Pulmonary arteries, capillaries and veins  contain approximately 9% of total blood volume.

   The heart in diastole normally contains about 7% of total blood volume.

8%

At any one point approximately 68% of blood vol is in the venous system (pulmonary + systemic veins), 7% is in the heart 17the arterial system (aorta and arteries and arterioles) in hand 8% in the capillaries.

The total cross-sectional area of the pulmonary capillary bed is normally equal to that of the systemic capillary bed.

True or False?

True

The total cross sectional area for passive blood gas diffusion inthe systemic capillary beds is normally matched by the area available in the lungs in order to assure optimal pulmonay oxygenation of blood to match tissue needs, and to prevent the deadly possibility of CO2 accumulation in body fluids.

Capillaries are generally more permeable on the venous end than on the arterial.

True or False?

True

There are a greater number of pores on the venous end of the capillary, so it is generally more permeable.

1 - 2 seconds

blood moves through a capillary at the rate of about 0.07 cm/sec in the resting state.

What equation best describes the relationship between blood flow and total cross-sectional area of blood vessels in the determination of linear velocity of blood flow?

a. v = QA

b. v = Q + A

c. v = Q/A

d. v = Q - A

e. v = A/Q²

C

Area (A) is in cm²

Velocity refers to rate of displacement with respect to time (cm/sec).

While blood flow is the volume per unit time. (Q cm³/sec or ml/sec)

so...

cm³/sec x 1/cm²

Which is true?

a. When a blood vessel is narrowed, the velocity of blood flow through it increases, as does lateral distending pressure on the vessel walls.

b. In the narrowed portion of a blood vessel, kinetic energy of blood flow is decreased, while the velocity and potential energy are increased

c. When a blood vessel dilates, velocity of blood flow through it increases, as does lateral distending pressure

d. When a blood vessel is narrowed, velocity of blood flow through it increases while lateral distending pressure on the vessel walls decreases.

e. In a closed tube, such as the blood vessel, when kinetic energy of flow is increased as velocity increases, potential energy also increases.

D

Bernouilli principle states that in a closed tube total energy must remain constant, Thus kinetic energy of flow plus pressure must remain constant.  Therefore if kinetic energy increases as velocity increases, potential energy must be reduced (i.e. the distending pressure on the wall of the blood vessel.)

Select False Statement:

a. Flow (Q) of blood through capillaries varies inversely with the viscosity (n) of blood contained therein (i.e. Q=1/n)

b. Measurements of Poiseuille revealed that the flow of fluid (Q) through a closed tube, like a blood vessel, varies directly with the fourth power of the tube radius (Q = r⁴)

c. Flow of blood (Q) through any given blood vessel is inversely proportional to the difference btwn the inflow (P_i) and outflow (P_o) pressures. (Q=1/(P_i-P_o))

d. Blood flow (Q) through a vessel is thought to vary inversely with the length (l) of that vessel (Q=1/l)

e. The viscosity of water at 20 degrees celcius is 1 centipose.

Q = ∏(P_i-P_o)r²/8nl

C is false.

Which rearrangement of Pouseuilles law gives us the most accurate definition of resistance (R) to blood flow?

a. R = (P_i - P_o) / Q = 8nl / ∏r⁴

b. R = ∏(P_i - P_o) / 8nl / r⁴

c. R = 8nl∏(P_i - P_o)r⁴

d. R = 8nl / ∏(P_i - P_o)r⁴

e. R = ∏r⁴ / 8nl = Q / (P_i - P_o)

Resistance to blood  flow is dependent on ratio of pressure drop to flow AND dependent on the dimensions of the blood vessel and the blood therein: (so A is correct)
a. R = (P_i - P_o) / Q = 8nl / ∏r⁴

n = viscosity

Q = flow

l = length

∏/8 = constant of proportionality

(P_i - P_o) = outflow - inflow pressures

r⁴ = fourth power of the radius

Which of the following is the primary determinate of resistance to blood flow in the vascular system?

a. Viscosity of blood

b. Inflow pressure into capillary beds

c. Outflow pressure from the capillary beds

d. Plasma osmolarity

e. The radius of blood flow

The answer is e

Resistance to flow is greatest in capillaries, and resistance diminishes as blood moves into venules and veins

Also changes in vascular resistance occure as a result of changes in radius (i.e. the contraction and relaxation of blood vessels)

Select False statement below:

a. Red blood cells travel faster then plasma through blood vessels

b. Hematocrit ratios of the blood contained in various tissues are lower that those in blood samples withdrawn from large arteries or veins in the same animal.

c. Greater pressure is required to force fluid through blood vessel when the flow is turbulent than when it's laminar.

d. The flexibility of erythrocytes is enhanced as the concentration of fibrinogen in plasma increases.

e. Where laminar flow exists within the cardiovascular system, a murmer is usually detected.

The amount of lymph formed per day in the body is roughly equivalent to the:

a. Extracellular fluid volume

b. Interstitial fluid volume

c. Intracellular fluid volume

d. Blood volume

e. Plasma volume

The answer is E

About 4% of the body weight moves through the lymphatic system every day (2-3 liters in a large dog or about 100 ml/hour)

Normal plasma volume is roughly 4% of body weight, whole blood 7%

interstitial fluid vol 16%

extracellular fluid vol 20%

intracellular fluid vol 30 - 40%

Over one-half of lymph formed in body normally comes from the

a. liver and intestinal tract

b. lungs and kidney

c. skeletal muscle and intestinal tract

d. liver and kidneys

e. brain and lungs

The answer is a

Lymphatics are a major route for absorption of nutrients in intestinal tract. it is largely responsible for absorption of fat.

All the following are known to increase lymph flow and potentially cause edema, EXCEPT:

a. Increased venous pressure

b. Increased arterial pressure

c. Decreased plasma colloid osmotic pressure

d. Increased capillary permeability

e. Increased interstitial fluid protein

B is correct

Arterial pressure does not change the overall sum of Starling's Forces in the cap bed is not the cause of edema

The answer is a. 5%

60% is in veins

NEFP = (Pc_a - Pif) - (¶p - ¶if)

NRP = (Pc_v - Pif) - (¶p - ¶if)

Pc = capillary hydrostatic pressure

Pif = interstitial hydrostatic pressure

¶p = plasma colloid osmotic (oncotic) pressure

¶if = interstitial colloid osmotic (oncotic) pressure

An estimated 16 ml/min (or 23 L/day) of fluid filters accros the arteriolar ends of all capillaries in the body .

T or F

Fluid filtration across all cap beds of the body accounts for only 0.3% of the cardiac output at any one time

T of F?

Unregulated fluid movement across cap membranes totals approximately 120 liters.min.

T or F

The percent of plasma filtered by a particular capillary bed depends on the tissue type, filtration is low across capillaries on the brain, yet high across capillaries in the intestine and lungs, as well as sinusoids of the liver.

T or F

The filtration and reabsorption of solutes and solvent across peripheral capillary membranes due to Starling's forces is normally far greater than the passive diffusion of these substances.

T or F

Lymph flow is facilitated by all the following EXCEPT:

a. Movement of the skeletam muscle

b. Rhythmic contractions of capillary beds

c. Suction effect of high velocity flow of blood in the veins where lymphatics terminate

d. Rhythmic contractions of the walls of large lymph ducts (i.e. lymph pump)

e. The negative intrathoracic pressure created during inspiration

25 - 50 %

The protein returned to circulation per day is equal to 25% - 50% of the total circulating plasma protein

Which of the following factors would be least likely to cause edema?

a. Increased capillary pressure

b. Decreased plasma colloid osmotic pressure

c. Increased interstitial fluid oncotic pressure

d. Increased capillary permeabilty

e. Hypertension

Agents that promote the production of lymph are called:

a. Cholagogues

b. Lymphagogues

c. Diuretics

d. Hydrocholeretics

e. Lymphocytes

The answer is b. Lymphagogues

fyi - Cholagogues = compounds that stimulate evacuation of the gallbladder

is caused by oscillation of blood in the ventricular chambers and vibration of the chamber walls.

detected during the onset of ventricular systole and is consistant with the QRS-complex of the EKG, not the T-wave

It is normally the loudest and longest of the heart sounds.

occures with the closure of the semilunar valves

conditions that bring a more rapid closure to the semilunar valves  like increases in pulmonary or aortic bp increase the intensity of the sound

The third sound of the cardiac cycle...

a. is normal in older animals

b. is particularly evident in the resting state

c. is associated with rapid inflow of blood into the ventricles.

d. normally occurs during the P-Q interval of the ECG

e. occurs due to closure of the mitral valve

The answer is C - Is associated with rapid inflow of blood into the ventricles.

not b bc it is more evident after exercise, when blood flow is rapid.

not a bc a faint third heart sound may be audible in young animals, but is rarely heard in adults

not e bc it is a result of a rapid inflow of blood into the ventricles

Resting external myocardial work efficiency is approximately:

a. 1% - 2%

b. 10% - 20%

c. 20% - 30%

d. 30% - 40%

e. 40% - 50%

Normal end-ventricular systolic volume (i.e. residual volume):

a. at rest is equal to that ejected during systole

b does not normally change following the onset of exercise

c. at rest is nearly zero

d. during exercise is about equal to that ejected during systole

e. at rest about equal to the end-ventricular diastolic volume

Answer is a

Ejection efficiency at rest is roughly 50%

It can go up to 85%-90% with exercise

Atrial Systole:

a. plays a minor role in filling the ventricles of patients exhibiting AV valvular stenosis

b. is not essential for normal ventricular filling at rest

c. normally occurs immediately following the QRS- complex of the ECG

d. normally precedes ventricular filling

e. normally occurs simultaneously with ventricular systole

Answer is b. is not essential for normal ventricular filling at rest

most of ventricular filling is complete before atrial systole - usually it is only responsible for around 10% of ventricular volume - atrial kick

Bainbridge

the venoatrial junctions of the heart (aka cardiopulmonary receptors) are mechano receptors that sense and increase in venous return to the atria (preload). They can increase heart rate and contractility via SNS output to the SA node

Thermoreceptors in the face sense immersion in water and induces:

a vagal (parasympathetic) response - HR slows and systemic blood flow is reduced

AND

a sympathetic (SNS) mediated vasoconstriction

This reduces O2 consumption while preserving coronary and cerebral blood flow.

Match the electrode to the limb

a. left forelimb        negative / positive / or both

b. right forelimb      negative / positive / or both

c. left hind limb       negative / positive / or both

a. left forelimb        negative and positive i.e. both

b. right forelimb      positive / positive

c. left hind limb       negative / negative

Describe the two baroreceptors aka "Buffer Nerves"

When stimulated,

Aortic Arch sends information via the vagus n (CN X)

Carotid sinus sends information via CN IX

Info is integrated in the nucleus tractus solitarius (NTS)

which direct changes in 3 different medullary CV centers

1) Cardiac Decelerator (parasympathetic) slows the SA node  -- this baroreceptor is active when P_mean increases and inactive when it decreases

2) Cardiac Accelerator center are part of the SNS and increase firing of SA node

3) Cardiac decelerator center (part of PNS) - senses decrease in P_mean It reduces TPR (total peripheral resistance)

Erythrocytes generally travel slower through blood vessels than plasma.

T or F?

False

RBCs tend to travel faster through blood vessels than plasma

An increase in contractility in the myocardium will increase

a. the width of the pressure volume loop

b. end-ventricular systolic volume EVSV

c. end-ventricular diastolic volume EVDV

d. All of the above

e. none of the above

If cardiac output (CO) is 4,500 ml/min, mean artierial is 94 mmHg and right atrial pressure is 4 mmHg, systemic vascular resistance (in peripheral resistance units) is:

a. .02

b. 20

c. 50

d. 4.05 x 10 to the 6th powera

Match:

1 Arterioles

2 Capillaries

3 Veins

Exchange Vessels

Resistance Vessels

Capacitance Vessels

1 Arterioles  -  Resistance Vessels

2 Capillaries  -  Exchange Vessels

3 Veins   -  Capacitance Vessels

How much fluid is actually filtered out of plasma in a systemic capillary be?

How much is normally reabsorbed on the venous end of the capillar?

How much of the filtered fluid enters lymphatic circulation?

0.5% of plasma entering the capillary bed = 16 ml/min

16ml/min x 60 min = 100 ml/hr x 24 hrs = 24 L/day

90% of the above fluid is reabsorbed = 14.4 ml/min

10% of the filtered fluid goes to the lymphatic system

1.6ml/min x 60 min = 100 ml/hr x 24 hrs = 2.4 L/day

1.6 ml/min x 60 min = 100 ml

100 ml/hr x 24 hrs = 2.4 L/day

Roughly equivalent to the plasma volume

Major contributors:
Liver

Small Intestine

Lungs

Movements of skeletal muscles

Suction effect of high velocity blood flow in the veins in which the lymphatics terminate

Rhythmic contractions of the walls of large lymphatic ducts (i.e. lymph pump)

Explain the relationship between

Blood Flow (ml/sec of cm3/sec)

Velocity of blood flow (cm/sec)

Arterial blood pressure (BP; distending pressure; mmHg)

V = Q / A

Contraction of an arteriole will not affect flow, but will increase flow velocity and decrease distending pressure / capillary hydrostatic pressure / and blood pressure.

Bernoulli's principle states that for a fluid flow, an increase in the speed of the fluid occurs simultaneously with a decrease in pressure - i.e. distending pressure or Blood Pressure.

What happens to filtration and/or reabsorption pressure in the capillary bed following arteriolar constriction (vasoconstriction)?

Could this play a role in hypertension, and/or the physiologic response to hemorrhage (i.e. hypovolemic shock)?

Starlings Forces

 and how to use them

P_c (plasma capillary hydrostatic pressure)

¶_p (plasma colloid osmotic (oncotic) pressure)

P_if (interstitial fluid hydrostatic pressure)

¶_if (interstitial fluid colloid osmotic (oncotic) pressure)

(P_c - P_if) - (¶P_p - ¶P_if)

alveolar end (25 - (-6)) - (28 - 5) = 8.3 mmHg

venular end (10 - (-6)) - (28 - 5) = -6.7 mmHg

Presence of protein in interstitial fluid is due to :

Cell turnover

Capillary protein leakage (e.g. albumin (liver) lungs)

Lipoprotein exocytosis (CM (intensive) VLDL (liver))

Slow removal by the lymphatics

Negative in most tissue beds (holds tissues together)

Lymph pump (helps to establish & maintain this negativity

Positive in the liver, kidney and brain

General Causes of Edema

↑P_c

↓¶_p

↑P_if

↓ Capillary Permeability

Lymphatic Obstruction

first four increase lymph flow

hypertension does NOT cause edema

Explain Ohm's Law

Ohm's law help us to understand how blood flow (Q) changes when resistance (R) is altered

Q = ΔP/R where ΔP = P1 - P2

rearranged

ΔP = QR

↑ Arterial BP = CO x ↑TPR

Pouseuille's equation

Helps us to understand how blood viscosity (n), length (l), and radius (r) of a blood vessel affects resistance (R) or (TPR) to blood flow?

R = 8nl/∏r⁴

radius much more influential than viscosity

Q = (P1 - P2)∏r⁴/8nl

(Q = ΔP/R is Ohms Law)

increased hemcrit (Hct) or an increase in plasma protein

(↑R due to ↑n)

↑n = ↓Q

Equation for Reynolds Number

N_R = pdv / n

N_R < 2000 = laminar flow

N_R < 2000 = turbulent flow

P = blood density

d = vessel diameter

v = blood flow velocity

n = viscosity

anemia → ↓Hct → ↓n → ↑CO or Q → ↑CO → ↓NR

Thrombi → ↓d → ↑v → N_R

Name the 7 phases of the Wiggers diagram

Phase A = Atrial Systole

Phase B = Isovolumetric Contraction

Phase C = Rapid Vetricular Ejection

Phase D = Reduced Ventricular Ejection

Phase E =Isovolumetric Ventricular Relaxation

Phase F = Rapid Ventricular Filling

Phase G = Reduced Ventricular Filling (Diastasis)

Describe events during

Phase A = Atrial Systole

Atria contract

Final phase of ventricular filling

Period of Atrial Kick = 10 - 40 % of ttl Ventricular vol

ECG = second half of P wave

and

PR interval

4th heart sound

Describe events in

Phase B = Isovolumetric Contraction

include relevent ECG information

Ventricles contract and Ventricular pressure increases

NO CHANGE in ventricular volume BUT ventricular chamber geometry changes

All valves are closed  (AV closes at begining and semilunar opens at the end)

corresponds to QRS-complex (no wave for repolarization of atria)

First heart sound heard - due to oscillation of blood against ventricular walls

Describe events in

Phase C = Rapid Vetricular Ejection

mention ECG events too

Starts with Semilunar Valves opening

Ventricles are contracting

increase in ventricular pressure reaches max

decrease in ventricular volume

increase in aortic pressure - reaches max

corresponds to ST segment of ECG

Descibe events in

Phase D = Reduced Ventricular Ejection

include info on ECG

Ventricles eject at a slower rate

decrease in ventricular volume - reaches min

decrease in aortic pressure

corresponds to t wave = ventricular repolarization

Describe events during

Phase E =Isovolumetric Ventricular Relaxation

begins when semilunar valves close (this creates a dicrotic notch aka incisura)

ventricles relaxed

decrease in ventricular pressure

NO CHANGE in vetricular volume

2nd heart sound heard here - due to oscillations of blood and tensed vessel walls caused by recoil of closed semilunar valves

Describe events during

Phase F = Rapid Ventricular Filling

Begins when AV valve opens

ventricle relaxed

ventricle fill passively

increased ventricular volume

ventricular pressure low

3rd heart sound heard here

Describe events during

Phase G = Reduced Ventricular Filling

AKA (Diastasis)

av valves open; aortic and pulmonic valves closed

ventricles relaxed

final phase of PASSIVE ventricular filling

end of overall cardiac diastole

What is

N_R = pdv/n

Reynold's number determines turbulent flow (and possiblity of murmer or bruit)

p is blood density

d is vessel diameter

v = blood velocity

and

n = blood viscosity

N_R < 2000 = Laminar Flow

N_R > 2000 = Turbulent Flow

Which contributes more to Reynolds number:

velocity of blood or vessel diameter?

N_R = pdv/n

since v = Q/∏r²

v increases as radius decreases - raised to the second power

thus

v contributes more to N_R than d (aka 2r)

Equation for Blood Vessel Compliance/Capacitance (C)

the volume (V) of blood a vessel can hold at a given pressure (P)

C is highest in veins

C is lowest in aging arteries

P_mean = P_dia + 1/3 PP

PP = P_sys - P_dia

Why?

Because greater fraction of cardiac cycle is spent in diastole

SA node = 0 msec

AV node = 60 msec _DELAY here

Bundle of His = 160 msec

Apex of heart = 200 msec

End of AP = 220 msec

SA and AV nodes have prepotentials caused by T-gated Ca⁺⁺ channels

Only has Phases 0, 4, and 3

no phase 1 nor 2

Phase 4 = depolarization (prepotential)=Ca⁺⁺ influx from fast T-channels creates a Ca++ current (I_CaT)

(Note: Na+ influx g_Na creates a "funny" current (I_f) which contributes very little to prepotential)

Phase 0 = rapid depolarization = Ca⁺⁺ conductance (g_Ca) through slow Ca⁺⁺ L-channels. It's the I_CaL that creates the impulse

Phase 3 = Repolarization by potassium current (I_K) due to K⁺ conductance (g_K)

As the I_K decays the prepotential (aka pacemaker potential) bring another AP

AV node and His-Purkinje system are "latent paecmakers" that are usually in "overdrive suppression"

SA node has the fastest rate of Phase 4 depolarization (i.e. prepotential) and the shortest refractory period

SNS stim increases the slope, brining AP to threshold faster

PNS stim decreases the slope by hyperpolarizing the RMP and slowing the entrance of Ca⁺⁺ into the cell

NE acts on ß1 receptors in the SA node and:

increase AC activity

increase cAMP formation

increase Ca⁺⁺ conductance (g_Ca) through both T&L Ca⁺⁺ channels

Depolarizes prepotential and increases rapidity of firing AP

decreases slope of prepotential

ACh acts on Muscarinic (M₂) receptors to:

1) increase K+ conductance (gK)

this hyperpolarizes the cell

AND

2) decrease cAMP which delays opening of Ca⁺⁺ T-channels

Both methods htperpolarize prepotential

Phase 0 = Rapid depolaization due to opening of Na⁺activation gates Na⁺ enters following chem and conc gradients

Phase 1 = Rapid Repolarization

Na+ inactivation gates close due to depolarization (keeping membrane from reachin E_Na

K⁺ gates open permitting I_TO K⁺ leaves following chem and conc gradients

Phase 2 = Plateau inward I_Ca through L-channels almost equal to outward I_K

Phase 3 = Repolarization: ↓I_CaL(until stops) and ↑I_K

Phase 4 = near EK an inward retifying K⁺ current maintains g_{K (net K⁺ out)}

Ca++ channel blocker

affects L-channels of smooth and cardiac mm and the SA node

used to treat high BP

relaxes vascular sm mm = vasodilation and ↓TPR (little effect on venous beds)

↓chronotropy = ↓phase 0 of SA and AV nodes

↓dromotropy & ↓inotropy=less Ca⁺⁺ influx during phase 2

Na⁺⁺/K⁺ ATpase (gate) inhibitors

(e.g. foxglove, Digitalis)

Na⁺⁺ can't leave cell, lowers g_Na and the Na/Ca exchange decreases.  Meaning more Ca⁺⁺ in cell and extended muscle contraction.

↑ chronotropy

↑ inotropy

↑ dromotropy

Myocytes                                         SA/AV nodes

I_{Na (Na+ fast, phase 0)}                                I_CaT (phase 4)

I_{TO (K+ phase1)}                                          If (phase 4)

I_CaL (phase 2)                                  I_CaL (phase 0)

I_K  (phases 2, 3, & 4)                        I_K phase 3

ARP absolute refractory period = Na+ activation gated closed

ERP effective refractory period = some Na+ gates are opening

RRP relative refractory period = even more Na+ gates are opening

SNP supranormal refractory period =gates fully recoverd and membrane potential close to threshold - APs more likely

Draw ECG for early ventricular depolarization

the vol of blood ejected in phase d and e depends on the vol present an the end of ventricular diastole

muscle stretchinf due to ↑ in preload increases:

- number of sites available for actin-myosin interaction

- Ca++ sensitivity of troponin

- Ca++ release from the SR

Hypercalcemia would shorten S-T segment

Hypocalcemia would lengthen the S-T segment

cause is the effect of Ca++ on Phase 2

diagram a pressure-volume loop

label axis and valve behavior

atria

pulmonary circulation

these sense volume or fullness

aka effective circulating volume (ECV)

carotid arteries

aortic arch

renal afferent arterioles (renin production)

sense pressure

carotid bodies

aortic bodies

sense Po₂ Pco₂ pH and BP

Supraoptic and paraventricular nuclei of the hypothalmus

sense osmolarity

they are sensitive to a 1% change in [Na⁺] of plasma

carotid and aortic bodies sense BP

send input to Medulary CV center

↑BP (due to ↑aortic or carotid P_mean) → PNS activation

↓BP → SNS activation

Describe the ADH and ANP Release Reflex

an increase in blood volume (BV) causes

↓antidiuretic hormone (ADH, vasopressin) from posterior pitutitary

↓ADH causes diuresis (urine production) and ↓BV

Also

Atria secrete ANP (atrial natriuretic peptide) that causes diuresis and inhibits ADH output

Nocireceptors:

describe the different reflexes to severe fear or pain versus simple fear or pain

Severe fear or pain stim PNS and cause vasovagal syncope (fainting)

Simple fear or pain stimulate SNS and cause sweating, tachycardia, and hypertension - can lead to left ventrical hypertrophy

chemoreceptors sense ↓PO2 ↑CO2 and ↓pH

the primary relfex effect on SA node is inhibitory (PNS) this lowered hr yet hypoxia (↓O2) also causes hyperpnea (↑breathing) hyperventilation causes both hypocapnia (↓CO2) and lung stretching both of which stimulate a SNS response that overrides the PNS response and the net effect is ↑HR

This is ONLY if the patient has working lungs

w/o the PNS would slow down heart and pos kill pt.

PNS presominates thus producing "vagal tone"

PNS stim: ACh binds to M2 receptors and decreases chronotropy, inotropy, and dromotropy, also has tendency to dilate coronary vasculature

ACh on M2 on blood vessels vasodilate, but there aren't many M2 on blood vessels

SNS stim: NE binds to ß1 receptors on heart and increase chronotropy, inotropy, and dromotropy

NE binds to α1 and α2 receptors on blood vessels and vasoconstrict

prejunctional β2 receptors facilitate NE release

prejunctional α2 receptors inhibit NE release

describe

active and reactive hyperemia

active hyperemia occurs when blood flow to an organ changes in direct proportion to its metabolic activity

reactive hyperemia occurs when there is an increase of blood flow in response to a prior period of decreased blood flow.  The loger the occlusion, the greater the debt.

histimine is released by mast cells in tissue in response to injury. It causes:

arteriolar vasodilation

venous constriction

and increased capillary permeabililty

decreases in systole

increases in diastole

as HR increases perfusion decreases

Autoregulatory vasodilation restores bf following exercise

adenosine most imp

NO next most imp

Desribe PNS stimulation on coronary blood flow

ACh direstly causes coronary vasodilation

BUT

PNS causes ↓HR, which ↓O2 demand, which indirectly causes vasoconstriction due to lack of vasodilator metabolites.

So PNS generally decreases coronary blood flow

hydrostatic pressure, oncotic pressure and permeability

Cardiogenic pumonary edema: increase in left arterial pressure causes ↑hydrostatic pressure and net outward fluid flux.

Pulmonary capillary wedge pressure is above normal

ARDS (adult respiratory distress syndrome): increased capillary permeability causes pulmonary edema, can be caused  by epithelial injury due to toxins or infection. Difficult to treat because protenatious fluid is hard to remove.

A pressure transducer ina catheter is introduced via the systemic venous circulation and measures pressures in the

right atrium

right ventricle

and

pulmonary arteries

Pulmonary arteries have large diameter and less smooth muscle. They do not regulate supply of blood to different organs and are not concerned with directing flow. High Flow, Low Resistance, Low Pressure.

The mean pulmonary arterial pressures are much lower (avg = 17mmHG)

pressure difference from inlet to outlet is only 15mmHG (17 - 2mmHg) while systemic is (100 - 2mmHg)

Pulmonary arteries are more compliant/distensible

pulmonary arteries vasoconstrict inresponse to hypoxia except for bronchial vessels, which, like systemic arteries, dilate.

Define subdivisions of total lung capacity

Which can be directly measured?

Which change with exercise?

• Tidal Volume (V_T) volume of single expired breath
  - increases with exercise
• Vital Capacity (VC) maximal volume expired after max inhalation
• Residual Volume (RV) vol remaining in lungs after max exhalation
  - measured using gas dilution techniques
  
• Functional Residual Capacity (FRC) vol in lungs at end of tidal exhale
  - measured using gas dilution techniques

PIO₂ = (P_total-PH₂O) x FIO₂

= (760-48) x 0.21

= 150mmHG

P_AO₂ = PIO₂ - PaCO₂/0.8

150mmHg - 40/0.8 = 100mmHg

the partial pressure of O₂ in alveolar gas is found by taking partial pressure of CO₂ in arterial blood, dividing it by respiratory exchange ratio (VCO₂/VO₂)which is 0.8

subtract this sum from pressure of inspired gas which is normally 150mmHg

How do you calculate the partial pressure of a gas?

Dalton's Law

P0₂ = FO₂ x P_total

the partial pressure of oxygen equals the fraction of oxygen in the ambient air times the barometric pressure for ambient air

changes for inspired air because of water vapor

PIO2 = (P_total - PH₂O) x FIO₂

(760-47) x 0.21 = 150mmHg

Ususally, the partial pressure of oxygen equals the fraction of oxygen in the ambient air times the barometric pressure for ambient air

With inspired air one must subtract out water vapor

PIO2 = (P_total - PH₂O) x FIO₂

(760-47) x 0.21 = 150mmHg

list two functions of surficant

how does it help maintain stable alveoli of unequal diameter?

surfactant reduces surface tension - reducing pressure needed to keep alveoli open

Surfactant allows surface tension to vary directly with radius, so smaller alveoli have smaller surface tension

thus pressures to keep alveoli open are equalized and both small and large alveoli can exist

at high lung volumes, the relaxed chest wall is compliant , but at low volumes it is stiff and thus resist lung collapse, and retains residual volume

at residual volume = chest wall has strong outward recoil and inward recoil of lung is small

at functional capacity = elastic recoils of lung and chest wall are equal, but opposite

at larger lung volume= elastic recoil of chest is smaller and recoil of lung increases

At TLC = elastic recoil of both lung and chest wall direct inward

Draw the relationship between ventilation and perfusion and height in the chest of a human

how is a dog and a horse different?

Causes for high V/Q ratio:
emphysema
canine heartworm disease
hemorhage
positive pressure ventillation
Causes for low V/Q ratio:
shunt
obstruction
extreme bronchitis

pulmonary fibrosis\

prolonged anesthesia

increase in PCO2 causes hyperventillation to already over-ventilated alveoli.

There is no limit to how low CO2 can go (i.e the blood-CO2 dissociation curve is nearly linear)

BUT

not much more oxygen can be dissolved into the plasma to make up for total oxygen content of the blood

How does PaCO2 influence ventilation?

How does hypoxia affect this response?

↑ in PaCo2 allows more to diffuse across BBB into CSF

this ↑[H+]

Central and peripheral Chemoreceptors stim ↑ ventillation

Hypoxia accentuates the stimulation of ↑↑↑ ventillation

stretch receptors in lung parenchyma and airway sm mm - terminate inspiration

irritant receptors in airway epithelial cells - promote rapid shallow breathing in response to noxious agents

J-receptors (juxta-capillary) in lung interstitium near capillaries - respond to interstitial edema

chest wall mechanoreceptors - increase inspirator mm activity to maintain tidal volume

tachnea - increases respiratory rate

Dyspnea - subjective sensation of breathlessness

define

Cheyne Stokes Respiration

regular rapid rate with large tidal volume

usually caused by metabolic acidosis

Bradykinin

Serotonin

PGE, PGF_2a

NE

Histamine?

Adenine nucleotides

Acetocholine (ACh)

Poor ventilation causes a buildup of CO₂ and an increase in [H⁺] causing respiratory acidosis

CO₂ + H₂O ↔ H₂CO₃ ↔ H⁺ + HCO₃

Amphibians

can use their skin for gas exchange

metomophisize from gills to "lungs"

have no necks so less dead air

their lungs are sac-like - no alveoli

their hearts have 2atria and one ventrical so deoxygenated and oxygenated blood mix.

Both mammals and amphibians have internal lungs where gas exchange takes place from pool of air to constantly flowing blood in capillaries

what are the anatomical differences between the avian and  mammalian respiratory system

Birds

lack a diaphram

ventilation is separate from gas exchange

pneumatization of bone

-Parabronchii - cross-current gas exchange

Air sacs

very efficient

draw the Hb-O2 dissociation curve

for a mouse and an elephant on same graph

Pores of Kohn allow alternate routes for air to travel in lungs

positive:

allow alternate routes for air to travel in lungs around an obstruction for example

negative:

allows infection to spread throughout lung

Explain the difference between FRC and VRX.  Which is the higher volume in a kitten? In a horse?

FRC - functional residual capacity

V_RX - relaxation volume = the volume at which the outward chest wall recoil is balanced by the lung's inward recoil

In small animals and newborns V_RX < FRC

i.e. the end of a tidal breath may not go as low as V_RX

In horses the VRX > FRC

i.e. the last part of the expiration may require energy