does angiotensin II increase the workload of the heart after a myocardial infarction (MI)?
By causing dysrhythmias as a result of hyperkalemia
By increasing the peripheral vasoconstriction
By stimulating the sympathetic nervous system
By reducing the contractility of the myocardium
The Correct Answer is B
A. By causing dysrhythmias as a result of hyperkalemia: Angiotensin II does not directly cause dysrhythmias through hyperkalemia. While hyperkalemia can lead to dysrhythmias, angiotensin II primarily acts as a vasoconstrictor and does not directly influence potassium levels.
B. By increasing peripheral vasoconstriction: Angiotensin II increases peripheral vascular resistance through vasoconstriction, which raises blood pressure. This increased resistance requires the heart to work harder to pump blood, thereby increasing the workload on the heart following a myocardial infarction.
C. By stimulating the sympathetic nervous system: Angiotensin II does stimulate the sympathetic nervous system, which can increase heart rate and contractility; however, the direct effect on increasing workload is more prominently due to peripheral vasoconstriction.
D. By reducing the contractility of the myocardium: Angiotensin II does not reduce contractility; in fact, it can enhance contractility in some contexts. It primarily increases the workload of the heart through vasoconstriction and increased afterload rather than reducing contractility.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
A. Carotid wall thinness: Carotid wall thinness is not considered a nontraditional risk factor for coronary artery disease (CAD). Traditional risk factors for CAD include age, gender, hypertension, hyperlipidemia, and smoking, while carotid wall thickness (rather than thinness) is often used as a marker for atherosclerosis and cardiovascular risk.
B. Chronic kidney disease: Chronic kidney disease (CKD) is recognized as a nontraditional risk factor for coronary artery disease. It is associated with increased cardiovascular risk due to factors like inflammation, mineral metabolism disorders, and increased vascular stiffness.
C. Coronary artery calcification: Coronary artery calcification is considered a nontraditional risk factor for CAD. It reflects the presence of atherosclerosis and is associated with an increased risk of cardiovascular events.
D. Markers of inflammation, ischemia, and thrombosis: Markers of inflammation (such as C-reactive protein), ischemia, and thrombosis (such as fibrinogen and D-dimer) are nontraditional risk factors for coronary artery disease. Elevated levels of these markers indicate increased cardiovascular risk and are used in risk stratification.
Correct Answer is D
Explanation
A. Inflammation: Inflammation refers to the body's immune response to injury or infection and does not specifically denote a temporary deprivation of blood supply to a cell. It is characterized by redness, swelling, heat, and pain in the affected area.
B. Necrosis: Necrosis is the process of cell death that occurs when cells are irreversibly damaged, often due to a lack of blood supply or other injury. It is a consequence of prolonged ischemia rather than the temporary condition itself.
C. Infarction: Infarction refers to the death of tissue due to prolonged ischemia, resulting from an irreversible loss of blood supply. It indicates permanent damage and is not synonymous with a temporary deprivation of blood supply.
D. Ischemia: Ischemia is the term used to describe a temporary reduction in blood flow to a tissue or organ, resulting in a deficiency of oxygen and nutrients. This condition can lead to symptoms and may cause damage if prolonged, making it the correct answer for this scenario.
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