critical incidence n.
Skip this Video
Loading SlideShow in 5 Seconds..
Critical Incidence PowerPoint Presentation
Download Presentation
Critical Incidence

Loading in 2 Seconds...

play fullscreen
1 / 60

Critical Incidence - PowerPoint PPT Presentation

  • Uploaded on

Critical Incidence. By : Azhar Faruqi Mohd Rasani Supervisor : Dr NORASLAWATI BINTI RAZAK. Madam N, G1 P0 at Date + 1 day No known medical illness antenatally just had one episode of albuminuria at 17W with UTI symptoms treat as UTI BP normotensive all over the pregnancy.

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about 'Critical Incidence' - skule

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
critical incidence

Critical Incidence

By : AzharFaruqiMohdRasani



Madam N, G1 P0 at Date + 1 day

  • No known medical illness
  • antenatally
    • 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 -rtfrontotemporalintraparenchymal 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
learning issues
Learning Issues
  • Decision regarding intubation
  • Physiological changes in pregnancy
objective measures indicating the need for intubation
Objective measures indicating the need for intubation
  • -RR > 35bpm
  • - VC < 15ml/kg
  • - PaO2 < 60
  • - PaCO2 > 50 (except in chronic retainers)
  • 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 intubate
Decision to intubate

Maintaining airway?

Airway manuevers, Adjuncts


Now maintained?





Protecting airway?


Ventilating / oxygenating



Deterioration / airway

compromise likely?

Consider intubation vs. close observation

Rapid transport



Supp. O2, Observe, Transport

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


  •  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


  • 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 airways

2. 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 FVC

5. 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

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)

 paO2by 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

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


  • 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 Output

    • decrease 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
SystemicVascular 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 section
Suggested procedure for GA for caesarean section
  • Ensure well functioning IV line
  • Administer non-particulate antacid and H2 receptor antagonist
  • Place patient in the supine with left uterine displacement
  • Apply standard ASA monitors
  • Preoxygenate, ideally 3-5 minutes
  • Administer induction agent with rapid sequence induction
    • Propofol 2mg/kg
    • Thiopental 4mg/kg
    • Etomidate 0.2-0.3mg/kg
    • Succinylcholine 1-1.5mg/kg
  • Apply cricoid pressure

Intubate with cuffed endotracheal tube

  • Confirm placement ETT
  • Administer 100% oxygen plus 0.5-1 MAC of halogenated agent
  • 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
  • Administer uterine contractile agent
  • Closely monitor uterine tone and bleeding
  • Extubate the patient once fully awake.