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149 Cards in this Set
- Front
- Back
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Law of Laplace
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Without Surfactant: small alveoli have more pressure inside b/c the pressure in a bubble is inversely related to it's radius
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Static Compliance
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measures pressure and volume
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Dynamic compliance
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pressure and volume when lungs are moving
in acute situation dynamic compliance decreases |
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Compliance
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the change in lung volume per unit change in transmural pressure gradient
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transmural pressure
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the difference between inside pressure and outside pressure
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Hysteresis
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compliance curve changes between inflation and deflation
small alveoli=surfactant close together=increased compliance |
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surfactant is mostly made of:
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DPPC: Dipalmitoyl Phosphatoyl Choline
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Advantages of Surfactant
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1. lowers surface tension
2. increase lung compliance 3. decreases work of breathing 4. Promotes stability of alveoli 5. Helps keep alveoli dry!!!! |
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interdependence of alveoli
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when alveoli surrounded and supported by each other, they tend to move closer together which contributes to stability of alveoli
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When is the lung Non-compliance
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at residual volume
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anatomic factors that influence the compliance of thoracic cage include:
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1. ribs
2. the state of ossification of the costal cartilages 3. obesity 4. abdominal distention 5. pathological skin conditions like burns (can decrease chest compliance) |
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2 linings of the lung
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1. Visceral pleura (inside)
2. Parietal pleura (outside of lung) |
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Normal Negative Intrapleural Pressure
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-5 (negative 5)
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pneumothorax
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air gets between the 2 layers of the lung causing the lung to recoil in and the chest to spring out and the pressure is then 0 (zero)
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FRC
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functional residual capacity
the equilibrium volume at which the elastic recoil of the lung is balanced by the tendency of the chest wall to spring out |
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Laminar flow
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the gas flow rate is directly proportional to the pressure gradient along the tube
- Heliox not helpful b/c it's dependent on density but laminar flow is: Dependent of Viscosity!!! - Pressure = constant x velocity - viscosity effects resistance to flow - occurs at level of alveoli with gas diffusion |
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Turbulent flow
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- occurs at level of trachea
- Heliox would be advantageous to decrease airflow resistance - Pressure = constant x velocity2 |
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Reynolds' number is > 2,000 what kind of flow is occurring?
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Turbulent Flow
- Increase air flow resistance, increase WOB, increase velocity, increase turbulence = bad = increased Re # |
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Reynolds' number
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linear velocity of gas x tube diameter x gas density divided by gas viscosity
Re=2rvd/n |
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Causes of increased airway resistance
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1. material within lumen
2. thickening or contraction of the wall of the passage 3. intraluminal obstruction of the lower respiratory tract |
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most common cause of increased airflow resistance
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Airway disease
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Does intrapleural pressure increase or decrease as you inhale?
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Decreases
- breath by negative pressure |
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Does alveolar pressure increase or decrease as you inhale?
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Decreases
- air goes from high to low pressure, which is why it moves into alveoli |
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Chief site of airway resistance
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Medium sized bronchi
- just a note: less 20% of airway resistance is attributed to airways less than 2mm in diameter |
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closing capacity
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volume at which airways close.
- includes residual volume, where as closing volume does not |
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Factors that Increase Closing Capacity
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1. Lung Disease
2. Age |
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Shunt
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Alveoli Perfused but not Ventilated
norm: <3% under anesthesia: 10% - clinical finding = O2 wouldn't be as high as expected and higher A:a gradient |
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Dead Space
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Alveoli Ventilated but not Perfused
- clinical finding = high A:a gradient, and end tidal CO2 would be lower than expected |
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4 pathways involved in controlling muscle tone in small bronchi and bronchioles are:
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1. Neural pathway
2. Humoral pathway 3. Direct physical and chemical effects 4. Local cellular mechanisms |
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Parasympathetic Nervous System involves what Nerve in body
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Vagus Nerve
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Sympathetic Nervous System is controlled by what?
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Humoral Control b/c bronchial smooth muscle contains Beta-2 adrenergic receptors, which are highly sensative to Adrenaline
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How is the Afferent System involved with bronchoconstriction?
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react to Noxious stimuli or mast cell degeneration causing bronchoconstriction
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How is the Efferent System involved with bronchoconstriction?
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releases Acetylcholine (Ach) causing smooth muscle contraction which is bronchoconstriction
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time constant
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product of resistance and compliance.
- if have problem with compliance or resistance the lung doesn't fill and empty as a unit which is called an altered time contant |
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The WOB overcomes 2 main sources of impedance:
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1. Elastic Work
2. Airflow Resistance |
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Normal RR with Minimal WOB
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15 breaths per minute
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RR with Minimal WOB in Stiff lungs (elastic WOB):
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18 breaths per minute
ex: pulmonary fibrosis: breaths shallow and fast |
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RR with Minimal WOB in an increased resistance situation
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10 breaths per minute
ex: asthmatics, COPD, emphysema: tend to breath less frequent but have large volumes |
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Where is basic rhythm of respiration controlled?
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Dorsal Respiratory Group
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Dorsal Respiratory Group
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plays most fundamental role in control of ventilation
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Where is the Dorsal Group located?
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Tactus Solarius of medulla
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Glosopharengeal and Vagus Nerves transmit to respiratory center of brain in 3 places to the dorsal respiratory group
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1. Peripheral Chemoreceptors
2. Barroreceptors 3. Lung Receptors |
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3 Major Collections of Neurons
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1. Dorsal Group
2. Ventral Group 3. Pneumotaxic center |
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Dorsal Group
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located in the dorsal portion of the medulla
- causes inspiration - controls inspiration and respiratory rhythm |
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Ventral Group
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located in the medulla
- causes inspiration and expiration depending on the neurons stimulated |
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Pneumotaxic Center
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located in the superior medulla
- controls ventilatory rate and pattern of breathing |
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Inspiratory Ramp controlled in 2 ways:
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1. Controls rate of increase of ramp
ex: exercise ramp to increase quicker so lung can fill quicker 2. Control of limiting point at which the ramp stops. ex: the earlier the ramp stops the shorter the inspiration and then resp. rate increases |
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Primary Affect of Pneumotaxic Center
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Switches off inspiratory ramp and limits resp. rate
- inhibit resp. ramp and cause less volume to lungs - Strong signal allows inspir. to last 0.5 seconds Weak signal allows inspir. to last 3-5 seconds |
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Secondary Affect of Pneumotaxic Center
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Increase respiratory rate
- Strong pneumotaxic signal can increase RR to 30-40bpm - Weak pneumotaxic signal can decrease RR to 3-5 bpm |
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Apneustic Center
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located in center of medulla
- plays no part in normal breathing, but causes inspiratory gasps seen in severe brain injury - only used in abnormal breathing |
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stretch receptors
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located in bronchi
- transmit signals thru vagus nerve into dorsal resp. group when lung is over streched - when lungs become over inflated the inspir. ramp is turned off and inspir. ends |
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Hering-Breuer Reflex
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a reflex triggered by stretch receptors that prevent overinflation of the lungs
- activated when tidal volume > 1L |
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The only ion that DIRECTLY affects Chemosensative area
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Hydrogen Ion
- it affects inspiration and increases respiration with increased Hydrogen ion levels |
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Peripheral Chemoreceptors Respond to what? What is the Role of Peripheral Chemoreceptors
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Low O2 levels, mainly <70mmHg
Role: transmit nervous signals to the respiratory center of the brain |
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Other Factors that Effect Respiration
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1. Voluntary control of respiration = in Cortex of brain
2. Effect of irritant receptors in the airways = pulmonary irritant receptors 3. Function of Lung "J Receptors" 4. Effects of Brain Edema 5. Anesthesia |
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Location of Voluntary Respiratory Control Center
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Located in:
1. Cortex of brain 2. Down Corticospinal tract to resp. muscles |
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Location of Pulmonary Irritant Receptors
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1. Epithelium
2. Bronchi 3. Bronchioles |
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J Receptors
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Located in Juxtaposition to Pulmonary Capillaries
- Sensory Nerve Endings in Alveolar Wall - Stimulated when pulmonary capillaries become engorged with blood or fluid and their excitation causes DYSPNEA |
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Paradoxical Respirations
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a rocking boat movement occurring in which there is out of phase depression of chest wall during inspiration.
Happens under very deep anesthesia - similar to airway obstruction and partial paralysis |
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How is Respiratory Rate Affected by Nitrous Oxide Narcotic technique?
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Respiratory rate is slow with Large tidal volumes
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How is Respiratory Rate Affected by Halogenated Agents?
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there is faster Respiratory Rate and Shallow breathing.
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Mechanism of Cheyne-Stokes Breathing
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1. Circulatory Problem (heart failure): where it takes a long time for the brain to get the blood that has altered CO2 and O2 levels
2. Problem with the Brain (brain damage): there is a problem in the respiratory control center that don't respond to changes in CO2 or O2 levels |
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most common measurement of lung function:
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Vital Capacity =
- largest volume measured after pt inspires to total lung capacity and exhales completely to residual volume into spirometer |
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Normal Lung Volume
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5 Liters
- but varies with age, height, & position - norm. noted as %. - abnormal if lung volume falls below 80% of its predicted value |
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a decreased vital capacity may be result from:
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1. lung pathology: pneumonia, atelectasis, pulmonary fibrosis
2. loss of distensible lung tissue: following surgical excision 3. Causes other than lung disease: muscle weakness, abdominal swelling, pain |
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Obstructive Defect
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characterized by decreased airflow rate relative to actual volume exhaled.
- this indicates Flow Limitation during expiration |
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Causes of early airway closure
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1. secondary to loss of radial traction from surrounding parenchyma (ex: emphysema)
2. edema of bronchial walls 3. secretions with in airway 4. obstructive disease (cause low FEV1) |
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Normal FEV1/FVC ratio (in percent)
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80%
we normally exhale 80% of our total vital capacity FEV1 = 4L FVC = 5L |
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FEV1/FVC ratio in Obstructive Disease (COPD)
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LOW
43% FEV1 is VERY LOW (1.3L) FVC is moderately low (3.1L) |
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FEV1/FVC ratio in Restrictive Disease (Pulmonary Fibrosis)
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Normal or High
80-90% FEV1 is moderately low (2.8L) FVC is moderately low (3.1L) |
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Maximal breathing capacity
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the largest volume that can be breathed per minute.
- comprehensive test of lung function which would be reduced by airway obstruction, poor lung compliance, decreased muscle strength, and decreased motivation - Normal Value = 150-175L/min (male) - gives info on: Coordination, Motivation, and Stamina |
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Measurements requiring pt effort
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1. Peek Flow
2. Maximum Ventilatory Volume |
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PiMAX
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- When inspiration is about to start/ end expiration
- Involves diaphragm (relaxed and stretched out) and low lung volume - normal male value = -100cmH2O |
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PEMAX
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- use of expiratory muscles. They are stretched & full inspiration is near total lung capacity
- Expiration is about to begin/ end inspiration - Pressure less than 40 suggests severe impaired coughing ability |
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Normal Static Pressure
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200cmH2O
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Negative Inspiratory Force must be at least?
What muscle are we testing? |
-25cmH2O in order for air to flow into lungs
- we b/c we breath by negative pressure. We need at least -25cmH2O for air to get into our lungs - tests strength of Diaphragm |
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Physiological Determinants of Maximum Flow Rates
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1. degree of effort, or the driving pressure generated by muscle contraction
2. the elastic recoil pressure of the lung 3. Airway Resistance |
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Expiratory flow is determined by
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1. Elastic recoil force of lungs
2. Resistance of airway flow |
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Variable Airway Obstruction affect Inspiration, Expiration or both?
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Only affects Expiration
ex. Lung Cancer |
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Fixed Airway Obstruction affect Inspiration, Expiration, or both?
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Affect Inspiration and Expiration
ex. Tracheal Stenosis |
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What does the Plateau Phase on the End Tidal CO2 of Capnograph stand for?
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it's mainly flat b/c pt is breathing out gas from alveoli that has a more constant CO2 level
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3 Phases of Expiration
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1. Breath out Dead Space with only O2 (CO2 free)
2. exhale mix of alveolar and dead space gas 3. Alveolar Plateau: all gas is from alveoli and none from dead space |
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Phase 3 Slope (Increased Alpha Angle)
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results from uneven emptying of alveoli caused by uneven time constants and gas trapping (seen in OR)
- lung not emptying as a unit (obstructive disease) - tx: give pt more time to exhale |
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Phase 4 Slope
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Seen in pregnant women and obesity
- small FRC, exhale CO2 fast from alveoli |
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Increased Beta Angle
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Occur with Rebreathing of pt's own CO2
- cause: too much dead space in ETT, anesthesia machine malfunction |
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3 Major Determinants of Flow
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1. Muscle Strength: PEMax
2. Lung Elastic recoil pressure 3. Airway Resistance |
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Early lung dysfunction include:
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1. Small airway disease
2. Early obstructive lung disease 3. Minimal airway dysfunction 4. Peripheral airway obstruction |
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Most airflow resistance comes from:
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Medium sized Bronchi
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Tests of Early Lung Dysfunction
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1. Alveolar:Arterial Oxygen Tension Difference
2. Frequency Dependence of Compliance 3. Nitrogen Washout 4. Closing Volume |
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Phase 4 of Expiration, using Closing Volume graph
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- end of expiration with abrupt increase in N2 (Nitrogen).
b/c: it shows the alveoli in the apex that are still exhaling N2 (Nitrogen) while to alveoli in the base have already closed and aren't contributing to expired gas |
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Closing Volume definition
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the difference between onset of Phase 4 and Residual Volume
- doesn't include residual volume - norm = 10% of vital capacity |
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3 factors that cause V/Q abnormalities
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1. A:a O2 gradient abnormality
2. Physiologic shunt and venous admixture 3. Alveolar dead space |
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Shunt moves Oxygen Dissociation curve to left or right?
What happens to V/Q? |
Moves curve to the Left with a Low V/Q ratio
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Dead Space move Oxygen Dissociation curve to left or right?
What happens to V/Q? |
Moves curve to Right with High V/Q ratio
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4 Main causes of Hypoxemia
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1. Pure Hypoventilation
2. Diffusion Impairment 3. Low V/Q ratio 4. Shunt |
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Pt's who need PFT's prior to surgery
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1. COPD pt's
2. Heavy smokers with hx of persistent cough 3. Pt's with wheezing/dyspnea on exertion 4. Patients with chest wall and spinal deformities 5. Morbidly obese 6. Pt's undergoing Thoracic surgery 7. Elderly (older than 70 y/o) 8. Pt's undergoing upper abdominal surgery |
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The efficiency of adaptation to high altitude depends on what factors?
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1. the normal altitude the person lives at
2. Rate of ascent 3. Altitude attained 4. Health of person |
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Acclimatization
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When over a few days the respiratory center in the brain looses its sensitivity to CO2 and H ions and low O2 that initially caused hyperventilation
- you now renally excrete bicrab and therefore the person will want respiratory alkalosis and hyperventilation b/c the renal system is controlling the rest of pH balance |
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Signs and Symptoms of High Altitude Sickness:
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Happens b/c of low PO2 levels
1. Impaired Night Vision 2. Headache 3. Fatigue 4. Dizziness 5. Palpitations 6. Insomnia 7. Loss of appetite 8. Impairment of Mental Performance 9. Loss of Consciousness |
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Adaptation
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refers to the physiologic differences in permanent residents at high altitudes
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Things that are Adapted in those who are permanent residents at high altitudes
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1. Increase in Hgb concentration and O2 affinity = Earliest adaptation
2. Pulmonary diffusion capacity increases 3. Maximum breathing capacity increases 4. Increased vascularity of the heart and striated muscles |
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HPV: Hypoxic Pulmonary Vasoconstriction
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When the blood flow constricts past unventilated/poorly ventilated alveoli and opens up while passing good ventilated alveoli to allow for gas exchange to happen
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Symptoms of Oxygen Toxicity
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1. Irritation of the tracheobronchial tree: cause sensation of retroperitonitis
2. sensation of retrosternal tightness 3. Chest pain 4. Cough 5. urge to take deep breaths 6. Reduced vital capacity 7. Structural changes which give rise to acute lung injury and changes in lung function |
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Deleterious Effects of Smoking
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1. Airway reflexes are more sensitive
2. Ciliary function is inhibited 3. Mucus production is increased 4. Airway diameter is reduced increases airway resistance 5. Ventilatory capacity is reduced 6. Integrity of the alveolar/capillary barrier is impaired 7. Dead space to tidal volume ratio is increased |
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Mechanism of Smoking Related to Lung Damage
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1. Direct irritation and toxic effects from compounds in cigarette smoke
2. Oxidative injury of the lungs: b/c of the tar in cigarettes 3. Activation of Neutrophil and Macrophage activity |
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2 groups of compounds with carcinogenic activity, found mostly in the tar phase of cigarettes
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1. Hydrocarbons
2. Nicotine derivatives |
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Primary Pollutants
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substances that are released into the atmosphere directly from the polluting source
- mostly derived from the combustion of fossil fuels - cause release of Free Radicals |
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Secondary Pollutants
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formed in the atmosphere from chemical changes to primary pollutants
- cause the release of Free Radicals |
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3 things that cause surfactant release
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1. High lung volume
2. increase in Vent Rate 3. Endocrine Stimulation (ex. adrenaline) |
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Hysteresis
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states that the compliance curve is different on inhalation and exhalation
- decreased compliance with inhalation - increased compliance with exhalation |
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what tissue in the lung is most metabolically active
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endothelium
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2 ways Arachidonic Acid is Metabolized
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1. Cyclooxygenase pathway
2. Lipoxygenase pathway |
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Product of Lipoxygenase metabolism
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Leukotrienes
- cause bronchoconstriction in some asthmatics |
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product of Cyclooxygenase metabolism
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1. Prostaglandins
2. Thromboxane A2 - cause pain and inflammation |
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Non-Respiratory Functions of the lungs
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1. secrete immunoglobulin: IgA
- secreted in bronchial mucous and defends against infection 2. Synthetic function: Surfactant, Collagen, and Elastin - collagen and elastin are proteins that are structural framework of the lungs 3. Reservoir for blood: - Pulmonary vascular pressure remains normal even with high blood volume b/c of recruitment and distention of blood vessels in the lungs |
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Hypoxemia
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an SaO2 < 90% lasting more than 30-60 seconds
- occurs in up to 60% of pt's breathing room air after surgery. |
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Severe Hypoxemia
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an SaO2 , 85% that long lasting
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Those people predisposed to Hypoxemia
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1. Obesity
2. Smokers 3. Pre-existing and current lung disease 4. Heart Disease 5. Extreme age (very young or old) 6. Thoracic and high abdominal surgery |
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Low Flow devises
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1. Nasal canula
2. face mask 3. face tent |
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High Flow devises
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1. special face mask
2. oxygen nebulizer 3. CPAP, BiPAP 4. Ventilatory |
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Venturi Principle
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have a dial to control the flow of FiO2 and entrained air
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BiPAP is most commonly used on what type of disease or pt population?
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Obstructive Sleep Apnea
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Benefits of adding Peep
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1. Increase FRC!!!!!
2. More stable alveoli 3. Better gas exchange b/c redistributes lung water 4. Prevents small airway collapse |
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Downside of adding Peep
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Decreases Cardiac Output
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Contraindications for adding PEEP
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1. Heart failure
2. hypotension 3. pneumothorax 4. increased ICP |
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Auto-Peep
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when gas is trapped in the alveoli and doesn't fully exhale
- breath stacking can occur. tx by increasing expiratory time |
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2 incidences respiratory failure causes hypercapnia
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1. hypoventilation
2. V/Q abnormality (Low V/Q) |
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Ventilatory Support is used most often in:
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1. Resuscitation following acute apnea
2. Anesthesia with Paralysis 3. ICU 4. Treatment of chronic ventilatory failure |
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2 forms of impedance for airflow
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1. Elastic Resistance
2. Non-elastic Resistance |
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Peek Inspiratory Pressure (PIP)
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the pressure it takes to overcome elastic and non-elastic work of breathing
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Zero-End Expiratory Pressure (ZEEP)
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expiration to ambient pressure
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Normal Tidal Volumes
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10-15 mL/kg
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Benefits of Large Tidal Volumes
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1. Prevent atelectasis (open alveoli)
2. Maintains near normal compliance and oxygenation 3. Compensate fro increased dead space caused by positive pressure ventilation 4. Large Tidal Volumes are better tolerated by conscious patients |
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Plateau Pressure is reflective of:
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Alveolar Pressure
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Normal Plateau Pressures
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less than or equal to 30 cmH2O.
- and increase above 40 cmH2O causes barotrauma |
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Explain Volume Control Ventilation
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- Set TIdal Volume that is always delivered
- Pressure varies with pt compliance - Can set a max pressure that will make vent "pop-off" if pressure goes above set value and the rest of the volume will not be delivered |
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Explain Pressure Controlled Ventilation
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- Set a Pressure that's constant
- the volume varies |
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Most common ventilator setting used in O.R.
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Volume Control with Pressure "Pop-off"
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Advantage and Disadvantage of using Pressure Controlled Ventilation
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Advantage = No Peek Pressure
Disadvantage = Tidal Volume Varies |
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2 Problems with reversing I:E ratio & What Vent mode must be used
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1. Breath stacking
2. Auto Peep - Must use Pressure Controlled Ventilation to reverse I:E ratio |
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Pressure Limit & what are the settings
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"pop-off"
when in Volume Control Ventilation you can set a pressure limit that the pt can't go over. If the pressure does get higher than set limit than the vent will "pop-off" and the rest of the volume will not be delivered to the pt - set it at 10-15cmH2O higher than the pt's Peek Inspiratory Pressure (PIP) |
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3 Triggers that cause vent to cycle an inspiration
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1. Time
2. Pressure 3. Flow/Volume |
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When is Controlled Mandatory Ventilation used? (CMV)
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in the OR when the pt is paralyzed
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Assist Control (AC)
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Volume and RR are preset but pt can breath over the the Volume and RR if they choose to
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Intermittent Mandatory Ventilation (IMV)
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the pt breaths on their own and draws in as much Volume as they want.
- the pt does not get a preset breath |
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Synchronized Intermittent Mandatory Ventilation (SIMV)
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All breaths are Synchronized to prevent breath stacking
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Manifestations of Pulmonary Barotrauma
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1. Pulm interstitial emphysema
2. Pneumomediatstinum 3. Pneumothorax 4. Sub-Q emphysema 5. Pneumoretropertioneum 6. Pneumoperitoneum 7. Pneumopericardium 8. Venous and arterial air embolism 9. Bronchopleural fistula |
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Ventilator discontinuance should be attempted when:
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1. underlying indication for vent support is reversed or significantly improved
2. Cardiovascular and Pulmonary stability 3. Labs suggest no factors that significantly increase vent demand |
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Weaning Parameters
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1. Rapid Shallow Breathing index is <100
2. Inspiratory Pressure is <-25cmH2O 3. Tidal volume >5mL/kg 4. Vital Capacity >10mL/kg 5. Minute Ventilation <10L |
