Ain Shams University MD of Anesthesia (AIP 7003)

Faculty of Medicine Semester Assessment (Part I & II)

Department of Anesthesia, Intensive 08/09/2015
Care & Pain Management 1 hour / 30 Marks

All questions are to be answered

1. Anesthetic management of patient with cardiac tamponade. (6 Marks)

2. Anesthesia for carotid artery surgery: Preoperative evaluation & considerations,

and regional anesthetic management. (6 Marks)

3. Pre-operative assessment and principles of anesthetic management for 45-year

lady presented for bronchial carcinoid tumor removal surgery. (6 Marks)

4. Minimally invasive and non-invasive cardiac output monitoring. (6 Marks)

5. Platelet transfusions: preparation, response to transfused platelets, indications

and adverse effects. (6 Marks)

GOOD LUCK
 MODEL ANSWER (Parta I & II, September 2015)

Q-1: Anesthetic management of patient with cardiac tamponade.

Preoperative Considerations
Volume of pericardial fluid is relatively fixed (20-50mL in adults).
Any increase in pericardial pressure diastolic filling. Pressure is applied equally to
each cardiac chamber. Thin walled atria and the Rt-ventricle are more susceptible to
pressure-induced abnormalities of filling than the Lt-ventricle.
Pericardial pressure is normally similar to pleural pressure {(- 4) and (+ 4) mmHg with
respiration}. The magnitude of the increased pressure depends on both the volume of
fluid (effusions or bleeding) and the rate of accumulation; sudden increases exceeding
100200mL precipitously pericardial pressure, whereas very slow accumulations up
to 1000mL allow the pericardium to stretch with minimal increases in pericardial
pressure.
Etiology: may be due to bleeding (after cardiac surgery; trauma); infections (viral,
bacterial, or fungal); malignancies; uremia; myocardial infarction; aortic dissection;
hypersensitivity or autoimmune disorders; drugs; or myxedema.
Hemodynamic features of cardiac tamponade include:
CO with CVP.
HR & contractility (reflex sympathetic activation) help maintain CO which
becomes dependent on HR (SV remains relatively fixed).
Arterial VC (increased SVR) supports systemic BP.
In the absence of severe LV dysfunction, equalization of diastolic pressure occurs
throughout the heart ([RAP] = [RVEDP] = [LAP] = [LVEDP]).
The CVP waveform is characteristic. Impairment of both diastolic filling and atrial
emptying abolishes the y descent; the x descent (systolic atrial filling) is normal
or even accentuated.
Acute cardiac tamponade usually presents as sudden hypotension, tachycardia, and
tachypnea.
Physical signs include:
Jugular venous distention, a narrowed arterial pulse pressure, and muffled heart
sounds.
Inability to lie flat.
A friction rub may be audible.
A prominent pulsus paradoxus (cyclic inspiratory in SBP 10mm Hg) represents
an exaggeration of a normal phenomenon related to inspiratory decreases in
intrathoracic pressure.
CXR: enlarged heart (or may appear normal).
ECG:
Decreased voltage in all leads,
Nonspecific ST-segment & T-wave abnormalities. Generalized ST elevation.
 Electrical alternans (cyclic alteration in magnitude of the P waves, QRS complex,
and T waves).
Echocardiography:
Diastolic compression or collapse of RA and RV, left-ward displacement of the
ventricular septum, and an exaggerated in RV size with a reciprocal in LV size
during inspiration.
Anesthetic Considerations
Pericardiocentesis: for tamponade 2ry to non-traumatic causes (infectious, malignant,
autoimmune, or uremia). It might be associated with a risk of myocardial or coronary
laceration or pneumothorax; through a subxiphoid approach under Local Anesthesia.
Surgical: for traumatic postoperative (thoracotomy) & also for large recurrent medical
pericardial effusions. Via Lt anterior thoracotomy, median sternotomy, or
thoracoscopy.
Large-bore IV access is mandatory.
Monitoring: invasive intra-arterial pressure, but should not delay pericardial drainage
if the patient is unstable.
Induction:
Induction of GA can precipitate severe hypotension and cardiac arrest.
Removal of even a small volume of pericardial fluid before induction (subxiphoid
approach; under LA) may be sufficient to greatly improve CO and allow safe
induction.
Ketamine is the agent of choice for induction & maintenance until the tamponade is
relieved. IV small doses (10 mg at a time) provide excellent supplemental analgesia.
It is useful to have an epinephrine infusion available and initiate it before induction.
Intubation: Awake intubation with maintenance of spontaneous ventilation is
theoretically desirable, but coughing, straining, hypoxemia, & respiratory acidosis are
equally detrimental & should be avoided.
Anesthetic technique:
Should maintain a high sympathetic tone until the tamponade is relieved; in other
words, deep anesthesia is not the object.
Cardiac depression, VD, & slowing HR should be avoided.
Similarly, increases in mean airway pressures can seriously jeopardize VR.
Thoracoscopy requires one-lung anesthesia.
Small doses of epinephrine (510 mcg) may be useful as a temporary inotrope and
chronotrope.
Generous IV fluid administration is useful in maintaining CO.
Q-2: Anesthesia for carotid artery surgery: Preoperative evaluation &
considerations, and regional anesthetic management.

Preoperative Considerations:
80% of cerebrovascular strokes are ischemic; usually a result of embolism or (less
commonly) thrombosis.
The bifurcation of the common carotid artery is the most common site of atherosclerotic
plaques that may lead to TIA or stroke (embolization of platelet-fibrin or plaque
material, stenosis, or complete occlusion).
Symptoms depend on the adequacy of collateral circulation. It is common for TIAs or
minor strokes to precede a major stroke.
Indications for open surgery or intravascular interventions include:
TIAs or minor (incomplete) stroke associated with ipsilateral severe carotid stenosis
(>70% occlusion),
Ipsilateral symptoms with 3070% occlusion (usually an ulcerated plaque).
In the past, carotid endarterectomy was recommended for asymptomatic with
significantly stenotic lesions (>60%). Currently, stenting is recommended.
Operative Mortality: For open surgery 14% (cardiac complications or infarction).
Peri-operative Morbidity:
410%; principally neurological; patients with preexisting neurological deficits
have the greatest risk of perioperative neurological events.
Risk factors to increase operative risk:
Age >75 years, Angina,
Symptomatic lesions, Carotid thrombus, and
Uncontrolled hypertension, Occlusions near the carotid siphon.
Preoperative Anesthetic Evaluation & Management
Patients usually elderly, hypertensive, diabetic with generalized arteriosclerosis.
Because most patients are elderly, enhanced sensitivity to premedication should be
expected.
Optimizing coexisting diseases:
Neuro: Evaluation & defining preexisting neurological deficit. Most post-operative
deficits appear to be related to surgical technique.
DM: Uncontrolled periop hyperglycemia can increase morbidity by enhancing
ischemic cerebral injury.
CVS: - BP should be controlled; (usual medications on schedule until time of surgery
except diuretics).
- Angina: should be stable and controlled, with absent signs of CHF.
Regional Anesthesia
The tremendous advantage of regional anesthesia is that the patient can be continually
examined intraoperatively; thus, the need for a temporary shunt can be assessed and
any new neurological deficits diagnosed immediately intraop.
Blockade of the superficial cervical plexus effectively blocks the C2C4 nerves.
 Deep cervical plexus block is not required.
LA by the surgeon into the carotid sheath may be required in some patients.
Intraop neurological examination is the most reliable method for assessing the adequacy
of cerebral perfusion during carotid cross-clamping. The examination minimally
consists of level of consciousness, speech, and contralateral handgrip.
Minimal sedation and conversation with the patient to monitor the neurological
status.
Some surgeons routinely use a shunt, but this may increase incidence of postop
neurological deficits (can dislodge emboli). Carotid stump pressure distal to the cross-
clamp <50 mmHg is an indication for a shunt.
Technique of Superficial Cervical Plexus Block
The cervical plexus is formed from the
anterior rami of C14, which emerge
from the platysma muscle posterior to
the sternomastoid.
It supplies sensation to the jaw, neck,
occiput, and areas of the chest and
shoulder.
The patient is positioned supine with
the head turned away from the side to
be blocked.
Identify and avoid the external jugular
vein.
The sternomastoid muscle is identified
and its lateral edge marked.
At the junction of the upper and middle thirds, a short (5-cm) block needle is inserted,
directed cephalad toward the mastoid process, and 5mL of LA is injected in a
subcutaneous plane.
The needle is turned to advance it in a caudad direction, maintaining a path along the
posterior border of sternocleidomastoid.
An additional 5mL of local anesthetic is infiltrated subcutaneously.
General considerations
The goal of anesthetic management is maintaining adequate perfusion to the brain and
heart (close regulation of BP & avoidance of tachycardia).
Monitoring:
ECG should include V5 (to detect ischemia). Invasive BP.
Continuous computerized ST-segment analysis is desirable.
Maintenance fluids should be glucose-free (adverse effects of hyperglycemia).
Procedure is not usually associated with significant blood loss or fluid shifts. MAP
should be maintained at (or slightly above) the patients usual range.
Management of hypertension:
 - Blocker Nitroglycerin beneficial for IHD
-B (prevents reflex tachycardia from Nicardipine or Nitroprusside (for
vasodilators) marked hypertension)
Management of Hypotension: vasopressors (phenylephrine the vasopressor of choice;
in small increments).
Reflex bradycardia or heart block caused by manipulation of the carotid baroreceptor
can be treated with atropine. (Infiltrate the area of the carotid sinus with LA by surgeon,
to prevent this response, but the infiltration itself can induce bradycardia).
ABG: PaCO2 should be in the normal range (PaCO2 intracerebral steal, extreme
PaCO2 cerebral perfusion).
Heparin (50007500 IU, IV) is usually administered prior to occlusion of the carotid
artery. Protamine, 50150 mg, to reverse heparin @ skin closure.
Postoperative:
Postoperative hypertension may be related to surgical denervation of the
ipsilateral carotid baroreceptor. Denervation of the carotid body blunts the
ventilator response to hypoxemia.
Postop wound hematoma can compromises the airway, the initial treatment maneuver
require opening the wound to release the hematoma.
Transient postop hoarseness & ipsilateral deviation of the tongue may be noted; they
are due to intraop retraction of the recurrent laryngeal or hypoglossal nerves,
respectively.

Q-3: Pre-operative assessment and principles of anesthetic management for 45-year

lady presented for bronchial carcinoid tumor removal surgery.

Carcinoid syndrome is the complex of symptoms & signs caused by the secretion of
vasoactive substances (e.g., serotonin, kallikrein, histamine).
Highest incidence in GIT (67%) & bronchopulmonary system (25%). GIT tumors
release their metabolic products into portal circulation destroyed by liver before
causing systemic effect, whereas the products of non-intestinal tumors (e.g. pulmonary,
ovarian) bypass portal circulation and therefore can cause variety of clinical
manifestations.
Mediators and their Clinical Manifestations:
Serotonin: Vasoconstriction (coronary artery spasm, hypertension), increased
intestinal tone, water and electrolyte imbalance (profuse diarrhea).
Histamine: Vasodilatation (hypotension, flushing), arrhythmias, bronchoconstriction.
Kallikrein: Vasodilatation (hypotension, flushing), bronchoconstriction.
So, the most common manifestations are cutaneous flushing, bronchospasm, profuse
diarrhea, dramatic unpredictable, swings in arterial blood pressure (usually
hypotension), and supraventricular arrhythmias.
 Carcinoid syndrome is associated with Rt-sided heart disease caused by valvular
and myocardial plaque formation, and, in some cases, implantation of tumors on
the tricuspid and pulmonary valves.
Symptomatic treatment; Somatostatin, an inhibitory peptide, reduces the release of
vasoactive tumor products.
Pre-operative assessment
Diagnosis & investigations:
Serology: 5-hydroxyindoleaceticacid (5-HIAA) (73% sensitivity & 100%
specificity). Chromagraffin-A (glycoprotein) is 95% specific & 80% sensitive.
Imaging: CT-scan for metastasis.
Routine labs & investigations + Echo.
There are 2 specific areas of concern for planning anesthetic management:
1. Cardiovascular history & assessment:
- Rt or biventricular heart failure (may complicate chronic, excessive hormone
release), pulmonary stenosis, or all may also be present.
- Coronary artery spasm may occur during flushing episodes.
- Carcinoid heart disease: Reduced exercise tolerance, orthopnoea, paroxysmal
dyspnoea, & peripheral edema.
2. Uncontrolled hormone release precipitated by surgical stimulus (hypo- or
hypertensive crises & hemodynamic collapse) unresponsive to conventional
inotrope & pressors. It is essential to minimize tumor activity preop using
octreotide (long-acting somatostatin analogue), infusion 50 mg/h for at least 12 h
immediately preop.
Anesthetic Considerations
The key to perioperative management is to avoid anesthetic & surgical techniques or
agents that could cause release of vasoactive substances.
Invasive monitoring is vital. If there is intrinsic heart disease caused by carcinoid
syndrome, TEE may be helpful.
Thoracic epidural insertion before GA induction may limit release of hormones
perioperatively and provide postop analgesia.
Large bolus doses of histamine-releasing drugs (eg, morphine & atracurium) should be
avoided.
One lung anesthesia (OLA) is essential for bronchial carcinoid tumor removal
surgery
Surgical manipulation of the tumor can cause a massive release of hormones.
Vasoconstrictors:
- Response to inotropic & vasopressor is unpredictable.
- Generally, nor-epinephrine and epinephrine can be HAZARDOUS in carcinoid
patients. Nor-epinephrine can activate kallikrein in the tumor & can even lead to
the synthesis & release of bradykinin, resulting in further VD and worsening
hypotension, although exaggerated hypertensive responses may be seen.
- Phenylephrine; cautious administration of small doses of has been found helpful.
 - Octreotide IV boluses of 2050mg titrated to hemodynamic response.
- Vasopressin if prolonged VC is required.
- Labetalol infusions have been used for prolonged hypertension, (as has alpha
blockade).
Hourly ABG & glucose monitoring which may become problematical. Alterations in
carbohydrate metabolism may lead to unsuspected hypoglycemia or hyperglycemia.
Post-operative high-dependency care
High-dependency care or ICU is recommended.
Care will focus on stable cardio-respiratory conditions and adequate analgesia
(Thoracic epidural).
As surgery may have been aimed at reducing the bulk of the tumor, rather than
eliminating it, ongoing hormonal control is important as postoperative crises are
possible.
48 hours of invasive monitoring, analgesia and fluid management may be required
to ensure safe recovery from the surgery.
IV then SC octreotide follow-up will be needed to help control any further hormone
release.

Q-4: Minimally invasive and non-invasive cardiac output monitoring.

The concept of determining blood flow over time (CO) by measuring the dilution of a
known substance in the blood has (Ficks principle) applied by PA catheter using the
thermodilution technique remains the gold standard approach of CO monitoring.
However it is not without risk.
I. Esophageal Doppler Ultrasonography
Principle:
- It measures blood flow velocity in the descending thoracic aorta by using the change in
frequency of US beam as it reflects off a moving object (Doppler shift).
- If this measurement is combined with an estimate of the cross-sectional area of the
aorta (derived value from pts age, height & weight using normograms), it allows
hemodynamic variables to be calculated (SV, CO & CI).
Advantage: provides continuous measurements
Limitations: the following three conditions must be met to guarantee accuracy:
- The cross sectional area must be accurate;
- The US beam must be directed parallel to the flow of blood;
- The beam direction cannot move to any great degree between measurements.
Variations in the above conditions lead to inaccuracies.
Disadvantages:
 - The main problem with its use as a continuous CO monitor relates to its precision which
indicates the reproducibility of a measurement.
- It is operator dependant and it is very easy for the position of the probe to change
between measurements which will reduce the precision.
- Need for frequent repositioning not well tolerated by an awake pt, and is therefore need
sedation.
II. Echocardiography (TransThoracic & TEE)
Principle:
- This technique can be used to calculate SV which can then be multiplied by HR to
give the CO.
- For the assessment of SV; 2 steps are necessary;
i) Calculation of flow velocity from the area under the Doppler velocity wave. This
represents the distance RBCs are projected forward in one cardiac cycle.
ii) Determination of area through which the flow is pushed forward (calculated from
the diameter assuming a circular shape or determined by direct planimetry).
Measurements can be performed at the level of the PA, MV or AV.
Advantage: good correlation with thermo-dilution cardiac CO measurements providing
that the MV is competent.
Limitations:
- it is very difficult to measure the diameter of the pulmonary artery,
- Measurement at the mitral valve is even more difficult because the shape & size of the
valve changes during the cardiac cycle
- The aortic valve is the third option for Doppler assessment which can be performed
using transgastric or deep transgastric views. In the absence of aortic stenosis this
method is the most accurate for CO measurements.
Disadvantages:
- TEE cannot be tolerated by an awake patient as a continuous CO monitor.
- Esophageal damage by the probe & mediastinitis.
III. Thoracic Electrical Bioimpedance
Principle:
- Changes in thoracic volume cause changes in thoracic resistance (bioimpedance) to
low amplitude, high frequency currents. If thoracic changes in bioimpedance are
measured following ventricular depolarization, SV can be continuously determined.
- Increasing fluid in the chest results in less electrical bioimpedance.
- This noninvasive technique requires 6-electrodes to inject microcurrents & to sense
bioimpedance on both sides of the chest.
- Mathematical assumptions and correlations are then made to calculate CO from
changes in bioimpedance.
Advantage: simple, quick, very non-invasive with minimal patient risk.
Limitations The accuracy is questionable in several groups of patients, e.g.; those with
aortic valve disease, previous heart surgery, or acute changes in thoracic sympathetic
nervous function (e.g., those undergoing spinal anesthesia).
 Disadvantages :
- Electrode susceptibility to electrical interference.
- Electrode placement is an important source of error.
- Measurements influenced by intrathoracic fluid shifts & changes in Hct.
IV. Lithium Dilution CO (LiDCO)
Principle
- Depends on indicator dilution technique which is minimally invasive, requiring
only venous (central or peripheral) & arterial lines.
- The indicator is isotonic lithium chloride (LiCl) which is injected as a very small
bolus (0.3mmol) via the venous line. LiCl is not normally present in the plasma &
not metabolized, and is excreted almost entirely in the urine.
- A LiCl sensitive sensor, attached to the peripheral arterial line, detects the
concentration of LiCl ion in the arterial blood.
- The LiCl indicator dilution wash-out-curve provides accurate absolute CO value.
Advantage
- Simple & minimally invasive,
- As accurate as, or more accurate than bolus thermodilution.
- Safe & does not elicit any hemodynamic changes that are sometimes seen with
injections of cold saline.
Limitations & Disadvantages
- The clinical margin of safety: Although the amount of LiCl injected is 100 lower
than the lowest clinical doses of lithium treated patients, it is recommended to
administer not more than 10-20 boluses of lithium.
- Side-effects of multiple injections over a short time need to be investigated.
V. Pulse Pressure Analysis Techniques (Pulse Contour Devices)
Principle
- Utilize the arterial pressure tracing curve to estimate the CO and other dynamic
parameters, (SV, SVR, and BP).
- It measures the area of the systolic portion of the arterial pressure trace from end
diastole to the end of ventricular ejection, together with an individual calibration
factor to account for individual vascular compliance.
- Some devices use thermodilution or lithium dilution for calibration for subsequent
measurements.
- Some devices (FloTrac; Edwards Life Sciences) do not require calibration with
another measure and relies upon a statistical analysis and algorithm.
Advantage
- Offers beat-to-beat non-invasive CO measurement.
- Reliable, accurate, precise and comparable to PA-thermodilution.
- Frequent recalibration, or even no-calibration (FloTrac) is not required.
Disadvantages: cost.
Q-5: Platelet transfusions: preparation, response to transfused platelets, indications
and adverse effects.

Platelet Preparation
Platelets are obtained either by pooling the platelets from multiple donors, or by from a
single donor using apheresis techniques.
Pooled Platelets:
- Platelets are separated from fresh whole blood by centrifugation, and the resulting
platelet concentrates from 5 units of whole blood (from 5 individual donors) are
pooled together prior to storage.
- The pooled platelet concentrate contains about 381010 platelets in 250mL plasma,
which is equivalent to a platelet count of about 130109/L. This is 6 times higher
than the normal platelet count in blood (150400103/L).
- Platelets are stored at 2024C, and can be stored for up to 5 days.
Apheresis Platelets:
- From a single donor and have a platelet count & volume equivalent to the pooled
platelets from 5 donors.
- The presumed benefit is a lower risk of transmitted infections and a lower incidence
of platelet alloimmunization (i.e., developing antibodies to donor platelets).
Leukoreduction:
- Leukocyte reduction before platelet transfusions (using specialized filters) has the
following advantages: a) lower incidence of cytomegalovirus transmission
(transmitted in leukocytes), b) fewer febrile reactions, and c) lower incidence of
platelet alloimmunization. Because of these advantages, leukocyte reduction is
becoming a routine practice for platelet transfusions.
Response to Transfused Platelets
- Platelets extracted from one unit of whole blood expected to raise the recipient count
by 7000-10000/L within one hour post-transfusion.
- Since an average of 5 whole blood platelet concentrates are pooled together for each
platelet transfusion, the expected increase in recipient platelet count is 35,000-
50,000/L at one hour post-transfusion.
- This count usually decreases by about 40% within 24 hours.
- Multiple Transfusions: Development of antiplatelet antibodies (directed at ABO-
Ag on donor platelets) creates platelet refractoriness with repeated transfusions
leads to decrease the expected post-transfusion raise in platelet count by about 25%
after 5 platelet transfusions. This can be reduced by transfusing ABO-matched
platelets.
Indications for Platelet Transfusions
Active Bleeding:
- Platelet transfusions are recommended to maintain a platelet count >50,000/L.
- For intracranial hemorrhage, higher platelet counts (>100,000/L) should be
maintained.
No Active Bleeding:
 - In the absence of bleeding (other than ecchymoses or petechiae), prophylactic
platelet transfusions are usually recommended when the platelet count reaches
10,000/L.
Platelet Count & Surgical Procedures:
- In the absence of associated coagulation abnormalities platelet count of:
>40,000/L is sufficient to perform, tracheostomy, percutaneous liver biopsy, &
bronchoscopic or endoscopic biopsy.
>50,000/L for major elective non-neuraxial surgery.
>50,000/L is sufficient to perform lumbar punctures.
>20,000/L is sufficient to perform CVL cannulation safely.
Adverse Effects
Bacterial Transmission: Bacteria flourish more in platelet concentrates than in
PRBC because platelets are stored at room temperature (22C), while RBCs are
refrigerated at about 4C.
Fever:
- Febrile nonhemolytic reactions reported to be 30% of platelet transfusions,
compared to 0.5% with RBC transfusions.
- Since antibodies to donor leukocytes (multiple donors) are implicated in this
reaction, leukocytic depletion of platelet products will reduce this problem.
Hypersensitivity Reactions:
- Hypersensitivity reactions (urticaria, anaphylaxis, anaphylactic shock) are also
more common with platelet transfusions that with RBC transfusions.
- This is due to reaction to donors plasma proteins, so; removing the plasma from
platelet concentrates will reduce this risk.
Transfusion-related acute lung injury (TRALI):
- It is an inflammatory lung injury similar to ARDS, most often associated with RBC
transfusions, but has also been reported in association with platelet transfusions.
- Believed to be antileukocyte antibodies in donor blood that activates neutrophils
in the recipient.
- TRALI usually appears within 6 hours after the start of a transfusion, and
management is supportive.

-<>*<>*<>*<>*<>*<>*<>*<>-