Physiology 2

This is a single gas exchanging unit consisting of an alveolus and its associated pulmonary capillary.

Acinus

How does respiratory alkalosis happen?

Increased alveolar ventilation leads to a drop in paCO2 HH ratio becomes larger. pH increases. All mechanisms opposite respiratory acidosis.

What is Zone 2 of pulmonary capillary perfusion?

Ppa > PA > Ppv (alveolar pressure is partially obstructing blood flow).

Can control anesthetized patients in terms of hypoventilation by controlling their Vmin (ventilates out CO2). How do we control Vmin?

Vmin = f x VT, so alter either.

What does the nose do?

Warms and humidifies air. Removes particles: Hairs at entrance of nostrils filter LARGE particles (nasopharynx). Deposited by impaction in the bends of the upper airways. Removed by mucociliary clearance. Turbulent precipitation or sedimentation removes medium sized particles (from small airways). Removed by mucociliary clearance. Diffusion deposits submicronic particles in the alveoli where they are removed by alveolar macrophages.

This is when you inhale air and use energy to inhale it, but the air never makes it out of the conducting airways for gas exhange.

Wasted ventilation (occurs all the way to terminal bronchioles). Wasted ventilation occurs in the "anatomic dead space."

What is the general pathogenesis of edema?

Water balance across any vascular endothelium is the result of 4 Starling forces: two of which favor water retention in the vascular compartment and two of which favor water movement out of the vascular compartment.

When the lung is not functioning as a gas exchanger, this is called?

lung consolidation

Transpulmonary pressure during inspiration becomes slightly more?

negative

Gas exchange is regulated by a ?

negative feedback loop.

At REST, in an open pneumothorax, what is the pressure inside the lungs and pleural cavity?

0 and 0 (both are equal to atmospheric pressure). The normally negative pleural cavity pressure has equilibrated with atmospheric. When PA = 0 and PL = 0 Then transpulmonary pressure (PA-PPL) = 0 and now the lungs have no opposing force holding them up. Atelectasis.

What is the solubility constant of O2 in blood?

0.003 ml O2/dL (dissolved O2)

Flow creates inflation and deflation of lungs. This is the PE for flow through a tube.

A pressure drop (conditions related to diaphragmatic contraction or relaxation create a pressure gradient condition).

This is the pressure difference between the mouth and the alveoli divided by a flow rate, or (Patm-Palv)/flow rate.

Airway resistance remember resistance is a pressure drop across a tube/ flow rate. Can only measure the pressure drop and flow and thus calculate R. We cannot measure R directly.

Microvascular leakage can lead to?

ARDS. Acute respiratory distress syndrome; which is acute development of frothy, high protein alveolar edema. How does the alveolar edema happen? Capillary endothelium normally keeps large molecules like albumin in the vessel. A disrupted "leaky" endothelium allows proteins out (mostly albumin), and these proteins carry water with them. Increased interstitial oncotic pressure, lead to water accumulating in the interstitial space and increasing interstitial hydrostatic pressure leads to water invading the alveoli. Once alveolar edema occurs, the survival rates are poor in all species, because the alveolar flooding is rapid.

What can make FRC increase?

Air trapping increases RV and thus FRC. Occurs during asthma, inflammation, infection, bronchoalveolar lavage, and mucus plugging. Air trapping = excessive constriction of smooth muscle in an airway, and air distal to that constriction can't escape. Can treat with bronchodilators. Also increased lung compliance in emphysema raises FRC. This is due to poor lung elasticity.

What are the causes of hypoventilation (which can lead to hypoxemia).

Airway obstruction (congenital abnormalities like in brachycephalic dogs, acquired anatomical defects like an elongated soft palate, collapsing trachea, inflammatory dzs, aspiration). Neuromuscular weakness or dysfunction (could be from neuromuscular blocking drugs like Nm antagonists, peripheral neuropathy, hypocalcemia, myasthenia gravis). Decreased chemoreceptor sensitivity from opioids, barbituates, inhalation anesthetics. There is an inverse relationship between decreasing paO2 and increasing paCO2.

These are facts about what receptor in the medulla? 1. Sensitive to increase in H+ in CSF/ECF 2. CO2 (not H+ or HCO3-) diffuses across the BBB into the CSF. 3. CO2 increases H+ concentration in the CSF via carbonic acid dissociation equation. 4. An increase in arterial pCO2 increases H+ in the CSF, which is detected by this receptor, and then send afferent impulses to: medulla respiratory centers, which send efferent impulses to respiratory mm, and those increase ventilation there by decreasing pCO2 and pH levels in the arteries back to normal.

CCRs. (mediate 70% of the CO2 response)

Why might a dog pant that does not have to do with thermoregulation?

Could be trying to compensate for acidemia from a metabolic problem. Eliminates CO2 Kidneys regulate acid-base balance by reabsorbing bicarbonate ions by the glomerulus. Kidneys put bicarbonate ions back in circulation to maintain balance. If kidneys aren't working well and not enough bicarbonate ions are being put back into circulation = metabolic acidosis. Animals compensate for this acidosis by increasing ventilation to get rid of more CO2.

This is an abnomal lung sound that is high-pitched, discontinous, and heard on inspiration (frequently louder during) AND expiration. Is the sound of air as it bubbles through mucus plugged airways.

Crackle

Cilia always beat in a power stroke towards the pharynx. Cilia in the lungs beat ? cilia in the pharynx beat?

Cranially, caudally

If the CO of the RV and LV are not equal what happens?

Congestion in the area behind the problem, which creates an increase in hydrostatic pressure in venous/capillary circulation and then extraversion of water at the site. Diffusion of water. The pulmonary circuit can handle the same output that the LV generates due to the fact that the pulmonary vasculature does not impose much resistance.

This law says that the rate of diffusion of gas through a surface is directly proportional to the gas solubility and inversely proportional to the square root of the molecular weight of the gas.

Graham's Law

PP of O2 in blood is ? than in interstitial fluid. PP of CO2 in interstitial fluid is ? than PP of CO2 in blood.

Greater, greater

This says that the concentration of a gas in SOLUTION is proportional to its partial pressure.

Henry's Law And thus, the transfer of gases across the respiratory surface is driven by a partial pressure gradient which is equivalent to a concentration gradient. Transfer of molecules of any kind between physiological compartments (across cell membrane etc) is driven by the concentration gradient between the 2 compartments.

How does your paO2 become low? (hypoxemia)

High altitude (O2 is always at 20% in the air but the barometric pressure is lower so you are not taking in as great of a density/amount of air). O2 supply malfunction during anesthesia. pAO2 decreases so paO2 decreases (disrupts paO2 and the concentration gradient is disrupted). As pAO2 becomes smaller, the PP gradient between the alveolar and blood compartments becomes smaller, so there is less PE for diffusion of O2 from alveoli to blood.

The shifting of the oxyhemoglobin dissociation curve to the left is related to what?

Higher saturation of hemoglobin with O2, at any given pO2. Hemoglobin has an increased affinity for O2. decreased H+ concentration (increase in pH) decreased pCO2 decreased temperature decreased concentration of 2,5 diphosphoglycerate Fetal hemoglobin is left shifted compared to an adult, so O2 will bind to the fetal Hb during placental circulation. Has a greater affinity for O2. Fetal hemoglobin.

What can low blood PaCO2 be caused by?

Hyperventilation, which can occur during hypoxemia. Decreases bicarbonate ions in blood (HCo3-)

This is when your paCO2 > 45 mmHg, and is determined by arterial blood gas analysis. Can cause hypoxemia (abnormally low paO2).

Hypoventilation normal paCO2 = 40 mmHg

What can cause PaO2 to be too low?

Hypoventilation. Pneumonia could cause this. Lung is not working well as a gas exchanger.

A less than normal PaO2 is called? It is also when an insufficient amount of O2 is dissolved in the blood. Should be between units of 80-100.

Hypoxemia (which is inefficient to saturate hemoglobin).

How does a pneumothorax cause a problem with preload?

In a pneumothorax, the normal negative pressure in the thorax is gone. The normal negative pressure potentiates venous return. If the pressure in the thorax becomes = 0 or + the vena cavae will conpress/collapse leading to a huge decrease in preload. Will be unable to circulate blood.

If the diaphragm contracts what is happening to the volume of the closed thoracic cavity?

Increasing and therefore is lowering P A. Air flows in.

Info slide about pulmonary circulation: The PP's of O2 and CO2 in blood are altered by alveolar perfusion and then systemic organ perfusion. Gas exchange in the pulmonary circulation rejuvenates the arterial gas tensions as both O2 and CO2 exchange between the pulmonary capillary blood and the alveolar gas which is renewed by ventilation.

Info slide

What are the forces favoring water movement out of the vascular space?

Interstitial oncotic pressure (pulls things out). Capillary hydrostatic pressure (pushes things out).

These receptors are in between airway epithelial cells. They respond to noxious gases, cigarette smoke, inhaled dusts, and cold air. They bronchoconstrict.

Irritant receptors.

What is an important characteristic of the CO2 dissociation curve?

It is much steeper than the oxyhemoglobin dissociation curve. That means that any incremental decrease in pCO2 caused by ventilation evokes a much more substantial decrease in total CO2 content.

These receptors are located in the alveolar walls of capillaries. They're activated when alveolar walls are thickened (e.g. due to edema). Cause rapid, shallow breathing, dyspnea.

J-receptors or Juxta-capillary receptors

The location of most airway resistance to flow occurs where?

Medium sized bronchioles (in the conducting zone). Very small bronchioles past these bronchi contribute little to resistance (small R) due to their incredible number (cross sectional area becomes so big, R is reduced, and flow increases). Dz can effect these smaller areas in terms of increasing R if those areas are filled with junk.

What cells secrete the pleural fluid into the potential space AS pleura is stretched?

Mesothelial cells

What is the 4th cause of pulmonary edema?

Microvascular leakage. This is damage to the pulmonary capillary endothelium secondary to inflammation, infection (pneumonia), or exposure to noxious substances (chlorine gas, sulfur dioxide). Albumin leaks into the alveolar interstitial space, which leads to an increase in hydrostatic and osmotic (oncotic) pressures outside the capillaries.

This occurs when all alveoli are ventilated equally, and blood flow through all pulmonary capillaries is the same for all alveoli, and the V/Q = 1 for all acini.

Perfect lung

This is a ventilation-perfusion abnormality that can cause hypoxemia. It is not anatomic but physiologic because the cardiovascular anatomy is normal. Blood does actually go to the lung via the pulmonary circulation. It is characterized by conditions wherein regional ventilation is impaired with no change in blood flow. Perfusion goes to where pAO2 is low, and O2 is not added to the blood in that region (blood exposed to the defective alveoli).

Physiologic right to left shunt (venous admixture). V/Q < 1

Lungs are covered by a layer of the pleura, and the chest wall is covered by a layer of pleura. The potential space between these 2 layers of pleura is filled with a thin layer of?

Pleural fluid (in pleural cavity)

This means the alveoli are filled with inflammatory things.

Pneumonia

What are some causes of physiologic right to left shunts? V/Q < 1

Pneumonia Pneumothorax Masses in lung Atelectasis (including absorption atelectasis from 100% O2 breathing). Diaphragmatic hernia Gravitational effects

This is an accumulation of air inside the pleural cavity.

Pneumothorax

What is Zone 3 of pulmonary capillary perfusion?

Ppa> Ppv > PA Most animals at rest are in this zone. A little near the hilus in zone 2. NONE in zone 1. Zone 3 = the alveolar pressure presents no effect on pulmonary circulation. During exercise, Ppa > Ppv > PA. However, blood flow improves in the dorsal part of the lung. Not so much in zone 2 anymore.

This is the number of molecules in a closed space and the number of collisions these molecules make with the walls of the space. More frequent collisions leads to a higher pressure. (The number of collisions is essentially the temperature or how fast the molecules move).

Pressure of a gas

Pv=nRT is the?

Pressure-Molecule relationship Lung volume and temperature are constants, so the equation can be reduced to: P =nC. P is pressure, n is number of molecules, C is constant everything else. Which says that gas pressures are essentially due to the number of molecules present.

The goals of respiration are?

Provide O2 to tissues and remove CO2 from tissues.

What are the 4 functional events of respiration?

Pulmonary ventilation (the inflow and outflow of air between the atmosphere and alveoli). Diffusion of O2 and CO2 between alveoli and blood Transport of O2 and CO2 between blood/body fluids to tissue/cells Regulation of respiration (nervous system control)

As alveolar size decreases, surface tension pressure of the fluid coating the inside of the alveoli ? but surfactant concentration increases as it is spread over a smaller surface area. Thus, the surface tension of the water is neutralized.

increases

The mechanics of lung expansion and contraction occur by 2 methods:

1. Caudal and cranial movement of diaphragm 2. elevation/depression of ribs

If the length of a tube doubles R increases by a factor of?

2

How long is the transit time for blood to go through a pulmonary capillary? From the arterial end to the venous end?

250 ms.

The venous end of a tissue capillary bed has a pCO2 of?

45mmhg

Oxidative metabolism in tissues leads to pCO2 of ? in CELLS.

46 mmhg

The pH of blood should be?

7.4

This says as the volume of a closed container increases, pressure decreases and vice versa, with everything else held constant.

Boyle's Law (breaks down if thorax is compromised).

This is the capacity that blood has for holding O2.

Hemoglobin saturation or SPO2/SO2. Should be 95% or higher.

The brainstem part of the central controller is located where? These areas control inspiration and expiration, are poorly defined collections of neurons, and are not nuclei.

pons and medulla

All physiological pressures (respiratory, circulatory, esophageal, etc) are expressed relative to a ? value reference atmospheric pressure.

zero

Abnormally low paO2 is? (should be higher than 80 mmHg)

hypoxemia

This is related to the dissociation of carbonic acid by the Henderson-Hasselbalch equation.

pH of blood. pH = pKa + log (HCo3-)/(o.o3 x pCO2) Normal pH is 7.4 As long as the HCO3-/0.03 x pCO2 ratio remains 20, pH will be 7.4

What are lungs suspended by in the thoracic cage?

Mediastinum

Air flow forces during quiet breathing: 1. at rest 2. during inspiration 3. during expiration

1 at rest = respiratory muscles are at rest. The recoil force of the lung and chest wall are equal but opposite. Pressure along the whole tracheobronchial tree is atmospheric. No flow. But beware! At rest the P PL (-4) and PA (0) are not the same. They are only the same in a pneumo. 2 during inspiration = inspiratory muscles contract and chest expands. Alveolar pressure becomes subatmospheric with respect to pressure at glottis. Air flows into lungs. 3. during expiration = inspiratory mm relax and the recoil of the lung causes alveolar pressure to exceed pressure at airway opening (more + compared to atmospheric pressure). Air flows out of the lungs.

What is the main force, and also the secondary force for negative pleural pressure?

1. (main force) responsible for negative pleural pressure, even during expiration = elastic recoil of the lungs. Lungs want to recoil further, but the elastic force outward from the thoracic wall prevents that. 2. secondary force that contributes to a slightly negative pleural pressure = continuous suction of excess pleural fluid into lymphatic channels causes a slightly negative P PL. Also the surface tension of the alveolar fluid draws alveoli in.

The normal position for mammal hemoglobin is determined by 3 key X, Y points: ?

1. 95-100% saturation of hemoglobin with O2 is at a paO2 of 100mmHg 2. 75% saturation of hemoglobin with O2 is at paO2 of 40 mmHg (normal venous circulation on its way back to the pulmonary artery, or in the pulmonary artery before gas exchange). 3. 50% saturation of hemoglobin with O2 at 28 mmHg. This is called the p50 value. *The partial pressure of oxygen in the blood at which the hemoglobin is 50% saturated.

What are conditions that affect the total O2 content in the blood?

1. Anemia. This is an abnormally low hemoglobin concentration. It can come from hemmorrhage, hemodilution, chronic diseases, cancers involving bone marrow, RBC production. 2. Polycythemia. This is when hemoglobin is abnormally elevated. Some cancers cause this. Adapting to altitude causes this. 3. Hypoxemia (from any cause). Hemoglobin loading is a dependent variable of pO2. When pO2 is abnormally low (hypoxemia) the Hb-O2 part of total O2 will be low also. Hemoglobin will not be as saturated with O2. and when... When Hb-O2 is less than 98% of blood O2, the concentration gradient for O2 to diffuse across the respiratory surface is disrupted. Which is why hypoxemia is so devastating. Not enough O2 is around to saturate hemoglobin.

What are the 2 types of pneumothorax?

1. Closed pneumothorax = a discontinuity of the lung parenchyma, without an opening between the chest and the atmosphere. Caused by rib fractures or a ruptured bulla. Bulla = a sac of air/gas in the lung tissue itself. 2. Open pneumothorax = a puncture wound to the chest. Pneumothorax = air in the pleural cavity

Describe the pulmonary circulation loop.

1. Deoxygenated blood is pumped from the right ventricle to the pulmonary artery. 2. Blood moves through smaller and smaller pulmonary arteries and arterioles until it goes through the pulmonary capillary beds which are intimately associated with the alveoli. 3. Blood returns to the left atrium via the pulmonary venules and veins. 4. Oxygenated blood is pumped to the systemic circulation from the left ventricle.

How is CO2 carried in blood? 3 forms.

1. Dissolved CO2 (which obeys Henry's Law -- says that the concentration of a gas in SOLUTION is proportional to its partial pressure.) Dissolved CO2 is about 20 times more soluble in blood than O2. Dissolved CO2 accounts for about 10% of the CO2 difference between arterial and venous blood. 2. Bicarbonate. CO2 + H2O catalyzed by carbonic anhydrase ----> H2CO3 ----> H+ and HCo3 - (which is bicarbonate). This is the carbonic acid dissociation equation. 90% of CO2 in arterial blood is carried as bicarbonate. It accounts for about 60% of the CO2 difference between arterial and venous blood. 3. Carbamino compounds. Hb . NH2 + Co2 <-----> Hb.NH.COOH Carbamino compounds makes up 5% of arterial CO2, and 30% of the A-V difference for CO2. *When carbon dioxide binds to haemoglobin, carbaminohemoglobin is formed, lowering haemoglobin's affinity for oxygen via the Bohr effect. In the absence of oxygen, unbound haemoglobin molecules have a greater chance of becoming carbaminohaemoglobin.

What are the 2 components of compliance?

1. Elastic forces of lung tissue. (e.g. how the elastin and collagen fibers are interwoven around the lung parenchyma. In a deflated lung the fibers are contracted and kinked. In an inflated lung, the fibers are stretched and unkinked with elastic PE for returning the lung to its resting volume). 2. Forces from surface tension. (e.g. the fluid on the inner surfaces of the alveoli also have surface tension, which is when water molecules are attracted to one another via hydrogen bonding and bead up. Contraction of H2o surface attempts to collapse alveoli as lungs deflate, but surfactant decreases the surface tension of the water which helps to prevent alveolar collapse. Surfactant reduces surface tension, is secreted by Type II alveolar epithelial cells (which make up 10% of alveolar surface) and surfactant is phospholipid containing).

Within elastic recoil. What are the forces promoting alveolar collapse?

1. Elasticity of the pulmonary connective tissue 2. Alveolar surface tension

Patterns of airflow include?

1. Laminar flow/Tubular flow = occurs mainly in small peripheral airways where the rate of airflow through an airway is low. Is a smooth sheet of molecules moving through a tube. Associated with less resistance. 2. Turbulent flow at high flow rates in the trachea and larger airways. Turbulent flow slows flow rate down, because resistance is increasing in the airway, since molecules are bumping into each other. *A large increase in pressure difference is required to maintain flow if it becomes turbulent. Lung dz is often characterized by things that create turbulent flow. 3. Transitional flow occurs in larger airways, especially at branches and at sites of narrowing. This occurs in most airways.

What are the requirements for gas exchange into the lung?

1. Movement of air to and from the air-blood barrier. (from ventilation, V). 2. Diffusion of gas across the respiratory barrier. 3. Movement of blood to and from the respiratory barrier (perfusion or Q) 4. A matching of ventilation and perfusion

What are the two main ways oxygen is carried in blood?

1. O2 dissolved in blood (this is about < or equal to 2% of all total O2 in blood). 2. O2 in combination with hemoglobin (> or equal to 98% of total O2 in blood).

What are the forces that favor water retention in the vascular space?

1. Plasma oncotic pressure -- a function of albumin concentration in plasma. With a lot of albumin in the plasma, water from outside will want to come into the capillary lumen. *Oncotic pressure = form of osmotic pressure exerted by proteins, notably albumin, in a blood vessel's plasma (blood/liquid) that usually tends to pull water into the circulatory system. 2. Tissue pressure -- Hydrostatic pressure of the interstitium.

What are the 3 important pressures that cause the movement of air into and out of the lungs?

1. Pleural pressure (or intrapleural pressure). = Pressure inside the pleural space or pleural cavity. Normally subatmospheric, or negative. Abbreviated P PL(subscript). Pressure lies external to lungs. Negative P PL is due to the elastic recoil forces of the lungs and the thoracic wall force directed outward. These are opposing forces. 2. Alveolar pressure = Pressure inside the alveoli. Abbreviated P A (subscript). Pressure inside alveoli at the END of passive exhalation (or glottis is open) is 0 (or atmospheric). If the alveolar pressure is different than atmospheric pressure, flow is moving in or out of the lungs. If alveolar pressure = to atmospheric or o = no flow is occurring. 3. Transpulmonary pressure= P TP (subscript) = P A - P PL. Normally P A > P PL (P A being greater than P PL contributes to lung inflation or non-collapse). This pressure is the difference between alveolar and pleural pressure. This is the pressure across the lung field. IS ALSO CALLED RECOIL PRESSURE.

What are the 3 pressures that cause movement of air?

1. Pleural pressure/intrapleural pressure (P pl) -- the pressure inside the pleural space. Is a negative pressure due to the elastic recoil forces of the lungs and thoracic wall in opposing directions. 2. Alveolar pressure/intrapulmonary pressure (Pa) -- the pressure inside the alveoli. Is atmospheric if glottis is open. 3. Transpulmonary pressure (Ptp). Is Pa-Ppl. Normally Pa > Ppl. Transpulmonary pressure is the difference between the alveolar pressure and the pleural pressure in the lungs.

How does pulmonary vascular resistance decrease as vessel pressure OR flow rises? (right ventricular output, CO, is increased).

1. Recruitment: capillaries closed under normal conditions begin to open and conduct blood as pressure rises. This accomodates flow increase. 2. Distension: the individual capillaries increase in size at high vascular pressures and obtain a larger cross-sectional area. There is a very small increase in pressure when right ventricle CO increases due to a lack of resistance by the aforementioned. Pressure and resistance are directly related. Key point: if you give a patient a positive ionotrope, SV increases out of both the right and left ventricles. Systemic arterial pressure will increase, but there will be VERY little increase in pulmonary arterial pressure, due to the lack of resistance change. If RV occurs it is because pulmonary resistance HAS increased. HW dz is an example. They obstruct the pul artery and RV does not have the contractile strength to deal with it. No hypertrophy, RV just gives up.

What is the physiology of a cough?

1. Subepithelial irritant receptors are stimulated. Send afferent nerve impulses up the vagus nerve to the brain. Triggers an automatic sequence of events: 2. Air is rapidly inspired into lungs. Air gets trapped in lungs when epiglottis and larynx close. 3. Expiratory and abdominal muscles contract. 4. Pressure in lungs goes up. 5. Larynx and epiglottis open, air in lungs under pressure explodes out (75-100 mph). 6.Intrapulmonary pressure (lung pressure) exceeds pressure in the airway lumen. Noncartilaginous parts of trachea and bronchi collapse. Air explodes through bronchial and trachial slits. Is a protective mechanism

What are the 4 lung volumes (component volumes) which are NOT discrete anatomical volumes?

1. Tidal volume (V T) = Volume of air inspired or expired with each normal breath. No effort to inhale or exhale. Occurs during normal quiet breathing. Can be estimated. 2. Inspiratory Reserve Volume (IRV) = maximum extra volume of air that can be inspired above normal tidal volume. (Is beyond tidal volume, so doesn't include tidal volume). 3. Expiratory Reserve Volume (ERV) = maximum extra volume of air that can be expired by forceful expiration after the end of normal tidal expiration. 4. Residual Volume (RV) = volume of air remaining in the lungs after the most forceful expiration. Volume left after ERV. We can combine these volumes in a few ways to create "capacities".

Within elastic recoil. What are the forces preventing alveolar collapse?

1. Transmural pressure gradient (or Transpulmonary Pressure) which is the transpulmonary pressure acting across the alveolar surface. P A should be 0 at rest and P PL is negative at rest. P A - P PL = a + number. 2. Pulmonary surfactant which opposes surface tension 3. Alveolar interdependence or pores of Kohn. These vary by species. This is a way to get alveoli to inflate if a tube is blocked. Alveoli are interdependent and communicate with one another via pores. Harder for atelectasis to happen bc there is enough alveolar interdependence so that they can inflate each other if one inflates. Smaller animals have way more of these than larger animals. When an alveolus can inflate because of a communication with its neighbor it is called collateral ventilation.

What is the general airflow pattern?

1. Upper airway (nose, pharynx, larynx) 2.Tracheobronchial tree 3. Alveoli (where gas exchange occurs between the lung and bloodstream).

What are the two components of compliance?

1. elastic forces of lung tissue: Elastin and collagen fibers are interwoven among the lung parenchyma. In deflated lungs fibers are contracted and kinked. In expanded lungs fibers become stretched and unkinked with elastic potential energy for returning the lung to its resting volume. 2. forces from surface tension: Fluid on inner surfaces of alveoli also have surface tension, contraction of the H2O surface attempts to force air out and collapse alveoli. Surfactant decreases surface tension of water, which helps to prevent alveolar collapse. Alveolar collapse is called atelectasis. *Pulmonary surfactant is a surface-active lipoprotein complex (phospholipoprotein) formed by type II alveolar cells. The proteins and lipids that make up the surfactant have both hydrophilic and hydrophobic regions. By adsorbing to the air-water interface of alveoli hydrophilic head groups in the water and the hydrophobic tails facing towards the air, reduces surface tension of fluid coating inner surface of alveoli. Reduces surface tension when added to a liquid = surfactant Is amphiphilic.

What is the pO2 of blood entering tissues capillaries?

100 mmhg

At rest, what is the average pAO2 of someone who has just inspired?

104 mmHg

As the radius of a tube is halved, R increases by a factor of?

16

At rest what is the average paO2 of blood that is on the arterial side of a pulmonary capillary bed (coming in for gas exchange).

40 mmHg

The arterial end of a tissue capillary (going into the capillary bed) has a pCO2 of?

40 mmhg

What is the pO2 of blood leaving tissue capillaries?

40 mmhg

The pCO2 of blood at the venous side of a pulmonary capillary bed is?

40 mmhg (extra CO2 left via diffusion into alveolus and out through ventilation). The diffusion part happened before the blood passed more than 1/3rd of the way through the capillary.

The pCO2 of blood entering arterial end of pulmonary capillary bed is?

45 mmhg

What is the R equation?

8nl/pir^4 where n = viscosity and l is the tube length

What is a sneeze?

A cough applied to the nasal passages. Stimulus = irritation of nasal pathway. Afferent nerve signals trigger sneeze reflex Physiology is similar to cough, but with uvula depressed so air is rapdily pushed through nose. Is a protective mechanism.

What is a shunt?

A fraction of CO where deoxygenated blood enters systemic circulation (e.g., an anatomic shunt can be a congenital defect, or an anatomic right to left shunt as witht the bronchopulmonary vein, is normal). Reduces systemic oxygenation. Another physiologic right to left shunt = in pneumonia, alveoli are not ventilated although they are perfused.

What is in the potential space between the visceral pleura of the lungs and the parietal costal pleura?

A thin layer of pleural fluid (in the pleural cavity, a potential space).

What is panting?

A way the respiratory system can regulate temperature. The animal's respiratory center responds to stimuli and core body temperature. Heat is dissipated by increasing anatomical dead space ventilation, which provides cooling by evaporation of water from the mucous membranes of the nose, mouth, and upper airway tissues. Dogs can only sweat on feet, which is a small surface area for dissipating heat. They cannot thermoregulate by sweating.

As lung volume decreases R (airway resistance imposed) does what?

Airway resistance increases logarithmically. At very low lung volumes, small airways may totally close. This is why you ventilate during anesthesia -- to keep airways open so gas can exchange. As a lung inflates there is traction from the surrounding tissue on the tubing contained within it. Pulls on tubing. This is called radial traction. Radial traction decreases as a person exhales and the size of the airways decrease (smaller r = greater R). Conductance is also related to volume, so as airway resistance increases, conductance decreases and vice versa. Conductance = the volume conducted over time per pressure drop. Conductance is inversely related to resistance.

Alveoli that are ventilated but not perfused is ?

Alveolar dead space. V/Q > 1. Alveolus is no longer functional due to altered pulmonary perfusion. Alveoli in this case are basically an extension of the conducting airways. Could occur in hypotension or ineffective circulating volume from any cause such as: dehydration, hemmorhage, sepsis, vasodilating drugs (reducing preload), pulmonary vascular obstruction (such as a pulmonary embolism, fat embolus, thrombus) positive pressure ventilation (which is lung inflation by positive airway pressure that can cyclically impede pulmonary blood flow), RHF, or HW stuck in the right ventricle and pulmonary artery (alveoli that are perfused by the restricted pulmonary artery are not being perfused well at all) ... all of these can lead to alveoli not being perfused as well.

Pulmonary edema is classified according to the location of fluid accumulation. Where are 2 types of pulmonary edema?

Alveolar edema = from fluid accumulation in the alveoli themselves, which is a serious problem. It obliterates the gas space, resulting in hypoxemia. It washes out surfactant, altering pulomonary compliance. How does alveolar edema happen? = Infection or toxin can disrupt the alveolar epithelium. Albumin can get out of the capillary and take water with it. Increased interstitial hydrostatic pressure recruits water into the alveoli. V/Q < 1. Creates a physiologic right to left shunt. Interstitial edema = fluid accumulation in the alveolar interstitial space, between the alveolar epithelium and capillary endothelium.

This relates the decrease in alveolar oxygen to the increase in alveolar CO2 during hypoventilation.

Alveolar gas equation paO2 = piO2 - (pACo2/R) piO2 = PP of inspired O2 R = respiratory quotient which refers to the molecular ratio of CO2 production/O2 consumption. A normal R is 0.8 The alveolar gas equation shows that when R = 0.8, the fall in alveolar pO2 is slightly greater than the rise in pCO2 during hypoventilation. Equation can also be pAO2 = FIO2 x (P baro press - PH2o) - (1.25 x PaCO2). This equation shows us that the paO2 should be at least 80, but normally the PaO2 should be 100 and the PaCO2 should be between 35-45.

Where exactly are Starling's forces operative in the lungs?

Alveolar interstital space (between the alveoli and pulmonary capillary). The 4 Starling forces direct the extraversion of water from pulmonary capillaries into the alveolar interstitum. Alveolar interstitial edema does not influence gas exchange because it is not in the alveoli. How does this water that gets into the alveolar interstitium during interstitial edema escape? There are no lymphatics in the alveolar interstitium . The water must migrate to the extraalveolar interstitial space (space around the bronchi and pulmonary arteries). Movement due to ventilation and pressure squeezes the alveolar interstitial space and water moved toward the extra alveolar interstial space, where there ARE lymphatics to drain the extra water. It is rare for water to get into the alveoli due to the alveolar epithelium being way less permeable than capillary endothelium. Can happen during ARDS when there is a disruption of the normal alveolar epithelial barriers. Even normally there is a continuous flow of fluid from the pulmonary capillaries through the capillary endothelium to the alveolar interstitial space. It is when water flow is excessive that edema occurs.

This is the total volume of new air entering the gas exchange areas of the lung per minute. This is EFFECTIVE ventilation. Not Vmin because Vmin is just the air per minute moving into the respiratory passages, not gas exchange areas. Some gas you inhale never gets to alveoli; some gas only makes it to the anatomic dead space. That gas is part of Vmin but not this value.

Alveolar ventilation Alveolar ventilation is one of the major determinants of the concentrations of O2 and CO2 in the alveoli and thus, the blood. Equation for alveolar ventilation rate = VA = (Vmin-VD) x f Where VA = the rate of alveolar ventilation per minute (cc/min) VD = physiologic dead space volume. The volume difference here is what got into the actual alveoli in cc/breath. and f = the amount of tidal breaths per minute.

Any volume of entire lung that is ventilated but not participating in gas exchange. *Airways that take no part in gas exchange because they don't have alveoli.

Anatomic dead space (synonomous with conducting airways). However, alveoli filled with water are not an anatomic dead space.

This area includes the trachea, the bronchi, and the bronchioles.

Anatomic dead space. The volume of the anatomic dead space is related to the tidal volume because the amount of traction on airways from surrounding tissue changes with changing tidal volume. Larger VT leads to greater traction so a larger anatomic dead space happens. Smaller VT leads to less traction so a smaller anatomic dead space happens. The volume of the anatomic dead space changes as a result of contraction or airway relaxation of airway smooth muscle. (affected by Beta 2 adrenergic which relaxes smooth muscle, muscarinic cholinergic which constricts, histamine 1).

This is the 4th cause of hypoxemia. It is a congenital defect in which exists a true anatomic route for blood flow from the venous (deoxygenated, right heart) circulation to the arterial (oxygenated, left heart) circulation. It is a variable fraction of cardiac output that never actually goes to the lungs. It is not oxygenated.

Anatomic right to left shunt Includes such defects like Tetraology of Fallot and Eisenmenger's physiology which is when you have a reversal of left to right shunts because of vascular hypertrophy (like a reversed PDA, reversed VSD). V/Q < 1

What can make FRC decrease?

Anesthesia due to the relaxation of the diaphragm and intercostal mm. Also gravitational effects. Won't take in as much air. Pressure less negative in alveoli. Thorax does not expand as much (greater volume) as well as the recoil force of the thorax is less effective at keeping lungs from collapsing. Post-operative pain (esp after thoracotomy) -- painful chest expansion during tidal breathing can result in decreased effort to take in air and FRC decreases. ANY pneumothorax (open or closed). You have a smaller lung volume. Diaphragmatic hernia. Absorption atelectasis: has 2 constraints: 1. patient is breathing 100% O2 2. patient hypoventilates Normally nitrogen moves in and out of the pulmonary capillaries freely. There is normally no gradient for diffusion of N2. When you put a patient on 100% O2, you set up a concentration gradient for N2; to move out of the pulmonary capillaries and into the alveoli. This denitrogenates the blood. If anesthesia is discontinued and patient hypoventilates, all the remaining 100% O2 in the alveoli diffuse back into the pul capillary blood, N2 has left the alveoli by breathing, and alveoli do not remain well expanded due to hypoventilation and nitogen loss, and they collapse. Ventilate patient manually to prevent this from occurring. *Nitrogen is a major component for the alveoli's state of inflation. If a large volume of nitrogen in the lungs is replaced with oxygen, the oxygen may subsequently be absorbed into the blood, reducing the volume of the alveoli, resulting in a form of alveolar collapse known as absorption atelectasis. Anything that decreases FRC reduces gas exchange efficiency, affecting O2 uptake, CO2 elimination and uptake of inhaled anesthetics.

What is the gold standard for how the lungs are functioning? Evaluates how well the respiratory system gets O2 and eliminates CO2.

Arterial sample

How does surfactant work?

As alveolar size decreases, surface tension increases, but surfactant concentration increases as it is spread over a smaller surface area. The surface tension of water is neutralized.

Why is elastic recoil the main force responsible for negative pleural pressure?

At rest, the lungs are elastic and want to recoil to asssume their normal resting conformation. However the lungs aren't as small as they could be during this time, because of 2 forces: 1. There is elastic recoil of lung force directed inward trying to make the lung smaller. 2. Force directed outward by the thorax trying to resist. When these 2 forces are equal to one another, that is the volume the lung assumes at the end of passive exhalation. This is also what occurs when there is no flow occurring.

When the glottis is open, pressure throughout the entire respiratory tree is equal to?

Atmospheric pressure

At rest what is the average paO2 of blood that is on the venous side of a pulmonary capillary bed?

Basically the same pO2 as in the alveoli (pAO2) which is 104 mmHg.

What is the utility of high compliance of pulmonary vasculature in exercise?

Big idea: CO increases, therefore SV and HR increase. Pulmonary artery flow increases. Increased flow leads to pulmonary artery distention. Capillary recruitment increases the surface area available for O2 absorption. The output between the 2 ventricles must be there same so the SV increases as much in the pulmonary circuit as in the systemic circuit. In the systemic circuit the increased pressure is controlled by vasodilation. CO x R = P In the lungs accomodation of higher SV occurs and the vasculature dilates a bit to accept increase in output. Lung areas that were previously not well perfused become recruited into perfusion. Distention happens bc of an accomodation for an increase in flow; more capillaries are recruited which increases surface area for diffusion. As the CO of the RV increases and vascular accomodations are made to accept an increase in flow -- the accomodation, distention, and recruitment of other vasculature in lungs ensures that pressure does NOT increase. Even though CO x R = P, there is no increase in pressure bc of distension capability and reduced R of the pulmonary circuit. There is no pressure increase with increasing RV output! Pulmonary hypertension is caused by other things; eg HWs where there is a much greater resistance to flow out of the RV. So the heart works harder.

Vessels account for pulmonary blood flow. How so?

Blood flow is normally due to the passive effects of the hydrostatic pressure gradient. (Ppa > Ppv). The pressures that occupy the pulmonary arteries are diminished by the time you get to the pulmonary capillaries.

How long does it take for the arterial blood to go through the capillary and go from 40 mmHg of paO2 to 104 mmHg of paO2 (basically come up to pAO2).

Blood only needs to travel 1/3rd of the way though a pulmonary capillary to achieve this.

In these conducting airways (consist of main, lobar and segmental) they have cartilage plates which give rigidity but allow motion as lungs move. The plates decrease along their length. Where there is no cartilage, walls are composed of smooth mucle.

Bronchi

This is SYSTEMIC circulation that supports the health of the lung tissue that does not participate in gas exchange. Makes up 1-2% of CO. It's a left-sided event with low PaO2 and high PaCO2 because that blood has already gone through a capillary bed. Its functions include: --Is important in fetal lung development --Adult lung is viable without it --Is increased in chronic inflammatory lung dzs and neoplasms.

Bronchial circulation

In these conducting airways there is no cartilage present, and the walls are made of smooth muscle.

Bronchioles

These represent the greatest resistance to flow of air in dz if they are too small, because: Their small size makes them easily occluded. A high percentage of smooth muscles in the walls causes them to constrict easily. *Their smooth muscle tone is governed by adrenergic beta 2 receptors (which cause bronchodilation). Beta 2 agonists can open them up in asthmatics... as well as governed by cholinergic muscarinic receptors which cause constriction when stimulated.

Bronchioles

The movement of gases through the tubes of the lungs (to the terminal bronchioles) is from? which follows a pressure gradient. After this, the velocity of air moving into the respiratory bronchioles and beyond is very slow which is related to the massive increase in total cross-sectional area of the tubing.

Bulk flow. Bulk flow of tidal air during normal inspiration is only enough to fill the respiratory passageways as far as the terminal bronchioles.

This is a lung bleb that forms and breaks through the visceral pleura. It leads to an open communication from the trachea to the thorax outside the lungs. Causes an internal pneumo, and creates a lot of pressure in thorax.

Bulla

CO2 uptake and O2 release from Hb in a RBC.

CO2 combines with H2o in an RBC. This happens fast when carbonic anhydrase is present. The binding of CO2 with H2o (to make H2CO3) creates a concentration gradient favoring the transfer of CO2 down its concentration gradient (from tissues to RBCs). Carbonic acid is now made and it spontaneously dissociates into its constituent ions: H+ and HCO3-. HCO3- diffuses out of the RBC easily, but the RBC membrane is much less permeable to H+ so it stay inside the RBC. Cl- moves into the RBC to maintain electroneutrality with the H+ in EXCHANGE for a HCO3- via an anion exchanger (this is "chloride shift"). The more acidic environment in the RBC (H+ ions) facilitates O2 unloading (reduced affinity of Hb for O2) and O2 leaves the RBC for the tissue. HBO2 ----> O2 + Hb. The newly available Hb (left over from when O2 left it) -- some of these Hbs become bound to H+ because deoxygenated Hb is a better proton acceptor than Hb-O2. Osmolar content of the RBC increases during CO2 going into cell and other stuff ocurring, so H2O enters the cell, and the RBC swells. The RBC shrinks when CO2 is offloaded at the respiratory surface.

What establishes the CO2 concentration gradient, allowing CO2 to move across the alveolar membrane?

CO2 is being continuously formed in the body as an aerobic metabolism product. It is highly soluble in blood so PaCO2 is large in capillary blood. Its elimination by ventilation maintains tension difference across a respiratory surface.

How do the various lung volumes combine into the 4 important capacities of the lungs? What are the 4 capacities?

Capacities are the combinations of 2 or more volumes. 1. Inspiratory capacity. (IC) = the amount of air breathed in beginning at a normal inspiratory level and distending lungs to a maximum. VT + IRV = IC. 2. Functional Residual Capacity (FRC) = The amount of air remaining in the lungs at the end of a normal expiration. ERV + RV = FRC. 3. Vital capacity (VC) = amount of air that can be expelled by filling lungs to maximum and then exhaling to a maximum. VT + IRV + ERV = VC 4. Total lung capacity (TLC) = the maximum volume to which lungs can be extended. VC + RV = TLC.

What do bronchial arteries do? (Makes up bronchial circulation).

Carries O2 via the systemic circulation to supply the supporting tissues of the lungs (CT, smooth muscle etc).

This is a receptor that responds to change in chemical composition of fluid surrounding it. They are bathed in brain ECF through which CO2 easily diffuses from blood vessels to CSF. The CO2 reduces the CSF pH thus stimulating the receptor. H+ and HCO3- ions cannot easily cross the BBB.

Central chemoreceptors (CCR). In the medulla

Surfactant is a "detergent" which is a ?

Chemical that decreases surface tension.

This is a discontinuity of the lung parenchyma, without an opening between the chest and the atmosphere. Thorax is still closed. Occurs and pressure in pleural cavity becomes > atmospheric. Air can't escape. You must relieve the pressure inside the pleural cavity or else the lungs can collapse (atelectasis) which makes the lungs stiff and non-compliant, and the great vessels can become obstructed. Caused by rib fractures or ruptured bulla. For this type of situation the pressure inside the pleural cavity is initially negative (at rest) which draws air into the pleural cavity, air builds up, pressure becomes more positive and air cant escape. If not treated decreases preload, CO and tissue perfusion due to possible great vessel obstruction. Causes a huge inefficiency of gas exchange.

Closed pneumothorax or tension pneumothorax

The volume change per unit transpulmonary pressure change. An indicator of how distensible (capable of distention) the lung is.

Compliance Themore compliant something is, the less stiff it is.

This is the volume change per unit of transpulmonary pressure change. It indicates how distensible the lung is. A change in volume/a change in pressure.

Compliance. Also, the more compliant something is, the less stiff it will be.

This is the volume of the respiratory tract where no gas exchange takes place (the conducting airways).

Dead space Dead space is also any volume of lung that is being ventilated but not participating in gas exchange.

How does respiratory acidosis happen?

Decreased alveolar ventilation leads to increased paCO2 (hypoventilation). Increased paCO2 disrupts the (HCO3-/paCO2) base/acid ratio of the HH equation, making the overall number smaller and thus decreasing pH of blood. With chronic respiratory acidosis the kidney eventually tries to conserve bicarbonate to up the numerator portion of the ratio to bring it back to 20 overall (when paCO2 is x by 0.03). The kidney also responds by excreting more H+ as fixed acids (phosphoric acid: H2PO4- and ammonia: NH4+). Increased H+ in blood can also stimulate greater ventilation by stimulating peripheral chemoreceptors. pH will rise a bit but never return to 7.4

What are 2 dz states that affect lung compliance?

Decreased compliance = alveolar edema (prevents alveolar inflation) and fibrosis. Increased compliance: old age, emphysema.

Dzs that affect lung compliance?

Decreased compliance = alveolar edema (prevents inflation of alveoli) and fibrosis (scarring of lung, washing out of surfactant). Increased compliance = old age, emphysema (elastic recoil of lung is reduced, elastin breaks down, patient has difficulties with exhalation).

What is another cause of pulmonary edema?

Decreased plasma oncotic pressure (protein concentration). Water leaves capillary. Decreased oncotic pressure can arise from: failure of albumin synthesis (hepatic dz, starvation such as not eating enough protein). Excessive loss of plasma proteins (renal, GI). Hemodilution due to IV fluid loading (iatrogenic).

How does anesthesia cause atelectasis?

Decreasing FRC (diaphragm not contracting as well, thorax volume not increasing enough for an adequate pressure decrease to draw enough air in). Also with decreasing FRC the lungs can get smaller under anesthesia and reach a critical volume point called "closing volume or closing capacity". The alveoli can collapse. If FRC > CV then the alveoli do not collapse which occurs during normal tidal breathing. CV is an inherent intrinsic property related to the elastic recoil of a lung. Decreasing FRC is bad because it can lead to atelectasis.

What is the goal of pulmonary blood flow?

Deliver blood in a thin film to gas exchange units so oxygen can be taken up and CO2 eliminated.

The formula for vascular resistance is?

Delta P (input pressure - output pressure)/blood flow Basically Delta P/Q The normal pulmonary vascular resistance is very small: imput pressure (pulmonary artery)-output pressure (left atrium) = 10 mmHg

What are the 3 zones of pulmonary capillary perfusion (the influence of alveolar pressure on the pulmonary capillaries)? Or the 3 zones of "pulmonary ventilation."

Dependent on where PA falls (air pressure in the alveolus) and how it exerts pressure on the pulmonary artery (inlet pressure of capillary bed) or pulmonary vein side (outlet pressure of capillary bed) -- is it larger than Pa (inlet pressure) intermediate to Pa or less than both Pa and Pv?

The single most important respiratory muscle is?

Diaphragm

During inspiration quiet breathing -- what happens?

Diaphragm contracts lungs expand caudally Diaphragm moves caudally Volume of thorax increases

During quiet breathing expiration -- what happens?

Diaphragm relaxes Gas is expelled by the elastic recoil of the lungs and chest wall.

Quiet breathing is primarily a function of?

Diaphragmatic movement (diaphragm is the primary muscle associated with ventilation in quiet breathing). Diaphragm is a skeletal m because you can choose to act on it (e.g. holding breath). You can voluntarily take over ventilation. Phrenic nerve controls diaphragm.

What maintains the O2 gas concentration gradient, allowing O2 to move across the alveolar membrane?

Difference in gas concentration gradient or partial pressure of O2 between alveolus and capillary blood. O2 PP in alveoli is controlled by the rate of entry of new oxygen into the lungs (ventilation) as well as the rate of absorption of O2 into the capillary blood. O2 that moves into the blood rapidly associates with hemoglobin which maintains pO2 concentration gradient (keeps PaO2 low). 99% of O2 is bound up in hemoglobin.

This is another cause of hypoxemia (an abnormally low paO2). This is only apparent when you exercise at a high altitude. The PP gradient favoring O2 diffusion from alveolar space to blood is reduced.

Diffusion impairment at the respiratory membrane.

This moves air across the alveoli.

Diffusion. The kinetic motion of gas molecules; the velocity of molecules so great and distance so short, the gas moves across in a fraction of a second.

This element of the respiratory control system includes the mm of respiration (the diaphragm).

Effectors

Lungs are elastic like a balloon. Without a force to keep them inflated, they deflate. The rebound of the lungs after having been stretched by inhalation; the ease with which they return to their original shape and deflate on their own.

Elastic recoil

Lungs are elastic like a balloon: without a force to keep them inflated, they deflate. This attribute is called?

Elastic recoil (the main force responsible for negative pleural pressure, even during expiration). *the rebound of the lungs after having been stretched by inhalation, or rather, the ease with which the lung rebounds. Lung elasticity is due to elastin and collagen fibers in the lung tissue.

What are the forces to overcome during breathing?

Elastic recoil and airway resistance

This is the property of something being able to go back to its original shape after being stretched, by itself. Lungs have wrinkled and curly proteins, and when these get stretched during stretching (inhalation) there is PE stored in these molecules. So the lungs recoil back to their original shape, on their own.

Elasticity (due to elastin and collagen fibers in lung tissue).

What can cause acidemia?

Elevated CO2 in blood (in the form of carbonic acid) which dissociates into H+ and bicarbonate (HCO3-). Either caused from making more CO2 than normal or not ventilating CO2 out well enough.

What is the 3rd cause of pulmonary edema?

Elevated interstitial oncotic pressure (elevation in interstitial osmotic force). Pulls water out of the capillaries. Can be due to lymphatic obstruction: silicosis, asbestosis (asbestos gets stuck in the interstitium and it has osmotic activity).

The CO of the right ventricle and left ventricle must be?

Equal --If not you have congestion which creates an increase in hydrostatic pressure in venous and capillary circulation, and where hydrostatic pressure increases you have extraversion of water out of the vessel. --The pulmonary circulation can accomodate the same output as the systemic portion due to the fact that the pulmonary ARTERIES do not impose much resistance. MPAP /CO = R -- the MPAP is always WAY lower in the pulmonary arteries than the systemic ones, leading to a greatly reduced resistance to flow in the pulmonary vessels. MAP/CO = R (systemic circuit) Veins are similar in distensibility so the difference here lies in the arteries. Pulmonary artery must be way more distensible.

What happens during expiration during heavy breathing?

Expiration still depends on elastic recoil forces? Normally expiratory muscles are not actively contracting except during forced expiration such as extreme exercise, or airway obstruction (e.g. heaves in horses). In this situation the abdominal mm contract and pull the abdominal contents against the diaphragm.

What are the muscles of inspiration used during heavy breathing (these raise the rib cage)?

External intercostals (contract between ribs). Serratus dorsalis cranialis (lifts many ribs). Dorsal scalenus (lifts some cranial ribs).

This is the amount of air left in the lungs after a passive exhalation. Is equivalent to RV + ERV.

FRC (functional residual capacity)

This states that the amount of gas moved is proportional to the area of the membrane it moves across, and inversely proportional to the thickness of that membrane

Fick's Law of Diffusion

This governs diffusion through the air-blood barrier. It says that the rate of diffusion of a gas through a surface that the gas can permeate is directly proportional to the area of the surface and inversely proportional to the thickness of the surface.

Fick's Law of Diffusion volume of gas per unit time = area of surface/thickness of surface x D x (P1-P2).

This occurs through the airways whenever there is a pressure difference between the proximal and distal ends of the airways, and its direction is always toward the area of lower pressure.

Flow

The air-blood barrier is also called the respiratory surface. What are its layers?

Fluid lining the alveolus, containing surfactant Alveolar epithelium Epithelial basement membrane Alveolar interstitial space Capillary basement membrane (can be fused with alveolar basement membrane in places). Capillary endothelium RBCs

Why is the lung never as small as it could be at the end of a passive exhalation?

From the thorax recoil force directed outward.

Gas left over in the lungs after a passive exhalation = ?

Functional residual capacity (FRC).

Past the terminal bronchioles sits the 17th generation of airway down. This is where?

Gas exchange occurs

What causes pulmonary edema?

Left-sided heart failure (LV). It raises pulmonary capillary hydrostatic pressure. First, the LA pressure rises with no initial effect on the pulmonary vessels, due to their high distensibility. With COMPLETE left heart failure, as pressure rises dramatically (pulmonary hypertension), you see equally great increases in pulmonary ARTERIAL pressure and load on the right heart. If RV fails you get a big vena cava and ascites. As left atrial pressure increases due to LV HF pulmonary arterial pressure increases exponentially. The normal pulmonary arterial pressure is around 13-15 mmhg. Complete HF can irritate subepithelial irritant receptors and cause a cough. When pulmonary capillary pressure rises to > 15 mmHg, the hydrostatic pressure gradient favors extravasation of water (vessel pressure > interstitial pressure). Eventually all the water filtration across the pulmonary capillary endothelium exceeds lymphatic removal capacity. Excess fluid is seen in pericapillary and peribronchovascular interstitial space. When both of these interstitial spaces are full, alveolar flooding occurs.

What causes alveolar dead space?

Low cardiac output Gravitational effects Vascular obstruction -- emboli (such as heartworms, thrombi, air, fat). Positive pressure ventilation (causes zone 1 flow in lungs, capillary flow halts).

Flow occurs through the airways whenever there is a pressure difference between the proximal and distal ends. The direction of flow is always toward the area of?

Lower pressure

The shifting of the oxyhemoglobin curve to the right denotes what?

Lower saturation of hemoglobin with O2, at any given pO2. Hemoglobin has decreased affinity for O2. These things cause a right shift: increased H+ concentration (decreased pH). increased pCO2 increased temperature increased concentration of 2,5 diphosphoglycerate The Bohr effect: 1. When hemoglobin is exposed to increased CO2 and H+ (decrease in pH), (and maybe increased temperature during exercise) in the peripheral tissue capillaries (as compared to the pulmonary circulation) -- thse conditions lower Hb affinity for O2 and favor off-loading of O2 along its partial pressure gradient. Oxyhemoglobin curve shifts to the right. A decrease in pH assists in unloading more O2 at the tissues. But the change in pH has little effect on the amount of O2 being unloaded into the blood (from hemoglobin) in the lungs. 2. Conditions and process are reversed in the pulmonary circulation favoring O2 loading. *The Bohr effect is a physiological phenomenon first described in 1904 by the Danish physiologist Christian Bohr, stating that hemoglobin's oxygen binding affinity (see Oxygen-haemoglobin dissociation curve) is inversely related both to acidity and to the concentration of carbon dioxide.[1] That is to say, an increase in blood CO2 concentration which leads to a decrease in blood pH will result in hemoglobin proteins releasing their load of oxygen. Conversely, a decrease in carbon dioxide provokes an increase in pH, which results in hemoglobin picking up more oxygen. Since carbon dioxide reacts with water to form carbonic acid, an increase in CO2 results in a decrease in blood pH.

If someone does not make surfactant what happens?

Lungs become very stuff and require way more work to inflate.

This is when the diaphragm contracts but a portion of the costal thorax moves inward.

Paradoxical ventilation

This is the amount of new air moved into the respiratory passages per minute (and the air must move through the anatomic dead space before reaching alveoli, so not all of the air reaches the alveoli).

Minute respiratory volume Vmin (is ventilation). Vmin = VT (tidal volume) x f (or respiratory rate). Units are volume per time. Ventilation is not just tidal volume, it has to do with the tidal volume x how often you take that in per minute. The effective alveolar ventilation is based on Vmin. Panting does not mean Vmin is high because you might be taking in much smaller tidal volumes. Vmin is dependent on BOTH tidal volume and frequency.

Gases get into and out of the alveoli by ?. A concentration gradient allows it to occur.

Molecular diffusion. *The cross sectional area of the airways is so large that forward velocity of the air slows and diffusion of gas is responsible for its movement into alveoli.

Where are subepithelial irritant receptors located?

Most numerous in larynx, trachea and bronchi carina (irritant sensitive) terminal bronchioles, alveoli (sensitive to corrosive gases)

The continual movement of cilia and the gel layer of mucus is known as the?

Mucociliary escalator

This is secreted by goblet cells and submucosal glands in the tracheobronchial mucosa. It is also secreted by apocrine, mucus-secreting (Clara) cells lining the respiratory bronchioles. Has 2 layers: gel and sol (cilia beat in this layer, which is below the gel layer). Traps particles, bacteria and viruses.

Mucus

Ciliated epithelium exists from where to where?

Nasal passage to terminal bronchioles

At the end of exhalation, the transpulmonary or recoil pressure is?

Negative to atmospheric pressure.

During inspiration during an open pneumothorax, there is a momentary point when there is ? pressure that draws air from the atmosphere into the thorax.

Negative. The pressure in the pleural cavity eventually equilibrates with atmospheric pressure during expiration. Open pneumothoraxes are better than closed because they at least let air out. Air does not accumulate in the pleural cavity and create positive pressure.

This is what you calculate when you resolve all of Starling's forces.

Net filtration pressure Remember, there are 4 starling forces: hydrostatic, osmotic: and both of them are active in the interstitium and vascular compartments. The same 4 are in effect in the lungs which is all about water balance. The substance influenced by Starling's forces is water. Migration of water osmotically is influenced by Starling's forces. This occurs in the lung.

If the elastic recoil force of the lung and recoil force of thoracic wall exactly neutralize one another, what happens?

No flow occurs. There is no pressure difference between atmospheric and alveoli pressures.

These are airway and lung sounds heard during quiet breathing. Barely perceptible in some animals (cats, horses).

Normal breath sounds.

What are the important things to know about dissolved O2 in blood or "Dis-O2"?

O2 is poorly soluble in water, so it follows Henry's Law that its concentration is proportional to its partial pressure. Henry's Law says that the concentration of a gas in SOLUTION is proportional to its partial pressure.

This is a puncture wound to the chest, an opening into the pleural cavity from the outside, OR from a diaphragmatic hernia (hole in diaphragm).

Open pneumothorax which causes the pleural cavity pressure to become more positive. Can lead to atelectasis.

Whar is important to know about hemoglobin-bound oxygen? (HB-O2).

Oxygen binds REVERSIBLY with the heme portion of hemoglobin. Hb-O2 accounts for 98%+ of total O2 in blood. Hb binding is saturable and cooperative There are only 4 O2 binding sites/hemoglobin molecule, therefore binding capacity of O2 varies with the hemoglobin concentration. About 15 mg/dL is normal. The binding of each successive O2 molecule facilitates the binding of the next O2 molecule (cooperativity). For each O2 bound, the next O2 will bind more easily. This trait confers the sigmoidal shape of the Hb-O2 dissociation curve. *The sigmoidal shape of hemoglobin's oxygen-dissociation curve results from cooperative binding of oxygen to hemoglobin.

During expiration, as thoracic volume decreases, this decrease puts pressure on the alveoli which causes what to occur?

P A> P atmospheric -- flow moves out of lungs.

What are the 3 pressures in the pulmonary system?

PA = Alveolar pressure, pressure of air in the alveolus. Pa or Ppa = pulmonary artery pressure Pv or Ppv = pulmonary vein pressure (also left atrial pressure).

What is Zone 1 of pulmonary capillary perfusion?

PA > Ppa> Ppv Pressure has exceeded inlet pressure (pulmonary arterial pressure). All flow stops. Alveolar dead space. Occurs in animals with positive pressure ventilation or hemorrhage. Can occur if CO is low, and patient is dehydrated (hypovolemic). Preload decreases, RV output decreases, Pa drops, and V/Q becomes greater than 1.

These receptors are located at the carotid bodies, and aortic bodies. They respond to : 1. a decrease in arterial pO2. The entire ventilatory response to arterial hypoxemia is mediated by these. 2. An increase in arterial pCO2. But these are less important than CCRs in controlling paCO2. Send afferent impulses to the medulla respiratory centers, which send efferent impulses to respiratory mm, which results in increased ventilation to rid body of more CO2 and arterial pCO2 and pH return to normal.

PCRs (mediate 30% of the CO2 response)

This is the PE for the diffusion of gases.

PP gradient

These receptors are in the airway smooth muscle (surrounding conducting airways). They respond with the Hering-Breuer Inflation Reflex: an increase in lung volume leads to these receptors firing, leads to a decrease in respiratory frequency by increasing expiratory time.

PSR or pulmonary stretch receptors.

How does the hypoxic pulmonary vasoconstriction reflex work? (HPV)

Pulmonary vessels constrict in areas of low pAO2. This reroutes pulmonary blood flow away from the low pAO2 alveoli toward alveoli where pAO2 is higher. HPV is an intrinsic negative feedback reflex to minimize the contribution of V/Q < 1 alveoli on gas exchange efficiency of whole lung. HPV reflex is inhibited by inhalation anesthetics, but not IV anesthetics or other drugs.

What causes a V/Q relationship of > 1?

Q gets smaller so perfusion is reduced or negligible and ventilation is normal. Efficiency of gas exchange is diminished.

These 2 constraints occur when?: 1. Inspiratory component of ventilation cycle is the active component (diaphragam contracts and you use ATP). 2. Exhalation is passive. Diaphragm relaxes.

Quiet breathing

What effects the pO2 and pCO2 in the alveoli?

Rate of ventilation Rate of oxygen and CO2 transfer through the respiratory membrane

What are the expiratory mm used during heavy breathing?

Rectus abdominus mm (compresses abdominal contents towards the diaphragm). Internal intercostal mm

What is the Hypoxic Pulmonary Vasoconstriction (HPV) reflex?

Reflex is initiated by the alveolar PP of O2 (going too low). The alveolar PP of O2 could go too low from pneumonia or atelectasis. Alveoli are pooly ventilated. It is a contraction of smooth muscle in the walls of small blood vessels in regions of the lung with alveolar hypoxia. Pulmonary arteries or capillaries feeding the alveoli vasoconstrict. Flow beyond those alveoli is reduced. This increases resistance to flow in that capillary bed. An increase in resistance in one area of the lung due to low PP of alveolar O2, shifts the blood flow of the RV to places where the O2 in the alveoli is greater; limiting the effect of mixing poorly oxygenated blood with oxygenated blood.The reflex occurs when pO2 of the alveolar gas is too low (PP of alveolar O2). The lungs can self-regulate ventilation and perfusion. All inhalation anesthetics inhibit HPV reflex but injectable anesthetics don't. This inhibition is a possible cause of hypoxemia during anesthesia. His words: HPV reflex is an obscure mechanism, with no CNS involvement. It is the pO2 in the alveolar gas and not the pO2 in arterial blood that determines the response. The reflex directs blood flow away from the hypoxic regions of lung to functional alveoli. The reflex reduces the amount of ventilation=perfusion inequality in a diseased lung. It limits depression of arterial O2.

Bicarbonate concentration in the body is determined chiefly by? and the pCO2 concentration is determined by ?

Renal function Effective alveolar ventilation

Epithelium here is cuboidal. Has a mixture of ciliated cells and apocrine secretory Clara cells. No goblet cells, no submucosal cells, no cartilage.

Respiratory bronchioles

These make up the "respiratory zone"

Respiratory bronchioles, alveolar ducts (lined with alveoli), and alveoli (where gas exchange occurs between lung and pulmonary capillaries).

What is past terminal bronchioles?

Respiratory bronchioles, alveolar ducts, alveolar sacs. At respiratory bronchioles gas exchange is possible, because occasional alveoli pop up.

If the reference atmospheric pressure is 0 -- what are the various alveolar pressures at different times?

Resting = 0 cm H2o Inspiration = -1 cm H20 (air goes into lungs, from an area of higher pressure to lower pressure) Expiration = + 1 cm H20 (air leaves the lungs from an area of higher pressure to lower pressure).

What is P PL at various parts of ventilation?

Resting pressure = -4 cm H20 (due to elastic recoil of the lungs). Inspiration = -6 cm H2O (creating a greater volume in the thorax, which lowers P PL, caused by contraction of diaphragm; Boyle's Law). Expiration = -4 cm H20 The decrease from -4 to -6 is the force that evokes expansion of the lung parenchyma, creates flow.

What are the 3 negative pleural pressures?

Resting pressure = -4 cm H2O Inspiration pressure = -6 cm H2O Expiration pressure = -4 cm H20 The decrease from -4 to -6 cm H20 is the force that evokes expansion of the lung parenchyma during inhalation.

What is the P A at various parts of ventilation?

Resting pressure = 0 cm H20 Inspiration pressure = -1 cm H20 (from volume of thorax increasing as diaphragm contracts; Boyle's Law). Expiration pressure = +1 cm H20 (from the elastic recoil of the lung creates pressure in the alveoli, which is greater than atmospheric pressure. Flow moves out of the alveoli. Lungs begin to deflate but eventually stop deflating due to elastic recoil of the lung and elastic recoil of the thorax eventually equaling and opposing one another. Stops pressure gradient).

How are the conducting airways kept open?

Rigid structural elements Traction from surrounding tissues Pressure gradient across walls

This element of the respiratory control system includes the central chemoreceptors (CCR), peripheral chemoreceptors (PCR) and lung receptors (pulmonary stretch receptors)

Sensors

Continuous suction of excess fluid into lymphatic channels gives a ? which holds the lungs and the pleura next to the thoracic wall.

Slightly negative pleural pressure.

Perfect lung really never occurs. Why is this?

Some acini are underventilated (V/Q < 1) and some are underperfused (V/Q >1). So the normal lung functions with a V/Q = 0.8 When an individial assumes their normal, upright posture (or sternal recumbency for quadrapeds) the uppermost acini operate at V/Q > 1 (alveolar dead space) and the lowermost acini operate at V/Q < 1 simply because of the gravitational effect on both regional V and Q. Therefore, altered body positioning (lateral or dorsal recumbency) alters the V/Q distribution. A homogenous lung is more efficient at adding O2 to blood than one having regional V/Q mismatching, but regional mismatching is reality. Patients with V/Q abnormalities generally present with normal paCO2 because the paCO2 drives global ventilation and the paCO2 rises and falls linearly with changes in ventilation whereas paO2 does not. Ventilation from the V/Q is a regional effect, not a global one. Global ventilation is how O2 is acquired and how CO2 is eliminated. Is equivalent to Vmin (VT x rr).

This device studies pulmonary ventilation; records movement of air into and out of the lungs. Records how volume changes with flow rate into and out of the lungs.

Spirometer.

What is a cough triggered by?

Stimulation of subepithelial irritant receptors. Occurs by material on epithelial surface bronchoconstriction (allergic rxn, noxious stimuli) a hyperactive response when respiratory tract is injured (e.g., from a virus). Is a protective mechanism

This reduces surface tension of fluid coating inner surface of alveoli. Is secreted by type II alveolar epithelial cells (which are about 10% of alveolar surface). It is a phospholipid containing fluid.

Surfactant

T or F you can hear crackles and wheezes at the same time.

T

T or F. Widely differing demands for O2 uptake and CO2 output occur, but the nervous system adjusts the rate of alveolar ventilation to almost exactly meet the demands of the body. Therefore pO2 and pCO2 are altered very little by exercise, stress, etc.

T

T or F: cyclic diapragmatic activity acts on alveolar, intrapleural and transpulmonary pressures during tidal breathing. Comes from a change in thoracic volume.

T

What causes interstitial pulmonary edema?

The 4 starling forces competing with one another for holding water or attracting it out into the vasculature.

This is the first element of the respiratory control system. Its main parts consist of the cerebrum (voluntary control), the brainstem (automatic control), the spinal cord (governs the respiratory mm to yield ventilation) and the limbic system and hypothalamus (change breathing pattern in response to rage, fear, etc).

The Central Controller (CNS)

What happens during heavy breathing?

The auxillary mm of inspiration are recruited. Inspiration relies on expanding the rib cage. Thoracic volume increases by 20%.

What is the ultimate goal of cardio-pulmonary activity?

The cyclic delivery of O2 to peripheral tissues in support of oxidative metabolism, and delivery of the CO2 produced by that metabolic process back to the respiratory surface for elimination.

What is the Haldane effect?

The deoxygenation of blood increases RBCs ability to carry CO2 as H+ becomes bound to Hb. Also, oxygenated blood has a reduced capacity to carry CO2.

Why does alveolar pressure increase during positive pressure ventilation?

The dynamics of how the lungs inflate is reversed. You squeeze a bag and flow of air goes into lungs because of the high external pressure you have created within the bag. The pressure in the lungs does not become more negative to inspire air. Creating positive pressure inside the alveoli such as this squeezes down on the capillaries feeding the alveoli, creating an intermittent obstruction to pulmonary blood flow. Alveolar pressure can also go up when gravity exerts on the lung parenchyma.

Why can we never eliminate the residual volume or RV?

The effort put into deliberately exhaling to achieve ERV eventually makes lungs so small that airways collapse and gas trapped distally to the collapsed airways in the alveoli can't get out.

Why does the pressure gradient reverse when the diaphragm stops contracting after inhalation?

The elastic recoil of the lung creates pressure in the alveoli, which is greater than atmospheric pressure. Flow moves out of the alveoli.

How do the lungs participate more in the body's acid-base balance than the kidney?

The lungs excrete more than 10,000 mEQ of carbonic acid a day compared to less than 100 mEQ of fixed acids by the kidney. Therefore, anything that alters alveolar ventilation alters CO2 elimination quickly. This effects the body's acid-base balance, all because of the carbonic acid equation. CO2 + H2O <----> H2CO3 <-----> H+ HCo3-

How do you quantify O2 delivery?

The product of TOTAL O2 content and cardiac output (CO). Total O2 in ml/dl x CO in dl/min = O2 delivery in ml/min If a patient becomes very anemic (like during a hemmorhage) so that Hb-O2 concentration is reduced by 50%, (therefore total O2 goes down) so the only way to continue delivering O2 at the same ml/min is to increase CO. Some patients can't do this; like if they are under anesthesia. Cardiovascular diseases and respiratory diseases are often characterized by lethargy because lethargy is a behavioral adaptation that reduces metabolic O2 requirement. Perhaps you have less ability to deliver O2 in that circumstance so you develop lethargy to compensate for that. Less O2 will be required so you don't have to deliver as much of it.

What happens with oxygen transport to tissues during exercise?

The pulmonary blood flow though a capillary increases, which decreases the transit time of the blood and the time RBCs spend in the capillary. This decreases the time available to reoxygenate blood. However, the diffusing capacity of O2 from the alveoli increases almost 3 FOLD due to capillary recruitment which increases the surface area for O2 absorption. Therefore, blood still becomes fully oxygenated with 1/3rd the time in the capillary. Stays in capillary for 83 seconds.

What are the hallmarks of the pulmonary circulation in terms of pressure and resistance?

The pulmonary circulation has high compliance and low resistance. The pressures in the vessels (arteries) are very low. The walls of the pulmonary artery and its branches are thin with little smooth muscle. The pulmonary arteries and arterioles have larger diameters than systemic arteries and arterioles. Why is all of this true? 1. The lung needs to accept all of the cardiac output all the time. 2. All of these conditions keeps right sided heart work low. 3. There is only enough pressure needed to lift blood to the top of the lung.

What are the hallmarks of the systemic circulation in terms of pressure and resistance.

The systemic circulation has higher resistance, and is less compliant than pulmonary circulation. The arteries have thick walls with arterioles having abundant smooth muscle. The blood must leave the LV and travel to the far reaches of the body so high pressures are required (pressure being the PE for flow).

This is a cause of hypoxemia. It occurs when there is a V/Q > 1.

The ventilation perfusion abnormality of Alveolar dead space. Occurs as a result of decreased blood flow to a particular lung region, with no change in regional ventilation. Ventilating fine, just not getting perfused.

How are capillaries and the alveoli connected (fused at a point)? There is no interstitial space at that point. However there is a potential space of interstitum in the non-fused area where interstitial pulmonary edema can happen. This edema does not cause hypoxemia or gas exchange inefficiency.

Their respective epitheliums (capillary, alveolar) are divided by a basement membrane. The alveoli are covered by a dense vascular capillary network.

Calculating the total O2 content of blood.

Total O2 content in blood = Hb bound O2 + dissolved O2 in blood. Total O2 content is expressed in ml of O2/dL The O2 bound to hemoglobin is calculated as Hb concentration in g/dL x 1.34 ml O2/g x % saturation (expressed as a fraction). The dissolved O2 in blood is calculated as pO2 mmHg x 0.003 ml O2/dL/mmHg. Both calculations above have final units of ml of O2/dl. You can add them together to get the total amount of O2 in blood in ml of O2/dl.

These are the conducting airways which are non-gas exchange tubes. The function of these conducting airways is to lead inspired air to the gas exchange portions of the lungs.

Trachea, bronchi, and bronchioles

Epithelium here is pseudostratified columnar, and has ciliated cells, goblet cells, basal cells, and a submucosal gland too. Cartilage is found here.

Tracheobronchial mucosa in trachea and bronchus

This is the pressure difference between the P A and P PL (outer surface of the lungs). P A - P PL. It is equal to the elastic forces of lung that want to collapse it. Also called recoil pressure. Keeps lungs from collapsing.

Transpulmonary pressure

This pressure is equal to the elastic forces of lung that want to collapse it, also called recoil pressure. Lung inflation is maintained by this pressure. Events that neutralize this pressure cause lung deflation.

Transpulmonary pressure (Pa-Ppl) Should be positive right after exhalation ends, since P PL is normally a negative number, it is like adding a positive number to PA. The positive Transpulmonary pressure is normally what inflates the lungs and opens the cavae up. *For a given lung volume the transpulmonary pressure is equal and opposite to the elastic recoil pressure of the lung.

Lung INFLATION (non-collapse) is maintained by?

Transpulmonary pressure. If it is not maintained the lungs deflate, which can happen in a pneumothorax.

Increased sounds during breathing denote?

Turbulent airflow

This is when air moving through the passageways of the nose hits obstructions (e.g., conchae/turbinates, septum, pharyngeal wall) causing the inspired air to change directions, but for the particles in the air (which are heavier) to strike surfaces and get stuck in mucus. The particles are removed by mucociliary clearance. As air moves through nose and sinuses its at a high velocity but then slows due to turbulence . Particles get "shaken out" of air due to striking the surfaces. Particles sediment out and get trapped in mucus.

Turbulent precipitation or sedimentation Prevents particles from getting into lungs (has an immune function).

How does the venous systemic blood supply (deoxygenated) from capillaries supplied by bronchial ARTERIES return to the heart?

Two ways: 1. Bronchial veins (found in lung hilus, come from the bronchial artery (high PaO2, low PaCO2), capillary bed, VEIN, flow back into RA). Flows into azygous vein. This flow going into the azygous vein PaO2 equivalent to systemic venous blood. 2. Bronchopulmonary veins (veins originating from bronchial arteries within lung tissue (high PaO2, low PaCo2), capillary bed, VEIN (now has low PaO2, high PaCO2) flow into the pulmonary vein (high O2, low CO2) and return directly to the LEFT atrium. This content of blood reduces systemic O2 tension Bronchopulmonary circulation is an ANATOMIC right to left shunt, which decreases arterial O2 tension by some fraction.

The opposing sides of the respiratory surface are fed by V/Q. What is V and what is Q?

V = ventilation Q = pulmonary artery perfusion Gas exchange efficiency is maximized when V/Q = 1 or V and Q are well-matched. V/Q is the rate of ventilation of an alveolus or group of alveoli.

What does the value of VD or Physiologic dead space volume take into account?

VD = alveolar dead space + anatomic dead space

Describe the ratio of dead space to tidal volume, or the fraction/percentage of tidal volume distributed to dead space. It effects alveolar ventilation.

VD/VT where VD = alveolar dead space + anatomic dead space and where VT = tidal volume. This equation is also expressed as the Bohr equation: (PaCO2 - PeCO2)/PaCo2. You calculate this and get a fraction like 1/8 or 0.125. Multiply by 100. That is 12.5%. So about 12.5% of tidal volume is distributed to dead space with every breath, or ventilation without perfusion. PeCO2 = partial pressure of CO2 in the gas exhaled during a normal tidal exhalation. The difference between PaCO2 and PeCO2 is never 0 because arterial CO2 > expired CO2. There will always be wasted ventilation, some portion of tidal volume will always be in the conducting airways, so VD is NEVER 0 and the ratio can NEVER be 0. He says about VD/VT never being 0: "even if alveolar gas exchange is 100% efficient, the anatomic dead space volume represents a fractional volume of CO2 that is reinhaled, therefore NOT lost from the body during tidal breathing."

This is the mechanical process that allows the lungs to expand and contract. The process of aerating the alveoli. The mechanical process by which the lung parenchyma is filled and emptied. Skeletal muscle accomplishes it. Skeletal muscle is active during inhalation and passive during expiration. Is not the same as respiration (which is mitochondria using O2).

Ventilation

What causes a V/Q relationship to be < 1?

Ventilation decreases. V gets small, Q is the same. Alveoli are taken out of gas exchange, but are still being perfuses. Efficiency of gas exchange is diminished. Includes atelectasis, pneumonia, alveolar edema.

What is the V/Q relationship?

Ventilation to perfusion relationship. Gas exchange efficiency is greatest when this ratio is 1 (doesn't mean they are the same numbers though, just matched equivalently).

How does air diffuse across a membrane?

Via a gas concentration/partial pressure gradient. It moves from high pp to low pp. The PE for diffusion is the concentration gradient of a substance.

This is an abnormal lung sound that is high-pitched due to small airway obstruction or collapse. The sides of airway vibrate and make a noise when they're close together. Is a continuous sound on expiration.

Wheeze

When is P A 0 (equal to atmospheric pressure)?

When no flow is occuring. At rest. The only way flow can occur is if there is a pressure drop. Pressure drop occurs when diaphragm contracts and expands volume of thoracic cavity. Diaphragmatic contraction creates the pressure gradient.

What are the traits of the oxyhemoglobin dissociation curve?

X axis is the independent variable or paO2 in mmhg. Y axis is the dependent variable and it is the % saturation of hemoglobin with O2. (hemoglobin saturation %). The position of the curve along the X-axis indicates the Hb affinity for O2. *The position of this curve may shift rightwards (lower saturation for given PaO2) or leftwards (higher saturation for a given PaO2).

Respiratory acidosis can cause ? which is an excessive amount of H ions in blood.

acidemia

How is air drawn into the lung?

diaphragmatic contraction and rib cage expansion, which increases intrathoracic volume, and lowers alveolar pressure relative to atmospheric pressure. Air flows into lungs following a high to low pressure gradient, which is created by diaphragmatic contraction.

As the pleura is stretched, these cells secrete pleural fluid into the potential space.

mesothelial cells. *The mesothelium is a membrane composed of simple squamous cells that forms the lining of the pleura.