Download - Critical Incidence
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Critical IncidenceBy : Azhar Faruqi Mohd Rasani
Supervisor : Dr NORASLAWATI BINTI RAZAK
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Madam N, G1 P0 at Date + 1 dayNo known medical illnessantenatally
◦ just had one episode of albuminuria at 17W with UTI symptoms
◦ treat as UTI◦ BP normotensive all over the pregnancy
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presented to hospital dungun on 10/5/14 with -severe headache for 3/7 +occipital headache +neck pain +vomitting x6 +fever for 3/7 a/w chills and rigor
+left side body weakness for 1/7 +numbness
no fitting episode no hx of trauma
then was referred to HSNZ for suspected encephalitis
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on examination GCS 14/15 (e4v5m5) orientated to time place and person look drowsy
+left facial assymetry +neck stiffness bilateral pupil reactive and equal 2mm Gag reflex present
bp 143/73 pr 80 t 37.7
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cns examination◦ right side
both upper and lower limbs normal power 5/5 normal tone reflex brisk, babinski equivocal
◦ left side hypotonia power 4/5 reflex brisk, babinski equivocal
Impression at this time space occupying lession, tro intracranial bleeding
Then proceed with CT brain plain
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ct brain -rt frontotemporal intraparenchymal with intraventricular extension with significant mass effect
abg : respiratory alkalosis◦ (ph 7.5 pco2 23 pos2 123 hco3 20.7)
was electively intubated for respiratory alkalosis and going for OP◦ premedication - given iv fentanyl 50mcg, iv midazolam 5mg, iv
scolene 50mg◦ intubated with ETT size 7mm anchored at 20cm◦ start on sedation iv midazolam 2mls/hr
then was sent to OT for EMLSCS + rt decompression craniectomy + EVD left side
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in OT was induce with sevoflurane gases and oxygen◦ iv esmeron 50mg
then connect to ventilator VC◦ VT 400 , rate 12, peep 4, I:E 1:2◦ maintained with sevofurane
intra operative given ◦ iv fentanyl 100mcg ◦ iv morphine 3mg + 3mg + 2 mg
EBL for emlscs - 500mls
◦ baby was born flat, intubated and was sent to NICU◦ able to extubate after arrive at NICU◦ and was put under headbox oxygen
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after EMLSCS proceed with neurosurgery operation
intraoperative findings◦ two yellowish soft tumour 3x3cm surrounded by blood clots◦ blood clot evacuate 40cc◦ pulsatile brain◦ pre op pupil rt 2mm lt 2mm◦ post op pupil rt 4mm lt 3mm
done rt craniotomy + evacuation of clots and tumour EBL 700mls
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intra op given ◦ 2 pint WB◦ 6 pints NS◦ started on iv noradrenaline single strength 2-5mls/hr
ABG at 7pm◦ ph 7.31 pco2 35 po2 257 so2 99 be -7.4 hco3 18.5◦ lactate 1.1
ABG at 10pm◦ ph 7.22 pco2 40 po2 200 so2 99 be -10 hco3 16.2◦ lactate 2
post operation was sent to ICU for weaning◦ not for CP
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over the night was sedated on mida morphine infusion
next morning GCS 11/15 obey command abg good on CPAP mode
then was extubate to VMO2 and was sent to radiology department to repeat
CT brain
repeated CT brain
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Decision regarding intubationPhysiological changes in pregnancy
Learning Issues
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-RR > 35bpm - VC < 15ml/kg - PaO2 < 60 - PaCO2 > 50 (except in chronic retainers)
Objective measures indicating the need for intubation
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Indications: For supporting ventilation in patient with pathologic
disease:◦ Upper airway obstruction,◦ Respiratory failure,◦ Loss of consciousness
For supporting ventilation during general anaesthesia:◦ Type of surgery:
Operative site near the airway, Thoracic or abdominal surgery, Prone or lateral surgery, Long period of surgery
Patient has risk of pulmonary aspiration Difficult mask ventilation
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Decision to intubateMaintaining airway?
Protecting airway?
Ventilating / oxygenating adequately?
Deterioration / airway compromise likely?
Airway manuevers, Adjuncts
Now maintained? Intubate
Consider intubation vs. close observationRapid transport
Supp. O2, Observe, Transport
no
noyes
yes
yes
yes
yes
no
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PHYSIOLOGICAL CHANGES IN PREGNANCY
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The changes in maternal homeostasis a/w pregnancy – adaptive & useful to the mother in tolerating the stresses of pregnancy, labour & delivery
It involved (virtually every organ system) -hormonal changes –physiological
preparation for pregnancy (after ovulation) progesterone
-↑ of bld volume meet the metabolic demand following conception
Maternal physiological changes return to normal following parturition
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PHYSIOLOGICAL CHANGES IN RESPIRATORY SYSTEM
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Anatomy ¨ vertical measurement of the chest as much as 4 cm
results from elevated position of the diaphragm its contraction not markedly restricted
¨ AP and transverse diameter (2-3 cm) in the subcostal angle from 68.5 to 103.5˚ at term
as a result of flaring out of lower ribs¨ in thoracic cage circumference by 5-7 cm (early
pregnancy)¨ Changes produce by relaxin (secreted by corpus luteum)
that relaxes the ligamentous attachments of the ribs
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Anatomy (Upper Respiratory Tract)◦ Hyperemia & edema induced by estrogen ◦ Nasal stuffiness & epistaxis ◦ Capillary engorgement throughout the resp.
tract (nasal, oropharyngeal mucosa & larynx), vocal cord may be swollen or edematous
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Anatomy Airway conductance - indicates dilation of
larger airway below the larynx◦ Factors contributing to airway dilation :
Direct effects of progesterone, cortisone & relaxin Possibly enhanced -adrenergic activity induced by
progesterone
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Mechanics of breathing
1. Dilatation of large airways2. No change in max. expiratory flow rate (PEFR)3. No change in forced expiratory volume in 1 sec
(FEV1)4. No change in ratio of FEV1 to FVC5. Flow-volume loops are unaffected & airway
resistance decreases
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Lung volumes & capacities Tidal volume: 40-45%
◦ with approx. half of the change occurring during the 1st trimester
◦ This early change is a/w a reduction in Inspiratory Reserve Volume (IRV)
◦ The changes during the later half is accompanied by a decline in FRC & increased in IRV
◦ Chest wall compliance & total lung compliance decrease 30% increase in minute volume (50%)
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Lung volumes & capacities
FRC : 20% begins by 5th month of pregnancy caused by elevation of the relaxed diaphragm occurs as the
enlarging uterus enters the abdominal cavity ↓ by 20% at term contributed by 25% reduction in ERV &
15% reduction in RV Return to normal 48H post delivery Decrease in FRC d/t reduction in ERV as a result of larger
than normal VT
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Lung volumes & capacities
Inspiratory capacity 15% ◦ during the 3rd trimester because of the in VT
and IRV Vital capacity & closing capacity is
unchanged ◦ because of corresponding in ERV
Total lung capacity ↓ slightly (0-5%)
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Lung volumes & capacities
minute ventilation by 45-50% results from in VT alveolar ventilation by 45%
-hormonal changes Progesterone & Estrogen- CO2 production-PaCO2 is closely related to the bld level of progesterone◦ this hormone the sensitivity of the central resp
center to CO2 & acts as a direct resp stimulant
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VARIABLE NON-PREGNANT TERM PREGNANTVT 450ml 650ml (45%)
RR 16 p/min 16 p/min
VC 3.2 L 3.2 L
IRV 2.05 L 2.05 L
ERV 700ml 500ml (-25%)
FRC 1600ml 1300ml (-20%)
RV 1.0 L 0.8 L (-20%)
paO2 /pH 11.3kPa/7.4 12.3kPa/7.44
pCO2 4.7-5.3kPa 4.0kPa
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Lung Functions in Pregnancy
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Anatomical dead space unchanged (until late pregnancy upper airway edema-reduction)
Physiological DS decreases but intrapulmonary shunting increases towards term
VD/VT ratio unchanged ↓ dead space narrows the arterial end-tidal CO2 gradient CXR: prominent vascular markings d/t ↑ pulm bld volume
& an elevated diaphragm
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Elevation of the diaphragm decreases the volume of the lungs in the resting state, reducing TLC by 5% and FRC by 20%
FRC mainly decreased by RV Vital capacity does not change
◦Spirometry is not changed in pregnancy
◦FEV1 is unchanged ◦Peak flow is unchanged
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paCO2 by 15 %◦ Decrease to 28-32 mmHg◦ Due to resp.alkalosis -every 0.13kPa increase in pCO2,ventilation
increase 6 l/min compare non-pregnant 2 l/min -compensates by ↓ plasma [HCO3]◦ Hyperventilation increase PaO2 slightly◦ During 2nd and 3rd trimester◦ Progesterone enhance the response of the resp.
centre to CO2 ◦ ODC curve shifted to Rt (rise in 2,3 DPG)
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paO2 by 10 %◦ results from in paCO2 and arteriovenous
oxygen difference, which reduces the impact of venous admixture on the paO2
◦ O2 consumption(Vo2) increases 250-500ml/min
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Arteriovenous oxygen difference - smaller in early pregnancy because
in CO is greater than the in O2 consumption- as pregnancy progresses, O2 consumption
continues to while CO to a lesser degree, resulting in decreased mixed venous O2 content and increased AV O2 difference
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Anaesthetic Implication Rapid alveolar & arterial hypoxia during periods of apnoea /
airway obst. d/t combination of FRC & O2 consumption-adequate preoxygenation
Easily atelectasis & hypoxemia when in supine position closing volume > FRC
-O2 supplement during supine
Accelerate the uptake of all inhalational agent combination of FRC & minute ventilation
- MAC by 15-40%
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Anaesthetic Implication As a result of capillary engorgement of the
mucosa:◦ ↑ risk upper airway trauma, bleeding &
obstruction apply gentle laryngoscopy & use smaller ETT
◦ ↑ risk URTI can further compromised the airway
◦ Avoid nasotracheal intubation◦ Mallampati score
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PHYSIOLOGICAL CHANGES IN CARDIOVASCULAR
SYSTEM
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Examination of the heart Grade 1 or 2 early to mid (ejection) systolic murmur
is commonly heard at the left sternal border D/t cardiac enlargement, which results in dilation
of tricuspid annulus that causes regurgitation ECG –Lt axis deviation, flattened/inverted T-waves,
occasionally ST depression
CXR appearance of enlarged heart d/t elevation of the
diaphragm, shifts the heart’s position
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Cardiac Output◦ accompanied increase the bld volume (to meet the
metabolic demand)◦ reaching 35-40% (1.5 L/min) by end of 1st trimester◦ continues to till 3rd trimester, until reaching 44-
50% as a result of increase in HR (15-20%) and SV (30%)
◦ Double during labour esp. 2nd stage◦ May further increase immediate post delivery (d/t
autotransfusion)◦ Return to normal after 2 wks post delivery
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Cardiac Outputdecrease in CO in supine position after 28th week
of pregnancy, 2° to impeded VR as the enlarging uterus compresses the IVC
At 38-40 weeks, there is a 25-30% fall in CO when turning from the side to the back
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Stroke volume ◦ approx. 20% between 5th and 8th week of gestation◦ by 25-30% by end of 2nd trimester till term
CVP, PA and PCWP ◦ similar to nonpregnant levels (relaxant effect of
progesterone on the smooth ms)
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Systemic Vascular Resistance
SVR is reduced during pregnancy average SVR in pregnancy is about 980
(1150 dynes.s cm−5 in non-pregnant women)
Decrease in SVR results from development of a low-resistance vascular bed (the intervillous space) & vasodilatory effects of oestrogens, prostacyclin & progesterone
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Regional blood flow Uterine blood flow
◦ before conception from 50-190 ml/min, to 700-900 ml/min at term
◦ 90% perfuse the intervillous space with the balance to myometrium
Skin perfusion ◦ begin to at 15 wks of gestation, reaching to 3-4
times the non-pregnant level at term◦ Results in an skin temperature
Blood flow to brain & liver do not change
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Distribution of CO◦ First trimester and non-pregnant state
Uterus receives 2-3%◦ By term
Uterus receives 17% Breasts 2%
◦ Reduction of the fraction of CO going to the splanchnic bed & skeletal ms
◦ CO to the kidneys, skin, brain and coronary arteries does not change
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Arterial and venous pressures
SBP -minimally affected◦ Max. about 8 % during early to mid-
gestation◦ Return to pre-pregnant level at term◦ Explained by aortic size & compliance in spite
of SV, lesser degree of reduce SVR
DBP◦ by 20 % at 2nd trimester◦ Return to pre-pregnant level at term◦ Consistent with decrease in SVR
Decrease in SVR – decrease both DBP and SBP
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Aortocaval Compression Degree of compression of the aorta and IVC
by term gravid uterus depends on the position of the pregnant women
Supine position ◦ Cause complete or nearly complete obstruction of
IVC - occur as early as 13-16 wks/28wks◦ causes 10-20% reduction in SV and CO (supine
hypotension synd) 20% of women @ term
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SUPINE HYPOTENSION SYNDROME Incidence: 1-10% of patients Hypotension a/w pallor, sweating or N/V D/t complete/near complete occlusion of IVC by
gravid uterus Turning the pt on her side restores VR from the
lower body & correct the hypotension Trendelenburg position exacerbate caval
compression gravid uterus also compresses the aorta in supine
position decrease bld flow to the lower extremities & uteroplacental circulation
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Aortocaval Compression Combination of systemic hypotension (d/t ↓ VR),
↑ uterine venous pressure & uterine arterial hypoperfusion severely compromises uterine & placental bld flows
When combined with the hypotensive effects of regional/GA, aortocaval compression can produce fetal asphyxia
Parturients should not be placed supine w/out left uterine displacement placed a wedge >15° under the right hip
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Aortocaval Compression◦ VR is not maintained in spite of collateral
circulation◦ Obstruction of the gravid uterus on illiac veins
and IVC, thus increase pressure in the femoral & other leg veins
◦ Developed varicose vein
Lateral decubitus position ◦ cause partial caval obstruction◦ VR maintains by collateral circulation reflected
by unaltered RV filling pressure
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Chronic partial caval obstruction In 3rd trimester Predisposes to venous stasis, phlebitis,
edema Compression of IVC distends &
increases blood flow through collateral venous drainage (paravertebral venous plexus)
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Suggested procedure for GA for caesarean section1. Ensure well functioning IV line2. Administer non-particulate antacid and H2 receptor
antagonist3. Place patient in the supine with left uterine displacement4. Apply standard ASA monitors5. Preoxygenate, ideally 3-5 minutes6. Administer induction agent with rapid sequence
induction◦ Propofol 2mg/kg◦ Thiopental 4mg/kg◦ Etomidate 0.2-0.3mg/kg◦ Succinylcholine 1-1.5mg/kg
7. Apply cricoid pressure
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8. Intubate with cuffed endotracheal tube9. Confirm placement ETT10. Administer 100% oxygen plus 0.5-1 MAC of
halogenated agent11. Once baby delivered, administered 50% NO2
and 50% oxygen, decrease volatile agent to < 0.5 MAC and consider adding opiods and/or muscle relaxants as necessary
12. Administer uterine contractile agent13. Closely monitor uterine tone and bleeding14. Extubate the patient once fully awake.
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Thanks for your attention!