UNIT 2 The Heart Part 2 of 2

Intrinsic and Extrinsic Control Electrocardiography Heart Sounds Cardiac Output Fetal Circulation Disorders of the Heart

(8th edition)

Intrinsic Conduction System of the Heart (fig. 18.14) - made up of modified cardiac muscle fibers (not neurons or nerves!); the heart can contract and beat independent of the nervous system; the nervous system only modifies the beat
SYNOATRIAL NOTE (SA Node) - the pacemaker; located in right atrial wall causes depolarization and contraction of the atria, and depolarization of the AV node ATRIOVENTRICULAR NODE (AV Node) - there is a slight delay at the AV node to allow the atria to contract completely before the ventricles contract; after the delay the BUNDLE OF HIS (AV BUNDLE) depolarizes within the atrioventricular septum BUNDLE BRANCHES (right and left) - carry the depolarization to the PURKINJE FIBERS in the right and left ventricles Purkinje Fibers - depolarize and contract the ventricles *An electrocardiogram (ECG or EKG) shows the electrical signals produced by the conduction system

(8th edition)

Extrinsic Innervation of the Heart (fig. 18.15)

The sympathetic and parasympathetic branches of the autonomic nervous system influence HEART RATE through antagonistic control Parasympathetic fibers from the vagus nerve release acetylcholine (ACh) which inhibits cardiac muscle of the heart; slows down the heart rate Sympathetic fibers from the sympathetic chain ganglia - release norepinephrine (NE) which excites cardiac muscle of the heart; speeds up the heart rate Thus, to decrease heart rate: the nervous system inhibits sympathetic neurons and stimulates parasympathetic neurons (analogous to taking your foot off the gas and applying the brakes) Thus, to increase heart rate: the nervous system inhibits parasympathetic neurons and stimulates sympathetic neurons (analogous to taking your foot off the brake and pushing the gas)

(8th edition)

Electrocardiography -- a lot of this section is not covered at the same level of detail in the textbook; please read carefully and know for the exam!
The Electrocardiogram (ECG or EKG) reflects the electrical activity of the heart An ECG is a recording of electrical activity of the heart made from electrodes placed on the surface of the skin the electrical signals are very weak by the time that they reach the level of the skin; peaks are measured in mV Einthovens triangle - a hypothetical triangle created around the heart when electrodes are placed on both arms and the left leg (see figure on this slide)

the three sides of the triangle represent three leads, or pairs of electrodes, used for recording you will record an ECG from lead 1 (across the chest) during your lab exercises in the BLC

(8th edition)

Electrocardiography -- a lot of this section is not covered at the same level of detail in the textbook; please read carefully and know for the exam!
 clinically, using 12 leads is most common: three limb electrodes plus nine electrodes placed on the chest and trunk each lead gives a different view of the threedimensional functioning heart when recording an ECG, one active surface electrode is the positive electrode, and the other active electrode is the negative electrode; the third electrode is inactive (ground) by convention, the net electrical current in the heart moves toward the positive electrode (from negative to positive, or from right arm toward left arm for lead 1), such that the tracing moves upward from the baseline

(8th edition)

Electrocardiography (fig. 18.16)

Waves, Segments, and Intervals of the ECG (from lead 1) (fig. 18.16) waves - appear as deflections above and below the baseline   P wave - corresponds to depolarization of the atria QRS complex - three waves representing the progressive wave of depolarization of the ventricles; note: the repolarization of the atria is obscured by this huge depolarization of the ventricles; thus, you cannot see the peak of the wave of atrial repolarization T wave - represents repolarization of the ventricles

segments - sections of baseline between waves   P-Q or P-R segment - measured from the end of the P wave to the beginning of the Q wave S-T segment - measured from the end of the S wave to the beginning of the T wave

intervals - combinations of waves and segments   P-Q or P-R interval - measured from the beginning of the P wave to the beginning of the Q wave; includes the P wave and P-Q or P-R segment Q-T interval - measured from the beginning of the Q wave to the end of the T wave; includes the QRS complex, S-T segment, and T wave

(8th edition)

Electrocardiography (fig. 18.17)

Because depolarization is the signal for contraction, the electrical events (waves) of an ECG can be associated approximately to contraction or relaxation of the atria and ventricles (fig. 18.17) mechanical events of the cardiac cycle lag slightly behind the electrical signals; thus, the contraction of the cardiac muscle comes just after the corresponding electrical signal atrial contraction begins during the latter part of the P wave, and continues during the P-R segment ventricular contraction begins just after the Q wave and continues through the T wave

(8th edition)

Interpretation of an ECG (fig. 18.18) - an ECG provides information on heart rate and rhythm, conduction velocity, and even the condition of tissues within the heart
questions to ask: What is the heart rate? Is it within the normal range of 60-100 beats per minute?   BRADYCARDIA = slower than normal heart rate TACHYCARDIA = faster than normal heart rate

Is the rhythm of the heartbeat regular or irregular? Are there regular intervals? ARRHYTHMIA = irregular rhythm:  ventricular fibrillation - rapid, random firing of electrical impulses in the ventricles (problem in the conduction system) atrial fibrillation - multiple waves of impulses randomly signal the AV node; signals ventricles to contract quickly and irregularly (problem in the conduction system -- the SA node has lost control of the pacemaking)

(8th edition)

Interpretation of an ECG (fig. 18.18) - an ECG provides information on heart rate and rhythm, conduction velocity, and even the condition of tissues within the heart
questions to ask: Are all normal waves present in recognizable form? Is there one QRS complex for each P wave?   if yes, is the P-Q or P-R segment constant in length? if no (there is more than one P wave for each QRS complex), it could signal HEART BLOCK; In heart block, action potentials from the SA node sometimes fail to be transmitted through the AV node to the ventricles; thus, one or more P waves may occur without initiating a QRS complex

(8th edition)

Heart Sounds - the 2 major heart sounds are caused by the closure of the valves; lubb -- dupp -- lubb -- dupp -- lubb -- dupp (fig. 18.20 shows the relationship between the heart sounds and closure of particular heart valves; it is also a good summary of the events during the cardiac cycle)
First Heart Sound (S1) - lubb; louder and longer than second heart sound; caused by the closure of the AV valves during systole Second Heart Sound (S2) - dupp; caused by the closure of the semilunar valves during diastole Heart Murmurs - abnormal heart sounds
 STENOSIS - constriction of the valve opening, causing a turbulent flow of blood; e.g. mitral stenosis or aortic stenosis REGURGITATION (=insufficiency) - leaky valve, causing some blood to flow backwards; e.g. mitral regurgitation or aortic regurgitation

(8th edition)

Cardiac Output, and Regulation of Stroke Volume and Heart Rate (and Blood Pressure)
Cardiac Output (CO) = Heart Rate (HR) X Stroke Volume (SV) Heart Rate = beats per minute Stroke Volume = mL per beat (ejected from each of the ventricles) Average CO: CO = 72 beats/min X 70 ml/beat CO = 5040 mL/min = approx. 5 L /min At rest the body pumps about 5 L, or the total volume of blood in the body During exercise, cardiac output may increase to 30-35 L/min *NOTE: an increase in EITHER stroke volume or heart rate will result in an increase in cardiac output (fig. 18.22)

(8th edition)

Cardiac Output, and Regulation of Stroke Volume and Heart Rate (and Blood Pressure)
Starlings Law and Stroke Volume - the more that cardiac muscle is stretched, the more forcefully it will contract; thus, as additional blood enters the heart, the heart contracts more forcefully, or more completely empties itself (higher stroke volume)  PRELOAD (end diastolic volume or EDV) - the degree to which the cardiac muscles in the ventricles are stretched just before they contract  VENOUS RETURN = the amount of blood returning to the heart, and thus stretching the ventricles; this is the most important factor causing stretching of cardiac muscle cells; an increase in venous return results in an increase in EDV, which causes a higher stroke volume, and thus a higher cardiac output (fig. 18.22)

(8th edition)

Cardiac Output, and Regulation of Stroke Volume and Heart Rate (and Blood Pressure)
BARORECEPTORS - stretch receptors are located in the carotid sinus and aorta (see figure below) when there is increased pressure to these receptors the cardioinhibitory center is stimulated and sends parasympathetic stimulation to the heart by way of the vagus nerve; this triggers the heart to slow down, thus decreasing blood pressure when there is decreased pressure to these receptors the cardioacceleratory center is stimulated and sends sympathetic stimulation to the heart; this triggers the heart to speed up, thus increasing blood pressure

(8th edition)

Cardiac Output, and Regulation of Stroke Volume and Heart Rate (and Blood Pressure)
Chemoreceptors - send the cardiac centers in the medulla oblongata of the brain information about O2 and CO2 levels in the blood; increased CO2 levels stimulate the cardioacceleratory center resulting in sympathetic stimulation to the heart and increased heart rate

(8th edition)

Fetal vs. Newborn (Adult) Circulation - the newborn and adult are essentially the same; I have included a good figure of fetal circulation below)
Very little blood is carried through the pulmonary circuit (to lungs) in the fetus; blood bypasses the lungs via the foramen ovale and ductus arteriosus in the fetus Blood bypasses the developing liver via the ductus venosus in the fetus Comparison of structures in the fetus and newborn (adult)  the ductus venosus (fetus) becomes the ligamentum venosum in the newborn (adult) the foramen ovale (fetus) becomes the fossa ovalis in the newborn (adult) the ductus arteriosus (fetus) becomes the ligamentum arteriosum in the newborn (adult)

(8th edition)

Fetal vs. Newborn (Adult) Circulation - the newborn and adult are essentially the same; I have included a good figure of fetal circulation below)
Very little blood is carried through the pulmonary circuit (to lungs) in the fetus; blood bypasses the lungs via the foramen ovale and ductus arteriosus in the fetus Blood bypasses the developing liver via the ductus venosus in the fetus Comparison of structures in the fetus and newborn (adult)  the ductus venosus (fetus) becomes the ligamentum venosum in the newborn (adult) the foramen ovale (fetus) becomes the fossa ovalis in the newborn (adult) the ductus arteriosus (fetus) becomes the ligamentum arteriosum in the newborn (adult)

(8th edition)

Other Disorders of the Heart

Coronary Artery Disease ATHEROSCLEROSIS fatty deposits in the arteries; hardening of the arteries ANGINA PECTORIS chest pain MYOCARDIAL INFARCTION blocked coronary artery; heart attack

Heart Failure - progressive weakening of the heart; the heart cannot meet the bodys demands for oxygenated blood CONGESTIVE HEART FAILURE heart enlarges and pumping efficiency declines

(8th edition)

This concludes the current lecture topic

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(8th edition)