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cardiac output has increased by 20% by 8wks pregnancy and now reaches a peak increase of around 40% at around 20-28 wks which helps offset the 25-30% fall in systemic vascular resistance due to vasodilatation which starts at 6wks. This arterial under-filling leads to lowered blood pressure and the stimulation of arterial baroreceptors, activating the RAA and the sympathetic nervous systems however there is also a relative resistance to angiotensin II
hence patients have an increase heart rate of 10-20bpm and an increased stroke volume
as pregnancy progresses, pressure from the gravid uterus upon the IVC restricts venous return and cardiac output by up to 25% when supine
colloid osmotic pressure/pulmonary capillary wedge pressure gradient is reduced by about 30%, making pregnant women particularly susceptible to pulmonary oedema
the ECG may show:
atrial and ventricular ectopics
small Q wave and inverted T in III
ST-segment depression and T-wave inversion in the inferior and lateral leads
left-axis shift of QRS
renal plasma flow and glomerular filtration rate (GFR) both increase, compared to non-pregnant levels, by 40–65 and 50–85% and increased renal blood flow leads to an increase in renal size of 1–1.5 cm, reaching the maximal size by mid-pregnancy
There is a significant increase in oxygen demand during normal pregnancy. This is due to a 15% increase in the metabolic rate and a 20% increased consumption of oxygen.
There is a 40–50% increase in minute ventilation, mostly due to an increase in tidal volume, rather than in the respiratory rate, this maternal hyperventilation causes arterial pO2 to increase and arterial pCO2 to fall, with a compensatory fall in serum bicarbonate to 18–22 mmol/l causing a normal mild fully compensated respiratory alkalosis.
the subjective feeling of breathlessness may develop and classically is present at rest or while talking and may paradoxically improve during mild activity