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Question 301Question →

A telemetry nurse is caring for an older adult client receiving a continuous intravenous infusion of furosemide for severe decompensated heart failure. Over the past 4848 hours, the client has experienced a net fluid loss of 4.5 L4.5\ \text{L}. The nurse notes the client is now exhibiting generalized muscle weakness, shallow respirations at 10 breaths/min10\ \text{breaths/min}, and frequent premature ventricular contractions on the cardiac monitor.

Laboratory TestResult
pH7.517.51
PaCO2\text{PaCO}_248 mmHg48\ \text{mmHg}
HCO3−\text{HCO}_3^-34 mEq/L34\ \text{mEq/L}
PaO2\text{PaO}_288 mmHg88\ \text{mmHg}
Serum Sodium136 mEq/L136\ \text{mEq/L}
Serum Potassium2.7 mEq/L2.7\ \text{mEq/L}
Serum Chloride92 mEq/L92\ \text{mEq/L}

Which physiological mechanism best explains the client's current clinical presentation and laboratory results?

Show answer & explanation

Answer: Excessive loss of fluid, chloride, and potassium has induced a primary metabolic alkalosis, prompting compensatory alveolar hypoventilation.

Answer

Excessive loss of fluid, chloride, and potassium has induced a primary metabolic alkalosis, prompting compensatory alveolar hypoventilation.
The client's ABG reveals a pH of 7.51 (alkalemia) with an elevated HCO3- (34 mEq/L), indicating a primary metabolic alkalosis. This is a classic complication of massive loop diuretic therapy (furosemide), which causes profound renal wasting of water, potassium, and chloride. The loss of chloride and fluid concentrates the extracellular bicarbonate, creating contraction alkalosis. The respiratory system compensates for metabolic alkalosis by hypoventilating (respiratory rate of 10 breaths/min) to retain CO2 (PaCO2 48 mmHg), which acts as an acid to help lower the pH. The concurrent severe hypokalemia (2.7 mEq/L) directly causes the muscle weakness and premature ventricular contractions.

Step-by-Step Solution

1
Analyze the Arterial Blood Gas (ABG) results.
The pH is 7.51 (alkalemia). The HCO3- is 34 mEq/L (elevated, indicating metabolic alkalosis). The PaCO2 is 48 mmHg (elevated, indicating a respiratory acid buffer response).
Determining the primary acid-base disturbance is required to understand the client's physiological state.
2
Identify the etiology of the acid-base and electrolyte disturbances.
Massive diuresis with furosemide caused profound renal excretion of water, potassium, and chloride. The disproportionate loss of chloride and fluid leads to contraction alkalosis (metabolic alkalosis), while potassium loss leads to severe hypokalemia.
Connecting the diuretic therapy to its expected physiological consequences explains the laboratory abnormalities.
3
Correlate the physical assessment findings with the laboratory data.
The severe hypokalemia (2.7 mEq/L) directly causes muscle weakness and premature ventricular contractions. To compensate for the metabolic alkalosis, the respiratory center decreases the respiratory rate (10 breaths/min) to retain CO2 and lower the pH.
This confirms that the clinical signs are physiological adaptations to the iatrogenic electrolyte and acid-base shifts.
4
Select the mechanism that encompasses all clinical data.
The only mechanism that explains the alkalotic pH, the compensatory hypoventilation, and the complications of diuresis is primary metabolic alkalosis with respiratory compensation.
The other options incorrectly identify the primary disturbance as acidosis or hyperventilation, contradicting the objective data.

Key Concept

Acid-Base Imbalances and Loop Diuretic Complications
Question 302Question →

A critical care nurse evaluates a client with severe sepsis who is receiving a continuous intravenous infusion of norepinephrine. The client has become increasingly restless and confused over the past hour, with new-onset mottling of the lower extremities. Current assessment data include:

- Blood pressure: 102/82102/82 mm Hg
- Heart rate: 128128 beats/min
- Respiratory rate: 3232 breaths/min
- Arterial blood gas (ABG): pH 7.287.28, PaCO 2_2 3030 mm Hg, HCO 3−_3^- 1414 mEq/L, PaO 2_2 8585 mm Hg
- Central venous oxygen saturation (ScvO 2_2): 48%48\%
- Serum lactate: 6.86.8 mmol/L

Based on these findings, which action should the nurse prioritize?

Show answer & explanation

Answer: Administer a rapid isotonic crystalloid fluid bolus.

Answer

The correct action is to administer a rapid isotonic crystalloid fluid bolus to increase cardiac output and tissue perfusion.
The clinical picture demonstrates profound, unresuscitated shock. Although the mean arterial pressure (MAP) is technically adequate (around 8888 mm Hg), the severely narrowed pulse pressure (2020 mm Hg), extremely low central venous oxygen saturation (ScvO 2_2 of 48%48\%), high lactate, and physical signs of poor perfusion (mottling, confusion) indicate that cardiac output is grossly inadequate. The blood pressure is only being maintained by extreme vasoconstriction from the norepinephrine. Administering an isotonic fluid bolus is the priority to increase intravascular volume, improve stroke volume, and enhance tissue oxygen delivery.

Step-by-Step Solution

1
Analyze the hemodynamic parameters in the context of the vasopressor infusion.
The mean arterial pressure (MAP) is technically adequate (~88 mm Hg), but the pulse pressure is severely narrowed (20 mm Hg) and ScvO2 is critically low (48%).
This combination indicates that the blood pressure is being maintained solely by extreme vasoconstriction, masking a severely depleted stroke volume and profound tissue hypoperfusion.
2
Evaluate the arterial blood gas (ABG) for compensation.
The ABG reveals a metabolic acidosis (HCO3- 14) with perfect respiratory compensation (PaCO2 30).
Using Winter's formula (1.5 x 14 + 8 = 29 +/- 2), the actual PaCO2 matches the expected value, indicating the respiratory system is working appropriately to buffer the acid and should not be suppressed.
3
Determine the highest priority intervention.
Fluid resuscitation is required immediately.
Reversing the root cause of the shock (inadequate intravascular volume leading to lactic acidosis) takes precedence over managing the numbers. Expanding the volume will increase stroke volume, improve ScvO2, and reduce reliance on vasoconstriction.

Key Concept

In severe sepsis, a 'normal' mean arterial pressure achieved via high-dose vasopressors can mask profound hypoperfusion. A severely narrowed pulse pressure, low ScvO2, and elevated lactate require volume expansion to improve cardiac output, rather than further vasoconstriction.
Question 303Question →

A nurse is evaluating a client who sustained a high-grade splenic laceration following blunt torso trauma. The client is currently being managed with non-operative, conservative therapy. Which clinical finding provides the most definitive evidence that the client's physiological status has transitioned from a compensatory state into a progressive state of hypovolemic shock?

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Answer: The client's mean arterial pressure decreases to 58 mm Hg, and the extremities become cold and mottled.

Answer

The client's mean arterial pressure decreases to 58 mm Hg, and the extremities become cold and mottled.
In the progressive stage of shock, the body's compensatory mechanisms begin to fail. This is clinically evidenced by an inability to maintain blood pressure (e.g., MAP dropping below the critical threshold of 65 mm Hg) and signs of profound peripheral hypoperfusion, such as cold, clammy, and mottled extremities. Anaerobic metabolism ensues, leading to widespread cellular injury.

Step-by-Step Solution

1
Analyze the question's requirement.
Identify findings that distinguish the progressive stage of hypovolemic shock from the compensatory stage.
Recognizing the transition between shock stages dictates the urgency and type of medical intervention required.
2
Evaluate the pathophysiology of the compensatory phase of shock.
The compensatory phase involves neural, hormonal, and biochemical mechanisms (like sympathetic activation) that maintain blood pressure and tissue perfusion. Symptoms include restlessness, tachycardia, narrowed pulse pressure, and respiratory alkalosis from tachypnea.
Understanding these early signs helps eliminate distractors that represent the compensatory phase.
3
Evaluate the pathophysiology of the progressive phase of shock.
The progressive phase occurs when compensatory mechanisms fail. Hallmarks include a drop in blood pressure (MAP < 65 mm Hg), altered mental status (lethargy rather than simple agitation), mottled skin due to profound vasoconstriction and sluggish capillary blood flow, and metabolic acidosis.
Matching these pathophysiological hallmarks to the correct option confirms the answer.

Key Concept

Hypovolemic Shock Stages and Progression
Question 304Question →

A nurse in the neuro-intensive care unit is assessing a client who sustained a complete spinal cord injury at the T3 level 2424 hours ago. The nurse is evaluating the client for potential complications. Which of the following clinical findings specifically indicate that the client is experiencing neurogenic shock rather than spinal shock or hypovolemic shock? Select all that apply.

Select all that apply

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Answer: Heart rate of 44 bpm44\text{ bpm}; Mean arterial pressure (MAP) of 50 mm Hg50\text{ mm Hg}; Warm, flushed, and dry skin below the level of the injury

Answer

The clinical findings that specifically indicate neurogenic shock are a heart rate of 44 bpm, a mean arterial pressure of 50 mm Hg, and warm, flushed, dry skin below the level of the injury.
Neurogenic shock is a severe hemodynamic complication that occurs after spinal cord injuries typically above T6. The injury severs the sympathetic nervous system pathways, leaving the parasympathetic nervous system unopposed. This results in massive peripheral vasodilation (causing severe hypotension and warm, flushed, dry skin) and vagal dominance (causing profound bradycardia). The correct options represent this classic clinical triad.

Step-by-Step Solution

1
Differentiate between the underlying pathophysiology of neurogenic shock and spinal shock.
Neurogenic shock is a systemic hemodynamic failure due to lost sympathetic tone, whereas spinal shock is a temporary, localized neurologic deficit (loss of reflexes, sensation, and motor function below the injury).
Understanding the core mechanism prevents confusing these two distinct complications of spinal cord injury.
2
Identify the classic hemodynamic triad of neurogenic shock.
The triad consists of profound hypotension (low MAP), bradycardia (low heart rate), and peripheral vasodilation (warm, dry skin).
These occur because the sympathetic nervous system cannot initiate vasoconstriction or increase the heart rate to compensate for positional changes or pooling of blood.
3
Evaluate the remaining options to rule out other pathophysiological states.
Flaccid paralysis points directly to spinal shock. The arterial blood gas demonstrates respiratory acidosis from muscle weakness, not the metabolic acidosis expected in shock. Finally, cool and clammy skin indicates hypovolemia, not neurogenic vasodilation.
Systematically analyzing distractors against the specific signs of different shock types ensures accurate clinical prioritization and diagnostic reasoning.

Key Concept

Differentiating the hemodynamic instability of neurogenic shock from the neurological deficits of spinal shock and the compensatory mechanisms of hypovolemic shock.
Question 305Question →

A client with severe emphysema requires mechanical ventilation via an endotracheal tube following acute respiratory failure. During continuous monitoring, the expiratory flow waveform fails to reach the zero baseline prior to the initiation of the next breath. Over the past fifteen minutes, the client's systolic blood pressure has trended down to 78 mmHg, and the heart rate is steady at 132 beats per minute with weak peripheral pulses. What is the immediate priority action for this client?

Show answer & explanation

Answer: Temporarily disconnect the endotracheal tube from the ventilator circuit to allow for prolonged exhalation.

Answer

Temporarily disconnect the endotracheal tube from the ventilator circuit to allow for prolonged exhalation.
The clinical presentation describes auto-PEEP (dynamic hyperinflation), a highly dangerous complication in clients with obstructive lung diseases like emphysema. When expiratory flow does not return to zero, air becomes progressively trapped in the alveoli with each breath. This trapped air drastically raises intrathoracic pressure, compressing the vena cava and severely restricting venous return. This cascade results in obstructive shock, evidenced by the sudden drop in blood pressure and compensatory tachycardia. The immediate, definitive action to reverse this life-threatening hemodynamic collapse is to temporarily disconnect the client from the ventilator circuit. This removes the positive pressure and allows the trapped air to passively exhale, rapidly restoring venous return and cardiac output.

Step-by-Step Solution

1
Analyze the mechanical ventilator waveform data.
The failure of the expiratory flow waveform to return to the zero baseline indicates dynamic hyperinflation (auto-PEEP), meaning air is progressively becoming trapped in the lungs.
Accurate interpretation of ventilator graphics is essential for identifying the underlying cause of sudden deterioration in mechanically ventilated clients.
2
Evaluate the client's hemodynamic status.
The client is exhibiting hypotension, tachycardia, and weak pulses, which are classic signs of obstructive shock.
The trapped air from auto-PEEP drastically increases intrathoracic pressure, which compresses the vena cava and severely restricts venous return to the heart.
3
Determine the highest priority, life-saving intervention.
The immediate action is to relieve the intrathoracic pressure by briefly disconnecting the client from the ventilator, allowing the trapped air to escape passively.
Restoring venous return and cardiac output takes absolute precedence over other supportive measures or ventilator adjustments.

Key Concept

Management of Auto-PEEP and Obstructive Shock in Mechanical Ventilation
Estimated Time:2m 0s
Question 306Question →

A nurse is evaluating a client who was admitted with a mechanical small bowel obstruction. For the past 48 hours, the client has been treated with a nasogastric (NG) tube set to continuous low wall suction, yielding high outputs of gastric drainage. The nurse notes the client is becoming lethargic with a respiratory rate of 10 breaths/min and shallow chest excursion. Based on these clinical findings, which of the following arterial blood gas (ABG) results should the nurse anticipate?

Show answer & explanation

Answer: pH 7.52, PaCO2 53 mm Hg, HCO3- 35 mEq/L

Answer

An ABG showing a high pH, high PaCO2, and high HCO3- (pH 7.52, PaCO2 53 mm Hg, HCO3- 35 mEq/L)
The correct ABG result demonstrates a high pH (>7.45) and a high HCO3- (>26 mEq/L), which correctly identifies the primary metabolic alkalosis caused by the continuous suctioning of gastric acid. Furthermore, the elevated PaCO2 (>45 mm Hg) accurately reflects the client's compensatory hypoventilation (retaining acidic CO2 to balance the alkalosis), which aligns with the nurse's assessment of a low respiratory rate and shallow breathing.

Step-by-Step Solution

1
Identify the primary acid-base disturbance based on the clinical scenario.
Prolonged nasogastric suction removes hydrochloric acid from the stomach, leading to a primary metabolic alkalosis.
Loss of gastric acid leaves a relative excess of bicarbonate in the blood, elevating both the pH and the HCO3- levels.
2
Determine the expected physiological compensation for the identified disturbance.
The respiratory system compensates for metabolic alkalosis by hypoventilating (decreasing respiratory rate and depth).
Hypoventilation retains CO2 in the blood. Since CO2 acts as an acid in the body, retaining it helps lower the alkaline pH back toward a normal range.
3
Correlate the client's current symptoms with the expected ABG changes.
The respiratory rate of 10 breaths/min and shallow excursion confirms compensatory hypoventilation, which will result in an elevated PaCO2 on the ABG.
The combination of elevated pH, elevated HCO3- (primary issue), and elevated PaCO2 (compensatory response) points exclusively to partially compensated metabolic alkalosis.

Key Concept

Acid-Base Imbalances and Compensatory Mechanisms
Question 307Question →

A triage nurse in the emergency department receives a client with acute kidney injury secondary to severe rhabdomyolysis. The client reports profound muscle weakness. A STAT 12-lead electrocardiogram reveals absent P waves, a heart rate of 42 bpm42\text{ bpm}, and markedly widened QRS complexes. Arrange the following nursing actions in the most appropriate priority order from first to last.

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Answer

The correct order is: Place the client on a continuous cardiac monitor, followed by administering IV calcium gluconate, then IV regular insulin with dextrose, then oral sodium polystyrene sulfonate, and finally drawing blood for a repeat potassium level.
The correct sequence aligns with the principles of acute physiological resuscitation: immediate safety monitoring (ECG), rapid stabilization of vital organ function (Calcium for the myocardium), acute temporizing treatment (Insulin/Dextrose for shifting), delayed definitive treatment (Sodium polystyrene sulfonate for elimination), and post-intervention evaluation (Repeat labs).

Step-by-Step Solution

1
Ensure continuous visualization of the cardiac rhythm.
The client is placed on a continuous cardiac monitor with defibrillator pads readily available.
The client has a symptomatic, life-threatening arrhythmia due to severe hyperkalemia. Continuous monitoring is required to immediately detect deterioration into a lethal arrhythmia.
2
Initiate myocardial membrane stabilization.
Intravenous calcium gluconate is administered.
Calcium gluconate is the absolute first-line pharmacological agent for hyperkalemia with ECG changes. It does not lower potassium but raises the myocardial threshold potential, protecting the heart from ventricular fibrillation within minutes.
3
Initiate intracellular potassium shifting.
Intravenous regular insulin and 50% dextrose are administered.
Once the myocardium is stabilized, the next priority is to rapidly lower the serum potassium level. Insulin drives potassium into cells (working in 15-30 minutes), and dextrose prevents profound hypoglycemia.
4
Initiate definitive potassium elimination.
Sodium polystyrene sulfonate is administered.
After temporizing measures are completed, a medication that permanently removes potassium from the gastrointestinal tract is given. Because this resin takes hours to days to significantly lower serum levels, it cannot be given before stabilization.
5
Evaluate the response to therapeutic interventions.
Blood is drawn for a repeat serum potassium level and basic metabolic panel.
Evaluation is the final step of the acute nursing process to determine if extracellular potassium has shifted adequately or if emergent hemodialysis is now required.

Key Concept

The physiological sequencing of hyperkalemia management prioritizes myocardial stabilization, followed by intracellular shifting, and finally bodily elimination.
Estimated Time:2m 0s
Question 308Question →

A nurse is evaluating a client who is 33 days post-operative following an exploratory laparotomy for a perforated appendix. The client appears restless and has warm, flushed skin.

AssessmentValue
Blood pressure84/42 mm Hg84/42\text{ mm Hg}
Heart rate126 beats/min126\text{ beats/min}
Respiratory rate32 breaths/min32\text{ breaths/min}
Temperature39.1∘C39.1^\circ\text{C} (102.4∘F102.4^\circ\text{F})
Arterial Blood GasResults
pH7.277.27
PaCO₂29 mm Hg29\text{ mm Hg}
HCO₃⁻14 mEq/L14\text{ mEq/L}
PaO₂85 mm Hg85\text{ mm Hg}

Based on these findings, which intervention should the nurse perform first?

Show answer & explanation

Answer: Rapidly infuse a prescribed intravenous bolus of isotonic crystalloid solution.

Answer

Rapidly infuse a prescribed intravenous bolus of isotonic crystalloid solution.
The client is experiencing early (hyperdynamic) septic shock, evidenced by profound hypotension, tachycardia, fever, and warm, flushed skin following an intra-abdominal infection. The ABG results indicate a severe metabolic acidosis (pH 7.277.27, HCO₃⁻ 14 mEq/L14\text{ mEq/L}) with appropriate respiratory compensation (PaCO₂ 29 mm Hg29\text{ mm Hg}). The metabolic acidosis is a result of lactic acid accumulation from systemic tissue hypoperfusion. According to sepsis management guidelines, the absolute first priority to restore tissue perfusion and clear the lactic acidosis is aggressive intravascular volume resuscitation with an isotonic crystalloid bolus.

Step-by-Step Solution

1
Evaluate the client's vital signs and physical assessment findings in the context of recent abdominal surgery.
The client demonstrates profound hypotension (84/42 mm Hg84/42\text{ mm Hg}), tachycardia, fever, and warm, flushed skin.
To identify the onset of a life-threatening complication, specifically early hyperdynamic septic shock resulting from the perforated appendix.
2
Analyze the arterial blood gas (ABG) values.
The ABG reveals a metabolic acidosis (pH 7.277.27, HCO₃⁻ 14 mEq/L14\text{ mEq/L}) with appropriate respiratory compensation (PaCO₂ 29 mm Hg29\text{ mm Hg}).
To determine the systemic impact of the shock state and ensure the respiratory system is appropriately attempting to compensate.
3
Correlate the metabolic acidosis with the clinical presentation to identify the root cause.
The acidosis is identified as lactic acidosis resulting from widespread tissue hypoperfusion caused by the septic shock state.
To ensure interventions target the underlying physiological failure (hypoperfusion) rather than simply attempting to correct the abnormal lab numbers.
4
Select the highest priority nursing intervention according to established sepsis protocols.
Aggressive fluid resuscitation with an isotonic crystalloid bolus is prioritized.
Intravascular volume expansion is the absolute first step required to restore mean arterial pressure, deliver oxygen to tissues, and halt the production of lactic acid.

Key Concept

Management of Septic Shock and Interpretation of Compensatory Acid-Base Imbalances
Question 309Question →

During bedside rounds in the intensive care unit, the nurse assesses a client admitted 2424 hours ago with acute necrotizing pancreatitis. The client is now profoundly lethargic. Current vital signs reveal a blood pressure of 82/4882/48 mm Hg, a heart rate of 136136 beats/minute, and a respiratory rate of 3636 breaths/minute. Auscultation identifies diffuse coarse crackles bilaterally. Arterial blood gas (ABG) results while receiving 100%100\% oxygen via a non-rebreather mask are: pH 7.287.28, PaCO 2_2 5454 mm Hg, PaO 2_2 4848 mm Hg, and HCO 3−_3^- 2020 mEq/L. Based on this client's physiological decompensation, which of the following actions should the nurse anticipate? Select all that apply.

Select all that apply

Show answer & explanation

Answer: Prepare the client for endotracheal intubation and mechanical ventilation with positive end-expiratory pressure.; Initiate rapid administration of prescribed intravenous isotonic crystalloids.; Evaluate for facial muscle twitching upon tapping the cheek.

Answer

The correct actions are preparing for endotracheal intubation, initiating rapid intravenous isotonic crystalloids, and evaluating for facial muscle twitching.
The client is experiencing severe, concurrent complications of acute necrotizing pancreatitis: Acute Respiratory Distress Syndrome (ARDS), distributive/hypovolemic shock from massive third-spacing, and risk for hypocalcemia. The ABG demonstrates refractory hypoxemia and mixed acidosis, necessitating immediate endotracheal intubation and mechanical ventilation. Profound hypotension and tachycardia require rapid isotonic crystalloid volume resuscitation to restore organ perfusion. Furthermore, tapping the facial nerve evaluates for the Chvostek sign, a classic indicator of hypocalcemia which is highly common in severe pancreatitis due to fat saponification.

Step-by-Step Solution

1
Analyze the arterial blood gas (ABG) and respiratory status.
The ABG reveals mixed respiratory and metabolic acidosis (pH 7.287.28, PaCO 2_2 5454, HCO 3−_3^- 2020) with severe refractory hypoxemia (PaO 2_2 4848 on 100%100\% FiO 2_2), indicating Acute Respiratory Distress Syndrome (ARDS).
To determine the severity of respiratory failure and establish the need for immediate invasive airway management.
2
Evaluate the systemic hemodynamic parameters.
Profound hypotension (82/4882/48 mm Hg) and marked tachycardia (136136 bpm) signify decompensated shock.
To identify massive third-spacing and fluid shifts inherent to necrotizing pancreatitis, prioritizing aggressive volume resuscitation.
3
Correlate the disease process with potential electrolyte emergencies.
Necrotizing pancreatitis frequently causes hypocalcemia due to fat necrosis and saponification.
To anticipate necessary physical assessments, such as testing for the Chvostek sign (facial muscle twitching).

Key Concept

Concurrent management of ARDS, hypovolemic shock, and hypocalcemia in acute necrotizing pancreatitis.
Estimated Time:2m 0s
Question 310Question →

A client is receiving care in the neuroscience unit on the second day following surgical clipping of a ruptured cerebral aneurysm. Assessment reveals increasing lethargy, a heart rate of 118 beats/min, a blood pressure of 88/54 mm Hg, and a central venous pressure (CVP) of 2 mm Hg. Laboratory results show a serum sodium of 122 mEq/L, serum osmolality of 258 mOsm/kg, and a urine sodium of 150 mEq/L. Which of the following is the priority nursing action?

Show answer & explanation

Answer: Start a prescribed continuous infusion of 0.9% sodium chloride.

Answer

The priority action is to start a prescribed continuous infusion of 0.9% sodium chloride to restore intravascular volume.
The client is exhibiting classic signs of Cerebral Salt Wasting (CSW) syndrome, a complication of subarachnoid hemorrhage. CSW is characterized by hyponatremia, high urine sodium, and profound hypovolemia (evidenced by hypotension, tachycardia, and a low CVP). The absolute priority is to restore intravascular volume with isotonic fluids (such as 0.9% sodium chloride) to maintain adequate cerebral perfusion pressure and prevent circulatory collapse.

Step-by-Step Solution

1
Analyze the client's vital signs and hemodynamic parameters.
A heart rate of 118 beats/min, blood pressure of 88/54 mm Hg, and CVP of 2 mm Hg indicate severe hypovolemia.
Identifying the client's perfusion status is critical for recognizing early signs of impending shock.
2
Correlate the hemodynamics with the laboratory findings.
The presence of hyponatremia (122 mEq/L) and high urine sodium (150 mEq/L) alongside hypovolemia points to Cerebral Salt Wasting (CSW) rather than Syndrome of Inappropriate Antidiuretic Hormone (SIADH).
CSW and SIADH both present with hyponatremia, but CSW causes hypovolemia due to renal salt loss, whereas SIADH causes euvolemia or hypervolemia.
3
Determine the most critical nursing intervention.
Isotonic fluid replacement (0.9% sodium chloride) is required immediately.
Addressing the profound intravascular volume deficit is the highest priority to maintain cerebral perfusion pressure and prevent hypovolemic shock following a subarachnoid hemorrhage.

Key Concept

Differentiating Cerebral Salt Wasting (CSW) from SIADH using hemodynamic indicators and prioritizing volume resuscitation.
Question 311Question →

A client is 6 hours post-coronary artery bypass graft (CABG) surgery and is receiving mechanical ventilation. The intensive care nurse notes that the mediastinal chest tube drainage, which had been steadily draining 100 mL/hr100\text{ mL/hr}, has abruptly ceased over the past 45 minutes. The client's blood pressure drops from 115/75 mmHg115/75\text{ mmHg} to 82/64 mmHg82/64\text{ mmHg}, heart rate increases from 85 bpm85\text{ bpm} to 128 bpm128\text{ bpm}, and central venous pressure (CVP) rapidly rises from 8 mmHg8\text{ mmHg} to 19 mmHg19\text{ mmHg}. Jugular venous distension is visible. The nurse suspects acute cardiac tamponade. Place the following collaborative and nursing actions in the correct priority sequence.

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Answer

The correct sequence is: 1) Auscultate the precordium for muffled heart sounds, 2) Notify the cardiothoracic surgeon, 3) Administer a rapid IV fluid bolus, 4) Facilitate a stat bedside echocardiogram, and 5) Assemble the pericardiocentesis tray.
The correct sequence strictly follows the nursing process and emergency prioritization (Assessment -> Escalation -> Temporizing Intervention -> Diagnostics -> Definitive Procedure). In obstructive shock from cardiac tamponade, immediate recognition (assessing Beck's triad) must precede calling the provider. Once help is activated, a fluid bolus is the priority medical intervention to increase preload and overcome pericardial compression. Diagnostics (echocardiogram) confirm the effusion, followed by preparation for the definitive procedure (pericardiocentesis or chest reopening).

Step-by-Step Solution

1
Assess for muffled heart sounds.
Completes the rapid focused assessment for Beck's triad.
Before calling the provider, the nurse must quickly gather all necessary clinical data to provide a comprehensive and accurate SBAR report.
2
Notify the surgeon and rapid response team.
Escalates the critical situation to providers.
Cardiac tamponade cannot be resolved with nursing interventions alone; it requires immediate procedural intervention to prevent cardiac arrest.
3
Administer the prescribed IV fluid bolus.
Increases right-sided cardiac preload.
A fluid bolus temporarily increases venous return to force blood into the compressed right heart, maintaining cardiac output until the effusion can be drained.
4
Facilitate a stat bedside echocardiogram.
Provides diagnostic confirmation.
The medical team uses ultrasound to visualize the pericardial fluid and right ventricular collapse prior to performing an invasive needle insertion.
5
Assemble the pericardiocentesis tray.
Prepares the environment for definitive treatment.
Once confirmed, the fluid must be physically drained via pericardiocentesis or emergency sternotomy to permanently relieve the obstructive shock.

Key Concept

Hemodynamic management and prioritization of obstructive shock (cardiac tamponade)
Question 312Question →

A nurse is monitoring a client who sustained a closed femur fracture and pelvic contusions following a motor vehicle collision. Serial assessments over a three-hour period reveal the following trends:

Parameter14:0015:0016:00
Blood Pressure124/72 mm Hg118/78 mm Hg110/86 mm Hg
Heart Rate76 beats/min88 beats/min104 beats/min
Respiratory Rate14 breaths/min18 breaths/min24 breaths/min
Hourly Urine Output55 mL40 mL25 mL
Neurological StatusAlert and orientedAlert, appropriately anxiousRestless and agitated

Based on the physiological mechanisms underlying these assessment trends, which action should the nurse prioritize?

Show answer & explanation

Answer: Ensure the patency of large-bore intravenous access and verify the availability of crossmatched blood.

Answer

Ensure the patency of large-bore intravenous access and verify the availability of crossmatched blood.
The client is exhibiting classic signs of the compensatory stage of hypovolemic (hemorrhagic) shock due to internal bleeding from the femur and pelvic fractures. The sympathetic nervous system responds to volume loss by inducing peripheral vasoconstriction, which raises the diastolic pressure and narrows the pulse pressure (from 52 mm Hg to 24 mm Hg). This vasoconstriction temporarily maintains the mean arterial pressure (MAP). However, the rising heart rate, increasing respiratory rate, dropping urine output (due to renal conservation of water), and new-onset restlessness (indicating mild cerebral hypoxia) confirm inadequate tissue perfusion. The priority action is to prepare for immediate intravascular volume expansion with crystalloids and blood products to prevent progression to decompensated, irreversible shock.

Step-by-Step Solution

1
Analyze the blood pressure trend to identify the pulse pressure and mean arterial pressure (MAP).
The pulse pressure narrows significantly from 52 mm Hg (124-72) to 24 mm Hg (110-86). The MAP remains relatively stable (around 89 to 94 mm Hg).
A narrowing pulse pressure with a maintained MAP is a hallmark sign of compensatory vasoconstriction in early shock.
2
Correlate the blood pressure findings with the heart rate, respiratory rate, and urine output.
Mild tachycardia (104 beats/min), tachypnea (24 breaths/min), and oliguria (25 mL/hr) are present.
The sympathetic nervous system increases the heart and respiratory rates while the kidneys conserve fluid (via aldosterone and ADH release) to maintain cardiac output.
3
Evaluate the change in neurological status within the context of the physical trauma.
The transition from alert to restless/agitated indicates decreasing cerebral perfusion.
Femur and pelvic fractures can conceal massive internal hemorrhage. The clinical picture confirms the compensatory stage of hypovolemic shock.
4
Determine the priority nursing intervention for compensatory hemorrhagic shock.
The priority is rapid restoration of circulating volume.
Large-bore intravenous access and blood products are essential to treat the underlying hemorrhage before the client decompensates into irreversible shock.

Key Concept

Recognition of early (compensatory) hemorrhagic shock through subtle vital sign trends, specifically a narrowing pulse pressure, despite a seemingly normal mean arterial pressure.
Estimated Time:2m 0s
Question 313Question →

A triage nurse in the emergency department receives a 4545-year-old client who was rescued from an enclosed structural fire. The client sustained deep partial-thickness and full-thickness burns to the face, anterior chest, and bilateral entire upper extremities.

The nurse assesses the following initial clinical data:

ParameterValue
Blood Pressure84/52 mmHg84/52\text{ mmHg}
Heart Rate136 beats/min136\text{ beats/min}
Respiratory Rate28 breaths/min28\text{ breaths/min}
SpO2SpO_298%98\% on room air
pH7.327.32
PaCO2PaCO_234 mmHg34\text{ mmHg}
PaO2PaO_292 mmHg92\text{ mmHg}
HCO3−HCO_3^-18 mEq/L18\text{ mEq/L}
Carboxyhemoglobin (COHbCOHb)22%22\%

Physical assessment reveals a hoarse voice, singed nasal hairs, and carbonaceous sputum.

Which interventions should the nurse anticipate incorporating into the immediate plan of care? (Select all that apply)

Select all that apply

Show answer & explanation

Answer: Prepare equipment for rapid sequence endotracheal intubation.; Initiate continuous 100%100\% oxygen via a tight-fitting non-rebreather mask.; Insert an indwelling urinary catheter to continuously monitor hourly urine output.

Answer

The correct interventions are preparing for rapid sequence intubation, administering continuous 100% oxygen via a non-rebreather mask, and inserting an indwelling urinary catheter.
The client is exhibiting classical signs of severe inhalation injury (hoarse voice, singed nasal hairs, carbonaceous sputum, and a history of an enclosed space fire). Prophylactic rapid sequence intubation is required before profound airway edema causes complete obstruction. Furthermore, the client has carbon monoxide poisoning, indicated by a carboxyhemoglobin level of 22%. Because standard pulse oximetry cannot differentiate between oxyhemoglobin and carboxyhemoglobin, the oxygen saturation reading of 98% is falsely reassuring. The standard treatment for carbon monoxide toxicity is the immediate application of 100% oxygen via a non-rebreather mask (prior to intubation) to rapidly decrease the half-life of the carboxyhemoglobin. Lastly, aggressive fluid resuscitation is required to combat hypovolemic burn shock. An indwelling urinary catheter is essential because hourly urine output is the most reliable physiological indicator of adequate tissue perfusion and fluid resuscitation.

Step-by-Step Solution

1
Analyze the primary survey and airway security.
The client has facial burns, singed nasal hairs, hoarseness, and carbonaceous sputum, all indicating impending airway loss.
Airway protection takes absolute priority in emergency burn management, especially with evident inhalation injuries.
2
Evaluate the arterial blood gas and oxygenation status.
Despite a normal pulse oximetry reading of 98%, the carboxyhemoglobin is dangerously elevated at 22%, indicating severe carbon monoxide poisoning.
Standard pulse oximetry cannot distinguish between oxygen and carbon monoxide bound to hemoglobin, necessitating 100% oxygen therapy to reduce the half-life of carboxyhemoglobin.
3
Assess the client's hemodynamic status and perfusion.
The client is in hypovolemic (burn) shock, evidenced by a blood pressure of 84/52 mmHg and a heart rate of 136 beats/min.
Massive fluid shifts into the interstitial space occur rapidly after severe burns, requiring aggressive, calculated fluid resuscitation.
4
Determine the prioritized nursing interventions based on the assessment.
The immediate needs are prophylactic intubation, 100% oxygen administration, and strict intake and output monitoring via a urinary catheter.
These actions directly address the life-threatening airway compromise, cellular hypoxia, and evaluation of fluid resuscitation adequacy.

Key Concept

Burn Shock Resuscitation and Inhalation Injury Management
Estimated Time:3m 0s
Question 314Question →

An intensive care nurse evaluates a mechanically ventilated client 2424 hours post-splenectomy who received a massive transfusion protocol for hemorrhagic shock. Over the last two hours, the client's urine output decreased to 10 mL/hr10\text{ mL/hr}, peak inspiratory pressure (PIP) increased from 24 cm H2O24\text{ cm H}_2\text{O} to 52 cm H2O52\text{ cm H}_2\text{O}, and blood pressure dropped from 118/72 mm Hg118/72\text{ mm Hg} to 82/46 mm Hg82/46\text{ mm Hg}. The current central venous pressure (CVP) is 21 mm Hg21\text{ mm Hg}. Which action should the nurse take first?

Show answer & explanation

Answer: Measure intra-abdominal pressure using the indwelling urinary catheter system.

Answer

Measure intra-abdominal pressure using the indwelling urinary catheter system.
The client's clinical presentation—severe oliguria, drastically elevated peak inspiratory pressures, hypotension, and a high central venous pressure following massive fluid resuscitation—is the hallmark triad of Abdominal Compartment Syndrome (ACS). Fluid resuscitation causes massive third-spacing and bowel edema, raising intra-abdominal pressure. This pressure compresses the renal vasculature (decreasing urine output), compresses the inferior vena cava (decreasing venous return and cardiac output, resulting in hypotension), and displaces the diaphragm upward, which increases intrathoracic pressure (manifesting as elevated PIP and a falsely elevated CVP). The immediate priority is to measure intra-abdominal pressure via the bladder catheter to confirm the diagnosis and prepare for decompression.

Step-by-Step Solution

1
Analyze the client's hemodynamic and respiratory trends.
The client is experiencing severe oliguria, hypotension, drastically elevated PIP, and elevated CVP after massive fluid resuscitation.
Identifying the pattern of multi-system decompensation is required to pinpoint the underlying etiology.
2
Synthesize the pathophysiological findings.
The massive fluid load caused bowel edema (third-spacing), severely increasing intra-abdominal pressure. This pressure compresses the renal arteries (oliguria), compresses the inferior vena cava (reduced venous return leading to hypotension), and pushes the diaphragm upward into the thoracic cavity (high PIP and falsely elevated CVP).
Connecting these specific signs points directly to Abdominal Compartment Syndrome (ACS) leading to obstructive shock.
3
Determine the priority nursing intervention.
The priority is to objectively measure the intra-abdominal pressure (IAP) via the bladder to confirm the diagnosis.
Accurate IAP measurement is essential before targeted medical or surgical decompressive interventions can be initiated.

Key Concept

Pathophysiological recognition of Abdominal Compartment Syndrome (ACS) and secondary obstructive shock.
Question 315Question →

A 3434-year-old client with a known history of Graves' disease is admitted to the progressive care unit exhibiting extreme restlessness, profound diaphoresis, and delirium. Current vital signs reveal a heart rate of 188 beats/min188\text{ beats/min}, blood pressure of 182/104 mmHg182/104\text{ mmHg}, and a core temperature of 40.6∘C40.6^\circ\text{C} (105.1∘F105.1^\circ\text{F}). The client is diagnosed with a thyrotoxic crisis (thyroid storm). The healthcare provider prescribes several emergent interventions. Arrange the following actions in the correct physiological priority order.

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Answer

The correct sequence is: 1) Apply supplemental oxygen, 2) Administer intravenous propranolol, 3) Administer enteral propylthiouracil (PTU), 4) Administer Lugol's iodine solution, 5) Administer intravenous hydrocortisone.
In a thyroid storm, the physiological hierarchy of needs dictates the sequence of care. The most immediate threat is cellular hypoxia and cardiovascular collapse from sympathetic overdrive. Therefore, oxygenation and beta-blockade (propranolol) are initiated first. Once hemodynamics are stabilized, the source of the crisis must be addressed pharmacologically. It is a critical physiological principle that new hormone synthesis must be blocked by propylthiouracil (PTU) before administering iodine. If iodine is given first, the hyperactive thyroid gland will rapidly use it to synthesize more hormone. Once synthesis is blocked, Lugol's iodine is given to halt the release of already-stored hormone. Finally, corticosteroids (hydrocortisone) are administered to replace depleted adrenal reserves and assist in decreasing peripheral hormone conversion.

Step-by-Step Solution

1
Prioritize tissue perfusion and oxygenation by applying supplemental oxygen.
Meets the escalated metabolic and cellular oxygen demands.
Airway and breathing are the foundational steps in any acute decompensation, especially when metabolic consumption is massively elevated.
2
Administer the prescribed beta-adrenergic antagonist (propranolol).
Rapidly decreases the heart rate of 188 beats/min188\text{ beats/min} and lowers blood pressure.
Sympathetic overdrive poses the most immediate threat to life via cardiovascular collapse.
3
Administer the thionamide derivative (propylthiouracil).
Halts the ongoing synthesis of new thyroid hormone in the thyroid gland.
Synthesis must be stopped before iodine is introduced to the system to prevent paradoxical worsening of the crisis.
4
Administer the iodine solution (Lugol's solution) at least one hour after the thionamide.
Inhibits the release of preformed, stored thyroid hormone into the bloodstream.
This exploits the Wolff-Chaikoff effect safely, provided synthesis has already been blocked.
5
Administer glucocorticoids (hydrocortisone).
Provides adrenal support and further blunts the peripheral conversion of T4T_4 to T3T_3.
The profound hypermetabolic state quickly depletes endogenous cortisol, requiring replacement after acute stabilization.

Key Concept

The management of thyrotoxic crisis requires a strict pathophysiological sequence: stabilizing oxygenation, controlling adrenergic overdrive, blocking hormone synthesis with thionamides, blocking hormone release with iodine, and providing adrenal support. Iodine must never precede thionamides.
Question 316Question →

An emergency department nurse is caring for a trauma client undergoing aggressive resuscitation for severe hemorrhagic shock. Over the last 120120 minutes, the client has received 1010 units of packed red blood cells (PRBCs) and 66 units of fresh frozen plasma (FFP). During the ongoing assessment, the nurse notes a core body temperature of 34.2∘C34.2^\circ\text{C} (93.5∘F93.5^\circ\text{F}) and new-onset facial muscle twitching. The telemetry monitor displays peaked T waves, a widening QRS complex, and a prolonged QT interval. Which of the following physiological adaptations and underlying mechanisms correlate with this client's current presentation? (Select all that apply.)

Select all that apply

Show answer & explanation

Answer: The citrate preservative in the transfused blood has chelated the client's ionized calcium, resulting in neuromuscular excitability and a prolonged QT interval.; Intracellular potassium released from stored erythrocytes has accumulated in the client's serum, causing the peaked T waves and widened QRS complex.; The client's decreased core body temperature has shifted the oxyhemoglobin dissociation curve to the left, impairing the release of oxygen to peripheral tissues.

Answer

The correct physiological interpretations include citrate chelation of calcium, potassium leakage from stored cells, and a leftward shift of the oxyhemoglobin dissociation curve due to hypothermia.
Massive transfusion protocols involve the rapid administration of large volumes of blood products, which carries specific physiological risks. The citrate used as an anticoagulant preservative in these products binds with the client's serum ionized calcium, leading to acute hypocalcemia. This manifests as neuromuscular excitability (e.g., facial twitching or Chvostek's sign) and a prolonged QT interval on the ECG. Additionally, as red blood cells are stored, they slowly break down and release intracellular potassium into the plasma. When massively transfused, this leads to significant hyperkalemia, which alters cardiac repolarization, causing peaked T waves and widened QRS complexes. Furthermore, the rapid infusion of refrigerated blood products frequently causes systemic hypothermia. Hypothermia shifts the oxyhemoglobin dissociation curve to the left, meaning hemoglobin binds more tightly to oxygen and releases less of it to the peripheral tissues, which exacerbates cellular hypoxia despite adequate blood volume replacement.

Step-by-Step Solution

1
Analyze the client's history and current clinical data.
The client has received massive amounts of PRBCs and FFP, is hypothermic (34.2∘C34.2^\circ\text{C}), exhibits facial twitching, and has an ECG showing peaked T waves, a wide QRS, and a prolonged QT interval.
Identifying the specific constellation of symptoms is required to differentiate between expected shock progression and iatrogenic complications from the massive transfusion protocol.
2
Correlate the facial twitching and prolonged QT interval with blood product pharmacology.
These are classic signs of hypocalcemia, caused by the citrate preservative in blood products chelating the client's ionized calcium.
Understanding the metabolic consequences of large-volume citrate administration is critical for recognizing hypocalcemia.
3
Correlate the peaked T waves and widening QRS complex with PRBC storage changes.
These are classic signs of hyperkalemia, which occurs because red blood cells slowly hemolyze during storage and release intracellular potassium into the plasma.
Hyperkalemia is a lethal complication of rapid, massive blood transfusion that requires immediate pharmacological reversal.
4
Evaluate the impact of the client's hypothermia on systemic oxygen transport.
Hypothermia causes a leftward shift in the oxyhemoglobin dissociation curve, meaning hemoglobin holds onto oxygen more tightly and releases less to the hypoxic tissues.
Nurses must recognize that cold blood products exacerbate tissue hypoxia through this physiological mechanism.
5
Identify and eliminate incorrect interpretations.
The findings are not caused by respiratory acidosis, they are not benign compensatory mechanisms of shock, and they do not reflect an acute hemolytic reaction.
Eliminating distractors ensures that interventions will be correctly targeted at correcting the electrolyte and temperature derangements.

Key Concept

Complications of Massive Transfusion Protocol (Electrolyte and Hemodynamic Shifts)
Estimated Time:2m 30s
Question 317Question →

A rapid response team is called for a client admitted with community-acquired pneumonia who began receiving an initial infusion of intravenous ampicillin-sulbactam 1515 minutes ago. The client presents with acute respiratory distress, audible stridor, and diffuse urticaria. Vital signs are: blood pressure 68/3868/38 mm Hg, heart rate 5252 bpm, respiratory rate 3232 breaths/min, and SpO2 86%86\% on room air. The client's medication history includes daily lisinopril, metoprolol succinate, timolol ophthalmic drops, and atorvastatin. The nurse immediately stops the antibiotic infusion and administers 0.50.5 mg of intramuscular epinephrine. Five minutes later, the client's blood pressure is 70/4070/40 mm Hg, heart rate is 5454 bpm, and severe wheezing persists. Which of the following is the most appropriate priority intervention?

Show answer & explanation

Answer: Administer intravenous glucagon

Answer

The most appropriate priority intervention is to administer intravenous glucagon.
The client is experiencing anaphylaxis but is refractory to standard epinephrine therapy due to systemic beta-adrenergic blockade from their home medications (metoprolol and timolol). Glucagon is the evidence-based antidote in this scenario because it directly activates adenylate cyclase to increase intracellular cAMP, functioning completely independently of beta receptors. This effectively reverses both the life-threatening bronchospasm and hypotension.

Step-by-Step Solution

1
Analyze the client's clinical presentation and vital signs.
The client is experiencing severe anaphylactic shock (stridor, urticaria, profound hypotension) but presents with paradoxical bradycardia (HR 52-54 bpm).
Identifying the mismatch between the expected compensatory tachycardia of shock and the actual bradycardic state is critical for diagnosing the underlying pathophysiology.
2
Correlate the clinical findings with the client's medication history.
The bradycardia and unresponsiveness to the first dose of epinephrine are caused by systemic beta-adrenergic blockade from the concurrent use of metoprolol and timolol.
Beta-blockers prevent epinephrine from binding to beta-1 and beta-2 receptors, blunting its inotropic, chronotropic, and bronchodilatory effects.
3
Determine the priority pharmacological intervention for refractory anaphylaxis.
Intravenous glucagon is selected as the antidote.
Glucagon directly activates adenylate cyclase independent of the beta-receptor, increasing intracellular cAMP to produce necessary bronchodilation and cardiovascular support.

Key Concept

Management of Refractory Anaphylaxis in Beta-Blocked Clients
Question 318Question →

A nurse is caring for a client with a complete T4T4 spinal cord injury. The client suddenly reports a severe, pounding headache and blurred vision. The nurse observes profuse diaphoresis and flushing above the level of the spinal lesion, accompanied by marked pallor and piloerection below the lesion. The client's blood pressure is 220/115220/115 mmHg and heart rate is 4848 bpm. Place the following nursing interventions in the correct sequence of priority to manage this acute complication.

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Answer

The correct sequence is: 1) Elevate the head of the bed, 2) Assess and relieve urinary obstruction, 3) Evaluate for bowel impaction, 4) Administer antihypertensive medication, and 5) Document the event.
The priority in managing autonomic dysreflexia is to rapidly lower the dangerously high blood pressure to prevent a hemorrhagic stroke. Elevating the head of the bed utilizes gravity to induce orthostatic pooling of blood in the lower extremities, providing an instant reduction in blood pressure. Once the client is safely positioned, the nurse must systematically identify and eliminate the noxious stimulus driving the sympathetic surge. Because bladder distension is the most common cause, the urinary system is assessed first. If the bladder is empty, bowel impaction (the second most common cause) is assessed next. If these physical measures fail to resolve the crisis, rapid-acting pharmacological antihypertensives are administered. Finally, once the client is stable, the nurse documents the entire event.

Step-by-Step Solution

1
Recognize the clinical presentation of autonomic dysreflexia.
The symptoms (severe hypertension, bradycardia, pounding headache, diaphoresis above the lesion) indicate a medical emergency requiring immediate reduction of blood pressure.
Identifying the syndrome dictates the specific crisis management protocol.
2
Prioritize immediate physical positioning over diagnostic assessment.
Elevating the head of the bed to 9090 degrees is selected as the absolute first action.
Positioning utilizes orthostatic principles to instantly lower blood pressure, mitigating the immediate risk of a catastrophic hemorrhagic stroke.
3
Systematically assess for and eliminate noxious stimuli, starting with the most common.
Checking the bladder is prioritized next, followed by checking the bowel.
Removing the underlying trigger (usually a distended bladder or bowel impaction) stops the unchecked sympathetic nervous system response.
4
Determine the role of pharmacological interventions.
Antihypertensive medications are placed after mechanical interventions.
Medications are used if the blood pressure remains dangerously elevated despite the removal of mechanical triggers.

Key Concept

Autonomic dysreflexia is a life-threatening sympathetic response in clients with spinal cord injuries at or above T6T6. Management requires immediate positioning to lower blood pressure via orthostasis, followed by rapid identification and removal of the noxious stimulus (usually bladder or bowel).
Question 319Question →

A nurse is caring for a client admitted with severe diabetic ketoacidosis (DKA). The client is receiving a continuous intravenous regular insulin infusion and 0.9% sodium chloride. The nurse observes that the client's deep, rapid breathing has transitioned to shallow, weak respirations over the last 3030 minutes, and the client is now profoundly lethargic and difficult to arouse.

Recent laboratory results:
- Blood glucose: 230230 mg/dL (12.812.8 mmol/L)
- Serum potassium: 2.72.7 mEq/L (2.72.7 mmol/L)
- Arterial Blood Gas (room air): pH 7.207.20, PaCO 2_2 4949 mm Hg, HCO 3−_3^- 1111 mEq/L, PaO 2_2 8282 mm Hg

Which of the following is the priority nursing action?

Show answer & explanation

Answer: Discontinue the regular insulin infusion and activate the rapid response team.

Answer

Discontinue the regular insulin infusion and activate the rapid response team.
The client is exhibiting signs of impending respiratory failure and severe hypokalemia. In DKA, the expected respiratory compensation for metabolic acidosis is hyperventilation (Kussmaul respirations), which lowers PaCO2. A PaCO2 of 49 mm Hg in this context indicates respiratory muscle fatigue, directly secondary to the profound hypokalemia (2.7 mEq/L). Because insulin actively shifts potassium into the intracellular space, continuing the insulin infusion will fatally worsen the hypokalemia. The nurse must immediately stop the insulin infusion to prevent cardiac and respiratory arrest, and activate the rapid response team to secure the airway and initiate emergency potassium replacement.

Step-by-Step Solution

1
Analyze the arterial blood gas (ABG) and respiratory assessment.
The client has a severe metabolic acidosis (HCO3- 11 mEq/L, pH 7.20) but an elevated PaCO2 (49 mm Hg), indicating a failure of the expected respiratory compensation (loss of Kussmaul respirations).
Identifying the mixed acid-base disorder reveals that the client is experiencing respiratory muscle fatigue and impending respiratory arrest.
2
Evaluate the serum electrolytes in the context of the prescribed treatment.
The serum potassium is critically low at 2.7 mEq/L. The continuous insulin infusion actively drives potassium into the intracellular space.
Severe hypokalemia causes profound muscle weakness, including paralysis of the diaphragm and intercostal muscles, which directly explains the shallow respirations and rising PaCO2.
3
Prioritize interventions based on the ABCs (Airway, Breathing, Circulation).
The most immediate threats to life are respiratory failure and fatal arrhythmias from hypokalemia. The nurse must stop the insulin to prevent further potassium shifts and call for emergency assistance to secure the airway.
Addressing the critical ABC threat supersedes standard DKA protocol actions, such as adding dextrose to the intravenous fluids.

Key Concept

Prioritization in DKA complications and recognition of hypokalemia-induced respiratory failure.
Question 320Question →

An older adult client is admitted with a severe urinary tract infection. Over the past hour, the client has become restless and confused. Current vital signs are: blood pressure 84/52 mm Hg84/52\text{ mm Hg}, heart rate 128 bpm128\text{ bpm}, respiratory rate 30 breaths/min30\text{ breaths/min}, and temperature 101.8∘F101.8^\circ\text{F} (38.8∘C38.8^\circ\text{C}). Oxygen saturation is 93%93\% on room air. An arterial blood gas (ABG) and serum lactate analysis reveal the following:

ParameterValue
pH\text{pH}7.527.52
PaCO2\text{PaCO}_226 mm Hg26\text{ mm Hg}
HCO3−\text{HCO}_3^-21 mEq/L21\text{ mEq/L}
PaO2\text{PaO}_274 mm Hg74\text{ mm Hg}
Lactate\text{Lactate}4.3 mmol/L4.3\text{ mmol/L}

Which of the following prescribed interventions should the nurse prioritize?

Show answer & explanation

Answer: Initiate a rapid intravenous infusion of 0.9%0.9\% sodium chloride at 30 mL/kg30\text{ mL/kg}.

Answer

The nurse should prioritize initiating a rapid intravenous fluid bolus of 0.9% sodium chloride.
The client is exhibiting classic signs of early septic shock: severe hypotension, tachycardia, altered mental status, and an elevated lactate level. In the initial stages of sepsis, systemic vasodilation and increased capillary permeability cause profound relative hypovolemia. According to evidence-based sepsis management guidelines, the absolute priority is aggressive fluid resuscitation (typically a 30 mL/kg bolus of isotonic crystalloid) to restore intravascular volume, increase cardiac output, and improve tissue perfusion.

Step-by-Step Solution

1
Analyze the client's clinical presentation.
The combination of infection, hypotension, tachycardia, altered mental status, and elevated lactate indicates early septic shock.
Recognizing the shock state dictates the urgency and sequence of interventions.
2
Interpret the arterial blood gas (ABG) results.
The pH is 7.52 (alkalemia) and PaCO2 is 26 mm Hg (respiratory alkalosis).
The client is hyperventilating in response to fever and early tissue hypoxia, creating a primary respiratory alkalosis despite the rising lactate level.
3
Determine the priority physiological need.
The client's profound relative hypovolemia from sepsis-induced vasodilation must be corrected immediately.
Without adequate intravascular volume, tissue perfusion cannot be restored, and secondary interventions like vasopressors will fail.
4
Select the most appropriate intervention.
Administering a 30 mL/kg isotonic crystalloid fluid bolus is the required first-line action.
Clinical guidelines mandate aggressive fluid resuscitation before the use of vasopressors in septic shock.

Key Concept

Early recognition and fluid resuscitation sequence in septic shock
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