Color Atlas of Physiology 2003 thieme

F. Wilson chest leads (unipolar)

V1–V6

V9 V8

V7

Vr6

V6

II

(ECG)

Vr5

R

V5

Vr4

V4

Electrocardiogram

1

2

Vr3

V1

V3

View from above

V2

G. Determination of largest mean QRS vector (QRS axis) using ECG leads I–III

1

“Vertical”

2

“Intermediate”

3

“Horizontal” (left axis)

II

III

II

III

II

III

QRS

8.7

I

I

I

Plate

QRS axis

α=90¡

QRS

α=50¡

α=0¡

(α= +60° to +90°)

(α=+30° to +60°)

(α= +30° to –30°)

I

+

+

I

–

–

II

+

+

II

–

–

III

–+

–+

III

H. Electrical axis of the heart

I. ECG changes in coronary infarction

Infarction

R

ECG

Left axis

P

4

–30°

deviation

Q

T

2

Left axis

P

R

1

0°

T

Stage 2

Q

(days to wks later)

Right axis

R

5

3

deviation

Inter-

+30°

P

mediate

Right

axis

Q S

T

Vertical

+120°

axis

axis

+60°

Stage 1

Stage 3

199

(few hrs to days later)

+90°

Normal

(months to yrs later)

range

(after Netter)

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8 Cardiovascular System

200

Cardiac Arrhythmias

Arrhythmias are pathological changes in cardiac impulse generation or conduction that can be visualized by ECG. Disturbances of impulse generation change the sinus rhythm. Sinus tachycardia (!A2): The sinus rhythm rises to 100 min–1 or higher e.g., due to physical exertion, anxiety, fever (rise of about 10 beats/min for each 1 !C) or hyperthyroidism. Sinus bradycardia: The heart rate falls below 60 min–1 (e.g., due to hypothyroidism). In both cases the rhythm is regular whereas in sinus arrhythmias the rate varies. In adolescents, sinus arrhythmias can be physiological and respiration-de- pendent (heart rate increases during inspiration and decreases during expiration).

Ectopic pacemakers. Foci in the atrium, AV node or ventricles can initiate abnormal ectopic (heterotopic) impulses, even when normal (nomotopic) stimulus generation by the SA node is taking place (!A). The rapid discharge of impulses from an atrial focus can induce atrial tachycardia (serrated baseline instead of normal P waves), which triggers a ventricular response rate of up to 200 min–1. Fortunately, only every second or third stimulus is transmitted to the ventricles because part of the impulses arrive at the Purkinje fibers (longest APs) during their refractory period. Thus, Purkinje fibers act as impulse frequency filters. Elevated atrial contraction rates of up to 350 min–1 are defined as atrial flutter, and all higher rates are defined as atrial fibrillation (up to 500 min–1). Ventricular stimulation is then totally irregular (absolute arrhythmia).

Ventricular tachycardia is a rapid train of impulses originating from a ventricular (ectopic) focus, starting with an extrasystole (ES) (!B3; second ES). The heart therefore fails to fill adequately, and the stroke volume decreases. This can lead to ventricular fibrillation (extremely frequent and uncoordinated contractions; !B4). Because of failure of the ventricle to transport blood, ventricular fibrillation can be fatal.

Ventricular fibrillation mainly occurs when an ectopic focus fires during the relative refractory period of the previous AP (called the “vulnerable phase” synchronous with T wave on the ECG; !p. 193 A). The APs triggered during this period have smaller slopes, lower

propagation velocities, and shorter durations. This leads to re-excitation of myocardial areas that have already been stimulated (re-entry cycles). Ventricular fibrillation can be caused by electrical accidents and can usually be corrected by timely electrical defibrillation.

Extrasystoles (ES). The spread of impulses arising from an supraventricular (atrial or nodal) ectopic focus to the ventricles can disturb their sinus rhythm, leading to a supraventricular arrhythmia. When atrial extrasystoles occur, the P wave on the ECG is distorted while the QRS complex remains normal. Nodal extrasystoles lead to retrograde stimulation of the atria, which is why the P wave is negative and is either masked by the QRS complex or appears shortly thereafter (!B1 right). Since the SA node often is discharged by a supraventricular extrasystole, the interval between the R wave of the extrasystole (RES) and the next normal R wave increases by the amount of time needed for the stimulus to travel from the focus to the SA node. This is called the postextrasystole pause. The RR intervals are as follows: RESR

" RR and (RRES + RESR) #2 RR (!B1).

Ventricular (or infranodal) ES (!B2, B3) distorts the QRS complex of the ES. If the sinus rate is slow enough, the ES will cause a ventricular contraction between two normal heart beats; this is called an interpolated (or interposed) ES (!B2). If the sinus rate is high, the next sinus stimulus reaches the ventricles while they are still refractory from the ectopic excitation. Ventricular contraction is therefore blocked until the next sinus stimulus arrives, resulting in a compensatory pause, where RRES + RESR = 2 RR.

Disturbances of impulse conduction: AV block.

First-degree AV block: prolonged but otherwise normal impulse conduction in the AV node (PQ interval "0.2 sec); second-degree AV block: only every second (2:1 block) or third (3:1 block) impulse is conducted. Third-degree AV block: no impulses are conducted; sudden cardiac arrest may occur (Adam–Stokes attack or syncope). Ventricular atopic pacemakers then take over (ventricular bradycardia with normal atrial excitation rate), resulting in partial or total disjunction of QRS complexes and P waves (!B5). The heart rate drops to 40 to 55 min–1 when the AV node acts as the pacemaker (!B5), and to a mere 25 to 40 min–1 when tertiary (ventricular) pacemakers take over. Artificial pacemakers are then used.

Bundle branch block: disturbance of conduction in a branch of the bundle of His. Severe QRS changes occur because the affected side of the myocardium is activated by the healthy side via abnormal pathways.

Despopoulos, Color Atlas of Physiology © 2003 Thieme

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A. Nomotopic impulse generation with normal conduction

SA

A

E R

Atria

Distance fromSA node

node

A

E

R

Lead II

f= 87min–1

AV node

R

1 Normal sinus rhythm

1s

Ventricles

Excitation

P

T

Trautwein)(After

Arrhythmias

Lead II

f= 140min

–1

S = Spreading

Q S

1s

C = Complete

R = Retrogression

0

0.1

0.2

0.3 0.4 s

2 Sinus tachycardia

Cardiac

B. Heterotopic impulse generation (1–5) and disturbances of impulse conduction (5)

Sinus

ES

Retrograde atrial and

SA node

SA node activation

R

R

RES

R

R

8.8

Lead II

Plate

1 Nodal (AV) extrasystole (ES)

Negative P

with post-extrasystolic pause

QRS

T

Sinus						SA node
ES	ES	Isolated
		ventricle activation
Lead II
1 s
2 Interpolated ventricular						QRS		P QRS	T
extrasystole (ES)
3 Ventricular tachycardia			ES					ES
following extrasystole (ES)
				f= 100min–1				f= 205min–1
		Lead I						Ventricular
								tachycardia
4 Ventricular fibrillation		Lead II
5 Total AV block with ventricular		R	R			R	R	R		R
escape rhythm
		P	P	(P)	P	P	P	P	P	P
		Lead II		1s			P= 75P/min		R= 45R/min		201
								(Partly after Riecker)

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Ventricular Pressure–Volume

Relationships

		The relationship between the volume (length)
		and pressure (tension) of a ventricle illustrates
		the interdependence between muscle length
		and force in the specific case of the heart
		(!p. 66ff.). The work diagram of the heart can
		be constructed by plotting the changes in
		ventricular pressure over volume during one
		complete cardiac cycle (!A1, points A-D-S-V-
		A, pressure values are those for the left ven-
	System	tricle).
		The following pressure–volume curves can be used to
		construct a work diagram of the ventricles:
	Cardiovascular	Passive (or resting) pressure–volume curve: In-
		dicates the pressures that result passively (without
		muscle contraction) at various ventricular volume
		loads (!A1, 2; blue curve).
		Isovolumic peak curve (!A1, 2, green curves):
		Based on experimental measurements made using
		an isolated heart. Data are generated for various
	8	volume loads by measuring the peak ventricular
		pressure at a constant ventricular volume during
		contraction. The contraction is therefore iso-
		volumetric (isovolumic), i.e., ejection does not take
		place (!A2, vertical arrows).
		Isotonic (or isobaric) peak curve (!A1, 2, violet
		curves). Also based on experimental measurements
		taken at various volume loads under isotonic
		(isobaric) conditions, i.e., the ejection is controlled in
		such a way that the ventricular pressure remains con-
		stant while the volume decreases (!A2, horizontal
		arrows).
		Afterloaded peak curve: (A1, 2, orange curves).
		Systole (!p. 190) consists of an isovolumic contrac-
		tion phase (!A1, A–D and p. 191 A, phase I) fol-
		lowed by an auxotonic ejection phase (volume
		decreases while pressure continues to rise) (!A1,
		D–S and p. 191 A, phase II). This type of mixed con-
		traction is called an afterloaded contraction (see also
		p. 67 B). At a given volume load (preload) (!A1,
		point A), the afterloaded peak value changes (!A1,
		point S) depending on the aortic end-diastolic pres-
		sure (!A1, point D). All the afterloaded peak values
		are represented on the curve, which appears as a
		(nearly) straight line connecting the isovolumic and
		isotonic peaks for each respective volume load (point
		A) (!A1, points T and M).
		Ventricular work diagram. The pressure–
		volume relationships observed during the car-
		diac cycle (!p. 190) can be plotted as a work
		diagram, e.g., for the left ventricle (!A1): The
	202	end-diastolic volume (EDV) is 125 mL (!A1,
		point A). During the isovolumetric contraction

phase, the pressure in the left ventricle rises (all valves closed) until the diastolic aortic pressure (80 mmHg in this case) is reached (!A1, point D). The aortic valve then opens. During the ejection phase, the ventricular volume is reduced by the stroke volume (SV) while the pressure initially continues to rise (!p. 188, Laplace’s law, Eq. 8.4b: Ptm " because r #and w "). Once maximum (systolic) pressure is reached (!A1, point S), the volume will remain virtually constant, but the pressure will drop slightly until it falls below the aortic pressure, causing the aortic valve to close (!A1, point K). During the isovolumetric relaxation phase, the pressure rapidly decreases to (almost) 0 (!A1, point V). The ventricles now contain only the end-systolic volume (ESV), which equals 60 mL in the illustrated example. The ventricular pressure rises slightly during the filling phase (passive pressure–volume curve).

Cardiac Work and Cardiac Power

Since work (J = N · m) equals pressure (N · m–2= Pa) times volume (m3), the area within the working diagram (!A1, pink area) represents the pressure/volume (P/V) work achieved by the left ventricle during systole (13,333 Pa· 0.00008 m3 = 1.07 J; right ventricle: 0.16 J). In systole, the bulk of cardiac work is achieved by active contraction of the myocardium, while a much smaller portion is attributable to passive elastic recoil of the ventricle, which stretches while filling. This represents diastolic filling work (!A1, blue area under the blue curve), which is shared by the ventricular myocardium (indirectly), the atrial myocardium, and the respiratory and skeletal muscles (!p. 204, venous return).

Total cardiac work. In addition to the cardiac work performed by the left and right ventricles in systole (ca. 1.2 J at rest), the heart has to generate 20% more energy (0.24 J) for the pulse wave (!p. 188, windkessel). Only a small amount of energy is required to accelerate the blood at rest (1% of total cardiac work), but the energy requirement rises with the heart rate. The total cardiac power (= work/time, !p. 374) at rest (70 min–1 = 1.17 s–1) is approximately 1.45 J · 1.17 s–1 = 1.7 W.

Despopoulos, Color Atlas of Physiology © 2003 Thieme

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A. Work diagram of the heart (left ventricle)

kPa	mmHg		1		Isovolumic (iso-	Relationships
40	300				volumetric) peaks
pressurebloodventricular			T	Isotonic (iso-		Pressure–VolumeVentricular
				pressureVentricular
				baric) peaks	Afterloaded
		Afterloaded		2
30		peak curve			peak curve
	200
20
		S =Systolic
Left		pressure				8.9
	100	= Aortic valve
		K
10		closure		Ventricular volume
			D =Aortic			Plate
				valve opening

				Systolic pressure/volume work		Resting
	M			A		tension curve
		V
				Diastolic pressure/volume work
0	00		100	200	mL
	End-systolic		Stroke	Blood volume in left ventricle
	volume		volume
	(ESV)		(SV)

End-diastolic volume (EDV)

B.Effects of pretension (preload) (1), heart rate and sympathetic stimuli (2) on myocardial force and contraction velocity

				Norepinephrine administered
	1		2	at heart rate of 60min–1
	force		force	Heart rate: 60min–1
		Resting tension:		Heart rate: 30min–1
	Myocardial	High	Myocardial
		Medium
		Low
	0		0
	0	0.5 Time (s)1.0	0	0.5 Time (s)1.,0
				203
		(See text on next page)		(After Sonnenblick)

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Regulation of Stroke Volume

Venous Return

		Frank–Starling mechanism (FSM): The heart
		autonomously responds to changes in ventric-
		ular volume load or aortic pressure load by ad-
		justing the stroke volume (SV) in accordance
		with the myocardial preload (resting tension;
		!p. 66ff.). The FSM also functions to maintain
		an equal SV in both ventricles to prevent con-
		gestion in the pulmonary or systemic circula-
		tion.
		Preload change. When the volume load
	System	(preload) increases, the start of isovolumic
		contraction shifts to the right along the passive
		P–V curve (!A1, from point A to point A1).
	Cardiovascular	This increases end-diastolic volume (EDV),
		stroke volume (SV), cardiac work and end-sys-
		tolic volume (ESV) (!A).
		Afterload change. When the aortic pressure
		load (afterload) increases, the aortic valve will
		not open until the pressure in the left ventricle
	8	has risen accordingly (!A2, point Dt). Thus,
		the SV in the short transitional phase (SVt) will
		decrease, and ESV will rise (ESVt). Con-
		sequently, the start of the isovolumic contrac-
		tion shifts to the right along the passive P–V
		curve (!A2, point A2). SV will then normalize
		(SV2) despite the increased aortic pressure
		(D2), resulting in a relatively large increase in
		ESV (ESV2).
		Preload or afterload-independent changes
		in myocardial contraction force are referred to
		as contractility or inotropism. It increases in
		response to norepinephrine (NE) and epineph-
		rine (E) as well as to increases in heart rate (!1-
		adrenoceptor-mediated, positive inotropic ef-
		fect and frequency inotropism, respectively;
		!p. 194). This causes a number of effects, par-
		ticularly, an increase in isovolumic pressure
		peaks (!A3, green curves). The heart can
		therefore pump against increased pressure
		levels (!A3, point D3) and/or eject larger SVs
		(at the expense of the ESV) ( !A3, SV4).
		While changes in the preload only affect the
		force of contraction (!p. 203 B1), changes in
		contractility also affect the velocity of contrac-
		tion (!p. 203/B2). The steepest increase in
		isovolumic pressure per unit time (maximum
		dP/dt) is therefore used as a measure of con-
	204	tractility in clinical practice. dP/dt is increased
		E and NE and decreased by bradycardia
		(!p. 203 B2) or heart failure.

Blood from the capillaries is collected in the veins and returned to the heart. The driving forces for this venous return (!B) are: (a) vis a tergo, i.e., the postcapillary blood pressure (BP) (ca. 15 mmHg); (b) the suction that arises due to lowering of the cardiac valve plane in systole; (c) the pressure exerted on the veins during skeletal muscle contraction (muscle pump); the valves of veins prevent the blood from flowing in the wrong direction, (d) the increased abdominal pressure together with the lowered intrathoracic pressure during inspiration (Ppl; !p. 108), which leads to thoracic venous dilatation and suction (!p. 206).

Orthostatic reflex. When rising from a supine to a standing position (orthostatic change), the blood vessels in the legs are subjected to additional hydrostatic pressure from the blood column. The resulting vasodilation raises blood volume in the leg veins (by ca. 0.4 L). Since this blood is taken from the central blood volume, i.e., mainly from pulmonary vessels, venous return to the left atrium decreases, resulting in a decrease in stroke volume and cardiac output. A reflexive increase (orthostatic reflex) in heart rate and peripheral resistance therefore occurs to prevent an excessive drop in arterial BP (!pp. 7 E and 212ff.); orthostatic collapse can occur. The drop in central blood volume is more pronounced when standing than when walking due to muscle pump activity. Conversely, pressure in veins above the heart level, e.g., in the cerebral veins, decreases when a person stands still for prolonged periods of time. Since the venous pressure just below the diaphragm remains constant despite changes in body position, it is referred to as a hydrostatic indifference point.

The central venous pressure (CVP) is measured at the right atrium (normal range: 0–12 cm H2O or 0–9 mmHg). Since it is mainly dependent on the blood volume, the CVP is used to monitor the blood volume in clinical medicine (e.g., during a transfusion). Elevated CVP (!20 cm H2O or 15 mmHg) may be pathological (e.g., due to heart failure or other diseases associated with cardiac pump dysfunction), or physiological (e.g., in pregnancy).

Despopoulos, Color Atlas of Physiology © 2003 Thieme

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A. Factors influencing cardiac action

1 Increase in filling (preload)

	(See preceding Plate A	T1
	for explanation of curves)
pressure	T	loaded
		New after-
Blood		peak curve

	S	S1
			D	D1
			Work
M	V			A1
			A	Ventricular volume
ESV			SV
		EDV
3 Increase			T3
in contractility
				New
pressureBlood			T	afterloaded
				peak curve
				Same stroke
				volume at
				higher pressure

	S3	or
		Higher stroke
	D3	volume
		(SV4>SV) at
		same pressure

S4

Arbeit

V4

Ventricular volume

SV

SV4

2 Increase in blood pressure (afterload)

		T	T2
pressure	Transitional phase (t):
	Blood pressure		Stroke volume
	rises while
			normalizes
	stroke volume
			(SV2=SV) despite
Blood	decreases
			increased
	S2
			blood pressure:
	St		Increased work

Dt	D2
Work
VÜ	A2

Ventricular volume

ESV	SV
ESVt	SVt
ESV2	SV2

B. Venous return

Venous return = cardiac output

Right		Left
	Pulmonary	heart
heart
	circulation

Suction via lowering of cardiac valve plane

Negative pressure in thorax

Venous	Inspiration
valves

Positive pressure in abdominal cavity

Muscle pump

Systemic

Blood pressure circulation ca. 15mmHg

Plate 8.10 Regulation of Stroke Volume

205

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Arterial Blood Pressure

		The term blood pressure (BP) per se refers to
		the arterial BP in the systemic circulation. The
		maximum BP occurs in the aorta during the
		systolic ejection phase; this is the systolic pres-
		sure (Ps); the minimum aortic pressure is
		reached during the isovolumic contraction
		phase (while the aortic valves are closed) and
		is referred to as the diastolic pressure (Pd)
		(!A1 and p. 191, phase I in A2). The systolic–
		diastolic pressure difference (Ps–Pd) represents
	System	the blood pressure amplitude, also called pulse
		pressure (PP), and is a function of the stroke
		volume (SV) and arterial compliance (C =
	Cardiovascular8	dV/dP, !p. 188). When C decreases at a con-
		If the total peripheral resistance (TPR, !p. 188) in-
		stant SV, the systolic pressure Ps will rise more
		sharply than the diastolic pressure Pd, i.e., the
		PP will increase (common in the elderly; de-
		scribed below). The same holds true when the
		SV increases at a constant C.
		creases while the SV ejection time remains constant,
		then Ps and the Pd will increase by the same amount
		(no change in PP). However, increases in the TPR nor-
		mally lead to retardation of SV ejection and a
		decrease in the ratio of arterial volume rise to periph-
		eral drainage during the ejection phase. Conse-
		quently, Ps rises less sharply than Pd and PP
		decreases.
		Normal range. In individuals up to 45 years of
		age, Pd normally range from 60 to 90 mmHg
		and Ps from 100 to 140 mmHg at rest (while sit-
		ting or reclining). A Ps of up to 150 mmHg is
		considered to be normal in 45 to 60-year-old
		adults, and a Ps of up to 160 mmHg is normal in
		individuals over 60 (!C). Optimal BP regula-
		tion (!p. 212) is essential for proper tissue
		perfusion.
		Abnormally low BP (hypotension) can lead to shock
		(!p. 218), anoxia (!p. 130) and tissue destruction.
		Chronically elevated BP (hypertension; !p. 216)
		also causes damage because important vessels (es-
		pecially those of the heart, brain, kidneys and retina)
		are injured.
		The mean BP (= the average measured over
		time) is the decisive factor of peripheral perfu-
		sion (!p. 188).
	206	The mean BP can be determined by continuous BP
		measurement using an arterial catheter, etc. (!A).

By attenuating the pressure signal, only the mean BP is recorded.

Although the mean BP falls slightly as the blood travels from the aorta to the arteries, the Ps in the greater arteries (e.g., femoral artery) is usually higher than in the aorta (A1 v. A2 ) because their compliance is lower than that of the aorta (see pulse wave velocity, p. 190).

Direct invasive BP measurements show that the BP curve in arteries distal to the heart is not synchronous with that of the aorta due to the time delay required for passage of the pulse wave (3–10 m/s; !p. 190); its shape is also different (!A1/A2).

The BP is routinely measured externally (at the level of the heart) according to the Riva-Rocci method by sphygmomanometer (!B). An inflatable cuff is snugly wrapped around the arm and a stethoscope is placed over the brachial artery at the crook of the elbow. While reading the manometer, the cuff is inflated to a pressure higher than the expected Ps (the radial pulse disappears). The air in the cuff is then slowly released (2–4 mmHg/s). The first sounds synchronous with the pulse (Korotkoff sounds) indicate that the cuff pressure has fallen below the Ps. This value is read from the manometer. These sounds first become increasingly louder, then more quiet and muffled and eventually disappear when the cuff pressure falls below the Pd (second reading).

Reasons for false BP readings. When re-measur- ing the blood pressure, the cuff pressure must be completely released for 1 to 2 min. Otherwise venous pooling can mimic elevated Pd. The cuff of the sphygmomanometer should be 20% broader than the diameter of the patient’s upper arm. Falsely high Pd readings can also occur if the cuff is too loose or too small relative to the arm diameter (e.g., in obese or very muscular patients) or if measurement has to be made at the thigh.

The blood pressure in the pulmonary artery is much lower than the aortic pressure (!p. 186). The pulmonary vessels have relatively thin walls and their environment (airfilled lung tissue) is highly compliant. Increased cardiac output from the right ventricle therefore leads to expansion and thus to decreased resistance of the pulmonary vessels (!D). This prevents excessive rises in pulmonary artery pressure during physical exertion when cardiac output rises. The pulmonary vessels also function to buffer short-term fluctuations in blood volume (!p. 204).

Despopoulos, Color Atlas of Physiology © 2003 Thieme

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	A. Arterial blood-pressure curve
			Pulse pressure (PS–PD)
	Blood pressure (mmHg)	120			Arterial mean pressure
						3
			F1			+F		F1
			F2	F3		2
						=F
						1	F2	F3	Blood Pressure
		80	Systolic blood			when F
			pressure (Ps)
			Diastolic blood
			pressure (Pd)
		0
			1 Aorta					2 Femoral artery	Arterial
	B. Blood-pressure measurement with sphygmomanometer (Riva–Rocci)
		Upper arm							8.11
	Brachial artery
					Korotkoff				Plate
		Cuff			sounds
					(at crook of elbow)

Systolic

Pressure

Manometer

150

reading

(brachial artery)

Pump

mmHg

125

100

Release valve

75

Diastolic

Cuff pressure

reading

0

Time

C. Age-dependency of blood pressure

D. Blood pressure and blood flow rate

Systolic

)

s

g

(L/min)

n

Mean pressure

u

l

(

R)

n

t

(mmHg)

o

an

Diastolic

i

t

.

a

onst

150

rateQ

t

la

i

(c

d

tube

o

s

Bloodpressure

125

Blood flow

a

t

e

d

v

Rigid

l a

neys)

e

ati

r

ul

75

-

g

re

r

e

to

u

s

u

A

s

e

00

r

20

40

60

80

P

Age (years)

Driving pressure gradient

P (mmHg)

207

(after Guyton)

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Endothelial Exchange Processes

		Nutrients and waste products are exchanged
		across the walls of the capillaries and post-
		papillary venules (exchange vessels; !p. 188).
		Their endothelia contain small (ca. 2–5 nm) or
		large (20–80 nm, especially in the kidneys and
		liver) functional pores: permeable, intercellu-
		lar fissures or endothelial fenestrae, respec-
		tively. The degree of endothelial permeability
		varies greatly from one organ to another. Vir-
		tually all endothelia allow water and inorganic
	System	ions to pass, but most are largely impermeable
		to blood cells and large protein molecules.
		Transcytosis and carriers (!p. 26f.) allow for
	Cardiovascular	passage of certain larger molecules.
		Filtration and reabsorption. About 20 L/day
		of fluid is filtered (excluding the kidneys) into
		the interstitium from the body’s exchange ves-
		sels. About 18 L/day of this fluid is thought to be
		reabsorbed by the venous limb of these vessels.
	8	The remaining 2 L/day or so make up the lymph
		flow and thereby return to the bloodstream
		(!A). The filtration or reabsorption rate Qf is a
		factor of the endothelial filtration coefficient Kf
		(= water permeability k · exchange area A) and
		the effective filtration pressure Peff (Qf = Kf · Peff).
		Peff is calculated as the hydrostatic pressure
		difference P minus	the oncotic pressure
		difference Δπ across the capillary wall (Star-
		ling’s relationship; !A), where		P = capillary
		pressure (Pcap) minus interstitial pressure (Pint,
		normally ! 0 mmHg). At the level of the heart,
		P at the arterial end of the systemic capillar-
		ies is about 30 mmHg and decreases to about
		22 mmHg at the venous end. Since Δπ (ca.
		24 mmHg; !A) counteracts		P, the initially
		high filtration rate (Peff = + 6 mmHg) is thought
		to change into reabsorption whenever Peff be-
		comes negative. (Since	P is only 10 mmHg in

the lungs, the pulmonary Peff is very low). Δπ occurs because the concentration of proteins (especially albumin) in the plasma is much higher than their interstitial concentration. The closer the reflection coefficient of the

plasma proteins (σprot) to 1.0, the higher Δπ and, consequently, the lower the permeability

of the membrane to these proteins (!p. 377).

According to Starling’s relationship, water reab-

208sorption should occur as long as Peff is negative. However, recent data suggest that a negative Peff re-

sults in only transient reabsorption. After several minutes it stops because the interstitial oncotic pressure rises due to “self-regulation”. Thus, a major part of the 18 L/d expected to be reabsorbed from the exchange vessels (see above) might actually be reabsorbed in the lymph nodes. Rhythmic contraction of the arterioles (vasomotion) may also play a role by decreasing Peff and thus by allowing intermittent capillary reabsorption.

In parts of the body below the heart, the effects of hydrostatic pressure from the blood column increase the pressure in the capillary lumen (in the feet !90 mmHg). The filtration rate in these regions therefore rise, especially when standing still. This is counteracted by two “self-regulatory” mechanisms:

(1) the outflow of water results in an increase in the luminal protein concentration (and thus Δπ) along the capillaries (normally the case in glomerular capillaries, !p. 152); (2) increased filtration results in an increase in Pint and a consequent decrease in P.

Edema. Fluid will accumulate in the interstitial space (extracellular edema), portal venous system (ascites), and pulmonary interstice (pulmonary edema) if the volume of filtered fluid is higher than the amount returned to the blood.

Causes of edema (!B):

Increased capillary pressure (!B1) due to precapil-

lary vasodilatation (Pcap"), especially when the capillary permeability to proteins also increases (σprot # and Δπ #) due, for example, to infection or anaphylaxis (histamine etc.). Hypertension in the portal vein leads to ascites.

Increased venous pressure (Pcap ", !B2) due, for example, to venous thrombosis or cardiac insufficiency (cardiac edema).

Decreased concentration of plasma proteins, especially albumin, leading to a drop in Δπ (!B3 and p. 379 A) due, for example, to loss of proteins (proteinuria), decreased hepatic protein synthesis (e.g., in liver cirrhosis), or to increased breakdown of plasma proteins to meet energy requirements (hunger edema).

Decreased lymph drainage due, e.g., to lymph tract compression (tumors), severance (surgery), obliteration (radiation therapy) or obstruction (bilharziosis) can lead to localized edema (!B4).

Increased hydrostatic pressure promotes edema formation in lower regions of the body (e.g., in the ankles; !B).

Diffusion. Although dissolved particles are dragged through capillary walls along with filtered and reabsorbed water (solvent drag; !p. 24), diffusion plays a much greater role in the exchange of solutes. Net diffusion of a substance (e.g., O2, CO2) occurs if its plasma and interstitial conc. are different.

Despopoulos, Color Atlas of Physiology © 2003 Thieme

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