Pulm Pharm and Phys Flashcards
Gas exchange is determined by _______ and _______.
Gas exchange is determined by ventilation and perfusion of the lungs and matching of these two independent variables
3 Types of Alveolar Cells
Type I - squamous cells make up the alveolar epithelium and cover 80% of the alveolar surface area
Type II - produce surfactant
Type III - alveolar macrophages
Law of LaPlace
Pr=2T for a sphere
P - pressure inside the alveoli
R - radius of the alveoli
T - surface tension trying to collapse the alveoli
alveoli do not directly follow the Law of LaPlace due to the effect of surfactant!
Diffusion of gases is determined by 5 things
1) membrane thickness (thicker the membrane the slower the diffusion)
2) surface area (more surface area = more area to diffuse through)
3) diffusion coefficient of the gas (blood:gas coefficient, more soluble agent means faster diffusion)
4) pressure difference between the two sides of the membrane (henry’s law)
5) distance (greater the distance the slower the diffusion - more of a problem w blocks)
Graham’s Law
(Molecular Weight and Diffusion of Gases)
difusion of gas through a semi-permeable membrane is inversely proportional to the square root of the molecular weight of that gas
the larger the molecule, the slower the diffusion
Henry’s Law
(Pressure difference and diffusion of gases)
the greater the pressure difference the greater the rate of diffusion
ie: when we want to increase our [] of anesthetic gases, we increase our delivered agent so more will diffuse across and deepen the anesthetic
At equal pressures, the rate of diffusion of a gas is dependent on the ________ of the gas divided by the _______ _______.
At equal pressures, the rate of diffusion of a gas is dependent on the solubility of the gas divided by the molecular weight.
- CO2 is 20x as diffusable as 02
- N2O is 19x as diffusable as 02
- N20 is 36x as diffusible as N2
- these principles are behind why N2O expands when we don’t want it to!*
Total body oxygen delivery (DO2) is the product of what 2 things?
- 02 content of arterial blood (Ca02)
- rate of delivery to the tissues (CO)
DO2 = CO x Ca02
Ca02 (oxygen content of arterial blood) calculation
Ca02 = Hgb x 1.39 Sa02 + (0.0031*Pa02)
Ca02: oxyen content of arterial blood
1.39: binding capacity of Hgb is 1.39mL 02 per gm of Hgb
Sa02: arterial oxygen saturation
0.0031: solubility of 02 in plasma (mL 02/ mmHg/100mL plasma)
Pa02: partial pressure of dissolved oxygen in arterial blood
Cv02 (oxygen content of venous blood) calculation
Cv02 = Hgb x 1.39 x Sv02 + (0.0031 x Pv02)
Cv02 - oxygen content of venous blood
Sv02 - venous oxygen saturation
Pv02 - partial pressure of dissolved oxygen in venous blood
VO2 calculation (total body oxyen consumption)
V02 = CO x (Ca02 - Cv02)
normal is 250mL/min or
2-4 cc/kg/min
In healthy individuals, what is oxygen delivery and consumption?
– Oxygen delivery (DO2) is 16 ml/kg/min
– Oxygen consumption is 4 ml/kg/min
– Therefore total body oxygen extraction fraction (OEF) is about 25%
– And returning oxygen SvO2 is about 65-80%
Sv02 (mixed venous oxygen concentration) calculation
- normal between 65-80%
Decreased Sv02 may indicate what 4 things?
- decreased Hgb (hemolysis/hemorrhage/ not enough oxygen on cells being carried around)
- decreased CO (MI, CHF, hypovolemia)
- decreased Pa02 (hypoxia, ARDS, inappropriate vent settings)
- increased oxygen demands (fever, MH, shivering, thyroid storm, exercise, agitation)
Increased SV02 suggests what 4 things?
- permanently wedged Sv02 S-G catheter
- decreased VO2 (sepsis, hypothermia, methmeglobenmia, CO poisoning, cyanide toxicity)
- increased CO (sepsis, burns, L-R shunt, AV fistula, inotropic excess, hepatitis, pancreatitis)
- increased Hgb or Sa02 (GA may increase Sv02 by decreasing VO2 and increasing Fi02)
an increased Sv02 may indicate issues w inability to utilize oxygen
Oxygen Consumption
- determined by basal metabolic rate, estimated by Brody Equation
- normal is 2-4 cc/kg/min or 250cc/min
- increased by fever, thyrotoxicosis, exercise, stress, shivering
- decreased by hypothermia, hypothyroidism, and ANESTHESIA
- GA reduces 02 consumption 10-15%
- hypothermia reduces by 50% at 31 degrees C
A-a gradient
if ventilation/perfusion were perfectly matched, PA02-Pa02 = 0 and PAC02-PaCO2 = 0.
the difference in PA02-Pa02 or PACO2-PaCO2 is a measure of the V:Q abnormality
PO2 estimation calculation
PA02 = percent Fi02 x 6 (about 120 Pa02 = percent Fi02 x 5 (105 ish)
ETCO2 = average PACO2
Normal A-a gradient (AaDO2) breathing room air and 100% oxygen
breathing room air:
PA02-Pa02 (AaDO2) = 5-15mmHg
- progressively increases w age up to 20-30mmHg
- AaDO2 in healthy elderly is 37.5
Pa02 guesstimate = 102-age/3 or Fi02x5
- Pa02 range 60-100
breathing 100% oxygen:
PA02-Pa02 <100mmHg
Forms of Hypoxemia
- hypoxemic hypoxemia: 2/2 inadequate arterial oxygenation (typically low Fi02)
- anemic hypoxia: 2/2 decreased Hgb
- circulatory hypoxia: 2/2 decreased perfusion
- histologic hypoxia: 2/2 cellular inability to utilize oxygen
Causes of low Pa02
- low inspired 02 (fi02)
- hypoventilation
- V:Q mismatch (low Hgb, low CO)
Treating Hypoxemia
• Increasing FiO2 alone may do little to increase PaO2 if the problem is due to absolute right to left shunt
– e.g. PDA, atelectasis
• Increasing FiO2 should increase PaO2 if the problem is primarily hypoventiation or increasing dead space
( e. g. PE).
• 100% FiO2 = absorption atelectasis (bad!)
Anatomic Deadspace
is normally 1/3 of tidal volume or 1 cc/lb. This is the inhaled air that sits in the conducting air passages and doesn’t participate in gas exchange.
ie: oropharynx, nasopharynx, trachea, 1st gen bronchi
Physiologic Deadspace
is anatomic deadspace plus alveolar deadspace. These terms are synonomous in the healthy person.
ie: deadspace in alveoli not being perfused
Pathologic Deadspace
refers to additional alveolar space which is being perfused but not ventilated. In persons with respiratory disease physiologic deadspace may be as high as 10x normal anatomic deadspace.
– An increased V/Q ratio indicates increased deadspace and may be caused by pulmonary emboli, hypotension, or ligation of a pulmonary vessel.
Shunt
refers to lung that is perfused but not ventilated (right mainstem intubation)
– A decreased V/Q ratio indicates increased shunt and can be caused by endobronchial intubation, mucus plug, or alveolar collapse
Compliance
- Compliance can be expressed as how much the volume in the lungs will increase for a given increase in alveolar pressure.
- Normal lungs will expand 130ml of volume for every 1cm increase in water pressure or 0.13 L/ cm H2O.
- The more compliant a lung is, the greater the volume that can by inspired at a lower PIP.
- The less compliant lung inspires smaller volumes at higher PIPs
Normal lungs will expand _____mL of volume for every 1cm increase in water pressure or 0.13 L/ cm H2O.
• Normal lungs will expand 130ml of volume for every 1cm increase in water pressure or 0.13 L/ cm H2O.
Boyle’s Gas Law
At a constant temperature, pressure is inversely proportional to volume
- as pressure increases, volume decreases
- as pressure decreases, volume increases
static compliance
p/v relationship when air is NOT moving
- decreases w conditions that make it difficult to inflate the lung, ie: obesity, fibrosis, edema, vascular engorgement, external compression (surgeons elbow)
- increases w emphysema which destroys lung tissue as wella s reduces elastic recoil, causing air trapping
dynamic compliance
P/V relationship when air IS moving
- decreases w airway obstruction such as foreign body and bronchospasm
Intrapulmonary pressure
- pressur ewithin the alveoli
- negative w inspiration, positive w expiration
Intrapleural pressure
- pressure in the potential space between the inside of the chest wall and lungs
- lungs recoil inward and chest recoils outward
- this is what fills w hemo or pneumothorax
- always negative during normal breathing*
- becomes MORE negative w inspiration and less negative w expiration*
- becomes positive w forced expiration/valsava*
Is intrapleural pressure more negative in the dependent or non-dependent lung?
- more nebative in the non-dependent lung
V:Q Ratio
- normal V/Q: 0.8 or 4L/min / 5L/min = 0.8
- Absolute Shunt: V/Q = 0
no ventilation, desaturated blood from R heart returns to L w/o being oxygenated
Absolute Dead Space: V/Q = infinity
NO perfusion (ie: pulmonary embolus)
FRC
functional residual capacity, lung volume at end of normal exhalation
- obese = lower FRC
RV
residual volume - volume remaining after maximal exhalation
VC
vital capacity - max volume of gas that can be exhaled following maximal inspiration
Normal PFT Values
FEV1 - 4L/sec
FVC - 5L/sec
FEV1/FVC = 4/5 = 0.8 or 80%
FEV1
normal 4 L/sec
- forced expiratory volume in 1 sec; the volume of gas that can be exhaled within one second of beginning a force expiration
FVC
- normal 5L/sec
- volume of gas that can be exhaled during a forced expiratory maneuver
FEV1/FVC
ratio used to distinguish between obstructive and restrictive diseases
- normal = 4/5 = 0.8 = 80%
FEF 25-75%
midmaximal expiratory flow (MMEF)
- rate of flow occuring in a forced expiratory flow from the point where 25% of the FVC has been exhaled to where 75% has been exhaled
- best test for assessing small airway disease, independent of respiratory effort!
Extrathoracic Obstruction
- inspiration is impaired
- ie: vocal cord paralysis w inspiratory stridor, pharyngeal muscle weakness, papilloma in airway
can be overcome by using ETT
Intrathoracic Obstruction
- expiration is impaired
- negative pressure of inspiration keeps trachea open, PPV will be difficult if ETT does not pass obstruction, often not compensated by intubation as obstruction is past carina
- usually tumors of trachea or bronchi
fixed large airway obstruction
ie: mucous plug in ETT, kinked ETT
Restrictive Pulmonary Disease
- decreased lung compliance = decreased lung volumes
- alveolar ventilation is restricted
- both FEV1 and FVC are decreased but FEV1/FVC ratio is normal
- compliance as low as 0.02 L/cmH20 in severe dx (normal is 0.10)
- types: acute intrinsic, chronic intrinsic and chronic extrinsic
Obstructive Pulmonary Disease
- pathologic conditions increase airway resistance which results in a decrease in max rate of exhalation
- exhalation is obstructed
- intralumenal and extralumenal airflow obstruction results in air trapping
- ie: COPD
Acute Intrinsic
- restrictive lung disease like pulmonary edema
- water and solutes accumulate in the interstitial tissues causing lungs to become stiff
- aspiration, ARDS, POPE, CHF
Chronic Intrinsic
- restrictive lung dx
- changes in elastic tissue in lung lead to decreased ompliance
- ie: sarcoidosis, drug-induced pulm fibrosis (amiodarone, bleomycin)
Chronic Extrinsic
- restrictive lung disease
- disorder of the chest wall and intra-abdominal changes
ie: obesity, pregnancy, kyphosis, SCI transection, muscular dystrophy
Indicators of Increased Risk of Post-op Pulmonary Dysfunction
- dyspnea that limits activity
- decrease in VC to <15ml/kg (normal is 70)
- FEV1 <50% of predicted or <2 L
- FC <50% of predicted
Anesthetic Mgmt of Restrictive Lung Dx
- treat reversible conditions preop (abx for pna, bronchodilators)
- baseline ABG, pulse ox, PFTs
- use large ETT (hagen-pouiselle)
- use higher inspiratory pressures
- smaller TV w higher rate, occasional “sigh” breaths w PIP 35-45 cmH20
- slow inspiratory flow rate
- prolong inspiration time
- PC vs VC
- consider PEEP
- consider regional (above T10 = resp block)
- maintain NMB
- when in doubt, don’t pull the tube out!
Laryngospasm
- mediated by superior laryngeal nerve in response to irritating glottic/supraglottic stimuli such as food, blood, vomitus or foreign body
- false cords and epiglottic body come together to prevent air flow and vocal sounds
- deepening anesthetic won’t work because you can’t ventilate anyways
Treatment of Laryngospasm
- forward displacement of jaw, PPV and 100% 02
- may need 20mg-ish of IV succx and re-intubation
- can give 40-60 mg IM or sublingual
POPE
- post obstructive pulmonary edema
- sudden onset of pulm edema following upper airway obstruction
Type I: follows a sudden severe episode of upper airway obstruction
Type II: develops after surgical relief of chronic upper airway obstruction
- laryngospasm during intubation or after anesthesia is the most common cause of upper airway obstruction leading to POPE Type I
High Negative Intrapulmonary Pressure
- increased venous return to RV
- increases pulmonary blood flow causing elevated pulmonary capillary hydrostatic pressure
- increased afterload and decreased EF and CO
- decreases pulmonary interstitial pressures
- increases pulmonary capillary hydrostatic pressure
How does pulmonary edema develop when an obstruction is relieved?
- forced inspiratory attempts alternated w forced expiratory attempts (Valsava) creates auto-PEEP which opposes transudation of fluid in the interstitium
- once obstruction is relieved, unopposed venous hydrostatic pressure leads to pulmonary edema
Tx of POPE
- self limited, clears within 48 hours
- tx depends on severity of hypoxemia
- re-establish airway (jaw thrust, chin lift)
- supplemental oxygen
- CPAP
- reintubate and use PEEP
Emphysema
• Destructive process involving the lung parenchyma that results in loss of elastic recoil of the lungs.
– Airway collapse happens during exhalation.
– Increase work of breathing.
• Can have relatively advanced disease with preservation of PaO2 , and usually do not retain CO2 .
– “Pink Puffers”
– Tendency to exhale through pursed lips to provide end-expiratory pressure.
Spirometry w Emphysema
– Decreased FEV1
• When FEV1 is < 40% of normal, dyspnea is seen during ADL’s
– Decrease in FEV1/FVC
– Decreased FEF 25-‐75%
– Diminished air flow at all volumes
– Increased RV
– Normal to increased FRC and TLC
Radiographically you will see hyperlucency and hyperinflation (flat diaphragm)
emphysema radiograph
- hyperlucency w hyperinflation (flat diaphragm)
Chronic Bronchitis
- Follows prolonged exposure to airway irritants.
- Characterized by hypersecretion of mucus and inflammatory changes in the bronchi.
- Copious secretions occlude airways.
- Diagnosed if a patient produces sputum 2 months out of the year for 2 years in a row.
- Unlike emphysematous patients, there is a marked tendency toward decreased PaO2 early in their disease course.
- CO2 diffusion is also impaired (increased PaCO2)
Blue Bloater
- seen in chronic bronchitis
- hypoxemia and respiratory acidosis lead to pulmonary vasoconstriction and pulm HTN
- may lead to cor pulmonale w RV hypertrophy and R axis deviation
Spirometry w Chronic Bronchitis
- FEV1/FVC decreased
- FEF 25-75% is decreased
- increased RV
- normal to increased FRC and TLC due to slowing of expiratory airflow and gas trapping behind prematurely closed airways
- greater WOB at high lung volumes
- chronic bronchitis x-ray
- non specifix w bronchial wall thickening
- increased bronchovascular markings, enlarged vessels and cardiomegaly
- scarring of tissue scauses irregular bronchovascular structures
- maintains curvature on diaphragm vs emphysema which is flat
Asthma
- chronic airway narrowing due to bronchial hyperactivity
- exacerbations
- patho not completely known, IGE mediated
- increased cAMP = bronchodilation and sympathetic stimulation of B2
- increased cGMP = bronchoconstriction and PS stimulation of muscarinic
- asthmatic x-ray
- normal cardiomediastinal contours
- no pleural abnormalities, no collapse or consolidation, unremarkable x-ray
Beta 2 agonists
- bronchodilator thearpy
- albuterol, metaproterenol, ceprenaline
- relatively free of a1 and b1 effects
phosphodiasterase inhibitors
methylzanthines
- oral or IV
- inhibit breakdown of cAMP
- aminophylline
Parasympatholytics
- block the effect of ACh on bronchial smooth muscle
- ipratroprium (does not have the same SE as atropine, less tachycardia)
COPD Anesthetic Mgmt
- intraoperatively, volatiles provide bronchodilation and may attenuate regional hypoxic vasoconstriction (R to L shunt)
- N20 use carefully in pts w pulmonary bulae, can cause diffusino hypoxia
- opioids be very careful, extreme sensitivity, opioids will exacerbate breathing difficulties
COPD and Mechanical Ventilation
- large TV (10-15 mL/kg)
- Slow RR (6-10)
- increased expiratory time
- avoid high PIP especially w pulmonary bullae
- PEEP not necessary, may impede expiratory air flow
- use sigh mode
- extubation, use post op vent FEV1/FVC ratio of <0.5, pre-p[ PaCO2 of >50
