History

Fact Explanation
Shortness of breath Increased pulmonary venous pressure (cardiogenic pulmonary edema) or decreased plasma oncotic pressure (non-cardiogenic pulmonary edema) lead to an imbalance in Starling forces that results in initiation of the process of pulmonary oedema. There are four stages of the development of pulmonary edema. Only interstitial edema is present at first, then filling of the the alveoli, thirdly alveolar flooding and finallly airway blockage. There is increased resistance of small airways and lung will become less compliant. [1] Later developing interstitial and alveolar oedema worsens the shortness of breath. [1]
Frothy sputum As the pulmonary venous pressure Increasing, there is severe disruption of alveolar-capillary membrane[1] leading to leakage of red blood cells into the alveoli. [7]
Anxiety Gas exchange gradually deteriorates and hypoxia worsens. [1] Also there can be acidemia and hypercapnia.
Risk factors:- History of valvular disease Valvular diseases like mitral stenosis, valvular regurgitation in infective endocarditis can also result in pulmonary edema. [2]
Risk factors:- History of myocardial infarction Myocardial infarction can weakens the ventricular wall, leading to left ventricular failure. As the cardiac output reduces, [5] effective circulatory volume is also decreasing, this causes activation of renin angiotencinogen aldesterone mechanism and sodium water retention. This results in expansion of extracellular volume and increase in pulmonary venous pressure.
Risk factors:- History of pneumothorax Large negative pressure develops while draining a pneumothorax [4] and that can cause unilateral pulmonary edema.
Risk factors:- History of liver disease, nephrotic syndrome, protein losing enterepothy In liver disease, protein production by the liver is decreased. in nephrotic syndrome, there is loss of macromolecular proteins through the glomerular-capillary basement membrane. Hypoalbuminaemia [1] is the net result of all these. Resulting reduced oncotic pressure will leads to pulmonary edema.[1] In addition there is a peripheral vasodilatation leading to activation of renin-angiotensinogen-aldosterone mechanism.
Risk factors:- History of filariasis Causes interstitial edema. [2]
Risk factors:- History of pancreatitis Haemorragic pancreatitis [6] can cause shock and non-cardiogenic pulmonary edema.
Risk factors:- History of hypertension Hypertensive acute heart failure [1] can presents with pulmonary oedema without left ventricular dysfunction.
Risk factors:- History of toxin inhalation Various toxins like ozone, chlorine [9] and smoke disrupts the alveolar-capillary membrane and causes leakage of fluid into the alveoli.
Risk factors:- History of drug usage Drugs like nitrofurontoin [3] can damage the alveolar-capillary membrane and causes leakage of fluid into the alveoli.
Risk factors:- History of central nervous system disease This causes non-cardiogenic pulmonary edema, [2] which is related to sympathetic activation and peripheral vasoconstriction.
Risk factors:- History of aspiration Is a cause for non-cardiogenic pulmonary edema. [2]
Risk factors:- History of kidney disease Both acute and chronic kidney disease can cause pulmonary edema due to fluid overload and reduced excretion by the kidney. [8]
References
  1. PERRY AW. The Management of Acute Pulmonary Edema Can Fam Physician [online] 1969 Oct, 15(10):49-50 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2281517
  2. KERR GW. Neurogenic pulmonary oedema. J Accid Emerg Med [online] 1998 Jul, 15(4):275-276 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1343146
  3. PINERUA RF, HARTNETT BJ. Acute pulmonary reaction to nitrofurantoin Thorax [online] 1974 Sep, 29(5):599-602 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC470207
  4. CURRIE GP, ALLURI R, CHRISTIE GL, LEGGE JS. Pneumothorax: an update Postgrad Med J [online] 2007 Jul, 83(981):461-465 [viewed 17 September 2014] Available from: doi:10.1136/pgmj.2007.056978
  5. KHALID L, DHAKAM SH. A Review of Cardiogenic Shock in Acute Myocardial Infarction Curr Cardiol Rev [online] 2008 Feb, 4(1):34-40 [viewed 17 September 2014] Available from: doi:10.2174/157340308783565456
  6. WARSHAW AL, LESSER PB, RIE M, CULLEN DJ. The pathogenesis of pulmonary edema in acute pancreatitis. Ann Surg [online] 1975 Oct, 182(4):505-510 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1344021
  7. Treatment of Pulmonary Oedema Br Med J [online] 1956 Dec 29, 2(5008):1531-1533 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2036040
  8. CANET EMMANUEL, OSMAN DAVID, LAMBERT JéROME, GUITTON CHRISTOPHE, HENG ANNE-ELISABETH, ARGAUD LAURENT, KLOUCHE KADA, MOURAD GEORGES, LEGENDRE CHRISTOPHE, TIMSIT JEAN-FRANçOIS, RONDEAU ERIC, HOURMANT MARYVONNE, DURRBACH ANTOINE, GLOTZ DENIS, SOUWEINE BERTRAND, SCHLEMMER BENOîT, AZOULAY ELIE. Acute respiratory failure in kidney transplant recipients: a multicenter study. Array [online] 2011 December [viewed 17 September 2014] Available from: doi:10.1186/cc10091
  9. CHANG W, CHEN J, SCHLUETER CF, RANDO RJ, PATHAK YV, HOYLE GW. Inhibition of Chlorine-Induced Lung Injury by the Type 4 Phosphodiesterase Inhibitor Rolipram Toxicol Appl Pharmacol [online] 2012 Sep 1, 263(2):251-258 [viewed 17 September 2014] Available from: doi:10.1016/j.taap.2012.06.017

Examination

Fact Explanation
Tachypnea [2] There is increased resistance in small airways and lung will become less compliant. There is impaired gas exchange at the alveolar capillary membrane leading to hypoxia. [1]
Dyspnoea, apnea There is difficulty in breathing as mentioned above in the history along with the extensive use of accessory muscles, and temporary episodes of no breathing (apnea),. [2]
Cyanosis Gas exchange is impaired due to disruption of alveolar capillary membrane. [1]
Bi-basal crepitations As the pulmonary edema progresses, alveolar edema develops with disruption of alveolar capillary membrane and leakage of red blood cells and macromolecules into the alveoli. [1] Then there will be fine end inspiratory crepitations occurring when the distal airways are opened at the end of inspiration .
Tachycardia Rapid heart beat [2] is also occurring in the pulmonary edema.
Elevated blood pressure This is seen in hypertensive acute heart failure. [1] Systolic blood pressure is an independent clinical predictor of morbidity and mortality after initial therapy during heart failure with reduced ejection fraction.
Associated plural effusion, [3] pericardial effusion and ascites. As the interstitial volume expands, there can be associated pleural effusion [3] pericardial effusion and ascites. Pleural effusion: reduced chest expansion and moments, stony dull percussion note, reduced vocal fremitus and bronchial breathing over the affected areas. Pericardial effusion :pericardial friction rub, this rub is that inflammation of the pericardial sac causes the parietal and visceral surfaces of the roughened pericardium to rub against each other. This rubbing produces an extracardiac sound. Ascites :flank, shifting and horseshoe dullness, and fluid thrill in severe cases.
Features of right heart failure Elevated jugular venous pressure, cardiomegaly (shifted cardiac apex), third heart sound, positive hepatojugular reflex and hepatomegaly are features of right heart failure. Sometimes left heart failure can be associated with right heart failure which is congestive heart failure. [1,4]
If associated with peripheral edema Ankle edema, sacral edema and facial puffiness can be seen if there is associated expansion of the extracellular fluid. [2]
Altered mental state [2] Hypoxia [1] , acidemia can results in confusion and mental alterations.
References
  1. PERRY AW. The Management of Acute Pulmonary Edema Can Fam Physician [online] 1969 Oct, 15(10):49-50 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2281517
  2. KERR GW. Neurogenic pulmonary oedema. J Accid Emerg Med [online] 1998 Jul, 15(4):275-276 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1343146
  3. CHAOUAT A, KESSLER R, WEITZENBLUM E. Pulmonary oedema and pleural effusion in two patients with primary pulmonary hypertension treated with calcium channel blockers. Heart [online] 1996 Apr, 75(4):383 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC484315
  4. JOSEPH SM, CEDARS AM, EWALD GA, GELTMAN EM, MANN DL. Acute Decompensated Heart Failure: Contemporary Medical Management Tex Heart Inst J [online] 2009, 36(6):510-520 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2801958

Differential Diagnoses

Fact Explanation
Myocardial ischemia [3] This is a type of cardiogenic pulmonary edema. Patient presents with symptoms such as central chest pain radiating to the arm/jaw and autonomic symptoms, also they might have a history of acute coronary events and co-morbidities such as diabetes mellitus, stroke, and hyperlipidaemia. ECG and cardiac biomarkers are helpful to diagnose and differentiate it from the other conditions. [4]
Cardiogenic shock [1] Systolic blood pressure is <90 mmHg/ reduction of mean arterial pressure by >30 mmhg lasting for more thatn 30 minutes that is due to the myocardial dysfunction. [1] Urine output <0.5ml/kg/hour are some of the features of cardiogenic shock. Also there can be associated elevation of jugular venous pressure, gallop rhythm and basal crepitations.
Pneumothorax [2] There is accumulation of air in the pleural cavity [2] and valve like mechanism developed with sucking of air into the pleural space during each inspiration, but not expelling during expiration creating a positive pressure inside the pleural cavity throughout the respiration. This can lead to tension pneumothorax. They can presents with sudden onset of unilateral chest pain, worsening breathlessness, and tachycardia.[2]
Pulmonary embolism [5] Thrombus is formed in the systemic veins or rarely on the right side of the heart. They presents with sudden onset of pleuritic chest pain, dyspnea and haemoptysis. [5] There can be new onset atrial fibrillation. Chest X-ray is often normal, sometimes may show pulmonary oligaemia, linear atelectasis and blunted costophrenic angle. Full blood count shows polymorphonuclear leukocytosis, ESR is elevated and lactate dehydrogenase is also elevated.
Respiratory failure [6] There are 2 types of respiratory failure, type 1 is acute hypoxia (low PaO2 with normal or low PaCO2) ,[usually occurs with pulmonary edema, pneumonia and acute lung injury, In type 2, there is low PaO2 with high PaCO2 and usually seen in chronic obstructive pulmonary disease and neurological conditions such as guillen bare syndrome. [6] Apart from the tachypnea, tachycardia and dyspnoea, [6] they also have sweating, pulsus paradoxus, paradoxical respiration and asynchronous respiration(abdominal and thoracic cages moving in opposite direction)are present.
Acute respiratory distress syndrome (ARDS) There will be a history of significant aetiological factors such as pneumonia, aspiration, toxic inhalation, near-drowning, or lung contusion; as well as indirect mechanisms, such as sepsis, burn, pancreatitis. [7] Severe shortness of breath is the main symptom of ARDS. Other features include, unusually rapid breathing, confusion and low blood pressure. PaO2/F iO2 ≤200 mmHg . [7]
Pneumonia [9] Patient presents with productive cough with whitish/yellowish sputum, fever, and pleuritic chest pain. [9] There are localized areas of consolidation on examination such as reduced chest expansion, dull percussion note, increased vocal fremitus and coarse early/mid inspiratory crepitations when compared to the fine end inspiratory crepitations in pulmonary edema. [9]
Goodpasture syndrome [8] Initial symptoms would be shortness of breath, persistent cough, sometimes with blood. [8] When Goodpasture syndrome affects the kidneys, it may cause, haematuria, proteinuria and hypertension. [8]
References
  1. KHALID L, DHAKAM SH. A Review of Cardiogenic Shock in Acute Myocardial Infarction Curr Cardiol Rev [online] 2008 Feb, 4(1):34-40 [viewed 17 September 2014] Available from: doi:10.2174/157340308783565456
  2. CURRIE GP, ALLURI R, CHRISTIE GL, LEGGE JS. Pneumothorax: an update Postgrad Med J [online] 2007 Jul, 83(981):461-465 [viewed 17 September 2014] Available from: doi:10.1136/pgmj.2007.056978
  3. JENNINGS RB. Myocardial ischemia: introduction. Am J Pathol [online] 1981 Feb, 102(2):239-240 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1903676
  4. HENG MK, SINGH BN, NORRIS RM, JOHN MB, ELLIOT R. Relationship between epicardial ST-segment elevation and myocardial ischemic damage after experimental coronary artery occlusion in dogs. J Clin Invest [online] 1976 Dec, 58(6):1317-1326 [viewed 17 September 2014] Available from: doi:10.1172/JCI108587
  5. MATTOX KL, FELDTMAN RW, BEALL AC JR, DEBAKEY ME. Pulmonary embolectomy for acute massive pulmonary embolism. Ann Surg [online] 1982 Jun, 195(6):726-731 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1352667
  6. BREDENBERG CE, JAMES PM, COLLINS J, ANDERSON RW, MARTIN AM JR, HARDAWAY RM 3RD. Respiratory failure in shock. Ann Surg [online] 1969 Mar, 169(3):392-403 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1387440
  7. LUH SP, CHIANG CH. Acute lung injury/acute respiratory distress syndrome (ALI/ARDS): the mechanism, present strategies and future perspectives of therapies J Zhejiang Univ Sci B [online] 2007 Jan, 8(1):60-69 [viewed 17 September 2014] Available from: doi:10.1631/jzus.2007.B0060
  8. A case of Goodpasture's syndrome. Br Med J [online] 1972 Apr 29, 2(5808):272-277 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1788937
  9. HOPSTAKEN RM, MURIS JW, KNOTTNERUS JA, KESTER AD, RINKENS PE, DINANT GJ. Contributions of symptoms, signs, erythrocyte sedimentation rate, and C-reactive protein to a diagnosis of pneumonia in acute lower respiratory tract infection. Br J Gen Pract [online] 2003 May, 53(490):358-364 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1314594

Investigations - for Diagnosis

Fact Explanation
Chest X-ray As the pulmonary edema progresses, alveolar edema develops with disruption of the alveolar capillary membrane. [5] There is bi-basal diffuse haziness of lung fields, Kerley B lines, loss of distinct vascular margins, increased bronchovascular margins (bat's wing sign) [5] and ares of consolidation, lung mottling and pleural effusion on chest x-ray. Cardiomegaly [5] may also be present. Acute respiratory distress syndrome, a type of non cardiogenic pulmonary edema may resemble cardiac pulmonary edema. But within next 24-48 hours following the onset of symptoms, ARDS becomes more uniform. Differentiation of cardiac pulmonary edema from non cardiogenic pulmonary edema, can be done by the time it takes for the edema to develop and to vanish. If substantial improvement occurs within 24 hours, it is usually cardiac pulmonary edema.
Computer tomography CT scan findings in non cardiogenic pulmonary edema are similar to those of ARDS. [5] High-resolution CT (HRCT) scan shows widespread airspace consolidation and a reticular pattern with a striking anterior distribution is a frequent finding of follow-up CT scan.
BNP and NTproBNP Natriuretic peptides are elevated in acute heart failure. [4] BNP >100pg/ml and NTproBNP >300pg/ml are findings in acute heart failure.
Cardiac enzymes and troponin These are important to detect ischaemic changes in the myocardium. Troponin is a complex made of 3 proteins called I, T and C. These are sensitive markers of myocardial necrosis. [6]
2D Echo Confirms the diagnosis of heart failure and can be used to identify the cause. [2]
Full blood count Infection is a precipitating cause for pulmonary edema, which will present as a leucocytosis(elevated white cell count, usually in bacterial infection) and lymphocytosis(elevated lymphocytes, usually in viral infection). Sometimes cardiac failure may be associated with low lymphocyte count. [4]
Serum creatinine and blood urea Both acute and chronic kidney diseases can cause pulmonary edema. [3]
Oxygen saturation In the acute stage of pulmonary edema SaO2 will be <90% in air. [1,2]
References
  1. PERRY AW. The Management of Acute Pulmonary Edema Can Fam Physician [online] 1969 Oct, 15(10):49-50 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2281517
  2. JOSEPH SM, CEDARS AM, EWALD GA, GELTMAN EM, MANN DL. Acute Decompensated Heart Failure: Contemporary Medical Management Tex Heart Inst J [online] 2009, 36(6):510-520 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2801958
  3. KUTE VB, SHAH PR, GOPLANI KR, GUMBER MR, VANIKAR AV, TRIVEDI HL. Successful treatment of refractory hypotension, noncardiogenic pulmonary edema and acute kidney injury after an overdose of amlodipine Indian J Crit Care Med [online] 2011, 15(3):182-184 [viewed 17 September 2014] Available from: doi:10.4103/0972-5229.84901
  4. VADUGANATHAN M., AMBROSY A. P., GREENE S. J., MENTZ R. J., SUBACIUS H. P., MAGGIONI A. P., SWEDBERG K., NODARI S., ZANNAD F., KONSTAM M. A., BUTLER J., GHEORGHIADE M.. Predictive Value of Low Relative Lymphocyte Count in Patients Hospitalized for Heart Failure With Reduced Ejection Fraction: Insights from the EVEREST Trial. Circulation: Heart Failure [online] December, 5(6):750-758 [viewed 17 September 2014] Available from: doi:10.1161/CIRCHEARTFAILURE.112.970525
  5. BOWSER B JR, STINSON JM. Spontaneous Unilateral Pulmonary Edema J Natl Med Assoc [online] 1986 Sep, 78(9):882-886 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2571366

Investigations - Fitness for Management

Fact Explanation
Full blood count To see any infection as a causative or aggravating factor for pulmonary edema. There will be leucocytosis in bacterial infections and elevated lymphocytes in viral infections. Anaemia [1] is important to treat as it can aggravates the heart failure.
Serum electrolytes Low serum sodium concentration is a poor prognostic factor in acute pulmonary edema. [1]
References
  1. GHEORGHIADE M, ABRAHAM WT, ALBERT NM, GATTIS STOUGH W, GREENBERG BH, O'CONNOR CM, SHE L, YANCY CW, YOUNG J, FONAROW GC, OPTIMIZE-HF INVESTIGATORS AND COORDINATORS. Relationship between admission serum sodium concentration and clinical outcomes in patients hospitalized for heart failure: an analysis from the OPTIMIZE-HF registry. Eur Heart J [online] 2007 Apr, 28(8):980-8 [viewed 13 June 2014] Available from: doi:10.1093/eurheartj/ehl542

Investigations - Followup

Fact Explanation
Chest X-ray Usually substantial improvement occurs within 24 hours, in the case of cardiac pulmonary edema. [2]
Serum electrolytes Serum electrolytes are important as there can be electrolyte imbalances during the treatment of diuretics. Sodium concentration is also important as marker of prognosis. [2]
Oxygen saturation Is monitored to see the response to treatment. [1]
The Pulmonary Edema Prognostic Score (PEPS) [3] The PEPS is a simple tool that can be easily calculated using common clinical diagnostic tests (electrocardiogram, blood pressure, heart rate, and white cell count) to determine in-hospital mortality risk in patients with an acute episode of cardiogenic pulmonary edema. [3] PEPS was defined as a sum of all points. Patients with a PEPS of 0 had good short-term prognosis with a 2% in-hospital mortality rate, whereas mortality in patients with a PEPS of 4 was 64%.
Lymphocyte count Low relative lymphocyte count during hospitalization for heart failure is an independent predictor of poor outcomes. [1]
References
  1. VADUGANATHAN M., AMBROSY A. P., GREENE S. J., MENTZ R. J., SUBACIUS H. P., MAGGIONI A. P., SWEDBERG K., NODARI S., ZANNAD F., KONSTAM M. A., BUTLER J., GHEORGHIADE M.. Predictive Value of Low Relative Lymphocyte Count in Patients Hospitalized for Heart Failure With Reduced Ejection Fraction: Insights from the EVEREST Trial. Circulation: Heart Failure [online] December, 5(6):750-758 [viewed 17 September 2014] Available from: doi:10.1161/CIRCHEARTFAILURE.112.970525
  2. NARCı H. Acute Pulmonary Edema Due to Excessive Water Intake in Pyschiatric Patient Iran Red Crescent Med J [online] 2013 Apr, 15(4):375-376 [viewed 17 September 2014] Available from: doi:10.5812/ircmj.2228
  3. INAMI TAKUMI, KATAOKA MASAHARU, SHIMURA NOBUHIKO, ISHIGURO HARUHISA, YANAGISAWA RYOJI, TAGUCHI HIROKI, FUKUDA KEIICHI, YOSHINO HIDEAKI, SATOH TORU. Pulmonary Edema Predictive Scoring Index (PEPSI), a New Index to Predict Risk of Reperfusion Pulmonary Edema and Improvement of Hemodynamics in Percutaneous Transluminal Pulmonary Angioplasty. JACC: Cardiovascular Interventions [online] 2013 July, 6(7):725-736 [viewed 17 September 2014] Available from: doi:10.1016/j.jcin.2013.03.009

Investigations - Screening/Staging

Fact Explanation
Electrocardiogram To see any changes suggestive of myocardial ischaemia, arrhythmias and valvular lesions. There can be ST elevations, ST depressions, T inversions in acute coronary syndrome. Atrial fibrillation can be associated with mitral stenosis. [1]
2D Echocardiogram This is important to see the ventricular size, function, ejection fraction and valvular stenosis. [3] In mitral stenosis, the M mode show restriction and reversal of direction of the posterior leaflet motion. Increase left ventricular end diastolic dimension on echocardiogram suggests a poor prognosis.
Cardiac magnetic resonance(CMR) Valvular stenosis produces signal void on gradient on gradient echo CMR. [4]
References
  1. ALWI I. Diagnosis and management of cardiogenic pulmonary edema. Acta Med Indones [online] 2010 Jul, 42(3):176-84 [viewed 13 June 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/20973297
  2. VADUGANATHAN M, AMBROSY AP, GREENE SJ, MENTZ RJ, SUBACIUS HP, MAGGIONI AP, SWEDBERG K, NODARI S, ZANNAD F, KONSTAM MA, BUTLER J, GHEORGHIADE M, EVEREST TRIAL INVESTIGATORS. Predictive value of low relative lymphocyte count in patients hospitalized for heart failure with reduced ejection fraction: insights from the EVEREST trial. Circ Heart Fail [online] 2012 Nov, 5(6):750-8 [viewed 13 June 2014] Available from: doi:10.1161/CIRCHEARTFAILURE.112.970525
  3. NARCı H. Acute Pulmonary Edema Due to Excessive Water Intake in Pyschiatric Patient Iran Red Crescent Med J [online] 2013 Apr, 15(4):375-376 [viewed 17 September 2014] Available from: doi:10.5812/ircmj.2228
  4. WEIR R. A. P., PETRIE C. J., MURPHY C. A., CLEMENTS S., STEEDMAN T., MILLER A. M., MCINNES I. B., SQUIRE I. B., NG L. L., DARGIE H. J., MCMURRAY J. J. V.. Galectin-3 and Cardiac Function in Survivors of Acute Myocardial Infarction. Circulation: Heart Failure [online] December, 6(3):492-498 [viewed 17 September 2014] Available from: doi:10.1161/CIRCHEARTFAILURE.112.000146

Management - General Measures

Fact Explanation
Resuscitation Airway, breathing, circulation, disability and exposure should be done in an order as and when necessary. [2]
Physical and mental rest In acute phase absolute bed rest is advised as this reduces the cardiac work load. [2] Mental rest also does the same.
Prop up This is to improve the pulmonary function by relieving the pulmonary congestion by changing the gravity. [1]
Oxygen therapy [1] Improves oxygen delivery to the hypoxic, dyspnoeic patient. Target is to maintain PaO2 >60mmHg. Oxygen can be delivered by face mask [1] , noninvasive pressure-support ventilation, and intubation and mechanical ventilation.
Fluid management Strict water restriction is advised only if serum sodium is <125 meq/L. Because to remove the extracellular fluid, water restriction is of little value. [2]
Monitoring of the patient Oxygen saturation, pulse rate , respiratory rate, blood pressure and temperature are continuously monitored during the acute phase .[1] Patient should be connected to a cardiac monitor. [1]
Looking for complications of treatment Main complications occurring during the treatment are hypovolemic, shock [1] and electrolyte imbalances. Hypovolaemia is due the rapid administration of diuretics. There can be hyponatraemia , hypokalaemia, altered glucose tolerance during the diuretic treatment.
Attention to co-morbidities Patient might be having acute coronary syndrome, atrial fibrillation , liver disease, renal disease [1] and or other problem in association with pulmonary edema, which need proper treatment in order to proper management of pulmonary edema.
Correct the precipitating and underlying factors Valvular heart diseases, ischaemic heart diseases, congenital heart diseases and infective endocarditis, need appropriate treatment. Some will need the elimination of the precipitating factors such as infection, drugs and toxins. Nephrotic syndrome patients may need albumin on some occasions. [1]
References
  1. PERRY AW. The Management of Acute Pulmonary Edema Can Fam Physician [online] 1969 Oct, 15(10):49-50 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2281517
  2. Treatment of Pulmonary Oedema Br Med J [online] 1956 Dec 29, 2(5008):1531-1533 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2036040

Management - Specific Treatments

Fact Explanation
Diuretics (furosemide, bumetanide) Loop diuretics are the mainstay of treatment in pulmonary edema. [1,3] Main action is venodilation causing increase in venous capacitance, and it also blocks the sodium potassium 2 chloride cotransport in thick ascending limb of loop of Henle. Side effects include urate retention (gout), hypokalemia, hypomagnesemia, reduced glucose tolerance, myalgia and ototoxicity. Diuresis usually occurs within one hour of administration. [1]
Vasodialators Glyceryl trinitrate(10-200micg/min,only if systolic blood pressure is >85mmHg) and nitroprusside are the vasodilators used in the management. [1]
Ionotropes [1] Inotropic agents are used to reduce the symptoms of severe heart failure. [3] Dobutamine, phosphodiesterase inhibitors, levosimendan are used if there is poor response to initial treatment. Dobutamine:-It is safely used in the treatment of congestive heart failure as it stimulate the β1-adrenoceptors of the heart, and increase the contractility and cardiac output. Infusion of dobutamine should be started at a low rate (0.5 to 1.0 mcg/kg/min) and guided by the patient's response, including systemic blood pressure, urine flow, heart rate and if possible measurements of cardiac output, central venous pressure, and pulmonary capillary wedge pressure. Phosphodiesterase inhibitors:- The cardiostimulatory and vasodilatory actions of these drugs are used for the treatment of heart failure. [3] Arterial dilation reduces afterload and leads to an increase in stroke volume and ejection fraction. Reducing the afterload leads to a then decrease the preload and improve the contractility of the heart.
Digoxin Some patients presenting with worsening of heart failure are having evidence of atrial fibrillation. [2] If it is not a medical emergency, several doses of intravenous digoxin [1] followed by a maintenance dose of oral digoxin (0.125 mg/day) can be used to reduce the ventricular rate and thus improve signs and symptoms. Even in the absence of atrial fibrillation, it is advised to add a maintenance dose of digoxin as it reduces the incidence of death or hospitalization, specially in patients who are already on diuretics and angiotensin-converting enzyme inhibitors.
Hypotension If there is hypotension noradrenaline is used and if it is profound hypotension, inotropes and vasopressors are used. [1]
Mechanical support This is used in patients who are unresponsive to the standard medical treatment, but having a chance of recovery with a transient myocardial ischaemia. [2] Ventricular assist device is an example of mechanical support. Thromboembolism, infection, bleeding are some of the problems with these devices.
References
  1. PERRY AW. The Management of Acute Pulmonary Edema Can Fam Physician [online] 1969 Oct, 15(10):49-50 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2281517
  2. Treatment of Pulmonary Oedema Br Med J [online] 1956 Dec 29, 2(5008):1531-1533 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2036040
  3. JOSEPH SM, CEDARS AM, EWALD GA, GELTMAN EM, MANN DL. Acute Decompensated Heart Failure: Contemporary Medical Management Tex Heart Inst J [online] 2009, 36(6):510-520 [viewed 17 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2801958