15B08: Exam Report
Compare and contrast the physiological changes in the cardiovascular system in pregnancy at term and morbid obesity (BMI > 30).
2% of candidates passed this question.
The question was very specific for the cardiovascular system and therefore answers that described respiratory changes and airway modulation failed to score marks. This answer leant itself to a tabular format. Candidates are reminded to ensure they document the facts in the correct column i.e. obesity facts in the obesity column. The cardiovascular changes associated with term pregnancy are well described in various texts. Those associated with morbid obesity required some integration from various sources and would include a structured series of comments such as heart rate (unchanged), blood pressure (tendency for hypertension), stoke volume (increased), cardiac output (increased), blood volume (increased – although perhaps decreased on a ml/kg basis), systolic function (preserved or increased), LV wall thickness increased. The pathological changes seen with the diseases associated with obesity are difficult to tease out and better answers identified this. Morbid obesity has a specific definition and stating this aided focus of the answers.
V1i / 15B08: Compare and contrast the physiological changes in the cardiovascular system in pregnancy at term and morbid obesity (BMI > 30)
Definition
PREGNANCY
From conception to delivery of fetus. Approx 40 weeks & consisting of 3 trimesters
MORBID OBESITY
Condition of excess body fat w BMI > 30kg/m2
Hormonal
Oestrogen. Progresterone
Proinflammatory cytokines
Atheroma
Increased risk with maternal smoking
Obesity & IHD both proinflammatory conditions
Fat tissue release adipocytokines which induce insulin resistance and a proinflammatory state
Elevated CRP associated with increase risk MI
HR
↑HR 25%
Increased across all trimesters
Increase in HR
Propensity to arrythmias
Multifactorial
Obesity & IHD both proinflammatory conditions
Fat tissue release adipocytokines which induce insulin resistance and a proinflammatory state
- Elevated CRP associated with increase risk MI Tissue hypertrophy/dilatation
- Hypoxia
- ↓K+ from diuretics
- CAD
- ↑Catecholamines
- Fatty infiltration of conducting tissue
BP
↓ SBP & ↓ DBP
BP = CO x SVR
- SVR ↓30% below normal values & stays there
- Vasodilation 2° Prgst, PGIs, downregulation α-receptors
- Necessary to feed placenta → low R circuit
↓HTN
Multifactorial;
↑blood vol → ↑CO → ↑BP
Hyperinsulinaemia → activates SNS → ↑Na+ reabsorption → BP
SV
↑SV 30%
Increased across all trimesters
Increase in SV
Activated RAAS
CO
- Steady ↑CO from:
↑VR → venodilation
↑circulating volume → Ostrg activated RAAS
Large amount of CO going to uteroplacental circulation which is 1L/min at term
Increased across all trimesters
RAAS activation
Blood Volume
Blood vol ↑1.5L 2° Ostrg induced RAAS activation
↑Red cell vol 2° ↑EPO
↑Plasma vol > red cell vol ∴ ↓HCt ~30%
↓Colloid osmotic P → oedema
Physiological anaemia of pregnancy
↑ Blood Volume & CO
Due to ↑metabolic demands of fat tissue
Extra blood vol is distributed to the fat tissue (cerebral & renal BF unchanged)
↑O2 consumption & CO2 production despite ↑CO
LV Systolic FN
Increased, but within normal range and higher than in non pregnant controls
LV Systolic Dysfunction
- ↑Wall stress from LVH → contributes to systolic dysfunction
- Impaired LV Diastolic Filling & ↑LV filling pressure
- LVEDP → most specific measure for LV diastolic function
- LV hypertrophy predisposes to impaired diastolic filling & ↑pressures
- LA dilatation
- ↑LA size 2° impaired LV filling
- PA Hypertension
- OSA → ↑CO2/↓O2 → RV enlargement → RV failure