Congestive Heart Failure (CHF) and Pulmonary Insufficiency

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What is congested in CHF?

The lungs.

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Why the lungs?

When cardiac output falls, the kidney releases renin. Renin converts angiotensinogen to angiotensin I in the liver. Angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE) in the lung. Angiotensin II stimulates release of aldosterone from the adrenal and antidiuretic hormone (ADH) from the posterior pituitary. Both aldosterone and AHD collaborate to increase blood volume. As the left ventricle fails, blood is backed up in the lungs. As the pulmonary vasculature fills, intravascular hydrostatic pressure pushes fluid into the pulmonary extravascular space, “congesting” the lungs. Lung congestion prevents ventilated alveoli (Va) from matching up with pulmonary capillary blood flow (Q).

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What is Va/Q?

The ratio of alveolar ventilation to perfusion.

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What should Va/Q be?

Equal, or one.

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What is the alveolar-capillary surface area of a healthy pair of lungs?

About the size of a singles tennis court.

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What is it called when alveoli are not ventilated (Va = 0) but are perfused?

A shunt.

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What is it called when alveoli are ventilated but are not perfused?

Dead space.

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What is functional reserve capacity (FRC)?

The volume of air left in your lungs when you stop exhaling after a normal breath.

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What is closing volume?

As we exhale down below FRC toward residual volume (RV), we reach a point at which we close off terminal airways so that alveoli are no longer ventilated but are perfused, creating a shunt. Closing volume (CV) is the minimum volume required to keep airways from collapsing.

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Why is closing volume important in CHF?

As our patients go into CHF their FRC decreases below the CV, so that alveolar collapse and the corresponding shunt become prominent during normal tidal breathing.

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