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. Deep vein thrombosis: Patients with deep vein thrombosis (DVT) are at a significantly higher risk for developing pulmonary embolism (PE) due to the potential for thrombus formation in the veins to dislodge and travel to the lungs. Assessing this patient as a priority is crucial, as timely intervention can prevent the development of PE.
B. Endocarditis: While endocarditis can lead to embolic events, it typically results in systemic emboli rather than specifically causing pulmonary embolism. The immediate priority for PE assessment is lower in patients with endocarditis compared to those with DVT.
C. Left heart failure: Left heart failure can lead to pulmonary congestion and respiratory symptoms but does not directly indicate a high risk of pulmonary embolism. While it is important to monitor these patients, assessing for PE is not the immediate priority.
D. Valvular disease: Valvular disease can increase the risk of thrombus formation, particularly if it results in atrial fibrillation. However, the direct connection to pulmonary embolism is not as pronounced as in patients with DVT. Therefore, assessing patients with valvular disease for PE is not the priority compared to those with DVT.
Correct Answer is A
Explanation
A. Myocardial infarction: Myocardial infarction involves the irreversible damage to the heart muscle due to prolonged ischemia, typically resulting from the occlusion of a coronary artery. The lack of oxygen and nutrients leads to cell death in the affected area of the heart, causing permanent damage.
B. Myocardial stunning: Myocardial stunning refers to a temporary reduction in the heart's function following reperfusion after a period of ischemia. The heart muscle may regain function over time, and this condition does not cause irreversible damage.
C. Stable angina: Stable angina is characterized by transient chest pain due to reversible ischemia, usually triggered by physical exertion or stress. The ischemic episodes do not lead to irreversible damage to the heart muscle, as blood flow is restored when the trigger is removed.
D. Unstable angina: Unstable angina involves episodes of chest pain that occur at rest or with minimal exertion and may signal an impending myocardial infarction. While it indicates a high risk of myocardial infarction, it does not cause irreversible damage to the heart muscle itself unless it progresses to an infarction.
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