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.
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Related Questions
Correct Answer is C
Explanation
A. Atherosclerotic lesion: An atherosclerotic lesion can lead to reduced blood flow to the myocardium, but it is not the direct trigger for angina pectoris. Rather, it is a contributing factor to the development of conditions that cause angina.
B. Myocardial necrosis: Myocardial necrosis refers to irreversible cell damage due to prolonged ischemia, such as in a myocardial infarction. This is not a trigger for angina pectoris but rather a consequence of severe and prolonged ischemia.
C. Myocardial ischemia: Myocardial ischemia is the primary trigger for angina pectoris. It occurs when there is an imbalance between the oxygen supply and demand in the heart muscle, typically due to narrowed coronary arteries. This insufficient blood flow results in chest pain or discomfort characteristic of angina.
D. Hyperlipidemia: Hyperlipidemia is a risk factor for atherosclerosis and subsequent coronary artery disease but does not directly trigger angina pectoris. It contributes to the underlying processes that lead to myocardial ischemia.
Correct Answer is D
Explanation
A. Obtaining a STAT electrocardiogram: While obtaining an electrocardiogram (ECG) can be important in evaluating a patient's cardiac status, it is not the highest priority in the context of suspected AAA rupture. Immediate management focuses on stabilizing the patient and addressing potential hemorrhagic shock.
B. Inserting an indwelling urinary catheter: Inserting a urinary catheter may be necessary for monitoring urine output, but it is not the immediate priority when managing a suspected AAA rupture. The focus should be on life-threatening conditions first.
C. Increasing cardiac contractility: Increasing cardiac contractility may be relevant in some clinical situations, but it does not directly address the urgent need to maintain hemodynamic stability and prevent shock in a patient with suspected AAA rupture.
D. Maintaining blood pressure: Maintaining blood pressure is the highest priority intervention in this scenario. Patients with a suspected AAA rupture are at high risk for hypovolemic shock due to internal bleeding. Ensuring adequate blood pressure is critical to perfusing vital organs and stabilizing the patient before surgical intervention.
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