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RESPIRATORY MECHANICS
PA = alveolar pressure PIP = intrapleural pressure PB = atmospheric pressure
Transmural Pressures:
PTP = PA - PIP PTC = PIP – PB PTT = PA - PB
Compliance: C = DV Clung = DV 1 = 1 + 1
DPTransmural DPTP CT CL CCW
Hysteresis- Expiration and inspiration curves are different - Takes less PTP to maintain a particular volume during expiration - Mainly due to surface tension forces at the air-liquid interface of alveolus - Small contribution due to elastic properties of lung tissue
Minimum volume = lung is removed from intrapleural space and allowed to collapse
Degassed lung- Lung has minimum volume removed - Alveoli are completely collapsed - PTP to get first inflation - Beginning with next inflation back to normal
Saline filled lung- ¯ pressure - lung compliance ( volume and ¯ PTP) - ¯ Hysteresis b/c air-liquid interface ruined
Surface Tension Forces
Law of Laplace P = 2 T r
Dilemma- bubbles with equal surface tensions - different radii - bubbles with ¯ radii will have pressure - \ smaller bubbles will empty into larger bubbles
Solution- surfactant adjusts the tension with changes in surface area - tension with area / ¯ Tension with ¯ area - \ PA is equal in all alveoli at the end of expiration - detergent decreases surface tension but is independent of the surface area
Lung with surfactant removed- resembles degassed lung - PTP needed each time the lung is inflated - ¯ hysteresis - lung contains less air at a particular pressure - resembles Respiratory Distress Syndrome
Functional Residual Capacity (FRC) - volume in lung at end of normal expiration - elastic forces of chest wall and lungs are exactly balanced
Interaction between Lung and Chest- Chest wants to expand - Lungs want to collapse - \ PIP is negative (subatmospheric) - \ In Pneumothorax (puncture) the lungs are collapsed to MV and chest is expanded (PIP = 0 = PB)
Lung Pressures in Normal Lung-Chest SystemAt FRC, PIP = -5 cm H2O PTP = PA – PIP 0 – (-5) = 5 cm H2O PA = 0 PTC = PIP – PB (-5) – 0 = -5 PB = 0 PTT = PA - PB 0 – 0 = 0
Fig. 7.11Above FRC - contribution of PTC towards PTT decreases until zero at the equilibrium point of the chest wall - up until the chest wall reaches its equilibrium it is helping to expand lung - after reaching the equilibrium point of the chest wall the respiratory muscles must do additional work to expand chest and lung - positive airway pressures
At FRC- airway pressure = 0 (atmospheric)
Below FRC - negative airway pressures - chest resists expiration
Poiseuille’s Law
Flow = DP r4 p inspiration: DP = PB - PA Flow = DP h l 8 expiration: DP = PA – PB R R=resistance
Re > 2000 = turbulent airflow ® DP ® resistance to breathing
Dynamics of Breathing1. diaphragm and intercostal muscles contract 5. respiratory muscles relax 2. volume of alveoli 6. ¯ volume 3. ¯ PA (PA < PB) 7. PA (PA > PB) 4. air flows into lungs 8. air flows out of lungs
Flow – Volume curves- airflow rises rapidly then declines during most of the expiration - it is virtually impossible to go outside of the curve - this is due to the compression of the airways by intrathoracic pressure (EPP) - there is no flow at the EPP \ transmural pressure = 0 - driving force of the upstream segment from the alveolus depends on lung volume and elastic recoil not on the force of expiratory muscle contraction
Base of Lung Apex of Lung compliance PIP is the most negative ventilation PTP is the most positive perfusion
SPIROMETRY
Measures - lung volumes - flow rates Results given as - flow-volume loops - volume-time curves
Max inspiratory volume (TLC) is decreased by - ¯ inspiratory muscle strength - in elastic recoil of lung or chest wall
Max expiratory volume is decreased by - residual volume - ¯ expiratory muscle strength - airway resistance - airways that close at higher volumes
Obstructive Lung Disease
Asthma COPD (emphysema)Chronic brochial inflammation Chronic brochial inflammation Episodic bronchospasm loss of alveolar- capillary wall ¯ x-sec area of bronchi, resistance, ¯flow ¯ x-sec area of bronchi, resistance, ¯flow
Normal inspiratory capacity Reduced expiratory flow Reduced expiratory flow ¯ flow rate (slope) ¯ flow rate (slope)
TLC TLC ¯ Lung markings, reduced elastic recoil ¯ Lung markings, reduced elastic recoil normal FVC normal FVC reduced FEV (and FEV/FVC) reduced FEV (and FEV/FVC)
¯ PO2 (low V/Q) ¯ PO2 (low V/Q) ¯ PCO2 (increased V in response to hypoxemia) variable PCO2
RESTRICTIVE PULMONARY DISEASE
Pulmonary Fibrosis Respiratory Muscle WeaknessInflammation and fibrosis Normal lung Reduced compliance Reduced muscle strength
Reduced inspiratory capacity Reduced inspiratory capacity normal expiratory flow normal expiratory flow flow rate (slope) abnormal ventilation perfusion relationships
¯ TLC ¯ TLC lung markings, elastic recoil abdominal paradox ¯ FVC ¯ FVC ¯FEV (ratio okay) ¯FEV (ratio okay)
¯ PO2 (low V/Q) ¯ PO2 (low V/Q) ¯ PCO2 (increased V in response to hypoxemia) variable PCO2 DIFFUSION
Mixed Venous BloodPO2 = 40 mmHg PCO2 = 45 mmHg
PO2 - of air = .21(PB – 47) » 150 mmHg - in alveolus (PAO2) » 100 mmHg
PCO2 in alveolus = 40 mmHg
Fick’s Law of Diffusion
Flow = (d) A (P1 –P2) diffusion capacity = (d) A = flowO2 T T PAO2 – PpcO2
d = diffusion constant A = area available for diffusion T = thickness of diffusion barrier PC = pulmonary capillary
DCO2 = 1.25 DCCO DCco = flowco PACO
Pulmonary capillary blood - equilibrates from 40 to 100mmHg in .25 sec - has until .75 sec so there is some slack
Factors determining PACO2
Vdot = FACO2 x VA
PACO2 = (863) VCO2 PACO2 means ¯ in ventilation VA
Hyperventilation = ¯ PCO2 Hypoventilation = PCO2
Alveolar Gas Equation
PAO2 = .21 (PB – 47) – PACO2 .82
BLOOD FLOWPulmonary Circulation vs. Systemic CirculationVery low Pressures Pressures 10x higher Mean pulmonary = 15 Mean systemic = 100 Right Ventricle (begins) = 25 Left ventricle = 120 Left atrium (ends) = 5 Right atrium = 2
Thin vessel walls Thick vessel walls Little smooth muscle Abundant smooth muscle
Extra – alveolar vessels¯ pressure Radial traction pulls these vessels open
Alveolar vesselsExposed to alveolar pressure Increasing PA squishes these vessels
Pulmonary vascular resistanceFlow = DP \ Resistance = DP R V(CO)
DPpul = 15 – 5 = 10 DPsys = 100 – 2 = 98 V (CO) is the same for both, \ pulmonary vascular resistance must be 1/10 that of systemic
Pulmonary vascular resistance = 15 – 5 = 1.7mmHg/L/min CO = 6 L/min 6 mean pulmonary arterial pressure = 15 left atrium pressure = 5
Pulmonary vascular resistance ¯ as pulmonary arterial or venous pressures 1. Recruitment – chief mechanism from low to high pressures 2. Distension – chief mechanism at relatively high pressures
Lung volumes ¯ resistance on pulmonary arteries (extra – alveolar) resistance on pulmonary capillaries (alveolar)
Measurement of Pulmonary Blood Flow
Blood flow through lung = VO2 (consumption) [O2]a - [O2]mV
Zone 1 Does not occur under normal conditions PA > Pa > Pv No blood flow is possible b/c capillaries are squashed flat Considered as alveolar dead space (ventilated but not perfused)
Zone 2Pa > PA > Pv Blood flow is determined by the difference between arterial and alveolar pressures (instead of venous)
Zone 3Pa > Pv > PA Blood flow is determined y the difference between arterial and venous pressures
Hypoxic pulmonary vasoconstriction“The lung is a noble organ” contraction of smooth muscle in hypoxic region depends on PO2 of alveolar gas (not pulmonary arterial blood)
Where does the fluid go when it leaves the capillaries?First: Interstitium of alveolar wall ® interstitial space ® perivascular and peribronchial spaces ® lymph Later: Alveolar spaces ® alveoli
Functions
1. Gas exchange 2. Reservoir for blood 3. Filter blood 4. Trap white blood cells 5. Synthesis of phospholipids (PC for surfactant) 6. Syntheses of proteins (collagen and elastin) 7. Carbohydrate metabolism (mucus) 8. Vasoactive substances metabolized (receives whole circulation so well suited to modify blood-borne substances) -activation: AI ® AII with ACE -deactivation: bradykinin with ACE serotonin from uptake and storage prostaglandins NE 9. Arachidonic acid metabolites (leukotrienes, prostaglandins, and thromboxane A2)
VENTILATION – PERFUSION RELATIONSHIPS
Hypoxemia = low PO2
1. Hypoventilation alveolar and arterial PCO2 PACO2 = (863) CO2 production (if ventilation is halved, then PCO2 is doubled) VA
Alveolar gas equation PAO2 = PIO2 - PaCO2 PIO2 = .21( PB – 47) R R = .82 2. Imcomplete Diffusion Part of the reason why PO2 of arterial blood is not the same as that in alveolar gas
3. Shunt Blood which enters the arterial system without going through ventilated areas of lung Contributes to why PO2 of arterial blood is not the same as that in alveolar gas Bronchial artery blood, coronary venous blood (Thesbian veins) Giving O2 to patient will not make a difference
4. Ventilation – Perfusion Ratio Most common cause of Hypoxemia
Inspired air PO2 = 150 mmHg Inspired air PCO2 = 0
Normal alveolar PO2 = 100 mmHg Normal alveolar PCO2 = 40 mmHg
Mixed venous blood PO2 = 40 mmHg Mixed venous blood PCO2 = 45 mmHg
VA/Q ratio is lower in base than apex Ventilation and perfusion are both increased in base However perfusion is increased more ¯ the ratio
CO2 retention b/c - chemoreceptors - ventilation
A-a gradient
PaO2 - PAO2
TRANSPORT
O2 transport
Carried in two forms 1. Dissolved in plasma [O2]dissolved = .03 PO2
2. Hemoglobin 14.7g of Hb in 100ml blood each gram of Hb has capacity to carry 1.39 ml of O2
O2 content = dissolved O2 + Hb-O2 = .03 PO2 + (1.39 x Hb x Sat.)
O2 capacity = 1.34 x [Hb]
% Hb-O2 saturation = O2 combined with Hb x 100 O2 capacity
Significance of shape of oxygen dissociation curveAt high PO2 values changes can occur in PO2 without altering % Hb saturation (flat portion of curve)
Shift to the rightDecreased affinity for O2 Increased temperature Decreased pH ( H+) Increased BPG Increased CO2
Carbon monoxideBinds Hb 210x more strongly than oxygen ¯ O2 carrying capacity O2 affinity
Carbon dioxide Transport1. Dissolved [CO2]dissolved = .7 PCO2 (20x more dissolvable than oxygen)
2. Carbamino – CO2
3. Bicarbonate Majority is carried as bicarbonate Chloride shift Haldane effect: blood increases its ability to carry CO2 when it is deoxygenated
CO2 dissociation curve is steeper and more linear
See schematic of Gas exchange in tissues (RBC) |