Cardiovascular Changes Across the Lifecyle-Lecture 5

• Study notes for Lecture 5, covering cardiovascular changes across the lifecycle.

Heart Development

• Heart development begins in week 3 of embryogenesis.
• Derived from the mesoderm, which forms the circulatory system.
• Endocardial tubes fuse to form a single primitive heart tube.
• The heart tube folds into C-shaped loops, then S-shaped loops, forming chambers.
• By day 35, the four chambers of the heart are fully developed.
• Bulbus cordis and primitive ventricle form ventricles.
• Primitive atrium forms atria.
• Sinus venosus contributes to atria and the SA node (pacemaker).
• Truncus arteriosus develops into the aorta and pulmonary artery.
• Atrioventricular (AV) and semilunar valves regulate blood flow by forming between weeks 5-9.
• Septal defects (ASD, VSD) and valve malformations are common congenital heart defects, affecting ~1% of newborns.

Fetal vs. Neonatal Circulation

• Feature differences exist in oxygenation site, lung function, liver function, shunts, main O2 transporter, and blood flow pathway.
• Oxygenation occurs at the placenta in fetal circulation, and the lungs in neonatal circulation.
• Fetal lungs are bypassed via shunts; neonatal lungs are fully functional.
• The fetal liver is bypassed via the ductus venosus; the neonatal liver is fully functional.
• Shunts are present in fetal circulation but absent in neonatal circulation.
• Fetal hemoglobin (HbF) is the main O2 transporter in fetal circulation; adult hemoglobin (HbA) in neonatal circulation.
• Umbilical cord clamping stops placental circulation, requiring the neonate to rely on its own heart and lungs.

Ventricular Fibrillation (VF)

• VF is a life-threatening arrhythmia where the ventricles quiver instead of contracting properly, preventing blood circulation.
• Electrical disruption in the ventricles is a cause.
• Calcium dysregulation (due to abnormal Ca²+ release leading to erratic contractions) is a cause.
• Severe heart failure, myocardial infarction (heart attack), or electrolyte imbalances is a cause.
• VF results in no effective contraction, no cardiac output, and sudden cardiac arrest.
• Treatment requires defibrillation (electric shock) to reset the heart's electrical activity.

Age-Induced Changes in Cardiac Function

• Functional, structural, and molecular changes associated with aging can lead to heart failure.
• Diastolic dysfunction (filling problems) occurs due to slow relaxation of stiffened heart muscle (cardiomyocytes).
• Reduced left ventricular filling leads to lower cardiac output (CO).
• Ventricular refilling occurs late, reducing oxygen delivery.
• Systolic dysfunction (pumping problems) occurs due to weaker contractions and myocardial remodeling, reducing ejection fraction.
• Poor circulation and symptoms like fatigue and breathlessness result from systolic dysfunction.
• Calcium mishandling and elevated SNS activity increase arrhythmia risk in aging hearts.
• Aging causes left ventricular hypertrophy (LVH)
• Fibrosis and stiffening occur as heart muscle cells die and are replaced by non-contractile fibrous tissue.
• Reduced coronary blood flow from stiffening blood vessels decreases oxygen supply to the heart.
• Aging reduces ATP production, leading to weaker contractions.
• Excess Reactive Oxygen Species (ROS) damage cardiac proteins, impairing heart function.
• Chronic beta-adrenergic receptor activation increases calcium mishandling and arrhythmia risk.

Estrogen's Protective Role

• Before menopause, estrogen helps regulate calcium release and reduce oxidative stress.
• Potentially lowering heart disease risk in younger women.

Fetal Heart Development - Germ Layers

• During gastrulation, the three primary germ layers are formed through the rearrangement and migration of epiblast cells.
• Ectoderm forms the nervous system, skin, and external structures.
• Mesoderm gives rise to the heart, muscles, bones, and circulatory system.
• Endoderm forms internal organs like the liver, pancreas, and gastrointestinal tract.
• The heart originates from mesodermal cells.

Adult Circulatory System revision

• The heart is a dual pump driving blood through two distinct circuits:
  • Systemic Circulation - Oxygenated blood travels: Pulmonary vein → Left atrium → Left ventricle → Aorta → Systemic arteries to the Body.
  • Pulmonary Circulation - Deoxygenated blood returns: Systemic capillaries → Vena cava→ Right atrium → Right ventricle → Pulmonary artery → Lungs.
• CO refers to the volume of blood the left ventricle pumps per unit time
• With age, CO decreases due to metabolic changes, and alterations in left ventricular function can significantly impact overall circulation.

Key Bypass Mechanisms (Foetal Shunts)

• Foramen Ovale (Right Atrium → Left Atrium)
• Ductus Arteriosus (Pulmonary Artery → Aorta)
• Ductus Venosus (Umbilical Vein -Inferior Vena Cava)

Physiological Adaptations for Oxygen Transport

• Foetal Haemoglobin (HbF) has a higher affinity for oxygen than Adult Haemoglobin (HbA).
• Double Bohr Effect causes Maternal blood to offload more oxygen due to changes in CO2 and pH levels.
• Higher haemoglobin concentration in foetal blood.

Circulatory System – Changes at Birth

• First breath and lung expansion is a significant change at birth.
• Increased left atrial (LA) pressure occurs
• Ductus venosus collapses and closes • Closure occurs via vasoconstriction.

Homeostatic Mechanisms Supporting Adaptation

• adjusts based on: ■ Aging ■ Illness/Injury ■ Exercise and metabolic demands

Heart Rate and Cardiac Output Changes Over Time

Resting Heart Rate (HR) Across Different Life Stages ■ Foetal HR: ~150 bpm ■ Newborn HR: ~130 bpm ■ Adult HR: ~60-100 bpm (stabilizes after teenage years)