What is the inherent rate of the AV (atrioventricular) node area?
40 to 60.
20 to 40.
60 to 80.
80 to 100.
The Correct Answer is A
The atrioventricular (AV) node is an essential component of the cardiac conduction system responsible for transmitting electrical impulses from the atria to the ventricles. The inherent rate of the AV node refers to its intrinsic ability to generate electrical impulses in the absence of external influences.
Here's a breakdown of each option:
A) 40 to 60:
Correct. The inherent rate of the AV node is typically 40 to 60 beats per minute (bpm). This rate is slower than that of the sinoatrial (SA) node, which has an inherent rate of 60 to 100 bpm. The AV node acts as a backup pacemaker, ensuring that the ventricles receive electrical impulses even if the SA node fails to function properly.
B) 20 to 40:
This range is not consistent with the typical inherent rate of the AV node. A rate of 20 to 40 bpm would be unusually slow and could indicate significant conduction system abnormalities rather than the normal functioning of the AV node.
C) 60 to 80:
This range is more characteristic of the inherent rate of the SA node rather than the AV node. The SA node is the primary pacemaker of the heart, and its inherent rate is typically 60 to 100 bpm.
D) 80 to 100:
Similar to option C, this range is more consistent with the inherent rate of the SA node rather than the AV node. The SA node typically has a faster intrinsic rate compared to the AV node.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is B
Explanation
Acute leukemia, including acute myeloid leukemia (AML), involves the proliferation of abnormal myeloblasts (immature white blood cells) in the bone marrow, leading to decreased production of normal blood cells. Here's the breakdown of the pathophysiology contributing to bruising in acute leukemia:
A) Oxyhemoglobin provides less oxygen to tissues:
Oxyhemoglobin refers to hemoglobin bound to oxygen, and its role is in oxygen transport, not in the process of bruising. Therefore, this option is not directly related to the pathophysiology of bruising in acute leukemia.
B) Insufficient platelets delay the clotting process:
Correct. Thrombocytopenia, or low platelet count, is a common complication of acute leukemia due to the replacement of normal bone marrow cells with leukemia cells, leading to inadequate production of platelets. Platelets play a crucial role in hemostasis and clot formation. Insufficient platelets result in delayed clotting, leading to easy bruising and bleeding tendencies in patients with acute leukemia.
C) Phagocytic cells are inadequate in fighting infection:
Leukopenia, or low white blood cell count, can occur in acute leukemia due to suppression of normal hematopoiesis by leukemia cells in the bone marrow. While leukopenia predisposes patients to infections due to impaired immune function, it is not directly related to the pathophysiology of bruising.
D) Lack of iron causes hypochromic blood cells:
Iron deficiency anemia can result in hypochromic red blood cells, but this is not typically associated with the pathophysiology of bruising in acute leukemia. Anemia may contribute to other symptoms such as fatigue and pallor, but bruising primarily results from thrombocytopenia-induced clotting abnormalities.
Correct Answer is C
Explanation
The ABG results indicate respiratory acidosis (pH 7.0, PaCO2 66 mmHg) with compensatory metabolic alkalosis (HCO3- 24 mEq/L). The low PaO2 (60 mmHg) suggests hypoxemia.
pH 7.0: The pH is below the normal range (7.35 to 7.45), indicating acidosis.
PaCO2 66 mmHg: The PaCO2 is elevated above the normal range (35 to 45 mmHg), indicating respiratory acidosis.
HCO3- 24 mEq/L: The bicarbonate level is within the normal range (21 to 28 mEq/L), indicating compensatory metabolic alkalosis.
PaO2 60 mmHg: The PaO2 is decreased below the normal range (80 to 100 mmHg), indicating hypoxemia.
These findings suggest that the client is experiencing respiratory failure, which is characterized by inadequate gas exchange resulting in hypoxemia and hypercapnia. In this case, the massive pulmonary embolus is causing ventilation-perfusion (V/Q) mismatch, leading to impaired gas exchange and respiratory compromise. Tachycardia, hypotension, and audible bilateral pulmonary crackles further support the diagnosis of respiratory failure in the context of a massive pulmonary embolus.
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