2.3 Blood Flow to the Lung Objectives.docx

2.3 Blood Flow to the Lung Objuectives Define the terms dead space and shuntsee 2.4 Objectives Describe bronchial circulation Bronchiole Circulation—2% Cardiac Output of LV Arises from aorta or intercostal arteries and supplies tracheobronchial tree and structures to terminal bronchioles (They also...

2.3 Blood Flow to the Lung Objuectives Define the terms dead space and shuntsee 2.4 Objectives Describe bronchial circulation Bronchiole Circulation—2% Cardiac Output of LV Arises from aorta or intercostal arteries and supplies tracheobronchial tree and structures to terminal bronchioles (They also provide blood flow to the hilar lymph nodes, visceral pleura, pulmonary arteries and veins, vagus, and esophagus.) Drainage by azygos system of veins (*proximal segment) + a substantial portion enters pulmonary veins (*distal segments) Part of the normal anatomic right-to-left shunt Functions - Air conditioning of inspired air May function as collateral circulation for gas exchange airways New vessels can branch from the bronchial veins if pulmonary circulation is blocked collaterals may supply other airways Regulation of bronchial circulation Some vasoconstriction Explain pulmonary circulation according to its functions Compare systemic and pulmonary circulation Pulmonary Circulation is Equal to 100% of Cardiac Output Entire output of the RV and supplies lung with mixed venous blood draining all tissues of the body Lung structures distal to terminal bronchioles (*aka anything involved in gas exchange) receive O2 directly by diffusion from alveolar air and nutrients from mixed venous blood of pulmonary circulation Pulmonary circulation holds ~500 ml of blood ~70 ml located in pulmonary capillaries Functional pulmonary capillaries are pulmonary arterial segments and capillaries 280 billion pulmonary capillaries supply 300 million alveoli (alveoli completely enveloped) Pulmonary capillary diameters average 6 um; average erythrocyte is ~ 8um (*so they have to “bend” to get through) An RBC takes 4-5 seconds to travel through at resting CO Functions of Pulmonary Circulation Major function is gas exchange Also: Blood reservoir - primarily for the left ventricle; Can transiently compensate Pulmonary circulation holds ~500 ml of blood ~70 ml located in pulmonary capillaries Filter to trap emboli, gas bubbles, and cellular debris etc. Absorption of exogenous fluid from inner surface of alveoli: Pulmonary capillary endothelium is much more permeable to water and solutes than is alveolar epithelium Edema fluid accumulates in interstitium before alveoli Similarities to the Systemic Circulation Pulmonary circulation has: A pump- the right ventricle The same circulating volume/min as cardiac output from the LV ~ 5L/min Similar vessel types: Distributing vessels - arteries and arterioles Exchange vessels - pulmonary capillaries Collecting vessels - venules and veins Normally there are four pulmonary veins that enter the left atrium One from each lobe Right upper and middle combine (*this is why we only have 4) Differences from systemic circulation Pulmonary vessels have thin walls & less vascular smooth muscle and offer much less resistance to blood flow*** ~ 1/10 the resistance of the systemic circulation Distribution of resistance: 1/3 in each vessel type: distributing, exchange, and collecting 70% of resistance of systemic circulation in distributing vessels Vessels are more compliant (more distensible) than systemic circulation*** And have lower intravascular pressures They are more compressible than systemic arteries Pulmonary vessels in the thorax are subject to alveolar and IPPs that can change greatly. Transmural pressure difference is a major determinant of PVR Permits for increases in blood flow without increasing blood pressure Allows for less resistance to flow compared to systemic BP Vasoconstrict in response to hypoxia = Hypoxic Pulmonary Vasoconstriction *different bc in systemic hypoxia actually causes dilation** **passive factors- distention & recruitment are the 2 things that allow a lot more blood flow without major increase in pressures!** Normal pressures in pulmonary circulation Pulmonary circulation conducts the entire CO from the pulmonary artery to the left atrium with a low driving pressure Drop in pressure in pulmonary circulation-from the PA to the left atrium is ~ 10 mmHg Drop in pressure in systemic circulation is ~ 100 mmHg Identify determinants of pulmonary vascular resistance (PVR must be CALCULATED) Pulmonary vascular transmural pressure difference is an important determinant of PVR “As the transmural pressure difference (which is equal to pressure inside minus pressure outside) increases, the vessel diameter increases and resistance falls; as the transmural pressure difference decreases, the vessel diameter decreases and the resistance increases. Negative transmural pres~ sure differences lead to compression or even collapse of the vessel.” Thin walls (compared to systemic circulation) Subject to alveolar and intrapleural pressures that can change greatly Vascular smooth muscle can actively contract or relax in response to neural and humoral factors- but Passive factors play a major role in determining PVR PVR is 1/10 SVR *bc it’s a low pressure system (sometimes called TPR) Distribution of resistance: 1/3 in each vessel type: distributing, exchange, and collecting (compared to systemic where 70% resistance is from arterial system) ” Gravity, body position, lung volume, alveolar and intrapleural pressures, intravascular pressures, and right ventricular output all can have profound effects on PVR without any alteration in the tone of the pulmonary vascular smooth muscle.” Describe the change in pulmonary vascular resistance at various lung volumes Alveolar capillary walls Distend when blood volume inside increases Compress when alveolar air pressure increases At high lung volumes: Extra-alveolar vessel resistance to blood flow decreases (bc the negative IPP increases the difference of the TMP thus, allowing the extra-alveolar vessels to expand—also, the radial traction pulls the vessels more open) Alveolar vessel resistance to blood flow increases (bc they become compressed by expanding alveoli & elongated inc in length & dec in radius = inc resistance) At forced low volumes: Extra-alveolar vessel resistance to blood flow increases (IPP becomes positive and compresses extra-alveolar vessels—smaller radius gives them less radial traction which also contributes to the inc in resistance) Alveolar vessel resistance to blood flow decreases *during insp IPP becomes more negative = dec resistance & better flow (same with extra-alveolar); but intra-alveolar are gonna be stretched and get inc resistance @high lung vol *at forced low vol- extra-alveolar will have inc resistance to flow bc of inc IPP; alveolar will have dec resistance to flow Describe how the location of vessels affects their resistance Location of alveolar vessels affects their resistance: Alveolar and extraalveolar vessels are two Groups of resistances in series Their resistances are additive at any volume PVR is usually lowest at FRC and increases at higher and lower lung volumes *graph is showing at RV (all air is forced out-aka low lung volumes) we have high extra-alveolar resistance and low alveolar resistance *at TLC (breathing in as much air as possible) we have low extra-alveolar resistance and high alveolar resistance *at FRC the resistance is lowest bc there is no extreme pressure changes *we want low PVR for forward flow Describe how increased cardiac output affects pulmonary vessels PVR decreases with increased CO (*bc of distention and recruitment) Allows for less resistance to flow compared to systemic arteries and arterioles Effects of increased cardiac output: Increasing blood flow to the lungs (eg exercise) only increases mean pulmonary artery pressure slightly Resistance to pulmonary blood flow decreases A passive event- not hormonal or nervous Understand distention and recruitment of vessels in pulmonary circulation PVR decreases with increases in pulmonary blood flow, pulmonary artery pressure, left atrial pressure, or pulmonary capillary blood volume because of: Distention of already open blood vessels (*engorgement/ inc volume) Recruitment of previously unopened vessels Or Both Distention increases diameter of vessels Increased perfusion pressure in capillaries Poiseuille’s law and r4 factor R = 8ηl/πr4 Recruitment opens “closed” capillaries Particularly in the apical region of the lung Blood flow is diverted to previously “closed” capillaries Newly opened vessels decrease resistance Both distention and recruitment occur: During exercise With removal of lung tissue (*so this is how we can have large inc of CO during things like exercise, without increasing PVR—from the passive (NOT neural or hormonal related) events of distention and recruitment) *helps with changed in removal of areas of perfusion to adapt (ie, lobectomy; hysterectomy) Identify the effects of gravity on pulmonary blood pressure and zones of the lung In physiologic person: Lungs are ~30cm in height Pulmonary artery enters at the hilum two vertical columns of blood each 15cm in height One above the pulmonary artery/hilum and One below the pulmonary artery/hilum Hilar region is approximately at the midpoint, ie 15cm below apex/15 cm above base A column of pulmonary blood of 15cm exerts a pressure of 11mm hg at its base Example if pulmonary arterial pressure is 25/8: From the pulmonary artery to apexblood must overcome a pressure = 11mm hg 25 - 11 = 14 is pulmonary arterial blood pressure at apex 8 - 11 = -3 From the pulmonary artery to base column of blood exerts a pressure of 11 mmHg higher 25 + 11 = 36 8 + 11 = 19 According to Starling’s forces base of the lung is the first place pulmonary edema occurs (*bc of higher pressures) Interaction of Gravity and Extravascular Pressure: Zones of the Lungs There is more blood flow in the lower regions of the lung than in upper regions. The effects of pulmonary artery pressure, pulmonary vein pressure, and alveolar pressure on pulmonary blood flow are described as the “zones of the lung”. Experiments done on excised lungs of experimental animals to demonstrated three zones of pulmonary blood flow Parameters: PA= alveolar pressure; Pa = pulmonary arterial pressure /Systolic Even in uppermost regions is normally > alveolar pressure Pv = pulmonary venous pressure /Diastolic *can effect pulmonary blood flow through relationships btwn arteries & veins (resistance) or with high alveolar pressures (aka inc fluid in alveoli) *note: Pa is ALWAYS > Pv Zone 1- No blood flow (PA>Pa>PV) Capillary pressure is never > alveolar P Ventilated but not perfused Alveolar dead space Does not normally exist Hypovolemic states / PPV *Zone 1: can occur w/ +pressure ventilation, hemorrhagic crisis, & anesthesia. Alveolar pressure exceeds arterial pressureno forward blood flow because of higher pressures in alveoli Zone 2- Intermittent blood flow(Pa>PA>PV) Normally from 10 cm above heart to apex *intermittent bc of effects from zone 1 and 3 *Zone 2- Higher pressure of pulmonary artery (compared to Alveoli) allows some blood flow but not as much as zone 3 Zone 3- Continuous blood flow(Pa>PV>PA) Normally from 10 cm above heart to base (*majority of lung bc higher blood flow/ventilation) During exercise and recumbent, all lung zone 3 (*bc of recruitment or gravity) PCWP is measured with the catheter tip in Zone 3 Lying down- blood flow per unit volume is still greater in the gravity-dependent regions of the lung *Zone 3: maintence of pul. Blood flow, matches with ventilation (aka no V/Q mismatch in normal pt here). Pulm artery pressures and pulmonary vein both > alveoli pressures so able to have best blood flow here (flow not impeded by high alveoli pressures) Understand the mechanism and contribution of hypoxic pulmonary vasoconstriction HPV redistributes blood to ventilated alveoli- Mitigates Shunt Mitigates shunt- it is a local response to alveolar hypoxia or hypercapnia Diverts blood away from poorly ventilated or unventilated alveoli Not CNS- effect persists in transplant patients (*local response) Arterioles supplying hypoxic alveoli constrict If PO2 of alveoli decreases, the smooth muscle in the arterioles will be exposed to decreased PO2s outside the vessel, causing them to constrict Inhibition of O2-sensitive voltage-gated K+ channels depolarizes smooth muscle cells in the small branches of the pulmonary artery The influx of calcium causes vascular smooth muscle contraction HPV occurs in response to alveolar hypoxia and alveolar hypercapnia (hypoventilation) *anesthetic GASES obliterate this HPV response Normal alveolar-capillary unit B. Perfusion of a hypoventilated alveolus sends venous blood to left atrium HPV increases the resistance to blood flow to the hypoventilated alveolus Blood is diverted away from the hypoventilated alveolus Describe hemodynamics during positive pressure breathing Effects of Mechanical Ventilation (PPV) on Pulmonary Blood Flow During negative-pressure (eupnea) breathing During inspiration decreased IPP increased venous return Decreased blood to left heart decreased LV filling and stroke volume Positive pressure ventilation decreases pulmonary blood flow Decreases CO by decreasing RV preload and increasing right atrial pressure IPP is positive during inspiration without PEEP IPP is positive throughout the respiratory cycle with PEEP Also increases intrathoracic pressure which compresses great veins/ lower venous return PPV increase afterload of RV by increasing PVR During inspiration, resistance to pulmonary blood vessels increases Alveolar pressure is also positive which compresses the capillaries Positive alveolar pressures and decreased venous return (*ie mechanical ventilation) Increase Zone 1 Increase alveolar dead space PPV (esp with PEEP) may decrease or prevent low ventilation-perfusion ratios (shunt) List and describe 5 main conditions that can produce pulmonary edema Pulmonary Edema – Extravascular Accumulation Of Fluid In The Lung Starling’s principle of capillary exchange- normal conditions Net reabsorption of water is into the pulmonary capillary at arteriolar and venule ends This net reabsorption is one mechanism for absorbing exogenous water from alveoli Plasma colloid osmotic pressure- does not change along the length of capillary The only force that can be measured clinically (*keeps fluid in vessel & out of alveoli) Hydrostatic pressure of plasma along capillary- remains less than πPC of plasma Factors Predisposing To Pulmonary Edema: Starling Forces and Surface Tension -Capillary endothelium is more permeable to water and solutes than alveolar epithelium In pulmonary edema: Fluid moves from capillaries interstitium alveolus Factors associated with Starling’s principle: Increased alveolar-capillary unit permeability allows fluid to flow alveolus Infection, O2 toxicity, circulating or inhaled toxins Increased pulmonary hydrostatic pressure (pc) - Pulmonary hypertension Fluid overload from excess IV fluids CHF, mitral stenosis, left ventricular MI, emphysema Decreased plasma colloid osmotic pressure (πpc) – Protein loss Renal and liver disease and malnutrition Surface tension: In surfactant deficiency, surface tension forces are increased Fluid is drawn from pulmonary capillary to inner surface of alveolus Factors Predispose To Pulmonary Edema: A Very Negative IPP A very negative IPP can lead to pulmonary edema Forceful inspiration against a closed glottis or other upper airway obstruction Laryngospasm can result in negative-pressure pulmonary edema: A very negative IPP is created to overcome resistance for inhalation Reduces the interstitial hydrostatic pressure creates a subatmospheric alveolar P Promotes transudate of fluid from capillaries interstitium alveoli Small vessel damage may result in frank hemorrhage into alveoli (pink froth) Laryngospasm is an airway obstruction- the spasm is maintained after stimulus passed Morbidity/mortality related immediately to hypoxemia and hypercapnia Obstructions not relieved immediately negative-pressure pulmonary edema Tx: Deepen anesthetic, Larson’s maneuver, give succinylcholine Clinical picture related to degree of obstruction and inspiratory effort: Partial airway obstruction produces high-pitched stridor Give positive pressure ventilation with a facemask, head extension, and jaw thrust Complete obstruction is silent Positive pressure mask ventilation forces air into piriform fossa *can give 1cc of succ if really bad Factors Predispose To Pulmonary Edema: Pulmonary Hypertension Pulmonary hypertension can lead to pulmonary edema Causes of pulmonary hypertension: Primary or idiopathic pulmonary hypertension Left heart failure Emphysema Destruction of alveolar septa/pulmonary capillaries H+ ions from acidosis causes vasoconstriction Hypoxia causes vasoconstriction in pulmonary vessels HPV Factors Predispose To Pulmonary Edema: Hypoxic Pulmonary Vasoconstriction Hypoxic pulmonary vasoconstriction Alveolar hypoxia or atelectasis active vasoconstriction in pulmonary circulation Vascular smooth m. constriction near the alveoli in the arterial, precapillary vessels May be localized to small region of lung or global Global hypoxia of the whole lung eg at high altitude pulmonary edema