Huffing and Puffing
Answer: E
A, B, C, and D are all examples of a circulatory shunt.
Normal cardiac shunts include:
Bronchial circulation – the bronchial arteries carry oxygenated blood at systemic pressures to the parenchyma; the bronchial veins drain into the pulmonary veins, where this poorly oxygenated blood mixes with oxygenated blood travelling to the left atrium to be pumped systemically.
Thebesian circulation – the coronary arteries perfuse the myocardium; the venae cordis minimae (Thebesian veins) drain into the cardiac chambers.
These two normal shunts account for the normal alveolar-arterial PO2 difference of 5-20 mm Hg.
Abnormal shunts include:
Cyanotic congenital heart disease – a wide spectrum of disorders that involve anatomical defects where poorly oxygenated blood bypasses the lungs and enters the systemic circulation (e.g. right-to-left shunt, bidirectional shunt, transposition of the great vessels).
Blood flow through atelectatic lung – the classic V/Q mismatch: pneumonia, asthma, ALI/ARDS, pulmonary embolus, interstitial lung disease, hemorrhage, among others.
Our child here has evidence of pulmonary edema. Recall that pulmonary edema may have various
etiologies:
Increased hydrostatic pressure – congestive heart failure causes increased chamber and pulmonary
hydrostatic pressures. The lymphatic system compensates by removing excess fluid in the pulmonary bed, until it is overwhelmed (left atrial pressure > 20 mm Hg). This is cardiogenic pulmonary edema.
Increased permeability – capillary or endothelial damage causes plasma proteins to leak into the interstitial space (e.g. ALI/ARDS, heroin overdose). This is non-cardiogenic pulmonary edema.
High surface tension – reduction in surfactant, fluid fills the alveoli. An example is newborn respiratory distress syndrome (hyaline membrane disease), seen mostly in premature infants.
Decreased osmotic pressure – loss of plasma proteins from liver disease, starvation, or hemodilution from resuscitation from large volumes of IV fluids or packed red blood cells (without other blood products).
Global hypoxia – right heart failure (cor pulmonale); examples include pulmonary hypertension, high altitude, pulmonary embolism, COPD.
Increased intrathoracic pressures – large negative intrathoracic pressures cause disruption of the
alveolar-capillary membrane, resulting in edema. Examples include drowning, laryngospasm, and post-obstructive edema following a choking episode.
Bottom line:
Not all that fluffs on chest xray is CHF!
Keeping the etiologies of pulmonary edema in mind will help the clinician to identify and treat the root cause of
the shunt early with the goal of improving morbidity.
References
McCullagh A, Rosenthal M, Wanner A et al. The bronchial circulation—worth a closer look: A review of the
relationship between the bronchial vasculature and airway inflammation. Pediatr Pulmonol. 2010; 45(1):1099-0496.
Wood SC. The ECC Book: Extracorporeal Circulation Continual Perfusion Education.
www.ecc-book.com.
A, B, C, and D are all examples of a circulatory shunt.
Normal cardiac shunts include:
Bronchial circulation – the bronchial arteries carry oxygenated blood at systemic pressures to the parenchyma; the bronchial veins drain into the pulmonary veins, where this poorly oxygenated blood mixes with oxygenated blood travelling to the left atrium to be pumped systemically.
Thebesian circulation – the coronary arteries perfuse the myocardium; the venae cordis minimae (Thebesian veins) drain into the cardiac chambers.
These two normal shunts account for the normal alveolar-arterial PO2 difference of 5-20 mm Hg.
Abnormal shunts include:
Cyanotic congenital heart disease – a wide spectrum of disorders that involve anatomical defects where poorly oxygenated blood bypasses the lungs and enters the systemic circulation (e.g. right-to-left shunt, bidirectional shunt, transposition of the great vessels).
Blood flow through atelectatic lung – the classic V/Q mismatch: pneumonia, asthma, ALI/ARDS, pulmonary embolus, interstitial lung disease, hemorrhage, among others.
Our child here has evidence of pulmonary edema. Recall that pulmonary edema may have various
etiologies:
Increased hydrostatic pressure – congestive heart failure causes increased chamber and pulmonary
hydrostatic pressures. The lymphatic system compensates by removing excess fluid in the pulmonary bed, until it is overwhelmed (left atrial pressure > 20 mm Hg). This is cardiogenic pulmonary edema.
Increased permeability – capillary or endothelial damage causes plasma proteins to leak into the interstitial space (e.g. ALI/ARDS, heroin overdose). This is non-cardiogenic pulmonary edema.
High surface tension – reduction in surfactant, fluid fills the alveoli. An example is newborn respiratory distress syndrome (hyaline membrane disease), seen mostly in premature infants.
Decreased osmotic pressure – loss of plasma proteins from liver disease, starvation, or hemodilution from resuscitation from large volumes of IV fluids or packed red blood cells (without other blood products).
Global hypoxia – right heart failure (cor pulmonale); examples include pulmonary hypertension, high altitude, pulmonary embolism, COPD.
Increased intrathoracic pressures – large negative intrathoracic pressures cause disruption of the
alveolar-capillary membrane, resulting in edema. Examples include drowning, laryngospasm, and post-obstructive edema following a choking episode.
Bottom line:
Not all that fluffs on chest xray is CHF!
Keeping the etiologies of pulmonary edema in mind will help the clinician to identify and treat the root cause of
the shunt early with the goal of improving morbidity.
References
McCullagh A, Rosenthal M, Wanner A et al. The bronchial circulation—worth a closer look: A review of the
relationship between the bronchial vasculature and airway inflammation. Pediatr Pulmonol. 2010; 45(1):1099-0496.
Wood SC. The ECC Book: Extracorporeal Circulation Continual Perfusion Education.
www.ecc-book.com.