Cardiovascular System Flashcards
functions of blood
- transport: gas, nutrients, wastes, processed molecules, regulatory molecules
- regulate pH (7.35-7.45) and osmosis
- maintain internal body temp
- protect against foreign substances
- clot formation
production of formed elements
- hematopoiesis: to make blood cells
- stem cells: all formed elements derive from here
- proerythroblasts -> erythrocytes
- myeloblasts -> basophils, neutrophils, eosinophils
- lymphoblasts -> lymphocytes
- monoblasts -> monocytes
- megakaryoblasts -> platelets (not cells but fragments)
erythropoiesis
production of red blood cells
-decreased O2 = kidney release erythropoietin = red bone marrow make more RBC = release more RBC
- stem cell –> proerythrocytes –> early erythrocytes –> intermediate erythrocytes –> late erythrocytes–> reticulocytes
erythropoietin
A hormone produced and released by the kidney that stimulates the production of red blood cells by the bone marrow.
hemoglobin breakdown
1) Hemoglobin is split into heme and globin
2) Globin’s amino acids are recycled to the blood
3) Heme’s iron is stored in the liver for future use (to spleen and bone marrow to make RBC)
4)Heme’s pigment, now bilirubin, is used in bile production
WBCs function and movement
protect body against microorganisms; remove dead cells and debris
- ameboid: pseudopod
- diapedesis: stretch to fit btwn cells or thru capillaries
- chemotaxis: attraction and mvmnt toward foreign material or injured cells
hemostasis
stoppage of bleeding by one of 3 ways:
- vascular spasm
- platelet plug formation
- clot formation / coagulation
vascular spasm
vasocontraction of the smooth muscle in the wall of a damaged blood vessel to prevent blood loss
- form of hemostasis
- caused by thromboxane from platelets and endothelin
platelet plug formation
platelet adhesion: when von Willebrand factor connects collagen and platelets
platelet release rxn: release ADP, thrombaxanes, other chemicals to activate platelets in cascade effect
platelet aggregation: activated platelets give out receptors to bind to fibrinogen to make a plug/bridge btwn platelets
expression of factor V and phospholipids
coagulation
blood clotting (hemostasis)
- activate prothrombinase > prothrombin to thrombin > fibrinogen to fibrin
- factors are proteins in plasma that circulate inactively until tissues are damaged; when platelets adhere the activations begin
- blood clot: fibrin fibers, trapped blood cells, platelets and fluid
extrinsic clotting pathway
- begin w chemicals outside of blood
stage 1: damaged tissues release TF3; Ca present makes TF3 + TF7 = TF 10; form prothrombinase
stage 2: prothrombinase turn prothrombin > thrombin
stage 3: thrombin turn fibrinogen > fibrin
and thrombin activate TF13 to stabilize clot
intrinsic clotting pathway
- begin with chemicals part of blood
stage 1: in damaged vessels TF12 comes in contact w collagen to activate TF12; TF11 is stimulated to turn on TF9; TF9 joins with TF8, platelets, Ca, to make TF10; prothrombinase made
stage 2: prothrombinase turn prothrombin > thrombin
stage 3: thrombin turn fibrinogen > fibrin
and thrombin activate TF13 to stabilize clot
control of clot formation
- anticoagulants: prevent coagulation factors from starting clot
- coagulation factors need to meet threshold
anticoagulants
prevent blood clot formation
- antithrombin: made in liver, slowly inactivates thrombin
- heparin: made from basophils and endothelial cells; increases antithrombin effectiveness
- prostacyclin: prostaglandin from endothelial cells,, cause vasodilation and inhibit release of coagulating factors from platelets
fibrinolysis
Breakdown and removal of a clot; how stop blood leave body
- fibrin threads of clot attach to vessel walls
- platelet processes attach to fibrin threads
- actin and myosin in platelets contract to pull edges in and allow serum to exit
clot dissolved by plasmin (enzyme that hydrolyzes fibrin)
antibodies
Specialized proteins that aid in destroying infectious agents by attaching to antigens
antigens
foreign substances that trigger the attack of antibodies in the immune response.
blood types
A: has B antibodies and A antigens
B: has A antibodies and B antigens
AB: no antibodies; A and B antigens
O: has A and B antibodies but no antigens
Rh blood group
Rh (+) : have these antigens on surface of RBCs
Rh (-) : do not have these antigens on RBCs
mean arterial pressure (MAP)
average BP in aorta
- MAP = CO x PR = (SV x HR) x PR
- low HR at rest = greater SV
- PR: total resistance blood pumped against
Decreased BP causes
1.) Decreased blood pressure, decreased blood pH, increased blood carbon dioxide, decreased blood oxygen, exercise, and emotions
↓
2.) Increased sympathetic stimulation, decreased parasympathetic stimulation, and increased epinephrine and norepinephrine secretion from the adrenal medulla
↓
3.) Increased heart rate
↓
4.) Increased cardiac output
↓
5.) Increased mean arterial pressure
increased BP causes
1.) increased BP, exercise, change sit/stand–>
2.) increased venous return increases end diastolic volume –>
3.) increased force of contraction and end diastolic volume –>
4.) increase SV –> increase CO–> increase MAP
intrinsic heart regulation
Normal heart functions (not neural or hormonal)
- preload: (Sterling’s Law) amount of stretch of ventricular walls; more stretch = more force contraction
- afterload: pressure contracting ventricles overcome to aortic pressure to move blood into heart
extrinsic heart regulation
neural and hormonal control of heart
- parasympathetic: vagus nerve decreases HR, ACh repolarizes heart
- sympathetic: cardiac nerves SA and AV nodes, increase HR, epinephrine and norepinephrine released.
increased HR = increase CO = low end diastolic = less refill
- hormonal: epinephrine and norepinephrine when increased PA, emotions and stress
heart homeostasis
- blood pressure: baroreceptors monitor BP, internal pressure of carotid and aorta, send info to medulla
- pH, CO2, O2: measurements taken in hypothalamus, chemoreceptors monitor low O2 to increase HR and O2 delivery
- extracellular ion conc: increase/decrease K = increase HR
- body temp: HR and temp both will increase or decrease
baroreceptor and chemoreceptor reflexes
- baroreceptors affect heart homeostasis and monitor BP
- chemoreceptors determine heart beat w O2
- CO2 receptors monitor pH in CSF (no bicarbonate in CSF)
dynamics of blood circulation
Interrelationships between
Pressure
Flow
Resistance
Control mechanisms that regulate blood pressure and blood flow
laminar flow
- interior of blood vessels is smooth
- outer layer is slow, middle is fast
- slow and easy (sound dissipates)
- no sound = no turbulence
turbulent flow
- interrupted blood flow
- rate of flow exceed critical velocity
- due to blockage, bend, rough surface
- sound is due to abnormal blood flowing; increase thrombosis
blood flow
rate of flow through tube expressed as volume pass specific point at certain time.
flow = (point1-point2/resistance)
- BP increase = blood flow increase
- resistance increase = blood flow decrease
- resistance = 8vl/(pi)r^4
blood pressure variables
viscosity (how much solute in solvent): more solute = more viscous
length of vessel (increase length = increase resistance)
radius: moves faster down middle of tube as sides have friction (decrease radius = more friction = slow) (increase radius = less friction = fast)
Poisuelle’s Law
- flow decrease when resistance increase (vise versa) (resistance is proportional to diameter)
Flow = (P1 -P2)/R - p(P1 -P2)r4/8vl
viscosity
resistance to liquid to flow
- More solute in solvent = higher viscosity
Viscosity increase = decrease in flow
Viscosity in humans from dehydration = more plasma
Reduce viscosity and resistance to blood flow if hydration (also increase BP)
Fill blood w more plasma = more volume = more pressure on walls of arteries/veins
critical closing pressure
Pressure at which a blood vessel collapses and blood flow stops
Laplace’s Law
-Forces act on blood vessel wall proportional to diameter of vessel times blood pressure
-F = D x BP
-Max dilation = max pressure on walls
vascular compliance
Tendency for blood vessel volume to increase as blood pressure increases
compliance
*increase in volume/Increase in pressure
-More easily the vessel wall stretches, the greater its compliance
-Venous system has a large compliance (24 times greater than that of arteries) and acts as a blood reservoir
capillary exchange
movement of substances between blood and interstitial fluid (most important is diffusion)
- lipid soluble thru PM (O2, CO2, hormones, FA)
- water soluble thru intercellular space (AA, glucose)
- BP drop if too much blood lost (thru fenestrated caps)
- some fluid is picked up by lymphatic system
fluid exchange across capillary walls
net filtration pressure (NFP) (force move fluid across)
- hydrostatic pressure higher at arterial end
- osmotic pressure remains the same thru out
- water flow out at arterial end; in at venous end
- more fluid escapes than is reabsorbed (lose plasma - picked up by lymph syst)
hydrostatic pressure
pressure of fluids in a closed space; generally higher in capillaries than tissues therefore fluid wants to escape capillaries
- mvmnt of blood flow due to heart beat
osmotic pressure
pressure that must be applied to the solution side to stop fluid movement when a semipermeable membrane separates a solution from pure water.
- more solute in blood than tissues; water enter capillaries
pressure equations
NFP = hydrostatic - osmotic
hydrostatic = BP - IFP
osmotic = BCOP - ICOP
BCOP
blood colloid osmotic pressure
- more colloids in blood (trapped (-) ions) that pull on water
- cause pull of fluid back into capillary
ICOP
interstitial fluid colloid osmotic pressure
- amount of colloids in IF
-If lose plasma (ICOP>BCOP) mean increase blood viscosity and increase resistance
capillary fluid exchange
- as blood enters arterial end BCOP will try to pull some fluid out since it is greater than ICOP
- hydrostatic pressure > osmotic pressure = some plasma leaves
- at the venous end osmotic > hydrostatic
- 10% taken by lymphatic system, other 90% by BCOP
edema
capillaries break and proteins move into IF which increases ICOP and so fluid moves from caps to IF = swelling
- inflammatory chem increase permeability
- decrease plasma protein = increase BCOP
veins
- move blood due to hydrostatic pressure in arterial end
- venous tone: continual state of partial contraction of veins as result of sympathetic stimulation (increase w activity)
Control of Blood flow in tissues
Local control: proportional to metabolic need of tissue
Nervous System: routing bf and maintaining bp
Hormonal Control: stimulate epinephrine and norepinephrine
Local Control of blood flow
Can increase 7-8x due to vasodilation and precap sphincters
Vasomotion: contract/relax of precap sphincter. Autoregulation
Long-term local control: capillaries more dense in areas with Increased metabolic rate
Regulate of Mean Arterial Pressure (MAP)
MAP slightly less than SBP and DBP bc DBP longer
- 70mmHg at birth; 100mmHg adult; 110mmHg elder
- MAP = (sv)(hr) x (pr) : all increase w each other
peripheral resistance
opposition to blood flow caused by friction of the blood vessel walls
stroke volume
The amount of blood ejected from the heart in one contraction
-More SV = greater systolic = close more rapid = leave heart faster harder
- affected by PR
baroreceptor reflex
change in peripheral resistance, HR, SV, in response to changes in BP (orthostatic hypotension) (lower BP>vasodilate>increase BP)
- sx standing or sitting
- Orthostatic hypotension
Chemoreceptors:
-sensory receptors to O2, CO2, pH of blood (to monitor pH is to monitor CO2 - behind pons)
CNS ischemic response
-Increase BP due to lack of blood flow to medulla oblongata
-In response to emerg (shock) and BP decrease to 50 mmHg
-Neurons of vasomotor center strongly stimulated; increase blood flow to vessels and also decrease oxygenation of blood as not go to lungs
-Blood O2 levels drop bc not getting to lungs to exchange
-Initial response: blood to brain ASAP>respiratory not stimulate, drop BP by vasodilation
Long-Term regulation of BP
RAA mechanism :
Vasopressin (ADH):
Atrial natriuretic mechanism:
Fluid shift mechanism
Stress-Relaxation Response
renin-angiotensin-aldosterone system
-release more Na into interstitial fluid in cells in kidney > more water out of kidney > increase osmotic gradient outside cell (less water leave)
- Decreased BP liver (want to increase plasma: drink water and reduce urine)
-Renin from kidney due to BP activate angiotensinogen to angiotensin 1 > lungs become angiotensin 2 > liver (adrenal gland) to release aldosterone back to kidney = increase extracellular Na and decrease volume of urine
Vasopressin (ADH) Mechanism
- collecting duct more permeable to water (osmotic gradient out) = more water goes out of collecting duct (decrease urine, increases plasma)
- Oxytocin and ADH
-Vasopressin released effect permeability of collecting duct (allows water)
-Vasopressin lack: collecting duct non permeable to water
-Increase permeability will decrease urine volume
atrial natriuretic hormone
cause decrease permeability of collecting duct by shut down ADH effects (increase urine, decrease plasma)
released from cardiac muscle cells when atrial blood pressure increases, simulating an increase in urinary production, causing a decrease in blood volume and blood pressure
blood at RA > RA walls swell > release ANH
Only on to control high blood pressure w/ urine
Fluid Shift
movement of fluid from interstitial spaces into capillaries in response to decrease in blood pressure to maintain blood volume and vice versa
BCOP increase and draw in fluid
