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Pulmonary Edema

Basic Mechanism and Classification

• Definition: Pulmonary edema is the accumulation of fluid in the lung interstitium and alveoli, caused by leakage of intravascular fluid.
• Types:
  1. Hydrostatic (Cardiogenic) Pulmonary Edema:
     • Cause: Increased capillary pressure due to elevated hydrostatic forces.
     • Mechanism: Commonly occurs due to left ventricular failure, leading to increased pulmonary venous pressure and fluid translocation into the alveoli.
  2. Increased Capillary Permeability (Non-Cardiogenic) Pulmonary Edema:
     • Cause: Increased permeability of the pulmonary capillaries.
     • Mechanism: Often a result of direct injury to the alveolar-capillary membrane from factors such as infections, inhaled toxins, or systemic inflammatory responses.
  3. Pulmonary Vasoconstriction:
     • Mechanism: Increases capillary pressure, leading to fluid translocation into the alveoli.
     • Examples:
       • Neurogenic: Can occur following acute brain injuries.
       • Drugs: Certain substances like cocaine can induce vasoconstriction and subsequent pulmonary oedema.

How to Get Pulmonary Oedema

Increased Capillary Permeability	Increased Hydrostatic Pressure	Decreased Plasma Protein	Decreased Interstitial Pressure	Lymphatic Obstructions
Oxygen toxicity	Increased LA pressure (mitral stenosis, or myocardial infarction)	Protein starvation	Unknown origin	Tumors
Inhaled toxins	Excess IV fluids	Excess IV fluids	Too rapid evacuation of pneumothorax or hemothorax	Interstitial fibrotic diseases
Circulating toxins		Renal injury	High altitude
ARDS			Neurogenic (head injury)
			Drug overdose

Anaesthesia Considerations for Pulmonary Oedema

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CXR Features

• Cardiomegaly
  • Cardiothoracic Ratio (CTR) = 18/30 (>50%)
• Upper Zone Vessel Enlargement
  • Sign of pulmonary venous hypertension
• Septal (Kerley B) Lines
  • Sign of interstitial oedema
• Airspace Shadowing
  • Due to alveolar oedema, acutely in a peri-hilar (bat’s wing) distribution
• Blunt Costophrenic Angles
  • Due to pleural effusions

Cardiogenic Pulmonary Edema

Pathophysiology

• Acutely reduced forward flow and subsequent neurohumoral activation augment LAP; pulmonary capillary engorgement promotes alveolar haemorrhage and oedema

Understanding the Ventricular Pressure-Volume Loops in Normal and Pathological Conditions

Key Points

• End-Systolic Elastance (Ees):

  • Steeper slope indicates higher contractility.
  • Depressed ventricular contractility leads to a reduced Ees, and thus, a reduced stroke volume.

• Effective Arterial Elastance (Ea):

  • Represents the arterial load the ventricle must overcome to eject blood.
  • Increased Ea indicates increased arterial impedance, resulting in higher ventricular pressure to eject the same volume of blood.
  • Therapies that reduce arterial impedance can decrease Ea and restore SV.

Pathological Implications

• Reduced Ventricular Compliance:

  • Reduces EDV and SV while EDV is maintained at the expense of elevated end-diastolic pressure (frequently seen in heart failure).
  • Nitrates and diuretics lower EDV and hence end-diastolic pressure (EDP); this has the desired effect of lowering left atrial pressure (LAP) and limiting pulmonary congestion but may reduce preload and SV.

• Increased Arterial Impedance:

  • Increases the ventricular pressure required to eject blood and decreases SV.
  • Therapies that reduce arterial impedance (e.g., nitrates, restoration of coronary perfusion) can reduce Ea and restore SV.

• Depressed Ventricular Contractility:

  • Leads to reduced Ees and thus a reduced SV.
  • Therapies that improve contractility (e.g., inotropes) can restore Ees and ventricular ejection pressure, decreasing ESV and boosting SV.

• Elevated Left Atrial Pressure (LAP):

  • Seen in the right shift of the EDV due to elevated LAP, indicative of heart failure and fluid overload.

Summary

• Normal Conditions: Balance between ventricular contractility (Ees) and arterial impedance (Ea) ensures effective stroke volume and pressure.
• Pathological Conditions: Disruptions in Ees or Ea lead to reduced SV and elevated ventricular pressures.
• Therapeutic Interventions: Aim to restore the balance by reducing arterial impedance, improving ventricular contractility, and managing preload and afterload to optimize cardiac output and reduce congestion.

Negative Pressure Pulmonary Oedema (NPPE)

Pathogenesis

• Cause: Generation of high negative intrathoracic pressures in an attempt to overcome airway obstruction.
• Hydrostatic Mechanism:
  • Increased Preload and LV Afterload: Augmented venous return due to high negative pressures.
  • Hypoxia: Causes hypoxic pulmonary vasoconstriction (HPV) and decreased myocardial contractility, increasing pulmonary pressure.
  • Sympathetic Tone: Increased systemic vascular resistance (SVR) due to sympathetic stimulation.
• Mechanical Stress Mechanism:
  • Reduced microvascular integrity leads to increased permeability.

Pathophysiology

1. Hypoxia:
   • Detected by peripheral chemoreceptors, triggering sympathetic stimulation.
2. Airway Obstruction:
   • Commonly due to involuntary biting of the endotracheal (ET) tube or laryngospasm.
   • Patient attempts to inspire forcefully against the obstruction, causing highly negative intrathoracic pressure.
3. Acute Increase in Systemic Venous Return to Right Heart:
   • Increases pulmonary blood volume, raising pulmonary arterial and capillary pressure.
   • Leads to increased pulmonary interstitial pressure and trans-capillary pressure gradient.
4. Fluid Movement:
   • Fluid is pushed out of pulmonary capillaries into the interstitium, causing NPPE.

Mechanisms and Effects

• Fluid Surrounds Alveoli:
  • Decreases diffusion of alveolar O2 into pulmonary capillaries.
• Severe Cases:
  • Pressure and fluid build-up damage capillaries and alveolar walls.
  • Fluid and red blood cells enter alveoli, potentially being coughed up as frothy pink sputum.

Signs, Symptoms, and Lab Findings

• Chest X-Ray (CXR):
  • Shows diffuse bilateral infiltrates.
• Blood Gases:
  • Decreased PaO2 and oxygen saturation (Sats).

Management of NPPE

1. Maintain a Patent Airway:
   • Oxygen supplementation.
   • PEEP (Positive End-Expiratory Pressure) / NIV (Noninvasive Ventilation) guided by physical examination and ABG (Arterial Blood Gas) results.
2. Mechanical Ventilation:
   • Reserved for severe cases that do not respond to NIV.
3. Preload Reduction:
   • Use GTN (Glyceryl Trinitrate) if adequate blood pressure (e.g., SBP >100 mmHg).
   • May also provide beneficial afterload reduction effects.
4. Diuretics:
   • Often used, but there is no evidence of their utility and may exacerbate hypovolemia and hypoperfusion.
5. Clinical Course:
   • NPPE usually resolves rapidly within 12-48 hours when recognized early and treated immediately.

Neurogenic Pulmonary Edema

Pathophysiology of Pulmonary Edema in Acute CNS Injury

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Links

• Heart failure
• Ventilation and Weaning
• Pulmonary Hypertension
• Acute Respiratory Distress Syndrome (ARDS)

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References:

1. The Calgary Guide to Understanding Disease. (2024). Retrieved June 5, 2024, from https://calgaryguide.ucalgary.ca/
2. Anesthesia Considerations. (2024). Retrieved June 5, 2024, from https://www.anesthesiaconsiderations.com/
3. Reddi, B. A. J., Shanmugam, N., & Fletcher, N. (2017). Heart failure—pathophysiology and inpatient management. BJA Education, 17(5), 151-160. https://doi.org/10.1093/bjaed/mkw067

Summaries:

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© 2025 Francois Uys. All Rights Reserved.

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