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. Assist with a chest tube insertion: A gunshot wound to the chest with a one-way valve pleural rupture indicates a tension pneumothorax, a life-threatening condition. Air enters the pleural space with each breath but cannot escape, leading to increased intrathoracic pressure, lung collapse, and mediastinal shift, which can compromise venous return and cardiac output. Immediate chest tube insertion or needle decompression is necessary to relieve pressure and restore normal lung function.
B. Give the patient low-flow oxygen: Oxygen therapy may help improve oxygenation, but it does not address the underlying issue of trapped air causing intrathoracic pressure buildup. Without intervention to release the trapped air, respiratory distress and cardiovascular collapse can occur.
C. Assess for clubbing of fingernails: Clubbing is a sign of chronic hypoxia seen in long-term respiratory diseases but is not relevant in the acute management of a tension pneumothorax. The priority is to relieve the trapped air and restore normal lung expansion.
D. Draw arterial gases: While arterial blood gases can help assess oxygenation and ventilation status, they do not treat the underlying tension pneumothorax. Immediate decompression is required before diagnostic tests to prevent rapid deterioration and potential cardiac arrest.
Correct Answer is B
Explanation
A. Septal: Septal cardiomyopathy typically refers to abnormalities in the interventricular septum and does not specifically address the rigidity and noncompliance of the myocardium that affects diastolic filling.
B. Restrictive: Restrictive cardiomyopathy is characterized by a rigid and noncompliant myocardium that impedes ventricular filling during diastole. This results in elevated pressures in the ventricles and may lead to heart failure symptoms due to poor filling capacity.
C. Infiltrative: Infiltrative cardiomyopathy involves the deposition of abnormal substances (such as amyloid or sarcoid) within the myocardial tissue, which can lead to stiffness. While this may contribute to restrictive physiology, "restrictive" is the more precise term for the condition described.
D. Hypertrophic: Hypertrophic cardiomyopathy is characterized by an abnormal thickening of the heart muscle, particularly the left ventricle. While this condition can affect diastolic filling, it is primarily due to muscle hypertrophy rather than rigidity and noncompliance of the myocardium.
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