PHYSIOLOGY -

CARDIOVASCULAR SYSTEM
 LEARNING OUTCOMES

By the end of this lecture you should be able to:

◾ Describe the characteristics of cardiac muscle

◾ Describe the conducting system of the heart

◾ Describe the extrinsic nerve supply to the heart

◾ Provide an interpretation of an ECG

◾ Define cardiac output and stroke volume

◾ Discuss the mechanisms that regulate blood flow and blood

pressure
 STRUCTURE OF CARDIAC MUSCLE
◾ cardiomyocytes - striated,short, thick, branched cells

◾ central nucleus surrounded by light-staining mass of glycogen

◾ striations of actin & myosin (as in skeletal muscle)

◾ intercalated discs - join cardiomyocytes end to end

◾ intercalated discs have three features that help propagate action potentials:

(i) interdigitating folds

(ii) mechanical junctions

(iii) electrical [gap] junctions

 STRUCTURE OF CARDIAC MUSCLE

Cardiac muscle fibre Branched cardiac muscle fibre

Intercalated discs Nucleus of cardiac muscle cell Perinuclear cytoplasm

STRUCTURE OF CARDIAC MUSCLE
 STRUCTURE OF CARDIAC MUSCLE

◾ depends almost exclusively on aerobic

respiration to makeATP
◾ rich in myoglobin & glycogen
◾ mitochondria - 25% of cell

◾ adaptable to different organic fuels

◾ vulnerable to O 2 deficiency

◾ fatigue resistant - little use of anaerobic

fermentation or O 2 debt mechanisms
 LEARNING OUTCOMES

By the end of this lecture you should be able to:

◾ Describe the characteristics of cardiac muscle√

◾ Describe the conducting system of the heart

◾ Describe the extrinsic nerve supply to the heart

◾ Provide an interpretation of an ECG

◾ Define cardiac output & stroke volume

◾ Discuss the mechanisms that regulate blood flow & blood pressure
 CONDUCTIO N SYSTEM OF THE HEART

◾ specialised muscle cells that control & coordinate heart beat

◾ cardiac muscle contracts on its own - auto-rhythmicity (without stimulation)
◾ maximum heart rate 230 beats per minute - maximum rate that AV node can
conduct impulses
◾ comprises an internal pacemaker & nerve-like conduction pathways through
myocardium
 CONDUCTI O N SYSTEM OF THE HEART
◾ system relies on membrane potential
Recall
◾ electrical potentials exists across cell membranes
◾ ‘potential’ quantity determining charge in electrical field
◾ field due to differently charged particles inside & outside cell membrane
◾ nerve & muscle cells capable of self-generation of electrochemical impulses at
membrane
◾ change in voltage across cell membrane when nerve impulse triggered – action
potential
◾ passage of charged particles across membrane - observable manifestation of
passage of impulse - transmit signals
 C O N D U C TION SYSTEM OF THE HEART

◾ generates & conducts rhythmic

electrical signals as follows:
(1) Sinoatrial (SA) node [pacemaker]:
modified cardiomyocytes
◾ SA node in right atrium near
opening of superior vena cava
◾ initiates each heartbeat &
determines heart rate
(2) impulses move along internodal
pathways in interatrial septum
(stimulates contraction of both atria)
◾ transmission of impulses in one
direction only
 CONDUCTION SYSTEM

(3)Atrioventricular (AV) node

◾ near rightAV valve at lower
end of interatrial septum
◾ electrical gateway to ventricles
◾ fibrous skeleton prevents
currents from reaching
ventricles by other route

Figure 19.12
 CONDUCTION SYSTEM

(4)Atrioventricular bundle (of His)

◾ divides into right & left bundle
branches
◾ branches pass through
interventricular septum toward
apex of heart
◾ delay atAV node - atria must
contract before ventricles

Figure 19.12
 CONDUCTION SYSTEM

(5) Subendothelial conducting networks

◾ Purkinje fibres spread through
ventricular myocardium
◾ cardiomyocytes pass signal from cell
to cell through gap junctions
◾ papillary muscles contract first,
Purkinje fibres second
◾ starts at apex & moves towards base
 LEARNING OUTCOMES

By the end of this lecture you should be able to:

◾ Describe the characteristics of cardiac muscle√

◾ Describe the conducting system of the heart √

◾ Describe the extrinsic nerve supply to the heart

◾ Provide an interpretation of an ECG

◾ Define cardiac output & stroke volume

◾ Discuss the mechanisms that regulate blood flow & blood pressure
 EXTRINSIC NERVE SUPPLY TO THE HEART

◾ autonomic nervous system [ANS]

◾ sympathetic and parasympathetic fibres

◾ sympathetic nerves increase heart rate &

contraction strength
◾ pathway to heart originates in lower
cervical to upper thoracic segments of the
spinal cord
◾ fibers pass through cardiac plexus in chest
& continue as cardiac nerves to the heart
◾ fibres terminate on SA &AV nodes, in the
myocardium & major vessels
 EXTRINSIC NERVE SUPPLY TO THE HEART

◾ parasympathetic nerves slow heart rate

◾ pathway begins with nuclei of the vagus

nerves in medulla oblongata
◾ extend to cardiac plexus & continue to
heart by way of cardiac nerves
◾ fibres of right vagus nerve lead to SA node

◾ fibres of left vagus nerve lead toAV node

◾ little/no vagal stimulation of myocardium

 ELECTRICAL & CONTRACTILE ACTIVITY OF HEART

In each cardiac cycle

◾ blood flows out of atria into ventricles - atrial systole lasts ± 0.1 second
◾ 70% passive,30% by atrial contraction

◾ ventricles contract - ventricular systole lasts ± 0.3 second

◾ closure ofAV valves - first heart sound (‘lub’)
◾ ventricles continue contraction - semilunar valves open

◾ ventricular relaxation (diastole)

▪ backflow of blood - closure of semilunar valves - second heart sound (‘dub’)

▪ entire cardiac cycle completed in less than 1 second

◾ sinus rhythm - normal heartbeat triggered by SA node quiescent period, when all
4 chambers are in diastole,lasts ± 0.4 second
◾ in adult at rest,there are typically 70-80 bpm (vagal tone)
 PACEMAKER PHYSIOLOGY

◾ SA node does not have a stable resting membrane potential

◾ starts at −60 mV & drifts upwards due to slow Na+ inflow
◾ gradual depolarisation is called pacemaker potential

◾ when it reaches threshold of −40 mV,voltage-gated fast Ca2+ & Na+ channels
open
◾ faster depolarisation occurs - peaking at 0 mV

◾ K + channels open & K + leaves the cell

◾ causes repolarisation
◾ once K+ channels close, pacemaker potential starts over

◾ When SA node fires it sets off heartbeat

◾ fires every 0.8 seconds, setting resting rate at 75 bpm
PACEMAKER PHYSIOLOGY
 IMPULSE C O N D U C TION TO MYO C ARDIUM

◾ signal from SA node stimulates both atria to contract almost simultaneously

◾ reachesAV node in 50 ms

◾ signal slows down throughAV node

◾ thin cardiomyocytes with fewer gap junctions

◾ delays signal 100 ms which allows ventricles time to fill

 IMPULSE CONDUCTI O N TO MYO C ARDIUM

◾ signals travel very quickly throughAV bundle & subendothelial conducting

network
◾ entire ventricular myocardium depolarises & contracts in near unison

◾ ventricular systole progresses up from apex of the heart

◾ spiral arrangement of myocardium twists ventricles slightly [wringing motion]

 ELECTRICAL BEHAVIOUR OF MYOCARDIUM:
C ARDIOMYOCYTE ACTION POTENTIAL

◾ cardiomyocytes have a stable resting potential of −90 mV

◾ depolarise only when stimulated
◾ Three phases to cardiomyocyte action potential:
(i) depolarization phase (very brief)
◾ stimulus opens voltage-regulated Na+ gates & membrane depolarises rapidly
◾ action potential peaks at +30 mV
◾ Na+ gates close quickly

(ii) plateau phase lasts 200 to 250 ms - sustained contraction for expulsion of blood
◾ voltage-gated slow Ca2+ channels open admitting Ca2+ which triggers
opening of Ca2+ channels on sarcoplasmic reticulum (SR)
◾ Ca2+ (mostly from the SR) binds to troponin triggering contraction
 ELECTRICAL BEHAVIOUR OF MYOCARDIUM:
C ARDIOMYOCYTE ACTION POTENTIAL

(iii) repolarisation phase:

▪ Ca2+ channels close, K+ channels open,rapid diffusion of K+ out of cell
returns it to resting potential

◾ long absolute refractory period of 250 ms (only 1-2 ms in skeletal muscle)

◾ prevents wave summation & tetanus which would stop pumping action
of heart
ELECTRICAL BEHAVIOUR OF MYOCARDIUM
 LEARNING OUTCOMES

By the end of this lecture you should be able to:

◾ Describe the characteristics of cardiac muscle √

◾ Describe the conducting system of the heart √

◾ Describe the extrinsic nerve supply to the heart √

◾ Provide an interpretation of an ECG

◾ Define cardiac output & stroke volume

◾ Discuss the mechanisms that regulate blood flow & blood pressure
 THE ELECTROCARDIOGRAM
◾ composite of all action potentials of nodal & myocardial cells detected,
amplified & recorded by electrodes on arms,legs & chest
 THE ELECTROCARDIOGRAM

P wave
◾ SA node fires, atria depolarise & contract
◾ atrial systole begins 100 ms after SA signal

QRS complex
◾ ventricular depolarization
◾ complex shape of spike due to different
thickness & shape of the two ventricles

ST segment - ventricular systole

◾ corresponds to plateau in myocardial action
potential

T wave
◾ ventricular repolarisation & relaxation
RELATIONSHIP BETWEEN C O N TRACTION CYCLE & ECG
 ECGS:NORMAL &ABNORMAL
Assessing ECG:
◾ height of waves,duration of waves,relationship between different waves
◾ amount of depolarisation in P wave & QRS complex
◾ e.g.large Q RS – enlarged heart
◾ smaller than normal electrical signal may mean heart mass reduced

Deviations of ECG from normal can indicate:

◾ myocardial infarction (MI)
◾ abnormalities in conduction pathways
◾ heart enlargement
◾ electrolyte & hormone imbalances
ECGS: NORMAL &ABNORMAL

(a) Sinus rhythm (normal)

CARDIAC RHYTHM
 LEARNING OUTCOMES

By the end of this lecture you should be able to:

◾ Describe the characteristics of cardiac muscle √

◾ Describe the conducting system of the heart √

◾ Describe the extrinsic nerve supply to the heart √

◾ Provide an interpretation of an ECG √

◾ Define cardiac output & stroke volume

◾ Discuss the mechanisms that regulate blood flow & blood pressure
 SOME IMPORTANT CONCEPTS

◾ cardiac output

◾ blood pressure

◾ blood flow through vessels

◾ regulation of flow
 CARDIAC OUTPUT

▪ volume blood ejected from heart per unit time (minute)

◾ 5-6 litres per minute in adults
◾ vigorous exercise increases C O to 21 L/min & up to 35 L/min for world-class
athlete

Combination of:
▪ volume blood pumped from ventricle per contraction = stroke volume [SV]
▪ number of beats per minute = heart rate[HR]

▪ Thus C O = SV x HR
 C ARDIAC OUTPUT:STROKE VOLUME
Stroke volume:volume of blood pumped out of each ventricle with each contraction

SV is difference between End-Diastolic volume & End-Systolic volume

▪ End-Diastolic volume:volume of blood in ventricles after diastole [i.e.before it

contracts]

▪End-Systolic volume:volume of blood remaining in ventricle after systole

End-Diastolic volume influenced by:

▪ filling time - duration of ventricular diastole
▪ depends on heart rate – if fast = less filling time
▪ venous return – rate of blood flow back to heart
▪ velocity of blood flow,pressure gradients,sympathetic nerve activity
 STROKE VOLUME

◾ Three variables govern stroke volume

◾ preload

◾ contractility

◾ afterload
 PRELO A D

◾ amount of tension in ventricular

myocardium immediately before it begins to
contract
◾ stretching of muscle cells during ventricular
diastole (increase EDV,increased preload)
◾ increased preload causes increased force of
contraction
◾ exercise increases venous return &
stretches myocardium
◾ cardiomyocytes generate more tension
during contraction
◾ increased cardiac output matches increased
venous return
◾ increase in stroke volume
 PRELO A D
Frank– Starling law of the heart:SV  EDV
◾ heart adapts to changing volume of incoming blood
◾ stroke volume is proportional to end diastolic volume [EDV]
◾ volume pumped out determined by venous return
◾ ventricles eject almost as much blood received

◾ the more the ventricles are stretched,the harder they contract

◾ relates to length-tension relationship of striated muscle

 CONTRACTILITY

◾ refers to strength of contraction of myocardium for given preload

▪ increased due to increased calcium entry into cardiac muscle cells

▪ chronotrophic effects – positive or negative factors that influence contraction
▪ Sympathetic NS increases contractility (positive inotropic action)
▪ Parasympathetic NS decreases contractility (negative inotropic action)
▪ hormones (e.g.epinephrine) have positive inotropic actions
▪ drugs can have positive inotropic actions (e.g.Dopamine) or negative
inotropic actions (e.g.Beta-blockers)
▪ digitalis raises intracellular calcium levels & contraction strength
 CHRONOTROPIC EFFECTS OF ELECTROLYTES

◾ Electrolytes
◾ K + has greatest chronotropic effect
◾ Hyperkalemia - excess K + diffuses into cardiomyocytes
◾ myocardium less excitable,heart rate slows & becomes irregular
◾ hypokalemia - deficiency in K +
◾ cells hyperpolarized, require increased stimulation
 CHRONOTROPIC EFFECTS OF ELECTROLYTES

◾ Electrolytes
◾ Calcium
◾ hypercalcaemia - excess of Ca2+
◾ decreases heart rate & contraction strength
◾ hypocalcaemia - deficiency of Ca2+
◾ increases heart rate & contraction strength
 AFTERLOAD
◾ sum of all forces opposing ejection of blood from
ventricle
◾ tension required to force open semilunar valve
◾ tension increased by factors that decrease blood flow

◾ largest component is blood pressure in aorta &

pulmonary trunk
◾ opposes opening of semilunar valves
◾ limits stroke volume
◾ hypertension increases afterload & opposes
ventricular ejection
◾ lung diseases can restrict pulmonary circulation
◾ cor pulmonale:right ventricular failure due to
obstructed pulmonary circulation
◾ emphysema,chronic bronchitis & black lung disease
 BLOOD PRESSURE
◾ pressure exerted by blood on walls of blood vessels that contain it
Two pressures are recorded
◾ systolic pressure: peak arterial BP taken during ventricular contraction
◾ diastolic pressure: minimum arterial BP taken during ventricular relaxation
◾ measured at brachial artery of arm using sphygmomanometer
◾ a close approximation of pressure at exit of left ventricle
◾ pulse pressure – difference between SBP & DBP
◾ mean arterial pressure (MAP): estimate of average blood pressure
 LEARNING OUTCOMES

By the end of this lecture you should be able to:

◾ Describe the characteristics of cardiac muscle √

◾ Describe the conducting system of the heart √

◾ Describe the extrinsic nerve supply to the heart √

◾ Provide an interpretation of an ECG √

◾ Define cardiac output & stroke volume √

◾ Discuss the mechanisms that regulate blood flow & blood pressure
 BLOOD PRESSURE
◾ pressure varies across the cardiac cycle - blood flow in arteries is pulsatile
◾ in capillaries & veins,blood flows at steady speed

◾ BP tends to rise with age

◾ Hypertension - high blood pressure

◾ chronic resting BP >140/90
◾ can weaken arteries,cause aneurysms, promote atherosclerosis

◾ Hypotension - chronic low resting BP

◾ caused by blood loss, dehydration,anemia
 BLOOD PRESSURE IS INFLUENCED BY:

◾ peripheral resistance:force that opposes movement of blood through a vessel

◾ vascular pressure gradients:pressure difference between ends of blood vessel
◾ blood flow & velocity:volume & speed of blood flow through vessel
◾ venous return:amount of blood arriving at right atrium each minute
◾ cardiac output & heart rate
 PERIPHERAL RESISTANCE

◾ opposition to flow that blood encounters in vessels away from the heart
◾ resistance dependent on:
◾ blood viscosity – ‘thickness’ of blood
◾ RBC count & albumin concentration elevate viscosity the most
◾ decreased viscosity with anemia & hypoproteinemia speed flow
◾ increased viscosity with polycythemia & dehydration slow flow

◾ Vessel length
◾ the further blood travels,the more cumulative friction it encounters
◾ pressure & flow decline with distance
BP CHANGES WITH DISTANCE
 PERIPHERAL RESISTANCE

◾ Vessel radius:most powerful

influence over flow
◾ markedly affects blood velocity
◾ small changes in blood vessel radius
can cause large changes in flow
(mL/min)
◾ vasoreflexes produce changes in
vessel radius
◾ vasoconstriction:smooth muscle of
tunica media contracts
◾ vasodilation:relaxation of muscle,
allowing vessel to expand
 PERIPHERAL RESISTANCE

◾ from aorta to capillaries,blood velocity (speed) decreases because:

◾ greater distance,more friction from vessel walls to reduce speed
◾ smaller radii of arterioles & capillaries offer more resistance

◾ from capillaries to venae cavae,velocity increases again:

◾ large volume of blood forced into smaller channels
◾ veins are larger so they create less resistance than capillaries

◾ blood in veins never regains velocity it had in large arteries

◾ veins are more compliant than arteries
 PERIPHERAL RESISTANCE

◾ Most significant are arterioles

◾ on proximal side of capillary beds
regulate flow into capillaries
◾ outnumber other types of artery
- provide most control points
◾ more muscular in proportion to
their diameter
◾ highly capable of changing radius

◾ Arterioles produce half of total

peripheral resistance
 REGULATION OF BLOOD PRESSURE & FLO W

◾ Vasomotion is a quick and powerful way of altering blood pressure and flow

◾ Three ways of controlling vasomotor activity

◾ Local control
◾ Neural control
◾ Hormonal control
 LOCAL CONTROL

◾ autoregulation - ability of tissues to regulate their own blood supply

◾ if tissues inadequately perfused, wastes accumulate - stimulates vasodilation
which increases perfusion
◾ bloodstream delivers O 2 & removes metabolites
◾ when wastes are removed,vessels constrict
◾ vasoactive chemicals - substances secreted by platelets,endothelial cells &
perivascular tissue to stimulate vasomotor responses
◾ histamine,bradykinin & prostaglandins stimulate vasodilation
 NEURAL CONTROL
◾ Central & autonomic nervous systems also
exert control over blood vessel size
◾ vasomotor centre of medulla
◾ exerts sympathetic control over vessels
throughout body
◾ stimulates vessels to constrict but can dilate
vessels in cardiac muscle during exercise
◾ vasomotor centre is integrating centre for
three autonomic reflexes
◾ Baroreflexes
◾ Chemoreflexes
◾ Medullary ischemic reflex
 NEURAL CONTROL
Baroreflex
◾ govern short-term regulation of BP
◾ adjustments for rapid changes in posture
◾ automatic
◾ negative feedback response to change in BP
◾ increases in BP detected by carotid sinuses
◾ glossopharyngeal nerve sends signals to brainstem

Results in:
1) inhibition of sympathetic cardiac & vasomotor neurons
2) excitation of vagal fibers - slow heart rate & reduce BP
◾ decreases in BP have the opposite effect
NEGATIVE FEEDBACK CONTROL OF BP
 NEURAL CONTROL
◾ chemoreceptors in aortic & carotid bodies
◾ automatic response to changes in blood
chemistry
◾ adjust respiration to changes in pH &
concentrations of O2 & CO2
◾ act through vasomotor centre
◾ cause widespread vasoconstriction,
increasing BP,lung perfusion & gas
exchange
◾ also stimulate breathing
 NEURAL CONTROL
◾ Medullary ischemic reflex
◾ automatic response to decrease in
perfusion of the brain
◾ medulla monitors own blood supply
◾ can detect ischaemia
◾ cardiac & vasomotor centres send
sympathetic signals to heart & vessels
◾ increases heart rate & contraction
force
◾ widespread vasoconstriction
◾ raises BP & restores normal
perfusion to the brain
 HORMONAL CONTROL

◾ Hormones influence blood pressure

◾ vasoactive effects
◾ regulate water balance

◾ Angiotensin II - potent vasoconstrictor

◾ raises blood pressure
◾ promotes Na+ & H 2O retention by kidneys
◾ increases blood volume & pressure

◾ Atrial natriuretic peptide - increases urinary sodium excretion

◾ reduces blood volume & promotes vasodilation
◾ lowers blood pressure
 HORMONAL CONTROL

◾ ADH promotes water retention & raises BP

◾ also a vasoconstrictor (vasopressin)

◾ Epinephrine & norepinephrine effects

◾ bind to 𝛼-adrenergic receptors in most blood vessels - vasoconstriction

◾ in cardiac muscle blood vessels
◾ bind to 𝛽-adrenergic receptors - vasodilation
 CAPILLARY EXCHANGE

◾ exchanges between blood & surrounding tissues occurs in capillaries

◾ two-way movement of fluid across capillary walls
◾ H2O, O2, CO2, glucose, amino acids,antibodies,hormones, wastes, ammonia
◾ diffusion,transcytosis, filtration & reabsorption
 ROUTES OF CAPILLARY FLUID EXCHANGE

Lipid-soluble substances -
steroid hormones,O2 &
CO2 diffuse easily across
plasma membranes

Water-soluble substances -
glucose & electrolytes must
pass through filtration pores
& intercellular clefts

Transcytosis - fatty acids,

albumin,& some hormones
(insulin)
 FILTRATION & REABSORPTION

◾ Hydrostatic pressure
◾ physical force exerted against a surface by a liquid
◾ blood pressure in vessels is hydrostatic pressure

◾ capillaries reabsorb about 85% of the fluid they filter

◾ other 15% is absorbed by lymphatic system & returned to the blood

 FILTRATION & REABSORPTION

◾ fluid filters from arterial end of capillary bed & osmotically reenters at venous
end

◾ delivers materials to the cell & removes metabolic wastes

◾ Opposing forces:
◾ blood hydrostatic pressure drives fluid out of capillary
◾ high on arterial end of capillary,low on venous end
◾ colloid osmotic pressure (COP) draws fluid into capillary
◾ results from plasma proteins (albumin) - more in blood
◾ oncotic pressure = net C O P (blood C O P − tissue C O P)
FILTRATION & REABSORPTION

Arterial end Forces (mm Hg) Venous end

Hydrostatic pressures
30 out Blood hydrostatic pressure 10 out
+3 out Interstitial hydrostatic pressure +3 out
33 out Net hydrostatic pressure 13 out
Colloid osmotic pressures (COP)
28 in Blood 28 in
-8 out Tissue fluid -8 out
20 in Oncotic pressure (net Cop) 20 in
13 out Net filtration or reabsorption pressure 7 in
 O VERVIEW OF VOLUME CHANGES

◾ right & left sides of heart eject same volume of blood despite different pressure

◾ congestive heart failure (CHF) - failure of either ventricle to eject blood effectively

◾ usually due to heart weakened by myocardial infarction,chronic hypertension,

valvular insufficiency,or congenital defects in heart structure
 O VERVIEW OF VOLUME CHANGES
◾ left sided failure - blood backs up into lungs causing pulmonary oedema

◾ right sided failure - blood backs up in venae cavae causing systemic or generalized
oedema
◾ enlargement of liver,ascites (pooling of fluid in abdominal cavity),distension of
jugular veins,swelling of fingers,ankles,feet
◾ Can eventually lead to total heart failure
 PULMONARY OEDEMA

1)right ventricular output exceeds left

ventricular output
2) pressure backs up

3) fluid accumulates in pulmonary tissue

▪ shortness of breath

▪ sense of suffocation
 SYSTEMIC OEDEMA

1) left ventricular output exceeds right ventricular output

2) pressure backs up
3) fluid accumulates in systemic tissue
 LEARNING OUTCOMES

By the end of this lecture you should be able to:

◾ Describe the characteristics of cardiac muscle √
◾ Describe the conducting system of the heart √
◾ Describe the extrinsic nerve supply to the heart √
◾ Provide an interpretation of an ECG √
◾ Define cardiac output & stroke volume √
◾ Discuss the mechanisms that regulate blood flow & blood pressure √