Types of Airways
+ negative pressure breathing explained v2
+ two types of alveoli
Conducting airways: trachea, bronchi, and all but last few brancioles
Respiratory airway: respiratory bronchioles, alveolar ducts and sacs – lots of SA for exchange
Negative pressure breathing explained:
Specific naming of serous membranes in regards to the cavity / organ (5)
Types of Alveoli (2)
+ Gas exchange
+ Gas diffusion
Alveoli:
Gas exchange:
Gases always diffuse from high partial pressure to low partial pressure
Types of Circuits for the Mammalian Cardiovascular System (2)
Pulmonary: pumps out O2 poor blood from the pulmonary artery to the right and left lungs → shorter pathway, therefore low pressure circuit
Systemic: pumping of O2 rich blood from the aorta to the systemic circuits / rest of body; can diffuse into respiring tissues → longer pathway, requires higher pressure
* also explains why left side of the heart is thicker in muscle than the right
Pulmonary and systemic circuits are completely separate in mammals and birds → closed circulatory system
– Circuits are in series (not parallel) → equal volumes of blood pumped BUT at different pressures (systemic is higher than pulmonary) bc of the locations that need to be oxygenated
Circulatory System
Functions:
Defining attributes: transport of oxygen is most pressing / urgent, therefore minute to minute changes in tissue demand for O2 will drive changes in the rate of blood flow
DIFFERENTIATION OF BLOOD CELLS (2)
+ erythrocytes
All blood cells are derived from the same connective tissue source (Stem cells in bone marrow) → yield lymphoid and myeloid
Erythrocytes:
Following the heart through a single cardiac cycle – pressure
+ ECG waves timeline
WHOLE HEART DIASTOLE: 0.4 seconds; AV valves open while SL valves closed bc P(atria) > P(ventricles); ventricles fill with deoxygenated blood
ATRIAL SYSTOLE and VENTRICULAR DIASTOLE: 0.4 seconds; AV valves open while SL valves closed bc P(atria) > P(ventricles); ventricles fill with deoxygenated blood
INITIAL OF VENTRICULAR DIASTOLE: P(ventricles) increase
END OF VENTRICULAR DIASTOLE: P(ventricles) decrease
(P) Signals from SA node spread throughout atria
(PQ) Signals are delayed at the AV node
(Q) Bundle branches pass signals to heart apex
(RS) Signals spread throughout ventricles via Purkinje fibers
(T) Relaxation as the signals stop contracting.
Heart anatomy
Valves maintain one-way flow of blood (no backflow)
1. Atrioventricular valves:
– Tricuspid: present in the right atrioventricular valve
– bicuspid: present in the left
⇒ “tri before you bi” make sure it’s “right before you leave (left)”
2. Semilunar valve: three flaps; bases of aorta and pulmonary artery
Right side receives venous return via VENA CAVA and pumps blood via PULMONARY ARTERY towards the lungs
– Veins will always return blood to the heart no matter the O2 content.
Left side receives oxygenated blood from lungs via PULMONARY VEINS and pumps blood into systemic circuit via the AORTA
Heart anatomy
Regarding venous return
Valves maintain one-way flow of blood (no backflow)
1. Atrioventricular valves:
– Tricuspid: present in the right atrioventricular valve
– bicuspid: present in the left
⇒ “tri before you bi” make sure it’s “right before you leave (left)”
2. Semilunar valve: three flaps; bases of aorta and pulmonary artery
Right side receives venous return via VENA CAVA and pumps blood via PULMONARY ARTERY towards the lungs
Left side receives oxygenated blood from lungs via PULMONARY VEINS and pumps blood into systemic circuit via the AORTA
Veins will always return blood to the heart no matter the O2 content. Venous return dependent on:
Influences that affect SA node
INCREASE:
DECREASE: extrinsic only
Influences that affect SA node
INCREASE:
DECREASE: extrinsic only
Arterioles (2)
Vasodilate in response to low [O2]m pH, high [CO2] and by release of nitric oxide from endothelial cells → local response
Constrict via sympathetic stimulation (and endothelin, a local paracrine) → basically control how much blood is passing through / at what pressure
Flow in mL/min = P(in) - P(out) / R
- pressure in minus pressure out, all over radius
Three sources of resistance:
Capillaries
Hydrostatic pressure pushes plasma out of the capillary via open clefts btwn endothelial cells (leakage) BUT osmotic pressure maintained by blood proteins (esp albumin) brings it back in
Interrelationship of Blood Vessels, Blood Flow Velocity, and Blood Pressure
Water example: Water doesn’t compress under pressure THEREFORE volume of water moving through a hose exits from a narrow nozzle at a higher speed so that volumes remain equal
Compare to capillaries: Capillaries are NARROWER than arteries THEREFORE velocity in capillaries is the slowest (0.1cm / sec) → Slow velocity in capillary is good bc then allows for exchange btwn capillaries and interstitial fluid
– compare to that of arteries, which is 50cm/sec
Blood pressure highest nearest course of contraction (ie ventricles) and then dissipates due to the resistance generated by narrowing diameters of the tiny arterioles and capillaries → largest drop off in pressure is btwn the arteries and arterioles
Monitoring and maintenance of blood pressure
SHORT TERM REGULATION
LONG TERM REGULATION
Hemoglobin
Polypeptide bc has two alpha globin + two beta globin chains, each of which can carry one iron containing heme → each heme can bind one molecule of O2
– HbO2 = oxyhemoglobin, HbCO2 = carbaminohemoglobin
HONORARY ENZYME bc O2 attaches to the defined bind site via noncovalent interactions causing a conformational shift in the hemoglobin structure → cooperativity: affinity for O2 increases via shape change
– Once released, will start to revert to the original shape and thus lose the other O2 molecules more readily → called something
O2 is poorly soluble in water, therefore hemoglobin can increases the O2 carrying capacity of the blood by 50X
Dissociation Curve for Hemoglobin
+ Bohr shift, defined sub 3
functional relationship btwn P(O2) and percent saturation of hemoglobin
Bohr shift, defined: change in hemoglobin’s affinity due to different pH values; triggered by H+ and CO2 binding to globin chains of hemoglobin (cooperativity)
CO2 Exchanges in systemic and pulmonary capillaries – the science-y bits
Two exchanges happen concurrently
Loading of CO2 and release of O2 from blood in systemic capillaries:
1. 8% of CO2 released from tissues dissolves in plasma; 20% binds to globin chains; 72% diffuses into RBC
2. Carbonic anyhydrase converts CO2 and H20 into H2CO3
3. Chloride shift reduces [HCO3-] inside RBC, which favors diffusion of even more CO2 into RBC
RESULT = binding of H+ to globin chains reduces affinity of hemoglobin to O-
Release of Co2 and loading of O2 into blood in pulmonary capillaries:
1. REVERSE chloride shift allows HCO3- to diffuse back inside RBC where carbonic anhydrase converts it back to CO2
2. CO2 will diffuse into alveoli
RESULT = Loss of H+ binding to hemoglobin increases its affinity for O2
Homeostatic control of breathing
Tidal ventilation
vs countercurrent
vs crosscurrent
Tidal ventilation: normal amount of volume inhaled and exhaled; allows for exchange of fresh air with stale air BUT v inefficient bc P(O2) blood exiting respiratory organ < P(O2) in exhaled medium = very inefficient system
– versus X-current exchanges where its the opposite, therefore more efficient
Countercurrent: opposing directions
– Fish: gill arch → water passes through gill filaments allowing for countercurrent gas exchange
Crosscurrent: same direction
– Bird: air passes through posterior air sacs, pick up oxygen in the lungs; air passes through anterior air sacs → two cycles of inhale, exhale to move through both air sacs