During a care conference for a patient with Acute Coronary Syndrome (ACS), which primary goal should guide the care team's selection of assessments, interventions, and treatments?
Achieving a balance between myocardial oxygen supply and demand to prevent ischemia
Regulating heart rate and contractility to optimize cardiac output and perfusion
Enhancing myocardial muscle strength to improve overall cardiac function
Minimizing myocardial energy consumption to reduce workload and stress on the heart
The Correct Answer is A
A. The cornerstone of ACS management is to prevent further ischemia by ensuring that myocardial oxygen supply meets the heart’s demand. This goal guides all interventions, including oxygen therapy, medications, and revascularization strategies.
B. While regulating heart rate and contractility helps optimize cardiac output, it is a secondary objective that supports the primary goal of oxygen balance.
C. Enhancing myocardial muscle strength is not immediately achievable in ACS and is not the primary focus of acute care.
D. Minimizing myocardial energy consumption is supportive but does not directly address the critical issue of ischemia prevention.
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Related Questions
Correct Answer is B
Explanation
A. Dopamine can increase cardiac output and BP but may worsen hypovolemia if the patient is volume-depleted.
B. Low CVP and PAP indicate hypovolemia; fluid replacement is the priority to restore preload, improve cardiac output, and stabilize blood pressure.
C. Nitroprusside sodium is a vasodilator and would further lower BP, which is contraindicated in this hypotensive, hypovolemic patient.
D. Furosemide is a diuretic and would worsen hypotension and low preload; it is not appropriate in this situation.
Correct Answer is B
Explanation
A. Morphine does not raise systemic vascular resistance; it primarily causes vasodilation.
B. Morphine reduces systemic and pulmonary vascular resistance (vasodilation), decreases preload and afterload, reduces cardiac workload, decreases myocardial oxygen demand, and alleviates pain, making it beneficial in acute MI.
C. Morphine does not increase myocardial contractility; increasing contractility would raise oxygen demand, which is undesirable in MI.
D. Morphine decreases venous return rather than increasing it, which helps reduce cardiac workload.
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