Why Valves?

• Valves provide a means to ensure that fluids (e.g., blood) only flows in one direction – when heart chambers contract, valves prevent blood from flowing backward.

• Heart valves are passive – i.e., they have no intrinsic opening or closing mechanism –they close from initial currents caused by pressure gradients, and also open by these.

Two different kinds of Valves:

• Atrio-ventricular (A-V) valves – between these chambers – the tricuspid (right), and the bicuspid or Mitral (left), are flimsy, and are supported by Chordae tendinae to prevent reversal and leakage.

• Semilunar valves (aortic and pulmonary) are more robust and are able to resist backflow because of well developed edges on the cusps.

Frank–Starling Law of the Heart

Strength ofContraction

cardiac

Amount of pre-contraction stretch of muscle

Ventricular (left vs right) imbalance

This is usually described as heart failure – not a sudden “heart attack” (most commonly an “infarct”

due to deprived blood flow) but rather an acute weakening of the myocardium (a consequence of

an infarct or other pathology) and its output capacity – and almost always also clarified as either left side or right side heart failure (since rarely are both sides of the heart equally damaged)

Ventricular (left vs right) imbalance

• If the right ventricle is damaged and cannot keep up (viz. flow rate) with the left vent.:

Ventricular (left vs right) imbalance

• If the right ventricle is damaged and cannot keep up (viz. flow rate) with the left vent.:

• If the left ventricle is damaged and cannot keep up with the right ventricle:

Cardiac Cycle

• Atrial press wave- a-wave - atrial contraction c-wave - ventricular contraction

(A-V valves bulge) v-wave - flow of blood into atria

Ventricular Pressure and Volume Curves

• DiastoleIsovolumic relaxationA-V valves openRapid inflowDiastasis - slow flow into ventricleAtrial systole - extra blood in and this

just follows P wave.

Ventricular Pressure and Volume Curves (cont’d)

• SystoleIsovolumic contractionA-V valves close (ventricular press >

atrial press)Aortic valve opensEjection phaseAortic valve closes

• During the latter part of the ejection phase how can blood still leave the ventricle if pressure is higher in the aorta?

• Total energy of blood = P + mV2/2 = pressure + kinetic energy

• Total energy of blood leaving ventricle is greater than in aorta.

Ventricular Pressure and Volume Curves (cont’d)

Aortic Pressure Curve

• Aortic pressure starts increasing during systole after the aortic valve opens.

• Aortic pressure decreases toward the end of the ejection phase.

• After the aortic valve closes, an incisura occurs because of sudden blockage of back-flow toward left ventricle by the closed valve.

• Aortic pressure decreases slowly during diastole because of the elasticity of the aorta.

50

100

150

200

50 100 150 2000

Intr

aven

tric

ula

r P

ress

ure

(m

mH

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Left Ventricular Volume (ml)Period of Filling

IsovolumicRelaxation

Period ofEjection

IsovolumicContraction

End Systolic Volume

End Diastolic Volume

Work Output of the Heart

Work Output graph variations:• Increased Preload: extends to the right (increased pressure) because there is

more venous return (volume and pressure), and this increases the swelling of the atrium and ventricle (more volume = right shift, more pressure, shift higher), increasing the mass of blood to be ejected.

• Increased Afterload: extends the diagram upward because there is greater than normal pressure in the aorta. Thus the semilunar valve cannot open at the usual pressure level (at the corner, #2), and blood cannot be ejected until the ventricle’s pressure rises higher to match the Aorta’s – thus its opening is delayed, and the curve rises higher on the diagram. However, the left side is shifted to the right because as the ventricle relaxes and ventricular pressure drops, the higher aortic pressure causes the semilunar valve to close earlier (normally, the corner, #3). Less blood is ejected, and more blood remains inside (smaller ejection fraction)!

• Increased Contractility: The ventricle contracts more forcibly (raising the curve upward to a higher pressure when the semilunar valve opens). Also, this increased contraction ejects more blood (higher ejection fraction), so the curve also extends farther left (to a lower volume for the start of isovolumic relaxation).

Ejection Fraction

• End diastolic volume = ___ ml• End systolic volume = __ ml• Ejection volume (stroke volume) = __ ml• Ejection fraction = 70ml/120ml = __%

(normally __%)• If heart rate (HR) is 70 beats/minute, what is

cardiac output?• Cardiac output = HR * stroke volume

= 70/min. * __ ml = ____ml/min.

Beats per minute50 160 200

Output per individual “beats”H

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Beats per minute50 160 200

Output per unit time (e.g., minute)H

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Ejection Fraction (cont’d)

• If HR =100, end diastolic volume = 180 ml, end systolic vol. = 20 ml, what is cardiac

output?• C.O. = ___/min. * ___ ml = _____ ml/min.

Cardiac Cells

In comparison to skeletal muscle:

Long contraction – to ensure emptying

Long refractory period – to prevent tetanus

Intercalated disks – obvious!

SA (and AV nodes), and ectopic pacemaker tissue (i.e.,conductive system cells) have leaky Ca2+ channels!

Reduced Sarcoplasmic Reticulum, Terminal Cisternæ;and enlarged T-tubules to facilitate intake –dependent on extracellular calcium

Myocardium controls

Concentration of Ca2+ is important, because normally thetroponin is not saturated with it, so extra calcium increasesthe number of cross-bridge formation.

Sympathetic stimulation (epinephrine and norepinephrine) increases the concentration of Ca2+ and increases forceof contraction and tachycardia, mainly of the ventricle.

1 adrenergic receptors (of both epinephrine and

norepinephrine) let Ca enter faster.

2 adrenergic receptors (of only epinephrine)increases force of contraction mainly of the Atria andthe speed of the SA node.

Digitalis stimulates the heart by raising intracellular calciumand increasing the force of contraction. It slows the Na-Ca pump (unique to heart muscle), and also increases the Ca “current” during stimulation.

“Electrical” events of the Cardiac Cycle

Action Potentials start by opening voltage-gated Nachannels; this is followed by rapid closure of the channels.

The sustained action potential is maintained by openingvoltage-gates Ca channels.

Final repolarization takes place by closing the Ca channelsand opening the potassium channels.

SA Node Controls

The SA node has the highest automaticity, about 90-120 bpm.

Firing rate increases with temperature, calorigenic hormonesand epinephrine and norepinephrine.

Right vagus nerve normally releases Acetylcholine (ACh) to it,hyperpolarizing it by increasing K+ conductance outwardand slowing Ca2+ inward, lowering it to 70 bpm.

Very strong vagal stimulation can actually eliminate SA nodeactivity completely (Sinus arrest, “asystole”) until someectopic pacemaker takes over.

Cardiac sympathetic nerves release Epinephrine, increasingautomaticity of the SA node as well as ectopicpacemakers, and also increases the strength ofcontraction.

SA Node Controls (continued)

Hyperkalemia (> 8 mEq/L) reduces concentration gradients ofpotassium and its outward flow (Bradycardia – in extremecases, Sinus Arrest, AV nodal block, ventricularfibrillation, etc.) – extreme: stops in diastole.

Hypokalemia also results in reduced K outflow andhyperpolarization: bradycardia, or stoppage in systole inextreme cases, but not for reasons given in your textbook (editorial mistake?).

Hypercalcemia decreases excitability of myocardial fibers andslows the sinus rhythm; it also increases muscle tensiondeveloped, and marked hypercalcemia can arrest the heartin mid-systole.

Hypocalcemia weakens contractions – it can stop the heart.

AV Node Controls

Vagal (left side) stimulation slows the conduction rate.

Normally the only “electrical” connection between the Atriaand the Ventricles.

Alternative pathways cause abnormal excitation of theventricles – Wolff-Parkinson-White syndrome.

Normally, causes a delay of up to 200 msec. between Atrialand Ventricular contraction; normally sets max. bpm atabout 200 or so, preventing inefficient filling andejection.

Sympathetic stimulation (e.g., Epinephrine) increases theconduction rate.

Leads for the Electrocardiogram

Standard or Bipolar:

These are to three limbs (two wrists and the left ankle), I,II, and III. Actually, these two wrists and left leg are“active” leads, while the right leg (a 4th lead) is a“reference” electrode.

Unipolar (no “reference” electrode – “reference” is electronically built into the ECG machine):

There are three Unipolar Limb Leads, right arm, left armand left foot, each called VR, VL, and VF.

There are six Unipolar Chest leads, V1 to V6, from theright side of the sternum across to the left side of the ribcage.

And there are three Augmented Limb leads, aVR, aVL,and aVF.

Details of the PQRST Waveform

P Atrial depolarization: The wave spreads across the atria from rightto left, causing a small positive signal in the three Bipolar Limbleads.

QRS ComplexQ Initial signal out of the AV node spreads from the Bundle of His

near the left side of the Interventricular Septum across to theright, giving a very small negative signal.

R Depolarization of the remainder of the Interventricular Septum,the right ventricle and most of the left ventricle – the large massof the left ventricle biases the signal to the left, and producesthe huge, positive R wave.

S The remainder of the left ventricle, the inferior posterior area,produces the negative S wave.

T Repolarization of the ventricles is a combination of the oppositeelectrically charged signal going in the opposite direction of theQRS, resulting in a polarity the same as the QRS.

It is extended (long duration), however, because the ventricularmuscle is slightly hypoxic (no blood flow during systole), so itsrefractory period is extended.

Bipolar Limb Leads

• Bipolar means that the EKG is recorded from two electrodes on the body.

Figure 11-6; Guyton & Hall

Bipolar Limb Leads (cont’d)

• Lead I - The negative terminal of the electrocardiogram is connected to the right arm, and the positive terminal is connected to the left arm.

• Lead II - The negative terminal of the electrocardiogram is connected to the right arm, and the positive terminal is connected to the left leg.

Bipolar Limb Leads (cont’d)

• Lead III - The negative terminal of the electrocardiogram is connected to the left arm, and the positive terminal is connected to the left leg.

• Einthoven’s Law states that the electrical potential of any limb equals the sum of the other two (+ and - signs of leads must be observed).

• If lead I = 1.0 mV, Lead III = 0.5 mV, then Lead II = 1.0 + 0.5 = 1.5 mV

Principles of Vectorial Analysis of EKG’s

• The current in the heart flows from the area of depolarization to the polarized areas, and the electrical potential generated can be represented by a vector, with the arrowhead pointing in the positive direction.

• The length of the vector is proportional to the voltage of the potential.

• The generated potential at any instance can be represented by an instantaneous mean vector.

• The normal mean QRS vector is 59o.

Principles of Vectorial Analysis of EKG’s (cont’d)

• The axis of lead I is zero degrees because the electrodes lie in the horizontal direction on each of the arms.

• The axis of lead II is +60 degrees because the right arm connects to the torso in the top right corner, and left leg connects to the torso in the bottom left corner.

• The axis of lead III is 120 degrees.

Principles of Vectorial Analysis of EKG’s (cont’d)

• When the vector representing the mean direct current flow in the heart is perpendicular to the axis of one of the bipolar limb leads, the voltage recorded in the electrocardiogram in this lead will be very low.

• When the vector has approximately the same direction as the axis of one of the bipolar limb leads, nearly the entire voltage will be recorded in this lead.

Other EKG Leads (cont’d)

Augmented Unipolar Limb Leads aVR, aVL, and aVF are also in use. For aVR the + electrode is the right arm, and the - electrode is the left arm + left leg; aVL + electrode is left arm; aVF + electrode is left foot.

Axes of the Unipolar Limb Leads

+

+

+I

aVLaVR

aVF

-

Principles of Vectorial Analysis of EKG’s (cont’d)

Axes of the Three Bipolar and Augmented Leads

+

_

__

+

+

60o

120o

0oI I

IIIII

IIIII

+

_

-30o

aVL

aVL+

_

210o

aVR

aVR

+

_ aVF

aVF

90o

Leads for the Electrocardiogram

Standard or Bipolar:

These are to three limbs (two wrists and the left ankle), I, II, and III. Actually, these two wrists and left leg are “active” leads, while the right leg (a 4th lead) is a “reference” electrode.

Unipolar (no “reference” electrode – “reference” is electronically built into the ECG machine):

There are three Unipolar Limb Leads, right arm, left arm and left foot, each called VR, VL, and VF.

There are six Unipolar Precordial Chest leads, V1 to V6, from the right side of the sternum across to the left side of the rib cage.

And there are three Augmented Limb leads, aVR, aVL, and aVF.

Atrial and Sinus Rhythm Defects

Normal: Sinus Rhythm

Sinus Arrhythmia – varies with respiration (effected by vagaltone) – incr. with inspiration (inhibits vagus), decreaseswith expiration.

Sinus Tachycardia – increases due to fever,hyperthyroidism, etc.

PATs – Paroxysmal Atrial Tachycardia – idiopathic, caffeineor nicotine or alcohol, anxiety; or reentry (alternativepathways).

PACs – Premature Atrial Contractions (aka, atrialextrasystoles) – benign – perfectly normal tooccasionally experience it.

Atrial and Sinus Rhythm Defects

Atrial Fibrillation – rapid, irregular rate affecting varyingparts of the Atria. Very common among the elderly.

SA Nodal Block or Sick Sinus Syndrome – p wavedisappears.

AV Node and Ventricular Defects

Permanent Junctional Rhythms – substituting for a lack ofSA Node stimulation

AV Nodal BlocksFirst Degree – PQ interval > .2 secondsSecond Deg. – some signals are skipped

Wenkebach block – successive increases Periodic – occasional failure (e.g., 8:7, a:v) Constant – almost always (e.g., 2:1, 3:1)

Third Deg. (complete) – Atria and Ventricles areindependent – beats can drop to 30 bpm and causedizziness and fainting. But in extreme cases,Ventricular escape may paradoxically save your life!

PVCs – Premature Ventricular Contractions – Ectopicpacemakers – Ischemia makes the cells more irritable!

AV Node and Ventricular Defects

Bundle Branch Blocks – conduction interupted or delayed –QRS >> .12 sec.., from overlap

Enlarged Ventricles – heightened “R”

PVTs – Paroxysmal Ventricular TachycardiaorV-Tach – Ventricular Tachycardia – sustained, not paroxys.

Circus Rhythms

V-Fib – Ventricular Fibrillation !

Defibrillator – Cardioversion

Long Q-T syndrome – may be responsible for idiopathicdeaths in the young!

Ventricular Fibrillation

• Some parts of ventricle contract while others relax, thus little blood flows out of the heart.

• Caused by electrical shock or cardiac ischemia.• Also called circus movements.• If pathway is long (dilated heart)• If conduction velocity is decreased (blockade of

Purkinje system, ischemia of muscle, and high K+ levels)

• If refractory period is shortened (epinephrine)

Other Pathologies, #1

Inflammation:

Endocarditis – usually results in complications that formscars on the valves, causing stenosis orincompetence; can be caused by as innocent asource as a dental procedure.

Myocarditis – can lead to heart failure.

Pericarditis – bacterial or viral.

Rheumatic disease – from streptococcal infection’stoxin. The immune system’s reaction will inflame theendocardium (rheumatic endocarditis), and especiallycan destroy the bicuspid valve (it’s better oxygenatedthan the tricuspid valve).

Other Pathologies, #2

Reduced flow to myocardium:

Angina pectoris: pain resulting from ischemia (reducedblood flow).

Coronary thrombosis: a clot blocking a vessel.

Infarct: damaged heart tissue.

Heart Failure: progressive weakening of themyocardium resulting in inadequate pumping ofblood.