A 36 week pregnant woman is involved in a car crash and suffers fractures to her left femur and tibia and left ribs 4-8. What are the cardiorespiratory changes in normal pregnancy?
How do they effect her response to these injuries?
This question had two parts. Lists would suffice. For example: (a) Cardiorespiratory changes include:
• Increased blood, plasma and Rd cell volume from 6 weeks. maximal at 28 to 32 weeks
• Increased cardiac output (33% by 10 weeks.to 40-50'/o by 28 to 32 weeks)
• Decreased blood pressure due to low SVR
• Susceptibility to aorto-caval compression develops during second trimester (maximal at 36-
• Cardiac hypertrophy with increased wall thickness and chamber volume.
• Left axis deviation, horizontal heart
• Hb decreased due to relative haemodilution
• Upper respiratory tract oedema and capillary engorgement
• Increased minute volume, respiratory rate, V, lV, RR. Chronic respiratory allcalosis
• Decreased FRC, RV, TLC, AWR
(b) The clinical effects on her response to the injury include:
• Larger blood volume allows blood loss to be relatively better tolerated
• Susceptible to supine hypotension
• Susceptible to basal atelectasis and hypoxia
• Difficult intubation
• High Vand low FRC means that hypoxia and hypercarbia develop rapidly with airway
obstruction. apnoea etc
This question forms a part of the "manage this pregnant trauma patient" spectrum of fellowship questions. For a general reference, one is directed to Question 3 from the first paper of 2007 (Outline the special considerations involved in the care of a pregnant patient involved in multi-trauma.). That answer also covers section (b) of the current question ("How do they effect her response to these injuries?")
The management of the pregnant poly-trauma patient is discussed elsewhere. The answer prepared for Question 3 from the first paper of 2007 is very similar: "Outline the special considerations involved in the care of a pregnant patient involved in multi-trauma.".
Bag-mask ventilation becomes more difficult:
- The nasal mucosa is engorged, which means there is greater resistance to flow
- The upper airway mucosa is oedematous
- There has been weight gain
Laryngoscopy becomes more difficult:
- Upper airway oedema
- Breast enlargement
- The Mallampatti grade changes during pregnancy, largely because of oedema of the pharynx, and due to weight gain. It gets even worse with labour.
Less time is available for intubation:
- Decreased FRC, less time to intubate
- Increased oxygen consumption, less time to intubate
Intubation is more risky
- Increased risk of aspiration, decreased stomach emptying
- The diaphragm is pushed up by 4cm
- Tidal volume increases by ~ 30-50%
- Respiratory rate increases to 15-17
- Minute volume increases by 20-50%.
- Chest wall compliance decreases
- Lung compliance remains the same
- FRC decreases during pregnancy, due to compression of the diaphragm by the gravid uterus.
- pH increases to 7.40-7.47
- PaCO2 decreases to 30 mmHg
- PaO2 increases to 105 mmHg
- HCO3- decreases to 20 mmol/L
- Maternal 2,3-DPG increases
- p50 remains the same because of alkalosis
- Cardiac output increases (from 5L/min to 7L/min)
- Stroke volume increases (from 65ml to 80-90ml)
- Heart rate increases (from 75 to 85-90)
- Systemic vascular resistance decreases (down by as much as 40%) - in fact, the vascular system becomes fairly refractory to the effects of vasoconstrictors such as angiotensin and vasopressin
- The IVC is compressed by the gravid uterus in the supine position, decreasing the preload
- Blood pressure decreases (and is lowest in the second trimester)
- Pulmonary vascular resistance decreases
- Pulmonary artery wedge pressure remains unchanged
- Blood volume is increased by 50%
- CVP remains unchanged
- Colloid oncotic pressure decreases
- Oxygen consumption increases by 20% during pregnancy
Electrolyte and endocrine changes
- Vasopressin release increases;
- Thus, there is water retention
- A hypervolemic hypoosmolar state develops
- In response to a decreased SVR, aldosterone release is increased. This is the major contributor to the 50% circulating volume expansion
- There is a relative iodine deficiency (the foetus is stealing it all)
- Cortisol secretion is increased, which has implications for all those people who still do random cortisol levels on their patients
- Renal blood flow increases: the renal arteries are also affected by the fall in SVRI, and this is mediated by relaxin (which influences endothelial nitric oxide production).
- GFR increases by as much as 85%
- Urea and creatinine decrease because of this
- Kidneys become enlarged; the renal pelvis dilates and there is a "physiological hydronephrosis" - more so on the right because the right ureter crosses iliac and ovarian vessels at an angle. This predisposes to pyelonephritis
- Tubular resorption of urate and glucose decreases
Gastrointestinal and nutritional changes
- Nausea and vomiting: in 50-90%.
- Oesophageal sphincter tone is decreased (aspiration is more likely)
- There is increased intragastric pressure due to upward displacement
- Gastric emptying is delayed, and is virtually non-existant during labour
- Thiamine supplementation is important, because prolonged hyperemesis can result in vitamin deficiency.
- Abdominal compartment pressure measurements are going to be wildly inaccurate.
- There is insulin resistance, particularly later in pregnancy
- Metabolic fuel use favours lipolysis, preserving the glucose and amino acids for use by the foetus.
- Protein catabolism is decreased
- There is a peak of calcium demand in the third trimester
Specific features of the cardiorespiratory changes in pregnancy can be found on the page dedicated to this topic. In brief summary, they are as follows:
|The diaphragm is pushed up||by 4cm|
|Tidal volume increases||by ~ 30-50%|
|Respiratory rate increases||to 15-17|
|Minute volume increases||by 20-50%.|
|Chest wall compliance decreases|
|Lung compliance remains the same|
|pH increases||to 740-7.47|
|PaCO2 decreases||to 30 mmHg|
|PaO2 increases||to 105 mmHg|
|HCO3- decreases||to 20 mmol/L|
|Maternal 2,3-DPG increases|
|p50 remains the same because of alkalosis|
|Heart rate||Increased (from 75 to 85-90)|
|Stroke volume||Increased (from 65ml to 80-90ml)|
|Cardiac output||Increased (from 5L/min to 7L/min)|
|Systemic vascular resistance||Decreased|
|Pulmonary vascular resistance||Decreased|
|Pulmonary artery wedge pressure||Unchanged|
|Blood volume||Increased by 50%|
|Renal blood flow||Increased by 30-80%|
|Resting oxygen consumption||Increased by 20-30%|
|Colloid oncotic pressure||Decreased|
Critical Care Medicine has dedicated an entire supplement to the influence of pregnancy in critical care: Volume 33 Supplement 10 October 2005 - pg. S247-S397
Additionally, UpToDate has an excellent summary for the paying customer.
Hunter, Stewart, and Stephen C. Robson. "Adaptation of the maternal heart in pregnancy." British heart journal 68.6 (1992): 540.
Metcalfe, James, and Kent Ueland. "Maternal cardiovascular adjustments to pregnancy." Progress in cardiovascular diseases 16.4 (1974): 363-374.