Sepsis and shock questions test whether you can recognize deterioration early and sequence interventions correctly under time pressure. The NCLEX builds these scenarios from subtle clues — a rising heart rate, a new confusion, a lactate creeping up — before the blood pressure ever drops, because septic shock is defined by vasopressor need and lactate above 2 mmol/L despite fluids, not by hypotension alone. You must know the hour-1 sepsis bundle cold: lactate, blood cultures before antibiotics, broad-spectrum antibiotics within one hour, and 30 mL/kg crystalloid for hypotension. Shock-type questions then ask you to match hemodynamic patterns to hypovolemic, cardiogenic, distributive, and obstructive causes and choose the priority treatment for each.
Quick Study Tips
Cultures before antibiotics, but antibiotics within one hour regardless.
Lactate 4 or higher, or hypotension: 30 mL/kg crystalloid.
Tachycardia and confusion precede hypotension in every shock type.
Norepinephrine is first-line for septic shock, after fluids.
Match the shock type to the fix: fill the tank, fix the pump, clamp the leak, or relieve the block.
Practice Quiz: Sepsis & Shock NCLEX Questions
Answer these exam-style questions to test your knowledge. Detailed rationales are shown after each answer.
Early Recognition: SIRS, qSOFA, and the Hour-1 Bundle
Sepsis is a dysregulated response to infection causing organ dysfunction, and the earliest clues are often subtle: tachycardia, tachypnea, fever or hypothermia, and new confusion — especially in older adults, where altered mentation may be the only sign. qSOFA flags risk with three criteria: respiratory rate 22 or higher, systolic blood pressure 100 or lower, and altered mentation. Once sepsis is suspected, the hour-1 bundle drives the sequence: measure lactate, obtain blood cultures before antibiotics (but never delay antibiotics to get them), administer broad-spectrum antibiotics within one hour, and infuse 30 mL/kg of IV crystalloid for hypotension or lactate of 4 or higher. A lactate above 2 mmol/L signals tissue hypoperfusion, and a repeat lactate tracks response to resuscitation. The NCLEX loves the ordering trap: cultures first, antibiotics second, but antibiotics within the hour regardless.
Septic Shock and Vasopressor Priorities
Septic shock is sepsis with persistent hypotension requiring vasopressors to maintain a mean arterial pressure of 65 mmHg or higher, plus lactate above 2 mmol/L despite adequate fluid resuscitation. Norepinephrine is the first-line vasopressor, given through a central line when available, with continuous blood pressure and urine output monitoring — urine output under 30 mL/hour signals worsening perfusion. Warm, flushed skin early in sepsis (warm shock) reflects vasodilation; cool, mottled extremities later signal decompensation. Source control matters as much as drugs: the NCLEX expects you to connect the infection source (a wound, a urinary catheter, a central line) to the treatment plan. Monitor for progression to MODS — rising creatinine, falling platelets, worsening oxygenation — because each new organ failure changes the priority list.
The Four Shock Types and Their Priorities
Hypovolemic shock (hemorrhage, burns, dehydration) shows decreased preload and low cardiac output: the priority is stopping the loss and replacing volume with isotonic fluids or blood products. Cardiogenic shock (massive MI, heart failure) shows high filling pressures with low output — pulmonary congestion plus hypotension — and fluids make it worse; the priority is inotropic support and afterload management. Distributive shock (septic, anaphylactic, neurogenic) shows massive vasodilation with warm skin early; the priority is fluids plus vasopressors, and for anaphylaxis, IM epinephrine immediately. Obstructive shock (tension pneumothorax, cardiac tamponade, massive pulmonary embolism) requires relieving the obstruction — needle decompression, pericardiocentesis — because fluids and pressors cannot fix a mechanical block. The universal early sign across all types is tachycardia and subtle mental status change; hypotension is a late finding, and waiting for it is the classic wrong answer.
Review each question with its correct answer and a rationale for every choice.
1. New sepsis alert: lactate 4.2, BP 84/48. Which intervention does the nurse complete FIRST?
A. Start broad-spectrum antibioticsInitiating broad-spectrum antibiotics is a critical component of sepsis management to combat the underlying infection. However, administering antibiotics *before* obtaining blood cultures can contaminate the cultures, leading to false negatives or masking the true causative organism. This delay in identifying the specific pathogen can hinder targeted antibiotic therapy and potentially lead to antibiotic resistance and prolonged treatment. Therefore, while essential, it should be done *after* cultures are drawn to ensure accurate diagnostic results.
B. Draw blood culturesDrawing blood cultures is the priority action in a patient presenting with suspected sepsis. Blood cultures are crucial for identifying the specific microorganism causing the infection, which then guides targeted antibiotic therapy. Obtaining cultures *before* administering antibiotics ensures the highest likelihood of isolating the causative pathogen, preventing false-negative results that could arise if antibiotics were started first. This diagnostic step is foundational for effective antimicrobial stewardship and improving patient outcomes in sepsis.
C. Begin norepinephrineBeginning norepinephrine is an intervention for septic shock to increase blood pressure and improve perfusion to vital organs by causing vasoconstriction. While the patient's blood pressure of 84/48 mmHg indicates hypotension consistent with septic shock, immediate initiation of vasopressors often follows fluid resuscitation, and in the *initial* phase, diagnostic steps like blood cultures are prioritized to identify the source of infection. Without identifying the pathogen, definitive treatment remains elusive, and starting vasopressors alone does not address the root cause of the septic state.
D. Insert an indwelling catheterInserting an indwelling catheter allows for accurate monitoring of urine output, which is a key indicator of renal perfusion and overall organ function in sepsis. It is also important for fluid balance management. While this is a valuable intervention in a critically ill patient, it is not the *immediate* priority over obtaining cultures to diagnose the underlying infection. Furthermore, inserting a catheter introduces a risk of infection, and this procedural step can be performed after the most critical diagnostic and initial therapeutic steps are underway.
Correct answer: B. Option A: Initiating broad-spectrum antibiotics is a critical component of sepsis management to combat the underlying infection. However, administering antibiotics *before* obtaining blood cultures can contaminate the cultures, leading to false negatives or masking the true causative organism. This delay in identifying the specific pathogen can hinder targeted antibiotic therapy and potentially lead to antibiotic resistance and prolonged treatment. Therefore, while essential, it should be done *after* cultures are drawn to ensure accurate diagnostic results.
Option B: Drawing blood cultures is the priority action in a patient presenting with suspected sepsis. Blood cultures are crucial for identifying the specific microorganism causing the infection, which then guides targeted antibiotic therapy. Obtaining cultures *before* administering antibiotics ensures the highest likelihood of isolating the causative pathogen, preventing false-negative results that could arise if antibiotics were started first. This diagnostic step is foundational for effective antimicrobial stewardship and improving patient outcomes in sepsis.
Option C: Beginning norepinephrine is an intervention for septic shock to increase blood pressure and improve perfusion to vital organs by causing vasoconstriction. While the patient's blood pressure of 84/48 mmHg indicates hypotension consistent with septic shock, immediate initiation of vasopressors often follows fluid resuscitation, and in the *initial* phase, diagnostic steps like blood cultures are prioritized to identify the source of infection. Without identifying the pathogen, definitive treatment remains elusive, and starting vasopressors alone does not address the root cause of the septic state.
Option D: Inserting an indwelling catheter allows for accurate monitoring of urine output, which is a key indicator of renal perfusion and overall organ function in sepsis. It is also important for fluid balance management. While this is a valuable intervention in a critically ill patient, it is not the *immediate* priority over obtaining cultures to diagnose the underlying infection. Furthermore, inserting a catheter introduces a risk of infection, and this procedural step can be performed after the most critical diagnostic and initial therapeutic steps are underway.
2. Warm, flushed skin with bounding pulses and a widened pulse pressure points to which shock?
A. HypovolemicHypovolemic shock results from a significant reduction in intravascular volume, such as from hemorrhage or severe dehydration, leading to decreased cardiac output and systemic hypoperfusion. Clinically, patients present with cool, clammy skin due to compensatory vasoconstriction aimed at shunting blood to vital organs, along with weak, thready pulses and a narrowed pulse pressure, as the heart struggles to maintain pressure against reduced volume. These symptoms directly contradict the warm, flushed skin and bounding pulses described in the question, making hypovolemic shock an unlikely cause.
B. CardiogenicCardiogenic shock occurs when the heart's pumping ability is severely impaired, often due to myocardial infarction, leading to decreased cardiac output and systemic hypoperfusion despite adequate intravascular volume. Patients typically exhibit signs of poor tissue perfusion, such as cool, clammy skin, weak and rapid pulses, and often a narrowed pulse pressure as the left ventricle struggles to eject blood efficiently. The presence of warm, flushed skin and bounding pulses is inconsistent with the primary pump failure characteristic of cardiogenic shock.
C. DistributiveDistributive shock, which includes septic, anaphylactic, and neurogenic shock, is characterized by widespread vasodilation and maldistribution of blood flow, leading to a relative hypovolemia despite normal or increased total blood volume. This systemic vasodilation causes warm, flushed skin as blood pools in the periphery, and the compensatory increase in cardiac output combined with low peripheral vascular resistance results in bounding pulses and a widened pulse pressure. This clinical presentation precisely aligns with the symptoms provided, making distributive shock the correct answer.
D. ObstructiveObstructive shock arises from a physical impediment to blood flow within the cardiovascular system, such as a pulmonary embolism, cardiac tamponade, or tension pneumothorax, which reduces venous return or impedes ventricular filling/ejection. The clinical presentation typically includes signs of impaired cardiac output, such as cool, clammy skin, weak and rapid pulses, and a narrowed pulse pressure, similar to cardiogenic shock, as the heart struggles against the obstruction. The warm, flushed skin and bounding pulses described are not characteristic findings of obstructive shock.
Correct answer: C. Option A: Hypovolemic shock results from a significant reduction in intravascular volume, such as from hemorrhage or severe dehydration, leading to decreased cardiac output and systemic hypoperfusion. Clinically, patients present with cool, clammy skin due to compensatory vasoconstriction aimed at shunting blood to vital organs, along with weak, thready pulses and a narrowed pulse pressure, as the heart struggles to maintain pressure against reduced volume. These symptoms directly contradict the warm, flushed skin and bounding pulses described in the question, making hypovolemic shock an unlikely cause.
Option B: Cardiogenic shock occurs when the heart's pumping ability is severely impaired, often due to myocardial infarction, leading to decreased cardiac output and systemic hypoperfusion despite adequate intravascular volume. Patients typically exhibit signs of poor tissue perfusion, such as cool, clammy skin, weak and rapid pulses, and often a narrowed pulse pressure as the left ventricle struggles to eject blood efficiently. The presence of warm, flushed skin and bounding pulses is inconsistent with the primary pump failure characteristic of cardiogenic shock.
Option C: Distributive shock, which includes septic, anaphylactic, and neurogenic shock, is characterized by widespread vasodilation and maldistribution of blood flow, leading to a relative hypovolemia despite normal or increased total blood volume. This systemic vasodilation causes warm, flushed skin as blood pools in the periphery, and the compensatory increase in cardiac output combined with low peripheral vascular resistance results in bounding pulses and a widened pulse pressure. This clinical presentation precisely aligns with the symptoms provided, making distributive shock the correct answer.
Option D: Obstructive shock arises from a physical impediment to blood flow within the cardiovascular system, such as a pulmonary embolism, cardiac tamponade, or tension pneumothorax, which reduces venous return or impedes ventricular filling/ejection. The clinical presentation typically includes signs of impaired cardiac output, such as cool, clammy skin, weak and rapid pulses, and a narrowed pulse pressure, similar to cardiogenic shock, as the heart struggles against the obstruction. The warm, flushed skin and bounding pulses described are not characteristic findings of obstructive shock.
3. Four clients need the nurse. Who is seen FIRST?
A. Post-op client rating pain 8 of 10A post-operative client experiencing an 8 out of 10 pain level requires prompt pain management to promote comfort, facilitate recovery, and prevent complications like increased stress response or delayed ambulation. While high pain levels warrant attention and intervention, they typically do not represent an immediate, life-threatening emergency in the same way as an acute respiratory crisis. The nurse would assess the pain further, administer analgesia, and evaluate its effectiveness, but this client's condition is not as immediately unstable as one experiencing a severe respiratory compromise.
B. Asthma client with a suddenly silent chestAn asthma client with a suddenly silent chest is experiencing a critical, life-threatening emergency known as status asthmaticus or impending respiratory failure. A silent chest indicates a severe reduction or absence of air movement, meaning that despite significant airway obstruction, the client is no longer able to move enough air to produce wheezing sounds. This is a dire sign of inadequate ventilation and impending respiratory arrest, requiring immediate and aggressive intervention to prevent complete airway collapse, hypoxemia, and death. This client's condition demands the nurse's immediate assessment and intervention above all others.
C. Diabetic client with a glucose of 232A diabetic client with a blood glucose of 232 mg/dL is experiencing hyperglycemia, which needs to be addressed through medication administration and further assessment. While hyperglycemia can lead to long-term complications and, if very high, acute complications like diabetic ketoacidosis or hyperosmolar hyperglycemic state, a glucose level of 232 mg/dL is not an immediate, life-threatening emergency demanding urgent attention over a respiratory crisis. The nurse would plan to administer insulin or oral hypoglycemics as ordered, educate the client, and monitor blood glucose, but this is a stable, non-emergent situation compared to acute respiratory distress.
D. Client asking about discharge teachingA client asking about discharge teaching indicates readiness for discharge and a need for education to ensure safe transition home. Providing comprehensive discharge teaching is a crucial nursing responsibility to promote self-management, prevent readmissions, and ensure client understanding of their care plan, medications, and follow-up appointments. However, this is a non-urgent educational need that can be addressed once clients with acute, life-threatening conditions have been stabilized. The nurse would prioritize immediate physiological needs over educational needs, regardless of their importance for continuity of care.
Correct answer: B. Option A: A post-operative client experiencing an 8 out of 10 pain level requires prompt pain management to promote comfort, facilitate recovery, and prevent complications like increased stress response or delayed ambulation. While high pain levels warrant attention and intervention, they typically do not represent an immediate, life-threatening emergency in the same way as an acute respiratory crisis. The nurse would assess the pain further, administer analgesia, and evaluate its effectiveness, but this client's condition is not as immediately unstable as one experiencing a severe respiratory compromise.
Option B: An asthma client with a suddenly silent chest is experiencing a critical, life-threatening emergency known as status asthmaticus or impending respiratory failure. A silent chest indicates a severe reduction or absence of air movement, meaning that despite significant airway obstruction, the client is no longer able to move enough air to produce wheezing sounds. This is a dire sign of inadequate ventilation and impending respiratory arrest, requiring immediate and aggressive intervention to prevent complete airway collapse, hypoxemia, and death. This client's condition demands the nurse's immediate assessment and intervention above all others.
Option C: A diabetic client with a blood glucose of 232 mg/dL is experiencing hyperglycemia, which needs to be addressed through medication administration and further assessment. While hyperglycemia can lead to long-term complications and, if very high, acute complications like diabetic ketoacidosis or hyperosmolar hyperglycemic state, a glucose level of 232 mg/dL is not an immediate, life-threatening emergency demanding urgent attention over a respiratory crisis. The nurse would plan to administer insulin or oral hypoglycemics as ordered, educate the client, and monitor blood glucose, but this is a stable, non-emergent situation compared to acute respiratory distress.
Option D: A client asking about discharge teaching indicates readiness for discharge and a need for education to ensure safe transition home. Providing comprehensive discharge teaching is a crucial nursing responsibility to promote self-management, prevent readmissions, and ensure client understanding of their care plan, medications, and follow-up appointments. However, this is a non-urgent educational need that can be addressed once clients with acute, life-threatening conditions have been stabilized. The nurse would prioritize immediate physiological needs over educational needs, regardless of their importance for continuity of care.
4. Fifteen minutes into a PRBC transfusion the client reports chills, flank pain, and dark urine. What does the nurse do FIRST?
A. Slow the transfusion rateSlowing the transfusion rate is an insufficient intervention because the client is exhibiting classic signs and symptoms of an acute hemolytic transfusion reaction, which is a life-threatening emergency caused by immune-mediated destruction of transfused red blood cells. Reducing the flow rate allows the damaging reaction to continue, albeit at a slower pace, potentially leading to further organ damage, acute kidney injury from hemoglobinuria, and disseminated intravascular coagulation (DIC). The priority is to immediately halt the introduction of the incompatible blood into the patient's system to prevent further harm and stabilize their condition.
B. Stop the transfusion and keep the line open with normal salineStopping the transfusion immediately and maintaining intravenous access with normal saline is the critical first action because the client's symptoms (chills, flank pain, dark urine) are highly indicative of an acute hemolytic transfusion reaction, a severe and potentially fatal immune response. By stopping the transfusion, the nurse prevents further infusion of incompatible blood, thereby minimizing ongoing hemolysis and subsequent kidney damage, shock, and DIC. Keeping the intravenous line patent with normal saline allows for rapid administration of medications and fluids, which may be necessary to manage the acute reaction and support organ perfusion.
C. Give acetaminophen and continueAdministering acetaminophen and continuing the transfusion is an inappropriate and dangerous action because acetaminophen is an antipyretic that would only mask the fever, a symptom of the severe transfusion reaction, without addressing the underlying immune response. Continuing the transfusion would allow more incompatible blood to enter the patient's circulation, escalating the hemolytic reaction and increasing the risk of acute renal failure, shock, and potentially death. The priority is to stop the causative agent, not merely treat a symptom while the harmful process continues.
D. Obtain a urine sample for the labWhile obtaining a urine sample is an important diagnostic step to confirm hemoglobinuria, it is not the *first* action a nurse should take when a client exhibits signs of an acute hemolytic transfusion reaction. The immediate priority is to stop the infusion of the incompatible blood to prevent further patient harm and preserve kidney function. After stopping the transfusion and maintaining IV access, then collecting a urine sample and sending the remaining blood product and tubing to the lab are crucial steps for investigation and diagnosis.
Correct answer: B. Option A: Slowing the transfusion rate is an insufficient intervention because the client is exhibiting classic signs and symptoms of an acute hemolytic transfusion reaction, which is a life-threatening emergency caused by immune-mediated destruction of transfused red blood cells. Reducing the flow rate allows the damaging reaction to continue, albeit at a slower pace, potentially leading to further organ damage, acute kidney injury from hemoglobinuria, and disseminated intravascular coagulation (DIC). The priority is to immediately halt the introduction of the incompatible blood into the patient's system to prevent further harm and stabilize their condition.
Option B: Stopping the transfusion immediately and maintaining intravenous access with normal saline is the critical first action because the client's symptoms (chills, flank pain, dark urine) are highly indicative of an acute hemolytic transfusion reaction, a severe and potentially fatal immune response. By stopping the transfusion, the nurse prevents further infusion of incompatible blood, thereby minimizing ongoing hemolysis and subsequent kidney damage, shock, and DIC. Keeping the intravenous line patent with normal saline allows for rapid administration of medications and fluids, which may be necessary to manage the acute reaction and support organ perfusion.
Option C: Administering acetaminophen and continuing the transfusion is an inappropriate and dangerous action because acetaminophen is an antipyretic that would only mask the fever, a symptom of the severe transfusion reaction, without addressing the underlying immune response. Continuing the transfusion would allow more incompatible blood to enter the patient's circulation, escalating the hemolytic reaction and increasing the risk of acute renal failure, shock, and potentially death. The priority is to stop the causative agent, not merely treat a symptom while the harmful process continues.
Option D: While obtaining a urine sample is an important diagnostic step to confirm hemoglobinuria, it is not the *first* action a nurse should take when a client exhibits signs of an acute hemolytic transfusion reaction. The immediate priority is to stop the infusion of the incompatible blood to prevent further patient harm and preserve kidney function. After stopping the transfusion and maintaining IV access, then collecting a urine sample and sending the remaining blood product and tubing to the lab are crucial steps for investigation and diagnosis.
5. A client with type 1 diabetes mellitus who takes propranolol for migraine prophylaxis is admitted to the intensive care unit with diabetic ketoacidosis (DKA). While managing the client's blood glucose, the nurse monitors for signs of hypoglycemia. Which symptom should the nurse recognize as remaining UNMASKED by non-selective beta-blocker therapy?
A. DiaphoresisDiaphoresis is mediated by the sympathetic cholinergic system rather than adrenergic beta-receptors, making sweating the primary clinical sign of hypoglycemia that remains unmasked by beta-blockers.
B. TachycardiaTachycardia is mediated by beta-1 adrenergic receptors; beta-blockers suppress this sympathetic response, effectively masking an elevated heart rate during an episode of hypoglycemia.
C. Muscle tremorsMuscle tremors are mediated by beta-2 adrenergic stimulation; administration of beta-blockers blunts this response, preventing the client from experiencing or recognizing hypoglycemia tremors.
D. PalpitationsPalpitations are driven by cardiac beta-adrenergic stimulation during sympathetic activation; beta-blocker therapy blocks these receptor responses, masking palpitations during hypoglycemia.
Correct answer: A. Beta-blockers inhibit sympathetic adrenergic responses such as tachycardia, tremors, and palpitations, masking key warning signs of hypoglycemia. Diaphoresis is mediated by cholinergic pathways and remains present.
6. A client is being discharged home on oral amiodarone for maintenance control of recurrent ventricular dysrhythmias. When providing discharge teaching, which symptom should the nurse instruct the client to report to the healthcare provider immediately?
A. New onset of dyspnea, dry cough, or pleuritic chest pain.Amiodarone carries a black box warning for pulmonary toxicity, which can manifest as fatal pulmonary fibrosis; prompt reporting of respiratory symptoms like dyspnea or cough is essential.
B. Mild peripheral edema in the lower extremities at the end of the day.While heart failure exacerbations cause edema, pulmonary fibrosis and organ toxicities are the primary unique long-term toxicities specific to chronic amiodarone therapy.
C. Darkened stool color after taking the medication with meal.Dietary vitamin K intake adjustment is critical for clients taking warfarin, not amiodarone, although amiodarone can interact with warfarin if co-administered.
D. Mild gastrointestinal upset when taken on an empty stomach.Taking amiodarone with meals helps reduce GI distress, but identifying signs of life-threatening organ toxicity like pulmonary fibrosis takes priority in discharge instruction.
Correct answer: A. Amiodarone is an effective antiarrhythmic but is associated with severe long-term toxicities, most notably pulmonary toxicity (fibrosis), thyroid dysfunction, hepatotoxicity, and corneal microdeposits. Clients must be taught to immediately report respiratory symptoms such as new or worsening dyspnea, cough, or pleuritic chest pain.
7. A client with an acute Type A aortic dissection is admitted to the intensive care unit (ICU). The healthcare provider orders a continuous intravenous (IV) infusion of esmolol to lower the client's blood pressure and heart rate. Which pre-existing clinical condition in the client's history requires immediate communication with the provider before initiating the infusion?
A. Severe, active asthma with recurrent bronchospasmsSevere active asthma or bronchospasm is a major contraindication for beta-blockers, as blocking beta-2 receptors can precipitate fatal bronchoconstriction and respiratory failure.
B. Mild generalized anxiety with diaphoretic skinMild anxiety and diaphoretic appearance are expected findings in acute aortic dissection due to severe pain and sympathetic stimulation; they do not contraindicate beta-blocker therapy.
C. Serum potassium level of 4.8 mEq/L (4.8 mmol/L)A potassium level of 4.8 mEq/L is within normal limits (3.5–5.0 mEq/L) and does not contraindicate the administration of esmolol in this critically ill client.
D. Urine output of 45 mL/hr over the past two hoursA urine output of 45 mL/hr is adequate (greater than 30 mL/hr) and reflects acceptable renal perfusion, presenting no immediate contraindication to initiating esmolol therapy.
Correct answer: A. In acute aortic dissection, beta-blockers like esmolol are used to decrease heart rate and blood pressure to reduce aortic wall stress. However, active severe asthma is a major contraindication due to bronchospasm risk.
8. A client with an acute anterior myocardial infarction is admitted to the cardiac intensive care unit. Upon assessment, the nurse notes a blood pressure of 82/50 mmHg, a heart rate of 118 beats/min, bilateral diffuse pulmonary crackles, an S3 gallop, and cold, clammy extremities. The client's medication orders include intravenous metoprolol. Which action should the nurse take first?
A. Withhold the metoprolol and immediately report signs of cardiogenic shock to the provider.The client displays signs of cardiogenic shock (hypotension, tachycardia, pulmonary crackles, S3 gallop, cold/clammy skin); beta-blockers decrease contractility and are strictly contraindicated in acute heart failure or shock.
B. Administer half of the prescribed metoprolol dose and reassess the client's vital signs in 15 minutes.Administering even half the dose of metoprolol to a client in decompensated cardiogenic shock can further reduce cardiac output, worsening tissue hypoperfusion and leading to cardiac arrest.
C. Administer the metoprolol as ordered to reduce the elevated heart rate and myocardial oxygen demand.Although tachycardia increases myocardial oxygen demand, administering a negative inotrope like metoprolol during acute cardiogenic shock will suppress compensatory mechanisms and precipitate collapse.
D. Infuse a rapid 1,000 mL normal saline bolus prior to administering the prescribed metoprolol.Giving a fluid bolus in the presence of severe pulmonary edema (crackles, S3 gallop) will exacerbate fluid overload and respiratory failure, and metoprolol remains strictly contraindicated.
Correct answer: A. Beta-blockers are contraindicated in decompensated heart failure and cardiogenic shock because their negative inotropic and chronotropic effects exacerbate cardiac collapse, despite the presence of compensatory tachycardia.
9. The nurse in the emergency department is assessing a client whose telemetry displays a third-degree (complete) atrioventricular (AV) block. The client has a heart rate of 32 beats/min, a blood pressure of 80/44 mmHg, and is difficult to arouse. Which nursing action is the highest priority?
A. Administer intravenous amiodarone bolus over 10 minutes.Amiodarone is an antiarrhythmic medication used to suppress tachyarrhythmias, and administering it during severe bradycardia or complete heart block will further depress cardiac output.
B. Apply transcutaneous pacemaker pads and initiate cardiac pacing.Third-degree (complete) AV block is a medical emergency that leads to severe bradycardia and compromised cardiac output; transcutaneous pacing is the immediate high-priority intervention.
C. Instruct the client to perform a vagal maneuver such as coughing.Vagal maneuvers stimulate the vagus nerve to slow down excessive heart rates in SVT and are strictly contraindicated in bradycardic states like complete heart block.
D. Prepare the client for immediate synchronized cardioversion.Synchronized cardioversion is indicated for rapid tachyarrhythmias with a pulse, not for profound bradycardia resulting from third-degree heart block.
Correct answer: B. Third-degree AV block represents complete AV dissociation where no atrial impulses reach the ventricles. This severely compromises cardiac output, leading to hypotension and altered mental status. Immediate transcutaneous pacing is required to restore an adequate heart rate until a permanent pacemaker can be inserted.
10. A client in the intensive care unit is receiving a continuous intravenous infusion of sodium nitroprusside alongside labetalol for a hypertensive emergency following an intracerebral hemorrhage. During assessment, the client reports new-onset tinnitus and abdominal pain, and displays acute confusion. Arterial blood gas results show uncompensated metabolic acidosis. Which complication should the nurse suspect?
A. Cyanide toxicity secondary to sodium nitroprusside infusionSodium nitroprusside metabolizes into cyanide; toxic buildup presents with metabolic acidosis, confusion, tinnitus, and abdominal pain, requiring immediate cessation of the infusion and provider notification.
B. Beta-blocker withdrawal syndrome secondary to labetalol administrationBeta-blocker withdrawal occurs after abrupt cessation of chronic therapy, not during active administration, and symptoms describe nitroprusside-induced cyanide toxicity rather than withdrawal.
C. Hypertensive encephalopathy secondary to inadequate blood pressure controlHypertensive encephalopathy involves severe hypertension with neurological symptoms, but metabolic acidosis and tinnitus paired with continuous nitroprusside strongly point to cyanide toxicity.
D. Cushing's triad secondary to rapidly increasing intracranial pressureCushing's triad consists of bradycardia, irregular respiration, and widening pulse pressure indicating increased intracranial pressure; it does not present with metabolic acidosis or tinnitus.
Correct answer: A. Continuous high-dose or prolonged infusions of sodium nitroprusside can cause cyanide or thiocyanate toxicity. Key features include altered mental status, metabolic acidosis, tinnitus, and abdominal pain; the infusion must be stopped immediately.