Sangram Patil
Cardiac output
§ Definition
§ Determinants
§ Ideal device
§ Gold standard- thermo dilution technique of PAC.
Clinical assessment
§ Low organ perfusion
§ CNS
§ Metabolic acidosis
§ R/S
§ GUT
§ CVS
§ CRT
Techniques
§ Fick partial rebreathing method
§ Dye dilution
§ Thermo dilution
§ Arterial pulse contour analysis
§ Combined Li dilution APCA
§ Thoracic impedance
§ Doppler ultrasound technique
Dye dilution
§ Diagram
§ Graph
§ CO= Computer analysis of AUC for concentration-time curve.
§ Indocyanine green
§ Lithium dilution technique.
Thermo dilution
§ Most widely used.
§ Technique
§ Recent advance- Continuous CO measurement.
§ Status
Arterial waveform analysis
§ Pulse contour analysis- PiCCO (aortic).
§ Arterial cannulation- pulse contour analysis.
§ CVP line- transcardiopulmonary thermo dilution CO measurement for calibration.
§ Beat to beat calculation of CO from AUC.
§ Problems-abnormal waveforms, arrhythmias.
Combined Li dilution-APCA
§ Li dilution-calibration.
§ APCA-Beat to beat CO calculation.
§ LiDCO
§ PulseCO
§ SVR, SV, CO.
Fick Partial rebreathing method
§ Fick principle + CO2 elimination--NICO
§ CO2 elimination = V CO2/ CaCO2 - CvCO2
§ V CO2, CaCO2, CvCO2
§ Technique
§ ETT+IPPV, Rebreathing valve cycles through 2 phases- baseline (non RB), second phase (rebreathing), CO2 / flow sensor, ratio of change in CO2 elimination- calculated as CO.
Thoracic electrical bio-impedance
§ Flow from ventricle to aorta changes the electrical impedance.
§ Xiphoid electrode, neck electrode.
§ Not good correlation with thermo dilution.
§ Problems- age, fluid shifts, pulmonary oedema, myocardial ischemia, electrical interference.
Doppler ultrasound
§ Velocity of BF in descending aorta
§ Frequency of reflected US is changed depending on flow velocity in aorta.
§ V= 2.F0 / (C). (Fd). (Cosine incident angle).
§ > 20 degree angle- underestimates V.
§ Sites- suprasternal, trachea, Oesophagus
§ Oesophageal- Doppler transducer, M mode transducer, SV, 70% CO, ETT.
TOE
§ Sophisticated endoscopic probe.
§ Doppler ultrasound technique.
§ CO, V function, Wall motion abnormality, anatomy, valve function.
§ Doppler- velocity across valve. AUC for flow- velocity curve gives VIT ( velocity time integral)
§ 2DECHO- valve cross sectional area, CSA.
§ SV =VTI . CSA
§ CO= SV. HR
Advantages
Wednesday, May 31, 2006
Wednesday, May 24, 2006
Non-obstetric surgery during pregnancy
Anaesthesia for non-obstetric surgery during pregnancy
Dr.Sathish Krishnan
YG
Introduction
1-2% of pregnant women undergo anaesthesia during their pregnancy for surgery unrelated to delivery
M.C – Appendicitis,ovarian cyst,trauma.
Physiological and pharmacological changes important.
Goals
Maintain normal maternal physiological function
Maintain uteroplacental flow and O2 delivery.
Avoid unwanted drug effects on the fetus
Avoid oxytocic effects
Avoid awareness during G.A
Use regional when possible
Preanaesthetic assessment
Liase with obst & neonatalogist
U.S –if delivery is imminent
Symptoms of cardiac disease & ECG changes are common in pregnancy.
Radiology- minimise fetal exposure.
Relevant blood tests
Premeds-always include aspiration prophylaxis
Avoid NSAIDS.
Drugs
Teratogenic effects- 15th -56 days of gestation
Studies- no increase in teratogenecity but increase in abortion, growth restriction and LBW
Problems were due to primary disease and surgery and not due to anaesthesia
Benzodiazepines not teratogenic & single dose is safe.
GESTATION
No elective surgery during pregnancy
Only tubal ligation in first 6 weeks after delivery
Emergency surgery-regardless of gestational age
Preserve the life of mother
If possible-surgery delayed until 2nd trimester- reduced abortion & teratogenecity - but no firm evidence.
Nonviable fetus
Same principles as for pregnant patient
Coagulopathy risk- should be corrected
Anaesthesia for conception & 1st trimester
IV sedation for invitro fertilisation, should not interfere with fertilisation & embryo development
Propofol – sedation, regional or G.A.N20 avoided
6-8 weeks-physiological changes occur , supplementary O2, hyperventilation.
Airway management- may be difficult. Nasal airways avoided
Reduced pseudocholinesterase (30%), balanced by increase in Vd.
Aspiration prophylaxis from beginning of 2nd trimester
Lower anaes.requirements.reduced MAC (30%) ,IV drugs in lower doses
Fetus assessed by U.S before & after surgery
Regional whenever possible
2nd Trimester
Aortocaval compression from 20 weeks (may be before)
Lateral displacement of uterus
Risk of intravascular injection
Reduce dose of LA
Hypercoagulable state-prophylaxis
3rd Trimester
C.section before major surgery
Surgery delayed for 48 hrs to allow steroid therapy for fetal lung maturation
Regional for section and then converted to GA if needed
Volatile agents in small doses- to prevent uterine atony
Lactation may be supressed, contraindications for breast feeding are patients on ergot, lithium etc
Fetal monitoring
After 24-26 weeks, FH should be monitored
Difficult in obese or abdominal surgery
Inhalation agents cause decrease in FHR variability
Plan of action if fetal distress diagnosed
Minimal uterine manipulation
No evidence to use prophylactic tocolytics
Anaesthetic technique
No evidence to show that regional is better than GA in terms of outcome
Regional minimises fetal drug exposure, airway management is simpler, blood loss reduced & overall risk is less to both mother & fetus
Risk of regional is hypotension- reduce uterine blood flow
Recent studies show that it is more important to treat the blood pressure than to worry about agent
GA only by well trained anaesthetist
Laparoscopic surgeries
Pregnancy is no longer a contraindication for LAP surgeries
Study in Sweden- 2 million deliveries- favoured lap surgeries than open surgeries
Why? Less exposure of fetus to toxic agents, small incisions, less pain, less analgesic needed, rapid recovery & mobilisation.
C02 pneumoperitoneum - risk of hypoxemia, hypercarbia & hypotension.
THANK YOU
Dr.Sathish Krishnan
YG
Introduction
1-2% of pregnant women undergo anaesthesia during their pregnancy for surgery unrelated to delivery
M.C – Appendicitis,ovarian cyst,trauma.
Physiological and pharmacological changes important.
Goals
Maintain normal maternal physiological function
Maintain uteroplacental flow and O2 delivery.
Avoid unwanted drug effects on the fetus
Avoid oxytocic effects
Avoid awareness during G.A
Use regional when possible
Preanaesthetic assessment
Liase with obst & neonatalogist
U.S –if delivery is imminent
Symptoms of cardiac disease & ECG changes are common in pregnancy.
Radiology- minimise fetal exposure.
Relevant blood tests
Premeds-always include aspiration prophylaxis
Avoid NSAIDS.
Drugs
Teratogenic effects- 15th -56 days of gestation
Studies- no increase in teratogenecity but increase in abortion, growth restriction and LBW
Problems were due to primary disease and surgery and not due to anaesthesia
Benzodiazepines not teratogenic & single dose is safe.
GESTATION
No elective surgery during pregnancy
Only tubal ligation in first 6 weeks after delivery
Emergency surgery-regardless of gestational age
Preserve the life of mother
If possible-surgery delayed until 2nd trimester- reduced abortion & teratogenecity - but no firm evidence.
Nonviable fetus
Same principles as for pregnant patient
Coagulopathy risk- should be corrected
Anaesthesia for conception & 1st trimester
IV sedation for invitro fertilisation, should not interfere with fertilisation & embryo development
Propofol – sedation, regional or G.A.N20 avoided
6-8 weeks-physiological changes occur , supplementary O2, hyperventilation.
Airway management- may be difficult. Nasal airways avoided
Reduced pseudocholinesterase (30%), balanced by increase in Vd.
Aspiration prophylaxis from beginning of 2nd trimester
Lower anaes.requirements.reduced MAC (30%) ,IV drugs in lower doses
Fetus assessed by U.S before & after surgery
Regional whenever possible
2nd Trimester
Aortocaval compression from 20 weeks (may be before)
Lateral displacement of uterus
Risk of intravascular injection
Reduce dose of LA
Hypercoagulable state-prophylaxis
3rd Trimester
C.section before major surgery
Surgery delayed for 48 hrs to allow steroid therapy for fetal lung maturation
Regional for section and then converted to GA if needed
Volatile agents in small doses- to prevent uterine atony
Lactation may be supressed, contraindications for breast feeding are patients on ergot, lithium etc
Fetal monitoring
After 24-26 weeks, FH should be monitored
Difficult in obese or abdominal surgery
Inhalation agents cause decrease in FHR variability
Plan of action if fetal distress diagnosed
Minimal uterine manipulation
No evidence to use prophylactic tocolytics
Anaesthetic technique
No evidence to show that regional is better than GA in terms of outcome
Regional minimises fetal drug exposure, airway management is simpler, blood loss reduced & overall risk is less to both mother & fetus
Risk of regional is hypotension- reduce uterine blood flow
Recent studies show that it is more important to treat the blood pressure than to worry about agent
GA only by well trained anaesthetist
Laparoscopic surgeries
Pregnancy is no longer a contraindication for LAP surgeries
Study in Sweden- 2 million deliveries- favoured lap surgeries than open surgeries
Why? Less exposure of fetus to toxic agents, small incisions, less pain, less analgesic needed, rapid recovery & mobilisation.
C02 pneumoperitoneum - risk of hypoxemia, hypercarbia & hypotension.
THANK YOU
medicine teacher
Hi friends,
Thank you for your interest in this website.
Most of the time our academic work goes unnoticed. Even we tend to forget about it after some time, though it is there with us in floppy or flash disc. Most of our academic material is for presentation or teaching a small or large group of audience.
Once the presentation is done nothing usually happens to the prepared material unless we are very enthusiastic to submit the same for publication in journals or books.How about publishing these presentations in the form of website? This will keep our hard work alive for ever.
Another aspect is we can have access to this material anywhere and anytime.On website, this material is open to the whole world. Sharing our knowledge and hard work with others on such a broad scale is excellent idea, isn’t it?
I would encourage you to contribute to this website by sending me your presentations or any other academic material. It might be your lecture, personal notes or audit work, or case presentation. You can send me without disclosing patient identity or department identification.
I wont be publishing any diagrams or photographs on this website, so no problem with copy rights.
Do let me know your suggestions and forward me as much material as you can.
Thank you again.
Dr S Patil
SpR Anaesthetics
All Wales rotation
UK
sangram@doctors.org.uk
Thank you for your interest in this website.
Most of the time our academic work goes unnoticed. Even we tend to forget about it after some time, though it is there with us in floppy or flash disc. Most of our academic material is for presentation or teaching a small or large group of audience.
Once the presentation is done nothing usually happens to the prepared material unless we are very enthusiastic to submit the same for publication in journals or books.How about publishing these presentations in the form of website? This will keep our hard work alive for ever.
Another aspect is we can have access to this material anywhere and anytime.On website, this material is open to the whole world. Sharing our knowledge and hard work with others on such a broad scale is excellent idea, isn’t it?
I would encourage you to contribute to this website by sending me your presentations or any other academic material. It might be your lecture, personal notes or audit work, or case presentation. You can send me without disclosing patient identity or department identification.
I wont be publishing any diagrams or photographs on this website, so no problem with copy rights.
Do let me know your suggestions and forward me as much material as you can.
Thank you again.
Dr S Patil
SpR Anaesthetics
All Wales rotation
UK
sangram@doctors.org.uk
Thursday, May 18, 2006
Neurocritical Care
Neurosurgery & neurocitical care
www.medicineteacher.blogspot.com
Unresolved issues
•IV versus inhalational
•Nitrous oxide
•Opioids
•Sitting Position
•Hypothermia
•Hyperventilation
•Hypotension
•Triple H therapy
•Colloid versus crystalloid
•HS, mannitol, steroids
•Non-anaesthetic drugs
IV versus inhalational
•Sevoflurane
•Propofol
•Etomidate
•Thiopental
•Research studies- failed to show any difference
Nitrous oxide
•Opponents
•Proponents
•Research studies- no specific study.
•Avoid in- air in ventricles, risk of embolism, pneumocephalus, reduced IC compliance & need of high FiO2
Opioids
•Morphine
•Fentanyl
•Sufentanyl
•Remifentanyl
Sitting position
•Risk of VAE
•Benefits
•Studies- relatively low incidence of complications reported
•Careful patient selection, expert anaesthetic team, intra-operative monitoring
Mild hypothermia
•Mild hypothermia, 2-3 degree Celsius
•Moderate to severe hypothermia
•Research studies- conflicting results
•NABIS- no benefits
•IHAST- no benefits
•Head injury with raised ICT- clear benefit
•Immediate management of cardiac arrest- helpful
Hyperventilation
•Logic behind this
•Studies- Cochrane library report
•PaCO2 >4.0 kPa
•Routine hyperventilation avoided except as a rescue measure for herniation of brain
Induced hypotension
•Induced hypotension for global cerebral effect- not used now
•In past brief periods of controlled hypotension for surgical dissections and aneurysm clippings
•Temporary clipping of major feeding vessel
•Research- Controversy over which is better
•Clip might cause ischaemia as well plus interference with surgical field.
Triple H therapy
•Hypervolaemia
•Hypertension
•Haemodilution
•Controversies- when, what fluids, how much BP, for how long
•Oxygen carrying capacity
Crystalloid versus colloid
•Volume required
•Response time
•Duration of effect
•Interference with clotting, allergy
•CPP
•ICT
HS Mannitol Steroids
•HS
•Mannitol
•Steroids
•Research evidence
Non-anaesthetic drugs
•Nimodipine
•Mg
•Remacemide
Summary
•Nitrous oxide use is controversial
•Limited indications for hypothermia
•No routine hyperventilation
•Strict BM control
•Nimodipine, remacemide might be helpful
•Modern trend is minimally invasive surgery, awake procedures (functional neurosurgery)
•Modern technology like TCD ultrasound, JB oximetry, NIRS, laser Doppler flowmeter
www.medicalaudits.blogspot.com
www.medicineteacher.blogspot.com
Unresolved issues
•IV versus inhalational
•Nitrous oxide
•Opioids
•Sitting Position
•Hypothermia
•Hyperventilation
•Hypotension
•Triple H therapy
•Colloid versus crystalloid
•HS, mannitol, steroids
•Non-anaesthetic drugs
IV versus inhalational
•Sevoflurane
•Propofol
•Etomidate
•Thiopental
•Research studies- failed to show any difference
Nitrous oxide
•Opponents
•Proponents
•Research studies- no specific study.
•Avoid in- air in ventricles, risk of embolism, pneumocephalus, reduced IC compliance & need of high FiO2
Opioids
•Morphine
•Fentanyl
•Sufentanyl
•Remifentanyl
Sitting position
•Risk of VAE
•Benefits
•Studies- relatively low incidence of complications reported
•Careful patient selection, expert anaesthetic team, intra-operative monitoring
Mild hypothermia
•Mild hypothermia, 2-3 degree Celsius
•Moderate to severe hypothermia
•Research studies- conflicting results
•NABIS- no benefits
•IHAST- no benefits
•Head injury with raised ICT- clear benefit
•Immediate management of cardiac arrest- helpful
Hyperventilation
•Logic behind this
•Studies- Cochrane library report
•PaCO2 >4.0 kPa
•Routine hyperventilation avoided except as a rescue measure for herniation of brain
Induced hypotension
•Induced hypotension for global cerebral effect- not used now
•In past brief periods of controlled hypotension for surgical dissections and aneurysm clippings
•Temporary clipping of major feeding vessel
•Research- Controversy over which is better
•Clip might cause ischaemia as well plus interference with surgical field.
Triple H therapy
•Hypervolaemia
•Hypertension
•Haemodilution
•Controversies- when, what fluids, how much BP, for how long
•Oxygen carrying capacity
Crystalloid versus colloid
•Volume required
•Response time
•Duration of effect
•Interference with clotting, allergy
•CPP
•ICT
HS Mannitol Steroids
•HS
•Mannitol
•Steroids
•Research evidence
Non-anaesthetic drugs
•Nimodipine
•Mg
•Remacemide
Summary
•Nitrous oxide use is controversial
•Limited indications for hypothermia
•No routine hyperventilation
•Strict BM control
•Nimodipine, remacemide might be helpful
•Modern trend is minimally invasive surgery, awake procedures (functional neurosurgery)
•Modern technology like TCD ultrasound, JB oximetry, NIRS, laser Doppler flowmeter
www.medicalaudits.blogspot.com
Friday, May 12, 2006
Post cord transection
Sangram Patil
Spinal cord anatomy
Physiology
Blood supply-
Single ASA, 2 small PSAs
Essentially no collateral supply between the two
Segmental vessels, large distance between them- watershed area between upper thoracic and lumbar region. Artery of Adamkiewicz (T8-L3).
Regulation of SC blood flow
SC perfusion pressure
Auto regulation- abolished by trauma
Pathophysiology of acute cord injury (ASCI)
Primary injury
Original impact and compression of SC.
No treatment
Secondary injury
Ischemia triggered by primary injury, and other mechanisms.
Systemic effects of ASCI
CVS, R/S, GIT, GUT, Temperature, CNS, Skin.
CNS- Central/ Anterior/Posterior/ Hemi section/ complete transection
Chronic cord injury/ transection
Spinal Shock
Autonomic dysreflexia
Other CVS changes
Blood Volume
Abnormal Valsalva response- no plateau, no overshoot.
Orthostatic hypotension- gradual adaptation d/t autoreg.
Increased renin-angiotensin response- salt-water retention.
Continued..
Respiratory system
C1/2, C3/4, lower cervical- intercostal.
Reduced VC- might recover to some extent;
Increased WOB, reduced ERV/FVC (better in head up position).
Abdominal muscle paralysis- cough, atelectasis, V/Q mismatch.
Muscles
Increased Ach receptors, K changes with suxamethonium.
Spasticity- due to intact spinal reflex arc below the level of lesion.
Bones
Reduced density below the level.
Temperature- perception, regulation.
Continued..
Skin-
decubitus ulcers, common reason for operations in them.
Blood-
Anaemia, DVT.
GUT-
emptying, shock-reflex phase (detrusor-sphinctor dyssynergia), predisposed to Renal Failure.
GIT- emptying delayed
Chronic Pain- 60% of them.
Anaesthetic implications:
Pre-anaesthetic checklist
Anaesthesia
Standby anaesthesia
Risk of AD- cervical injury, history of AD, urological procedures.
Spasm- proprioceptive/ cutaneous stimuli cause spasm of muscles.
Patient wish- IV sedation is a choice.
Previous procedures done as standby anaesthesia.
General anaesthesia
Premedication
Sedatives, nifedipine 10 mg S/L.
Monitoring- routine, CVP/PAC.
Drugs-reduced circulating BV, small VOD for anaesthetics, more sensitive to IV agents, reduced ability to tolerate CVS effects, reduced renal clearance.
Propofol is well established now, ketamine- spasm, NDMR single dose usually sufficient.
Sux- avoid 3days to 9months.
Induction- large vein, preload, RSI not routine.
Maintenance- IPPV, risk of more drop in CO with IPPV.
Positioning- pressure points
Fluids- preload, meticulous attention to balance.
Anticholinergics at induction for low HR.
Temperature
Autonomic dysreflexia- Halothane, enflurane/ isoflurane equally well. Increase the depth under GA.
Spasm- increase depth, relaxants rarely.
Penile erections- metaraminaol, increase depth.
Recovery- temperature, respiration. AD may occur in recovery.
Pregnancy- Increased changes of SCI, reduced CVS/RS reserve when there is increased demand
Regional anaesthesia..
Reliable prevention of AD with spinal.
Difficult to decide level of block
Dose-response relationship is not well established.
Epidural not very satisfactory blockade.
Procedures usually needing anaesthesia
Spine fixation
Intrathecal baclofen infusion apparatus
Ant sacral root stimulators, phrenic nerve pacing.
Urological procedures
Limbs, ulcers.
Other procedures.
Spinal cord anatomy
Physiology
Blood supply-
Single ASA, 2 small PSAs
Essentially no collateral supply between the two
Segmental vessels, large distance between them- watershed area between upper thoracic and lumbar region. Artery of Adamkiewicz (T8-L3).
Regulation of SC blood flow
SC perfusion pressure
Auto regulation- abolished by trauma
Pathophysiology of acute cord injury (ASCI)
Primary injury
Original impact and compression of SC.
No treatment
Secondary injury
Ischemia triggered by primary injury, and other mechanisms.
Systemic effects of ASCI
CVS, R/S, GIT, GUT, Temperature, CNS, Skin.
CNS- Central/ Anterior/Posterior/ Hemi section/ complete transection
Chronic cord injury/ transection
Spinal Shock
Autonomic dysreflexia
Other CVS changes
Blood Volume
Abnormal Valsalva response- no plateau, no overshoot.
Orthostatic hypotension- gradual adaptation d/t autoreg.
Increased renin-angiotensin response- salt-water retention.
Continued..
Respiratory system
C1/2, C3/4, lower cervical- intercostal.
Reduced VC- might recover to some extent;
Increased WOB, reduced ERV/FVC (better in head up position).
Abdominal muscle paralysis- cough, atelectasis, V/Q mismatch.
Muscles
Increased Ach receptors, K changes with suxamethonium.
Spasticity- due to intact spinal reflex arc below the level of lesion.
Bones
Reduced density below the level.
Temperature- perception, regulation.
Continued..
Skin-
decubitus ulcers, common reason for operations in them.
Blood-
Anaemia, DVT.
GUT-
emptying, shock-reflex phase (detrusor-sphinctor dyssynergia), predisposed to Renal Failure.
GIT- emptying delayed
Chronic Pain- 60% of them.
Anaesthetic implications:
Pre-anaesthetic checklist
Anaesthesia
Standby anaesthesia
Risk of AD- cervical injury, history of AD, urological procedures.
Spasm- proprioceptive/ cutaneous stimuli cause spasm of muscles.
Patient wish- IV sedation is a choice.
Previous procedures done as standby anaesthesia.
General anaesthesia
Premedication
Sedatives, nifedipine 10 mg S/L.
Monitoring- routine, CVP/PAC.
Drugs-reduced circulating BV, small VOD for anaesthetics, more sensitive to IV agents, reduced ability to tolerate CVS effects, reduced renal clearance.
Propofol is well established now, ketamine- spasm, NDMR single dose usually sufficient.
Sux- avoid 3days to 9months.
Induction- large vein, preload, RSI not routine.
Maintenance- IPPV, risk of more drop in CO with IPPV.
Positioning- pressure points
Fluids- preload, meticulous attention to balance.
Anticholinergics at induction for low HR.
Temperature
Autonomic dysreflexia- Halothane, enflurane/ isoflurane equally well. Increase the depth under GA.
Spasm- increase depth, relaxants rarely.
Penile erections- metaraminaol, increase depth.
Recovery- temperature, respiration. AD may occur in recovery.
Pregnancy- Increased changes of SCI, reduced CVS/RS reserve when there is increased demand
Regional anaesthesia..
Reliable prevention of AD with spinal.
Difficult to decide level of block
Dose-response relationship is not well established.
Epidural not very satisfactory blockade.
Procedures usually needing anaesthesia
Spine fixation
Intrathecal baclofen infusion apparatus
Ant sacral root stimulators, phrenic nerve pacing.
Urological procedures
Limbs, ulcers.
Other procedures.
Nutrition
Owen McIntyre
DEFINITIONS
•Basal metabolic rate
•Amount of energy liberated by catabolism of food per unit time under standardized conditions, ie relaxed, room temp, 12-14 hours post-prandial
•Corrected for age, sex and surface area
•Normal adult male= 197 Kj/m2/hr; 40Kcal/m2/hr
DEFINITIONS
•Calorie
•1 calorie=energy reqired to heat 1gram of water by 1o C
•1 Cal=1Kcal
1 kg of water by 1o C
•1 kcal= 4.18 kjoules
•Joule
•SI unit of energy
•1 joule=energy expended in moving a resistive force of 1 newton a distance of 1 metre
DEFINITIONS
•Nitrogen Balance
•1 gram of nitrogen=6.2 grams of protein
=30 grams of muscle
•Normal losses=0.15-0.2g/kg/day
•ITU losses can be> 0.5g/kg/day
•Mainly in urinary urea
•Approx 4g/day in skin/hair/faeces
•Also: proteinuria, GIT fistula
•Measured by 24 hour urea collection with corrections for other losses
DEFINITIONS
•Malnutrition
•Multiple nutrient deficiencies
•Common in hospital patients
•Impaired healing
•Reduced immune system function
•Reduced muscle mass/poor mobility and weaning
•Anaemia
•Electrolyte disturbances
•Starvation
•Carbs- hepatic and muscle glycogen = 24-48 hrs
•Protein- from skeletal muscle = 10-12 days
•Fat- from adipose tissue = 20-25 days
DEFINITIONS
•Catabolism
•Form of accelerated starvation with glycogenolysis, lipolysis and proteolysis/gluconeogenisis
•Malnutrition is a predisposing factor
•Assoc with severe illness, sepsis, burns, trauma and stress response to surgery
Common mechanism: catabolic hormones
insulin resistance
increased metabolic rate
increased oxygen demand
NORMAL DAILY REQUIREMENTS
•Energy: 30- 40 kcal/kg
carbs= 50% (4kcal/g)
lipids= 35% (9kcal/g)
protein= 15% (4kcal/g)
•Water: 30- 40 ml/kg
1000ml of water for 1000kcal expended
•Nitrogen: 0.2 g/kg=1.5 g/kg
•Fat: 2 g/kg
•Glucose: 2 g/kg
NORMAL DAILY REQUIREMENTS
•Na+ 1mmol/kg
•K+ 1
•Cl- 1.5
•Mg+ 0.1-0.2
•Ca+ 0.1-0.2
•Phos 0.2-0.5
NUTRITIONAL ASSESSMENT
•Careful history and exam
•Objective tests
•Subjective global assessment
•Experimental
•All difficult in ITU setting
•Nutritional Risk Screening
•Impaired nutritional status
•Severity of disease
QUESTIONS?
•What routes are available for nutritional support?
•List the pros and cons for each route
•List the contraindications for each
•List the complications of each
ENTERAL FEEDS
•Polymeric
•Normal gut function
•Nitrogen source is protein
•Energy from triglycerides and glucose polymers
•Elemental
•GI failure,pancreatic insufficiency, often NJ
•Nitrogen from amino acids or oligopeptides
•Energy from short glucose polymers, no lipid
•Specialist, Disease specific
PARENTERAL FEEDS
•Nitrogen from L-amino acids
•Energy from glucose-50% lipid emulsion-50%
•Electrolytes
•Trace elements and minerals
•Bespoke
MONITORING
•Fluid balance, calorie intake, ?weight
•Urea and electrolytes, phosphate
•Blood glucose
•FBC
•LFTs, Ca and Mg
•Plasma triglycerides
FINAL POINTS
•Glutamine
•Significantly reduce mortality and ITU stay?
•Prevents gut atrophy, direct fuel for enterocytes and lymphoid tissue
•Conditionally essential in critical illness
•Re-feeding Syndrome
•Previously malnourished
•Low K+, Mg+, Phosphate
DEFINITIONS
•Basal metabolic rate
•Amount of energy liberated by catabolism of food per unit time under standardized conditions, ie relaxed, room temp, 12-14 hours post-prandial
•Corrected for age, sex and surface area
•Normal adult male= 197 Kj/m2/hr; 40Kcal/m2/hr
DEFINITIONS
•Calorie
•1 calorie=energy reqired to heat 1gram of water by 1o C
•1 Cal=1Kcal
1 kg of water by 1o C
•1 kcal= 4.18 kjoules
•Joule
•SI unit of energy
•1 joule=energy expended in moving a resistive force of 1 newton a distance of 1 metre
DEFINITIONS
•Nitrogen Balance
•1 gram of nitrogen=6.2 grams of protein
=30 grams of muscle
•Normal losses=0.15-0.2g/kg/day
•ITU losses can be> 0.5g/kg/day
•Mainly in urinary urea
•Approx 4g/day in skin/hair/faeces
•Also: proteinuria, GIT fistula
•Measured by 24 hour urea collection with corrections for other losses
DEFINITIONS
•Malnutrition
•Multiple nutrient deficiencies
•Common in hospital patients
•Impaired healing
•Reduced immune system function
•Reduced muscle mass/poor mobility and weaning
•Anaemia
•Electrolyte disturbances
•Starvation
•Carbs- hepatic and muscle glycogen = 24-48 hrs
•Protein- from skeletal muscle = 10-12 days
•Fat- from adipose tissue = 20-25 days
DEFINITIONS
•Catabolism
•Form of accelerated starvation with glycogenolysis, lipolysis and proteolysis/gluconeogenisis
•Malnutrition is a predisposing factor
•Assoc with severe illness, sepsis, burns, trauma and stress response to surgery
Common mechanism: catabolic hormones
insulin resistance
increased metabolic rate
increased oxygen demand
NORMAL DAILY REQUIREMENTS
•Energy: 30- 40 kcal/kg
carbs= 50% (4kcal/g)
lipids= 35% (9kcal/g)
protein= 15% (4kcal/g)
•Water: 30- 40 ml/kg
1000ml of water for 1000kcal expended
•Nitrogen: 0.2 g/kg=1.5 g/kg
•Fat: 2 g/kg
•Glucose: 2 g/kg
NORMAL DAILY REQUIREMENTS
•Na+ 1mmol/kg
•K+ 1
•Cl- 1.5
•Mg+ 0.1-0.2
•Ca+ 0.1-0.2
•Phos 0.2-0.5
NUTRITIONAL ASSESSMENT
•Careful history and exam
•Objective tests
•Subjective global assessment
•Experimental
•All difficult in ITU setting
•Nutritional Risk Screening
•Impaired nutritional status
•Severity of disease
QUESTIONS?
•What routes are available for nutritional support?
•List the pros and cons for each route
•List the contraindications for each
•List the complications of each
ENTERAL FEEDS
•Polymeric
•Normal gut function
•Nitrogen source is protein
•Energy from triglycerides and glucose polymers
•Elemental
•GI failure,pancreatic insufficiency, often NJ
•Nitrogen from amino acids or oligopeptides
•Energy from short glucose polymers, no lipid
•Specialist, Disease specific
PARENTERAL FEEDS
•Nitrogen from L-amino acids
•Energy from glucose-50% lipid emulsion-50%
•Electrolytes
•Trace elements and minerals
•Bespoke
MONITORING
•Fluid balance, calorie intake, ?weight
•Urea and electrolytes, phosphate
•Blood glucose
•FBC
•LFTs, Ca and Mg
•Plasma triglycerides
FINAL POINTS
•Glutamine
•Significantly reduce mortality and ITU stay?
•Prevents gut atrophy, direct fuel for enterocytes and lymphoid tissue
•Conditionally essential in critical illness
•Re-feeding Syndrome
•Previously malnourished
•Low K+, Mg+, Phosphate
Carbon Monoxide Poisoning
Andy Ketchin
History
•Mr MJ,
56 year old male.
•House fire mid morning. Patient unharmed.
•Found with GCS 4 in house 5pm same day.
•Evidence of aspiration. No evidence self harm.
Background
•PMHx No significant past.
•DHx No regular meds, or allergy.
•SHx Lives alone.
? Learning difficulties.
Unemployed.
Smoker, no alcohol.
On Examination
•A Soot Intubated
•B Reduced air entry right lower zone.
•C Hypotensive Normal ECG.
•D GCS 4 Normoglycaemic/thermic.
•E No burns/trauma.
Investigations
•U&E,CRP NAD
•FBC WCC 43, HB16.0
•ABG pH 7.26 pO2 7.9 pCO2 4.6 BE - 12.0
•Toxicology COHb 43.5% à 12.8%
•CXR Right lower zone diffuse opacity.
Problem List & Plan
CO Poisoning - Presentation
Mild – constitutional / viral symptoms.
Severe – seizures, syncope, coma myocardial ischaemia ventricular arrhythmias pulmonary oedema profound lactic acidosis
“Cherry red” insensitive
CO Poisoning - Pathophysiology
•Affinity COHb 240 : HbO2
•(Non smokers < color="#ff0000">DO = CO x CaO2
CaO2 = (k1 x Hb x SaO2) + (k2 x PaO2)
{k1 = 1.32, k2 = 0.23}
CO Poisoning - Management
Hyperbaric therapy:
•Reduced COHb t1/2
•PaO2 increased from 0.3 à 6.0 ml/dl.
Hyperbaric Therapy
Recommended:
•CO level > 40%
•CO level > 20% in pregnancy
•LOC
•Severe acidosis, pH <>
Considerations:
•Delay < 6 hr
•Logistics
•Concomitant cyanide poisoning
History
•Mr MJ,
56 year old male.
•House fire mid morning. Patient unharmed.
•Found with GCS 4 in house 5pm same day.
•Evidence of aspiration. No evidence self harm.
Background
•PMHx No significant past.
•DHx No regular meds, or allergy.
•SHx Lives alone.
? Learning difficulties.
Unemployed.
Smoker, no alcohol.
On Examination
•A Soot Intubated
•B Reduced air entry right lower zone.
•C Hypotensive Normal ECG.
•D GCS 4 Normoglycaemic/thermic.
•E No burns/trauma.
Investigations
•U&E,CRP NAD
•FBC WCC 43, HB16.0
•ABG pH 7.26 pO2 7.9 pCO2 4.6 BE - 12.0
•Toxicology COHb 43.5% à 12.8%
•CXR Right lower zone diffuse opacity.
Problem List & Plan
CO Poisoning - Presentation
Mild – constitutional / viral symptoms.
Severe – seizures, syncope, coma myocardial ischaemia ventricular arrhythmias pulmonary oedema profound lactic acidosis
“Cherry red” insensitive
CO Poisoning - Pathophysiology
•Affinity COHb 240 : HbO2
•(Non smokers < color="#ff0000">DO = CO x CaO2
CaO2 = (k1 x Hb x SaO2) + (k2 x PaO2)
{k1 = 1.32, k2 = 0.23}
CO Poisoning - Management
Hyperbaric therapy:
•Reduced COHb t1/2
•PaO2 increased from 0.3 à 6.0 ml/dl.
Hyperbaric Therapy
Recommended:
•CO level > 40%
•CO level > 20% in pregnancy
•LOC
•Severe acidosis, pH <>
Considerations:
•Delay < 6 hr
•Logistics
•Concomitant cyanide poisoning
Inhaled Anaesthetics
Jason Koerber
Definitions
Gas
A substance above its critical temperature.
Volatile
A substance in a gaseous state but below its critical temperature.
Definitions - Anaesthesia
“Anaesthesia” was first used by the Greek philosopher Dioscorides in the 1st century to describe the narcotic effect of the plant mandragora.
The word reappeared in the 1771 Encyclopaedia Britannica, where it was defined as “privation of the senses”.
After introduction of ether by Morton in 1846, Oliver Wendell Holmes coined the word to describe the new phenomenon that made surgical procedures possible.
Definitions - Anaesthesia 2
We measure the response to stimulation.
Does the patient move when their name is called?
Does the response to incision suggest conscious perception?
Does the heart of BP go up in response to surgical manipulation?
Does the patient remember events, conversations, or pain?
Regional or General?
Definitions - Anaesthesia 3
Anaesthetic agent: reversible.
General consists of the following components:UnconsciousnessAmnesiaAnalgesiaMuscle relaxation
Regional: blockade of pain transmission.
MAC
Measure of potency.
Minimum alveolar concentration at steady state that prevents reaction to a standard surgical stimulus (skin incision) in 50% of subjects at sea level.
Meyer-Overton hypothesis
Name the Anaesthetic Agent!
H H H H
H C C O C C H
H H H H
Diethyl ether
Ethanol and sulphuric acid.
Flammable/explosive.
High blood:gas and oil:gas coefficients.
10% metabolised to ethanol and aldehydes.
Nausea and vomiting.
Seizures can occur.
Increased salivation.
Increased gluconeogenesis
Name the Anaesthetic Agent!
F H F
H C O C C F
F Cl F
Isoflurane
Halogenated ethyl methyl ether.
Resp: dep, pungent, bronchodil.
CVS: dec SVR, tachy,
? coronary steal.
CNS: best balance of reduction cerebral consumption and minimal increase in cerebral blood flow.
Met: 0.2% (trifluroacetic acid, F-, CO)
Name the Anaesthetic Agent!
F F H
H C O C C F
F F Cl
Enflurane
Halogenated ethyl methyl ether.
Resp: most dep, non-irritant
CVS: dec SVR, tachy, heart not sensitized.
CNS: high conc in presence of hypocarbia produce 3Hz spike and wave pattern. Increase ICP.
Met: 2% (F-)
Name the Anaesthetic Agent!
Cl F
H C C F
Br F
Halothane
Halogenated hydrocarbonThymol 0.01% preservative.Dissolves into rubber.
Resp: dep, sweet, bronchodil.
CVS: dec SVR, brady, sensitizes to catecholamines.
CNS: increases cerebral blood flow more than other volatiles.
Met: 25% (trifluroacetic acid, Cl-, Br-, F-). Hepatitis?
Name the Anaesthetic Agent!
F H F
H C O C C F
F F F
Desflurane
Fluorinated ethyl methyl ether.Tec 6 vaporizer.
Resp: dep, pungent, coughing and breath holding.CVS: Similar to isoflurane but at conc above 1 MAC may produce stimulation.
CNS: increased cerebral blood flow
Met: 0.02% (Trifluroacetic acid)
Name the Anaesthetic Agent!
F CH3
H C O C H
H CH3
Sevofluorane
Polyfluorinated isopropyl methyl ether.Achiral - unlike other volatiles.
Resp: dep, pleasant odour bronchodilationCVS: dec SVR, HR unchanged, heart not sensitized.
CNS: increases cerebral blood flow. ? Post-op agitation in children
Met: 3.5% (F-), compound A
Name the Anaesthetic Agent!
H F Cl
H C O C C H
H F Cl
Methoxyflurane
Halogenated ethyl methyl ether.
BP 105 degrees.
Very soluble in blood.Blood:gas coefficient 13.MAC 0.2.
Fluoride ion caused renal failure.
Nitrous oxide (N2O)
lManufacture: heating ammonium nitrate to 250 degrees. May contain impurities NH3, N2, NO, NO2, HNO3. These are removed by scrubbers, water and caustic soda.
lBlue cylinders. Filling ratio.
lConcentration effect, second gas effect and diffusion hypoxia.
lResp: small fall in VT and increase in rate.
lCVS: mild direct cardiac depressant. Normally counterbalanced by central sympathetic stimulant effects.
lCNS: increases cerebral blood flow. Produces analgesia.
lToxicity.
Xeon
lInert, odourless gas.
lMakes up 0.0000087% of atmosphere.
lFastest onset.
lResp: increases VT and decreases rate.
lCVS: no effect on contractility but may cause small decrease in HR.
lCNS: increases cerebral blood flow. May be used to enhance CT images of brain.Produces analgesia.
lNot metabolised.
The bloody table!!
Definitions
Gas
A substance above its critical temperature.
Volatile
A substance in a gaseous state but below its critical temperature.
Definitions - Anaesthesia
“Anaesthesia” was first used by the Greek philosopher Dioscorides in the 1st century to describe the narcotic effect of the plant mandragora.
The word reappeared in the 1771 Encyclopaedia Britannica, where it was defined as “privation of the senses”.
After introduction of ether by Morton in 1846, Oliver Wendell Holmes coined the word to describe the new phenomenon that made surgical procedures possible.
Definitions - Anaesthesia 2
We measure the response to stimulation.
Does the patient move when their name is called?
Does the response to incision suggest conscious perception?
Does the heart of BP go up in response to surgical manipulation?
Does the patient remember events, conversations, or pain?
Regional or General?
Definitions - Anaesthesia 3
Anaesthetic agent: reversible.
General consists of the following components:UnconsciousnessAmnesiaAnalgesiaMuscle relaxation
Regional: blockade of pain transmission.
MAC
Measure of potency.
Minimum alveolar concentration at steady state that prevents reaction to a standard surgical stimulus (skin incision) in 50% of subjects at sea level.
Meyer-Overton hypothesis
Name the Anaesthetic Agent!
H H H H
H C C O C C H
H H H H
Diethyl ether
Ethanol and sulphuric acid.
Flammable/explosive.
High blood:gas and oil:gas coefficients.
10% metabolised to ethanol and aldehydes.
Nausea and vomiting.
Seizures can occur.
Increased salivation.
Increased gluconeogenesis
Name the Anaesthetic Agent!
F H F
H C O C C F
F Cl F
Isoflurane
Halogenated ethyl methyl ether.
Resp: dep, pungent, bronchodil.
CVS: dec SVR, tachy,
? coronary steal.
CNS: best balance of reduction cerebral consumption and minimal increase in cerebral blood flow.
Met: 0.2% (trifluroacetic acid, F-, CO)
Name the Anaesthetic Agent!
F F H
H C O C C F
F F Cl
Enflurane
Halogenated ethyl methyl ether.
Resp: most dep, non-irritant
CVS: dec SVR, tachy, heart not sensitized.
CNS: high conc in presence of hypocarbia produce 3Hz spike and wave pattern. Increase ICP.
Met: 2% (F-)
Name the Anaesthetic Agent!
Cl F
H C C F
Br F
Halothane
Halogenated hydrocarbonThymol 0.01% preservative.Dissolves into rubber.
Resp: dep, sweet, bronchodil.
CVS: dec SVR, brady, sensitizes to catecholamines.
CNS: increases cerebral blood flow more than other volatiles.
Met: 25% (trifluroacetic acid, Cl-, Br-, F-). Hepatitis?
Name the Anaesthetic Agent!
F H F
H C O C C F
F F F
Desflurane
Fluorinated ethyl methyl ether.Tec 6 vaporizer.
Resp: dep, pungent, coughing and breath holding.CVS: Similar to isoflurane but at conc above 1 MAC may produce stimulation.
CNS: increased cerebral blood flow
Met: 0.02% (Trifluroacetic acid)
Name the Anaesthetic Agent!
F CH3
H C O C H
H CH3
Sevofluorane
Polyfluorinated isopropyl methyl ether.Achiral - unlike other volatiles.
Resp: dep, pleasant odour bronchodilationCVS: dec SVR, HR unchanged, heart not sensitized.
CNS: increases cerebral blood flow. ? Post-op agitation in children
Met: 3.5% (F-), compound A
Name the Anaesthetic Agent!
H F Cl
H C O C C H
H F Cl
Methoxyflurane
Halogenated ethyl methyl ether.
BP 105 degrees.
Very soluble in blood.Blood:gas coefficient 13.MAC 0.2.
Fluoride ion caused renal failure.
Nitrous oxide (N2O)
lManufacture: heating ammonium nitrate to 250 degrees. May contain impurities NH3, N2, NO, NO2, HNO3. These are removed by scrubbers, water and caustic soda.
lBlue cylinders. Filling ratio.
lConcentration effect, second gas effect and diffusion hypoxia.
lResp: small fall in VT and increase in rate.
lCVS: mild direct cardiac depressant. Normally counterbalanced by central sympathetic stimulant effects.
lCNS: increases cerebral blood flow. Produces analgesia.
lToxicity.
Xeon
lInert, odourless gas.
lMakes up 0.0000087% of atmosphere.
lFastest onset.
lResp: increases VT and decreases rate.
lCVS: no effect on contractility but may cause small decrease in HR.
lCNS: increases cerebral blood flow. May be used to enhance CT images of brain.Produces analgesia.
lNot metabolised.
The bloody table!!
Obesity and anaesthesia
Obesity
BMI = mass (kg)/[height (m)]2
BMI>28 obese, BMI >35 morbidly obese
17% of UK population are obese
Associated with BP, IHD, NIDDM, peripheral vascular disease, gallstones, etc…
Pathophysiology
Obesity is associated with
Increase in absolute blood volume, but it’s low relative to body mass
Increase O2 consumption by metabolically active adipose tissue & work of supporting ms.
Reduced FRC in awake pt, and significantly decreased following induction
Rapid desaturation.
OSA
Obesity hypoventilation syndrome, causing loss of CO2 resp drive & hypoxia, polycythemia and pulmonary hypertension
Increase gastric volume, raised intra-abdominal pressure, and a higher incidence of hiatus hernia pose a significant risk of aspiration.
Insulin resistance may cause peri-operative diabetes.
Vd for drugs is altered due to a smaller proportion of TBW, greater proportion of adipose tissue,
Increase lean body mass, and
Increase blood volume and cardiac output.
Conduct of anaesthesia
Difficult intubation
IV access
Operating table
Thromboembolic events.
Premedication.
Ventilation
Positioning
Regional anaesthesia
Post op
Post op mortality is doubled
Mobilize as soon as possible
Pulmonary atalectasis is common
Early physiotherapy.
Nocturnal nasal CPAP
PCA more predictable than IM morphine
HDU care should be available
Obstructive Sleep Apnoea
At least 5% of morbidly obese patients will have OSA particularly if they have associated risk factors such as large collar size (over 16.5 inches), evening alcohol consumption and pharyngeal abnormalities.
The disease is cause by passive collapse of the pharyngeal airway during deeper planes of sleep, resulting in snoring and intermittent airway obstruction.
Resultant hypoxaemia and hypercapnia results in arousal and disruption of quality sleep thus causing the characteristic daytime somnolence.
Cont.
Pulmonary and systemic vasoconstriction, polycythaemia, right ventricular failure and cor pulmonale can all occur.
lIndeed the relative hypoventilation can cause a progressive desensitisation of the respiratory centres to hypercapnia with resultant Type II respiratory failure.
Formal diagnosis is by sleep studies and treatment includes removal of precipitants, weight loss and nocturnal CPAP.
BMI = mass (kg)/[height (m)]2
BMI>28 obese, BMI >35 morbidly obese
17% of UK population are obese
Associated with BP, IHD, NIDDM, peripheral vascular disease, gallstones, etc…
Pathophysiology
Obesity is associated with
Increase in absolute blood volume, but it’s low relative to body mass
Increase O2 consumption by metabolically active adipose tissue & work of supporting ms.
Reduced FRC in awake pt, and significantly decreased following induction
Rapid desaturation.
OSA
Obesity hypoventilation syndrome, causing loss of CO2 resp drive & hypoxia, polycythemia and pulmonary hypertension
Increase gastric volume, raised intra-abdominal pressure, and a higher incidence of hiatus hernia pose a significant risk of aspiration.
Insulin resistance may cause peri-operative diabetes.
Vd for drugs is altered due to a smaller proportion of TBW, greater proportion of adipose tissue,
Increase lean body mass, and
Increase blood volume and cardiac output.
Conduct of anaesthesia
Difficult intubation
IV access
Operating table
Thromboembolic events.
Premedication.
Ventilation
Positioning
Regional anaesthesia
Post op
Post op mortality is doubled
Mobilize as soon as possible
Pulmonary atalectasis is common
Early physiotherapy.
Nocturnal nasal CPAP
PCA more predictable than IM morphine
HDU care should be available
Obstructive Sleep Apnoea
At least 5% of morbidly obese patients will have OSA particularly if they have associated risk factors such as large collar size (over 16.5 inches), evening alcohol consumption and pharyngeal abnormalities.
The disease is cause by passive collapse of the pharyngeal airway during deeper planes of sleep, resulting in snoring and intermittent airway obstruction.
Resultant hypoxaemia and hypercapnia results in arousal and disruption of quality sleep thus causing the characteristic daytime somnolence.
Cont.
Pulmonary and systemic vasoconstriction, polycythaemia, right ventricular failure and cor pulmonale can all occur.
lIndeed the relative hypoventilation can cause a progressive desensitisation of the respiratory centres to hypercapnia with resultant Type II respiratory failure.
Formal diagnosis is by sleep studies and treatment includes removal of precipitants, weight loss and nocturnal CPAP.
LAMINAR FLOW
FLOW- the quantity of fluid i.e. gas or liquid passing a point in unit time.
F= Q/T
Where-
F- Mean flow
Q- Quantity (mass or volume)
T- Time.
LAMINAR FLOW
In Laminar flow-fluid moves in a smooth manner and there are no eddies or turbulence.
The flow is greatest at the centre, being about twice the mean flow.
As the side of the tube is approached the flow becomes slower, until it becomes zero at the wall.
In order to drive fluid thru the tube a pressure difference, must be present across the ends.
Laminar flow has got a CONICAL VELOCITY PROFILE.
HAGEN-POISEUILLE equation.
Laminar flow is not the only type of flow occurring in anaesthesia. App., breathing systems, airways and circulation.
Laminar flow may change to TURBULENT FLOW if a constriction is reached which results in the fluid velocity increasing.
Fluid no longer exists in smooth manner, but, swirls in eddies and the resistance is higher than for the same laminar flow.
Turbulent flow has a FLAT VELOCITY PROFILE.
Although bronchi and smaller air passages are smaller than the trachea, air flow thru them is slower so laminar flow is usual in the LOWER RESP. TRACT.
Laminar flow-VISCOSITY.
Turbulent flow-DENSITY.
ROTAMETER
Anaesthetists require a continuous of gas flows in the anaesthetic machine and this is provided by a VARIABLE ORIFICE FLOWMETER.
This is often referred to by the trade name ROTAMETER.
A BOBBIN is supp. In the middle of a glass or plastic tube which is tapered.
As the gas flow increases, the bobbin rises in the tube and the clearance round the bobbin increases.
In other words, there is a variable orifice around the bobbin which depends on the gas flow.
The pressure across the bobbin remains CONSTANT because it gives rise to a force which balances the force of gravity on the bobbin.
The increase in area of the annular orifice as the bobbin rises reduces the flow resistance at higher flows and so the pressure across the bobbin stays constant, despite the flow increase.
VENTURI PRINCIPLE
The entrainment of a fluid thru the side arm into an area of low pressure caused by a constriction in a tube is the basis of the venturi principle.
It is called the BERNOULLI EFFECT.
Some equipment may include a tube with a constriction in which the cross section gradually decreases and then increases –this is known as VENTURI.
This principle is employed in gas mixing devices, including fixed performance oxygen devices, suction equipment and scavenging equipment.
F= Q/T
Where-
F- Mean flow
Q- Quantity (mass or volume)
T- Time.
LAMINAR FLOW
In Laminar flow-fluid moves in a smooth manner and there are no eddies or turbulence.
The flow is greatest at the centre, being about twice the mean flow.
As the side of the tube is approached the flow becomes slower, until it becomes zero at the wall.
In order to drive fluid thru the tube a pressure difference, must be present across the ends.
Laminar flow has got a CONICAL VELOCITY PROFILE.
HAGEN-POISEUILLE equation.
Laminar flow is not the only type of flow occurring in anaesthesia. App., breathing systems, airways and circulation.
Laminar flow may change to TURBULENT FLOW if a constriction is reached which results in the fluid velocity increasing.
Fluid no longer exists in smooth manner, but, swirls in eddies and the resistance is higher than for the same laminar flow.
Turbulent flow has a FLAT VELOCITY PROFILE.
Although bronchi and smaller air passages are smaller than the trachea, air flow thru them is slower so laminar flow is usual in the LOWER RESP. TRACT.
Laminar flow-VISCOSITY.
Turbulent flow-DENSITY.
ROTAMETER
Anaesthetists require a continuous of gas flows in the anaesthetic machine and this is provided by a VARIABLE ORIFICE FLOWMETER.
This is often referred to by the trade name ROTAMETER.
A BOBBIN is supp. In the middle of a glass or plastic tube which is tapered.
As the gas flow increases, the bobbin rises in the tube and the clearance round the bobbin increases.
In other words, there is a variable orifice around the bobbin which depends on the gas flow.
The pressure across the bobbin remains CONSTANT because it gives rise to a force which balances the force of gravity on the bobbin.
The increase in area of the annular orifice as the bobbin rises reduces the flow resistance at higher flows and so the pressure across the bobbin stays constant, despite the flow increase.
VENTURI PRINCIPLE
The entrainment of a fluid thru the side arm into an area of low pressure caused by a constriction in a tube is the basis of the venturi principle.
It is called the BERNOULLI EFFECT.
Some equipment may include a tube with a constriction in which the cross section gradually decreases and then increases –this is known as VENTURI.
This principle is employed in gas mixing devices, including fixed performance oxygen devices, suction equipment and scavenging equipment.
PONV
Dr Owen McIntyre
Define PONV
•NAUSEA
•Sensation that precedes vomiting
•VOMITING
•Rapid expulsion of stomach contents through the mouth
•PONV
•Multifactorial
•Incidence in GA with volatile between 20-40%
(Anywhere between 10-90%)
•Early: within first 6 hours
•Late: within first 24 hours
Neural pathways mediating N+V?
•CTZ: medulla, floor of 4th ventricle, outside BBB
•Primary NT is Dopamine, D2 (+5HT3)
•Vestibular afferents
•Raised ICP via direct action
•Metabolic abnormalities; uraemia, hypernatraemia
• Drugs: opiates, volatiles, etomidate, neostigmine
sympathomimetics; ketamine, ephedrine
cytotoxics, cardiac glycosides, apomorphine
•Efferents to VC
Neural pathways mediating N+V?
•Vomiting Centre: medulla, same level as CTZ
inside BBB
•Primary NT is Acetylchloine, M3 (+H1, ?mu opioid)
•Cortical affferents, limbic, olfactory,visual
•Visceral afferents, gut and heart (X and symp)
•Occulovestibular afferents
•Efferent compose Vomiting reflex pathway
Neural pathways mediating N+V?
•Substance P
•Slow excitatory neurotransmitter
•Acting at Neurokinin-1 receptors
•Loads of NK-1 receptors at key sites in medulla
•Could be final common pathway
•Vofopitant
Describe the vomiting reflex
•Complex: central, peripheral and enteric NS
•Reflex is preceded by retrograde peristalsis
•Increased salivation
•Forceful inspiration, breath held mid-insp
•Raise hyoid and larynx; closes glottis and opens crico-oesophageal sphincter
•Elevation of soft palate closes nasopharynx
•Contraction of diaphragm, abdo muscles
•Opening of LOS and relaxation of oesophagus
What are the risk factors for PONV?
•Patient factors
•Female(2-4x)
•Past history of PONV(3x)
•History of motion sickness
•Non smoker
•Obesity
•Children
•Early ambulation
What are the risk factors for PONV?
•Anaesthetic factors
•Volatiles
•Opiates
•N2O
•Etomidate, Thiopentone
•Neostigmine
•Sympathomimetics
•Hypotension
•Hypoxia
•Bag-mask ventilation
How would you manage PONV?
•Assessment of risk
•Prevention
•Pre
•Peri
•Post-op
•Pharmacotherapy
•Multimodal, ‘Balanced anti-emetic therapy’
•Prophylaxis vs. treatment
•Others
•Acupuncture
Prevention
•Pre-operative
•Optimize fasting; clear fluid 2hours pre-op
•Pre-med; benzos, ?metoclopramide
•Peri-operative
•Regional anaesthesia
•Avoid volatiles and N2O in favour of Propofol TCI
•Avoid thio, etomidate, ketamine
•Avoid NMBAs and therefore neostigmine
•Avoid opioids if possible, alternate analgesia
•Generous fluid therapy
•Post-operative
•Adequate analgesia
Can you classify antiemetics?
•Mode of action or site of action
•Anti-dopaminergic(D2)
•Anti-histamines(H1)
•Anti-cholinergic(M3)
•Anti-serotinergic(5HT3)
•Others
•Corticosteroids
•Cannabinoids
•Propofol
What are the side effects of the anti-emetics you commonly use?
•Cyclizine
•Ondansetron
•Dexamethasone
•?Prochlorperazine
•?Others
Strategy for the management of PONV
•A Simplified Risk Score for Predicting Postoperative Nausea and Vomiting
–Apfel et al, Anesthesiology 1999 91:693-700
•4 patient risk factors were as accurate at predicting PONV as more complicated equations
Female
Past history of PONV or Motion Sickness
Non smoker
Post-op opiates
•No association with type or duration of surgery
Strategy for the management of PONV
•Number of Risk Factors Incidence of PONV
0 10%
1 21%
2 39%
3 61%
4 79%
•If 2+ present risk is high
•Modify anaesthetic technique
•?Prophylaxis
•Multimodal approach
Evidence for the management of PONV
•Too much information!!
•Cost effectiveness: Individual drugs
Prophylaxis vs Treatment
•Patient satisfaction
•NNT much better for high risk patients
•Single antiemetic: Ondansetron NNT 5-6
•Combination therapy significantly better than monotherapy with no increased SE (Ondan + dex /drop)
Evidence for the management of PONV
•Multimodal Approach
•Scuderi et al, Anaest Analg 2000; 91
•TIVA: Propofol and remifentanil
•No nitrous
•No NMBA
•Aggressive IV fluids(25ml/kg)
•3x prophylactic anti-emetics
•98% response rate
Define PONV
•NAUSEA
•Sensation that precedes vomiting
•VOMITING
•Rapid expulsion of stomach contents through the mouth
•PONV
•Multifactorial
•Incidence in GA with volatile between 20-40%
(Anywhere between 10-90%)
•Early: within first 6 hours
•Late: within first 24 hours
Neural pathways mediating N+V?
•CTZ: medulla, floor of 4th ventricle, outside BBB
•Primary NT is Dopamine, D2 (+5HT3)
•Vestibular afferents
•Raised ICP via direct action
•Metabolic abnormalities; uraemia, hypernatraemia
• Drugs: opiates, volatiles, etomidate, neostigmine
sympathomimetics; ketamine, ephedrine
cytotoxics, cardiac glycosides, apomorphine
•Efferents to VC
Neural pathways mediating N+V?
•Vomiting Centre: medulla, same level as CTZ
inside BBB
•Primary NT is Acetylchloine, M3 (+H1, ?mu opioid)
•Cortical affferents, limbic, olfactory,visual
•Visceral afferents, gut and heart (X and symp)
•Occulovestibular afferents
•Efferent compose Vomiting reflex pathway
Neural pathways mediating N+V?
•Substance P
•Slow excitatory neurotransmitter
•Acting at Neurokinin-1 receptors
•Loads of NK-1 receptors at key sites in medulla
•Could be final common pathway
•Vofopitant
Describe the vomiting reflex
•Complex: central, peripheral and enteric NS
•Reflex is preceded by retrograde peristalsis
•Increased salivation
•Forceful inspiration, breath held mid-insp
•Raise hyoid and larynx; closes glottis and opens crico-oesophageal sphincter
•Elevation of soft palate closes nasopharynx
•Contraction of diaphragm, abdo muscles
•Opening of LOS and relaxation of oesophagus
What are the risk factors for PONV?
•Patient factors
•Female(2-4x)
•Past history of PONV(3x)
•History of motion sickness
•Non smoker
•Obesity
•Children
•Early ambulation
What are the risk factors for PONV?
•Anaesthetic factors
•Volatiles
•Opiates
•N2O
•Etomidate, Thiopentone
•Neostigmine
•Sympathomimetics
•Hypotension
•Hypoxia
•Bag-mask ventilation
How would you manage PONV?
•Assessment of risk
•Prevention
•Pre
•Peri
•Post-op
•Pharmacotherapy
•Multimodal, ‘Balanced anti-emetic therapy’
•Prophylaxis vs. treatment
•Others
•Acupuncture
Prevention
•Pre-operative
•Optimize fasting; clear fluid 2hours pre-op
•Pre-med; benzos, ?metoclopramide
•Peri-operative
•Regional anaesthesia
•Avoid volatiles and N2O in favour of Propofol TCI
•Avoid thio, etomidate, ketamine
•Avoid NMBAs and therefore neostigmine
•Avoid opioids if possible, alternate analgesia
•Generous fluid therapy
•Post-operative
•Adequate analgesia
Can you classify antiemetics?
•Mode of action or site of action
•Anti-dopaminergic(D2)
•Anti-histamines(H1)
•Anti-cholinergic(M3)
•Anti-serotinergic(5HT3)
•Others
•Corticosteroids
•Cannabinoids
•Propofol
What are the side effects of the anti-emetics you commonly use?
•Cyclizine
•Ondansetron
•Dexamethasone
•?Prochlorperazine
•?Others
Strategy for the management of PONV
•A Simplified Risk Score for Predicting Postoperative Nausea and Vomiting
–Apfel et al, Anesthesiology 1999 91:693-700
•4 patient risk factors were as accurate at predicting PONV as more complicated equations
Female
Past history of PONV or Motion Sickness
Non smoker
Post-op opiates
•No association with type or duration of surgery
Strategy for the management of PONV
•Number of Risk Factors Incidence of PONV
0 10%
1 21%
2 39%
3 61%
4 79%
•If 2+ present risk is high
•Modify anaesthetic technique
•?Prophylaxis
•Multimodal approach
Evidence for the management of PONV
•Too much information!!
•Cost effectiveness: Individual drugs
Prophylaxis vs Treatment
•Patient satisfaction
•NNT much better for high risk patients
•Single antiemetic: Ondansetron NNT 5-6
•Combination therapy significantly better than monotherapy with no increased SE (Ondan + dex /drop)
Evidence for the management of PONV
•Multimodal Approach
•Scuderi et al, Anaest Analg 2000; 91
•TIVA: Propofol and remifentanil
•No nitrous
•No NMBA
•Aggressive IV fluids(25ml/kg)
•3x prophylactic anti-emetics
•98% response rate
Fluid Balance
Body Organization
Cells exist in “internal sea” of ECF
Composition – primordial oceans
ECF = Interstitial Fluid + Blood plasma
TBW = ECF + ICF
18% protein,7% mineral,15% fat
60% - WATER
Body Water
60% Total body weight
40% intracellular
20% extra cellular
Extracellular – 25% intravascular
- 75% interstitial
Body Water
70 kg normal adult
TBW = 42 l
ICF = 28 l
ECF = 14 l
Measurements – fluid vol.
Inject subs that stay in one comp.
Vd = amount injected/conc. of subs
Mix evenly through the comp.
No effect on the dist of H20
Must be unchanged
Easy to measure
Plasma Volume
Dyes bound to plasma proteins
Evans blue (t-1824)
Sr. Alb labeled with radioactive iodine
Average value = 3500ml(70kg adult)
Blood vol.
Hematocrit (Hct)- % of blood vol made up of cells
Total blood vol. = plasma volume x 100/100- Hct
Red cell volume = total blood vol.-plasma volume
ECF Volume
Difficult to measure
Limits of the space are ill defined
Transcellular fluids
Inulin
Mannitol and sucrose
20% of body weight
Interstitial fluid vol.
Cannot be measured directly
ECF VOL – Plasma vol.
ECF: ICF - infants & children>adults
ICF VOLUME
Cannot be measured directly
ICF = TBW – ECF
TBW – Deuterium oxide D2O
Tritium oxide and aminopyrine
Water content of lean body tissue – 71 to72 ml/100gm of tissue
Conc. Of Solutes - Units
Mole
Millimoles, micromoles
Molecular weight
Equivalents
Moles
Gram molecular weight of a substance
One mole = 6 x 1023 molecules
SI unit for amount of substance
Mol. Wt – ratio of mass of one molecule of a substance to the mass of 1/12 the mass of an atom of carbon-12
Dalton – unit of mass equal to 1/12 the mass of an atom of carbon-12
Equivalents
1 eq is 1 mol of an ionized substance divided by its valence.
Water
Small, highly diffusible, polar molecule
Solvent – hydrate proteins, sugars and other substances-
Dissolving properties
Thermal properties
Ionizes very slightly (pH 7.0)
Bulk Flow & Diffusion
Bulk flow –movement of the solution mass in the direction of hydrostatic pressure gradient
Diffusion – molecular movement down conc. Gradient
Disperse local accumulation of molecules if it is free to move
Osmotic Pressure
Fluid compartment – principal solute
Mainly restricted to that compartment
K+ ICF
Na+ ECF
Plasma proteins: intra vascular space
Osmotic pressure – total number of particles
Osmosis
Solution – stable mixture of solute & solvent
Solute– dispersed individual molecules
Solvent – liquid bulk
Solute mol. Occupy space
Water mol. Net movement by diffusion.
Osmosis
Water – diffuse from region of high solvent conc. to low conc.
The extent of tendency for solvent to move – measured by use of semi permeable membrane. -hydrostatic pressure to produce equal and opposite bulk flow
Sum of conc. of all solute particles
Oncotic Pressure
Plasma proteins – albumin, globulin
Large mol wt & size –unable to leave intravascular space
Pressure diff between plasma and interstitial fluids
Colloid osmotic pressure
Amounts to only 0.7 mosmol/kg water
Thank you
Cells exist in “internal sea” of ECF
Composition – primordial oceans
ECF = Interstitial Fluid + Blood plasma
TBW = ECF + ICF
18% protein,7% mineral,15% fat
60% - WATER
Body Water
60% Total body weight
40% intracellular
20% extra cellular
Extracellular – 25% intravascular
- 75% interstitial
Body Water
70 kg normal adult
TBW = 42 l
ICF = 28 l
ECF = 14 l
Measurements – fluid vol.
Inject subs that stay in one comp.
Vd = amount injected/conc. of subs
Mix evenly through the comp.
No effect on the dist of H20
Must be unchanged
Easy to measure
Plasma Volume
Dyes bound to plasma proteins
Evans blue (t-1824)
Sr. Alb labeled with radioactive iodine
Average value = 3500ml(70kg adult)
Blood vol.
Hematocrit (Hct)- % of blood vol made up of cells
Total blood vol. = plasma volume x 100/100- Hct
Red cell volume = total blood vol.-plasma volume
ECF Volume
Difficult to measure
Limits of the space are ill defined
Transcellular fluids
Inulin
Mannitol and sucrose
20% of body weight
Interstitial fluid vol.
Cannot be measured directly
ECF VOL – Plasma vol.
ECF: ICF - infants & children>adults
ICF VOLUME
Cannot be measured directly
ICF = TBW – ECF
TBW – Deuterium oxide D2O
Tritium oxide and aminopyrine
Water content of lean body tissue – 71 to72 ml/100gm of tissue
Conc. Of Solutes - Units
Mole
Millimoles, micromoles
Molecular weight
Equivalents
Moles
Gram molecular weight of a substance
One mole = 6 x 1023 molecules
SI unit for amount of substance
Mol. Wt – ratio of mass of one molecule of a substance to the mass of 1/12 the mass of an atom of carbon-12
Dalton – unit of mass equal to 1/12 the mass of an atom of carbon-12
Equivalents
1 eq is 1 mol of an ionized substance divided by its valence.
Water
Small, highly diffusible, polar molecule
Solvent – hydrate proteins, sugars and other substances-
Dissolving properties
Thermal properties
Ionizes very slightly (pH 7.0)
Bulk Flow & Diffusion
Bulk flow –movement of the solution mass in the direction of hydrostatic pressure gradient
Diffusion – molecular movement down conc. Gradient
Disperse local accumulation of molecules if it is free to move
Osmotic Pressure
Fluid compartment – principal solute
Mainly restricted to that compartment
K+ ICF
Na+ ECF
Plasma proteins: intra vascular space
Osmotic pressure – total number of particles
Osmosis
Solution – stable mixture of solute & solvent
Solute– dispersed individual molecules
Solvent – liquid bulk
Solute mol. Occupy space
Water mol. Net movement by diffusion.
Osmosis
Water – diffuse from region of high solvent conc. to low conc.
The extent of tendency for solvent to move – measured by use of semi permeable membrane. -hydrostatic pressure to produce equal and opposite bulk flow
Sum of conc. of all solute particles
Oncotic Pressure
Plasma proteins – albumin, globulin
Large mol wt & size –unable to leave intravascular space
Pressure diff between plasma and interstitial fluids
Colloid osmotic pressure
Amounts to only 0.7 mosmol/kg water
Thank you
Bronchoscopy & Inhaled Foreign Bodies
Bronchoscopy & Management of Inhaled Foreign Bodies
Objectives-
Anatomy of Tracheobronchial tree
General Indications & Contraindications
Discuss problems & Options for management
How to manage a patient with a foreign body in the airway
Tracheobronchial Anatomy
Airway generations 0-23
0 – Trachea
1-4 – Main Lobar & segmental
5-11 – Small Bronchi
12-16 – Bronchioles
17-19 – Respiratory bronchioles
20-22 – Alveolar ducts
23 – Alveolar sacs
Tracheobronchial Anatomy
Indications for bronchoscopy
Diagnostic
Initial diagnosis (Flexible > Rigid)
Staging of disease
Indications continued
Therapeutic
R/O Foreign Body
Stent Insertion
Diathermy Resection
Airway Management
Insertion of DLT
Contraindications
Absolute
Don't exist?
Relative
Anaesthetic Risk
Surgical Risk - Biopsy
Tracheal Stenosis – Flexible type
Potential problems
Shared airway
Ventilation & Oxygenation
Potential for awareness
Scavenging
Concurrent disease
Work up
As for pneumonectomy especially if pre thoracotomy
What are they?
Minimal pulmonary function test criteria
Pre op Pneumonectomy criteria
PAP with unilateral occlusion
< 25 mmHg rest
< 35 mmHg exercise
Anaesthetic technique
Method of choice
TCI (Propofol +/- Remifentanil) for all but the shortest procedures
Exceptions
Upper airway obstruction
Bronchopleural fistula
Ventilation
Venturi – Sanders Injector
Ventilating bronchoscope
High Frequency Jet ventilation
Questions?
Inhaled Foreign Bodies
Who?
Children < 3y.o.
Elderly
Debilitated
Drunks
What?
Anything small enough to enter the airway
Organic e.g. Peanuts
Inorganic e.g. Coin
Case Example 1
2 y.o child presents after having coughing fit, stridor and shortness of breath
What is your management?
Case example 2
77 y.o man with a 6 week history of persistent cough
What are the findings on CXR?
X-Ray Findings
CXR
Acute presentation- Ipsilateral Obstructive Emphysema on Expiratory film
Chronic presentation - Features of collapse / consolidation distal to the FB
Anaesthetic technique
Inhalational Vs Intravenous
Upper airway obstruction or not?
Post operatively
When to Extubate?
Monitor for complications
Laryngospasm, Bronchospasm & pneumothorax
Summary
Anatomy
Indications / Contraindications
Problems & Management options
Specific management of inhaled foreign body
Objectives-
Anatomy of Tracheobronchial tree
General Indications & Contraindications
Discuss problems & Options for management
How to manage a patient with a foreign body in the airway
Tracheobronchial Anatomy
Airway generations 0-23
0 – Trachea
1-4 – Main Lobar & segmental
5-11 – Small Bronchi
12-16 – Bronchioles
17-19 – Respiratory bronchioles
20-22 – Alveolar ducts
23 – Alveolar sacs
Tracheobronchial Anatomy
Indications for bronchoscopy
Diagnostic
Initial diagnosis (Flexible > Rigid)
Staging of disease
Indications continued
Therapeutic
R/O Foreign Body
Stent Insertion
Diathermy Resection
Airway Management
Insertion of DLT
Contraindications
Absolute
Don't exist?
Relative
Anaesthetic Risk
Surgical Risk - Biopsy
Tracheal Stenosis – Flexible type
Potential problems
Shared airway
Ventilation & Oxygenation
Potential for awareness
Scavenging
Concurrent disease
Work up
As for pneumonectomy especially if pre thoracotomy
What are they?
Minimal pulmonary function test criteria
Pre op Pneumonectomy criteria
PAP with unilateral occlusion
< 25 mmHg rest
< 35 mmHg exercise
Anaesthetic technique
Method of choice
TCI (Propofol +/- Remifentanil) for all but the shortest procedures
Exceptions
Upper airway obstruction
Bronchopleural fistula
Ventilation
Venturi – Sanders Injector
Ventilating bronchoscope
High Frequency Jet ventilation
Questions?
Inhaled Foreign Bodies
Who?
Children < 3y.o.
Elderly
Debilitated
Drunks
What?
Anything small enough to enter the airway
Organic e.g. Peanuts
Inorganic e.g. Coin
Case Example 1
2 y.o child presents after having coughing fit, stridor and shortness of breath
What is your management?
Case example 2
77 y.o man with a 6 week history of persistent cough
What are the findings on CXR?
X-Ray Findings
CXR
Acute presentation- Ipsilateral Obstructive Emphysema on Expiratory film
Chronic presentation - Features of collapse / consolidation distal to the FB
Anaesthetic technique
Inhalational Vs Intravenous
Upper airway obstruction or not?
Post operatively
When to Extubate?
Monitor for complications
Laryngospasm, Bronchospasm & pneumothorax
Summary
Anatomy
Indications / Contraindications
Problems & Management options
Specific management of inhaled foreign body
Heart Failure due to Systolic Dysfunction
Basic Principals
• Heart failure has a poor prognosis, worse than most forms of cancer
• Major risk factor - Goldman
• Seek aetiology
• Avoid it happening in the first place
– Modify risks
– Treat Myocardial infarction
Aims
• Reduction of mortality
• Relief of symptoms
Some advances in disease modification improved both morbidity and mortality
Aetiology
• IHD
• VHD
• Idiopathic – dilated cardiomyopathy
• Hypertension
• C2H5OH
• Viral - Coxsackie’s
• Systemic disease Haemochromatosis, Sarcoidisis
• Connective tissue disorders – SLE etc
Epidemiology
• Increases with age
• Men > Women
• 3% of population 65-74 years
• 9% over 90 years
• 2,9% 25-74 impaired ejection fraction
• ??? Tip of Iceberg
Pathophysiology
• Definition not of much use – “inability…oxygen…metabolising tissue…adequate filling pressure”
• A Syndrome – not a diagnosis
• Breathlessness, fatigue, fluid retention
• Secondary to adrenergic and Renin-AT-Aldosterone
Treatment directed at antagonism of these systems
Investigations
• ECG
• CXR
• ECHO
• Biochem – Haematolgy
• Angiogram
• Nuclear Imaging
• Exercise ECG, VO2, MET’s
• MRI
• BNP – strong negative predictive value
Investigations
• ECG
– Abnormal in 93%
• Previous MI
• Non specific ST and T changes
• Conduction abnormalities
• ST
• Dysrythmias – AF, VE
Investigation
• ECHO
– Dilation of Ventricles
– Global dysfunction
– Wall motion
• CXR
– Cardiac enlargement
– Pulmonary Oedema
Management
Disease modifying therapy
ACE-I
1st line drugs – given to all patients with systolic dysfunction whether symptomatic or not – 25% relative risk reduction
Combined with diuretic with evidence of cardiac compression – fluid retention
Disease modifying therapy
B-Blockers
Many trials showed benefit with all grades of CHF, post MI
Must be free of decompensation and titrated up – start slow go slow
COPD – without reversible component - not contraindicated
Disease modifying therapy
Aldosterone Antagonists
Spironolactone been shown as effective in reduction of M&M with moderate to severe CHF
In addition to ACE/B-blocker
Caution – renal impairment – hyper K
Disease modifying therapy
AT-II receptor antagonists
ACE intolerant patients – shown to be effective
In addition - Mortality reduced 15%
Management
Symptomatic Therapy
Diuretics
Well established place
Over treatment can have adverse effect on outcome – low dose
Fluid restriction may be needed
Monitor renal function
Symptomatic Therapy
Digoxin
Role less clear
Introduce when symptomatic despite maximal medical therapy or AF
Studies excluded AF – no benefit
For symptomatic, frequent hospitalisation, large hearts
Avoid in Ventricular Dysrythmias
Other Pharmacological Therapy
IHD – Aspirin (AF – Warfarin)
Statin – Benefit in prevention IHD proven – recently safety aspects.
Anaemia – Predicts mortality independently
EPO and Iron therapy been shown to be of benefit
Avoid NSAID’s, Ca antagonists, steroids, TCA, class I anti-arrhythmic - exacerbate
Non Pharmacological Intervention
• Lifestyle modifications
• Smoking
• C2H5OH
• Weight loss
• Exercise
• Immunisation Influenza, Pneumococcus
• Fluid/salt restriction – daily weighing
Device Therapy
Automatic Implantable Cardioverter
Defibrillators (AICD’s)
When L-V-dysfunction, EF < 35%, IHD – benefits in terms of mortality
Cost implications
Currently only if dysrythmias
Device Therapy
Cardiac Resynchronisation Therapy (CRT)
Combine with optimal medical therapy may improve well being by correcting ventricular dysynchrony
Pacing in DDD mode
Device Therapy
LV Assist Devices
Help – take over pump function in series
Bridge to transplantation
Surgical Options
Revascularization
Ventricular remodelling
Transplantation
Significant 1 year mortality – 19%
Life expectancy 10 years
Must be otherwise well
• Heart failure has a poor prognosis, worse than most forms of cancer
• Major risk factor - Goldman
• Seek aetiology
• Avoid it happening in the first place
– Modify risks
– Treat Myocardial infarction
Aims
• Reduction of mortality
• Relief of symptoms
Some advances in disease modification improved both morbidity and mortality
Aetiology
• IHD
• VHD
• Idiopathic – dilated cardiomyopathy
• Hypertension
• C2H5OH
• Viral - Coxsackie’s
• Systemic disease Haemochromatosis, Sarcoidisis
• Connective tissue disorders – SLE etc
Epidemiology
• Increases with age
• Men > Women
• 3% of population 65-74 years
• 9% over 90 years
• 2,9% 25-74 impaired ejection fraction
• ??? Tip of Iceberg
Pathophysiology
• Definition not of much use – “inability…oxygen…metabolising tissue…adequate filling pressure”
• A Syndrome – not a diagnosis
• Breathlessness, fatigue, fluid retention
• Secondary to adrenergic and Renin-AT-Aldosterone
Treatment directed at antagonism of these systems
Investigations
• ECG
• CXR
• ECHO
• Biochem – Haematolgy
• Angiogram
• Nuclear Imaging
• Exercise ECG, VO2, MET’s
• MRI
• BNP – strong negative predictive value
Investigations
• ECG
– Abnormal in 93%
• Previous MI
• Non specific ST and T changes
• Conduction abnormalities
• ST
• Dysrythmias – AF, VE
Investigation
• ECHO
– Dilation of Ventricles
– Global dysfunction
– Wall motion
• CXR
– Cardiac enlargement
– Pulmonary Oedema
Management
Disease modifying therapy
ACE-I
1st line drugs – given to all patients with systolic dysfunction whether symptomatic or not – 25% relative risk reduction
Combined with diuretic with evidence of cardiac compression – fluid retention
Disease modifying therapy
B-Blockers
Many trials showed benefit with all grades of CHF, post MI
Must be free of decompensation and titrated up – start slow go slow
COPD – without reversible component - not contraindicated
Disease modifying therapy
Aldosterone Antagonists
Spironolactone been shown as effective in reduction of M&M with moderate to severe CHF
In addition to ACE/B-blocker
Caution – renal impairment – hyper K
Disease modifying therapy
AT-II receptor antagonists
ACE intolerant patients – shown to be effective
In addition - Mortality reduced 15%
Management
Symptomatic Therapy
Diuretics
Well established place
Over treatment can have adverse effect on outcome – low dose
Fluid restriction may be needed
Monitor renal function
Symptomatic Therapy
Digoxin
Role less clear
Introduce when symptomatic despite maximal medical therapy or AF
Studies excluded AF – no benefit
For symptomatic, frequent hospitalisation, large hearts
Avoid in Ventricular Dysrythmias
Other Pharmacological Therapy
IHD – Aspirin (AF – Warfarin)
Statin – Benefit in prevention IHD proven – recently safety aspects.
Anaemia – Predicts mortality independently
EPO and Iron therapy been shown to be of benefit
Avoid NSAID’s, Ca antagonists, steroids, TCA, class I anti-arrhythmic - exacerbate
Non Pharmacological Intervention
• Lifestyle modifications
• Smoking
• C2H5OH
• Weight loss
• Exercise
• Immunisation Influenza, Pneumococcus
• Fluid/salt restriction – daily weighing
Device Therapy
Automatic Implantable Cardioverter
Defibrillators (AICD’s)
When L-V-dysfunction, EF < 35%, IHD – benefits in terms of mortality
Cost implications
Currently only if dysrythmias
Device Therapy
Cardiac Resynchronisation Therapy (CRT)
Combine with optimal medical therapy may improve well being by correcting ventricular dysynchrony
Pacing in DDD mode
Device Therapy
LV Assist Devices
Help – take over pump function in series
Bridge to transplantation
Surgical Options
Revascularization
Ventricular remodelling
Transplantation
Significant 1 year mortality – 19%
Life expectancy 10 years
Must be otherwise well
Wednesday, May 10, 2006
Carotid Endarterectomy
Indications for CEA
(NASCET & ECET trials)
• TIA & ipsilateral lesion >70%
• Failure of medical mix with >40% stenosis
• Established stroke- should be perceptible benefit
• Asymptomatic with bruit & >70% stenosis
Neurological Monitoring- Why?
• 1° goal - Identify patients that would benefit from placement of a shunt.
• 2° goal - Identify patients who may benefit from BP augmentation.
• N.B.- The concept of selective shunting not accepted by all surgeons.
• Most intra-operative strokes are thomboembolic and most peri-operative strokes are postoperative.
Neurologic Monitoring- Types
Monitors of function
• Awake patient
• EEG- Standard Vs processed.
• Somatosensory evoked potentials
Monitor of O2 supply & demand
• Jugular SvO2/ Cerebral Oximetry
Neurologic monitoring_ Types
Monitors of blood flow
• Internal carotid artery stump pressures
• Transcranial doppler
• Radioactive Xe 133
Awake patient
• At first glance the simplest and most non-invasive methods is to maintain direct contact with the patient.
• Requires some form of loco-regional anaesthesia, a spare nurse and the ability to communicate well with the patient.
• 2-3% conversion rate to GA
Stump pressures
• Represents back pressure from collateral flow through the circle of Willis.
• Advantage of being cheap, continuous and little expertise is required.
• Criticisms
– Inaccurate
– Critical stump pressure unknown (? <50mmHg)
Standard EEG
• 16-20 channel continuous in real-time.
• No false negatives in a series of >2000 patients @ Mayo Clinic.
• Gold standard of EEG analysis but requires an experienced electroencephalographer.
• Minimum of 2 channels per hemisphere provided territory of MCA included.
• 100% sensitivity and specificity.
Normal a wave EEG
Processed EEG- what is it?
• Resurgence because of increased power of microprocessors to do the algorithms.
• 2 types - Power or Bispectral analysis.
• Power analysis uses Fourier transformation to convert raw EEG signal into its component sine waves of an identifiable frequency and amplitude.
Processed EEG- what is it?
• These amplitudes and frequencies are plotted for against time and displayed as either a compressed or density spectral array CSA or DSA.
• Bispectral is a recent development finding a niche as an anaesthetic depth monitor.
Technique to generate Compressed spectral array
CSA during hypotension
Processed EEG- Why use it?
• Cross-clamp during CEA is a unilateral time specific event involving a large part of the hemisphere.
• These are the best circumstances for interpreting the processed EEG.
• Allows ‘black box’ approach to EEG interpretation by novices. 91-98% sensitivity and specificity
Processed EEG
• Criticisms
– Electronically remote from original.
– Less information.
– Bilateral Vs Unilateral. Not 100% reliable.
– Data acquisition period. Not 100% real-time.
Limitations of EEG generally
• EEG not ischemia specific.
• May not detect subcortical or small cortical infarcts.
• Patients with pre-existing, bilateral or contralateral cerebrovascular disease.
• False negatives
• False positives
Somatosensory evoked potentials
• Sensory cortex is primarily supplied by the MCA
• Repetitive electrical stimuli applied to a peripheral nerve and the responses are averaged to produce the evoked response.
• Generally 4 channels are necessary
• A control site should be monitored as well to differentiate global factors- Anaesthetic & metabolic
SSEP
• Characteristic changes of ischemia are a decrease in amplitude and/or increase in latency.
• Validated in animals but not in humans intra-operatively.
• Usually median nerve at the wrist chosen for CEA- Short latency more resilient.
Short latency SSEP from median nerve at the wrist
Jugular venous Saturation & Cerebral Oximetry
• Both are measures of the balance between cerebral oxygen supply and demand.
• However, limited benefit in this setting because they are a measure of global oxygenation and regional variations would go undetected.
Transcranial Doppler
• Use of doppler shift phenomenon
• Temporal bone used as window (relatively thin) to measure flow velocity in the MCA.
• Assumptions
– Flow µ flow velocity only if diameter of vessel and measurement angle of doppler probe remain constant.
– CBF in basal arteries µ cortical CBF.
Transcranial doppler
• Not only allows continuous measurement of mean blood flow but also detection of embolic events.
• Postoperative TCD has been used in one centre as a basis to treat with dextrans.
Normal TCD trace
Transcranial doppler
• Criticisms
– Doesn’t allow for normal variation in flow velocities, which appears to be large.
– CBF and MCAv not well correlated.
– Cross clamping a relatively short period and most strokes occur at other times during or after surgery.
Radioactive Xenon
• Injected intravenously or into ipsilateral carotid typically pre, during and post clamping.
• Detectors placed over the ipsilateral area supplied by the MCA.
• Decay curves are then analysed.
• Expense and expertise required are the limiting factors.
Conclusion
• Each has its pros and cons.
• Use some form of neurologic monitor.
• One that suits you and your surgeon.
(NASCET & ECET trials)
• TIA & ipsilateral lesion >70%
• Failure of medical mix with >40% stenosis
• Established stroke- should be perceptible benefit
• Asymptomatic with bruit & >70% stenosis
Neurological Monitoring- Why?
• 1° goal - Identify patients that would benefit from placement of a shunt.
• 2° goal - Identify patients who may benefit from BP augmentation.
• N.B.- The concept of selective shunting not accepted by all surgeons.
• Most intra-operative strokes are thomboembolic and most peri-operative strokes are postoperative.
Neurologic Monitoring- Types
Monitors of function
• Awake patient
• EEG- Standard Vs processed.
• Somatosensory evoked potentials
Monitor of O2 supply & demand
• Jugular SvO2/ Cerebral Oximetry
Neurologic monitoring_ Types
Monitors of blood flow
• Internal carotid artery stump pressures
• Transcranial doppler
• Radioactive Xe 133
Awake patient
• At first glance the simplest and most non-invasive methods is to maintain direct contact with the patient.
• Requires some form of loco-regional anaesthesia, a spare nurse and the ability to communicate well with the patient.
• 2-3% conversion rate to GA
Stump pressures
• Represents back pressure from collateral flow through the circle of Willis.
• Advantage of being cheap, continuous and little expertise is required.
• Criticisms
– Inaccurate
– Critical stump pressure unknown (? <50mmHg)
Standard EEG
• 16-20 channel continuous in real-time.
• No false negatives in a series of >2000 patients @ Mayo Clinic.
• Gold standard of EEG analysis but requires an experienced electroencephalographer.
• Minimum of 2 channels per hemisphere provided territory of MCA included.
• 100% sensitivity and specificity.
Normal a wave EEG
Processed EEG- what is it?
• Resurgence because of increased power of microprocessors to do the algorithms.
• 2 types - Power or Bispectral analysis.
• Power analysis uses Fourier transformation to convert raw EEG signal into its component sine waves of an identifiable frequency and amplitude.
Processed EEG- what is it?
• These amplitudes and frequencies are plotted for against time and displayed as either a compressed or density spectral array CSA or DSA.
• Bispectral is a recent development finding a niche as an anaesthetic depth monitor.
Technique to generate Compressed spectral array
CSA during hypotension
Processed EEG- Why use it?
• Cross-clamp during CEA is a unilateral time specific event involving a large part of the hemisphere.
• These are the best circumstances for interpreting the processed EEG.
• Allows ‘black box’ approach to EEG interpretation by novices. 91-98% sensitivity and specificity
Processed EEG
• Criticisms
– Electronically remote from original.
– Less information.
– Bilateral Vs Unilateral. Not 100% reliable.
– Data acquisition period. Not 100% real-time.
Limitations of EEG generally
• EEG not ischemia specific.
• May not detect subcortical or small cortical infarcts.
• Patients with pre-existing, bilateral or contralateral cerebrovascular disease.
• False negatives
• False positives
Somatosensory evoked potentials
• Sensory cortex is primarily supplied by the MCA
• Repetitive electrical stimuli applied to a peripheral nerve and the responses are averaged to produce the evoked response.
• Generally 4 channels are necessary
• A control site should be monitored as well to differentiate global factors- Anaesthetic & metabolic
SSEP
• Characteristic changes of ischemia are a decrease in amplitude and/or increase in latency.
• Validated in animals but not in humans intra-operatively.
• Usually median nerve at the wrist chosen for CEA- Short latency more resilient.
Short latency SSEP from median nerve at the wrist
Jugular venous Saturation & Cerebral Oximetry
• Both are measures of the balance between cerebral oxygen supply and demand.
• However, limited benefit in this setting because they are a measure of global oxygenation and regional variations would go undetected.
Transcranial Doppler
• Use of doppler shift phenomenon
• Temporal bone used as window (relatively thin) to measure flow velocity in the MCA.
• Assumptions
– Flow µ flow velocity only if diameter of vessel and measurement angle of doppler probe remain constant.
– CBF in basal arteries µ cortical CBF.
Transcranial doppler
• Not only allows continuous measurement of mean blood flow but also detection of embolic events.
• Postoperative TCD has been used in one centre as a basis to treat with dextrans.
Normal TCD trace
Transcranial doppler
• Criticisms
– Doesn’t allow for normal variation in flow velocities, which appears to be large.
– CBF and MCAv not well correlated.
– Cross clamping a relatively short period and most strokes occur at other times during or after surgery.
Radioactive Xenon
• Injected intravenously or into ipsilateral carotid typically pre, during and post clamping.
• Detectors placed over the ipsilateral area supplied by the MCA.
• Decay curves are then analysed.
• Expense and expertise required are the limiting factors.
Conclusion
• Each has its pros and cons.
• Use some form of neurologic monitor.
• One that suits you and your surgeon.
Methods to reduce blood transfusion
Alternative Therapies to Reduce Blood Transfusion
Blood Conservation
Preop –
Intra op –
Post op –
Pre Op
Assessment of patient, review blood results.
Drug treatment.
Donation of Autologous blood.
Relatively fit patients with Hb >10g/dl.
Up to 4 units.
Needs a good team, funding for programme.
Decline in popularity.
Pre Op
Iron – deficiency 14% women and 3% men.
iron – iron sucrose and iron dextran preparations.
iv bolus or iv infusion.
Can reduce blood transfusions and prepare patients for surgery in anticipation of blood loss.
Erythropoietin.
Acute normovolaemic haemodilution.
Anaesthetic Techniques
Deliberate Hypotension
Arterial pressure
Patient selection
Various agents, techniques
Invasive monitoring
MAP – 55 to 60 mm hg
Venous Pressure
Patient positioning- elevate op site, avoid obstruction to venous drainage,coughing, straining.
IPPV, PEEP and CPAP.
Avoid Hypervolemia in certain cases.
Hypothermia
T< 35.5 C – impairs haemostasis.
Reduce heat loss – inc ambient temp, keep patient covered, short procedures, minimally invasive surgery.
Increase heat input – warm fluids, skin warming.
Monitor temperature.
Pre, intra op, post op warming.
General Vs Regional Anaesthesia
Regional – low arterial BP,CVP, peripheral venous pressure.
Evidence is equivocal.
Fluid Therapy
Effect on coagulation – dilutional
Crystalloids less effect than colloids
Gelatins less effect than starches and dextran
Surgical Methods
Operative Techniques
Avascular planes
Progressive haemostasis
Patient position
Limb exanguination
Minimally invasive procedures- endovascular AAA repair, laproscopic surgeries, laser prostatectomy etc
Surgical Haemostasis
Diathermy
Lasers
Ultrasound dissectors
Water - jet dissectors
Haemostatic swabs
Fibrin sealents
Cell Salvage
Surgical blood loss anticoagulated, filtered and collected.
Separated concentrated and washed.
Re suspended in saline and re infused.
Best if loss > 1 litre.
Major vascular, orthopaedic and trauma, hepatic surgeries.
Capital costs, disposables, training.
Aprotinin
Reversible inhibitor of serine proteases.
Antifibrinolytic – inhibitory action on plasmin by directly binding to plasmin.
Supresses inflammation by inhibiting kallikrein.
Uses - orthopedic surgeries.
Reduction in blood loss ~ 50%.
Tranexamic Acid
Binds to lysine binding sites of plasminogen.
Blocks its binding to fibrin.
Prevents plasminogen activation.
Delays fibrinolysis.
Uses – joint replacement surgeries specially revision surgeries.
Post Op
Drain salvage.
Transfusion trigger.
Drug therapy – iron, erythropoietin,tranexamic acid.
Summary
Assess patients – optimise conditon.
Reduce blood loss.
Conserve blood.
Reduce threshold.
Team effort – consult hematologist.
Thank You
Blood Conservation
Preop –
Intra op –
Post op –
Pre Op
Assessment of patient, review blood results.
Drug treatment.
Donation of Autologous blood.
Relatively fit patients with Hb >10g/dl.
Up to 4 units.
Needs a good team, funding for programme.
Decline in popularity.
Pre Op
Iron – deficiency 14% women and 3% men.
iron – iron sucrose and iron dextran preparations.
iv bolus or iv infusion.
Can reduce blood transfusions and prepare patients for surgery in anticipation of blood loss.
Erythropoietin.
Acute normovolaemic haemodilution.
Anaesthetic Techniques
Deliberate Hypotension
Arterial pressure
Patient selection
Various agents, techniques
Invasive monitoring
MAP – 55 to 60 mm hg
Venous Pressure
Patient positioning- elevate op site, avoid obstruction to venous drainage,coughing, straining.
IPPV, PEEP and CPAP.
Avoid Hypervolemia in certain cases.
Hypothermia
T< 35.5 C – impairs haemostasis.
Reduce heat loss – inc ambient temp, keep patient covered, short procedures, minimally invasive surgery.
Increase heat input – warm fluids, skin warming.
Monitor temperature.
Pre, intra op, post op warming.
General Vs Regional Anaesthesia
Regional – low arterial BP,CVP, peripheral venous pressure.
Evidence is equivocal.
Fluid Therapy
Effect on coagulation – dilutional
Crystalloids less effect than colloids
Gelatins less effect than starches and dextran
Surgical Methods
Operative Techniques
Avascular planes
Progressive haemostasis
Patient position
Limb exanguination
Minimally invasive procedures- endovascular AAA repair, laproscopic surgeries, laser prostatectomy etc
Surgical Haemostasis
Diathermy
Lasers
Ultrasound dissectors
Water - jet dissectors
Haemostatic swabs
Fibrin sealents
Cell Salvage
Surgical blood loss anticoagulated, filtered and collected.
Separated concentrated and washed.
Re suspended in saline and re infused.
Best if loss > 1 litre.
Major vascular, orthopaedic and trauma, hepatic surgeries.
Capital costs, disposables, training.
Aprotinin
Reversible inhibitor of serine proteases.
Antifibrinolytic – inhibitory action on plasmin by directly binding to plasmin.
Supresses inflammation by inhibiting kallikrein.
Uses - orthopedic surgeries.
Reduction in blood loss ~ 50%.
Tranexamic Acid
Binds to lysine binding sites of plasminogen.
Blocks its binding to fibrin.
Prevents plasminogen activation.
Delays fibrinolysis.
Uses – joint replacement surgeries specially revision surgeries.
Post Op
Drain salvage.
Transfusion trigger.
Drug therapy – iron, erythropoietin,tranexamic acid.
Summary
Assess patients – optimise conditon.
Reduce blood loss.
Conserve blood.
Reduce threshold.
Team effort – consult hematologist.
Thank You
Septic Shock
Shock – Syndrome in which tissue perfusion is inadequate in supplying tissue metabolic requirements:
• Hypovolaemic
• Cardiogenic
• Distributive e.g. septic, anaphylaxis
• Obstructive e.g. tensionpneumothorax, PE
Septic shock:
Definitions
Sepsis: source of infection, temperature >38 ‘C, heart rate >90, resp. rate > 20 or PaC02 < 4,3kPa, WCC . 12000 or > 10% immature forms
Septic shock: Sepsis plus hypotension, despite adequate fluid resuscitation, plus organ perfusion abnormalities e.g. lactic acidosis, oliguria and mental impairment
Definitions continue
SIRS: Systemic inflammatory response syndrome has the same definition as sepsis but can occur as a response to insults other than infection, e.g. pancreatitis or multiple trauma
Pathology
Severity of illness determined more by nature of inflammatory response than by infection itself
Chemical mediators, complex interactive pathways, some are pro and others anti-inflammatory
Gram negative bacteria endotoxins activate mediators e.g. TNF, PG, interleukin, NO, macrophages
Pathological effects
Vasodilatation
Increased capillary permeability
Impaired tissue oxygen utilization
Myocardial depression
Clinical signs
Pyrexia, tachycardia, warm bounding peripheries and hypotension
Other: confusion, drowsiness, cool peripheries, tachypnoea and oliguria
BEWARE: young children
elderly
pre-existing pathology
steroids or beta blockers
moribund advanced sepsis
Investigations
FBC: high WBC neutrophilia, low WBC and low platelets indicate severe sepsis
U&E: dehydration and renal impairment
Coagulation: raised INR indicate septic coagulopathy
Bloodsugar: usually raised
Bloodgas: metabolic acidosis, low C02 and hypoxia
Lactate: high due to tissue hypoxia
CXR: ‘ wet lungs’ or ARDS changes
Monitoring: Oxygenation & Perfusion
Routine non invasive monitors
CVP and arterial line
CO monitoring e.g. PiCCO
Urine output
Mixed venous oxygenation via PA catheter, normal >75%
Regular bloodgasses, U&E, lactate, clotting
Peripheral – core temperature difference, normal < 2 ‘C (more useful in low cardiac output states
Treatment: Restoration & maintaining tissue oxygenation
IV fluid therapy
Inotropes/vasoconstrictors
Oxygen and PEEP
Ventilation
Treatment: continue
Appropriate antibacterial and antifungal drugs, microbiology input
Nutrition
Maintain normo- glycaemia
Activated Protein C
Steroids?
Prevent stress gastric ulcers
Other: PG’s, nalaxone, thyrotropin releasing hormone?
Complications
Multi-organ failure including ARDS, renal failure, hepatic failure, pancreatitis & DM, DIC, cardiac failure and coma
DEATH: Mortality 50%
• Hypovolaemic
• Cardiogenic
• Distributive e.g. septic, anaphylaxis
• Obstructive e.g. tensionpneumothorax, PE
Septic shock:
Definitions
Sepsis: source of infection, temperature >38 ‘C, heart rate >90, resp. rate > 20 or PaC02 < 4,3kPa, WCC . 12000 or > 10% immature forms
Septic shock: Sepsis plus hypotension, despite adequate fluid resuscitation, plus organ perfusion abnormalities e.g. lactic acidosis, oliguria and mental impairment
Definitions continue
SIRS: Systemic inflammatory response syndrome has the same definition as sepsis but can occur as a response to insults other than infection, e.g. pancreatitis or multiple trauma
Pathology
Severity of illness determined more by nature of inflammatory response than by infection itself
Chemical mediators, complex interactive pathways, some are pro and others anti-inflammatory
Gram negative bacteria endotoxins activate mediators e.g. TNF, PG, interleukin, NO, macrophages
Pathological effects
Vasodilatation
Increased capillary permeability
Impaired tissue oxygen utilization
Myocardial depression
Clinical signs
Pyrexia, tachycardia, warm bounding peripheries and hypotension
Other: confusion, drowsiness, cool peripheries, tachypnoea and oliguria
BEWARE: young children
elderly
pre-existing pathology
steroids or beta blockers
moribund advanced sepsis
Investigations
FBC: high WBC neutrophilia, low WBC and low platelets indicate severe sepsis
U&E: dehydration and renal impairment
Coagulation: raised INR indicate septic coagulopathy
Bloodsugar: usually raised
Bloodgas: metabolic acidosis, low C02 and hypoxia
Lactate: high due to tissue hypoxia
CXR: ‘ wet lungs’ or ARDS changes
Monitoring: Oxygenation & Perfusion
Routine non invasive monitors
CVP and arterial line
CO monitoring e.g. PiCCO
Urine output
Mixed venous oxygenation via PA catheter, normal >75%
Regular bloodgasses, U&E, lactate, clotting
Peripheral – core temperature difference, normal < 2 ‘C (more useful in low cardiac output states
Treatment: Restoration & maintaining tissue oxygenation
IV fluid therapy
Inotropes/vasoconstrictors
Oxygen and PEEP
Ventilation
Treatment: continue
Appropriate antibacterial and antifungal drugs, microbiology input
Nutrition
Maintain normo- glycaemia
Activated Protein C
Steroids?
Prevent stress gastric ulcers
Other: PG’s, nalaxone, thyrotropin releasing hormone?
Complications
Multi-organ failure including ARDS, renal failure, hepatic failure, pancreatitis & DM, DIC, cardiac failure and coma
DEATH: Mortality 50%
Tuesday, May 09, 2006
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