CARDIOVASCULAR PHYSIOLOGYDr J. du ToitRoom 511

Fisan building

Text books: Human Physiology – An Integrated Approach. Silverthorn.Human Physiology. Rhodes and Pflanzer.

Functions of the CVS1.Transport of: 1) nutrients and water and, 2) gases

DS Lungs

Cells Liver Cells

Kidneys2. Cell cell communication - hormones3. Transport – fatty acids from adipose tissue & glucose from the liver4. Transport WBC & antibodies5. NB in temperature regulation

Anatomy of the Heart

Size of fist Between lungs - base under sternum and apex on diaphram

Epi- en pericardium – fibrous and serous tissue

Wall Myocardium - contractile cells

Endocardium – endothelium –continuous with blood vessel endothelium

2 Atria 4 Chambers

2 Ventricles

Right – Tricuspid valve (3-leaflets)

• Atria & ventricles separated by AV valves Cordae tendinae en papillary muscles Left – Bicuspid – Mitral valve (2 leaflets)

Ventricles of pulmonary artery and aorta – separated by – semilunar valves: Aortic valve and Pulmonary valve

Arteries oxygenated blood - red

VASCULAR SYSTEM

Veins deoxygenated blood - blue

B. Anatomy and direction of blood flow through the heart

The Heart wall

a) Epicardium/Pericardium: 2 layers nl. i) Outside fibrous pericardium ii) Inside serous pericardiumFunctions: 1) Prevents excess stretching of heart2) Provides smooth, lubricated outside surface

b) Myocardium: Contractile part of the heart wall.

c) Endocardium: Connective tissue attaches the myocardium to the endothelium. The latter provides smooth surface and prevents clotting.

ELECTRICAL ACTIVITY OF THE HEARTStructure of the cardiomyocyte

Properties of the cardiomyocyte:

•Is striated•Contains one or more nuclei•Cells are branched•More mitochondria than skeletal muscle•Contains tight junctions and gap junctions.

2 Types of cardiomiocytes: 1) normal cardiomyocytes2) pacemaker and conducting cardiomyocytes

AP of Skeletal and Heart muscle

•Depolarisation due to Na+ influx•Repolarisation due to K+ efflux•Heart muscle AP – has plato due to Ca2+ influx longer AP

Importance of the Refractory Period

Prevents tetanus• Ensures diastolic relaxation

SA node wall of the RA near superior vena cava. primary pacemaker at rest = 70bpm. Parasympathetic: ACh - heart rate Sympathetic: adren. & nor-adren. - heart rate and contractile forceSensitive to – temp., stretch, touch and chem. stimulation

AV node Bottom wall of the RA - interatrial septum Firing frequency: 40-60bpm 1) Delays heart impulse: 0.1 sec complete ventricular filling 2) Delays frequency of impuls propagation

AV bundle From the AV-node to interventricular septum. Right bundle branch – right of the septum to the apex of the heart Left bundle branch – posterior/inferior branch

-anterior/superior branch functional link between atria and ventricles

Purkinje fibres branches of the left and right bundle branch impulse propagation to contractile cells in ventricle

AP – Origin and Propagation

SA-node propagation speed fast (1 m/sec) AV-node propagation speed slow (0.05-0.1 m/sec)

no direct conduction from atria to ventricle muscle – Fibrous plate/sheathBundle of His propagation speed fast Purkinje system propagation speed fast (2 m/sec) Ventricular contractile cells

Wave of depolarization over heart creates a potential difference - dipole Dipole (hart) surrounded by conductor (elektroliete & water)• Elektrodes on surface attached to galvanometer – measures potential differences

ECG – measures electrical changes in heart

ECG• The sum of all the potentials that are created by the cells of the heart at any given moment• Each component of the ECG reflects a de- or repolarisation of a part of the heart can associate parts of the ECG with parts of the cardiac cycle.

Clinical application of the ECGDetermination of: • HR, heart rhythm• Presence of hypertrophy or atrophy• Abnormal conduction paterns• The cardiac axis (electrical axis)

Normal heart rhythmSinus rhythm – bradycardia or tagycardia

ECG Leads

• Position of the electrodes = leads • 6 peripheral leads and 6 precordial leads

a) 3 bipolar limb leads (standard leads) measure the potential differences between 2 points (Einthoven triangle)

b) 9 unipolar leads measure the potential at a point on the body

•3 unipolar limb leads: aVR, aVL en aVF • 6 unipolar chest leads: V1-V6

Normal heart rhythm

Sinus rhythm: • Sinus tachycardia: > 100 bpm Causes: exercise, emotional excitement, heart failure, fever, anemia.• Sinus bradycardia: < 60 bpm Causes: long term exercise, hypothyroidism.

Sinus arrhythmias: irregular firing of the SA-node (fast and slow beats)

Ectopic heart beats: the impulse that causes heart contraction originates outside the SA-node and causes extrasystoles.

1. The QRS complex may be abnormally large (ventricular hypertrophy) or abnormally small (ventricular atrophy).

2. The QRS complex does not follow the P-wave. Sometimes several P-waves followed by the QRS-complex. Causes, heart block. The impulse is not

always conducted through the AV-node.3. The Q-wave is enlarged, abnormal QRS-complex, ST-segment is

elevated above baseline and inverted T-waves are indicative of necrotic heart muscle. Therefore MI.

Abnormal ECG

Heart defect ECG DefectVentricular hypertrophy QRS complex with high amplitude

Ventricular atrophy QRS complex with low amplitude

Ischaemia and infarction Abnormal QRS complex, ST segment elevated, T-wave inverted.

Bundle branch block wide QRS complex due to delayed conduction

Heart block P wave not followed by QRS complex

1st degree delayed QRS complex2nddegree absent QRS complex3rd degree total AV dissosiasionVT Abnormal QRS complex, no P waveVF No QRS complex distinguishable

Heart sounds and Heart murmurs

Heart sounds

1st heart sound – during ventricular systole – low tone – closing of AV valves

2nd heart sound – end of ventricular systole – sharp with high tone – closing of the semilunar valves.

3rd heart sounds – end of systole - AV valves open – blood flows through

4th heart sounds – artial systole – vibrasion of the ventricular wall

Heart murmurs

• Due to abnormalities of the heart

• Narrowed valves (stenosis) and/or leaking valves (incompetence)

Whistle Swish

Aortic valve stenosis – Rheumatic feverType of murmur – loud coarse systolic murmur – max. intensity middle systole Ventricular systolic pressure – very highECG – Hypertrophy – Large QRS komplex Aortic pressure – stays relatively low during systole

Mitral valve stenosis• Type of murmur – long rumbeling diastolic murmur, intensity high - end diastole• Pressure in LV and aorta – low or normal• Right venticle – hypertrophic

Aortic valve incompetence• Type of murmur – Soft, high pitched diastolic murmur• Pressure in aorta – systolic pressure high• Left ventricle – end-diastolic pressure high

Mitral valve incompetence• Type of murmur – systolic murmur• Pressure in left atrium – elevated• Left ventricle – elevated end-diastolic pressure

Pulmonary Circulation

• Pressure changes qualitatively similar – pressures however far lower• Pulmonary artery diastolic and systolic pressure 8-24mmHg • Pulmonary circulation – low pressure system

CARDIAC OUTPUT (CO)

Vol blood that leaves LV per min into systemic circulation - 5-6 L/min - adultstrenuous exercise - 35-50 L/min

by exercise, fever, stress, anemia, gender, and thyroid defects.

CO – determined by two variables nl. 1) Heart rate (HR) and, 2) Stroke volume (SV)

SV and HR - regulated by two mechanisms:1) Intrinsic (auto-regulation), eg. Stretch of muscle fibers, frequency of

contraction, tension and temperature.2) Extrinsic, eg. by nerves, hormones and electrolytes.

Stroke volume (SV): volume of blood leaving ventricle per heartbeat.

End-diastolic volume (EDV) – End systolic volume (ESV) = SV 120 ml –50 ml = 70 mlThe Ejection fraction is : SV/EDV = 70/120 = 0.58 of 58%

Factors that determine SV:1. Preload (intrinsic mech.)2. Afterload (intrinsicmech.)3. Contractility of the myocardium (exstrinsic mech.)

Preload – degree of stretch of muscle fiber which is determined by the EDV = volume blood entering ventricle during diastole.

EDV is influenced by: 1) filling pressure venous return

06h00-08h00 24h00-05h00

2.5 bar 3.5 bar

1.5 L/min

0.75 L/min

2) Filling time HR Pressure in A = Pressure in B

Time in A- 1sec Time in B – 0.6 sec

Filling pressure function of central venous pressure (CVP) = pressure in RA

During diastole CVP = 0mm Hg

During systole CVP = 8 mm Hg

CVP determined by:1. the ability of the heart to pump blood away – heart failure - CVP2. Volume of the system.3. The pressure around the heart also influences the CVP

Significance of the CVP

1. Determines RV filling EDV SV CO2. Controls venous return - CVP venous return

edema3. Clinically present with heart abnormalities and lung

diseases• Asthma en emphysema CVP• Accumulation of fluid in vascular system CVP

Preload also influenced by compliance of the heart chambers. venous return EDV preload compliance EDV preload

INTRINSIC CONTROL OF SV

blood volume in ventricles

stretch of the ventricular fibers

Stronger contraction during

systole

Stroke volume

cardiac output

better tissue perfusion

20 mmHg 20 mmHg 40 mmHg

Afterload on the Heart

Pressure against which the ventricle must eject blood.Influenced by: Arterial BP Elasticity of the arterial bloodvessel wall Arterial resistance

5 liter/min 2.5 liter/min 5 liter/min

CONTRACTILITY

Extrinsic factors – Adrenalin en Noradrenalin influenced by intracellular Ca2+ levels

Chemical substances influence contractility – positive en negative inotropic agents

Catecholamines & digitalis Anaesthetics & ACh

Regulation of heart rate (HR)

Heart rate is regulated – not controlled. Factors that determine HR:

a) Inside the heart temperature• anemia, hipoxia, blood loss

b) Outside the heart1. Nerves• parasimpathetic stimulation - vagal-nerve - ACh• sympathetic stimulation (T1-T6) - noradrenalin2. Hormones• particularly adrenalin en noradrenalin

BLOOD FLOW

F P

Pressure declines due to resistance (R) in blood vessels

R= 8 L r 4 - Poiseuille Law

r very NB in determining the resistance to flow.

vasoconstriction vasodilatation

BLOOD FLOW AND THE CIRCULATORY SYSTEM

Blood flow – influenced by BP & resistance to flow.F P, where P = P1 - P2 ……. (1)

F= 1/R………………(2)

Resistance to blood flow influenced by:• The length of the blood vessel (L)• The radius of the blood vessel (r)• The viscosity of the blood ()

Factors in Poiseuille’s law:R= 8 L r4

With: 8 a constant = blood viscosity = constant L = Length of the tube = constant = constant r = radius of the tube

Change in the radius of the tube makes the biggest difference to resistance to flow. 1. in radius = vasodilatation2. in radius = vasoconstriction

Flow (F) = volume of blood that flows past a point in a given time (L/min)F = P/R

Flow velocity of blood

Flow velocity is the distance a given volume of blood will move in a given time (mm/sec).

The cross-sectional area of all the capillaries together is very large - flow velocity is the slowest in the capillaries.

H2O uit

Flow of flow rate = F = P - liters/min R

Flow velocity = distance that a given volume of blood moves in a given time – mm/sec

H2O in

Cross-sectional area NB for flow velocity – see capillaries

TYPE OF BLOOD VESSELS

Arteries arterioles capillaries venules veins1. Arteries (distribution vessels: large diameter, little resistance)

Large arteries:• Aorta en pulmonary arteries• Elastic vessels: lots of elastin and collagen – little smooth muscle

Functions:• Temporary reservoir• Pump of blood • Monitor system for BP

Medium arteries:•Cerebral and brachial arteries•Muscle type arteries (little elastin and more smooth muscle)

Functions: link between large and small arteries

2. Arterioles (NB for regulation of blood flow to capillaries)• Distribution arteries and resistance vessels• Thick layer of smooth muscle – supplied with sympathetic nerves; also

sensitive to some hormones and chemical changes in blood• Always partially constricted

Functions: control vascular resistance and determines distribution of blood to different organs.Assists with regulation of BP

3. Veins

• Walls are thinner and their diameter larger than arteries• Veins are more compliant than arteries• Does not have much smooth muscle and connective tissue• Valves: prevents backflow of blood Functions: i) transport blood from distal vascular bed to the heart.ii) Serves as reservoir (66 % of blood)

4. Capillaries• Capillaries branch out of arterioles or metarterioles (serve as throughway/canal

between arterioles and venules).• Has largest cross-sectional area – flow velocity is very slow• Walls very permeable• Diameter: 3-8 m; thichness: 1-2 m

• 3 layers:1. Endothelial cells2. basal membrane of proteoglycans3. thin collagen and reticular fibers. NB: no smooth muscle layer

Functions: link between blood and tissue for exchange of: water, gasses, electrolytes, nutrients etc.

• Tissue that is metabolically more active has larger capillary bed.

ARTERIAL SYSTEM

•Conduction vessels •Pressure buffer/reservoir•Regulates blood distribution

Pressure in arteries serves as driving force for blood through the vascular system back to the heart.

F = P RF = P (aorta) – P (vena cava)

RF = MAP – 0 mmHg

R

MAP = Diastolic pressure + systolic pressure – diastolic pressure 3

F = MAP or MAP F X R (F = CO) R

MAP is influenced by : •F and R in arteriole•Blood volume•Blood volume distribution – veins contain 60% of total blood volume

Pulse pressure - ‘n function of SV and compliance of the aorta.

•an increase in SV - stretch of the aorta - systolic BP and consequent high pulse pressure. •The less compliant the aorta, the larger the systolic BP - pulse pressure.•Heart rate - diastolic filling - MAP and pulse pressure

Tachycardia – reduction in pulse pressure (small SV)Bradycardia – increase in pulse pressure (larger SV).

TOTAL PERIPHERAL RESISTANCE

Mean pressure in arteriesF = MAP R

Resistance in blood vessels from aorta to the heart = TPR

Due to changes in R

1. Changes in MAP 2. Changes in blood distribution

MAP = F X R R – Achieved by arterioles – (60% van TPR)

NEURAL CONTROL OF BLOOD DISTRIBUTION

? Vasodilatation of all vascular beds – heat exhaustion

Inadequate perfusion of vital organscommunication NB – nerve and hormone control

Arterioles are well supplied with nerves– nor-epinephrine receptor contraction

At rest all arterioles stimulated by sympathetic nervous system.

Parasympathetic nerves don’t play a role in the control of blood flow

How is vasodilatation achieved ?

Short term processes that control BP

Receptor – baroreceptor

Nerve

Integrator

Nerve (ONS)

Heart of arteriole

Long term processes that control BP

Receptor – baroreceptor

Nerve

Integrator

Nerve (ANS)

Endocrine gland or kidney

Hormone fluid retention or excretion

Baroreceptors

•In aortic arch and carotid sinus

•Reacts to stretch of the elastic walls of the arteries

•Reseptors always tonically active

Systemic BP determination

TOTAL RERIPHERAL RESISTANCE

Resistance that blood vessels present against blood flow - TPR – arterioles contribute 60% to TPR

R = 8 L 1 r 4 r4

Radius controlled by: A Local control mechanisms (intrinsic). B. Reflex control (exstrinsic).

Myogenic autoregulation, due to in pressure or in pressureRESTING TONE – depolarises spontaneously

MAP Blood flow and blood vessel diameter vasoconstriction blood vessel diameter and blood flow or,

MAP Blood flow and blood vessel diameter vasodilatation blood vessel diameter and blood flow

B. Reflex (exstrinsic) control mechanisms. Hormones•Bradykinin, histamin – vasodilators•Noradrenalin, Angiotensin II en ADH – vasoconstrictors

Venous System • Thin walls and very compliant• Degree to which blood is stored in the veins – dependent on smooth muscle tone – sympathetic nerve activity.

Venous return dependent on:• Pressure in RA• Total blood volume• Sympathetic activity on veins• Skeletal muscle and respiratory pump

SYSTEMIC BLOOD PRESSURE

MAP = diast BP + pulse pressure 3

Normal BP = 120/80 mmHg

Method of measuring:• Indirect • Direct Low in children, women and when lying downHigh in elderly, obese, with stress and severe exercise

Factors that determine BP

BP = CO X TPR1. CO = SV X HR2. TPR3. Elasticity of blood vessels4. Volume of blood5. Viscosity of blood

Question1) Why would MAP rise as HR rises even if diastolic filling of the ventricle decreases (at an increased CO)?

NB MAP = CO X TPR

CO TPR = CO MAP

1. CO = SV and HR• SV and HR can only change BP if CO changes• If CO then BP decreases if TPR remains constant• If CO then BP will be maintained by increasing TPR• If CO as with exercise, then BP rises unless TPR decreases (this is the

normal situation)

2. Peripheral resistance – dependent on diameter of the arteriole (and therefore resistance in arterioles)

3. The BP will increase with a decrease in compliance of the elastic blood vessels.

Pulse pressure will rise as a result of a decrease in compliance of the blood vessels MAP

Hipertensie

•BD van 140/90 mmHg = skeidingslyn tussen normaal en hipertensief•Gewoonlik agv verlaagde radius van die arteriole •Gewoonlik is die oorsaak onbekend – essensiële hipertensie

Moontlike oorsake:•Baie wetenskaplike bewyse dat oormaat natrium “retension” kan hipertensie veroorsaak•Behandeling met ‘n lae natrium dieet of die gebruik van “diuretikums” (diuretics) verlaag BD•Vetsug risiko faktor vir hipertensie – oefening en gewig verlies kan die hoë BD laat afneem

Gevolge:Hipertrofie van hart en beroerte (stroke)

Behandeling van hipertensie

• Diuretika - water en natrium uitskeiding (niere) KO• -blockers KO ( ? effek op oefeningsvermoeë)• Kalsium antagoniste baie spesifiek vir gladdespier kalsium kanale TPW• ACE inhibeerders

Angiotensienogeen Angiotensien I Angiotensien II vasokontriksie

ACE

ACE - inhibeerder

Control of BP

+ Chronotropicand dromotropic

vasoconstrictor

- Chronotropic

Sensor Baroreseptor (carotid sinus, aortic arch, RA, LA LV en pulmonary art.)

Volume en chemoreceptors Brain cortex en Hypothalamus

Cardiovascular control centre – in medulla Sensory area Vasomotor center

SA en AV node A en V muscle fibers Blood vessel and smooth muscle

Pressor area Depressor area

Afferent impulses from other centers Cerebral cortex (limbic region)

Excitement and rage anxiety, fear, sadness

CMC CMC ( vagal act.) ( vagal act.)

BP; HR BP; HR

MICROCIRCULATION AND LYMPH

Molecular exchange at the capillaries

• Transcytosis en endocytosis • Diffusion • Bulk flow

Filtration and Absorption