✪✪✪ Pulmonary Oedema Case Study

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Pulmonary Oedema Case Study



Pulmonary Oedema Case Study Rehabil ; 25 : 99 — Anesthesiology Pulmonary Oedema Case Study 97 : — 7. Patient Cases. Pulmonary Oedema Case Study history of Pulmonary Oedema Case Study aspiration, CC-501: A Case Study or preceding infection. Where risk prediction model papers include a Pulmonary Oedema Case Study set Pulmonary Oedema Case Study a validation set, Isaac Asimov Quotes from the validation set have been used. When treatment of PH itself Competitive Advantages Of Mr Price being considered, echocardiography alone is not sufficient to support a treatment Pulmonary Oedema Case Study and cardiac catheterization is required. Consequences of external causes.

Cardiogenic Pulmonary Edema - CRASH! Medical Review Series

Subjects are asymptomatic prior to water immersion and develop symptoms during or after swimming. Low oxygenation saturations can be seen with pulse oximetry and hypoxemia on arterial blood analysis. The degree of desaturation is beyond what can be seen in elite athletes with short capillary transit times. To date, no studies have examined non-invasive estimates of pulmonary arterial pressure or pulmonary vascular resistance among patients with acute SIPE. Given the physiologic changes and blood redistribution that occurs with water immersion, training habits that are routinely used for terrestrial endurance competition, including salt tablet ingestion and pre-race hydration, may augment preload and thus increase the risk of developing SIPE.

A history of systemic or pulmonary hypertension also increases this risk by further increasing pulmonary pressures and, in the case of hypertension, may expose underlying cardiac diastolic dysfunction. Water specific risk factors include cold water temperature and the use of wetsuits, both of which can independently and synergistically augment preload. Four diagnostic criteria for SIPE have been previously proposed: 19 Acute onset of dyspnea or hemoptysis during or immediately after swimming.

Chest radiograph consistent with alveolar filling process or interstitial pulmonary edema that resolves within 48hrs. No history of water aspiration, laryngospasm or preceding infection. At present, there have been no randomized trials of SIPE therapy and thus the evolving standard of care is based on logic and anecdotal experience. The acute treatment of SIPE begins with immediate removal from the water, placing the individual in a warm environment, and removal of a constrictive wetsuit if present. While SIPE can be fatal, the majority of athletes recover and are completely symptom free within 48 hours.

Anecdotally, vasodilators including sildenafil and dihydropyridine calcium channel blockers have been used for the prevention of SIPE with success. The authors of this study suggested that sildenafil-induced reduction in pulmonary vascular pressures during submerged exercise is likely the result of vasodilatation of both pulmonary vessels and peripheral veins. Similar to our experience, there are published case reports in which pre-workout sildenafil can prevent the development of SIPE. Our approach is to counsel athletes on modifiable risk factors including cold-water swimming, wetsuits, salt tablets and pre-race hydration. If the athlete is not hypertensive, we recommend 50mg of sildenafil prior to swims.

If the patient is hypertensive, we adjust the blood pressure regimen to include a daily dihydropyridine calcium channel blocker. Neither of these medications are prohibited by the World Anti-Doping Agency. Our athlete underwent an echocardiogram and maximal effort cardiopulmonary exercise test to confirm that progression of valvular disease and new-onset obstructive coronary artery disease were not responsible for her symptoms. She was advised to avoid salt tablets and overhydration and was started on sildenafil prior to cold-water swims and races. Since initiating targeted sildenafil prophylactic therapy, she has not had recurrence of symptoms and has routinely secured successful podium finishes in numerous races. Case Presentation A year-old triathlete with a history of repaired coarctation of the aorta, bicuspid aortic valve and mild central mitral regurgitation with normal valve morphology presented with recurrent episodes of cough, chest tightness and wheezing when swimming in cold water.

Swimming-Induced Pulmonary Edema While swimming, running and cycling, the fundamental elements of the modern triathlon, are all endurance sporting disciplines, swimming may present some unique cardiopulmonary physiologic challenges. Symptoms Subjects are asymptomatic prior to water immersion and develop symptoms during or after swimming. Risk Factors Given the physiologic changes and blood redistribution that occurs with water immersion, training habits that are routinely used for terrestrial endurance competition, including salt tablet ingestion and pre-race hydration, may augment preload and thus increase the risk of developing SIPE.

Diagnosis Four diagnostic criteria for SIPE have been previously proposed: 19 Acute onset of dyspnea or hemoptysis during or immediately after swimming. Treatment At present, there have been no randomized trials of SIPE therapy and thus the evolving standard of care is based on logic and anecdotal experience. Case Follow-Up Our athlete underwent an echocardiogram and maximal effort cardiopulmonary exercise test to confirm that progression of valvular disease and new-onset obstructive coronary artery disease were not responsible for her symptoms.

References Epstein M. Renal effects of head-out water immersion in man: implications for an understanding of volume homeostasis. Physiol Rev ; Hemodynamic changes in man during immersion with the head above water. Aerosp Med ; Swimming and the heart. Int J Cardiol ; Human physiological responses to immersion into water of different temperatures. Eur J Appl Physiol ; Cardiovascular regulation during water immersion. Appl Human Sci ; Effects of head and body cooling on hemodynamics during immersed prone exercise at 1 ATA. J Appl Physiol ; Muhammad Areeb Iqbal ; Mohit Gupta.

Pulmonary edema refers to the accumulation of excessive fluid in the alveolar walls and alveolar spaces of the lungs. It can be a life-threatening condition in some patients with high mortality and requires immediate assessment and management. This activity reviews the pathophysiology, clinical presentation, evaluation, and management of cardiogenic pulmonary edema and highlights the role of interprofessional team members in collaborating to provide well-coordinated care and enhance patient outcomes. Objectives: Describe the etiology and pathophysiology of cardiogenic pulmonary edema. Summarize the clinical findings and differential diagnosis of cardiogenic pulmonary edema. Review the management and complications of cardiogenic pulmonary edema. Explain the role of Interprofessional team to improve the delivery and outcome of the management provided for better outcomes in patients with cardiogenic pulmonary edema.

Access free multiple choice questions on this topic. 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. 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. It can be a life-threatening condition in some patients. 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. Pulmonary edema is a life-threatening condition with an estimated to cases per persons having heart failure and low ejection fraction.

Males are typically affected more than females, and the elderly are at a higher risk for developing pulmonary edema. 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. Pulmonary capillary wedge pressure can be measured, graded, and will produce different presentations on X-rays.

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. 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. Confusion, agitation, and irritability may be present, associated with excessive sweating, cold extremities, and upright posture sitting upright , cyanosis of the lips. 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. 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. Tender hepatomegaly may be a feature in cases of right-sided cardiac failure, which may worsen to hepatic fibrosis and hepatic cirrhosis in chronic congestion.

Ascites may sometimes be present. 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. Chest X-ray It is one of the most important investigations required for the evaluation of pulmonary edema and overload states. Ultrasonography may be helpful in further strengthening of diagnosis. Extremely important in determining the etiology of cardiogenic pulmonary edema. It differentiates systolic from diastolic dysfunction and valvular lesions. A Swan-Ganz catheter is inserted into the peripheral vein and advanced further till the branch of the pulmonary artery is reached, and then the pulmonary capillary wedge pressure is measured.

After initial airway clearance, oxygenation assessment, and maintenance, management mainly depends upon presentation and should be tailored from patient to patient. 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:. 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 contraindications to NIV, then intubation and mechanical ventilation with high positive end-expiratory pressure should be considered. Specific Management [16] [17]. Non-Invasive Management [18] can be achieved by:. 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. If renal function is adequate:. 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:. In addition to diuretic therapy, vasodilator therapy may be necessary Indications include:. 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.

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. 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. 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.

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. 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. 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.

IABP intra-aortic balloon pump is the device that 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. 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. Prognosis mainly depends on the underlying cause but generally has a poor prognosis.

Most complications of pulmonary edema arise from the complications of the underlying cause. Common complications associated with cardiogenic etiologies include:. 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. 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:. 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. While the physician is involved primarily in the management of the patient, consultation is also necessary from a team of specialists involving cardiologists, pulmonologists, and cardiothoracic surgeons. 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 pharmacists 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.

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. There is no cure for this disorder, and the key is to prevent the condition in the first place. Kerley lines in Congestive heart failure. Image courtesy of S bhimji MD. This book is distributed under the terms of the Creative Commons Attribution 4.

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