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The CVS Physiology

By Mariam A. (MSc.)
Outlines
• General Introduction: structure and functions of the heart
• The cardiac cycle
• Electrophysiology of the heart muscle
• The E.C.G.
• The heart sounds
• The heart rate and its regulation
• The cardiac output in normal and in failing heart
• The arterial blood pressure and its control
• Tissue fluid formation and drainage, EDEMA
• The coronary circulation
• Hypertension: causes, types, complication
• Shock: stages and types
General Introduction: structure and functions of the heart
4. Systemic fluid & electrolyte homeostasis via the
Function of CVS: Tissue blood flow:
renal circulation.
mass movement of fluid caused by
5. Distribute agents that regulate cell function
pressure gradient.
(hormones, NTs & drugs).
Principal functions of tissue blood flow: 6. Secretion of hormones like ANP to regulate BP
1. Delivery of metabolic substrates (O2, & blood volume via increases renal Na+
excretion.
glucose etc) to cells
7. Vital role in reproduction - penile erection.
2.‘Washout’ of tissue metabolic by-
8. Contribution to defense mechanisms (by
products (CO2, H,+ amines, etc).
delivering antibodies, platelets & leucocytes to
3. Systemic heat exchange via cutaneous & affected areas of the body.

pulmonary circulation.
Cont.…
Structures/components of CVS: pump, distributive
channel, micro-vascular network and reservoirs

1. THE HEART (pump): Generate driving force


for blood.

2. THE ARTERIES : Blood distribution


channels to the organs.

3. CAPILLARIES-The microcirculation:
Exchange region.

4. THE VEINS: Blood reservoirs and return of


blood to the heart
THE HEART
• Physiological anatomy of the heart
 The HEART is a muscular pump that drives the
blood through the blood vessels.

 Is located b/n the lungs in the center and a bit to the left
mid-line of the body.
 The heart has right & left partitions completely
separated by a partition called the septum (Interatrial
septum and Interventricular septum)
 The heart also have four chambers:
o 2 receiving chambers (Atria)
o 2 pumping chambers (Ventricles).
Cont.…
Each of the Rt. & Lt. hearts has a pulsatile two-
chamber pump composed of an atrium and a
ventricle.
• Each atrium is a weak primer pump for the
ventricle, helping to move blood into the ventricle.
• The ventricles then supply the main pumping
force that propels the blood either: Through the
pulmonary circulation by the right ventricle or
through the Systemic/peripheral circulation by
the left ventricle.
Cont.…
• The heart also have structures called valves.
 Valves of the Heart:- four
• Thin flaps of flexible, endothelium-covered fibrous tissue
firmly attached to fibrous rings at the base of the heart.
• It’s fibrous connective tissue important to: Prevent
enlargement of valve opening and Anchor valve flaps.
• Since the ventricles are the pumping chambers, the
valves which are all one way, are located at the
entrance & exit of each ventricle.
 Function: Responsible for the unidirectional flow of
blood through the heart ( to direct blood flow).
Cont.…

• 2 group valves:
1. The atrioventricular valves/ entrance
valves/ Inlet valves
• Tricuspid & mitral
2. The semilunals valves/ exit valves/outlet
valves
• Aortic and Pulmonary valves
 Valve closure prevents backflow of blood
during and after contraction.
The heart and the dual pump
1. The right atrium: Receives the venous blood
returning from the body tissues thru vena cava.
• No valve between RA & vena cava;
2. The right ventricle: Received venous blood
from the RA
• Pumps it to the lungs thru pulmonary artery.
3. The left atrium : Receives blood rich in O2
from the lungs thru pulmonary vein.
• No valve between LA & pulmonary vein.
4. The left ventricle : Pumps oxygenated blood to
all parts of the body tissues.
Cont.…
The heart has actually two separate pumps
(“dual pump”) that drives blood into two
serial circuits.
Right heart receives deoxygenated blood
via venae cava pumps blood to the lungs
via pulmonary artery, drive the
pulmonary circulation
The Left heart receives oxygenated blood
from the lungs via Pulmonary vein and
pumps blood to the peripheral organs,
systemic circulation.
Cont.…
 Generally,
1. Systemic Circulation: deliveries oxygen to
all cells of the body & carries away wastes.
2. Pulmonary Circulation: oxygenate the
blood & eliminates CO2 via lungs.
Cont.…
Physiologic Anatomy of Cardiac Muscle

• Cardiac muscle fibers arranged in a latticework, with the


fibers dividing, recombining, and then spreading again.
 Similarity: Cardiac muscles are almost identical to skeletal
muscle in the following:
o Similar arrangement of myofibrils (actin & myosin
filaments) - These filaments lie side by side & slide
along each another during contraction.
o Striated.
 Difference: Nature of muscle contraction

• Skeletal muscle: Tetanic contraction possible b/c of Short


refractory period

• Cardiac muscle: No tetanic contraction b/c has long


refractory period
Properties of cardiac muscle
Cont.… 1. Excitatory & conductive muscle fibers

 Forms the Pacemaker & conducting tissues:


• The heart is composed of two major types
• Generate excitatory impulse and send to
of cardiac muscle fibers (based on
working (contractile) myocardial cells.
morphology & functional criteria):
1. Excitatory & conductive muscle • Contract only feebly because they contain few
contractile fibrils.
fibers
• Sinoatrial node, Atrioventricular node • Ruther, they exhibit either automatic

& His-Purkinje system systems (1%). rhythmical electrical discharge in the form of

2. Contractile muscle fibers APs or conduction of the APs that controls

• Atrial & ventricular muscle fibers the rhythmical beating of the heart.

(99%) .
Cont..

• Pacemaker & conductive tissues: Specialized heart-


muscle tissue in the wall of the heart that sends out
rhythmic electrical impulses to regulate the heartbeat.

• Natural, local (intrinsic) heartbeat regulator tissues.


 Includes:

1. Sinoatrial node (SA node)

2. Atrioventricular node (AV node)

3. His bundle, bundle branches & purkinje fibers


Cont.…
 Sinoatrial node (SA node):

 Small, flattened, ellipsoid band of specialized cardiac muscle tissue.

 Located in upper portion of right atrium at junction of superior vena cava & right atrium.

 Normal pacemaker, drive heart at a rate of 70 bpm at rest.

 (Self excitatory nature) due to they have:

o Less negative & unstable RMP


o Leaky membrane to Na+/Ca++
o Spontaneously depolarizes at fastest rate.
• So, they can do overdrive suppression of…
 Excitation spreads over working myocardium of atria.

 Contracts feebly
Cont.…

2. Contractile muscle fibers

• Form the Atrial and Ventricular muscle wall

 Do mechanical work of pumping.

 Contract when electrically stimulated.

 They contract in much the same way as skeletal


muscle, except that the duration of contraction is
much longer in cardiac muscles.
Cont.…
At each intercalated disc
o The cell membranes fuse with one another
o They form permeable “communicating” junctions (gap junctions)
o This gap junctions allow almost totally free diffusion of ions along the longitudinal
axes of the cardiac muscle fibers,
o So that, Aps travel easily from one cardiac muscle cell to the next past the intercalated
discs.
Thus, cardiac muscle is a syncytium of many heart muscle cells in which the cardiac
cells are so interconnected that when one of these cells becomes excited, the AP
spreads to all of them, spreading from cell to cell throughout the latticework
interconnections...Synchronous excitation
Cardiac Muscle as a Syncytium
• Cardiac muscle tissue forms two functional syncytia:

(a) The atrial syncytium .......constitutes walls of the atria

(b) The ventricular syncytium ............................ventricles.

• These are separated from each other by fibrous tissue ( electric resistant, surrounds
valves).

• APs are conducted from atrial syncytium to ventricular syncytium through the AV
bundle (Bundle of His) only.

• This division of the muscle of the heart into two functional syncytium allows the atria to
contract a short time ahead of ventricular contraction, which is important for
effectiveness of heart pumping.
Ionic Basis of Cardiac Action Potential (Reading assignment)

 Various phases of cardiac AP are associated with changes in membrane permeability of


cardiac cells to different ions, mainly, Na, K, & Ca ions.

 The shape of AP of myocardial cells depend upon whether the AP recorded from the
CMCs (atria or ventricles) or the pacemaker conducting tissues (SAN, AVN or His-
Purkinje System).

 Based on this fact, the AP of cardiac muscle cells are of two types:
1. Fast response type (based on depolarization rate)
2. Slow response type
Ionic Basis of Cardiac Action Potential

 Various phases of cardiac AP are


• Based on this fact, the AP of cardiac
associated with changes in membrane
muscle cells are of two types:
permeability of cardiac cells to different
ions, mainly, Na, K, & Ca ions. 1. Fast response type (based on
depolarization rate)
 The shape of AP of myocardial cells
2. Slow response type
depend upon whether the AP recorded
from the CMCs (atria or ventricles) or
the pacemaker conducting tissues
(SAN, AVN or His-Purkinje System).
AP in contractile and auto-rhythmic cells
Fast response AP
• Seen in atria and ventricles
• More negative RMP
• Depolarize and repolarize when
stimulated (not spontaneously active).
• Steep upstroke (due to opening of fast
Na+ channel) and Plateau due to calcium
Cont.…
Slow response AP • Phase 4: Pacemaker Potential:

 The Funny Sodium channels starts to be opened (If


• Seen in SAN and AVN
or f channels )… Inward, depolarizing Na current
• Less negative unstable RMP
• Phase 0: The Rising Phase (Depolarization):
• Depolarize spontaneously
 Opening of Long-lasting voltage-gated Calcium
(due to the presence of
channels (L-type Ca2+ channels).
spontaneously opening Na+
 Large influx of Calcium.
and Ca2+ channels)
• Phase 3: The Falling Phase or Repolarization:
• More gradual upstroke
 Opening of voltage-gated K channels & Closing of
L-type Ca channels….. → Potassium Efflux
Cont.….
AP of pacemaker conducting tissues: authorhythemic fibers, slow response type

• A membrane potential of auto rhythmic cells of the heart do not have a stable RMP.

• Instead they have an unstable membrane potential that starts at – 60mv and slowly drifts

upwards towards threshold.

• Shows slow depolarization due to the presence of low, leaky Na & Ca ions

channels…..membrane potential never rests at a constant value….. it is called a

Pacemaker Potential rather than a RMP.


Excitation-Contraction Coupling in Cardiac muscles

• Is the mechanism by which the cardiac muscle membrane AP causes contraction of the
myofibrils of cardiac muscle.
• When an AP passes over the cardiac muscle membrane, the AP spreads to the interior of
the cardiac muscle fiber along the membranes of the transverse (T) tubules.
• The T tubule APs opens VG calcium channels (DHPR) which are found on T- tubules…..
Influx of calcium from ECF.
• Then this calcium in turn opened the RyR calcium receptor found in Sarcoplasmic
reticulum (SR)…..Calcium release to sarcoplasm.
• These calcium ions diffuse into the myofibrils and promote sliding of the actin and
myosin filaments along one another producing the muscle contraction.
Cont.…
Cont.…
 Steps in Excitation-contraction-coupling: 
Relaxation/diastole
 Contraction (systole). • The clearance of calcium from the sarcoplasm
 Spread of excitation (AP) from cell-to cell via gap terminates the contraction and starts the relaxation
junctions also spread to interior via T-tubules. process.
 APs opens VG calcium channals (DHPR) which are • Calcium is cleared from the sarcoplasm by :
found on T- tubules resulting increases Ca++ 1. Na+/Ca2+ Exchanger (3:1) + Na+/K+ ATPase
permeability (3:2):
 This Ca++ triggers release of Ca++ from SR which 2. SERCA Pump (Sarco-endoplasmic reticulum
causes Ca++ level increases in cytosol calcium ATPase) that is inhibited by phospholimbin.
 Ca++ binds to Troponin C. and Troponin-C -Ca++
3. ATP dependant calcium pump (Ca2+ ATPase):
complex interacts with tropomyosin to unlock active
 Sarcolemma that pumps calcium out into the ECF.
site between actin & myosin.
 Cross bridge cycling = contraction (systole).
Physiological regulation of Ca2+ during muscle contraction & relaxation
1. Hormonal /NT (Catecholamines, NA):
2. Drugs (Cardiac glycosides)- enhance
• Contraction
contraction
 Phosphorylation of Ca++ channels
 Increase Ca++ into cells by  Inhibit Na+/K+-ATPase=> increase in
phosphorylation of Ca++ channels by
cAMP dependent protein kinase intracellular [Na++] => decreasing the
(cAMP-PK)…..↑IC [Ca2+] availability of sodium to pump
…..contraction
• Relaxation (diastole): As result of Ca++ calcium out through the Na+/Ca++
removal. exchanger => leads to increase in
 Ca++ removed By:
 re-uptake by SR (SERCA) intracellular Ca++ =>enhanced
 Extrusion by Na+-Ca++ exchanger contractility.
 Ca++ pump (to limited extent)
Cont.…
The Cardiac Cycle
• Frank-Starling Mechanism-
Although the right and left side of the heart are separated
extra amount of blood flows
from each other, they work together.
into the ventricles, the cardiac
 The blood is squeezed through the chambers by a

contraction of heart muscles, contraction beginning in muscle is stretched to a greater


the atria, followed by a contraction of the ventricles.
length. This stretching in turn
• This active phase is called the systole, and in each case
causes the muscle to contract
it is followed by a resting period/filling period known as

diastole. with increased force.


•This sequence of the heart relaxation & contraction is

called the cardiac cycle.


Phases of cardiac cycle

• The cardiac cycle involves 4 major


stages of activity:

1) Period of filling

2) Isovolumic contraction

3) Period of Ejection

4) Isovolumic relaxation
Definitions of terms
Regulation of the heart pumping

Innervations of the heart


Sympathetic  all parts of the heart.

 Parasympathetic (from vagus)- mainly:


 SA node
 Atria
 AV node
 No Ventricular innervations.
 Strong stimulation of vagus
has no effect on ventricles
(Vagal escape or Ventricular escape).
Cont.…
• Sympathetic & Parasympathetic effects
Receptors in CVS
Parasympathetic (vagal): cholinergic
Sympathetic: Adrenergic Heart:
 Heart: Ach binds to pre junctional
NE (NA) binds to adrenoceptors in the
muscarinic receptors (M2 ),
heart (affinity : β1 > > β2 and α1)
inhibit NE discharge.
Produce positive inotropy, chronotropy,
and dromotropy.
Ach also binds to post junctional
 Blood vessels: M2 receptor to decrease Inotropy,
 α-adrenoceptors – vasoconstriction chronotropy & dromotropy.
(affinity : α1 > > α2)
• Blood vessels:
 β2 adrenoceptors - vasodilatation
 M2 Ach-R - vasodilatation
Cont.…
The Normal Electrocardiogram (ECG)

• ECG: Electrical impulse of heart recorded on the surface of body.

• It is a record of overall spread of electrical activity through the heart


Cont.…

Difference b/n AP and ECG


AP one electrical event in a single cell

ECG is summed electrical activity of all

cells

AP recorded using intracellular electrode

ECG recorded from surface of body


Cont.…
Information obtained from ECG
 Anatomical orientation of the heart

 Relative size of chambers

 Origin of excitation

 HR=1/cycle length

 Rhythm and conduction disturbance

 Extent, location and progress of ischemic


damage
 Electrolyte disturbance

 Influence of drugs
Cont.…
• Electrodes- conductive pads used to
detect small electrical changes due to
cardiac muscle depolarization and
repolarization.

• Actual recording sites are arms legs


and the chest.

• Conventionally, 10 electrodes are placed


on patients limbs and the chest surface.

• The Right leg is always a reference


electrode ground (earth).
Cont.….
Cont.…  Categorized in 3 groups :
• LEADS: any pair of electrodes which helps to
• Limb leads (I,II,III)
measure electrical potential difference b/n 2
• Augmented Limb Leads
corresponding locations of attachment.

• The 10 electrodes will be connected in such away (aVR, a VL, aVF)


forming a 12 lead ECG. • Pericordial Leads (V1-V6)
• The overall magnitude of the heart’s electrical
potential is measured in 12 different angles and
recorded as a period of time.
Cont.…
Limb Leads

• One limb is connected to the negative


terminal of the electrocardiograph, and the
second limb to the positive terminal.

• Leads I, II and III are called the limb


leads.

• The limb leads form the points of what is


known as Einthoven's triangle.
Augmented Limb Leads

• In this type of recording, two of the limbs


are connected through to the negative
terminal of the electrocardiograph, and the
third limb is connected to the positive
terminal.

• Is known as the Lead augmented vector:


aVR, aVL, aVF lead.
CHEST LEADS (PRECORDIAL LEADS)

• Often ECGs are recorded with one electrode

placed on the anterior surface of the chest

directly over the heart at one of the points

shown
Cont.…

• Chest electrode connected to the positive


terminal of the electrocardiograph, and the
negative electrode, called the indifferent
electrode, is connected to the right arm, left
arm, and left leg all at the same time

• Usually six standard chest leads are recorded,


one at a time, from the anterior chest wall, with
the chest electrode being placed sequentially.

• The different recordings are known as leads V1,


V2, V3, V4, V5, and V6.
ECG Conventions

• Voltage Vs time graph will be formed from the electrical activity detected using
electrodes on the skin.
• ECG is recorded from specific sites of the body in graphic form relating voltage (vertical
axis) with time (horizontal axis).
1. Right leg  ground (earth)
reference electrode
2. Recording points  wrist,
ankle, skin on chest
3. 1mV input→10mm deflection
4. Paper speed  25mm/sec.
Cont.…
Cont.…
Cont.…
Cont.…

Deflections in the ECG correspond to electrical events in the heart

1) The AP begins within the SAN


 The mass of the SAN is too small so no contribution in the ECG
2) AP propagate across the atria.
 The first electrical signal on a normal ECG originates from the atria and is known as
the P wave.
 The sum of the electrical signals from the two atria, representing atrial
depolarization
 The duration of the P wave indicates the speed of propagation of action potentials through
the atria.
Cont.…

3) The AP reach the AVN


• A short, physiological delay AVN slows the electrical depolarization before it proceeds
to the ventricles.
• This delay cause the PR segment, a short period where no electrical activity is seen on
the ECG (a straight horizontal/‘isoelectric’ line).
 PR segment - Represents AV node delay (between the end of the P wave and the start of
the QRS complex).
 PR interval- Represents atrial depolarization+ the AVN delay (from the onset of the P
wave to the start of the QRS complex)
 The normal PR interval is between (0.12-0.20s) in duration (3-5 small squares). ( > 200 ms, first degree
heart block).
Cont.…
Cont.…
4) Propagation of AP to ventricles thru His Purkinje system
• Results in the largest ECG signal (greater muscle mass) known as the QRS complex.
• Ventricular depolarization
 ST Segment=> Interval between ventricular depolarization and repolarization (end
of the S wave and the beginning of the T wave)
 Q-T Interval=> beginning of the QRS complex to the end of the T wave
(Representing ventricular depolarization + ventricular repolarization).
Cont.…
5. Repolarization of ventricular muscle mass => T- wave
 The T wave in most leads is an upright deflection of variable amplitude and duration

6. U-wave: is a small rounded upright wave following the T wave.


o Mostly seen in slow HR.

o Represents repolarization of Purkinje fibres.


Summary
Cont.…
Heart sounds Third heart sound (sometimes)-due
NORMAL HEART SOUNDS
to rapid ventricular filling
• Heart sounds are associated (usually)
Fourth heart sound (occasionally)-
with valve closure
during atrial contraction.
First heart sound -Closure of AV valves
 Third and fourth sounds occur
(at beginning of Isovolumic contraction)
Second heart sound- Closure of normally in children (abnormal in
Semilunar valves (at end of ejection/ at adult)
onset of diastole)
- Sometimes splitted, since Aortic valve
closes slightly before Pulmonic valve
Pathological heart sounds

 Heart murmurs are sounds such as whooshing or swishing made by turbulent blood
in or near your heart (may be normal when flow increases) or valvar disease

 Diagnosed by

 The time they occur in cardiac cycle (systolic vs diastolic)

 The changes in intensity over time (shape)

 Auscultation site where they are best heard (A,P,T,M)

 The type of valvular disease (Stenotic vs Regurgitation)


Cont.…
• The type of valvular disease :Can be due to:-Regurgitation or Stenosis

 Stenosis: - narrowing

- Swish sound= murmur

 Regergitations (Insufficiency, incompetency)

-valve does not close properly

-whistle sound = murmur


Cont.…

 The time they occur in cardiac cycle (systolic vs diastolic)

 Systolic murmurs: Murmur throughout systole

• Can be due to: Regurgitation ( MV, TCV) or Stenosis (AV, PV)

 Diastolic murmurs: Murmur throughout diastole

• Can be due to: Regurgitation ( AV, PV) or Stenosis (MV,TCV)


 Timing of murmur indicate which valve damaged

 Eg. Mitral insufficiency regurgitation of blood into left atrium during ventricular systole
associated murmur between 1st and 2nd heart sound.
The Heart Rate and its regulation

• Heart rate: The number of heartbeats per unit of time.

• Is based on the number of contractions of the ventricles.

• Can be affected by different factors: physical exercise, sleep, anxiety, stress, illness,
drugs etc.…

• The normal resting Adult human HR ranges from 60-100bpm.

• For Endurance Athletes =33-50bpm. (Bradycardic, WHY?)

• Slow HR(<60bpm) is called bradycardia.

• Fast HR(>100bpm) is called tachycardia.


Regulation of the HR
• While the rhythm entirely is regulated by SA node under normal conditions

• HR is controlled by the sympathetic and parasympathetic input to SAN.

• Stimulation by SNS accelerates the HR while PSN stimulation slows it down.


The cardiac out put in normal and in failing heart

Defn = Liters of blood pumped trough the CVS per min

CO (L/min)= HR (beasts/min) x SV (L/beat)

• SV: volume ejected from either ventricles during each beat, depends on venous return,
can be equal to venous return

• CO (at rest) = 5-6 L/min (HR=72 beats/min , SV=0.07L/min (70ml))

• All blood pumped around circuit once each min.

• CO increases when need be (eg. Exercise), Therefore, HR or SV or both can increase


• CO decreases in heart failure
Factors influencing CO

 Intrinsic:

Venous filling pressure(preload)

 Aortic pressure (afterload)

 Extrinsic :

Parasympathetic

 Sympathetic effects
Cont.…
Ejection fraction(EF)

• EF=Measurement of ventricular performance

• Is fraction of EDV ejected from ventricles

EF= SV/EDV

A healthy man has EF of 50% or more

• Is primary clinical index of contractility


Cardiac index

• Adequacy of cardiac out put(CO) considered in relation to tissue metabolic


demand, which varies by body size and activity

• Thus, CO expressed relative to body surface area (BSA) as Cardiac index (CI)

• CI= CO/BSA

CI= cardiac index (L/min./m2)

CO= cardiac out put (L/min.)

BSA= body surface area (m2)

=3.8 L(male), 7-10% less in female


The Circulation
• Components of Circulatory System
Cont.…
Functional parts of the circulation

The distribution channels


2. Arteries … (muscular, low resistance vessels)
• Control distribution of the blood/blood flow (Q) &
 Less elastic & have a thicker layer of smooth ms.
BP by adjusting their luminal diameters as their walls

actively contract or relax.  Diameter changes slightly as BP raises & falls.

1. Aorta … (elastic recoil)- the largest 3. Arterioles … (high resistance vessels)

artery in the body (Numerous layers of  Contain highest %ge of smooth muscle.

elastin fibers b/n smooth ms.)  It Expands less under pressure (less compliance).

 Expand when the pressure of the  Called resistance vessels (greatest resistance to flow).

blood rises.
 Act as recoil system when ventricles
relax.
 Micro-vascular network (Capillaries): Exchange systems

• Smallest blood vessels/(exchange vessels)

• Has single endothelial cell thickness.

• Provide direct access to cells.

• Permits exchange of nutrients & wastes.

From arterioles, blood enters, the capillaries


and post capillary venules.

 These vascular segments are under low

pressure & their walls allow O2 & CO2,

nutrients & metabolic products, hormonal


discharges etc. to pass back & forth between
tissues & vascular segment.
 The Blood reservoirs

• Are blood reservoirs and return of blood to the


heart
1. Venules
 Formed when capillaries unite.
 Very porous.
2. Veins … (capacitance vessels)
■ Contain little smooth muscle or elastin.
 Capacitance vessels (blood reservoirs).
 Contain 1-way valves that ensure
blood flow to the heart.
■  2/3 of total blood volume is located in
veins ( 60-70%).
3. Vena cava
Summary
The coronary circulation

• The circulation of blood in the blood


vessels that supply the heart muscle

• The heart receives its own blood from


the coronary arteries

• Coronary arteries supply


oxygenated blood to the heart muscle
and cardiac veins drain away the
blood once it is deoxygenated.
Biophysics of blood flow (Hemodynamic)

• Hemodynamic: the general term • Biophysics of BF: focuses on the


referring to the movement/flow of biophysical aspects of BF
blood in the body (The flow of  Includes the arrangement and the
blood through the vessels) characteristics of the blood vessels
 Specifically, the measurement and
the general principles governing
the BF in the human body.
Cont.…

• BF is dependent on many factors.

• Blood flow (Q) determined specially by 2 factors:

1. Pressure difference (P)


2. Vascular resistance (R) acting along blood vessels.
• The flow through the vessel can be calculated by the following formula, which is
called Ohm’s law:
Cont.… 2. Vascular resistance (R) acting along
1. Pressure difference (P) blood vessels.

• Q depends on pressure gradient (P), P1-P2 • R= measure of friction between

•  Blood vessel & moving fluid.


Flow(Q) from high pressure to low
pressure.  Fluid molecules within themselves
Summary
Cont.…

Blood flow Vs blood flow velocity


• Flow = volume/time
• Velocity = distance /time
 Rapid flow velocity = aorta

(smallest cross-sectional area)


 Slowest flow velocity =

capillaries

(largest cross-sectional area)


Types of blood flow

1. Laminar flow
• Normal and noiseless

• All elements of the fluid move in a stream line, that


are parallel to the axis of the tube

• No fluid move in radial or circumferential direction

• Layer of fluid in contact with the wall is motionless


(thin layer, adherent to wall, hence motionless)

• Fluid that move along the axis of the tube has


max.Velocity
2.Turbulent blood flow
• Various elements of fluid move irregularly in
axial, radial and circumferential direction

• More pressure required to drive blood than


laminar

• Energy wasted in propelling blood radially


and axially

• Often accompanied by noise(murmurs)

• Occur at valves and aorta(normal), at site of


blood clot(pathological)
Summary
Arterial system: The arterial BP and its control

• Arterial BP- Pressure exerted by circulating blood upon the walls of blood vessels
in millimeters of mercury (mmHg).

 During each beat: BP varies between maximum (systole) & minimum (diastole)
….120/80mmHg

 Average blood pressure (mmHg) increases with age.

95/65 → for 1 year

100/65 → for 6-9 years

110-140/65-90 → for Adults


Mean Arterial and Venous pressure

• MAP: the average BP in individual during


1 cardiac cycle (90 – 100 mmHg).
Cont.…
Cont.…
• Mean venous pressure: the average BP in the venous compartment
• Is only 2 mmHg (low).

Due to:
1. Pressure drop b/n arteries & capillaries.
2. High venous compliance.
N.B. Venous pressure is highest in venules (10 mmHg), & lowest at
junction of venaecavae with Rt atrium (0 mmHg).
Measurement of ABP
Cont.…
Factors influencing tissue BP and Tissue BF
ABP Control Mechanisms
Short-term control mechanisms

Predominantly vasomotor adjustment and neuronal control


 Include:

A. Baroreceptor/Stretch reflexes:
B. Chemoreceptor reflexes
C. Ischemic reflexes of CNS
• Common characteristics:
 Rapid onset of action (within few sec.)
 Response vigorous, but if activated continuously, within a few days, it either dies out
completely- (baroreceptors) or attenuated- (chemoreceptors, CNS Ischemic response)
A. Baroreceptor/stretch reflexes
 Location:
• Wall of large thoracic arteries
• Wall of cervical arteries
• Aortic arch greater functional
importance
• Carotid sinus
 Baroreceptors convey information
about:
• Mean arterial pressure (MAP)
• Amplitude of pressure fluctuation
Steepness of pressure rise rate of
pressure change
• More sensate to than pressure
(P/t)
• More sensitive to sudden change
Cont.…
• More sensitive to decrease than increase pressure → Stimulation of baroreceptors
→discharges of sensory aortic and carotid sinus nerves → vagus & glossopharyngial nerves
→centers in medulla.
Cont.…
B. Arterial chemoreceptors

• Location:- carotid and aortic bodies


(near aortic sinus & carotid sinus)
• Stimulus: decreased PO2,
increased PCO2, & H+
• Response: hyperventilation
(increased minute volume)
• Secondary effect: increased O2 delivery
to tissues (heart, brain)
• General vasoconstriction
• Increased arterial pressure
C. CNS ischemic response

· Cerebral ischemia (diminished blood flow in vasomotor center of the brain,

Or increases PCO2 which stimulates sympathetic area of medulla of brain.

· This causes increase in arterial pressure (as high as heart can pump)
· This system is emergency arterial pressure control system i.e acts rapidly
and very powerfully.
· Thus prevent further decline in arterial pressure when blood flow to
brain decreases dangerously.
· This control system is “last ditch” mechanism for blood pressure control.
Intermediate term control

 Transcapillary volume shifts in response to changes in capillary


pressure
  capillary Pressure   stress on veins  veins relax& 
pressure (stress relaxation)
  intravascular volume  opposite effect.
3. Long term control regulation (volume regulation)

• Renin-Angiotension-Aldosterone system (long-term control (RASS)


Hypertension

• High BP (SBP>=140 mmHg and DBP>= 80 mmHg)

• Can lead to increase risk of heart disease, stroke and death

• STAGES OF HYPERTENSION (Reading Assignment)

• TWO types :

1) Primary/Essential

2) Secondary
Types of Hypertension
A) PRIMARY (ESSENTIAL) HYPERTENSION

 The hypertension is of unknown origin.

 About 90- 95 % of all people who have hypertension

Treatment of Essential Hypertension.


 Lifestyle modifications that are aimed at increasing physical activity
and weight loss in most patients. (If unable to lose weight
pharmacological treatment with antihypertensive drugs must be
initiated.
Cont.…

 Cause of the hypertension is


clarified (cause is known)

Renal, endocrine, cardiovascular


diseases are main causes

Pregnancy or drugs are also


related

• 80% of all cases is due to renal


disorder
Hypotension: Low BP
Shock  Absolute hypovolemia: Blood loss, plasma loss

• Def. General circulatory insufficiency (fall in arterial - Dehydration (water deprivations severe diarrhea, or
vomiting excessive sweating, intestinal obstruction with
pressure, inadequate tissue perfusion), associated by
luminal fluid accumulation, urinary loss of
rapid HR, RR, With pale, moist and grey skin, proteins/salt/water, excessive use of diuretics,

• Clinical syndrome that results from inadequate tissue hypoaldosteronism)

 Relative hypovolemia: due to Vasodilation


perfusion
- Septic shock from viral, or bacterial infection
• A condition of profound hemodynamic and metabolic
- Anaphylactic shock
disturbance characterized by failure of circulatory
- Neurogenic shock (vasodilatation by severe pain
systems to maintain adequate perfusion of vital
or stress, anesthetics or brain stem lesions close to
organs.
vasoconstrictor center.
Cont.…

• Hypovolemic Shock
• Cardiogenic shock
• Obstructive Shock
• Distributive Shock
Septic Shock
Anaphylactic shock
Neurogenic Shock
Acute adrenal insufficiency
Types of shock

1. Hypovolemic shock: a condition in which rapid body fluid loss results


in inadequate circulation and multiple organ failure.

• Causes: severe dehydration (burns -plasma loss), fluid loss in vomiting


and diarrhea or blood loss (Hemorrhage -rapid loss of blood) due to
Trauma.

• Symptoms: anxiety, confusion, decreased UOP, cool clammy skin etc.

• Management: REPLACEMENT THERAPY


Cont.…
2. Distributive shock (vasogenic/vasodilatory or low resistant shock)

• Circulatory failure caused by excessive vasodilation and/ or vasoplegia resulting


in inadequate blood supply to body’s tissues ad organs.

• Causes: vascular hypo-reactivity with reduced vascular smooth muscle


contraction in response to alpha1 adrenergic agonists

• Sign and symptoms: confusion, weak pulse, decreased UOP cool clammy skin
etc.

• Management: reverse the underline cause, stabilize hemodynamic and organ


failure from hypo-perfusion.
Cont.…
 Underline conditions of distributive shock

• Neurogenic shock- loss of vasomotor tone through out body due to sever autonomic
dysfunction, thus increasing vascular capacity characterized by hemodynamic triad
(hypotension, bradycardia, peripheral vasodilation)

• Anaphylactic shock- sever allergic reaction i.e. histamine induced to food, insect bite and
medications resulting in:

-Increase capillary permeability

-Increase vascular resistance

-Arteriolar dilation

• Septic shock- dissemination of bacterial (toxin) resulting in sepsis. This increase capillary
permeability
Cont.…

3. Cardiogenic shock: inadequate blood supply to body’s tissues and organs


caused by cardiac dysfunctions

• Causes: Inability of the heart to function properly due to different disease


conditions (Myocardial infraction, Cardiac tumor, Pulmonary embolic).

• Sign and symptoms: hypotension, tachycardia, rapid breathing, weak pulse,


pale skin etc.

• Management: medications that increase heart’s pumping activity and reduce


risk of blood clot
Cont.…
4. Obstructive shock inadequate blood supply to body’s tissues and organs
caused by Obstruction of blood vessels in systemic or pulmonary circulation
reducing blood flow.

• Cause: Obstruction of blood flow associated with Pulmonary embolism,


Tension Pneumothorax, Cardiac tumor)

• Sign and symptoms: hypotension, tachycardia, oliguria, consciousness


disturbance etc.

• Management: fluid administration+ medications that constrict blood vessels.


Stages of shock
Lymphatic system

• Almost all tissues of the body have special lymph channels that drain
excess fluid directly from the interstitial spaces.

• The exceptions include the superficial portions of the skin, the CNS, the
endomysium of muscles, and the bones.

• However, even these tissues have minute interstitial channels called


prelymphatics through which interstitial fluid can flow;

• This fluid eventually empties into lymphatic vessels and then directly back
into blood venous system
Cont.…

• Lymphatic vessels present between capillaries.

■ 3 basic functions:
 Drain excess interstitial (tissue) fluid back to the blood, in
order to maintain original blood volume.
Transports absorbed fat from small intestine to the blood.
 Helps provide immunological defenses against pathogens.
Tissue fluid formation and drainage, EDEMA

• When lymphatics system fails to function, excess fluid accumulates in the extracellular
spaces and the condition known as edema occurs.

• There are two general causes of extracellular edema:

(1) Abnormal fluid leakage from the plasma to the interstitial spaces across the capillaries

(2) Failure of the lymphatics to return fluid from the interstitium back into the blood
(lymphedema).

The most common clinical cause of interstitial fluid accumulation is excessive capillary
fluid filtration.
Causes of Edema
References
1. Guyton and Hall Textbook of Medical Physiology by Hall, 13th Edition,
2016.

2. Ganong’s Review Medical Physiology by Kim E. Barrett et al., 25th


Edition, 2016.

3. Medical Physiology by Rhoades et al., 4th Edition, 2013.

4. Berne and Levy Physiology by Koeppen and Stanton, 7th Edition, 2018.

5. Medical Physiology by Boron et al., 3rd Edition, 2017.

6. Vander’s Human Physiology: The Mechanism of Body Function by


Widmaier et al., 14th Edition, 2016.
11/18/2024 General introduction and cell physiology 119

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