Canonical Question
CVS – Responses
Master answer
Pregnancy at Term
Morbid Obesity
- Pregnancy is a time of increased metabolic demand, which cardiovascular changes reflect.
- Changes begin from week 8 and ↑ to plateau at 32 weeks → return to normal 2-8 weeks post delivery
- excessive fat accumulation in adipose tissue
- WHO/NIH classification based on BMI:
- Overweight: BMI 25 – 30
- Obesity: BMI ≥ 30
- Obesity Class 1: 30 to 34.9 kg/m2
- Obesity Class 2: 35 to 39.9 kg/m2
- Obesity Class 3: BMI ≥40 kg/m2
- Alternate classifications:
- Severe Obesity: ≥ 35 or 40 kg/m2
- Morbidly Obese: BMI ≥ 40 (or) Obesity related disease and a BMI ≥ 35
- Super Obesity: ≥ 45 or 50 kg/m2
- Changes depend on stage of pregnancy
- Hormonal changes: ↑ circulating concentrations of oestrogen, progesterone, hCG
- ↑ metabolic demand esp. during labour: ~↑60% O2 consumption/ CO2 production during labour
- Mechanical effects from gravid uterus
- Changes depend on extent + duration of obesity
- Complex genetic and environmental causes
- Increased caloric intake
- Increased metabolic rate (normal for BSA)
- associated with HTN, HF, IHD, cardiomyopathy, sudden cardiac death, arrhythmias, PVD, DVT, CVD
- Thoracic changes:
- Anatomical compression of chest
- Diaphragm pushed upwards by 4cm
- ↑ AP + transverse diameter of chest wall (2-3cm)
- placental circulation: ↓pressure, ↓resistance AV shunt
- Aortocaval compression
- Collateral blood flow via collateral paravertebral epidural veins
- Compression of abdominal + leg vessels
- ↓ VR → supine hypotension + ↑ risk DVTs
- ↑ circulating concentrations of oestrogen, progesterone, hCG
- Oestrogen stimulation of RAAS
- Increased plasma volume (40% or 1~1.5L positive)
- Erythropoietin secretion
- Increased erythropoiesis and red blood cell volume (20%)
- ↑ SNS
- ↑ HR + ↑ SV
- ↑ RAAS → Na+ retention → ↑ blood vol → ↑ MAP (Systemic HTN)
- ↑ MAP → LVH → LV dilation → LV failure
- LV diastolic failure + ↑ PVR → RV hypertrophy
- ↑ Leptin → Cardiac remodelling + LVH
- Plasminogen Activator Inhibitor-1 → ↓ fibrinolysis → predisposes to VTE
- Inflammatory Adipokines → Impairs endothelial function → ↑ SVR
- insulin resistance + hyperlipidaemia → inflammatory mediator upregulation → disrupt endothelial function → IHD + cerebrovascular disease + PVD
- Anaemia of pregnancy
- Disproportionate plasma volume expansion relative to erythropoiesis
- Increased cardiac output (40%)
- Increased uterine blood flow (750ml/min)
- Increased renal blood flow
- Increased HR (25% by second trimester)
- Increased SV (25% in first trimester)
- Increased VO2 : Due to increased LBM and fat mass.
- Increased Cardiac Output: To maintain DO2.Initially with preserved ejection fraction
- Increased Stroke Volume: Due to:
- Increased preload (major factor)
- Increased contractility (minor factor) due to increased circulating adrenal hormones.
- Decreased peripheral vascular resistance (30%)
- Progesterone
- Prostaglandins
- Down-regulation of α receptors
- Decreased plasma oncotic pressure (15%) → peripheral oedema
- ↑ Peripheral vascular resistance
- Inflammatory Adipokines → Impairs endothelial function
- ↑ SNS
- Diastolic dysfunction: Due to myocardial fibrosis impairing relaxation.
- direct deposition of fat in myocardium → conduction disease (& predisposition to arrhythmias) + cardiomyopathy
- OSA
- Pulmonary HTN → cor pulmonale
- Polycythaemia → ↑ viscosity
Sakurai / Kerr / JC 2020
Exam appearances
| Exam | Exact wording | Relationship | Success |
|---|---|---|---|
| 2015B Q08 | Compare and contrast the physiological changes in the cardiovascular system in pregnancy at term and morbid obesity (BMI > 30). | historical_member | — |