V1i / 15B08: C+C CVS Pregnancy and morbid obesity

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 Wall Thickness

Increased, but within normal range

Ventricular remodelling well described

LVH

  • ↑LV wall thickness & myocyte size
  • Hypertrophy to compensate for ↑CO
  • ↑LV size & dilatation → ↑LV wall stress as per Law of LaPlace:

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