Chapter 17 The Cardiovascular system: The Heart
Objectives:
1. Describe the size and shape of the heart, and indicate its location and orientation in the thorax.
2. Name the coverings of the heart.
3. Describe the structure and function of each of the three layers of the heart wall.
4. Describe the structural and functional properties of cardiac muscle, and explain how it differs from skeletal muscle.
5. Briefly describe the events of cardiac muscle cell contraction.
- Name the components of the conduction system of the heart, and trace the conduction pathway.
7. Draw a diagram of a normal electrocardiogram tracing; name the individual waves and intervals, and indicate what each represents. Name some abnormalities that can be detected on an ECG tracing.
8. Describe the timing and events of the cardiac cycle.
9. Name and explain the effects of the various factors involved in regulating stroke volume and heart rate.
10. Explain the role of the autonomic nervous system in regulating cardiac output.
11. Describe fetal heart formation, and indicate how the fetal heart differs from the adult heart.
Location: in mediastinum (medial cavity of thorax) along w/ esophagus, trachea, great vessels and nerves. Apex points into left lung. See figure 17.1
Pericardium: protective sac around heart. Double layered
· Fibrous: protects, anchors, and prevents overfilling
· Serous: produces fluid that fills pericardial cavity for lubrication
Layers of Heart See figure 17.2
· Epicardium: also called the visceral/serous pericardium; outer layer of heart, infiltrated with fat.
· Myocardium: made of cardiac muscle. Makes up the fibrous skeleton of the heart
· Endocardium: simple squamous epithelium, lines chambers, covers valves.
Microscopic Anatomy See figure 17.11
· Intercalated discs and gap junctions for cell-cell communication
· Cylindrical cells, striated w/ single nucleus
· Branching fibers
Mechanism and events of contraction
· Means of stimulation: autorhythmicity, self excitable cells
· Organ vs. motor unit contraction
· Length of absolute refractory period: 250 ms. Prevents tetanic contractions.
Electrical events in contractile cells See figure 17.12
1. Na+ channels open very briefly and gates close quickly for initial depolarization
2. Ca2+ gates (slow Ca2+ channels) open to allow Ca2+ in from ECF to help open channels in SR.
3. Ca2+ prolongs depolarization (plateau). As long as Ca2+ enters cells, they continue to contract.
4. Tension develops during plateau and peaks just after. Contractile phase and action potential are longer in cardiac muscle to help eject blood from heart.
5. After 200 ms, Ca2+ gates close and K+ open for repolarization.
Energy requirements
· More mitochondria carry out aerobic respiration, uses glucose, fatty acids, lactic acid.
· GREATEST THREAT TO CARDIAC MUSCLE: LACK OF O2 NOT FUEL!!!!
· Ischemia: lack of blood supply and O2 starvation causes pH to drop (too many H+ ) that impairs ATP production to pump Ca2+ in ECF. Gap junctions close, cells are electrically isolated, and action potentials cannot connect to cells beyond ischemic areas.
Intrinsic conduction system: independent but coordinated activity of heart. See figure 17.13
· Noncontractile cardiac cells have an unstable resting potential that continuously depolarizes toward threshold.
· Gradually reduced membrane permeability to K+ and Na+ make membrane hypopolarized. Fast Ca2+ gates open and action potential occurs. Cells then initiate and distribute impulses through heart.
Sequence of Excitation See figure 17.14
1. SA (sinoatrial) Node: in upper right atrial wall. Typically generates 75 impulses/min. It is the heart’s pacemaker w/sinus rhythm.
2. Internodal tracts: depolarization wave spreads across and through via internodal tracts (through gap junctions) to AV node above tricuspid valve. Impulse is delayed 0.1 s @ AV node to allow atria to respond before ventricles contract.
3. AV bundle (Bundle of His): in inferior interatrial septum, then into right and left branches through interventricular septum.
4. Purkinje fibers: found in ventricular walls. Signals begin in apex and travels upward.
Arrhythmia: defects in intrinsic conduction system.
Fibrillation: rapid and irregular or out of phase contractions. Shocking is used to stop everything and allow SA node to start again.
Ectopic focus:
· Abnormal pacemaker may appear if SA node is defective.
· May appear even when SA node is functioning (too much nicotine or caffeine)
· Leads to extrasystole (premature contraction) and PVC’s (premature ventricular contractions) result.
Heart block: damage to AV node, interferes with the ability of the ventricles to receive pacing impulses. In total heart block, the ventricles beat at their intrinsic rate, which is too slow to maintain adequate circulation. In partial heart block, only some of the atrial impulses reach the ventricles.
Pacemakers are used to recouple the atria to the ventricles. The programmable devices speed up in response to increased physical activity like a normal heart.
Electrocardiography: deflection waves caused by electrical activity of cardiac muscle. See figure 17.16, 17.17, 17.18
1. P wave: lasts 0.08 s. SA node thru internodal tracts to atria (0.1 s later atria contract)
2. QRS complex: lasts 0.08 s. Ventricular depolarization just before ventricular contraction.
3. T wave: 0.16 s. Ventricular repolarization, lasts longer since repolarization is slower. Atrial repolarization is lost in the QRS complex.
4. P-Q interval: 0.16 s. From beginning of atrial excitation to beginning of ventricular excitation.
5. ST segment: entire ventricular myocardium is depolarized.
6. QT interval: 0.38 s. Beginning of ventricular depolarization to end of repolarization.
Heart sounds: associated with closing of heart valves. The first sound occurs as the AV valves close, when ventricular pressure rises above atrial pressure (the beginning of ventricular systole). The second heart sound is heard as the semilunar (SL) valves close, at the beginning of ventricular relaxation. See figure 17.19
Cardiac cycle: systole = contraction, diastole = relaxation See figure 17.20
1. Ventricular filling: mid to late diastole – 70% filling occurs here.
· AV valves open since pressure is higher in atria than in ventricles
· P wave occurs; atrial contraction begins
· Semilunar valves are closed
· At the end the AV valves begin drifting closed
· At end diastolic volume in ventricles
· Finally, atria relax and QRS wave occurs
2. Ventricular systole:
· Ventricular pressure increases due to ventricular contraction beginning
· AV valves are closed and produce the first heart sound
· Isovolumetric contraction phase begins (no blood leaves the heart)
· Semilunar valves are forced open
· The ventricular ejection phase begins and blood leaves the ventricles
3. Isovolumetric relaxation:
· Early diastole, ventricles relax
· T wave occurs
· End systolic volume is left in heart
· Ventricular pressure drops
· Semilunar valves close and produce the second heart sound
· Atria are filling and pressure is increasing.
Length of cardiac cycle
· About 0.8s
· Atrial systole = 0.1s
· Ventricular systole = 0.3s
· 0.4s is quiescent period or total relaxation
Cardiac output (CO): See Figure 17.23
· The amount of blood pumped out by each ventricle in one minute. HR x SV = CO (heart rate times stroke volume equals cardiac output.
Stroke volume:
· The volume of blood pumped out by a ventricle with each beat. It equals about 70 ml/beat.
· So, 75 bpm x 70 ml/beat = average adult CO (5.25 L/min or the entire blood supply pumped every minute)
· CO increases with either an increase in HR or SV or both.
Cardiac reserve:
· How much more blood we can pump with exertion.
· In nontrained individuals it is 4-5x CO (or 20-25 L/min)
· In athletes it is 7x CO (or 35 L/min)
Regulation of stroke volume:
· SV = EDV – ESV
· EDV or end diastolic volume is how much blood is in the ventricle after it is filled by the atrium and is approx. 120 ml.
· ESV or end systolic volume is how much blood is left in the ventricle after it contracts and the blood leaves the heart and is approx. 50 ml.
· So SV ends up about 70 ml. How do you change that?
Preload: See figure 17.21
· a measure of the degree of stretch of the heart muscle.
· Frank-Starling law of the heart says that the greater the stretch of cardiac muscle cells, the greater the force of contraction.
· The EDV increases this stretch and EDV increases with slow heart rate (more time to fill ventricles) or exercise (speeds up venous return).
· Stroke volume may double due to these factors
Contractility: See figure 17.22
· Slow calcium channels and greater calcium from SR allows more complete ejection of blood and a lower ESV.
· Contractility increases with an increase in sympathetic stimulation by epinephrine and an increase in calcium permeability of membrane
· Decreased contractility comes from acidosis (too many H+), increased K+, and calcium channel blockers
Afterload See figure 17.21b
· Pressure from blood on pulmonary and aortic semilunar valves may affect the amount of pressure that must be produced by the ventricles to eject blood.
· This is not a major determinant on stroke volume, but may have some effect on patients with hypertension because more blood remains within the heart.
· The result of afterload is an increased ESV and decreased SV
Autonomic Nervous System Regulation
1. Extrinsic innervation of heart: ANS modifies heart beat. Sympathetic division increases rate and force with NE. Parasympathetic division decreases rate with vagus nerve. (Intrinsic rate of heart is actually 25 bpm faster when vagus nerve is cut). See figure 17.15
2. Cardiac centers in the medulla:
1. Cardioacceleratory center: works with sympathetic division to increase HR and force
2. Cardioinhibitory center: works with parasympathetic division to decrease HR and force
Both centers act on the SA and AV nodes to regulate heart rate.
3. Norepinephrine: binds to beta-adrenergic receptors, threshold of cardiac muscle cells is reached more quickly and relaxation is accelerated, the pacemaker fires more rapidly and the heart beats faster. NE also allows enhanced Ca2+ entry into contractile cells for greater contractility. This lowers ESV, and even though heart rate is faster, SV doesn’t drop (like it would if only rate increased and decreased time for filling and decreased EDV).
4. ACh: the NT of the vagus nerve hyperpolarizes membranes of SA and AV node effector cells by opening K+ channels. Under resting conditions, both sympathetic and parasympathetic send signals, but the dominant signal is inhibitory. Vagal tone (through the vagus nerve) slows the heart rate to less than what it would be without it. If vagal tone is too great, the heart will experience vagal escape, where heart seems to ignore the stimulus to slow and returns to a normal rate.
5. Baroreceptors/Bainbridge reflex: sensory input generated by baroreceptors that respond to changes in systemic blood pressure result in the Bainbridge reflex. Increased venous return and blood congestion in atria stretch atrial walls. This in turn stimulates SA node and baroreceptors that trigger a reflex that increases sympathetic stimulation of the heart.
6. Chemical Regulation
a. hormones: epinephrine: enhances heart rate and contractility (like NE). Thyroxine, in large quantities, causes a slower but more sustained increase in heart rate.
b. ions: Hypocalcemia (low calcium) depresses the heart. Hypercalcemia (high calcium) prolongs the plateau phase of the action potential to dramatically increase heart irritability, which can lead to spastic heart contractions that permit the heart little rest. Hypernatremia (high sodium) inhibits transport of calcium into cardiac cells, thus blocking heart contraction. Hyperkalemia (high potassium) interferes with depolarization by lowering resting potential and may lead to heart block and cardiac arrest. Hypokalemia causes a feeble and arrhythmic heart beat.
Tachycardia: abnormally fast HR due to increased body temperature, stress, drugs, heart disease
Bradycardia: slower than 60 bpm; due to decreased body temperature, drugs, parasympathetic stimulation, or endurance-type athletic training.
Congestive heart failure: CO of heart is so low that blood circulation is inadequate to meet tissue needs. It is usually a worsening condition; weakening of myocardium (due to atherosclerosis), high blood pressure, multiple MI’s. The coronary arteries are susceptible to atherosclerosis because the blood entering them is the most oxygenated and nutrient-rich (full of fat!). The coronary arteries also branch very quickly and often, and in the bifurcations the plaques build up.
Dilated cardiomyopathy: ventricles stretch and become flabby, myocardium deteriorates; see:
http://www.americanheart.org/presenter.jhtml?identifier=4468
Left side failure: pulmonary congestion. Blood vessels in lungs become engorged, pressure increases, fluid leaks, edema results.
Right side failure: peripheral congestion. Blood stagnates in body organs. Tissues cannot rid themselves of wastes, and don’t receive nutrients and oxygen. Edema is most noticeable in extremities.
Heart Murmur: blood flowing back into atria during ventricular systole due to leaky atrioventricular valves (bicuspid and tricuspid). Semilunar valves rarely have murmurs. Can result in atrial congestion.