Cardiogenic vs noncardiogenic pulmonary edema (ARDs)

Pulmonary edema cardiogenic and noncardiogenic (ARDs)

1. Differential Diagnosis and Treatment of Cardiogenic and Noncardiogenic (ARDs ) Pulmonary Edema

2. Overview Pulmonary edema is a condition characterized by abnormal fluid accumulation in the lungs caused by extravasation of fluid from pulmonary vasculature into the interstitium and alveoli of the lungs This process leads to diminished gas exchange at the alveolar level, progressing to potentially causing respiratory failure Respiratory failure occurs when lungs fail to maintain ventilation, in which PaO2 <60 mmHg and/or PaCO2 >50 mmHg Due to either a cardiogenic process with the inability to remove sufficient blood away from the pulmonary circulation or non-cardiogenic precipitated by injury to the lung parenchyma The most recognized form of non-cardiogenic pulmonary edema is acute respiratory distress syndrome ( ARDS) Clinical features include progressive worsening dyspnea, rales on lung auscultation, and worsening hypoxia More than 1 million patients are admitted each year with a diagnosis of pulmonary edema secondary to cardiac causes (heart failure ). An estimated 190,000 patients are diagnosed with acute lung injury each year.

3. Non-cardiogenic Pulmonary Edema Etiology Acute respiratory distress syndrome (ARDS) High altitude pulmonary edema (HAPE) Neurogenic pulmonary edema Opioid overdose Salicylate toxicity  Pulmonary embolism Reexpansion pulmonary edema  Reperfusion pulmonary edema Transfusion-related acute lung injury (TRALI)

4. ARDs Has an acute onset secondary to an underlying inflammatory process Such as sepsis, pneumonia, gastric aspiration, blood transfusion, pancreatitis, multisystem trauma or trauma to the chest wall, drug overdose, fractures with fat embolism, burns, or head injury It’s defined as an acute disorder that starts within 7 days of the inciting event and is characterized by bilateral lung infiltrates and severe progressive hypoxemia in the absence of any evidence of cardiogenic pulmonary edema Characterized by widespread inflammation in the lungs, poor oxygenation, and is life-threatening 40% mortality rate Healing may result in interstitial fibrosis

5. Clinical features of ARDs Acute severe dyspnea Tachypnea Cyanosis Gasping Bilateral crackles Severe hypoxemia unresponsive to oxygen Bilateral infiltrates on chest radiograph Absence of signs of left ventricular failure

6. Diagnosis of ARDs Based on following criteria: Acute onset Bilateral lung infiltrates on chest radiography of a non-cardiogenic origin PaO2/FiO2 ratio of less than 300 mmHg Laboratory tests Arterial blood gas: hypoxemia (PaO2 <60 mmHg), respiratory alkalosis or respiratory acidosis as the condition progresses and PaCo2 rises. Metabolic acidosis can be present in the context of sepsis, with or without respiratory compensation.

7. CBC In case of sepsis leukopenia or leukocytosis may be noted Thrombocytopenia may be observed in the presence of disseminated intravascular coagulation (DIC) Cytokines - Multiple cytokines, such as interleukin (IL)–1, IL-6, and IL-8, are elevated in the serum of patients at risk for ARDS . Chest Radiography Bilateral pulmonary infiltrate, may be diffuse and symmetric or asymmetric Initially, the infiltrates may have a patchy peripheral distribution, but soon they progress to diffuse bilateral involvement with ground glass changes or frank alveolar infiltrates. Bronchoscopy: To evaluate the possibility of infection, alveolar hemorrhage, or acute eosinophilic pneumonia in patients with acute bilateral pulmonary infiltrates Bronchoalveolar lavage analysis: fluid is analyzed for cell differential, cytology, silver stain, gram stain, and quantitative culture.

8. Diagnosis, Continued…… Doppler Echocardiography To assess pulmonary circulation and biventricular function Invasive Hemodynamic Monitoring : central venous catheter to facilitate fluid management in patients who are hypotensive or with associated renal failure Other laboratory and/or radiographic tests will be guided by the underlying disease process, which has triggered the inflammatory process that has led to the development of ARDS.

9. Treatment No specific medical treatment exists Treatment is supportive: Supplemental oxygen Mechanical ventilation Positioning therapy: prone position has shown benefits in about 50% to 70% of patients Fluid management Corticosteroids: methylprednisolone may improve oxygenation but does not decrease mortality, studies report that it increases mortality in patients who have had ARDS for >14d

10. Cardiogenic Pulmonary Edema Cardiogenic pulmonary edema (CPE) is defined as pulmonary edema due to increased capillary hydrostatic pressure secondary to elevated pulmonary venous pressure caused by left heart disease Etiology Disorders that increase pressure in the left side of the heart and pooling of blood can cause cardiogenic pulmonary edema Coronary artery disease with left ventricular failure (myocardial infarction) Congestive heart failure: left ventricular volume overload Cardiomyopathy Valvular heart diseases on the left side of the heart (stenosis and regurgitation) Cardiac arrhythmias Right to left shunts

11. Pathophysiology

12. Clinical Features Acute onset Sudden onset of extreme dyspnea, anxiety, and feelings of drowning Hypoxia and increased sympathetic tone Profuse diaphoresis Pink colored frothy sputum in very severe disease Chest pain (myocardial infarction, or aortic dissection) Gradual onset Dyspnea on exertion Orthopnea Paroxysmal nocturnal dyspnea Fatigue

13. Physical exam Confusion, agitation, irritability, diaphoresis, cyanosis, upright posture, cold extremities Tachypnea with gasps for breath Bilateral crackles Rhonchi and wheezing may also be present Pedal edema with pulmonary edema, in chronic heart failure

14. Cardiovascular findings Hypertension, but if hypotension is present it indicates severe left ventricular systolic dysfunction and cardiogenic shock must be ruled out Jugular venous distension Tachycardia On auscultation - several different types of murmurs can be heard depending upon the cause of the valvular lesion . S3 gallop is present in volume overload states Aortic stenosis produces a harsh crescendo-decrescendo ejection systolic murmur at the aortic area, increasing on expiration usually radiating towards the right side of the neck . Aortic regurgitation is associated with a short, high-pitched soft diastolic murmur, best heard at the aortic area during expiration. Mitral stenosis typically produces a loud S1, opening snap, and diastolic rumble at the cardiac apex. M itral regurgitation produces a loud high-pitched systolic murmur heard best at the apex or lower sternal border .

15. Investigations Blood Tests CBC (to rule out anemia and sepsis) Serum electrolytes (patients on diuretic therapy may have disturbances) Pulse oximetry and ABGs (to assess hypoxia and oxygen saturation) BNP (brain natriuretic peptide levels: low levels rule out cardiogenic type) ECG : to rule out ischemic changes and rhythm abnormalities . Radiology Echocardiography : to differentiate systolic from diastolic dysfunction and valvular lesions . LA enlargement and LV hypertrophy are sensitive indicators of chronic LV dysfunction. Transthoracic lung ultrasonography may be useful for differentiating between chronic obstructive pulmonary disease and chronic heart failure as causes of exacerbation of chronic dyspnea

16. Chest x-ray findings Cardiomegaly Kerley B lines Basilar or central edema (perihilar) Absence of air bronchograms Presence of pleural effusion Broad vascular pedicle Vascular redistribution   Thickened interlobular septae Pulmonary arterial catheter : a PCWP exceeding 18 mm Hg in a patient not known to have chronically elevated LA pressure indicates CPE.

17. Treatment ABC must be addressed initially as the patient arrives. Airway assessment  ( Make sure the airway is clear for adequate oxygenation and ventilation) Breathing  ( Note the pattern of breathing and oxygen saturation.) Circulation  ( Vital signs and cardiac assessment and management ) Oxygen delivery and ventilatory support  (Through nasal cannula, face mask, non-rebreather mask, noninvasive pressure support ventilation, and mechanical ventilation as required) Prop up Intra-venous access Urine output monitoring

18. Treatment, continued…. Supplemental oxygen (in risk of hypoxemia, SPO2 is <90%) Medical treatment: Preload reduction (reduction of pulmonary venous return) Afterload reduction (reduction of systemic vascular resistance) Inotropic support: in case of hypotension in severe LV dysfunction or acute valvular disorders Preload reduction Intravenous diuretics is the mainstay of treatment in acute settings, with or without vasodilator therapy Furosemide is the usual drug of choice: 20-40 mg IV, or up to 200 mg in severe heart failure Daily weight, serum electrolytes, and O2 saturation should be monitored Vasodilator therapy may be necessary in urgent afterload reduction (severe hypertension), as an adjunct to diuretics, and in patients with refractory heart failure. Nitroglycerin can be used at 5 to 10 mcg/min initially and can be increased gradually to the maximum recommended dose (200 mcg/min)

19. Afterload reduction therapy: ACE inhibitors: captopril 25mg sublingually, or enalapril (1.25mg IV) ARBs: valsartan, candesartan Inotropic agents: is usually used if preload and afterload therapies are unsuccessful, and if patient is hypotensive Catecholamines : Dobutamine (avoided in patients with severe hypotension systolic BP <90 mmHg) Norepinephrine: used in profound hypotension (systolic BP <60 mmHg) Phosphodiesterase inhibitors: milrinone   Calcium sensitizers: levosimendan – is an effective and safe alternative to dobutamine * IV inotropic agents are associated with an increased long-term mortality, and should therefore be reserved for patients with heart failure and a markedly depressed cardiac index and stroke volume . * In general, ACE inhibitors should be started as an oral vasodilator therapy after the patient’s condition has been stabilized.

20. Invasive management IABP (intra-aortic balloon bump): not a definitive therapy but is widely used as a bridge therapy for patients with cardiogenic shock and also as an adjunct to thrombolysis in acute myocardial infarction for stabilization . Ultrafiltration : can be crucial in patients with heart failure and resistance to diuretic therapy and can serve to optimize the volume status.

21. Cardiogenic pulmonary edema

22. Cardiogenic pulmonary edema

23. Kerley B lines

24. Bibliographies Medscape.com ncbi.nlm.nih.gov Radiopaedia.org Semanticscholar.org