Watching this resources will notify you when proposed changes or new versions are created so you can keep track of improvements that have been made.
Favoriting this resource allows you to save it in the “My Resources” tab of your account. There, you can easily access this resource later when you’re ready to customize it or assign it to your students.
Left ventricular failure which may be termed congestive heart failure and may be due to a heart attack leading to left ventricular failure, arrhythmias (tachycardia/fast heartbeat or bradycardia/slow heartbeat) and fluid overload.
Example - from kidney failure or intravenous therapy which may cause dilatation and failure of the left ventricle or may cause pulmonary edema in the absence of heart failure.
Pulmonary edema is fluid accumulation in the air spaces and parenchyma of the lungs and it leads to impaired gas exchange which may cause respiratory failure.
It is due to either failure of the left ventricle of the heart to adequately remove blood from the pulmonary circulation ("cardiogenic pulmonary edema") or an injury to the lung parenchyma or vasculature of the lung ("noncardiogenic pulmonary edema").
Treatment is focused on three aspects: improving respiratory function, treating the underlying cause, and avoiding further damage to the lung.
Pulmonary edema, especially in the acute setting, can lead to respiratory failure, cardiac arrest due to hypoxia, and death.
The overwhelming symptom of pulmonary edema is difficulty breathing, but may also include coughing up blood, excessive sweating, anxiety, and pale skin.
Shortness of breath and/or paroxysmal nocturnal dyspnea also happen.
The chronic development of pulmonary edema may be associated with symptoms and signs of "fluid overload," this is a non specific term to describe the manifestations of left ventricular failure on the rest of the body and includes peripheral edema (swelling of the legs, in general, of the "pitting" variety, wherein the skin is slow to return to normal when pressed upon), raised jugular venous pressure and hepatomegaly, where the liver is enlarged and may be tender or even pulsatile.
Other signs include end-inspiratory crackles (sounds heard at the end of a deep breath) on auscultation and the presence of a third heart sound.
There is no one single test for confirming that breathlessness is caused by pulmonary edema.
Indeed, in many cases, the cause of shortness of breath is probably multifactorial.
Low oxygen saturation and disturbed arterial blood gas readings support the proposed diagnosis by suggesting a pulmonary shunt.
Chest X-ray will show fluid in the alveolar walls, Kerley B lines, increased vascular shadowing in a classical batwing peri-hilum pattern, upper lobe diversion (increased blood flow to the superior parts of the lung), and possibly pleural effusions as shown in Figures 1 and 2.
In the case of cardiogenic pulmonary edema, urgent echocardiography may strengthen the diagnosis by demonstrating impaired left ventricular function, high central venous pressures, and high pulmonary artery pressures.
In certain circumstances, the insertion of a Swan-Ganz catheter may be required to aid diagnosis.
Blood tests are performed for electrolytes (sodium, potassium) and markers of renal function (creatinine, urea).
Liver enzymes, inflammatory markers (usually C-reactive protein), and a complete blood count as well as coagulation studies (PT, aPTT) are also typically requested.
B-type natriuretic peptide (BNP) is available in many hospitals, sometimes even as a point-of-care test.
Low levels of BNP (<100 pg/ml) suggest a cardiac cause is unlikely.
fluid accumulation in the lung's air spaces leading to impaired gas exchange, failure of left ventricle of heart to adequately remove blood from pulmonary circulation, causes difficulty breathing, peripheral edema, raised jugular venous pressure, hepatomegaly, and failure of right ventricle of heart to adequately remove blood from systemic circulation