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Send Home Our method Usage examples Index Contact StatisticsWe do not evaluate or guarantee the accuracy of any content in this site. Amiodarone is an antiarrhythmic drug which is commonly used to treat ventricular and supraventricular arrhythmias, in particular following pulmonary and cardiac surgery, due to a higher incidence of postoperative atrial fibrillation in these patients. Cytotoxicity- a direct toxic injury to lung cells: Amiodarone may induce the production of toxic O2 radicals, which can directly damage cells.
Micrograph of hyaline membranes, as seen in diffuse alveolar damage (DAD), the histologic correlate of adult respiratory distress syndrome (ARDS). Histopathological image of pulmonary fibrosis representing chronic interstitial pneumonitis.
Some individuals were noted to develop pulmonary fibrosis after a week of treatment, while others did not develop it after years of continuous use. Typically, patients who have been on amiodarone for months or even several years develop progressive dyspnea, nonproductive cough, malaise, fever, and occasionally pleuritic chest pain.[19][2][20] However, clinicians evaluating patients with possible amiodarone-induced pulmonary toxicity must obtain a thorough drug exposure history, maintain a high index of suspicion, and use a systematic diagnostic approach to make the correct and firm diagnosis.
Use the alternative medications and procedures to treat supraventricular arrhythmias and the implantable cardioverter-defibrillator for potentially life-threatening ventricular arrhythmias. Patients who are to begin amiodarone therapy should be informed about potential adverse effects and told to report any new respiratory symptoms promptly. It is an iodine-containing compound that tends to accumulate in several organs, including the lungs.
Patients on higher doses and one who have been taking the drug for a long period of time appear to have a higher risk, and some evidence suggests that individuals with underlying lung disease are also more likely to develop toxicity with amiodarone. Common practice is to avoid the drug if possible in individuals with decreased lung function. These symptoms are easy to mistaken for heart disease or the effects of aging, as many patients taking amiodarone have a history of heart disease.
Symptoms can persist or worsen despite drug withdrawal as elimination half-life averages 40-55 days. Unexplained pulmonary conditions for which no other likely cause can be identified should be judged as probable amiodarone lung toxicity. The only strategy that appears to be efficacious is that of using the smallest dose possible for any particular patient. They should have an initial chest x-ray and pulmonary function test, including a DLCO for the baseline reference points. Any new pulmonary symptom in patient taking amiodarone should raise the suspicion of toxicity. Sometimes, however, pulmonary edema is observed in swimmers and divers when no underlying medical cause is apparent. Most individuals administered amiodarone on a chronic basis will experience at least one side effect. This condition, immersion pulmonary edema (IPE), presents as a rapid onset of shortness of breath, cough and sometimes blood-tinged, frothy sputum. Because the fluid builds up in the air-containing spaces of the lungs and interrupts gas exchange, IPE resembles drowning.


The important difference is that the obstructing fluid comes from within the body rather than from inhalation of surrounding water.The DAN Medical Information department receives a few calls each month in which divers report symptoms suggestive of IPE. Anyone who experiences sudden shortness of breath or persistent cough while diving should abort the dive in as safe a manner as possible and breathe 100 percent oxygen on the surface. It was originally described in cold-water diving and called "cold-induced pulmonary edema." However, it has now been reported in warm-water diving as well. An absence of chest pain helps differentiate IPE from pulmonary decompression sickness ("chokes").
The exact mechanism is not known, but it is thought to be due to a combination of the increased hydrostatic pressure in the pulmonary capillaries that occurs with immersion in water and the presence of a gradient between the hydrostatic pressure at mouth level and at chest level when a diver is upright. Additionally, diving causes increased negative pressure in the alveoli due to denser breathing gas and when using a poorly tuned regulator.Immersion in water causes a number of physiologic effects including a rapid distribution of blood from the legs to the thorax, which can increase blood volume in the thorax by up to 700 ml.
This additional blood causes an increase in pressure in the right atrium by 16-18 mm Hg, a 30-percent increase in cardiac output and a slight increase in blood pressure. Divers with conditions such as hypertension or underlying cardiovascular disease, especially those with weakened heart muscle function, are less able to tolerate these physiologic changes and are thus more prone to pulmonary edema.
No large studies have been performed, but review of the medical literature shows several small case studies of patients with IPE. In some cases, the diver relates a tight-breathing regulator, and in others no evident stress or equipment problems are noted. Reduced diastolic relaxation (usually a result of long-standing hypertension) can lead to increased venous pressure in the lungs — the usual cause of pulmonary edema from cardiac problems. Measurements of both systolic and diastolic heart function can be readily obtained from an echocardiogram. One theory suggests that prolonged immersion in cold water causes peripheral blood vessels to constrict and shunt blood to the heart and central circulation, which then leads to fluid leaking into the lungs. However, one would think that otherwise healthy individuals should be able to compensate for this fluid shift. Another theory, similar to the first, is that hydrostatic pressure from the water causes blood to be shunted to the core.
Yet again, one would think this volume would not be enough to overwhelm a young, healthy circulatory system. None of these theories explains why IPE may occur in an individual during a particular dive while other divers diving the same profile and wearing the same thermal protection remain unaffected.Yet another theory suggests IPE is the result of respiratory mechanics. This idea is that a strong, forced inhalation against resistance (essentially overbreathing a snorkel or regulator) may cause the lungs to respond by leaking fluid out of the capillaries and into the alveoli (pulmonary edema). This may explain why young, healthy swimmers with strong lungs may develop IPE especially during particularly strenuous swims. In other words, some individuals may have the potential to develop IPE under certain conditions, yet others may never develop IPE even under the same stress. Though there may be a genetic predisposition, I have seen and treated cases of IPE and then returned the diver to full duty with no recurrence. The diver went on to complete identical dive profiles, wearing the same thermal protection and breathing the same regulator, but never again developed IPE.


In triathletes who develop IPE, excess hydration and rapid onset of extreme exercise while immersed should be avoided. Divers are advised to ensure normal regulator function and not to use regulators that allow breathing resistance to be increased. After an episode of IPE, there is often spontaneous recovery once the diver leaves the water. Whether or not a diver should return to diving after an episode of IPE should be determined on a case-by-case basis.
The decision should be based on the physical condition of the diver, a history of hypertension or cardiovascular disease and the type of diving being considered.
This person should be counseled that futures dives should be aborted if they again develop signs of IPE. Again, I have treated many cases and subsequently returned these divers to full duty without recurrence. A person who has known or potential cardiac disease (hypertension, advanced age, diabetes) and develops IPE is a different matter.
These people should have further cardiac evaluation prior to diving to make sure they do not have heart valve problems or underlying blockages in their coronary arteries.
A person who experiences recurrent episodes of IPE should probably refrain from diving again in the future. What do we not understand about IPE — in what ways is it still a mystery?Bove: The mechanisms of IPE are not well understood.
The phenomenon of negative-pressure pulmonary edema is well known in anesthesia and likely contributes to IPE in divers.
The development of pulmonary edema in swimmers is better understood and has a model in the well-known pulmonary edema problem found in highly motivated racehorses.
Until we better understand the mechanism of the disorder and who is predisposed to it, it is difficult to make recommendations to divers as to how to avoid it or when to return to diving after an episode.Witucki: The cause! We do not know what causes IPE nor can we currently predict which people are at increased risk of developing this condition. We know the disease involves fluid leaking out of pulmonary capillaries and into the alveoli.
He is board certified in cardiology, internal medicine, and undersea and hyperbaric medicine.
Richard Moon of the Duke Center for Hyperbaric Medicine and Environmental Physiology, in collaboration with DAN, is currently conducting research on IPE. The goal of the study is to identify susceptible individuals and develop methods to prevent the condition.
DNA samples from participants who have experienced IPE will be compared with samples from those who have not, and the effects of cold-water immersion on blood pressure, cardiac output and pulmonary artery pressures will be compared between the two groups.



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