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Respiratory failure
during pregnancy
By
Samiaa Hamdy Sadek
Professor of chest diseases
Assiut University
 Introduction
 Respiratory physiology during
pregnancy
 Causes of respiratory failure during
pregnancy
 Management of respiratory failure
during pregnancy
Agenda:
 Although estimated frequency of respiratory
failure during pregnancy is low (ranged
between 0.2-0.3% of pregnancies), it has
significant morbidity and mortality for both
mother and fetus.
Introduction:
 Physiological and mechanical changes during
pregnancy in addition to increased metabolic
requirement of the fetus, and impaired native
immunity, all of these expose pregnant women to
greater risk of respiratory failure even with trace
insult.
 Careful assessment and early management can
significantly improve the prognosis
Introduction:
Respiratory physiology during
pregnancy
 Enlarging uterus and elevation of the diaphragm
are compensated by increase in the
circumference of the lower chest wall by 5-7cm ,
increase in anteroposterior and transverse
diameters, resulting in widening of the costal
angle from 68° to 103.
 Increase in tidal volume (TV) 30-50% accounts
for mild respiratory alkalosis despite normal
respiratory rate.
Anatomical and lung volume
changes:
 NB. tachypnea often is a sign of underlying
pathology even during pregnancy.
 Total lung capacity decreases by 4-6%
 Functional residual capacity (ERV+RV)decreases
by 15-25%
 Inspiratory capacity increased 5-10%
 Minute ventilation increases by 20-45%
 Dead space ventilation increased
 Alveolar ventilation increased 45%
Anatomical and lung volume
changes:
 Pregnancy associated with 30% decrease in
chest wall, total respiratory compliance despite
that lung compliance unchanged.
 Elevation of the diaphragm, and reduced FRC
resulting in small airway closure even with
minimal decrease in lung volume, leading to
basal atelectasis.
 The above factors in addition to increased
oxygen requirement significantly increased risk
of desaturation during pregnancy.
Respiratory mechanics during
pregnancy
 Colloid osmotic pressure of both serum and
pulmonary capillary wedge decreased, so
pregnant women more susceptible to
pulmonary edema if there is increase in
cardiac preload or pulmonary capillary
permeability
Continue:
‫الرحيم‬ ‫الرحمن‬ ‫هللا‬ ‫بسم‬
 Mild compensated respiratory alkalosis
 The normal partial pressure of carbon dioxide (PaCO2) during
pregnancy is 27-34 mmHg as a result of respiratory center
stimulation by the progesterone and increased minute
ventilation.
 The partial pressure of oxygen (PaO2) is between 90 and 110
mmHg.
 Serum bicarbonate (HCO3) decreased between 18 mEq/L to
21 mEq/L
 The alveolar-arterial gradient increases 26 mm Hg
Arterial blood gases during
pregnancy:
Anatomical and functional changes
during pregnancy
Anatomical
changes:
• Airway edema and
friability
• Elevated
diaphragm and
widened AP and
transverse D
• Widened
subcostal angle
• Enlarged uterus
Functional
changes:
• Increased
respiratory
derive
• Decreased TLC,
FRC, and
increased IC, VE
• Increased O2
consumption and
CO2 output
• Widened (A-a) O2
gradient.
Obstetric causes Non obstetric causes
Hypertensive disorder Venous thromboembolism
Amniotic fluid embolism Cardiovascular disease
Ovarian hyper-stimulation
syndrome
Pulmonary artery hypertension
Acute fatty liver of pregnancy Bronchial asthma
Peripartum cardiomyopathy Respiratory infection
Chemical pneumonitis Neuromuscular disorders
Tocolytic induced pulmonary
edema
Sepsis
Septic abortion, chorioamnionitis,
endometritis
Causes of respiratory failure
during pregnancy:
 Aspiration of gastric content, more common with
general anesthesia.
 Pregnancy related weak gastroesphageal sphincter,
delayed gastric emptying, and increased gastric
pressure all potentiate incidence.
 ARDS , possibly complicated by PE and deteriorating
ventilatory parameters common presentation.
 Regional anesthesia, and fair use of antacid a H2
blocker with rapid sequence induction(RSI) can
decrease the risk.
NB. High antacid dose increase risk of vomiting
RSI means rapid intubation following induction of anesthesia
Mendelson’s syndrome(chemical
pneumonitis)
 As a result of disruption of maternal-fetal barrier
fetal antigens enter maternal vasculature, where
anaphylactic inflammatory response occurs.
 Increased both systemic, and pulmonary
vascular resistance, decreased COP, RF, and
shock.
 Treatment mainly supportive through MV, careful
use of IV fluid, blood product, and correction of
coagulopathy
 Prognosis poor.
Anaphylactic syndrome of
pregnancy(amniotic fluid embolism)
 It occurs as a result of air entry through sub-
placental venous sinus during any of the
following maneuvers (douching, vaginal
insufflation, criminal abortion, or normal labor)
 Sudden death is common, also PAH, right heart
failure, or PE can developed.
Air embolism:
 With increasing use of assisted reproductive
techniques OHSS is increasingly observed.
 Increased capillary permeability as a side effect of
gonadotropin, and clomiphene citrate is possible
mechanism.
 CP include dyspnea, rapid weight gain, anasarca,
nausea, vomiting, abdominal pain ,
thromboembolism, and organ failure.
 Treatment include gonadotropin releasing hormone
antagonist, loop diuretics, albumin, anticoagulant,
fluid as needed, and ventilatory support.
Ovarian hyper-stimulation
syndrome(OHSS)
 From 3rd trimester to the fifth month following labor
is period of risk.
 Oxidative stress secondary to the breakdown of
prolactin hormone is possible mechanism.
 Loop diuretics, ACE inhibitors, vasodilator, inotrops,
b blockers, vasodilators, ventricular assist, and
heart transplantation are suggested lines of
treatment.
Peripartum cardiomyopathy
 Risk factors: cardiac, blood diseases, smoking, DM,
obesity, hormonal replacement therapy, CS, age>35,
personal and family history, multiple pregnancy.
 IV unfractionated heparin is 1st choice, LMWH is the
agent of choice in the antenatal period.
 Warfarin can be initiated 5-7 days post-labor.
 Treatment continue 3-6 months.
 Thrombolytic therapy may be life saving in presence
of unstable hemodynamics.

Venous thromboembolism
Ventilatory support during
pregnancy
 The fetus is sensitive to both hypoxemia and
acidosis.
 Whatever the cause of respiratory failure, the
aim of ventilatory support in pregnant female is
SaO2 >95%, and PaO2>70mmHg.
 The fact that level of carbon dioxide is lower
during pregnancy, and poor tolerance to period
of apnea associated with increased oxygen
consumption makes great recommendation for
not deferred and elective intubation in cases
not responding to initial ventilatory support
General consideration:
 ARF not responding to conventional oxygenation
 Dyspnea , nasal flaring, and use of accessory
muscle of respiration.
 Respiratory muscle fatigue and rising PaCO2
 Failure of improved oxygenation and presistent
hypoxemia despite oxygenation.
 Hemodynamic instability
 Disturbed conscious level
Indications of mechanical
ventilation during pregnancy:
 In sever PAH pregnancy should be avoided or
terminated as recommended in guidelines.
 Prostaglandins mainly epoprostinol is the 1st
choice, phosphodiastrase 5- inhibitor also safe.
 Riociguat, and endothelin receptor antagonists
are cotraindicated.
 Patient should be hospitalized in 20week of
gestation with close monitoring, bed rest,
anticoagulant, and pulmonary vasodilators.
Pulmonary arterial hypertension:
 Non adherence with medication and infection are
major causes of worsening asthma.
 Maternal and fetal outcome are the same in patients
with well controlled asthma, and non asthmatics.
 Indications for hospitalization, ICU admission, and MV
are more or less similar in pregnant asthmatic and
non asthmatic females.
 Sever restrictive lung disease (VC<1 liter) is
contraindication for pregnancy and indication for
termination.
 If pregnancy continued CS is preferred, and post
labor MV may be required.
Bronchial asthma and restrictive
disorders:
 Some studies documented successful outcome of
NIV in controlling ARF during pregnancy.
 Pregnant woman at increased risk of aspiration as a
result of decreased tone of lower esophageal
sphincter, increased intra-gastric pressure, and
delayed gastric emptying.
 Inspiratory pressure (12-15)cmH2O, and expiratory
pressure (5-8) cmH2O are recommended.
Non invasive positive pressure
ventilation
 Failure of improvement within 30-45 minutes is
indication for intubation.
 Meticulous observation fetal heart rate, and
maternal pattern of respiration is highly
recommended.
Non invasive positive pressure
ventilation
Contraindications of NIV in pregnancy include:
 Disturbed conscious level
 Inability to protect the airway
 Hemodynamic instability
 Severe acid base disturbance
 Poor respiratory derive
 GIT bleedng
Non invasive positive pressure
ventilation
Invasive mechanical
ventilation:
The following factors contribute to difficult
intubation in pregnancy:
 Mucosal edema
 Increased mucosal vascularization and risk of
bleeding
 Increased risk of aspiration
So smaller size of endotracheal tube is
recommended (7 mm)
Endotracheal tube:
 The minimum FiO2 required to maintain SaO2 94-98% and
PaO2 60-100mmHg is recommended.
 Hyperoxia (PaO2 >120 mmHg)produce superoxide radicals,
,cytokines, and potentiate lung injury.
 Recommended initial PEEP is 5-8cmH2O to, it can be
increased or decreased according to oxygenation level,
and hemodynamics.
 PEEP guard against alveolar collapse and cyclic
atelectrauma which exaggerated in 3rd trimester duo to
anatomical and physiological changes of pregnancy.
Parameters of invasive
ventilation:
 Recommended Vt is 6-8 ml/kg ideal body weight
in cases other than ARDS.
 IBW=(Height in meter)2*21.5
 For cases associated with ARDS start with Vt
4ml/kg predicted body weight up to 6 ml
 Predicted BW=[(height in cm-152.4)*0.91]+45
Parameters of invasive
ventilation:
 Pplat pressure should be <25-30cmH2O, better to
be measured every 12hour.
 In cases Pplat pressure higher than 30cmH2O Vt
should be decreased to minimum 4ml/kg.
 Another important parameter is the driving
pressure (DP) [ideally 12-16cmH2O]. In presence
of ARDS, it is better to be ≤12cmH2O if higher
decrease Vt.
Parameters of invasive
ventilation:
 Driving pressure =
 Vt/CRS(compliance of respiratory system.
 =Pplat - PEEP
 The driving pressure (DP) [ideally 12-16cmH2O]. In
presence of ARDS, it is better to be ≤12cmH2O if
higher decrease Vt.
Driving pressure:
Aims of mechanical
ventilation during
pregnancy
In VC mode:
PAP≤ 35cmH2O
Pplat ≤ 28cmH2O
DP ≤ 12cmH2O
In case of PC mode:
PI or PS ≤12- 15cmH2O
 PIP peak inspiratory pressure should be adjusted at
≤35cmH2O. Barotrauma is increased with PIP> 35cmH2O
 PIP is the pressure of gas to overcome resistance of the
airway(RAW), so its value is dependent on RAW, lung
compliance, and Vt.
 PIP is the maximum pressure in the airway.
 Bronchospam, mucus plug, occlusion of orotracheal tube,
and more seriously pneumothorax, all of them causing
increased PIP.
Parameters of invasive
ventilation:
 Prone positioning in combination with
neuromuscular blocking agents are
recommended if PaO2/FiO2<150
 Two drugs should be avoided in pregnant women
presented with moderate to severe ARDS in need
for tocolytics: beta agonist and magnisium
sulfate, increase cardiac demand, capillary
permeability, and risk of pulmonary edema.
Parameters of invasive
ventilation:
 Once the patient thermodynamically and
clinically stable, and insult that leads to MV is
controlled weaning process should be initiated.
 pregnant patients have airway and mucosal
edema, so cuff leak test is mandatory for them
before weaning to avoid risk of post extubation
stridor.
Weaning:
Cuff leak test
 Deflating cuff and observe volume time curve leakage.
 >20% or 110ml leak indicate negative test and absence
of post-extubation stridor risk.
 Lower values indicate need for treatment and subsquent
reassessment.
 In case of failed cuff leak test give three doses
20 mg methylprednisolone 12hours apart and
reassess cuff leak test from 2nd or 3rd dose.
Cuff leak test
Cuff leak test
 Deloya-Tomas E, Mondragon-Labelle T, Lopez-Fermin J, Perez-Nieto OR, et al. (2020). Considerations for Mechanical
Ventilation inthe Critically III Obstetric Patient. Crit Care Obst Gyne Vol.6 No.4:10.
 Bhatia PK, Biyani G, Mohammed S, Sethi P,Bihani P. Acute respiratory failure and mechanical ventilation in pregnant
patient: A narrative review of literature. J Anaesthesiol Clin Pharmacol 2016;32:431-9.
 Lapinsky SE (2017) Management of acute respiratory failure in pregnancy. In Seminars in respiratory and critical care
medicine 38:
 201-207.
 Soma-Pillay P, Catherine NP, Tolppanen H, Mebazaa A, Tolppanen H, et al. (2016) Physiological changes in pregnancy.
Cardiovasc J Afr 27:89.
 Amato MB, Meade MO, Slutsky AS, Brochard L, Costa EL, et al.(2015) Driving pressure and survival in the acute
respiratory distress syndrome. N Engl J Med 372: 747-755.
 Guérin C, Papazian L, Reignier J, Ayzac L, Loundou A, et al. (2016) Effect of driving pressure on mortality in ARDS
patients during lungprotective mechanical ventilation in two randomized controlled trials. Crit Care 20: 384.
 Lapinsky SE, Rojas-Suarez JA, Crozier TM, Vasquez DN, Barrett N, et al. (2015) Mechanical ventilation in critically-ill
pregnant women: a case series. Int J Obstet Anesth 24: 323-328.
 Fanelli V, Ranieri MV, Mancebo J, Moerer O, Quintel M, et al. (2016) Feasibility and safety of low-flow extracorporeal
carbon dioxide removal to facilitate ultra-protective ventilation in patients with moderate acute respiratory distress
syndrome. Crit Care 20: 1-7.
 Girard TD, Alhazzani W, Kress JP, Ouellette DR, Schmidt GA, et al. (2017) An official American Thoracic
Society/American College of Chest Physicians clinical practice guideline: liberation from mechanical ventilation in
critically ill adults. Rehabilitation protocols, ventilator liberation protocols, and cuff leak tests. Am J Respir Crit Care
Med 195: 120-133.
 Zein H, Baratloo A, Negida A, Safari S (2016) Ventilator weaning and spontaneous breathing trials; an educational
review. Emergency 4:65.
References:
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Respiratory failure during pregnancy.ppsx

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  • 2. Respiratory failure during pregnancy By Samiaa Hamdy Sadek Professor of chest diseases Assiut University
  • 3.  Introduction  Respiratory physiology during pregnancy  Causes of respiratory failure during pregnancy  Management of respiratory failure during pregnancy Agenda:
  • 4.  Although estimated frequency of respiratory failure during pregnancy is low (ranged between 0.2-0.3% of pregnancies), it has significant morbidity and mortality for both mother and fetus. Introduction:
  • 5.  Physiological and mechanical changes during pregnancy in addition to increased metabolic requirement of the fetus, and impaired native immunity, all of these expose pregnant women to greater risk of respiratory failure even with trace insult.  Careful assessment and early management can significantly improve the prognosis Introduction:
  • 7.  Enlarging uterus and elevation of the diaphragm are compensated by increase in the circumference of the lower chest wall by 5-7cm , increase in anteroposterior and transverse diameters, resulting in widening of the costal angle from 68° to 103.  Increase in tidal volume (TV) 30-50% accounts for mild respiratory alkalosis despite normal respiratory rate. Anatomical and lung volume changes:
  • 8.  NB. tachypnea often is a sign of underlying pathology even during pregnancy.  Total lung capacity decreases by 4-6%  Functional residual capacity (ERV+RV)decreases by 15-25%  Inspiratory capacity increased 5-10%  Minute ventilation increases by 20-45%  Dead space ventilation increased  Alveolar ventilation increased 45% Anatomical and lung volume changes:
  • 9.  Pregnancy associated with 30% decrease in chest wall, total respiratory compliance despite that lung compliance unchanged.  Elevation of the diaphragm, and reduced FRC resulting in small airway closure even with minimal decrease in lung volume, leading to basal atelectasis.  The above factors in addition to increased oxygen requirement significantly increased risk of desaturation during pregnancy. Respiratory mechanics during pregnancy
  • 10.  Colloid osmotic pressure of both serum and pulmonary capillary wedge decreased, so pregnant women more susceptible to pulmonary edema if there is increase in cardiac preload or pulmonary capillary permeability Continue:
  • 12.  Mild compensated respiratory alkalosis  The normal partial pressure of carbon dioxide (PaCO2) during pregnancy is 27-34 mmHg as a result of respiratory center stimulation by the progesterone and increased minute ventilation.  The partial pressure of oxygen (PaO2) is between 90 and 110 mmHg.  Serum bicarbonate (HCO3) decreased between 18 mEq/L to 21 mEq/L  The alveolar-arterial gradient increases 26 mm Hg Arterial blood gases during pregnancy:
  • 13. Anatomical and functional changes during pregnancy Anatomical changes: • Airway edema and friability • Elevated diaphragm and widened AP and transverse D • Widened subcostal angle • Enlarged uterus Functional changes: • Increased respiratory derive • Decreased TLC, FRC, and increased IC, VE • Increased O2 consumption and CO2 output • Widened (A-a) O2 gradient.
  • 14. Obstetric causes Non obstetric causes Hypertensive disorder Venous thromboembolism Amniotic fluid embolism Cardiovascular disease Ovarian hyper-stimulation syndrome Pulmonary artery hypertension Acute fatty liver of pregnancy Bronchial asthma Peripartum cardiomyopathy Respiratory infection Chemical pneumonitis Neuromuscular disorders Tocolytic induced pulmonary edema Sepsis Septic abortion, chorioamnionitis, endometritis Causes of respiratory failure during pregnancy:
  • 15.  Aspiration of gastric content, more common with general anesthesia.  Pregnancy related weak gastroesphageal sphincter, delayed gastric emptying, and increased gastric pressure all potentiate incidence.  ARDS , possibly complicated by PE and deteriorating ventilatory parameters common presentation.  Regional anesthesia, and fair use of antacid a H2 blocker with rapid sequence induction(RSI) can decrease the risk. NB. High antacid dose increase risk of vomiting RSI means rapid intubation following induction of anesthesia Mendelson’s syndrome(chemical pneumonitis)
  • 16.  As a result of disruption of maternal-fetal barrier fetal antigens enter maternal vasculature, where anaphylactic inflammatory response occurs.  Increased both systemic, and pulmonary vascular resistance, decreased COP, RF, and shock.  Treatment mainly supportive through MV, careful use of IV fluid, blood product, and correction of coagulopathy  Prognosis poor. Anaphylactic syndrome of pregnancy(amniotic fluid embolism)
  • 17.  It occurs as a result of air entry through sub- placental venous sinus during any of the following maneuvers (douching, vaginal insufflation, criminal abortion, or normal labor)  Sudden death is common, also PAH, right heart failure, or PE can developed. Air embolism:
  • 18.  With increasing use of assisted reproductive techniques OHSS is increasingly observed.  Increased capillary permeability as a side effect of gonadotropin, and clomiphene citrate is possible mechanism.  CP include dyspnea, rapid weight gain, anasarca, nausea, vomiting, abdominal pain , thromboembolism, and organ failure.  Treatment include gonadotropin releasing hormone antagonist, loop diuretics, albumin, anticoagulant, fluid as needed, and ventilatory support. Ovarian hyper-stimulation syndrome(OHSS)
  • 19.  From 3rd trimester to the fifth month following labor is period of risk.  Oxidative stress secondary to the breakdown of prolactin hormone is possible mechanism.  Loop diuretics, ACE inhibitors, vasodilator, inotrops, b blockers, vasodilators, ventricular assist, and heart transplantation are suggested lines of treatment. Peripartum cardiomyopathy
  • 20.  Risk factors: cardiac, blood diseases, smoking, DM, obesity, hormonal replacement therapy, CS, age>35, personal and family history, multiple pregnancy.  IV unfractionated heparin is 1st choice, LMWH is the agent of choice in the antenatal period.  Warfarin can be initiated 5-7 days post-labor.  Treatment continue 3-6 months.  Thrombolytic therapy may be life saving in presence of unstable hemodynamics.  Venous thromboembolism
  • 22.  The fetus is sensitive to both hypoxemia and acidosis.  Whatever the cause of respiratory failure, the aim of ventilatory support in pregnant female is SaO2 >95%, and PaO2>70mmHg.  The fact that level of carbon dioxide is lower during pregnancy, and poor tolerance to period of apnea associated with increased oxygen consumption makes great recommendation for not deferred and elective intubation in cases not responding to initial ventilatory support General consideration:
  • 23.  ARF not responding to conventional oxygenation  Dyspnea , nasal flaring, and use of accessory muscle of respiration.  Respiratory muscle fatigue and rising PaCO2  Failure of improved oxygenation and presistent hypoxemia despite oxygenation.  Hemodynamic instability  Disturbed conscious level Indications of mechanical ventilation during pregnancy:
  • 24.  In sever PAH pregnancy should be avoided or terminated as recommended in guidelines.  Prostaglandins mainly epoprostinol is the 1st choice, phosphodiastrase 5- inhibitor also safe.  Riociguat, and endothelin receptor antagonists are cotraindicated.  Patient should be hospitalized in 20week of gestation with close monitoring, bed rest, anticoagulant, and pulmonary vasodilators. Pulmonary arterial hypertension:
  • 25.  Non adherence with medication and infection are major causes of worsening asthma.  Maternal and fetal outcome are the same in patients with well controlled asthma, and non asthmatics.  Indications for hospitalization, ICU admission, and MV are more or less similar in pregnant asthmatic and non asthmatic females.  Sever restrictive lung disease (VC<1 liter) is contraindication for pregnancy and indication for termination.  If pregnancy continued CS is preferred, and post labor MV may be required. Bronchial asthma and restrictive disorders:
  • 26.  Some studies documented successful outcome of NIV in controlling ARF during pregnancy.  Pregnant woman at increased risk of aspiration as a result of decreased tone of lower esophageal sphincter, increased intra-gastric pressure, and delayed gastric emptying.  Inspiratory pressure (12-15)cmH2O, and expiratory pressure (5-8) cmH2O are recommended. Non invasive positive pressure ventilation
  • 27.  Failure of improvement within 30-45 minutes is indication for intubation.  Meticulous observation fetal heart rate, and maternal pattern of respiration is highly recommended. Non invasive positive pressure ventilation
  • 28. Contraindications of NIV in pregnancy include:  Disturbed conscious level  Inability to protect the airway  Hemodynamic instability  Severe acid base disturbance  Poor respiratory derive  GIT bleedng Non invasive positive pressure ventilation
  • 30. The following factors contribute to difficult intubation in pregnancy:  Mucosal edema  Increased mucosal vascularization and risk of bleeding  Increased risk of aspiration So smaller size of endotracheal tube is recommended (7 mm) Endotracheal tube:
  • 31.  The minimum FiO2 required to maintain SaO2 94-98% and PaO2 60-100mmHg is recommended.  Hyperoxia (PaO2 >120 mmHg)produce superoxide radicals, ,cytokines, and potentiate lung injury.  Recommended initial PEEP is 5-8cmH2O to, it can be increased or decreased according to oxygenation level, and hemodynamics.  PEEP guard against alveolar collapse and cyclic atelectrauma which exaggerated in 3rd trimester duo to anatomical and physiological changes of pregnancy. Parameters of invasive ventilation:
  • 32.  Recommended Vt is 6-8 ml/kg ideal body weight in cases other than ARDS.  IBW=(Height in meter)2*21.5  For cases associated with ARDS start with Vt 4ml/kg predicted body weight up to 6 ml  Predicted BW=[(height in cm-152.4)*0.91]+45 Parameters of invasive ventilation:
  • 33.  Pplat pressure should be <25-30cmH2O, better to be measured every 12hour.  In cases Pplat pressure higher than 30cmH2O Vt should be decreased to minimum 4ml/kg.  Another important parameter is the driving pressure (DP) [ideally 12-16cmH2O]. In presence of ARDS, it is better to be ≤12cmH2O if higher decrease Vt. Parameters of invasive ventilation:
  • 34.  Driving pressure =  Vt/CRS(compliance of respiratory system.  =Pplat - PEEP  The driving pressure (DP) [ideally 12-16cmH2O]. In presence of ARDS, it is better to be ≤12cmH2O if higher decrease Vt. Driving pressure:
  • 35. Aims of mechanical ventilation during pregnancy In VC mode: PAP≤ 35cmH2O Pplat ≤ 28cmH2O DP ≤ 12cmH2O In case of PC mode: PI or PS ≤12- 15cmH2O
  • 36.  PIP peak inspiratory pressure should be adjusted at ≤35cmH2O. Barotrauma is increased with PIP> 35cmH2O  PIP is the pressure of gas to overcome resistance of the airway(RAW), so its value is dependent on RAW, lung compliance, and Vt.  PIP is the maximum pressure in the airway.  Bronchospam, mucus plug, occlusion of orotracheal tube, and more seriously pneumothorax, all of them causing increased PIP. Parameters of invasive ventilation:
  • 37.  Prone positioning in combination with neuromuscular blocking agents are recommended if PaO2/FiO2<150  Two drugs should be avoided in pregnant women presented with moderate to severe ARDS in need for tocolytics: beta agonist and magnisium sulfate, increase cardiac demand, capillary permeability, and risk of pulmonary edema. Parameters of invasive ventilation:
  • 38.  Once the patient thermodynamically and clinically stable, and insult that leads to MV is controlled weaning process should be initiated.  pregnant patients have airway and mucosal edema, so cuff leak test is mandatory for them before weaning to avoid risk of post extubation stridor. Weaning:
  • 39. Cuff leak test  Deflating cuff and observe volume time curve leakage.  >20% or 110ml leak indicate negative test and absence of post-extubation stridor risk.  Lower values indicate need for treatment and subsquent reassessment.
  • 40.  In case of failed cuff leak test give three doses 20 mg methylprednisolone 12hours apart and reassess cuff leak test from 2nd or 3rd dose. Cuff leak test
  • 42.  Deloya-Tomas E, Mondragon-Labelle T, Lopez-Fermin J, Perez-Nieto OR, et al. (2020). Considerations for Mechanical Ventilation inthe Critically III Obstetric Patient. Crit Care Obst Gyne Vol.6 No.4:10.  Bhatia PK, Biyani G, Mohammed S, Sethi P,Bihani P. Acute respiratory failure and mechanical ventilation in pregnant patient: A narrative review of literature. J Anaesthesiol Clin Pharmacol 2016;32:431-9.  Lapinsky SE (2017) Management of acute respiratory failure in pregnancy. In Seminars in respiratory and critical care medicine 38:  201-207.  Soma-Pillay P, Catherine NP, Tolppanen H, Mebazaa A, Tolppanen H, et al. (2016) Physiological changes in pregnancy. Cardiovasc J Afr 27:89.  Amato MB, Meade MO, Slutsky AS, Brochard L, Costa EL, et al.(2015) Driving pressure and survival in the acute respiratory distress syndrome. N Engl J Med 372: 747-755.  Guérin C, Papazian L, Reignier J, Ayzac L, Loundou A, et al. (2016) Effect of driving pressure on mortality in ARDS patients during lungprotective mechanical ventilation in two randomized controlled trials. Crit Care 20: 384.  Lapinsky SE, Rojas-Suarez JA, Crozier TM, Vasquez DN, Barrett N, et al. (2015) Mechanical ventilation in critically-ill pregnant women: a case series. Int J Obstet Anesth 24: 323-328.  Fanelli V, Ranieri MV, Mancebo J, Moerer O, Quintel M, et al. (2016) Feasibility and safety of low-flow extracorporeal carbon dioxide removal to facilitate ultra-protective ventilation in patients with moderate acute respiratory distress syndrome. Crit Care 20: 1-7.  Girard TD, Alhazzani W, Kress JP, Ouellette DR, Schmidt GA, et al. (2017) An official American Thoracic Society/American College of Chest Physicians clinical practice guideline: liberation from mechanical ventilation in critically ill adults. Rehabilitation protocols, ventilator liberation protocols, and cuff leak tests. Am J Respir Crit Care Med 195: 120-133.  Zein H, Baratloo A, Negida A, Safari S (2016) Ventilator weaning and spontaneous breathing trials; an educational review. Emergency 4:65. References: