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PHYSIOLOGICAL PROPERTIES OF HEART

FORMATION OF NORMAL ELECTROCARDIOGRAM

PUMPING WORK OF THE

Objectives for Students’ Independent Studies

You should prepare for the practical class using the existing textbooks and lectures. Special attention should be paid to the following:

List:

I Physiological properties of heart

1. Morphology and functional organization of heart

2. Automaticity of the heart

3. Conductibility of the heart

4. Excitability of heart

5. Contractibility of the heart

6. Mechanism of contraction and relaxing of the heart muscle.

II Formation of normal electrocardiogram

1. ECG leads

2. Algorithm of ECG registration:

3. ECG analysis

14. ECG analysis begins with estimation of control voltage and paper speed. Another analysis at usual performs in this order.

5. Investigation of conductive system in the heart

6. ECG registration

7. ECG analysis

III Pumping work of the heart

1. The heart:

2. Cardiac cycle

3. Cardiac volumes

4. Physiological analysis of cardiac output

5. Heart sounds

Regulation of the heart pumping

 

 

PHYSIOLOGICAL PROPERTIES OF HEART

1. Morphology and functional organization of heart

a) Structure of heart.

The heart contains four chambers: two upper atria, which receive venous blood and two lower ventricles, which eject blood into arteries. The right ventricle pumps blood to the lungs, where the blood becomes oxygenated. The left ventricle pumps oxygenated blood to the entire body.

The right and left atria receive blood from the venous system. The right atrium and ventricle are separated from the left one by septum, which is the muscular wall. This septum normally prevents mixture oxygenated and not oxygenated blood.

Between the atria and ventricles there is a layer of dense connective tissue known as fibrous skeleton of the heart. The connective tissue of skeleton also forms rings, called annuli fibroses around two pairs of one-way valves.

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b) Structure of myocardium.

Bundles of myocardial cells in the atria attach to the upper margin of this fibrous skeleton and form a myocardium. The myocardial cell bundles of the ventricles attach to the lower margin and form a different myocardium. As a result, the myocardium of the atria and ventricles are structurally and functionally separated from each other.

Weight of whole myocardium consist 250-300g. Atria myocardium has two layers of muscle cells – circular and

 longitudinal. Circular cells layers surround mouth of vessels, which fall into atria and may cover again it in constriction.

Ventricles myocardium has three layers of muscle cells. External and internal layer have spiral form and are common for both ventricles. Middle layer has circular orientation and is separated in every ventricle.

c) Functional specialties of myocardial cells.

Myocardial cells contain actin and myosin filaments and contracts by means of the sliding filament mechanism. Myocardial cells are joined by gap junctions, due to which electrical impulses can spread to all cells in the mass. Sarcoplasmatic reticulum in myocardial cells is developed slightly. That is why some amount of calcium may enter the myocardial cell from the outside.

Besides contractive myocardial cells there are modified cells of the conduction system of the heart. They can generate and conduct impulses through myocardium.

d) Electrophysiological properties of the contractive myocardium.

The main electrophysiological properties of the contractive myocardium are automaticity, contractility, conductability and excitability.

Automaticity is property to contract replying to electrical impulses, originated in pacemaker cells of the conduction system of the heart.

Contractility is property to contract replying to irritation.

Conductibility is property to spread electrical impulses through the conduction system and contractive myocardium.

Excitability is property to reply the irritation.

2. Automaticity of the heart

a) Structure of conduction system.

Action potentials that originate in the sinoatrial node (SA-node) spread to adjacent myocardial cells of the right and left atria through the gap junction between these cells.

Since the myocardium of the atria is separated from the myocardium of ventricles by the fibroses skeleton of the heart, the impulse cannot be conducted directly from the atria to the ventricles. Besides that atria have to contract before ventricles to guarantee pumping of blood.

Once the impulses spreads through the atria, it passes to the atrio-ventricular node (AV-node), which is located on the inferior portion of the internal septum. From here, the impulse continues through the atrio-ventricular bundle, or bundle of His, beginning at the top of the interventricular septum. The atrio-ventricular bundle divides into right and left bundle branches, which are continues with Purkinje fibers within the ventricular walls.

Specialized excitatory and conductive system of the heart: consists of:

1. Sinus node “SA” node: also called sinoatrial node, located in the right atrium. It is concerned with the generation of rhythmical impulse; it is the pacemaker of the heart that initiates each heart beat. This automatic nature of the heart beat is referred to as automaticity.

2. Internodal pathways conduct the impulse generated in SA node to the AV node.

3. The AV node (atrioventricular node), located near the right AV valve at the lower end of the interatrial septum, in the posterior septal wall of the right atrium. At which impulse from the atria is delayed before passing into the ventricles.

4. The AV bundle (bundle of His) conducts the impulse from the atria into ventricles.

5. The left and right bundles of purkinje fibers, which conduct the cardiac impulse to all parts of the ventricles. The purkinje fibers distribute the electrical excitation to the myocytes of the ventricles.

 

 

Figure: The cardiac conduction system.

 

 

Figure: organization of the AV node.

The SA node as the pacemaker of the heart:

(Automaticity & rhythmicity)

Automaticity is the property of self-excitation (i.e. the ability of spon­taneously generating action potentials independent of any extrinsic stimuli) while rhythmicity is the regular generation of these action potentials. In other words, the cardiac impulse normally arises in the SA node, which has the capability of originating action potentials and functioning as pacemaker. This action potential then spreads from the SA node throughout the atria and then into and throughout the ventricles.

The contractile cardiac muscle cells don’t normally generate action potentials but they can do in certain pathological conditions. This mean that all parts of the conduction system are able to generate a cardiac impulse; (autorhythmicity), but the normal primary pacemaker is the SA node, while the AV node is a secondary pacemaker and the Purkinje system is a tertiary (or latent) pacemaker. The AV node acts only if the SA node is damaged or blocked, while the tertiary pacemaker takes over only if impulse conduction via the AV node is completely blocked.

The SA node discharges at an intrinsic rhythmical rate of 100-110 times per minute (sinus rhythm). Under abnormal condition; the AV nodal fibers can exhibit rhythmical discharge and contraction at a rate of 40 to 60 times/minute. While those of purkinje fibers discharge at a rate between 15 and 40 times/minute.

Autorhythmicity is a myogenic property independent of cardiac innervation. This is evidenced by the following:

·        Completely denervated heart continues beating rhythmically.

·        Hearts removed from the body and placed in suitable solutions continue

·        beating for relatively long periods.

·        The transplanted heart (denervated heart) has no nerve supply but they beat regularly.

Self-excitation of SA node:

What causes the SA node to fire spontaneously?

Although the SA node discharges at an intrinsic rhythmical rate of 100-110 times per minute but the pulse rate averages 70 or 80 times per minute, this is because of the effect of vagal tone. SA node does not have a stable resting membrane potential which starts at about – 60 mV. This is due to the inherent leakiness of the SA nodal fibers to Na⁺ ions that causes this self-excitation (Na⁺ influx). in other words, because of the high Na⁺ ions concentration in the ECF as well as the negative electrical charge inside the resting sinus nodal fibers, the positive Na⁺ ions outside the fibers tend to leak to the inside, rising the membrane potential up to a threshed to fire an action potential.

Atrioventricular node (AV node):

The conductive system is organized, so that cardiac impulse will not travel from the atria into ventricles too rapidly. There is a delay of transmission of the cardiac impulse in the AV node to allow time for the atria to empty their blood into the ventricles before ventricular contraction begins.

 

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b) Electrophisiological properties of conduction system.

The cells of SA-node do not keep a resting membrane potential in the manner of resting neurons or skeletal muscle cells. The membrane potential begins at about -60 mV and gradually depolarizes to -40 mV, which is the threshold for producing an action potential in these cells. This spontaneous depolarization is produced by the diffusion of Ca²⁺ through openings in membrane called slow calcium cannels. At the threshold level of depolarization, other channels, called fast calcium channels, open and calcium rapidly diffuses into the cells. The opening of voltage regulated sodium gates, and the inward diffusion of sodium that results, may also contribute to the upshot phase of the action potential in pacemaker cells.

The opening of potassium gates and outward diffusion of potassium, as in the other excitable tissues produce repolarization.

Once repolarization to -60 mV has been achieved, a new pacemaker potential begins, again culminating with a new action potential.

Action potential of SA node

The resting membrane potential of SA node is of -55 to -60 mV (millivolts). The cause of this reduced negativity “less negative” is that the cell membrane of the sinus fibers are naturally leaky to sodium ions “Na⁺ influx”. Therefore; Na⁺ influx causes    a rising membrane potential “gradual depolarization” which when reaches a threshold voltage at about – 40 mV, the fast calcium and sodium channels opened, leading to    a rapid entry of both Ca⁺² and Na⁺ ions causing the action potential to about 0 mV (zero), to be followed by repolarization which is induced by K⁺ efflux out of the fiber because of the opening of K⁺ channels. This repolarization carries the resting membrane potential down to about -55 to -60 mV at the termination of action potential.

 

 

Figure: Action potentials of the SA node.

 

Action potential of ventricular cardiac muscle fiber

The membrane potential of cardiac ventricular muscle fiber cells is about -90 mV; the interior of the cell is electrically negative with respect to the exterior due to disposition; distribution of ions mainly Na⁺, K⁺ and Ca⁺² ions across its membrane.

The action potential (AP) is an electrical signal or impulse produced by ionic redistribution that the potential changes into positive inside the cell (depolarization), to be followed by restoration of the ions; returning back to the resting potential (repolarization). Stimulation of cardiac muscle cells by SA produces a propagated action potential, that is responsible for muscle contraction i.e., excitation-contraction coupling.  In other words, stimulation of cardiac muscle cells specifically those of the ventricles is performed by the propagated AP of the SA node from which the electrical impulses originating and propagated over the heart. According to the figure (a), the propagated AP of the SA node depolarized the ventricular muscle fiber cells rapidly with an overshoot (phase 0), followed by a plateau at around zero potential level (phase 2). This plateau is unique for the heart muscle; and is followed by phase 3 and 4; as final repolarization i.e., for the potential to return to baseline.

 

Ionic basis of the action potential of the cardiac ventricular muscle fiber cell:

The action potential of cardiac ventricular muscle fiber cell includes the following phases (a):

 

·        Phase 0 (upstroke): initial rapid depolarization with an overshoot to about   +20 mV are due to opening of the voltage-gated Na⁺ channels with rapid Na⁺ influx.

·        Phase 1 (partial repolarization): initial rapid repolarization is due to K⁺ efflux (K⁺ outflow) followed the closure of Na⁺ channels when the voltage reaches at nearly +20 mV.

·        Phase 2 (plateau): subsequent prolonged plateau is due to slower and prolonged opening of the voltage-gated Ca⁺² channels with Ca⁺² influx, Ca⁺² enter through these channels prolong depolarization of the membrane.

·        Phase 3 (rapid repolarization): final repolarization is due to opening of the voltage-gated K⁺ channels at zero voltage with rapid K⁺ outflow (K⁺ efflux)  followed the closure of Ca⁺² channels and, this restores the membrane to its resting potential.

·        Phase 4 (complete repolarization): The membrane potential goes back to the resting level (-90 mV) i.e., restoration of the resting potential. This is achieved by the Na⁺-K⁺ pump that works to move the excess K⁺ in and the excess Na⁺ out.

 

Figure (a): The action potential of the ventricular muscle fiber.

     

Figure: Rhythmical action potentials from a purkinje and ventricular muscle fibers.

 

Figure: Rhythmical discharge of SA nodal fiber, compared with action potential of ventricular muscle fiber.

c) Function of pacemaker centers.

Some other regions of the heart, including the area around SA-node and the atrio-ventricular bundle can potentially produce pacemaker potentials. The rate of spontaneous depolarization of these cells however is slower, than that of SA-node.

As it determined SA-node produce 60-90 impulses per minute, AV-node – 40-50, bundle of His – 20-30 and Purkinje fibers 10-20 impulses per minute. The potential pacemaker cells are stimulated by action potential from SA-node before they can stimulate themselves through their own pacemaker potentials. If action potentials from the SA-node are prevented from reaching these areas (through blockade of conduction), they will generate pacemaker potentials at their own rate and save as sites for the origin of action as pacemakers.

A pacemaker other than SA-node is called as ectopic pacemaker or ectopic focus.

If the heart of a frog is removed from the body, and put in physiological solution, it will still continue to beat as long as the myocardial cells remained alive.

At a result of experiments with isolated myocardial cells and clinical experience with patients who have specific heart disorders, many regions within the heart have been shown to be capable of originating action potentials and functioning as pacemakers.

In a normal heart, however, only one region demonstrates spontaneous electrical activity and by this means functions as a pacemaker – SA-node.

3. Conductibility of the heart

a)     Conduction of impulses in atria. After excitation of SA-node impulses conduct by bundle of Thorel, Venkenbuh and Buhman to AV-node.

 

Action potentials from SA-node spread at a rate of 0,8-1,0 m/s across the myocardial cells of both atria. At first the right atrium is excited and left is the second.

b) Peculiarities of conduction through AV-node. The conduction rate slows considerably as the impulse passes into the AV-node. Slow conduction of impulses (0,03-0,05 m/s) through the AV-node is caused by special form of AV-node and peculiarities of impulse development in cells of AV-node, as absence of rapid diffusion of ions. Slow conduction in AV-node is necessary for proper order of contracting atria and ventricles.

c) Excitation of ventricles. After the impulses spread through the AV-node, the conduction rate increases in the atrio-ventricular bundle and reaches 5 m/s in the Purkinje fibers. As a result of this rapid conduction of impulses, ventricular contraction begins 0,1-0,2 s after the contraction of atria.

High velocity of impulses in ventricles is caused by rapid Na⁺-gates.

At first middle part of septum is excited, than impulses spread to apex of heart, than to the right ventricle wall, to the left ventricle wall and to basal parts of ventricles myocardium.

4. Excitability of heart

a)    Excitability changing during excitation.

Once contractive myocardial cell has been stimulated by action potentials origin in SA-node, it produces its own action potentials. The majority of myocardial cells have resting membrane potentials of about -90 mV. When stimulated by action potentials from a pacemaker region these cells become depolarized to threshold. At this point their voltage – regulated Na⁺-gates open.

The upshot phase of the action potential of no pacemaker cells is due to the inward diffusion of Na⁺. This period called depolarization.

Following the rapid reversal of the membrane polarity, the membrane potential quickly declines to about -15 mV. Opening K⁺ and Cl^– gates and inward diffusion of K⁺ and Cl^– causes it. This period called quickly initial repolarization.

Then this level potential maintained for 200-300 ms and cells plato phase. It’s due to opening of slow Ca2+ gates. Gradually slow Ca2+ diffusion stops and than diffusion of K⁺ increases. Rapid repolarization at the end of the plato is achieved by rapid outward diffusion of K⁺. During last phase of rest initial distribution of ions inwards and outwards is recovered by function of the sodium-potassium pumps. The heart normally cannot be stimulated until after it has relaxed from its previous contraction because myocardial cells have long refractory periods. It corresponds to the long duration of their action potentials. Summation of contractions is thus prevented and myocardium must relax after each contraction. The rhythmic pumping action of the heart is thus ensured.

Refractory period:

·        Absolute refractory period (ARP), it is the interval during which no action potential can be produced, regardless of the stimulus intensity i.e., no stimulus however strong, can produce a propagated action potential. It lasts the upstroke plus plateau and initial repolarization till mid-repolarization at about -50 to -60 mV. It means that the cardiac muscle caot be exited during the whole period of systole and early part of diastole. This period prevents waves summation and tetanus.

·        Relative refractory period (RRP), it is the interval during which a second action potential can be produced but at higher stimulus intensity i.e., the heart responds only to stronger stimuli. It lasts from the end of ARP (midrepolarization) and ends shortly before complete repolarization i.e., it lasts for a short period during diastole.

 

 

b) Excitability of the heart and skeletal muscles. Electrical impulses that originate at any point of myocardium can spread to all cells, according to ruler “all or nothing”. Because all cells in myocardium are electrically joined a myocardium behaves as a single functional unit. Unlike it, in skeletal muscle contraction depends oumber of excited neurons, which stimulate motor unit. Unlike skeletal muscles, cardiac muscle capable to produce action potentials by pacemaker cells. The rate of heartbeat is regulated by autonomic nervous system. In difference, skeletal muscles are regulated by somatic nervous system.

5. Contractibility of the heart

a) Mechanism of contraction and relaxing of the heart muscle.

Like skeletal muscle cells, cardiac muscle cells are striated. They contain actin and myosin filaments arranged in the form of sarcomeres. They contract by means of the sliding filament mechanism. Myocardial cells are short, branched and interconnected. Gap junctions join adjacent myocardial cells. That is why a myocardium contracts to its full extent each time and all of its cells contribute to the contraction. After opening Ca²⁺– gates contraction begins. The mechanism of contraction is similar to skeletal muscles. Sliding on thin filaments they produce shortening of the sarcomeres. In the process of contraction, the thin filaments slide deeper and deeper toward the center, producing increasing amounts of overlap with thick filaments. Sliding of the filaments is produced by the action of numerous cross brigs that extend out from the myosin toward the action. Before the cross brigs combine with actin the globular head function as myosin ATP-ase enzymes. Then cross brigs combine with actin and can attach to actin.

 

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6. Mechanism of contraction and relaxing of the heart muscle.

b)    Contractibility cardiac and skeletal muscles:

Contractility is the ability of the cardiac muscle to contract.

The effect of various factors on contractility is called inotropism; a positive (+ve) inotropic effect means an increase in myocardial contractility, whereas a negative  (-ve) inotropic effect means a decrease in myocardial contractility. 

– In skeletal muscles long fibrose cells are separated from each other functionally and structurally. But myocardial cells are short, branched and interconnected by gap junctions.

– Skeletal muscle produce contractions, which are graded depending on the number of cells stimulated. But a myocardium contracts as a single functional unit.

– Skeletal muscles require external stimulation by somatic motor nerves before they can produce action potentials and contract. But cardiac muscle is able to produce action potentials automaticity.

– Skeletal muscle capable to summation of contraction, but myocardial muscle pumps the blood by rhythmic contractions.

Excitation-Contraction coupling in the heart muscle:

As in skeletal muscles, the depolarization wave reaching via the T tubules causes the opening of Ca⁺² channels in the sarcoplasmic reticulum adjacent to the T-tubules. The released Ca⁺² from the cisternae of the sarcoplasmic reticulum (activator Ca⁺²; aCa⁺²) binds to troponin C, leading to cross bridge formation between actin and myosin, which results in contraction.

In cardiac muscle, the amount of this activator Ca⁺² is often insufficient to initiate contraction, but it can be increased indirectly by the following mechanism:

The depolarization wave in the T-tubules opens the long-lasting Ca⁺² chann­els in the T-tubule membrane, and sarcolemma, Ca⁺² diffuses from the ECF through these channels into the cardiac muscle fibre cell causing a small increase in the cytosolic (fluid of the cytoplasm) calcium concentration in the region of the T-tubules and adjacent sarcoplasmic reticulum. This Ca⁺² is called depolarizing Ca⁺², and although its amount is normally very small, yet it is important because it acts as a signal for the release of large amount of activator Ca⁺² from the cisternae of sarcoplasmic reticulum, it is mainly this cytosolic Ca⁺² that causes the contraction, i.e. once Ca⁺² is in the cytoplasm, it binds to troponin and stimulates contraction. As a result, myocardial cells contract when they are depolarized. The force of contraction is directly proportional to the amount of cytosolic Ca⁺².

Contraction ends when the cytosolic Ca⁺² concentration restored to its original level. In other words, relaxation of the cardiac muscle occurs as a result of release of the actin-myosin combination, this is achieved by decreasing the intracellular Ca⁺² to its pre- contraction level, which occurs by:

1- Active re uptake of Ca⁺² into the sarcoplasmic reticulum by Ca⁺² pump (primary active transport of Ca⁺²).

2- Active pumping of excess Ca⁺² outside the fibres by Na⁺– Ca⁺² exchanger carrier protein (secondary active transport ; counter transport).

The heart normally cannot be stimulated again until after it has relaxed from its previous contraction because myocardial cells have long refractory periods that correspond the long duration of their action potentials. Summation of contractions and tetanus are thus prevented, and the myocardium must relax at each contraction to ensure the rhythmic pumping action of the heart.

 

Factors that affect cardiac contractility:

1) mechanical, 2) cardiac, 3) extracardiac

1). Mechanical factors:

* Preload (venous return)

* Afterload

The preload:

The preload is the load that determines the initial length of the resting muscle before contraction. The level of the preload is rep­resented by the end-diastolic volume (EDV) i.e., by the venous return (VR). It affects the tension developed in the muscle. When the venous return (EDV), increases, the strength of ventricular contraction increases too, leading to an increa­se in the stroke volume (Frank-Starling law).

Frank-Starling’s law of the heart

This law describes the length-tension relationship in muscles; it states that the force of contraction of the ventricles depends on the initial length of ventricular muscle fibers. In such a way, that the force of myocardial contraction is directly proportional to the initial length of the cardiac muscle fibres (i.e. to the preload (VR) or EDV). This means that the greater the degree of stretching of the myocardium before contraction, the greater the force of contraction. In other words, Frank-Starling law reflects the relationship between ventricular end-diastolic volume (EDV) and stroke volume; when the blood returns to the heart during the filling phase, this blood will distend the ventricles so the ventricles will produce more powerful contraction to pump the increased volume of the blood.

The Significance of Frank-Starling’s law

The Starling’s law allows autoregulation of myocardial contractility (regulation of the contractility by changing the length of the muscle fibers), in the following conditions:

(1) Iormal hearts. Starling’s law allows changes in the right ventricular output to match changes in the venous return (VR), and maintains equa outputs from both ventricles. For example, if the systemic VR increases, the EDV of the right ventricle increases, leading to a forceful contraction that increases its output to match the increased VR. At the same time, the increased right ventricular output increases the pulmonary VR to the leftventricle, which also increases its EDV, resulting in an increase of its output, which balances the increased right ventricular output.

 (2) In denervated hearts (e.g. transplanted hearts); autoregulation of myocardial contractility becomes the main mechanism.

(3) In cases of rise of the arterial blood pressure: the stroke volume of the left ventricle would decrease. However, the retained blood in the left ventricle plus blood returning to it from the left atrium during the next diastole increase the EDV. This leads to a forceful contraction, thus the accumulated blood in the left ventricle will be ejected in spite of the increased arterial blood pressure.

The Afterload:

The afterload is the load that the muscle faces when it begins to contract. In the intact heart, the afterload is produced by the aortic impedance which is determined by:

·        The aortic pressure (arterial systolic blood pressure).

·        The arterial wall rigidity (arteriosclerosis).

·        Blood viscosity (polycythemia).

2). Cardiac factors:

·        The myocardial mass.

·        The heart rate.

The myocardial mass:

A significant injury or loss of the functioning ventricular muscle (e.g. due to ischemia or necrosis) decreases the force of myocardial contractility. This also occurs in cases of heart failure.

The heart rate:

The force of cardiac contractility is affected by the frequency of stimulation. An increase in the frequency of stimulation (i.e. shortening the intervals between the stimuli) causes a proportional increase in the force of contraction.

Accordingly, tachycardia causes a positive inotropic effect while bradycardia exerts a negative inotropic action. The positive inotropic effect in tachycardia is due to the increase in the number of depolarization (which increases the intracellular Ca⁺² content and its availability to the contractile proteins (troponin C).

3). Extra cardiac factors:

These factors affect the cardiac inotropic state and they include the following:

a). Neural

b). Physical

c). Chemical

a). Neural factors:

Sympathetic stimulation and noradrenaline exert a +ve inotropic eff­ect by increasing;

·        Cyclic-AMP in the cardiac muscle fibres (which leads to activation of the Ca⁺² channels and more Ca⁺² influx from the ECF).

·        The heart rate.

Conversely, parasympathetic stimulation and acetylcholine exert a -ve inotropic effect (by opposite mechanism) but on the atrial muscle only (since the vagi nerves don’t supply the ventricles).

b). Physical factors:

A moderate rise of the body temperature strengthens cardiac contractility (by increasing the Ca⁺² influx and ATP formation in the muscle) while an excessive rise of the body temperature (e.g. in fever) exhausts the metabolic substrates in the cardiac muscle and decreases its contractility. Hypothermia also decreases cardiac contractility.

c). Chemical factors:

(A) Hormones:

Catecholamines (epinephrine, norepinephrine and dopamine), glucagon and the thyroid hormones; all exert a +ve inotropic effect.

(B) Blood gases:

Moderate hypoxia (O₂ lack) and hypercapnia (CO₂ excess) increase the cardiac contractility, whereas severe hypoxia and hyper­capnia directly depress the cardiac muscle and decrease its contractility.

(C) H ⁺ ion concentration (pH):

An increase of the blood [H⁺] i.e. drop of the blood pH (acidosis) produces a -ve inotropic effect, whereas  a decrease of the blood [H⁺] i.e. rise of the blood pH (alkalosis) produces a + ve inotropic effect.

 

(D) Inorganic ions:

·        Sodium: Hypernatraemia favors Na⁺ influx and Ca⁺² efflux by the

·        Na⁺-Ca⁺² exchanger carrier, thus it has a -ve inotropic effect. On the other

·        hand, hyponatraemia exerts a +ve inotropic effect by an opposite mechanism.

·        Potassium: Hyperkalaemia has a -ve inotropic effect (weakens the myocardial contractility; flaccidity) and may stop the heart in diastole. This is because the excess K⁺ in the ECF decreases the resting membrane potential (more positive resting membrane potential; closer to the threshold)) in the cardiac muscle fibers, so the amplitude of the action potential is reduced leading to less influx of the depolarizing Ca⁺² and in turn less release of activator Ca⁺² from the sarcoplasmic reticulum. In addition, Hyperkalaemia increases excitation and decreases conduction leading to ectopics and dilated, flaccid heart. On the other hand, hypokalaemia produces a +ve inotropic effect by an opposite mechanism.

·        Calcium: Hypercalcaemia exerts a +ve inotropic effect as a result of more cytosolic Ca⁺². Whereas hypocalcaemia has a little (or no) -ve inotropic effect, since lowering of the serum Ca⁺² level causes fatal tetany before affecting the heart. However, hypocalcaemia causes cardiac flaccidity like Hyperkalaemia.

 

(E) Toxins:

Several toxins (e.g. certain snake venoms and the toxin released by the diphtheria microorganisms) produce a-ve inotropic effect (mostly by a direct action on the contractile mechanism of the cardiac muscle).

(F) Drugs:

·        Cardiac glycosides (e.g. digitalis; Digoxin): These drugs inhibit the Na⁺-K⁺ ATPase in the sarcolemma of the cardiac muscle fibres, so the intracellular Na⁺ concentration increases. This decrease the Na⁺ influx, thus Ca⁺² efflux through the Na⁺-Ca⁺² exchanger is also decreased. Accordingly, the intra­cellular Ca⁺² concentration increases, producing a +ve inotropic effect. Digitalis also increases the slow Ca⁺² influx during the action potential.

·        Xanthines (e.g., caffeine and theophylline; bronchodilator): They exert a +ve inotropic effect.

·        Ouinidine, barbiturates, procainamide (and other anesthetic drugs) as well as Ca⁺² blocker drugs all have a -ve inotropic effect by decreasing Ca⁺² influx into the cardiac muscle fibres.

7. Separate myocardial cell electricity.

Potential changes on cell membrane, which is recorded separately called electro gram. During resting potential membrane charge is positive. If two electrodes will dispose on membrane surface the voltage difference is absent and baseline is recorded. In irritation the cell membrane is depolarized some part firstly. The voltage between two electrodes increased and electro gram line deflects upward. The positive wave of electro gram is formed. After depolarizing all the membrane its surface charge becomes negative. The voltage under both electrodes temporarily becomes the same. Electro gram line returns downward to baseline level. Then repolarization begins from the same point as depolarization and in the same order. Polarity of cell membrane changes and electro gram deflects downward. The negative wave is formed. After depolarization of hole the membrane surface the voltage returns to rest potential level and baseline on electro gram record.

FORMATION OF NORMAL ELECTROCARDIOGRAM

1. Electrogram and action potential of one myocardial cell.

An electrocardiograph is an instrument that measures and records the electrocardiogram (ECG), the electrical activity generated by the heart. Electrodes placed on various anatomical sites on the body help conduct the ECG to the electrocardiograph. The ECG alone is not sufficient to diagnose all abnormalities possible in the pacing or conduction system of the heart. The interpretation of the 12-lead ECG provides a differential diagnosis for many arrhythmias

During the depolarization phase the rapid Na⁺ gates open and inward diffusion of Na⁺ occur. This event corresponds to formation upward part of positive wave on electro gram line. The next fast initial repolarization begins with inward Cl^– diffusion. Then electro gram returns to baseline level. When opening slow Ca²⁺ gates the potential difference temporarily isn’t essential and baseline continues. During the next phase outward K+ diffusion increases and external surface of membrane becomes positive. Voltage fluctuation leads to deflection of electro gram downward further returning to baseline level. In rest period all the membrane has positive charge on external surface and baseline is recorded. Through this period ion pumps restore initial distribution of ions.

2. Formation of EEG waves

Unexcited part of cell has already positive charge. Depolarized part has already negative charge. Between positive and negative charges the electrical power is recorded. Electrical power directs towards positive voltage. When changing polarity, electrical power of entire heart has different volume and direction in every moment of cardiac cycle.

To understand formation of ECG waves in different leads it is necessary to remember some rulers of this process:

– When electrical power directs towards positive pole of lead the upward wave is recorded;

– When electrical power directs towards negative lead pole, the downward wave occurs;

– If electrical power directs perpendicular to lead axis the baseline is recorded.

 

3. ECG as a representation of heart depolarization

Every cardiac cycle produces ECG waves designated as P, Q, R, S and T. These waves are not action potentials. They represent potentials between rested and depolarized or depolarized and repolarized parts of whole heart. Amplitude and duration of these waves correspond to electrical power fluctuation in entire heart.

 After producing impulse in SA-node depolarization begins at first in cells of right atrium and ascend part of P wave is recorded. When depolarization spreads into left atrium, the ECG line returns to baseline level. Delay of depolarization in AV-node recorded as PQ-interval in baseline. Then impulse spreads into middle part of septum and heart apex. This event recorded as descend part of Q wave. Iext depolarization of right ventricle wall ECG line deflexed upward and formation of R wave begins. When impulse spreads into left ventricle wall, the ECG line returned in contrary side towards the lowest point of S wave. Depolarization of ventricles basis afterwards caused formation of S wave, which continues to baseline.

 

Repolarization of atria is failed to record in ECG because of greater depolarization of ventricles. Repolarization of ventricles develops firstly in right part of heart and then in left one. That is why ascend and descend parts of T wave are formed.

In diastole normally baseline is recorded but U wave may occur.

 

 

Electrocardiography as a method of observation

1. ECG leads:

The electrical current generated by the heart is conducted through the pairs of electrodes and leads, and is amplified, recorded, and processed by the electrocardiograph. The wires connecting the pairs of electrodes on the surface of the body to the electrocardiograph are called leads. The different features and modules of a typical electrocardiograph include the protection circuitry, lead selector, calibration signal, preamplifier, isolation circuit, driver amplifier, memory system, microcomputer, and recorder or printer.

Twelve leads usually comprise a diagnostic ECG recording: six limb leads (three bipolar and three unipolar), and six unipolar precordial leads. The instantaneous cardiac scalar voltages resulting from the electrical activity in the heart is measured in each of the 12 leads. Since the cardiac vector varies in magnitude with time over a three-dimensional space, it is important to know its presentation (i.e. appearance or projection) in each of the 12 leads of the ECG.

a) Bipolar limb leads.

The bipolar limb leads record the voltage between electrodes placed on the wrists and legs. These leads were proposed by Einthoven in 1913.

I lead: left arm (+) – right arm (-);

II lead: left leg (+) – right arm (-);

III lead: left arm (+) – left leg (-).

For recording limb leads we put red electrode on right arm, yellow – on left arm, green – on left leg and black – on right leg. Black electrode has zero potential (ground).

b) The unipolar limb leads were proposed by Goldberger in 1942. They record voltage between single “exploratory electrode” fro one limb and zero joined electrode from two other limbs. So there are three leads AVR, AVL, AVF. In fact zero electrodes records middle voltage of two limbs. Bipolar limb leads and unipolar limb leads record electrical power in frontal projection.

c) The unipolar chest leads were suggested in 1934 by Vilson. One electrode, which is active, situated on the chest in six standard positions. They labeled V1 – V6. Joined zero electrode records middle potential of right arm, left arm and left leg. That is why every chest lead records voltage between active chest electrode and Vilson’s joined zero electrode.

These standard positions of active chest electrode are:

V1 – in crossing right IV right intercostal space and parasternal line;

V2 – in crossing left IV intercostal space and parasternal line;

V3 – between V2 and V4;

V4 – in crossing V left intercostal space and medioclavicular line;

V5 – in crossing V left intercostal space and anterior axilar line;

V6 – in crossing V left intercostal space and middle axilar line.

Unipolar chest leads records changes of heart polarity in horizontal projection.

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2. Algorithm of ECG registration:

 Registration performs fare from electric motors and other electrical devices.

Tested person may have rest before registration in 10-15 minutes. This procedure needs 2-hour interval after eating or worm procedures.

For better contact between electrodes and skin use solution NaCl 5-10 % or special electrode past or electrode gel. Otherwise hindrances in ECG curve may occur. They will stand in the way of ECG analysis

ECG registration performs in quiet breathing in patients.

Registration begins from standard voltage 1 mV from the electrocardiograph for regulation of amplitude in ECG. Usually standard voltage amplitude is 10 mm. Then continue registration of bipolar limb leads, the next – unipolar limb leads and afterwards – unipolar chest leads.

3. ECG analysis:

In order to interpret the 12-lead ECG and use it to diagnose abnormalities, it is important to know the normal characteristics of the ECG, and understand the mechanisms underlying the generation of each segment of the ECG. Figure 1 shows the various fiducial points in the ECG, and typical values of the various intervals measured from the ECG.

Fig. 1. – Points various and intervals in the ECG

The main elements of ECG curve are:

– Waves P, Q, R, S and T. Sometimes U wave may occur;

– Segments – P-Q (from the end of P wave to beginning of Q wave), S-T (from the end of S wave until beginning of T wave);

– Intervals, which characterize certain time period of heart activity – P-Q (from the beginning of P wave to beginning of Q wave), Q-T (from beginning of Q wave to end of T wave);

– Complexes – atrial, which is presented by P wave, and ventricular -QRST.

a) P wave in healthy persons, is obligatory positive in I, II, AVF, V₂-V₆ leads. P wave may be negative in III, AVL and V1, either positive or biphasic. If it is diphasic, then the negative component comes after the positive component and is not excessively broad or deep. An absent P wave in the ECG may signify sinoatrial block, an abnormality in which the impulse from the SA node is not conducted to the AV node. Normally in II lead its amplitude is 2,5 mm, duration – 0,1 s (not greater than 110 ms).

The P wave is caused by atrial depolarization. The normal shape of the P wave does not include any notches or peaks.

b) P-Q interval reflects duration of AV-conduction, which is spreading of potential by AV node, His bundle and its branches. This interval lasts 0.12-0.20 s and depends on heartbeat rate.

c) QRST complex reflects spreading of excitation by ventricles. It hole amplitude is higher 5 mm of the waves are signed by capital letters. Otherwise it used little letters. ORS duration in II lead is not more than 0.1 s.

d) Q wave normally in II lead is less then 1/4 of R amplitude duration is 0.03 s. Normally in AVR deep and wide Q waves may be recorded. In V₁, V₂ – Q wave is particularly absent.

 

e) R-view usually is recorded in all leads; exalt AVR, which may be absent. In unipolar chest leads R amplitude gradually increases from V₁ to V₄ and some decreases in V5 and V6. So normally in unipolar chest leads both increasing R-amplitude and S-amplitude occurs. S-wave has amplitude not more than 20 mm, but it varies from lead to lead.

j) S-T –segment corresponds to excitation of both ventricles. Normally in bipolar and unipolar leads it lies on baseline and don’t move more than 0.5 mm. In V1-V3 deviation upward to 2 mm may occur.

h) T-wave normally is positive in I, II AVF, V₂-V₆, T_I>T_III, T_V6>T_V1. T-wave has sloping ascend part and sleep descending part. In III, AVL, V₁ T-wave may either be positive, negative or bipolar. In II lead T-amplitude is 5-6 mm, duration – 0.16-0.24 s.

i) Q-T interval is electrical systole of ventricles. Its duration directly depends on heartbeat rate. Proper duration may calculated by Buzett formula:h0

Q-T=K√¯R-R¯, where

K=0.37 in male or 0,40 in female

f) U-wave may be recorded in unipolar chest leads, which reflects excitation fare of excitability after electrical systole of ventricles myocardium. U-wave usually is positive and small.

4. ECG analysis begins with estimation of control voltage and paper speed. Another analysis at usual performs in this order.

1) Determining of impulse origin. Pay attention to proper order of waves in ECG. If P wave in II lead is positive and recorded before QRS complex is believed to determine pacemaker in SA node.

2) Heart rhythm evaluation by measuring of R-R duration. Normally adjacent R-R intervals duration may differ from each other not more 0.1 s. Usually II lead is examined.

3) Determining of heart rate. In proper rhythm 60 s is divided to R-R duration in seconds, which is calculated using paper speed.

4) Evaluation of ECG voltage. If in bipolar limb leads the lowest R wave is smaller than 5 mm and RI+RII+RIII less than 15 mm, the ECG voltage is decreased. Otherwise it is normal.

5) EMP direction determining.

– Visual method: needs measuring R amplitude in all bipolar limb leads. If true, that R_II>R_I>R_III, the EMP direction is near 30º-69º, that is normal;

– Graphic method use Baily co-ordinate. If in Einthoven’s triangle put through the center parallel to leads axes we’ll get Baily’s co-ordinate. Than in any two bipolar limbs leads it is necessary to determine summary amplitude of QRS waves. Upward waves have positive meaning and downward are negative. Summary amplitude put on corresponding axis with (+) or (-) sign. In this point lined perpendicular to lead axis. Next time determined cross point of two drown perpendiculars. When join this point to Baily’s co-ordinate center we’ll obtain the EMP direction outward the center.

6) ECG elements analysis. Pay attention to form, amplitude and duration of waves and intervals. Measure deviation from baseline if it occurs. Compare the results with normal rate.

5. Investigation of conductive system in the heart

After distraction brain in spinal cord by probe enter to thoracic cavity. Calculate rate of heartbeat in intact heart. Put the first Stannius’s ligature and calculate heartbeat upper and lover this one. Also put the II and III ligature. Every case calculate rate of heartbeat for venous sinus, atria and ventricles.

In the conclusioote would the automaticity gradient is characteristic for heart of frog. Describe, what is automaticity gradient.

6. ECG registration

Registration performs fare from electric motors and other electrical devices.

Tested person may have rest before registration in 10-15 minutes. This procedure needs 2-hour interval after eating or worm procedures.

VIDEO ECG 1

For better contact between electrodes and skin use pieces of bandage, wet by solution NaCl 5-10 % or special electrode past or electrode gel. Otherwise hindrances in ECG curve may occur. They will stand in the way of ECG analysis

ECG registration performs in quiet breathing in patients.

Registration begins from standard voltage 1 mV from the electrocardiograph for regulation of amplitude in ECG. Usually standard voltage amplitude is 10 mm. Then continue registration of bipolar limb leads, the next – unipolar limb leads and afterwards – unipolar chest leads.

 

 

VIDEO ECG 2

17. ECG analysis

1) Determining of impulse origin. Pay attention to proper order of waves in ECG. If P wave in II lead is positive and recorded before QRS complex is believed to determine pacemaker in SA node.

2) Heart rhythm evaluation by measuring of R-R duration. Normally adjacent R-R intervals duration may differ from each other not more 0.1 s. Usually II lead is examined.

3) Determining of heart rate. In proper rhythm 60 s is divided to R-R duration in seconds, which is calculated using paper speed.

4) Evaluation of ECG voltage. If in bipolar limb leads the lowest R wave is smaller than 5 mm and RI+RII+RIII less than 15 mm, the ECG voltage is decreased. Otherwise it is normal.

5) Electrical magnetic power (EMP) direction determining.

– Visual method: needs measuring R amplitude in all bipolar limb leads. If true, that RII>RI>RIII, the EMP direction is near 30º-69º, that is normal;

– Graphic method use Baily co-ordinate. If in Einthoven’s triangle put through the center parallel to leads axes we’ll get Baily’s co-ordinate. Than in any two bipolar limbs leads it is necessary to determine summary amplitude of QRS waves. Upward waves have positive meaning and downward are negative. Summary amplitude put on corresponding axis with (+) or (-) sign. In this point lined perpendicular to lead axis. Next time determined cross point of two drown perpendiculars. When join this point to Baily’s co-ordinate center we’ll obtain the EMP direction outward the center.

6) ECG elements analysis. Pay attention to form, amplitude and duration of waves and intervals. Measure deviation from baseline if it occurs. Compare the results with normal rate.

PUMPING WORK OF THE HEART

ECHOCARDIOGRAPHY EVALUATION OF HEART FUNCTION

REGULATION OF THE HEART PUMPING

 

Physiology of cardiac muscle.

The heart is composed of three major types of cardiac muscle.

1- The atrial muscle.         

2- The ventricular muscle.

3- Specialized excitatory and conductive muscle fibers; an excitatory system of the heart that helps spread of the impulse (action potential) rapidly throughout the heart.

 

Physiologic anatomy of cardiac muscle

Cardiac muscle cells (myocytes) are striated as they have typical myofibrils containing thin actin and thick myosin filaments, similar to those found in skeletal muscle, which slide along each other during the process of contraction.

Unlike skeletal muscle (no gap junction), adjacent myocardial cells are joined end to end at structures called intercalated discs, which are cell membranes that have very low electrical resistance. Within the intercalated discs, there are electrical synapses or gap junctions, these gap junctions are protein channels that allow ions to flow from the cytoplasm of one cell directly into the next cell and, therefore action potentials to move with ease from one cardiac myocyte to another. That is, when one of these cells becomes excited, the action potential spreads rapidly throughout the intercalated discs and gap junctions to stimulate the neighbor cell, so the myocardium act almost as if it is a single cell; a syncytium, i.e., the cardiac muscle contracts or behaves as a single functional unit (syncytium property).

Innervation of the heart

The heart receives a rich supply of sympathetic and parasympathetic nerve fibers. The parasympathetic contained in the vagus nerves release acetylcholine which acts on the muscarinic receptors. The sympathetic postganglionic fibers release norepinephrine (noradrenaline) which acts on beta one (β₁) adrenergic receptors distributed on cardiac muscle. The circulating epinephrine hormone from adrenal medulla also combines with the same receptors (β₁ receptors).

Blood supply of the heart

The myocardial cells receive their blood supply through arteries that branch from the aorta, named coronary arteries.

Coronary veins drain into a single large vein, the coronary sinus, which drain into the right atrium.

b). The function of the heart valves

The atrioventricular valves (AV valves) are composed of thin membranous cusps (fibrous flaps of tissue covered with endothelium), which hangdown in the ventricular cavities during diastole. After atrial contraction and just before ventricular contraction, the AV valves begin to close and the leaflets (cusps) come together by mean of backflow of the blood in the ventricles towards the atria.

The AV valves include:

·        The mitral valve; the left AV valve; bicuspid valve, which consists of two cusps (anterior and posterior), located between left atrium and left ventricle.

·        The tricuspid valve; the right AV valve, which consists of three cusps, located between right atrium and right ventricle.

The function of AV valves is to prevent backflow (prevent regurgitation; leakage) of blood into the atria during ventricular contraction. Normally they allow blood to flow from the atrium to the ventricle but prevent backward flow from the ventricle to the atria. The atrioventricular valves contain and supported by papillary muscles.

The aortic and pulmonary valves each consist of three semilunar cusps that resemble pockets projecting into the lumen of aorta and pulmonary trunk. They contaio papillary muscle. During diastole the cusps of these valves become closely approximated to prevent regurgitation of blood from aorta and pulmonary arteries into the ventricles. During systole the cusps are open towards arterial wall, leaving a wide opening for ejection of blood from the ventricles. In other words, the pulmonary and aortic valves allow blood to flow into the arteries during ventricular contraction (systole) but prevent blood from moving in the opposite direction during ventricular relaxation (diastole).

*All valves close and open passively. That is, they close when a backward pressure gradient pushes blood backward, and they open when a forward pressure gradient forces blood in the forward direction.

*There are no valves at entrance of superior, inferior vena cava and pulmonary veins into the atria. What prevents the backflow of blood from the atria toward the veins is the compression of these veins by the atrial contraction. However little blood is ejected back into veins, this represents the venous pulse seen in the neck veins (jugular veins) when the atria contracting.

 

          c). The function of papillary muscles

The AV valves (mitral and tricuspid) are supported by papillary muscles that attach to the flaps of these valves by the chordae tendineae.The papillary muscles originated from the ventricular walls and contract at the same time when the ventricular walls contract, but these muscles do not help the valves to close or open. Instead, they pull the flaps of the valves inward, toward the ventricles to prevent too much further bulging of the flaps (cusps) backward toward the atria during ventricular contraction, to prevent leakage of blood into the atria (keep the valve flaps tightly closed). In other words, contractions of papillary muscles prevent evertion of the flaps of the AV valves into the atria which could be induced by high pressure produced by contraction of the ventricles.

 

 

Figure: Mitral (two cusps) and Aortic (three cusps) valves.

          d). Heart Sounds

When the stethoscope is placed on the chest wall over the heart, two sounds are normally heard during each cardiac cycle (1st & 2nd heart sounds). Heart sounds are associated with closure of the valves with their associated vibration of the flaps of the valves and the surrounding blood under the influence of the sudden pressure changes that develop across the valve. That is, heart sound does not produced by the opening of the valve because this opening is a slow developing process that makes no noise.

1-The first heart sound (S₁): is caused by closure of the AV valves when ventricles contract at systole. The vibration is soft, low-pitched lub.

2-The second heart sound (S₂): is caused by closure of the aortic and pulmonary valves when the ventricles relax at the beginning of diastole. The vibration is loud, high-pitched dup. It is rapid sound because these valves close rapidly and continue for only a short period i.e., rapid, short and of higher pitch dup.

3-The third heart sound (S₃): is caused by rapid filling of the ventricles, by blood that flow with a rumbling motion into the almost filled ventricles; at the middle one third (1/3) of diastole i.e., it is caused by the vibrations of the ventricular walls during the period of rapid ventricular filling that follows the opening of AV valves. It is a low-pitched sound and can be heard after the S₂. It is heard iormal heart; in children and in adult during exercise. It is also heard in anemia, and AV valve regurgitation.

4-The fourth heart sound (S₄): it is an atrial sound when the atria contract (at late diastole). It is a vibration sound (similar to that of S₃) associated with the flow of blood into the ventricle. It is not heard iormal hearts but occurs during ventricular overload as in severe anemia, Thyroitoxicosis (hyperthyroidism) or in reduced ventricular compliance and in hypertension. If present, it is heard before S₁. (S₄, S₁, S₂, S₃).

 

 

 

          e) Heart murmurs

They are abnormal sounds, can be produced by blood flowing rapidly in the usual direction but through an abnormally narrowed valve (stenosis), by blood flowing backward through a damaged, leaky valve (incompetent, regurgitant valve) or by blood flowing between the two atria or two ventricles through a small hole: ASD (atrial septal defect), VSD (ventricular septal defect).

f). Properties of the cardiac muscle

In addition, to the syncytium property, the cardiac muscle has the property of:

·        Automaticity and rhythmicity (Autorhythmicity).

·        Excitability and conductivity.

·        Contractility

Contractility – is the ability of the cardiac muscle to contract.

The effect of various factors on contractility is called inotropism; a positive (+ve) inotropic effect means an increase in myocardial contractility, whereas a negative     (-ve) inotropic effect means a decrease in myocardial contractility.

Factors that affect cardiac contractility:

a). Mechanical

b). Cardiac

c). Extra cardiac

a). Mechanical factors:

          * Preload (venous return)

          * Afterload

b). Cardiac factors:

          * The myocardial mass.

          * The heart rate.

c). Extra cardiac factors:

These factors affect the cardiac inotropic state and they include the following:

     * Neural

     * Physical

     * Chemical

 

2. CARDIAC CYCLE

Functional analysis.

Period from end of one heart contraction to end of next, is called cardiac cycle. Each cycle is initiated by spontaneous generation of an action potential in the sinus node which travels rapidly through both atria and then through the A-V bundle into the ventricles.

Because of this special arrangement of the conducting system from the atria into the ventricles, there is a delay of more than 0,1 second during passage of the cardiac impulse from the atria into the ventricles. This allows the atria to contract, pumping blood into the ventricles before the strong ventricular contraction begins. Thus, the atria act as primer pumps for the ventricles, and the ventricles in turn provide the major source of power for moving blood through the body’s vascular system.

There are two phases: systole, when heart contracts and diastole, when heart dilates.

In a normal heart, cardiac activity is repeated in a regular cycle. Heart rate is about 72 beats/minute; for the atria, the cycle lasts for about 0,15 second in systole and 0,65 second in diastole. For the ventricles, the duration of each cardiac cycle lasts about 0,8 second. If the heart rate increases, the diastole decreases, which means that the heart beating very fast may not remain relaxed long enough to allow complete filling of the ventricles before the next contraction.

For the ventricles, the two major phases of the cardiac cycle are:

·        The diastole; a period of ventricular relaxation in which the ventricles fill with blood and it last for about 0,5 second.

·        The systole; a period of ventricular contraction and blood ejection, lasting   about 0,3 second.

 

Diastole can be divided into:

– Period of isometric relaxation, during which ventricles begin to relax and pulmonary valves close;

– Period of rapid filling of ventricles, when AV valves open;

– Atria systole, when atria contract and pump 20-30 % blood into ventricles.

Systole is composed by:

– Period of isometric contraction, when ventricles begin to contract and AV valves are closed;

– Period of ejection: during rapid ejection 70 % empting occur and in slow ejection last 30 % empting occur;

– Protodiastole.

b) Intra cardiac pressure

 

Wiggers Diagram

During period of isometric relaxation intra ventricular pressure falls. In period of rapid filling of ventricles atria pressure becomes grater than intra ventricular pressure. In atria systole pressure in right atrium rises to 4-6 mm Hg, in left atrium – 7-8 mm Hg.

Systole begins. In period of isometric contraction ventricular pressure rises. In period of ejection left ventricular pressure rises to 125 mm Hg and right ventricular pressure to 25 mm Hg. In protodiastole ventricular pressure falls, below aortic and pulmonary pressure.

 

a). Phases of the cardiac cycle:

The cardiac cycle starts by atrial systole followed by ventricular systole then by diastole of the whole heart.

Atrial systole (atria as a pump):

It is the first phase of cardiac cycle. Blood normally flows continually (passively) from the veins into the atria and about 75% of the blood in the atria flow directly into the ventricles even before the atrial contraction. Then, atrial contraction usually causes an additional 25% filling of the ventricles. So the heart can continue to operate satisfactorily under most condition without this extra 25%, yet this 25% is needed in case of exercise.

Pressure changes in the atria during cardiac cycle

During atrial contraction; right atrial pressure raises 4 to 6 mmHg, while the left atrial pressure raises 7 to 8 mmHg. In the atrial pressure curve, there are 3 major pressure elevations called the a, c and v atrial pressure waves:

·        a wave is caused by atrial contraction.

·        c wave is caused by bulging of the tricuspid valve into the right atrium during ventricular contraction because of increasing pressure in the ventricles.

·        v wave result from slow flow of blood into the right atrium from the veins while the AV valve are closed during ventricular contraction. So the v wave is due to atrial filling.

 

Figure: Atrial pressure curve.

 

Clinical importance of atrial waves

 

Venous pulsations occur only in large veins near the heart like the jugular veins in the neck (the jugular venous pulsations). The jugular venous pulse reflects changes in right atrial pressure (the central venous pressure), i.e. the pressure changes within the right atrium are communicated to the neck jugular veins. To make the jugular venous pulsations visible in the neck, the person has to be supine with his back at a slight angle to the horizontal (45 degree). In this position, the a and v waves can be seen in the jugular veins when the neck is carefully examined. When the venous pressure is raised as in heart failure disease, the jugular veins become more prominent and the pulsation can be observed in the neck.

·        x-descent is caused by pulling the AV ring down during ventricular systole; drop in right atrial pressure.

·        y-descent is caused by the opening of the AV valve and the escape of the blood from the atrium into the ventricle; drop in right atrial pressure.

Ventricular cardiac cycle

The ventricular cardiac cycle consists of three phases:

·        Phase one: Ventricular filling.

·        Phase two: Ventricular systole.

·        Phase three: Isovolumic, isometric relaxation.

 

1.     Ventricular filling

During ventricular systole, the accumulated large amounts of blood in the atria because of the closed AV valves push the AV valves open and allow blood to flow rapidly into the ventricles. During atrial contraction, an additional amount of blood flows into the ventricles represent 25% of the filling of the ventricles.

 

Figure: Ventricular pressure curve.

 

2.Ventricular systole:

Subdivided into two phases:

1). Isovolumic, isometric contraction (isovolumetric contraction). Ventricles begin to contract, pushing AV valves close, SL valves still closed, pressure in ventricles rises. Pressure in ventricles is not enough to open semilunar valves. Therefore, All Valves Are Closed

2). Ventricular ejection – second (and last) phase of ventricular contraction. Pressure in ventricles rises and forces semilunar valves open. Blood is ejected into arteries. Ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected.

 

Isovolumetric contraction

It is ventricular contraction but without blood ejection (no emptying) just to close the AV valves and to open semilunar valves by the rise in intraventricular pressure (from 0 to 80 mmHg in the left ventricle). It is the isovolumetric contraction, which means only the tension is increasing in the ventricular muscle without shortening of the muscle and with no change in blood volume.

 

Ventricular ejection

The blood ejected from the ventricles into pulmonary trunk and aorta when the ventricular pressure rises and forces the semilunar valves open.

Left ventricular pressure rises above 80 mmHg.

Right ventricular pressure rises above 8 mmHg.

Figure: Ventricular volume curve.

 

2.     Isovolumetric relaxation:

Isovolumic, isometric relaxation; following ventricular systole, ventricular relaxation begins suddenly and ventricular pressure falls. The blood in the aorta and pulmonary trunk backflows toward the heart closing the semilunar valves. For another 0.03 to 0.06 second, the ventricular muscle continues to relax, even though the ventricular volume does not change giving rise to the period of isovolumic relaxation in which the intraventricular pressure falls rapidly back to their low diastolic levels. Meanwhile, the atria have been filling with blood. When the pressure exerted by the blood on the atrial side of AV valves exceeds that in the ventricles, AV valves forced open and the ventricular filling phase begins again for a new cycle of ventricular pumping.

b). Aortic pressure curve:

When the left ventricle contracts, the intraventricular pressure rises rapidly until the aortic valve opens. So blood immediately flows out of the ventricle into the aorta, causes the wall of this artery to stretch and the pressure rise. Then, at the end of the systole, after the left ventricle stops ejecting blood and the aortic valve closes, the elastic recoil of the arteries maintains a high pressure even during diastole (diastolic pressure = 80 mmHg).The systolic pressure inside the aorta is equal to 120 mmHg. Incisura: is caused by a short period of backward flow of blood from the ventricle immediately before closure of the valve followed then by sudden cessation of the backflow.

 

Figure: Aortic pressure curve.

 

c). Relationship of the ECG to the cardiac cycle (Timing):

The ECG (electrocardiogram) shows the P, QRS and T waves. They are electrical voltages generated by the heart and recorded by the ECG:

·        P-wave is caused by atrial depolarization; this is followed by atrial contraction, which causes a slight rise in the atrial pressure curve after the P wave.

·        About 0.16 second after the onset of the P wave, the QRS waves appear as a

result of electrical depolarization of the ventricles, which initiates contraction of the ventricles and causes the ventricular pressure to begin rising, as shown in the figure. Therefore, the QRS complex begins slightly before the onset of ventricular systole.

·        T-wave represents ventricular repolarization at which the ventricles begin to

relax. Therefore, the T wave occurs slightly before the end of ventricular contraction.

 

d). Relationship of the Heart Sounds to Heart Pumping

When listening to the heart with a stethoscope, one does not hear the opening of the valves because this is a relatively slow process that normally makes no noise. However, when the valves close, the cusps of the valves and the surrounding blood vibrate under the influence of sudden pressure changes, giving off sound that travels in all directions through the chest. When the ventricles contract, one first hears a sound caused by closure of the A-V valves. The vibration is low in pitch and relatively long-lasting and is known as the first heart sound. When the aortic and pulmonary valves close at the end of systole, one hears a rapid snap because these valves close rapidly, and the surroundings vibrate for a short period. This sound is called the second heart sound.

 

 

Cardiac volumes

During period of isometric relaxation ventricular volume does not change. During rapid filling of ventricles period blood flows rapidly into respective ventricles. In atria systole ventricle volume increases on 20-30 %. Systole begins. In period of isometric contraction there is no volume change. In period of ejection stroke volume output occur. In protodiastole blood flows into aorta and pulmonary trunk, due to momentum.

3. PHYSIOLOGICAL ANALYSIS OF CARDIAC OUTPUT

Stroke work output is the amount of blood that left ventricle pump to aorta during each cardiac cycle. Volume of blood on each ventricle at end of diastole is called end-diastolic volume and measures 120-140 ml. Volume of blood in the each ventricle at end of systole is called end systolic volume and measures 50-60 ml.

Blood volume, which heart pumps per minute called as minute blood volume. It may be calculated by multiply stroke volume to rate of heartbeat and normally equal to 4-6,5 l/min. In physical exercises it rises to 10 l/min and more.

Cardiac output is the amount of blood pumped by each ventricle per minute, expressed in liters/minute. Normally, it is about 5 liters per minute.

The cardiac output (CO) is determined through multiplying the heart rate (HR) by the stroke volume (SV).

 

CO = HR X SV

 

Heart rate = the number of heart beats/minute (aveage; 72 beat/minute).

Stroke volume  = the volume of blood ejected by each ventricle with each beat.

If the HR = 72 beats/min., and the SV is of 70 ml;

Cardiac output = 72 X 70 = 5.04 Liters.

As the cardiovascular system is a closed system, cardiac output of the left ventricle equals to the cardiac output of the right ventricle i.e., the two sides of the heart have the same output per minute. It is also the volume of blood flowing through either the systemic or pulmonary circulation per minute. In other words, cardiac output is the quantity of blood pumped into the aorta each minute by the heart. This is also the quantity of blood that flows through the circulation.

cardiac output= arterial blood flow = pulmonary blood flow.

Cardiac output varies widely with the level of activity of the body. Therefore, the level of body metabolism, exercise, age and size of the body influence the cardiac output. For young, healthy men, the resting cardiac output averages about 5.6 liter/min., for young women, this value is 10-20% less, but it is not constant. It might be increased even up to 30 liters/min., depending on the activity of the body. Therefore, cardiac output is a variable parameter usually it is not less than 5 liter/min., at rest to supply the body with oxygen and to maintaiormal BMR (basal metabolic rate). The highest cardiac output recorded is 48 liters/min., in the Roadrunners (Hyperdynamic circulation which mean the same blood volume; 5 liters circulating at a higher speed). Blood volume is about 5 – 6 liters. So the heart pumps the whole blood in one minute.

 

a). Control of cardiac output:

The cardiac output is controlled (either increased or decreased or maintained) by the following factors.

1). Venous return (preload).

2). Heart rate (HR)

3). Myocardial contractility.

4). Cardiac compliance.

5). Afterload.

 

1). Venous return:

The venous return (VR) is the amount of the blood flowing from the tissues into the veins and then into the right or left atrium each minute. So in steady state, they are equal (CO = VR) because what is pumped out from the left ventricle equals to what returned to the right side of the heart. In other words, It is the quantity of blood flowing from the veins into the right atrium each minute. It represents the preload. The venous return and CO must be equal to each other.

The CO is controlled by venous return through the following mechanisms:

 

Frank-Starling law; the heart pumps automatically whatever amount of blood flows into the right atrium from the veins. This law states that when increased quantities of blood flow into the heart, this stretches the walls of the heart chambers. As a result of the stretch, the cardiac muscle contracts with increased force to empty the expanded chambers i.e. the extra blood that flows into the heart (VR) is automatically pumped without delay into the aorta and flows again through the circulation.

The effect of the venous return on the heart rate by mean of stretching the heart. Stretch of the SA node in the wall of the right atrium has a direct effect on the rhythmicity of the SA node itself to increase heart rate 10 – 15% .

Another factor, the stretched right atrim initiates a nervous reflex called the Bainbridge reflex, passing first to the medullary vasomotor center and then back to the heart by sympathetic nerves, to increase the heart rate. The increase in the heart rate then helps to pump the extra blood.

Decrease in Cardiac Output Caused by Decreased Venous Return.

Anything that interferes with venous return also can lead to decreased cardiac output. Some of these factors are the following:

1. Decreased blood volume.

Resulting most often from hemorrhage. Loss of blood decreases the filling of the vascular system to such a low level that there is not enough blood in the peripheral vessels to create peripheral vascular pressures high enough to push the blood back to the heart.

2. Acute venous dilation.

In case of sudden and acute vasodilatation especially the peripheral veins involved. This results most often when the sympathetic nervous system suddenly becomes inactive. For instance, fainting often results from sudden loss of sympathetic nervous system activity, which causes the peripheral vessels, (veins), to dilate markedly. This decreases the filling pressure of the vascular system because the blood volume cao longer create adequate pressure in the flaccid peripheral blood vessels. As a result, the blood “pools” in the vessels and does not return to the heart.

3. Obstruction of the large veins.

When the large veins leading into the heart become obstructed, so that the blood in the peripheral vessels cannot flow back into the heart. Consequently, the cardiac output falls markedly.

4. Decreased tissue mass, especially decreased skeletal muscle mass.

With normal aging or with prolonged periods of physical inactivity, there is usually a reduction in the size of the skeletal muscles. This, in turn, decreases the total oxygen consumption and blood flow needs of the muscles, resulting in decreases in skeletal muscle blood flow and cardiac output.

* Regardless of the cause of low cardiac output, if the cardiac output falls below that level required for adequate nutrition of the tissues, the person is said to suffer circulatory shock. This condition can be lethal within a few minutes to a few hours.

2). Control of cardiac output:

Heart rate and cardiac output:

In resting state, (the venous return is constant), changes in heart rate between 100-200 beats/min., not affect CO markedly. However, high heart rate (more than 200 beats/minute) in patient with ventricular tachycardia (VT) or supraventricular tachycardia (SVT) may affect CO to be insufficient to maintain the nutritional needs of the body because such increase in heart rate will reduces the duration of ventricular diastole and so reduce the time available for ventricular filling that will reduce the stroke volume. On the other hand, slow heart rate may also reduce CO, as in complete heart block disease (HR < 40 beats/minute).

 

In exercise, (the venous return is increased), cardiac output is increased to meet the body need by increasing in both heart rate and stroke volume, the increase in heart rate is through sympathetic stimulation as the exercise is a stressful situation, while the increase in stroke volume is through the increase in venous return by the action of skeletal muscles that squeezed and pumped the blood toward the heart, and through the increased myocardial contractility.

So, the heart rate is effective in increasing the CO if the venous return is increased, otherwise the stroke volume will be decreased and so the decreased  CO.

Stroke Volume

Stroke volume (SV) is defined as the amount of blood pumped out by each ventricle per beat. It is about 70 ml/beat at rest but may increase to 150 ml/beat with exercise.

The stroke volume equals to the amount of blood present in the ventricle when systole starts just before the initiation of ventricular contraction. However, the ventricles don’t completely empty themselves of blood during contraction (2/3 of blood is ejected, 1/3 is left there) therefore, a more forceful contraction can produce an increase in stroke volume.

Substruction of end-systolic volume (ESV) from end-diastolic volume (EDV) produce stroke volume (SV).

SV = EDV – ESV.

 

EDV: the ventricular blood volume at the end of the diastole; normally                     EDV = 110  to 120 ml.

ESV: the ventricular blood volume at the end of the systole; normaly  ESV = 40 ml.

* Strok volume = 70  to  80 ml.

Regulation of Stroke Volume

 

The stroke volume is regulated by three variables:

·        The end-diastolic volume (EDV).

·        Sympathetic nervous system input to the ventricles (myocardial contractility; strength of ventricular contraction).

·        The total peripheral resistance.

The end-diastolic volume is the amount of blood in the ventricles immediately before they begin to contract (preload). The stroke volume is directly proportional to the preload; an increase in EDV results in an increase in stroke volume. This relationship is known as the Frank-Starling law. In other words, the ventricle contracts more forcefully during systole when it has been filled to a grater degree during distole.

The stroke volume is also directly proportional to the myocardial contractility which is influenced by cardiac sympathetic nerves (norepinephrine) and circulating epinephrine secreted from adrenal medulla. Thus, when the ventricles contract more forcefully as a result of sympathetic nerve stimulation or epinephrine which is independend of a change in end-diastolic ventricular  volume, they pump more blood (increased stroke volume).

The total peripheral resistance which is the impedance to blood flow in the arteries (aortic impedance). The pressure in the arterial system before the ventricle contracts is, in turn, a function of the total peripheral resistance. The higher the peripheral resistance, the higher the pressure. Thus, an increased arterial pressure tends to reduce stroke volume. The total peripheral resist­ance thus presents an impedance to the ejection of blood from the ventricle, or an afterload imposed on the ventricle after con­traction. This means that the stroke volume is inversely proportional to the total peripheral resistance; the greater the peripheral resis­tance, the lower the SV.

Ejection Fraction (EF%):

The proportion of the end-diastolic volume that is ejected against a given afterload depends on the strength of ventricular contraction. Normally, contraction strength is sufficient to eject 70 to 80 ml of blood out of a total end-diastolic volume of 110 to 120 ml (2/3 of blood is ejected). The ejection fraction is thus about 65%.

In other words, the ejection fraction is the ratio of stroke volume to end-diastolic volume (EDV) and it reflects the ventricular contractility, expressed as percentage, normally it averages at rest  65% (again, about 2/3 of the EDV is ejected).

Increased ventricular contractility causes an increase in ejection fraction.

EF% = SV / EDV X 100. 

EF% = 80/120 X 100 = 2/3 %.     (more than 55% considered as normal).

In heart failure, the EF is reduced;  < 50%.

EF can be measured by Echocardiogram (Echo) that can measure the EDV, ESV and so the SV.

3). Myocardial contractility:

It is defined as the strength of contraction at any given EDV.

Myocardial contractility exerts a major influence on stroke volume and in turn on the cardiac output. It is reduced in heart failure.

It is measured by Ejection Fraction.

Myocardial contractility is affected by the following factors :

·        The preload (i.e., EDV): controls the power of cardiac contractility by Frank-Starling’s law.

·        Sympathetic nerve supply: The resting cardiac sympathetic tone increases the

·        cardiac pumping power to 13-15 litres/minute, and maximal sympathetic stimula­tion (e.g. in severe muscular exercise) increases it to about 25 litres/ minute.

·        The afterload (i.e., aortic impedance): An increase in the afterload

·        (e.g. due to rise of the arterial blood pressure, aortic stenosis or polycythaemia) reduces the cardiac pumping power, and vice versa.

·        Ventricular hypertrophy; This may normally occur in some athletes as a result of prolonged strenuous exercises, and it can increase the cardiac pumping power up to about 35 litres minute.

 

4). Cardiac compliance:

It is the stretchability, elasticity, it is the change in volume per unit change in pressure = ∆V/∆P, decreased compliance in which there is a myocardial stiffness, this is in disease condition which will affect cardiac output as in cases of cadiomyopathies, and pericardial effusion.

5). Afterload:

It is the resistance that oppose cardiac output, e.g., increased arterial systolic pressure (systolic hypertension), valve disease that obstruct the outflow of blood as in case of aortic stenosis disease. So increased afterload will reduce cardiac output.

On the other hand, reduced total peripheral resistance (reduced afterload) causes high cardiac output. Conditions that can decrease the total peripheral resistance and at the same time increase the cardiac output to above normal include:

1. Beriberi

2. Arteriovenous

3. Hyperthyroidism

4. Anemia

Low cardiac output: (Abnormalities)

·        Fainting: low cardiac output leads to ischemia of the brain; causing fall down (fainting). It is a protective mechanism to correct the brain ischemia through increasing blood supply to the brain.

·        Shock: also low cardiac output that may cause hypotension, again leading to ischaemia to the brain.

 

b). Methods for measuring cardiac output:

In animal experiments, cardiac output can be measured using any type of flowmeter (electromagnetic, or ultrasonic flowmeter) which can be placed on the aorta or pulmonary arteries i.e., blood flow in the root of aorta can be recorded by an electromagnetic flowmeter.

In the human, CO is measured by indirect methods that do not require surgery. Two methods commonly used are:

1)The oxygen fick method

2)The indicator dilution method

Another method is by 3) Echocardiography; it consists of emitting Ultrasonic waves to the heart. Such echoes record the ventricular movements, from which both the EDV and ESV and so the SV can be calculated. The CO then can be measured by multipling the SV X HR.

 

ESV è contractility and afterload.

 

EDV è cardiac compliance and preload (venous return).

 

5. HEART SOUNDS

Movement of heart structures in heart contraction produces heart sounds.

First heart sound occurs at beginning of systole, mainly due to closure of AV valves.

First heart sound or “lubb” – AV valves close and surrounding fluid vibrations at systole

Second heart sound occurs at the end of systole, mainly due to closure of semi lunar valves.

Second heart sound or “dupp”

Results from closure of aortic and pulmonary semilunar valves at  diastole, lasts longer

Third heart sound occurs at beginning of middle third diastole is produced by oscillation of blood back and forth between walls of ventricles initiated by inrushing blood from atria.

Fourth heart sound occurs when atria contracts.

First and second heart sounds can head by ear. Abnormal heart sounds are known as heart murmurs. Functional murmurs appear because of insufficient function of heart valves.

Auscultation of heart sounds

Use stethoscope for listen to heart sounds. Listen to I heart sound in V intercostal space through medioclavicular line and 1 cm medially from the left ventricle. Listen to I heart sound over the end of sternum bone – from the right ventricle. Listen to II heart sound over the pulmonary trunk in II intercostal space on the left side. Listen to II heart sound over aorta in II intercostal space on the right side. In performing auscultation compare appearance II and I heart sounds to apex push and pulsation of carotid arteries.

 

 

 

Congestive Heart Failure (CHF)

 

      Congestive heart failure (CHF) is caused by:

● Coronary atherosclerosis

● Persistent high blood pressure

● Multiple myocardial infarcts

● Dilated cardiomyopathy (DCM)

 

 

REGULATION OF THE HEART PUMPING

The activity of the heart is regulated by two centers present in the medulla oblongata.

1) Cardiac Inhibitory centre, which is connected with the vagus nerve i.e. parasympathetic nervous system: C.I.C. It is a part of the dorsal nucleus of vagus, the axons of their neurons leave the medulla as preganglionic fibers. They relay in terminal ganglia present in the heart.

2) Cardiac accelerator (activation) centre, which is connected with the sympathetic nervous system: CAC. It lies near the inhibitory center, the axon of their neurons descend in the white matter of the spinal cord and synapse in lateral horn cells (L.H.C) of upper 5 thoracic segment. Preganglionic fibers arise from L.H.C and relay in the three cervical sympathetic ganglia. Postganglionic fibers pass from these ganglia to supply the whole heart.

Nerve supply to the heart:

I. Parasympathetic innervation: (vagus nerve)

Preganglionic fibers of vagus arise from the neurons of C.I.C. They reach the heart as preganglionic fibers and relay in terminal ganglia present in the substance of the atrial muscle particularly the nodal tissues. Postganglionic fibers supply SA node, A-V node and main stem of A-V bundle (but not its branches),  atrial muscle, and coronary blood vessels. Vagus nerve does not supply the ventricles, branches of A-V bundle and Purkinje fibers.

Function of vagus nerve: (Parasympathetic supply to the heart)

1)       It inhibits all cardiac properties; contractility, rhythmicity, excitability, and conductivity.  

2)       Constriction of coronary blood vessels.

Vagus escape phenomenon: Stimulation of vagus slow HR, strong stimulation of vagus stops the heart completely. If the strong stimulus is maintained, the ventricles begin to beat by its own rhythm “Idio-ventricular rhythm” (25 – 40 / min). This phenomenon is called vagus escape. It means escape of the ventricle from the inhibitory effect of vagus. It is a proof that the vagus does not supply the ventricles.

Physiological significance of absent vagal supply to the ventricles:

In case of idio-ventricular rhythm, the ventricular rhythm is (25-40 beats/min) which is inadequate to maintain sufficient circulation. If vagus supplies the ventricle, it will further ” the rate which is not desirable.

Vagus tone: During rest vagus nerve continuously discharge inhibitory impulses to the heart to ” the high rhythm of  S-A node ( from 110-120 beat / min’ 70 beat/ min), this is called “Vagus tone”.

Mechanism of vagus tone:

It is a reflex mechanism in which the stimulus is the resting A.B.P. Receptors: baroreceptors or pressure receptors present in carotid sinus and Aortic arch. Afferents: through sinus nerve which is a branch of Glossopharyngeal nerve (IX.C) and Aortic nerve which is a branch of vagus nerve (X.C). Centre : C.I.C. Efferent: vagus nerve which ” the high rhythm of S-A node.

Proof: Cutting of both vagi in animal result in “ in HR. ( from 70 to 120). Stimulation of the cut end of vagus ’ ” in HR.

Vagus tone “ : In man more than women, in athletes more thaon athletes, and in adult more than children.

Physiological significance of vagus tone: Vagus tone ” HR from 120 – to 70 beat / min. This ” in HR will be a reserve to be used at times of need as in muscular exercise.

II. Sympathetic supply to the heart:

It begins at C.A.C in the medulla oblongata near C.I.C. The axons of their neuron descend in the white matter of the spinal cord, and relay at L.H.C of upper 5 thoracic segment. Preganglionic fibers of L.H.C pass in sympathetic chain and ascend upwards to relay in the three cervical sympathetic ganglia (superior, middle and inferior cervical sympathetic ganglia. Postganglionic fibers pass from the ganglia to the heart where they supply all the structures of the heart including the ventricles.

Function of sympathetic supply to the heart:

1- It increases all cardiac properties; contractility, rhythmicity, excitability, and conductivity.

2- Vasodilatation of coronary vessels.

Humoral regulation

a) Effects of catecholamynes are transmitted by alfa- and bita-adrenoreceptors.

Adrenalin and noradrenalin stimulate heat activity and cause positive regulatory effects:

– Positive inotropic effect – increasing strength of heart contractions;

– Positive chrono-tropic effect – increasing heartbeat rate;

– Positive dromo-tropic effect – increasing heart conductibility;

– Positive bathmo-tropic effect – increasing excitability of heart muscle.

Nor-epinephrine increases permeability of cardiac fiber membrane to Na⁺ and Ca²⁺.

 

b) Effects of acetylcholin leads to increase of K⁺ permeability through cell membrane in conductive system, which leads to hyper-polarisation and cause such effects to the heart activity:

– Negative inotropic effect – decreasing strength of heart contractions;

– Negative chrono-tropic effect – decreasing heartbeat rate;

-Negative dromo-tropic effect – decreasing heart conductibility;

– Negative bathmo-tropic effect – decreasing excitability of heart muscle.

c) Effects of ions:

VIDEO

(Effects of Ca²⁺ – ions)

-Ca²⁺ causes spastic contraction of heart. Decreasing Ca²⁺ causes cardiac flaccidity.

Excessive concentration of K⁺ causes decreasing heart rate. Impulse’ transmission through AV bundle is blocked. If K⁺ level was previously decreased, increasing Concentration of K⁺ capable normalize cardiac rhythm. Na⁺ competes Ca²⁺ in contractile process. So increasing Na⁺ may depress cardiac contraction.

d) Effects of thyroid hormones.

Thyroid hormones increase transmission process in ribosome and nucleus of cells. Intracellular enzymes are stimulated due to increasing protein synthesis. Also increases glucose absorption and uptake of glucose by cells, increases glycolisis and gluconeogenesis. In blood plasma increases contents of free fatty acids. All these effects of thyroid hormones lead to increase activity of mitochondria in heart cells and ATP formation in it. So, both activity of heart muscle and conduction of impulses are stimulated.

e) Effects of adrenocortical hormones.

Aldosterone causes increasing Na⁺ and Cl^– in blood and decreases K⁺. This is actually for producing action potential in the heart. Cortisol stimulates gluconeogenesis and increase blood glucose level. Amino acids blood level and free fatty acids concentration in blood increases also. Utilization of free fatty acids for energy increases. These mechanisms actual in stress reaction. So heart activity is stimulated.

f) Hormones of islets of Langerhans effects.

Insulin promotes facilitated diffusion of glucose into cells by activation glucokinase that phosphorilates glucose and traps it in the cell, promotes glucose utilization, causes active transport of amino acids into cells, promote translation of mRNA in ribosome to form new proteins. Also insulin promotes glucose utilization in cardiac muscle, because of utilization fatty acids for energy. Clucagone stimulate gluconeogenesis, mobilizes fatty acids from adipose tissue, promotes utilization free fatty acids foe energy and promotes gluconeogenesis from glycerol. So both hormones can increase strength of heartbeat.

g) Endocrine function of heart. Myocardium, especially in heart auricles capable to secretion of regulatory substances as atria Na-ureic peptide, which increases loss of Na⁺ in increase of systemic pressure, or digitalis-like substances, which can stimulate heart activity.

3. Mechanisms of heart auto regulation

a) Greater rate of metabolism or less blood flow causes decreasing O₂ supply and other nutrients. Therefore rate of formation vasodilator substances (CO₂, lactic acid, adenosine, histamine, K⁺ and H⁺) rises. When decreasing both blood flow and oxygen supply smooth muscle in precapillary sphincter dilate, and blood flow increases. Moderate increasing temperature increases contractile strength of heart. Prolonged increase of temperature exhausts metabolic system of heart and causes cardiac weakness. Anoxia increases heart rate. Moderate increase CO₂ stimulates heart rate. Greater increase CO₂ decreases heart rate.

b) Intrinsic regulation is performed in response changes of blood volume, flowing into the heart. It is known as Frank Starling low. Within physiological limits heart pumps all blood that comes to it without allowing excessive damming of blood in veins. Cardiac contraction is directly proportional to initial length of its fibers. In end-diastolic volume over 180 ml excessive stretching heart fibers occurs and strength of next cardiac contraction decreases.

 

 

 

c) Anrep’s low. Increase of blood flow in aorta and so coronary arteries leads to excessive stretching surrounding myocardial cells. According to Frank Starling low cardiac contraction is directly proportional to initial length of its fibers. So increase of coronary blood flow leads to stimulation heartbeat.

 

d) Boudichi phenomenon. In evaluation heart beat rate increase of every next heart contraction is observed. It caused by rising of Ca²⁺ influx into myocardial cells without perfect outflow, because of shortening of cardio cycle duration.