Myocardial conducting cells have
The Correct Answer is {"dropdown-group-1":"B"}
A. the same number of: Myocardial conducting cells do not have the same density of myofibrils as contractile cells. While they contain some contractile proteins, their primary function is impulse conduction rather than force generation, so their myofibril content is significantly lower.
B. fewer: Myocardial conducting cells, including those in the sinoatrial node, atrioventricular node, and Bundle of His, have fewer myofibrils compared to contractile cardiomyocytes. This structural adaptation allows them to focus on rapid generation and conduction of electrical impulses rather than strong contraction.
C. no: Conducting cells are not completely devoid of myofibrils. They retain some actin and myosin filaments, enabling minor contractile activity, but this is minimal compared to contractile myocardial cells.
D. more: Conducting cells do not require additional myofibrils, as their primary role is impulse initiation and propagation, not forceful contraction. Excess filaments would impede their conduction efficiency and slow electrical signal transmission.
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Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
Correct answer: True
Heart failure is a clinical condition in which the heart is unable to maintain adequate cardiac output to meet the metabolic needs of the body. This can occur either because the ventricular myocardium is too weak to contract effectively (systolic heart failure), reducing the amount of blood ejected during systole, or because the ventricles cannot relax and fill properly during diastole (diastolic heart failure), limiting stroke volume. Anatomically, this involves the left, right, or both ventricles, and physiologically it results in inadequate tissue perfusion, fluid retention, and compensatory mechanisms such as increased heart rate and vasoconstriction, which further stress cardiac function.
Correct Answer is B
Explanation
Correct answer: False
Afterload refers to the resistance the ventricles must overcome to eject blood into the aorta and pulmonary artery during systole. Vasoconstriction of blood vessels increases systemic vascular resistance, which raises afterload and makes it more difficult for the heart to pump blood effectively. Conversely, vasodilation decreases vascular resistance, lowering afterload and reducing cardiac workload. Anatomically, the aorta and systemic arteries are the primary sites where afterload is influenced, and physiologically, increased afterload can lead to higher ventricular pressure, reduced stroke volume, and increased myocardial oxygen demand.
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