HEMODYNAMICS

Physical principles governing blood

flow
 BLOOD PRESSURE
Lateral pressure exerted by the blood on the vessel walls

• Static pressure/Lateral pressure

• Dynamic component

Static pressure = Hemodynamic PR + Hydrostatic pressure

TOTAL PRESSURE = P + Hdg + Pd

RELATIONSHIP BETWEEN VELOCITY AND PRESSURE
Total energy = PE + KE
Bernoulli’s principle
 Inverse relationship
between velocity and
CS

12/22/2023 Dr S.Rajam Krishna 5

Pressure in aorta and large arteries is referred to as arterial BP
WINDKESSEL EFFECT

Arterioles – convert pulsatile inflow to a steady outflow

Pressure drop occurs at arterioles – resistance vessels
MAP – Average arterial pressure during one cardiac cycle
(averaged over time)

MAP = DBP + 1/3 PP

 How are BP, blood flow and blood volumes
established in CVS?

Model of systemic
circulation

Q α ∆P
Q α 1/R

C = ∆V/∆P
 POISEUILLE’S LAW – FLOW OF FLUID
THROUGH RIGID TUBES
Ohm’s law analogy: Q = ∆P/R

• Resistance is determined by properties of both

the fluid and the tube

R = 8 ηL/πr4

Q = ∆Pπr4/8ηL
 Q a = ∆Pπr4/8ηL

Q b= ∆Pπr4/8η2L
Small changes in arteriolar radius will
have a greater influence on resistance

Q B = ∆Pπr4/8ηL

Q A= ∆Pπ(2r)4/8ηL
Q A= ∆Pπ16r4/8ηL
LAMINAR FLOW (Movement of fluid through a tube
in concentric layers
Velocity is highest in the centre of the stream

AXIAL STREAMING
EFFECT (As flow rate
increases, viscosity of
blood decreases)
LAMINAR FLOW OCCURS ONLY
UPTO CRITICAL VELOCITY

Turbulent flow
Work load of the heart increases
(Greater pressure needed to produce
the same flow through the same vessel

Velocity = 1/CS Area

REYNOLD’S NUMBER: NR

NR = ρDV/η

ρ = Fluid density
D = Diameter of the cylindrical vessel
V = Mean velocity
η = Viscosity of blood
• NR less than 2000 – laminar flow

• NR more than 3000 – turbulent flow

• Laminar flow – silent

• Turbulent flow – Noisy

• Turbulent flow occurs at branching points of

arteries and at regions of vessel constriction
MURMURS:
Noisy flow causing vibrations to be transmitted to the
surface of the body

• Structural causes – Valvular causes/narrowing of

arteries

• Functional causes
Anaemia (reduced viscosity and a high fluid velocity)
 LAW OF LAPLACE
• Relationship between distending pressure and
tension
• Cylindrical vessel:
P = T (1/(r1 + r2))
• Sphere:
• P = 2T/r
• Distending pressure – Pressure to keep the
vessel wall open
• Transmural pressure = Pressure inside –
Pressure outside the cylinder

• Transmural pressure = Pressure inside (Since

pressure outside is low and ignored)

• Smaller the radius of the vessel, lower the

tension in the wall to keep the distending
pressure a constant
• Critical closing pressure – Pressure at which
flow ceases
Applications of Laplace law:
1. Thin walled capillaries can withstand high
internal pressure without bursting. When the
radius decreases, tension decreases to
maintain pressure a constant.
2. Dilated hearts – Tension increases thereby
increasing the workload of the heart
3. Alveoli
4. Urinary bladder
 Q = ∆P/R

∆P = Q × R

MAP - RAP = CO × TPR

MAP = CO × TPR

MAP – Mean arterial pressure

CO - Cardiac output
TPR - Total peripheral resistance
RAP – Right atrial pressure ≃ 0
 Determinants of MAP

Cardiac output TPR

1. Radius of the vessel
wall
Heart rate Stroke volume 2. Length of the vessel
wall
1. ANS 3. Viscosity of the fluid
2. Hormones
Myocardial
3. Drugs Preload contractility Afterload
(Venous return)
Major determinant when the cardiac
1. Blood volume performance decreases
2. Venomotor tone
3. Respiratory and calf muscle pump TPR
4. Posture

FRANK STARLING’S LAW

 Factors affecting the radius of the vessel
wall
Extrinsic regulation:
• Neural – Sympathetic
• Hormones – catecholamines, Angiotensin

Intrinsic regulation:
• Autoregulation by myogenic mechanism
• Local factors – hypoxia, hypercarbia, acidosis
 LOCAL CONTROL OF PERIPHERAL BLOOD
FLOW
AUTOREGULATION:
Capacity of the tissues to regulate their own blood flow
Changes in perfusion pressure

Vascular resistance is altered

Blood flow is maintained

Autoregulation is well developed in kidneys
Other areas where autoregulation occurs – Brain, Heart,
skeletal muscle, gut
THEORIES OF AUTOREGULATION:

Myogenic mechanism

Metabolic mechanism
 MYOGENIC MECHANISM

MAP increases – Increased

tissue blood flow(TBF)

Q = ∆P/R Increased stretch of

arteriolar walls -

Stretch activates mechanically gated

channels – Calcium release – Muscle
contraction
VASOCONSTRICTION – increased
vascular resistance
 METABOLIC THEORY OF AUTOREGULATION

Increased demand in the tissues –

Exercise

Increased tissue metabolism – accumulation of

metabolites – K+, Adenosine, H+, lactates
Other factors – Hypoxia, hypercarbia, high temperature

Potent vasodilators – Resistance decreases

Blood flow increases and the

metabolites are washed away
• Substances released by the endothelial cells:

• Thromboxane A2 - Vasoconstrictor

• Prostacyclin – Vasodilator

• Nitric oxide - Vasodilator

REGULATION OF BLOOD
PRESSURE
 MAP – Provides the perfusion pressure for
tissue perfusion

• Short term regulation of blood pressure

Neural mechanism

• Long term regulation of blood pressure

Hormonal mechanism
Neural reflexes:
1. Baroreceptor reflex

2. Peripheral chemoreceptor reflex

3. Central CNS ischaemic response

4. Cardiopulmonary receptors
 MEDULLARY CENTRES – CARDIOVASCULAR CONTROL

CARDIAC ACCELERATORY AREA CARDIAC INHIBITORY AREA

Present in the rostroventerolateral area Vagal centre – Nucleus Tractus

– RVLM - VASOMOTOR AREA solitarius
Afferents to RVLM: Afferents:
- Limbic cortex, Motor cortex
- Baroreceptors
- Hypothalamus - Chemoreceptors
- Lung afferents - Lung afferents
- Baroreceptors
Efferents:
- Chemoreceptors
Preganglionic PS fibres in the Nucleus
- Medullary RS centres
Ambiguus
- Direct effect of hypoxia, hypercarbia
Efferents:
- Intermediolateral horn of thoracic SC Preganglionic sympathetic
fibres arise
 BARORECEPTORS

Firing of baroreceptors
CAROTID SINUS

Sympathetic inhibition

Parasympathetic activation

AORTIC ARCH
 NUCLEUS TRACTUS
SOLITARIUS
CONNECTIONS TO THE
RVLM

Carotid
sinus nerve
Activation of RVLM: Aortic depressor ROSTRAL VENTRO-LATERAL
-Hypoxia nerve MEDULLA
-Hypercarbia
CARDIAC ACCELERATORY AREA
-Limbic system thr
hypothalamus VASOMOTOR AREA
-Chemoreceptors

Inhibition of RVLM:
-Baroreceptors
-Lung inflation afferents
CARDIO-INHIBITORY AREA
 + VAGAL CENTRE

NTS VMC
- -
+ +
+
VEINS ARTERIOLES HEART
(venoconstriction) HR
SV

Baroreceptors TPR

MAP CO
MAP INCREASES MAP DECREASES

Baroreceptor firing Baroreceptor firing

increases Decreases –
UNLOADING OF BARORECEPTORS
Sympathetic inhibition Less inhibition of Sympathetics
Parasympathetic activation Less activation of Parasympathetics

Activation of sympathetics

Arteriolar dilation
Arteriolar constriction
Heart rate decreases Heart rate increases
Stroke volume decreases Stroke volume increases

MAP decreases MAP increases

RESETTING OF BARORECEPTORS

ADAPTATION OF BARORECEPTORS
CARDIOPULMONARY BARORECEPTORS:
• Located in atria, ventricles, pulmonary vessels – low
pressure areas

• Vagal and sympathetic afferent nerves arise from these

areas

• Type A and B receptors – Atrial stretch receptors

(Venoatrial junctions)

• Activated by atrial stretch during venous return – Bain

bridge reflex

• Response: Vasodilation and fall in BP, Increased heart rate

Atrial stretch – Increased ANP – Natriuresis and reduction in TPR

Reduction of ADH and reduced sympathetic activity

Bezold-Jarisch reflex:
• Juxtacapillary region of alveoli, ventricles,
atria, great veins, pulmonary artery –
Chemosensitive vagal C fibres

• Activated by chemicals like capasaicin

• Activated during myocardial ischaemia

• Response – Bradycardia, hypotension,

apnoea followed by shallow breathing
Peripheral chemoreceptor reflex:
• Carotid and aortic bodies
• Important when the MAP decreases to 60
mmHg
• Vasoconstriction
Central CNS ischemic response:
• Occurs when the MAP decreases to 60 mmHg
• Hypoxia, hypercarbia – Direct stimulation of
VMC
• Cushing’s reflex – Raised ICT, High BP, Reflex
bardycardia
 HORMONAL REGULATION
• Renin – Angiotensin mechanism

• Vasopressin

• ANP
 HYPERTENSION
• Sustained elevation in arterial blood pressure

Types:

• Primary hypertension

• Secondary hypertension
PRIMARY HYPERTENSION:

• No definable cause

• Essential/Idiopathic/Primary HT

• Genetic causes, obesity

SECONDARY CAUSES:
Renal:
• Vascular
• Parenchymal
Endocrine:
• Primary hyper aldosteronism
• Oral contraceptives
• Cushing’s syndrome
Miscellaneous:
Pregnancy induced HT