Which strategy has been shown to counteract the effects of stress on heart rate?
Meditation and deep breathing exercises
Increased cortisol production
Rapid and shallow breathing
Ignoring emotional distress
The Correct Answer is A
A. Meditation and deep breathing exercises: Techniques such as meditation, mindfulness, and slow, deep diaphragmatic breathing activate the parasympathetic nervous system via the vagus nerve. This reduces sympathetic stimulation, lowers heart rate, decreases blood pressure, and promotes relaxation, counteracting the cardiovascular effects of acute and chronic stress.
B. Increased cortisol production: Cortisol is a stress hormone released by the adrenal cortex in response to sympathetic activation. Elevated cortisol levels during stress can increase heart rate and blood pressure, so increasing cortisol would exacerbate, not reduce, stress-related cardiovascular effects.
C. Rapid and shallow breathing: Hyperventilation or rapid shallow breathing typically occurs during stress or anxiety. It increases sympathetic activity, may cause tachycardia, and does not mitigate the physiological effects of stress on heart rate.
D. Ignoring emotional distress: Suppressing or ignoring stress does not engage mechanisms that reduce sympathetic activity. Chronic unaddressed stress can increase heart rate, elevate blood pressure, and contribute to cardiovascular strain over time.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
A. Chordae tendinae: The structure pointed to by the line is the chordae tendineae. The chordae tendineae are strong, fibrous collagen cords that connect the atrioventricular valve leaflets (mitral and tricuspid valves) to the papillary muscles within the ventricles. They prevent valve prolapse during ventricular systole. When the ventricles contract, papillary muscles also contract, maintaining tension on the chordae tendineae to keep the valves closed and prevent backflow into the atria.
B. Papillary Muscles: Papillary muscles are cone-shaped projections from the ventricular walls that anchor chordae tendineae. During ventricular contraction, they prevent valve prolapse by maintaining tension on valve leaflets, ensuring unidirectional blood flow
C. Septal leaflet: The septal leaflet is part of the tricuspid valve attached to the interventricular septum. Chordae tendineae connect it to papillary muscles, stabilizing the valve during systole and preventing backflow into the right atrium.
D: Pulmonary vein: Pulmonary veins are vessels transporting oxygenated blood from the lungs to the left atrium. They are not directly connected to chordae tendineae but are adjacent to atrial structures influencing left atrial filling and valve dynamics.
Correct Answer is A
Explanation
A. Sympathetic stimulation releases norepinephrine (NE), which binds to beta-1 receptors, increasing heart rate: Sympathetic nerve fibers release norepinephrine, which binds to beta-1 adrenergic receptors on the sinoatrial node and ventricular myocardium. This increases the rate of depolarization in pacemaker cells, enhancing heart rate (positive chronotropy), and also increases contractility (positive inotropy), preparing the heart for increased cardiac output.
B. Parasympathetic stimulation releases norepinephrine (NE), which binds to beta-1 receptors, increasing heart rate: Parasympathetic fibers do not release norepinephrine; they release acetylcholine. Norepinephrine is specific to sympathetic innervation. Therefore, this description incorrectly attributes sympathetic neurotransmission to parasympathetic activity.
C. Sympathetic stimulation releases norepinephrine (NE), which binds to muscarinic receptors, slowing heart rate: Muscarinic receptors are activated by acetylcholine released from parasympathetic fibers, not by norepinephrine. Sympathetic stimulation increases heart rate, rather than slowing it, through beta-1 receptor activation.
D. Parasympathetic stimulation releases acetylcholine (ACh), which binds to the beta-1 receptors, increasing heart rate: Parasympathetic stimulation releases acetylcholine, but it binds to muscarinic receptors on pacemaker cells, not beta-1 adrenergic receptors. Activation of muscarinic receptors slows the heart rate (negative chronotropy) rather than increasing it.
Whether you are a student looking to ace your exams or a practicing nurse seeking to enhance your expertise , our nursing education contents will empower you with the confidence and competence to make a difference in the lives of patients and become a respected leader in the healthcare field.
Visit Naxlex, invest in your future and unlock endless possibilities with our unparalleled nursing education contents today
Report Wrong Answer on the Current Question
Do you disagree with the answer? If yes, what is your expected answer? Explain.
Kindly be descriptive with the issue you are facing.