This document discusses respiratory physiology and causes of respiratory failure during pregnancy. It notes the anatomical and functional changes that occur during pregnancy, including elevated diaphragm, increased lung volumes, and decreased functional residual capacity. Causes of respiratory failure include conditions like preeclampsia, amniotic fluid embolism, and pulmonary embolism. The document provides guidance on managing respiratory failure with non-invasive ventilation when possible and invasive mechanical ventilation if needed, emphasizing proper settings and monitoring to support both mother and fetus.
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.
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
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