Pulmonary Oedema Flashcards
Define Pulmonary Oedema
Increased pulmonary vessel permeability results in fluid from the blood plasma migrating into the lung parenchyma (tissue that make up the walls of the capillaries and alveoli), interstitial space and alveoli. The accumulation of the fluid results in gas exchange abnormalities.
What are the 2 causes of pulmonary oedema?
Cardiogenic and Non-Cardiogenic
Cardiogenic Pathophysiology of Pulmonary Oedema (3 reasons it occurs)
Result of a problem with the heart ejecting blood, can occur due to 3 reasons
- Increase of cardiac preload pressure (due to over infusion of fluids/ pulmonary hypertension)
- Failure of co-ordinated muscular contraction of the myocardium (caused by MI or arrythmias)
- Increased afterload pressure (from hypertension/aortic stenosis)
Non-Cardiogenic Pathophysiology of Pulmonary Oedema - Oncotic Pressure
- Blood must have sufficient oncotic pressure to ensure fluid doesn’t migrate into the lungs
- Albumin is a key protein in maintaining oncotic pressure
- A decrease in Albumin can result in pulmonary oedema
- This can happen from burns, liver failure or renal conditions
Cardiogenic Pathophysiology of Pulmonary Oedema - 3 reasons result in:
Any of these reasons can result in left sided heart failure as capillary hydrostatic pressure is increased:
- LVF results in the heart being unable to pump blood through aorta properly
- Resulting in an increase in pressure in the Left Ventricle and Atria
- The pressure then increases in pulmonary veins and finally in pulmonary capillaries raising hydrostatic pressure
- High hydrostatic pressure in capillaries causes fluid to be forced out into interstitial space, across the parenchyma, then into alveoli
- Alveolar pulmonary oedema develops
Non-Cardiogenic Pathophysiology of Pulmonary Oedema - Increased Permeability
- Direct injury of alveolar epithelium or capillary endothelium causes increased pulmonary vascular permeability
Non-Cardiogenic Pathophysiology of Pulmonary Oedema - EXOGENOUS Causes
(e. g. Aspirations/ Toxic/ Noxious gas inhalation/ Direct trauma)
- Direct injury of the alveolar epithelium results in rapid leakage of interstitial proteins and fluid into the alveoli.
- Proteins deactivate surfactant
- Blood flow is normal but no ventilation due to fluid filled alveoli (pulmonary shunt)
Non-Cardiogenic Pathophysiology of Pulmonary Oedema - ENDOGENOUS Causes
(e. g. Pneumonia/ Sepsis)
- These damage alveolar capillaries
- As a result, neutrophils leak out into interstitial fluid
- Neutrophils damage alveolar walls resulting in fluid and proteins filling the alveoli
Signs and Symptoms of Pulmonary Oedema
- Dyspnoea (difficulty in breathing) /Respiratory failure
- Tachycardia
- Orthopnoea (shortness of breath when laying down)
- Hypoxaemia (reduced saturations)
- Increased JVP
- Productive cough (pink frothy)
- Hypotension
- Use of accessory muscles
- Reduced GCS
Risk Factors for Pulmonary Oedema
- Hypertension
- Family history of heart disease
- Diabetes
- Chest infections
Assessment for Pulmonary Oedema
DRA(c)BCDE
DANGER assessment for Pulmonary Oedema
- Assess for any potential dangers?
- Manage any bleeds
RESPONSE assessment for Pulmonary Oedema
AVPU - assess
AIRWAY assessment for Pulmonary Oedema
- Clear?
- Correct if compromised
C-SPINE assessment for Pulmonary Oedema
Is this a concern based on MOI?
BREATHING assessment for Pulmonary Oedema
- Respiration rate?
- Bubbling on expiration?
- Accessory muscle use
- Assist with ventilation if required
CIRCULATION assessment for Pulmonary Oedema
- Heart rate?
- Palpable radial pulse?
- Capillary refill?
- Oxygen saturations?
- Blood pressure?
- Skin colour?
DISABILITY assessment for Pulmonary Oedema
- Temperature
- Blood glucose
- PEARL
- Equal and bilateral air entry?
- Crackles?
- 12 ECG
- Altered GCS?
EXAMINATIONS assessment for Pulmonary Oedema
- Peripheral oedema
- Distended jugular vein
Past Medical History
- Does the patient have a history of heart failure?
Treatment for Pulmonary Oedema
Treat as per JRCALC
- Correct any ABC problems immediately
- Administer oxygen if saturations are below 94%
- Sit patient upright to alleviate left atrial pressure
- 12 lead ECG
- Consider GTN (400-800 mcg – max 2.4 mg) and IV furosemide (40mg – max 40mg) - if due to heart failure
- If time critical - Pre- alert and convey to the nearest A&E with continuous monitoring and management on route
Dosage of GTN (if due to heart failure)
400-800 mcg – max 2.4 mg
Dosage of IV furosemide (if due to heart failure)
40mg – max 40mg
