the electrocardiogram (ecg)

THE ELECTROCARDIOGRA

M (ECG)

Introduction

• ECG is a crucial diagnostic tool in clinical practice• Useful in diagnosing rhythm disturbances, changes in electrical

conduction, and myocardial muscle condition• Electrical currents are measured by an array of electrodes placed

at specific locations on the body surface• The repeating waves of the ECG represent the sequence of

depolarization and repolarization of the atria and ventricles

• ECG does not measure absolute voltages, but voltage changes from a baseline (isoelectric) voltage.

• ECG are generally recorded on paper at a speed of 25 mm/sec and with a vertical calibration of 1 mV/cm.

• Light lines describe small squares each of 1 x 1 mm size.

• Dark lines describe large squares each of 5 x 5 mm size.

• X axis denotes time – 1 small square = 0.04 seconds.

• Y axis denotes the amplitude of the wave produced – 1 small square = 0.1 mV.

Methods for Recording Electrocardiograms• The electrical currents generated by the cardiac muscle during each

beat of the heart change electrical potentials and polarities on the respective sides of the heart in less than 0.01 second

• Apparatus for recording electrocardiograms be capable of responding rapidly to these changes in potentials

• Measures the flow of electric current around the heart during the cardiac cycle

• Flow of electrical currents in the chest around the heart

ECG Leads: Placement of RecordingElectrodes• on each arm and leg, and six electrodes are placed at defined locations

on the chest

• three types of leads – standard Limb leads, augmented and precordial (chest) leads

• Each leads views the heart at a unique angle enhancing its sensitivity to a particular region of the heart.

• are connected to a device that measures potential differences between selected electrodes to produce the characteristic ECG tracings.

Electrocardiographic Leads

• Three Bipolar Limb Leads • Bipolar means that the electrocardiogram is recorded from two

electrodes located on different sides of the heart• “lead” is not a single wire connecting from the body but a

combination of two wires and their electrodes to make a complete circuit between the body and the electrocardiograph.

• unipolar leads because they have a single positive electrode with the other electrodes coupled together electrically to serve as a common negative electrode augmented leads and chest leads

ECG Limb Leads

• Lead I = has the +VE electrode on the LA and –VE RA

therefore measuring the potential difference across the chest between the two arms. electrode on the right leg is a reference electrode for recording purposes

• the lead II configuration, the positive electrode is on the left leg and the negative electrode is on the right arm.

• Lead III has the positive electrode on the left leg and the negative electrode on the left arm.

• Form Equilateral triangle

Einthoven’s Law

• is drawn around the area of the heart• Einthoven’s law states that if the electric potentials of any two of

the three bipolar limb electrocardiographic leads are known at any given instant, the third one can be determined mathematically by simply summing the first two.

• The augmented limb leads are,• AVR – (-50 degrees): Right arm is +ve and other limbs are –ve.• AVL – (-30 degrees): Left arm +ve and other limbs are –ve.• AVF – (90 degrees): Legs are +ve and other limbs are –ve.• Note these augmented are so named as they amplify the tracings

to get an adequate recording.

Precordial leads

• view the electrical forces moving anteriorly and posteriorly• These are,• V1: Placed in the 4th intercostal space right to the sternum.• V2: Placed in the 4th intercostal space left to the sternum.• V3: Placed between leads V2 and V4.• V4: Placed in the 5th intercostal space in the mid clavicular line.• V5: Placed between the leads V4 and V6.• V6: Placed in the 5th intercostal space in the mid axillary line.

• leads V1 and V2, the QRS recordings of the normal heart are mainly negative because nearer to the base of the heart than to the apex,

• QRS complexes in leads V4, V5, and V6 are mainly positive because the chest electrode in these leads is nearer the heart apex, which is the direction of electropositivity during most of depolarization

wave of the ECG

• P wave. It represents the wave of depolarization that spreads from the SA node throughout the atria; it is usually 0.08 to 0.1 seconds

• a small, rounded, upward (positive) deflection

• the P-R interval The period of time from the onset of the P wave to the beginning of the QRS complex, 0.12 to 0.20

• Represents the time between the onset of atrial depolarization and the onset of ventricular depolarization

• QRS complex and is caused by depolarization of the ventricles

• normally 0.06 to 0.1 seconds, indicating that ventricular depolarization occurs rapidly

• ST segment: The isoelectric period (following the QRS is the period at which the entire ventricle is depolarized and roughly corresponds to the plateau phase of the ventricular Action potential

• Important to diagnosis of Ventricular ischemia

• Can become either depressed or elevated indicating non uniform membrane potentials in ventricular cells.

• T wave represents ventricular repolarization (phase 3 of the action potential) and lasts longer than depolarization.

• Q-T interval, both ventricular depolarization and repolarization occur

• roughly estimates the duration of ventricular action potentials.

• The Q-T interval can range from 0.2 to 0.4 seconds depending on heart rate.

Cardiac Electrical Activity

Sequence and procedure of ECG analysis

Determination of the excitation source.

Evaluation of correctness of heart rate – based on duration comparing of R-R-intervals. Normally observed an insignificant difference of duration within 0,1 sec

Determination of heart rate. With normal heart rate you should divide 60 seconds by the duration of R-R-interval in seconds

Determination of the electrical axis direction

Analysis of ECG elements

Interpretation of ECG

1. cardiac rhythm, by recording a rhythm strip •a consistent, one-to-one correspondence exists between P waves and the QRS complex •P wave is followed by a QRS complex (ventricular depolarization is being triggered by atrial depolarization) →sinus rhythm

• SINUS RYTHM • Normal rhythm of heart • Cardiac impulse originated in SA

node, atria depolarize • Represented by P wave • Travel down to AV node • AV nodal delay • Represented by PR interval

•Impulse travel down to purkinje fibers •Ventricles depolarize •Represented by QRS complex •Then repolarize •Represented by T wave • Again SA node send another impulse and cycle repeats •Sinus node discharge these impulse at a pace of 60-100/min

• Rhythm that originated by SA node

• on ECG, P wave followed by QRS complex

• QRS complex followed by P wave

• @ 60-100 impulses per min

• SINUS BRADYCARDIA

• Sinus rhythm

• Originated in SA node

• P wave followed by QRS complex

• Rate < 60BPM

• SINUS TACHYCARDIA

• Sinus rhythm

• Originated in SA node

• P wave followed by QRS complex

• Rate more than 100/min

• SINUS ARRHYTHMIA • Normal physiological mechanism • Minimal variation in pace of SA node

with respiration • Minimal increase in heart rate with

inspiration • Inspiration- activated sympathetic

stimulation of SA node • Minimal decrease in heart rate with

expiration • Expiration –activated

parasympathetic stimulation of SA node

Detects abnormalities related to rhythm • Abnormal rhythmicity of the pacemaker.

• Shift of the pacemaker from the sinus node to another place in the heart.

• Blocks at different points in the spread of the impulse through the heart.

• Abnormal pathways of impulse transmission through the heart.

• Spontaneous generation of spurious impulses in almost any part of the heart

Sinoatrial Block

• Atrioventricular Block

• Incomplete Atrioventricular Heart Block

• Prolonged P-R (or P-Q) Interval First-Degree Block.

• a delay of conduction from the atria to the ventricles but not actual blockage of conduction.

Second-Degree Block

• conduction through the A-V bundle is slowed enough to increase the P-R interval to 0.25 to 0.45 second

• there will be an atrial P wave but no QRS-T wave, and it is said that there are “dropped beats”

Complete A-V Block (Third-Degree Block).• complete block of the impulse

from the atria into the ventricles occurs

• the P waves become dissociated from the QRS-T complexes

• the ventricles have “escaped” from control by the atria

Left Bundle Branch Block.

• Block of the left bundle or both fasicles of the left bundle.

• Electrical potential must travel down RBB.

• Depolarisation from right to left via cell transmission.

• Cell transmission longer due to LV mass.

Left Bundle Branch Block (LBBB).

ECG Criteria for LBBB.

• QRS Duration >0.12secs.• Broad, mono-morphic R wave leads I and V6.• Broad mono-morphic S waves in V1 (can also have small 'r' wave).

LBBB consequence.

• Mostly abnormal ECG finding - indicates heart disease.• Coronary artery disease (indication for thrombolysis - if associated with chest

pain and raised Troponin).• Valvular heart disease.• Hypertension.• Cardiomegaly.• Heart failure.• Impacts on prognosis - QRS duration.• Use of Bi-Ventricular Pacemakers.

Right Bundle Branch Block.

• Impulse transmitted normally by left bundle.

• Blocked right bundle results in cell depolarisation to spread impulse (slower).

• Impulse to IV septum and RV delayed.

• Results in an additional vector.

Right Bundle Branch Block (RBBB).

ECG Criteria RBBB.

• QRS duration >0.12 secs.• Slurred 'S' wave in leads I and

V6.• RSR' pattern in V1 - bunny ears!!

• Premature Contractions is a contraction of the heart before the time that normal contraction would have been expected.

• This condition is also called extra systole, premature beat, or ectopic beat →result from ectopic foci in the heart

• Possible causes of ectopic foci are 1. local areas of ischemia 2. small calcified plaques at different points in the heart 3. toxic irritationPremature Atrial Contractions & Premature Ventricular

Contractions

• Paroxysmal Tachycardia abnormalities in different portions of the heart, including the atria, the Purkinje system, or the ventricles, can occasionally cause rapid rhythmical discharge of impulses that spread in all directions throughout the heart.

• Atrial Paroxysmal Tachycardia

• Ventricular Paroxysmal Tachycardia

Ventricular Fibrillation

• most serious of all cardiac arrhythmias

• cardiac impulses that have gone berserk within the ventricular muscle mass, stimulating first one portion of the ventricular muscle, then another portion,

• never a coordinate contraction of all the ventricular muscle at once, which is required for a pumping cycle of the heart

2. Detects mean electrical axis

•the preponderant direction of the vectors of the ventricles during depolarization is mainly toward the apex of the heart

•this axis can swing even in the normal

•heart from about 30 degrees to about 100 degrees.

• When one ventricle greatly hypertrophies, the axis of the heart shifts toward the hypertrophied ventricle for two reasons.

1. Greater quantity of muscle exists → allows generation of greater electrical potential on that side.

2. More time is required for the depolarization wave to travel than normal

• LVH

• mean electrical axis pointing in the −15-degree direction

• hypertension

• Pregenancy

• Obesity

• Infract right ventricles

• RVH

• intense right axis deviation, to an electrical axis of 170 degrees

• congenital pulmonary valve stenosis.

• tetralogy of Fallot and interventricular septal defect

• Infarct in left ventricle.

ECG changes seen in electrolyte imbalances• Hyperkalemia

• Tall peaked T waves across the entire 12 lead ECG.

• PR interval is prolonged and gradually it flattens or disappears

• QRS complexes widens and merges with the T waves

• Ventricular fibrillation

• Hypokalemia

• ST segment depression.

• Flattening of the T wave.

• Appearance of U wave

• Hypo/Hyper calcemia

• Hypo with prolonged QT interval

• hyper is associated with short QT interval

Heart sounds:• The mechanical activities of the heart during each cardiac

cycle, cause the production of some sounds, which are called heart sounds.

Factors involved in the production of heart sounds

are:

• The movement of blood through chambers of the heart.

• The movement of cardiac muscle.

• The movement of valves of the heart.

First heart sound:• It is produced during isometric

contraction and earlier part of ejection period.

• It resembles spoken word ‘LUBB’.Characteristics:• It is long, soft, low pitched sound.• Duration of this sound is 0.10 – 0.17

secCauses:• It mainly occurs due to sudden

closure of atrioventricular valves.First heart sound and ECG:• It coincides with peak of ‘R’ wave of

ECG

Second heart sound:• It produces during the onset of diastole.

• It resembles the spoken word ‘DUBB’

Characteristics:

• It is short, sharp and high pitched sound.

• Duration of this sound is 0.10 – 0.14 seconds.

Causes:

• It mainly produces during sudden closure of the semilunar valves.

Second heart sound and ECG:

• It coincides with the ‘T’ wave of ECG.

Third heart sound:• It is produced during rapid filling period of the cardiac cycle.

Characteristics:

• It is short and low pitched sound.

• Duration of this sound is 0.07 – 0.10 seconds.

Causes:

• It is produced due to the vibrations which set up in ventricular wall, due to rushing of blood in to ventricles during rapid filling phase.

Third heart sound and ECG:

• It appears between ‘T’ and ‘P’ waves of ECG.

Fourth heart sound:• It is produced during atrial systole

and considered as physiologic heart sound.

Characteristics:• It is short and low pitched sound.• Duration of the sound is 0.02 – 0.04

seconds.Causes:• It occurs due to vibrations which set

up in atrial musculature during atrial systole.

Fourth heart sound and ECG:• It coincides with interval between

end of ‘P’ wave and onset of ‘Q’ wave in ECG.

Triple heart sound:• In some conditions like myocardial

infarction and severe hypertension, the intensity of third and fourth heart sounds increases and they could be heard as a single sound along with the first and second heart sound. This is known as triple heart sound.

Importance of the heart sounds:

• Heart sound generally alters during cardiac diseases involving the valves of the heart. That’s why heart sounds are having important diagnostic value.

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Murmurs:• Intensity: see grading scale

• Quality: Blowing, harsh, grating, rumble.

• Pitch: High vs low pitched

• Timing: Early/mid/late systolic vs. holosystolic. Early/mid diastolic.

• Configuration: Crescendo-decrescendo, decrescendo, plateau, others.

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Characteristic Systolic Murmurs

• Innocent or functional murmurs: arise from pulmonic or aortic outflow tracts in the presence of normal pulmonic/aortic valves. Common in young, healthy individuals. Usually Grade I or II, get louder with squatting and very soft or absent with standing/valsalva. Mid-systolic, short.

• Aortic stenosis: harsh, often loud, best heard base/aortic area, C/D (crescendo/decrescendo), radiate to neck/carotids. Length of murmur correlates with severity of obstruction. Best heard with diaphragm.

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Characteristic Systolic Murmurs

• Mitral regurgitation: high pitched, blowing, best heard at apex, holosystolic (if not acute), radiates to axilla. Best heard with diaphragm.

• MV prolapse with MR: high pitched, blowing, best heard at apex, mid to late systolic and often preceded by valve click. Best heard with diaphragm.

• Pulmonic stenosis (congenital defect): harsh, best heard at base/pulmonic area, radiates down. Louder in inspiration.

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Characteristic Diastolic Murmurs

• Aortic regurgitation/insufficiency: high pitched, blowing, best heard, 2nd/3rd ICS, begins with S2, radiates down. Best heard with diaphragm.

• Mitral stenosis: low pitched, rumbling, best heard at apex, mid diastolic. Best heard with bell- easily missed with diaphragm.

Methods to study heart sounds:• There are three methods to study heart sounds:1. By using stethoscope2. By using microphone3. By using phonocardiogramStethoscope:• The chest piece of the stethoscope is placed over 4 areas

of the chest, which are called auscultatory areas. The auscultatory areas are as follow:

1. Mitral area or bicuspid area: • Situated in the left V intercostal space about 3 inches

from midline. This is the area of apex beat. Mitral valve sound best heart near this region.

2. Tricuspid area:• Present over xiphoid process . Tricuspid valve sound best

heart near this region.3. Pulmonary area:• Present over the left II intercostal space close to the

sternum. Semilunar valve sound best heart near this region.

4. Aortic area:• Situated over right II intercostal space near to the

sternum. Semilunar valve sounds are best heard near this region.

First heart sound is best heard in mitral and tricuspid area where second heart sound is best heard in pulmonary and aortic areas.

Cardiac cycle

• The cardiac cycle is a period from the beginning of one heart beat to the beginning of the next one.

• The cardiac cycle describes pressure, volume and flow phenomena in the ventricles as a function of time.

• Similar for both LV and RV except for the timing, levels of pressure.

• Ventricular contraction called systole. • Ventricular relaxation called diastole • Each part of the cardiac cycle consists of several phases characterized

by either a strong pressure change with constant volume or a volume change with a relatively small change in pressure

Systole includes: •Isovolumic contraction. •Ejection. •Diastole includes: •Isovolumic relaxation. •Rapid ventricular filling. •Slow ventricular filling (diastasis). •Atrial contraction

• The duration of the cardiac cycle is inversely proportional to the heart rate

• At a normal heart rate, one cardiac cycle lasts 0.8 second. • Under resting conditions, systole occupies ⅓ and diastole ⅔ of the

cardiac cycle duration

• Mechanical events in the heart • Pressure and volume changes in both the atria and the ventricles.• The pressure changes in the right atrium are seen in the recording of

the venous pulse. • Pressure changes in the arteries – arterial pulse. • Electrical activity of the heart – electrocardiogram (ECG) • Heart sounds or phonocardiogram

1. Isovolumic Contraction

1.1. Heart •the pressure inside the ventricles rapidly increases due to the ventricular depolarization → ventricles contract → after a ventricular contraction begins, the pressure in the ventricles exceeds the pressure in the atria •the atrioventricular valves shut → semilunar valves are closed because the ventricular pressure is lower than that in the aorta

1.2. Pressure and volume changes Ventricles ventricles contract and all valves are closed, so no blood can be ejected ventricular pressure rises considerably without any change in the ventricular blood volume – isovolumic contraction blood volume in the ventricles equals to the end-diastolic volume (≈130 ml).

• Atria • The atrioventricular valves are bulged backward into the atria

because of increasing pressure in the ventricles. This event causes the c wave in the venous pulse

• Arteries • Pressures in arteries of both systemic and pulmonary circulations

decrease constantly

1.3. Electrocardiogram

• depolarization spreads from the atrioventricular node to the septum and the walls of both ventricles through the bundle of His and Purkyne fibres

• The ventricular depolarization causes the QRS complex in the ECG

1.4. Heart sounds

• the first heart sound appears • caused by vibrations of the

atrioventricular valves • due to the closure of the

atrioventricular valves

2. Ejection

• 2.1. Heart • ventricular contraction continues Both left and right ventricular

pressure > the pressure in the aorta and in the pulmonary artery respectively → the semilunar valves open.

• blood is ejected from the left and the right ventricles to the aorta and the pulmonary artery

2.2. Pressure and volume changes• Ventricles • rapid ejection: first part of the ejection, the ventricular pressure rises

and blood is intensively ejected to the arteries • decreased or slow ejection: the blood volume in the ventricles ↓, the

ventricular pressure starts to decline • maximum ventricular pressure at the top of the ejection reaches 120

mmHg and 25 mmHg in the left and right ventricles, respectively• systolic pressure.

• about 70 ml of blood is ejected from each ventricle during ejection; this volume is called the stroke or systolic volume

• 60 ml of blood remains in each ventricle at the end of systole – the end-systolic volume

• ratio of the stroke volume and the end-diastolic one is called the ejection fraction.

• It is the fraction of the ventricular blood which is ejected during systole. Its physiological value is about 60 %.

• Atria • As the ventricles contract they also shorten. The shortening ventricles

elongate the atria and the big veins, lowering their pressure. • This pressure decrease is represented by the x wave in the venous

pulse

Ejection - pressure and volume changes Red line - pressure in the left ventricle, black - the aortic pressure, dark blue - the pressure in the right atrium, light blue - the ventricular volume.

2.3. Electrocardiogram

• ventricles are completely depolarized at the beginning of the ejection – segment ST in the ECG.

• The T wave appears due to the ventricular repolarization in the second half of this phase

3. Isovolumic Relaxation

• 3.1. Heart• At the end of systole, the ventricles relax and the ventricular pressure

decreases rapidly• the elevated pressures in the aorta and the pulmonary artery push

the blood back toward the ventricles to close the semilunar valves.• atrioventricular valves are closed because the pressure in the atria is

lower than the ventricular pressure

• 3.2. Pressure and volume changes• Ventricles :ventricles relax without changing blood volume in

ventricles • ventricular relaxation leads to a significant pressure decrease→ is

close to zero in both ventricles • Atria : Blood flows from the veins to the atria while the AV valves are

closed • Arteries : dicrotic notch that is seen in the aortic pulse.

Electrocardiogram

• ventricular repolarization is being completed and the end of the T wave

Heart sounds

• the second heart sound appears• due to the closure of the

semilunar valves

4. Rapid Ventricular Filling

4.1. Heart •the ventricular pressure falls bellow the atrial pressure, •the atrioventricular valves open. Blood flows rapidly from the atria to the ventricles.• The semilunar valves are closed

4.2. Pressure and volume changes Ventricles

ventricles are rapidly filled with the blood cumulated in the atriaventricular volume increases, the ventricular pressure is not changed significantly due to the ventricular relaxation

• Atria • the blood will be evacuated from the atria to the ventricles →

negative y wave in the venous pulse• Arteries • diastolic pressure is about 80 mmHg and 8 mmHg in the systemic and

the pulmonary circulations, respectively • After the semilunar valves close, the arterial pressure slowly

decreases, the pressure in the large arteries never falls to zero due to their elastic property

Rapid ventricular filling - pressure and volume changes Red line - pressure in the left ventricle, black - the aortic pressure, dark blue - the pressure in the right atrium, light blue - the ventricular volume

4.3. Electrocardiogram

• No electrical activity is produced by cardiac cells thus the isoelectric line is present in the ECG

4.4. Heart sounds

• The third heart sound, which occurs rarely, is probably caused by the rapid blood flow

5. Slow Ventricular Filling

5.1. Heart : The atrioventricular valves remain open while the semilunar valves are closed 5.2. Pressure and volume changes: the middle part of a diastole a small volume of blood flows into the ventricles. the blood flowing from veins and passing the atria to fill the ventricles.Since the pressure in both ventricles is close to zeroArteries •The pressures in arteries of both systemic and pulmonary circulations decrease constantly

5.3. Electrocardiogram

• the end of slow ventricular filling, depolarization spreads from sino-atrial node in all directions over the atria to produce the P wave in ECG

6. Atrial Systole

• 6.1. Heart • the last phase of a diastole

during which the ventricular filling is completed.

• The atrioventricular valves are open; the semilunar valves are closed

• The atria contract to eject blood into the ventricles

6.2. Pressure and volume changes • Ventricles • 25 % of the ventricular filling

volume is ejected from the atrium to the ventricle

• ventricular myocardium is relaxed, the ventricular pressure does not change significantly

• the end of the atrial systole each ventricle contains 130 ml of blood; end-diastolic volume

6.3. Electrocardiogram

• atrial depolarization is completed and the end of the P wave appears at the beginning of the atrial systole.

• the PR segment is visible in the ECG

6.4. Heart sounds

• fourth heart sound is a soft sound due to an increase in the ventricular pressure following an atrial systole

• rarely occurs in a healthy person

The cardiac cycle of the LV can be divided into four basic phases : .

• Isovolumetric contraction phase.

• Ejection phase.

• Isovolumetric relaxation phase.

• Ventricular filling phase

Pressure-Volume loop

Point 1 on the PV loop is the pressure and volume at the end of ventricular filling (diastole), and therefore represents the end-diastolic pressure and end-diastolic volume (EDV) for the ventricle.

Pressure-Volume loopAs the ventricle begins to contract isovolumetrically (phase b), the LVP increases but the LV volume remains the same, therefore resulting in a vertical line (all valves are closed).

Once LVP exceeds aortic diastolic pressure, the aortic valve opens (point 2) and ejection (phase c) begins.

Pressure-Volume loopDuring this phase the LV volume decreases as LVP increases to a peak value (peak systolic pressure) and then decreases as the ventricle begins to relax.

When the aortic valve closes (point 3), ejection ceases and the ventricle relaxes isovolumetrically - that is, the LVP falls but the LV volume remains unchanged, therefore the line is vertical (all valves are closed).

Pressure-Volume loop

The LV volume at this time is the end-systolic volume (ESV).

When the LVP falls below left atrial pressure, the mitral valve opens (point 4) and the ventricle begins to fill.

Initially, the LVP continues to fall as the ventricle fills because the ventricle is still relaxing.

However, once the ventricle is fully relaxed, the LVP gradually increases as the LV volume increases.

Cardiac Output and Venous Return

•Cardiac  output  is  the  quantity  of  blood pumped  into  the  aorta  each  minute.

Cardiac  output  =  stroke  volume  x  heart  rate

•Venous  return  is  the  quantity  of  blood  flowing from  the  veins  to  the  right  atrium.

•Except  for  temporary  moments,  the  cardiac output  should  equal  the  venous  return

Normal  Cardiac  Output

•Normal  resting  cardiac  output: - Stroke  volume  of  70 ml

- Heart  rate  of  72 beats/minute

- Cardiac  output  ~ 5 litres/minute

•During  exercise,  cardiac  output  may  increase to  >  20  liters/minutes

Cardiac Output

• Stroke Volume = the vol of blood pumped by either the right or left ventricle during 1 ventricular contraction.

SV = EDV – ESV

CO = SV x HR

5,250 = 70 ml/beat x 75 beats/min

CO = 5.25 L/min

Cardiac Output• Regulation of Stroke volume

• Preload: Degree of stretch of heart muscle (Frank-Starling) – greatest factor influencing stretch is venous return (see Below)

• Contractility – Strength of contractionIncreased Ca2+ is the result of sympathetic

nervous system

A Simple Model of Stroke Volume

Cardiac Output• Other chemicals can affect contractility:

- Positive inotropic agents: glucagon, epinephrine, thyroxine, digitalis.

- Negative inotropic agents: acidoses, rising K+, Ca2+ channel blockers.

Afterload: Back pressure exerted by arterial blood.

Regulation of Heart Rate

• Autonomic nervous system

• Chemical Regulation: Hormones (e.g., epinephrine, thyroxine) and ions.

Regulation of Cardiac Output

• Frank-Starling  Mechanism  - ‐ Cardiac  output changes  in  response  to  changes  in  venous return.

• Autonomic  control  - ‐ Control  of  heart  rate  and strength  of  heart  pumping  by  the  autonomic

nervous system.

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

Regulation of Stroke Volume

• SV: volume of blood pumped by a ventricle per beat SV= end diastolic volume (EDV) minus end systolic volume

(ESV); SV = EDV - ESV

• EDV = end diastolic volume• amount of blood in a ventricle at end of diastole

• ESV = end systolic volume• amount of blood remaining in a ventricle after contraction

• Ejection Fraction - % of EDV that is pumped by the ventricle; important clinical parameter

• Ejection fraction should be about 55-60% or higher

Factors Affecting Stroke Volume

• EDV - affected by• Venous return - vol. of blood returning to heart• Preload – amount ventricles are stretched by blood

(=EDV)• ESV - affected by

• Contractility – myocardial contractile force due to factors other than EDV

• Afterload – back pressure exerted by blood in the large arteries leaving the heart

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; EDV leads to stretch of myocardium.

• preload stretch of muscle force of contraction SV• Unlike skeletal fibers, cardiac fibers contract MORE FORCEFULLY when

stretched thus ejecting MORE BLOOD (SV)• If SV is increased, then ESV is decreased!!

• Slow heartbeat and exercise increase venous return (VR) to the heart, increasing SV.

• VR changes in response to blood volume, skeletal muscle activity, alterations in cardiac output

• VR EDV and in VR in EDV• Any in EDV in SV

• Blood loss and extremely rapid heartbeat decrease SV.

Frank-Starling Law of the Heart

• Relationship between EDV, contraction strength, and SV.

• Intrinsic mechanism:• As EDV increases:

• Myocardium is increasingly stretched.

• Contracts more forcefully.

• As ventricles fill, the myocardium stretches:

• Increases the number of interactions between actin and myosin.

• Allows more force to develop.

• Explains how the heart can adjust to rise in TPR.

Figure 14.3

Extrinsic Control of Contractility• Contractility:

• Strength of contraction at any given fiber length.

• Sympathoadrenal system:• NE and Epi produce an

increase in contractile strength.

• + inotropic effect: • More Ca2+ available

to sarcomeres.• Parasympathetic stimulation:

• Does not directly influence contraction strength. Figure 14.2

Frank-Starling Mechanism

The force of cardiac muscle contraction

increases as the muscle stretches,

within limits.

Due to more optimal overlap of actin

and myosin filaments during stretch -

same in skeletal muscle

So, with increase venous return and

increased stretching, the force of

contraction increases and the stroke

volume increases.

Moreover, stretching of the SA node

increasing the firing rate of the pacemaker

(increasing heart rate).

Frank- Starling ‐

Summary: within physiological limits, the heart pumps all the blood that returns to it from the veins.

Venous return increases when there is an increase in the blood flow through peripheral organs. So, peripheral blood flow is a major determinant of cardiac output

Factors Affecting Stroke Volume

Extrinsic Factors Influencing Stroke Volume• Contractility is the increase in contractile strength, independent of stretch and EDV

• Referred to as extrinsic since the influencing factor is from some external source

• Increase in contractility comes from: • Increased sympathetic stimuli• Certain hormones• Ca2+ and some drugs

• Agents/factors that decrease contractility include:• Acidosis• Increased extracellular K+

• Calcium channel blockers

• Sympathetic stimulation• Release norepinephrine from symp. postganglionic fiber• Also, EP and NE from adrenal medulla• Have positive ionotropic effect• Ventricles contract more forcefully, increasing SV, increasing

ejection fraction and decreasing ESV

• Parasympathetic stimulation via Vagus Nerve -CNX• Releases ACh• Has a negative inotropic effect

• Hyperpolarization and inhibition• Force of contractions is reduced, ejection fraction decreased

Effects of Autonomic Activity on Contractility

Contractility and Norepinephrine

• Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP 2nd-messenger system

Figure 18.22

Autonomic Nervous System

Preload and Afterload

Figure 18.21

Effects of Hormones on Contractility

• Epi, NE, and Thyroxine all have positive ionotropic effects and thus contractility

• Digitalis elevates intracellular Ca++ concentrations by interfering with its removal from sarcoplasm of cardiac cells

• Beta-blockers (propanolol, timolol) block beta-receptors and prevent sympathetic stimulation of heart (neg. chronotropic effect)

Autonomic Control of Cardiac Output

Sympathetic increases cardiac output ‡Can increase heart rate 70 to 180-200 BPM ‡Can double force of contraction

Sympathetic nerves release norepinephrine ‡Believed to increase permeability of Ca2+ and Na+.

Parasympathetic (vagal) decreases cardiac output ‡Can decrease heart rate to 20-40 BPM ‡Can decrease force of contraction by 20-30%

Parasympathetic nerves release acetylcholine ‡Increases permeability to K+

Cardiac Output and Peripheral Resistance

Increasing the peripheral resistance decreases cardiac output.

cardiac output = arterial pressure

total peripheral resistance

Other Factors Affecting Cardiac Output

• Age• Gender• Exercise/body temperature

Blood Vessels

Blood Vessels: Overview• Structure of blood vessel wall

• Tunica externa – outer covering mostly collagen• Tunica media – elastin & encircling smooth muscle• Tunica interna – endothelium

• Lumen – the channel• Vasa Vasorum – in large vessels, supplies blood to the outer layers

of the vessel wall

Figure 19.1b

Types of Blood Vessels• Arteries – carry cardiac outflow.

• Thicker walled & more muscular.• Repeated bifurcation (divisions): elastic arteries muscular arteries

arterioles then to:• Capillaries – wall has single cell thickness. Repeated anastomosis (merging) yield: • Venules which then anastomose to form:• Veins – thin wall, less muscle, more expansible, large lumen, carry venous return

to heart

Figure 19.1b

Arteries: Types

• Elastic arteries – expand & contract passively to accommodate blood volume. Smoothes out pulsatile flow

• Muscular arteries – distribution arteries. Deliver blood to organs. Less elastic / more muscle (vasoconstriction)

• Arterioles – smallest; endothelium & a single layer of smooth muscle – regulate flow to capillary beds

Figure 19.1b

Capillaries: Types• Continuous: Endothelium with

occasional intercellular clefts

Capillaries: Types• Fenestrated: Endothelial cells full of pores. Very

permeable. Absorption / filtration

Capillaries: Types• Sinusoids: large irregular lumen, fenestrations &

intercellular clefts. Allow movement of large molecules / plasma between circulatory system & extracellular space

Capillary Beds• True capillaries are exchange vessels

• Precapillary sphincter: smooth muscle that controls blood flow between metarteriole & true capillary

• Vascular Shunt: arteriole metarteriole venule

• Pericytes: spaced along capillaries to anchor & stabilize Figure 19.4a,b

Veins

• Venules: small caliber, porous; allow fluid & WBC movement out of circulation

• Veins: capacitance vessels which hold 65% of blood supply. Pressure is low.

• Venous valves: one way valves that inhibit retrograde flow• Small amount of smooth muscle or elastin• Venous sinuses – thin walled flattened veins supported by

surrounding tissue (coronary sinuses, dural sinuses)

Figure 19.1b

Anastomoses

• Anastomoses: collaterals, bypasses & shunts• Arterial• Arteriovenous• Venous

Physiology of Circulation

• Introduction to hemodynamics:• Blood flow (F)

• Blood pressure (BP) &

• Resistance (R)

Blood flow

• Blood flow = volume of blood flowing through a structure; ml/min

• Total blood flow = Cardiac Output• Individual structure blood flow varies

• example: skin (hot vs. cold); gut (digestion)

Blood pressure

• Blood pressure: force of blood against vessel walls (i.e. 120 mmHg systolic)

• Pressure gradient keeps blood moving

ARTERIAL BLOOD PRESSURE

• Systolic pressure• Pressure peak after

ventricular systole. Ave = 120 mm Hg.

• Diastolic Pressure• Pressure drop during

ventricular diastole. Ave = 80 mm Hg.

BP = 120/80 mm Hg

Resistance

• Resistance: opposition to flow; friction of blood moving through vessels

• Blood viscosity = blood’s internal resistance to flow• Laminar flow: blood at the wall moves slower than blood

in center

Resistance

• Blood vessel length:• increased length = increased resistance

• Blood vessel diameter:• decreased diameter = increased resistance

Resistance

• Resistance varies inversely to the radius4

(i.e. 1/r4)

• Doubling the radius:• Decreases resistance to R/16

• Halving the radius• Increases resistance to 16R

Relationships: Flow, Pressure & Resistance• F = rP

R• rP = Phigh - Plow

• Increased rP yields:• Increased Flow

• Decreased rP yields:• Decreased Flow

Relationships: Flow, Pressure & Resistance• F = rP

R • Increased R yields:

• Decreased Flow• Decreased R yields:

• Increased Flow

• Resistance has a greater influence than change in Pressure on Flow

Systemic Blood Pressure

• Systemic BP• Arterial BP: depends upon distensibility of the great vessels

& the volume of blood pumped into them (pulsatile)• Ventricular contraction blood flow to aorta aortic

stretch pressure:

Systemic Blood Pressure

• Systolic Pressure: peak pressure with aortic filling increases to ~120 mmHg.

• Blood run off begins & flows down the pressure gradient into the systemic circulation.

• Diastolic pressure: lowest pressure. As aorta recoils, pressure decreases to ~80 mmHg.

Systemic Blood Pressure

• Pulse pressure - Difference between systolic & diastolic pressures. Felt as a pulse during systole.

PP = 120 - 80 = 40 mm Hg

Systemic Blood Pressure

• Pulse pressure = systolic - diastolic

• Mean Arterial Pressure = average pressure throughout the cycle• MAP = diastolic + pulse pressure

3• MAP = ~90 mmHg

Capillary BP

• Capillary BP• ~40 mmHg at the start of the capillary bed• ~20 mmHg at the end

• Higher pressure would destroy capillaries

• Capillary permeability is high enough that exchange process occurs at low pressure

Venous BP / Venous Return

• Venous BP (non pulsatile)

• Respiratory pump: pressure changes in the thorax & abdomen b/c of breathing

• Muscular pump: skeletal muscle activity

Maintaining BP• Maintaining BP: CO = P

R

• P = CO x R

• Alteration of BP depends on CO & R

• CO = HR x SV; a function of venous return; under neural & hormonal influences

• P = (HR x SV) x R

Neural Effectors of CO

Resistance: Short Term Control

• Short term control by neural & chemical factors• Alters blood distribution• Maintains MAP by changes in vessel diameter

• Operate via baroreceptors & chemoreceptors

Short Term: Neural Control

• Vasomotor center (medulla): exerts vasomotor tone via vasomotor fibers that innervate smooth muscle of vessels

• SNS activity generalized vasoconstriction

• Input from baroreceptors & chemoreceptors to vasomotor center modifies vasomotor output

Short Term: Neural Control

• Baroreceptors:• Carotid sinuses (monitor blood flow to brain)• Aortic (monitor blood flow to periphery)

• Detect changes in MAP• Chemoreceptors: detect [O2], [CO2] & pH (carotid & aortic bodies)

MAINTAINING BLOOD PRESSURE

Short Term Mechanisms: Chemical• Epinephrine and Norepinephrine -

• Enhances the sympathetic nervous system. Epi increases cardiac output; NE is a vasoconstrictor.

MAINTAINING BLOOD PRESSURE

Short Term Mechanisms: Chemical• Atrial Natriuretic Peptide (ANP) -

• Antagonist of aldosterone. Causes excretion of Na+ and H2O from body

• Reduces blood volume and blood pressure

MAINTAINING BLOOD PRESSURE

Short Term Mechanisms: Chemical• Antidiuretic Hormone (ADH) -

• Released at high amounts when MAP drops to low levels; it acts as a vasoconstrictor (its other name is vasopressin).

It also conserves water, but this is not an important short-term mechanism.

MAINTAINING BLOOD PRESSURE

Short Term Mechanisms: Chemical• Angiotensin II - A potent vasoconstrictor

produced within the blood.

ACE

Angiotensinogen

Angiotensin I

MAINTAINING BLOOD PRESSUREShort Term Mechanisms: Chemical• Nitric Oxide (NO) -

• Promotes vasodilation, lowering MAP.• Secreted by endothelial cells in response

to high flow rate

MAINTAINING BLOOD PRESSURE

Short Term Mechanisms: Chemical• Inflammatory chemicals - Histamine and

other chemicals released during inflammation are vasodilators.

MAINTAINING BLOOD PRESSUREShort Term Mechanisms: Chemical• Alcohol -

• Antagonist of ADH (lowers blood volume and blood pressure)

• Promotes vasodilation (thereby reducing resistance and blood pressure).

Long term control: Renal

• Direct renal• Increased renal flow & BP increased filtrate from

kidney which results in decreases in volume & in pressure• Decreased renal flow & BP decreased filtrate;

conservation of volume & increases in BP• Indirect renal

• Decreased BP results in renin release• Angiotensin II (vasoconstrictor) which stimulates:• Aldosterone & ADH release which conserve Na & water

MAINTAINING BLOOD PRESSURE

Long Term Mechanisms: Renal

Alterations in BP

• Hypotension (low BP): systolic <100 mmHg• Hypertension (high BP) systolic >140/90

• Primary HTN – no specific cause; lifestyle & heredity

• Secondary HTN – identifiable cause; increased renin, arteriosclerosis, endocrine disorders

Alterations in BP

• Autoregulation; local changes in blood flow• Intrinsic: modifying diameter of local arterioles• Metabolic: endothelial response (NO, etc)• Myogenic: smooth muscle responds to increased stretch

with increased tone

Blood Flow Through Capillaries

• Fluid exchange: • Hydrostatic pressure vs. colloid osmotic pressure

• Hydrostatic Pressure pushes fluid out down pressure gradient (HPc)• Interstitial Hydrostatic Pressure (HPif) pushes fluid into capillaries• Colloid Osmotic Pressure: large molecules pull H2O toward themselves. Interstitial

(OPif) & Capillary (OPc)

• NFP = (HPc – HPif) – (OPc – OPif)

Figure 19.16

Net Filtration Pressure of Capillaries

• Net Filtration Pressure of capillaries• NFP = (HPc – HPif) – (OPc – OPif)

• NFP at arterial end of capillary bed = 10 mmHg• Hydrostatic

• NFP at venous end of capillary bed = -8 mmHg• Oncotic

Figure 19.16

Circulatory Shock• Circulatory Shock: marked decrease in blood

flow• Symptoms: increased HR, thready pulse,

marked vasoconstriction; • Marked fall in BP is a late symptom

Circulatory Shock: Causes

• Hypovolemic: inadequate volume (hemorrhage, dehydration, burns)

• Vascular: normal volume but global vasodilation• Anaphylaxis: allergies (histamine)• Neurogenic: failure of autonomic nervous

system• Septic: bacteria (bacterial toxins are

vasodilators)• Cardiogenic pump failure