Circulation

Dara Rosmailina Pabittei, MD, PhD

Dept. of Physiology, UnHas

Dept. of Cardiothoracic Surgery, AMC-UvA
 Introduction
 Name : Dara R. Pabittei, MD, PhD

 Education : UGM - MD
Academic Medical Center (AMC),University of
Amsterdam (Department of Cardiothoracic
surgery) - PhD

 Staff : FK Unhas (2010), Post-doc AMC Dept. of

Cardiothoracic Surgery
 Circulation
 The body’s transport system, transport & distribute
 nutrient & O2
 waste removal
 hormon signaling
 Highlights:
 Arteries: transport blood heart to organs; pressure
reservoir
 Arterioles: supply the organs; adjustable caliber,
resistance vessels
 Capillaries: site of exchange blood & cells
 Veins: highly distensible; return blood to heart; blood
reservoir
Patterns & physics of blood
flow
 Circulation
 Circulations: systemic &
pulmonary
 Blood: constantly reconditioned
 maintain composition
 Reconditioning organs:
 digestive, kidneys, skin
 receives more blood
 withstand temporary << blood
flow

 Other organs:
 meets the basic metabolic needs
 adjusted to activity level
 can’t withstand << blood flow
 Brain: 4min  permanent
damage
Flow rate, pressure gradient,
vascular resistance
Flow rate (Q/F)
“volume darah yang melewati titik tertentu dalam pembuluh
darah pada waktu tertentu”

Q = ΔP/R
Q : blood flow (L/min; mil/min; ml/sec)  5L/min
ΔP : pressure gradient
R: resistance
 Flow rate, pressure gradient,
vascular resistance
Blood pressure
Kekuatan darah melawan setiap luas dinding pembuluh
darah. Tekanan pemb.drh 50mmHg  mampu mendorong
air raksa setinggi 50 mmHg.

Pressure gradient ( ΔP )
 Δ pressure at the beginning and the end of blood vessel
 heart contraction  frictional losses on blood vessels  ΔP
 ΔP : forward flow of blood
 Flow rate, pressure gradient,
vascular resistance
Resistance
 hindering blood flow
 friction of moving fluid &
vascular wall

η = viscosity,
L = vessel length,
r= vessel radius
 Rtot
Seri: R1 + R2 + R3
Paralel: 1/R1 + 1/R2 + 1/R3
Flow rate, pressure gradient,
vascular resistance
Konduktansi
ukuran dari jumlah darah yang mengalir setiap
pemberian tekanan yang berbeda, dan dinyatakan
dalam ml/detik/mmHg. Secara singkat konduktans
merupakan kebalikan dari resistensi.

Konduktansi = 1/resistensi
Konduktansi = diameter 4 d=1 1 ml/mnt

d=2
P=100 mmHg 16 ml/mnt

d=4 256 ml/mnt

Flow rate, pressure gradient,
vascular resistance
Poiseuille’s law
summarizes factors that influence flow

Q =pr 4

8nl

p = tekanan
 r 4 = Luas penampang
r = diameter
l = panjang
n = kekentalan/viscocity
Flow rate, pressure gradient,
vascular resistance
The vascular tree
Systemic:
LV  aorta  big arteries 
small arteries  (organs)
arterioles – capillaries –
venules – small veins  big
veins  v. cava  RA

Pulmonary:
RV  pulmonary a. 
arterioles  capillaries 
venules  pulm. v  LA
Vascular tree
3 different types, all with different functions:
1. Distributing system : Aorta, arteri, and arteriole

2. Diffusion and filtration system : kapiler.

metaarteriole, venule (in the organs
“microcirculations”)

3. Collecting system : vena

 Arteries
 # several hundreds; thick,
highly elastic

 Rapid-transit passageway
heart  organs

 Pressure reservoir: provide

driving force when heart is
relaxing

 Pressure fluctuates in
relation to ventricular
systole & diastole

Elastic recoil
Arteries
Mean arterial pressure (MAP)
The average pressure driving blood forward into
the tissues throughout the cardiac cycle

MAP = diastolic pressure + 1/3 pulse pressure

Arteries: little resistance  pressures = in all arteries

“Blood pressure” : pressure of the arteries

Pressures along circulatory system
 Arterioles
 # 500.000; >> SMC ; innervated; small radii

 Resistance vessels  distribution CO

 MAP : 93 mmHg  37 mmHg

 Allow blood to flow from heart  organs
 Pulsatile to non-fluctuating pressures

 Vasoconstriction & vasodilatation

 Distribute CO to organs
 Regulate arterial BP
Arterioles –
vasoconstriction & vasodilatation
Smooth muscle cells:
Sympathetic nerves, sensitive to chemical
changes, circulating hormones, stretch
Vascular tone: (half constricted)
Myogenic activity (Ca2+ channels)
Norepinephrine (symp.actv)
Vasoconstriction & vasodilatation:
Local (intrinsic) controls: Distribute CO
based on the needs
Extrinsic controls: Regulate arterial BP
 Local controls
Numbers and caliber of arteries  distribution of CO
Local controls: Changes within an organ  adjust Q by
affecting SMCs (affecting R)

Chemical :
1. Local metabolic changes (exp: exercise)
Active hyperemia, reactive hyperemia
2. Histamine releases

Physical :
 How much the vessels is stretched
 Extent of shear stress
 Heat/cold
 Local controls (chemical)
1. Active hyperemia: respons thdp perubahan komposis
kimia lokal yg diakibatkan o/ perubahan aktv. metabolik
lokal
Chemical changes:
decreased O2, increased CO2, increased acid (carbonic acid
from CO2 & lactate acid), increased K+, increased osmolarity,
adenosine release (cardiac muscle)  relaxation of smc 
vasodilatation
Endothelial vasoactive paracrine:
Paracrine: secreted by EC and acted on SMC
Nitric oxide  vasodilatation
Endothelin  vasoconstriction
 Local controls (Chemical)
2. Reactive hyperemia: respons for suppply-demand
imbalance due to cut of blood supply (metabolic activity
remain constant). c/ tourniquet

Chemical changes:
 decreased O2,
 increased CO2, acid and other metabolites

 Vasodilatation  blockage is removed  blood flow >>

Active Hyperemia Reactive Hyperemia
 Local controls (chemical)
Histamine release
 Influences smc  dilates arterioles
 Not release in response to local metabolic changes
 Not derived from EC
 Important for pathological condition
 Allergic reaction: histamine  vasodilation  redness
& swelling
Local controls (physical)
1. Myogenic autoregulation:
Myogenic response to stretch
helps tissue to autoregulate
their blood flow

2. Shear stress
release of NO  vasodilatation

3. Heat/cold
 Heat  vasodilatation
 Cold  vasoconstriction
 Extrinsic control
Regulating blood flow; Sympathetic & hormonal.
1. Sympathetic innervation
Generalized vasoconstriction
Control center: Cardiovascular control center in medulla brain
stem
Total peripheral resistance (TPR) influence MAP
ΔP = Q x R  MAP = CO x TPR
Norepinephrine
 α1-adrenergic receptors on smc: vasoconstriction
 Brain: no α1-adrenergic receptors. Cerebral arterioles (local control)
No parasympathetic innervation to arterioles; MAP increases 
reflex reduction of sympathetic activity.
 Extrinsic control
2. Hormones:
 Sympt stim medulla adrenal
Norepinephrinie + α1 adrenergic  vasoconstrinction
Epinephirine (more abundant of adrenal medullary hormones)
+ β2 receptors (heart & skeletal) : vasodilatation
 Vasopressin: regulate water retention in the kidney
 Angiotensin II : Renin – angiotensin – aldosterone  salt
retention
Vasopressin & angiotensin II: potent vasoconstrictors

3. Others
 Hypothalamus
Apart of temp. regulating system  controls blood to the skin to
adjust heat loss
Capillaries
 Capillaries
Site of materials exchange between blood and tissue
cells
Materials exchanges: mainly via diffusion
Factors that enhance diffusion:
1. Short distance: capillaries – cells
 Capillaries: very thin walls, single layer of flat EC,
narrow
 Extensive branching
2. Large surface area: 10-40 x 109 capillaries
3. Blood flow more slowly in capillaries
 extensive branching
 Allows exchange of nutrients & metabolic products
 Capillaries pores

Brain: tight
junction, BBB

Skeletal muscle:
pores +

Liver cells: EC
discontinuous
(sinusoids) 
protein can pass
 Precapillary sphincters (PS)
 Branching of cap 
depending on the tissue
Directly from arterioles or
from metarteriole
(between arterioles and
venules)

 PS: innervated (-),

myogenic tone (+),
sensitive to local metab
changes
 Control Q to capillary
Interstitial fluid (IF)
Blood – IF – cells

Cells - IF.
 Passive : diffusion down electrochemical gradient or carrier-
mediated facilitated diffusion
 Active: carrier mediated active transport or vesicular transport

Capillary – IF: passive

Capillary – tissue:
 Passive diffusion down concentration gradient
(individual solutes)
 Bulk flow  determine distribution of ECF
 Exchange of individual solutes

Independent exchange of individual solutes down their

own concentration gradients across capillary wall
 Bulk flow
Extracelullar fluid distribution

Ultrafiltration & reabsorption

Forces influencing bulk flow:

 Capillary bp (PC): hydrostatic pressure, inside the cap  blood

outward; 37 mmHg

 Plasma-colloid osmotic pres (πP): colloidal dispersion of

plasma protein, fluid inward; 25 mmHg

 IF hydrostatic pressure (PIF): IF inward

 IF – colloid osmotic pressure (πIF): outward

 Bulk flow
Net exchange = (PC + πIF) – (πP + PIF)

Bulk flow: regulate distribution of ECF btw plasma-IF

Veins
 Veins
 Passageway to the heart

 # several hundred, thin walled, highly

distensible, large radii

 Capacitance vessels
 Thinner SMC, more collagens, SMC less myogenic tone
 Veins: highly distensible, little/no elastic recoil

 Blood reservoir : low demands  store more; increase

demands  increase venous return
Distribution of cardiac output
 Venous capacity & venous return
Venous capacity:
 Volume of blood that veins can accommodate
 Dispensability of veins walls & external pressure

Venous return:
Vol. of blood/minute entering atrium from veins
Influenced by:
1. Sympathetic induce vasoconstriction
2. Skeletal muscle pump
3. Venous valves
4. Respiratory pump
5. Cardiac suction
 Venous return (VR)
1. Sympathetic stimulation
Veins SMC  innervated with sympathetic nerves
Vasoconstriction  elevates venous pressure  increase
press gradient  increase VR

2. Skeletal pump
Countering gravity of venous system
Large veins: btw skeletal muscle
Muscle contraction  compress veins  decrease venous
capacity, increase venous pressure
Venous return (VR)
3. Venous valve
One way valve  blood move forward & prevent back flow
Varicose veins : incompetent valves; prolonged standing >>

4. Respiratory pump
Pressure in the chest 5 mmHg < atmospheric pressure
ΔP between lower veins & chest pressure: push blood forward

5. Cardiac suction
Ventricular contraction, AV valves drawn downward  atrial
cavity >>, atrial pressure drops < 0 mmHg  push blood from
vein  RA
 Thank you
d.pabitei@gmail.com