Hemodynamic readings for a client awaiting a heart transplant are

P-114

B/P-94/52

CO (cardiac output) - 3.5 L/min

CI (cardiac index) - 1.8 L/min

CVP (central venous pressure) - 12

SVR (systemic vascular resistance) - 1500 dynes/sec/cm2

The client would most benefit from an IV infusion of

A. Nitroglycerine and dobutamine: The client’s hemodynamic profile shows low cardiac output and low cardiac index, indicating poor perfusion, with elevated systemic vascular resistance (SVR). Dobutamine increases myocardial contractility and cardiac output, while nitroglycerine is a vasodilator that reduces afterload, helping to lower SVR. This combination improves tissue perfusion and decreases cardiac workload.

B. Amiodarone and levophed: Amiodarone is used for arrhythmias, and levophed (norepinephrine) is a vasopressor that increases SVR. Since this client already has an elevated SVR, adding levophed could worsen afterload and further reduce cardiac output. Amiodarone does not address the low perfusion indicated by the low cardiac index.

C. Atropine and epinephrine: Atropine increases heart rate, and epinephrine provides inotropic and vasoconstrictive effects. While they can raise cardiac output, epinephrine also increases SVR, which is already elevated in this client, potentially worsening cardiac workload.

D. Phenylephrine and dopamine: Phenylephrine is a pure vasoconstrictor that would increase SVR further, which is already high. Dopamine can improve cardiac output, but the vasoconstrictive effect of phenylephrine could offset this benefit. This combination could increase afterload and strain the heart rather than improving perfusion.

A. Normal ABG results: The ABG shows a pH of 7.50 (alkalemia) and PaCO₂ of 30 mmHg (hypocapnia), indicating respiratory alkalosis, which is not normal. PaO₂ is slightly low at 76 mmHg, and SaO₂ is decreased at 90%, further confirming abnormal gas exchange.

B. Early acute respiratory distress syndrome: Early ARDS is characterized by hypoxemia (PaO₂ < 80 mmHg) and respiratory alkalosis caused by hyperventilation as the patient compensates for impaired oxygenation. Restlessness and tachypnea are also typical early clinical signs. These ABG findings align with the early compensatory phase of ARDS.

C. Acute ventilatory failure: Acute ventilatory failure usually presents with respiratory acidosis (elevated PaCO₂) and hypoxemia, indicating insufficient ventilation. This client has low PaCO₂, which indicates hyperventilation rather than ventilatory failure.

D. Late acute respiratory distress syndrome: Late ARDS is marked by worsening hypoxemia, hypercapnia, and respiratory acidosis due to alveolar collapse and decreased lung compliance. This client’s ABG shows alkalosis and mild hypoxemia, consistent with early, not late, ARDS.