Critical IncidenceBy : Azhar Faruqi Mohd Rasani

Supervisor : Dr NORASLAWATI BINTI RAZAK

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

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

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

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

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

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

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

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

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

Decision regarding intubationPhysiological changes in pregnancy

Learning Issues

-RR > 35bpm - VC < 15ml/kg - PaO2 < 60 - PaCO2 > 50 (except in chronic retainers)

Objective measures indicating the need for intubation

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

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

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PHYSIOLOGICAL CHANGES IN PREGNANCY

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

PHYSIOLOGICAL CHANGES IN RESPIRATORY SYSTEM

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

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

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

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

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%)

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

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%)

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

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

Lung Functions in Pregnancy

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

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

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)

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

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

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%

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

PHYSIOLOGICAL CHANGES IN CARDIOVASCULAR

SYSTEM

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

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

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

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)

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

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

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

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

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

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

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

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

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)

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

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.

Thanks for your attention!