Advanced heart failure and transplantation US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Advanced heart failure and transplantation. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Advanced heart failure and transplantation US Medical PG Question 1: A 10-year-old boy is presented to the hospital for a kidney transplant. In the operating room, the surgeon connects an allograft kidney renal artery to the aorta, and after a few moments, the kidney becomes cyanotic, edematous, and dusky with mottling. Which of the following in the recipient’s serum is responsible for this rejection?
- A. Macrophages
- B. CD4+ T cells
- C. IgA
- D. CD8+ T cells
- E. IgG (Correct Answer)
Advanced heart failure and transplantation Explanation: ***IgG***
- The rapid onset of tissue necrosis and the immediate signs of rejection (cyanotic, edematous, dusky with mottling) upon vascular anastomosis are characteristic of **hyperacute rejection**.
- **Hyperacute rejection** is mediated by pre-formed recipient antibodies, primarily **IgG**, targeting donor ABO or HLA antigens. These antibodies activate complement, leading to rapid thrombosis and graft destruction.
*Macrophages*
- While macrophages play a role in chronic allograft rejection and delayed type hypersensitivity, they are not the primary mediators of **hyperacute rejection**.
- Their involvement typically presents with a more delayed and less immediate profound tissue damage than seen in this scenario.
*CD4+ T cells*
- **CD4+ T cells** are central to acute cellular rejection, which typically manifests days to weeks after transplantation.
- They are not responsible for the immediate, pre-formed antibody-mediated response seen in **hyperacute rejection**.
*IgA*
- **IgA antibodies** are primarily involved in mucosal immunity and are generally not implicated in solid organ transplant rejection, especially hyperacute rejection.
- While IgA can contribute to immune complex formation, it's not the main antibody type driving hyperacute allograft destruction.
*CD8+ T cells*
- **CD8+ T cells** (cytotoxic T lymphocytes) are key players in acute cellular rejection, mediating direct lysis of donor cells.
- Their action is part of a cellular immune response that takes days to weeks to develop and is not responsible for the immediate, antibody-mediated hyperacute rejection.
Advanced heart failure and transplantation US Medical PG Question 2: A 56-year-old man comes to the emergency department because of progressively worsening shortness of breath and fever for 2 days. He also has a nonproductive cough. He does not have chest pain or headache. He has chronic myeloid leukemia and had a bone marrow transplant 3 months ago. His current medications include busulfan, mycophenolate mofetil, tacrolimus, and methylprednisolone. His temperature is 38.1°C (100.6°F), pulse is 103/min, respirations are 26/min, and blood pressure is 130/70 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 93%. Pulmonary examination shows diffuse crackles. The spleen tip is palpated 4 cm below the left costal margin. Laboratory studies show:
Hemoglobin 10.3 g/dL
Leukocyte count 4,400/mm3
Platelet count 160,000/mm3
Serum
Glucose 78 mg/dL
Creatinine 2.1 mg/dL
D-dimer 96 ng/mL (N < 250)
pp65 antigen positive
Galactomannan antigen negative
Urinalysis is normal. An x-ray of the chest shows diffuse bilateral interstitial infiltrates. An ECG shows sinus tachycardia. Which of the following is the most appropriate pharmacotherapy?
- A. Levofloxacin
- B. Ganciclovir (Correct Answer)
- C. Valganciclovir
- D. Azithromycin
- E. Acyclovir
Advanced heart failure and transplantation Explanation: ***Ganciclovir***
- The patient's **positive pp65 antigen** confirms **cytomegalovirus (CMV) infection**, the most common viral infection in immunocompromised bone marrow transplant recipients.
- This patient has **severe, life-threatening CMV pneumonitis** evidenced by hypoxia (O2 sat 93%), tachypnea, and diffuse bilateral interstitial infiltrates.
- **Intravenous ganciclovir** is the **first-line treatment** for severe CMV disease due to its potent antiviral activity and reliable bioavailability in critically ill patients.
*Valganciclovir*
- **Valganciclovir** is an **oral prodrug of ganciclovir** with excellent bioavailability, but it is primarily reserved for **CMV prophylaxis** or **maintenance therapy** after initial IV treatment.
- In this patient with **acute, severe CMV pneumonitis** requiring urgent intervention (hypoxia, respiratory distress), **IV ganciclovir is strongly preferred** for faster, more reliable drug delivery and higher tissue concentrations.
*Levofloxacin*
- This **fluoroquinolone antibiotic** treats **bacterial infections**, not viral pathogens like CMV.
- The **positive pp65 antigen** specifically identifies CMV as the etiology, and negative galactomannan rules out invasive aspergillosis.
- While empiric antibacterial coverage might be considered in febrile neutropenic patients, the clear viral diagnosis directs therapy toward antivirals.
*Azithromycin*
- **Azithromycin** is a macrolide antibiotic effective against atypical bacteria (Mycoplasma, Chlamydophila) and some other bacterial pathogens.
- It has **no activity against CMV** and would not address the confirmed viral etiology.
*Acyclovir*
- **Acyclovir** is effective against **herpes simplex virus (HSV)** and **varicella-zoster virus (VZV)**, but has **poor activity against CMV** due to inadequate phosphorylation by CMV enzymes.
- The positive pp65 antigen specifically indicates CMV, for which ganciclovir (not acyclovir) is required.
Advanced heart failure and transplantation US Medical PG Question 3: A 43-year-old woman presents to the emergency department complaining of palpitations, dry cough, and shortness of breath for 1 week. She immigrated to the United States from Korea at the age of 20. She says that her heart is racing and she has never felt these symptoms before. Her cough is dry and is associated with shortness of breath that occurs with minimal exertion. Her past medical history is otherwise unremarkable. She has no allergies and is not currently taking any medications. She is a nonsmoker and an occasional drinker. She denies illicit drug use. Her blood pressure is 100/65 mm Hg, pulse is 76/min, respiratory rate is 23/min, and temperature is 36.8°C (98.2°F). Her physical examination is significant for bibasilar lung crackles and a non-radiating, low-pitched, mid-diastolic rumbling murmur best heard at the apical region. In addition, she has jugular vein distention and bilateral pitting edema in her lower extremities. Which of the following best describes the infectious agent that led to this patient’s condition?
- A. A bacterium that induces partial lysis of red cells with hydrogen peroxide
- B. A bacterium that requires an anaerobic environment to grow properly
- C. A bacterium that does not lyse red cells
- D. A bacterium that induces heme degradation of the red cells of a blood agar plate
- E. A bacterium that induces complete lysis of the red cells of a blood agar plate with an oxygen-sensitive cytotoxin (Correct Answer)
Advanced heart failure and transplantation Explanation: ***A bacterium that induces complete lysis of the red cells of a blood agar plate with an oxygen-sensitive cytotoxin***
- This describes **Group A Streptococcus (GAS)**, specifically *Streptococcus pyogenes*, which causes **rheumatic fever** leading to **mitral stenosis**. Mitral stenosis is characterized by a **mid-diastolic rumbling murmur** at the apex, left atrial enlargement causing **palpitations**, and **pulmonary congestion** leading to dyspnea, cough, and bibasilar crackles.
- The delayed onset of symptoms (immigrated at 20, symptoms at 43) is typical for **rheumatic heart disease**, where repeated GAS infections in childhood/adolescence lead to valve damage that manifests years later. GAS produces **streptolysin O**, an **oxygen-labile cytotoxin** responsible for **beta-hemolysis** (complete lysis) on blood agar.
*A bacterium that induces partial lysis of red cells with hydrogen peroxide*
- This describes **alpha-hemolytic** bacteria like *Streptococcus pneumoniae* or *Viridans streptococci*, which cause **partial hemolysis** (greenish discoloration) on blood agar due to **hydrogen peroxide** production.
- While *Viridans streptococci* can cause **infective endocarditis**, the clinical picture of **rheumatic mitral stenosis** is more consistent with a history of recurrent streptococcal pharyngitis (GAS).
*A bacterium that requires an anaerobic environment to grow properly*
- This description typically refers to **anaerobic bacteria**, such as *Clostridium* or *Bacteroides* species.
- These bacteria are generally not associated with the primary cause of acute rheumatic fever or the subsequent development of chronic valvular heart disease like mitral stenosis.
*A bacterium that does not lyse red cells*
- This describes **gamma-hemolytic** (non-hemolytic) bacteria, such as *Enterococcus faecalis* or some *Staphylococcus* species.
- These organisms do not cause the characteristic hemolysis seen with the streptococci responsible for rheumatic fever.
*A bacterium that induces heme degradation of the red cells of a blood agar plate*
- This description is **too vague** and does not specifically identify the organism. While heme degradation occurs with various types of hemolysis, the key distinguishing feature of **Group A Streptococcus** is **complete lysis (beta-hemolysis)** combined with production of the **oxygen-sensitive toxin streptolysin O**.
- This option lacks the specificity needed to identify GAS as the causative agent of rheumatic fever. Both alpha- and beta-hemolytic organisms can degrade heme, but only beta-hemolytic GAS causes rheumatic heart disease.
Advanced heart failure and transplantation US Medical PG Question 4: A 72-year-old woman is brought to the emergency department by ambulance after an unexpected fall at home 1 hour ago. She was resuscitated at the scene by paramedics before being transferred to the hospital. She has a history of ischemic heart disease and type 2 diabetes mellitus. She has not taken any sedative medications. Her GCS is 6. She is connected to a mechanical ventilator. Her medical records show that she signed a living will 5 years ago, which indicates her refusal to receive any type of cardiopulmonary resuscitation, intubation, or maintenance of life support on mechanical ventilation. Her son, who has a durable power-of-attorney for her healthcare decisions, objects to the discontinuation of mechanical ventilation and wishes that his mother be kept alive without suffering in the chance that she might recover. Which of the following is the most appropriate response to her son regarding his wishes for his mother?
- A. “We will take every measure necessary to prolong her life.”
- B. “She may be eligible for hospice care.”
- C. “The opinion of her primary care physician must be obtained regarding further steps in management.”
- D. “Based on her wishes, mechanical ventilation must be discontinued.” (Correct Answer)
- E. “Further management decisions will be referred to the hospital’s ethics committee.”
Advanced heart failure and transplantation Explanation: ***Based on her wishes, mechanical ventilation must be discontinued.***
- A **living will** is a legally binding document that outlines a patient's wishes regarding medical treatment, including **refusal of life support**.
- In this scenario, the patient’s clear and documented wishes in her living will take precedence over the son's objections, even though he holds **durable power of attorney for healthcare** (DPA).
*“We will take every measure necessary to prolong her life.”*
- This statement directly contradicts the patient's **documented wishes** in her living will to refuse intubation and maintenance on mechanical ventilation.
- Ignoring a patient's advance directive can lead to ethical and legal issues, as it undermines the principle of **patient autonomy**.
*“She may be eligible for hospice care.”*
- While hospice care is a relevant consideration for patients with terminal illnesses, suggesting it prematurely without addressing the immediate issue of the **living will** can be dismissive of the patient's explicit directives.
- The primary concern is upholding the patient's autonomy, which includes addressing her advance directive regarding **withdrawal of life support**.
*“The opinion of her primary care physician must be obtained regarding further steps in management.”*
- While the **primary care physician's** input is valuable for understanding the patient's overall health and discussing goals of care, the existence of a clear and legally binding **living will** simplifies the decision-making process concerning life support.
- The patient's advance directive is paramount and generally does not require further medical negotiation unless there's ambiguity or new information suggesting a change in her wishes.
*“Further management decisions will be referred to the hospital’s ethics committee.”*
- An **ethics committee** consultation may be appropriate in cases of ambiguity surrounding an advance directive, conflict among surrogates, or uncertainty about the patient's capacity at the time of signing the directive.
- However, in this case, the **living will** explicitly states her wishes regarding mechanical ventilation, making the patient's intent clear and generally overriding the need for an ethics committee in the initial response.
Advanced heart failure and transplantation US Medical PG Question 5: A 71-year-old woman with a past medical history of type 2 diabetes, hypercholesterolemia, and hypertension was admitted to the hospital 8 hours ago with substernal chest pain for management of acute non-ST-elevated myocardial infarction (NSTEMI). The ECG findings noted by ST-depressions and T-wave inversions on anterolateral leads, which is also accompanied by elevated cardiac enzymes. Upon diagnosis, management with inhaled oxygen therapy, beta-blockers and aspirin, and low-molecular-weight heparin therapy were initiated, and she was placed on bed rest with continuous electrocardiographic monitoring. Since admission, she required 2 doses of sublingual nitroglycerin for recurrent angina, and the repeat troponin levels continued to rise. Given her risk factors, plans were made for early coronary angiography. The telemetry nurse calls the on-call physician because of her concern with the patient's mild confusion and increasing need for supplemental oxygen. At bedside evaluation, The vital signs include: heart rate 122/min, blood pressure 89/40 mm Hg, and the pulse oximetry is 91% on 6L of oxygen by nasal cannula. The telemetry and a repeat ECG show sinus tachycardia. She is breathing rapidly, appears confused, and complains of shortness of breath. On physical exam, the skin is cool and clammy and appears pale and dull. She has diffuse bilateral pulmonary crackles, and an S3 gallop is noted on chest auscultation with no new murmurs. She has jugular venous distention to the jaw-line, rapid and faint radial pulses, and 1+ dependent edema. She is immediately transferred to the intensive care unit for respiratory support and precautions for airway security. The bedside sonography shows abnormal hypodynamic anterior wall movement and an ejection fraction of 20%, but no evidence of mitral regurgitation or ventricular shunt. The chest X-ray demonstrates cephalization of pulmonary veins and pulmonary edema. What is the most appropriate next step in the stabilization of this patient?
- A. Obtain blood cultures and start preliminary broad-spectrum antibiotics
- B. Start intravenous fluids and epinephrine therapy
- C. Intubate the patient and perform an emergency cardiocentesis
- D. Initiate dopamine therapy and diuresis (Correct Answer)
- E. Insert two large-bore intravenous catheters and start rapid fluid resuscitation
Advanced heart failure and transplantation Explanation: ***Initiate dopamine therapy and diuresis***
- This patient is presenting with **cardiogenic shock** secondary to extensive NSTEMI, characterized by **hypotension**, signs of **end-organ hypoperfusion** (confusion, cool clammy skin), **pulmonary edema** (crackles, dyspnea, elevated jugular venous pressure), and **severely reduced ejection fraction**. Dopamine is a vasopressor that can increase cardiac output and blood pressure.
- **Diuresis** with loop diuretics such as furosemide is crucial to reduce the fluid overload contributing to the pulmonary edema and jugular venous distention.
*Obtain blood cultures and start preliminary broad-spectrum antibiotics*
- While infection is a concern in critically ill patients, there are **no signs of infection** in this clinical presentation. The patient's symptoms are clearly attributable to acute cardiac decompensation.
- A delay in treating cardiogenic shock to investigate for infection would be detrimental and potentially fatal.
*Start intravenous fluids and epinephrine therapy*
- Intravenous fluids would **worsen the existing pulmonary edema and fluid overload** in a patient with an ejection fraction of 20% and clinical signs of volume overload (crackles, JVD, S3 gallop).
- Epinephrine is a potent vasopressor but is generally reserved for more severe shock refractory to other inotropes, or in cases of **cardiac arrest**, not typically first-line for cardiogenic shock with significant pulmonary congestion.
*Intubate the patient and perform an emergency cardiocentesis*
- While the patient is confused and has respiratory distress, **intubation** should be considered after hemodynamic stabilization, if respiratory failure persists or worsens.
- **Cardiocentesis** is indicated for **cardiac tamponade**, which is not supported by the absence of an effusion on bedside sonography and the finding of hypodynamic anterior wall movement, which points to pump failure.
*Insert two large-bore intravenous catheters and start rapid fluid resuscitation*
- This patient is in **cardiogenic shock with clear evidence of fluid overload**, including pulmonary edema and elevated jugular venous pressure.
- **Rapid fluid resuscitation would exacerbate heart failure** and worsen respiratory compromise due to increased preload.
Advanced heart failure and transplantation US Medical PG Question 6: A 72-year-old woman comes to the emergency department because of a 2-week history of worsening shortness of breath, lower extremity swelling, and a 3-kg (6.6-lb) weight gain. Crackles are heard on auscultation of the chest. Cardiac examination shows a dull, low-pitched early diastolic sound at the 5th left intercostal space that becomes louder in the left lateral decubitus position at end-expiration. Which of the following is the most likely cause of these auscultation findings?
- A. Increased ventricular contractility
- B. Increased capacity of the pulmonary circulation
- C. Decreased left-ventricular filling pressure
- D. Increased left ventricular end-systolic volume
- E. Decreased left myocardial compliance (Correct Answer)
Advanced heart failure and transplantation Explanation: ***Decreased left myocardial compliance***
- A dull, low-pitched early **diastolic sound (S3 gallop)**, heard best in the left lateral decubitus position at end-expiration, indicates **rapid ventricular filling** into a ventricle with altered diastolic properties. This finding, along with worsening shortness of breath, lower extremity swelling, and weight gain, suggests **heart failure with impaired ventricular filling**.
- Decreased left myocardial compliance (increased stiffness) means the left ventricle cannot **relax and fill properly** during diastole. The S3 occurs when blood rapidly decelerates as it enters the stiff, non-compliant ventricle, creating the characteristic sound.
- This represents **diastolic dysfunction** (heart failure with preserved ejection fraction - HFpEF), which is common in elderly patients with hypertension and is characterized by a stiff ventricle with increased filling pressures.
*Increased ventricular contractility*
- Increased ventricular contractility would lead to a more forceful ejection of blood during systole, not an early diastolic filling sound.
- This would not explain the S3 gallop or the signs of heart failure with fluid retention.
*Increased capacity of the pulmonary circulation*
- Increased pulmonary circulation capacity would help accommodate fluid and prevent pulmonary congestion, which contradicts the symptoms of crackles and shortness of breath.
- The patient has **decreased** capacity to handle the fluid volume, leading to pulmonary edema.
*Decreased left-ventricular filling pressure*
- Decreased LV filling pressure would imply less fluid overload and better cardiac function, contrary to the clinical presentation.
- An S3 gallop and signs of heart failure (crackles, edema, weight gain) indicate **increased** filling pressures from impaired ventricular function.
*Increased left ventricular end-systolic volume*
- Increased end-systolic volume indicates **systolic dysfunction** (reduced ejection fraction), where the ventricle cannot adequately eject blood, leaving residual volume after contraction.
- While systolic dysfunction can also produce an S3 gallop due to volume overload, the specific clinical description emphasizes a **diastolic filling abnormality** (sound during early diastole in a specific position that optimizes detection of ventricular filling).
- The S3 in systolic dysfunction is primarily due to **volume overload**, whereas the S3 here is attributed to blood entering a **stiff ventricle** with impaired compliance, which is the primary pathophysiologic mechanism being tested.
Advanced heart failure and transplantation US Medical PG Question 7: The serum brain natriuretic peptide and N-terminal pro-BNP are elevated. A diagnosis of heart failure with preserved ejection fraction is made. In addition to supplemental oxygen therapy, which of the following is the most appropriate initial step in management?
- A. Intravenous dobutamine
- B. Intravenous furosemide therapy (Correct Answer)
- C. Intravenous morphine therapy
- D. Thoracentesis
- E. Intermittent hemodialysis
Advanced heart failure and transplantation Explanation: ***Intravenous furosemide therapy***
- Heart failure with **preserved ejection fraction (HFpEF)** often presents with **pulmonary congestion** due to elevated filling pressures.
- **Furosemide**, a loop diuretic, effectively reduces fluid overload and associated symptoms by increasing renal excretion of sodium and water.
*Intravenous dobutamine*
- **Dobutamine** is an inotropic agent that increases myocardial contractility and heart rate.
- It is typically used for **acute decompensated heart failure with low cardiac output** and is generally avoided in HFpEF unless there is significant hypoperfusion, as it can worsen myocardial oxygen demand and diastolic dysfunction.
*Intravenous morphine therapy*
- **Morphine** can be used in acute heart failure to reduce preload and anxiety, but it is not a primary treatment for the underlying fluid overload.
- It can cause respiratory depression and hypotension, and its use is typically reserved for patients with severe pain or dyspnea not adequately managed by other therapies.
*Thoracentesis*
- **Thoracentesis** is indicated for symptomatic **pleural effusions** causing respiratory distress.
- While pleural effusions can occur in heart failure, initial management of generalized fluid overload typically involves diuretics, making thoracentesis a secondary intervention if diuretic therapy is insufficient.
*Intermittent hemodialysis*
- **Intermittent hemodialysis** is an invasive procedure primarily used for severe renal failure or refractory fluid overload that has not responded to maximal diuretic therapy.
- It is not the initial step in managing heart failure with preserved ejection fraction and would only be considered in highly selected cases with **acute kidney injury** or diuretic resistance.
Advanced heart failure and transplantation US Medical PG Question 8: A 59-year-old woman presents to the physician for a 3-month history of progressively worsening shortness of breath on exertion and swelling of her legs. She has a history of breast cancer that was treated with surgery, followed by doxorubicin and cyclophosphamide therapy 4 years ago. Cardiac examination shows an S3 gallop, but there are no murmurs or rubs. Examination of the lower extremities shows pitting edema below the knees. Echocardiography is most likely to show which of the following sets of changes in this patient?
Aorto-ventricular pressure gradient
Diastolic function Ventricular cavity size Ventricular wall thickness
A Normal ↓ Normal Normal
B Normal Normal ↑ ↑
C Normal ↓ ↑ ↑
D ↑ ↓ ↑ ↑
E Normal Normal ↑ ↓
- A. C Normal ↓ ↑ ↑ (Correct Answer)
- B. E Normal Normal ↑ ↓
- C. B Normal Normal ↑ ↑
- D. D ↑ ↓ ↑ ↑
- E. A Normal ↓ Normal Normal
Advanced heart failure and transplantation Explanation: ***C Normal ↓ ↑ ↑***
- The patient's history of **doxorubicin chemotherapy** with symptoms of **progressive dyspnea, leg edema, and S3 gallop** indicates **dilated cardiomyopathy (DCM)** from anthracycline cardiotoxicity.
- Echocardiographic findings in DCM include: **normal aorto-ventricular gradient** (no valvular stenosis), **impaired diastolic function** (both systolic and diastolic dysfunction occur), **increased ventricular cavity size** (dilated chambers), and **increased wall thickness** due to **eccentric hypertrophy** (volume overload causes chamber dilation with proportional wall thickening, though the wall appears relatively thin compared to the enlarged cavity).
- The S3 gallop reflects elevated filling pressures and ventricular dysfunction characteristic of heart failure with reduced ejection fraction.
*E Normal Normal ↑ ↓*
- This option incorrectly suggests **normal diastolic function**, which contradicts the pathophysiology of dilated cardiomyopathy where both systolic and diastolic dysfunction are present.
- Decreased wall thickness is also incorrect; in DCM, there is **eccentric hypertrophy** with absolute wall thickness that is normal-to-increased, not decreased (though relative wall thickness may appear reduced given the marked chamber dilation).
*B Normal Normal ↑ ↑*
- While this option correctly identifies increased cavity size and wall thickness, it incorrectly suggests **normal diastolic function**.
- In dilated cardiomyopathy, **diastolic dysfunction is present** due to impaired ventricular compliance and elevated filling pressures, as evidenced by the S3 gallop.
*D ↑ ↓ ↑ ↑*
- This option suggests an **elevated aorto-ventricular pressure gradient**, which would indicate **aortic stenosis**.
- The clinical presentation shows no murmur, making significant aortic stenosis unlikely; dilated cardiomyopathy does not cause valvular gradients.
*A Normal ↓ Normal Normal*
- This pattern suggests **diastolic heart failure with preserved ejection fraction (HFpEF)** or **restrictive cardiomyopathy** with normal chamber size and wall thickness.
- However, the patient's anthracycline exposure and clinical picture are classic for **dilated cardiomyopathy with reduced ejection fraction**, which features ventricular dilation.
Advanced heart failure and transplantation US Medical PG Question 9: A 66-year-old man presents to the emergency department with dyspnea. Two days ago, he hosted his grandchild's birthday party, and since has noticed general malaise, fever, and dry cough. He does not know if he feels more dyspneic while supine or standing but has noticed difficulty breathing even while watching television. He has a past medical history of congestive heart failure and hypertension, for which he takes aspirin, metoprolol, furosemide, lisinopril, and spironolactone as prescribed. His blood pressure is 90/50 mmHg, pulse is 120/min, and respirations are 30/min. His radial pulse is barely palpable, and his wrists and ankles are cold and clammy. Physical exam reveals a S3 and S4 with a soft holosystolic murmur at the apex, decreased breath sounds up to the middle lung fields, jugular venous distention to the auricles, and 3+ pitting edema to the mid thighs. EKG shows ST depressions consistent with demand ischemia. Bedside echocardiogram shows global akinesis with an ejection fraction (EF) of 20%; previous reports show EF at 40%. A portable chest radiograph shows bilateral pulmonary edema. Metoprolol is held, dobutamine and furosemide drips are started, and BiPAP is started at 20/5 cm H2O. After 15 minutes, the nurse reports that urine output is minimal and blood pressure is now 75/40 mmHg and pulse is 130/min. What is the best next step in management?
- A. Decrease furosemide rate
- B. Resume home metoprolol
- C. Decrease positive inspiratory pressure (Correct Answer)
- D. Decrease dobutamine rate
- E. Decrease positive end-expiratory pressure
Advanced heart failure and transplantation Explanation: ***Decrease positive inspiratory pressure***
- The patient is experiencing worsening **hypotension** and **tachycardia** despite initial treatment, suggesting that the current BiPAP settings, particularly a high **positive inspiratory pressure (PIP)**, might be exacerbating the hemodynamic instability.
- High intrathoracic pressure from BiPAP can decrease **venous return** and **cardiac preload**, further compromising an already struggling heart with reduced ejection fraction, leading to decreased cardiac output and worsening hypotension.
*Decrease furosemide rate*
- The patient has significant signs of **fluid overload** (pulmonary edema, JVD, pitting edema), and minimal urine output suggests inadequate diuresis, not over-diuresis.
- Decreasing the furosemide rate would likely worsen fluid overload and pulmonary congestion, which is detrimental given his acute heart failure exacerbation.
*Resume home metoprolol*
- The patient is already hypotensive (90/50 mmHg initially, dropping to 75/40 mmHg) and in **cardiogenic shock**, and beta-blockers like metoprolol are **contraindicated** in this acute setting.
- Resuming metoprolol would further depress myocardial contractility and worsen bradycardia (although he is currently tachycardic), significantly exacerbating his hypotension and shock state.
*Decrease dobutamine rate*
- **Dobutamine** is an **inotropic agent** used to improve cardiac contractility and cardiac output in patients with cardiogenic shock, especially with a low EF.
- Decreasing the dobutamine rate would reduce inotropic support, likely leading to a further decline in cardiac output and worsening his profound hypotension and shock.
*Decrease positive end-expiratory pressure*
- While PEEP can increase intrathoracic pressure, the given BiPAP setting of 20/5 cm H2O indicates a PIP of 20 cm H2O and a **PEEP of 5 cm H2O**. A PEEP of 5 cm H2O is relatively low and often beneficial for oxygenation and reducing preload in pulmonary edema.
- The primary concern for hemodynamic compromise with BiPAP is more often related to high peak inspiratory pressure reducing venous return, rather than a low PEEP which can help keep alveoli open and improve gas exchange.
Advanced heart failure and transplantation US Medical PG Question 10: A 70-year-old male presents for an annual exam. His past medical history is notable for shortness of breath when he sleeps, and upon exertion. Recently he has experienced dyspnea and lower extremity edema that seems to be worsening. Both of these symptoms have resolved since he was started on several medications and instructed to weigh himself daily. Which of the following is most likely a component of his medical management?
- A. Lidocaine
- B. Verapamil
- C. Carvedilol (Correct Answer)
- D. Aspirin
- E. Ibutilide
Advanced heart failure and transplantation Explanation: ***Carvedilol***
- The patient exhibits classic symptoms of **heart failure**, such as **dyspnea on exertion**, **orthopnea** (shortness of breath when he sleeps), and **lower extremity edema**.
- **Beta-blockers** like carvedilol are essential for managing **chronic heart failure** by reducing myocardial oxygen demand and improving cardiac function.
*Lidocaine*
- **Lidocaine** is primarily an **antiarrhythmic drug** used for acute treatment of **ventricular arrhythmias**, not for chronic heart failure management.
- It works by blocking sodium channels and has no direct benefit in addressing the underlying pathophysiology of heart failure.
*Verapamil*
- **Verapamil** is a **non-dihydropyridine calcium channel blocker** typically used for hypertension, angina, and supraventricular tachyarrhythmias.
- It can have **negative inotropic effects**, which are generally contraindicated or used with extreme caution in patients with **systolic heart failure** due to its potential to worsen cardiac function.
*Aspirin*
- **Aspirin** is an **antiplatelet agent** used for primary or secondary prevention of **atherosclerotic cardiovascular disease** (e.g., in patients with coronary artery disease).
- It does not directly manage the symptoms or pathophysiology of **heart failure** unless there is a coexisting ischemic etiology.
*Ibutilide*
- **Ibutilide** is an **antiarrhythmic drug** specifically used for the rapid conversion of **atrial flutter and atrial fibrillation** of recent onset to sinus rhythm.
- It is not a medication used for the long-term management of **heart failure** symptoms described in the patient.
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