Cardiogenic Pulmonary Edema


Article Author:
Muhammad Areeb Iqbal


Article Editor:
Mohit Gupta


Editors In Chief:
Kranthi Sitammagari
Mayank Singhal


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Trevor Nezwek
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes


Updated:
7/9/2019 2:38:09 PM

Introduction

Edema refers to excessive fluid accumulation in the interstitial spaces, beneath the skin or within the body cavities caused by any of the following and producing significant signs and symptoms.[1] 

  • An imbalance among the "Starling forces" 
  • Damage/blockage of the draining lymphatic system

The affected body part usually swells if edema is present beneath the skin or produces significant signs and symptoms related to the body cavity involved.

There are several different types of edema, and few important are the peripheral edema, pulmonary edema, cerebral edema, macular edema, and lymphedema. The atypical forms are the idiopathic edema and hereditary angioneurotic edema.

Pulmonary edema refers to the accumulation of excessive fluid in the alveolar walls and alveolar spaces of the lungs. It can be a very life-threatening condition in some patients.[2] Pulmonary edema can be:

  • Cardiogenic (disturbed starling forces involving the pulmonary vasculature and interstitium)
  • Non-Cardiogenic (direct injury/damage to lung parenchyma/vasculature)

Etiology

All the factors which contribute to increased pressure in the left side and pooling of blood on the left side of the heart can cause cardiogenic pulmonary edema.[3] The result of all these conditions will be increased pressure on the left side of the heart: increased pulmonary venous pressure--> increased capillary pressure in lungs--> pulmonary edema.[4]

  • Coronary artery disease with left ventricular failure (myocardial infarction)
  • Congestive heart failure
  • Cardiomyopathy
  • Valvular heart diseases on the left side of the heart (stenosis and regurgitation)
  • Cardiac arrhythmias

Epidemiology

Pulmonary edema is a life-threatening condition with an estimated 75000 to 83000 cases per 100000 persons having heart failure and low ejection fraction. A trial showed an alarming 80% prevalence of pulmonary edema in patients with heart failure.[5] It is a troublesome condition with the rate of discharge being 74% and the rate of survival after one year of 50%.[6]. The mortality rate at six years follow up was 85% with patients of congestive heart failure. Males are typically affected more than females, and the elderly are at a higher risk for developing pulmonary edema.[7]

Pathophysiology

Cardiogenic form of pulmonary edema (pressure induced) produces a non-inflammatory type of edema by the disturbance in Starling forces. The pulmonary capillary pressure is 10mm Hg (range: 6 to 13) in normal conditions, but any factor which increases this pressure can cause pulmonary edema.[8] The alveoli are normally kept dry because of the negative pressure in extra-alveolar interstitial spaces, but when there is[9]:

Increased pressure/pooling--> Increased pulmonary venous pressure--> Increased pulmonary capillary pressure--> fluid in interstitial spaces--> Increased pressure in Interstitial spaces--> fluid in alveoli (pulmonary edema).

Pulmonary capillary wedge pressure can be measured, graded, and will produce different presentations on X-rays.

Histopathology

The main features seen on microscopy are[10]:

  • Alveolar wall thickening
  • Dilated capillaries and interstitial edema
  • Transudation in the alveolar lumen (granular and pale eosinophilic)

History and Physical

Patients usually present with shortness of breath, which may be acute in onset (from minutes to hours) or gradual in onset occurring over hours to days, depending upon the etiology of pulmonary edema.

Acute pulmonary edema will have[11]:

  • Excessive shortness of breath worsening on exertion or lying down
  • A feeling of the sinking of heart and drowning/anxiety worsening on lying down
  • Gasping for breath
  • Blueness of lips
  • Dizziness and excessive sweating
  • A cough may be associated with worsening edema
  • Blood tinged/pink colored frothy sputum in very severe disease
  • Chest pain (myocardial infarction and aortic dissection)
  • Cold, clammy skin

Chronic pulmonary edema will have:

  • Shortness of breath on exertion
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
  • Swelling of the body/lower extremities
  • Weight gain
  • Fatigue

Ortner syndrome, which refers to hoarseness due to compression of recurrent laryngeal nerve because of an enlarged left atrium, may also be occasionally present in some patients.

Physical Examination

On examination, the positive findings include:

  • General appearance

Confusion, agitation, and irritability may be present, associated with excessive sweating, cold extremities, and upright posture (sitting upright).

  • JVP/JVD      

Usually raised.

  • Blood Pressure

Hypertension is more often present, but if hypotension prevails, it is an indicator of severe left ventricular systolic dysfunction, and cardiogenic shock must be ruled out. Cold extremities are a feature of low perfusion and shock.

  • Respiratory Rate

Tachypnea usually present.

  • Pulse

Tachycardia (increased heart/ pulse rate) and associated finding of the cause in the pulse.

  • Pedal Edema

Usually co-exists with pulmonary edema in chronic heart failure.

  • Respiratory Findings

Dyspnea and tachypnea are usually present, may be associated with the use of accessory muscles of respiration. Fine crackles are usually heard at the bases of lungs bilaterally, and progress apically as the edema worsens. Ronchi and wheeze may also be presenting signs. 

  • Cardiovascular Findings      
    • Tachycardia and hypotension may be present along with jugular venous distention. Auscultation of the heart helps to differentiate between the various causes of valvular lesions causing pulmonary edema.
    • Auscultation typically reveals an S3 gallop in volume overload states, which may be associated with accentuation of the pulmonic component of S2.
    • Several different types of murmurs can be heard depending upon the cause of the valvular lesion.
    • Mitral stenosis produces a low pitched, rumbling diastolic murmur associated with an opening snap at the apex which accentuates on expiration and produces loud S1.
    • Mitral regurgitation produces a blowing, high pitched pan-systolic murmur best heard at the apex, radiating to left axilla and accentuating on expiration, produces soft S1.
    • Aortic stenosis produces a harsh crescendo-decrescendo ejection systolic murmur at the aortic area, increasing on expiration usually radiating towards R side of the neck.
    • Aortic regurgitation produces a high pitched blowing early diastolic murmur best heard during expiration heard of the aortic area.
  • Gastrointestinal System

Tender hepatomegaly may be a feature in case of right-sided cardiac failure, which may worsen to hepatic fibrosis and hepatic cirrhosis in chronic congestion. Ascites may sometimes be present.

Evaluation

No single definitive test is available for diagnosing pulmonary edema but clinically one proceeds from simple to the more complex tests while searching for the diagnosis and the associated etiology.

        Blood Tests[12]

  • CBC (to rule out anemia and sepsis)
  • Serum electrolytes (patients on diuretic therapy may have disturbances )
  • Pulse oximetry and ABGs (assessing hypoxia and oxygen saturation)
  • BNP (brain natriuretic peptide levels: low levels rule out cardiogenic type )

       ECG 

Used to rule out ischemic changes and rhythm abnormalities.

       Radiologic Investigations[13]

Chest X-ray (It is one of the most important investigations required for the evaluation of pulmonary edema and overload states.

Early Stage

  • In the early stages, cardiomegaly is present, usually identified as an increase of cardiothoracic ratio over 50%.
  • Broad vascular pedicle
  • Vascular redistribution
  • Cephalization

 Intermediate Stage

  • Interstitial edema
  • Kerley B lines
  • Peribronchial cuffing
  • Thickened interlobar fissure    

 Late Stage

  • Alveolar edema
  • Perihilar Bat wing appearance
  • Pleural effusion 

Ultrasonography

Ultrasonography may be helpful in further strengthening of diagnosis. Transthoracic ultrasound usually differentiates COPD from CCF as a cause of acute exacerbation of chronic dyspnea.

Echocardiography[14]

Extremely important in determining the etiology of cardiogenic pulmonary edema. It differentiates systolic from diastolic dysfunction and valvular lesions.

  • Cardiac tamponade
  • Acute papillary muscle rupture
  • Acute ventricular septal defect
  • Valvular lesions

Invasive Technique

Pulmonary Arterial Catheter

A Swan-Ganz catheter is inserted into the peripheral vein and advanced further till branch of the pulmonary artery is reached, and then the pulmonary capillary wedge pressure is measured.

Treatment / Management

General Management[15]

ABC must be addressed initially as the patient arrives.

  • Airway assessment ( Make sure the airway is clear for adequate oxygenation and ventilation)
  • Breathing ( Note the pattern of breathing and oxygen saturation.)
  • Circulation ( Vital sign and cardiac assessment and management )
  • Oxygen delivery and ventilatory support (Through nasal cannula, face mask, non-rebreather mask, noninvasive pressure support ventilation, and mechanical ventilation as required)
  • Prop up
  • Intra-venous access
  • Urine output monitoring

After initial airway clearance, oxygenation assessment, and maintenance, management mainly depends upon presentation and should be tailored from patient to patient. Supplemental oxygen is a requirement if the patient is at risk of hypoxemia (SPO2 less than 90% ). Unnecessary oxygen should not be administered as it causes vasoconstriction and reduction in cardiac output. Supplemental oxygen if necessary should be given in the following order:

Nasal cannula and face mask ---> Non-rebreather mask ---> Trial of non-invasive ventilation (NIV) ---> Intubation and mechanical ventilation

If the respiratory distress and hypoxemia continue on oxygen supplementation, a trial of non-invasive ventilation should follow if there are no contraindications of NIV, as evidence suggests that it lowers the need for intubation and improves respiratory parameters. If the patient does not improve or have contra-indications to NIV, then intubation and mechanical ventilation (with high positive end-expiratory pressure) should be considered.

Specific Management[16][17]

  • Treatment of the underlying cause.
  • Non Invasive Management
  • Invasive Management

Non-Invasive Management[18] can be achieved by:

  • Pre-Load Reduction which can be achieved by:
  1. Nitroglycerin
  2. Sodium nitroprusside
  3. Isosorbide dinitrate
  4. Loop diuretics (furosemide, torsemide, bumetanide) 
  5. Morphine and nesiritide require extreme care.
  6. BIPAP can help move the fluid out of the lungs by increasing the intrapulmonary pressure

After initial resuscitation and management, the mainstay of treatment in acute settings is diuresis with or without vasodilatory therapy. The aggressiveness of treatment depends upon the initial presentation, hemodynamic, and volume status of the patient. VTE prophylaxis is generally indicated in patients admitted with acute heart failure. Sodium restriction is also necessary for patients with HF.

Patients presenting with acute decompensated heart failure (ADHF) with features of pulmonary edema should be treated with intravenous diuretics initially, regardless of the etiology. Patients with HF and features of pulmonary edema receiving treatment with early administration of diuretics had better outcomes according to guidelines of the American College of Cardiology Foundation/ American Heart Association Task Force.[19] A prospective observational study suggested that early treatment with furosemide in patients with AHF lowers the in-hospital mortality, and the mortality increased with delay in the time of administration.[20] Diuretic therapy for patients who have not received diuretics previously is as follows:

If renal function is adequate:                                    

  • Furosemide: 20 to 40 mg IV                     
  • Torsemide: 10 to 20 mg IV 
  • Bumetanide: 1 mg IV

If renal function is deranged/severe HF:

  • Furosemide: up to 160 to 200 mg IV bolus, or can be given as 5 to 10mg/hr drip.
  • Torsemide: up to 100 to 200 mg IV bolus
  • Bumetanide: 4 to 8 mg IV bolus

If the patient shows normal renal function, and there is very little/no response to initial treatment, the dose of diuretics should be doubled at 2-hour intervals until achieving the maximum recommended.

The patients who are on chronic diuretic therapy should receive higher doses of diuretics in acute settings. The initial dose for such patients should be greater than two times of daily maintenance dose. A continuous infusion can also be used as an alternative to bolus therapy if the patient responds to the bolus dose. 

While being managed in hospital for pulmonary edema IV diuresis can be used using loop diuretics. Furosemide is the usual drug of choice. While diuresis, one should monitor the following:

  1. Daily weight
  2. Strict intake and output measures
  3. Telemetry
  4. A basic metabolic panel including kidney functions and electrolytes
  5. Keep serum potassium above 4.0 mEq/L and Mg over 2.0 mEq/L.
  6. Continuous pulse ox if indicated 
  7. Renal functions   

In addition to diuretic therapy, vasodilator therapy may be necessary  Indications include:

  1. Urgent afterload reduction ( severe hypertension )
  2. Adjunct to diuretics when the patient doesn't respond to diuretic therapy alone
  3. For patients with refractory heart failure and decreased cardiac output

Vasodilator therapy has to be used with great caution since it can cause symptomatic hypotension, and the evidence of its efficacy and safety is very limited. When they are needed, they should be used with great caution while monitoring hemodynamic response under expert opinion.

Nitrates (Nitroglycerin and isosorbide dinitrate) cause greater venodilation than arterio-dilation and can be used intravenously in recommended doses. Nitroglycerin can be used at 5 to 10 mcg/min initially and can be increased gradually to the maximum recommended dose (200 mcg/min) while closely monitoring the hemodynamic responses. Isosorbide dinitrate has a much longer half-life than nitroglycerin, which puts it at a disadvantage if the drug requires discontinuation because of the symptomatic hypotension.

Sodium nitroprusside causes both venous and arterio-dilation and can significantly lower the blood pressure. It requires close hemodynamic monitoring through an intra-arterial catheter. It is used initially in a dose of 5 to 10 mcg/min, which can be titrated up to 400mcg/min, which is the maximum recommended dose. At higher doses, it increases the risk of cyanide toxicity. Hence it has to be used with extreme caution and with close monitoring under expert supervision.

Nesiritide should not routinely be a therapeutic option for the treatment of HF. A large randomized trial fusing nesiritide in patients of acutely decompensated heart failure (ADHF)  shows that it was not associated with any change in the rate of death or rehospitalization, increased risk of hypotension and a small non-significant change in dyspnea.[21]  Nesiritide, if used, should be used initially as an intravenous bolus of 2mcg/kg and afterward a continuous infusion 0.01mcg/kg.

Salt and water restriction is generally indicated for patients with HF.

Vasopressor receptor antagonist (tolvaptan) can also be used with caution and under supervision.

  • After-Load Reduction which can be achieved by:
  1. ACE inhibitors or angiotensin receptor-neprilysin inhibitor (ARNI):  captopril, enalapril, lisinopril, perindopril, etc.
  2. ARBs (angiotensin receptor blockers): valsartan, telmisartan, olmesartan, candesartan, etc.
  3. Sodium nitroprusside

ACE inhibitors or ARNI is the mainstay of chronic treatment for patients with HFrEF. If the patient doesn't tolerate ACE-inhibitors or ARNI, then ARB should be considered the first line choice for prolonged treatment. Beta blockers and mineralocorticoid receptor antagonists require extra care if used. 

If blood pressure is low, start ionotropic agents, and vasopressors (catecholamines and phosphodiesterase inhibitors) should commence. The treatment for heart failure with reduced ejection fraction (HFrEF) differs from heart failure with preserved ejection fraction. (HFpEF).

For patients of HFrEF presenting with hypotension, intense hemodynamic monitoring is necessary. The patient should undergo evaluation for signs of shock (confusion, cold extremities, decreased urine output, etc.). If the patient of HFrEF has signs of hypotension and/or blood pressure less than 80mmg, Ionotropes should be added immediately and titrated accordingly. For patients of persistent shock, vasopressors also have to be added. 

For the patients of HFpEF, only vasopressors are necessary. Inotropes are NOT indicated in patients with HFpEF and dynamic left ventricular obstruction (most commonly hypertrophic obstructive cardiomyopathy). 

Invasive Management[14]

  • IABP (intra-aortic balloon pump)
  • Ultrafiltration
  • Ventricular assist devices
  • ECMO (extracorporeal membrane oxygenation) 
  • Cardiac transplant
  • Valve replacement (in case of valvular issues)
  • PCI (percutaneous coronary intervention)
  • CABG (coronary artery bypass graft)
  • Intubation (if required to maintain the airway and also helps in moving the fluid out)

In a patient of severe HFrEF with acute hemodynamic compromise and cardiogenic shock, mechanical cardiac support is available while waiting on a decision or waiting on recovery hence called " bridge to the decision and "bridge to recovery." The patients usually have blood pressure less than 90mmHg, PCWP greater than 18mmHg, and a cardiac index of less than 2L/min per meter square. 

IABP (intra-aortic balloon pump) is the device which is used most commonly among the mechanical circulatory devices as it is least expensive, easily insertable, and readily available. It consists of a balloon in the aorta that inflates and deflates synchronously with the heartbeat causing increased cardiac output and coronary flow. IABPs are used commonly for temporary circulatory support with patients of advanced heart failure while waiting for a heart transplant or VADs. It is not a definitive therapy but is widely used as a bridge therapy for patients with cardiogenic shock and also as an adjunct to thrombolysis in acute myocardial infarction for stabilization.

Ventricular assist devices as compared to IABP have greater efficacy in increasing the hemodynamic parameters. These have more complications and require more expertise, take longer to insert and cost more in comparison. They are an option in acute decompensated heart failure. They can also be useful in complications of acute heart failure like cardiogenic shock, mitral regurgitation, and VSDs. They can be different kinds like left ventricle to the aorta, left atrium to the aorta, right ventricular assist device, etc. 

Ultrafiltration (UF) is the most effective approach for sodium, and water removal effectively improves hemodynamics in patients of heart failure. UF is the process of abstracting plasma water from the whole blood across a hemofilter because of the transmembrane pressure gradient. It is preferred over diuretics because it removes sodium and water more effectively and does not stimulate the neurohormonal activation through macula densa. UF is used in patients with HF as it decreases PCWP, restores diuresis, reduces diuretic requirements, corrects hyponatremia, improves cardiac output, and thus improves congestion.[22]  In some patients of heart failure, UF was associated with improved cardiac index and oxygenation capacity, decreased PCWP, and less need for inotropes.[23] Several types of UF are isolated, intermittent, and continuous. The continuous type can work in an arterio-venous or veno-venous mode, which is the most common type.

UF can be crucial in patients with heart failure and resistance to diuretic therapy and can serve to optimize the volume status. Many questions regarding UF require examination in further studies, and the evidence does not support its widespread use as a substitute for diuretics.[24]

Differential Diagnosis

Differential Diagnosis includes[25]:

  • Respiratory failure
  • Myocardial ischemia/infarct
  • Pulmonary embolism
  • Neurogenic pulmonary edema
  • High altitude pulmonary edema
  • Acute respiratory distress syndrome

Prognosis

Prognosis mainly depends on the underlying cause but generally has a poor prognosis. Cardiogenic pulmonary edema is an alarming condition with the rate of discharge being 74% and the rate of survival after one year of 50%.[6] The mortality rate at 6 years follow-up is 85% with patients of congestive heart failure.[7]

Complications

Most complications of pulmonary edema arise from the complications of the underlying cause. Common complications associated with cardiogenic etiologies include:

  • Risk of arrhythmias (atrial fibrillation, ventricular fibrillation, ventricular tachycardias)
  • Thromboembolism (pulmonary embolism, DVT, stroke)
  • Pericarditis
  • Rupture
  • Valvular heart disease
  • Cardiogenic shock
  • Tamponade
  • Dressler syndrome
  • Death

Pulmonary edema can cause severe hypoxia and hypoxemia leading to end organ damage and multi-organ failure. Respiratory failure is another common complication of cardiogenic pulmonary edema.

Deterrence and Patient Education

As cardiac events are the prime factors for the development of pulmonary edema, patients are advised to control and prevent the progression of heart disease by :

  • Healthy lifestyle and exercise
  • Smoking cessation
  • Alcohol cessation
  • Weight reduction and monitoring
  • Proper diet control
  • Low cholesterol diet
  • Reducing salt intake
  • Blood pressure control
  • Good glycemic control

Enhancing Healthcare Team Outcomes

Pulmonary edema can be a very life-threatening condition, and specialized consultation is a requirement for diagnosis and management. Considering a very high short term mortality rate, an Interprofessional team approach is recommended in the management of these patients to improve outcomes.

Starting from the diagnosis, etiological factor, and management of the patient, a well-coordinated team needs to work for better patient care involving all the related departments. All the available treatment options need to be discussed to avoid any complications and improving the outcome. The use of non-invasive positive pressure ventilation has a significant benefit in acute cardiogenic pulmonary edema.[26] [Level-2]

While the physician is involved primarily in the management of the patient, consultation is also necessary from a team of specialists involving cardiologist, pulmonologist, and cardiothoracic surgeon. The nurses are also a vital member of the interprofessional group, as they will monitor the patient's vital signs, and communicate back to the team with results. The nurse practitioner, like the primary care provider, follows these patients in an outpatient setting and should try and reduce the risk factors for ischemic heart disease. Patients should be urged to quit smoking, enroll in cardiac rehabilitation, maintain healthy body weight, become physically active, and remain compliant with follow up appointments and medications. A dietary consult should be obtained to educate the patient on a healthy diet and what foods to avoid.

Since most patients with heart failure are no longer able to work, social work assistance is crucial so that the patient can get the much needed medical support.

The role of pharmacist will be to ensure that the patient is on the right medication and dosage. The radiologist can also play a vital role in determining the cause of dyspnea. A mental health nurse should consult with the patient because depression and anxiety are common morbidities, leading to poor quality of life.

As shown above, cardiogenic pulmonary edema requires an interprofessional team approach, including physicians, specialists, specialty-trained nurses, other ancillary therapists (respiratory, social worker), and pharmacists, all collaborating across disciplines to achieve optimal patient results. [Level V]

If the patient is deemed to be a candidate for a ventricular assist device or heart transplant, the transplant nurse should be involved early in the care. With a shortage of organs, one also has to be realistic with patients.

At the moment, the role of morphine and nesiritide remain questionable and requires further evaluation.[27][28]

Outcomes

Unfortunately, despite optimal treatment, the outcomes for cardiogenic pulmonary edema/heart failure are abysmal. There is no cure for this disorder, and the key is to prevent the condition in the first place.


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Cardiogenic Pulmonary Edema - Questions

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A 70-year-old patient with diabetes mellitus and hypertension presents with the complaints of progressive shortness of breath gradually worsening from the last five days associated with pedal swelling and cough. Blood pressure is 140/90 mmHg, pulse 100/min, RR 24/min, and SpO2 88% on room air. Chest auscultation reveals normal S1 and S2 with an added S3 and fine inspiratory crackles at bases. Two plus pedal edema is also present. She is currently on lisinopril, rosuvastatin, and low dose aspirin. Echocardiography shows an ejection fraction of 35% with global hypokinesia. What is the agent of choice for her current condition?



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A 67-year-old female with diabetes mellitus and hypertension presents to with severe shortness of breath from 2 hours which is associated with orthopnea and feeling of the sinking of the heart. She is also having bluish-grey discoloration of fingers. Blood pressure is 80/50 mmHg, pulse 115/min, and respiratory rate 27/min. There is the use of accessory muscles of respiration and SpO2 is 84% on room air which increased to 87% with supplemental oxygen. Chest auscultation reveals fine inspiratory crackles up to mid-chest. There are jugular venous distension and generalized edema. What will be the most appropriate next step in the management of this patient?



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A 75-year-old male with a history of diabetes mellitus, hypertension, and ischemic heart disease presents in an altered state with severe shortness of breath associated with bluish discoloration of fingers and raised jugular venous pressure. The blood pressure is 100/60 mmHg, pulse 100/min, respiratory rate 26/min, SpO2 of 82% on room air which increases to 85% with high flow supplemental oxygen. There are normal S1 and S2 but an added S3 with fine inspiratory crackles till mid zones of the chest. There is 2+ pedal edema. What is the best available management option?



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A 65-year-old male is brought to the emergency department with severe shortness of breath for two hours. Vital signs are blood pressure 180/100 mmHg, heart rate 115 bpm, and respirations 30. Oxygen saturation on room air is 87 percent but increases to 95 percent on 100 percent oxygen by mask. The exam shows S1S2 tachycardic with gallop but no murmurs. The lungs show bilateral rales to midlung. Select the most appropriate initial treatment.



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A 63-year-old male presents with severe shortness of breath and chest pain on inspiration with bluish discoloration of the fingers. On exam, his blood pressure is 100/70 mmHg, pulse 105/min, respiratory rate 26/min, and SpO2 is 81% on room air and 83% on supplemental oxygen. On auscultation, S1 and S2 are normal with no added sounds. Chest auscultation reveals fine inspiratory crepitations. The differentials include cardiogenic edema and acute respiratory distress syndrome. Which of the following differentiates cardiogenic pulmonary edema can be differentiated from acute respiratory distress syndrome?



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A 65-year-old male with a history of smoking, hypertension and heart failure presents in the emergency department with severe shortness of breath from the last two days worsened now from last 1 hour. On presentation, his vitals are BP 160/90 mmHg, pulse 105/min, RR 26/min, afebrile, and Spo2 = 86% at room air, S1, S2, and S3 gallop, raised jugular venous pressure, fine inspiratory crepitations to mid-chest, tender hepatomegaly, and two pulse pedal edema. What will be the next step in the management of this patient?



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A 65-year-old male with known congestive heart failure presents to the emergency department with severe dyspnea for the last two hours that is worsening. On presentation, his BP is 165/95 mmHg, P 115/min, RR 32/min, afebrile, and Spo2 = 86% at room air which increases to 93% with supplemental oxygen. Examination reveals a raised jugular venous pressure with fine inspiratory crackles at the lung bases, tender hepatomegaly, and two plus pedal edema. Pulmonary capillary wedge pressure (PCWP) is between 18 and 25 mmHg. What are the expected x-ray findings?



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A 65-years-old female presents to you in the emergency department with slow onset shortness of breath associated with orthopnea and paroxysmal nocturnal dyspnea. She has a history of hypertension, diabetes, and ischemic heart disease. Her medications include insulin, aspirin, atorvastatin, lisinopril, furosemide, and metformin. On examination she has a blood pressure of 155/85, pulse 115/min, respiratory rate 24/min, temperature 37 C, and SpO2 86% which increased to 93% with 2 L supplemental oxygen. Jugular venous distension is noted, a soft S1 and an S3 gallop associated with a pan-systolic murmur at the mitral area radiating to the axilla are also noted. Fine inspiratory crackles are also heard at the lung bases bilaterally. Which of the following factors is most likely to worsen her current condition?



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A 72-year-old female with a history of diabetes mellitus, hypertension, smoking, and previous myocardial infarction and multivessel disease presents with a history of central chest pain for 1 hour, severe in intensity, associated with nausea, vomiting diaphoresis, shortness of breath, and radiating to left jaw. Vital signs are BP 165/90 mmHg, pulse 127/min, RR 26/min, and afebrile. The chest is clear, and no significant findings on the cardiovascular exam are noted. ECG shows anterolateral myocardial infarction. Thrombolytics were given, and the patient improved. One day later she develops shock with BP 80/60 mmHg, pulse 140/min, RR=32/min, and SpO2=86% on room air. Auscultation of the chest reveals a blowing, high pitched pan-systolic murmur best heard at the apex, radiating to left axilla and accentuating on expiration with soft S1. There are fine inspiratory crackles to the mid-zone of the lungs. What is the initial treatment in this case?



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A 67-year-old female with a history of diabetes mellitus and hypertension presents with worsening shortness of breath for the last ten days, which is exertional and positional. It is increased by lying flat and decreased by propping up or sitting. It is also associated with body swelling of the feet. She is tachycardiac with a heart rate of 110/min, blood pressure of 150/85 mmHg, and respiratory rate of 22/min. She is afebrile with pedal edema and body swelling. Jugular venous pressure is raised, and chest examination reveals normal S1 and S2, but there is an added S3 gallop. Bilateral fine inspiratory crackles are also heard till the mid zones of lungs. Her previous echocardiogram shows an ejection fraction of 35%. Which of the following investigations is the most appropriate to assess this patient's prognosis?



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Cardiogenic Pulmonary Edema - References

References

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