How much blood is in each portion of the circulation in the body?
Systemic circulation 84%
Pulmonary circulation 9%
What are the functional parts of the circulation?
What is the distribution of blood in the systemic circulation?
64% in the veins
13% in the arteries
7% in the arterioles.
**Majority of blood is in systemic circulation, in the majority of that is in the veins
Even though the smallest amount of blood at any time is in the ___________ they represent
the largest cross sectional surface area of the body.
The fact that there is more of the blood in systemic circulation in the ____, this is where most of the blood volume capacity needs to be.
What is the role of the conduit vessels?
Transport blood to & from regions of
the body (Aorta and vena cava)
What is the role of the distribution vessels?
Distribute & return blood to & from various organs
Name relates to structure served
What is the role of the resistance vessels?
Responsible for most of the resistance in the circulation
What is the role of the exchange vessels?
Allow for movement of gases, fluids, & nutrients between blood and organs
What is the role of the capacitance vessels?
Reservoir for blood; can hold a large volume at low pressure (high compliance vessel)
What is the role of the lymphatic vessels?
Help maintain fluid balance
Structure of blood vessels, they all have similar structures. Most cases, involves 3 layers. What are they?
tunica intima (inner layer)
tunica adventitia (outer layer)
Tell me about the tunica initima
Inner most layer.
Most intimate with the blood. This is where (in all vessels) there is a continuous layer of endothelial cells (Connecting end to end) and those form the lumen of the vessel. There is a difference in different tissues. So liver & kidney vessels have larger pores (slit junctions) permit capacity for large amount of exchange to occur in contrast to BBB where only lipid soluble things can pass d/t tight junctions.
What are the two important substances released from the endothelium
Endothelin (Causes vasoconstriction)
NO (causes vasodilation)
It’s really the balance of the two that contributes in a major way to changes in resistance and therefore blood flow through the vessel.
Tell me about the tunica media
where the vascular smooth muscle is.
Smooth muscle cells are connected end to end circumferentially around the vessel. Its contraction of that smooth muscle in tunica media, helps to regulate BP and vascular resistance.
Both arteries & veins!
Why is venoconstriction (contraction of the smooth muscle in the tunica media.
If venoconstriction (constriction of veins specifically) important regulator of venous return, constriction enhances venous return.
Conversely, if we have venodilation (dilation of veins), we’re talking about pooling of blood in the veins.
What is good about vasodilation of the smooth muscle in the tunica media of the arteries?
Enhance blood flow through. This layer, also has elastic tissue, or elastin, helps contribute to elastic recoil in the blood vessels.
Tell me about the tunica adventitia
This layer contains connective tissue as well as small arteries and nerves from the autonomic nervous system.
Blood vessels themselves need oxygen and nutrients, there are small blood vessels that
perfuse blood vessels, penetrate the walls of the blood vessel (go into the muscle). What are these called?
What are the key structural features of the conduit vessels (Aorta)
Wall contains all 3 layers with large diameter for flow (this helps to reduce resistance to flow) t. media has thick muscle & elastic fibers. (elastic fibers support BP during diastole). Elastic fibers are helpful during systole, allows Aorta to expand and accept that volume of blood ejected. When ventricle relaxes, the elastic recoil of the Aorta helps maintain BP between contractions.
Aorta moves blood at high pressure away from the heart. Essentially what it does during systole. It has elastic recoil in diastole to support BP between contractions of the ventricle.
What are the key structural features of the distribution vessels? (Femoral artery or Brachial artery)?
Wall contains 3 layers but fewer elastic fibers in the walls . Large amount of muscle in t. media assists with dilation/constriction balance (in order to distribute blood to various vascular beds according to requirements)
What are the key structural features of the resistance vessels? (Arterioles)
Have a large amount of smooth muscle for their size so can constrict or dilate as needed
Arterial resistance vessels really help us out, they respond to various needs like acute blood loss in the OR. They are also helpful in other situations (exercise) we need blood more preferentially to certain areas than others. Because of the differential constriction of resistance vessels, vasoconstriction not universally supplied but to where we need it. To muscle in exercise as opposed to GI tract
What are the key structural features of the exchange vessels? (capillaries)
Single layer of endothelial cells
Exchange vessels, are capillaries. No tunica media, no tunica adventitia. They allow exchange at the cellular level of oxygen, nutrients, CO2 and a certain amount of fluid. They also produce endothelin (vasoconstrictor) and NO (Vasodilator) to help w/constriction and vasodilation
What are the key structural features of the capacitance vessels? (veins)
Contain all 3 layers but have relatively thin walls with less smooth muscle in the t. media. Contain unidirectional valves so they tend to be more floppy.
They have a large capacity to hold a large volume of blood. Veins have unidirectional valves. Help w/forward flow. If breakdown of valves = get varicose veins. Veins in leg are also supported by skeletal muscle which also helps to facilitate blood flow back to the heart.
There are technically 3 types of capillaries. What are they?
1st is the continuous capillaries (tight junctions like in brain)
2nd is fenestrated capillaries (these are in the kidneys, the intestinal villa, and some endocrine glands- they have pores (fenestrations-swiss cheese) between the endothelial cells, allows small substances to cross the cell membrane pretty easily).
3rd type: discontinuous, or sinusoids. (These have really large gaps between the endothelial cells, considered the leakiest kinds of capillaries) found in liver, spleen, and bone marrow.
This shows the changes in pressure within the circulatory system (hydrostatic pressures) Heart pumps to Aorta (highest pressure, MEAN 100, systolic 120, diastolic 80). Then as blood flows through systemic circulation, ultimately the mean pressure reaches 0 as it gets to vena cava and then empties into RA. If we look at pressure just in capillaries, naturally pressure is higher at arterioles (30 mean) vs. venous (10) actual pressure in capillaries at about 17mmHg. Because the pressure is relatively low, even
though nutrients will pass but not fluid will pass. All comes back to starlings forces again.
Looking at R side of diagram. We have pressures in pulmonary circulation. Pa sys 25, Pa diastolic 8, Mean Pap around 16. The blood flow permitted is the same through both despite the major difference in pressures of
PA and Aorta.
What are normal PA pressures?
What is the pressure in the Aorta
What is the pressure in the arterioles? venules? capillaries?
Because Aorta has more ______, it offers low resistance to stretch so it has the greatest compliance.
**but Aortic compliance will decrease with age and with atherosclerotic disease
Aortic pulse is determined by
ventricular stroke volume & Aortic compliance.Anything that changes SV, (preload, afterload, inotropy, HR), or anything that changes compliance (Age, atherosclerotic disease, HTN) will alter pulse pressure.
So if there is an increase in SV, it will ______pulse pressure. A decrease in Aortic compliance, will ______ pulse pressure.
Blood flow must be regulated the tissues metabolic needs. We can't just increase CO, different tissues need different amounts, so smaller vessels must __________ to control the local flow
constrict or dilate
TRUE or FALSE. Arterial pressure is autoregulated
So there can be a change in the force of contraction, an increase in venous return, because of venoconstriction (and/or arteriolar vasodconstriction)
Kidneys play an important role in autoregulation.
Describe Ohm's Law
blood to flow through the vessel need gradient, to push blood along.
For individual vessel, talking about the pressure gradient along the individual vessel
(its not just MAP and CVP)
What are the units of resistance?
What is the normal value for systemic vascular resistance?
What is the normal value for pulmonary vascular resistance?
What is general equation for Ohm's law that we use to get resistance?
MAP-CVP x80 = ____ dynes/sec/cm5
Blood vessesl can be arranged in what two ways that can affect resistance?
series or parallel arrangments
How do you calculate the resistance for a series of blood vessels?
the flow through each vessel is the same, resistance of flow is the sum of the individual vessel resistance.
What's nice about the parallel arrangement regarding blood flow resistance?
permits the individual tissue to control it’s own blood flow, according to it’s requirements.
So resistance in parallel arrangement is lower because they can each be controlled separately. This provides an alternate pathway for flow
How do we calculate the Reynold's #?
Re = 2rvd
Used for LAMINAR FLOW
How do we calculate poiseuille's #?
Flow = p (P1- P2) r4
*shows the diameter of the vessel effect on flow
Viscosity has an impact on flow, what could increase viscosity?
Increased Hct, increased plasma proteins, etc. all of which would DECREASE flow
Name 5 reasons we care about the regulation of blood flow
An increase in metabolic rate of tissue will ________blood flow pretty dramatically
As O2 saturation declines, blood flow also _______
The acute control is rapid vasodilation (or rapid vasoconstriction) that happens within _____________. In contrast to longer term control that can take _________.
seconds to minutes; days to months
What are the TWO proposed theories regarding blood flow regulation
Oxygen (& other nutrients) lack theory
Explain the vasodilator theory
Greater the rate of metabolism (less availability of O2) the greater the formation of vasodilators in various tissue cells.
Things that are considered to be vasodilators:
- Adenosine (important vasodilator particularly in coronary circulation)
- Carbon dioxide
- Adenosine phosphate compounds
- Potassium ions
- Hydrogen ions
Explain the Oxygen lack theory (Really same as vasodilator but explained differently)
There is a cyclical opening & closing of precapillary sphincters, along with the metaarterials that happen several times every minute.
This is the vasomotion that normally occurs. So what happens is the smooth muscle involved needs O2 in order to stay contracted, with enough O2the sphincter closes and stays closed until O2 is consumed, when O2 falls to certain level the sphincter will open again and flow will happen again.
Distance factors include which two things?
Autonomic nerves (SNS and PNS)
Hormones (angiotensin and vasopressin)
How does the ANS (distance factor) control blood flow & vascular resistance?
-post ganglionic fibers of SNS release norepi, which acts mostly on alpha 1 post junctional receptors on the vascular smooth muscle.
-release of norepi also causes beta 1 stimulation that will ↑ HR
-release of epinephrine from adrenal medulla (medulla effectively a SNS ganglion). Epi in
particular will act on Beta 2 receptors in vascular smooth muscle to cause vasodilation.
- Alpha receptors also found in veins, can also get venoconstriction (SNS effect on veins is venoconstriction) ↑ venous return,↑ preload & ↑SV.
-post ganglionic fiber releases Ach, this will cause vasodilation. Either d/t direct stimulation or indirect action because of NO release (vasodilator).
So if Norepi mostly constricts and Epi mostly vasodilates, how do we figure out the effect of SNS?
What it comes down to is how many alpha receptors and how many beta receptors are there. The effect at any given part of vascular system is dependent on the ratio of the alpha and beta receptors. Which receptors are available to be stimulated.
How the hormonal distance factors (Angiotensin and Vasopressin) control blood flow and vascular resistance?
Angiontensin II part of RAAS & causes vasoconstriction. Vasopressin is also a vasocontrictor and it’s role in inserting water channels (aquaporins) and retaining water.
Local factors can be divided into three categories, what are they?
-Oxygen & nutrients
- Property of vascular smooth muscle
- Part of autoregulation
- Nitric oxide
There are metabolic local factors. How do they work?
refers to everything necessary to ensure thereis adequate O2 and nutrients.
Active hyperemia: During exercise, increase in lactic acid production and vasodilation in order to bring more blood flow to the tissues. Because there is also ↑ O2 requirement (↑ O2 consumption) that also causes vasodilation. Sequence of events that occurs, that vasodilation and ↑ blood flow.
There are myogenic local factors. How do they work?
intrinsic property of vascular smooth muscle.
To protect the muscle against high pressures.
If perfusion pressure increases, those vascular smooth muscle cells respond by contracting. Get stretch of muscle cells, and they respond by contracting, stretch induced depolarization. Part of autoreuglation (will occur when BP falls acutely in the arterial, this is the opposite of stretch, now we have relaxation. The fall in perfusion pressure, decrease blood flow to tissues, decrease O2, increase metabolic byproducts of anaerobic metabolism, that also causes vasodilation. All of theses things help to maintain flow at the lower level of perfusion pressure.
There are limits to autoregulation (discussed during myogenic local factors). What is the limit
Usually autoregulation is intact between MAP 60-170 (Guyton70-175mmHg).
So compensatory mechanisms can’t operate outside of those limits.
What organs have particularly tight autoregulation?
Heart, brain, kidneys
The third local factor is endothelial. How does this work?
Acute factors that regulate blood flow work within a few minutes of a change in conditions. What are the acute factors?
distance and local factors
K+ and H+ ions
lack of glucose and various vitamins.
What is reactive hyperemia?
Happens when blood supply to a tissue is blocked for a few seconds to an hour or more and then becomes unblocked. When this occurs, (becomes unblocked again), there is an increase in blood flow up to 4-7x normal (immediately). If that flow has been stopped for 1hr or more, that increase in flow can continue for potentially many hours. That increase in flow is just about enough to repay the oxygen debt that has accumulated.
What clinical situation may we see reactive hyperemia?
We see in OR, for a total knee arthroplasty use a tourniquet, inflated to 300-350mmHg stopping arterial flow. The tourniquet, (CRNA monitors time) in 1hr the alarm goes off, our responsibility to say to surgeon that’s an hour of tourniquet, if only 15min then keep going but if longer let it down then re-inflate. When tourniquet goes down we see an increase in EtCO2 because we’ve isolated this leg for 1hr. There has been this build up of lactic acid (anaerobic metabolism). There is also a certain amount of vasodilation that goes on (CO2).
Acute control mechanisms (even w/max utilization of these mechanisms) blood flow is usually only about___% of the way to exact tissue requirements. Over next period for hours, today, to weeks, there is more complete regulation.
What is the mechanism for long term control?
Increase in vascularity
Angiogensis is a long term control mechanism for control blood flow. How does this work?
Angiogenesis: increase in vascularity if metabolism in a particular tissue is increased for a prolonged period of time. The reverse also occurs & vascularity decreases if metabolism decreases. This angiogenesis that occurs is same thing in cancer tissue or normal scar formation.
*The time required for angiogenesis is a little dependent on age of patient, days in newborn or months in geriatric population. Also less efficient in geriatric, doesn’t quite match the metabolic requirements.
Oxygen debt or excess can effect vascularity (and long term control of blood flow). Explain this situation in a premature infant.
Retrolental fibroplasia (RLF), now called retinopathy of the prematurity (ROP) excess oxygen causes decreased vascularity in retina (including some degeneration of small blood vessels already formed) when O2 discontinued extensive overgrowth of new vessels to compensate for decrease of oxygen supply and this overgrowth of tissue causes the retinal vessels to grow beyond retina to aqueous humor and eventually causing blindness
What are the peptides found to increase vascularity
Vascular endothelial growth factor (VEGF)
Fibroblast growth factor
What do antiangiogenic factors do? How can they be useful?
dessolution of blood vessels or block the growth of blood vessels.
Use of these antiangiogenic factors trying to be exploited to stop growth of blood vessels to cancerous tissues, try to cut off blood supply to tumor in cancer
We increased our vascularity, what happens to vessels if they aren't needed?
increase in vascularity goes along with maximum requirements for blood flow, oxygen, and nutrients, not average flow, maximum flow.
If those additional vessels aren’t needed, they can stay constricted until needed again to supply oxygen
Collateral circulation is another part of the long term mechanism to control blood flow (increase in vascularity). What does Guyton say about this?
says all people by age 60 probably have some degree of coronary occlusion not recognized because of the collateral development of vessels that normally occurs
Humoral control (etc.) agents that cause vasodilation
↑ Potassium ion
↑ Magnesium ion
↑ Hydrogen ion
↑ Acetate & citrate ions
↑ Carbon dioxide
Humoral control (etc.) agents that cause vasoconstriction
Norepinephrine (profound vasoconstrictor)
Epinephrine (less vasoconstriction than norepi, could cause vasodilation depending on Alpha 1/Beta 2 receptor ratio)
Angiotensin II (powerful vasoconstrictor-part of RAAS)
Vasopressin (vasoconstrictor & ↑H2O absorption)
↑ Calcium ion
↓ Hydrogen ion
Vasopressin is a vasoconstrictor and causes an increase in water reabsorption. How much can it improve BP by these mechanisms?
It can help increase BP by 60mmHg following an acute blood loss
Neuronal control of circulation: SNS fibers leave the spinal cord by the ____________
thoracic spinal nerve and the 1st one or two lumbar nerves. Because of that, the SNS can be referred to as the thoracolumbar. Pre-ganglionic fibers will go immediately into the sympathetic chain that lies on each side of the spinal column.
Neuronal control of circulation: see that sympathetic nervous stimulation goes to which vessels?
arteries, veins, arterioles and venules
(everything but the capillaries).
Neuronal control of circulation: Pre-ganglionic parasympathetic efferent nerves exit the medulla at the ______________ and go to heart within the R and L vagus nerves. They also innervate blood vessels where they cause vasodilation and release of _____.
10th cranial (Vagus nerve); Ach
What part of the brain is responsible for transmitting parasympathetic impulses by way of vagus to the heart & sympathetic impulses
through the spinal cord and to peripheral nerves to all of the vessels (except the capillaries)??
Vasomotor center in the brain
Located bilaterally, its in the medulla and lower 1/3 of the pons.
What three areas are in the vasomotor area of the brain?
Where does the sensory area of the vasomotor area in the brain get its signals from?
(nerves in sensory area get signals from the circulation by way of the vagus and the glossopharyngeal nerves. Then output helps to control vasoconstriction/vasodilation as a reflex (Baroreceptors-baroreflex is really important)
What creates the vasomotor tone?
continuous firing of the sympathetic vasoconstrictor fibers at slow rate that maintains a certain amount of tone (certain partial state of contraction in the smooth muscle blood vessels)
Explain “Sympathectomy” with spinal anesthesia
differential blocked, do it for sensory block (no pain during surgery) but also motor block (no movement during procedure-surgeon likes this) but with it we get autonomic nervous system blockade as well, called sympathectomy. Blood vessels vasodilate and the patient becomes hypotensive.*Some patient w/severe peripheral vascular disease get surgical sympathectomy to help improve flow to their poor vasculature by cutting off sympathetic supply selectively.
Arteries there is much _____volume and ____ pressure.
In veins, the pressure is low but the volume is high
Circulation can operate almost normally with asmuch as 25% of blood volume loss. How does this work??
Because of SNS stimulation blood can be transferred from one area of circulation to another, that sympathetic activity can help maintain blood flow to vital organs in setting of acute blood loss.
How doe we respond to an increase in blood volume?
Initially rise in intravascular pressure, distention of elastic fibers, but eventually the veins will adapt and there will be a decrease in intravascular pressure.
The ability to adapt is of course somewhat limited dependent to normal A&P and with disease that ability gets lost.
What is the single most important requirement for an effective CV system to function?
maintaining appropriate BP.
If BP is not adequate, then the brain and heart won’t receive O2 and nutrients no matter what the local mechanisms try to do.
Opposite is also true, if excessive pressure is there, that puts unnecessary demand on heart and presents hazards to brain.
Is the Baroreflex system long or short term?
What is the SINGLE most important mechanism for short term BP control?!
The usual pieces of reflex pathway include the sensory receptors, afferent pathways, integrating sensors in CNS, efferent pathways, and ultimately the effector organ. So we’re taking about baroreceptor system specifically, the sensors are:
in carotid sinus and aortic arch!!!!
(she repeated this-locations of baroreceptors, aka know them!)
The baroreceptors referred to as mechanoreceptors. Why?
they are stimulated by stretch.
The degree of stretch within the elastic arterial walls. So when the elastic arterial wall stretches there is an increase in the rate of action potential generation. It’s not just the absolute stretch but also the rate of change of stretch. So both mean pressure and systolic arterial pressure will affect the baroreceptor firing.
If a period of pressure happens over period of days, do the baroreceptors serve as mechanism for control of blood flow?
The baroreceptor adapts to change. SHORT TERM only
How does the AP generated by the carotid and aortic barorecptor get to the CNS?
The AP generated by carotid sinus baroreceptor travel through the carotid sinus nerves (afferent pathway) (aka herings nerve) this joins with glossopharyngeal nerves (Cranial nerve 9) before entering the CNS.
Similarly, the aortic nerve baroreceptor afferents run to the CNS and the vagus.
Explain the effect of stimulation of baroreceptors in the carotid sinus
Stimulation of baroreceptors
Impulse goes to medulla via tractus solitarius
Inhibition of vasoconstrictor center in medulla
PNS stimulation via vagus
Vasodilation & ↓ HR ↓ contractility
(end result is an decrease in BP)
At what pressure are the carotid baroreceptors stimulated?
aren’t stimulated for pressures up to 50-60mmHg at higher pressure the response becomes progressively more rapid reaching a pressure 180mmHg (kind of within that autoregulation).
The receptors (Aortic arch) respond similarly but at pressure 30mmHg higher, carotid are a little sensitive.
Is it the rate of change or the amount of change that stimulate the baroreceptors?
THE RATE OF CHANGE!
They respond more rapidly if the pressure change in rapid, again it’s the rate of change, the rate of firing, the rate of stimulation on the receptor, not the absolute value
Do we use baroreflex in emergent situations or all the time?
use baroreflex all the time, helps to mediate even postural changes.
Important for minute to minute control of BP but tend to reset within 1-2days to whatever pressure they are exposed so limited in terms of long term BP control.
What are the two chemoreceptors and where are they located?
located in several small chemoreceptor organs (2 carotid bodies and 1-3 Aortic bodies)
Carotid bodies are at bifurcation of L and R common carotid artery.
Aortic bodies are adjacent to the Aorta.
How do the chemoreceptors work to regulate blood flow
sensitive to things like lack of O2, too much CO2, elevated levels of H+ ions.
They will stimulate nerves that go along w/baroreceptor fibers (go through Hering’s nerves) into vasomotor center of the brain stem. There is a small nutrient artery that supplies the chemoreceptors, and so if the arterial pressure falls below a certain point, there is a decrease in O2 level, the CO2 and H+ ion level increases
What are the thresholds for the chemoreceptor stimulation?
PO2 threshold is around 80mmHg
PCO2 around 40mmHg
So if PO2 goes below 80 the CO2 above 40, & the pH below 7.4,that will cause a firing of the carotid bodies. That will excite the vasomotor center and increase BP
Describe the arterial and pulmonary artery reflexes in control of blood flow (BP)
low pressure stretch receptors in walls of Atria and pulmonary arteries. These are similar to the baroreceptors in the large systemic arteries. Again they play a role in minimizing pressure changes and changes in volume. So the atrial reflexes will cause dilation of afferent arterial in the kidney, they also will send signal in hypothalamus to decrease ADH secretion. So increase in blood flow through afferent arterial will increase GFR, decrease in ADH secretion will decrease water reabsorption. Both of which will return BP back down to normal. The other thing that happens w/stretch of atria release of atrial natriuretic peptide (hormone) that will also increase excretion of fluid in the urine.
Explain the Bainbridge Reflex
reflex along w/stretch of atria will cause an increase in HR when the RA is stretched about 10-20%.
It will increase the HR by an additional 40-60%. Because of this reflex afferent signals by vagus to medulla, efferent by SNS to effect HR and contractility
Explain the CNS Ischemic Response
Decrease on blood flow to brain that results in CNS ischemia will also cause excitation of vasoconstrictor, & the cardiac accelerator fibers of the vasomotor center and the result again would be an increase in BP. Mechanism of that is the accumulation of CO2 & lactic acid.
So decrease in CBF, cerebral ischemia, causes SNS stimulation which then causes an increase in BP. This is an extremely powerful activator of the SNS.
What is a problem with the CNS Ischemic Response
Problem is it doesn’t take effect until arterial pressure drops to around 60mmHg (systolic). Considered to be an emergency control system, to protect the brain in a real hypotensive event. Greatest stimulation is a pressure of 15-20mmHg.
Explain the cushing reflex
Cushing Reflex is a special type of CNS ischemic response d/t increase in ICP from increase CSF in the brain. Increase in CSF pressure & ICP will interfere w/blood supply to the brain, initiates ischemic response, once BP goes above ICP the brain will be perfused again.
What three reflexes are mechanoreceptors? Where are they located?
Arterial Baroreceptor (Internal carotids and Ao Arch)
Bainbridge (Venoatrial junctions)
Cardiac (Atria & Ventricle)
What three reflexes are chemoreceptors? Where are they located?
Chemoreceptor Reflex (Brain)
Bezold-Jarisch (Ventricle and coronaries)
What is the stimulus for the aterial baroreceptor? What happens to SNS and PNS activity?
Increased arterial pressure
What is the stimulus for the Bainbridge reflex? What happens to SNS and PNS activity?
Increased Venous return
What is the stimulus for the Cardiac (Atria Reflex)? What happens to SNS and PNS activity?
Increased chamber pressure
What is the stimulus for the chemoreceptor reflex? What happens to SNS and PNS activity?
Hypoxia, hypercapnia, acidosis
What is the stimulus for the CNS ischemic response? What happens to SNS and PNS activity?
What is the stimulus for the Cushing Reflex? What happens to SNS and PNS activity?
What is the stimulus for the Bezold-Jarisch reflex? What happens to SNS and PNS activity?
Ventricles and coronaries
Clinically, when might we see the Bezold-Jarisch reflex?
stimulated when dye injected into the coronary artery during cardiac catheter. Its ischemia within the inferior posterior wall of LV that can also produce that reflex. And its bradycardia and hypotension that are mediated by the vagus
How big is the diameter of the capillary? Why is this important?
*Sue loves her #s....
diameter is only 4-9 dichrometers, barely allows the RBC to pass. What the capillaries do though is permit efficient exchange mechanism for passive diffusion from high concentration to areas of low concentration.
And all the factors include Fick’s law that relate to diffusion across the membrane.
Substances are delivered through the circulation and to the capillary and going through the capillary to the interstitial fluid. Name some factors involved
Size of pores
Gradient across the membrane
(STARLINGS FORCES) Balance between capillary hydrostatic pressure, plasma colloid oncotic pressure and interstitial hydrostatic and the osmotic pressure in the intersitial fluid as well.
Blood is what % of body weight?
6-8% of body weight
What is the estimated blood volume of neonates?
What is the estimated blood volume of infants?
What is the estimated blood volume of adults?
Does blood contain both extracellular and intracellular fluid?
YES!!! (plasma and RBC)
In the blood, a _________ is cells and
_________ is plasma.
What is the normal Hct for males and females?
Hgb is ___of Hct
We want to evaluate the patient’s starting Hct and think about how low we’ll let their Hct go
and how much blood lost in the field would it take for Hct to get that low.
To estimate the RBC volume, we first need to
know pt hct and pt blood volume.
Starting Hct is 35%. Pt is 70kg. First decide RBC volume. Then figure out now how much blood loss will we transufse at (when Hct hits 30%)
75ml/kg x 70 kg = 5250ml (total blood volume)
Take 5250 x 0.35 = 1838ml
Blood loss we'd transfuse at (Hct 30%)
5250ml x 0.3 = 1575
If we subtract these two, 1838-1575 = 263ml that’s the RBC lost to get Hct to go from 35 to 30%. Then multiply by 3 which gives up 789ml because can’t loose RBC by itself, losing everything. So 263 x 3 =789ml allowable blood loss.
decrease in O2 carrying capacity in the blood (For us in OR it’s usually blood loss) but can be other types of anemia (nutrient deficiency). Could have chemo or radiation therapy and have bone marrow suppression as a result. There are certain situations where RBC become fragile & tend to lyse or rupture easily (hemolytic anemia-sickle cell disease)
How many types of WBC are there? Name a few
macrophages/monocytes attack & destroy bacteria and other infectious agents as part of inflammation.
Dry mucous membranes are a sign of intravascular volume fluid loss. What happens at 5%, 10% and 15% of body weight loss?
10% Very dry
Sensorium is a sign of intravascular volume fluid loss. What happens at 5%, 10%, and 15% of body weight loss?
Orthostatic changes (HR and BP) are a sign of intravascular volume loss. What happens at 5%, 10%, and 15% of body weight loss.
15% marked! >15bpm ↑ >10mmHg ↓
Urinary output decreases as a sign of intravascular volume loss. What happens at 5%, 10%, and 15% of body weight loss?
HR increases as a sign of intravascular volume loss. What happens at 5%, 10%, and 15% of body weight loss?
5% Normal or↑
10% ↑ >100bpm
15% markedly ↑ >120
BP decreases as a sign of intravascular volume loss. What happens at 5%, 10% and 15% of body weight loss?