2.4 Ventilation-Perfusion relationships.pptx

Ventilation- Perfusion Ratios Lecture Outline I. Concept of Matching Ventilation and Perfusion II. Consequences of High and Low Ventilation (V) and Perfusion (Q) III. Testing for Nonuniform Distribution of Inspired Gas and Pulmonary Blood Flow IV. Regional V/Q Differences and Their Consequences in t...

Ventilation- Perfusion Ratios Lecture Outline I. Concept of Matching Ventilation and Perfusion II. Consequences of High and Low Ventilation (V) and Perfusion (Q) III. Testing for Nonuniform Distribution of Inspired Gas and Pulmonary Blood Flow IV. Regional V/Q Differences and Their Consequences in the Lung 1 Ventilation- Perfusion Ratios Objectives 1.Identify the major components of gas exchange 2.Identify the contributions of normal ventilation and perfusion 3.Explain ventilation:perfusion ratio both in excess and less than 0.8 4.Describe the reasons for nonuniform ventilation of the alveoli 5.Review the measurement of pulmonary blood flow using a Swan-Ganz catheter 6.Describe nonuniform distribution of pulmonary blood flow 7.Understand mismatch regarding physiologic, anatomic, and absolute shunts 8.Identify the purpose of the shunt equation 9.Explain physiologic dead space 10.Summarize regional differences in ventilation and perfusion 11.Identify compensatory mechanisms for abnormal VA/Q ratios 12.Identify how V/Q ratios related to gravity 2 References Assigned reading from your text: Levitzky Chapter 5 3 I. Concept of Matching Ventilation and Perfusion 4 Gas Exchange  Gas exchange between alveoli and pulmonary capillary blood maintained by matching of Alveolar ventilation brings O2 into the lung and removes CO2 Mixed venous blood brings CO2 into the lungs and takes up alveolar O2 Influences on Mixed Venous Blood  Influences on mixed venous blood brings CO2 into the lungs and takes up alveolar O2 (Active factor) (table 4-2 Levitzky) Neural regulation; - Pulmonary vasculature is sparsely innervated compared to systemic - Larger, less muscular vessels more innervated - Sympathetic innervation may increase PVR and decrease distensibility - Parasympathetic Innervation produces vasodilation Humoral/chemical regulation: - Drug effects on pulmonary vascular smooth muscle and PVR - Pulmonary vasoconstrictors increase PVR – Alveolar hypoxia and hypercapnia – Low pH of mixed venous blood – Catecholamines NE and epinephrine; NE > Epi – Histamine (systemic vasodilator- pulmonary vasoconstrictor), PGF2a, PGE2 - Pulmonary vasodilators decreased PVR increases blood volume - Acetylcholine, NO, β-adrenergic agonist isoproterenol, PGE1 and PGI2 Intrinsic autoregulation produces vasoconstriction - HPV constricts precapillary pulmonary vessels; alveolar hypoxia or hypercapnia II. Consequences of High and Low Ventilation (V) and Perfusion (Q) 8 Normal Ventilation And Perfusion  Alveolar ventilation is normally ~ 4.2-5 L /min  Mixed venous blood is normally ~ 5 L/min Qc= pulmonary capillary perfusion  VA/Qc (the ratio of alveolar ventilation to capillary perfusion) – PAO2 and PACO2 are determined by the relationship between VA and Qc – Alterations in the ratio result in changes in PAO2 and PACO2 – V/Q for the whole lung approximates VA/Qc for all alveolar-capillary units – V/Q for the whole lung is roughly 0.8-1.2 Altered ventilation-perfusion  Ventilation-perfusion ratio: relationship between alveolar ventilation & pulmonary blood flow Expressed quantitatively: VA alveolar ventilation Q cardiac output (pulmonary blood flow)  VA/Q in excess of 0.8 – – – High VA/Q indicates alveolar ventilation exceeds perfusion Delivery of O2 relative to its removal increases Removal of CO2 relative to its delivery increases – Result PAO2 increases and PACO2 decreases Alveolar gases become more like ambient air  VA/Q ratio less than 0.8 – – – Low VA/Q indicates perfusion is in excess of alveolar ventilation Delivery of CO2 relative to its removal increases Removal of O2 relative to its delivery increases – Result PAO2 decreases and PACO2 increases Alveolar gases become more like mixed venous blood Consequences of High and Low V/Q  Effect of changes in the ventilation-perfusion ratio on the alveolar PO2 and PCO2 Ventilation-perfusion ratios: – – – Close to 1.0 Result in alveolar PO2s of approximately 100 mmHg and PCO2s close to 40 mmHg Greater than 1.0 increase the PO2 and decrease the PCO2 Less than 1.0 decrease the PO2 and increase the PCO2  V/Q Along a Continuum- Alveolar dead space (infinite) and intrapulmonary shunt (zero) represent the two extremes of ventilation-perfusion ratios A. Normal B. Airway occluded – V/Q = 0 – A right-to-left shunt C. Pulmonary embolus – V/Q approaches infinity – Alveolar dead space 11 Ventilation-perfusion ratio line on an O2-CO2 diagram O2-CO2 diagram and the ventilation-perfusion ratio curve (line) A. Normal O2/CO2 diagram B. Zero PO2 and PCO2 of mixed venous blood C. Infinite Has the PO2 and PCO2 of inspired air The position of the V/Q ratio line is altered if the partial pressures of the inspired gas or mixed venous blood are altered 12 Dead Space and Shunt  Matched ventilation and perfusion = optimal gas exchange at the alveolar-capillary unit Dead Space Normal- physiologic dead space Shunt Normal- physiologic shunt Allows fresh gas to reach alveoli that lack perfusion Allows some blood to reach the arterial system without passing through ventilated regions of the lung More ventilation than circulation More circulation than ventilation Alveoli are overventilated or underperfused; eg hypotension Intrapulmonary shunts- alveoli are underventilated or overperfused (a major cause of hypoxemia) eg atelectasis Shunts may be extrapulmonary- CHD/VSD Increased a-A CO2 difference Increases the required minute ventilation for gas exchange Increased A-a O2 difference Does not respond to increased FiO2 Small shunts can be detected by measuring PaO2 during FiO2 1.0 (100%) 13 III. Testing for Nonuniform Distribution of Inspired Gas and Pulmonary Blood Flow 14 Nonuniform Ventilation Of The Alveoli  Can be caused by: Uneven resistance to airflow due to: – collapse of airways- emphysema – bronchoconstriction- asthma – decreased lumen – inflammation – obstruction- mucus – compression- edema/tumors Nonuniform compliance in different parts of the lung – fibrosis – regional variations in surfactant production – pulmonary vascular congestion or edema – emphysema – diffuse or regional atelectasis – pneumothorax – compression by tumors or cysts 15 Nonuniform Distribution of Pulmonary Blood Flow  Nonuniform distribution of pulmonary blood flow may be due to: embolization or thrombosis compression of pulmonary vessels by high alveolar pressures, tumors, exudate, edema, PTX destruction or occlusion of pulmonary vessels by various disease processes  Angiograms with radiolabeled macroaggregates of albumin Lung scans after IV administration of dissolved Xe 16 Expired Nitrogen Concentration Versus Number Of Breaths During A Nitrogen Washout A. Normal subject: N decreases predictably- straight line B. Normal subject after inhalation histamine Maldistribution of airways resistance produces a complex curve After initial period of rapid N washout, there is a longer period of slow N washout indicating a population of poorly ventilated “slow alveoli” Indicates nonuniformity of ventilation 17 Testing for mismatched ventilation& perfusion includes calculations for:  Physiologic shunt – – Right-to-left shunt is the mixing of venous blood that has not been oxygenated into arterial blood Physiologic shunt should = physiologic dead space Anatomic Shunts = venous blood that enters LV without entering pulmonary capillaries – Normal physiologic, anatomical shunts = 2-5% CO from bronchial, thebesian, and pleural veins – LV output normally greater than RV – Pathological right-to-left intracardiac shunts can occur, eg tetralogy of Fallot Absolute Intrapulmonary shunts- aka true shunts – Mixed venous blood perfuses pulmonary capillaries of unventilated or collapsed alveoli Shuntlike States– Shunt-like states are alveolar-capillary units with low VA/Qc lower arterial O2 content – Blood draining these units has a lower PO2 than blood from well-matched unit 18 Intrapulmonary Shunting  That part of the cardiac output that does not exchange with alveolar air – Right-to-left shunting Physiological shunt corresponds to anatomic dead space – Physiologic shunt = Anatomic shunt + Intrapulmonary shunt – Intrapulmonary shunt = Absolute shunt and Shunt-like states 19 Anatomic Shunts  Systemic venous blood entering the LV without entering pulmonary vasculature 2-5% of CO and includes venous blood from bronchial, pleural, and thebesian veins Output of the LV is normally greater than that of the RV in adults  Contributions from: Blood from bronchiolar capillaries from lower respiratory airways Thebesian veins drain musculature of the heart into all four chamber – Smallest cardiac veins of the left atrium and ventricle deoxygenated  oxygenated Visceral pleural capillaries anastomose with pulmonary venules oxygenated blood 20 Intrapulmonary Shunts  Absolute intrapulmonary shunts Mixed venous blood perfusing pulmonary capillaries associated with unventilated or collapsed alveoli  aka “true shunts” Supplemental O2 will not improve an anatomic or absolute -“true”-shunt  Shunt-like state Alveolar-capillary units with perfusion in excess of ventilation – Most variable and complex type of shunt Occurs in an alveolar-capillary units that have: – An excess of pulmonary blood flow – Decreased or poorly ventilated alveoli – Impedance to oxygen perfusion Blood leaving this unit has an O2 content < blood from a normal unit – Supplemental O2 should improve a shuntlike state 21 The Shunt Equation  Shunt equation conceptually divides all alveolar-capillary units into two groups: – Shunt- all – Well matched V/Qs – Venous admixture = the ratio of shunt flow to cardiac output May be CO perfusing absolutely unventilated alveoli Or a larger portion of CO could be overperfusing poorly ventilated alveoli – Arterial blood determined from a systemic artery – Mixed venous blood from a pulmonary artery (mixed venous) sample – O2 content at end of pulmonary capillaries calculated from alveolar air equation – Using varying FiO2s will saturate alveoli with very low V/Qs; – Only areas of absolute shunt will contribute to the Qs/Qt *Very high inspired O2 concentrations may lead to absorption atelectasis 22 Dead Space  Physiologic dead space Bohr equation is used to determine the physiologic dead space Physiologic- anatomic dead space = alveolar dead space (infinite V/Q) Alveolar dead space results in increased arterial-alveolar CO2 difference Arterial PCO2 > end tidal PCO2 usually indicates alveolar dead space  Alveolar and arterial PO2 treat as equal although the PaO2 is a few mmHg < PAO2 Normal (A-a) DO2 is due to: – some degree of ventilation-perfusion mismatch (most important) – normal anatomic shunt (small contribution) – diffusion limitation in some parts of the lung (slight) Normal (A-a) Do2 is 5-15 mmHg in a young healthy person at sea-level and increases about 20 mmHg between ages 20-70 Clinical estimate of alveolar-arterial PO2 difference = Age/4 + 4 mmHg – Another estimate is ratio of PaO2 / FiO2 should be > 200 < 200 = ARDS 23 Examples of Distributions of V/Q Ratios in Normal Subjects X-axis = V/Q ratios displayed logarithmically Y-axis = amount of V or Q going to alveolar-capillary units with the V/Q ratios on the x-axis Almost all blood flow and ventilation go to alveolar-capillary units with V/Q ratios near 1 Younger subject- There is no V or Q of units with ratios below 0.3 or above 3.0 Middle-aged subject- wider dispersion with more perfusion going to units with ratios >3.0 and much more going to units with ratios apex – There is normally more gas exchange in the lower regions of the lung because they receive more blood Apical regions of lungs have high VA/Q ratios (>1.0)  Greater ventilation: blood flow PAO2 increased to ~ 130 mmHg; PACO2 decreased Basal regions of lungs have low VA/Q ratios (