Chapter 44 Gas Exchange and Circulation

Important points… •  Animals take in oxygen and expel carbon dioxide to sustain cellular respiration. •  Terrestrial animals and aquatic animals face different challenges in performing gas exchange. •  Gas exchange organs maximize the rate of oxygen and carbon dioxide diffusion by presenting a large, thin surface area to the environment. •  Gas exchange organs maintain a steep partialpressure gradient that favors entry of oxygen and elimination of carbon dioxide.

44.1 Air and Water as Respiratory Media

•  Air or Water is the medium. The medium contains oxygen & carbon dioxide •  Ventilation of gas exchanger (=breathing; but confused by use of term “respiration rate” when correct would be “ventilation rate”) •  Gas exchange at a surface – interface between medium & gas exchanger •  “Respiration” is equivalent to oxidative metabolism

(and CO2)

Does Freeman need a geography lesson ;)

Sea level barometric pressure is 760 mmHg. Since oxygen is 21% of air, the partial pressure of oxygen is 0.21 x 760 = 160 mmHg.

The amount of oxygen and carbon dioxide in water varies also. The source of gases in water is the atmosphere (mostly), and gas diffuses from the atmosphere into water at the air/water surface. Factor 1 à surface/depth ratio Factor 2 à mixing AIR AIR AIR AIR

AIR

Deep water, relatively small surface area, expect O2 & CO2 gradient with little at bottom.

Shallow water, relatively large surface area, most of water will have O2 & CO2.

FACTOR 2: MIXING

Gas exchange in water is much more difficult than in air. Oxygen solubility in water is much less: O2 in air 100-130 ml O2/liter of air

O2 in water 0-10 ml O2/liter of water.

(But CO2 is 20X more soluble in water than O2 – this is why elaborate aqueous transport mechanisms evolved for O2 only, not for CO2.) Aquatic: Just move more of the medium past your gas exchanger to compensate for the reduced amount of O2 in water?

…oops: water is 1000X more dense than air and 100X more viscous!!!!! A terrestrial animal may use 1 – 2% of its energy budget to ventilate its gas exchanger. A fish may use 20% of its energy budget for ventilation! Warm water holds less O2 than cold water and salt water holds less than fresh water. So… tropical salt water fish have the greatest burden.

Fick’s law controls the rate of diffusion

Diffusion occurs across the medium ß à gas exchanger epithelium

This is the interface between: water and gill (aquatic gas exchange organ) or air and lung (terrestrial gas exchange organ)

There are many adaptations for ventilating gill gas exchangers.

Counter-current exchanger in fish gills.

Two basic strategies in fish for ventilating gills: l 

Ram jet ventilation

l 

Buccal pumping Extreme ram jet ventilators: some species of sharks. They will suffocate if they stop swimming. Extreme buccal pumpers: sit-and-wait predators.

How the buccal pump works.

Insect terrestrial gas exchange -Insects are relatively small, have relatively lower metabolic rates. After invading land ‘discover’ that oxygen is relatively abundant. So… a simple system of internal tubing, with spiracles opening to the outside, is sufficient to keep open circulatory system (hemocoel) perfused with oxygen. This system is limiting, though, and has prevented larger (modern) insects from evolving.

Hmm, “some sort of breathing mechanism”. What could it be?

Of course you would jump right to the hypothesis that flying is the answer. Not!

Note: No antagonist muscle: exoskeleton provides restoring force à faster operation

How about vertebrates invading land? Amphibians are the first to do so…

Amphibians inherit the fish buccal pump – replace oral valve with a nasal valve! Buccal pumping uses positive pressure to inflate lungs. Amphibians also use highly vascularized dorsal skin as a gas exchange organ.

Reptile invention: Replace positive pressure system with a negative pressure mechanism to inflate lungs. Muscles move back liver, this expands the body cavity, and creates a vacuum.

From reptiles… •  Birds evolve a unique ventilatory mechanism •  Mammals expand on reptile system: l 

l 

Divide body cavity into abdominal and thoracic sections (diaphragm separates the two) Use intercostal muscles and diaphragm to expand thoracic cavity and create negative pressure.

First mammals, then birds…

Basic mammalian lung plan

More detail next slide

?

Note extremely thin wall - this improves the speed of diffusion

Surface tension of the water film on the inside of alveolus tries to collapse the alveolus. This forces out air when muscles, expanding the body cavity, relax.

From amphibians on, surfactant is produced in lungs to control water surface tension. The surface tension is potentially so great it would cause alveolar collapse and no reasonable positive or negative pressure could inflate lungs.

The surfactant produced in human lungs is very effective. Normal water surface tension is 70 mN/m. Laundry detergent reduces this to 25 mN/m Lung surfactant reduces it to 1 mN/m !!

Specialized Bird Lungs

Ventilation of the Bird Lung

(Caudal sacs)

(Cranial sacs)

1

Cycle 1 inhalation 1: New air fills caudal sacs.

2

3

Cycle 2 inhalation 2: Expansion of anterior sac pulls new air across and out of lungs

4

Cycle 1 exhalation 1: New air forced out of caudal sacs into lungs.

Cycle 2 exhalation 2: Contraction of cranial sacs forces “new” air out of bronchus.

Each cycle is similar but valves control flow direction. Flow always same direction across lungs (not tidal) Cross-current exchange improves performance.

Recent research alert! Alligators and Crocodiles – sister groups to birds – and large Varanids also have one-way lung airflow!!

Elaborate branching patterns in lungs. Use probe to measure airflow during artificial inhalation and exhalation.

Crocs & Gators

Birds

One way flow in monitor lizards too

CIRCULATION

CIRCULATION - topics 1. Blood cells & gas transport 2. Circulatory systems l  Blood Vessels l  Hearts 3. Control of circulation

After diffusion at lungs, oxygen carried by hemoglobin (Hb), and hemoglobin contained within red blood cells. Less diffusion distance without RBCs, but the high concentration of Hb free in blood would create a huge osmotic pressure problem!

Sigmoidal curve

“cooperativity”

Due to interaction of peptide chains in hemoglobin (Hb)

One (1) Hb molecule

Four (4) polypetide chains One polypeptide chain: l  150 aa globin l  One heme group 3+ atom l  Contains one Fe l  Binds 1 O molecule 2

So four (4) O2 molecules bound per Hb molecule

Extra delivery due to sigmoidal function

Increased oxygen delivery to tissues if there is a greater demand. How do tissues express their increased need? Reduced oxygen means slower mitochondrial function

Build up of lactate and pyruvate

Drop in pH

Due to the higher solubility of carbon dioxide, no special transport proteins needed.

LUNGS

TISSUES

Blood Pumping

Don’t memorize all the numbers, just understand the concepts: where is the PO2 higher, lower etc.

Many animals have hearts, not just vertebrates.

There may be blood vessels, but also large open spaces where blood flows à lower pressure system

ß This minimizes the diffusion distance

Note: one cell layer only, thus only very small hydrostatic pressures are tolerated

Variable-width gaps between endothelial cells allow some plasma to escape

Is there diffusion of gas here?

Thick walls of arteries tolerate very high pressures.

A portion of plasma forced out under hydrostatic pressure, returns via osmotic pressure. Pressure drop

Hearts need a pressurizing element and at least one valve to prevent backflow.

Muscle/tendon provide constant small tension to keep valves open during filling phase.

Hearts & circulation pattern increase in complexity with increased aerobic needs

SV = SINUS VENOSUS CA = CONUS ARTERIOSUS

Improved performance by total separation of pulmonary and systemic circuits.

Too complicated – just learn next slide!

Heart Contraction sequence Atria contract – move about 20% of the blood that will ultimately be ejected to systemic circulation, into ventricles. Ventricles contract à pressure builds à A-V valves forced closed à pressure builds à ventricle pressure exceeds artery backpressure à semilunar valves open

Systolic pressure during ejection Diastolic pressure during filling

The cardiac cycle as a loop, independent of time. Abbreviations: AVVC = atrioventricular valve closure AVVO = atrioventricular valve opening EDV = end-diastolic volume ESV = end-systolic volume IVVC = Isovolumic ventricular contraction IVVR = isovolumic ventricular relaxation SLVC = semi-lunar valve closure

Note that TIME is not on the graph!

SLVO = semi-lunar valve opening.

Stroke Volume (SV) is the amount of blood ejected on each beat. CO = S.V. x H.R. Where S.V. = stroke volume, H.R. = heart rate Starling’s law – heart pumps all the blood that fills it… so only control over CO is HR!

The mean pressure is estimated like this: M.A.P. = 0.67*DP + 0.33*SP Suppose DP = 60 mm Hg, SP = 120 mm Hg. M.A.P. = .67*60 + .33*120 = 80 mm Hg (60 mmHg is about the minimum to sufficiently perfuse all tissues in humans)

Why is M.A.P. not just the average of DP and SP?

Starling: •  As resting muscle is stretched, the tension increases exponentially so… •  …increasing venous return to the heart stretches the ventricle, which in turn results in more forceful ejection of blood at the very next heart beat.

Typical intrinsic heart rate is 70 beats per minute. Typical stroke volume is 70 mls So… typical CO is 70 x .07 = 5 liters per minute. Human blood volume (all of it) is 5 liters, so your entire blood volume circulates every minute!

Stroke volume is less than the total volume filled.

SV = 60-70 mls Healthy human ejection fraction = 55 – 70% So 30+ % remains in heart each stroke. Weakened heart, early pathology EF = 40 – 55% Heart failure < 40%

How the heart synchronizes contraction

Regulation of Blood Pressure and Blood Flow

Pressure = F/A. For given force of contraction, as x.s. area increases, pressure decreases

Flow = vA. Flow must stay the same, so as x.s. area increases velocity decr.

Blood shunting is critical because vascular volume much greater than blood volume.

Too much vasodilation à blood pressure drops to zero!!!

Why do you feel faint (perhaps) when you stand up quickly (or raise head up quickly)? Shunting takes time and gravity drains blood from brain in less time! How do giraffes do it? Giraffe up

Giraffe down

1.  Heart weighs 25 lbs (vs ¾ lb for human) & has much thicker walls. 2.  Jugular vein (drains brain) has a valve that blocks outflow due to gravity. 3.  Fast blood shunting of blood in head away from facial muscles, tongue, etc and just to brain.

Blood shunting particularly important for diving mammals (but humans have diving reflex too)

For mammals adapted for diving, the change in heart rate can be dramatic. Fur seals go from 120 to 18 beats per minute! By closing off all unnecessary capillary beds, mean arterial pressure remains high even with low C.O.

M.A.P. = C.O. * total peripheral resistance So as heart rate drops, C.O. drops, but TPR goes up.

Human clinical hypertension control 1. Based on controlling salt Normal: Eat extra salt (any prepared food!) à drink more à increase blood volume à increase blood pressure. Don’t care if BP not too much. Hypertensive: Give diuretics à dump waterà lower blood volume à lower BP Normal: Eat extra salt à renin mech. conserve H20 à hypervolemic à higher BP. Don’t care if BP not too much. Hypertensive: Remove salt in diet à renin system can’t work, reduces blood volume à decr. BP

Human clinical hypertension control 2. Based on preventing BP increase Normal: If low BP à renin à angiotensin II à pump more salt out of filtrate à drag more water out of filtrate à incr. blood pressure. Hypertensive: Block angiotensin converting enzyme (ACE inhibitor) à block mech. to increase BP à keep BP low. Normal: Stress, etc à adrenalin release à binds to β type “adrenergic” receptors on heart à increase contraction strength & rate à incr. BP. Hypertensive: Take β-blocker à prevent incr. in rate à decr. BP

Congestive Heart Failure -- 1. Early stage

Decr. heart pumping strength

Decr. arterial pressure

Neg. Feedback control loop: Restores pressure BUT there will be excess blood volume and excess tissue fluid. Incr. arterial pressure

Activate renin/ angiotensin, aldosterone, sympathetic n.s.

Sodium retention water retention

Congestive Heart Failure -- 2. Late stage

Much decr. heart pumping strength

Decr. arterial pressure

Little/no urine flow, edema due to water retention. Heart stress greater due to greater blood volume. Can’t incr. arterial pressure – heart too weak

Activate renin/ angiotensin, aldosterone, sympathetic n.s.

Sodium retention water retention

Congestive Heart Failure -- 3. End stage Much decr. heart pumping strength Positive feedback: Ever increasing load on heart à imbalance of O2 need vs O2 delivery à successive minor heart attacks à  weaker heart à more blood volume

Hypervolemia Lung fluid build-up Incr. diffusion distance Less O2

Incr. load on heart

Incr. heart O2 demand