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
Polycystic kidney disease (PKD) is a genetic disorder characterized by the formation of multiple fluid-filled cysts in the kidneys. One of the complications associated with PKD is hypertension, which often occurs due to activation of the renin-angiotensin-aldosterone system (RAAS). Here's how the pathophysiological process of the RAAS contributes to the client's elevated blood pressure:
A) Intravascular fluid deficit:
In polycystic kidney disease, the development of multiple cysts in the kidneys can impair renal function and lead to decreased filtration and reabsorption capacity. However, this impairment typically leads to fluid retention rather than intravascular fluid deficit, contributing to hypertension rather than hypotension.
B) Renin angiotensin mechanism:
Correct. In PKD, the cysts disrupt normal kidney architecture and function, leading to activation of the renin-angiotensin-aldosterone system (RAAS). Reduced renal blood flow and glomerular filtration rate (GFR) stimulate the release of renin from the juxtaglomerular cells of the kidneys. Renin acts on angiotensinogen to convert it into angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasoconstrictor that increases peripheral vascular resistance, leading to elevated blood pressure. Additionally, angiotensin II stimulates the secretion of aldosterone, which promotes sodium and water retention, further contributing to hypertension.
C) Inflammatory process of bladder mucosa:
This option is not directly related to the pathophysiological process of hypertension in polycystic kidney disease. Flank pain and hematuria in PKD are often associated with cyst rupture or hemorrhage within the cysts rather than an inflammatory process of the bladder mucosa.
D) Mineral precipitation in urine:
Mineral precipitation in urine, such as the formation of kidney stones, can occur in polycystic kidney disease but is not directly associated with hypertension. Kidney stones may contribute to flank pain and hematuria but do not typically cause systemic hypertension.
Correct Answer is A
Explanation
A. Gastric carcinoma:
Helicobacter pylori infection is a known risk factor for the development of gastric carcinoma, or stomach cancer. Long-term follow-up is essential for clients treated for gastric ulcers caused by H. pylori infection to monitor for any signs or symptoms of gastric malignancy, such as persistent abdominal pain, unexplained weight loss, dysphagia, or gastrointestinal bleeding. Regular surveillance with endoscopic examinations may be recommended to detect any precancerous or cancerous changes in the gastric mucosa.
B. Hypokalemia:
Hypokalemia, or low potassium levels, is not directly associated with gastric ulcers caused by H. pylori infection. While certain medications used in the treatment of gastric ulcers, such as proton pump inhibitors (PPIs) or H2-receptor antagonists, may increase the risk of hypokalemia, it is not a long-term complication specifically related to H. pylori infection.
C. Kidney stones:
Kidney stones, or nephrolithiasis, are not directly associated with gastric ulcers caused by H. pylori infection. Kidney stones typically form in the kidneys and urinary tract due to factors such as dehydration, dietary factors, or metabolic disorders. While certain conditions, such as chronic kidney disease, may be associated with gastric ulcers, kidney stones are not a typical long-term complication.
D. Celiac disease:
Celiac disease is an autoimmune disorder characterized by an abnormal immune response to gluten, a protein found in wheat, barley, and rye. It is not directly associated with gastric ulcers caused by H. pylori infection. Celiac disease primarily affects the small intestine, leading to inflammation and damage to the intestinal lining in response to gluten ingestion. While individuals with celiac disease may experience gastrointestinal symptoms, they are not at increased risk for gastric ulcers specifically related to H. pylori infection.
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