The scenario describes a patient experiencing symptoms indicative of acute decompensated heart failure (ADHF) complicated by possible cardiogenic shock. The key findings are hypotension (systolic BP <90 mmHg), altered mental status (confusion), severe dyspnea, and crackles in the lungs, all suggesting inadequate tissue perfusion due to the heart's inability to pump effectively.

The immediate priority is to improve cardiac output and blood pressure to restore adequate tissue perfusion. Options such as Trendelenburg positioning are generally contraindicated in heart failure as they increase preload, potentially worsening pulmonary edema. High flow oxygen via a non-rebreather mask is appropriate but may not be sufficient to address the underlying hemodynamic instability. Rapid fluid boluses are dangerous in ADHF, especially with pulmonary edema, as they can exacerbate fluid overload and worsen respiratory distress.

Initiating vasopressor support with close hemodynamic monitoring is the most appropriate initial intervention. Vasopressors like norepinephrine or dopamine can increase blood pressure by increasing systemic vascular resistance and, in some cases, contractility. However, it is crucial to administer vasopressors judiciously and monitor the patient's response closely, as excessive vasoconstriction can increase afterload and further impair cardiac output. The placement of an arterial line allows for continuous blood pressure monitoring and facilitates frequent arterial blood gas analysis to assess oxygenation and acid-base balance. A central venous catheter can provide information about central venous pressure (CVP), which can help guide fluid management and assess the patient's response to treatment. This approach addresses the immediate life-threatening problem of inadequate tissue perfusion while allowing for careful monitoring to prevent further complications.

The scenario describes a patient with known aortic stenosis who is scheduled for a dental extraction. Patients with valvular heart disease, including aortic stenosis, are at increased risk of developing infective endocarditis (IE) following procedures that can cause bacteremia, such as dental extractions. The American Heart Association (AHA) provides guidelines for antibiotic prophylaxis to prevent IE in high-risk patients undergoing certain procedures.

While previous guidelines recommended antibiotic prophylaxis for a wider range of patients and procedures, current guidelines have narrowed the indications. Prophylaxis is now recommended only for patients with prosthetic heart valves, a history of IE, certain congenital heart defects, or a heart transplant with valvular disease. Since this patient has aortic stenosis but does not fall into any of these high-risk categories, antibiotic prophylaxis is not routinely recommended. However, maintaining good oral hygiene is essential for all patients, especially those with valvular heart disease, to reduce the risk of bacteremia. Consulting with the cardiologist is not necessary in this case, as the AHA guidelines provide clear recommendations. Delaying the dental extraction could have negative consequences for the patient’s oral health. The nurse’s role includes educating the patient about the current AHA guidelines and the importance of maintaining good oral hygiene.

The scenario describes a patient experiencing chest pain that is unrelieved by nitroglycerin and associated with ST-segment elevation on an ECG. This presentation is highly suggestive of an acute ST-segment elevation myocardial infarction (STEMI). Current guidelines recommend that patients with STEMI receive reperfusion therapy as quickly as possible to restore blood flow to the affected myocardium. The two main reperfusion strategies are percutaneous coronary intervention (PCI) and thrombolytic therapy. PCI, involving angioplasty and stenting, is generally preferred if it can be performed within a timely manner by experienced operators. The American Heart Association (AHA) recommends a “door-to-balloon” time (time from arrival in the emergency department to balloon inflation) of 90 minutes or less. If PCI is not available within this timeframe or is contraindicated, thrombolytic therapy (e.g., alteplase, tenecteplase) should be considered, ideally within 30 minutes of arrival (“door-to-needle” time). In this scenario, the closest PCI-capable hospital is 3 hours away, making PCI outside the recommended timeframe. Therefore, the most appropriate intervention is to administer a thrombolytic medication to attempt to restore blood flow as quickly as possible. Transferring the patient to the PCI center would delay reperfusion, which could lead to increased myocardial damage. Administering more nitroglycerin is unlikely to be effective in relieving the pain associated with STEMI.

The scenario describes a patient with an abdominal aortic aneurysm (AAA) who is experiencing back pain and hypotension. These are concerning signs of a potential AAA rupture, which is a life-threatening emergency. The priority is to stabilize the patient hemodynamically and prepare for immediate surgical intervention. Rapid fluid resuscitation with crystalloid solutions (e.g., normal saline or lactated Ringer’s) is crucial to maintain blood pressure and tissue perfusion. Type and crossmatch for blood products should be done immediately as the patient is likely to need a blood transfusion. Calling the vascular surgeon is essential to prepare for surgical repair of the aneurysm. Applying oxygen via nasal cannula is important, but it is not the priority in this situation.

The scenario describes a patient with a history of heart failure who is now experiencing acute decompensated heart failure (ADHF). The key signs and symptoms are indicative of fluid overload and impaired cardiac function. The most appropriate initial intervention focuses on rapidly addressing the pulmonary edema and improving oxygenation. Administering a rapid IV bolus of normal saline would exacerbate the fluid overload and worsen the patient’s respiratory distress. Initiating continuous positive airway pressure (CPAP) is a non-invasive ventilation method that can help improve oxygenation and reduce the work of breathing by providing positive pressure to keep the airways open. While furosemide is a loop diuretic used to reduce fluid volume, it takes time to take effect and may not provide immediate relief for acute respiratory distress. Obtaining a 12-lead ECG is important for assessing cardiac function and identifying potential arrhythmias or ischemia, but it does not address the immediate respiratory compromise. Therefore, the priority is to improve oxygenation and ventilation with CPAP before addressing fluid overload or obtaining further diagnostic information. CPAP helps to reduce preload and afterload, improving cardiac output and reducing pulmonary congestion, aligning with the immediate needs of the patient in ADHF.

The patient is experiencing signs and symptoms suggestive of cardiac tamponade, a life-threatening condition where fluid accumulation in the pericardial sac compresses the heart, impairing its ability to pump effectively. Key indicators include hypotension (low blood pressure), muffled heart sounds, and jugular venous distension (JVD), collectively known as Beck’s triad. Pulsus paradoxus, an exaggerated decrease in systolic blood pressure during inspiration, is another significant finding.

In this scenario, the priority nursing intervention is to prepare for pericardiocentesis. Pericardiocentesis involves inserting a needle into the pericardial sac to drain the excess fluid, relieving the pressure on the heart and improving cardiac output. While other interventions like administering vasopressors or increasing intravenous fluids might be considered to support blood pressure, they do not address the underlying cause of the tamponade. Similarly, administering diuretics would not be effective in rapidly resolving the fluid accumulation in the pericardial sac. Obtaining a 12-lead ECG is important for monitoring, but it does not directly address the immediate life-threatening situation. Therefore, preparing for pericardiocentesis is the most appropriate and crucial initial action to stabilize the patient. The nurse must also be prepared to assist with continuous hemodynamic monitoring during and after the procedure.

The scenario describes a patient with advanced heart failure experiencing worsening symptoms despite optimal medical therapy, including guideline-directed medical therapy (GDMT). The patient’s NYHA Class III-IV heart failure, reduced ejection fraction (HFrEF), and recurrent hospitalizations indicate a need for advanced therapies. Cardiac Resynchronization Therapy (CRT) is specifically indicated for patients with HFrEF, a wide QRS complex (typically >120ms), and NYHA Class II-IV symptoms despite optimal medical therapy. CRT aims to improve cardiac function by coordinating ventricular contractions, leading to increased cardiac output and reduced mitral regurgitation. Left Ventricular Assist Device (LVAD) is considered for patients with end-stage heart failure who are not candidates for heart transplantation or as a bridge to transplant. While heart transplantation remains the gold standard for end-stage heart failure, it is limited by donor availability and patient eligibility. Palliative care focuses on symptom management and improving quality of life for patients with advanced heart failure who are not candidates for other therapies or who choose to focus on comfort. Given the patient’s HFrEF, wide QRS complex, and persistent symptoms despite GDMT, CRT is the most appropriate initial intervention to improve cardiac function and quality of life. The decision to proceed with LVAD or heart transplant would depend on further evaluation and the patient’s overall condition and goals of care. The current ESC guidelines state that CRT is recommended in symptomatic patients (NYHA class II-IV) with LVEF ≤35%, sinus rhythm, LBBB with QRS duration ≥130 ms or QRS duration of 130-149 ms.

The scenario describes a patient with a new onset of a second-degree AV block Mobitz Type II. This type of block is characterized by intermittent non-conducted P waves without progressive PR interval prolongation, indicating a block below the AV node, often in the His-Purkinje system. This is an unstable rhythm that can quickly progress to a third-degree AV block or asystole. The appropriate initial intervention is to prepare for transcutaneous pacing, as this provides immediate electrical stimulation to the heart to maintain adequate cardiac output. Administering atropine is generally ineffective in Mobitz II blocks and may paradoxically worsen the block. Observing the patient is not appropriate given the potential for rapid deterioration. Administering a beta-blocker is contraindicated as it can further slow the heart rate and exacerbate the AV block. The priority is to ensure adequate cardiac output by preparing for immediate pacing.

This scenario involves a patient experiencing symptomatic bradycardia with dizziness and altered mental status, which is a medical emergency. The patient has a third-degree AV block, also known as complete heart block, where there is no communication between the atria and ventricles. This results in a slow ventricular rate, which is causing the patient’s symptoms.

According to Advanced Cardiovascular Life Support (ACLS) guidelines, the initial treatment for symptomatic bradycardia unresponsive to atropine is transcutaneous pacing. Transcutaneous pacing delivers electrical impulses through the skin to stimulate the heart and increase the heart rate. While awaiting transcutaneous pacing, it is also appropriate to prepare for transvenous pacing, which is a more definitive treatment for complete heart block. Administering another dose of atropine is unlikely to be effective in third-degree AV block, as atropine primarily works on the AV node, which is completely blocked in this case. Synchronized cardioversion is used for tachyarrhythmias, not bradycardia.

The scenario describes a patient with a history of heart failure who is experiencing increased shortness of breath and lower extremity edema. These symptoms are indicative of fluid overload, a common complication of heart failure. The initial nursing intervention should focus on assessing the patient’s fluid status and oxygenation. This includes measuring vital signs (heart rate, blood pressure, respiratory rate, oxygen saturation), auscultating lung sounds for rales (crackles), assessing for peripheral edema, and monitoring urine output. Administering oxygen is appropriate if the patient is hypoxic (low oxygen saturation). Elevating the legs can help reduce edema. However, obtaining a weight and notifying the physician are important but should follow the initial assessment to provide the physician with accurate and timely information. The nurse must quickly assess the patient’s condition to determine the severity of the fluid overload and guide further interventions.

The scenario presents a patient with a known abdominal aortic aneurysm (AAA) who is experiencing sudden, severe back pain and hypotension. These are classic signs of AAA rupture, a life-threatening emergency. While obtaining a 12-lead ECG is important to rule out myocardial infarction, it is not the priority in this situation. Administering oxygen is a standard intervention for patients with chest pain or respiratory distress, but it does not address the underlying cause of the patient’s symptoms. Starting an IV line is a necessary step to prepare for fluid resuscitation and medication administration, but it should not delay the most critical action. The most important and time-sensitive action is to prepare the patient for immediate transfer to the operating room for surgical repair of the ruptured AAA. AAA rupture is associated with high mortality, and prompt surgical intervention is essential to improve the patient’s chances of survival. The nurse’s role is to recognize the signs and symptoms of AAA rupture and act quickly to facilitate appropriate intervention.

The scenario presents a patient with known heart failure experiencing increased dyspnea and edema, indicative of acute decompensated heart failure (ADHF). The patient’s medication regimen includes furosemide, an aldosterone antagonist, and a beta-blocker. The key concern is the potential for further decompensation due to medication interactions or inadequate management. Administering an additional dose of the beta-blocker at this stage could worsen the patient’s condition. Beta-blockers, while beneficial in chronic heart failure, can reduce cardiac output and exacerbate symptoms in ADHF, particularly if the patient is already experiencing fluid overload and reduced contractility. The increased dyspnea suggests worsening pulmonary congestion, and the edema indicates fluid retention. A beta-blocker would further reduce the heart’s ability to compensate for these challenges. The most appropriate initial action is to assess the patient’s fluid status and consider adjusting the diuretic dosage. Furosemide is a loop diuretic that promotes sodium and water excretion, helping to alleviate fluid overload. Increasing the furosemide dosage can help reduce pulmonary congestion and edema, improving the patient’s respiratory status. This approach aligns with guidelines for managing ADHF, which prioritize addressing fluid overload and optimizing hemodynamic stability before making changes to beta-blocker therapy. Furthermore, continuous monitoring of vital signs, oxygen saturation, and urine output is essential to evaluate the patient’s response to treatment and guide further interventions. The nurse should also consider other potential causes of decompensation, such as medication non-adherence, dietary indiscretions, or underlying infections.

The scenario describes a patient with a known abdominal aortic aneurysm (AAA) presenting with sudden, severe abdominal and back pain, along with signs of hemodynamic instability (hypotension, tachycardia). These are classic signs of a ruptured AAA, which is a life-threatening emergency. The priority is to prepare the patient for immediate surgical intervention to repair the aneurysm and stop the bleeding. Administering pain medication is important for comfort, but it should not delay the preparation for surgery. Obtaining a CT scan of the abdomen would confirm the diagnosis, but it would delay definitive treatment and is not the priority in this unstable patient. Monitoring vital signs frequently is essential, but it is not the primary intervention. The focus should be on stabilizing the patient and getting them to surgery as quickly as possible.

The scenario describes a patient with a known abdominal aortic aneurysm (AAA) who presents to the emergency department with sudden onset of severe abdominal and back pain, along with hypotension and tachycardia. These findings are highly suggestive of a ruptured AAA. A ruptured AAA is a life-threatening emergency that requires immediate surgical intervention to repair the aneurysm and prevent exsanguination. The primary goal of initial management is to stabilize the patient hemodynamically and prepare for emergent surgical repair. The most appropriate initial nursing intervention is to administer intravenous fluids and prepare for immediate transfer to the operating room. Rapid fluid resuscitation is essential to maintain blood pressure and tissue perfusion. However, it is important to avoid over-resuscitation, as this can increase bleeding from the rupture site. Obtaining a CT scan of the abdomen may be helpful to confirm the diagnosis, but it should not delay transfer to the operating room. Calling for a cardiology consult is not the priority in this situation, as the primary problem is a surgical emergency. Administering pain medication is important for patient comfort, but it should not delay definitive treatment.

The correct response is to prepare for pericardiocentesis. The patient’s presentation (hypotension, tachycardia, muffled heart sounds, and pulsus paradoxus) is highly suggestive of cardiac tamponade. Pulsus paradoxus, an exaggerated decrease in systolic blood pressure during inspiration, is a classic sign of tamponade. Cardiac tamponade occurs when fluid accumulates in the pericardial space, compressing the heart and impairing its ability to pump effectively. This leads to decreased cardiac output and subsequent hypotension. Pericardiocentesis, the aspiration of fluid from the pericardial sac, is the definitive treatment for cardiac tamponade. Administering a fluid bolus may transiently improve blood pressure, but it does not address the underlying cause of the tamponade and may worsen the condition. Increasing the oxygen flow rate is important for supporting oxygenation, but it does not treat the tamponade. Initiating vasopressor support may temporarily increase blood pressure, but it does not address the underlying cause and can have adverse effects. The priority is to relieve the pressure on the heart by removing the fluid from the pericardial space. The nurse’s ability to recognize the signs and symptoms of cardiac tamponade and promptly prepare for pericardiocentesis is crucial in ensuring timely intervention and improving patient outcomes.

The scenario describes a patient with a newly implanted permanent pacemaker. The key is to identify the MOST important instruction regarding potential electromagnetic interference (EMI) with the pacemaker.

a) Mobile phones can cause EMI with pacemakers if held too close to the device. Current guidelines recommend holding mobile phones on the ear opposite the side of the pacemaker and avoiding carrying the phone in a pocket directly over the pacemaker.

b) Microwaves generally do not interfere with pacemakers as long as they are functioning properly.

c) Airport security wands can potentially interfere with pacemakers. Patients with pacemakers should inform security personnel and may request a hand search instead of going through the metal detector or being scanned with a security wand.

d) Electric blankets generally do not interfere with pacemakers.

Therefore, the MOST important instruction regarding potential electromagnetic interference for a patient with a newly implanted permanent pacemaker is to hold mobile phones on the ear opposite the side of the pacemaker and avoid carrying the phone in a pocket directly over the pacemaker.

The scenario involves a patient who has undergone coronary artery bypass grafting (CABG) and is now 24 hours post-operative. A key concern after CABG is the potential for atrial fibrillation (AFib), which is a common complication due to surgical stress, inflammation, and electrolyte imbalances. Prophylactic administration of amiodarone or beta-blockers is often used to reduce the risk of post-operative AFib. Monitoring electrolytes, particularly potassium and magnesium, is crucial because imbalances can predispose to arrhythmias. While chest tube patency and pain management are important aspects of post-operative care, they are not specifically targeted at preventing AFib. Early ambulation is encouraged to prevent complications like pneumonia and deep vein thrombosis, but it does not directly prevent AFib. Therefore, the most important nursing intervention to prevent atrial fibrillation in this patient is to monitor electrolyte levels and administer prophylactic antiarrhythmic medications as prescribed. This question tests the knowledge of common post-operative complications following CABG and the specific interventions aimed at preventing atrial fibrillation.

The scenario describes a patient with a history of mitral valve stenosis who is now experiencing signs and symptoms suggestive of pulmonary hypertension (dyspnea, fatigue, edema) and atrial fibrillation (irregularly irregular rhythm). Mitral stenosis, a narrowing of the mitral valve, obstructs blood flow from the left atrium to the left ventricle, leading to increased left atrial pressure. This elevated pressure is transmitted backward into the pulmonary vasculature, causing pulmonary hypertension. Over time, the increased pulmonary pressure can lead to right ventricular hypertrophy and failure, resulting in systemic congestion (edema). The enlarged left atrium in mitral stenosis also predisposes the patient to atrial fibrillation due to structural and electrical remodeling of the atrial tissue. Therefore, the most likely underlying cause of the patient’s current presentation is the progression of mitral valve stenosis leading to pulmonary hypertension and atrial fibrillation. While heart failure with preserved ejection fraction (HFpEF) can cause similar symptoms, it is less likely given the patient’s known history of mitral stenosis. Coronary artery disease (CAD) could contribute to heart failure, but it does not directly explain the atrial fibrillation or the pulmonary hypertension in the context of mitral stenosis. Hyperthyroidism can cause atrial fibrillation and heart failure, but it is less likely than the known valvular pathology.

The scenario describes a patient with known CAD experiencing symptoms suggestive of unstable angina or NSTEMI. The key is to differentiate between the immediate actions and the long-term strategies. While all options are potentially relevant in the broader management of CAD, the *most* appropriate immediate action focuses on addressing the acute ischemic event. Obtaining a 12-lead ECG is crucial to assess for ST-segment elevation or depression, which helps differentiate between unstable angina, NSTEMI, and STEMI, guiding immediate treatment decisions like percutaneous coronary intervention (PCI) or thrombolytics. Administering a statin is important for long-term management of hyperlipidemia in CAD patients, but it’s not the priority in the acute setting. Scheduling a stress test is useful for assessing the extent of CAD and guiding long-term management, but it’s not indicated during an acute ischemic event. Recommending lifestyle modifications is essential for secondary prevention of CAD, but it is not the immediate action needed when a patient presents with chest pain suggestive of ACS. The focus should be on rapid assessment and intervention to minimize myocardial damage. In addition, this action adheres to established protocols and guidelines for managing patients presenting with chest pain, ensuring timely and appropriate care. The prompt acquisition and interpretation of the ECG are paramount in directing subsequent treatment strategies.

The scenario presents a patient with a history of paroxysmal supraventricular tachycardia (PSVT) who is currently experiencing an episode. Vagal maneuvers are the first-line treatment for PSVT, aiming to increase parasympathetic tone and slow down the heart rate by affecting the AV node conduction.

The Valsalva maneuver is a specific vagal maneuver that involves the patient attempting to exhale forcefully against a closed airway (e.g., by bearing down as if straining during a bowel movement). This increases intrathoracic pressure, stimulating the vagus nerve. Asking the patient to cough forcefully is another vagal maneuver, but not the primary one. Administering adenosine is a pharmacological intervention used if vagal maneuvers are ineffective. Applying ice to the face can stimulate the vagus nerve, but it’s less commonly used as a first-line maneuver compared to the Valsalva maneuver. The nurse should initially attempt the Valsalva maneuver to try to terminate the PSVT episode.

This question tests knowledge of antiarrhythmic drug classifications and their effects on cardiac action potentials. Potassium channel blockers (Class III antiarrhythmics) prolong the repolarization phase of the cardiac action potential. This prolongation increases the effective refractory period (ERP), making the heart less susceptible to arrhythmias. Sodium channel blockers (Class I) affect the depolarization phase. Beta-blockers (Class II) primarily affect the slope of phase 4 depolarization in pacemaker cells. Calcium channel blockers (Class IV) affect the plateau phase of the action potential and slow conduction through the AV node.

This question focuses on the nurse’s understanding of the management of acute cardiogenic shock, a life-threatening condition characterized by severe heart failure and inadequate tissue perfusion. In cardiogenic shock, the heart is unable to pump enough blood to meet the body’s needs, leading to hypotension, decreased cardiac output, and end-organ dysfunction. The priority in managing cardiogenic shock is to improve cardiac output and tissue perfusion. Inotropic support, such as dobutamine or milrinone, can help to increase contractility and improve cardiac output. However, inotropic agents can also increase myocardial oxygen demand, potentially worsening ischemia. An intra-aortic balloon pump (IABP) is a mechanical circulatory support device that can improve cardiac output and reduce afterload, thereby decreasing myocardial oxygen demand. The IABP works by inflating during diastole, increasing coronary perfusion, and deflating during systole, reducing afterload. While vasopressors may be necessary to maintain blood pressure, they can also increase afterload and worsen cardiac output. Administering a fluid bolus is generally not recommended in cardiogenic shock unless there is evidence of hypovolemia, as it can worsen pulmonary congestion. Placing the patient in Trendelenburg position is also not recommended, as it can increase preload and worsen pulmonary edema.

The scenario presents a patient with a history of heart failure (HF) who is now experiencing increased shortness of breath and lower extremity edema, indicative of acute decompensated heart failure (ADHF). The patient’s medication regimen includes furosemide, an ACE inhibitor, and digoxin. The addition of metoprolol, a beta-blocker, requires careful consideration due to its potential effects on cardiac contractility and heart rate. In ADHF, the heart’s ability to pump effectively is already compromised. Beta-blockers can further reduce contractility, potentially worsening the patient’s condition, especially in the acute phase. While beta-blockers are beneficial in chronic HF to reduce remodeling and improve long-term outcomes, initiating them during an acute exacerbation can be detrimental. The nurse must assess the patient’s current clinical status, including blood pressure, heart rate, and signs of hypoperfusion, before administering metoprolol. Contacting the provider to discuss the appropriateness of administering the beta-blocker at this time is crucial. The provider may choose to hold the medication, reduce the dose, or initiate it only if the patient’s condition stabilizes. Failing to recognize the potential negative impact of beta-blockers in ADHF and administering the medication without further evaluation could lead to further decompensation, including hypotension, bradycardia, and worsening heart failure symptoms. The nurse’s actions must prioritize patient safety and evidence-based practice, considering the specific context of ADHF and the potential risks associated with beta-blocker initiation. The goal is to optimize the patient’s hemodynamic status and prevent further deterioration.

Cardiac tamponade is a life-threatening condition characterized by the accumulation of fluid in the pericardial sac, leading to compression of the heart and impaired cardiac filling. Beck’s triad, a classic sign of cardiac tamponade, consists of hypotension (due to decreased cardiac output), jugular venous distension (JVD) (due to impaired venous return to the heart), and muffled heart sounds (due to fluid surrounding the heart). Pulsus paradoxus, an exaggerated drop in systolic blood pressure during inspiration, is another important finding in cardiac tamponade. Tachycardia is a compensatory mechanism to maintain cardiac output. Bradycardia is not typically associated with cardiac tamponade, as the heart attempts to compensate for reduced stroke volume by increasing heart rate. Hypertension is not a typical finding, as cardiac output is compromised. Bounding peripheral pulses are also not expected due to the decreased stroke volume.

The scenario describes a patient with symptomatic bradycardia (dizziness and lightheadedness) unresponsive to atropine, indicating a significant conduction system issue likely at or below the AV node. Transcutaneous pacing (TCP) is the immediate next step to provide temporary electrical stimulation and improve cardiac output until a more permanent solution (transvenous or permanent pacemaker) can be implemented. While epinephrine and dopamine can increase heart rate, they do not address the underlying conduction problem and are generally used after pacing is initiated or if pacing is ineffective. Administering another dose of atropine is unlikely to be effective, as the patient has already demonstrated a lack of response. Atropine primarily works on the SA and AV nodes, and if the block is infra-nodal, it will not be effective. Preparation for transvenous pacing involves gathering necessary equipment and potentially administering sedation, but it is not the immediate first action. TCP provides immediate electrical stimulation to improve cardiac output. The CV-BC nurse must understand the principles of advanced cardiac life support (ACLS) and the algorithms for bradycardia, as well as the indications and contraindications for various interventions. The nurse must also be knowledgeable about pacemaker types and settings to provide appropriate care. The CV-BC nurse should also understand the legal implications of delaying treatment in a symptomatic patient. Standards of care require prompt intervention to prevent further harm.

The scenario describes a patient with a known abdominal aortic aneurysm (AAA) who is experiencing sudden onset of severe abdominal and back pain, along with signs of hemodynamic instability (hypotension and tachycardia). These findings are highly suggestive of AAA rupture, a life-threatening emergency. The immediate priority is to stabilize the patient and prepare for emergent surgical intervention to repair the ruptured aneurysm. While obtaining a CT angiogram can confirm the diagnosis, it should not delay transfer to the operating room, as time is of the essence. Aggressive fluid resuscitation is necessary to maintain blood pressure and tissue perfusion, but it should be done cautiously to avoid exacerbating bleeding. Administering pain medication is important for patient comfort, but it should not be the primary focus. The key is to recognize the signs of AAA rupture and expedite surgical intervention to improve the patient’s chances of survival. The nurse should immediately notify the surgeon and prepare the patient for transfer to the operating room.

The scenario describes a patient with a history of heart failure who is experiencing increased shortness of breath and lower extremity edema. These are classic signs of fluid overload and decompensated heart failure. The best indicator of fluid volume status in this patient is daily weights. Daily weights provide a trend of fluid retention or loss, allowing for timely adjustments in diuretic therapy. While monitoring blood pressure, assessing skin turgor, and measuring intake and output are important assessments, they do not provide as accurate and comprehensive an assessment of fluid volume status as daily weights. The rationale for prioritizing daily weights is that they provide a reliable and objective measure of fluid balance, enabling the healthcare team to effectively manage the patient’s fluid overload and prevent further decompensation.

The scenario describes a patient experiencing a hypertensive emergency complicated by aortic dissection. The primary goal is rapid blood pressure reduction to prevent further aortic damage. While all listed medications can lower blood pressure, the key consideration is their suitability in the context of aortic dissection. Nitroprusside is a potent vasodilator that rapidly lowers blood pressure. However, its use can be problematic in aortic dissection because it can cause reflex tachycardia, increasing the shear stress on the aortic wall and potentially worsening the dissection. Beta-blockers are crucial in managing aortic dissection because they reduce heart rate and contractility, decreasing the force of the blood against the weakened aortic wall (dP/dt). Labetalol is particularly useful because it has both alpha- and beta-blocking effects, providing both afterload reduction and heart rate control without the reflex tachycardia associated with pure vasodilators. Hydralazine, a direct vasodilator, can also cause reflex tachycardia, making it less desirable as a first-line agent in aortic dissection. While nicardipine, a calcium channel blocker, is effective in lowering blood pressure, it does not provide the same heart rate control as labetalol, which is critical in this scenario. Therefore, labetalol is the most appropriate initial medication because it effectively lowers blood pressure while also reducing heart rate and the force of ventricular contraction, thereby minimizing stress on the aortic wall. The prompt administration of labetalol helps to prevent further propagation of the aortic dissection and reduces the risk of life-threatening complications such as aortic rupture or end-organ ischemia.

The correct response is to monitor the patient for signs and symptoms of bleeding. Heparin-induced thrombocytopenia (HIT) is a serious complication of heparin therapy characterized by a decrease in platelet count and an increased risk of thrombosis. The initial drop in platelets is a key indicator. Although thrombosis is a major concern, the immediate nursing action focuses on monitoring for bleeding due to the thrombocytopenia. Administering protamine sulfate is the antidote for heparin overdose, but it is not indicated in HIT unless there is active bleeding. Increasing the heparin dosage would be contraindicated in HIT, as it could worsen the thrombocytopenia and increase the risk of thrombosis. Discontinuing heparin and initiating warfarin is the standard treatment for HIT, but it requires confirmation of the diagnosis and is not the most appropriate initial nursing action.

The correct response is to prepare for transcutaneous pacing. The patient’s presentation of symptomatic bradycardia (heart rate of 40 bpm with dizziness and hypotension) requires immediate intervention to increase the heart rate and improve cardiac output. Transcutaneous pacing is a noninvasive method of delivering electrical impulses to the heart to stimulate contraction. While atropine is a first-line medication for symptomatic bradycardia, it may not be effective in all cases, particularly in the presence of AV block. Administering a fluid bolus may help to improve blood pressure, but it does not address the underlying bradycardia. Preparing for synchronized cardioversion is not appropriate for bradycardia; it is used for tachyarrhythmias. The nurse must understand the management of bradyarrhythmias and the indications for transcutaneous pacing. The underlying concept is the understanding of cardiac conduction disturbances and the ability to initiate appropriate interventions based on the patient’s clinical presentation.