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281 Cards in this Set

  • Front
  • Back
very, very basic, describe how blood flows
right atrium> right ventricle > lungs > left atrium > left ventricle > body > right atrium
What does cardiovascular system consist of
heart
blood vessels
blood
central wall
septum
artery where blood is pumped out of the left ventricle
aorta
why is blood lost in the cardiovascular system
because of resistance due to the walls of the blood vessels
Why does blood flow?
liquids and gases flow down pressure gradients
what is the pressure gradient like as one moves from the heart?

the cross sectional area?

the velocity of blood flow?
csarea: max at cappilaries...min at aorta and venea cava

velocity: max at aorta and vena cava
hydrostatic pressure
the pressure a fluid (normally not moving) exerts on its container
name 2 things that are derivatives of coelomic cavities
-kidneys
-reproductive organs
-pleural cavities
-cardiac sack
what is an alternate to diffusion
stirring
what does the cardio system have the highest priority in delivering blood too?
brain
heart
kidney
What part of the body has the most amount of blood?
veins
how is a fish's heart?
-2 chamber
-heart, gills, and systemic organs are in the same loop


**second loop arose when fish came to land and had dual oxygen exchange between lungs and gills at the same time
flow rate
volume of blood that passes a given point in the system per unit time
velocity of flow
distance fixed volume of blood travels in a given period of time
What acts as a pressure reservoir during the heart's relaxation phase?
arteries
MAP
mean arterial pressure

primary driving force of blood flow

MAP=CO*PR

CO=volume of blood the heart pumps per minute

PR=resistance of the blood vessels to blood flow through them.
velocity of flow equation
v=flow rate/AREA crosssec
connection in series vs, connection in parallel
series...
D(change in)P(total) = DP1 + DP2 + DP3
R(total) = R1 + R2 + R3
F1 = F2 = F3
DPn ~ Rn

Parallel...
1/R(total) = 1/R1 + 1/R2 + 1/R3

DP(total) = DP1 = DP2 = DP3

F(total) = F1 + F2 + F3

Fn ~ 1/Rn
how is a fish's heart?
-2 chamber
-heart, gills, and systemic organs are in the same loop


**second loop arose when fish came to land and had dual oxygen exchange between lungs and gills at the same time
flow rate
volume of blood that passes a given point in the system per unit time
velocity of flow
distance fixed volume of blood travels in a given period of time
What acts as a pressure reservoir during the heart's relaxation phase?
arteries
MAP
mean arterial pressure

primary driving force of blood flow

MAP=CO*PR

CO=volume of blood the heart pumps per minute

PR=resistance of the blood vessels to blood flow through them.
velocity of flow equation
v=flow rate/AREA crosssec
connection in series vs, connection in parallel
series...
DP(total) = DP1 + DP2 + DP3
R(total) = R1 + R2 + R3
F1 = F2 = F3
DPn ~ Rn

Parallel...
1/R(total) = 1/R1 + 1/R2 + 1/R3

DP(total) = DP1 = DP2 = DP3

F(total) = F1 + F2 + F3

Fn ~ 1/Rn
laminar flow
a
turbulent flow
a
what does pouiseuille's law work for?
only for laminar flow

flow=pressure/resistance

R = 8Ln/pir4

R ~ Ln/r4

L=length
n=viscosity
r=radius
tough membranous sac encasing heart
pericardium
pericardium
tough membranous sac encasing heart
peri
around
kardia
heart
myo
muscle
how does the apex of the heart point?
to the left side ofthe body, while the broaer base lies just behind the breastbone or sternum
what lubricates the heart?
a thin layer of clear pericardial fluid inside the pericardium
pulmonary trunk
directs blood to the lungs
where is the thyroid gland?
right below adams apple

rostral to trachea

superior to heart
coronary arteries
branch very early on aorta and supply blood to the heart
coronary veins
after blood is supplied to the heart, they return the deoxygenated blood to via the vena cava
chart of different vessels with the following

diameter
wall thickness
endothelium
elastic tissue
smooth muscle
fibrous tissue
aa
draw the heart in the rib cage
aa
what does color of blood indicate?
red: well oxygenated blood

blue: not very good oxygenated blood
picture of heart open
aa
what prevents blood on one side of heart from mixing with blood on the other side of the heart?
interventricular septum
how must ventricles contract and why
they must contract bottom up because the aorta and pulmonary trunk are both at the top of the heart...this contracting makes sure blood is squeezed out of the heart
where does left atrium receive blood from?
pulmonary veins
what encases heart?
a membranous fluid-filled sac called the pericardium
what happens to valves during ventricular contraction?
right AV or tricuspid valve: closed

mitral, left AV, or bicuspid valve: closed

aortic semilunar valve: open

pulmonary semilunar valve: open
what happens to valves during relaxation
left and right AV valve open

semilunar valves closed
main purpose of valves?
prevent the backflow of blood

ensure that blood flows in only one direction
talk about valves
-four fibrous connective tissue rings surround the four heart valves
-form the origin and insertion for cardiac muscle
-acts as electrical insulator
-
right side of heart has what A-V valves?
tricuspid

mn...RST
left side of the heart has what valves
bicuspid

or mitral valve
how do valves work?
AV:
-have chordae tendineae on the inside of the ventrical that holds the valve to the papillary muscle that branches from the wall of the ventricle

-valves move passively when flowing blood pushes on them

-when ventricle contracts, blood pushes on ventricular side and causes valve to close...chordae holds the valve from going into the atrium

semilunar valves:
-seperate ventricles from major arteries
-have 3 cuplike leaflets that snap sloces when blood attempting to flow back into the ventricles fills them
-due not need connective tendons because of their shape
why are funny channels called funny channels?
because they allow both potassium and sodium in and researchers were unsure as to how they worked.

-sodium enters more rapidly because it has a higher driving force when the cell is at -60mv

-these channels cause the pacemaker potential and when the Vm reaches -40mv an AP is fired

-
what is heart rate determined by?
the rate at which the pacemaker cells depolarize

-increased potassium P or decreased Ca P slows down heart pace
How does NE speed up the heart rate?
it binds to B1 adrenergic receptors and causes cAMP to bind to If channels and make them remain open longer...thus they are open at the same time as Ca2+ channels are open
2 types of cardiac cells?
-autorhythmic
-contractile
SA node
autorhythmic cells in the top of the right atrium that serve as the main pacemaker of the heart
AV node
autorhythmic cells near the floor of the right atrium
draw the picture of how the heart pacemaker works
autorhythmic cells fire slower as you move down the chain...pacemaker is set by the fastest firing cells:normally the SA node
what insulates atria from the ventricles?
Fibro-tendonous ring
describe cardiac cells
-branched
-single nucleus
-attached to each other by junctions called intercalated disks: have gap junctions
what aids in ejection of blood from ventricle?
the spiral arrangement of muscles in the walls
mnemonic to remember nodes?
nodes SAAV the heart
second function of the AV node?
delays transmission of AP slightly allowing the atria to complete their contraction before ventricular contractino begins

-AP's move at only 1/20 the speed of AP's in the atrial internodal pathway.
what cells set the pace of the heart
SA node

-other autorhythmic cells can act as pacemakers but their rhythm is slower than that of the SA node so they normally have no chance to set the heartbeat

the fastest autorhythmic cells will set the pace

if the SA node fails, the AV node will set the pace
how are electrodes attached in an ECG
Einthoven's triangle

-right arm all negative
-left leg all positive
-left arm positive and negative

- a normal ECG uses a 12-lead...3 limbs + 9 on the chest and trunk
what is P wave?
depolarization of the atria
QRS complex
progressive wave of ventricular depolarization
T wave
represents the repolarization of the ventricles
how do the mechanical events of the cardiac cycle relate to the electrical signals?
they lag slightly behind
can you tell if an ecg represents repolarization or depolarization?
no
what does the ecg represent
extracellular recording that represents the sum of multiple action potentials taking place in many heart muscle cells
faster than normal heart rate
tachycardia
slower than normal heart rate
bradycardia
how do you measure heart rate
go from one peak on ECG to next peak.....R to R
how do the lines occur during an ecg
when the electrical wave moving through the heart is directed toward the positive electrode, the wave points up

-negative electrode will point down
where does atrial repolarization occur?
the qrs wave
name some things an ecg can tell u
heart rate

rhythm

analyze the waves
how can blood going through capillaries avoid some of them?
sphincters contracting and blood traveling through metarterioles
is blood an ideal fluid?
no
law of laplace
T=pr/2 for a sphere

T=pr for a cylinder

T is tension
p is pressure difference
what assists passive filling of the heart
7-12 mmHg positive pressure that is always present in the circulation system irrespective of the pumping....systemic filling pressure
left ventricular pressure vs. left ventricular volume diagram
a
wigger's diagram
a
explain coronary circulation
Both, the left and the right coronary arteries branch from the aorta right above the semilunar valve

They provide blood to the epicardial (outer) layer of myocardium. The coronary arteries are interconnected with the inner network of smaller arteries named Subendocardial plexus. Endocardium receives part of its oxygen from the blood inside the heart

Venous blood is discharged via cardiac veins into both left and right atria

Blood flow in the coronary circulation is in counterphase relative to the systemic loop: it slows down during the systole
angiogenesis
growth of new blood vessels from old ones
infarction
tissue that becomes necrotic because of inadequate blood supply
after a heart attack, what are the new passage ways that blood travels through?
collaterals
draw a diagram of the rapid homeostatic response to a sudden increase in arterial pressure

sudden decrease in bp?
discussion questions set 5
draw the homeostatic loop that would provide long-term compensation for reduced blood pressure. Now give the loop for long-term compensation of increased blood pressure.
discussion 5
draw the o2/hb dissociation curve..label important things

what will make the curve shift to the right or left?
discussion 5
draw the chloride shift mechanism, where does this occur....now draw the reverse of this...
discussion 5 and pg600
How do you know if HR will increase?
parameter sheet
how do you know if TPR will increase?
parameter sheet
how do you know if SV will increase?
parameter sheet
how do you know if will CO increase?
parameter sheet
how do you know if VR will increase?
parameter sheet
how do you know if DP will increase?
parameter sheet
How do you know if PP will increase?
parameter sheet
how do you know if MAP will increase?
parameter sheet
describe the heart cells....basic
-contain desmosomes that transfer force from one cell to adjacent cell

-also contain gap junctions to transfer impulses
describe pacemaker
-fibro-tendonous ring electrically insulates atria from the ventricles

-AV node is the only pathway in which ventricles can be reached
what are gap junctions formed by and what happens when different ones bind?
connexins

if different connexins bind, the gap will not be present and the electrical signal will not be conducted
draw cardiac E-C coupling
5% of Ca2+ required for contraction enters cardiomyocytes during the action potential from outside

other 95% comes from SR
draw action potential of a contractile cell in the heart
pg473

-calcium helps to prevent tetanus from occuring...

-a normal muscle cell finishes its entire AP before the muscle cell is done contracting and relaxing...this is not the case with cardiac muscles
why does skeletal muscle twitch occur?
why doesn't cardiac twitch occur?
where does excitation begin
SA node
draw ap in autorhythmic cells
-first part is known as the funny channel
-second part is the Ap
-...-60, -40, +20 are the big numbers
-permeable to both sodium and potassium but sodium has a larger driving force
another name for funny channels?
HCN channel

-hyperpolarization-activated cyclic-nucleotide gated channel
what would happen to the autorhytmic AP if stimulated by sympathetic response?

PS response?
draw the pathway for epi and ACh interaction on heart autorhythmic cells

also contractile cells
In the pacemaker (chronotropic effect):
a b1 stimulation increases [cAMP], which shifts the activation curve of the ‘funny’ channel, so it activates earlier and faster. It also increases the conduction velocity in the AV node
a cholinergic stimulation through the right vagus (SA node) directly activates KACh channel (via mAChR and Gbg), hyperpolarizing the cell. At the same time, Ga inhibits Adenylyl Cyclase, reduces [cAMP], which downregulates the ‘funny’ channel. The left vagus slows down conduction in the AV node and the bundle of His

...right side through PKA affects contractile cells

In the contractile myocradium (inotropic effect):
a b1 stimulation increases [cAMP], activates PKA which phosphorylates several targets:
-L-type Ca2+ channel (DHPR), letting more Ca2+ in
-Phospholamban, which increases Ca2+ re-uptake into SR
-TnC, which re-sets its Ca2+ binding curve to higher Ca2+ concentration

As a result, a more forceful contraction is followed by a deeper relaxation, and the stroke volume increases.
what does each part of a ecg mean?
draw an ecg with a ventricular action potential
CO=
CO= SVxHR

SV=EDV-ESV
what does EDV depend on

ESV?
rate of filling (degree of relaxation, ventricular filling pressure and time between strokes)

ESV depends on the contractility and the back pressure on the aorta
what does HR depend on?
state of the pacemaker, balance of sympathetic and parasympathetic inputs, or alternatively it may rely on an artificial pacemaker
another name for effects on heart rate?
chronotropic
another name for effects on heart contraction
inotropic
abnormal electrical activity of the heart
arrhythmias

ex.
tachycardia
bradycardia
ectopic focus
Any part of the heart that initiates an impulse without waiting for the sinoatrial node is called an ectopic focus
types of arrhythmias
Tachycardia (elevated HR - high sympathetic tone, fever or intoxication)

Bradycardia (reduced HR - under vagal stimulation or abnormally high sensitivity of baroreceptors)

Premature atrial or ventricular contractions due to the presence of an ectopic focus - additional pacemaker spot

Accessory conduction pathways between atria and ventricles - premature ventricular systole

Reentrant tachycardia (AVNRT) - early atrial systole due to re-entry back to atria

Fibrillation-uncoordinated contraction of heart muscles
how to normalize (usually reduce) the heart rate
use anti-arrhythmic effects

Cardiac glycosides, digoxin (Digitalis, Foxglove extract) – Na/K pump blocker (increases the force of contractions, slows the pacemaker down)

Propranolol - b-blocker

Adenosine – has parasympathomimetic effect
- (both ACh and Adenosine reduce cAMP levels, see the messenger cascade)

Lidocaine - Na+ channel blocker (prolongs refractory period)

Verapamil, Diltiazem - cardiac L-type Ca2+ channel blockers (increase the excitation threshold)
how to get rid of bad spots and fibrillation
use surgery to remove the following
-ectopic foci
-some accessory pathways
-some points of re-entry


use electric defibrillator to deliver a strong discharge through the chest, re-polarizing (and thus stopping) the entire heart. A minute after the heart has a chance to resume paced contractions.
how does digotoxin work?
blocks the sodium/k+ pump

increases the force of contraction while slowing the pacemaker down

..positve inotropic effect on myocardium

..negative chronotropic effect on pacemaker..reduces driving force for sodium in funny channels
draw p-r and qt interval
long q-t syndrome
-recessively inherited disorder
-bilateral deafness and cardiac arrhythmias (prolonged q-t interval)
-mutation in potassium channel that is expressed in both the ear and the heart

-heart k+ is involved in repolarization
(defects in timing repolarization is deadly)

-the inner ear requires a special compartment filled with K+ rich endolymph...this fluid saves hair cells from sodium poisoning
what is the refractory period?
the time that the action potential occurs in and no other action potentials can occur
early afterdepolarization that predisposes to a severe arrythmic condition called
exam 2 study sheet (1)

early afterdepolarization that predisposes to a severe arrythmic condition called

called Torzade de Pointes
what do mutations in potassium channels do to heart cells?
-prolonged cardiac action potentials beyond the refractory period

-via LQT 1 and 2
explain of blood coming from the left and right heart
must pump blood at the same rate
starling law of the heart
the more fibers are stretched, the more the fibers will contracts
compensation
increase of SV and CO following following the pressure buildup in front of the left or right heart
lack of compensation=
heart failure

causes congestive disease and edema
besides starling law of the heart, what else did starling publish?
capillary filtration and absorption is set by osmotic difference between the interstitium and plasma
osmotic pressure=
RTC
relationship between capillaries and lymph vessels
lymph vessels have openings that allow fluid to flow in via bulk flow
MAP through cardiovascular system
starling's capillary hypothesis
-red is the colloid osmotic pressure...occurs from there being more protein in the capillaries and water following its natural gradient
-capillary hydrostatic pressure decreases because of friction that takes away energy
what can cause edema
valve regurgitation

cardiac tamponade

weak heart

infarction

heart hypertropy

low concentration of serum albumin (malnutrition or liver cirrhosis)

dysfunction of lympatics
left heart failure
pulmonary edema
right heart failure
systemic edema
filling is what?
passive...no venous pressure....no venous returnm
why is blood loss dangerous
hypovolumea reduces the systemic filling pressure which fills the heart
what to do when there is no spare blood to transfuse
inject physiological solutions supplemented with plasma expanders

-large molecules such as dextrans will provide onctotic pressure

-salt solution will not stay in the blood, but will distribute into tissues and cause a massive systemic edema
edema
fluid accumulating in the interstium
draw pressure profile throughout the systemic loop
what does the SP and DP really measure?
the pressure in the aorta
arterial compliance
change in volume/ change in pressure
why is there still pressure during diastole
because of elastic recoil that sends blood forward
what happens if heart becomes too big?
laplacian disadvantage

T=pr/2

must generate larger tension to achieve sufficient pressure and eject the required amount of blood. After a certain size the heart fails.
pulse pressure=
PP=SP-DP
Mean arterial pressure=
the average of the DP and SP....takes into account DP more because it lasts longer

MAP= DP + pp/3
CO=
CO=HR*SV

CO=MAP/TPR
how is bp measured
by a sphygmomanometer

-korotkoff sounds are created when pulsatile blood flows through compressed artery
what happens to DP, SP and MAP w/ increased HR? at constant TPR
they will all increase because the aorta will fill up and the resistance will still be the same
what will Increased TPR do to DP, SP, MAP?
increase all of them because more hyrdrostatic will be allowed to act

-to determine, just view the picture of the aorta filling because of increased HR and then filling more because of more TPR
what does increased SV do to Sp, DP, and MAP
larger increase in SP, smaller increase in DP and MAP
what causes increased sympathetic outflow?
worries, excitement, anxiety and a static load (weight with no muscles contracting)
respnonse to worries, excitement, anxiety or static load?
increase in pressure values
what does exercise do?
incresed SP
decreased DP
decreased TPR
only slightly raised MAP
what does increase to SV and TPR do to BP values
increase all
what is complience and what does a decrease of this do to sp?
increased SP, decreased DP

complience is how contractile the arteries are....non-complient arteries stiff
hyperemia
increased perfusion to tissues
vasodilators and vasoconstrictors...these will affect tpr and ap
Vasodilators:
CO2, H+, K+ (metabolic)

NO, histamine, adenosine

ANP (atrial natriuretic peptide)

Epi (on b2 receptors)

Vasoconstrictors:
Serotonin
Endothelins

Angiotensin II

Vasopressin
NE, (on a1 receptors)
autoregulation of perfusion in tissues
1. Myogenic autoregulation adjusts blood flow

2. Paracrines (H+, K+, CO2, NO, histamine, adenosine) relax vascular smooth muscle
Relationships between major cardiovascular parameters
CO = VR (cardiac output = venous return)

CO = HRxSV, 70 beats/min x 70 ml = 4900 ml/min

SV= EDV-ESV

CO = mAP/TPR (blood flow=mean DPressure/Total Peripheral Resistance)

PP = SP - DP (pulse pressure = Syst. P - Diast. P)

mAP = DP+(1/3)PP,

Arterial Compliance = DV/DP = SV/PP
image of baroreceptor reflex
cardio big receptors
pacemaker
para: mACh
symph: b1

mycoardium
para: none
symph: b1

vessels are either a1 or b2 depending on what is needed...there is no psympathetic innervation

skeletal muscle also has mACh and a1
what neurotransmitters are involved with alpha

beta?
NE

epi and NE
draw ne epi effect on pulse, bp, and TPr
how is blood volume regulated by kidneys
Blood Loss, BP decrease::::

hypovolumea +
sympathetic stimulus

Renin is released by kidney

Stimulates activation of Angiotensin II

Vasoconstriction, thirst,
release of ADH (vasopressin)
increased H2O reabsorption

Release of Aldosterone
(increases Na+ reabsorption)

BV and BP increase

...too much volume, BPincrese

Atrial pressure increases

ANP is released by endocardium

ANP reduces H2O and Na+ reabsorption (which stimulates excretion)

More water is lost into urine together with Na+

BV decreases to normal
Ach, epi, and Ne on...
Hr
sv
tpr
vr
dp
sp
pp
co
ACh......
Hr;d
sv;i
tpr;d
vr;d
dp;d
sp;d
pp;?/nc
co;d

epi...
Hr i
sv i
tpr d
vr i
dp d
sp i
pp i
co i

NE...
Hr d
sv i
tpr i
vr i
dp i
sp i
pp i
co i

alpha is Ne
beta is epi and Ne

NE increases Hr at first which will increase BP, baroreceptors detect this and then cause a decrease...thus, NE will decrease bp if asked on exam
hypertension in experimental animals
Renal hypertension (by constriction of renal arteries)

Neurogenic hypetension (by denervation of baroreceptors)

Spontaneous (in genetically-predisposed animals)

Salt-induced hypertension (in salt-sensitive strains)
statistics and treatability in humans of hypertension
90% -essential (the cause is not firmly established) -treatable, but not really curable
corrected by administering a1- and b-blockers, inhibitors of angiotensin-converting enzyme (ACE), Ca2+ channel blockers and diuretics

10% - secondary, usually caused by either an endocrine disorder and/or higher retention of fluid. This includes hypersecretion of aldosterone or other mineralocorticoids. Hypersecretion of catecholamines (tumors of adrenal medulla). Narrowing of renal arteries and other renal disorders, which reduce filtration/excretion
how do atheroslerosis plaques form?
1)ldl cholesterol accumulates
2)macrophages ingest and become foam cells
3)release cytokines that causes smooth muscle to uptake cholesterol
3)lipid core accumulates below endothelium
4)fibrous scar tissue walls off endothelium
5) calcium deposits occur in fat deposit
6)if plaque ruptures, platelets will cause a blood clot
arteriosclerosis
general hardening of arteries due to fat deposition usually followed by calcification
atherosclerosis
formation of atheromatous plaque due to inflammation, macrophage accumulation, and cholesterol (LDL) deposition followed by stenosis (narrowing) of arteries and arterioles. Increases the chance of thrombosis
thrombosis
aggregation

formation of a blood clot inside a vessel
what are some complications of hypertension?
High pressure damage of vascular wall platelet
aggregation thrombosis
arteriosclerosis = general hardening of arteries due to fat deposition usually followed by calcification
atherosclerosis = formation of atheromatous plaque due to inflammation, macrophage accumulation, and cholesterol (LDL) deposition followed by stenosis (narrowing) of arteries and arterioles. Increases the chance of thrombosis

Fat depositions may ‘eat up’ the elastic layer, resulting in weak bulged areas called aneurysms..bad because of laplace's law
aneurysm
bad because of laplace law that says that

T=pr/2
angioplasty
medical procedure to repair diseased artery

-inflatable ballon techneque to compress blockage

-a stent can also be inserted to keep the vessel open
vicious circle of hypertension
High TPR High BP, but tissues still require the same amount of perfusion, thus the heart generates stronger stokes the heart becomes stronger, the arterioles become stiffer, the heart becomes bigger which leads to hypertrophy, Laplacian disadvantage and failure


...caused by positive feedback
perfussion
In physiology, perfusion is the process of nutritive delivery of arterial blood to a capillary bed in the biological tissue
anaphylaxis
Anaphylaxis is an acute systemic (multi-system) and severe Type I Hypersensitivity allergic reaction in humans and other mammals

Anaphylactic shock, the most severe type of anaphylaxis, occurs when an allergic response triggers a quick release from mast cells of large quantities of immunological mediators (histamines, prostaglandins, leukotrienes) leading to systemic vasodilation (associated with a sudden drop in blood pressure) and edema of bronchial mucosa (resulting in bronchoconstriction and difficulty breathing). Anaphylactic shock can lead to death in a matter of minutes if left untreated.
septic shock
Septic shock is a serious medical condition caused by decreased tissue perfusion and oxygen delivery as a result of infection and sepsis, though the microbe may be systemic or localized to a particular site[1]. It can cause multiple organ dysfunction syndrome (formerly known as multiple organ failure) and death[1]. Its most common victims are children, immunocompromised individuals, and the elderly, as their immune systems cannot deal with the infection as effectively as those of healthy adults. The mortality rate from septic shock is approximately 50% [
tamponade
is a condition of blood flow stoppage into a blood vessel by a constriction of the vessel by an outside force.

Tamponade is a useful method of stopping a hemorrhage. This can be achieved by applying an absorbent dressing directly onto a wound, thereby absorbing excess blood and creating a blockage, or by applying direct pressure with a hand or a tourniquet.
circulatory shock

and treatment
- a condition of inadequate perfusion due to insufficient cardiac output

Hypovolumic shock: hemorrhage, trauma or surgery, fluid loss due to diarrhea or vomiting....dehydration or blood loss

Distributive shock: anaphylaxis, septic shock

Cardiogenic, obstructive or congested shocks: heart failure due to a loss of ventricular or valve function, tamponade, or fibrillation.

Low O2 supply may lead to lactic acidosis, kidney failure and coma

Refractory shock = condition beyond the “point of no return”

With hypovolumic and distributive shocks the major problem is to increase BV and Venous Return

- Immediate blood transfusion (when available)
- Transfusion of physiological solution with plasma expanders
- Injections of NE
why is pressure lost as fluid moves through a container
friction between the fluid and the blood vessel walls
hydrostatic pressure
pressure that a fluid exerts on its container
what do arteries do during the hearts relaxation phase?
act as a pressure reservoir
pericytes
secrete factors that influenc
coronary heart disease
narrowing of the lumen of blood vessels...would like to promote angiogenesis
high bp considered?
140/90
how does stuff get out of the capillary
hydrostatic pressure forces stuff out through leaky junctions
colloid osmotic pressure?
more proteins in the cappilaries so water will want to move in from the interstitual fluid
why does capillary hydrostatic pressure decrease along the length of a cappilary?
energy is lost to friction
how does fluid enter lymph vessels from interstitual fluid?

how does flow occur
there are large gaps that all fluid to flow in by bulk flow

flow occurs by contractile fibeers in endothelial
..one way valves
.contraction of skeletal muscle:patients who havent moved in a while will have edema because of this
what causes edema
1) inadequate drainage of lymph or
2) blood dapillary filtration that greatly exceeds capillary absorption

..increased hydrostatic pressure
..decrease in plasma protein concentration
..increase in interstitial proteins
what does a heart attack do
-oxygen starved cells rely on glycolysis
-calcium can't be pumped out of cells so gap junctions close because of high ca and h to isolate damaged cells
-action potentials must now find a different route
draw the respiration track
microanatomy of airway at bronchiole level
muscles used in ventilation
expiration muscles are only used during forced experation...otherwise experation is passive because of recoil
how do ribs increase with lateral motion
inhalation cause it to lift up and out
diaphragm
what is the pleural cavity
fluid filled with negative pressure

fluid acts to keep lungs attached to thoracic wall like 2 panes of glass
air leakage into pleural cavity

and different lung values
pneumothorax

causes air to rush into pleural cavity and causes lung to deflate
tell about all of the lung values
draw ciliated respiratory epithelium of airways
microscopic view of alveolar and endothelial cell of capillary interaction
exchange surface of alveoli and capillary
2 components of tension in alveolar walls?
elastic and surface
surfactants
they do not disrupt cohesive forces between water molecules...they, compress the monolayer and because of this decrease surface tension

-DPPC or lecithin is the surfactant in lungs

surface pressure of surfactant=surface tension of pure water-surface tension in the presence of surfactant

Lung surfactant proteins facilitate fast equilibration between the micellar and surface fractions of surfactant
what kinds of alveoles are at disadvantage?
P=2T/r

has a greater inward pressure so they won't fill with air as easily

t=surface tension
r=radius
p=pressure
surfactant and infants
lack of it causes respiratory distress of infants (collapse of lungs
fibrosis
replacement of lung epithelium and elastic fibers with a fibroblast scar tissue (stiff lungs)
Emphysema
loss of elastic fibers (lungs are too compliant)
compliancy
the rate at which the alveoli will expand
...bag vs.balloon picture

bag is very compliant, but not elastic

balloon is somewhat compliant, but also elastic
rank these in order of distensibilities

normal, no surfactant, water filled
highest to lowest

water-filled, normal, no surfactant
draw a graphic summary of mechanical pulmonary disorders
2
what is cystic fibrosis
-a disfunction of a chloride channel
-causes thick mucous
-Cystic Fibrosis (CF)
- is not only pulmonary, but a congenital systemic disorder that hits many epithelial functions in sweat and salivary glands, pancreas and kidney.
-caused by mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR), which is a cAMP-regulated Cl- channel (1480 a.a. protein, 12 TM domains, two nucleotide binding sites, requires cAMP and ATP for proper activity)
- one out of 2000 Caucasians carry the DF508 mutation which makes the channel insensitive to cAMP. There are other mutations that prevent intracellular targeting of the channel to the apical membrane. The main cause of death among CFTR patients is lung infection and pneumonia
air composition
partial pressure and gas solubility of 02
partial pressure and gas solubility of CO2
diagram showing basic alveoli, capillary and lung exchange
gas flow through the boundary and layer of fluid depends on what?
1) solubility
2) rate of diffusion
diffusion coefficient=
D=S/sroot of MW
po2 changing from 100 to 40 mmhg does what to saturation
98% to 75%
50% o2 hb saturation?
28 mmHg
physiological range of o2 hb curve
40-100 mmhg
what percent of o2 is carried as oxyhemoglobin
97% hb02

3% dissolved in plasma
how many oxygen bind to Hb and talk about equation
4

B=x/(kd+x)

x is ligand concentration
each x also has an n which is the hill coefficient...

* n > 1 - Positively cooperative reaction: Once one ligand molecule is bound to the enzyme, its affinity for other ligand molecules increases.

* n < 1 - Negatively cooperative reaction: Once one ligand molecule is bound to the enzyme, its affinity for other ligand molecules decreases.

* n = 1 - Noncooperative reaction: The affinity of the enzyme for a ligand molecule is not dependent on whether or not other ligand molecules are already bound.

oxygen bind in a cooperative manner
carbon monoxide poisoning
Oxygen (O2) is coordinated between the Fe ion and the imidazole ring of Histidine E7. Carbon monoxide (CO) binds exactly the same way with a 300 times higher affinity. It displaces O2 and dissociates slowly.
talk about hb
4 globular chains with a heme ring that contains iron
when does an increase of 2,3-dpg take place?
-high altitude or under the action of growth hormones

-23dpg shifts curve to the right
3 ways co2 is transported
~7% is carried as CO2 dissolved in plasma

~70% is in the form of bicarbonate. The conversion is catalyzed by carbonic anhydrase
CO2+H2O = H2CO3 = H+ + HCO3-

~23% as carbamino compound at the N-terminus of Hb
-C-NH2 + CO2 = -C-NH-COOH
haldane effect

bohr effect
Deoxygenation of the blood increases its ability to carry carbon dioxide; this property is the Haldane effect. Conversely, oxygenated blood has a reduced capacity for carbon dioxide. This is a consequence of the fact that reduced (deoxygenated) hemoglobin is a better proton acceptor than the oxygenated form.

bohr:Bohr effect is a property of hemoglobin first described in 1904 by the Danish physiologist Christian Bohr (father of physicist Niels Bohr), which states that in the presence of carbon dioxide, the oxygen affinity for dissociation of respiratory pigments, such as hemoglobin, decreases; because of the Bohr effect, an increase in blood carbon dioxide level or a decrease in pH causes hemoglobin to bind to oxygen with less affinity.
hematocrit
fraction of blood that is taken up by rbc's when centrifuged
chloride shift
an electrically neutral Cl-/HCO3- exchange occurs via the Band 3 anion exchanger.
what is special about blood in the lungs
blood is not fully oxygenated...20% remains venous...creates a physiologic shunt
hypoventilation vs. hyperventilation
ventilation vs perfusion rates
Ventilation (V) = 4.2 L/min

Perfusion (Q) = 5 L/min

V/Q = 0.84 (normal)

this indicates shunting because the perfused blood (blood reaching the lung) is not being properly ventillated

shunting is when some blood remains venous and does not pick up oxygen
effects of high altitude
Plasma CO2 decreases, pH increases and this leads to alkalosis. To correct for this condition acids need to be taken (citric acid).

At high altitude (low PO2) Erythropoietin is released, increasing hematocrit. Blood viscosity does up, making circulation less efficient
when the blood flow is insufficient in a certain locus this is equivalent to ?
increase in dead space...space in airways with no gas exchange
when the ventilation is insufficient, this is equivalent to increased amount of?
shunted blood
a decrease in ventilation in a certain locus leads to
constriction of corresponding arterioles and diverting blood to better ventilated alveoli
table of gas compositin vs. bronchioles, pulmonary arterioles, systemic arterioles
common sense if you think about it...just the gas component
pulmonary loop of circulation is characterized by?
low pressure and high throughput
the boundary between the dry and blood compartments is
very thin and delicate
what keeps alveoli dry
low capillary pressure

-powerful lympatic system that keeps interstitial pressure negative (-4 to -8 mmHg)
what follows alveolar edema
interstitial edema...lethal in 30 min

when left atrial pressure rises above 23 mmHg it becomes dangerous
scheme for how respiratory muscles control respiration
comment on respiratory muscle innervation
third forth and fifth cervical segments throgh the thoracic cavity to the diaphragm

intercostal muscles are innervated by the spinal segmental nerves of the 1st through 11th spinal segments, they don't branch from the phrenic nerve
respiratory chemoreceptors
Chemoreceptors
O2 Receptors in the aortic arch and carotid bodies, reside in glomus cells (K+ channels directly sensitive to [O2], non-adaptable, fire when PO2 gets below 60 mm Hg)

Peripheral CO2 (pH) Receptors (in the aortic arch and carotid bodies) fire when plasma pH is low

Central CO2 Receptors are located in the medulla, next to the inspiratory center. They are bathed in CSF and sensitive to the pH of CSF, which depends on plasma CO2

Central receptors are insensitive to plasma pH (H+ can not permeate through the blood brain barrier).

All CO2 receptors are adaptable, i.e. during sustainrd stimulation their firing declines with time. In contrast, O2 receptors do not adapt.
what type of channel is the oxygen receptor?
potassium channel
inspiratory ramp
functional anatomy of the respiratory center
feedback loop that leads to intercostal muscles and diaphragm contracting
4
chemoreceptor reflex
Low arterial oxygen levels cause bardycardia and elevated TPR

Vasoconstriction in response to low O2 compensates the vasodilatory effect of accumulated CO2
respiratory sinus arrhythmia
During inspiration - sympathetic stimulation increases (tachycardia)
During expiration- parasympathetic activity increases (bradycardia)
respiratory sinus arrhythmia
During inspiration - sympathetic stimulation increases (tachycardia)
During expiration- parasympathetic activity increases (bradycardia)
physiolgy of diving

diving animals and scuba divers
Diving reflex: temporary brdycardia on exposure to cold water, usually combined with peripheral vasoconstriction

The skeletal muscles are forced to draw on its store of O2 in myoglobin and then shift to anaerobic glycolysis
- O2 is therefore spared for the heart and brain

Lactic acid is accumulated in muscles and washed out at the end of the dive


Diving animals exhale before they dive. Deep in the seas their lungs collapse and the residual gas is stored in the ‘dead’ space. No N2 dissolved in the blood at high pressure.

Scuba divers breathe air which is exactly at the same pressure as is in the surrounding water. At depths greater than 30 m, a considerable amount of N2 gets dissolved in the plasma, so on decompression (assent) it may form bubbles. The bubbles cause ‘divers bends’.
Therefore, decompression must be slow. There are tables stipulating safety stops during assent to allow time to clear N2 from the blood.
4 types of immune hypersensitivity
There are four types of immune hypersensitivity reactions:

1. IgE - mediated mast cell degranulation (histamine and leukotriene release)

2. Cytotoxic action of killer cells and complement mediated by IgG directed against ‘self’ antigen (autoimmune IgG)

3. Immune complex deposition in tissues (antigen-antibody clot), attracting complement and polymorphonuclear cells that cause local damage of tissue

4. Sensitization of T-cells on the first exposure to antigen and massive release of cytokines followed by inflammatory reaction on the second contact

Asthma is type 1
asthma
-type 1
-strongly hereditary

in the young (70%) - allergic reaction to pollen and other inhaled allergens (dust mite feces, cat dander particles, fungal spores, rat urine)
- in older individuals (30%) - reaction to persisting irritants in the polluted air

Allergic reaction= development of sensitivity to the irritant and generation IgE against it. Mast cells and basophils reside in the mucus layer close to the airway lining. They carry IgE receptors (Fc) on their surface which bind IgE’s from the plasma. On arrival of the stimulus (irritant) crosslinking of Fc receptors occurs, the mast cells degranulate and release histamine and a mix of leukotrienes and prostaglandins (substance of anaphylaxis), then also release IL-4 and TNF-a.


-edema and brochospasm occur. airway resistance increases which makes it difficult to inhale and especially exhale

-asthma is an allergan induced bronchial edema and bronospasm
corticosteroids
Corticosteroids (Cortisol, Hydrocortisone) generally suppress inflammation and immune response
- in macrophages and monocytes they induce the protein called lipocortin, which blocks PLA2 and the production of arachidonic acid, prostaglandins and leucotriens
- block IgE-dependent degranulation of basophils and mast cells
- in endothelial cells they prevent release of molecules that mediate leukocyte adhesion and tissue penetration
- suppress adhesion and proliferation of fibroblasts that form scar tissue (fibrosis, sclerosis).
- inhibit release of cytokines (IL’s) from lymphocytes
obstructive lung disease
narrowing of the bronchioles
pneumothorax
air in the pleural sac
boyles law
pv=pv
solubilities of O2 and co2 in water
co2 is 20x more soluble

at 100 mmhg

co2= 3 mmol/L
o2=.15 mmol/l

both have a conc of 5.2mmol o2/L air
trained vs. untrained o2 consumption curve
exercise
O2 consumption reliably measures the intensity of exercise

~ 5 kcal of metabolic work per liter O2

During the most strenuous exercise we spend ~20 kcal/min, and consume 4-5 L O2/min

Ventilation increases to 120-150 L/min, in proportion with the aerobic (oxidative) metabolism
- both inspiration and expiration become active processes

Ventilation increases faster when we reach the anaerobic threshold (AT)
glycolysis
glucose > 2 pyruvate or 2 lactic acid

2 ADP + 2 Pi +NAD > 2ATP + 2 NADH
oxidative phosphorylation
glucose +602 > 6co2 + 6 h20

30 adp + 30 pi > 30 atp + 30 H + 30h20

process is 32 percent effective
fatty acids can only be used in what metabolism?
aerobic
where does glucose come from
glycogen or dietary intake
what and where can lactic acid be converted to
glucose by the liver
cardiovascular adjustments to exercise
Cardiac output increases 4-5 times (to 20-25 L/min)
- SV increases insignificantly
- HR increases up to 200 beats/min
- Systemic filling pressure (SFP) increases from 7 to 18 mm Hg, a small increase in pulmonary AP occurs
- blood is diverted from skin and other organs (but perfusion remains constant in the brain)
- TPR decreases 4-5 times, in some muscles perfusion increases 40 times
- Due to SFP and TPR, the venous return matches CO
- BP increases insignificantly (~20%)
energy supply
1. Easily consumable energy is stored in fat (adipose tissue)
2. Carbohydrates (glycogen) is consumed next. We have 55-90 g in liver and 12g/kg in muscles
3. Under extreme conditions ~ 10 kg of muscle protein is available too (consumed under exhaustion)

At <60% of work load: 80% extramuscular fat is consumed, 20% glycogen (aerobic slow-twitch)

60-90% of load: 30% extramuscular carbohydrate, 70% local glycogen

>90% load - mostly local glycogen (glycolytic metabolism)