Midterm 2 Flashcards
What happens if the V/Q ratio is low in humans?
Sending too much blood for the air to carry C02 away or not sending enough air to a particular region of the lung. CO2 levels rise in the body. Cause bronchiolar smooth muscle to relax which increases air flow to that particular region of the lung. Increase V/Q ratio back to 1 by matching!
- low 02 levels in blood cause vascular smooth muscle to constrict. This reduces Q so O2 levels in both alveoli and blood can increase. decrease blood flow to match ventilation.
rapid anion protein exchanger (BAND lll)
This exchanges bicarbonate for chloride in the RBC membrane and helps reaction move forward when Co2 is being transferred from the tissues to the blood
Haldone effect
ability of deoxy Hb to carry more CO2 and H+
respiratory alkylosis
Individual is hyperventilating which causes a decrease in CO2 levels - shifts rxn to the left (decrease in H+ but increase in pH). hypocapnia
respiratory acidosis
individual is hypoventilating - this increases CO2 levels in the body and also increase H+ in our body because increase in CO2 shifts the reaction to the right - > Increase in H+ causing a decrease in pH - fall in pH as a result of breathing. hypercapnia.
peripheral sensors in mammals
detect changes in oxygen levels - these are found in the aortic arch and the carotid arteries (these are called carotid bodies ) which detect the blood going to the brain. The can also detect RBC volume/hematocrit. These only get activated when oxygen levels are very low.
central receptors
found in the central nervous system (medulla). These monitor pH primarily but also CO2. Detect cerebrospinal fluid. Dominant control element is CO2 and pH (H+)
normoxia
normal body conditions for that particular animal. This varies with the animal and which environment they live in
hypoxia
LOW oxygen levels. This is unusual in air breathers bc of the abundance of oxygen in the environment we live in. If O2 levels were low however, this is when those peripheral receptors would kick in. Hypoxia can be caused by conditions in the lung that limit the diffusion of gases –> lung/gill diffusion limitation. Usually something that reduced functional surface area of the gas exchange surface. Water breathers are much better suited to deal with hypoxic conditions (decrease metabolic processes like protein synthesis to lower needs for oxygen)
Fish (water breathing circulation)
Has a sinus venosus chamber that helps collect blood and has electrical pacemaker machinery - paces rhythmic contractions. Generates depolarizations that trigger contractions of the heart
Sinus venosus
helps collect blood and has electrical pacemaker machinery - paces rhythmic contractions. Generates depolarizations that trigger contractions of the heart
bulbous arteriosus
teleosts . Elastic chamber that stretches and then recoils. Non-muscular chamber after the ventricle.
conus arteriosus
elasmobranchs/bowfins/lungfish. Weak muscular chamber following the ventricle that has weak muscular contractions
aortic valve
at junction between the aorta and the left ventricle. Triscuspid, semilunar valve
pulmonary valve
at junction between right ventricle pulmonary artery. Tricuspid, semilunar valve
left atrioventricular valve
bicuspid mitral valve, has chordae tendonae attached to make sure that no prolaspse occurs
right atrioventricular valve
tricuspid valve
ductus arteriosus
connection from pulmonary artery to the aorta in fetal hearts. Allows them to bypass the lungs as they are not in use.
ligamentum arteriosum
Ligament that represents the remnants of the ductus arteriosus
cardiac glycosides
Block the sodium potassium ATPase, thereby increasing intracellular which influences a sodium - calcium exchange to exchange sodium out of the cell, thereby increase calcium content inside the cell - this causes increased force of contractions
pacemaker cell action potential
-60 mV - 0 mV. W/threshold at -40mV. Upward drift of membrane potential is caused by a reduced potassium conductance. There is also an increase in calcium conductance. Once threshold is reached, VG calcium channels open for the spike (DHP). Potassium channels open to let potassium out of the cell - membrane hyperpolarizes.
sinoatrial node (SA) node
Cluster of pacemaker cells. This cluster is remnant of the sinus venosus we saw in frogs. This is near where the vena cava enters the right atrium. Depolarizes at about 70-80 beats per minute. It gets to express it’s inherent rate of spontaneous depolarization moreso than the other pacemaker cell clusters because it is the fastest .
atrioventricular (AV) node
Cluster of pacemaker cells between the right atrium and right ventricle. (40-60 beats per min)
Bundle of His
tract of pacemaker cells (conducting fibres) that runs down the septum dividing the ventricles. (20-40 beats per min)
Purkinje fibres
tract of pacemaker cells (conducting fibres) that pick up where the Bundle of His left off - carry the signal from the apex of the hear up the ventricular walls (20-40 beats per min)
atrioventricular (AV) node
Forms the electrical ring between the atria and the ventricles - gives the atria time to pump blood into the ventricles before they contract. This time pause is called the AV nodal delay (100-200 ms) in human heart. The AV nodal delay is caused by a very high resistance in the AV node muscle cells. This increase in resistance increases the time constant- takes more time for each cell to reach threshold .
chronotropic effects
affecting the speed of contraction/heart rate
inotropic effects
affecting the strength of contracton
lusitropic effects
controlling the ability of heart to relax and fill with heart
dromotropic effects
affecting the speed of the spread of depolarization on the heart
parasympathetic control of the heart
controlled via the vagus nerve. Acetylcholine is released from the nerve terminals of the vagus nerve - cholinergic effects - Ach binds to receptors on the heart cells
- Increases potassium conductance by opening up ion channels - tends to hold pacemaker cells in a HYPERPOLARIZED state bc more K+ is flowing out of the cell - SLOWS THE HEART RATE DOWN
PS tone
There is always some background level of parasympathetic stimulation. This holds back the heart rate from the inherent rate of the SA node (70-80 beats per min). So decreasing this PS tone would have the effect of increasing the heart rate.
M receptors
These are muscarinic (Ach) receptors on the pacemakers cells in the heart. Ach binds to these receptors, causing second messenger pathways to be stimulated, ultimately resulting in the increase in potassium conductance in the heart and thus a decrease in the heart rate!
sympathetic nervous stimulation of the heart
primary sympathetic nerve that innervates the heart = cardiac sympathetic nerve - catecholamines
- chronotropic effect: increase the heart rate by decreasing potassium conductance (cell can reach threshold faster)
- dromotropic effect - increase speed of spread of depolarization across the heart. *decrease potassium conductance
- increase force of contraction - E and NE bind to B1 receptors on working myocardium - this activates protein kinases which phosphorylate:
- Ca channels - causes more intracellular release of calcium
- troponin - causes troponin to bind more readily to calcium
- both of these lead to increased cross bridge formation
Cardiac Output
CO= heart rate x stroke volume
