Questions from the past

1. Spinal anatomy
a. Draw and label the diagram of lumbar vertebra. Enumerate the layers of spinal
canal from skin to dural space.

b. What is the blood supply of spinal cord?

Spinal cord and nerve roots receive blood supply from:
1. Anteriorly: Anterior spinal artery, formed from vertebral artery at the base of
the skull; supply anterior 2/3rd of the spinal cord.
2. Posteriorly: 2 posterior spinal arteries. Supply the posterior one third. These
are formed from posterior inferior cerebellar arteries and course down along
the dorsal surface of the cord medial to dorsal nerve roots.
3. In addition to these, in the thorax spinal cord receives blood supply from
intercostal arteries and in the abdomen via branches from lumbar arteries.
One of these radicular arteries is large arteria radicularis magna which
supplies the anterior part of the spinal cord.

c. How will you prepare a case for spinal anesthesia?

2. Spinal anesthesia
a. What is spinal anesthesia?
Spinal anesthesia also called subarachnoid block is a form of regional anesthesia
involving the injection of local anesthetic (with or without adjuvants) into the
subrachnoid space generally through a fine needle.

b. What are the contraindications of central blockade? What are the complications of
central blockade?
The following are the contraindications of central blockade:
Absolute contraindications:
1. Patient refusal
2. Known allergic reactions to local anesthetic of choice
3. Infection at the site of injection
4. Severe hypovolemia
5. Coagulopathy or bleeding diathesis
6. Increased ICP
7. Severe aortic stenosis
8. Severe mitral stenosis
Relative contraindications:
1. Sepsis
 2. Unco-operative patient
3. Preexisting neurological deficit
4. Severe spinal deformity
5. Stenotic valvular lesions

c. What are the factors affecting the level block?

The following are the factors affecting the level of block:
Important factors:
1. Baricity of the anesthetic solution
2. Position of the patient: during injection/immediately after the injection
3. Dose of the anesthetic agent
4. Site of injection
Other factors:
1. Age
2. CSF
3. Curvature of the spine
4. Drug volume
5. Intraabdominal pressure
6. Patient height
7. Pregnancy

3. Neurophysiology
a. What is the importance of cerebral blood flow?
Cerebral blood flow varies with the metabolic activity of the brain. In gray mater the
flow is around 80 ml/100g/min and in white mater it is 20 ml/100g/min thus the
average of 50 ml/100g/min. Skull is a rigid structure with fixed volume of blood, CSF,
and cells. Increase in one component directly increases the intracranial pressure. On
the other side, flow rates below 20-25 ml/100g/min are usually associated with
cerebral impairment, flow between 15-20 ml/100g/min produce flat EEG, and flow
rates below <10 ml/100g/min usually associated with irreversible brain damage.

b. What are the factors regulating cerebral blood flow?

Factors regulating CBF:
1. Cerebral Perfusion Pressure: CPP is MAP-ICP (or CVP whichever is higher).
CPP is normally around 80-100 mm Hg. Since ICP is normally <10 mm Hg
CPP is mostly determined by MAP.
2. Autoregulation: Like other organs, brain tolerates a much larger range of BP
with little change in blood flow. This is due to inherent property of cerebral
vasculature. CBF remains nearly constant between MAPs of 60 and 160 mm
Hg. Myogenic and metabolic mechanisms are responsible for this
autoregulation.
3. Extrinsic Mechanisms:
a. Respiratory gas tensions: CBF is directly proportional to PaCO2
between tensions of 20 and 80 mm Hg. Blood flow changes
approximately 1-2 ml/100g/min per mm Hg changes in PaCO2. This
effect is almost immediate and is due to changes in pH of CSF and
cerebral tissue.
 b. Temperature: CBF changes 5% to 7% per every degree Celsius rise in
temperature. Hypothermia decreases both CBF and CMRO2 and
reverse with hyperthermia.
c. Viscosity: Most important determinant of blood viscosity is hematocrit.
Elevated hematocrit as seen with polycyathemia increases blood
viscosity and can reduce CBF.
d. Autonomic influences: sympathetic is vasoconstrictive and
parasympathetic vasodilatory.

4. Respiratory physiology
a. What are the devices used for oxygen therapy? What are the indications of 100%
oxygen?
Devices used for oxygen therapy are:
Low flow or Variable performance devices:
a. Nasal canula: FiO2 range from 0.21 to 0.44 with oxygen flow rate
ranging from 1 to 5-6 L/min. However, the actual FiO2 delivered to the
patient is determined by oxygen flow, nasopharyngeal volume, and the
patients inspiratory flow (depends both on Vt and inspiratory time)
b. Simple mask: with FiO2 ranging from 0.3 to 0.6 at oxygen flow rate 5
to 8 L/min.
c. Mask with reservoir: At flow 5 L/min can deliver FiO2 upto 0.5.
d. Nasal mask
e. Partial rebreathing mask
f. Nonrebreathing mask: with flow upto 15 L/min can provide FiO2 upto
1.0.
Fixed performance or High flow devices:
a. Anesthesia Bag-Mask-Valve system
b. Air entraining venture masks
c. Air entraining nebulizers

Indications of 100% oxygen therapy:

1. Decompression sickness
2. Gas embolism
3. Gas gangrene
4. Carbon monoxide poisoning
5. Cyanide poisoning
6. Treatment of certain wounds
7. Acute Myocardial infarction, acute severe asthma, etc.

b. What are the causes of hypoxemia? What is the management of hypoxemia?

Causes of hypoxemia:
1. Hypoxic hypoxia:
a. Low Patm/Low FiO2 (<0.21): high altitude, oxygen equipment error
b. Alveolar hypoventilation: COPD, opioid drug overdose
c. Pulmonary diffusion defect: eg. Emphysema, fibrosis
d. Pulmonary V/Q mismatch: asthma, pulmonary emboli
e. RL shunt: atelectasis, cyanotic congenital heart disease
2. Circulatory hypoxia:
 a. Reduced cardiac output: severe heart failure, dehydration
b. Microvascular dysfunction: sepsis, SIRS
3. Hemic hypoxia:
a. Reduced Hb content: anemias
b. Reduced Hb function: carboxyhemoglobinemia, methemoglobinemia
4. Demand hypoxia: fever seizures
5. Histotoxic hypoxia: cyanide toxicity, late sepsis, etc.

c. What are the toxicities of oxygen therapy?

Toxicities of oxygen therapy:
Hypoventilation
Absorption atelectasis
Pulmonary toxicity
Retinopathy of prematurity
Hyberbaric oxygen therapy hazard
Fire hazards

5. Day case surgery

a. What are the patient selection criteria for day care surgery?
Patient factors:
Patient willingness
Easy access to a telephone (24 hours)
Should be living in a convenient distance
A responsible adult should accompany the patient at least for the first 24 hours
Patients home must be compatible with postoperative care.
ASA I and II preferably
Preexisting problem (in case of ASAII patient) should have been stable for the
past 3 months.
Surgical factors:
Type of surgery: should preferable be a minimally invasive surgery with less
effects on patients hemodynamics, less expectation of post-operative nausea
vomiting and no chances of pos-op ongoing bleeding.
Surgical duration: <90 minutes
Less post-op physiologic disturbance and less blood loss
Patient should be able to be mobilized after the surgery
Contraindications to day case surgery:
Potentially life threatening condition (brittle diabetes, unstable angina,
symptomatic asthma)
Morbid obesity complicated by symptomatic cardio-respiratory problems
(angina, asthma)
Multiple chronic active centrally acting drug therapies (eg. MAO inhibitors)
and/or active cocaine use.
Ex-premature infants <60 postconceptual weeks requiring general ET
intubation
No responsible adult to take care of the patient at home on the evening after
surgery.

b. What are the discharge criteria?

Recovery from day case surgery is divided into:
Early recovery: The time interval during which patients emerge from
anesthesia, recovery control of their protective reflexes, and resume early
motor activity. Eg. Aldrete score (OT)
Intermediate recovery: (Recovery room) begin to ambulate, drink fluids, void,
and prepare for discharge.
Late recovery: starts when the patient is discharged home and continues until
when full functional recovery is gained and patient is able to resume normal
activities of daily living.
Discharge criteria include:
mPADSS:
Vital signs
Activity level
Nausea and vomiting
Surgical bleeding
Pain

6. Hypothermia
a. What is hypothermia?
b. What are the adverse effects of hypothermia?

7. A 72 year male under beta-blocker for systemic hypertension is planned for

hemicolectomy?
a. What is your plan of anesthesia and why?
The patient did not regain consciousness till 40 minutes after the surgery is over
b. What is delayed recovery?
c. How do you manage this case?

8. Capnography
a. What is capnography?
b. Capnograph show a reading of 0 after intubation. What may be the possible
causes and how do you manage them?
c. What other information does a capnograph provide?

9. Muscle relaxants
a. What are the properties of an ideal muscle relaxant?
b. How do you classify muscle relaxants?
c. Explain the differences between them.

10. TIVA
a. What is TIVA?
b. What are the benefits of TIVA?

3rd Year Final Assessment 7th Batch Paper II From my memory bank
1. Early recovery after surgery
a. What are the elements of ERAS?
b. What will be your intraoperative management?
c. What are the benefits of ERAS?
2. Sepsis
a. Write down the criteria for SIRS and sepsis.
b. What will be your approach to prevent organ dysfunction?

3. Hyperthyroidism
a. A 25 year male with h/o trauma 3 days back. On traction for fracture of lower limb
planned for surgery. He has fever, tachycardia, and hypertension. On OT, pethidine 50
mg + Phenargan 25 mg given but still hes hypertension, and tachycardia. Hes
sweating and anxious. On examination of the neck, slightly enlarged thyroid is found.
b. What are the possible causes in this case?
c. What additional investigations will you order for this case?
d. What are the features in favor of thyroid storm?

4. AKI
a. What is AKI?
b. What are diagnostic criteria for AKI?
c. What are the risk factors present in this patient?

5. VAE
a. What is paradoxical air embolism?
b. How will you diagnose venous air embolism?
c. What are the preventive measures and how will you treat a case of venous air
embolism?

6. You are asked to place a central venous catheter in a 3 year child in ICU. After one
hour of catheter placement, the child had hypotension and fall in oxygen saturation.
What is the possible cause? Outline your approach to management of this case.

7. A 3 years child is planned for an ophthalmic surgery. He has runny nose and cough
but looks ok otherwise.
a. What will be your approach to preanesthetic assessment?
b. Will you take this case or not? Why?
c. What will be your anesthetic management?

8. A 9 year old child is planned for bilateral tonsillectomy.

a. What will you assess this case in the preoperative period?
b. Intraoperative management?
c. Outline your management of tonsillectomy re-bleeding.

9. Neuropathic pain.
a. What is neuropathic pain? Give examples
b. What are the signs and symptoms of neuropathic pain?
c. What is the pharmacological management of neuropathic pain?

10. A 25 years full term pregnant parturient has non-progress of labor and is kept on
oxytocin infusion. She complains of acute severe tearing abdominal pain which
subsided after some time. But she developed PV bleeding. Her BP 80/40 mmHg;
Pulse 130/min.
a. What is the diagnosis?
b. How will you prepare this case?
c. Anesthetic management?

Other questions:
1. Criteria for home discharge after day care surgery.
2. List strategies for postoperative pain management in day care surgery.
Multiple factors, including the type of surgery, pain threshold, patient age, and
expectations, affect the experience of postoperative pain
Patients with high anxiety, chronic pain and opioid tolerance experience
difficult postoperative pain control and should be identified early.
Postoperative pain management in day care surgery should begin before the
patient goes for surgery.
Patient should be provided with information about the likely extent and
duration of pain after surgery.
Should be advised about simple measures to reduce pain like maintaining
comfortable position, raising the swollen limbs, and benefits of distraction
technique.
Prevention is the mainstay of management of pain.

For pharmacological therapy:

Multimodal analgesia is the preferred one which relies on the additive and
synergistic effects of different modalities at different location along pain
pathways.
Includes:
LA wound infiltrations and regional anesthesia technique, routine use
of NSAIDs.

PCM:
Oral paracetamol displays peak plasma concentration within 3060 min; i.v.
paracetamol instantaneously with onset of pain relief after 510 min.

NSAIDs:
Have opioid sparing effect.

Opioids:
Intraoperative administration of short-acting opioids remains the mainstay of
treatment (to reduce the incidence of PONV)

Other analgesia:
NMDA receptor antagonists and alpha 2 agonists: have opioid dose reduction effect as
part of balanced multimodal analgesia; esp the use of gabapentin.

Neuraxial block and regional anesthesia:

Properly planned and executed regional anesthesia provides a good means of post-
operative pain control after day care surgery.

3. Differentiating points between depolarizing and non-depolarizing agents.

 Depolarizing
Non-competitive antagonism
Also called phase I block
Block is preceded by fasciculations
Drugs are also called leptocurare
Neostigmine addition: potentiation of
blockade
Effect of other NM blockers:
decreased effect
Serum potassium levels: rise in levels
Cardiac M2 receptor: stimulation
Response to tetanic stimulation: no
fade
Post tetanic facilitation: no
Rate of recovery: variable depending
upon drugs
Non-depolarizing
Competitive antagonism
No fasciculations
Drugs are also called pachycurare
Neostigmine addition: antagonism of
blockade
Effect of other NM blockers:
increased effect
No change in potassium levels
No stimulation of such receptors.
Response to tetanic stimulation: fade
Post tetanic facilitation: present
Rate of recovery: 3-8 min

4. Enumerate the side effects of succinylcholine

The side effects of succinylcholine are:
a. Cardiovascular:
i. Bradycardia: particularly in children and with repeated doses in
adults.
ii. Negative ionotropic effect
b. Fasciculations
c. Hyperkalemia
d. Muscle pain
e. Rise in Intraocular pressure
f. Masseter muscle rigidity
g. Malignant hyperthermia
h. Intracranial pressure
i. Histamine release

5. What are the hazards of patient being placed in lithotomy position?

a. CVS effects:
i. While placing in lithotomy position: autotransfusion from legs
thus increasing preload to the heart.
ii. Minimal changes unless IVC is compressed.
iii. On removing from stirrup: reperfusion of blood in the legs
hypotension.

b. Respiratory effects: Decr. FRC, decr. VT and lung compliance

Hazard: supine hypotension syndrome,
increased likelihood of aspiration,
patients of heart failure may not tolerate autotransfusion.

c. Nerve injuries in lithotomy position:

i. Femoral nerve: angulation of thigh and stretching of the
inguinal ligament and compression of the nerve
ii. Obturator nerve: greater degree of thigh flexion, stretching of
nerve as it exits the obturator foramen.
 iii. Saphenous nerve: medial condyle of tibia
iv. Common peroneal nerve: pressure on the head of fibula
Complications:
Compartment syndrome in lower limbs during lithotomy position
1. Long duration of lithotomy
2. Tightening of leg straps
3. Dorsiflexion of the ankle
4. Surgeon leaning on suspended leg for long duration
Upper limb injury in lithotomy position:
1. Compartment syndrome of upper limb by tucking of hand under
OT table or buttocks
2. Extension of upper limb >90 deg causes traction of brachial plexus.

Hazards of tilting the bed to Trendelenburg position:

1. Respiratory system:
a. Decr. lung compliance and decr. FRC
b. Increased work of breathing in spontaneous ventilation and airway
pressures higher during mechanical ventilation
c. Increased V/Q mismatch and atelectasis
d. Engorgement of mediastinal vessels: increased left atrial pressures
risk of pulmonary edema
2. CVS:
a. Increased venous return increased CO transiently
b. Increased CVP and JVP
c. Reflex decrease in HR, CO and SVR
3. CNS:
a. Incr. CVP and ICP decr. CPP
4. Others:
a. Incr IOP and increased likelihood of passive regurgitation.

Complications of Trendelenburg position:

1. Slipping of patient on OT table
2. Brachial plexus injury by certain devices
3. Raised ICP, IOP and decreased CPP
4. Barotrauma and respiratory fatigue
5. Increased incidence of atelectasis
6. ETT displacement: endo-bronchial
7. Increased risk of passive regurgitation.

What solutions are available for restoration of circulating volume in patient

suffering from acute blood loss.
Ans: Various solutions are available for restoration of volume in acute blood loss.
Principally:
1. Isotonic crystalloids
2. Hypertonic saline
3. Synthetic colloids (6% hetastarch, Dextran40/70, 10% pentastarch)
4. Blood and blood products
Crystalloids:
Are aqueous solutions of ions (salts) with or without glucose.
 These solutions distribute between intracellular and extracellular fluid
compartments.
These are usually considered as the initial resuscitation fluid in patients with
hemorrhagic and septic shock, burn patients, etc.
Isotonic electrolyte solutions are replacement type solutions whereas
hypotonic solutions are maintenance type solutions.
Glucose is added to the solution to maintain tonicity or prevent ketosis and
hypoglycemia.

Differences between colloid and crystalloid solutions:

Crystalloids Colloids
Are aqueous solutions of LMW ions with Are aqueous solutions of HMW
or without glucose substances similar to plasma proteins
Readily pass through the semi permeable Molecular size is large and do not easily
membrane thus extra-vascular cross the semi-permeable membrane thus
expanders are intravascular volume expanders
Intravascular half life: 20-30 mins IV half life is: 2-8 hours
Reduce plasma colloid oncotic pressure Maintain plasma colloid oncotic pressure
Have poor capillary perfusion Have good capillary perfusion
Complications associated with large No such risk
volume administration during
resuscitation:
Tissue/pulmonary edema, hypothermia,
hemodilution, risk of rebleeding, longer
time to resuscitate
No anaphylactic reactions Anaphylactic reactions
No issues of induction of coagulopathy Chances of inducing coagulopathy
Inexpensive Expensive
Readily available, easy to store and well Not so
tolerated by patients- advantages

Colloids:
Are either derived from
1. Plasma proteins: eg. Albumin 5% and 25%; plasma protein fractions 5% (both are
heated to 60 deg Celsius to decrease the transmission of hepatitis and other infections)
2. Synthetic glucose polymers:
Dextrose starches: (Dextran 40 and Dextran 70), have anti-platelet actions;
infusion >20 ml/kg/day can interfere with blood typing, prolong bleeding times and
are associated with kidney failure; can be antigenic as well.
Hetastarch (HES): multiple formulations based on concentration, molecular
weight, degree of starch substitution, and ration of hydroxylation between C2 to C6
positions. It is non antigenic. Coagulation studies and bleeding times are not
significantly altered.
Gelatins: associated with histamine mediated allergic reactions

Q. Relate the clinical use of STP and Propofol to their pharmacological

properties.
Ans:
Uses of STP:
 1. Induction of anesthesia: 3-5 mg/kg IV, d/t property of rapidity of induction
and short duration of action in case of a bolus dose
2. Anticonvulsant: blockade of the synaptic action of excitatory
neurotransmitters eg. Glutamate, adenosine, etc.
3. Barbiturate coma (in cases of massive brain swelling): because of long
context sensitive half time
4. To decrease ICP: because of the drugs effect of cerebral vasoconstriction,
decreasing the CMRO2 (by the facilitation of inhibitory NT GABA) and
by maintenance of flow-metabolism coupling in the brain.
5. An a neuroprotective agent: because of its action at NMDA receptor (via
NT glutamate)

Uses of Propofol:
1. Induction of anesthesia
2. Maintenance of anesthesia: Because of small context sensitive half time;
10 minutes when infused for less than 3 hours and 40 minutes when
infused upto 8 hours of infusion.
3. Antiemetic
4. Antipruritic
5. Treatment of laryngospasm
6. Anticonvulsant property

Q. Write 5 major functions of liver.

Ans: The major functions of liver are:
1. Synthetic function: Liver synthesizes plasma proteins (albumin, globulins),
clotting factors, etc.
2. Storage of glycogen, vitamins and minerals
3. Bile production and excretion
4. Metabolism of fats, proteins and carbohydrates and drugs

Q. Write down the blood and oxygen supply to the liver.

Ans: The liver receives blood supply from two sources: and receives around 25% of
CO
1. Hepatic artery (25-30%): which is a branch of celiac artery; blood flow is
around 500 ml/min. The oxygen saturation of hepatic artery is 98%. Liver
receives 50% of its oxygen supply from this source.
2. Portal vein (70-75%): Portal vein is formed from venous drainage from
stomach, small and large intestine and receives blood supply from celiac
artery, superior and inferior mesenteric artery. The total blood flow in portal
vein is around 1300 ml/min. Liver receives 50% of its oxygen supply from this
source. The oxygen saturation of portal vein is around 60-70%.

Q. Regulation of blood flow to the liver:

Ans: Regulated by two sets of mechanisms:
a. Intrinsic mechanism:
a. Pressure-flow autorgulation
b. Metabolic control
c. Hepatic artery buffer response
b. Extrinsic Mechanism:
a. Neural control
 b. Hormonal control
c. Effect of anesthesia

Q. Factors which can decrease blood flow to the liver

Ans: The factors which can decrease the blood flow to the liver are:
1. Effect of anesthetic agents like:
a. Halothane (and other inhalational agents to some extent)
b. Intermittent positive pressure ventilation (with PEEP further
accentuating the effect)
c. Central neuraxial blockade: spinal block upto T5 can decrease upto
23%.
2. Hypoxia, hypocapnia, and sympathetic stimulation: by causing
vasoconstriction
3. Surgical procedures near the liver: sympathetic activation, local reflexes, and
direct compression of the vessels in the portal and hepatic circulations.
4. Decrease in blood pressure with disruption of autoregulation.

Q. Define capnography.
Ans: Capnograph is an instrument that displays, in addition to digital data, a
capnogram the graphic representation of CO2 concentration or partial pressure over
time (time capnography) or displayed in terms of volume (volume capnography)
Two types: Mainstream and Sidestream (aspirate gas from the system at 50-
400mL/min)

Mechanism:
CO2 strongly absorbs IR light particularly at wavelength 4.3 micrometer. The IR light
absorbed is proportional to the concentration of the absorbing molecules, such as
CO2, such that concentration of the molecule can be determined by comparing the
measured absorbance against a known standard.

Q. In a capnograph if the inspiratory baseline is elevated (not 0) CO2 is being

rebreathed. What are the possible causes?
Ans: Incompetent expiratory valve, exhausted soda lime, gas channeling through the
absorbent and imperfectly calibrated capnometer.

Q. Draw a labelled diagram of a normal capnogram trace:

Ans:

Q. Why is capnography useful during general anesthesia

Ans: Capnography is useful during capnography to assess the following things.
1. To confirm the proper placement or misplacement of an endotracheal tube.
2. Real time monitoring of patients ventilator status and pulmonary perfusion
status of the patient.
 3. Volume capnography can also be used for measuring dead space and alveolar
ventilation as well as for assessing V/Q matching.
4. To immediately identify disconnections in the system.
5. To see for intraoperative complications like bronchospasm, pulmonary
embolism, respiratory depression, venous air embolism etc.
6. As a guide to look for rebreathing (by looking at the inspired CO2)

Q. What is 2,3 DPG? How is it produced in the RBC? List the causes that
increase the production of 2,3 DPG?
Ans: 2,3 DPG is a special intermediate of glycolysis especially in RBC which is
rapidly consumed under conditions of normal oxygen tension. But, when hypoxia is
present in peripheral tissues, 2,3 DPG can accumulate to a significant levels within
hours. At these concentrations, it binds to Hb and decreases the affinity of Hb to
oxygen molecules. There is rightward shift of the oxygen-Hb dissociation curve
which implies that the affinity of Hb to oxygen is reduced, thus there is increased
unloading of oxygen to tissues exposed to hypoxic condition.

Mechanism of production:
Glucose--- (Hexokinase) Glucose-6-phosphate(Phosphogluco isomerase)
Fructose 6-phosphate 2,3 DPG

Cause that increase the 2,3 DPG are:

1. Hyperthyroidism
2. Chronic anemia
3. Chronic respiratory disease with hypoxia

Q. Describe Boyles machine regarding

a. Gas cylinder: consists of the following components

1. Body:
Medical gas cylinders are storage devices made principally of steel along with other
alloys like molybdenum and aluminium (MRI compatible) and carbon fibers.
These have flat or concave base with tapered screw that attaches to a valve.
2. Valve:
Cylinders are filled and discharged through a valve attached to the neck of the
cylinder. Valves are made of bronze or brass. Parts of valve include: 1. Port: this is the
point of exit for the gas from the cylinder. 2. Stem: is rotated during opening and
closing of the valve.
3. Pressure relief valve:
Every cylinder is fitted with a pressure relief valve whose purpose is to vent the
cylinders contents to the atmosphere if enclosed gas increase to dangerous level
commonly of ruptured disc or fusible plug type.

Medical gas cylinders are available in different sizes and capacities named E, H, D.
The gases are stored in either gaseous form (oxygen, air, N2) at pressures ranging
from 1800-2000 psig or in liquid form (N2O) at pressure of 760 psig.

B. Yoke assembly:
Yoke assembly is a device that provides attachment of gas cylinders to anesthesia
machine maintaining a unidirectional flow of gases from cylinder to machine and
provides adequate sealing to prevent leakage. The assembly is indexed and each one
is specific to a cylinder of a particular gas preventing accidental connection of a
wrong gas cylinder. It consists of the following parts:
1. Body: Principle framework and supporting structure.
2. Screw: tighten cylinder in the yoke
3. Nipple: Through which gas enter the machine
4. Index pin: prevent attaching of a wrong cylinder. The index pin for different
gases are: oxygen (2,5), N2O (3,5), CO2 (1,6), Air (1,5), Heliox (2,4)
5. Washer: make seal between cylinder and the yoke
6. Filter: removes the particulate mater
7. Check valve assembly: for unidirectional flow of gases.

c. Pressure Gauge:
Cylinder pressure is usually measured by Bourdons pressure gauge which is a
flexible tube which straightens when exposed to a gas pressure causing a gear
mechanism to a move a needle pointer.
The pointer reads zero when the cylinder is empty, the cylinder is turned off and when
all the gas has been removed from the machine.

Q. What is FRC? How do you measure FRC? What are the factors that affect
FRC? What is the implication of FRC in general anesthesia and central
neuraxial blockade?
Ans: FRC is the amount of air that remains in the lungs at the end of normal
exhalation. At this volume the inward elastic recoil of the lung matches with the
outward elastic recoil of the chest (including the resting diaphragmatic tone)

FRC can be measured by the following techniques:

1. Nitrogen washout technique
2. Helium washin technique
3. Body plethysmography technique

The various factors which affect FRC are as follows:

1. Body habitus: FRC increases with increase in height whereas obesity
markedly decreases FRC as a result of change in chest wall compliance.
2. Gender: FRC is almost 10% less in females as compared to males.
3. Posture: FRC decreases as patient moves from upright to supine or prone
posture. There is reduced chest wall compliance as the abdominal contents
push up against the diaphragm.
4. Lung disease: Decrease compliance of the lung, chest or both is characteristic
of restrictive pulmonary disorders which decrease FRC.
5. Diaphragmatic tone: This normally contributes to FRC.

Implications of FRC in general anesthesia:

When a patient is kept in supine position for general anesthesia, there is already a
decrease in FRC by upto 1L. Further reduction of FRC occurs when the anesthesia is
induced (upto 0.5L) and there is loss of tone of the inspiratory muscle (causing
alveolar collapse and compression atelectasis), change in chest wall rigidity, and
upward shift of the diaphragm.
Steep head down position may further reduce the FRC as intrathoracic blood volume
increases.
Implications of FRC under central neuraxial anesthesia:
Unless patient is induced after neuraxial anesthesia FRC is not significantly altered in
patients under central neuraxial blockade. Vital capacity and ability to cough and clear
out secretions is however, diminished.

Q. What is GFR? What is normal GFR and how is urine formed?

Ans:
GFR is the volume of fluid filtered from the glomerular capillaries into the Bowmans
capsule per unit time. It is normally about 20% of the RPF. It is ideally estimated by
clearance of inulin (which is only filtered neither reabsorbed or secreted). However,
calculation of GFR based on clearance of creatinine is a more practical approach of
measuring GFR (though it overestimates it).
Tone of the afferent arteriole is mainly responsible for maintaining a relatively
constant GFR over a wide range of blood pressure.
Ratio of GFR to RPF is filtration fraction and it is 20% normally.

Normal GFR is 120 +/- 25 ml/min in men and 90 +/- 20 ml in women.

Q. Enumerate the contraindications and complications of STP.

Ans:
The contraindications to the use of STP are:
1. Known/documented allergic reaction to STP.
2. Septic/cardiogenic/hemorrhagic shock
3. Severe hypovolemic patient
4. Hypereosinophilia patient
5. Restrictive or dilated cardiomyopathy
6. Pericardial tamponade
7. Variegate porphyria
8. Acute intermittent porphyria

The complications of STP use are:

1. Cardiovascular system:
a. Decrease BP: CVS depression and peripheral vasodilation
2. Respiratory system:
a. Double apnea: decrease ventilator responses to hypercapnia and
hypoxia, decreased tidal volume and RR during awakening
3. CNS: Antanalgesic effect
4. Renal: Reduction in RBF and GFR
5. Immunological: Anaphylactic reaction due to histamine release from
degranulation of mast cell and basophils.
6. Other side effects: garlic or onion taste, local tissue irritation, tissue necrosis,
etc.
7. Serious reaction due to Intraarterial injection accidentally.

Treatment of Accidental intraarterial injection:

a. Stop the injection but leave the needle in the artery.
b. Dilute with infusion of NS
c. Vasodilate by:
i. Arterial injection of Lidocaine (5 ml 1%)
 ii. Brachial plexus block or stellate ganglion block
iii. Papaverine (40-80 mg in 20 ml saline)
iv. Anticoagulation with Heparin (1000U)

Q. Risk factors for PONV. Management of PONV.

Ans:
The risk factors for PONV are:
Female gender-1 (single most important independent risk factor)
Nonsmoker-1 (because smokers are desensitized to nausea; Nicotine actually
stimulates the release of dopamine in the brain via action at GABA sudden
stoppage of nicotine in the perioperative period, there is less dopamine less action
of dopamine to stimulate the vomiting center in the brain and thus less vomiting)
Postoperative opioid use-1
History of PONV-1

Risks of PONV is: 10% with no risk factors, 20%, 40%, 60%, and 80% with 1, 2, 3,
and 4 risk factors.

Post discharge nausea and vomiting (PDNV) risk factors:

Female gender: 1
Age <50 years: 1
History of PONV: 1
Use of opioids in the PACU: 1
Nausea in the PACU: 1

Risks of PDNV is: 10% with no risk factors, 20%, 30%, 50%, 60% and 80% with 1,
2, 3, 4, and 5 risk factors.

POV in children risk factors:

Children <3 years of age
Duration of surgery >30 min
Strabismus surgery
History of POV in sibling, parents or self

Strategies for control of PONV:

1. Prophylactic antiemetic therapy:
a. Antiemetic drugs
b. Perioperative pain control: LA, regional anesthesia, non-opioid
c. Balanced general anesthesia
2. Strategies to reduce baseline risk
a. Avoidance of general anesthesia and preference of regional anesthesia
(9X decrease risk)
b. Use of propofol for induction and maintenance
c. Avoidanc of nitrous oxide
d. Avoidance of volatile anesthetics (if possible)
e. Minimization of intraoperative and postoperative opioid use
f. Adequate hydration.
3. Antiemetic therapy:
a. Dopamine antagonist
 i. Metoclopramide- possess antidopaminergic, antiserotoninergic,
and prokinetic function; dose: 0.15 mg/kg,
ii. Droperidol: highly active antiemetic- MAO and D2 antagonist;
dose 0.625 -1.25 mg, S/E: anxiety, akathisia, restless, dystonia,
severe arrhythmias-torsade de pointes, prolongation of QT)
iii. Others: Prochlorperazine
b. Histamine antagonist
i. Dimenhydrinate: H1 receptor antagonism; weak anticholinergic
activity; 1 mg/kg S/E: drowsiness, dry mouth, urinary retention,
etc.
c. Anticholinergics
i. Scopolamine: centrally acting anticholinergic; prevents motion
induced nausea and vomiting. S/E: anticholinergic side effects.
d. Serotonin antagonists
i. Onansetron: Centrally acting antiemetic; milestone for
chemotherapy induced nausea and vomiting; short half life (so
given at end of surgery); dose: 0.1 mg/kg children (adults: 4
mg) S/E: QTc prolongation by 10-17 msec, abnormal LFTs,
headache and constipation.
e. Dexamethasone
i. Centrally inhibits nucleus tractus solitarius; slow onset so given
at the beginning; efficacy similar to ondansetron.
f. Neurokinin antagonists
i. Mechanism: Substance P binds to NK1 receptors located in
vagal afferents of GIT and CNS (NTS, area postrema) which is
responsible for vomiting
ii. Drugs: Aprepitant (40 mg), casopitant, Rolapitant
iii. Start 3-4 hrs before surgery

Q. What are the basic and advanced airway management in ACLS?

What are the reversible causes of cardiac arrest? How do you manage them?
Q. What is A-a gradient? Why do we need to know about A-a gradient? Factors
affecting A-a gradient.
Ans: A-a gradient is a measure of the difference between alveolar concentration of
oxygen and arterial concentration of oxygen. It is useful in diagnosing the source of
hypoxemia.
It is also helpful in the assessment of integrity of alveolar capillary unit. For example,
in high altitude, PaO2 is low only because PAO2 is also low and A-a gradient is
essentially normal (5-15 mm Hg). However, in cases like V/Q mismatch, there is
discrepancy between PAO2 and PaO2 signifying the non-integrity of alveolar-
capillary interface.
A-a gradient is: PAO2-PaO2

An abnormality in A-a gradient arises because of the following factors:

1. Defect in diffusion
2. V/Q mismatch
3. Right to left shunting

Q. Anesthetic concerns in patients for Strabismus surgery.

Ans.
1. Preoperative visit: Patients may have associated congenital anomalies along
with strabismus problem which may pose difficulties during airway
management and use of muscle relaxants. Common congenital syndromes are
Aperts syndrome, Cri du chat syndrome, Downs syndrome, etc.
2. Forced duction testing: If requested for this test, use of muscle relaxants
should be tailored. The use of Succinylcholine which results in sustained
contraction of the EOM for upto 20 minutes may alter the results, thus
avoided.
3. Oculocardiac and Oculorespiratory reflexes: These reflexes happen by the
same afferent innvervation of ophthalmic division of Trigeminal nerve and
efferent response by Vagus nerve or Phrenic nerve respectively in OCR and
ORR. Anticipation, identification and immediate intervention (including
asking the surgeon to hold the stimulation) are necessary thus close vigilance
is required.
4. Suspicion of Malignant hyperthermia: Strabismus surgery is supposedly
associated with increased incidence of malignant hyperthermia though the
documents supporting are very scant. However, this risk is to be taken into
mind and a close observation is required throughout the procedure.
5. Increased incidence of PONV: strabismus surgery is by far one of the most
important risk factor in children for PONV. Thus according to the other risks
involved, use of anti emetics should be done along with avoidance of other
emetogenic drugs like opioids in the perioperative period.

Q. Orthostatic hypotension. Causes and Management.

Ans:
Causes:
1. Neurogenic: Diabetes mellitus, autonomic neuropathies, Parkinsons disease,
2. Non-neurogenic cause: Cardiac impairment (from MI or AS), reduced IV
volume (dehydration, hemorrhage, adrenal insufficiency), vasodilation (fever,
systemic mastocytosis), drugs (diuretics, alpha blockers, beta blockers, insulin,
TCA, etc)
Treatment:
A: Abdominal compression (compression of venous capacitance vessels in legs and
splanchnic vessels (20-30% of blood volume) in the abdomen.
B: boluses of water (upto 500 ml bolus at a time)
B: Bed up (keeping at 30 degree head up)
C: Counter maneuvers (isometric contraction of muscles below the waist for upto 30
seconds at a time increases peripheral resistance, reduces venous capacitance and
augments venous return to heart.
D: Drugs: eg. Midodrine- a vasopressor, Fludrocortisone- mineralocorticoid,
Pyridostigmine
E: Education
E: Exercise
F: Fluid and salt expanders

Q. Features of autonomic dysfunction.

Ans:
1. Hypertension
2. Painless MI
3. Orthostatic hypotension
4. Lack of heart rate variability
5. Reduced heart rate response to Atropine and Propranolol
6. Neurogenic bladder
7. Early satiety
8. Impotence
9. Resting tachycardia
10. Lack of sweating

Q. Landmarks for:
1. Supraclavicular Brachial Plexus Block:
Place the patient in a supine position with the head turned toward the non-
operative side.
Palpate the posterior border of the sternocleido - mastoid muscle at the C6
level and roll your fingers laterally over the anterior scalene muscle until they
lie in the interscalene groove (the groove may be harder to identify below the
C6 level because of the overlying omohyoid muscle).
Then move your fingers laterally down the interscalene groove until they are
approximately one centimeter from the mid-clavicle.
This location is the initial insertion site for the needle.
Standing at the patients head, direct the needle toward the axilla, as
demonstrated.


2. Interscalene Approach:
Place the patient supine with the head turned toward the nonoperative side.
Identify the cricoid cartilage, which indicates the C6 level.
Palpate the lateral border of the sternocleidomastoid muscle (SCM), and move
your fingers laterally into the interscalene groove (between the anterior and
middle scalene muscles).
Ensure that the clavicular head of the SCM, rather than the more medial
sternal head, is being palpated.
The external jugular vein often crosses the border of the SCM muscle at this
point.
If this is the case, the initial needle insertion should be posterior to the vessel
Initial needle insertion (at the level of C6) is indicated by an X.
Q. What is statistical error?
Ans: Statistical error is defined as the discrepancy or uncontrolled variation between
an observed (or measured) value and the value predicted by a specification, standard
or model.

Q. What is p value?
Ans: The P value, or calculated probability, is the probability of finding the observed,
or more extreme, results when the null hypothesis (H 0) of a study question is true
the definition of 'extreme' depends on how the hypothesis is being tested.

Q. Components of RSI
Ans:
1. Preparation for expected intubation and also for the potential complication of a
difficult or failed intubation.
a. Environment: resuscitation room, monitoring, IV access, position on
trolley, drugs- drawn up, labelled, ready.
 b. Equipment: two functioning laryngoscopes fitted with appropriate
blade, ET tube- including one size smaller.
2. Preoxygenation
3. Pretreatment: with lidocaine, atropine or opioids, fluid bolus
4. Paralysis with induction: STP 5 mg/kg, Sux 1.5 mg/kg
5. Protection and positioning
6. Placement with proof
7. Post-intubation management

Q. Conditions requiring RSI are.

Ans:
1. Patients with full stomach with <8 hrs of fasting
2. Patients with unknown time since last oral intake
3. Morbid obesity: gastroparesis, incr. IAP
4. Severe GERD
5. Intra-abdominal processes: abscess, obstruction, bleeding etc.
6. Trauma:
a. NPO status unknown
b. Patients may be unable to protect their airway because of depressed
status
c. Delayed gastric emptying
7. Pregnancy: delayed gastric emptying, more acidic gastric contents, incr. IAP
8. Decreased gag reflex or depressed mental status
9. Gastric outlet obstruction: eg. Pyloric stenosis, Ca stomach/bowel, etc.

Contraindications to RSI:
1. Difficult airway
2. Contraindications to Sux
3. Cervical spine injury (do awake fiberoptic intubation)

Q. Local anesthetics. Factors determining- a) Potency b) Onset c) Duration of

action
Ans.
1. Determinants of potency
a. Hydrophobicity
b. Vasodilator vs vasoconstrictor properties
c. Charge
2. Determinants of onset
a. Related to physicochemical properties of individual drugs
b. Dose: higher the dose, faster the onset
c. Concentration: higher the concentration faster the onset
d. pKa (ionization): higher the uncharged fraction faster the onset
e. site of injection: longest latency and duration observed with BPB
3. Determinants of duration
a. Peripheral vascular effects of LA: vasodilation vs vasoconstriction
b. Dose
c. Protein binding major determinant

Q. Factors determining the delivery of oxygen to tissues are

1. FiO2
2. V/Q ratio
3. Alveolar wall thickness and pulmonary circulation
4. Cardiac output
5. Hb concentration and its saturation
6. Tissue perfusion pressure
7. Partial pressure of arterial oxygen
8. Integrity of central and peripheral circulation

Q. Preanesthetic concerns in a case of Mitral Stenosis

Ans.
Preanesthetic concerns in a case of MS
1. Assessment of the severity of MS
2. Assessing the degree of decompensation: History, physical examination, CXR,
Echo: valve area, PG, atrial clot, pulmonary HTN, IE
3. Medications and S/E
4. Effect on other organ systems: Respiratory, hepatic, renal and thromboembolic
complications.

Advice with reassurance

- Low dose BZD hypoventilation hypercarbia increase PAP

Intra-operative goals and measures to achieve them:

1. Sinus rhythm: maintain if present pre-operatively but these patients are usually
in AF in which case ventricular rate control should be the goal.
2. HR:
a. maintain between 60-80 bpm
b. use beta-blocker or digoxin if needed
c. cardioversion may be necessary
3. Preload:
a. Keep on the upper limit of normal value.
b. Go on preloading until there is no backflow, CVP 10-12 cm H2O
4. Afterload: Maintain afterload, if low coronary circulation will be
compromised; use vasopressors if needed
5. Contractility: usually not a problem
6. PVR: do not allow to increase in PVR, avoid hypoxia, hypercarbia, acidosis.

Q. Factors for prediction for perioperative pulmonary complications.

Ans:
a. Patient related factors
i. Age >50
ii. Patient with known h/o COPD
iii. Smoking within 8 weeks of surgery
iv. CCF
v. Physical dependence
vi. ASA PS >2
vii. OSA
viii. Pulmonary hypertension
ix. Preoperative albumin <3 g/dl
b. Procedure related factors
i. Prolonged surgery
 ii. Residual NMB agents effects
iii. Upper abdominal and thoracic surgery
iv. Neurosurgery, head and neck surgery
v. Emergency surgery
vi. Vascular surgery esp. aortic aneurysm repair

Roizens classification of dyspnea

Grade 0: No dyspnea while walking on level at normal pace
Grade 1: I am able to walk as far as I like, provided I take my time
Grade 2: Specific street block limitation eg. I have to stop after one or two blocks
Grade 3: dyspnea on mild exertion eg. Going from one room to the other
Grade 4: dyspnea at rest

Should also be supported (if possible) by formal assessment of exercise tolerance eg.
Stair climbing or 6MWT (Where CPET is unavailable, a 6min walk test distance of
>563m indicates an anaerobic threshold of >11mL/kg/min)

Whom to order for spirometry?

1. Those with dyspnea or exercise intolerance that remains unexplained after
clinical evaluation. The D/Ds may include cardiac diseases.
2. In patients with COPD or asthma if the clinical evaluation cannot determine if
the patient is at their best baseline and that airflow obstruction is optimally
reduced. In this case, spirometry will identify patient who will benefit from
more aggressive preoperative management.
3. Patients in whom functional ability cannot be determined because of lower
extremity disability.
4. As a part of assessment of patients for lung parenchymal resection.

Role of flow-volume loops.

1. Provide more accurate information regarding ventilator function.
2. Provide information about severity of restrictive and obstructive pulmonary
diseases.
3. Used in the assessment of airway obstruction from both extrinsic and intrinsic
causes.

DLCO and its role

Measurement:
- Measures diffusion of CO into the lung
- Single breath of gas containing 0.3% CO and 10% helium held for 20s.

Importance:
1. Restrictive lung disease: differentiate between intrinsic lung disease vs other
causes of restriction (eg. Chest problems)
2. Obstructive lung disease: differentiate between emphysema and other causes
of obstructive airway.
3. Normal value is 17-25 ml/min/mm Hg.

Who should be subjected to preoperative ABG?

1. For any patient breathless on minimal exertion.
 a. Why: detects CO2 retention. (a value >45 mm Hg at rest is predictive
or post operative pulmonary complications and suggests ventilator
failure)
b. To see for usual level of oxygenation and set a realistic goal of
parameter for the post operative management.

Who should be receiving pre-operative CXR?

1. Insufficient evidence to support which groups of patient will benefit from pre-
op CXR.
2. It is reasonable to obtain CXR in patient with known cardiopulmonary
disease: to reveal lung pathology, cardiac size and outline, and as a baseline
should postoperative problem arise.
3. Those patients >50 years of age undergoing high risk surgical procedures
including upper abdominal, aortic, esophageal and thoracic surgery.

Indications for CT Thorax.

1. In patients with lung cysts or bullae to accurate estimate the size and extent of
the disease.
2. Impingement of mass lesions on major airway and likely extent of the lung
resection.
3. Interstitial lung disease, anterior or posterior pneumothorax- not easily seen on
CXR.
4. Spiral CT can detect PE and dissecting aortic lesions.

V/Q scan.
1. Reports the likelihood of PE.
2. Useful in the assessment of patients for lung parenchymal resection to predict
the effect of resection on overall pulmonary performance (like improvement of
lung function after resection of non-ventilated/perfused lung segment)

Pulmonary risk indices.

1. Arozullah Risk Index: predicts post-operative respiratory failure
a. Procedure related risk factors: type of surgery, emergency surgery
b. Patient related risk factors: COPD, albumin <3 g/dl, BUN >30 mg/dl,
dependent functional status and advanced age (60-69 and >70 yrs)
2. Casnet Risk Index: predicts post-operative pulmonary complications
a. Seven factors to classify risk into low, intermediate and high risk
b. Procedure related: upper abdominal or thoracic surgery, surgery > 2hrs,
emergency surgery
c. Patient related factors: low preop saturation, respiratory infection
within the past 1 month, preoperative anemia

Strategies for reducing post-operative pulmonary complications

Pre-operatively:
1. Smoking cessation as early as possible- at least for 8 weeks
2. Regular ipratropium bromide or tiotropium bromide for patient with clinically
significant COPD
3. Inhaled beta agonists as required for patients with COPD who have wheeze or
dyspnea
 4. Pre-op glucocorticoids for patients with COPD or asthma who are not
optimized and whose airway obstruction has not been fully reversed.
5. Delay elective surgery in patients with RTI.
6. Antibiotics for patients with LRTI.
7. Preoperative inspiratory muscle training and chest physiotherapy.
Intra-operatively:
1. Choose alternative procedure lasting < 4 hrs.
2. Surgery other than upper abdominal or thoracic whenever possible.
3. Regional anesthesia- if that is an option.
4. Avoidance of long acting muscle relaxant in very high risk patient.
5. Choosing laparoscopic rather than open surgery, if feasible.
6. Lung protective ventilation strategies:
a. Vt: 6-8 ml/kg of IBW
b. PEEP: 6-8 cm H2O
c. Recruitment maneuvers every 30 mins.
Post-operatively:
1. If possible, aim for upright posture
2. Early mobilization- to reduce risk of the VTE
3. Early post-op chest physiotherapy- including incentive spirometry, breathing
exercise
4. Administer supplemental oxygen for upto 72 hours post-operatively
particularly if the patient is receiving opioids. Anesthetic agent exert a dose
dependent depression of central chemoreceptors particularly to CO2 and this
can last for up to 72 hours.
5. Consideration should be given to patient with COPD who are more dependent
on hypoxemic drive for ventilation- use of fixed performance oxygen delivery
device such as venture mask helps.
6. Humidification of oxygen helps in physiotherapy and sputum clearance.
7. Accurate management and documentation of fluid balance.
8. Good analgesia for the maintenance of efficient respiratory function,
compliance with physiotherapy, early mobilization, etc.

Respiratory problem patients requiring post-operative ICU

1. Electively
a. Borderline or established respiratory failure of gas exchange pre-
operatively.
b. Intercurrent respiratory infection (for emergency cases)
c. Chest disease productive of large amount of sputum (eg.
Bronchiectasis)
d. Major abdominal or thoracic surgery
e. Long duration of surgery
f. Major surgeries not amenable to regional analgesia and requiring post-
operative opioids.
2. Upredictably
a. Unexpected perioperative complications (hge, fluid overload, etc.)
b. Unexpectedly prolonged procedure.
c. Acidosis
d. Hypothermia
e. Depressed conscious level/slow recovery from anesthesia/poor cough
Q. What precautions should be taken regarding drug transfer in breast milk for
a lactating mother.
Ans:
Drug Comment
Opioids Minimal drug transfer to neonatal serum.
Precautions to be taken regarding
pethidine and codeine if mother or
neonate is excessively drowsy.
NSAIDs Most NSAIDs are safe during breast
feeding. Some caution regarding aspirin
(for fear of Reyes syndrome)
Antibiotics Penicillins and Cephalosporins are safe.
Unsafe agents are:
Tetracycline (although minimal
absorption because of chelation with Ca
in the milk)
Chloramphenicol (avoided for fear of
BMS in case of neonate)
Ciprofloxacin (present in high
concentration in breast milk and should
be avoided)
Antipsychotics Should be avoided
Cardiac drugs Amiodarone is present in breast milk in
significant amount- DISCONTINUE
BREASTFEEDING
Beta blockers: avoid Sotalol and
Celiprolol
ACE inhibitors: Except for Enalapril and
Captopril, other ACE inhibitors, ARBs
and Amlodipine should be avoided
Anticonvulsants Avoid phenobarbital and Diazepam.
Carbamazepine may be considered safe
but close observation for evidence of
neonatal sedation is important.

Q. What is an anesthetic vaporizer?

Vaporizers are special devices which are designed to convert liquid anesthetic agent to
vapor and add a controlled amount of that vapor to the fresh gas flow and to the
breathing system.

Q. Classify vaporizers.
Vaporizers are classified as:
a. Location
a. In circuit/low resistance/Draw over: OMV, EMO
b. Out of circuit/high resistance/plenum vaporizer: TEC, Penlon, Aladdin
b. Specificity
a. Agent specific: TEC, Vapor 19.1, Penlon
b. Agent non specific: Goldman
c. Method of vaporization
a. Flow over: TEC, Penlon, Vapor 19.1, Goldman
 b. Injection: TEC 6, Siemens
c. Bubble through: Copper Kettle
d. Flow over or bubble through: Boyles bottle
d. Temperature compensation:
a. Automatic thermocompensation: TEC- bimetallic strip (bronze,
nickel), Vapor 19.1- metal rod, EMO: ether filled bellows
b. Supplied heat: TEC 6
c. No thermocompensation: Boyles bottle, Goldman
d. Manual compensation: Copper kettle
e. Electronic: Aladdin
e. Concentration calibrated vs measured flow (copper kettle)

Q. What does a low resistance vaporizer mean to you? What are the four advantages
of low resistance vaporizer?
Low resistance vaporizer (eg. EMO, OMV) are in-circuit vaporizer used in draw over
anesthesia.
They have several advantages:
1. Low cost
2. Simple design, compact
3. Agent non specific
4. Not affected by altitude
5. Can be used in mass casualties

Q. Why is Copper used to construct vaporizer?

Ans:
1. Because of high specific heat (quantity of heat required to raise the temp of 1
gm of substance by 1 degree Celsius)
2. Because of high thermal conductivity: to achieve thermostabilization (heat lost
due to vaporization quickly replaced because of high thermal conductivity)

Q. State Bernoullis principle.

Ans: Bernoullis principle states that: For a non-compressible, non-viscous fluid
undergoing laminar flow, the sum of the pressure, kinetic energy, and potential energy
per unit volume remains constant at all points along the line of flow.

Q. Classify anti platelets and its anesthetic implications.

Ans: Antiplatelets are classified based on their mechanism of action.
1. COX inhibitors: eg. Aspirin
a. Directly and irreversibly inhibit COX enzyme in platelets thus
decreasing the activation of platelets and stopping the progression of
formation of clot.
2. Blocking of ADP receptors on platelets: eg. Ticlopidine, Clopidogrel
a. These agents also decrease the activation of platelets.
3. GP IIb/IIIa antagonists: eg. Abciximab, Tirofiban, Eptifibatide
a. These agents by acting on GP receptors halt the aggregation of
platelets by inhibiting cross linking reactions.

Q. Checklist for determining Brain Death.

Ans:
1. Prerequisites (all must be fulfilled)
 a. Coma, irreversible and cause known
b. Neuroimaging explains coma
c. CNS depressant effect of drugs absent
d. No evidence of residual muscle paralysis
e. Absence of severe acid base, electrolyte, endocrine abnormality.
f. Temperature: normothermia or mild hypothermia (core temperature
>36 degree Celsius)
g. SBP >100 mm Hg
h. No spontaneous respiration
2. Examination (all must be checked)
a. Absent pupillary reaction to bright light.
b. Absent corneal reflex
c. Absent oculocephalic reflex (provided integrity of C-spine is present)
d. Absent oculovestibular reflex
e. No facial movement to noxious stimulus at supraorbital ridge or
temporomandibular joint.
f. Absent Gag reflex
g. Absent cough reflex to tracheal suctioning
h. Absent motor response to noxious stimulus at all four limbs (spinally
mediated reflexes are permissible)
3. If all the above conditions are fulfilled, then proceed for Apnea testing.

Q. Define neuropathic pain. Give examples. What are the signs and symptoms of
neuropathic pain? How do you manage neuropathic pain?
Ans.
Neuropathic pain is a very common component of a wide range of pain states, usually
resulting from neural damage, including acute and chronic post-operative pain and
pain secondary to advanced malignancy. It is a complex condition which often has
profound negative physical, psychological, and social impacts.

Common examples include:

a. Peripheral disorders
a. Painful polyneuropathies: diabetic, non-diabetic
b. Post herpetic neuralgia
c. Trigeminal neuralgia
d. Post-surgical post traumatic neuralgia
e. Radiculopathy
f. Complex regional pain syndrome
b. Central disorders
a. Post stroke pain
b. Spinal cord injury
c. Multiple sclerosis

Common symptoms suggestive of neuropathic pain include:

1. Allodynia
2. Hyperalgesia
3. Hypoalgesia
4. Paresthesia
5. Hypoesthesia
6. Dysesthesia
Management:
Principal aim is to improve the patients quality of life by attaining pain relief while
minimizing adverse drugs effects and improving physical function.
The requirement of drug dose to achieve pain relief and similarly occurrence of side
effects varies from individual to individual.
Global assessment should include pain levels, psychological, environmental, and
behavioral factors.

General approach to management:

1. Commence with ONE medicine
a. Consider initiating with Amitriptyline with 10-25 mg at night
titrate every 7 days to a maximum of 150 mg at night
IF UNSUITABLE
b. Gabapentin can be considered initiated at 100-300 mg at night
titrating every 3-7 days according to response from once per day to 3
times/day. Maximum dose is 2400 mg/day.
OR
c. Pregabalin can be considered: Initiated at 75 mg daily, increase twice
daily after 2-3 days to titrate to a maximum 300 mg twice daily.
OR
d. Duloxetine can be considered: initiated at 30 mg daily, increase after
7 days to 60 mg daily. Titrate to a maximum dose 60 mg twice daily
if tolerated.
2. Initiated at a low dose and titrated accordingly
a. Allow adequate time to assess the response for each medicine
(approx. 2-8 weeks with 2 weeks at the maximum tolerated dosage)
b. Be alert to the possibility of adverse effects (for example falls,
urinary retention and cognitive impairment)
3. Monitor closely and reassess regularly
a. Assess for pain and overall improvement, adverse effects, mood,
quality of sleep, etc.
4. Consider changing to another medicine if initial medicine is inadequate
a. Rather than abrupt cessation, ensure dosage tapering when changing
medicines
b. Gradual reduction of dose over 7 days is recommended for
Gabapentin and Pregabalin to avoid anxiety, insomnia, nausea, pain
and sweating. Gradual reduction over at least 2 weeks for duloxetine.
For amitriptyline gradually over 4-7 days to avoid cholinergic
rebound symptoms.
5. Consider adjuvant therapy
a. When a medicine provides partial but inadequate pain relief and is
well tolerated, consider adding a second medicine
b. Introduce at low doses and titrate to a maximum dose required or
adverse effects are problematic
6. Re-evaluate regularly
a. Re-evaluate pain status, physical emotional issues, cognition and co-
ordination regularly
7. Consider Opioids only when:
a. Severe disabling neuropathic pain
 b. Episodic exacerbations of severe neuropathic pain
c. When titrating another medication requiring immediate pain relief is
required.
d. Withdraw opioid treatment if there is not benefit after a trial of 2-4
weeks.

Q. What are the causes of intraoperative wheezing during GA?

Ans.
The following are the causes of intraoperative wheezing during GA.
1. Partial obstruction of the ETT including ETT abutting the carina or
endobronchial intubation
2. Bronchospasm
3. Pulmonary edema
4. Aspiration of gastric contents
5. Anaphylaxis
6. Light plane of anesthesia
7. Pulmonary embolism
8. Tension pneumothorax
9. Foreign body in the tracheobronchial tree

Q. How will you manage a case of intraoperative wheezing in case of asthmatic

patient?
Ans:
The management of intraoperative wheezing in case of asthmatic patient includes:
Q. Comparison of Thoracic epidural, Intercostal blocks, and Intrapleural blocks.
Ans.
Thoracic epidural Intercostal block Intrapleural block
Merits: Merits:
Technically easier to
perform
Less discomfort to the
patient
Flexibility in post-
operative pain control
Demerits:
More extensive
sympathetic blockade
B/L blockade of nerve
fibers
Risk of pneumothorax
Inability to place catheter
in patients with
coagulopathy

Other alternatives to thoracic epidural are:

1. Intercostal block
2. Paravertebral block
3. Intrapleural block
4. Cryo analgesia
5. Lumbar epidural block
6. Intrathecal or epidural narcotics
7. IV narcotics
8. NSAIDs
9. Transcutaneous nerve stimulation
OBSTETRIC NOTES
Pain pathways during labor:
Pain in labor arises from:
1. Contraction of the myometrium against the resistance of the cervix and
perineum.
2. Progressive dilatation of the cervix and LUS.
3. Stretching and compression of pelvic and perineal structures.

Pain during 1st stage of labor:

- Viscreal pain from uterine contractions and cervical dilation.
- Confined to T10-12 during latent phase, T10-L1 during active phase.
- Visceral afferent fibers travel with sympathetic nerves uterine and cervical
plexus hypogastric and aortic plexuss enter the spinal cord with T10-L1
nerve roots.
- Pain initially in lower abdomen lumbosacral area, gluteal area, thighs, etc.
- Nulliparous and h/o dysmenorrhea greater pain.

Pain during 2nd stage of labor:

- Onset of perineal pain signals the beginning of second stage of labor.
- Stretching and compression of the pelvic and perineal structures intensifies
the pain.
- Sensory innervation of the perineum by pudendal nerve (S2-S4) thus pain
involves the T10-S4 dermatomes.

Pain management during labor:

1. Psychological and Non-pharmacological techniques:
- Suppressed by reorganizing ones thoughts.
- Patient education and positive conditioning about the birthing process.
- Techniques like Lamaze (coaching parturient to take deep breath at the
beginning of each contraction f/b rapid, shallow breathing for the duration of
contraction)
- Other techniques: hypnosis, TENS, biofeedback and acupuncture.
2. Parenteral agents:
- Concern of fetal depression limits the use of opioid analgesic and sedatives.
- Problem of using opioids to fetus: prolonged time to sustain respirations, respi
acidosis, loss of beat to beat variability in FHR, decreased fetal movements,
etc.
- Other effects of opioids in mother: respiratory depression, maternal N & V,
delay gastric emptying.
- Doses of opioids (preferably using PCA:
o Meperidine: 10-25 mg IV or 25-50 mg IM. Maxm maternal and fetal
respiratory depression within 10-20 min following IV and 1-3 h
following IM thus administer when delivery not expected for up to 4
hr.
o Fentanyl: 25-100 mcg, has 3 to 10 min analgesic onset. Lower doses
not associated with respiratory depression.
o Morphine: not used
 o Butorphanol: 1-2 mg, Nalbuphine: 10-20 mg: have no respiratory
depression but sedation with repeated doses.
o Ketorolac and NSAIDs not recommended because they suppress
uterine contractions and promote closure of ductus arteriosus.
o Ketamine: low doses 10-15 mg IV. Useful adjuvant to regional
anesthesia or just prior to delivery.
o Inhaled nitrous oxide-oxygen has minimal effect on uterine blood
flow or uterine contractions.
3. Local anesthesia:
- Pudendal nerve block (using special needle Koback or guide Iowa trumpet):
often combined with perineal infiltrations of LA during 2nd stage of labor.
- Paracervical plexus blocks: not used because of high chance of fetal
bradycardia, uteroplacental insufficiency, increased levels of LA in fetal blood
due to close proximity of uterine artery.
4. Regional anesthesia:
- Epidural
- Spinal
- Combined Spinal Epidural
Drugs in regional:
- Opioids alone:
o In patients who cant tolerate functional sympathectomy eg.
Hypovolemia, significant CV diseases such as severe AS, TOF,
Eisenmengers syndrome or pulmonary HTN.
- Intrathecal opioids: in dose of 0.1 -0.5 mg onset is slow (45-60 min) and
dose may not be adequate in all.
- Others: fentanyl, meperidine.
- Hypotension following intrathecal opioids is due to resultant analgesia and
decreased circulating catecholamines levels.
- Epidural opioids:
- Morphine: relatively large dose required >7.5 mg and also it is only effective
in 1st stage of labor thus no recommended.

- LA/LA-opioid mixtures:
o Continuous lumbar epidural analgesia most versatile and commonly
employed technique analgesia for first as well as for subsequent
vaginal delivery/CS if necessary.

Walking epidural:
Very dilute LA mixtures in epidural (0.625%) generally do not produce motor
blockade and may allow some patients to ambulate.
Test dose in epidural:
Should be injected between contractions to help reduce the false positive signs of IV
injection (tachycardia due to painful contraction)

Drug given: after 5 min when signs of IV and intrathecal injection is absent total
10 ml of 0.0625%-0.125% of Bupivacaine or 0.1-0.2% of Ropivacaine combined with
50-100 mcg Fentanyl (in 5 ml increments waiting 1-2 min between doses). OR
alternatively, continuous epidural infusion using 0.0625-0.1% Bupi and 1-5 mcg/ml
Fentanyl at 10 mL/h
OR, a patient controlled epidural analgesia (PCEA).

F/b monitoring with frequent BP for 20-30 min or until the patient is stable.

Possible indications for GA during vaginal delivery

1. Fetal distress during the second stage.
2. Tetanic uterine contractions.
3. Breech extraction.
4. Version and extraction.
5. Manual removal of retained placenta.
6. Replacement of an inverted uterus.

Deaths due to GA are related to airway problems (inability to intubate, inability to

ventilate, or aspiration pneumonia).

Advantage of RA over GA in obstetrics:

1. Less neonatal exposure to potentially depressant drugs.*
2. Less chances of manipulation of airways and related complications.
3. Decreased risk of maternal pulmonary complications.
4. An awake mother at the birth of her child.
5. Option for using regional anesthesia for post op pain relief.
*regardless of the technique neonates delivered more than 3 min after uterine
incision have lower Apgar scores and pH values.

Advantages of GA over RA:

1. Very rapid and reliable onset.
2. Control over airway and ventilation.
3. Greater comfort the parturients who have morbid fears of needles and
surgery.
4. Potentially less hypotension than RA.
5. Also is helpful in the event of severe hgic complications such as placenta
accreta.

Signs of fetal distress:

1. Non reassuring FHR pattern.
a. Repetitive late deceleration.
b. Loss of fetal beat-to-beat variability associated with late or deep
deceleration.
c. Sustained fetal heart rate <80/min.
 2. Fetal scalp pH <7.20
3. Meconium stained amniotic fluid.
4. IUGR

Predisposing factors for umbilical cord prolapse:

1. Excessive cord length.
2. Malpresentation
3. Low birth weight.
4. Grand parity (more than five pregnancies)
5. Multiple gestations
6. Artificial rupture of membranes.

Diagnosis suspected: after sudden fetal bradycardia or profound decelerations.

Treatment:
- Immediate steep Trendelenburg or keen chest position
- Manual pushing of the presenting fetal part back up into the pelvis until
immediate CS under GA can be performed.
- If the fetus is not viable, vaginal delivery is allowed to continue.

Dystocia and Abnormal Fetal Presentations and Positions:

Prolonged latent phase: Latent phase exceeding 20 h in a nulliparous parturient and 14
h in a multipara. The cervix usually remains at 4 cm or less but is completely effaced.

Arrest of dilation: when the cervix undergoes no further change after 2 h in the active
phase of labor.

Protracted active phase: slower than normal cervical dilation defined as less than 1.2
cm/h in a nulliparous and less than 1.5 cm/h in multiparous.

Prolonged deceleration phase: when cervical dilation slows markedly after 8 cm. The
cervix becomes very edematous and appears to lose effacement.

Prolonged 2nd phase (disorder of descent): as a descent of less than 1 cm/h and 2 cm/h
in nulliparous and multiparous respectively.

Arrest of descent: Failure of the head to descend 1 cm in station after adequate

pushing.

Drug of choice:
Oxytocin is DOC in the treatment of uterine contractile abnormalities.
Administration: IV at 1-6 mU/min and increased in increments of 1-6 mU/min every
15-40 min depending on the protocol.
Use of amniotomy is controversial.
Management is expectant: as long as the fetus and mother are tolerating the prolonged
labor.
When trial of oxytocin is unsuccessful or when malpresentation or CPD is also
present, operative vaginal or CS delivery is indicated.
Breech presentation
- Occur in 3-4% of deliveries.
- Increase neonatal mortality and incidence of cord prolapse >10X.
Management:
- ECV may be attempted after 34 weeks of gestation and prior to the onset of
labor (obstetrician may administer tocolytic agent at the same time)
o Role: ECV can be facilitated and its success rate improved by providing
epidural analgesia with 2% lidocaine and fentanyl.
o When unsuccessful: it can also cause placental abruption and
umbilical cord compression necessitating immediate CS.
o Role of epidural in Breech:
Need for breech extraction doesnt appear to be increased
when epidural is used for labor if labor is established prior to
activation of epidural.
Epidural anesthesia may decrease the likelihood of trapped
head because of relaxation of the perineum.
o If at all, head gets trapped even during regional, urgent RSI and GA to
relax uterus OR alternatively, Nitroglycerin 50-100 mcg IV may be
administered.

Obstetric Hge:
Placenta Previa:
- Occurs if the placenta implants in advance of the fetal presenting part.
- 0.5% of pregnancies.
- Increase risk in females with:
o Previous CS or uterine myomectomy
o Multiparity
o Advanced maternal age
o Larger placenta
- Anterior lying placenta previa increases the risk of excessive bleeding for CS.
C/F:
o usually presents as painless vaginal bleeding.
o Often severe hge can occur at any time.

Management:
- When gestation <37 weeks and bleeding is mild to moderate: treated with
bed rest and observation.
- When >37 weeks: delivery by CS.
- Patient with low-lying placenta may rarely be allowed to deliver vaginally if
bleeding is mild.
- Active bleeding or unstable patients: require immediate CS under GA.

Preparation:
- Two large-bore IV catheters inplace
- Replacement of IV volume deficits.
- Blood must be available for transfusion.
 Abruptio Placenta:
- Premature separation of normal placenta complicates approximately 1-2% of
pregnancies.
- Mild (grade I), moderate (II), severe (grade III)- 25%.
- Risk factors:
o HTN
o Trauma
o Short umbilical cord
o Multiparity
o Prolonged premature rupture of membrane
o Alcohol abuse
o Cocaine use
o Abnormal uterus
C/F:
- Painful vaginal bleeding
- Uterine contraction and tenderness
- An abdominal USG can help in the diagnosis
Choice of anesthetics:
- Based on urgency for delivery, maternal hemodynamic stability and any
coagulopathy (severe abruption may cause coagulopathy particularly after
fetal demise- fibrinogen levels <150 mg/dL d/t activation of circulating
plasminogen (fibrinogen) and the release of tissue thromboplastins that
precipitate DIC; platelet counts low and factors V and VIII are low, Fibrin split
products increased.).
- Bleeding may remain concealed inside the uterus and cause underestimation
of blood loss.
Management:
- Life threatening condition
- Emergency CS
- Massive blood transfusion
- Replacement of coagulation factors and platelets.

Uterine rupture
- Relatively uncommon.
- Occurs d/t:
o Dehiscence of scar from previous CS, extensive myomectomy or
uterine reconstruction.
o Intrauterine manipulations or use of forceps (iatrogenic)
o Spontaneous rupture following prolonged labor in patients with
hypertonic contractions (oxytocin use), fetopelvic disproportion, or
very large thin and weakened uterus.
C/F:
- Frank Hge
- Fetal distress
- Loss of uterine tone
- Hypotension
- Occult bleeding into the abdomen
 - Abrupt onset of continuous abdominal pain and hypotension.
T/t:
- Volume resuscitation
- Immediate laparotomy typically under GA
- Ligation of internal iliac arteries (hypogastric) with or without hysterectomy.

PROM and Chorioamnionitis

PROM is present when leakage of amniotic fluid occurs before the onse of
labor.
Diagnosis: The pH of amniotic fluid changes Nitrazine paper from BLUE to
YELLOW.
Complicates 10% of all and 35% of premature deliveries.
Predisposing factors:
o Short cervix
o Prior h/o PROM or preterm delivery
o Infection
o Multiple gestation
o Polyhydramnios
o Smoking
Spontaneous labor commences in 90% of patients within 24 hrs of PROM.
Issues in PROM: Risk of prematurity versus risk of infection.
Longer the interval between PROM and onset of labor higher the incidence of
chorioamnionitis.
PROM also predisposes to placental abruption and post partum endometritis.
Management:
Gestation <34 weeks: Expectant management with prophylactic antibiotics
and tocolytics for 5-7 days.

Chorioamnionitis:
Principal maternal complications are:
o Premature or dysfunctional labor
o Intra-abdominal infection
o Septicemia
o PPH
Fetal complications:
o Acidosis
o Hypoxia
o Septicemia
C/F:
Fever (>38 deg C)
Maternal and fetal tachycardia
Uterine tenderness
Foul smelling or purulent amniotic fluid
Lab: TLC (only if markedly elevated >15000/micL), CRP (>2 mg/dl), Gram staining
of amniotic fluid

Considerations:
 Use of regional anesthesia in chorioamnionitis is controversial (chance of
development of meningitis or epidural abscess)
Concerns over hemodynamic stability: particularly in patients with chills, high
fever, tachypnea and changes and mental status or borderline hypotension.
May have covert signs of septicemia, thrombocytopenia, or coagulopathy.

Issues in Preterm Delivery:

PROM and Preterm predispose to umbilical cord compression fetal
hypoxemia and asphyxia
Preterm with breech: prone to prolapse of umbilical cord during labor
Inadequate surfactant production: HMD after delivery
Soft, poorly calcified cranium predisposes to intracranial Hge during vaginal
delivery
Management: Based on gestational age, fetal maturity.

a. Preterm labor before 35 WOG:

Bed rest and tocolytic therapy initiated.
Labor is inhibited until the lungs are mature and sufficient
pulmonary surfactant is produced.
When amniotic fluid L/S ratio is >2, the risk of prematurity is
reduced.
Glucocorticoid may be given to induce production of
pulmonary surfactant which req minimum of 24-48 hours.
Most commonly used tocolytic therapies are:
Beta adrenergic agonists: Ritodrine (IV 100-350
mcg/min or Terbutaline (oral 2.5 5 mg every 4-6 hr);
maternal S/E: tachycardia, arrhythmia, MI,
hyperglycemia, and rarely pulmonary edema.
Magnesium (6 g IV over 30 min f/b 2-4 g/hr)
Others: calcium channel blockers (Nifedipine), PG
synthetase inhibitors, oxytocin antagonist (Atosiban),
and Nitric oxide.
When tocolysis fails to arrest labor, anesthesia becomes
necessary.

(Role: know that above mentioned drugs are given, eg.

Magnesium given (interaction with NMBD, vasodilation), its
role, beta adrenergic agonists are given thus their
interaction, fetal is premature thus need to resuscitate may
be- eg. Ketamine/ephedrine should be used cautiously).

Hypertensive Disorders:
HTN during pregnancy can be classified as:
o Pregnancy induced HTN: also referred to as preeclampsia
o Chronic HTN: that preceded pregnancy
o Chronic HTN with superimposed preeclampsia
Preeclampsia:
 o Is defined as SBP >140 mm Hg or DBP >90 mm Hg after the 20th WOG
accompanied by proteinuria (>300 mg/d) and resolving within 48 h
after delivery.
o Complicates about 7-10% pregnancies.
o Severe preeclampsia causes 20-40% of maternal deaths and 20% of
perinatal deaths.
o Maternal deaths are usually d/t stroke, pulmonary edema, hepatic
necrosis or rupture.
o Severe features: BP >160/110 mm Hg, Proteinuria >5g/d, Oligura <500
ml/day, elevated serum creatinine, IUGR, pulmonary edema, CNS
manifestations (headache, visual disturbances, seizures, stroke),
hepatic tenderness, or HELLP syndrome.
o Proposed theories for Preeclampsia:
Increased pressor response: increased sensitivity to AII
preceding onset of PIH
Prostaglandins: Decreased PGI2 and
Eclampsia:
o Preeclampsia + Seizure
Pathophysiology and Manifestations:
o Vascular dysfunction of the placenta resulting in abnormal metabolism
of prostaglandin.
o In preeclampsia: Elevated TXA2 and decreased PGI2
TXA2 is a potent vasoconstrictor and promoter of platelet
aggregation, PGI2 is a potent vasodilator and inhibitor of
platelet aggregation.
o Endothelial dysfunction may reduce production of NO and increase
production off ET-1 (a potent vasoconstrictor and platelet aggregator)
o Marked vascular reactivity and endothelial injury reduce placental
perfusion and lead to widespread systemic manifestations.
 T/T:
o Bed rest
o Sedation
o Repeated administration of antihypertensives
Labetalol: 5-10 mg IV
Hydralazine: 5 mg IV
Magnesium sulphate

Q. How do anesthetic agents cross the placenta? Examples of agents crossing and
not-crossing the placenta.
Ans.
Anesthetic agents enter the fetus side through placenta by way of diffusion.
Diffusion of anesthetic agents through the placenta is mostly dependent upon:
Diffusion constant which is dependent upon
o Molecular weight of substance
o Protein binding
o Lipid solubility
o Degree of ionization
Membrane surface area
Concentration of drugs on maternal side
Concentration of drug on fetal side
Membrane thickness
Timing of administration
Drugs that easily cross the placenta are:
Induction agents: STP, Propofol, Ketamine (however at conventional doses,
these drugs do not cause fetal depression)
Opioids
Drugs that do not easily cross the placenta are:
Muscle relaxants- big molecules (gallamine however crosses)

Q. Assessment of a trauma patient.

Ans:
ATLS scheme to assess trauma patient:
1. Overview:
a. Visual scan of the patient for obvious injuries.
b. Obtaining hx from prehospital personnel and patient.
2. Primary survey:
a. A: airway (with cervical spine control)
i. Chest wall movements, breath sounds, feeling for air
movements.
b. B: Breathing (giving supplemental oxygen)
i. Is ventilation adequate?
ii. B/L chest sounds?
iii. Provide assist ventilation for ventilator failure.
c. C: Circulation
i. Check peripheral pulses
ii. Grading of shock according to vital signs
iii. Correction of hypovolemia and obtaining blood samples.
d. D: Disability (determining neurological status)
i. AVPU (Alert, responding to Verbal stimulus, responding to
Painful stimulus (~GCS<8), Unresponsive) OR GCS
ii. Pupillary response to light
e. E: Expose the patient for complete examination.
3. Resuscitation phase
4. Secondary survey
5. Definitive Care Phase

Who should be intubated promptly?

1. Patients with GCS <8
2. Rapidly worsening GCS
3. Presence of hgic shock
4. Need to transport the patients for imaging or surgery

Things to keep in mind during laryngoscopy and intubation.

1. C-spine protection- until ruled out by radiological evidence
2. Manual-in-line immobilization
3. Decreasing the dose of induction agents (STP preferably, or Propofol)
4. In cases of Maxiollofacial trauma, or fracture of mandible: surgical airway
preferred (cricothyroidotomy or tracheostomy) over intubation of trachea
5. Ryles tube: preferably orogastric application.
 6. If anticipated difficult intubation, opt for surgical airway rather than struggle
with intubation.
7. Prevention against aspiration of gastric contents
8. Blunting of airway reflexes to prevent the rise in ICP (along with gentle and
prompt laryngoscopy)

Primary and Secondary Brain Injuries.

1. Primary brain injury:
a. Occur at the moment of trauma
b. Contusion, damage to blood vessels, axonal shearing and torn,
disruption of BBB, damage to meninges, neuronal death.
c. Eg. ICH, SDH, SAH, EDH, contusion, laceration, etc.
2. Secondary brain injury:
a. Occur d/t low blood pressure, cerebral swelling, hypoxia, hypercarbia,
etc.
b. Eg. Edema, Impaired metabolism, free radical formation,
excitotoxicity (excessive release of glutamate from neuronal cells in
the CSF incr. intracellular calcium activation of protein kinase,
PL, protease proteolysis, free radical formation neuronal death),
etc.

Principles of resuscitation of head injury patient.

1. Airway
2. Breathing
3. Circulation
4. Lower ICP
5. Maintain CPP

Triphasic response to head injury.

Is sequential derangement of water balance. May also be seen post
neurosurgery (esp. pituitary surgery).
Patients display Polyuria (d/t DI with rising sodium)- hypothalamic dysfunction,
followed by Oliguria (d/t SIADH and low sodium)- vasopressin from damaged
pituitary, followed by lastly return of normalcy or polyuric response again-
exhaustion of vasopressin.

ANESTHESIA FOR THE ELDERLY PATIENTS

Q. Physiological changes in the elderly.
Ans.
1. Cardiovascular:
Vascular
a. arterial elasticity- hyperplasia of intima, collagenization of media,
accumulation of calcium and phosphate in elastic fibers.
b. Decrease in arterial compliance SVR, afterload.
c. Atherosclerosis of vessels prone for periop MI, stroke, etc.
Cardiac
d. Calcification of valves- aortic valve sclerosis and mitral annular
calcification.
e. interstitial fibrosis of myocardium diastolic dysfunction and
impaired diastolic filling.
 f. Fibrotic changes of SA node and conduction system more prone to
dysrhythmias
Implication
g. In response to stress: Decr. in maximal heart rate, SV, CO, EF and
oxygen consumption.
h. in hearts inotropic and chronotropic response to endogenous and
exogenous catecholamines
i. SBP roughly 6-7 mm Hg per decade, whereas very little change in
DBP.
2. Respiratory system
Airway
a) in function of pharyngeal and laryngeal structures prone for upper
airway obstruction
b) Periodic breathing during sleep prone for apnea and airway obstruction
in recovery room
c) protective airway reflexes
d) Loss of ciliary function
e) Osteoporotic mandibles
f) Nuisance/peg/loose teeth
g) Temporo-mandibular joint stiffness
h) Cervical spondylosis
i) Arthritis of atlanto-occipital joint
Sometimes it is best to leave dentures in place to provide support for facemask ventilation or
laryngeal mask stability
j)
Lungs
a) Kyphosis of thoracic spine AP diameter and lateral diameter
barrel chest deformity
b) Flattening of diaphragm, loss of muscle mass difficult ventilation
c) Costochondral joints calcification less compliant lung, WOB
d) elastic support to airway collapsible airways during expiration, esp at
lung bases
e) PAP by 30%
f) in VC and in RV
g) in CV and CC
h) in motor power of accessory muscle of breathing FEV1 by 30
ml/year.
i) V/Q mismatch
j) Blunting of HPV reflex d/t rigid pulmonary vasculature
k) Ventilatory response to hypercapnia and hypoxia is blunted d/t reduced
neuronal output to respiratory muscles making them sensitive to
respiratory depressant effects of opioids and BZDs.
3. CNS
a. CBF and CMRO2 in proportion to decrease brain mass but intact
cerebral autoregulation in patients without neurological disease
b. neuronal substance esp tissues that synthesize NT depletion of
DA, NE, 5HT, etc. thus symptoms of depression, loss of memory
and motor dysfunction
c. Sleep: increased latency to sleep onset, increased awakenings during
night
d. Memory: decline with age
 e. Age related CNS diseases: cerebral arteriosclerosis, Alzheimers, and
Parkinsons.
4. PNS:
a. in threshold for all forms of perception- vision, hearing, touch, sense
of joint position prone to injury, smell, and peripheral pain
decrease requirement of analgesics, and temperature response
hypothermia chance.
5. ANS:
a. sensitivity of baroreceptor orthostatic hypotension and syncope
b. in autonomic end organ responsiveness eg. Endogenous beta
blockade of aging d/t reduced number of reeptors, reduced affinity
for agonist molecules
c. Affected thermoregulation in heat loss and heat tolerance
6. Renal system:
a. in renal mass in GFR and RBF
b. in number of functional glomeruli
c. However, serum creatinine normal d/t concomitant in muscle mass
serum creatinine levels are poor indicators of GFR in geriatric patients.
d. ability to concentrate urine or conserve sodium
e. total body stores of potassium leading to hypokalemia d/t loss of
lean body mass
7. Protein binding:
a. in albumin
8. Body compartments:
a. Loss of skeletal muscle in lean body mass
b. in TBW mainly d/t in ICW
c. in % of body fat reservoir for deposition of lipid soluble anesthetic
drugs
9. MSK system:
a. muscle mass, bone density stiffness of the joints, osteoporosis.
b. subcut fat, and poor skin turgor, fragile skin prone for injury
10. Endocrine:
a. Impairement of glucose homeostasis, decrease thyroxin clearance or
production, decrease production of renin, aldosterone
b. incidence of DM, thyroid dysfunction, sodium retention, etc.
11. Hematological and immune system
a. hematopoietic response to anemia
b. Susceptibility to life-threatening infection d/t depression of immune
system.
12. Metabolism:
a. BMR
b. Impaired thermoregulation
Older patients have:
An impaired ability to sense a colder temperature
Less subcutaneous fat
Impaired autonomic homeostasis
Reduced heat generation due to a decline in BMR
Reduced ability to increase their metabolic rate
Reduced ability to vasoconstrict and shiver

Q. Alterations in Pharmacokinetics and dynamics in elderly.

Ans:
1. in lean body mass small central compartment higher peak concn.
2. in TBW small equilibrating peripheral compartment dose
requirement
3. body fat large slowly equilibrating peripheral compartment longer
duration of drug effect
4. Changes in CVS:
a. More susceptible to hypotensive effects of anesthetic drugs
b. Delayed induction of anesthesia following IV agents d/t reduction in
CO
c. Faster inhalational inductions d/t rapid rise of alveolar partial
pressure
5. Renal and Hepatic effects:
a. renal clearance delay in offset of drugs (for drugs with renal
metabolism/excretion, eg. Pancuronium, pethidine, etc.)
b. metabolism of drugs in liver higher steady state plasma concn in
elderly
6. IV protein binding:
a. albumin thus acid drugs (eg. Pethidine, diazepam) have reduced
dose requirements in elderly d/t increase free fraction of drug
b. Alpha 1 acid GP: of drugs bound to AAG (eg. Lignocaine)
retarding the clearance in the elderly.
Individual drugs:
1. STP: in Vd induction dose by 15%, avoiding prolonged infusion
2. Propofol: Vd, sensitivity induction dose (~1.7 mg/kg), maintenance
dose (30-50%)
3. BZD: Higher clearance rate of Midazolam thus preferred choice, but to
about 75% suggested.
4. Opioids: 2X potent in elderly, 50% dose reductions, preferably shorter acting
opioids.
5. Muscle relaxants:
a. Unchanged numbers of Ach receptors and sensitivity unchanged
dose of NDMR.
b. But metabolism of these drugs in d/t renal and hepatic effects of
ageing

Factors influencing regional anesthesia techniques in the old age.

Ans:
1. Size of epidural space in
2. Permeability of dura is
3. Volume of CSF is
4. in size and number of myelinated fibers in the dorsal and ventral nerve roots
5. in transforaminal escape of LA injected during epidural anesthesia
6. permeability of extraneural tissues to LA rapid onset of analgesia
For LA/peripheral nerve blocks:
1. in conduction velocity of peripheral nerves
2. number of axons in the peripheral nerve
Both leading to reduction in the requirements of LA in different regional
techniques.
Epidurals and spinals are technically more difficult in the elderly due to spondylosis, osteoarthritis and patient
positioning.
Important post-op problems in the elderly.
Ans:
1. Oxygenation
2. Post-op analgesia:
a. NSAIDs avoided in those >70 yrs of age, with pre-existing renal
dysfunction and those who have suffered hemodynamic instability or
major blood loss.
3. Hemodynamics:
a. Hypothermia, hypovolemia may exist without tachycardia and may
manifest with profound hypotension.
b. Volume of fluid that may be necessary to support circulation during
anesthetic may prove excessive once the anesthetic is eliminated and
sympathetic tone returns risk of volume overload and pulmonary
edema thus administer volume in small intermittent boluses
watching for response in CVP, BP and UO.
c. Arrhythmias are common may be d/t hypokalemia,
hypomagnesemia, hypocalcemia, hypoxia or hypercarbian.
4. Hypothermia:
a. May manifest as altered mental status, delayed recovery, sluggish
DTRs, and slow or shallow respiratory pattern.
b. May lead to metabolic disturbances, reduce liver and renal perfusion,
induce coagulopathy and make NDMR reversal difficult, wound
healing, impaired immune function
5. Post-op confusion/mental dysfunction:
a. Esp with use of anticholinergic drugs, antihistaminics, phenothiazines,
and TCAs.
b. Other predisposing factors: hypoxia, hypercarbia, acidosis,
hypoglycemia, hyponatremia and liver and renal diseases AND also
sepsis.
Mnemonic:
DIM-TOP
Drugs
Infection
Metabolic
Trauma: hypoperfusion, FES in ortho
Oxygen: hypoxia, hypercarbia
Psychiatric and pain.
No difference in frequency can be reliably demonstrated with general or regional anaesthesia.

Treatment is of underlying cause e.g. antibiotics for infection and oxygen if hypoxic.
Haloperidol 2.5mg IV increased to 5mg PRN can be used to settle an agitated patient.
Thiamine and diazepam might also useful.
Repeated orientation, familiar surroundings, family, sensory aids and re-establishing day-night cycles are
useful non medical therapies.

6. Post-op CVA/TIA
7. Sleep disordered breathing:
a. Reason unclear
b. 2/3rd of elderly have frequent episodes of desaturation and apnea
during sleep and diminished response both to hypercapnia and
hypoxia.
8. Renal system:
 a. Risk of renal failure
b. Reasons: pre-renal causes, drugs, and sepsis, etc.
9. DVT:
a. More prone for DVT and PE
b. Advanced age, prior thromboembolism, malignancy, immobility,
pelvic, hip and orthopedic surgery, central lines, are risk factors.
c. Appropriate pharmacologic and non-pharmacologic prophylaxis
recommended.
10. Nutrition

CASE OF TURP
Prostate gland:
A fibromuscular gland weighing 20 g and underlies the apex of the male
bladder and surrounds the prostatic portion of the urethra.
Developmentally 2 lobes, anatomically 5 lobes median and 2 lateral lobes
most commonly undergo BPH
Nerve supply: From prostatic plexus (from inferior hypogastric plexus)
Afferent pain fibers from prostate, urethra and bladder mucosa from S2, 3,
and 4.
Pain fibers from over stretched bladder travel with sympathetic fibers T12,
L1 and L2.

Lithotomy position during TURP: Complications

1. Venous stasis: at points of compression by equipment or at the groin due to
thigh flexion Prevention: Elastic stockings (if >15 min duration)
2. Peripheral nerve injury:
a. Obturator nerve (L1,2,3): d/t acute flexion of the thigh to the groin
weakness and paralysis of adductors of thigh difficulty in walking
and outward swing of leg
b. Saphenous nerve (L1,2,3): d/t compression of medial aspect of leg
against knee brace sensory loss to medial side of thigh
c. Common peroneal nerve (L4,5, S1, 2): courses around head of fibula
prone to pressure injury to its nutrient vessel foot drop.
3. Cardiorespiratory compromise:
a. Results in 18% reduction in VC, further reduced by Trendelenburg
b. Abrupt return of blood to central circulation during lowering of legs
cardiopulmonary compromise in patients with pre-existing cardiac
diseases.

Pre-operative concerns in case of TURP

1. Old age: comorbidities, drug use
2. Chronic prostatic hypertrophy: obstructive renal insufficiency
3. Presence of UTI
4. Use of anticoagulants and antiplatelets
5. Presence of electrolyte imbalances, dehydration
6. Size of prostate
7. Blood arrangement
8. Type of anesthesia

Preparation of the patient:

 - NPO advice
- Blood arrangement:
o Type and screen
o Arrange and crossmatch if patient is anemic and/or prostate size >40
gm
- Anxiolytics
- Antibiotic prophylaxis: Genta 2-4 mg/kg slow IV

Problems during TURP:

During intra-operative period:
a. TURP syndrome: within 15 mins into procedure to 24 hours post-
procedure
i. D/t:
1. Acute changes in IV volume
2. Osmolality
3. Direct effects of irrigating fluid
ii. Factors influencing the absorption of irrigation fluid:
1. Hydrostatic pressure of irrigating fluid (Maximum
allowable irrigation pressure of 60 cm of water)
2. Duration of procedure (limit the resection time to < 1
hr)
3. Nos. of open venous sinuses (10-30 ml fluid absorbed
per minute)
4. Size of gland (25 ml/gm of tissue)
5. Low venous pressure at irrigant-blood interface
iii. C/F of Hyponatremia:
1. 120 mEq/L: CNS: Restlessness, mental confusion,
CVS: Hypotension, bradycardia
2. 115 mEq/L: CNS: Nausea, vomiting, dizziness,
headache, unresponsiveness or transient visual changes,
CVS: Cardiac depression
3. 110 mEq/L: CNS: seizures, coma, CVS: CHF
iv. C/F of Hyperglycinemia:
1. Toxic effects on heart, retina
2. Nausea, headache, malaise, seizure, encephalopathy
3. Treatment with arginine: increases ammonia
metabolism via urea cycle.
4. Trial of magnesium therapy for treatment: magnesium
exerts negative control on NMDA receptor.
5. Normal value of glycine approaches within 24 hours
6. Thus reassurance is needed when patient complains of
vision difficulty in glycine toxicity.
v. C/F of Hyperammonemia:
1. Nausea, vomiting, comatose for 10-12 hrs, awakens
when blood NH3 <150 mmol/L
vi. Management of TURP syndrome:
1. Stop surgery
2. Stop IV fluids
3. Airway and breathing: intubate and ventilate if
necessary
 4. Circulation: Hypotension treated with vasopressors,
bradycardia: glycopyrrolate
5. Seizures: Mida, STP, Phenytoin, IV Magnesium
6. Investigations: S.Na, S. osmolality, ABG, glucose,
creatinine
7. Diuretics: Frusemide 40 mg IV, Mannitol
8. If severe hyponatremia (S.Na <120 mOsm/L)
a. Hypertonic saline (3% at <100 ml/h) or 8.4%
sodium bicarbonate
b. Hemoflitration if CRF
9. Management in ICU/HDU
10. Invasive hemodynamic monitoring
vii. Prevention of TURP syndrome:
1. Preparation of the patient: adequate hydration,
electrolyte analysis, coagulation profile.
2. Hemodynamic monitoring
3. Limitation of duration of surgery < 1hr
4. Limitation of hydrostatic pressure of irrigation fluid to
<60 cm
5. Limitation of extent of bladder distention caused by
surgeon
6. Preservation of capsule of the prostate by careful
resection by the surgeon
7. Maintenance of BP
8. Intraprostatic vasopressin injection bleeding and
absorption of irrigating fluid
9. Use of bipolar electrode resection, laser excision of
prostate (nd-YAG laser)
10. Strict vigilance for early detection of symptoms
b. Hypothermia:
i. Continuous fluid irrigation: temp 1 deg C/hr
ii. Elderly: reduced thermoregulatory capacity
iii. Assoc. with incidence of MI
iv. Post-op shivering dislodge clots and post-op bleeding
c. MI: 1-3% incidence
d. Bleeding:
i. in hypertrophied prostate (>45 gm)
ii. Estimation:
1. Resection time 2-5 ml/min
2. Size 20-50 ml/gm
3. Nos. of open venous sinuses
iii. Prevention: use of adrenergic agonists
e. Bladder perforations:
i. 1%
ii. Causes:
1. Trauma by surgical instrument
2. Overdistention of bladder with irrigating fluid
iii. Manifestations:
1. in return of irrigation solution from bladder
 2. Extraperitoneal: pain in periumbilical, inguinal, and
suprainguinal region.
3. Intraperitoneal: generalized pain abdomen, shoulder tip
pain, abdominal rigidity, pallor, nausea and vomiting.
4. Capsular tear will cause supra-pubic pain (if spinal level
is <T10)

Post-operative period:
a. TURP syndrome
b. Clot retention
c. Bleeding
d. Post-operative cognitive dysfunction
e. Transient bacteremia/sepsis
i. Causes
1. Release of bacteria from prostatic tissue
2. Pre-op indwelling urinary catheter
3. Pre-op UTI
f. Coagulopathy:
i. < 1%
ii. Causes:
1. Dilutional thrombocytopenia
2. DIC d/t release of prostatic particles rich in
thromboplastin into blood
3. Local release of fibrinolytic agents (plasminogen and
urokinase)
iii. Treatment: FFP, platelets, ACA

Properties of Ideal irrigating fluid for TURP

a. Iso-osmolar and non-hemolytic
b. Non-eletrolytic
c. Non-toxic
d. Transparent
e. Non-metabolizable
f. Rapidly excretable
g. Inexpensive and sterile

Common fluids used for irrigation:

1. Distilled water osmolality (hypo 0)
2. Glycine (1.5%, 1.2%) 220 (iso), 175 (hypo)
3. Mannitol (5%) 275 (iso)
4. Sorbitol (3.5%) 165 (hypo)
5. Cytal (Sorb 2.7% + Man 0.54%) 178 (iso)

CASE OF THYROID SWELLING

Things to consider in history and examination of thyroid swelling:

Size and duration of swelling;
o Pressure effects on trachea: dyspnea, stridor (incl. effects of change
in position)
o Pressure effects on esophagus: dysphagia
 o Pressure effects on RLN: hoarseness
o Duration: long standing thyroid may be associated with
tracheomalacia
Retrosternal extension:
o Dysphagia, dyspnea
o Unable to get under the swelling
o SVC obstruction/thrombosis: dilated veins in the nect and upper
part of the chest, facial edema
Intratracheal extension:
o Dyspnea
o Hemoptysis
Thyroid hormone status:
o Hyperthyroidism
Common causes: Graves disease, thyroiditis, toxic MNG,
toxic adenomas, struma ovarii, thyroxine overdose, etc.
Symptoms: hyperactivity, weight loss, tremor- on
outstretched hands and tongue, palpitations, diarrhea,
intolerance to heat, large muscle group weakness, menstrual
irregularities
Signs: tachycardia (esp high sleeping PR), warm moist skin,
irregularly irregular HR, MVP, HF, and IHD, etc.
Drugs used are: PTU, Carbimazole, Methimazole, etc.
Iodides:
Decrease hormone release at high concn (Wolff-
Chaikoff effect)
Block coversion of T4 to T3
Dose: 3 drops of SSKI given 8 hrly.

o Hypothyroidism:
Causes: Hashimotos thyroiditis, thyroid destruction (from
radioactive iodine or surgery), pituitary or hypothalamic
disease.
Symptoms: CVS: Bradycardia, pericardial effusion,
reduced plasma volume, RS: pleural effusions, CNS: slow
development, mental slowing, excessive sleepiness,
depressed mood, GI: delayed gastric emptying,
constipation, impaired hepatic drug metabolism, Others;
fatigue, modest weight gain, cold intolerance, menorrhagia,
muscle cramps, dry coarse hair, dry skin, large tongue,
swelling of legs, etc.
Associated endocrine disorders:
o MEN 2A: Medullary Ca of thyroid, Pheochromocytoma,
Parathyroid hyperplasia
o MEN 2B: Medullary Ca of thyroid, Pheochromocytoma, Mucosal
Neuromas
o MEN 1: Pituitary adenoma, Parathyroid hyperplasia, Pancreatic
tumors like insulinoma
Thyroid malignancies:
o Papillary, medullary, follicular, and anaplastic
 o Sx of distant metastasia- lung, bones, liver, etc.
History of taking of any medications: dose, duration, previous TFT
o Common S/E of antithyroid drugs:
Agranulocytosis
Hepatotoxicity: Immunoallergic hepatitis seen with PTU
Vasculitis: arthritis, vasculitic rash, skin ulcerations, etc.

Presenting the Case in Exam:

o ____ year old (M/F) with (size/side) thyroid swelling with/out
airway compromise (eg. With tracheal deviation/compression)
with/out complications (retrosternal extension/SVC syndrome)
with/out normal thyroid function (or controlled/uncontrolled
hypo/hyperthyroidism) with/out comorbidities scheduled for
subtotal thyroidectomy

Thyroid hormone synthesis physiology:

(In thyroid gland, under the influence of TSH)

Active uptake of iodide in exchange for Na+

Iodide is oxidated for active iodine hydrogen peroxide (catalyzed by TPO)

Iodine actively transported across apical surface of follicular cells

Active iodine incorporated into the tyrosine residues of thyroglobulin to form
MIT/DIT

Thyroglobulin is taken up into the colloid of the follicle where coupling reaction
between pairs of iodinated tyrosine molecule occurs (catalyzed by TPO)

Stored in this form until taken up back into follicular cells (as droplets) by pinocytosis

Fusion of droplets with lysosomes result in hydrolysis of thyroglobulin and release of
T4 and T3

Approximately 100 mcg of thyroid hormone synthesized from gland each day
(90% T4 and 10% T3)
99.98% of T4 and 99.8% of T3 is bound to protein in blood.

Eye signs in Thyroid disorders:

o Dalrymple sign (Stare sign): white of the sclera is seen d/t upward
retraction of the eyelids
o Lid-lag (von Graefes sign): lid lag when looking downward
o Joffroys sign: absence of forehead wrinkling when looking upwards
with face tilted downwards.
o Exophthalmus (Graves disease): d/t immune mediated inflammation
of the retro-orbital fat.
o Moebius sign: lack of convergence of eyeball
What is sick euthyroid syndrome?
Ans:
Euthyroid sick syndrome is described as abnormal thyroid function tests that occur in
the setting of acute and severe nonthyroidal illness without preexisting hypothalamic-
pituitary and thyroid gland dysfunction. Most common findings are low T3, T4 and
TSH. Reversible after recovery from the illness. Administration of thyroid hormones
in this situation is controversial and not shown to improve outcomes. May be an
adaptive response or a maladaptive response.

Thyroid storm:
o Is a condition in which patients metabolic, thermoregulatory and
cardiovascular compensatory mechanisms fail in a patient with
hyperthyroidism.

C/F: Its manifestations include

CNS: agitation, and confusion
CVS: tachycardia, dysrhythmias, myocardial ischemia, congestive heart
failure
Hyperthermia

Also remove the precipitating cause

If intraop: stop the surgery, notify the surgeon

7 Ps:
Phluid
PTU
Potassium Iodide
Prednisolone (steroid)
Propranolol
Paracetamol
Precipitating factors

Note: PTU to be started before sodium iodide.

Role of steroid in thyroid storm:
Inhibit hormone release, peripheral conversion (T4 to T3)
To provide adrenal support
Precipitating factors:
Stress: surgical, emotional, mechanical stress to the gland, DKA, CHF, Pregnancy
Trauma
Infection, sepsis
Acute withdrawal of antithyroid drugs
Iodide therapy, contrast agents
Drugs containing iodine: eg. Amiodarone

Assessment for tracheal deviation and compression

Ans:
History: difficulty breathing, stridor or stridor on lying down
Examination:
o For deviation: palpation of and auscultation on anterior neck
o For compression: positive Kochers test (sligh push on lateral lobes
causes stridor)
Investigations:
o X-ray neck: AP, lateral
o CT scan of neck and upper thorax
o Flow-volume loops

Myxedema coma.
Loss of brain function as a result of severe, longstanding hypothyroidism.
Mostly seen in elderly, more in females.
Triggers:
o Drugs (sedatives, narcotics, anesthesia, lithium, and amiodarone)
o Infections
o Stroke
o Trauma
o Heart failure
o GI bleeding
o Hypothermia
o Missing thyroid medications

Some important things for VIVAs

Breathing system filters (HME filters)
a. Use:
i. Prevention of contamination of breathing system.
ii. Prevention of cross-infection
b. Mechanisms of filtration of micro-organisms:
i. Interception: particles with diameters larger than pore size are
intercepted by the filter pores.
ii. Inertial impaction: particles strike the fibers because of inertia
iii. Diffusion: particles less than 0.1 micron undergo Brownian
motion and are captured.
iv. Gravity: large particles settle on the fiber because of gravity
v. Electrostatic attraction of the particles
c. Types of filters:
i. Pleated hydrophobic membrane filters
ii. Electrostatic or composite filters
d. Filtration performance:
i. Determined by penetration: nos. of particles passing through
the filter as a percentage of particles in challenge to the filter.
ii. Efficiency is (100-penetration)%
e. Pore size in standard blood filter.
i. 170 micron to filter clots and debris
ii. Cannot filter micro-aggregates (20-40 micron) are implicated
in causing febrile transfusion reactions, pulmonary injury and
thrombocytopenia.