Physiological Integrity

1960 soru

Soru 101Soru →

An older adult client who underwent a right total hip arthroplasty (posterior approach) 2 days ago has developed acute delirium. The client is restless, frequently attempts to get out of bed unassisted, and requires assistance with activities of daily living. When updating the client's plan of care, what interventions should the nurse implement to safely address the client's basic care and comfort needs? Select all that apply.

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Cevap: Maintain an abduction wedge between the client's legs while resting in a supine position.; Implement a scheduled toileting routine and provide a well-lit environment during waking hours.

Cevap

The correct actions are to maintain an abduction wedge between the client's legs while resting in a supine position, and to implement a scheduled toileting routine while providing a well-lit environment during waking hours.
The correct interventions focus on safely meeting the client's fundamental physiological needs without compromising surgical integrity. Maintaining an abduction wedge is essential to prevent hip adduction and dislocation after a posterior approach arthroplasty. A scheduled toileting routine combined with a well-lit environment addresses the client's elimination needs proactively and serves as a highly effective, non-pharmacologic intervention to manage delirium and reduce restlessness.

Adım Adım Çözüm

1
Analyze the client's surgical history and associated precautions.
The client had a posterior approach total hip arthroplasty, which requires maintaining hip abduction and avoiding hip flexion greater than 90 degrees.
Identifying post-operative precautions dictates safe positioning and mobility interventions during basic care.
2
Evaluate the client's cognitive and behavioral status.
The client is experiencing acute delirium, restlessness, and attempts to get out of bed unassisted.
Understanding the cognitive impairment helps in selecting appropriate non-pharmacological safety and comfort measures without prematurely resorting to restraints.
3
Review the proposed nursing interventions against the client's needs and safety guidelines.
Maintaining an abduction wedge and implementing a scheduled toileting routine safely address the client's physical and cognitive needs while avoiding contraindicated positions, improper delegation, and premature restraint use.
Basic care must align with both orthopedic precautions and evidence-based delirium management protocols.

Anahtar Kavram

Basic Care and Comfort Integration for Complex Postoperative Clients
Soru 102Soru →

A registered nurse is managing the care of a young adult diagnosed with diabetic ketoacidosis. The individual has been receiving a continuous intravenous drip of regular insulin alongside isotonic saline for several hours. A recent metabolic panel and arterial blood gas analysis show a pH of 7.26, PaCO2 of 28 mm Hg, bicarbonate of 14 mEq/L, and a serum potassium level of 3.2 mEq/L. Electrocardiogram monitoring reveals flattened T waves and emerging U waves. Current hemodynamics demonstrate a systolic pressure of 108 mm Hg, diastolic of 70 mm Hg, and a pulse of 110 beats per minute. Which of the following clinical interventions should the nurse prioritize?

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Cevap: Suspend the continuous insulin infusion and initiate prescribed intravenous potassium replacement.

Cevap

The correct intervention is to immediately suspend the continuous insulin infusion and initiate prescribed intravenous potassium replacement.
The individual is experiencing profound hypokalemia, a highly dangerous complication of diabetic ketoacidosis treatment. Regular insulin drives potassium into the intracellular space, rapidly depleting serum levels. When serum potassium falls below 3.3 mEq/L, standard protocols dictate immediately suspending the insulin infusion to prevent fatal cardiac dysrhythmias—as evidenced by the flattened T waves and emerging U waves—and initiating potassium replacement. Continuing insulin would exacerbate the life-threatening hypokalemia.

Adım Adım Çözüm

1
Analyze the arterial blood gas (ABG) and metabolic panel results.
The ABGs reveal a partially compensated metabolic acidosis, but the critical and immediately life-threatening finding is the serum potassium level of 3.2 mEq/L.
Identifying the most life-threatening physiological abnormality is the first step in clinical prioritization.
2
Correlate laboratory findings with the clinical presentation and electrocardiogram (ECG).
The flattened T waves and emerging U waves confirm clinically significant and dangerous hypokalemia.
Potassium plays a vital role in cardiac action potentials, and uncorrected hypokalemia can quickly progress to lethal ventricular dysrhythmias.
3
Evaluate the impact of current pharmacological therapy on the client's physiological status.
The continuous insulin infusion is actively driving the remaining extracellular potassium into the cells, exacerbating the hypokalemia.
Understanding the systemic physiological mechanisms of action of insulin is required to anticipate its adverse effects.
4
Determine the immediate priority intervention based on established treatment guidelines.
The nurse must immediately hold the insulin infusion and prepare to administer intravenous potassium.
Standard diabetic ketoacidosis protocols mandate holding insulin therapy when serum potassium falls below 3.3 mEq/L to prevent cardiac arrest.

Anahtar Kavram

Management of life-threatening hypokalemia as a physiological complication of insulin therapy in diabetic ketoacidosis.
Tahmini Süre:2m 0s
Soru 103Soru →

A critically ill client is admitted to the intensive care unit with a diagnosis of severe diabetic ketoacidosis. Initial laboratory results reveal a serum glucose of 815815 mg/dL (45.245.2 mmol/L), an arterial pH of 7.087.08, and a serum potassium of 3.03.0 mEq/L (3.03.0 mmol/L). The client exhibits profound lethargy, deep and rapid respirations, and poor skin turgor. Arrange the following therapeutic interventions in the correct physiological priority sequence to safely manage this client's acute decompensation.

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Cevap

The correct priority sequence is: 1) Initiate 0.9%0.9\% sodium chloride, 2) Administer potassium chloride, 3) Commence regular insulin, 4) Evaluate blood glucose until it reaches 250250 mg/dL, 5) Incorporate 5%5\% dextrose into fluids.
The management of diabetic ketoacidosis requires a precise sequence to adapt to the physiological crisis. First, severe osmotic diuresis causes profound hypovolemia, making rapid fluid resuscitation with 0.9%0.9\% sodium chloride the absolute priority to restore perfusion. Second, the client's potassium is critically low (3.03.0 mEq/L). Because insulin drives potassium into the cells, administering insulin before replacing potassium would trigger life-threatening hypokalemia and cardiac dysrhythmias. Therefore, potassium chloride must be administered next. Third, a continuous regular insulin infusion is started to halt ketogenesis and correct the metabolic acidosis. Fourth, serial blood glucose levels are monitored closely. Finally, when the blood glucose decreases to 250250 mg/dL (13.913.9 mmol/L), 5%5\% dextrose is added to the intravenous fluids. This prevents hypoglycemia and cerebral edema while allowing the insulin infusion to continue until the anion gap closes and acidosis resolves.

Adım Adım Çözüm

1
Initiate a rapid intravenous infusion of 0.9%0.9\% sodium chloride.
Restores intravascular volume and organ perfusion.
Severe osmotic diuresis leads to profound hypovolemia; fluid resuscitation is the absolute first priority to stabilize blood pressure, reverse shock, and improve renal function.
2
Administer the prescribed intravenous potassium chloride.
Corrects the severe hypokalemia.
The client's potassium is critically low at 3.03.0 mEq/L. Because insulin shifts potassium intracellularly, administering insulin first would worsen hypokalemia and potentially trigger lethal cardiac dysrhythmias.
3
Commence a continuous intravenous infusion of regular insulin.
Halts ketogenesis and lowers blood glucose.
Once intravascular volume is expanding and potassium is safely being replaced, insulin is required to drive glucose into cells, thereby correcting the metabolic acidosis.
4
Evaluate serial blood glucose levels until they reach 250250 mg/dL (13.913.9 mmol/L).
Identifies the threshold for modifying fluid therapy.
As insulin works, glucose drops rapidly. Monitoring identifies the critical inflection point to prevent hypoglycemia while allowing insulin to continue clearing ketones.
5
Incorporate 5%5\% dextrose into the intravenous maintenance fluids.
Prevents rapid shifts in serum osmolality and hypoglycemia.
Adding dextrose provides a continuous substrate for the insulin infusion (which must continue until the anion gap closes) and prevents cerebral edema from a rapid drop in osmolality.

Anahtar Kavram

In severe diabetic ketoacidosis, priority management follows a strict physiological sequence: restore intravascular volume first, correct severe hypokalemia prior to administering insulin (to prevent lethal dysrhythmias), initiate insulin to reverse acidosis, and add dextrose when glucose reaches 250250 mg/dL to prevent hypoglycemia.
Tahmini Süre:2m 0s
Soru 104Soru →

A nurse in the emergency department evaluates the arterial blood gas (ABG) results of a client who intentionally ingested a toxic amount of acetylsalicylic acid 8 hours ago. The client is lethargic, diaphoretic, and breathing deeply at a rate of 34 breaths/minute.

ABG results (on room air):
- pH: 7.42
- PaCO2: 24 mm Hg
- HCO3-: 14 mEq/L
- PaO2: 95 mm Hg

Based on these clinical findings, which conclusion about the client's physiological acid-base status is most accurate?

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Cevap: A mixed acid-base disorder consisting of concurrent primary respiratory alkalosis and primary metabolic acidosis.

Cevap

The client is experiencing a mixed acid-base disorder consisting of concurrent primary respiratory alkalosis and primary metabolic acidosis.
A normal pH (7.35-7.45) accompanied by significantly abnormal PaCO2 and HCO3- values moving in opposite pH directions indicates a mixed acid-base disorder. Physiological compensatory mechanisms never completely normalize the pH. Salicylate toxicity causes two concurrent primary disorders: direct stimulation of the medullary respiratory center (primary respiratory alkalosis) and uncoupling of oxidative phosphorylation, which leads to the accumulation of organic acids (primary metabolic acidosis).

Adım Adım Çözüm

1
Analyze the pH to determine the primary direction of the acid-base imbalance.
The pH is 7.42, which is within the normal range (7.35-7.45) but leans slightly toward the alkalotic side.
Evaluating the pH is the first step in the standard ABG interpretation process.
2
Analyze the PaCO2 and HCO3- values.
The PaCO2 is 24 mm Hg (indicating respiratory alkalosis) and the HCO3- is 14 mEq/L (indicating metabolic acidosis).
This determines which systems are contributing to the acid-base derangement.
3
Evaluate for physiological compensation versus a mixed acid-base disorder.
Physiological compensatory mechanisms do not completely normalize the pH. A normal pH accompanied by significantly abnormal opposing PaCO2 and HCO3- values indicates a mixed acid-base disorder.
This differentiates a simple compensated disorder from a complex mixed disorder.
4
Correlate the ABG interpretation with the pathophysiology of salicylate toxicity.
Aspirin overdose causes direct medullary stimulation (primary respiratory alkalosis) and uncouples oxidative phosphorylation leading to organic acid accumulation (primary metabolic acidosis).
Clinical context confirms the presence of two concurrent primary disorders, matching the ABG findings.

Anahtar Kavram

Advanced Interpretation of Mixed Acid-Base Disorders in Salicylate Toxicity
Tahmini Süre:1m 30s
Soru 105Soru →

A nurse is caring for a client experiencing a severe asthma exacerbation. The client is highly agitated, visibly using accessory muscles to breathe, and has a respiratory rate of 34 breaths/min34 \text{ breaths/min} and a heart rate of 118 beats/min118 \text{ beats/min}. The most recent arterial blood gas (ABG) results on room air are:

ParameterValue
pH7.367.36
PaCO2\text{PaCO}_244 mm Hg44 \text{ mm Hg}
HCO3−\text{HCO}_3^-24 mEq/L24 \text{ mEq/L}
PaO2\text{PaO}_264 mm Hg64 \text{ mm Hg}

Based on these findings, which of the following is the priority nursing action?

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Cevap: Prepare the client for immediate endotracheal intubation and mechanical ventilation.

Cevap

Prepare the client for immediate endotracheal intubation and mechanical ventilation.
During a severe asthma exacerbation, a client typically hyperventilates, which blows off carbon dioxide and initially leads to respiratory alkalosis (low PaCO2\text{PaCO}_2). If the client remains in severe distress with a high respiratory rate, but the PaCO2\text{PaCO}_2 level has risen to a 'normal' range (35−45 mm Hg35-45 \text{ mm Hg}), this phenomenon is known as pseudonormalization. It indicates severe respiratory muscle fatigue; the client can no longer maintain the extreme work of breathing. This is a classic sign of impending respiratory arrest, making immediate airway securement via intubation the absolute priority.

Adım Adım Çözüm

1
Analyze the client's clinical presentation.
The client is exhibiting severe respiratory distress with a respiratory rate of 34 breaths/min34 \text{ breaths/min}, accessory muscle use, and significant agitation.
Clinical assessment provides the crucial context needed to accurately interpret laboratory values.
2
Evaluate the arterial blood gas (ABG) results in relation to the clinical picture.
The ABG values appear numerically normal, but a severely tachypneic client should have a low PaCO2\text{PaCO}_2 due to hyperventilation (blowing off carbon dioxide).
Identifying the discrepancy between the expected ABG results (respiratory alkalosis) and actual results ('normal' PaCO2\text{PaCO}_2) is essential for detecting physiological decompensation.
3
Determine the physiological cause of the 'normalizing' PaCO2\text{PaCO}_2.
The rising PaCO2\text{PaCO}_2 indicates that the client's respiratory muscles are fatiguing and they can no longer maintain the work of breathing necessary to eliminate carbon dioxide.
Recognizing muscle fatigue leads to the conclusion that respiratory arrest is imminent.
4
Select the priority nursing intervention.
The immediate priority is to collaborate with the healthcare provider to secure the airway via endotracheal intubation and initiate mechanical ventilation.
Airway management takes precedence over all other interventions in a client with impending respiratory failure.

Anahtar Kavram

During a severe asthma exacerbation, a 'normal' or rising PaCO2 in the presence of severe tachypnea and increased work of breathing indicates respiratory muscle fatigue and impending respiratory failure.
Soru 106Soru →

A nurse evaluates a client with severe acute pancreatitis who has become increasingly restless over the last 44 hours. Current vital signs are: blood pressure 88/46 mm Hg88/46 \text{ mm Hg}, heart rate 124 beats/min124 \text{ beats/min}, respiratory rate 28 breaths/min28 \text{ breaths/min}, and temperature 101.8∘F101.8^\circ\text{F} (38.8∘C38.8^\circ\text{C}). The nurse suspects the client is manifesting early distributive shock secondary to systemic inflammatory response syndrome (SIRS). Which of the following clinical and diagnostic findings are consistent with this specific early physiological state? Select all that apply.

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Cevap: Bounding peripheral pulses; Central venous pressure (CVP) of 2 mm Hg2 \text{ mm Hg}; Arterial blood gas (ABG) showing a pHpH of 7.497.49, PaCO2PaCO_2 of 30 mm Hg30 \text{ mm Hg}, and HCO3−HCO_3^- of 22 mEq/L22 \text{ mEq/L}

Cevap

The correct findings for early distributive shock are bounding peripheral pulses, a low Central Venous Pressure (CVP), and respiratory alkalosis on an Arterial Blood Gas (ABG) analysis.
Early distributive (septic or SIRS) shock represents a hyperdynamic, 'warm' state characterized by massive systemic vasodilation and a compensatory increase in cardiac output. This physiological adaptation results in bounding pulses, a low central venous pressure due to relative hypovolemia (expanded vascular space), and tachypnea that leads to primary respiratory alkalosis (pH>7.45pH > 7.45, PaCO2<35 mm HgPaCO_2 < 35 \text{ mm Hg}).

Adım Adım Çözüm

1
Analyze the pathophysiological phase based on the scenario.
The client is in the 'early' phase of distributive shock (SIRS/sepsis).
It is critical to distinguish early (hyperdynamic or 'warm') shock from late (hypodynamic or 'cold') shock, as their clinical presentations are physiologically opposite.
2
Evaluate hemodynamic and peripheral perfusion signs.
Identify that massive vasodilation causes relative hypovolemia (low CVP), widened pulse pressure, and a compensatory high cardiac output leading to bounding pulses and warm skin.
Unlike hypovolemic or cardiogenic shock, early distributive shock is characterized by a failure of vascular tone rather than a primary pump or volume failure.
3
Analyze the acid-base disturbances associated with the phase.
Identify that the initial tachypnea (28 breaths/min28 \text{ breaths/min}) will cause carbon dioxide washout, leading to respiratory alkalosis (pH>7.45pH > 7.45, PaCO2<35 mm HgPaCO_2 < 35 \text{ mm Hg}).
Metabolic acidosis (lactic acidosis) does not typically accumulate to pathological levels until the shock progresses to the late, decompensated phase where tissue oxygen extraction completely fails.

Anahtar Kavram

Early hyperdynamic phase of distributive shock presents with signs of vasodilation (low CVP, bounding pulses, warm skin) and respiratory alkalosis, distinguishing it from late or hypovolemic shock states.
Soru 107Soru →

A client is being treated in the emergency department for a severe asthma exacerbation. Upon admission, the client was highly anxious, tachypneic, and audibly wheezing. Initial arterial blood gas (ABG) results were: pH 7.52, PaCO2 28 mm Hg, HCO3- 24 mEq/L, and PaO2 68 mm Hg. Two hours later, the nurse notes that the client has become lethargic and the respiratory effort is shallow. A repeat ABG reveals: pH 7.36, PaCO2 44 mm Hg, HCO3- 24 mEq/L, and PaO2 58 mm Hg. Which of the following is the priority nursing action?

Cevabı ve açıklamayı göster

Cevap: Prepare the client for immediate endotracheal intubation and mechanical ventilation.

Cevap

Prepare the client for immediate endotracheal intubation and mechanical ventilation.
In the early stages of an asthma exacerbation, clients hyperventilate in an attempt to increase oxygenation, resulting in a low PaCO2 (respiratory alkalosis). As the client becomes fatigued, they can no longer maintain this increased respiratory effort. The breathing becomes shallow, and CO2 begins to be retained. A PaCO2 that rises from a low level to a 'normal' level (35-45 mm Hg), accompanied by clinical signs of deterioration such as lethargy, is a classic warning sign of impending respiratory failure. The priority action is to prepare for immediate intubation and mechanical ventilation to secure the airway and ensure adequate gas exchange.

Adım Adım Çözüm

1
Analyze the initial presentation and ABGs.
The client initially presented with hyperventilation (tachypnea), leading to respiratory alkalosis (pH 7.52, low PaCO2 28), which is a typical early physiological adaptation to hypoxemia in an asthma attack.
Establishing the baseline helps identify trends in the client's respiratory status.
2
Evaluate the current clinical signs and repeat ABGs.
The client is now lethargic with shallow breathing. The ABG shows a 'normal' pH (7.36) and PaCO2 (44), but worsening hypoxemia (PaO2 58).
Clinical assessment must always be correlated with laboratory values to determine the client's actual condition.
3
Synthesize the findings to determine the pathophysiological state.
The increase in PaCO2 from 28 to 44 mm Hg, combined with lethargy, means the client is no longer able to maintain the compensatory hyperventilation due to respiratory muscle fatigue.
A normalizing PaCO2 in a previously hyperventilating asthmatic is an ominous sign of impending respiratory failure.
4
Determine the highest priority intervention.
The client requires immediate airway protection and mechanical ventilation to prevent respiratory arrest.
Airway and breathing are the highest priorities in the ABCs of resuscitation.

Anahtar Kavram

Impending Respiratory Failure in Asthma
Tahmini Süre:1m 30s
Soru 108Soru →

Following a complex cystoscopy procedure, a client develops a systemic infection. While performing a reassessment, the nurse notes several changes in the client's clinical presentation. Which assessment findings should alert the nurse that the client is experiencing the early, hyperdynamic phase of septic shock? Select all that apply.

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Cevap: Warm, flushed skin; Heart rate of 118 beats/min118\text{ beats/min}; Respiratory rate of 28 breaths/min28\text{ breaths/min}

Cevap

The correct findings indicating early (hyperdynamic) septic shock are warm, flushed skin; a heart rate of 118 beats/min118\text{ beats/min}; and a respiratory rate of 28 breaths/min28\text{ breaths/min}.
During the early (hyperdynamic) phase of septic shock, inflammatory endotoxins cause massive systemic vasodilation. This lack of vascular resistance presents clinically as warm, flushed skin and a widened pulse pressure. To compensate for the loss of vascular tone and maintain tissue perfusion, the sympathetic nervous system initiates an increase in heart rate (tachycardia) and respiratory rate (tachypnea). Therefore, hyperthermia or flushed skin, a rapid heart rate, and increased respirations are classic early indicators that differentiate early septic shock from other shock states.

Adım Adım Çözüm

1
Identify the phase of shock described in the clinical scenario.
The scenario specifies the 'early, hyperdynamic phase' of septic shock.
Different phases of shock present with distinct physiological signs, requiring precise recognition for proper intervention.
2
Recall the physiological mechanisms that characterize the hyperdynamic phase of septic shock.
This phase is characterized by the release of inflammatory mediators causing massive systemic vasodilation and a compensatory increase in cardiac output and respiratory effort.
Understanding the underlying pathophysiology allows you to predict the resulting clinical signs.
3
Evaluate each option to determine if it aligns with vasodilation and early compensatory mechanisms.
Vasodilation causes warm, flushed skin. Compensatory mechanisms cause an elevated heart rate (tachycardia) and elevated respiratory rate (tachypnea).
Matching physiological principles directly to assessment data distinguishes correct early indicators from late signs or distractors.

Anahtar Kavram

Presentation of Early (Hyperdynamic) Septic Shock
Soru 109Soru →

An adult client is admitted to the surgical step-down unit following a motor vehicle collision involving blunt abdominal trauma. During the initial shift assessment, the nurse notes the client has become increasingly restless and diaphoretic, and is reporting new-onset pain in the left shoulder. The client's vital signs are heart rate 118118 bpm, blood pressure 98/6298/62 mmHg, and respiratory rate 2424/min. Which of the following is the priority nursing action to reduce the client's risk for physiological deterioration?

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Cevap: Initiate large-bore intravenous access and prepare for rapid isotonic fluid volume expansion.

Cevap

The priority action is to initiate large-bore intravenous access and prepare for rapid isotonic fluid volume expansion to address impending hypovolemic shock.
The correct answer addresses the immediate life-threatening complication of hypovolemic shock resulting from internal bleeding. The client is demonstrating Kehr's sign (left shoulder pain caused by diaphragmatic irritation from intraperitoneal blood, classically seen in splenic rupture) alongside compensatory shock symptoms (restlessness, diaphoresis, tachycardia, and hypotension). Establishing large-bore IV access to facilitate rapid fluid and blood replacement is the priority action to maintain tissue perfusion and reduce the risk of mortality.

Adım Adım Çözüm

1
Analyze the client's history and presenting clinical symptoms.
The client has blunt abdominal trauma, new left shoulder pain (Kehr's sign), restlessness, diaphoresis, tachycardia (118118 bpm), and hypotension (98/6298/62 mmHg).
Recognizing patterns in clinical presentation is necessary to identify the potential complication.
2
Correlate the assessment findings with potential pathophysiological processes.
The combination of referred shoulder pain and signs of systemic hypoperfusion indicates a high probability of a ruptured spleen and internal hemorrhage.
Kehr's sign is caused by blood irritating the diaphragm, and the vital sign changes reflect early compensatory mechanisms for hypovolemic shock.
3
Prioritize nursing actions using the Airway, Breathing, Circulation (ABC) framework.
The most immediate life-threatening issue is circulatory collapse from active internal blood loss.
Without adequate intravascular volume, the client will rapidly progress to uncompensated shock and multisystem organ failure.
4
Determine the most appropriate immediate intervention to stabilize circulation.
Securing large-bore IV access for the administration of isotonic fluids or blood products is the highest priority.
Rapid volume resuscitation is required to maintain perfusion while preparing the client for definitive surgical intervention.

Anahtar Kavram

Early Recognition of Hemorrhagic Shock and Spleen Rupture
Tahmini Süre:1m 30s
Soru 110Soru →

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?

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

Cevap

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.

Adım Adım Çözüm

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.

Anahtar Kavram

Acid-Base Imbalances and Loop Diuretic Complications
Soru 111Soru →

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?

Cevabı ve açıklamayı göster

Cevap: Administer a rapid isotonic crystalloid fluid bolus.

Cevap

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.

Adım Adım Çözüm

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.

Anahtar Kavram

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.
Soru 112Soru →

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?

Cevabı ve açıklamayı göster

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

Cevap

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.

Adım Adım Çözüm

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.

Anahtar Kavram

Hypovolemic Shock Stages and Progression
Soru 113Soru →

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.

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Cevabı ve açıklamayı göster

Cevap: 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

Cevap

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.

Adım Adım Çözüm

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.

Anahtar Kavram

Differentiating the hemodynamic instability of neurogenic shock from the neurological deficits of spinal shock and the compensatory mechanisms of hypovolemic shock.
Soru 114Soru →

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?

Cevabı ve açıklamayı göster

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

Cevap

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.

Adım Adım Çözüm

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.

Anahtar Kavram

Management of Auto-PEEP and Obstructive Shock in Mechanical Ventilation
Tahmini Süre:2m 0s
Soru 115Soru →

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?

Cevabı ve açıklamayı göster

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

Cevap

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.

Adım Adım Çözüm

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.

Anahtar Kavram

Acid-Base Imbalances and Compensatory Mechanisms
Soru 116Soru →

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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Cevabı ve açıklamayı göster

Cevap

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).

Adım Adım Çözüm

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.

Anahtar Kavram

The physiological sequencing of hyperkalemia management prioritizes myocardial stabilization, followed by intracellular shifting, and finally bodily elimination.
Tahmini Süre:2m 0s
Soru 117Soru →

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?

Cevabı ve açıklamayı göster

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

Cevap

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.

Adım Adım Çözüm

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.

Anahtar Kavram

Management of Septic Shock and Interpretation of Compensatory Acid-Base Imbalances
Soru 118Soru →

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.

Geçerli olan tümünü seçin

Cevabı ve açıklamayı göster

Cevap: 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.

Cevap

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.

Adım Adım Çözüm

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).

Anahtar Kavram

Concurrent management of ARDS, hypovolemic shock, and hypocalcemia in acute necrotizing pancreatitis.
Tahmini Süre:2m 0s
Soru 119Soru →

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?

Cevabı ve açıklamayı göster

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

Cevap

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.

Adım Adım Çözüm

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.

Anahtar Kavram

Differentiating Cerebral Salt Wasting (CSW) from SIADH using hemodynamic indicators and prioritizing volume resuscitation.
Soru 120Soru →

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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Cevabı ve açıklamayı göster

Cevap

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).

Adım Adım Çözüm

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.

Anahtar Kavram

Hemodynamic management and prioritization of obstructive shock (cardiac tamponade)
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Physiological Integrity Alıştırma Soruları — NCLEX-RN — Sayfa 6 | Examkin