Physio 3 Flashcards
what determines total amount O2 bound and carried by Hb?
% saturation Hb (amount O2 bound) and total [Hb] blood
Lower than normal blood [Hb] =
anemia
Describe relationship between PO2 and % Hb saturation
directly proportional
What’s shape/what variables determine (IV/DV) of O2-Hb dissociation (association) curve?
sigmoidal curve
% Hb saturation and PO2
B/c of cooperative binding of O2:
—0-40 mm Hg = large magnitude change in % saturation
—40-120 mm Hg = very small change in % saturation
normal systemic PO2 = 104 mm Hg (arterial) and 40 mm Hg (venous) –> thus, since arterial
Why will Hb never reach 100% saturation in systemic arterial blood?
due to chemical nature (kinetics) of molecules - constantly moving = constantly colliding (possibly forming bonds) and weak intermolecular interactions = constantly dissociating –> thus, all molecules are constantly forming bonds/dissociating
significance of “plateau at the right end” of O2-Hb dissociation curve and how does it act as safety factor?
Provide an example where safety factor would be useful.
Due to cooperative binding of O2 = large mag. change PO2 in arterial blood = small mag. change in % saturation
“plateau” = safety factor for supply O2 –> tissues if ever large decrease in PO2 of arterial blood (= decrease overall [O2] in blood)
example - regions HIGH ALTITUDE = LESS O2 = less O2 in alveoli = decrease net [O2] diffuses into arterial blood = decrease PO2 (O2 dissociated in blood plasma)
Describe how increase in altitude does not dramatically effect % saturation
high altitude –> O2 molecules in atmosphere farther apart (less dense, so inhale less O2 each breath) –> alveolar PO2 decreases –> systemic arterial PO2 decreases –> small decrease % saturation
due to “plateau at right end” dissociation curve - aka cooperative binding O2
If constant PO2, what 3 other variables effect % Hb saturation and why? What impact have on hemoglobin at molecular level?
Alter Hb affinity for O2 via altering bond strength
- changes in: [H+], [CO2], temperature, and [2,3-bisphosphoglycerate (2,3-BPG)
% Hb saturation =
( [HbO2] / total [Hb] ) X 100
Or
(# O2 molecules bound / total # O2 molecules total [Hb] capable of binding)
what determines % Hb saturation
affinity / bond strength between Hb & O2
List changes in variables that would cause O2-Hb dissociation curve to “shift to the right” (decrease % saturation):
- increase [H+]
- increase [CO2] (direct effect = increase [H+])
- increase temperature
- increase [2,3-bisphosphoglycerate]
How are metabolically active tissues able to “extract” more O2 from blood?
Increase [CO2] (carbohydrate metabolism / cell respiration product) –> increase [H+] –> decrease pH = local increase acidity –> local decrease Hb affinity O2 = local region causes increase HbO2 dissociation –> increased [O2] diffuse into metabolically active tissues
Increase temperature = decreased Hb affinity O2;
HEAT = product carbohydrate metabolism = metabolically active tissues = regions increase temperature
Metabolically active tissues create localized regions of increased [H+], increased [CO2], and increased temperature - all DECREASE Hb affinity to O2 = local increase HbO2 dissociation = increased [O2] diffusion into cells
How does increased [2,3-bisphosphoglycerate] effect O2 -Hb affinity? Give examples when elevated [2,3-BPG]
2,3-BPG binds to heme groups on Hb, decreases available binding sites on Hb –> decrease % Hb saturation
important for adaptation to poor blood flow certain regions/tissues or high altitude
How does carbohydrate metabolism increase [CO2] and subsequently [H+]?
C6H12O6 + O2 –> H2O + CO2 + ATP
Carbon dioxide reacts w/ H2O in blood create bicarbonate - equilibrium rxn = carbonic acid + H+
Blood circuit:
LEFT ventricle - aorta - systemic capillaries - superior and inferior venae cavae - RIGHT atrium
= Systemic blood circulation
Blood circuit:
RIGHT ventricle - pulmonary trunk - right and left pulmonary arteries - pulmonary capillaries - pulmonary veins (4) - LEFT atrium
= Pulmonary blood circulation
Total blood volume of adult?
5 liters
Hematocrit
List normal values (adult, male, female)
% total blood volume = RBCs
Average adult ~ 40%
Male ~ 43%
Female ~ 39%
Why is hematocrit different for males and females?
testosterone stimulates kidneys which produces more EPO = increase RBC production in bone marrow \
Only site of transport into or out of blood circulation:
crossing CAPILLARY WALLS
Does more blood pass through the systemic than pulmonary circuit in a given period of time?
NO - both pump same volume of blood/unit time
Rate = same
Portal circulatory pathway =
List examples
2 capillary beds in a series instead of 1 capillary bed.
heart - arteries - 1 capillary bed - blood vessel - 2nd capillary bed - veins - heart
ex. - Hypothalamus capillaries - blood vessel - anterior pituitary - 2nd capillaries; all digestive organ blood dumps into hepatic portal vessel - 2nd capillary bed
What is responsible for majority of ventricular filling?
gravity
why you can live with atrial fibrillation ~ weak primer pumps ~
List the formed elements of blood:
erythrocytes
leukocytes
platelets
all suspended in liquid called plasma
List structural components of pericardium.
SEROUS pericardium + Outer FIBROUS pericardium
Serous pericardium = 2 continuous layers (parietal + visceral) separated by pericardial cavity
What tissue = bulk of heart walls
myocardium - cardiac muscle
Muscular interventricular septum
divides the heart into right and left fxnal halves
Heart Valves
Prevent backflow = ensure unidirectional blood flow
Atrioventricular valves
Tricuspid valve - between RIGHT atrium and ventricle
Bicuspid or Mitral valve - between LEFT atrium and ventricle
Prolapsepushing of AV valve into atrium while closed + ventricle contracting - restricts the movement of valve
chordae tendineae + papillary muscles
prevent backflow into atria - unidirectional flow
Open = atrium higher pressure Closed = ventricle higher pressure
Semilunar valves
Pulmonary valve - between RIGHT ventricle + Pulmonary trunk
Aortic valve - between LEFT ventricle + aorta
prevents backflow from pulmonary or aortic arteries into ventricles
lack chordae tendineae + papillary muscles
Open - higher ventricular pressure
Closed - higher pulmonary or aortic pressure
Is the opening / closing of heart valves a passive process?
YES - driven via pressure gradient across valves caused by blood filling spaces on either side
bicuspid / mitral valve
left atrium/ventricle
chordae tendineae + papillary muscles (extension of myocardium from ventricular walls)
-prevent prolapse
tricuspid valve
right atrium/ventricle
chordae tendineae + papillary muscles (extension of myocardium from ventricular walls)
-prevent prolapse
Prolapse
= inappropriate pushing of AV valves into atrium while closed/ventricular contraction; restricts range of motion - papillary muscle contraction during ventricular contraction pulls cusps down toward ventricle
no role in opening/closing just prevents valve from being pushed into atrium
chordae tendineae + papillary muscles allow this
papillary muscles
attaches to AV valves to contract and prevent prolapse
extension of myocardium of the ventricles
chordae tendineae
fibrous tendons that link AV valves to papillary muscles
Coronary arteries
1st 2 branches of aorta
provide blood supply to heart muscle (myocardium)
All of the cardiac muscle fibers of the heart need to be coordinated, simultaneous contraction.
= all cardiac muscle fibers must be simultaneously depolarized
Volume of blood pumped by each ventricle per unit time (minutes)
Cardiac Output
2 factors directly determine the cardiac output
Heart Rate (HR) stroke volume (SV)
Volume of blood ejected by each ventricle during each contraction (mL)
Stroke Volume (SV)
Equation to calculate Cardiac Output
CO = HR x SV