CARDIOGENIC PULMONARY EDEMA

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CARDIOGENIC PULMONARY EDEMA

  1. 1. IN THE NAME OF GODCARDIOGENIC PULMONARY EDEMA 1
  2. 2. Cardiogenic pulmonary edema 2
  3. 3. CPECPE due to:• increased capillary hydrostatic pressure secondary to elevated pulmonary venous pressure 3
  4. 4. following major pathophysiologic mechanisms:• Imbalance of Starling forces - Ie, increased pulmonary capillary pressure, decreased plasma oncotic pressure, increased negative interstitial pressure• Damage to the alveolar-capillary barrier• Lymphatic obstruction• Idiopathic (unknown) mechanism 4
  5. 5. Mechanism of CPE• alveolar-capillary membrane• Increase of net flux of fluid from the vasculature into the interstitial space• Net flow of fluid across a membrane is determined by applying the following equation: Q = K(Pcap - Pis) - l(Pcap - Pis)• 5
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  7. 7. Lymphatics• 10-20 mL/h• acute rise in pulmonary arterial capillary pressure (ie, to >18 mm Hg)• chronically elevated LA pressure, the rate of lymphatic removal can be as high as 200 mL/h 7
  8. 8. StagesStage 1• elevated LA pressure→ distention and opening of small pulmonary vessels• blood gas exchange does not deteriorate 8
  9. 9. Stage 2• fluid and colloid shift into the lung interstitium from the pulmonary capillaries→but an initial increase in lymphatic outflow efficiently removes the fluid• may overpower the drainage capacity of the lymphatics 9
  10. 10. Stage 2• mild hypoxemia• Tachypnea→stimulation of juxtapulmonary capillary (J-type) 10
  11. 11. Stage 3• alveolar flooding• abnormalities in gas exchange• vital capacity and other respiratory volumes are substantially reduced• hypoxemia becomes more severe 11
  12. 12. Cardiac disorders manifesting as CPE• Atrial outflow obstruction• LV systolic dysfunction• LV diastolic dysfunction• Dysrhythmias• LV hypertrophy and cardiomyopathies• LV volume overload• Myocardial infarction• LV outflow obstruction 12
  13. 13. Presentation• History• Physical Examination 13
  14. 14. HistorySymptoms• Sudden (acute)• Long-term (chronic) 14
  15. 15. Sudden (acute)• Extreme shortness of breath or difficulty breathing (dyspnea) that worsens when lying down• A feeling of suffocating or drowning• Wheezing or gasping for breath• Anxiety, restlessness or a sense of apprehension• A cough that produces frothy sputum that may be tinged with blood 15
  16. 16. Sudden (acute)• Excessive sweating• Pale skin• Chest pain, if pulmonary edema is caused by heart disease• A rapid, irregular heartbeat (palpitations) 16
  17. 17. Long-term (chronic)• Having more shortness of breath than normal when youre physically active• Difficulty breathing with exertion, often when youre lying flat as opposed to sitting up• Wheezing• Awakening at night with a breathless feeling that may be relieved by sitting up• Rapid weight gain 17
  18. 18. Long-term (chronic)• Swelling in your legs and ankles• Loss of appetite• Fatigue• Ortner sign? 18
  19. 19. Physical Examination• Tachypnea• Tachycardia• sitting upright→air hunger• Confuse• agitate• anxious• diaphoretic 19
  20. 20. • Hypertension• Hypotension indicates severe LV systolic dysfunction and the possibility of cardiogenic shock• Cool extremities may indicate low cardiac output and poor perfusion. 20
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  22. 22. Auscultation• fine, crepitant rales• rhonchi or wheezes may also be present• Cardiovascular findings→S3,accentuation of the pulmonic component of S2, jugular venous distention• Auscultation of murmurs→acute valvular disorders 22
  23. 23. Auscultation• Aortic stenosis→ harsh crescendo- decrescendo systolic murmur, which is heard best at the upper sternal border and radiating to the carotid arteries• acute aortic regurgitation→short, soft diastolic murmur• Acute mitral regurgitation produces a loud systolic murmur heard best at the apex or lower sternal border 23
  24. 24. • Mitral stenosis typically produces a loud S1, opening snap, and diastolic rumble at the cardiac apex• skin pallor or mottling→peripheral vasoconstriction, low cardiac output 24
  25. 25. Severe CPE→mental status→hypoxia or hypercapniahypercapnia with respiratory acidosis may be seen in patients with severe CPE or underlying chronic obstructive pulmonary disease (COPD). 25
  26. 26. Diagnostic ConsiderationsCardiogenic pulmonary edema (CPE) should be differentiated from pulmonary edema associated with injury to the alveolar-capillary membrane, caused by diverse etiologies. 26
  27. 27. DDx• Acute Respiratory Distress Syndrome• Asthma• Cardiogenic Shock• Chronic Obstructive Pulmonary Disease• Emphysema• Goodpasture Syndrome• Myocardial Infarction 27
  28. 28. DDx• Pneumothorax• High-altitude pulmonary edema• Neurogenic pulmonary edema• Pulmonary embolism• Respiratory failure 28
  29. 29. DDx• Pneumocystis (carinii) jiroveci Pneumonia• Pneumonia, Bacterial• Pneumonia, Viral 29
  30. 30. differentiate CPE from NCPE• In CPE, a history of an acute cardiac event is usually present• low-flow state• S3 gallop• jugular venous distention• crackles on auscultation 30
  31. 31. differentiate CPE from NCPEPatients with NCPE have a warm periphery, a bounding pulse, and no S3 gallop or jugular venous distentionDefinite differentiation is based on pulmonary capillary wedge pressure (PCWP) measurements. The PCWP is generally >18 mm Hg in CPE and < 18 mm Hg in NCPE, but superimposition of chronic pulmonary vascular disease can make this distinction difficult to assess. 31
  32. 32. WorkupLab studies• Complete blood count• Serum electrolyte measurements• Blood urea nitrogen (BUN) and creatinine• Pulse oximetry• Arterial blood gas analysis 32
  33. 33. Electrocardiography• LA enlargement• LV hypertrophy• acute tachydysrhythmia• bradydysrhythmia• acute myocardial ischemia or infarction 33
  34. 34. BNPEFFECTS1.Vasodilation2. Diuresis3. Natriuresis4. Suppression of Renin Angiotensin Sys 34
  35. 35. BNP testing• high negative predictive value; that is, in patients with BNP value of under 100 pg/mL, heart failure is unlikelyValues of 100-400 pg/mL may be related to various pulmonary conditions, such as cor pulmonale, COPD, and pulmonary embolism. 35
  36. 36. RadiographyChest radiography is helpful in distinguishing CPE from other pulmonary causes of severe dyspnea.Features that suggest CPE rather than NCPE and other lung pathologies include the following:• Enlarged heart• Inverted blood flow• Kerley lines• Basilar edema (vs diffuse edema)• Absence of air bronchograms• Presence of pleural effusion (particularly bilateral and 36 symmetrical pleural effusions)
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  42. 42. Echocardiographyimportant diagnostic tool in determining the etiology of pulmonary edemahelpful in identifying a mechanical etiology for pulmonary edema, such as the following:• Acute papillary muscle rupture• Acute ventricular septal defect• Cardiac tamponade• Contained LV rupture• Valvular vegetation with resulting acute severe 42 mitral, aortic regurgitation
  43. 43. Pulmonary Arterial CatheterPCWP can be measured with a pulmonary arterial catheter (Swan-Ganz catheter)This method helps in differentiating CPE from NCPEA PCWP exceeding 18 mm Hg in a patient not known to have chronically elevated LA pressure indicates CPE. 43
  44. 44. TreatmentFollowing initial management, medical treatment of CPE focuses on 3 main goals(1) reduction of pulmonary venous return (preload reduction)(2) reduction of systemic vascular resistance (afterload reduction)(3) inotropic support 44
  45. 45. TreatmentPatients with severe LV dysfunction or acute valvular disorders may present with hypotension. These patients may not tolerate medications to reduce their preload and afterload. Therefore, inotropic support is necessary in this subset of patients to maintain adequate blood pressure. 45
  46. 46. Ventilatory Support• Noninvasive pressure-support ventilation• Mechanical ventilation 46
  47. 47. Preload Reduction• Nitroglycerin• Diuretics• Morphine sulfate• Nesiritide 47
  48. 48. Afterload Reduction• ACE inhibitors• Angiotensin II receptor blockers• Nitroprusside• Phosphodiesterase inhibitors 48
  49. 49. Inotropic support• Dobutamine• Dopamine• Norepinephrine• Phosphodiesterase inhibitors• Calcium sensitizers 49
  50. 50. SUMMARYABCREDISTRIBUTE FLUID OUT OF LUNGS!1ST Line: Nitrates2 ND Line: ACE Inhibitors3RD Line: DiureticsNIPPV – use early !Milrinone – preferred inotrope 50
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