Pulmonary Vascular Resistance, Cardiac Output, and Gas Exchange (Pulmonary Pt. 2)

Flashcards covering pulmonary vascular resistance, cardiac output measurement, regional blood flow, gas exchange, V/Q matching, pulmonary edema mechanisms, diffusion capacity, and acid-base balance.

Pouseille's Law (Pulmonary Vascular Resistance)

Pi – Po = Q x R, where Pi is pressure at the arterial side, Po is pressure at the venous side (e.g., mean arterial pressure for pulmonary), Q is pulmonary blood flow, and R is resistance.

Factors Contributing to PVR

Transmural pressure, gravity, body position, lung volume, alveolar and intrapleural pressures, intravascular pressures, and right ventricular output.

PVR and Lung Volume

PVR is lowest at Functional Residual Capacity (FRC) when all pressures are balanced.

Increased Lung Volume (above FRC) Effect on PVR

Increases PVR due to lengthening and compression of alveolar vessels while extraalveolar vessels expand.

Decreased Lung Volume (below FRC) Effect on PVR

Increases PVR due to increased intrapleural pressure, compression of extraalveolar vessels, and less traction on them.

Response to Increased Cardiac Output (Exercise)

Cardiac output can increase up to 3-fold, but mean pulmonary artery pressure (MPAP) increases by only a few mmHg, meaning PVR must fall passively through recruitment and distension of vessels.

Recruitment (PVR Reduction)

Opening of previously closed pulmonary vessels, increasing gas exchange surface and significantly affecting dead space.

Distension (PVR Reduction)

Widening of existing pulmonary vessels, increasing their diameter and decreasing resistance.

Positive-Pressure Ventilation Effect on PVR

Increases PVR due to compression and derecruitment of alveolar vessels.

Hypoxic Pulmonary Vasoconstriction

Principle mechanism of V/Q match where vessels in areas with low oxygen concentration constrict, helping in total lung hypoxia but poorly executed due to low smooth muscle content.

Active Regulators of PVR (Increase PVR)

Sympathetic innervation, norepinephrine, epinephrine, alpha-adrenergic agonists, PGF2, PGE2, thromboxane, endothelin, angiotensin, histamine, alveolar hypoxia, alveolar hypercapnia, and low pH of mixed venous blood.

Active Regulators of PVR (Decrease PVR)

Parasympathetic innervation, acetylcholine, beta-adrenergic agonists, PGE1, prostacyclin (PGI2), nitric oxide, bradykinin.

Fick Principle (Cardiac Output)

VO2 = Qt x (CaO2 - CvO2), where VO2 is oxygen consumption, Qt is cardiac output, CaO2 is arterial oxygen content, and CvO2 is mixed venous oxygen content. Allows calculation of cardiac output.

Swan-Ganz Catheter

A multiple lumen catheter with a float balloon used to measure pulmonary artery pressure (PAP) and cardiac output via dilution of cold liquid from a central vein to the pulmonary artery.

Regional Pulmonary Blood Flow (PBF)

Measured using methods like pulmonary angiography (detect emboli), radiolabeled microaggregates (lodge and image), or 133Xe (enters alveoli and imaging shows flow per unit area, often greater at the bottom of the lung due to gravity).

Dependence of Flow on Pa to PA Ratio

Flow is minimal or zero if alveolar pressure (PA) is greater than arterial pressure (Pa), and increases as Pa exceeds PA. This impacts ventilation/perfusion matching.

Mechanisms of Pulmonary Edema

Involves capillary filtration (Kf), capillary hydrostatic pressure (Pc), interstitial hydrostatic pressure (Pis), reflection coefficient (σ), plasma colloid osmotic pressure (πpl), and interstitial colloid osmotic pressure (πis). Increased Pc leads to fluid movement into lung tissue.

V/Q Mismatch

A continuum where ventilation-perfusion ratio (V/Q) above 1 indicates high V/Q (more ventilation than perfusion, higher O2, lower CO2), and V/Q below 1 indicates low V/Q (more perfusion than ventilation, lower O2, higher CO2).

Nitrogen Washout

A test involving inhaling 100% O2 and examining relative nitrogen content in expired air; the rate is proportional to V/Q match.

Shunts (Qs/Qt Ratio)

Indicates the fraction of cardiac output that does not participate in gas exchange, increasing with right-to-left shunts (anatomic or intrapulmonary), V/Q mismatch, impaired diffusion, and other factors.

Lung Structure and V/Q Match (Top vs. Bottom)

Due to gravity, the top of the lung has more negative intrapleural pressure, larger, less compliant alveoli (less ventilation) and lower vascular pressures (less blood flow, higher resistance). The bottom has less negative intrapleural pressure, smaller, more compliant alveoli (more ventilation) and greater vascular pressures (more blood flow, lower resistance).

Diffusion Capacity (DLCO)

A measure of gas transfer across the alveolar-capillary epithelium, specifically using carbon monoxide (CO) uptake. It is low when the barrier is thickened or alveolar surface area is decreased.

Causes of Reduced Diffusional Capacity

Thickening of the barrier (interstitial/alveolar edema or fibrosis, sarcoidosis, scleroderma), decreased surface area (emphysema, tumors, low cardiac output, low pulmonary capillary blood volume), or decreased uptake by erythrocytes (anemia, low pulmonary capillary blood volume, V/Q mismatch).

Elements Maintaining Acid-Base Balance

Lungs (regulate CO2, a weak acid, quickly), kidneys (regulate HCO3, a base, more slowly), and blood/tissues (buffering capacity).

Alveolar Ventilation and pCO2 Relationship

Inversely related: pCO2 = K / VAlv, where pCO2 is the partial pressure of CO2 in blood, K is a constant, and VAlv is alveolar ventilation.

Respiratory Acidosis

Caused by inadequate ventilation leading to increased pCO2, which results in a decrease in blood pH (acidemia). The kidneys compensate by increasing HCO3 reabsorption.