1. Prepared by: South West Education Committee
PULMONARY EDEMA
Prepared by:
South West Education Committee

2. “The Power of 7” Base Hospital Programs
Cambridge
Grey Bruce
Hamilton
Lambton
London
Niagara
Windsor
South
West
Education
Committee

3. SWEC MEMBERS Cambridge – Lori Smith Grey Bruce – Andy Whittemore
Hamilton – Ken Stuebing, Tim Dodd
Lambton – Judy Potter
London – Tre Rodriguez
Niagara – Greg Soto
Windsor – Cathie Hedges
RTN – Peter Deryk

4. Congestive Heart Failure or Acute Pulmonary Edema
SWEC Base Hospitals
Credit: W.A. (Bill) Penhallurick Southeastern Regional BH 1

5. OUTLINE
Review the pathophysiology and etiology of Congestive Heart Failure
Review the pathophysiology, etiology and emergency treatment of Acute Pulmonary Edema
Review cardio-respiratory assessments
Review the Acute Pulmonary Edema protocol and the use of Nitroglycerin

6. OBJECTIVES Describe the possible causes of pulmonary edema.
Explain the indications for NTG treatment
Describe the limitation to treatment
Explain the treatment procedure.

7. Congestive Heart Failure (CHF)??? :
INTRODUCTION
Congestive Heart Failure (CHF)??? :
A syndrome resulting from an imbalance in pump function in which the heart fails to maintain an adequate circulation of blood.
Results in retention of fluid “congestion”.

8. PULMONARY CIRCULATION
Blood flows from the right ventricle through the pulmonary artery
Blood reaches the capillaries surrounding alveoli where gas exchange occurs
Oxygenated blood returns by pulmonary veins to the left ventricle where it is pumped into systemic circulation

10. Results from conditions such as:
-Increased pulmonary capillary pressure
-Increased pulmonary capillary permeability
-Decreased oncotic pressure
-Lymphatic insufficiency
-mixed or unknown mechanisms

11. -Lymphatic insufficiency

12. ETIOLOGY AND PATHOPHYSIOLOGY
Syndrome usually results from LV dysfunction and compensatory mechanisms
Cardiac performance is a function of 4 primary factors. What are they? 4

13. 4 FACTORS DETERMINING CARDIAC PERFORMANCE
Preload (define)
Afterload (define)
Contractility
Heart Rate 5

14. Compensatory Mechanisms to Maintain Cardiac Output:
The Frank-Starling mechanism
Myocardial hypertrophy
Increased sympathetic tone
All result in increased myocardial O2 demand!
Kidneys 6

15. CAUSES OF Congestive Heart Failure
Conditions that increase preload, e.g. aortic regurgitation, ventricular septal defects, fluid overload
Conditions that increase afterload, e.g. aortic stenosis, systemic hypertension (vasoconstriction),
Conditions that decrease myocardial contractility, e.g. MI, cardiomyopathies, pericarditis, tamponade

16. SIGNS &SYMPTOMS OF Congestive Heart Failure
Exertional dyspnea usually with Crackles
- fatigue may be the first sign
Increased respiratory rate and effort
Orthopnea and/or PND
Cyanosis and pallor
Tachycardia
JVD
Dependant edema

17. CATEGORIZING FAILURE Left or Right sided heart failure
Forward or Backward ventricular failure
Backward failure is secondary to elevated systemic venous pressures.
Forward ventricular failure is secondary to left ventricle failure and reduced flow into the aorta and systemic circulation

18. LV BACKWARD EFFECTS Decreased emptying of the left ventricle 
Increased volume and end-diastolic pressure in the left ventricle
Increased volume (pressure) in the left atrium
Increased volume in pulmonary veins

19. LV BACKWARD EFFECTS con’t
Increased volume in pulmonary capillary bed = increased hydrostatic pressure 
Transudation of fluid from capillaries to alveoli
Rapid filling of alveolar spaces
Pulmonary edema

20. LV FORWARD EFFECTS Decreased cardiac output 
Decreased perfusion of tissues of body
Decreased blood flow to kidneys and glands
Increased reabsorption of sodium and water and vasoconstriction

21. LV FORWARD EFFECTS con’t
Increased secretion of sodium and water-retaining hormones 
Increased extracellular fluid volume
Increased total blood volume and increased systemic blood pressure

22. RV BACKWARD EFFECTS Decreased emptying of the right ventricle 
Increased volume and end-diastolic pressure in the right ventricle
Increased volume (pressure) in right atrium
Increased volume and pressure in the great veins

23. RV BACKWARD EFFECTS con’t
Increased volume in the systemic venous circulation 
Increased volume in distensible organs (hepatomegaly, splenomegaly)
Increased pressures at capillary line
Peripheral, dependant edema and serous infusion

24. RV Forward Effects Decreased volume from the RV to the lungs 
Decreased return to the left atrium and subsequent decreased cardiac output
All the forward effects of left heart failure

25. Congestive Heart Failure Can Be Defined Based on:
How rapid the symptoms onset
Which ventricle is primarily involved
Overall cardiac output 3

26. Left Heart Failure and Pulmonary Edema
LVF occurs when the left ventricle fails to function as an effective forward pump, causing a back-pressure of blood into the pulmonary circulation
May be caused by a variety of forms of heart disease including ischemic, valvular, and hypertensive heart disease
Untreated, significant LVF culminates in pulmonary edema

27. Left Heart Failure and Pulmonary Edema
Signs and symptoms
Severe respiratory distress
Severe apprehension, agitation, confusion
Cyanosis (if severe)
Diaphoresis
Adventitious lung sounds
JVD
Abnormal vital signs

28. Right Heart Failure
Occurs when the right ventricle fails as an effective forward pump, causing back-pressure of blood into the systemic venous circulation
Can result from:
Chronic hypertension (in which LVF usually precedes RVF)
COPD
Pulmonary embolism
Valvular heart disease
Right ventricular infarction
RVF most commonly results from LVF

29. Right Heart Failure Signs and symptoms Tachycardia Venous congestion
Engorged liver, spleen, or both
Venous distention; distention and pulsations of the neck veins
Peripheral edema
Fluid accumulation in serous cavities
History-common signs and symptoms of acute right-sided heart failure include chest pain, hypotension, and distended neck veins

30. CARDIOGENIC SHOCK The most extreme form of pump failure
Occurs when left ventricular function is so compromised that the heart cannot meet the metabolic needs of the body
Usually caused by extensive myocardial infarction, often involving more than 40% of the left ventricle, or by diffuse ischemia
MAP drops below 70mmHg

31. New York Heart Association’s functional classification of CHF

32. CLASS I
A patient who is not limited with normal physical activity by symptoms but has symptoms with exercise.

33. CLASS II
Ordinary physical activity results in fatigue, dyspnea, or other symptoms.

34. CLASS III
Characterized by a marked limitation in normal physical activity.

35. CLASS IV
Defined by symptoms at rest or with any physical activity.

36. Three Stages of Pulmonary Edema
Stage 1 - Fluid transfer is increased into the lung interstitium; because lymphatic flow also increases, no net increase in interstitial volume occurs.
Stage 2 - The capacity of the lymphatics to drain excess fluid is exceeded and liquid begins to accumulate in the interstitial spaces that surround the bronchioles and lung vasculature (which yields the roentgenographic pattern of interstitial pulmonary edema).

37. Three Stages of Pulmonary Edema
Stage 3 - As fluid continues to build up, increased pressure causes it to track into the interstitial space around the alveoli.
Fluid first builds up in the periphery of the alveolar capillary membranes and finally floods the alveoli .
During stage 3 the x-ray picture of alveolar pulmonary edema is generated and gas exchange becomes impaired.

38. Three Stages of Pulmonary Edema
Stage 3 cont. Additionally gravity exerts an important influence on the fluid mechanics of the lung.
Blood is much denser than air and air-containing tissue
Under normal circumstances more perfusion occurs at the lung bases than at the apices; however, when pulmonary venous pressures rise and when fluid begins to accumulate at the lung bases the blood flow begins to be redistributed toward the apices.

39. Acute Pulmonary Congestion/ Pulmonary Edema

40. Mechanisms to Keep Interstitium and Alveoli Dry
Plasma oncotic pressure
Connective tissue and cellular barriers relatively impermeable to plasma proteins
Extensive lymphatic system

41. Acute Pulmonary Edema May be CARDIAC or NON-CARDIAC in origin.
Results from conditions such as:
Increased pulmonary capillary pressure
Increased pulmonary capillary permeability
Decreased oncotic pressure
Lymphatic insufficiency
mixed or unknown mechanisms 7

42. Etiology of Pulmonary Edema
Increased fluid in lung interstitium
Interstitial edema
Pulmonary hydrostatic pressure exceeds colloid osmotic pressure
Fluid tracks into interstitial spaces around alveoli
Fluid enters alveoli

43. Differential Diagnosis for APE:
Cardiac causes of acute CHF
COPD exacerbation
Non-cardiac pulmonary edema:
Tansudate vs. Exudate
fluid overload
infection
ARDS
High altitude
Pulmonary Embolism
Pneumonia 8

44. CLINICAL PRESENTATION:
History
Physical Exam
EKG
This should provide enough information to establish a cardiac etiology, if one exists! 10

45. HISTORICAL INFORMATION
Maintain a high clinical suspicion for ischemia or infarction
[# 1 cause of CHF (think ASA)]
Search for cardiac etiology
A study of circadian patterns for Cardiogenic acute pulmonary edema shows a significant peak for progressive symptoms and AMI between 06: :59 (D.D. Buff, M.D. et all) 11

46. HISTORY Why did you call? What has changed?
How long has the dyspnea been present?
Was the onset gradual or abrupt?
Is the dyspnea better or worse with position? Is there associated orthopnea?
Has the patient been coughing?
- If so, was the cough productive?
- What was the character and colour?
- Is there any hemoptysis?
- recent fever?

47. HISTORY Is there pain associated with the dyspnea?
- OPQRST for the pain
Pt’s past history?
Allergies
Current Medications (pay close attention to O2 therapy, oral bronchodilators, corticosteriods,Beta Blockers, Digitalis, ACE Inhibitors, Diuretics)

48. HISTORY What is the patients normal level of activity?
How has the patient changed his/her environment to adjust to the disease?
- Pillow props
- Strategically placed chairs
- Meds within easy reach

49. Symptoms Suspicious of Pulmonary Congestion
Any complaint of dyspnea/ decreased exercise tolerance
PND/ Orthopnea
Feeling of “suffocation” or air-hunger
Restlessness and anxiety
Cyanosis/Diaphoresis
Pallor 12

50. Symptoms Suspicious of Pulmonary Congestion
Crackles
Wheezing (Cardiac Asthma)
Tachypnea
Coughing (Dry cough may be med related)
Retractions, accessory muscle use
Frothy pink-tinged sputum 15

51. Physical Findings
Varying degrees of pulmonary and systemic vascular congestion and hypoperfusion
Classic patient with APE presents sitting “bolt” upright 13

52. Physical Findings ( cont. )
JVD
Edema - ankle/pretibial vs sacral
Ascites
- Positive Hepato-jugular reflex test
BP and P are often markedly elevated
Cardiac exam
S3 or intermittent S4 may be present?
PMI may be shifted left 14

53. EKG Analysis: Search for evidence of infarction or ischemia
Non-specific findings may include:
hypertrophy
chamber enlargement
conduction disturbances 18

54. CHEST XRAY: Usually demonstrates increased heart size
Progression of pulmonary congestion:
first: Cephalization
second : Interstitial edema
third: Pulmonary (alveolar) edema 19

55. Cephalization on Right
- Due to pulmonary hypertension
- Pulmonary veins become visible due to increased blood congestion
- Decreases or clears after treatment

57. Pulmonary Edema Pulmonary edema is common in congestive heart failure.
As pulmonary capillary pressures increase, the initial fluid excess is removed by increased lymphatic drainage.
When lymphatic system capacity is exceeded, pulmonary edema occurs. Radiographic signs include septal lines, bronchial wall thickening and subpleural pulmonary edema.
Top radiograph illustrates generalized fissural thickening and lack of clarity of intrapulmonary vessels.
Figure and description from "Imaging Diseases of the Chest" , p. 388, by Peter Armstrong, Alan G. Wilson, and Paul Dee, Yearbook Medical Publishers, Inc

58. Treatment of APE: First and foremost is to increase oxygen saturation
a reasonable approach is to base therapy on the Systolic Blood Pressure
Decrease the preload on the heart
Shift and then eliminate excess fluids 20

59. Prehospital Management:
Patient sitting with legs dependent
Supplemental O2 provided
Cardiac monitoring/ Pulse oximetry
Initiate necessary supportive therapy
Nitroglycerin for APE if patient matches protocol
Be prepared to assist ventilations
PPV is an effective treatment
Stress DEPENDANT limbs
Iterate suction vs. PPV 21

60. Acute Pulmonary Edema Protocol - Indications
Patient in moderate to severe respiratory distress
Patient is assessed by the paramedic as being in Acute Pulmonary Edema

61. Acute Pulmonary Edema Protocol - Conditions
Weight > 40 Kg
Patient has NOT taken any erectile dysfunction medication within 48 hours
Heart rate greater then 60 & < 160 bpm
Initial and subsequent BP > 140 mmHg systolic

62. Acute Pulmonary Edema Protocol - Procedure
If the systolic blood pressure remains >140 mmHg - administer Nitroglycerin 0.4 mg spray SL every 5 minutes to a maximum of 6 doses.
Check the vital signs before administering EACH dose
NOTE: Do not administer further NTG if the systolic BP drops below 140 mmHg

63. Treatment Procedure Patient in sitting position
100% oxygen via NRB or BVM
Cardiac monitor

64. Limitations Max of 6 doses of Nitro by Paramedic Stop if
Systolic BP <140 mmhg
Drop in SBP by 1/3
Heart rate <60 or >160

65. Frequently Asked Questions
Q: If the patient is in Pulmonary Edema with crackles, can I give Salbutamol?

66. Answer
A. Continue with oxygen administration and NTG. Salbutamol is not the drug of choice.

67. Frequently Asked Questions
Q: What if I can only hear wheezing but suspect the patient is in Pulmonary Edema. Should I give Salbutamol?

68. Answer
A. Continue with oxygen administration. Consider the Acute Pulmonary Edema protocol and consult a BHP before administering Salbutamol if still uncertain.

69. QUESTIONS?