Cardiovascular physiology The objectives are to know the following: 1. Functional anatomy of the heart 2. The basics of heart physiology& the origin of heart beat 3. Changes that occur during cardiac cycle 4. Cardiac output & factors affecting it 5. Hemodynamics 6. Physiological abnormalities causing diseases
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Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
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Cardiovascular physiology The objectives are to know the following: 1. Functional anatomy of the heart 2. The basics of heart physiology& the origin of
heart beat 3. Changes that occur during cardiac cycle 4. Cardiac output & factors affecting it 5. Hemodynamics 6. Physiological abnormalities causing diseases
Cardiovascular system Functions of cardiovascular system include: 1. Transport of O2, glucose,A.A, F.A, vitamines,
drugs & water to the tissues. 2. Rapid washout of metabolic waste products like
CO2, urea & creatinine 3. CVS is part of a control system in that it
distributes hormones to the tissues & even secrete hormones by itself e:g ANP
4. Plays vital role in temperature regulation
Cardiovasular system Consists of: Heart: A pump that pumps blood under high
pressure A set of blood vessels for conduction of blood
from & back to the heart
Physiology of heartThe heart is a muscular organ. It’s wall consists of three layers:
1.Endocardium
2. Myocardium
3. Pericardium:
a.Visceral ( Epicardium)
b.Parietal:
1.Inner serous layer
2.Outer fibrous layer
PERICARDIUM&HEART WALL
Three Layers of Heart WallFrom the outside-in
- Epicardium- visceral pericardium
- Myocardium- the muscular wall
- Endocardium
Architecture Pericardial cavity Pericardium
Viscreal-epicardium-in direct contact with the heart
Pericardial cavity contains a small amount of fluid
Attached to diaphragm by fibers
Location Lies near anterior
chest wall, behind sternum
Tilted slightly to the left
Rotated slightly to the left
This causes the anterior surface to consist of the right atria and ventricle
Functional anatomy of heart Heart is divided into 2 halves: Rt.& Lt. Each half consists of an atrium & a ventricle Atrium & ventricle of the same side connect
through atrioventricular opening. AV opening guarded by presence of a valve
[ Atrioventricular valves- AV valves] Mitral valve on Lt.side Tricuspid valve on Rt.side
Heart ( functional anatomy) From Lt.ventricle arises the aorta From Rt.ventricle arises The pulmonary artery Openings of the large arteries are guarded by
semilunar valves: Aortic & pulmonary valves Valves are passive structures: they open when
there is a forward pressure to allow forward flow of blood
They close when there is a backward pressure to prevent backward flow of blood
Heart functional anatomy Blood reaches Rt. atrium via superior &
inferior vena cava Blood reaches Lt. atrium via pulmonary veins Opening of the veins are not guarded by
valves
Atrial Ventricular
Cardiac Muscle Almost totally dependant on aerobic
metabolism Each cell connected to its neighbor by
intercalated discs Gap junctions connect one cardiac muscle
fiber to another,act as functional syncytium- In the gap junction there is a channel that
allow movement between adjacent m.f- Diameter of channel is affected by
intracellular calcium concentration
FUNCTIONAL SYSCYTIUM
Cardiac muscle- Striated muscle- Arrangement of Actin, Myosin, Troponin &
Tropomyosin is similar to those in skeletal muscle.
- Excitation contraction coupling is similar to skeletal muscle
- Source of calcium ions: Sarcoplasmic reticulum+I.S.F through calcium channels
Cardiac muscle Because of presence of gap junctions, when
one cardiac muscle fiber is depolarized the wave of depolaization pass to other cardiac muscle fibers,acting as functional syncytium
All or None law applies to the whole cardiac muscle & not to a single muscle fiber as in skeletal muscle.
Sarcomeres are composed of myosin and actin
Several proteins mediate the interaction of myosin heads with the actin filament
Calcium signaling triggers contraction
ACTION POTENTIAL IN CARDIAC MUSCLE It is characterized by the presence of action potential
plateau ( 0.1-0.3 sec) Plateau keeps the membrane depolarized for longer
time than depolarization in skeletal muscle Plateau is due to inward calcium movement through
calcium channels Long refractory period No tetanization of cardiac muscle
REFRACTORY PERIOD
Conducting System Cardiac cells contract in the absence of neural
or hormonal stimulation. This is known as Self excitation or Rhythmicity.automaticity
Property of self excitation is obvious in the conducting system of the heart which is made of modified cardiac muscle fibers.
Path of the Action Potential Conducting system of heart: SA Node ( Pace maker of the heart)
- Atrial conducting pathways AV Node
- Impulse slows down to allow for blood movement and ventricular filling
Bundle of His Left and right bundle branches Purkinje fibers
Heart Physiology: Sequence of Excitation
Figure 18.14a
Heart Physiology: Intrinsic Conduction System Autorhythmic cells: Pace maker
Initiate action potentials Have unstable resting potentials called pacemaker
potentials Use calcium influx (rather than sodium) for rising
phase of the action potential
Pacemaker and Action Potentials of the Heart
Figure 18.13
Conducting system of heart Coducting system perform 2 functions: 1. Generation of impulses 2. Conduction of these impulses Rate of different parts of conductive system: SA node: 70-80/min AV node: 40-60/min Purkinje fibers: 15-40/min SA node dominates because of it’s high rate of
discharge & is the pace maker of the heart. The other parts function in conducting the impulses.
Heart Physiology: Sequence of Excitation Sinoatrial (SA) node generates impulses about
75 times/minute Atrioventricular (AV) node delays the
impulse approximately 0.1 second (allow atria to contract before ventricles)
Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His)
Heart Physiology: Sequence of Excitation AV bundle splits into two pathways in the
interventricular septum (Rt.& Lt.bundle branches) Bundle branches carry the impulse toward the
apex of the heart Purkinje fibers carry the impulse to the heart apex
and ventricular walls ( fast conduction allow the ventricle to contract as one unit)
Extrinsic Innervation of the Heart
Heart is stimulated by the sympathetic cardioacceleratory center
Heart is inhibited by the parasympathetic cardioinhibitory center
Figure 18.15
Cardiac cycle An action potential generated in the SA
node,travelling to the atria depolarizing them & bringing contraction of atria.
Action potential spreading to the ventricles through AV node,bundle of His & bundle branches depolarizing the ventricles & bringing contraction of the ventrices.
Contraction will be followed by relaxation
Cardiac Cycle Cardiac cycle refers to all events associated
with blood flow through the heart Cardiac cycle consists of systole &diastole
Systole – contraction of heart muscle Diastole – relaxation of heart muscle Duration: 0.8 sec if HR 72 ( 60/72) SYS: atrial (0.1sec), ventricular (0.3sec) DIAS: atrial (0.7sec), ventricular (0.5sec)
FUNCTIONAL ANATOMY OF HEART
Phases of the Cardiac Cycle Ventricular systole
Atria relax
1.Isometric ventricular contraction (0.06 sec)Rising ventricular pressure results in closure of AV
Phases of the Cardiac Cycle Ventricular diastole 1.Protodiastole (0.02 sec) ends by closure of semilunar
valves(2nd heart sound) 2.Isometric ventricular relaxation (0.05 sec) ends by
opening of AV valves 3.Rapid ventricular filling (0.16sec) 4.Slow ventricular filling (0.23sec) 5.Atrial systole (0.1sec) a new wave of depolarization
Changes during cardiac cycle 1. PRESSURE CHANGES A. in ventricles Rt ventricle 22/0 mm Hg Lt ventricle 120/0 mm Hg B. Aorta 120/80 mm Hg C. Pulmonary artery 22/8 D. Atria Rt.4-6, Lt.7-8 mmHg (a,c,v waves)
Changes during cardiac cycle 2.VOLUME CHANGES End Diastolic Volume (120-130ml) Stroke Volume 70 ml End Systolic Volume (50-60ml)
EDV- SV= ESV
Changes during cardiac cycle 3.HEART SOUNDS First heart sound LUP at beginning of systole Second heart sound DUP at beginning of
Changes during cardiac cycle 4.ELECTRICAL CHANGES Electrical changes originating in the heart
spreads to the surrounding tissue & some reaches the body surface & can be recorded
ELECTROCARDIOGRAPHY ECG
Phases of the Cardiac Cycle
Figure 18.20
Electrocardiography Electrical activity is recorded by
electrocardiography (ECG) P wave corresponds to depolarization of SA node QRS complex corresponds to ventricular
depolarization T wave corresponds to ventricular repolarization Atrial repolarization record is masked by the
larger QRS complex
Electrocardiography
Figure 18.16
Action potential in ventricular muscle
Heart Excitation Related to ECG
Figure 18.17
Recording ECG Recording is done by using two types of leads. 1. Bipolar leads: The potential difference between 2
active electrodes is recorded. Also called standard limb leads: Lead I,II,III
2. Unipolar leads: One active electrode called Exploring electrode is put on different points on body surface. The other electrode( indifferent electrode) is kept at zero potential
A. Unipolar limb leads( aVR, aVL, aVF) B. Unipolar chest leads( precordial leads):
V1,V2,V3,V4,V5,V6
Standard limb leads & Einthoven triangle
Einthoven law: I + III = II
Unipolar chest leads( precordial)
Precordial leads
Augmented limb leads: waves inverted in aVR
Waves & Intervals P wave: duration:0.1sec,voltage, 0.1-0.3mv P-R interval: 0.12-0.2 sec ORS complex: duration 0.08sec, voltage 0.5-
1.5mv T wave: duration 0.27sec, voltage 0.2-0.3mv Q-T interval: 0.35sec
Most ventricular activity that is recorded is activity in the left ventricle. The same activity gives different shapes in different leads because a wave of depolarization moving toward an electrode will cause an upward deflection on the ECG needle while if depolarization is moving away from an electrode that electrode records a negative wave.
Generation of the ECG complexes
READING ECG 1. Find heart rate 2. Detection of conduction defects 3. Detection of abnormality in rhythm
(arrhythmias) 4. Detection of signs of ischemia 5. Detection of atrial or ventricular
hypertrophy
Heart rate Is found by dividing 300 by the no. of large
squares between 2 successive R waves Normal HR 60-90/min Below 60/min. Bradycardia Above 90/min. Tachycardia
Calculation of heart rate
CONDUCTION DEFECTS 1.SA node .Sick sinus syndrome ( Stoke’s Adam
syndrome) :atrial escape.Corrected by artificial pacemaker. 2. AV node,bundle of His. (Heart block) a. Incomplete heart block: 1. 1st degree HB ( prolongation of P-R interval) 2. 2nd degree HB ( 2:1 or 3:1 block) b. Complete heart block (3rd degree HB) ( ventricular escape ventricles beat by their idioventricular
rhythm) 3. Bundle branch block ( RBBB, LBBB)
Sinoatrial block with AV nodal rhythm
First degree heart block
Second degree heart block
Complete heart block
ARRHYTHMIAS 1. SUPRAVENTRICULR a. Sinus ( tachycardia, bradycardia) b. Atrial ( extrasystole, paroxysmal atrial
Arrhythmias If the irritable ectopic focus discharges once,
the result will be a premature beat or extrasystole
If the focus discharges repetitively at a rate more rapid than SA node, it produced rapid regular tachycardia
A very rapidly & irregularly discharging focus or more likely group of foci can produce fibrillation
Sinus tachycardia
Sinus bradycardia
Supraventricular extrasystole (premature beat)
Ventricular extrasystole
Paroxysmal atrial tachycardia
Paroxysmal ventricular tachycardia
Ventricular fibrillation
Circus movement A common cause of paroxysmal arrhythmias
is a defect in conduction that permits a wave of excitation to propagate continuously within a closed circuit producing circus movement or Re-entry movement
Re-entry ( circus movement)
Atrial flutter & atrial fibrillation
SIGNS OF ISCHEMIA Decreased blood flow to the myocardium Angina pectoris Myocardial infarction
Signs of ischemia
Atrial hypertrophy Right atrial hypertrophy: Tall & peaked p
wave
Left atrial hypertrophy: Broad & Bifid p wave
Ventricular hypertrophy Estimating the electrical axis of the heart or
the main direction of the cardiac vector Estimated from the QRS deflection in 2
standard limb leads usually lead 1 & lead 3 Normal electrical axis of the heart +59
degrees [ normal range (-30)-(+110) ]
Visualization of the generation ofthe Left Ventricular portion ofthe ECG complex in Lead II
1. Septum depolarizes from the inside out and the resulting depolarization wave moves away from the electrode recording Lead II
2. The rest of the ventricle depolarizes counter-clockwise from the inside out and creates the (large arrow) which is essentially, the algebraic sum of all of the small depolarization vectors. This vector is, in a normal heart, almost always moving directly toward Lead II, generating a mostly positive QRS complex
main cardac vector
Lead II electrode60 downwardrotation angle from the horizontal 0
o
o
60o
Note: compared tothe left ventricle, the right ventricle is muchsmaller and contributeslittle to the overall mainvector of depolarization
(DEPOLARIATION)
Cardiac vector
Estimation of electrical axis
Electrical axis of different leads
Electrical axis estimated from 2 bipolar leads
Electrical axis of heart
Left axis deviation
Right axis deviation
Cardiac Output (CO) and Reserve CO is the amount of blood pumped by each
ventricle in one minute CO is the product of heart rate (HR) and stroke
volume (SV) HR is the number of heart beats per minute SV is the amount of blood pumped out by a
ventricle with each beat Cardiac reserve is the difference between resting
and maximal CO
Cardiac Output: Example CO (ml/min) = HR (75 beats/min) x SV (70
ml/beat) CO = 5250 ml/min (5.25 L/min) Change in HR or change in SV or change in
both of them can change the CO
Regulation of Stroke Volume SV = end diastolic volume (EDV) minus end
systolic volume (ESV) EDV = amount of blood collected in a
ventricle during diastole ESV = amount of blood remaining in a
ventricle after contraction
Factors Affecting Stroke Volume Preload – amount ventricles are stretched by
contained blood[EDV] .increase EDV increases SV Contractility – cardiac cell contractile force due to
factors other than EDV Afterload – Is the resistance to ventricular ejection
caused by resistance to flow in systemic circulation Increase afterload decreases SV
Frank-Starling Law of the Heart Preload, or degree of stretch, of cardiac muscle
cells before they contract is the critical factor controlling stroke volume. The heart can pump a small or a large volume of blood depending on blood reaching it.
Slow heartbeat and exercise increase venous return to the heart, increasing SV
Blood loss and extremely rapid heartbeat decrease SV
Venous return to the heart Venous return &EDV increase by: 1. Skeletal muscle contraction 2. Increased negative intrathoracic pressure
during inspiration 3. venoconstriction 4. Increased blood volume
Contractility of myocarium Contractility is the increase in contractile
strength, independent of preload & afterload Increase in contractility comes from:
Increased sympathetic stimuli Certain hormones:g Noradrenaline Ca2+ and some drugs ( sympathomimetic drugs)
Contractility and Norepinephrine
Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system
Figure 18.22
Afterload Resistance offered to ventricular ejection Hypertension, Aortic stenosis Stroke volume is inversely proportional to
afterload
Regulation of Heart Rate Positive chronotropic factors increase heart
rate Negative chronotropic factors decrease heart
rate HR is affected by: Nervous & Hormonal
factors
Sympathetic nervous system (SNS) stimulation is activated by stress, anxiety, excitement, or exercise. Increases HR
Parasympathetic nervous system (PNS) stimulation is mediated by acetylcholine and opposes the SNS. Decreases HR
PNS dominates the autonomic stimulation, slowing heart rate and causing vagal tone
Regulation of Heart Rate: Autonomic Nervous System
Atrial (Bainbridge) Reflex Atrial (Bainbridge) reflex – a sympathetic
reflex initiated by increased blood in the atria Causes stimulation of the SA node Stimulates baroreceptors in the atria, causing
increased SNS stimulation
Chemical Regulation of the Heart The hormones epinephrine and thyroxine
increase heart rate Intra- and extracellular ion concentrations
must be maintained for normal heart function
Factors Involved in Regulation of Cardiac Output
Figure 18.23
MEASUREMENT OF CO Clinical exam. Gives a good indication of
cardiac function. For example: Skin temperature Capillary refill. Pulse rate & pulse volume. Urine output level of consciousness are reliable markers of
CO
Measurement of C.O 1. Fick method ( O2 consumption method) Total O2 consumption in one min. C.O= Art.O2 content- Venous O2 content
250ml/min e:g =5L/min 190-140
Measurement of C.O 2. Dye dilution method A known amount of dye or radioactive isotope is
injected to an arm vein & the concentration of the indicator in serial samples of arterial blood is determined
mg dye injected C.O= mean conc. X time from appearance to
disappearance of dye
Measurement of C.O 3.Doppler method with Echocardiography Pulses of ultrasound are directed at the blood
flowing in ascending aorta & reflected back to the probe by red cells in the blood. The velocity of blood in aorta is measured & if the cross sectional area of aorta is measured by echocardiography the stroke volume & C.O can be calculated
Effect of various conditions on C.O NO CHANGE: 1. Sleep 2. Moderate change in environmental temp.
Increase C.O 1.Anxiety & excitement 50-100% 2.Eating 30% 3.Exercise up to 700% 4.High environmental temp. 5.pregnancy
Decrease C.O 1.Sitting or standing from lying position 20-30% 2.rapid arrhythmias 3.Heart disease
Oxygen consumption of the heart At rest: 9ml/100gm/min [ normal wt.250-300gm] Increases during exercise & in a no. of different conditions Cardiac muscle obtain energy mainly from metabolism of
fatty acids & to a lesser extent from glucose & lactate. Energy expenditure determined by: 1. Heart rate 2. Arterial B.P Energy expenditure can increase when these 2 parameters
increase even though the cardiac output is not changed.
Vascular system
Circulation
Systemic circulation
HEMODYNAMICS Include the study of : 1. Mean pressure 2. Type of flow 3. Speed of flow In different parts of the circulation [systemic
circulation]
HemodynamicsBLOOD VESSELS:
[anatomical & functional classification]
A. Arteries (high pressure vessels)[conducting vessels]
1. structure a. thick-walled b. large diameter c. elastic
HEMODYNAMICS
B. Arterioles [resistance vessels][1]. structure a. small diameter b. smooth muscle in wall 1. vasoconstriction, vasodilatation 2. vascular tone[2]. function: to regulate blood flow to capillary beds
HEMODYNAMICS
C. Capillaries [exchange vessels] 1. structure a. thin-walled; porous b. narrow c. Large surface area 2. function: exchange 3. capillary blood flow: regulated by presence of a. precapillary spincters
HEMODYNAMICS
D. Veins [storage or capacitance vessels]1. low pressure vessel2. structure a. large diameter b. distensible c. thin-walled d. Valve3. function: storage4. venous return mechanisms a. skeletal muscle pump b. sympathetic vasoconstriction c. Thoracic pump
Blood Flow Blood flow is defined as the quantity of blood
passing a given point in the circulation in a given period and is normally expressed in ml/min
Overall blood flow in the total circulation of an adult is about 5000 ml/min….The cardiac output
FORWARD BLOOD FLOW
Mechanisms – Movement of Blood1.Forces imparted by rhythmic contractions of the heart2.Elastic recoil of arteries following filling by the action
of the heart3.Squeezing of blood vessels during body movements4.Peristaltic contractions of smooth muscle surrounding
Slight changes in the diameter of a vessel cause tremendous changes in the vessel's ability to conduct blood when the blood flow is streamlined
Although the diameters of these vessels increase only fourfold, the respective flows are 1, 16, and 256 ml/mm, which is a 256-fold increase in flow. Thus, the conductance of the vessel increases in proportion to the fourth power of the diameter
Peripheral resistance Blood flow is determined by: 1. Pressure difference between the 2 ends of
the vessel 2. Peripheral resistance: A. Vessel diameter: Resistance is inversely
proportional to the fourth power of radius B. Blood viscosity: determined by no. of RBC
& by plasma proteins
HEMODYNAMICS Mean pressure: average pressure during the
whole cardiac cycle In the arteries it is obtained by : 1 systolic pressure+2diastoloic pressures 3 The mean pressure is important for proper
tissue perfusion.
MEAN PRESSURE Arteries: 95mmHg Beginning of arterioles: 85mmHg Leaving arterioles: 30mmHg Venular end of capillary: 10mmHg Rt atrium: around zero mmHg All these values are for blood vessels at the
level of the heart.
MEAN PRESSURE
TYPE & SPEED OF FLOW Arteries:Pulsatile flow Capillaries & Veins: Continuous flow Systolic BP-Diastolic BP= Pulse pressure Pulse pressure enables us to feel pulse Arteries: speed of flow 40cm/sec Capillaries: 0.07cm/sec Veins: 10cm/sec
LAMINAR & TURBULENT BLOOD FLOW Normally blood flow is laminar flow[silent] If blood passes by an obstruction or rough
surface or if it’s speed increases , it changes to Turbulent flow[ noisy flow]
Modes of flow in vessles Blood flow can either be laminar or turbulent
Laminar Flow
When blood flows through a long smooth vessel it flows in straight lines, with each layer of blood remaining the same distance from the walls of the vessel throughout its length
When laminar flow occurs the different layers flow at different rates creating a parabolic profile
The parabolic profile arises because the fluid molecules touching the walls barely move because of adherence to the vessel wall. The next layer slips over these, the third layer slips over the second and so on.
LAMINAR or STREAMLINE FLOW
P2P1
P1 > P2
-Cone Shaped Velocity Profile-Not Audible with a Stethoscope
Turbulent flow
When the rate of blood flow becomes too great, when it passes by an obstruction in a vessel, when it makes a sharp turn, or when it passes over a rough surface, the flow may then become turbulent
Turbulent flow means that the blood flows crosswise in the vessel as well as along the vessel, usually forming whorls in the blood called eddy currents. When eddy currents are present, the blood flows with much greater resistance than when the flow is streamline because eddies add tremendously to the overall friction of flow in the vessel.
Turbulent blood flow Turbulent blood flow is a noisy flow It produces sounds that can be heard by a
stethoscope The fact that turbulent flow produces sound is used
in measurement of arterial blood pressure Sounds produced by turbulence to blood flow during
blood pressure measurement are called : Korotkoff sounds
BLOOD PRESSURE Arterial blood pressure: It is the force of blood on the wall of arteries.
Blood pressure is important because it provides a forward driving force to the flow of blood & it ensures proper blood perfusion to all organs in the body specially the vital organs :
[brain, heart, kidneys]
Blood pressure Systolic BP: pressure of blood on the wall of
arteries during ventricular systole. Normal range is 100-140 mmHg
Diastolic BP: pressure of blood on wall of arteries during ventricular diastole. Normal range is 60-90 mmHg
Pulse pressure: difference between systolic & diastolic BP
Peripheral Resistance Blood viscosity Diameter of arterioles: Vasomotor tone [sympathetic tone] Arterioles are kept in a state of partial
vasoconstriction because of activity of VMC through sympathetic NS
Increased sympathetic activity= vasoconstriction Decreased sympathetic activity= vasodilatation There is no parasympathetic supply to blood vessels
BLOOD PRESSURE
B.P = C.O X P.R Changes in C.O affect systolic B.P Changes in P.R affect diastolic B.P
Neural regulation of blood pressure
Regulation of blood pressure 1. Neural control [ VMC, Sympathetic, Baroreceptors] Baroreceptors found in aortic arch & carotid sinus They are stimulated by increased blood pressure When stimulated they cause inhibition of VMC Inhibition of VMC decrease sympathetic discharge to blood
vessels This leads to vasodilatation and decreased peripheral
resistance = decreased blood pressure Baroreceptors have a buffering action on blood pressure
Aortic & carotid baroreceptors
Effect of increased BP on baroreceptor stimulation
Regulation of B.P 2. Hormonal regulation A. Epinephrine & Norepinephrine B. Antidiuretic hormone [ ADH] or
vasopressin C. Renin-Angiotensin- Aldosterone
system
The Adrenal MedullaActs very much like a part of the sympathetic
nervous system (fight or flight)Secretes two amines:
norepinephrine (20%) epinephrine (80%)
Stimulated by preganglionic neurons directly, so controlled by the hypothalamus as if part of the autonomic nervous system.
Effects of ADH
Renin-Angiotensin –Aldosterone system Decrease in BP or Decrease plasma sodium Stimulates cells in Juxtaglomerular apparatus
in the kidney to secrete renin Renin acts on angiotensinogen to form
angiotensin I Angiotensin I is activated to Angiotensin II
to heart =Increase CO 3. Stimulates adrenal cortex to secrete
Aldosterone which increases sodium reabsorption from renal tubules
Regulation of BP by renin-angiotensin
Regulation of BP by Renin-angiotensin
Blood pressure Effect of gravity on blood pressure: (+) or (-) 0.77mmHg/cm distance from heart level It is (+) for blood vessels below heart level It is (– )for blood vessels above heart level All values mentioned for mean blood pressure are
for blood vessels at level of heart Critical closing pressure: Blood flow stops if the pressure difference between
the 2 ends of a vessel is lower than peripheral resistance
Effects of gravity on arterial and venous pressures.Each cm of distance produces a 0.77 mmHg change.
Sphincters protectcapillaries
VENOUS PUMP keeps PV < 25 mm Hg
Veins Arteries
190 mm Hg
100 mm Hg0
HYPERTENSION Blood pressure levels above the generally
accepted normal according to age. 20 year: 140/90mmHg 50 year: 160/95mmHg 70 year: 170/105 Exercise,anxiety,discomfort & unfamiliar
surrounding can lead to to a transient rise in BP
ETIOLOGY OF HYPERTENSION 85-90% : Essential HT 10-15%: Secondary HT ,could be due to: 1. Renal diseases 2. Endocrine disorders& hormone therapy 3. Pregnancy 4. Coarctation of aorta( Ht in upper limb &
normal pressure in lower limb)
COMPLICATIONS OF H.T. 1. Left ventricular hypertrophy & MI 2. hypertensive encephalopathy & CVA 3. Hypertensive retinopathy 4. Hypertensive nephropathy Treatment aims at decreasing CO, or PR
or total blood volume & eventually decreasing BP
CAPILLARY CIRCULATION Types of capillaries: Throughfare, True Receives 5% of total CO Thin walled Speed of flow: 0.07cm/sec Exchange: by diffusion ( lipid sol.,water sol.),
pinocytosis. Water movement: by Filtration
Filtration of water Depends on Starling forces: 1. Filtration pressure= Hydrostatic pressure in capillaries-hydrostatic
pressure in I.S.F. 2. Osmotic pressure gradient= Colloid osmotic pressure in plasma-colloid
osmotic pressure in I.S.F.
Filtration
Filtration
ACTIVE & INACTIVE Capillaries Normally flow is through the throughfare vessels When there is an increased demand for blood flow,
blood pass through true capillaries as well. Vasodilator metabolites can cause capillary
Decreased sympathetic activity: Vasodilatation & relaxation of precapillary sphincter
VENOUS CIRCULATION Function: 1. Storing large quantities of blood(64%) of total C.O 2. Regulating C.O
Factors affecting venous flow: 1. Skeletal muscle contraction[ muscle pump] 2. Negative I.T.pre. During inspiration[thoracic pump] 3. Sympathetic venoconstriction 4. Presence of valves in limb veins.
VENOUS PRESSURE Central venous pressure is affected by a balance
between: 1. Pumping of blood by heart 2. Venous return Rt.atrial pressure & hence central venous pressure is
increased in: 1. Serious HF 2. Following massive transfusion of blood 3. Straining While it decreases in shock
VENOUS PRESSURE Effect of gravity on venous pressure is the
same as on arterial pressure Veins collapse when their pressure is zero or
below zero Measurement of venous pressure: Central venous pressure Peripheral venous pressure
LYMPHATIC CIRCULATION Constitute a one way route for the movement
of I.S.F to blood Lymphatic system; made of an extensive
network of thin vessels resembling veins arise as a group of blind end lymph capillaries permeable to all I.S.F. constituents
LYMPH FLOW Assisted by: 1. Pumping action of skeletal muscles 2. Effect of respiration on I.T.Pressure 3. Presence of valves 4. Rhythmic contraction of walls of large
lymph ducts
Functions of lymphatic system 1. Return of excess fluid from the
I.S.compartment 2. Return of proteins [ some capillaries are
permeable to protein] 3. Specific transport function for fat 4. lymph nodes & defence
4. Lymphatic obstruction e;g Filariasis or Elephantiasis
Cardiovascular regulatory mechanisms The aim of these mechanisms is to: 1. Increase blood supply to active tissues. 2. To increase or decrease heat loss from the
body by redistributing the blood. 3. In the face of challenges, e:g hemorrhage,
they maintain blood flow to vital organs at the expense of the rest of the body.
Cardiovascular regulatory mechanisms Cardiovascular adjustments are affected by: 1. Altering the cardiac output. 2. Changing the diameter of resistance vessels 3. Or changing the amount of blood pooled in
the capacitance vessels
Cardiovascular regulatory mechanisms Diameter of arteiole & amount of blood flow
can be regulated by; 1. Systemic regulation [affecting large
segment of circulation] 2. local regulation [ Auto-regulation]
hormones Vasodilator Vasoconstrictor Kinin Adr & Norad ANP Angiotensin II VIP ADH, Natriuretic F
AUTOREGULATION [local] Most tissues have an intrinsic capacity to
compensate for moderate changes in perfusion pressure by changes in vascular resistance so that blood flow remains constant.
This capacity is well developed in the kidneys,skeletal muscle, brain, liver & myocardium
Myogenic theory of autoregulation
AUTOREGULATION Local autoregulation could be due to: 1. Accumulation of metabolites: [ metabolic theory of autoregulation] Increase : CO2, H+, K+, lactic acid, Adenosine.
Or decrease O2
All lead to vasodilatation
AUTOREGULATION 2. Substances secreted by endothelium: a. Prostacycline [ vasodilatation] b. Endothelin [ vasoconstriction].Stretching of
blood vessels causes the release of endothelin c. EDRF [ Nitric oxide NO ]: vasodilatation
EndothelinEndothelin Biosynthesis Endothelin (ET-1) is a 21 amino acid peptide that is
produced by the vascular endothelium from a 39 amino acid precursor, through the actions of an endothelin converting enzyme (ECE) found on the endothelial cell membrane. ET-1 formation and release are stimulated by angiotensin II antidiuretic hormone (ADH), thrombin, cytokines, reactive oxygen species, and shearing forces acting on the vascular endothelium. ET-1 release is inhibited by prostacyclin and
atrial natriuretic peptide as well as by nitric oxide.
Endothelin Intracellular Mechanisms Once ET-1 is released by the endothelial cell, it binds to
receptors on the target tissue (e.g., adjacent vascular smooth muscle). There are two basic types of ET-1 receptors: ETA and ETB. Both of these receptors are coupled to a G-protein and the formation of IP3 . Increased IP3 causes calcium release by the sarcoplasmic reticulum, which causes smooth muscle contraction. In blood vessels, the ETA receptor is dominant under normal conditions in terms of ET-1 effects on contraction.
Nitric Oxide in the Muscular Nitric Oxide in the Muscular SystemSystem NO was orginally called EDRF (endothelium
derived relaxation factor) NO signals inhibition of smooth muscle contraction
Ca+2 is released from the vascular lumen activating NOS
NO is synthesized from NOS III in vascular endothelial cells
This causes guanylyl cyclase to produce cGMP A rise in cGMP causes Ca+2 pumps to be activated,
thus reducing Ca+2 concentration in the cell This causes muscle relaxation
Nitric Oxide in the Circulatory Nitric Oxide in the Circulatory SystemSystem
NO serves as a vasodilator Released in response to high blood flow rate and
signaling molecules (Ach and bradykinin) Highly localized and effects are brief If NO synthesis is inhibited, blood pressure rises During O2 delivery, NO locally dilates blood
vessels to aid in gas exchange
Nerve cells target the endothelial cells lining of blood vessels
Acetylcholine activates NO synthase & production of NO in endothelial cells that surround the smooth muscle cells surround the blood vessel.
Role of NO in smooth muscle relaxation of blood vessel walls
NO diffuses into smooth muscle, binds to heme group in guanylyl cyclase and activated synthesis of cGMP
Nitroglycerin is used to prevent chest pain (angina) because it is rapidly converted to NO
Synthesis of Nitric Oxide Nitric oxide is synthesized from L-arginine This reaction is catalyzed by nitric oxide
synthase, a 1,294 aa enzyme
COO-
C
(CH2)3
NH
C
H2N
H
NH2+
+H3N
Arginine
NOS
NADPH
+ O2
NAD+
COO-
C
(CH2)3
NH
C
H+H3N
N+
H2NH
OH
N-w-Hydroxyarginine
COO-
C
(CH2)3
NH
H+H3N + NO
NOS
C
O NH2
Citrulline
Types of NOS NOS I
Central and peripheral neuronal cells Ca+2 dependent, used for neuronal communication
NOS II Most nucleated cells, particularly macrophages Independent of intracellular Ca+2 Inducible in presence of inflammatory cytokines
NOS III Vascular endothelial cells Ca+2 dependent Vascular regulation
Synthesis & release of nitrous oxide (NO)
Nitric oxide synthase (NOS) catalyzes the synthesis of NO from the terminal nitrogen atom of L-arginine in the presence of O2
Once synthesized, NO can freely diffuse across plasma membranes reaching neighboring cells
NO acts locally, and has a very short half-life (5-10 secs)
PULMONARY CIRCULATION Receives same cardiac output= 5L/min Pulmonary a: Thin [1/3rd that of aorta] Branches of pulmonary a., smaller a. &
arterioles have larger diameter than corresponding systemic vessels.
Thinness+ Distensibility= very large compliance which permits the pul.a. to accommodate the C.O. of Rt.ventricle
PULMONARY CIRCULATION Pulmonary veins : compliance to similar to
those in systemic circulation Bronchial a.[oxygenated blood] : supply
connective tissue, septa, large & small bronchi. It empties in pul.vein & enters Lt. atrium.[ decreasing arterial PO2=physiological shunt]
The pulmonary circulation
tissue
CO2 O2
Pulmonary artery
RV
LA
Pulmonary vein
Pulmonary capillaries
PULMONARY CIRCULATION Pulmonary pressure= 22/8 mmHg Pulse pressure= 14 mmHg Pulmonary capillary pressure= 7mmHg Mean pressure at Lt.atrium & major
pul.veins= 2mmHg Blood volume in the lungs: 450ml[9% of CO] 70 ml of this blood is in the capillaries Remainder in the a. & v.
PULMONARY CIRCULATION Blood flow regulation: Local factors [ major role] & autonomic N.S.
[minor role] Pul.blood vessels constrict when PO2
decreases[ in systemic circulation there is vasodilatation when PO2 decreases]
Increase Lt.atrial pressure= slows venous return=increased pul. Cap.pre.=pul.edema
CIRCULATION THROUGH SPECIAL REGIONS
CORONARY CIRCULATION Coronary blood: 5% of resting C.O Major coronary vessels travel in the
epicardium & subdivide sending separate branches through the myocardium.
During Systole the myocardial wall tension compresses the vessels increasing resistance to flow
importance L > R (lower RV pressures) maximal L flow in early diastole
Coronary circulation Maximum flow in left coronary vessels
occurs during isometric ventricular relaxation while the arterial pressure is still relatively high & the myocardium is relaxed
Control of coronary flow: 1. Autoregulation [ Adenosine] 2. Sympathetic stimulation through ß
receptors
Coronary blood flow
SNS stimulation Receptors:
(vasoconstrictor) (vasodilator)
Direct SNS effect: vasoconstriction Overcome by vasodilation due to
metabolic activity (local regulation dominant)
Coronary circulation Energy obtained mostly through aerobic
pathway Normally Hb releases approximately half of
it’s arterial O2 content to myocardium in contrast to the remainder of the body [25%]
Becomes even higher during exercise or stress
Coronary circulation PO2 % Hb saturationArterial B 95mmHg 97%Venous B 40mmHg 75%Coronary 25-30mmHg 50%Venous BDuring exercise cardiac O2 consumption may increase
5-6 folds in well trained athletes due to:1. Increase coronary blood flow2. Widening of arterio-venous O2 difference
Cutaneous circulation Low metabolism
Blood flow serves mainly thermoregulatory role
Numerous AV anastomoses
Thick muscular layer Rich nerve supply No basal tone (can constrict maximally) No metabolic autoregulation Exclusively under SNS control (can close
completely) thermoregulation
Skin circulation
Effect of changes in environmental temp. on heat conductance from body core to skin surface
Cerebral circulationUnique features:
contained within rigid structure inflow/outflow inbalance pressure Cushing’s phenomenon: systemic BP with intracranial pressure
(e.g. tumor) - by ischemic stimulation of vasopressor center in medulla (helps maintain brain flow)
Absolute requirement for adequate flow tissue least tolerant to ischemia
5 sec ischemia loss of consciousness 3-4 min permenant brain damage
glucose-dependent
Cerebral circulation Important features: 1. Intracranial pressure [ Cushing reflex] 2. Effect of gravity 3. Blood Brain Barrier [BBB]: A. Protect against changes in ionic composition B. Protection of brain from endogenous &
exogenous toxins C. Prevention of escape of neurotransmitters into the
general circulation
Cushing reflex
Neural regulation of brain vessels Minimal importance (local mechanisms
Heart Failure Symptoms of Lt.HF: 1. Orthopnoea 2. Paroxysmal nocturnal dyspnoea 3. Crepitation at the base of lung Symptoms of Rt.HF: 1. Raised jugular venous pressure 2. Peripheral edema
SHOCK A term used to describe the clinical
syndrome that develops when oxygen delivery is inadequate to meet the metabolic needs of the tissues due to some form of acute circulatory failure
Clinical features of shock 1. Sweating 2.reduced conscious level:drowsiness 3. Tachypnoea 4. Hypotension 5. Tachycardia with weak pulse 6. Cold skin 7. Oliguria
Causes & Types of Shock 1. Fainting [Syncope] or vasovagal attack Caused by pain,stress ,fear ,excessive heat or