The term Flash Pulmonary Edema reflects a common misconception. This is a cardiovascular illness not a pulmonary illness. It appears in the acute setting much like a respiratory or pulmonary illness and most providers in the pre-hospital and even emergency department setting take it to be. This is understandable and it fools just about everybody. There is a lot of information that will only be available later but the initial providers must do the best they can with the limited information in a difficult situation. The moniker of flash pulmonary edema comes from the mistaken impression of the initial providers both in the pre-hospital setting and the emergency department. When additional information becomes available and a better understanding is possible the moniker still remains. This is however a cardiovascular disease not a pulmonary disease as the name suggests.
The usual situation is the sudden development of severe respiratory distress in someone who has long standing hypertension. The patient arrives by ambulance in the emergency department with severe shortness of breath and breathing rapidly. The blood pressure is greatly elevated. This is not thought to be important because the common wisdom is that elevated blood pressure does not cause shortness of breath. It does not, but it is a clue to greatly elevated peripheral vascular resistance which can and does. Blood pressure and peripheral resistance are not the same. Most clinicians believe that because blood pressure is elevated then flow must be good. In this case the blood pressure is very high but the resistance to blood flow is extreme. The heart is working against a very high afterload which impairs the flow of blood and the delivery of oxygen.
J81.0 Acute pulmonary edema is for a non-cardiogenic etiology. This situation, flash pulmonary edema is cardiogenic, mostly vascular – high resistance and poor oxygen delivery, just mistaken as non cardiogenic or respiratory. There is often some edema in the lungs but the illness with this moniker, flash pulmonary edema is still cardiogenic, cardiovascular in etiology, mechanism and progression.
I50.1 Left ventricular failure with congestive heart failure. The problem with this code is that flash pulmonary edema is mostly a problem with very high peripheral resistance not ventricular dysfunction. Fluid retention does not affect peripheral resistance and edema, and if visible in the extremities is misleading. The dyspnea is from stagnant tissue hypoxia producing an acidemia. Patients with this presentation may not have anything that would suggest congestion. Edema may not be present either in the extremities, or on the chest X-ray. Many patients have edema in the lungs but this is a result of the problem not the cause. The proximate cause is high peripheral resistance in the cardiovascular system. Abnormalities in the pulmonary system including the edema are secondary.
One of these two codes is usually used out of necessity. Unfortunately there is no code for acute dyspnea of a primarily vascular nature due to a sudden increase in peripheral resistance. High blood pressure does not cause dyspnea but high peripheral resistance can and does. These two measurements are not the same. The heart pumps forcefully creating severe elevations of blood pressure. Considering the force and pressure the heart generates, this in not left ventricular failure. Congestion may be present but is not the primary reason for dyspnea.
Despite the appearance of severe respiratory distress and labored breathing there is good airflow. We don’t measure airflow but the visual appearance of dyspnea is so striking that airflow is usually judged to be poor. Here the moniker with pulmonary in the description introduces bias in this subjective assessment. A blood gas analysis is much more difficult than an oxygen saturation by pulse oximetry which means that the acidemia is not apparent whereas any degree of hypoxia is. The moniker with pulmonary in the phrase induces a biased attitude to judging the labored breathing from hypoxia and a lack of airflow. Hypoxia induces a respiratory drive but so does acidemia. In the usual emergency situation we can perceive hypoxia which may be mild but not acidemia which could be severe.
When an emergency situation occurs there is great pressure to intervene is a way that convinces the patient that a positive step is in action and gives a hopeful attitude to everyone affected. A intervenion that visibly gives this impression and is immediately applied will do this. We need to show immediately that we care, are applying a treatment and that it will work. The possibility that what we have to offer is not effective is an unpleasant thought but applying it anyway makes sense in the way of gaining control and encouraging a positive attitude. A very high resistance or afterload on the flow of blood at the heart of this condition is difficult to treat. The best way to reduce peripheral resistance is intravenous nitroglycerin. Medications given intravenously don’t have the same visual effect as a mask and positive pressure. and are are not immediately noticed by the patient. In this sense, they don’t work because it is not immediate and visual.
Treatments such as bronchodialators, and CPAP or BIPAP is given for respiratory illness because it appears to be a respiratory illness. We have to intervene immediately and the patient needs to see that something is done. When edema of the lungs is discovered, confirmation bias is a powerful force that prevents a reevaluation with a more in depth evaluation to be considered as it should. There is only a subjective impression of respiratory disease and there is the moniker, pulmonary. With our minds made up, the edema has to be the cause of the problem not the result of it.
Many such patients have edema of the lower extremities. This is a chronic finding and does not interfere with respiration. The problem is that it is noticeable and deceiving. Edema of the lungs is a result of the problem not the cause of the problem. A portable plain film chest X-ray is easily done in an Emergency Department. The usual semi upright PA (front to back) image commonly creates or exacerbates the appearance of edema. A standing chest X-ray from back to front is a better technique that is done in non emergency cases but might if possible show little or no edema of the lungs. Edema is visible and noticeable which gives the impression of importance. Edema is not important functionally although it is a clue to circulatory insufficiency that causes the edema. There is hypoxia of the tissues because of the lack of oxygen delivery but not so much the oxygen content of the arterial blood.
For many years this scenario has been treated with IV furosemide. This is considered to be a diuretic which it is, but it also has vascular effects which are much less appreciated. The use of IV furosemide as a vascular agent has been forgotten and since the effect is not immediate and dramatic, it is generally discounted. The improvement is not seen for at least 20 to 30 minutes. We have become an instant society and everything has to be instantaneous. Unless one has lived in the era when this was the sole treatment, this is not appreciated. IV furosemide has a role as a vascular agent but many people pressed into service in the emergency department think of it only as a diuretic. It does not work quickly so in today’s consideration it is not thought to be effective at all. When IV furosemide is given and that is all that is available in about 20 to 30 min. the patient will almost always begin to improve.
Oxygen is delivered to the tissues in two steps. First oxygen is added to the blood in the lungs by the respiratory system. Second the oxygenated blood has to be delivered to the tissues by the cardiovascular system. Both steps are necessary. The delivery of oxygen is resisted by the peripheral resistance to blood flow. Flow is related to resistance by the equation CO = BP/SVR. If blood pressure increases and the resistance goes up more than blood pressure then flow will decrease. Elevated blood pressure is a clue that the resistance to blood flow is elevated. The poor circulation of blood due to elevated resistance will reduce the delivery of oxygen. This is perceived as dyspnea when combined with an acidemia produced by the production of lactic acid.
In addition to acidemia and breathlessness as the disease progresses edema of the lungs often develops. This gives the mistaken impression that the illness is a respiratory and not a cardiovascular illness. If the edema could somehow be removed we would still have a cardiovascular illness that is the root cause of this disorder. The acidosis would still be present and elevated pulmonary venous pressure that accompanies the edema would still be present. A focus on the edema of the lungs is easy but incorrect.
The plain film CXR is often an easy thing to accomplish. The edema that is seen is much easier to demonstrate than the most significant problem which is the inadequate flow of blood. Cardiac output can easily be calculated with a pulmonary artery catheter in place. Without one too much reliance of the blood pressure to assess peripheral perfusion is almost universal. Acidemia due to anaerobic metabolism and the production of lactate is a stronger but less obvious clue than is edema of the lungs. The clinical picture that is usually referred to as Flash Pulmonary Edema creates confusion because it gives the appearance of a disorder of breathing. The patient is distressed by the lack of oxygen but instead of a lack of oxygen in the blood stream the lack of oxygen is due to a lack of delivery because of limited blood flow. Some patients with this presentation are severely distressed but any edema on an X-ray is minimal or sometimes altogether absent. The distress comes primarily from the impaired delivery of oxygen by the cardiovascular system. This produces a feeling of dyspnea. This will not be obvious as the flow of blood and the delivery of oxygen is essentially impossible to measure. It is commonly assumed that a patient with high blood pressure cannot be in shock (low flow). They can because the total vascular resistance is so high that the elevated blood pressure is overwhelmed. Patients with severe elevations to blood flow, high peripheral resistance will have the impairment of oxygen delivery. This is perceived as dyspnea. Eventually edema of the lungs may develop and contribute to respiratory distress. Resolving the edema will not resolve the cardiovascular dysfunction.
The term pulmonary is misleading. This causes a type of confirmation bias or diagnostic closure. Because of this label that is incorrect it is assumed that this has to be respiratory system disease. This is a type of consensus science that leads to an unscientific conclusion. Since the majority of people believe in edema as the cause of dyspnea it is undemocratic conspiracy to believe otherwise. This is a cardiovascular disease not a pulmonary disease. The edema of the lungs is a problem but the edema is not the origin of the distress nor is the major abnormality causing respiratory distress. That the edema is the root of the problem is a long held and almost universal misconception.
Flash is an appropriate descriptor as the illness flashes or feeds itself similar to the proverbial snowball. Sometimes the adjectives, sympathetic and crashing is applied. These give the appropriate connotation. Severe vasoconstriction from sympathetic outflow is accelerating, crashing or snowballing. These presentations are not seen by appointment in the clinic. Such presentations are seen as urgent ambulance visits to the emergency department.
The introduction of non-invasive ventilation to treat acute cardiovascular insufficiency known by the colloquialism, flash pulmonary edema has contributed to the misunderstanding of the disease. Usually non-invasive ventilation is utilized in every severely distressed patient that presents to the emergency department. Little to no thought is given to the origin of the distress before this treatment is instituted. Usually a nurse with call for “bi-pap” and a respiratory therapist will initiate it before a doctor examines the patient. This often gives the doctor the excuses to delay as the impression is given that the therapy has begun which “buys them time”. The image of a patient severely short of breath with a mask connected to positive pressure paints a picture that is misleading. This is not a respiratory or pulmonary illness as it appears in this situation. Everyone in the room where this treatment is employed gets the wrong impression. It might be that only the doctor that knows that this is a cardiovascular disease. He is pressured by the panic of other providers. The cause of this illness despite the fact that edema of the lungs is a part of it, is insufficiency of the cardiovascular system. If we removed the edema of the lungs we would still have the inadequate flow, the tissues of the body would still be starved of the flow of blood and oxygen and there would still be the feeling of shortness of breath. The body feels a lack of oxygen at the tissue level. This still occurs if the oxygen in the arterial blood is normal or near normal. Edema of the lungs is the result of the problem not the proximate cause of the illness.
Evaluating the patient before this treatment is initiated would give a better picture of the problem. This is a very difficult diagnosis and the best information is necessary if the nature of this illness is to be appreciated. Blindly using BiPaP on every severely distressed patient is confusing. Most casual observers, students and lay individuals will have the wrong impression by observing Bi-Pap being used. This has an effect on even the educated observer. A physician who examines a patient with scenario who is already on BiPaP will have an even more difficult time understanding the nature of the illness. It is difficult in any case because it appears to be a respiratory illness only more so when Bi-Pap is already applied.
Acute Cardiovascular Insufficiency is not simply a dysfunction of the heart or heart failure but insufficiency of the entire cardiovascular system, the heart and also the blood vessels. Typically there is extremely high resistance to the flow of blood and the delivery of oxygen. Often it is assumed that a person with high blood pressure cannot have low perfusion and therefore be in shock. They can and they are is this disorder.
It is a common misunderstanding the initiating event is the development of edema in the lungs. The circular reasoning that leads to this conclusion is propagated because of the incorrect naming of this condition as pulmonary edema. It is also erroneously believed that resolving the edema would resolve the illness also. This is also incorrect. Rather, it is true that if the cardiovascular illness resolved, the edema would also. The edema is the result of the illness not the cause of it. It is not possible to create a proper understanding of the illness with the moniker of Flash Pulmonary Edema. Because of this misnomer, a type of misinformed closure interferes with a critical analysis of the origin and progression of the illness.
It is difficult to understand how financial arrangements can influence well meaning individuals. People
tend to do what will allow them to survive.
Edema of the lungs is easily observed. The flow of blood and the resistance to it is not.
Blood pressure is easily measured. Too much reliance is placed on the observation of blood pressure. Monitoring of the blood pressure continuously or in real time does not solve this problem. In all setting outside the ICU, the insufficiency of blood flow, and the resistance to flow cannot be measured.
The appearance of the most easily obtained image, the semi-recumbent portable plain film chest X-ray is misleading. We need measurements of blood flow which we don’t have and as a practical matter can’t be obtained. The true nature of this illness is difficult to appreciate.
The heart can be imaged. The vascular tree cannot. Severe high blood pressure is not the same as severe high resistance to blood flow.
The importance of oxygen is at the tissue level not in blood of the arteries. When the demand for oxygen overwhelms the supply the tissues will be starved of oxygen especially highly metabolic tissue like muscle.
Anaerobic metabolisms begins to supplement the aerobic metabolism already at its limit. The patient will begin to perceive dyspnea. Anaerobic metabolism generates lactic acid and lowers the pH. Respiratory compensation to the low pH drives ventilation and tachypnea.
The skin is not a highly metabolic tissue and the requirements for oxygen are not as high as the muscle and internal organs. The imbalance of supply and demand for oxygen is not seen in the skin. WE cannot see the problem.
Pulmonary Edema is a pathological or radiological finding. Many medical conditions are characterized and defined by a collection of findings known as a syndrome. The term pulmonary edema is but one finding and is not a complete syndrome, not a diagnosis. The insufficient delivery of oxygen to meet metabolic demand along with the acidosis from anaerobic metabolism is the cause of shortness of breath not the edema of the lungs. In the typical scenario this looks like a breathing disorder. It is not. The delivery of oxygen is impaired.
The majority of people believe that Flash Pulmonary Edema is a respiratory illness and the source of the problem is edema of the lungs. One should not be able to vote in this political discussion without certain prerequisites of knowledge. Consensus Science means that the most arrogant are the heard not the most knowledgeable. Arrogance wins the day in this sphere. It is likely that the majority will still continue to believe in Flash Pulmonary Edema.
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