Transport in Animals
The Structure of the Heart
External Features
Internal Features
Blood Presure
Cardiac Muscle Structure
The Cardiac Cycle
The Action of the Valves
Pressure Changes
Coordination of the Cardiac Cycle
Transport of Oxygen
Transport of Carbon Dioxide
Cardiac Muscle: specialised muscle found in the walls of the heart chambers
Coronary Arteries: Supply oxygenated blood to the heart
If constricted, can cause angina (chest pains) or myocardial infarction (heart attack)
Tendinous cords prevent the valves from turning inside out when walls contract.
Atria
Right Ventricle
Left Ventricle
Has fibres that branch, creating cross-bridges to spread stimulus so the muscle can squeeze chambers
Many mitochondria between muscle fibrils (myofibrils) to supply energy for contraction
Each cell has a nucleus and is divided into contractile units called sarcomeres.
Thick walls contract to push blood around the body
Sufficient enough pressure needed to overcome resistance of the systemic circulation
Pumps blood to the lungs, low pressure to prevent damage to alveoli
Thin walls to push blood into ventricles
The need for Coordination
Initiation and Control of the Heartbeat
Electrocardiograms
Haemoglobin
Fetal Haemoglobin
Atrio-ventricular Valves
Semilunar Valves
Heart Chambers
Blood Vessels
Heart muscle is myogenic, meaning it can initiate its own contractions
Fibrillation is uncoordinated contractions of the heart, it needs a mechanism which can coordinate all 4 chambers
The sino-atrial node (SAN), located at the top of the right atrium, generates a wave of electrical excitation at regular intervals. It is known as the pacemaker
Atrial Systole
Ventricle Systole
As the atria is unable to conduct a wave of excitation, at the top of the interventricular septum is the atrio-ventricular node (AVN). This wave is delayed to allow time for the artia to finish contracting
The wave of excitation spreads over the walls of both atria, travelling along causing cardiac muscle cells to contract
The wave of excitation is carried away from the AVN down specialised conducting tissues called Purkyne tissue. It runs down the intrerventricular septum and spreads over the ventricle walls from the base upwards
Electrocardiograms (ECG) measure electrical activity by attaching sensors to the skin
P - wave of excitation at atria
QRS - excitation of the ventricles
T - diastole
Abnormal ECGs
Bradycardia: slow heart rate
Tachycardia: fast heart rate
Ectopic Heartbeat: an extra beat or an early beat of the ventricles
Fetal haemoglobin has a higher affinity to oxygen than adult haemoglobin, therefore its disassociation curve is more to the left
Oxygen tension is low in the placenta so when the fetal haemoglobin associates with the oxygen, the oxygen tension lowers in the mother blood, further dissociating oxygen from the mother's erythrocytes
haemoglobin + oxygen -> oxyhaemoglobin
partial pressure of oxygen (pO2) = oxygen tension (kPa)
Disassociation Curve
At low oxygen tension, haemoglobin doesn't readily associate with oxygen; the haem group is at the centre of the haemoglobin molecule making it difficult to combine with the first oxygen.
As oxygen tension rises, so goes the diffusion gradient causing the first oxygen to bind. This causes a conformational change in the haemoglobin shape so oxygen more readily associates with oxygen
At the highest oxygen tension, haemoglobin never becomes 100% saturate due to decreased probability of oxygen binding with the last haem group and that the partial pressure is never high enough for long enough to associate with the last oxygen
Transport
5% dissolved directly into plasma
10% combined with haemoglobin forming carbaminohaemoglobin
85% transported in the form of hydrogencarbonate ions (HCO3-)
Hydrogencarbonate Ions
carbon dioxide + water --(carbonic anhydrase enzyme)-> carbonic acid
carbonic acid -> hydrogencarbonate ions + hydrogen ion
The hydrogencarbonate ions diffuse out the RBCs into the plasma and are replaced by chloride ions in a chloride shift
The build-up of H+ ions causing the RBC to become very acidic, therefore the hydrogen ions associate with haemoglobin (acting as a buffer) to form haemoglobinic acid (HHb)
hydrogen ions + haemoglobin -> haemoglobinic acid (HHb)
Bohr Effect
Increased CO2 levels means more H+ ions are released causing the haemoglobin to become more acidic
More acidic conditions alter the tertiary shape of the protein, lowering it's affinity for oxygen and shifting the dissociation curve right - the Bohr shift
Therefore oxygen is released at respiring tissues