Physiology Summary

First Year

By

Dr. M. Fayez

Lecturer Physiology
Ain Shams University
2017
 : ‫ صفحة فقط ويشمل‬178 ‫ملخص لكل أجزاء النظري في‬

1) Autonomic: 9 pages

2) Nerve: 4 pages

3) Muscle : 15 page

4) Blood: 16 pages

5) CVS: 83 pages

6) Respiration: 35 pages

7) Biophysics: 9 page

8) Biostatistics: 8 Pages

9) Collection: 8 pages
Autonomic

1
2
3
4
5
6
7
8
9
10
Nerve

11
12
13
14
15
16
Muscle

17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
Blood

1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
Cardiac

1
 CVS ‫ يحًذ فايس‬/‫د‬

Function
Characters of vessels

Homeostasis Temperature
Communication Aorta Capillaries Veins
regulation Arteriole

Elastic Smooth
fibers muscles Thin
(wall) wall
Capacitance

V
:ُٗ‫انًؼ‬
C= P ‫يًرهٗء تاكثش دجى دو‬
ٍ‫تالم ظغط يًك‬ Windkessel Resistance Exchange Capacitance
MCQ
Function
Stopcock
54% blood (vein) : ‫انذنيم‬
)‫(يذثظ‬

2
 CVS ‫ يحًذ فايس‬.‫د‬

Arrangement Portal vessel

Brain Hypothalamus
Series Parallel

Capillaries
Blood moves in
serial manner from Aorta Upper
Limb
Heart  Aorta  Arteriole  Capillaries  Vein

Lower
Limb Post pituitany

Parallel Homeostasis Blood flow

Capillaries
Arrangement ًٗ‫يؼُاْا انؼه‬
 Resistance Perfusion

3
 CVS ‫ يحًذ فايس‬.‫د‬
P1 Flow (F) P2

F=  P/R  Resistance
Intermittent
(LV  Aorta)
Vessels Aorta (93 mmHg)  Arteriole (32 mmHg)
 Capillaries  veins (10 mmHg) 
Types Velocity
Right atrium (0 mmHg)

High Pressure
Pulsatile Steady Rapid Slow
Ventricles (Systole)
+
Capillaries Veins Aorta Capill. orta
rteries
rterioles
rterial side of capillaries

Velocity  1/CSA Low Pressure

Atria + ‫انؼكظ‬
Pulmonary circulation

4
 Cardiac Anatomy ‫يحًذ فايس‬/‫د‬

Atrial muscle Valves

A-V ring

A-V Semilunar Cardiac Electric

Push Restrict
blood )‫(يًُع‬ Skeleton insulator
from atria Back flow
Mitral Aortic
of blood
from atria LV, Aorta
Ventricle LA, LV

Vena cava Pulmonary

Tricuspid
RV, pulmonary
Allow atria
RA, RV
to
finish
contraction
Uni direction ‫أٔال‬
flow only

5
 Cardiac Anatomy ‫ يحًذ فايس‬/‫د‬

Ventricular
muscle

Wall Papillary
muscle

Chorda tendinae

A-V Valve

‫األهًيح‬

Prevents AV Valve
to be forced into
atrium

Epicardium prevents Incompetence

(Regurge)

6
Cardiac Anatomy ‫ يحًذ فايس‬/‫د‬

Visceral
Pericardium
Layers
Parietal

Prevents acute
Fix Lubricate distension of heart

Pericardium

Left ventricular
ّ‫إرا صاد فيّ انًي‬ aid
(Effusion) LV compress IV septum VS
Rv Wall →RV pump
Tamponade ‫إخرُاق‬ ‫ال يىجذ انعكص‬ )RV ً‫(هاو ارا حذز فشم ف‬

 Filling

7
 ‫ يحًذ فايس‬/‫د‬

Fast Response Slow response

Phase 4 Stable RMP Unstable (Prepotential)

Cause K+ efflux > Na+ influx = Diastolic depolarization

Early: Na+ influx > K+ efflux

Late: Ca++ influx (T-channels)
Value -90 mV - 55 mV
Depolarisation
Phase 0
Cause Na+ influx (voltage gated Na+ channels) Ca++ influx (L-type Ca++ channels)

Firing level - 70 mV (Peak: +30 mv) - 45 mV (Peak: +10 mV)

Phase 1 Open voltage gated k+channels ------------

Repolarisation

Phase 2 Early: ca++Influx = K+ efflux

(platau) Late: Na+ influx = K+ efflux ----------------

Phase 3 Open voltage gated k+ channels

8
 Refractory Periods ‫ يحًذ فايس‬/‫دكرىر‬

Fast Response Slow response

Shorter Longer → Start phase 4

Refractoriness
(post repolar. Refractoriness)

ARP Time Phases (0, 1, 2, upper 1/2 (3)) Safety against tetanisation Phase (0) → 2/3 phase (3)
Significance
Voltage dependent refractoriness

ARP Time Lower 1/2 (phase 3) Partial recovery of fast Na+ Late 1/3 phase (3) → start phase (4)
Significance channels Pathological importance of AVN (2)

ERP Time ARP + 1st 10 mv of RRP → 60 mv

Significance
As ARP + cardioversion ‫ـــــــــــــــــــــــــ‬

(2000-3000 volt) in V.F (‫ نطثيعره‬SAN ‫)انهذف انغائه حرً يرجع‬

Supernormal
period
Short at end of phase (3), start phase (4(
Time
Significance Propagated AP → ↑ excitability

9
Relation between Fast response, ECG ‫ يحًذ فايس‬.‫د‬

Upper half of
(1) phase (3)
(2)
Lower half of
(0) phase (3) Vulnerable period
Lower 1/2 phase 3:
(4) Ectopic ‫يًكٍ اٌ يظٓش فيٓا‬
(4)
(Some fibers depolar./others repolar)
R

Q
S

QRS complex S-T Segment T-wave

Coincide with Coincide with
Upper 1/2 Lower 1/2
phase 0 "Depolar." phase 2 "Plateau"
Coincide with
Upper 1/2 phase (3) Lower 1/2 phase (3)

10
 SAN ‫ يحًذ فايس‬.‫د‬
RMP = Phase 4 = Prepotential = S S D D SAN is Normal Pacemaker
Slow Diastolic
Spontaneous Depolarization
Slope
Highest Discharge
Repolarized
Low Amplitude
Firing level

 SAN firing  SAN firing

Nervous Sympathetic Parasymp.

Sympathetic Parasympathetic
Ions Hypocalcemia Hyperkalemia calcemia

drenaline Muscarine
Na+ inward

++
c.AMP  Open L-Ca Channels
Na+ inward

c.AMP
Drug
A tropine -Blockers

Temperature Warming Cooling

K+ efflux K+ efflux

11
 Conductivity
Highest rate

Highest slope SA node

Pacemaker
AN → Maximal Delay
N → Slowest conduction
ً‫ عشيؼا‬Reach firing
AV node NH

A) Physiological
Beats/min Right
AV Bundle
SAN AVN Purkinye Delay impulse conduction in
Left
atria 0.1 second
90 60 30 4-5m/sec Purkinje fibers B) Pathological
Rich in Gap 1- Protect ventricle from atrial ectopic
Junctions Ventricular wall focus ‫صذيخ‬ ‫ٔانؼكظ‬
(Slow conduction) 2- 180-200 bpm/min ٍ‫ال يغًخ تًشٔس أكثش ي‬
Interventricular septum (Voltage, time refractoriness)

1st part to be depolarised in ventricle 3- Post repolarization refractoriness

Base of LV: Last depolarised

12
 Factors Affecting Contractility ‫ يحًذ فايس‬.‫د‬

Intrinsic Extrinsic

Preload Afterload Force Inotropic ‫أَظر انصفحح انقاديح‬

frequency state

Def.: ‫انمهة يًرهٗء‬ Def.: Healthy myocardium

Contr. ‫تانذو لثم‬ Resistance Vs Stair-case
Starling law ‫أركش‬ which blood is phenomena Intracellular Ca++
expelled
Parallel elastic element

Faced by
Redundant
(Stretch ‫)يمأو‬
Iso Iso
Muscle developed tension
metric tonic
=
S D
Cont.

13
 Extrinsic Factors Affecting Contractility ‫ يحًذ فايس‬.‫د‬

Nervous Hormonal Drugs Ions

 Hypercalcemia
Sympathetic Parasymp. Thyroid Increase Decrease
Insulin
Ca++ rigor
‫انعكص‬ Glucagon
Ca++ channel  Hyperkalemia
Bind to Channels Digitalis blocker
1 receptor e.g.
+ +
Inhibit Na - K Adalat
Stop heart in
Open Close pump .
++ diastole
Ca K+
 c.AMP (L-type)  Na+ intracellular

Keep Ca++ inside

 Force – Frequency relationship
Na+/Ca++ exchanger ‫ال يؼًم‬
)‫(يفيذ جذًا فٗ ػالج فشم انمهة‬

14
 Einthoven Triangle ‫ يحًذ فايس‬.‫د‬

Final Einthoven  ECG ‫فكرج تذايح‬

(a) (b) (a) (b)

(c) (c)

‫ َقاط‬3 ‫ذى ذغيير‬ ‫يًكٍ ذطجيم كهرتاء انُاذجح يٍ انقهة‬ :‫أضاش فكرج رضى انقهة‬
 Final Einthoven : :‫ َقاط‬3 ٍ‫الَه يقع عهً اتعاد يرطاويح ي‬ Axis of heart is directed
a) Rt arm. a) Rt shoulder. downward, to left
b) Lt arm ‫يعظى انىصالخ‬ b) Lt shoulder.  Einthoven 
‫شًال‬ c) Symphysis pubis.
c) Lt foot ‫يعظى انىصالخ َاحيح انشًال‬

15
 ECG Leads ‫ يحًذ فايس‬.‫د‬

Bipolar Unipolar
%50 ‫صىرج يكثرج‬
ً‫زيادج عٍ انطثيع‬
Chest Augmented
I II III
V1: 4th right I.C space aVR aVL aVF
VR-VL VR-VF VL-VF
V2: 4th left I.C. space
aVR
V3: V2, V4 ٍ‫تي‬

V4, V5, V6 ‫ انزٖ يغجم انكٓشتا‬Electrode

Right ‫َاحيح‬
5th Left I.C ‫كههى‬
ٍ‫ٔنك‬
‫انفشق‬
‫ فٗ انمهة‬impulse ِ‫اذجا‬
V4: Mid clavicular line Left ‫َاحيح‬
V5: Ant. axillary line ‫نزنك‬

V6¨Mid Axillary line

‫سعى انمهة كهه يقهىب‬

16
 Unipolar Lead
L
R

Indifferent
(0) Exploring
F
Resistance

‫) ذطاوي صفر‬In different( ٖ‫) أيا انُمطح األخش‬Exploring( ‫ يؼُاْا أعجم انكٓشتا ػُذ َمطح ٔادذج‬Unipolar lead
Indifferent = (R – L) + (L – F) + (F – R) = 0
‫ انكهرتا عُذها ذطاوي صفر‬،‫ال ذىجذ َقطح فً جطًك‬

It can be applied only by high resistance (5000 ohm) to be indifferent

Limb (unipolar Limb Lead)

Exploring electrode
Chest (unipolar chest Lead)

17
 Normal ECG ‫ يحًذ فايس‬.‫د‬

Waves Segments Intervals

Atrial Isoelectric
Depolar. P-R Q-T T-P
P QRS T

Ventricular AV Electric Electric

Repolar. conduction systole diastole
Postero
Septal basal
of P-R S-T T-P
LV
Apex,
wall
of
ventricles A-V Both ‫َهايح‬
nodal ventricles Ventricle
conduction depolar. repolar.
ٗ‫ف‬ ٔ
Ventricular ‫َفظ انٕلد‬ ‫قثم تذايح‬
depolarisation Atrial Depol.

18
 ECG Notes ‫ يحًذ فايس‬.‫د‬

Not recorded Waves

SA node Atrial repolarization

+ve -ve

Direction Direction
Small Masked by to to
left right
Muscle mass Ventricular depolarization
with against
)‫(جاء فٗ َفظ انٕلد‬

Axis
T wave in same direction as
QRS Complex
‫هــاو‬
Duration ‫حفظ‬

1st part depolarized ‫اخرــالف‬ of

is ٗ‫فــ‬
Last part repolarised Charges Waves Segments Intervals

19
 Proof: Augmented Unipolar Leads = 50%  Unipolar Lead ‫ يحًذ فايس‬.‫د‬

avR avL

avF

VL + VF)
avR = VR – ( )
2
 2 avR = 2 VR – (VL + VF)
 VR + VL + VF = Zero (Kirchhoff's 2nd law)
 (VL + VF) = - VR
 2 avR = 2 VR – (-VR) = 3 VR
 avR = 3/2 VR

20
 Notes on ECG ‫ يحًذ فايس‬.‫د‬

Atrium Ventricle

Endocardium Epicardium Endocardium Epicardium

Depolarised 1st Last 1st Last

Repolarised 1st Last Last 1st

Premature atrial contractions not followed by compensatory pause

Premature ventricular contractions followed by compensatory pause

21
 Cardiac Axis ‫ يحًذ فايس‬.‫د‬

Calculation Value

Normal Deviation

-- 30°  + 100° Right Left

Value Causes
> + 100°

Left axis deviation Physiological Pathological

Value Causes Tall, thin Rt BBB

> - 30° person
Lt Ectopic
Physiological Pathological focus
Lt Ventricular
ٍ‫ طخي‬، ‫لصيش‬ (Rt ‫)ػكظ‬
extrasystole

22
 Classification of Arrhythmia ‫ يحًذ فايس‬.‫د‬

Disturbed Impulse Disturbed Impulse

Formation Conduction

Sinus Ectopic No Short Prolonged

‫أَظر انصفحح‬ Beats Tachycardia SA block WPW

‫انقاديح‬

Atrial Ventricular
AV block BBB

PAC PNC PVC

Atrial Ventricular

PAT Flutter Fibrillation PVT VF

23
 Sinus Arrhythmia ‫ يحًذ فايس‬.‫د‬
Respiratory sinus
Sinus Tachycardia Sinus Bradycardia
arrhythmia
 (Inspiration)
Heart rate >100 bpm <60 bpm
 (Expiration)
1. Sympathetic 1. Vagal tone Inspiration

Stretch receptors
2. Regulation of  BP 2. Regulation of  BP (Lung)

Causes
3. Hyperthyroidism 3. Hypothyroidism  CIC

4. Fever 4.  blockers  Vagal tone

 Heart rate

N o r m a l
ECG Short c. cycle
(Inspiration)
Short c. cycle Long c. cycle ‫ٔانؼكـــظ‬
(Expiration)

24
 Ectopic Focus ‫ يحًذ فايس‬.‫د‬

hat ? Strong Stimulus

here ? AV node/Septum/wall
hy ? Inhibits SAN (over drive suppression)
hen ?

RRP ‫يثذأ‬ ARP ً‫يُره‬

1
Atrial Re-entry (Circus)
‫تذايح‬

‫أَظر انصفحح انقاديح‬

1 Slow
Conduction
Ventricular
>1 ‫ يضداد ػذدْا‬ ‫ ذؼٕد نُمطح انثذايح فررجذد‬ ARP ٗٓ‫درٗ يُر‬

25
 Ectopic beats ‫ يحًذ فايس‬.‫د‬
PAC PNC PVC (V. extrasystole)
Origin AV node 1) His-Purkinje
2) Ventricular wall
E C G
ً‫ذخرفــ‬
P wave A b n o r m a l
Before After
PR interval Short Short or absent

QRS complex Normal Normal 1. High voltage

2. Wide prolonged (Bizarre)

Compensatory Un common Common

pause ‫تؼذْــا‬ ‫تؼذْــا‬
T wave Normal Normal Inverted
Axis Normal Normal ‫يُذشف نهُاديح انؼكغــيح‬
Premature: weak
Pulse Weak
Post extrasystole: strong

26
 Ectopic Tachycardia ‫ يحًذ فايس‬.‫د‬
PAT PNT PVT A. flutter A.F V.F
1. Ectopic
Cause 2. ‫صذيح كٓشتيح‬
3. Ischemia
Heart rate: Heart rate: Heart rate: A. Rate: A. rate: Vulnerable
250-350 350-500 period:
140-220 150-220 150-250
V. rate:125-175 V. rate:100-150 Coincide which
Character-
‫دائًا ذذذز فٗ انشاب‬ ٍ‫صؼة ذفشلٓا ػ‬ ‫ال٘ ٔجذ أٖ دلاخ‬ Rhythm: Rhythm: mid part of
ised by
rregular T wave
‫انغهيى‬ PAT ‫طثيؼيح فيًا تيُٓا‬
Regular
Irregular
Irregular

E C G
P Abnormal ٗ‫ذخرــف‬ 2:1 / 3:1 (F wave)

Bizzar
Slurred, Notch,
QRS Normal
Wide
Normal
Opposite to
T Normal Normal
QRS
Contraction Synchronus A synchronous (Bag of worm)
Serious
Seriousness Not serious Serious  VF Not serious
)‫(يًيرح‬
 Vagal Tone
Treatment Cardioversion As PAT, PNT As PVT
Carotid Oculo-cardiac
Massage reflex

27
 Disturbance in Impulse Conduction ‫ يحًذ فايس‬.‫د‬

Systolic Systolic Systolic

SA block = WPW AV block BBB

Sick sinus $

Cause Types

Accessory bundle of Enters His bundle Inserted in V. 1st degree 2nd degree 3rd degree
kent bypass AVN myocardium
reduces AV delay
PR interval P/QRS:
Normal P > 0.2 sec 2:1/3:1
AV block causes Short PR

Purkinje (Pace maker) 

AVN AV bundle ‫ عهيًح‬QRS Prolong. QRS
Short PJ ‫ عهيًح‬PJ Idiovent. Rhythm (35-45 bpm)
 Stocks – Adam $
schemia car
I nflammation S urgery

28
 Effect of Ions on ECG ‫ يحًذ فايس‬.‫د‬

Na+ K+ Ca++

Hypo Hypo Hyper Hypo Hyper

QRS PR interval: QT interval

‫انؼكظ‬
Amplitude Prolonged Prolonged

Low T wave

1st Change >8 mEq/L

Atrial standstill
Tall, Peak T AV block V.F
Re-entry

29
 Cardiac Cycle ‫ يحًذ فايس‬.‫د‬
Atrial Isovol. Maximum Reduced Proto Iso vol. Rapid Slow
systole contraction ejection ejection diastolic relaxation filling filling
Atrial Pr. Increased (VR) No change
Ventricle Slow
Constant Constant
Vol.
Ventricle
Slight
Press.
Aortic ‫تذايح ثى يمم‬
Press.
CBF
Open (A-V)
Open: Semilunar Open: A-V
Valves Close Semi All closed All closed
Close: A-V valves Closed: Semilunar
lunar
Heart
`4th 1st 1st - - 2nd 3rd -
sounds
P-wave * Q-wave
before ST segment 1st ½ T- End T-wave
ECG before T-P segment
(0.02 sec) T ‫تذايح‬ wave TP segment ‫تذايح‬
(0.02 sec) * QRS

30
 LV Pressure Volume Loop ‫ يحًذ فايس‬.‫د‬
Points
A B C D
Valves MVC AVO AVC MVO
Lines
AB BC CD DA
Significance Phase of Isovolumetric Rapid, Reduced Isovolumetric
Rapid, slow filling
1. Area under curve = SW c. cycle contraction ejection relaxation
Ventricular
= SV X MAP Constant Constant
volume
2. BC represents SV
3. DA represents ventr. Filling. Rapid ejection Rapid filling
4. RV pressure volume loop (as LV) Ventricular  (80-120 mmHg) ‫يمم درٗ يصم صفش‬
(Systolic RV pressure: 25 mmHg) pressure Slow filling
Reduced ejection
5. Heart failure: ‫يمــم‬  up to (5-8 mmHg)
Contractility curve (Shirt to Rt)

31
 Heart Sounds ‫ يحًذ فايس‬.‫د‬

Audible by stethoscope Audible by phonocardiogram

3rd 4th
1st 2nd
Very low pitch

Rapid filling Atrial systole

L S
ub hort
ugmented 3rd, 4th sounds
ong
ow pitch
emilunar valve closure
econd A udible by stethoscope

Cause of S1 Costo sternal junction Left intercostal space Gallop rhythm

‫(ذغًغ انصٕخ كأَّ خطٕاخ‬

V
asculohaemic Pulmonary Aortic
ibrations ٗ‫رجم انحصاٌ ُْٔا يذذز ف‬
)LV failure
A-V valve closure
Muscle itself

32
 Splitting of heart sounds ‫ يحًذ فايس‬.‫د‬

1st 2nd

Physiological Pathological Physiological Pathological

‫يغًغ انصٕخ‬ ‫يذذز انؼكظ‬ ‫يغًغ انصٕخ‬ ‫يذذز انؼكظ‬

ٌ‫كأَّ صٕذيٍ أل‬ Cause: ٌ‫كأَّ صٕذيٍ أل‬ Cause:
Mitral valve closes Mitral stenosis Aortic valve closes Aortic stenosis
before tricuspid before pulmonary
LV failure

Cause:
Than splitting of S1
Inspiration   VR to
Physiological splitting 'S2' Easy heard Pulmonary area
RV  Delay closure of
Children
tricuspid valve

33
 Murmurs ‫ يحًذ فايس‬.‫د‬

Systolic Diastolic

Stenosis Regurge Stenosis Regurge

Aortic Pulmonary Mitral Tricuspid Mitral Tricuspid Aortic Pulmonary

Systolic Time Intervals

QS2 LVET PEP QS2 - LVET

Normal: 0.35
QRS 2nd H.S  Carotid press.
complex
Measure LV Function
Dicrotic notch

34
 Arterial Pulse Wave ‫ يحًذ فايس‬.‫د‬
Anacrotic Catacrotic Dicrotic notch Dicrotic
limb limb (Incisura) wave
Aortic pr.    

Opening of Less vibrations Sudden Aortic

Cause
Aortic valve Set up in Aorta AVC Elasticity
Phase of Maximum * Reduced ejection ‫َٓـايــــح‬ Iso vol.
c. cycle ejection * Ventricular diastole Protodiastolic relaxation

Notes
Factors affecting

Pulse wave Pulse volume

Rate Periphery

Elasticity Strong Weak

4-8 16 ً‫ال يعرًذ عه‬ ‫ذثذأ‬ ٗ‫يؼه‬
if decreased (Aorta) (Artery) Blood flow Notch Anacrotic
(Atherosclerosis)
A therosclerosis
.I
‫َضيف‬
‫يرأخشًا‬ ‫يرأخشًا‬

 Conduction

35
 Jugular Venous Pulse (JVP) ‫ يحًذ فايس‬.‫د‬

"a" wave "c" wave "x" descent "v" wave "y" descent
Wave + + - + -
Atrial ms contract
Down ward VR Opening of
Bulge of
Displacement While Tricuspid valve
Cause Tricuspid valve
of Tricuspid valve and
Atrial press. Into Rt atrium
AV ring is closed Rapid emptying
JVP
Iso volumetric Isovolumetric
Phase Atrial systole Rapid ejection Rapid filling
contraction relaxation

No  AF Note
Signif- a-c interval prolonged
Large  Tricuspid stenosis Giant
icance
Giant  3rd AV block Tricuspid regurge
1st degree AV block

36
 Definitions ‫هايــح‬
COP ‫ يحًذ فايس‬.‫د‬
* Volume of blood pumped by each ventricle

Beat Minute

COP = SV x HR SV COP

COP = (EDV – ESV) x HR * Cardiac Index = COP/SA = 3.2 L/m2

* Ejection Fraction (EF) = SV/EDV x 100 (N=55%)

EDV ESV HR
Rest 130 mL 60 mL 60-90 bpm
Exercise 240 mL 30 mL 180 bpm
o
Limited by Starling Law N of catecholamine vesicles Filling Time
Physiological ( Venous Return = VR) Physiological
1. Blood volume
2. Venous tone. Vagal Tone (-ve Inotropic)
3. Skeletal muscle contraction
4. Intrathoracic negativity Pathological ‫أَظــش‬
5. Atrial contraction HR Regulation
6. Ventricular compliance Heart Failure
Pathological (Vascular)
Physiological
Pericardial effusion Heart failure MI
Exercise
Cardiac Tamponade

37
 Cardiac Output (COP) ‫ يحًذ فايس‬.‫د‬

Filling one cycle

‫انمهة يعخ يُٓى‬ Ventricle
130 mL
SV 70 mL (EDV)
X
HR
(70)
Effects of HR variations on COP
COP

HR SV COP Notes
Physiological  Decreased
Range (EDV-ESV)

osture (Recumbent)
60-90 bpm  ‫ال يرغـيش‬ ‫ٔادذ صاد‬
Physiological Pathological
‫ٔادذ لم‬

P regnancy
ost prandial
hysical (Exercise)

Temperature
Standing Heart failure
()
100-160 bpm
()
200 bpm






‫االثُيٍ صادٔا‬

:ٍ‫فٗ انذانري‬
 ٍ‫انُمص أكثش ي‬
Hormones, Drugs (regulation ‫)أَظش‬
‫انضيادج نزنك يمم‬
40 bpm  
COP


38
 COP Measurments ‫ يحًذ فايس‬.‫د‬

Experimental Animal Human

Heart-lung Fick's Method Dye Dilution

Anesthetized preparation (Indocyanine) ‫* ذى دمٍ انًشيط تصثغح خعشاء‬
Venous Tissue Arterial
Amount = 6 mg Conc. = 2 mg/L
140 mL O2/L 190 mL O2/L
Ultrasonic flow Ventricle volume ‫ذذغة‬  Volume of blood pumped by Heart =

Meter on Aorta SV = EDV - ESV (Amount / conc.) = 3 L  30 sec.

Tissue use 50 ml O2 /L
COP = HR x SV = Heart pumps 1 L  50 mL O2
‫* كيف ذى حطاب انسيٍ؟‬

Conc. (mg/L)
Heart pumps ? L  250 mL
O2/min ٗ‫ الٔل يشج ف‬dye ‫ ظٓشخ‬-
Non Invasive Human measurements 5 ‫ تؼذ‬Pulmonary artery
O2 consump.
 ? (COP) = ---------------------- ،‫ثٕاَٗ ثى تذأ انمهة يرخهص يُٓا‬
A-V difference
‫ صاد‬،‫لثم يا ذصم إنٗ انصفش‬
Radionuclide Imaging Echocardiography = 5 L/min .ٖ‫ذشكيضْا يشج أخش‬ 0 5 35
‫ كاٌ انًفشٔض انمهة يرخهص‬-
Injected IV * Detect ultrasonic waves Thermodilution ‫ ثاَيح‬35 ‫ تؼذ‬dye ٍ‫ي‬
reflected on cardiac ‫ (ْيفمذ‬cold saline ‫* َذمٍ انًشيط‬
Visualise Heart (Systole, valves. ‫ نزنك ُْميظ‬،)‫تشٔدذّ نًا يزْة نهُغيخ‬  ? L pumped by heart to remove dye 
Diastole)  SV, EF 60 sec
)‫(يرى دغاتٓى‬ * Calculate EDV, ESV, Blood Temp.
SV, EF Adv.: 1) Not Toxic  COP = 6 L / min
* Adv.: Accurate, Non Invasive.
2) No 2nd Rise.
* Disadv.: Allergy.

39
 Regulation of COP ‫ يحًذ فايس‬.‫د‬
Intrinsic Extrinsic

Heterometric Homeometric  
Phenomenon Pre Load After Load Sympathetic
Stimulus  VR Ino chrono
Parasymp.
‫يثذأ أٔال‬ ‫ثاَيا‬ 1. Nervous Tropic ‫انؼكــظ‬
Time Transient Prolonged
(2-5 minutes) (Not Time Limit)  receptor   c.AMP
EDV  Constant Glucagon
ESV  
2. Hormonal  c.AMP Tropic
SV Increased Ino chrono
(strong) (weak)
 c.AMP  c.AMP

 adrenergic inhibit  Blockers

agonist break down
Significance Physiological (Exercise) 3. Drugs  Ca++
Caffeine
Pathological (Heart Failure) Theophylline
Ca++ channel blockers
 Ca++ intracellular: Digitalis (Adalat)
ypoxia
Heterometric = Pre Load =  EDV = Starling law 4. Ions
H ypercapnia
yperkalemia

40
 Compare Between MCP, CVP ‫ يحًذ فايس‬.‫د‬

Mean Circulatory Pressure (MCP) Central Venous Pressure (CVP)

Definition Average pressure (Intravascular) Pressure in thoracic veins (‫)يرصهح تانقهة‬
Normal 7 mmHg 0-5 mmHg
Static Dynamic
olume
Determinants
V olume
enous capacity

Physiological
V R
entricular Pump
Pathological
 Blood volume Gravity Venodilatation
Decreased
 Venous capacity Inspiration Shock
Physiological Pathological
ypervolemia
 Blood volume Expiration H eart Failure
Increased  Venous capacity (Forced) xcess blood Transf.
(Venoconstriction) Sympathetic
E mbolism (Pulmonary)
Shock (Cardiogenic)

41
 Function Curves ‫ يحًذ فايس‬.‫د‬
Combined
Ventricular VR (Vascular)
(Ventricular, VR)

Direct (RAP, COP) Inverse (VR, RAP) VR or COP (Vertical scale)

RAP (Horizontal scale), VR (Vertical)
RAP (Preload on Horizontal) VR = MCP - CVP RAP (Horizontal scale)
Static 7 mmHg
COP (Vertical scale) Equilibrium point:
)ٖٔ‫ يرغا‬circulation ‫ يصثخ انعغط فٗ كم‬،‫(ػُذيا يرٕلف انمهة‬
Relation CVP: Pressure in great veins (‫)يذخم انمهة‬
COP ‫ يضداد‬ RAP ‫كهًا يضداد‬ Point of intersection 2
= RAP = 0-5 mmHg
(Unlimited) ٖٔ‫ يغــــا‬RAP ‫ درٗ يصثخ‬RAP ‫ كهًا يقم‬VR ‫ * يسداد‬curves.
Gradual collapse of veins :‫ انغثة‬،(-2 mmHg)
CVP, MCP ٖٔ‫ ػُذيا يرغا‬VR ‫* يرىقف‬
Downward (-ve Inotropic
Shift to right Vagal Upward ( MCP due to veno constriction) -ve Inotropic (Heart failure)
Heart failure
Shift to left Upward (+ve Inotropic = Sympathetic) Downward ( MCP due to venodilatation, Hge). +ve Inotropic (Sympathetic)

42
 Cardiac Reserve ‫ يحًذ فايس‬.‫د‬

Short Term Long Term

 COP
Volume overload Pressure overload
Within Permissive Beyond Permissive
(5-12 L) (> 12 L)
VSD LV
Heart Failure Hypertrophy
HR SV HR SV Aortic Incompetence (Aortic stenosis)
to overcome
 (60-90 bpm)  EDV,  ESV  EDV  ESV
 After load
(Heterometric)
 Vagal Tone 60  180 pbm 130 ml  240 ml 60 ml  30 ml
then
Bain-Bridge
reflex
Homeometric L i m i t e d By

Filling Time Starling law No of catecholamine No of capillaries

vesicles
Permissive
Beyond permissive ٕ‫انؼكظ ْــ‬
Unlimited No Adrenergic

43
 Heart Failure (HF) ‫ يحًذ فايس‬.‫د‬

Low output High output

COP: Normal (Rest)

Causes Mechanism Effects Forward failure
=
Dysfunction COP:  (Rest)
Backward failure
1ry 2ry
(MI) * Over load
Right side HF Left side HF
Volume Pressure
* AF, VF
LL edema Pulmonary edema

Systolic Diastolic
Treatment
Causes MI & Valve stenosis Hypertension

Pressure-
volume loop

EF
Shifted to right
Moderate:
Upward to Left


C ause
onsider Meals
D igitalis
iuretics
ecrease
50%, Not  by exercise
Severe: <20% Pre load After load

44
Vascular

45
 Arterial Blood Pressure (ABP) ‫ يحًذ فايس‬.‫د‬
Pulse Mean arterial Proof: MAP = D + 1/3 PP
Systolic Diastolic
pressure pressure O. cycle S . D . D
(S) (D)
(PP) (MAP)
MAP = (S + D + D)/3
Highest pressure Lowest pressure Average
Def. on Arterial wall on Arterial wall S-D pressure in  PP = S – D
(Cardiac Cycle) (Cardiac cycle) Cardiac cycle
 S = PP + D
Normal 100-140 mmHg 60-90 mmHg 30-50 mmHg 93 mmHg
 MAP = (PP + D + D + D)/3
Average 120 mmHg 80 mmHg 40 mmHg` 90-95 mmHg
= D + 1/3 PP

Factors that affect

MCQ ‫هــاو‬
SV  Systolic TPR Diastolic  PP
Aortic  SV S+D
valve ------------ ٖٔ‫ ال يغا‬MAP
2
Elasticity of artery A therosclerosis
I

46
 ABP ‫ يحًذ فايس‬.‫د‬

Physiologic Determinants

Increased Decreased
COP TPR Blood volume Elasticity

* Old age New born Capacity BV

X
* Male Female
SBP
* Afternoon Morning ABP Prevents
MCP PP
* xercise Rest ==
* E xpiration Inspiration
8 L
r 4
MSFP  SBP
or
DBP

* Below level Above level

of heart 1 cm of heart  DBP
0.77 mmHg
Peripheral arteries

Inspiration:  capacity of pulmonary vessels 

Atherosclerosis:  PP (Water Hammer Pulse)
 VR (LA)   EDV   SV   COP   BP

47
 Regulation of Blood Pressure ‫ يحًذ فايس‬.‫د‬

Short Term Intermediate Long Term

Nervous (Main) Hormonal Renal

Capillary Artery Renin-Angiotensin System

Fluid shift

Baroreceptor Peripheral CNS

chemoR Ischemic
Response Stress relaxation Reverse stress relaxation

48
 Baroreceptor ‫ يحًذ فايس‬.‫د‬

Pressure

Physiological  Posture
Physiological
(Exercise) Increased Decreased Recumbent  Standing
Pathological
(Hypertension) Pathological  Hemorrhage

Mild Severe

Sensitivity of Hypothalamus Sensitivity of

Baroreceptors (VD center) Baroreceptors
Sympathetic
Cholinergic

(+) (-) (-) (+)

CIC VMC
CIC VMC

CIC: Cardiac Inhibitory Center

Skeletal ms
Arteriole VMC: Vasomotor Center

49
 Baroeceptor Reflex ‫ يحًذ فايس‬.‫د‬
Medulla Pulse pressure ٗ‫ذغيش ف‬
Stimulus
- +  Discharge (Sustained pressure)
IX Carotid sinus
Aortic arch
VMC CIC X Aortic arch, carotid sinus
Receptor
Type: Mechano (Stretch)
Start firing at 50 mmHg

Maximum firing at 200 mmHg

Afferent IX, X (Buffer nerves)

Center CIC, VMC
Efferent Vagus
Response (-)
(+)
CIC VMC

 HR Artery Vein  Dilatation

Vein Dilatation VR
Decreased COP, BP   SV   EDV   VR
(Below Heart Level)

50
 Baroreceptor )‫ يحًذ فايس (ذكًهح‬.‫د‬

Baroreceptor ‫إرا فشم‬ Carotid sinus Evaluation

Syndrome

Resetting
Pressure on carotid artery Valsalva (Deep Expiration
against closed glottis)

BP: 200/130 Phase BP Cause

(-)
(4) Straining
Stress

Shaving Tight collar

(3) 1st  Intrathoracic press.
(2)  Aortic pressure

Glottis
Baroreceptor

Close
BP: 160/110
adapt  Intrathoracic press.
to new pressure (-) VMC 2nd Compress Veins
‫دذز فشــم‬

as if it is normal
(1) (+) Vasodilator center  VR   COP
 Intrathoracic press.,

BP: 120/80 3rd Normal VR, COP

Glottis
ٗ‫يؼٕدٔا نهطثيؼ‬

Open
 TPR
‫األرقاو ذعثر عٍ ذرذية األحذاز‬ 4th
 BP

51
 Baroreceptor (2 ‫ يحًذ فايس )ذكًهــح‬.‫د‬
Other Types Effect on Respiratory Center
Atrial Receptors Ventricular Receptors
High Pressure Low Pressure High Pressure Bezold-Jarisch
(A) (B) volume reflex Adrenaline Apnea ‫أَظــش صـ‬
* MI
VR * Injection of
Ventricular
Stimulus Atrial Systole  BP
Blood volume Systole Veratridine
Seretonin
Nicotine  HR
* Reflex VD

 capillary Pr.
VD VD
Capillary fluid shift HR Marys' Law
HR (Intermediate) HR
Response
BP
Contractility *  ADH,  ANP Contractility

 urine
(Long Term)

Low Pressure (Act as Atrial Type B) Cardiac Stimulatory Center ‫ال يٕجــذ‬
Adrenaline Apnea
High Pressure

52
 Peripheral Chemoreceptor Reflex ‫ يحًذ فايس‬.‫د‬
Medulla
Stimulus MAP <80 mmHg
- +
IX Carotid Bodies Receptor Bodies (Aortic, Carotid)

VMC CIC X Afferent IX, X

Center CIC, VMC

Aortic Bodies
Efferent Sympathetic

Response

ICI VMC

EDV
SV Artery Vein

COP

Vein Venoconstriction
VR Venoconstriction

53
 Cerebral Ischemia ‫ يحًذ فايس‬.‫د‬

CNS Ischemic Cushing

Response Normal CSF Brain Tumor Reflex

* Stimulus: MAP <50 mmHg

 Blood flow to VMC  BP
* Last ditch ==

Ischemia ‫آخش خط دفاع ظـذ‬  HR

(+) Ischemic Neurons of Pressor Area (VMC)

Strong VC

 ABP

 Blood flow (VMC)

Prevent death of brain neurons (‫ دقائق‬3 ‫)قثم‬

54
 Rapdily Acting Hormones ‫ يحًذ فايس‬.‫د‬

Catecholamines ADH Renin-Angiotensin

ynthesis: Hypothalamus

HR
Adrenaline Noradrenaline
S tore: Posterior pituitary
Short Term
(20 min)
Long Term
(Years)

SV Action

COP
V1 receptors V2 receptors
TPR Slight affected

BP Less affected

SBP VC H2O reabsorption

DBP Slight  (Renal Collecting Duct)

PP Unchanged or
slight   BP
MAP Not or little
affected

55
 Intermediate Regulation of ABP ‫ يحًذ فايس‬.‫د‬

Capillary fluid shift Artery

 BP  BP  BP  BP

Response Response

 Filteration  Reabsorption VD (Myogenic) VC (Myogenic)

 Plasma  Plasma Reverse

volume volume Stress relaxation Stress relaxation

Reabsorp.
Filtration

Artery Vein

Tissue

56
 Long term regulation (Renal) ‫ يحًذ فايس‬.‫د‬

 BP  BP

Renal Ischemia  Na=, H2O loss (urine)

Blood volume
 Renin VR
Angiotensinogen Angiotensin I COP
(Liver) BP
ACE

Angiotensin II
Peptide

VC Stimulates Inhibits ANP

Natruretic
Atrial Urine
Na+
 TPR Thirst center DH

 SBP, DBP
A ldosterone   Na+ reabsorption (Distal Tubules)

ACE: Endothelium of Pulmonary Capillary

57
 Compare Regulation of BP ‫ يحًذ فايس‬.‫د‬

Shot-Term Long-Term

Rapid Slow

Act Seconds or Minutes Hours or Days

Control BP Moment to Moment Days/Weeks/Months

Regulate BP Change Capacity of BV Change ECF Volume

Mainly Nervous Renal, Hormonal

Effectiveness (Adaptation)

Potency Moderate Extreme

58
 Vasomotor Center (VMC) ‫ يحًذ فايس‬.‫د‬

Areas Factors affecting

Sensory Pressor Depressor Cardiac

Stimulatory Inhibitory

Direct:  CO2,  O2 ----

Receives from (Cushing R)
Baro, chemo
Receptors VC VD Tachycardia Chemo Receptors Baro Receptors

Emotions (Alarm) Emotions (Grief)

Pain (Mild or Pain (Severe)

Hypothalamic Sympathetic VD Moderate)
---- Lung inflation
(vagus)
No Normal Tone Activated

Physiological Pathological
(Baroreceptors in Exercise) (Carotid Sinus $)

59
 Hypertension ‫ يحًذ فايس‬.‫د‬

Experimental Human

Gold blatt Neurogenic Treat with DOCA

Unknown 1ry
2ry

Complications CNS CVS Endocrine Renal Others

Cushing Coarctation of Glomerulo- olycythemia vera

Reflex Aorta nephritis

 Renin P regnancy
(Toxemia)
ills (Contraceptive)

I
ncrease after load
schemic heart disease
nfarction
A DH
ldosterone
SIADH
Conn's $
C
ortisol  Cushing $
atecholamines  Pheochromocytoma

60
 Hypotension ‫ يحًذ فايس‬.‫د‬

Acute Chronic

 COP  COP   VR   TPR

Adequate Perfusion

S hock
yncope )ٗ‫(فمذاٌ يؤلد نهٕػ‬

Syncope

Vascular Cardiac Postural (Orhtostatic Hypotension) Others

Vasovagal Carotid Stoke VF Cough Micturition

attack sinus $ Adam's $

* Blood pools in lower  Intrathoracic

Emotions
(+)
(-) VMC ‫أَظر يا ضــثق‬
limb. pressure
Cortex (Pressor area)
(+)
Hypothalamic VD (+) Hypothal. VD * Cause:
Compress veins
VD of Skeletal ms VD (Skel. Ms 1. Loss of symp. Tone. VR
arterioles Arterioles
2. Barorecep. ‫غيش شغانح‬ COP
 BP  BP
BP

61
 Hemorrhage ‫ يحًذ فايس‬.‫د‬

Compensatory Reactions

Short Term (Immediate) Long Term

1)  Baroreceptor discharge

(+) VMC Sympathetic

Venoconstrict VC Heart Adr. Med.

VR Arterioles   TPR  HR  Catechol.

EDV ‫إشـــــرح‬
Correct  BP Skin  Pale, cold
SV Rapid, weak Restless Renin-Angiotensin System
COP Renal   urine vol. pulse

Compensatory VC   DBP   Pulse Pressure

2)  Peripheral chemoreceptor reflex (‫)إششح‬

3) Capillary fluid shift (‫)إششح‬
4) Reverse stress relaxation (‫)إششح‬
5)  Angiotensin II, ADH (‫)إششح‬
Plasma volume restored by capillary fluid shift Plasma vol. restored (½-3 days) by Thirst, ADH
Plasma proteins restored by moving liver proteins to Plasma ptn restored (3-4 dys) by hepatic synthesis
Correct  Volume plasma
RBCs restored by spleen contraction RBCs restored (4-8 weeks) by  erythropoietin

62
 Shock (Tissue Underperfusion) ‫ يحًذ فايس‬.‫د‬

Cause Course
Other Types
Hemorrhagic
Low resistance Cardiogenic Septic Traumatic Surgical
(Cold Shock)
Vasodilatation
loss of fluid: Severe bacteria Crush
infection
Emotions Loss of Antigen- injury
* Hemorrhage Vasomotor tone Antibody

* Burn Sympathetic Spinal cord  Histamine

Endotoxins
‫يشًـــــــــم‬
VD center Lesions
* Severe vomiting 1) VD (General)
Cause Anaphyl-
Heart
2)  Capillary ‫َفاريح‬
Neurogenic
* Diarrhea failure
Neurogenic Spinal actic 3) Cardiac Hypovolemic
depression
S h o c k
* Include
Low Resistance Vasogenic
features:
===== Hypovolemic
Distributive Warm shock Low resistance
Cardiogenic
CVP Decreased Increased

N.B.: ABP not a good measure for progression of shock.

63
 Course of Shock ‫ يحًذ فايس‬.‫د‬

Non progressive Progressive Irreversible

Compensated (Decompensated) (Refractory)

 BP (Stimulus)   BP (Response)
‫أَظر انصفحح انقاديح‬

-ve feed back MCQ

-ve feed back

Compensatory Mechanisms Hemorrhage ‫يثم‬

Cellular Deterioration Deleterious Substances

Baroreceptor reflex
hemoreceptor reflex Lactic acid

C NS Ischemic response
apillary fluid shift
onstrictors (BV)
Glucose metabolism
Mitochondria
ATP
Histamine
Serotonin

T
issue enzymes

A drenaline
DH
Na+ / K+ pump NF

64
 Course of Shock ‫ يحًذ فايس‬.‫د‬
Irreversible
Progressive (Decompensated)
(Refractory)
Decreased (BP) as stimulus  Decreased BP (Response) (+ve feed back = Viscious circle)

‫االرقاو ذعثر عٍ ذرذية‬

‫األحذاز‬  BP
(1)
(7) (5)  Lactic acid
Hyper coagulability (DIC)  Blood Flow (13)
(Metabolic acidosis)

(2) (8) (6)

Decompensatory VMC Pancreas Heart ‫أَظر انصفحح‬

Mechanisms (11) ‫انقاديح‬

Autodigest
Release MTF

(10)
VR
(9) EDV
Vasomotor SV
Failure Activate Trypsin COP

(12)
(3) Inhibit Excitation contraction

(4)
Venodilatation

65
 Irreversible (Refractory Shock) ‫ يحًذ فايس‬.‫د‬

Decompensatory Mechanisms

Pre Post
Capillary
1 X X Sympathetic constricts (pre, post capillary sphincters) in
(Hypovolemic and Cardiogenic shock)

Pre Post
Capillary

Severe local hypoxia  Accumulation of VD substances

2 X  Dilate precapillary sphincter (Post capillary closed)

Pre Post
Capillary

Post capillary sphincter relax  Packed RBCs and small

fragmented clots reach circulation  Pulmonary embolism
3

66
 Course of Shock ‫ يحًذ فايس‬.‫د‬
Brain, Heart
Spared for Long time
Organ Failure (although  flow 75% in others)

Liver Kidney Lung Intestine RES

Metabolism Opsonisation
Burn shock
Crush injury
Detoxification Renal Failure sepsis
Break down of Phagocytosis
intestinal barrier

Decreased Pulmonary Sepsis, Infection

bronchial flow Albumin

Surfactant
Embolism Edema

ARDS

67
 Factors Affecting HR ‫ يحًذ فايس‬.‫د‬

Tachycardia Bradycardia
Higher centers Pain (Mild or Moderate) Pain (Severe)
cortex Emotions (Alarm reaction) Emotions (Grief)
1) chemo Receptors 1) Baroreceptors
Reflexes 2) Atrial Type B 2) Ventricular, Atrial Type A
3) Muscle, joint receptors 3) Cushing.

Respiration Inspiration Expiration

Hormonal Adrenaline, NA, Thyroxine --

Thyroxine -Blockers
Drugs
Sympathomimetics Ca++ Blockers

Heat  Temperature Fever

HR ً‫ أقىي عه‬Adrenaline ‫ ٔنكٍ ذـأثير‬BP ٗ‫ ػه‬Adrenaline ٍ‫ أقىي ي‬NA ‫ ذأثيش‬:‫هـاو‬

68
 Notes on HR ‫ يحًذ فايس‬.‫د‬

Bain Bridge Reflex  O2,  CO2, H+

(-) (+)
Stimulus:  VR SA node CIC ChemoRecep.
Receptor: Type B 'Atrial', Pulmonary
Afferent: X
Center: CIC
 HR  HR  HR
Efferent: X , Sympathetic then
 HR

Response:  CIC (+) SA node

New Born (HR = 100 bpm)

Tachycardia

No inhibitory vagal Pressure < threshold of

Part of baroreceptor reflex
Vagal Tone tone baroreceptor
Prevented by 1) Vagotomy
2) Atropine

69
 Regulation of blood flow ‫ يحًذ فايس‬.‫د‬

Local Systemic

Acute Chronic Nervous Chemical

VC VD
Angiogenesis
Vasomotor tone drenaline Adrenaline

Autoregulation Vasoactive
sympathetic VD
Antidromic
A
N.A
DH
ng. II (skeletal)
Kinins
Seretonin
reflex
Vital organ maintains flow constant PGF2 PGI2
over wide range of pressure change
through  or  resistance VC VD O2 C.choline

Mechanisms
Seretonin
PH

CO2, H+
A denosine
NP
Brady kinin
Lactate
* Thromboxane A2 (+)
Adenosine Histamine

M etabolic
yogenic
Tissue pressure hypothesis
* Endothelin K+
Histamine
Osmolality
* : Endothelium vasoactive substances * NO (Nitric oxide)
* Prostacyclin

70
 Regulation of Coronary Blood Flow (CBF) ‫ يحًذ فايس‬.‫د‬

Adenosine (‫)األهى‬
 CO2, H+, NO

etabolic P otassium
rostaglandins
Autoregulation

M HR
yogenic
echanical
Vascular Smooth ms Contract/Relax

Cardiac Cycle
Maintain constant flow over
P (60-140 mmHg)

F =  P/R

‫ ثاتد‬F =   P/R
 HR   CBF CBF  Aortic Pressure

 R (Vascular Smooth ms Contract)

Nervous Reflexes
Phase Aortic P. CBF
Atrial systole
Isovolumetric Cont.
Symp. Parasymp.
Maximum ejection (Right)
(VD) (VC) Anrep
Reduced ejection
Bezold Jarisch
Proto diastolic
Direct Indirect Gastrocoronary
Isovolumetric relax. (Left)
(2) (Metabolites) Rapid filling
Slow filling

71
 Coronary Cicrulation (1) ‫ يحًذ فايس‬.‫د‬

Supply Characteristics

Arterial Venous 2/3 Coronary sinus, anterior cardiac veins *  Blood flow.
*  O2 Reserve.
Heart chambers
* Aerobic.

Arterio-
sinusoidal
Arterio-
luminal Thebesian
*
* No Anastomosis
O2 debt.
* Systole supply all tissues except LV.
Right Left

50% 20%

RV LV
Supply Inferior and Surfaces ant 250 ml/min (Rest) 
Measurement of Coronary Blood Flow
post surfaces lat septum 1000 ml/min (Exercise)

Experimental Kety Method Radionucleotides Angiography

N2O uptake
A-V difference

72
 Coronary Cicrulation (3) ‫ يحًذ فايس‬.‫د‬

Coronary artery insufficiency Angina pectoris )‫(يخرفٗ االنى يغ انشادح ٔيظٓش يغ انًجٕٓد‬
‫ػالج‬ Nitrite (VD   Preload)
Slight exercise (O2 lack   Adenosine  VD)
M.I.
1. Cardiogenic shock.
ECG Causes of Death 2. V.F.
)‫(أَظش يا عثك‬
3. Cardiac Tamponade.

Cardiac Work Mechanical efficiency of Heart

% Work done ( by sympathetic)

Potential Kinetic Total energy expenditure
-----
----- Cardiac O2 Consumption 60-80 ml/100 gm/minute
MAP x COP
Rest Exercise
D e t e r m i n e d
4-5% 50% Inotropic HR Tension = P x r
W
Direct proportional

 r (radius) = Volume overload   Tension   O2 Consump.  w (wall thickness) = Hypertrophy   Tension   O2 Consump.

73
 Coronary Insufficiency (M.I) ‫ يحًذ فايس‬.‫د‬

T wave inversion S-T elevation Deep Q

1st Change

Cause Cause Cause

Last part depolarized Current of injury Electric silent area

between
pathological depolar.
Last part repolarised Normal repolarized Electric window

Abnormal Q Old M.I.

74
 Capillary Circulation ‫ يحًذ فايس‬.‫د‬

True Non True

Through fare vessels or terminal arterioles Meta-arterioles, through fare vessels, A-V shunt
No Exchange (Capacitance, ‫)ذُظيى انذشاسج‬
Exchange

Alternate open, close

Vasomotion
capillaries
Types Mechanism )‫(دغة إدرياجاخ األَغجح‬

Flow
limited
Diffusion
limited
1. Diffusion (‫)األهى‬
2. Filtration.
M etabolic
yogenic
Temperature

3. Vesicular transport (ptn). Chemicals

4. Diapedesis (WBCs)
Constrict Dilate
Precapill.
Structure of True capillary
Sphincter
Catechola-
Fenestrated Sinusoidal Non fenestrated mines
Nervous ‫ال يرأثر تـ‬ Histamine
Bradykinin
substance P
Endocrine Villi Kidney Liver BM Brain Muscles
Rest: <25% of capillaries (Open = Active)

75
 Capillary Circulation )‫ يحًذ فايس (ذكًهح‬.‫د‬

Capillary Pressure Capillary Permeability

30-35 17 10-12 Increased Decreased

Liver, Kidney, Glands Muscle, Brain

Venular end Arteriolar end

Arteriolar end Mean Pressure Venous end
Hypoproteinemia (Liver, Renal
diseases) Increased
Increased Inflammation (subs. P, Pyrogens)

Dilated capillaries (Fragile) Pulse Pressure (5 mmHg)

Arteriolar VD  Venous Pressure Gravity

Capillary pressure nearer to venous than arterial press. Laplace law ecrease (Arteriolar VC)

Precapillary resistance = 4-5 post capillary Resistance

(T = P x r) D isappear (Post
resistance)
capillary

76
 Tissue Fluid Formation ‫ يحًذ فايس‬.‫د‬

Physiological (Starling Forces) Edema  Tissue fluid

Arteriolar end Venous end

Capillary pressure: 30 Capillary pressure: 10 Causes Types

Filtration -ve ISF pressure: 3 -ve ISF pressure: 3 *  Filtration

(mmHg) Pitting Non Pitting
ISF colloid pressure: 8 ISF colloid pressure: 8 Arteriolar dilate  Venous Pr.
‫صثاػك يذٔط‬ ٗ‫صثاػك يذٔط ػه‬
Reabsorption Colloid OP of plasma: 28 ‫ػهٗ ييّ فيغشط‬ ‫تشٔذيٍ فال يغشط‬
 Capillary ‫َفاريح‬ Pregnancy H.F
Net effect 13 mmHg 7 mmHg *  OP of plasma Ptn
(Filtration) (Reabsorption
Inflammation
Nutritional Hepatic Renal

Tissue fluid = ISF = Lymph * Obstruct lymph duct: Filaria Elephantiasis

Lymph Plasma Factors which  lymph flow: Edema Safety Factors

Lymphatic pump (VR ‫)يثم‬
Albumin 0.5-1 gm% 4.5 gm%
ISF pressure
A/G ratio   Activity of tissues Lymph flow 27 mmHg 17 mmHg

ISF
Composition N e a r er Pressure
Protein Pulmonary Systemic
ry
Lymphagogues ( Lymph)
1 : Bacterial Toxins, Peptones
2ry: Hypertonic Solutions
77
 Cerebral Circulation ‫ يحًذ فايس‬.‫د‬

Arterial Capillary Venous

2 internal carotid 2 vertebral * Non fenestrated Dural Sinus

Basilar * Basement membrane

* Tight junction
* Membrane
Circle of Wills
Astrocytes Glia

6 Cerebral arteries
Blood Brain Barrier (BBB)

Allow passage of

CO2 mmonia
O2
Lipids
A naesthetics

78
 Cerebral Blood Flow (CeBF) ‫ يحًذ فايس‬.‫د‬

Value Characteristics

Normal Regional Constant (Arterial in = Venous out)

Brain, CSF are incompressible

750 ml/min  Frontal Left Motor,
Grey = 2 White matter
Rest, awake Premotor cortex Skull enclose brain, CSF, Cerebral Vs
(Clench right hand)

Kety Method: N2O uptake /A-V difference in N2O uptake

Measurement Monro-Kellie Doctorine
Radioactive Xenon (133Xe)

5 seconds  loss of consciousness

Cerebral ischemia
2-4 minutes  Irreversible damage

79
 Factors Affecting Cerebral Blood Flow (CeBF) ‫ يحًذ فايس‬.‫د‬

P Resistance

CPP = ABP (Head) – VP (Internal Jugular Vein) Autoregulation Blood Gases

Physiolo- Patholo- PO2 PCO2

Increase Constant Decrease gical gical (VD)

 ABP  VP  VP  ABP

M
Physiolo- Patholo-
aintain CeBF  ABP
(60-160 mmHg) (100-200 mmHg) gical gical
yogenic
Upright  Volume No effect 30 mmHg
etabolic
( CeBF double)

CO2
Upward Acceleration Downward Acceleration D Substances
NO
iscosity Adenosine
ABP ABP ‫ راجــع‬: ‫هــاو‬
== ==  Resistance
VP VP Cushing Reflex, CNS Ischemic
asomotor nerves (Symp.)
Intra Arterial, Venous, Cranial Pressures are all balanced

Minimal or No control on Hypertension:

Upright:  MAP (Brain) by 25 mmHg   CeBF 20% Resistance Protects BBB

80
 Pulmonary Circulation ‫ يحًذ فايس‬.‫د‬
Pulmonary Systemic
Flow More Pulsatile Less Pulsatile
Pressure:
SBP 24-25 mmHg 100-140 mmHg
DBP 8-9 mmHg 60-90 mmHg
PP 15 mmHg 30-50 mmHg
PP/SBP 15/25 = 60 % 40/120 = 33% Transient Time
MAP 15 mmHg 93 mmHg
Hypertension Mitral stenosis 1ry, 2ry
MCP 10 mmHg 17 mmHg
Precapillary R. = Post capillary R 4-5 Post Capil. R
 Capillary ressure Time which RBC take to
Edema Permeability Traverse pulmonary Cap.
Edema Safety Factors 27 mmHg 17 mmHg
Apex : 5 mmHg Each 1 cm below heart level 0.75 sec. (Rest) 0.3 sec. (Exerc.)
Gravity Mid zone : 15 mmHg
Base : 25 mmHg   Pressure 0.77 mmHg
Less High
Resistance 600-700 (Erect)
Blood Reservoir 1000-1200 (Supine)
* Inspiration:  VR * Inspiration:  VR
* Expiration:  VR * Expiration:  VR
Respiration *  O2  VC of pulmonary artery *  O2  VD
  RV press.  RV Hypertrophy
(Corpulmonale)

81
 Venous Circulation ‫ يحًذ فايس‬.‫د‬

Effect of volume VR = MCP - CVP Hydrostatic in different point (HIP)

Increased Decreased 2-3 inches below vena

cava in Diaphragm
venous pr. ‫* ال يرغير عُذها‬
Flat Stiff .‫يهًا ذغير وضع انجطى‬
 VR
Elliptical Sympathetic
Shift down Shift up
 MCP  CVP
Oval Symp. Tone  Symp. Tone
Blood volume Water immersion
Circular Blood volume Thoracic pump
venoconstrict (Symp.)
Vis-A-Tergo Skeletal ms (contract) cardiac suction Vis-A-Fronto
Pressure gradient

0-2 (vena cava) Rapid venous velocity ( CSA) Flow of veins (2 Descent) Cardiac activity  VR
Venous Pressure 6-8 (large veins)
Reference Point X Y Both  Both 
8-10 (small veins) th
4 sternocostal jolint (middle of
10-12 (venules) Rt atrium = CVP = Zero). Rapid ejection Rapid filling Symp. HF

82
 Splanchnic Circulation ‫ يحًذ فايس‬.‫د‬

Hepatic Intestinal
Hepatic artery Portal vein

Flow 350 ml/min 1000 ml/min

Regulation of Both
PO2  

O2 Required 30-40% 60-70%

Mainly Neural (Sympathetic)
Exercise More O2 taken Less O2 taken
VC ( receptor)

Portal Venous Pressure No VD fibers to Liver

8-10 mmHg 15-20 mmHg Portal Hypertension

(Normal)
Splenomgealy
Bilharziasis Cause Complications  Albumin
Ascites
 Venous Pr.

Portal
Splanchnic Circulation 30% of COP, Blood reservoir, low pressure
Circulation

83
 Other Circulations ‫ يحًذ فايس‬.‫د‬

Cutaneous (Skin) Skeletal

Autoregulation Rest Exercise

No 6-8 ml/min/100 gm 60-80 ml/min/100 gm

VD fibers

‫ ؟‬VD ‫ إصاٖ يذصم‬:‫ضــؤال‬ Increased Skeletal Ms Flow (Exercise)

Sympathetic (+)
Sweat glands Before During After

Kininogen Kallikrein Kinin (VD)

Triple Response Hypothalamic  B.P Reactive

Symp. VD center
(+) Baroreceptor Hyperemia
Red line Flare Wheal
 Vasomotor Tone (Vasomotion)
Duration 5-10 seconds 30-45 seconds 3 minutes VD of skeletal ms
Arterioles VD of skeletal ms
Cause Capillary dilate Local Axon R.  Capillary
Arterioles
Permeability

84
 Circulatory Response to Exercise ‫ يحًذ فايس‬.‫د‬

Isometric Isotonic
Blood flow
HR
SV Little change
SBP
DBP
PP No or little change
MAP The same

Sympathetic
 HR (Exercise) Temperature
VR (Bain-Bridge Reflex)

Vagal Tone

Proprioceptors

85
Respiration

1
 Respiratory System ‫ يحًذ فايس‬.‫د‬

Lungs
Air ways

Upper Lower Branched Pleura Alveoli

Airways

Nose Pharynx Larynx 300 million 70 m2

Conducting Respiratory
zone zone Type II
secretes
surfactant
Site Trachea  Terminal Resp. bronchioles  Alveolar sac

Alveoli -- +

Functions Air (conduct, warm, Gas exchange

moisten), Defencive + Phonation

2
 Respiratory ‫ يحًذ فايس‬.‫د‬

Functions Processes

General Others Internal External

Diffusion
(4)
Conducting, Regulation Surfactant ‫* يصنغ‬ Ventilation
respiratory (1)
bradykinin ‫* يقهم مه وشاط‬ Exchange Gas
zones
Acid ‫حزارج‬ (2) Transport
Serotonin
(3)
base PG
Ach. ‫* يتخهص مه‬
Norepi.

* Angiotensin I ACE
Angiotensin II

3
 Mechanism of Respiration ‫ يحًذ فايس‬.‫د‬
Inspiration Expiration
Start: Tend to recoil Start: Distension
Lung
End: Distension End: Recoil
all all
Thoracic cavity
Dimensions Dimensions
IPP -6 -3
IAP -1 +1
Air moves in out
Respiratory Muscles
1. Diaphragm (75%)
 Vertical Relaxation of inspiratory
Normal
2. External Intercostal: Diameter muscles
 Transverse, AP
Accessory Muscles 1. Internal Intercostal
Deep (External ‫)ػكــس‬

(Forced)
S ternomastoid
calenus
2. Abdominal Muscles

Vertical diameter

4
 Respiratory Pressures ‫ يحًذ فايس‬.‫د‬

Atmospheric Intra Alveolar Intra Pleural Transpulmonary Trans

(Barometric) (IAP) (IPP) = Transmural Thoracic

760 mmHg
(0 mmHg) ‫أنظر انصفحت‬ IAP-IPP IPP-Atmosph.
‫انقاديت‬
Pause Inspiration Expiration +4 -4

Importance Importance

760 759 761 Measure Compressing

(0) (-1) (+1) Lung elastic pressure
recoil

Distending
pressure of alveoli

5
 Intra-pleural Pressure (IPP) ‫ يحًذ فايس‬.‫د‬

Values Importance Measurement

-4
Lung Venous,
-6 -3 Lymphatic Intra oesophageal
return balloon connected
Elasticity ‫يًنغ‬
)‫(مقياس‬ collapse to Manometer
Pneumothorax

Air in Types Effects

pleural sac Lung collapse (Atelectasis)

Chest wall (Distension)

Traumatic Spontaneous
(open) (closed) Mediastinum: shift ‫نهناحيت انؼكسيت‬

6
 Respiratory ‫ يحًذ فايس‬.‫د‬

States Applications

Pnea (‫)نفـس‬ Capnea = CO2 Paralysis Cut spinal cord

A Eu Dys Ortho Hyper Tachy

‫يفيش‬ ‫طبيؼى‬ ‫صؼىبت تنفــــــس‬ ‫زيـــــــــــــــــــــادة‬

Diaphragm Intercostals > C3 < C5

Orthopnea: recumbent ‫مش قادر تتىفش وأوت‬

Death ‫ال يتأثز التىفـش‬ ‫ال يتأثز التىفـش‬

Hyperpnea: Rate, depth

Tachypnea: Rate only

7
 Airway Resistance ‫ يحًذ فايس‬.‫د‬

R = 8 L / r4 Distribution Factors affect

Length
Maximal Minimal Nervous Local
Viscosity Radius

Trachea Bronchi Terminal Symp. Parasymp.  CO2 Histamine

Bronchiole SRSA
s

Chronic bronchitis Bronchoconstriction

COPD Bronchial Asthma

Emphysema  1 antitrypsin  elastase  Compliance

Collapse of small airways break alveolar wall

8
 Surfactant ‫ يحًذ فايس‬.‫د‬

Secreted by Structure Functions   RDS

Premature Adult
Type II DPPC Ca++ Apoptn
* Hypoxia
alveolar
* Smoking
Causes  Cortisone * Occlusion of
 S. Tension of fluid Stabilize
lining alveoli alveolar size pulmonary artery
* 100% O2
Keep alveoli dry
Small Large * Premature: 1. PEEP
Prevents pulmonary edema Surfactant ‫وصىع له‬ 2. Diuretics
(Lung collapse) Treatment
* Pregnant: 3. Cortisone
Cortisone ‫وعطً لها‬
P: Distending pressure (alveoli)
‫تبؼا نـ‬
 S. tension  Surfactant
T: Tension (alveoli ‫)الذي يصغز‬
Laplace law
r: Radius of alveoli P = 2T/r

9
 Compliance (C) ‫ يحًذ فايس‬.‫د‬

:‫انًؼنى‬ Normal values Elasticity ‫ػكس‬ Factors affect

‫تمتلًء الزئح تاكثز حجم هىاء‬
)P( ‫) تاقل ضغظ ممكه‬V(
Lung Lung + Thoracic cage Decreased Increased
C = V / P

 Compliance ‫نيس ييسة‬ Pulmonary Physiolo- Patholo-

Factors which cause alveoli
edema gical gical
 Transmural pressure congestion
Open Collapse fibrosis ‫كثز الضه‬ Emphysema
Surfac-  Diameter of small airways
tant S. Tension Elast-
(2/3) icity  Expiratory resistance
TPP

Alveolar  Work of breathing

Interdependence
65% 25% 10%

10
 Lung Volumes and Capacities ‫ يحًذ فايس‬.‫د‬

Static Dynamic

TV IRV ERV RV FVC FEV1 PV MBC

Maximum air ‫أنظر انصفحت انقاديت‬

Volume remain after
of air IC Forced expired
inspired TLC = TV + IRV + ERV + RV
or expired Forced Forced
inspired expired Volumes
‫ حفظ أرقاو‬:‫هاو جذًا‬
Vital Capacity Capacities
FRC
RV

Lung Chest Left side Diaphragm Measured Importance

COPD
wall H.F ‫أي حاجح تعىقه‬
‫يقللها‬
Athletes ‫يقللها‬ ‫يقللها‬ Dilution
‫يزودها‬ principle

11
 Importance of RV ‫ يحًذ فايس‬.‫د‬

Physiological Pathological Medicolegal

Respiratory Rate 12-16/minute  (COPD)

=
Heart rate 60-90/minute

15
Average =
75

=
5 ‫انًؼنى‬
1 exchange ‫ يحذث‬Deoxy blood ‫ يراث انقهب يضخ فيهى‬5 ‫* ين كم‬
Prevents ‫ أثناء‬exchange ‫ يضًن استًرار‬RV( ‫يرة واحذة فقط‬
)O2 Fluctuations

12
 Dynamic Lung Volumes ‫ يحًذ فايس‬.‫د‬

FVC FEV1 PV MBC

Timed VC 80% TV X RR
Deep, Fast Normal
of FVC
breathing for
6 L/min
15 seconds
‫يفرقىا بيــن‬
Male Female
80-170 60-120
Obstructive Restrictive L/min L/min
lung diseases lung diseases
BR MBC - PV
Lung
 
compliance
Air way   Normal >90%
resistance "Expiration" "Inspiration ً‫صعىتح ف‬ BR/MBC Dyspneic index
TLC  or N. 
RV, FRC   or N. Dyspnea <70%
FVC Decreased
FEV1  
FEV1/FVC <80% >80% N.B: RV, FRC, TLC (not measured by spirometer)

13
 Pulmonary Function Tests ‫ يحًذ فايس‬.‫د‬

Lung volumes, Ventilation, Arterial blood

capacities Diffusion perfusion gases

Static Dynamic Direct Inverse

131
Xenon

Proportional

Volumes (4) Capacities (4) FVC

FEV1
PV
CO uptake is Diffusion Limited
TV IC MBC
IRV FRC
ERV VC Index for Diffusion capacity
RV TLC

14
 Gas Exchange ‫ يحًذ فايس‬.‫د‬

Alveolar – Capillary membrane

6 Layers
/10 Micron
Factors which affect
Gas Diffusion

Epith- BM 2 fluids Endo- BM

elium thelium Direct Inverse
proportional proportional

Diffusion capacity P SA Temper. Solubility Thickness MW

Volume of gas diffusion via
membrane / min / mmHg
O2 CO2 CO2 24 times soluble > O2

But
Increase Decrease Arterial Venous Arterial Venou MW (CO2): 1.4 > O2
s

100 40 40 46 Diffusion coefficient

Exercise mphysema Fibrosis
E dema
60 6
CO2 = 20 times O2

15
 O2 Transport ‫ يحًذ فايس‬.‫د‬

Coefficient of
O2 Content O2 Capacity % Hb saturation O2 utilisation

Physical Chemical ‫ ػهى‬Hb ‫قذرة‬ O2 content x 100

+ O2 ‫حًم‬
O2 capacity

0.3 ml 19.5 ml 1 gm Hb  1.33 mlO2 -----

-----

15 gm Hb  20.1 mlO2 97.5%

19.8

Tissues ‫مذي اصــتفادج‬

O2 ‫مــه‬

Venous Arterial
% Hb saturation Tissue use % Hb Saturation
(75) (97.5-75 = 22.5%) (97.5)

16
 O2 Dissociation Curve ‫ يحًذ فايس‬.‫د‬

HB Myoglobin ‫أنظر انصفحت انقاديت‬

Plateau part of curve Steep part of curve

PO2 (100  60)

% Hb saturation (97.5  90)

PO2 % Hb

< 60  rapidly
Significance
40 75

Physiological Pathological 20 30

High altitude Significance

Lung diseases

Safety against PO2 changes Small  PO2   O2 release at tissues

17
 O2 Dissociation Curve )‫ يحًذ فايس (تكًهت‬.‫د‬

Hb Myoglobin

Shift to Right Shift to Left Store 1 Rectangular Left to O2

molecule O2 Dissociation curve
Hyperbolic

CO2 CO2
H+ H+ Hb
Temperature Temperature
2,3 DPG 2,3 DPG Adult Fetal
P50 P50 Hb () O2 Hb () O2
+
+
p50: PO2 = 27 mmHg when Hb 50%
2,3 DPG
Saturated with O2
‫ال يتفاػم مع‬
Acidosis
(-)
2,3 DPG
(+)
A ndrogen
lkalosis Hb-2,3 DPG + O2
2,3 DPG

(An aerobic glycolysis)

18
 CO2 ‫ يحًذ فايس‬.‫د‬

Transport Content

Arterial Venous
90% 5% 5%

48 ml 52 ml
HCO3 Physical Carbamino

Chloride shift phenomena ‫أنظر انصفحت انقاديت‬ 52

CO2

CO2 content
Dissociation
 Hb affinity 48 Curve

O2 CO2 40 46
PCO2

Bohr effect Haldane effect Linear relation (PCO2, CO2 content)

At any PCO2, Reduced Hb carries  CO2

19
 Chloride shift phenomena at Tissue ‫ يحًذ فايس‬.‫د‬

RBC Plasma Tissue

H2O +  CO2 Diffusion
 CO2 Diffusion  CO2
2 1
CA 3 (Tidal CO2 = 4.8 mL)
NaCL
 H2 CO3

4 8 CL-
Na+
KHb +  H+  Hco3- 7 HCO3-
5

(Weak acid) H. Hb + K+ buffer ‫ ك‬K+ ‫قـذرج‬ 9

6 (30%)

Note Number of ions (RBCs) > Plasma   Osmotic pressure  attract water to move
inside RBC   HV (Venous > Arterial blood)
‫سؤال هــاو ػًــهى‬

Chloride shift phenomena at lung ‫هــاو‬

is the reverse ‫االرقاو تؼبر ػن ترتيب األحذاث‬

20
 Dead Space (DS) ‫ يحًذ فايس‬.‫د‬

No exchange 150 mL Types Measurement

Anatomical Alveolar
Fowler Bohr's
Method equation
Pathological

Importance
Physiological

(Total) 1st 2nd 3rd

Conducting zone TV – Alveolar air

) 1 ‫(أنظر ص‬ Pure O2  N2 N2 reaches plateau

 O2  CO2
Clinical:
Most air remains in DS
(Rapid shallow breathing)

21
 Ventilation/Perfusion Ratio ‫ يحًذ فايس‬.‫د‬

Normal Abnormal

Average Apex Base

> Normal < Normal

0.8 3 0.6

Wasted 2% COP pass through

Regional distribution ventilation bronchial vessels

Ventilation Perfusion

Physiologic Physiologic
DS shunt
Apex Base Upright Recumbent

Apex = Base Local VC of local

IPP more –ve Apex Base bronchconst. BV
More compliant
 TPP
Low High
Shift ventilation away Shunt blood away from
 volume better ventil. from poor perfused area hypoxic area

22
 Control of Respiration ‫ يحًذ فايس‬.‫د‬

Respiratory Centers

Medulla Pons

DRG VRG Apneustic Pneumotaxic

Lower Upper

Inherent Rhythm (pacemaker) of respiration Pre-Bötzinger Complex

23
 Control of Respiration ‫ يحًذ فايس‬.‫د‬

Involuntary Voluntary

Pre-Bötzinger complex Cortex

(-)
DRG DRG DRG

(+) (+) (-)

Insp. Muscles Insp. Muscles VRG VRG

contraction relaxation
(Inspir. Neurons) (Expir. Neurons)

Inspiration Expiration Accessory Insp. Expiratory

Muscles Muscles

+ : Stimulation
- : Inhibition
Deep Inspiration Deep Expiration

24
 Pontine Centers ‫ يحًذ فايس‬.‫د‬

(3) off switches )‫(فزامل‬

Pneumotaxic Center ‫يثذأ‬ to Apneustic center:
(-) (4) Expiration
Pons 1. Pneumotaxic center.

Apneustic Center 2. Hering Breuer reflex.

Prevented by

(+) (1) 3. Vagii.

Medulla DRG if all

Damaged
(+) (2)
Apneusis

Inspiratory Muscles
Stretch Receptor
(3)
‫صمــيت‬
Apnea
Hering Breuer reflex
)‫(إرا نى يتى إيقافه‬
Protect against ً‫ليش لها دور ف‬
Bilateral vagotomy  Deep, slow breathing over Normal
distension ventilation

25
 Regulation of Respiration ‫ يحًذ فايس‬.‫د‬

Chemical Non chemical

CO2
O2, H+
‫أنظر انصفحت انقاديت‬
Increased
Decreased

Mild Chronic disease >70-80% ‫هــاو‬

Central chemo R. ‫ال يعمل‬
‫االرقاو تعثز عه تزتية االحذاث‬

BBB + = Stimulation
1 Medulla
 CO2 CO2 + H2O (CSF)
2 CA R = Receptor
H+ does not 3
H2CO3
cross BBB +
H
+
+
4
5
Central chemo Receptor 6
Inspiratory Muscles Hyperventilation

26
 Ventilatory Response to PO2, H+ (PH) ‫ يحًذ فايس‬.‫د‬

Hyperventilation
Respiratory Carotid
center bodies

CO2 O2
Receptors * Central chemo
)‫(أصاصًا‬ Peripheral
stimulated chemo Aortic
* Peripheral
chemo (weak) bodies

 PCO2 5%  PCO2 (100 mmHg)

‫أرقاو‬ Peripheral chemo
receptors
‫هايــت‬

Ventilation <60 mmHg to Stimulated by

3-4 times  Ventilation
O2  H+  CO2
(Metabolic (Weak)
acidosis)
‫ال يتأثر بــ‬
PCO2 is Main Respiratory Stimulus Anemia or Co poison Dissolved Decreased
O2 %100 ‫يًنىع إػطاء انًريض‬

Physiological Pathological
(PO2<60 mmHg) (Chronic lung disease)
27
 Non Chemical Regulation of Respiration ‫ يحًذ فايس‬.‫د‬

Stimulatory RC Inhibitory

High centers Lung R. Mechano R. Muscles ‫أنظر انصفحت انقاديت‬

Joints
Tendons
Cortex Hypothal. Irritant R. J receptor
Ligaments

Hyperventilation Rapid shallow ‫وفش‬

Pulmonary congestion Bradycardia

Alveoli
Upper Lower Capsaicin Hypotension
Pulmonary capillary
Sneezing Coughing

Deep inspiration followed by Deep expiration R Receptor

RC Respiratory center

28
 Non Chemical (Inhibitory) Regulation of Respiration ‫ يحًذ فايس‬.‫د‬

Cortex Lung CVS GIT

Breath Voluntary apnea Stretch R. Adrenaline apnea Swallowing apnea

holding test

 PCO2 Hering-Breuer Reflex

(+) Central ChemoR.

RC
(Medulla) Carotid sinus
Breaking Point

‫هــاو‬
Aortic arch
Apnea is prolonged by
Baro receptors

Hyperventilation Breathing
Before 100% O2
Apnea Adrenaline IV
Breath Holding Test

29
 Nonchemical Regulation of Respiration (Respiratory) ‫ يحًذ فايس‬.‫د‬
R e f l e x e s Lung irritant Chest wall
J receptors
Sneezing Coughing Swallowing Hering-Breuer receptors receptors

Irritant inhalation Pulmonary

Irritation of Stretch of chest
Irritation of Stimulation of e.g. ammonia congestion
Stimulus respiratory Lung inflation wall muscles,
nasal mucosa pharyngeal mucosa dema
mucosa
E mbolism
tendons

Irritant R. Stretch R. Irritant R. Alveolar wall Ms spindles of

Irritant R Mechano R.
Receptor (Trachea, (wall of (wall of close to chest wall
(Nasal mucosa) (Pharynx)
larynx, Bronchi) bronchi/oles) bronchi/oles) pulmonary cap. muscles
Afferent Trigeminal Vagus Glossopharyngeal Vagus Vagus Vagus Intercostal
Deep inspiration  *inhibit insp. *Shallow rapid *Inhibit Insp.
Shallow rapid
Forced Expiration against Apnea Center. breathing. Center.
Response breathing
*Start expiration *Broncho const. *Start expiration
Open glottis Closed glottis

30
 Hypoxia ‫ يحًذ فايس‬.‫د‬
Hypoxic Anemic Stagnant Histotoxic
1.  PO2  High altitude 1. Anemia
General
Block of cellular
2. 2. CO poisoning Oxidative enzymes
Lung Diseases
Heart failure

Causes  Gas VA/Q

Hypoventil. Local
Cyanide Alcohol
Diffusion Imbalance

neumonia Vascular spasm

P ul. Congestion
ul. fibrosis
Emphysema
Treated by
Nitrite, Methylene blue
(react with cyanide) 
Morphine Cyan Hb (Non Toxic)

P oliomyelitis
neumothorax
ulmonary (Obstructive)
3. Shunt of Venous blood into Arterial blood
PO2 
(VSD) Normal
O2 Therapy Beneficial except "shunt" Limited Hyperbaric

Cyanosis + - + -

31
 Notes ‫ يحًذ فايس‬.‫د‬

Hypoxia
(clinical) O2 Toxicity Cyanosis

80-100% 100% Bluish discolor. Threshold

CNS Cardio- GIT

pulmona > 5 gm reduced Hb
ry Nose congested Bronchi ‫إثارج‬ /100 ml blood
onvulsions
‫دوخح‬ ‫صذاع‬ ‫فقذان شهيح‬ sore throat

cough
C oma
achypnea Dizziness
T achycardia
Cyanosis

‫ال يحذث أيضا مع‬ ‫يحذث أيضا مع‬

Severe cold Moderate cold
Co poisoning Asphyxia

32
 Barometric Pressure ‫ يحًذ فايس‬.‫د‬

Decreased Increased

High Altitude
Nitrogen High pressure Oxygen
Narcosis nervous $ toxicity
10.000 feet > 10.000 feet

Headache *  PN2 * O2 + Helium

onvulsions
(+) Peripheral
chemoR.
 Hb
Satur.
Acute Mountain
Sickness
‫ فقذان‬Appetite
nsomnia
‫كأوه شارب خمز‬ ‫تأثيز مخذر‬
C oma

I rritability
* ttt: O2 + Helium Tremor Drowsy

Rapid HR Decompression sickness

Compensatory Mechanisms to (Caisson's Disease)
Acclimatization to  Altitude
*  Pressure 1 atmosphere every 10 m depth diving.
MCQ ‫هاو‬ Ventilation, Pulmonary flow   Diffusion * Rapid ascent (Diver breathes compressed air
Resp. Alkalosis Erythropoietin   Hb   O2 carriage (80% N2)  N2 escapes from Tissues 
corrected by 2,3 DPG  shift O2-Hb curve (Right) rthritis
HCO3 excretion itochondria, oxidative enzymes Bubbles  A rterial obstruction  Pain
M yoglobin
* ttt: Immediate recompression  Slow decompression.

33
 Respiratory Adjustment in Health, Disease ‫ يحًذ فايس‬.‫د‬

Barometric
Exercise pressure

O2
Ventilation

Causes
Arterial

P CO2
H
Slight
Constant (Moderate Exercise)
Severe Exercise
Shift O2-Hb curve (Right)

Lactic
acid

ً‫وفض‬ Cortex Hypothal. ‫حزارج‬

+  H+
+
Carotid bodies
Respiratory +
center (Medulla) Peripheral chemo Rec.

Aortic bodies
Muscle Receptors
X J receptor
Pulmonary blood flow 5.5 L  20-35 L/min
Alveoli + Means Stimulation

Ventilation (End) till O2 debt is paid Pulmonary capillary

34
 Respiratory ‫ يحًذ فايس‬.‫د‬

Abnormalities Failure

)‫(أنظر انصفحت انقاديت‬

Resp. effort
sphyxia caused by drowning, paralysis of respiratory muscles
A pnea
HR

Nervous Chemical Sleep

Voluntary Swallowing Adrenaline Central Air way obstruction

Apnea Hyperventilation
O2 lack Apnea  Hyperventil. Chyne-stoke

Uremia Brain injury

35
 Respiratory Failure ‫ يحًذ فايس‬.‫د‬

PO2 <60 mmHg (Hypoxemia)

+
PCO2 >45 mmHg (Hypercapnia)

Hypercapnic Normocapnic

Resp. (Center, Muscle Paralysis) neumonia

COPD P ulmonary "edema, fibrosis"

Artificial Respiration

outh to mouth breathing

M echanical ventilation PEEP
Positive end expiratory pressure

36
Biophysics

1
 Homeostasis ‫ محمد فايز‬.‫د‬

Definition: Stability of internal environment

[1] [2] [3]

Characteristics Receptors Controller Effector

[4]
Advantages MCQ ‫هــام‬ Response (feedback)

1) Not unlimited Negative Positive

2)  Chance of survival Antagonistic to stimulus Same as stimulus

Viscious circle
3) Allows freedom to work

4) Permit proper function of brain seful Fatal

U terine constractions (Irreversible shock)

2
 Pressure, Resistance ‫ محمد فايز‬.‫د‬

Carbohydrates Lipid Proteins

Receptors Barrier (Selective) Receptors

Blood group markers ence arriers ( Pmps)

F
C
Membrane
dentity markers luidity hannels (Ion)

I mmune reactions ell adhesion molecules

atalyze chemical reactions

Endoplasmic Reticulum Homeostasis -ve feedback

Smooth Rough
Maintenance of internal
Steroid Protein
environment relative stable
Synthesis

3
 Total Body Water ‫ محمد فايز‬.‫د‬

Decreases with age Weight of adult male 70 Kg Females: Less ( fat)

60%
Volume of Injected Substance ===
=== 42 L
Amount injected – Amount removed
Concentration 28 L 14 L

ISF: 10.5 L
ICF ECF
 ECF/ICF (Infant, Child)
Plasma: 3.5 L

More severe dehydration

TBW ECF Plasma I CFSF
nulin
Proteins ICF > Plasma > ISF
* Labeled water I sotopes
Evans Blue Not
Measured a) Deutrium oxide
hiosulphate Albumin labeled measured
by: b) Tritum oxide
* Aminopyrine
TSucrose,
hiocyanate with 131I Directly

Mannitol

4
 Transport ‫ محمد فايز‬.‫د‬

Lumen Cell Plasma

Na+ 2 Ka+
Glucose 3 Na+

2ry active (-) Na+-K+ pump (+)

(Symport = Co-transport)

Lumen Cell Thyroid hormones

Ouabain Aldosterone
+ Insulin
Na
H+
Treat Heart Failure

Low  High conc.

2ry active Transport Active Transport
(Antiport = Counter transport)
Needs (Energy, Carrier)

5
 Transport ‫ محمد فايز‬.‫د‬

D i f f u s i o n Primary (1ry) Secondary (2ry)

(Simple) (Facilitated)
High  Low Conc. Energy provided Uses energy of 1ry
from ATP active Na+ to
Characters No Energy Characters hydrolysis transfer ‫مواد‬
Carrier Vs conc. gradient
No carrier Transport Max.
1) Na+-K+ pump 1) Co transport
Lipid bilayer
* Electrogenic * Glucose
O2 CO2 Glucose Urea * 3 Na+ out: 2K+ in * Amino acid
* Importance:
Ion channels Maintain (RMP, 2) Antiport
Example Glucose Example * Na+-Ca++
cell volume)
Leakage Gated exchanger
2) Ca++ pump. * Na+-H+
Ligand Voltage exchanger
3) H+-K+ pump

Macromolecules
Endocytosis Exocytosis

Phagocytosis Pinocytosis
(cell eating) (cell drinking)

6
 Movement of Water ‫ محمد فايز‬.‫د‬
Water Diffusion
( H2O   H2O Conc.) Osmosis Prevented by osmotic pressure Filtration
( Solute   Solute)
Water moves from Fick's Law
Mole MW of substance (gram) high  Low
hydrostatic press.

Definitions Equivalent Mole (Ionized substance)/Valence

Filtration rate
====
Osmole Conc. of osmotic active particles  P x S A X filtration coefficient

Osmolarity Number of osmoles/Liter Ultra filtration Plasma - colloid

Osmolality Number of osmoles/Kg solvent Solvent drage Solvent takes some

molecules of solute

‫عندما يتحرك فى إتجاه معين‬

Plasma Described by Tonicity Small force
 290 mosomol/L
Iso
Tonic Hyper
Hypo

7
 Non Diffusible Ions (Proteins) ‫ محمد فايز‬.‫د‬

Before equilibrium At equilibrium

Side X Side Y Side X Side Y

5 Na+ 10 Na+ 9 Na+ 6 Na+

5 Protein- 10 Cl- 4 Cl- 6 Cl-

5 Protein-

CONC
gradient equals, opposes electric gradient
Gibbs Donnan Equilibrium
product of Diffusible ions equal (6x6 = 9x4)
of Diffusible cation (Na+) greater in side X

Cationic charges = Anionic charges (Side X = Side Y)

Cl- shift phenomena Fluid reabsorption

8
 Blood Volume ‫ محمد فايز‬.‫د‬

8% BW Calculation

100 100
RBCs volume x Plasma volume x
HV 100-HV

Plasma 5% of TBW

Cation: Na+
ECF
Anion: Cl-
Main
Cation: Na+
ICF
Anion: hsophate
P rotein

9
 Physics Control Blood Flow ‫ محمد فايز‬.‫د‬

Flow (F) =  P / Resistance (R)

Blood flow

Type Velocity

Korotkoff's sounds
Laminar Turbulence Relation with Pressure
Murmers )‫(أنظر الصفحة القادمة‬

Reynold number VPD


V : Velocity of blood
<2000 >2000 >3000 P : Density of blood
D : Diameter of tube

Laminar flow Transitional Turbulent flow  : Viscosity

10
 Pressure relation with ‫ محمد فايز‬.‫د‬

Velocity of blood flow Tension (T)

Bernoulli's Principle Laplace law

Resistance (Middle of tube) Alveoli Capillaries Dilated heart

Pressure

Potential energy (PE)

P = 2T/r T=Pxr T= P x r/w
Kinetic energy (KE)

PE + KE = Constant

Importance Importance

Small alveoli Small capillaries Dilated heart ( r)

Atherosclerosis Small tension Small tension  Tension

Not ruptured Not ruptured Maintain same press.

11
 Pressure, Resistance ‫ محمد فايز‬.‫د‬

Pressure at which no flow

Systemic Pulmonary

MAP – CVP MPP – PVP

Critical closing Pressure

P === ===

90-0 = 90 mmHg 15-0 8= L15mmHg

Poiseuille's law R= R : Resistance
r4 L : Length
 : Viscosity
r : Radius
Length, viscosity (constant) while radius is variable

MCQ If radius is doubled, resistance will decrease:

a) 2 Times.
b) 4 Times.
c) 8 Times.
 d) 16 Times.

12
Biostatistics

1
 Data

‫وصف تذوى أرقام‬ Qualitative Quantitative

Nominal Ordinal Discrete Continuous

‫لها إسن‬ ‫ليس لها إسن‬ ‫رقن تذوى كسر‬ ‫رقن ته كسر‬
‫ال يىجذ ترتية‬ ‫لها ترتية‬ e.g: number of e.g: weight
e.g: Blood e.g: severe Children (2-3) (58.5 kg)
groups head injury
(A,B,AB,O) ‫يوكن تصنيفها حسب‬
‫الحالت‬

Any Numerical Data (Age, Weight) is Quantitative

2
 )‫ (جمموعة أرقام يتم متثيلها برقم واحد‬Central tendency

Mean Median Mode

ً‫الوجوىع الكل‬ ‫الرقن األوسط‬ ً‫أكثر األػذاد تكرارا‬

‫ػذد األرقام‬

Advantage 1) ‫أفضل هقياس‬ 1) Not affected by extreme values 1) Not affected by extreme values

2) ‫ال تحتاج لترتية‬ 2) Used for data 2) Nominal data )‫(األفضل‬

‫ترتية األرقام‬
Disadvantages 1) Affected by extreme
(Ascending or Descending)
values

N.B: 1) Mode is easily located by finding peak in Frequency Distribution graph

2) Mode may be  1 e.g: 3, 4 , 5 , 6 , 4 , 6 (4 , 6)

3

Range
s
‫يساوي أكثر رقن – أصغر رقن‬
imple
ensitivity (Not)
cores (Extreme Limit)
 Mean Deviation = SD ,
Dispersion Measures
Mean Deviation Standard Deviation (SD) Variance
(Most Common)
‫الخطــــىات‬
‫ لألرقام‬Mean ‫) إحسة‬1
)×( ‫×) هن كل رقن‬-( Mean ‫) إطرح‬2
‫) إضرب ناتج طرح كل رقن فى نفسه‬3 ‫انظر هسألة الصفحة القادهة‬
‫) إجوغ الناتج هن الحطوة الثالثت‬4
‫ للخطوة الرابعت‬Mean ‫) إحسة‬5
 SD = Variance
4
 Central Tendency ‫مسائل عن‬

4, 5, 6 , 4 , 7 4 , 7 , 5 , 12 , 6 , 10

3rd + 4th number

Median = ‫ = ــــــــــــــــــــــــــــــــــــــــ‬6.58
2
Arrange numbers 1st (Ascending)
Arrange numbers 1st (Ascending)
1) 4
2) 4 1) 4

3) 5 2) 5
3) 6
4) 6 4) 7
5) 7 5) 10
6) 12
Mode = 4. Mode )‫(ال يوجذ‬

5
 Calculate Mean Deviation, Standard Deviation
x x –x - (x – x -)2
12 12 – 9 = 3 9
11 11 – 9 = 2 4
10 10 – 9 = 1 1
9 9–9=0 0
9 9–9=0 0
9 9–9=0 0
8 8 – 9 = –1 1
7 7–9=–2 4
6 6–9=–3 9
X : Number
X- : Mean = 81 / 9 = 9
Mean Deviation = Sum of (x – x-)2 / 9 = 28 / 9 = 3.11
Standard Deviation (SD) =  3.11 = 1.76

6
 Calculate Mean Deviation, Standard Deviation

Table Graph

Simple Frequency Distribution Complex Frequency Distribution

Distribution of 20 child according to weight (kg)

14,12,22,15,16,20,18,19,23,11,16,22,24,23,26,14,26,17,26,27,24,18

Relative Cumulative
weight (kg) Frequency Lung Cancer
Frequency % Frequency Total
1 10 – 14 3 15 15 Case Control
2 15 – 19 7 35 50 N % N % N %
3 20 – 24 6 30 80 Smoker 15 75 8 20 23 38.33
4 25 – 30 4 20 100 Non Smoker 5 25 32 80 37 61.67
Total 20 100 Total 20 100 40 100 60 100

Frequency: Range ‫عذد األرقام التى توجذ فى‬

Frequency
Relative Frequency %: ‫ ــــــــــــــــــــــــ‬x 100
Total

Cumulative Frequency: ‫ هع ها قبلها‬Relative Frequency ‫جوع‬

7
 Graph

Line graph Histogram Bar Chart Pei Chart

(Temperature chart) (Continuous Variable)

Frequency %
0 %
C

50 -
40 -

39 - 80 -

38 - 70 - 30 -

37 - 60 -
Time ABP

3 6 9 12 100 120 140 160

Quantitative Qualitative
8
Collection

1
 Compare ‫ محمد فايز‬.‫د‬
Anemia Polycythemia
1. Aplastic. Primary polycythemia (Polycythemia vera),
2.  Iron, vitamin B12. e.g. Tumors of BM
Causes 3. Hemolytic. Secondary polycythemia (Physiological)
4. Hemorrhagic. e.g. High altitude
5. Anemia of renal failure.
Hb < 11 gm% > 20 gm%
HV 30% 70-80% (1ry)
Blood indices Detect its type --
ESR Increased except iron deficiency Decreased
Cyanosis Absent Present
Pulse Water hammer --
Heart sounds 3rd --
ABP --  ( Viscosity   TPR)

2
 Physiology Laws ‫ محمد فايز‬.‫د‬
All or Non Starling Laplace
Threshold  firing level  Length of muscle   Force of contraction Alveoli  P = 2 T/r

Definition Maximal stimulus will give Within limit Capillary  T = PXr

the same response Dilated heart  T = PXr
W

Skeletal, Cardiac Muscle: * Alveoli, capillaries

* Tension  force of contraction. Small radius (r)
* Best contraction at length 2.2 . Small tension (r)
* > 2.2    force of contraction. Resist rupture

Significance Action potential Cardiac Muscle * Dilated heart

*  Length =  EDV =  COP (RV) = COP
(LV) = 5 L. r
* Not applied in Normal Heart.
* Applied in (Denervated, Transplant, T
Failing) heart.
O2 consumption

3
 Physiology Laws
Poiseuille Fick's

Resistance (R) = Diffusion rate (DR) =

8L P x SA x Solubility x Temp.

 r4  MW x thickness

Applied * Increased (Exercise)

Air way Blood vessels

P
Significance Radius is variable factor SA (open of closed
which determines either alveoli)
Resistance  or 
* Decreased e.g. pulmonary edema

( Thickness)

N.B.: Mareys' law ( BP   HR)

4
 CVS Reflexes
CNS Ischemic reflex Cushing Reflex Bezold-Jarisch Reflex

* Myocardial infarction
MAP <50 mmHg
Stimulus * Injection of:
Decreased Blood flow to VMC Veratridine
Nicotine
Normal CSF Brain Tumor
Serotonin
Stimulate Ischemic Neurons (Pressor area VMC)
Strong VC
BP HR
Response
Blood flow to VMC BP

Prevent death of brain neurons

(‫ دقائق‬3 ‫)قبل‬

5
 CVS Reflexes

Baroreceptor reflex Peripheral chemoreceptor Bain Bridge Reflex

reflex
Pulse pressure fluctuations MAP <80 mmHg VR
Stimulus
 Discharge (sustained press.)
Receptor Aortic arch, carotid sinus Bodies (Aortic, carotid) Type B "Atrial", Pulmonary
Afferent IX, X IX, X X
Center CIC, VMC CIC, VMC CIC
Efferent Vagus Sympathetic X, Sympathetic

* Stimulates CIC   HR * Stimulates CIC   HR X Sympathetic

* Inhibits VMC * Inhibits VMC
 CIC  SA node
Vaso- veno- Vaso- veno-
Response dilatation dilatation constriction constriction Tachycardia
VR VR
EDV EDV
SV SV
 BP COP  BP COP

6
 Compare CO2, O2
CO2 O2
No Exchange Nose Terminal Bronchioles (Dead Space)
90% (HCO3) Hb, Myoglobin
Transport 5% (Carbamino compound)
5% (Hb)
% Hb Saturation 2.5% 97.5%
Dissociation curve Linear Sigmoid
Shift to right
 release
From tissues  Hb unloads O2 (Bohr effect) From Hb   Hb affinity to CO2 (Haldane effect)
Receptors stimulated: (Central: Main), Receptors stimulated: Peripheral chemo R. only
Peripheral: Weak
Effect on 5%   Ventil. 3-4 Times  PO2 < 60 mmHg   Ventilation
ventilation Increased
70-80%  RC depression
Decreased  Apnea
Respiratory failure Hypercapnic Hypoxemia (Normocapnic)
Effect on BV VD Lack causes VC
Effect on cerebral VD Physiological: No or limited effect
circulation Pathological: PO2 (30 mmhg)  2 CeBF.

7
 Compare CO2, O2
CO2 O2
Content
Arterial 48 ml/100 ml 19.8 ml/100 ml
Venous 52 ml/100 ml --
Pressure
Arterial 40 mmHg 100 mmHg
Venous 46 mmHg 40 mmHg
MW High Low
Solubility 24 Times more
Diffusion
20 Times more
coefficient
VA/Q
Local Homeostatic  CO2  Bronchoconstriction  O2  VC

Imbalance  CO2  Shift ventilation away from

poor perfused alveoli

Exchange Alveoli

8
 Note the difference
Boyle's effect Boyle's equation Ficks law Ficks principle
 CO2 release Measures dead space Diffusion rate (DR) Measures COP
% CO2 expired - % CO2 Alveolar air
X 500 === ===
 Hb affinity to O2 % CO2 expired
 P x SA x Sol. X Temp Tissue O2 consumption
(Hb unloads O2) 6% - 4%
X 500 =  150 ml
 Mw x Thickness A-V difference
6% = 5 L/minute

Active hyperemia Reactive hyperemia Local potential Local response

 Blood flow to tissue Blood flow returns to tissue after  Subthreshold When cathode (+) produce 7 mv

temporary occlusion of BV  Graded, summated

 NO LL or none law Some voltage gated

e.g. 1) Skeletal muscle.

2) Cardiac muscle
A RP Na+ channels open

 Decremental conduction
Magnitude of depolarization greater
 Site: Receptor than expected.

Orthodromic: Same direction

Antidromic: Opposite direction