A. Assess the cause of the agitation: This is the most appropriate action. Agitation in a mechanically ventilated patient can be due to multiple causes, such as pain, hypoxia, or discomfort. It is crucial to assess and identify the underlying cause to address it appropriately.

B. Reassure the client that he or she is safe: While reassurance is important, it may not address the root cause of the agitation, especially if it is related to a physical issue such as hypoxia or tube displacement.

C. Restrain the client's hands: Restraining should be a last resort after other interventions have failed. Restraints can cause further agitation and distress.

D. Sedate the client immediately: Sedating the client without assessing the cause of the agitation could mask serious issues and lead to inappropriate treatment.

A. Partially compensated Metabolic Alkalosis: This is incorrect because the pH is within normal limits (7.35-7.45), and the elevated PaCO2 and bicarbonate suggest a respiratory issue rather than a metabolic one.

B. Fully compensated Metabolic Acidosis: This is incorrect because the primary disturbance is respiratory, not metabolic. A compensated metabolic acidosis would typically show a low PaCO2 as compensation.

C. Fully compensated Respiratory Acidosis: Correct. The pH is within the normal range, indicating full compensation. The elevated PaCO2 and bicarbonate reflect a chronic respiratory acidosis that has been compensated by the kidneys.

D. Partially compensated Respiratory Alkalosis: This is incorrect because in respiratory alkalosis, the PaCO2 would be low, not high.

A. Notify the health care provider: While it may eventually be necessary to notify the healthcare provider, the immediate action should involve confirming the balloon pressure, which is within the scope of respiratory therapy.

B. Call respiratory therapy to obtain the pressure within the balloon: This is the most appropriate action. Respiratory therapists are skilled in managing and measuring the cuff pressure to ensure it is within the correct range (typically 20-30 cm H2O).

C. Add air to the balloon port: Adding air without knowing the current pressure could lead to over inflation, which might cause tracheal injury.

D. Remove air from the balloon port: Similarly, removing air could lead to underinflation, increasing the risk of aspiration or inadequate ventilation.

A. Near-drowning: This is a direct cause of ARDS. Inhalation of water can lead to pulmonary edema, which triggers ARDS.

B. Aspiration: Aspiration of gastric contents can directly injure the lungs and is a well-known cause of ARDS.

C. Pancreatitis: Pancreatitis is associated with ARDS, but it is an indirect cause, not a direct one. The inflammatory response from pancreatitis can lead to ARDS, but it is not due to direct lung injury.

D. Toxic inhalation: Inhaling toxic substances can cause direct damage to the alveoli and lead to ARDS.

A. Hypertension: This is not a cause of high-output heart failure. Hypertension typically leads to low-output heart failure due to increased afterload, which causes the heart to work harder.

B. Severe anemia: Severe anemia causes high-output heart failure because the body compensates for the decreased oxygen-carrying capacity by increasing cardiac output.

C. Sepsis: Sepsis can lead to high-output heart failure as the body attempts to maintain perfusion in the face of widespread vasodilation.

D. Hyperthyroidism: Hyperthyroidism increases metabolic demands, which can cause high-output heart failure as the heart attempts to meet the increased needs.

A. Decreases contractility: This is incorrect because ACE inhibitors do not directly affect myocardial contractility. They primarily work on the vascular system.

B. Increases preload: This is incorrect as ACE inhibitors do not increase preload. They may decrease preload by reducing fluid retention.

C. Decreased afterload: ACE inhibitors lower systemic vascular resistance (afterload) by inhibiting the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. This reduces the workload on the heart.

D. Increases sympathetic stimulation: This is incorrect because ACE inhibitors actually reduce sympathetic stimulation by preventing the vasoconstrictive and sodium-retaining effects of angiotensin II.

A. Administer a stat fluid challenge: This might temporarily improve cardiac output in tamponade, but it is not the primary intervention. The fluid challenge may be used as a temporary measure, but it does not address the underlying cause.

B. Place the patient in a prone position: This is incorrect and could worsen the patient's condition. The patient should be in a semi-recumbent position to decrease venous return and reduce pressure on the heart.

C. Draw a stat CBC: A CBC is not relevant to the immediate management of cardiac tamponade and does not address the urgent need to relieve the pressure on the heart.

D. Perform a stat pericardiocentesis: Pericardiocentesis is the definitive treatment for cardiac tamponade, as it removes the fluid from the pericardial space, relieving the pressure on the heart and allowing it to function properly.

A. Pulmonary crackles/rales: Left-sided heart failure leads to a buildup of fluid in the lungs, causing pulmonary congestion and crackles/rales on auscultation.

B. Weight gain: This is more commonly associated with right-sided heart failure due to fluid retention, though it can be seen in both types of heart failure.

C. Hepatomegaly: Hepatomegaly is typically associated with right-sided heart failure due to congestion in the systemic circulation.

D. Jugular vein distention: JVD is a sign of right-sided heart failure, as it indicates increased central venous pressure.

A. ST segment elevation: ST segment elevation is a classic sign of myocardial injury, indicating that a portion of the heart muscle is not receiving enough oxygen and is actively injured.

B. Q wave: A Q wave typically appears later, representing a previous myocardial infarction (necrosis), not acute injury.

C. Inverted T wave: This indicates myocardial ischemia, which is a precursor to injury but not indicative of injury itself.

D. ST segment depression: This is typically associated with ischemia or subendocardial infarction, not full-thickness myocardial injury.

A. "Now you can eat whatever you want": This is incorrect and dangerous advice. Lifestyle changes, including diet, are crucial for preventing the progression of coronary artery disease even after a CABG.

B. "A CABG is not a cure - It may improve your quality of life": This response educates the patient that while CABG can relieve symptoms and improve quality of life, it does not cure the underlying disease. Continued management and lifestyle changes are essential.

C. "I am happy for you": While this might express empathy, it does not provide the necessary education or correction of the patient’s misconception about CABG.

D. "A CABG is not a cure - but now you can stop taking your medications": This is incorrect. Most patients will need to continue taking medications such as antiplatelets, statins, and antihypertensives to manage their condition post-CABG.