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Physiological Changes in Pregnancy and Its Anaesthetic Implications.
PHYSIOLOGICAL CHANGES IN
PREGNANCY AND ITS
DR. MOHTASIB MADAOO
DEPARTMENT OF ANAESTHESIOLOGY,
PHYSIOLOGICAL CHANGES IN
• Pregnancy produces profound physiological changes that
alter the usual responses to Anesthesia .
• Unique challenges - two patients are cared for
• Failure to take care can be disastrous for one or both of
Blood Volume Increases by 30%
Plasma Volume Increases by 45%
Cardiac Output Increases by 30-50%
Stroke Volume Increases by 25%
Heart Rate Increases by 15-25%
Peripheral Vascular Resistance Decreases by15-20%
• Enlarged uterus compresses IVC and Lower Aorta when the
patient lies supine Obstruction of IVC Decreases Venous
Return leads to Decrease in Cardiac Output
• When awake most women are capable of compensating for the
decrease in stroke volume by increasing Sytemic Vascular
Resistance and Heart rate. There are also alternative venous
pathways : the paravertebral and azygos systems.
• During Anaesthesia compensatory mechanisms are reduced or
• Obstruction of lower aorta causes reduced blood flow to
kidneys, uteroplacental unit and lower extremities.
SUPINE HYPOTENSION SYNDROME
8 to 15% of pregnant women have Overt Caval
Compression (supine hypotension syndrome)
Prevention of SHS: Uterus should be displaced by placing a
rigid wedge under the right hip and tilting the table left side
Regional anaethesia – Profound Hypotension
The patient can be turned to full left lateral position.
Oxygen consumption Increases by 20 to 50%
Minute ventilation Increases by 50%
Tidal volume Increases by 40%
Respiratory rate Unchanged/Slightly Increases
PaO2 Increases by 10%
PaCO2 Decreases by 15%
HCO3 Decreases by 15%
FRC Decreases by 20%
• Decreased FRC and Increased oxygen consumption
promotes rapid oxygen desaturation during periods of
apnea. This is more marked in obese patients.
• The reduced FRC causes airway closure in 50% of
parturients at term in the supine position making pre-oxygenation
• Regional block further diminishes FRC which leads to
rapid development of Hypoxemia.
• Preoxygenation prior to induction of general anesthesia is
therefore mandatory to avoid hypoxemia in pregnant
Factors affecting Smooth Intubation
• There is capillary engorgement and edema of the upper
airway down to the pharynx, false cords, glottis and
• The increase in chest diameter and enlarged breasts can
make laryngoscopy difficult.
Failure to intubate the trachea is 7 times more common in the
term parturient compared to non pregnant patients.
A smaller diameter endotracheal tube may be required for
intubation especially in cases of pre eclampsia.
Blood flow to the nasal mucosa is increased so
Oropharyngeal intubation is preferred over Nasal intubation.
Fibrinogen Increased from 2.5g/l to 5g/l
Factor 2 Slightly Increased
Factor 5 Slightly Increased
Factor 7 Increased 10 folds
Factor 8 Increased 2 folds
Factor 9 and 10 Increased
Factor 11 Decreased by 70%
Factor 12 Increased by 40%
Factor 13 Decreased by 40%
Bleeding time, PT, PTT is unchanged.
Pregnancy is a hypercoagulable state.
There is increased risk of thromboembolic episode.
The parturient should be considered a full stomach patient
during most of gestation because
• Upward & anterior displacement of the stomach by the uterus
leads to increase in intragastric pressure and decrease in
• Reduction of lower esophageal sphincter pressure due to
increased progesterone levels.
Risk of Regurgitation and aspiration of gastric contents.
Increased placental gastrin secretion which worsens gastric
• Prophylaxis in the form of H2 blocking drug and Prokinetic
drugs to all pregnant patients for surgery from 2nd
trimester onwards is a must.
• During GA airway protection by means of cuffed ETT is
mandatory; So is rapid sequence induction from 2nd
trimester of pregnancy till 48hrs post partum.
• Extubation should be done when the patient is awake and
on their side to reduce the risk of aspiration.
• The danger of aspiration is almost eliminated when
regional anaethesia is used.
CNS CHANGES & ITS IMPLICATIONS
Decrease in minimum alveolar concentrations secondary to
increased levels of progesterone and β- endorphin levels.
• Rapid induction with inhalation agents – The increased
minute ventilation combined with decreased FRC and
CNS CHANGES & ITS IMPLICATIONS
The amount of local anaesthetic drug required in a pregnant
woman is less compared to the non pregnant state. (Approx
two-thirds of the normal dose is adequate)
• Exaggerated lumbar lordosis contribute to cephalad
spread of the local anaesthetic.
• Engorged epidural plexus of veins will decrease the
volume of the epidural and subarachnoid space.
• The CSF pressure is increased due to compression from
the epidural veins in the epidural space.
• Increased sensitivity to opiods, sedatives, and local
anaesthetics when used for neuraxial anaesthesia.
• Renal vasodilatation increases renal blood flow early
• Increased Cardiac output leads to Increased GFR &
Increased renal plasma flow by 50% which increases
clearance of urea, uric acid and Creatinine.
• Increased Renin & Aldosterone level promotes Na+
retention leading to volume overload.
• Decreased Renal tubular threshold for glucose & amino
acids → mild glycosuria & proteinuria (< 300mg/d).
• Progesterone mediated ueretetic smooth muscle
relaxation can lead to urinary stasis making pregnant
women prone to urinary tract infections.
There is increase in the volume of distribution for drugs and
may have to be given in higher than normal dosages.
• Hepatic function and blood flow are unchanged.
• A mild decrease in serum albumin is due to an expanded
plasma volume. Thus, the free fraction of albumin-bound
medications is increased.
• A 25—30% decrease in serum pseudocholinesterase
activity is also present at term,but it rarely produces
significant prolongation of SCh action.
• Increased cholesterol gall stone formation(progesterone).
• Simple diffusion – 02 and CO2 transport occurs due to the
difference between partial pressures on both sides. Ffatty
acids are also transported by means of simple diffusion.
• Secondary active transport – amino acids are transferred
mostly as linked carriers.
• Pinocytosis – Placenta is Impermeable to proteins, only
IgG is transported.
• Bulk transport – Water and electrolytes moves across bulk
FACTORS AFFECTING PLACENTAL
TRANSFER OF DRUGS
• Lipid solubility – The placental membrane is freely
permeable to lipid soluble substances, which undergo
flow dependent transfer. Higher the lipid solubility , higher
the transfer of drugs.
• Molecular weight – Drugs with smaller molecular weight
diffuse easily (<600da)
• Degree of ionization – Ionized form will not cross the
barrier easily. The degree of ionization of acidic drugs is
greater on the maternal side and lower on the fetal side.
• Protein binding – protein bound drugs will not diffuse
easily, only free drug would cross the placental barrier
easily. Acidosis reduces the protein binding of local
anaesthetic. Reduced albumin concentration increases
the proportion of unbound drug
Opioids – All opioids cross the placenta in significant
amounts. They are weak bases, bound to α-glycoprotein.
Pethidine – Longer half life is due to its active metabolite
norpethidine, which may lead to respiratory depression in the
Morphine – It is poorly lipid soluble but readily crosses the
placenta due to low protein binding.
Fentanyl – It is highly lipid soluble and albumin bound, so
crosses the placental barrier easily.
IV Induction agents – Sodium thiopentone is highly lipid
soluble, weakly acidic, 75% protein bound and less than 50%
ionized at physiological pH. It crosses the placenta easily.
Propofol – It is highly protein bound and lipophilic.
Inhalational Agents – These agents are highly soluble with low
Muscle relaxants – These are quaternary ammonium compounds
and fully ionized. These drugs are fully ionized as well as have
low lipid solubility, hence they do not cross the placenta.
Local Anaesthetics – These drugs have low molecular weights
and also are lipid soluble. Different drugs have different protein