11.2B Transport of substances Flashcards
The mechanism of cardiac automaticity
LO: Explain the mechanism of cardiac automaticity
Functional syncytium
the heart consists of individual cells, the entire mass normally responds as a unit, and all cells contract together
Myogenic
- cardiac muscle can contract without nervous input, BUT the strength and the rate of contraction is modified by nervous input
- muscles or tissues that can contract on their own, without any external electrical stimulus from the brain or nervous system.
Automaticity
the cardiac cell’s ability to `spontaneously generate an electrical impulse (depolarize)
4 Valves
open only one way:
-high pressure behind – open
-high pressure in front – closed
- Aortic valve
- Plumonary valve
- Tricuspid valve
- Mitral(Biscupid) valve
Chordae tendinae
– prevents the valves from turnig inside out under the pressure
Transverse section of the heart apex
right ventricle| septum |left ventricle
LEFT ventricle is thicker because it needs to pump blood all the way around the body
Whereas the RIGHT ventricle only has to get blood to the lungs
Electrical Activity of the Heart
1) SAN node
2) AV node
3) Bundle of HIS
4) Righ/Left Branch Bundles
5) Purkinje fibers
Atrioventrical valves
link the atria to the ventricles
Semi-lunar
valves link the ventricles to the plumonary artery & aorta
Bundle of HIS
- heart muscle cells specialized for electrical conduction
- transmit electrical impulses from AV node to apex via bundle branches
Purkinje fibers
cardiomyocytes that are able to conduct cardiac action potential more efficiently than other heart cells
* allow syncronized contraction of the heart ventricles
* essential for **maintaining a consistent heart rhythm **
Heart muscle DEPOLARIZATION
- Influx of Na+ & Ca++ causes depolarization (positive charge inside the cell)
contraction depolarization → influx of Na+ & Ca++ → negative charge at the rest
– is when a cell membrane’s charge becomes positive to generate an action potential. This is usually caused by positive sodium and calcium ions going into the cell
REPOLARIZATION
– is when a cell membrane’s charge returns to negative after depolarization. This is caused by positive potassium ions moving out of the cell
The control of heart rhythm: SA node
- Signals from SA node spread through atria
- The cluster of cells — sinoatrial (SA) node or pacemaker, sets the rate and timing at which all cardiac muscle cells contract
- Impulses from the SA node first spread rapidly through the walls of the atria, causing both atria to contract in unison
- During atrial contraction, the impulses originating at the SA node reach other autorhythmic cells located in the wall between the left and right atria
SA node → atria (walls) → other autorhythmic cells
The control of heart rythm: AV node
- Signals are DELAYED at AV node
- Atrioventricular (AV) node – the cells that form a relay point
- The impulses are delayed for about 0.1 second before spreading to the heart apex.
- This delay allows the atria to empty completely before the ventricles contract
AV node → impulse delayed → //atria empty// → heart apex
The control of heart rythm: Bundle branches
- Bundle branches pass signals to heart apex
- Then the signals from the AV node are conducted to the heart apex and throughout the ventricular walls by specialized structures called bundle branches and Purkinje fibers
AV node → signal → Bundle branches → heart apex
The control of heart rythm: Purkinje fibers
- Signals spread throughout ventricles
signal → heart apex → Purkinje fibers → ventricles
Cardiac conduction/Cardiac cycle
1) Atrial DEpolarization, initiated by the SA node, causes P wave
2) with atrial DEpolarization complete, the impulse is delayed at the AV node
3) Ventricular DEpolarization begins at apex, causing the QRS complex. Atrial REpolarization occurs
4) Ventricular DEpolarisation is complete
5) Ventricular REpolarization begins at apex, causing the T wave
6) Ventricular REpolarisation is complete
Ventricle contraction
wave of DEPOLARIZATION flows through the Bundle of HIS
Cardiac cycle step by step
1)
* The cardiac cycle begins in the right atrium.
* The sinoatrial node (SAN) in the right atrium wall contracts and relaxes automatically, making it myogenic.
* The pacemaker’s rate can be adjusted by nerves.
2)
* The SAN produces an electrical excitation wave that sweeps through the muscle in the atrial walls, causing them to contract.
3)
* The excitation wave reaches the atrioventricular node (AVN), the only way the impulse can get down to the ventricles.
* The AVN delays the impulse for a fraction of a second, allowing the ventricles to contract after the atria.
4)
* The excitation wave moves swiftly down through the septum of the heart along Purkyne tissue fibers.
* The excitation wave arrives at the base of the ventricles and sweeps upwards through the ventricle walls, causing them to contract.
5)
* The ventricles then relax.
* The SAN contracts again, and the sequence starts anew.
Wolff-Parkinson White Syndrome
- is a disorder due to a specific type of problem with the electrical system of the heart which has resulted in symptoms.
- the electrical connection passes through another accessory pathway called the bundle of Kent between the atrium and the ventricle of the heart. This pathway does not cut down the electrical activity nor delay the electrical transmission going to the ventricles. This leads to extremely rapid heartbeats.
Facts
- SAN initiates heartbeat
- Beat of heart is myogenic – spontaneous not started by nervous system stimulus
- Rate of heartbeat is influenced by nervous system
- Wave of electrical activity, impulses over atria triggers contraction of atrium
- Electrical activity may only pass to the ventricles via AVN and bundle of HIS (septum)
- Fibrous tissue prevents passage beyond atria
- Delay at AVN allows ventricles to fill completely from atria
The cardiac cycle and ECG
LO: Use and electrocardiogram to describe the cardiac cycle
Cardiac cycle
1) An electrical impulse travels from the SA node to the walls of the atria, causing the to contract
2) The impulse reaches the AV node, which delays it by about 0.1 sec
3) Bundle branches carry signals from the AV node to the heart apex
4) The signal spread through the ventricle walls, causing them to contract
3 stages in cardiac cycle
- Atrial systole
- Ventrical systole
- Ventical diastole
Systole
contraction & ejection of blood into the aorta & plumonary trunk
Diastole
relaxation & fillin gif heart chambers with blood
Atrial systole
– the heart is filled with blood & the muscule in the atrial walls contract
- both atria contract
- blood flows from the atria into the ventricles
- backflow of blood is prevented by the closure of the valves in the veins
The pressure developed by this contraction is not very great, because the muscular walls of the atria are thin, but it is enough to force the blood in the atria down through the atrioventricular valves into the ventricles.
The blood from the atria does not go back into the pulmonary veins or the venae cavae, because these have semilunar valves to prevent backflow.
Venticular systole
– about 0.1 sec after the atria contract, the ventricles contract
- Both ventricles contract.
- The atrioventricular valves are pushed SHUT by the pressurised blood in the ventricles. (“LUB”)
- The semilunar valves in the aorta and pulmonary artery are pushed OPEN. Blood flows from the ventricles into the arteries.
The thick, muscular walls of the ventricles squeeze the blood, increasing its pressure and pushing it out of the heart.
When the pressure in the ventricles becomes greater than the pressure in the atria, the atrioventricular valves shut, preventing blood from going back into the atria.
The blood rushes upwards into the aorta and pulmonary artery, pushing open the semilunar valves in these vessels.
Ventricular diastole
– themuscle relaxes (lasts for about 0.3 sec)
- Atria & ventricles relax.
- The semilunar valves in the aorta & pulmonary artery are pushed SHUT. (“DUB”)
- Blood flows from the veins through the atria and into the ventricles.
As the heart muscle relaxes, the pressure in the ventricles drops, and the semilunar valves snap SHUT to prevent backflow of blood.
During diastole, the whole of the heart muscle relaxes, and blood from the veins flows into the two atria at a very low pressure.
The atria have thin walls that are easily distended, so they provide very little resistance to the low-pressure blood flow.
Blood flow
→ Oxygenated blood to all the cells IN body via aorta
→ Deoxygenated blood FROM body to RA through Vena Cava
→ Blood from RA to RV through tri-cuspid valve
→ Deoxygenated blood from RV through plumonary arteries TO lungs
→ Oxygenated blood RETURNS to LA via plumonary veins
→ Oxygenated blood TO LA via bi-cuspid valve
ECG: ElectroCardioGram
– a recording of the electrical events/changes during a cardiac cycle
- Assess your heart rhythm
- Diagnose poor blood flow to the heart muscle (ischemia)
- Diagnose a heart attack
- Evaluate certain abnormalities of your heart, such as an enlarged heart
To detect and record the waves of excitation flowing through heart muscle electrodes placed on the skin over opposite sides of the heart, and the electrical potentials generated recorded with time.
The result, which is essentially a graph of voltage against time, is an electrocardiogram (ECG).
- The part labelled P represents the wave of excitation sweeping over the atrial walls.
- The parts labelled Q, R and S represent the wave of excitation in the ventricle walls.
- The T section indicates the recovery of the ventricle walls.
/Graph pic/
P- wave: Depolarization of atria in response to SA node triggering (Artial contraction – systole)
PR interval: Delay of AV node to allow filling of ventricles
QRS complex: Depolarization of ventricles, triggers main pumping contractions (Ventricular contraction – systole)
ST segment: Beginning of ventricle repolarization, should be FLAT
T-wave: Ventrical (myocardium) repolarization
Wiggers diagram
– shows events during systole, mainly ventricular systole or contraction
The isovolumetric contraction phase begins at the R peak of the QRS complex on the electrocardiogram graph-line.
The isovolumetric contraction phase lasts for about 0.03 seconds.
After the isovolumetric contraction, the ejection phase begins immediately.
During the ejection phase, ventricular volume (red graph-line) decreases as ventricular pressure (light blue graph-line) continues to increase.
Once the blood is ejected from the ventricles, the pressure drops, and the heart enters diastole.
The oxygen dissociation
LO: Explain oxygen dissociation curves haemoglobin and myoglobin for adults and embryos
Haemoglobin
- transport oxygen from the gas exchange surfaces of the alveoli in the lungs to tissues all over the body.
- supplies oxygen for aerobic respiration.
- oxygen is transported inside red blood cells in combination with the protein haemoglobin.
- each haem group can combine with one oxygen molecule.
Hb + 4O2 ⇌ HbO8 (oxyhaemoglobin)
Oxygen Binding Affinities to Haemoglobin
Lungs:
* Oxygen high
* CO2 low
* pH high
Tissue:
* Oxygen low
* CO2 high
* pH low
Cooperative Binding of Haemoglobin
Oxygen dissociation curves show the relationship between oxygen levels (as partial pressure) and haemoglobin saturation.
Because binding potential changes with each additional O2 molecule, the saturation of haemoglobin is not linear.
oxygen binding affinity: low → high
Hb < HbO2 < HbO4 < HbO6 < HbO8
S-shaped curve
– due to shape of molecule being altered as each O2 molecule is taken up.
- After binding of first molecule shape changes so the binding of the others is easier.
- Steep part of the curve - small decrease in pp oxygen results in a big fall in % saturation.
Adult vs Fetal haemoglobin
- Adult hemoglobin is made up of four subunits. The most common form of adult hemoglobin, Hb A, consists of two alpha and two beta subunits (α2 β2).
- Mammals have a unique form of hemoglobin for fetuses, known as fetal hemoglobin (Hb F), consisting of two alpha and two gamma subunits (α2 γ2).
- Hb F has a higher affinity for oxygen compared to adult hemoglobin, allowing it to extract oxygen from maternal circulation.
- This results in a left-shifted hemoglobin-oxygen dissociation curve for Hb F compared to Hb A. A left-shifted curve means that oxygen loading occurs at lower oxygen concentrations.
Fetal oxygen transport
*Fetal blood has a very low PO2, but oxygen transport from placenta to sites of fetal need is efficient.
* Fetal Hgb has high O2 affinity.
- Hemoglobin transports oxygen in blood while myoglobin transports or stores oxygen in muscles.
- Myoglobin consists of a single polypeptide chain and hemoglobin consists of several polypeptide chains.
- Hemoglobin concentration in red blood cells is very high compared to myoglobin.
- Myoglobin is a monomeric protein that binds one oxygen molecule tightly
- Hemoglobin is a tetrameric protein that can bind four oxygen molecules and offload both oxygen and carbon dioxide.
- Hemoglobin initially binds oxygen with difficulty
- Myoglobin binds oxygen rapidly.
Adult haemoglobin
- rapid saturation of oxygen in the lungs
- rapid dissociation of oxygen as the oxygen concentration decreases
- oxygen released in the tissues where it is needed
Fetal haemoglobin
- fetal haemoglobin curve to the left of adult haemoglobin
- higher affinity for oxygen than adult haemoglobin
- oxygen moves from adult haemoglobin to fetal haemoglobin
Myoglobin
- myoglobin to the left of fetal haemoglobin
- higher affinity for oxygen than adult haemoglobin
- only releases oxygen at very low oxygen concentrations in tissues
- acts as oxygen reserve in muscle cells
high altitude where there is little O2.
- greater affinity to bind O2
- greater affinity to hold on to O2
Different Haemoglobins
- Haemoglobins with a high affinity for oxygen.
These take up oxygen more easily but release it less readily - Haemoglobins with a low affinity for oxygen.
These take up oxygen less readily but release it more readily
Q: What happens if we have an iron deficiency?
Answer: Hypochromic Anemia
Is a generic term for types of anemia in which the red blood cells are paler than normal.
Hypo – less, chromic – color.
Bohr effect
LO: Describe and explain the significance of the Bohr effect
The effect of pH on oxygen-haemoglobin loading and unloading is known as the Bohr effect.
the decrease in the oxygen affinity of a hemoglobin in response to decreased blood pH resulting from increased carbon dioxide concentration in the blood.
* the oxyhemoglobin dissociation curve is displaced to the right because of higher partial pressure of carbon dioxide and lower pH.
haemoglobin’s oxygen binding affinity is inversely related both to acidity and to the concentration of carbon dioxide.
- blood [CO2] ↑ blood pH ↓ Hb losing O2 (release)
CO2 + H2O → (HCO3)- + (H)+ - blood [CO2] ↓ blood pH ↑ Hb gaining O2 (hold)
(HCO3)- + (H)+ → CO2 + H2O
Since CO2 reacts with water to formcarbonic acid, an increase in CO2 results in a decrease in blood pH.
bohr effect
the formation of haemoglobinic acid means that in the presence of high CO2 conc. the dissociation curve shifts to the right (decrease in affinity for oxygen)
CO2 transport
- 85% is transported in the plasma as dissociated hydrogen carbonate
H2O + CO2 ⇌ H2CO3 ⇌ (H)+ + (HCO3)- - 15% is carried by haemoglobin as haemoglobinic acid
HbNH2 + CO2 ⇌ (HbNHCO2)- + (H)+ - carriage of CO2 by the plasma catalysed by carbonic anhydrase. Increased H+ conc. causes blood pH to drop so more oxygen is released from the haemoglobin
- chloride shift balances the movement if (HCO3)- ions into the plasma
CO2 is carried in the blood(tissues to lungs):
1) Bound to haemoglobin
2) Dissolved in the blood plasma
3) In erythrocytes(RBC’s) as carbonic acid(85% of CO2 carried)
- CO2 diffuses into erythrocyte
- CO2 + H2O ⇌ H2CO3, catalyzed by carbonic anhydrase; form carbonic acid which is more soluble
- H2CO3 dissociates (H)+ and (HCO3)-
- Chloride shift: bicarbonate ions pumped OUT of erythrocytes & Cl- ions are pumped IN (overall charge remains the same)
- Bicarbonate ions combine with sodium ions in the blood plasma (NaHCO3) – these are carried to the lungs
- H+ ions in the erythrocyte lower the pH, causing haemoglobin to release oxygen (to respiring cells/tissues)
- Haemoglobin binds excess H+ ions to restore pH in the erythrocyte (H+ released in lungs)
