الفهرس 
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Abstract
Acute cardiogenic pulmonary edema (ACPE) is a common cause of acute respiratory distress among patients presenting to intensive care units. Hypoxemia, sometimes associated with hypercapnia, is a common feature in the clinical presentation of acute cardiogenic pulmonary edema.
(ACPE) is a leading cause of hospitalization in patients over 65 years of age, in both the USA and Europe, with 20–30% of patients dying within 6 months after discharge (Go AS et al., 2013) and (Jhund PS et al., 2009).
The pathogenesis of acute cardiogenic pulmonary edema (ACPE) is related to a critical interaction between progressive decrease in left ventricular systolic function and acute increase in systemic vascular resistance, with the resultant migration of fluid from the intravascular compartment into the lung interstitium and alveoli.
ACPE is characterized by an increase in extravascular lung water, which causes a decrease in respiratory system compliance, increased airway resistance, air trapping, arterial hypoxaemia, and decreased diffusing capacity (Gehlbach BK and Geppert E, 2004).
The progression of fluid accumulation in CPE can be identified as 3 distinct physiologic stages (Weissleder R et al., 2007):
Stage 1: In stage 1, elevated LA pressure causes distention and opening of small pulmonary vessels.
Stage 2: In stage 2, fluid and colloid shift into the lung interstitium from the pulmonary capillaries.
Stage 3: In stage 3, as fluid filtration continues to increase and the filling of loose interstitial space occurs, fluid accumulates in the relatively noncompliant interstitial space. With further accumulations, the fluid crosses the alveolar epithelium in to the alveoli, leading to alveolar flooding.
Causes of ACPE can be divided into left atrial dysfunction causes and left ventricular dysfunction causes.
Left atrial dysfunction can be due outflow obstruction or dysrhythmia, outflow obstruction may be due to mitral stenosis or thrombosis of mitral valve or atrial myxoma.
Left ventricular dysfunction can be systolic or diastolic, systolic dysfunction may be due to acute myocardial infarction or myocarditis or acute rapid ventricular tachycardia or fibrillation or due to outflow obstruction like acute aortic stenosis due to thrombosed prosthetic aortic valve or acute elevation of systemic blood pressure
Diastolic dysfunction can be due to acute myocardial infarction or constrictive pericarditis or tamponade or endocarditis or due to iatrogenic causes like rupture of ventricular septum.
It is recommended that initial diagnosis of ACPE should be based on a thorough history assessing symptoms, prior cardiovascular history and potential cardiac and non-cardiac precipitants, as well as on the assessment of signs/symptoms of congestion and/or hypoperfusion by physical examination and further confirmed by appropriate additional investigations such as ECG, chest X-ray and echocardiography and laboratory assessment with specific biomarkers; cardiac biomarkers like (BNP, NT-proBNP, CK-MB, Troponin, myoglobin) and non cardiac biomarkers like (Na, K, TSH, urea, creatinine, liver function tests). In patients presenting with ACPE, early initiation of appropriate therapy (along with relevant investigations) is of key importance (Maisel AS et al., 2008).
Initial evaluation and continued non-invasive monitoring of the patient’s vital cardiorespiratory functions, including pulse oximetry, blood pressure, respiratory rate and a continuous ECG instituted within minutes, is essential to evaluate whether ventilation, peripheral perfusion, oxygenation, heart rate and blood pressure are adequate. Urine output should also be monitored. PICCO can be used for monitoring cardiac output and pulmonary edema.
Identification of precipitants/causes leading to decompensation that needs urgent management. The next step should comprise the identification of major precipitants/ causes leading to decompensation, which should be managed urgently according to 2016 ESC guidelines to avoid further deterioration like acute coronary syndrome or hypertensive emergency or rapid arrysthmia or acute pulmonary embolism.
Identification of acute etiologies/precipitants with subsequent initiation of specific treatments should be done within the immediate phase of (ACPE) management (initial 60–120 min).
Standard medical therapy includes diuretics, vasodilators, and inotropes results in rapid improvement of the respiratory symptoms. In this context, oxygen delivered through a face mask is the basic respiratory support. Although many patients respond rapidly to standard treatment, a significant number progress to severe respiratory distress leading to endotracheal intubation with its associated complications (Jessup & Broneza, 2003).
Non-invasive positive pressure ventilation reduces respiratory distress (Weng C-L et al., 2010) and (Gray A et al., 2008) and may decrease intubation and mortality rates (Vital FMR et al., 2013), although data regarding mortality are less conclusive. CPAP is a feasible technique in the pre-hospital setting, because it is simpler than (BiPAP) and requires minimal training and equipment. On hospital arrival, patients who still show signs of respiratory distress should continue with non-invasive ventilation, preferably (BiPAP), in case of acidosis and hypercapnia, particularly in those with a previous history of COPD or signs of fatigue (Mebazaa A et al., 2015).
There is no significant clinical benefit of (BiPAP) over (CPAP), so the modality chosen should be guided by local availability (van Riet EES et al., 2016). Non-invasive ventilation should be commenced at 100% oxygen with recommended initial settings of 10 cm of water pressure for CPAP and 10/4 cm water pressure (inspiratory positive airway pressure/expiratory positive airway pressure) for BiPAP (McMurray JJ V. 2010).
This work studied comparison between oxygen therapy delivered by face mask and CPAP in patient with ACPE to evaluate both intervention and which has the best outcome in treatment of ACPE.
This work included 20 patients with ACPE according to the inclusion criteria and exclusion criteria. Then these patient received the standard medical therapy of pulmonary edema including (diuretic, nitrates, morphine) then they are divided randomly into two groups (control group) received oxygen therapy by ordinary face mask, the other group (CPAP group) received CPAP mask then the respiratory rate (RR), heart rate (HR), blood pressure (BP), SPO2 and arterial blood gases (PaCO2, PaO2, and pH) recorded at different time points (0, 1hr, 6hrs, 12hrs, 24hrs).
The results of this work revealed that there is highly significant decrease in average follow up HR and RR and highly significant increase in O2 saturation with highly significant increase in average follow up PaO2 in CPAP group compared to control group
In conclusion CPAP has better clinical and laboratory outcomes than ordinary mask oxygen in treatment of ACPE.