Which statement is true regarding myocardial functioning in the normal heart, based upon the Frank Starling law?
An increase in afterload results in decreased systolic pressure, which creates a decreased cardiac output.
A decrease in afterload causes the cardiac muscles to hypertrophy, resulting in increased diastolic volume.
An increase in preload results in greater shortening of myocardial fibers, thereby increasing contractility.
A decrease in preload results in increasing diastolic muscle fiber length, which impedes contractility.
The Correct Answer is C
A) An increase in afterload results in decreased systolic pressure, which creates a decreased cardiac output:
This statement is not consistent with the Frank-Starling law. Afterload refers to the resistance against which the heart must pump blood during systole. An increase in afterload typically results in increased systolic pressure, not decreased, as the heart works harder to overcome the increased resistance. However, increased afterload can lead to decreased cardiac output due to the increased work of the heart.
B) A decrease in afterload causes the cardiac muscles to hypertrophy, resulting in increased diastolic volume:
This statement is not consistent with the Frank-Starling law. Afterload refers to the pressure or resistance against which the heart must pump blood during systole. A decrease in afterload typically reduces the workload on the heart, which may lead to reverse remodeling and a reduction in cardiac hypertrophy. Increased diastolic volume may occur due to reduced afterload, but it's not the direct result of hypertrophy.
C) An increase in preload results in greater shortening of myocardial fibers, thereby increasing contractility:
Correct. According to the Frank-Starling law, an increase in preload (end-diastolic volume or stretch of myocardial fibers) leads to greater overlap of actin and myosin filaments within myocardial fibers during systole. This increased overlap results in stronger myocardial contraction (increased contractility), leading to an increased stroke volume and cardiac output.
D) A decrease in preload results in increasing diastolic muscle fiber length, which impedes contractility:
This statement is not consistent with the Frank-Starling law. Preload refers to the degree of stretch of the myocardial fibers at the end of diastole. A decrease in preload would lead to decreased stretch of the myocardial fibers, not increasing diastolic muscle fiber length. Decreased preload typically results in decreased contractility rather than impediment to contractility due to reduced myocardial stretch.
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) Deficiency of factors VIII or IX.
Hemophilia is a genetic disorder characterized by deficient or defective clotting factors, specifically factors VIII (hemophilia A) or IX (hemophilia B). These clotting factors are essential for the formation of stable blood clots. Therefore, if hemophilia is present, the deficiency of factors VIII or IX can lead to impaired clot formation and prolonged bleeding.
B) Diminished amount of vitamin K:
Vitamin K deficiency can lead to impaired blood clotting due to inadequate synthesis of clotting factors in the liver. However, hemophilia is specifically associated with deficiencies in factors VIII or IX, not vitamin K.
C) Decreased amount of platelets:
Platelets play a crucial role in primary hemostasis and initial platelet plug formation at the site of vascular injury. While decreased platelet count or dysfunction can lead to bleeding disorders such as thrombocytopenia or platelet function disorders, hemophilia specifically involves deficiencies in clotting factors, not platelets.
D) Missing factors V and VII:
Factor V and VII are other clotting factors involved in the coagulation cascade, but they are not deficient in hemophilia. Hemophilia is specifically characterized by deficiencies in factors VIII (hemophilia A) or IX (hemophilia B).
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