Chronic heart failure management US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Chronic heart failure management. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Chronic heart failure management US Medical PG Question 1: 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
Chronic heart failure management 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.
Chronic heart failure management US Medical PG Question 2: A 70-year-old Caucasian male visits your office regularly for treatment of New York Heart association class IV congestive heart failure. Which of the following medications would you add to this man's drug regimen in order to improve his overall survival?
- A. Spironolactone (Correct Answer)
- B. Furosemide
- C. Amiloride
- D. Acetazolamide
- E. Hydrochlorothiazide
Chronic heart failure management Explanation: ***Spironolactone***
- **Spironolactone** is an **aldosterone antagonist** that has been shown to reduce mortality and morbidity in patients with **NYHA Class III and IV heart failure**.
- It works by blocking the harmful effects of **aldosterone** on the heart, such as **fibrosis** and remodeling, improving cardiac function and survival.
*Furosemide*
- **Furosemide** is a **loop diuretic** primarily used to relieve **symptoms of congestion** (edema, dyspnea) in heart failure by promoting fluid excretion.
- While it improves symptoms, **furosemide** alone does not significantly improve long-term survival in patients with heart failure.
*Amiloride*
- **Amiloride** is a **potassium-sparing diuretic** that works by blocking sodium channels in the collecting duct, leading to modest diuresis.
- It is often used to prevent **hypokalemia** caused by other diuretics but does not have the same proven mortality benefit in heart failure as spironolactone.
*Acetazolamide*
- **Acetazolamide** is a **carbonic anhydrase inhibitor** primarily used for glaucoma, metabolic alkalosis, and altitude sickness.
- It has a weaker diuretic effect and is not a commonly used or recommended medication for improving long-term survival in patients with heart failure.
*Hydrochlorothiazide*
- **Hydrochlorothiazide** is a **thiazide diuretic** primarily used for hypertension and mild to moderate edema.
- While it can help manage fluid retention, it does not offer the same mortality benefit in advanced heart failure as aldosterone antagonists like spironolactone.
Chronic heart failure management US Medical PG Question 3: A 59-year-old man presents to his primary care provider with the complaint of daytime fatigue. He often has a headache that is worse in the morning and feels tired when he awakes. He perpetually feels fatigued even when he sleeps in. The patient lives alone, drinks 2-3 beers daily, drinks coffee regularly, and has a 10 pack-year smoking history. His temperature is 99.0°F (37.2°C), blood pressure is 180/110 mm Hg, pulse is 80/min, respirations are 13/min, and oxygen saturation is 98% on room air. Physical exam is notable for a BMI of 39 kg/m^2. The rest of the patient's pulmonary and neurological exams are unremarkable. Which of the following is the best next step in management?
- A. Caffeine avoidance
- B. Screening for depression
- C. Alcohol avoidance in the evening
- D. CT head
- E. Weight loss (Correct Answer)
Chronic heart failure management Explanation: ***Weight Loss***
- The patient's **BMI of 39 kg/m²** indicates **class III obesity**, which is the strongest modifiable risk factor for **obstructive sleep apnea (OSA)**. The clinical presentation—**daytime fatigue**, morning headaches, unrefreshing sleep despite adequate sleep duration, and hypertension—strongly suggests OSA.
- While **polysomnography** is the gold standard for confirming OSA, the clinical diagnosis is evident in this case. **Weight loss** is the most important initial therapeutic intervention, as even modest weight reduction (10% of body weight) can significantly improve or resolve OSA in obese patients.
- Weight loss reduces upper airway collapse by decreasing fatty tissue deposition around the pharynx and improving lung volumes. This addresses the underlying pathophysiology rather than just treating symptoms.
- This intervention also addresses his **hypertension** (180/110 mm Hg), which is commonly associated with and exacerbated by OSA.
*Caffeine avoidance*
- While excessive caffeine can disrupt sleep architecture, the patient's symptoms—particularly **morning headaches** and **unrefreshing sleep despite sleeping in**—are not characteristic of caffeine-induced insomnia, which typically presents with difficulty initiating sleep.
- These symptoms, combined with obesity and hypertension, point strongly to a sleep-related breathing disorder rather than a stimulant effect.
*Screening for depression*
- Fatigue is indeed a cardinal symptom of major depressive disorder, but the specific pattern here—**morning headaches** (from nocturnal hypercapnia/hypoxemia), **unrefreshing sleep**, and **obesity with hypertension**—is far more consistent with OSA.
- Depression screening could be considered if symptoms persist after addressing the sleep disorder, as untreated OSA can contribute to or worsen mood disorders.
*Alcohol avoidance in the evening*
- **Alcohol consumption** (2-3 beers daily) does worsen OSA by relaxing upper airway dilator muscles and suppressing arousal responses to hypoxemia. Evening alcohol avoidance would be a beneficial **adjunctive measure**.
- However, while helpful, this intervention is less impactful than weight loss. The patient's **severe obesity** (BMI 39 kg/m²) is the predominant and most modifiable risk factor, making weight loss the priority intervention that will have the greatest effect on reducing OSA severity.
*CT head*
- CT head would be indicated if there were focal neurological deficits, papilledema, or features suggesting increased intracranial pressure or structural brain pathology.
- This patient's **neurological exam is unremarkable**, and his headaches are characteristic of OSA (worse in the morning due to nocturnal CO₂ retention, improving throughout the day). Imaging is not warranted.
Chronic heart failure management US Medical PG Question 4: A 56-year-old woman comes to the physician for follow-up after a measurement of elevated blood pressure at her last visit three months ago. She works as a high school teacher at a local school. She says that she mostly eats cafeteria food and take-out. She denies any regular physical activity. She does not smoke or use any recreational drugs. She drinks 2 to 3 glasses of wine per day. She has hypercholesterolemia for which she takes atorvastatin. Her height is 165 cm (5 ft 5 in), weight is 82 kg (181 lb), and BMI is 30.1 kg/m2. Her pulse is 67/min, respirations are 18/min, and blood pressure is 152/87 mm Hg on the right arm and 155/92 mm Hg on the left arm. She would like to try lifestyle modifications to improve her blood pressure before considering pharmacologic therapy. Which of the following lifestyle modifications is most likely to result in the greatest reduction of this patient's systolic blood pressure?
- A. Walking for 30 minutes, 5 days per week
- B. Reducing sodium intake to less than 2.4 g per day
- C. Losing 15 kg (33 lb) of body weight (Correct Answer)
- D. Adopting a DASH diet
- E. Decreasing alcohol consumption to maximum of one drink per day
Chronic heart failure management Explanation: ***Losing 15 kg (33 lb) of body weight***
- **Weight reduction** is the most effective lifestyle modification for lowering blood pressure, correlating directly with the amount of weight lost.
- A loss of 15 kg (33 lb) in this patient, who is **obese (BMI 30.1)**, could significantly reduce her systolic blood pressure, potentially by 5-20 mmHg per 10 kg weight loss.
*Walking for 30 minutes, 5 days per week*
- Regular **aerobic physical activity** is beneficial for blood pressure reduction, typically resulting in a 4-9 mmHg decrease in systolic pressure.
- While helpful, the magnitude of reduction from exercise alone is generally less than that achieved with significant weight loss in an obese individual.
*Reducing sodium intake to less than 2.4 g per day*
- **Sodium restriction** is an effective strategy, often leading to a 2-8 mmHg reduction in systolic blood pressure.
- Given the patient's diet of cafeteria and take-out food, high sodium intake is likely, making this a relevant intervention, but typically less impactful than substantial weight loss.
*Adopting a DASH diet*
- The **Dietary Approaches to Stop Hypertension (DASH) diet** emphasizes fruits, vegetables, and low-fat dairy, and can significantly lower blood pressure, by 8-14 mmHg.
- This diet is highly effective, but for an obese individual, the blood pressure reduction from achieving a healthy weight is often greater.
*Decreasing alcohol consumption to maximum of one drink per day*
- Reducing **excessive alcohol intake** can decrease systolic blood pressure by 2-4 mmHg, as the patient reports 2-3 glasses of wine daily.
- While beneficial, this reduction is likely to be less substantial compared to major weight loss or other dietary changes.
Chronic heart failure management US Medical PG Question 5: A 36-year-old man presents to his primary care physician because of shortness of breath. He is an office worker who has a mostly sedentary lifestyle; however, he has noticed that recently he feels tired and short of breath when going on long walks with his wife. He also has had a hacking cough that seems to linger, though he attributes this to an upper respiratory tract infection he had 2 months ago. He has diabetes that is well-controlled on metformin and has smoked 1 pack per day for 20 years. Physical exam reveals a large chested man with wheezing bilaterally and mild swelling in his legs and abdomen. The cause of this patient's abdominal and lower extremity swelling is most likely due to which of the following processes?
- A. Excessive protease activity
- B. Damage to kidney tubules
- C. Hyperplasia of mucous glands
- D. Defective protein folding
- E. Right ventricular dysfunction secondary to pulmonary hypertension (Correct Answer)
Chronic heart failure management Explanation: ***Right ventricular dysfunction secondary to pulmonary hypertension***
- This patient's long history of smoking, chronic cough, and wheezing suggest significant **chronic obstructive pulmonary disease (COPD)**, which leads to **hypoxemia** and **pulmonary hypertension**.
- **Pulmonary hypertension** increases the workload on the **right ventricle**, eventually leading to **right heart failure** (cor pulmonale), characterized by peripheral edema (leg swelling) and ascites (abdominal swelling).
*Excessive protease activity*
- While excessive protease activity (e.g., elastase) is implicated in the pathogenesis of **emphysema** by destroying alveolar walls, it does not directly cause peripheral edema and ascites.
- This process primarily leads to **airflow obstruction** and **gas exchange abnormalities**, which can indirectly contribute to pulmonary hypertension but is not the direct cause of the peripheral edema.
*Damage to kidney tubules*
- **Acute tubular necrosis** or chronic kidney disease can cause edema due to impaired fluid and electrolyte balance, but the patient's symptoms (dyspnea, wheezing, smoking history) point strongly to a primary pulmonary and cardiac etiology.
- While diabetes can cause nephropathy, there is no information to suggest acute kidney injury or chronic kidney disease leading to such severe edema.
*Hyperplasia of mucous glands*
- **Hyperplasia of mucous glands** in the bronchi is characteristic of **chronic bronchitis**, contributing to the chronic cough and airway obstruction.
- This pathology primarily affects airway clearance and airflow, rather than directly causing systemic edema or ascites.
*Defective protein folding*
- **Defective protein folding**, such as in **alpha-1 antitrypsin deficiency**, can lead to early-onset emphysema and liver disease.
- While this could fit with a pulmonary presentation, it is less common than smoking-induced COPD and does not directly explain the edema and ascites caused by right heart failure.
Chronic heart failure management US Medical PG Question 6: 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
Chronic heart failure management 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.
Chronic heart failure management US Medical PG Question 7: A 36-year-old man with a history of a stab wound to the right upper thigh one year previously presents to the emergency department with complaints of difficulty breathing while lying flat. Physical examination reveals an S3 gallop, hepatomegaly, warm skin and a continuous bruit over the right upper thigh. Which of the following is most likely responsible for his symptoms?
- A. Decreased sympathetic output
- B. Increased pulmonary resistance
- C. Increased peripheral resistance
- D. Decreased contractility
- E. Increased venous return (Correct Answer)
Chronic heart failure management Explanation: ***Increased venous return***
- The combination of **orthopnea**, **S3 gallop**, and **hepatomegaly** indicates **heart failure**. The **continuous bruit** over the historical stab wound points to an **arteriovenous (AV) fistula**.
- An AV fistula causes a substantial volume of blood to bypass the systemic circulation and return rapidly to the right heart, leading to **increased venous return** and subsequently **high-output heart failure**.
*Decreased sympathetic output*
- **Decreased sympathetic output** would typically lead to **vasodilation**, reduced heart rate, and decreased cardiac output, which contradicts the symptoms of **heart failure** observed here.
- Heart failure often involves compensatory **increased sympathetic activity** to maintain cardiac function.
*Increased pulmonary resistance*
- While **increased pulmonary resistance** (as in pulmonary hypertension) can cause right-sided heart failure, it doesn't explain the presence of a **continuous bruit** or the **high-output nature** of the heart failure suggested by the AV fistula.
- Pulmonary resistance would typically reduce venous return to the left side of the heart, not primarily increase early venous return to the right heart like an AV fistula.
*Increased peripheral resistance*
- **Increased peripheral resistance** would make it harder for the heart to pump blood forward (increased afterload) and would not directly cause the **high-output state** seen with an AV fistula.
- The **warm skin** observed in this patient is actually more consistent with **vasodilation** and **low systemic vascular resistance**, common in high-output heart failure.
*Decreased contractility*
- **Decreased contractility** (systolic dysfunction) is a common cause of heart failure, but in the context of an **AV fistula**, the primary issue is the **excessive volume load** on the heart, leading to high-output failure, rather than intrinsic myocardial weakness.
- The heart initially attempts to compensate for the increased preload, but eventually fails due to the sustained high volume.
Chronic heart failure management 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
Chronic heart failure management 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.
Chronic heart failure management 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
Chronic heart failure management 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.
Chronic heart failure management US Medical PG Question 10: A 65-year-old male with multiple comorbidities presents to your office complaining of difficulty falling asleep. Specifically, he says he has been having trouble breathing while lying flat very shortly after going to bed. He notes it only gets better when he adds several pillows, but that sitting up straight is an uncomfortable position for him in which to fall asleep. What is the most likely etiology of this man's sleeping troubles?
- A. Left-sided heart failure (Correct Answer)
- B. Amyotrophic lateral sclerosis (ALS)
- C. Obstructive sleep apnea
- D. Right-sided heart failure
- E. Myasthenia gravis
Chronic heart failure management Explanation: ***Left-sided heart failure***
- The patient's inability to breathe while lying flat (orthopnea) and the relief obtained by elevating his head with pillows is a classic symptom of **left-sided heart failure**.
- In this condition, accumulation of fluid in the lungs (pulmonary congestion) due to the heart's inability to pump blood effectively leads to difficulty breathing, especially in the recumbent position.
*Amyotrophic lateral sclerosis (ALS)*
- ALS primarily affects **motor neurons**, leading to progressive muscle weakness, atrophy, and spasticity.
- While it can eventually cause respiratory muscle weakness, it typically presents with more generalized motor symptoms and does not specifically manifest as acute orthopnea relieved by elevating the head of the bed shortly after lying down.
*Obstructive sleep apnea*
- Obstructive sleep apnea is characterized by recurrent upper airway collapse during sleep, leading to **pauses in breathing** and loud snoring.
- While it can cause fragmented sleep and daytime sleepiness, the primary relief is not typically from simply adding pillows but rather from CPAP therapy or surgical interventions to open the airway.
*Right-sided heart failure*
- Right-sided heart failure primarily leads to **systemic venous congestion**, causing symptoms like peripheral edema, ascites, and jugular venous distension.
- It does not typically cause orthopnea as a primary symptom, as pulmonary congestion is not the predominant feature.
*Myasthenia gravis*
- Myasthenia gravis is an **autoimmune disorder** characterized by fluctuating weakness of voluntary muscles, which worsens with activity and improves with rest.
- While it can affect respiratory muscles in severe cases, leading to respiratory compromise, the symptom presentation is more varied than isolated orthopnea, and it does not typically manifest acutely only when lying flat to sleep.
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