Ch 16: Respiratory System
SLOs: Explain how intrapulmonary pressures change during breathing Explain surface tension and the role of surfactant in respiratory physiology. Compare and contrast compliance and elasticity Apply math relationships to predict behaviors of gases and changes in air flow in the resp. system: Dalton s law: Partial pressure of an atmospheric gas = P atm % of gas in atmosphere Define lung volumes and lung capacities (see also lab!) Explain ventilation perfusion matching. Review key diseases and conditions that can affect respiratory function. Compare the solubility of O 2 and CO 2.
SLO cont: Describe the structure and function of HbA, HbF, and myoglobin Draw the oxyhemoglobin dissociation curve (for normal conditions) and explain the physiological significance of the shape of this curve. Draw the shifts and explain the significance in the oxygenhemoglobin dissociation curve that result from changes in ph and temperature Write the chemical reaction for the conversion of CO 2 to HCO 3 -. Explain how HCO 3 - acts as a buffer Describe normal physiological pressures of O 2 and CO 2 in the following locations: alveoli, arterial blood, resting cells, and venous blood. Diagram the pressure gradients at the sites of gas exchange and show the direction of O 2 and CO 2 movement. List factors that influence the diffusion of gases across the alveoli.
External Respiration Ventilation = ( + ) Gas Transport Gas exchange between and and Oxygen utilization
Review Anatomy on your own Relationship Between Alveoli and Capilaries Fig 16.1
16.2 PHYSICAL ASPECTS OF VENTILATION Key Terms: Boyle s Law Compliance Elasticity Surface Tension Surfactant Movement of air into and out of lungs is consequence of.. HOW??
Boyle s law: P 1 V 1 = P 2 V 2 Pressure-volume relationship Gases move.
Intrapulmonary and Intrapleural Pressures Lungs unable to expand and contract independently During development: Intrapleural pressure becomes subatmospheric necessary to keep lungs inflated Lungs stuck to thoracic cage by pleural fluid bond Pneumothorax?
Right sided tension pneumothorax with right sided lucency and leftward mediastinal shift. This is a medical emergency. Spontaneous vs. Tension Pneumothorax
Therapy? Tube thoracostomy
Physical Properties of the Lungs Compliance: ability of lungs to stretch Low compliance in restrictive lung diseases (e.g.: fibrotic lungs and not enough surfactant) Elasticity: ability to return to original shape Low Elasticity in case of emphysema due to destruction of elastic fibers. Normal lung is both compliant AND elastic
Surfactant = detergent-like complex of PLs (80%) & proteins: Disrupts cohesive forces between water molecules surface tension? Surface Tension at all air-fluid boundaries due to? Unequal attraction produces tension at liquid surface opposes alveolar expansion/distension
The Production of Pulmonary Surfactant Fig 16.11
Normal pregnancy takes... (I)RDS
16.3 MECHANICS OF BREATHING Pulmonary ventilation = Air flows due to pressure gradients (analogous to blood) Inspiration: Contraction of 60-75% volume change Remaining 25-40% due to other inspiratory muscles (?) Expiration Relaxation of inspiratory muscles Elastic recoil of pleura and lung tissue
The Airways: Conduction of Air from Outside to Alveoli 3 upper airway functions: Mucociliary escalator depends on secretion of watery saline note: (genetic disease) Effectiveness of nose vs. mouth breathing (Respirators!) CFTR channels!
Fig 16.13 P o = P i P o vs P i? P o vs P i?
Mechanisms of Pulmonary Ventilation Fig 16.14
Spirometry For pulmonary function tests Measures lung volumes during ventilation Perform measurements in lab
Lung Volumes and Capacities spirogram Fig 16-15
Efficiency of Breathing: Rate and Depth How is heart efficiency measured? Analogous: Total Alveolar/Pulmonary Ventilation = Anatomic dead space = ml
Airways Resistance Also influences work of breathing Primary determinant: Adjustable via? Under nervous, hormonal and paracrine control CO 2 : Parasympathetic neurons: No sympathetic neurons but 2 receptors (?): Histamine: Review Table 17-1
Examples? Table 17-2
Pulmonary Disorders: Asthma Symptoms: Dyspnea (shortness of breath) and wheezing Cause: Inflammation due to allergic reaction, mucus secretion, and constriction of bronchioles Possible allergens? Types of cells and IGs involved? Obstructive disorder, but distinguished from COPD because reversible with bronchodilator medications
Pulmonary Disorders: Emphysema Destruction of alveolar walls Reduced Decreased pulmonary elastic recoil permanent enlargement of air spaces distal to terminal bronchioles. COPD Smoking!
Pulmonary Disorders: Fibrosis PF and IPF May be due to inhalation of small particles Increased membrane thickness Example: Aspestosis and black lung (anthracosis) in miners
16.4 GAS EXCHANGE IN LUNGS
Dalton s Law Total P = Ps of individual gases % N 2 P N2 = mmhg Total atmospheric pressure at sea level = mmhg Air is a mix of gases % O 2 P O2 = mmhg
Fig 16-19
Fig 16-22 Gas Exchange in Lungs and Tissues Movement from higher partial pressure to lower partial pressure
Pulmonary Circulation Low pressure Flow rate equal to flow rate in systemic circuit has to be low resistance Less filtration pressure protects from edema Normal heart/lungs When a lung problem is not a lung problem: CHF in 5 Mio Americans
Ventilation Perfusion Matching Lung has collapsible capillaries Reduced blood flow at rest in lung apex [O 2 ] in ECF around pulmonary arterioles vasoconstriction of arteriole (blood diverted) opposite of systemic circulation!
Lung Ventilation/Perfusion Ratios Fig 16-23
Disorders Caused by High Partial Pressure of Gases Oxygen toxicity: 100% oxygen is dangerous due to oxidation of enzymes Scuba Diving: 1 atm / 10 m ( ft) of water Nitrogen narcosis (raptures of the deep): occurs if N 2 is inhaled under pressure; results in dizziness and drowsiness Decompression Sickness (the bends): Diver comes up too fast N 2 bubbles form in blood, blocking small vessels Also if airplane suddenly loses pressure
16.6 HEMOGLOBIN AND O 2 TRANSPORT Total O 2 content of blood depends on P O2 and Hb concentration O 2 -carrying capacity of blood measured by its [Hb] Anemia Polycythemia
Oxygen Content of Blood Fig 16-31
Oxygen Transport in Blood 98% carried by Called Law of mass action applies Rest dissolved in plasma
Oxyhemoglobin Dissociation Curve Demonstrates relationship between P O2 and Hb binding of O 2 Expressed as % saturation of Hb Explain physiological significance of curve shape Compare to Fig 16-33
Fig 16-33
Other Factors Affecting O 2 -Hb Dissociation Curve O 2 unloading during exercise : 22% at rest 39% light exercise 80% heavy exercise Compare to Fig 16-34
Myoglobin and Hemoglobin Dissociation Curves Fig 16.37
CO 2 Transport in Blood 1. 10% directly dissolved in plasma 2. 70% transported as HCO 3 - dissolved in plasma (acts as a ) 3. 20% bound to Hb Carbaminohemoglobin As with O 2 : Law of mass action applies Excess CO 2 in blood = Hypercapnia Leads to, CNS depression & coma
16.8 ACID BASE BALANCE OF THE BLOOD Blood ph? HCO 3- is weak base and major buffer in the blood excess H + CA + HCO 3- H 2 CO 3 CO 2 + H 2 O H 2 CO 3 volatile acid regulated by breathing. Lactic acid, fatty acids, ketone bodies nonvolatile/fixed acids kidneys regulate
Bicarbonate as a Blood Buffer Fig 16-40
Acidosis Respiratory acidosis due to alveolar hypoventilation (accumulation of CO 2 ) Possible causes: Respiratory depression, increased airway resistance (?), impaired gas exchange (emphysema, fibrosis, muscular dystrophy, pneumonia) Metabolic acidosis due to gain of fixed acid or loss of bicarbonate Possible causes: lactic acidosis, ketoacidosis, diarrhea Buffer capabilities exceeded once ph change appears in plasma. Options for compensation?
Alkalosis much rarer Respiratory alkalosis due to alveolar hyperventilation in the absence of increased metabolic CO 2 production Possible causes: Anxiety with hysterical hyperventilation, excessive artificial ventilation, aspirin toxicity, fever, high altitude Compensation? Metabolic alkalosis due to loss of H + ions or shift of H + into the intracellular space. Possible causes: Vomiting or nasogastric (NG) suction; antacid overdose Compensation? Buffer capabilities exceeded once ph change appears in plasma.
Body deals with ph changes by 3 mechanisms Buffers 1 st defense, immediate response Ventilation 2 nd line of defense, can handle ~ 75% of most ph disturbances Renal regulation of H + & HCO 3 - final defense, slow but very effective
See lab High Altitude Physiology