Cardiovascular System. Functional Organization of Cardiovascular system CARDIOVASCULAR SYSTEM HEART (PUMP) VESSELS (DISTRIBUTION SYSTEM) Blood.

Cardiovascular SystemCardiovascular System

Functional Organization of Functional Organization of Cardiovascular systemCardiovascular system

CARDIOVASCULAR SYSTEM

HEART(PUMP)

VESSELS(DISTRIBUTION

SYSTEM)

Blood

Functions of Cardiovascular Functions of Cardiovascular System:System:

I. Primary (main) function of the heart:I. Primary (main) function of the heart:

♥♥ Acts as a muscular pump:Acts as a muscular pump: in order to maintain adequate level of blood in order to maintain adequate level of blood

flow flow throughout CVS by pumping blood under throughout CVS by pumping blood under

press into press into vascular system.vascular system.

♥♥ Responsible for the mass movement of fluid Responsible for the mass movement of fluid in in

body.body.

Functions of Cardiovascular System Functions of Cardiovascular System (continued)(continued)

II. Secondary functions:II. Secondary functions: 1. Transportation:1. Transportation: delivers Odelivers O22 to tissues, & brings back CO to tissues, & brings back CO22 to lungs. to lungs. carries absorbed digestion products to liver & carries absorbed digestion products to liver &

tissues.tissues. carries metabolic wastes to kidneys to be excreted.carries metabolic wastes to kidneys to be excreted. distribution of body fluids. distribution of body fluids.

2. Regulation:2. Regulation: Hormonal: carries hormones to target tissues to produce Hormonal: carries hormones to target tissues to produce

their effects.their effects. Immune: carries antibodies, leukocytes (WBCs), Immune: carries antibodies, leukocytes (WBCs),

cytokines, & complement cytokines, & complement to aid body defense mechanism against pathogens.to aid body defense mechanism against pathogens. Protection: carries platelets, & clotting factors to aid Protection: carries platelets, & clotting factors to aid

protection of the bodyprotection of the body in blood clotting mechanism.in blood clotting mechanism. Temperature: helps in regulation of body temperature, Temperature: helps in regulation of body temperature,

by diverting blood by diverting blood to cool or warm the body.to cool or warm the body.

Anatomy of the heart:Anatomy of the heart:

Positioned between two bony structures – sternum and vertebrae

(CPR)

Hollow, muscular organ.Hollow, muscular organ.

AtriumAtrium: weak primer pump for the ventricle: weak primer pump for the ventricleVentricleVentricle: the main pumping force: the main pumping force Rt. Ventricle Lt. ventricleRt. Ventricle Lt. ventricle Pulmonary circulation Systemic circulationPulmonary circulation Systemic circulation

Valves of the heart:Valves of the heart:♥ 2 atrioventricular (AV) valves: ■ One way valves. ■ Allow blood to flow from atria into ventricles. ■ Tricuspid (Rt) & Mitral (Lt).

♥ 2 semilunar valves : ■ One way valves. ■ At origin of pulmonary artery & aorta. ■ Pulmonary (Rt) & Aortic (Lt). ■ Open during ventricular contraction.

Heart ValvesHeart Valves One way flow in One way flow in

heart is ensured by heart is ensured by heart valvesheart valves

Valves open & Valves open & close passivelyclose passively

-- open open by by forward P by bloodforward P by blood

- - closeclose by by backward P by backward P by bloodblood

Atrioventricular Valve Atrioventricular Valve FunctionFunction

Semilunar Valve Semilunar Valve FunctionFunction

No valves between atria No valves between atria and veinsand veins ReasonsReasons

Atrial pressures Atrial pressures usually are not usually are not much higher than much higher than venous pressuresvenous pressures

Sites where venae Sites where venae cavae enter atria cavae enter atria are partially are partially compressed during compressed during atrial contractionatrial contraction

The fibrous skeleton of the The fibrous skeleton of the heartheartServes 3 roles:Serves 3 roles: A mechanical base: A mechanical base:

atria anchored atria anchored above and above and ventricles belowventricles below

Perforated by 4 Perforated by 4 apertures, each apertures, each containing a valvecontaining a valve

Insulates the Insulates the ventriclesventricles

Blood Flow Through and Pump Action Blood Flow Through and Pump Action of the Heartof the Heart

Pulmonary circulation systemic circulation

Starts at right Starts at right ventricleventricle

Ends at left atriumEnds at left atrium

Receives blood Receives blood from right side of from right side of heartheart

Carries blood Carries blood between heart and between heart and lungslungs

Blood perfusing the Blood perfusing the lungs is partially lungs is partially deoxygenateddeoxygenated

All blood flows All blood flows through lungsthrough lungs

Low pressure, low Low pressure, low resistanceresistance

Starts at left ventricleStarts at left ventricle

Ends at right atriumEnds at right atrium

Receives blood from Receives blood from left side of heartleft side of heart

Carries blood Carries blood between heart and between heart and other organ systemsother organ systems

Blood perfusing the Blood perfusing the organ systems is organ systems is oxygenatedoxygenated

Part of the blood go Part of the blood go to different organ to different organ systemssystems

High pressure, high High pressure, high resistanceresistance

Vascular TreeVascular Tree Closed system of vesselsClosed system of vessels Consists of Consists of

ArteriesArteries Carry blood away from heart to tissuesCarry blood away from heart to tissues

ArteriolesArterioles Smaller branches of arteriesSmaller branches of arteries

CapillariesCapillaries Smaller branches of arteriolesSmaller branches of arterioles Smallest of vessels across which all exchanges Smallest of vessels across which all exchanges

are made with surrounding cellsare made with surrounding cells VenulesVenules

Formed when capillaries rejoinFormed when capillaries rejoin Return blood to heartReturn blood to heart

Veins Veins Formed when venules mergeFormed when venules merge Return blood to heartReturn blood to heart

ArteriesArteries

Structure of arterial wallStructure of arterial wall Plentiful of elastic Plentiful of elastic

fibers….high fibers….high compliancecompliance

Function: Rapid transit passage-ways for blood from heart to tissuesPressure reservoir

Arteries as a Pressure Arteries as a Pressure ReservoirReservoir

Arterioles (resistance vessels)Arterioles (resistance vessels) Very small arteries that Very small arteries that

delivers blood to delivers blood to capillariescapillaries

StructureStructure Very little elastic tissue Very little elastic tissue

but thick layer of smooth but thick layer of smooth musclemuscle

Function Function Regulating Regulating blood flow from arteries blood flow from arteries to capillaries by to capillaries by regulating resistance regulating resistance according to tissue according to tissue metabolic needs.metabolic needs.

CapillariesCapillaries Microscopic vessels that Microscopic vessels that connectsconnects

arterioles to venulesarterioles to venules StructureStructure

Single wallSingle wall layered vessels layered vessels (endothelial cells)(endothelial cells)

Undergoes extensive branchingUndergoes extensive branching Maximized surface area and Maximized surface area and

minimized diffusion distanceminimized diffusion distance Velocity of blood flow through Velocity of blood flow through

capillaries is relatively slowcapillaries is relatively slow Provides adequate exchange Provides adequate exchange

timetime Function:Function:

Exchange Exchange of nutrients and wastes of nutrients and wastes between blood and tissue cellsbetween blood and tissue cells

Capillaries cont.Capillaries cont.

Under resting conditions many capillaries are not Under resting conditions many capillaries are not openopen

Capillaries surrounded by precapillary sphinctersCapillaries surrounded by precapillary sphincters Contraction of sphincters reduces blood flowing into Contraction of sphincters reduces blood flowing into

capillaries in an organcapillaries in an organ Relaxation of sphincters has opposite effectRelaxation of sphincters has opposite effect

VeinsVeins Carry blood Carry blood from tissues to from tissues to

heartheart

Structure:Structure: Thin wallThin wall Less smooth muscle and Less smooth muscle and

considerable amount of considerable amount of collagencollagen

Less elastic fibersLess elastic fibers

Function:Function: Passage waysPassage ways back to back to

heartheart Blood reservoir Blood reservoir

(capacitance vessels)(capacitance vessels)

Properties of Properties of Cardiac Cardiac MuscleMuscle

22

Heart Composed of Three Heart Composed of Three LayersLayers

23

Properties of Cardiac Properties of Cardiac Muscle FibersMuscle Fibers

24

Exhibit branching Adjacent cardiac cells are joined end

to end by specialized structures known as intercalated discs

Within intercalated discs there are two types of junctions Desmosomes Gap junctions..allow action

potential to spread from one cell to adjacent cells.

Heart function as syncytiumwhen one cardiac cell undergoes an action potential, the electrical impulse spreads to all other cells that are joined by gap junctions so they become excited and contract as a single functional syncytium.

Atrial syncytium and ventricular syncytium

Histological Properties of Histological Properties of Cardiac Muscle FibersCardiac Muscle Fibers

25

THE CARDIAC MUSCLETHE CARDIAC MUSCLE

Contractile muscle fibres (myocardium 99%) Atrial muscle fibres & Ventricular muscle fibres

- Both contract same as in sk. Muscle - Duration of contraction much longer Excitatory & conductive muscle fibres (autorhythmic

1%) - Few contractile fibrils (v.weak contraction) - Exhibit either automatic rhythmic discharge(AP) OR Conduction of the AP through heart

26

Properties of Cardiac Muscle Properties of Cardiac Muscle FibersFibers1. Autorhythmicity: The ability to initiate a heart

beat continuously and regularly without external stimulation

2. Excitability: The ability to respond to a stimulus of adequate strength and duration (i.e. threshold or more) by generating a propagated action potential

3. Conductivity: The ability to conduct excitation through the cardiac tissue

4. Contractility: The ability to contract in response to stimulation

27

1. Autorhythmicity1. Autorhythmicity

myogenic myogenic (independent of nerve supply)(independent of nerve supply)

due to the due to the specialized excitatory & conductive systemspecialized excitatory & conductive system of the of the heartheart

intrinsic ability of self-excitationintrinsic ability of self-excitation (waves of depolarization)(waves of depolarization) cardiac impulsescardiac impulses

Definition: the ability of the heart to initiate its beat continuously and regularly without external stimulation

28

Have two important functions1. Act as a pacemaker (set the rhythm of electrical excitation)2. Form the conductive system (network of

specialized cardiac muscle fibers that provide a path for each cycle of cardiac excitation to progress through the heart)

Autorythmic fibersAutorythmic fibers

Forms 1% of the cardiac muscle fibers

29

Sinoatrial node (SA node)Specialized region in right atrial wall near opening of superior vena cava.

Atrioventricular node (AV node)Small bundle of pecializedcardiac cells located at base of right atrium near septum

Bundle of His (atrioventricular bundle)Cells originate at AV node and enters interventricular septumDivides to form right and left bundle branches which travel down septum, curve around tip of ventricular chambers, travel back toward atria along outer walls

Purkinje fibersSmall, terminal fibers that extend from bundle of His and spread throughout ventricular myocardium

Locations of autorythmic cellsLocations of autorythmic cells

30

Mechanism of Mechanism of AutorythmicityAutorythmicity Autorythmic cells do not

have stable resting membrane potential (RMP)

Natural leakiness to Na & Ca spontaneous and gradual depolarization

Unstable resting membrane potential (= pacemaker potential)

Gradual depolarization reaches threshold (-40 mv) spontaneous AP generation

31

Rate of generation of AP at different sites of the heartRate of generation of AP at different sites of the heart

SITESITE RATERATE

(Times/min)(Times/min)

SA nodeSA node 100100

AV nodeAV node 40 - 6040 - 60

AV bundle, bundle AV bundle, bundle branches,& Purkinje branches,& Purkinje fibresfibres

20 - 3520 - 35

SA node acts as heart pacemaker because it has the fastest rate of generating action potentialNerve impulses from autonomic nervous system and hormones modify the timing and strength of each heart beat but do not establish the fundamental rhythm.

32

2. Excitability2. Excitability

Definition: The ability of cardiac muscle to respond to a stimulus of adequate strength & duration by generating an AP

AP initiated by SA nodetravels along conductive

pathway excites atrial & ventricular muscle fibres

34

Action potential in Action potential in contractile fiberscontractile fibers

35

Refractory periodRefractory period LongLong refractory period (250 refractory period (250

msec) compared to skeletal msec) compared to skeletal muscle (3msec)muscle (3msec)

During this period During this period membrane membrane is refractory to further is refractory to further stimulationstimulation until contraction until contraction is over.is over.

It lasts longer than muscle It lasts longer than muscle contraction, contraction, prevents tetanusprevents tetanus

Gives time to heart to relax Gives time to heart to relax after each contraction, after each contraction, prevent fatigueprevent fatigue

It It allows timeallows time for the heart for the heart chambers to fill during chambers to fill during diastole before next diastole before next contractioncontraction

AP in skeletal muscle : 1-5 msecAP in cardiac muscle :200 -300 msec36

3. Contractility3. ContractilityDefinition: ability of cardiac muscle to contract in

response to stimulation

37

Excitation-Contraction Excitation-Contraction Coupling in Cardiac Coupling in Cardiac Contractile CellsContractile Cells

Similar to that in Similar to that in skeletal musclesskeletal muscles

38

4. Conductivity4. ConductivityDefinition:Definition: property by which excitation is conducted property by which excitation is conducted

through the cardiac tissuethrough the cardiac tissue

39

Criteria for spread of excitation & Criteria for spread of excitation & efficient cardiac functionefficient cardiac function

1. Atrial excitation and contraction should be complete before onset of ventricular contraction

- ensures complete filling of the ventricles during diastole

2. Excitation of cardiac muscle fibres should be coordinated ensure each heart chamber contracts as a unit accomplish efficient pumping

- smooth uniform contraction essential to squeeze out blood

3. Pair of atria & pair of ventricles should be functionally co-ordinated both members contract simultaneously

- permits synchronized pumping of blood into pulmonary & systemic circulation

40

Tissue Conduction rate (m/s)

Atrial muscle

0.3

Atrial pathways

1

AV node 0.05

Bundle of His

1

Purkinje system

4

Ventricular muscle

0.3-0.5

41

Cardiac impulse originates at SA nodeCardiac impulse originates at SA node Action potential spreads throughout right and left atriaAction potential spreads throughout right and left atria Impulse passes from atria into ventricles through AV Impulse passes from atria into ventricles through AV

node (only point of electrical contact between chambers)node (only point of electrical contact between chambers) Action potential briefly delayed at AV node (ensures Action potential briefly delayed at AV node (ensures

atrial contraction precedes ventricular contraction to atrial contraction precedes ventricular contraction to allow complete ventricular filling)allow complete ventricular filling)

Impulse travels rapidly down interventricular septum by Impulse travels rapidly down interventricular septum by means of bundle of Hismeans of bundle of His

Impulse rapidly disperses throughout myocardium by Impulse rapidly disperses throughout myocardium by means of Purkinje fibersmeans of Purkinje fibers

Rest of ventricular cells activated by cell-to-cell spread of Rest of ventricular cells activated by cell-to-cell spread of impulse through gap junctionsimpulse through gap junctions

Spread of Cardiac ExcitationSpread of Cardiac Excitation

42

Normal conduction pathway:

SA node -> atrial muscle -> AV node -> bundle of His -> Left and Right Bundle Branches -> Ventricular muscle

Electrocardiography

• A recording of the electrical activity of the heart over time

• Gold standard for diagnosis of cardiac arrhythmias

• Helps detect electrolyte disturbances (hyper- & hypokalemia)

• Allows for detection of conduction abnormalities

• Screening tool for ischemic heart disease during stress tests

• Helpful with non-cardiac diseases (e.g. pulmonary embolism or hypothermia

Electrocardiogram Electrocardiogram (ECG/EKG)(ECG/EKG)

Is a recording of electrical activity of heart conducted Is a recording of electrical activity of heart conducted thru ions in body to surfacethru ions in body to surface

Fig 13.22a

13-60

Recording of the ECG:Leads used:• Limb leads are I, II, II. So called because at one time subjects had to literally place arms and legs in buckets of salt water.• Each of the leads are bipolar; i.e., it requires two sensors on the skin to make a lead.• If one connects a line between two sensors, one has a vector.• There will be a positive end at one electrode and negative at the other.• The positioning for leads I, II, and III were first given by Einthoven. Form the basis of Einthoven’s triangle.

Types of ECG RecordingsTypes of ECG Recordings

Bipolar leadsBipolar leads record record voltage between voltage between electrodes placed on electrodes placed on wrists & legs (right leg wrists & legs (right leg is ground)is ground)

Lead ILead I records records between right arm & between right arm & left armleft arm

LeadLead IIII: right arm & : right arm & left legleft leg

LeadLead IIIIII: left arm & : left arm & left legleft leg

Fig 13.23

13-61

Fig. 13.22bFig. 13.22b

3 distinct waves are 3 distinct waves are produced during produced during cardiac cyclecardiac cycle

PP wavewave caused by caused by atrial atrial depolarizationdepolarization

QRSQRS complexcomplex caused by caused by ventricular ventricular depolarizationdepolarization

TT wavewave results from results from ventricular ventricular repolarizationrepolarization

ECG

Fig 13.2413-63

Elements of the ECG

Fig. 13.24bFig. 13.24b

Fig. 13.24cFig. 13.24c

Fig. 13.24dFig. 13.24d

Elements of the ECG:

• P wave• Depolarization of both atria;• Relationship between P and QRS helps distinguish various cardiac arrhythmias• Shape and duration of P may indicate atrial enlargement

•QRS complex: • Represents ventricular depolarization

• Larger than P wave because of greater muscle mass of ventricles

• Normal duration = 0.08-0.12 seconds

• Its duration, amplitude, and morphology are useful in diagnosing cardiac arrhythmias, ventricular hypertrophy, MI, electrolyte derangement, etc.

• Q wave greater than 1/3 the height of the R wave, greater than 0.04 sec are abnormal and may represent MI

• PR interval: • From onset of P wave to onset of QRS

• Normal duration = 0.12-2.0 sec (120-200 ms) (3-4 horizontal boxes)

• Represents atria to ventricular conduction time (through His bundle)

• Prolonged PR interval may indicate a 1st degree heart block

Fig. 13.24gFig. 13.24g

T wave: • Represents repolarization or recovery of ventricles• Interval from beginning of QRS to apex of T is referred to as the absolute refractory period

ST segment:• Connects the QRS complex and T wave• Duration of 0.08-0.12 sec (80-120 msec

QT Interval• Measured from beginning of QRS to the end of the T wave• Normal QT is usually about 0.40 sec• QT interval varies based on heart rate

Ischemic Heart DiseaseIschemic Heart Disease

Is most commonly due to atherosclerosis Is most commonly due to atherosclerosis in coronary arteriesin coronary arteries

IschemiaIschemia occurs when blood supply to occurs when blood supply to tissue is deficienttissue is deficient Causes increased lactic acid from anaerobic Causes increased lactic acid from anaerobic

metabolismmetabolism Often accompanied by Often accompanied by angina pectoris angina pectoris

(chest pain)(chest pain)

13-78

Ischemic Heart DiseaseIschemic Heart Disease

Detectable by changes in S-T segment of ECG Detectable by changes in S-T segment of ECG MyocardialMyocardial infarctioninfarction (MI) is a heart attack (MI) is a heart attack

Diagnosed by high levels of creatine phosphate Diagnosed by high levels of creatine phosphate (CPK) & lactate dehydrogenase (LDH)(CPK) & lactate dehydrogenase (LDH)

Fig 13.34

13-79

Arrhythmias Detected on Arrhythmias Detected on ECGECG

ArrhythmiasArrhythmias are abnormal heart rhythms are abnormal heart rhythms Heart rate <60/min is Heart rate <60/min is bradycardiabradycardia; ;

>100/min is >100/min is tachycardiatachycardia

Fig 13.35

13-80

Arrhythmias Detected on Arrhythmias Detected on ECG ECG continuedcontinued

In In flutterflutter contraction rates can be 200-300/min contraction rates can be 200-300/min In In fibrillationfibrillation contraction of myocardial cells is contraction of myocardial cells is

uncoordinated & pumping ineffectiveuncoordinated & pumping ineffective Ventricular fibrillationVentricular fibrillation is life-threateningis life-threatening

Electrical defibrillationElectrical defibrillation resynchronizes heart by depolarizing resynchronizes heart by depolarizing all cells at same time all cells at same time

Fig 13.35

13-81

AV node blockAV node block occur when node is damagedoccur when node is damaged First–degree AV node blockFirst–degree AV node block is when conduction is when conduction

through AV node > 0.2 secthrough AV node > 0.2 sec Causes long P-R intervalCauses long P-R interval

Second-degree AV node blockSecond-degree AV node block is when only 1 out of 2-4 is when only 1 out of 2-4 atrial APs can pass to ventriclesatrial APs can pass to ventricles Causes P waves with no QRSCauses P waves with no QRS

In In third-degree or complete AV node blockthird-degree or complete AV node block no atrial no atrial activity passes to ventriclesactivity passes to ventricles Ventricles driven slowly by bundle of His or PurkinjesVentricles driven slowly by bundle of His or Purkinjes

Arrhythmias Detected on Arrhythmias Detected on ECG ECG continuedcontinued

13-82

AV node blockAV node block occurs when node is damagedoccurs when node is damaged First–degree AV node blockFirst–degree AV node block is when is when

conduction thru AV node > 0.2 secconduction thru AV node > 0.2 sec Causes long P-R intervalCauses long P-R interval

Arrhythmias Detected on Arrhythmias Detected on ECG ECG continuedcontinued

Fig 13.36

13-83

Second-degree AV node blockSecond-degree AV node block is when only 1 is when only 1 out of 2-4 atrial APs can pass to ventriclesout of 2-4 atrial APs can pass to ventricles Causes P waves with no QRSCauses P waves with no QRS

Arrhythmias Detected on Arrhythmias Detected on ECG ECG continuedcontinued

Fig 13.36

13-84

In In third-degree or complete AV node blockthird-degree or complete AV node block, no , no atrial activity passes to ventriclesatrial activity passes to ventricles Ventricles are driven slowly by bundle of His or Ventricles are driven slowly by bundle of His or

PurkinjesPurkinjes

Arrhythmias Detected on Arrhythmias Detected on ECG ECG continuedcontinued

Fig 13.36

13-85

THE CARDIAC THE CARDIAC CYCLECYCLE

ISOVOLUMETRIC ISOVOLUMETRIC CONTRACTIONCONTRACTION

The The

Beginning of systoleBeginning of systole

ISOVOLUMETRIC ISOVOLUMETRIC CONTRACTIONCONTRACTION

HeartHeart The atrioventricular (AV) valves The atrioventricular (AV) valves

close at the beginning of this close at the beginning of this phase.phase.

Electrically, ventricular systole Electrically, ventricular systole is defined as the interval is defined as the interval between the QRS complex and between the QRS complex and the end of the T wave (the Q-T the end of the T wave (the Q-T interval).interval).

Mechanically, ventricular Mechanically, ventricular systole is defined as the systole is defined as the interval between the closing of interval between the closing of the AV valves and the opening the AV valves and the opening of the semilunar valves (aortic of the semilunar valves (aortic and pulmonary and pulmonary valves). valves).

RAPID EJECTIONRAPID EJECTION

RAPID EJECTIONRAPID EJECTIONHeartHeart

The semilunar The semilunar (aortic and (aortic and pulmonary) valves pulmonary) valves open at the open at the beginning of this beginning of this phase. phase.

REDUCED EJECTIONREDUCED EJECTION

The end of The end of

systolesystole

REDUCED EJECTIONREDUCED EJECTIONHeartHeart

At the end of this At the end of this phase the semilunar phase the semilunar (aortic and (aortic and pulmonary) valves pulmonary) valves close.close.

ISOVOLUMETRIC ISOVOLUMETRIC RELAXATIONRELAXATION

The The

beginning of Diastolebeginning of Diastole

ISOVOLUMETRIC ISOVOLUMETRIC RELAXATIONRELAXATION

HeartHeart At the beginning of this At the beginning of this

phase the AV valves are phase the AV valves are closed. closed.

RAPID VENTRICULAR RAPID VENTRICULAR FILLINGFILLING

REDUCED REDUCED VENTRICULAR VENTRICULAR

FILLINGFILLING (Diastasis) (Diastasis)

Cardiac Cardiac OutputOutput

When the heart contractsWhen the heart contracts

Cardiac OutputCardiac Output

Cardiac OutputCardiac Output is the volume of blood is the volume of blood pumped each minute, and is expressed by pumped each minute, and is expressed by the following equation:the following equation:

CO = SV x HRCO = SV x HR Where:Where:

COCO is cardiac output expressed in L/min  is cardiac output expressed in L/min (normal ~5 L/min)(normal ~5 L/min)

SVSV is stroke volume per beat is stroke volume per beat HRHR is the number of beats per minute is the number of beats per minute

PreloadPreload

PreloadPreload:  Preload is the muscle length prior to :  Preload is the muscle length prior to contractility, and it is dependent of ventricular contractility, and it is dependent of ventricular filling (or filling (or end diastolic volumeend diastolic volume…EDV) …EDV) 

This value is related to right atrial pressure.This value is related to right atrial pressure.

    The most important determining factor for The most important determining factor for

preload is preload is venous returnvenous return..

afterloadafterload

AfterloadAfterload:  Afterload is the tension (or the :  Afterload is the tension (or the arterial arterial pressurepressure) against which the ventricle must contract. ) against which the ventricle must contract. 

If arterial pressure increases, afterload also increases. If arterial pressure increases, afterload also increases.

Afterload for the left ventricle is determined by aortic Afterload for the left ventricle is determined by aortic pressurepressure

Afterload for the right ventricle is determined by Afterload for the right ventricle is determined by pulmonary artery pressure.pulmonary artery pressure.

Inotropic and Inotropic and chronotropicchronotropic

Homometric regulationHomometric regulation

Regulation of heart and Regulation of heart and blood vesselsblood vessels

SignificanceSignificance::

To maintain normal blood To maintain normal blood pressure, pressure,

blood flow to be relativity blood flow to be relativity constant.constant.

To redistribute blood supply to To redistribute blood supply to

different tissue and organs.different tissue and organs.

To redistribute blood supply to To redistribute blood supply to

different tissue and organs.different tissue and organs.

Copyright 2009, John Wiley & Sons, Inc.

CV CenterCV Center

A. Neural regulation A. Neural regulation

1. Innervation of the 1. Innervation of the

heart heart

dual innervationdual innervation

(1) cardiac sympathetic (1) cardiac sympathetic

nervenerve

(2) cardiac (2) cardiac

parasympathetic nerveparasympathetic nerve

Cardiac Symp nCardiac Symp n Cardiac Cardiac

Vagal nVagal n IML1-5 Amgiguus IML1-5 Amgiguus N, Dorsal N, Dorsal motor N motor N

of vagusof vagus Preganglionic fPreganglionic f Preganglionic fPreganglionic f ACh ACh ACh ACh

Postganglionic N Postganglionic N N receptorN receptor Postganglionic f Postganglionic f Postganglionic fPostganglionic f NE NE Effects Effects AchAch inotropic inotropic receptor receptor chronotropic chronotropic M M receptorreceptor dromotropic dromotropic propranolol propranolol Blocker Blocker atropineatropine

(1) (1) Effects of vagal nerveEffects of vagal nerve

Vagal nerve ending → Vagal nerve ending → ACh.ACh.

→ binds to M cholinergic → binds to M cholinergic

receptor →receptor →↑permeability ↑permeability

to Kto K++ results results

in:in:

↓↓automaticity of S-A nodeautomaticity of S-A node::

↓↓contractilitycontractility due to : due to :

↑↑KK++ efflux at phase 3 efflux at phase 3 repolarizationrepolarization

→↓ →↓AP duration → CaAP duration → Ca2+2+ influx ↓ influx ↓

→ → [Ca[Ca2+2+]]ii↓;↓;

ACh inhibits CaACh inhibits Ca2+2+ influx influx → [Ca → [Ca2+2+]]i i

↓→ ↓↓→ ↓contractility.contractility.

↓ ↓conductivityconductivity

TheThe left left Vagus Vagus

n:↓conductivity in n:↓conductivity in

A-V node A-V node

The The rightright Vagus n: Vagus n:

↓automaticity ↓automaticity

in S-A node. in S-A node.

(2) (2) Effects of cardiac sympathetic Effects of cardiac sympathetic nerve: nerve:

Cardiac sympathetic nerve ending Cardiac sympathetic nerve ending

→ → noradrenaline → binds to noradrenaline → binds to ββ--

adrenergic adrenergic receptor→↑permeabilityreceptor→↑permeability

to Cato Ca2+2+ leads to:leads to:

↑ ↑AutomaticityAutomaticity

↑↑ConductivityConductivity

↑↑ContractilityContractility

The The leftleft Symp n Symp n：：↑↑ contractility.contractility.

The The rightright Symp n Symp n ↑：↑： HR.HR.

Sympathetic input - HEARTSympathetic input - HEART

ACTIONSACTIONS Nerve fibers Nerve fibers

release NE release NE SA, atria, and SA, atria, and

ventriclesventricles ↑ ↑ HR and HR and

contractilitycontractility R side SA nodeR side SA node L side contractilityL side contractility

MECHANISMMECHANISM ß1 receptors – ß1 receptors –

pacemaker activitypacemaker activity ß1 myocardium ß1 myocardium

contractioncontraction

Parasympathetic input - Parasympathetic input - HEARTHEART

ACTIONSACTIONS Vagus nerve Vagus nerve

releases ACHreleases ACH SA and myocardiumSA and myocardium HR and conduction HR and conduction

velocityvelocity R side SA node (HR)R side SA node (HR) L side contractility L side contractility

(slight)(slight)

MECHANISMMECHANISM Muscarinic Muscarinic

receptors (M2)receptors (M2) ßßγγ subunit (HR) subunit (HR) Nitric oxide (weak Nitric oxide (weak

inotropic effect) inotropic effect)

Cardiac reflexesCardiac reflexes

Bainbridge ReflexBainbridge Reflex

Infusion of volume causes an Infusion of volume causes an increase in heart rate due to increase in heart rate due to activation of atrial stretch activation of atrial stretch receptors which causes receptors which causes medullary center activation medullary center activation of sympathetic output to the of sympathetic output to the SA nodeSA node

Reflex from atria Reflex from atria Type AType A Type BType B

Reflex from left ventricleReflex from left ventricle Coronary chemo reflex Coronary chemo reflex Sino Aortic reflex Sino Aortic reflex Reflex from peripheryReflex from periphery Reflex from higher centersReflex from higher centers

Arterial blood pressure Arterial blood pressure

Systolic pressureSystolic pressure

Diastolic pressureDiastolic pressure

Mean pressureMean pressure

MAP = DP + 1/3 (SP-DP)

REGULATION OF ARTERIAL REGULATION OF ARTERIAL BLOOD PRESSUREBLOOD PRESSURE

Regulation of Blood Pressure

NervousMechanis

m

Renal Mechanis

m

HormonalMechanis

m

LocalMechanis

m

By Vasomotor Center

and Impulses

from Periphery

By Regulation of ECF Volume

and renin –

angiotensin

mechanism

By Vasocons-

-trictor and

Vasodilator

Hormones

By Local Vasocons--trictors

and Vasodilato

rs

REGULATION OF ARTERIAL REGULATION OF ARTERIAL BLOOD PRESSUREBLOOD PRESSURE

SHORT-TERM CONTROLSHORT-TERM CONTROL

(IN SEC – MIN)(IN SEC – MIN)

INTERMEDIATE-TERM INTERMEDIATE-TERM CONTROLCONTROL

(30 MIN – HOURS)(30 MIN – HOURS)

LONG – TERM CONTROLLONG – TERM CONTROL

SHORT-TERM CONTROL OF SHORT-TERM CONTROL OF APAP

CNS ISCHAEMIC RESPONSECNS ISCHAEMIC RESPONSE

BARORECEPTOR REFLEXBARORECEPTOR REFLEX

CHEMORECEPTOR REFLEXCHEMORECEPTOR REFLEX

INTERMEDIATE CONTROL INTERMEDIATE CONTROL OF APOF AP

RENIN - ANGIOTENSIN – RENIN - ANGIOTENSIN – VASOCONSTRICTOR MECH.VASOCONSTRICTOR MECH.

STRESS RELAXATION OF STRESS RELAXATION OF VASCULATUREVASCULATURE

FLUID – SHIFT THROUGH FLUID – SHIFT THROUGH THE CAPILLARY WALLTHE CAPILLARY WALL

LONG – TERM CONTROL OF LONG – TERM CONTROL OF APAP

RENAL FLUID SHIFT RENAL FLUID SHIFT (THROUGH ADH / VOLUME (THROUGH ADH / VOLUME RECEPTORS)RECEPTORS)

RENIN – ANGIOTENSIN – RENIN – ANGIOTENSIN – ALDOSTERONE MECH.ALDOSTERONE MECH.

Sequential events by which increased Sequential events by which increased salt intake increases the arterial salt intake increases the arterial

pressure.pressure.Increased salt intakeIncreased salt intake

Increased extracellular volumeIncreased extracellular volume

Increased arterial pressureIncreased arterial pressure

Decreased renin and angiotensinDecreased renin and angiotensin

Decreased renal retention of salt and waterDecreased renal retention of salt and water

Return of extracellular volume almost to Return of extracellular volume almost to normalnormal

Return of arterial pressure almost to normalReturn of arterial pressure almost to normal

LOCAL MECH. FOR CONTROL LOCAL MECH. FOR CONTROL OF APOF AP

A.A. VasodilatosVasodilatos

1. 1. EDRFEDRF

2.2. Bradykinin Bradykinin

3.3. Histamine Histamine

4.4. ANP ANP

5.5. VIP VIP

6.6. Substance Substance PP

7. Prostacyclin8. Adenosine

9. K+

10. Acidosis [ CO2]

11. Hypercapnia12. Hypoxia13. Temperature

B.B. Vasoconstrictors Vasoconstrictors

1.1. Endothelin-1Endothelin-1

2.2. Angiotensin IIAngiotensin II

3.3. NorepinephrineNorepinephrine

4.4. ADHADH

5.5. SerotoninSerotonin

6.6. Thromboxane A2Thromboxane A2

7.7. Neuropeptide-YNeuropeptide-Y

8.8. ColdCold

HORMONAL MECH. FOR HORMONAL MECH. FOR CONTROL OF APCONTROL OF AP

HORMONES RAISING APHORMONES RAISING AP ADRENALINEADRENALINE NORADRENALINENORADRENALINE THYROXINETHYROXINE ALDOSTERONEALDOSTERONE VASOPRESSINVASOPRESSIN ANGIOTENSINANGIOTENSIN SEROTONINSEROTONIN

HORMONAL MECH. FOR HORMONAL MECH. FOR CONTROL OF APCONTROL OF AP

HORMONES DECREASING APHORMONES DECREASING APVIPVIPBRADY KININBRADY KININPROSTAGLANDINPROSTAGLANDINHISTAMINEHISTAMINEACETYLCHOLINEACETYLCHOLINEANPANP