Rosalind Franklin 1920-1958Had a crucial role in the discovery of the helix structure of DNA
Rosalind Franklin is most associated with the discovery of the structure of DNA. At 26, after she had her PhD, Franklin began working in x-ray diffraction - using x-rays to create images of crystallized solids. She pioneered the use of this method in analyzing complex, unorganized matter such as large biological molecules, and not just single crystals.
Franklin made marked advances in x-ray diffraction techniques with DNA. She adjusted her equipment to produce an extremely fine beam of x-rays. She extracted finer DNA fibers than ever before and arranged them in parallel bundles. And she studied the fibers' reactions to humid conditions. All of these allowed her to discover crucial keys to DNA's structure. Maurice Wilkins, her laboratory's second-in-command, shared her data, without her knowledge, with James Watson and Francis Crick, at Cambridge University, and they pulled ahead in the race, ultimately publishing the proposed structure of DNA in March, 1953.
It is clear that without an unauthorized peek at Franklin's unpublished data, Watson and Crick probably would neither have published their famous paper on the structure of DNA in 1953, nor won their Nobel Prizes in 1962. Franklin did not share the Nobel Prize; she died in 1958 at the age of 37.

Physics in Anesthesiology: Basic Science Review

Physics in Anesthesiology: Basic Science Review
Jeffrey B. Gross, M.D. Farmington, Connecticut
Why Physics?
a) Understand how our equipment is SUPPOSED to work
b) Understand what might happen if things go WRONG
c) Function as a CONSULTANT in the medical specialty of Anesthesiology
d) Do well on Content Outline Section 1B of the In-Training and Part I American Board of
Anesthesiology Examinations
Pressure
a) Pressure= Force per unit of area
b) Units
• Pounds / in2 (PSI)
- Atmospheric Pressure PATM=14.7 PSI)
• Pascals (nt / m2) (PATM~100 KPa)
• mmHg (7.5 mmHg = 1 KPa)
• cmH2O (1 mmHg = 1.36 cmH2O)
c) Implications
• Even a small pressure exerts a large force if area is large
• A small force can exert a lot of pressure if the area is small
d) Absolute vs. Gauge Pressures
• Gauge pressures: relative to ambient pressure
- Tire pressure, pressure in compressed gas cylinder, blood pressure
• Absolute pressures
- Vapor pressure of anesthetics, H2O
- Blood gases
- Other cases where you need to use gas laws
e) Pressure Gauges
• Bourdon tube (for high pressure gases such as compressed gas cylinders)
- Deformable tube changes shape when filled with pressurized gas causing pointer to move
• Diaphragm (for low pressures such as aneroid blood pressure cuffs--the kind with a pointer)
- Diaphragm at top of a "pancake" shaped cylinder moves outward causing pointer to move
f) Pressure Regulators
• Reduces high pressure in compressed gas cylinder to approximately 50 PSIG
Gas Cylinders
a) E Cylinder (back of machine)
• For ideal gases (air, nitrogen, oxygen)
- Full cylinder pressure = 2000 PSI
- Full cylinder volume = 660 liters
- Volume remaining is proportional to pressure
- 1000 PSI --> 330 L 500 PSI-->165 L
• For pressurized liquids (N2O, CO2, C3H8 [propane--barbecue grill], C3H6 [cyclopropane])
- Pressure depends on vapor pressure of liquid at tank temperature until liquid is “gone” (740
PSI) for N2O at room temperature
- Full cylinder of N2O – 1590 L
- Remaining quantity of gas best determined by weight
• The N2O in a full E cylinder weighs about 3 Kg
- Critical temperature (Tc): gas cannot be liquefied above this temperature regardless of
pressure
• For N2O TC = 36.5o C

b) Some Simple Calculations
• What is the weight of N2O in an E-cylinder?
• What is the internal volume of an “E” Cylinder?
- Use Boyle's Law: P1V1=P2V2
c) More Simple Calculations
• How many ml of sevoflurane vapor come from 1 ml of sevoflurane liquid?
• If the fresh-gas flow is 2 l/min, how many minutes of 2% sevoflurane anesthesia will 5 ml of
liquid provide?
Adiabatic Compression
a) Rapid compression of gas without giving heat a chance to escape
• Principle of diesel engine (no spark plugs)
b) If there is oil / grease in valve or regulator and tank opened quickly, explosion can occur :-(
Flows of Liquids and Gases
a) Laminar (streamlined)
• Pressure=Flow x Resistance
b) Turbulent
• Pressure α Density x Flow2
• Transition from laminar to turbulent flow when Reynold's number > 2300
Flowmeters
a) Tapered tube with diameter increasing toward the top
b) Bobbin position determined by equilibrium
• Upward force from flowing gas = downward force from gravity
- At low flow rates (laminar flow) upward force depends on viscosity of gas
- At high flow rates (turbulent flow ) upward force depends on density of gas
c) Always want O2 flow tube nearest to the common gas outlet
- Minimizes risk of hypoxia if a flow tube is cracked
η=viscosity of liquid
R=radius of tube
L=length of tube
ρ=density of liquid
V=velocity of flow
D=diameter of tube
η=viscosity of liquid

Fail Safe Valve
a) Cuts off N2O if O2 supply fails
• Does NOT prevent accidental or intentional “dialing in” of a hypoxic gas mixture
b) Testing
• Turn on O2 and N2O flows
• Disconnect wall O2 supply (be sure O2 tank is "off")
• Press O2 flush valve
• Verify that N2O flow ceases when O2 pressure drops to zero
Proportioning Systems
a) Limit N2O flow to 3 times O2 flow
b) Link vs. pressure operated systems
• Link system: mechanically turns down N2O needle valve if O2 flow reduced
- N2O flow will NOT return to initial value if O2 flow increased
• Pressure system: pneumatically decreases N2O flow if O2 flow reduced
- N2O flow will return to initial value if O2 flow increased
Anesthetic Vaporizers
a) Ye Olde Copper Kettle
• Vapor output depends on O2 inflow and vapor pressure of anesthetic
• For sevoflurane, Pv=190 mmHg = 1/4 ATM
- 1/4 of output molecules will be Sevoflurane; 3/4 of output molecules will be O2
- For every 100 ml O2 input, will get 133 ml of total output
• 100 ml O2 (3/4 of total)
• 33 ml sevoflurane (1/4 of total)
- If you use a total gas flow of 3.3 l/min (magic number :-), each 100 ml of O2 through the
vaporizer gives you 1% of sevoflurane concentration
b) Desflurane “Vaporizer”
• Boiling point of desflurane 23.5o C (vapor pressure at room temp nearly atmospheric
• Variable bypass vaporizer not controllable
- Each 100 ml of O2 through vaporizing chamber would give about 900 ml of desflurane output
- Large output swings with changes in temperature
• Alternative: Use a “boiler” and deliver as a gas
- Desflurane output determined by a "needle" valve, just like O2 and N2O
- Uses electronics to make desflurane flow proportional to total gas flow, so a constant
percentage is given regardless of fresh gas flow settings
c) Vaporizers at Altitude
• Recall that MAC is really a partial pressure
- Sevoflurane MAC = 2% x 760 mmHg =15.2 mmHg
• In Tibet PATM = 380 mmHg
• 15.2 / 380 = 4% (MAC of sevoflurane in Tibet)
- Vapor pressure of sevoflurane in Tibet (depends on temperature only) = 190 mmHg (same as
at sea level)
• Since vapor pressure = 1/2 barometric pressure, for every 100 ml of O2 flowing into
vaporizer the output will be 100 ml of sevoflurane plus 100 ml of O2
• This is 3 times as much as at sea level--vaporizer output triples
• Since MAC is only twice as great as at sea level, actually need to turn vaporizer DOWN
to 1.33% in order to get 1 MAC of anesthetic effect
• Desflurane “vaporizer”
- Percentage output unaffected by altitude
- MAC of desflurane in Tibet is 12%
- Need to “dial in” 12% desflurane to get 1 MAC of anesthetic effect

Low pressure leak test
a) Checks for leaks in flowmeters, vaporizers, common gas manifold
b) Check valve just before common gas outlet on many machines
• Allows patient to be ventilated with O2 from flush valve even if there is a leak in low pressure
system--therefore, the fact that the breathing circuit "holds pressure" does not guarantee that there
are no low-pressure leaks
• To check for leaks
- Turn machine fully off (otherwise minimum mandatory O2 flow will look like a leak
- Apply suction bulb to common gas outlet and verify that it remains deflated for at least 5 sec
Breathing Circuits
a) Open (non-rebreathing)
• Simple face mask or nasal cannula (CO2 diffuses away from the face)
• Bag-Valve-Mask system (Ambu®): uses 3 valves to allow either spontaneous or controlled
ventilation while preventing rebreathing
b) Semi-Open (Mapleson / Bain)
• Most efficient removal of CO2 for a given gas flow when the "pop off" valve is nearest the source
of the ventilatory power
- Spontaneous ventilation: Mapleson A
- Controlled ventilation: Mapleson D
• However, the "A" system is very inefficient (requires high gas flows) to prevent rebreathing
during controlled ventilation, while the "D" system is reasonably efficient for both controlled and
spontaneous ventilation, so the "D" is preferred for most applications.
- Bain circuit is a coaxial Mapleson D
c) Semi Closed Circle System
• Patient gas uptake < fresh gas flow < minute ventilation
• Some rebreathing of exhaled gas (following removal of CO2 by absorber)
d) Closed System
• Gas inflow = Patient Uptake
• If using sidestream agent / CO2 analyzer, must route exhaust back into circuit
• Starting values
- O2: 3-4 ml/kg/min
- Anesthetics: First minute uptake / √time (minutes)
• N2O (80% concentration, 80 kg patient): First minute uptake 1600 ml
• Sevoflurane (2%, 80 kg patient): First minute uptake 50 ml
• Desflurane (6%, 80 kg patient): First minute uptake 100 ml
• Closed System-Adjustments
- Total flow: Adjust N2O and O2 in proportion to keep volume of bag or bellows constant
- FIO2 : Adjust ratio of N2O and O2 to maintain desired FIO2 keeping total flow constant
- Depth of anesthesia: Adjust vaporizer setting to maintain desired depth or inspired
concentration
CO2 Absorption
a) Granules
• Small enough to have large surface area but large enough to avoid “channeling”
• Typically 4-8 mesh
b) Composition
• Sodalime: NaOH, Ca(OH)2
• Baralyme: KOH, Ca(OH)2, Ba(OH)2
- More likely to react with anesthetics to form CO (desflurane) or compound A (sevoflurane)
c) Moisture
• Necessary for CO2 absorption
• Reduces likelihood of anesthetic breakdown
d) Absorption Chemistry
• CO2 + H2O-->H2CO3
• H2CO3 + 2 NaOH-->Na2CO3+2H2O + heat
• Na2CO3 + Ca(OH)2 -->CaCO3 +2NaOH
• When the NaOH is gone, acidification causes indicator (ethyl violet) to turn “violet”
e) Zone of maximum absorption feels warm to touch (may be “hot” if malignant hyperthermia)

Pressure Transducer Systems
a) Accuracy with which transducer system reproduces actual intravascular pressure depends on
• Resonant frequency (higher is better)
• Degree of damping (most important if resonant frequency similar to 1/rise-time of waveform)
b) Zeroing Pressure Transducers
• Height of patient relative to transducer must remain constant after zeroing
• At time of zeroing
- Transducer may be at any height relative to patient (need not be at heart level)
- System should be “opened to air” by a stopcock at heart level before zeroing is performed
c) Site of Arterial Pressure Measurement
• Wave reflection causes systolic pressure to be higher and diastolic pressure to be lower when there
is an acute change in vessel diameter (radial / dorsalis pedis)
• This does NOT affect the mean pressure
• Resistance to flow causes a (very slight) decrease in mean pressure as pressure measurement
progresses from aorta to more distal vessels
Non-Invasive Blood Pressure Measurement
a) Most “standard cuff” systems use oscillometry
• Pulsations in the cuff pressure monitored as cuff deflates
• Initial pulsations--just above systolic pressure
• Maximal pulsations--mean arterial pressure
• Diastolic pressure by mathematical algorithm
b) Continuous non-invasive monitoring
• Most systems require intermittent calibration with a cuff
Cardiac Output Measurement
a) Fick Principle
• Conservation of mass
• Q=VO2/[CaO2-CvO2]
• Required measurements
- VO2 (Oxygen uptake--difficult to measure during anesthesia)
- CvO2 (requires PA catheter)
• NICO
- Fick formula applied to CO2 elimination
- Partial rebreathing to estimate mixed venous CO2
- Requires constant ventilatory pattern (controlled ventilation only)
b) Esophageal Doppler Monitor
• Doppler: Change in frequency of sound / ultrasound / light waves when reflected from a moving
object (e.g., RBC)
•
- v=RBC velocity fd= Doppler shift fi=frequency of ultrasound
- θ=angle between ultrasound beam and direction of blood flow
• CO = HR x CSA x VTI
- CO=Cardiac Output CSA=Cross Sectional Area VTI=Velocity-Time Integral
c) Thermodilution
• Quantity of indicator = Volume x (TPATIENT-TINDICATOR)
• Sources of error
- Quantity of indicator is "dialed in" to the C.O. computer based on the intended volume and
temperature of injectate

- If volume injected is lower than intended, then will be too low and the Cardiac
Output reading will be falsely high
- If the temperature of the indicator is colder than intended (e.g. using iced rather than room
temperature saline) then will be too high, and the Cardiac Output reading will
be falsely low

Management of the Parturient With Cardiovascular Disease

Management of the Parturient With Cardiovascular Disease
Lisa M. Councilman, M.D. Temple, Texas

Introduction
The incidence of clinically significant cardiac disease in the pregnant population ranges from 0.1-4%,
unchanged in decades; however, the most frequently seen etiology is now congenital heart disease (70-80%)1 due in part to advances in surgical techniques for these patients and advances in medical therapy, allowing these women to survive into childbearing age.2 Ischemic heart disease is also seen more commonly today due to both the increasing number of women of advanced maternal age who are electing to undergo pregnancy and childbirth as well as advances in medical therapy for ischemic heart disease, allowing women with this condition to carry a pregnancy to term. While the incidence of cardiac disease in pregnant patients has remained relatively unchanged, the maternal mortality from cardiac disease has decreased from 6% in the 1930s to 0.5-2.7% today.1 The last decade has shown a decline in maternal mortality from congenital heart disease, and now acquired heart disease has risen to be the leading cardiac cause of maternal death, with myocardial infarction, aortic dissection, and cardiomyopathy as the main processes.3 Unfortunately, the  cardiovascular changes of pregnancy may place additional stress on patients with underlying cardiac disease, increasing the risk of peripartum morbidity and mortality when compared with the general population, with the actual risk depending on the underlying cardiac disease process.1,2 Taking the altered physiologic processes into account, women with congenital heart disease and those with a history of ischemic heart disease require special attention and a multidisciplinary cooperation for optimal outcome during vaginal delivery or
cesarean section. The decision to perform regional or general anesthesia will ultimately depend on a thorough
understanding of the cardiac condition and condition-specific hemodynamic goals.2

Practice Guidelines

Practice Guidelines for the Prevention, Detection, and Management of Respiratory Depression Associated with Neuraxial Opioid Administration

 Summary of Recommendations

I. Identification of Patients at Increased Risk of Respiratory Depression

* The anesthesiologist should conduct a focused history and physical examination before administering neuraxial opioids.

○ Particular attention should be directed toward signs, symptoms, or a history of sleep apnea, coexisting diseases or conditions (e.g., diabetes, obesity), current medications (including preoperative opioids), and adverse effects after opioid administration.

○ A physical examination should include, but is not limited to, baseline vital signs, airway, heart, lung, and cognitive function.

II. Prevention of Respiratory Depression after Neuraxial Opioid Administration

* Noninvasive positive-pressure ventilation

○ Patients with a history of sleep apnea treated with noninvasive positive airway pressure should be encouraged to bring their own equipment to the hospital.

* Drug selection

○ Single-injection neuraxial opioids may be safely used in place of parenteral opioids without altering the risk of respiratory depression or hypoxemia.

○ Single-injection neuraxial fentanyl or sufentanil may be safe alternatives to single-injection neuraxial morphine.

○ When clinically suitable, extended-release epidural morphine may be used in place of intravenous or conventional (i.e., immediate-release) epidural morphine, although extended monitoring may be required.

○ Continuous epidural opioids are preferred to parenteral opioids for anesthesia and analgesia for reducing the risk of respiratory depression.

○ When clinically suitable, appropriate doses of continuous epidural infusion of fentanyl or sufentanil may be used in place of continuous infusion of morphine or hydromorphone without increasing the risk of respiratory depression.

○ Given the unique pharmacokinetic effect of the various neuraxially administered opioids, appropriate duration of monitoring should be matched with the drug.

○ Neuraxial morphine or hydromorphone should not be given to outpatient surgical patients.

* Dose selection

○ The lowest efficacious dose of neuraxial opioids should be administered to minimize the risk of respiratory depression.

○ Parenteral opioids or hypnotics should be cautiously administered in the presence of neuraxial opioids.

○ The concomitant administration of neuraxial opioids and parenteral opioids, sedatives, hypnotics, or magnesium requires increased monitoring (e.g., intensity, duration, or additional methods of monitoring).

III. Detection of Respiratory Depression

* All patients receiving neuraxial opioids should be monitored for adequacy of ventilation (e.g., respiratory rate, depth of respiration [assessed without disturbing a sleeping patient]), oxygenation (e.g., pulse oximetry when appropriate), and level of consciousness.##

* Single-injection neuraxial lipophilic opioids (e.g., fentanyl)

○ Monitoring should be performed for a minimum of 2 h after administration.

○ Continual (i.e., repeated regularly and frequently in steady rapid succession***) monitoring should be performed for the first 20 min after administration, followed by monitoring at least once per hour until 2 h has passed.

○ After 2 h, frequency of monitoring should be dictated by the patient’s overall clinical condition and concurrent medications.

* Continuous infusion or patient-controlled epidural analgesia (PCEA) with neuraxial lipophilic opioids

○ Monitoring should be performed during the entire time the infusion is in use.

○ Monitoring should be continual for the first 20 min after initiation, followed by monitoring at least once per hour until 12 h has passed.

○ From 12 to 24 h, monitoring should be performed at least once every 2 h.

○ After 24 h, monitoring should be performed at least once every 4 h.

○ After discontinuation of continuous infusion or PCEA with neuraxial lipophilic opioids, frequency of monitoring should be dictated by the patient’s overall clinical condition and concurrent medications.

* Single-injection neuraxial hydrophilic opioids (e.g., morphine, not including sustained- or extended-release epidural morphine)

○ Monitoring should be performed for a minimum of 24 h after administration.

○ Monitoring should be performed at least once per hour for the first 12 h after administration, followed by monitoring at least once every 2 h for the next 12 h (i.e., from 12 to 24 h).

○ After 24 h, frequency of monitoring should be dictated by the patient’s overall clinical condition and concurrent medications.

* Continuous infusion or PCEA with neuraxial hydrophilic opioids

○ Monitoring should be performed during the entire time the infusion is in use.

○ Monitoring at least once every hour should be performed for the first 12 h after initiation, followed by monitoring at least once every 2 h for the next 12 h.

○ After 24 h, monitoring should be performed at least once every 4 h.

○ After discontinuation of continuous infusion or PCEA, frequency of monitoring should be dictated by the patient’s overall clinical condition and concurrent medications.

* Sustained- or extended-release epidural morphine

○ Monitoring at least once every hour should be performed during the first 12 h after administration, and at least once every 2 h for the next 12 h (i.e., from 12 to 24 h).

○ After 24 h, monitoring should be performed at least once every 4 h for a minimum of 48 h.

* Increased monitoring (e.g., intensity, duration, or additional methods of monitoring) may be warranted in patients at increased risk of respiratory depression (e.g., unstable medical condition, obesity, obstructive sleep apnea,††† concomitant administration of opioid analgesics or hypnotics by other routes, extremes of age).

IV. Management and Treatment

* Supplemental oxygen

○ For patients receiving neuraxial opioids, supplemental oxygen should be available.

○ Supplemental oxygen should be administered to patients with altered level of consciousness, respiratory depression, or hypoxemia and continued until the patient is alert and no respiratory depression or hypoxemia is present.

○ Routine use of supplemental oxygen may increase the duration of apneic episodes and may hinder detection of atelectasis, transient apnea, and hypoventilation.

* Reversal agents

○ Intravenous access should be maintained if recurring respiratory depression occurs.

○ Reversal agents should be available for administration to all patients experiencing significant respiratory depression after neuraxial opioid administration.

○ In the presence of severe respiratory depression, appropriate resuscitation should be initiated.

* Noninvasive positive-pressure ventilation

○ Noninvasive positive-pressure ventilation may be considered for improving ventilatory status.

○ If frequent or severe airway obstruction or hypoxemia occurs during postoperative monitoring, noninvasive positive-pressure ventilation should be initiated.

source: Anesthesiology:February 2009 - Volume 110 - Issue 2 - pp 218-230

February 2009 - Volume 110 - Issue 2 - pp 218-230

PRACTICAL GUIDELINES FOR MECHANICAL VENTILATION

PRACTICAL GUIDELINES FOR MECHANICAL VENTILATION
IN DIFFERENT CLINICAL SETTINGS
Regardless of the specific issues associated with each of the following settings, the following general principles should be followed when mechanically ventilating acutely-ill patients:
•Maintain peak alveolar pressure (end-inspiratory plateau pressure) ≤ 30 cm H2O
•Look for and avoid the development of dynamic hyperinflation and auto-PEEP
•Use the lowest FIO2 necessary to maintain acceptable arterial PO2
Short-Term Ventilatory Support in Pts with Normal Underlying Lung Function
In this category are post-operative patients, patients requiring heavy sedation for procedures or to control muscular activity, and patients with acute ventilatory failure following accidental or intentional drug overdose. Almost any approach to mechanical ventilation is acceptable in this setting since no acute or chronic lung disease is present.
•AMV or SIMV (PCV requires more monitoring and ventilator adjustment)
•Tidal volume 10-12 mL/kg (note: the "lung protective" strategy does not apply
here; the use of lower tidal volumes may lead to atelectasis)
•Initial rate 10-15 breaths/min, adjusted to maintain arterial PCO2 35-45 mm Hg
•Peak inspiratory flow 60-80 L/min
•PEEP 5 cm H2O (optional)
•FIO2 = 0.30-0.50 (as required to maintain arterial PO2 > 70 mm Hg)
Intracranial Hypertension in Closed Head Injury
These patients generally have normal lungs, so that the above guidelines apply but with the following exceptions:
•No PEEP (may raise intracranial pressure) unless needed for hypoxemia
•If PEEP necessary, head of bed raised to counteract increased hydrostatic
pressure, and use as little PEEP as possible
•Insure appropriate sedation during suctioning to prevent patients from coughing
violently or fighting the ventilator
•Avoid "routine" chest physical therapy, especially in head-down position
•Optional: Hyperventilate to reduce acutely increased intracranial pressure: rate
>15 breaths/min in order to keep arterial PCO2 30-35 mm Hg [controversial;
usually used only short-term until other measures can be employed]
Acute Respiratory Failure in Obstructive Lung Disease (especially COPD)
This is the ideal setting for noninvasive positive-pressure ventilation (NPPV), and whenever possible this should be tried prior to intubation unless the patient has a complicating process like pneumonia or is too obtunded or agitated to cooperate.
Dynamic hyperinflation and auto-PEEP are common and may produce life-threatening cardiac compromise, especially on initial intubation or when patients become agitated. Rapid cycling rates and large tidal volumes (>10 mL/kg) should be avoided.
Work of breathing is already acutely increased in these patients, and is generally the reason mechanical ventilation has become necessary. Thus, the ventilator should be adjusted to maximize their comfort and minimize imposed (external) work of breathing.
A major goal should be to avoid alkalemia: arterial PCO2 should be lowered only enough to correct acutely life-threatening acidosis, and generally not to "normal" in these patients. Shoot for an arterial pH in the 7.30-7.35 range.
•Either assist-control or SIMV; pressure support also effective but harder to avoid
over-ventilation and keep tidal volume down
•Tidal volume 5-8 mL/kg
•Initial rate 6-8 breaths/min
•Pressure support 5 cm H2O (to minimize work of breathing during
spontaneous breaths if SIMV used)
•Peak inspiratory flow 70-90 L/min (note: this is higher than traditionally used)
•PEEP adjusted to about 80 percent of measured auto-PEEP level
•FIO2 sufficient to maintain arterial PO2 ≥ 60 mm Hg (avoiding hyperoxic ventilatory
depression is not an issue once the patient is intubated)
•Sedation as necessary to insure that patient rests during first 24 hours
Most COPD patients can be weaned and extubated within 48-72 hours, which should be the goal unless they have pneumonia or other serious complicating problem. Alkalemia, over-sedation, and iatrogenic auto-PEEP are the commonest reasons for failure.
Acute Neuromuscular Disease
Patients with spinal cord injury and other neurologic problems typically require larger tidal volumes than normal to provide the sensation of full inspiration. As such patients usually have normal lungs, tidal volumes larger than in other settings do not pose a significant threat of barotrauma. Neuromuscular patients also usually prefer a rapid inspiratory flow. Repeated adjustments of tidal volume, inspiratory flow, mode, and other settings may be necessary to achieve optimal comfort in these patients, who are typically fully awake.
•Assist-control or SIMV (with sufficient mandatory rate to prevent hypercapnia)
•Tidal volume 10-12 mL/kg (sometimes 15-18 mL/kg or more for optimum comfort)
•Initial rate 8-12 breaths/min; avoid acidosis
•Peak inspiratory flow adjusted to patient comfort; may require > 80 L/min
•PEEP 5 cm H2O (optional)
•FIO2 sufficient to keep arterial PO2 ≥ 80 mm Hg. Even mild hypoxemia is often
distressing to neuromuscular patients.
•Sedation as needed to avoid severe alkalosis
Acute Lung Injury
Current definitions and criteria for diagnosis:
•Acute clinical illness
•Bilateral diffuse infiltrates on chest X-ray
•Absence of left atrial hypertension (e.g. wedge pressure <18 mm Hg if
available; otherwise no clinical evidence of heart failure as explanation)
•Appropriate risk factor or clinical setting; no other apparent explanation
When the above conditions are met, the patient has either acute lung injury (ALI) or the acute respiratory distress syndrome (ARDS), depending on the severity of oxygenation impairment:
ALI: PaO2/FIO2 < 300 mm Hg ARDS: PaO2/FIO2 < 200 mm Hg
Of all the clinical scenarios requiring ventilatory support, this one is most challenging to the clinician. In severe acute lung injury it can be expected that normal gas exchange cannot be achieved, and new targets for both PO2 and PCO2 must be set. In addition, because of the extent of the injury, small tidal volumes are necessary in order to prevent local pulmonary overdistension and to maintain peak alveolar pressures below the "damage threshold" of 30 cm H2O.
•Assist-control (AMV) or SIMV (or PCV)*
•Tidal volume 6 mL/kg or less per ARDS Net protocol
•Rate 20-35 breaths/min, limited by development of auto-PEEP
•Peak inspiratory flow 60-80 L/min, higher if auto-PEEP develops
•PEEP: adjusted according to ARDS Net PEEP-FIO2 ladder; at least 8-10 cm H2O
initially; most patients need 15 cm ± 5 cm H2O
•Consider other means of augmenting tissue oxygen delivery (e.g. RBC
transfusion; dobutamine) if the above measures do not produce PO2
> 50-55 mm Hg
•Sedate patient to prevent fighting the ventilator and/or increased respiratory
rates over those set (to minimize auto-PEEP); the great majority of patients
do not need to be paralyzed, however
•FIO2: as low as possible to maintain arterial PO2 ≥ 50 mm Hg. The PaO2 target
should be 55-70 (SpO2 85-92%), not higher, to minimize FIO2 and PEEP;
use of ARDS Net PEEP-FIO2 ladder is strongly recommended.
•Permissive hypercapnia: allow arterial PCO2 to increase into the 60-90 mm Hg
range if necessary to achieve the target tidal volume and pressures.
Bicarbonate infusion is optional when pH falls below 7.25-7.30 but is
unnecessary unless patient has acute intracranial pathology or severe
cardiac dysfunction.
Care must be taken when decreasing PEEP once patients improve, as premature reduction worsen atelectasis and require a return to even higher levels of PEEP. Titrating PEEP according to the ARDS Net PEEP-FIO2 ladder is strongly recommended.
*Pressure control (PCV) is an acceptable alternative here (although not proven to be better), but tidal volume is harder to keep in the “lung-protective” range, and its use requires closer monitoring, more frequent ventilator adjustments, and a trained team familiar with its problems and idiosyncrasies.

A doctor is to give a speech at the local AMA dinner. He jots down notes for his speech. Unfortunately, when he stands in front of his colleagues later that night, he finds that he can't read his notes. So he asks, "Is there a pharmacist in the house?" A miracle drug is one that has now the same price as last year. Lady says to pharmacist: "Why does my prescription medication have 40 side effects?" Pharmacist replies: "Cause that's all we've documented so far." A man went to see his doctor because he was suffering from a miserable cold. His doctor prescribed some pills, but they didn't help. On his next visit the doctor gave him a shot, but that didn't do any good. On his third visit the doctor told the man, "Go home and take a hot bath. As soon as you finish bathing throw open all the windows and stand in the draft." "But doc," protested the patient, "if I do that, I'll get pneumonia." "I know," said the doctor, "I can cure pneumonia." A guy walks into work, and both of his ears are all bandaged up. The boss says, "What happened to your ears?" He says, "Yesterday I was ironing a shirt when the phone rang and shhh! I accidentally answered the iron." The boss says, "Well, that explains one ear, but what happened to your other ear?" He says, "Well, jeez, I had to call the doctor!" If it is dry - add moist; if it is moisten - add dryness. Congratulations, now you are a dermatologist. Patient to the eye doctor: "Whenever I drink coffee, I have this sharp, excruciating pain." "Try to remember to remove the spoon from the cup before drinking." A man goes to the eye doctor. The receptionist asks him why he is there. The man complains, "I keep seeing spots in front of my eyes." The receptionist asks, "Have you ever seen a doctor?" and the man replies, "No, just spots."

           

Ancient Egyptian Medicine

Ancient Egyptian MedicineAncient masters of human anatomy and healing
The Ancient Egyptians were advanced medical practitioners for their time. They were masters of human anatomy and healing mostly due to the extensive mummification ceremonies. This involved removing most of the internal organs including the brain, lungs, pancreas, liver, spleen, heart and intestine. The Egyptians had a basic knowledge of organ functions within the human body (save for the brain and heart which they thought had opposite functions).
The practices of Egyptian medical practitioners ranged from embalming to faith healing to surgery and autopsy. Among the curatives used by the Egyptians were all types of plant (herbs and other plants), animal (all parts nearly) and mineral compounds. The use of these compounds led to an extensive compendium of curative recipes, some still available today. For example, yeast was recognized for its healing qualities and was applied to leg ulcers and swellings. Yeast's were also taken internally for digestive disorders and were an effective cure for ulcers.
Though the Egyptians were effective healers, they did not have a clear knowledge of cellular biology or of germ theory, so it would be inappropriate to attribute the use of Yeast's as an antibiotic; as the curative effects behind the use of antibiotics were not known until well into modern times.

Neonatal Anesthesia

Ain Shams Journal of Anesthesiology                                         Vol 4-1; Jan 2011

Neonatal Anesthesia 
Hany M. El-Zahaby, MD
Department of Anesthesia, Intensive Care and Pain Management, Faculty of
Medicine, Ain Shams University, Cairo, Egypt.
Safe and effective neonatal anesthesia is one of the most challenging tasks presented to anesthesiologists. Knowledge of  the neonate's unique features, great manual skills and continuous practice are required for the
anesthesiologist to perform such task.
Neonatal Physiology Related to Anesthesia
Nociceptive System and Stress Response
The central nervous system is incompletely developed at birth. However, studies in preterm and term
neonates reported a fully competent neuroendocrine stress reaction in response to surgical stimulation.
Neonatal pain is capable of producing a "pain memory" as a result of plasticity changes within the central
nervous system or a psychological process.
 This confirms that a nonanalgesic technique practice is no longer acceptable.  The potential incompletely developed autoregulation of cerebral blood flow together with fragile infant's cerebral blood vessels
are important factors in the development of intraventricular hemorrhage.
 The spinal cord extends to a lower segment of the spine in neonates than in older children and adults. The volume of cerebrospinal fluid and the spinal surface area are proportionally larger in neonates, whereas the amount of myelination is less than in older children and adults.
These factors explain the increased amount of local anesthetics (mg/kg) required for a successful spinal
anesthetic in infants.   Hyperoxia has been associated with retinopathy of prematurity (ROP).
 However, ROP has been reported in full-term infants, in preterm infants never exposed to greater than ambient oxygen, may affect retina of one eye only, and even in infants with congenital cyanotic heart disease who has low oxygen tension in their blood.

fiberoptic intubation

Abdominal compartment syndrome

williams airway

The Airway Intubator is cylindrical on the proximal half and open on the distal half of the lingual surface.

The Airway Intubator is indicated for use as:

• An oropharyngeal airway
• A means of intubating the trachea
• A guide for fiber optic laryngoscope placement

For adult females (Williams Airway 9cm), recommended for use up to 7.5mm I.D. Endotracheal Tubes

For adult males (Williams Airway 10cm), recommended for use up to 8.5mm I.D. Endotracheal Tubes

Non obstetric surgery during pregnancy

Non obstetric surgery during pregnancy is relatively common.

The most common indications for surgery during pregnancy are either pregnancy related or pregnancy non related. Pregnancy related surgery include interventions for cervical incompetence and surgery for ovarian cyst problems.

The most common non pregnancy related indications are acute abdominal problems( most commonly appendicitis and cholecystitis), maternal trauma and surgery for malignancies.

Anaesthetists who care for pregnant patients undergoing non-obstetric surgery must provide safeanaesthesia for both the mother and the foetus.  To maintain maternal  safety the physiological and anatomical changes of pregnancy must be considered and anaesthetic techniques and drug administration modified accordingly.  Foetal wellbeing is related to avoidance of foetal asphyxia, teratogenic drugs and preterm labour.

Physiological Changes during Pregnancy

Central Nervous System Effects

The minimal alveolar concentration (MAC) progressively decreases during pregnancy—at term, by as much as 40%—for all general anesthetic agents; MAC returns to normal by the third day after delivery. Changes in maternal hormonal and endogenous opioid levels have been implicated. Progesterone, which is sedating when given in pharmacological doses, increases up to 20 times normal at term and is probably at least partly responsible for this observation. A surge in -endorphin levels during labor and delivery also likely plays a major role

At term, pregnant patients also display enhanced sensitivity to local anesthetics during regional anesthesia; dose requirements may be reduced as much as 30%. This phenomenon appears to be hormonally mediated but may also be related to engorgement of the epidural venous plexus.

Obstruction of the inferior vena cava by the enlarging uterus distends the epidural venous plexus and increases epidural blood volume. The latter has three major effects: (1) decreased spinal cerebrospinal fluid volume, (2) decreased potential volume of the epidural space, and (3) increased epidural (space) pressure. The first two effects enhance the cephalad spread of local anesthetic solutions during spinal and epidural anesthesia, respectively, whereas the last may predispose to a higher incidence of dural puncture with epidural anesthesia

Neurosurgery in children

Neurosurgery in children

Intracranial Physiology and Pathophysiology

There are a number of anatomic differences between children and adults that affect central nervous system physiology, especially intracranial pressure (ICP).

 At birth, the dura mater is covered by the calvaria, which consist of ossified plates connected by fibrous sutures and open fontanelles. The fontanelles close by approximately 10 to18 months of age but do not fully ossify until the teenage years. Thus, the infant skull is more compliant and may slowly expand in response to increasing ICP. These same structures offer a great deal of resistance to acute elevations in ICP. Infants and young children may not exhibit clinical signs of intracranial hypertension until the process is significantly advanced and the cranium can no longer accommodate a further increase in ICP.

 By the time an infant demonstrates the classic clinical signs of elevated ICP such as bradycardia, hypertension, papilledema, and pupillary changes, the disease process is likely very advanced. In contrast to adults, infants and young children may present with vague signs and symptoms such as increased head circumference, expanding sutures, bulging fontanelles, “sundowning” of eyes, lethargy, poor feeding, irritability, and possibly lower motor deficit.

 After ossification of the fontanelles, for a time, children may be more vulnerable to brain injury from increased ICP because of a relatively higher brain tissue to blood and cerebrospinal fluid intracranial volume than in the adult.

The limits of autoregulation are also different in infants and children. In adults, normal ICP ranges between 8 and 15 mmHg, whereas in infants, it may be as low as 2 to 4 mmHg. The cerebral autoregulation limit is shifted to a significantly lower value of mean arterial blood pressure (20 to 60 mmHg). The “margin of safety” may be narrower because infants are less able to compensate for the changes in blood pressure. Global cerebral blood flow (CBF, measured as ml/min/100 g of brain tissue) in children is greater than in adults, but in infants and premature babies, it is lower. The lower limit of CBF needed to sustain neuronal integrity is unknown in these patients. In infants with pathologic conditions resulting in a shift of the intracranial compliance curve to the right, cerebrospinal fluid production alone may be a significant contributor of increased ICP. Infants are at risk for ischemia when mean arterial pressure is low, whereas systemic hypertension may result in intraventricular hemorrhage; therefore, large fluctuations in systemic blood pressure may be deleterious. The response to hyperventilation may, also, be exaggerated and ischemia may ensue with very low PCO2 levels (less than 20 mmHg).

Twin-to-twin transfusion syndrome (TTTS)

Ain Shams Journal of Anesthesiology                                         Vol 4-1; Jan 2011
99
Twin-to-twin transfusion syndrome (TTTS)
 
Mohammed Abdel-Galil Sallam MD
Department of Anesthesiology, Intensive Care, and Pain Management, Faculty of
Medicine, Ain-Shams University, Cairo, Egypt
TTTS only occurs in monozygotic
(identical) twins with a monochorionic
placenta. It is the result of an
intrauterine blood transfusion from one
twin (donor) to another twin
(recipient). The donor twin is often
smaller with a birth weight 20% less
than the recipient’s birth weight. The
donor twin is often anemic and the
recipient twin is often plethoric with
hemoglobin differences greater than 5
gm/dL. The blood transfusion from the
donor twin to the recipient twin occurs
through placental vascular anastomoses.
The most common vascular anastomosis
is a deep, artery-to-vein anastomosis
through a shared placental cotyledon.
The clinical feature es of TTTS are
the result of hypoperfusion of the donor
twin and hyperperfusion of the recipient
twin.

Some Games on Anaesthetist.com

Some Games on Anaesthetist.com

Asthma Cardiac Arrest

Asthma Cardiac Arrest

In the early 1990’s at  the Alfred Hospital in Melbourne a young man was admitted in extremis with severe asthma. He had had many previous admissions some requiring ICU. He was intubated and ventilated, and given salbutamol and adrenaline.

However he went into asystole and was given all resuscitation measures but a rhythm could not be established. His pupils became dilated and fixed and further resuscitation was considered futile.

He was disconnected from the self-inflating bag and most of the staff left the room. After a few minutes a nurse noted that the patient had developed sinus rhythm. Staff were recalled and ventilation was recommenced.

However shortly afterwards he became pulseless  and again went into asystole. After some time resuscitation was again declared unsuccessful. Following disconnection from the breathing system the patient again developed a rhythm and pulses. Each subsequent time he was ventilated the same thing happened.

The staff realized that IPPV was causing the problem. Gentle ventilation with a slow respiratory rate was continued. The patient subsequently made a full recovery. This cases was written up in the journal “Anaesthesia and Intensive Care” in 1991 Vol 19 pp 118-121. Similar cases have since been published.

The problem here was gas trapping leading to high intrathoracic pressure which prevented venous return to the heart and resulted in cardiac arrest.

It is now appreciated that care must be taken with ventilation in asthma to allow ample time for expiration. A low respiratory rate of perhaps 6 breaths per minute should be combined with a long I:E ratio (say 1:6) to prevent gas trapping. Some level of “permissive” hypoxia and hypercarbia  is now considered to lead to better outcomes in ventilated asthmatic patients in preference to gas trapping.

There is not much point having oxygen in the lungs if there is no cardiac output to deliver it to vital organs.

Take Home Message:

Avoid high intra-thoracic pressures and gas trapping in ventilated patients with asthma.

This also applies to shocked patients where blood is returning to the thorax at very low pressure.

 source: http://www.anaesthesiacases.com.au/cases/asthma_cardiac_arrest

Anaesthesia Points to Remember

Beware of conus injuries from needling the spinal cord during spinal anaesthesia. It can lead to lifelong disability and pain. Once you insert your spinal needle more than one space above a line joining the iliac crests then the risks start to escalate.

Maintain adequate levels of blood pressure during anaesthesia. Hypotension  under anaesthesia  continues to be associated with increased morbidity and mortality. Patient age and co-morbidities should influence the minimum acceptable blood pressure. 

The recommended dose of morphine for an IV PCA  should not be greater than 1 mg with a 5 minute lockout, except in opiate dependent patients.

There is no point giving a test dose of antibiotic IV unless you perform minute dilutions into one litre of crystalloid and run it into the patient slowly.

Blood needs to be carefully checked to ensure the correct patient is receiving the correct blood. Errors continue to occur. Mismatched blood transfusion carries a high mortality rate.

When injecting significant amounts of LA it is recommended to have patients awake and communicative to reduce the likelihood of LA toxicity

Aspiration prior to injection does not rule out being intravascular (the side of the vessel wall can be sucked against the bevel of the needle).

Slow injection of LA is essential while maintaining communication with the patient: “Tell me if you are experiencing anything unusual”.

Longer acting LA’s such as bupivacaine  and ropivacaine have a higher incidence of LA toxicity than shorter acting ones such as lignocaine or prilocaine.

LA toxicity with mortality and major morbidity continues to occur.

Laryngeal tumours can create major airway difficulties for anaesthesia with airway obstruction and bleeding

Patients with laryngeal tumours ideally should have an MRI prior to anaesthesia.

Beware of gas trapping with IPPV in patients with respiratory conditions such as asthma and cystic fibrosis. This can lead to cardiovascular collapse. Such patients require reduced respiratory rates and longer I:E ratios to allow sufficient time for gas to be exhaled.

In patients with gastric outlet obstruction be prepared for regurgitation of large volumes of gastric fluid or blood.

Naloxone can precipitate massive sympathetic response with pulmonary oedema. Giving divided doses may diminish this effect.

Take care not to have malleable stylets protruding out the end of ETTs as they can also cause tracheal damage.

Jet ventilation must be used with considerable caution as surgical emphysema and pneumothoraces have been frequently reported. Care must be taken to ensure the upper airway is not obstructed. Gas needs to be able to get out as well as get in.

TIVA continues to be associated with awareness under anaesthesia.

Gas insufflation at laparoscopy can cause asystole or profound bradycardia. Careful monitoring is required. Treatment may require allowing the gas to escape rapidly.

Negative pressure pulmonary oedema may occur following emergence from anaesthesia in younger patients. CPAP or IPPV will usually be required.

Syringe swap continues to cause problems. Take extra care with muscle relaxants and vasopressors.

If your patient is hypotensive consider anaphylaxis, particularly if you have given muscle relaxants or antibiotics. There are many case reports of patients receiving  significant doses of metaraminol and ephedrine prior to anaesthetists starting definitive treatment of anaphylaxis with adrenaline.

source: http://www.anaesthesiacases.com.au/opinion/topics/anaesthesia_points_to_remember