CH 18 The Heart

BSC 216 Chapter 18: Heart Student Goals Students should be able to: Know the layers of the heart Fibrous pericardium- loosely fitting superficial part of the sac Serous pericardium- thin slippery two-layer serous membrane Parietal layer- lines the internal surface of the fibrous pericardium Visceral layer (epicardium)- covers the external heart surface Describe the pericardium The pericardium fibrous layer protects the heart, anchors it to the surrounding structures, and prevents overfilling of the heart with blood Know the anatomy of the heart (use picture from activity) Know the flow of blood through the heart Superior and inferior vena cava > right atrium > tricuspid valve > right ventricle > pulmonary semilunar valve > pulmonary artery > lungs > pulmonary veins > left atrium > Mitral (bicuspid) valve > left ventricle > aortic semilunar valve > aorta > rest of body Describe how the flow of blood of a fetal heart differs from the flow of blood in a newborn heart The fetal heart has a foramen ovale that connects the two atria and allows blood entering the heart to bypass the pulmonary circuit (fetal lungs are nonfunctional). The ductus arteriosus exists between the pulmonary trunk and the aorta which is another lung bypass. At birth (when the baby takes its first breath) the shunts close. Describe coronary circulation Arteries supply the heart with blood (right and left coronary arteries) Blood drains through the cardiac veins and the coronary sinus Know how cardiac muscle contraction differs from skeletal muscle contraction Some cardiac cells are self-excitable In skeletal muscle all cells of a given motor unit are stimulated and contract at the same time so impulses do not travel from cell to cell, the heart contracts as a unit or does not contract at all Skeletal muscle has a short refractory period, cardiac muscle has a long refractory period Know the sequence of cardiac excitation Sinoatrial node (right atrium, pacemaker) > atrioventricular node (interatrial septum) > atriventricular bundle (Bundle of His in the superior part of the interventricular septum) > Purkinje fibers (run through ventricular walls and supplies the papillary muscle) Describe how the ANS controls heart rate The sympathetic system increases rate and force of heart beat Parasympathetic system slows heart rate Cardiac centers are located in the medulla oblongata Describe how chemicals and hormones regulate heart rate Ephedrine is released by the adrenal medulla during sympathetic nervous system activation, produces cardiac effects as norepinephrine Thyroxine is released by the thyroid, increases metabolic rate and body heat, when released in large quantities it causes slower more sustained increase in heart rate than epinephrine, enhances the effect of epi and norepi Ions Reduced Ca++ depresses heart rate Increased Ca++ increases heart rate Increased K+ interferes with depolarization, lowers resting membrane potential, may lead to heart block and cardiac arrest Decreased K+ is life threatening because it will cause the heart to beat weakly Read an ECG P wave ? atrial depolarization QRS- ventricular depolarization T wave- ventricular repolarization PQ- time from beginning of atrial excitation to beginning of ventricular excitation QT- beginning of ventricular depolarization through ventricular repolarization QRS wave masks the repolarization of the atria Know the terms tachycardia, bradycardia Tachycardia- abnormally fast heartbeat, >100 beats per minute, promotes fibrillation so can be considered pathological. Results from elevated body temp, stress, certain drugs, heart disease Bradycardia- low heartbeat, <60 beats per minute, results from low body temp and certain drugs. Known to be a desirable consequence of endurance training. Resting rate may be lower but it provides the same cardiac output. Persistent bradycardia in poorly conditioned individuals may result in inadequate blood circulation to body tissues Describe congestive heart failure ? definition, conditions that cause congestive heart failure, difference between pulmonary congestion and peripheral congestion, treatment Weakening of the myocardium by various conditions Coronary atherosclerosis- blockage of coronary vessels with fatty build up, impairs blood and oxygen delivery to the cardiac cells, heart muscle becomes hypoxic, contractions are ineffective Persistent high BP- left ventricle exerts only slightly over 80mmHg to eject blood from the chamber. When aortic diastole blood pressure rises to 90mmHg, ventricle has to exert more force to open aortic semilunar valve and pump the same amount of blood. If this becomes chronic and systolic volume rises, the myocardium hypertrophies. Eventually the myocardium becomes progressively weaker Multiple myocardial infarct- succession of MIs depresses the pumping efficiency because the dead heart cells are replaced by scar tissue Dilated Cardiomyopathy (DCM)- ventricles stretch and become flabby, myocardium deteriorates. Thought to be due to alcohol, cocaine, chemotherapeutic agents, hyperthyroidism, inflammation of the heart due to infection. Heart attempts to work harder resulting in increasing levels of Ca++ in cardiac cells. Ca++ activates calcineurin which initiates a cascade of events leading to heart enlargement. Ventricle contraction is impaired, cardiac output is poor and the condition progressively worsens. Pulmonary Congestion- occurs if the left side of the heart fails. Right side propels blood to the lungs but the left side does not eject enough blood into the systemic circulation. Blood vessels in the lungs become engorged with blood and pressure increases. Fluid leaks into the lung tissue, this results in pulmonary edema and can lead to suffocation. Peripheral Congestion- blood stagnates in the body organs. Pooled fluids in tissue spaces impair the ability of body cells to obtain adequate amounts of nutrients and oxygen. Edema is noticeable in feet, fingers, and ankles. Failure of one side of the heart puts a greater strain on the other side of the heart. Ultimately the heart fails. Treatment- removing excess leaked fluids with diuretics, reducing overload with drugs that decrease blood pressure, conserving heart energy with digitalis derivatives (reduces heart rate). Understand fetal heart development; congenital heart defects Fetal heart begins as 2 endothelial tubes that fuse to form a single chamber. Day 23 heart starts beating. Day 25 the single heart tube forms 4 bulges. Sinus venosus- forms smooth part of right atrium, coronary sinus, SA node Atrium- forms pectinate muscles of the atria Ventricle- forms the left ventricle Bulbus Cordis- forms the pulmonary trunk, part of the aorta, and right ventricle Day 30 looping of the heart occurs. 2 shunts form to take blood away from the lungs (foramen ovale- becomes the fossa ovalis. Ductus arteriosus- becomes the ligamentum arteriosum. Both shunts close shortly after birth. Congenital heart defects Heart abnormalities are the most common birth defect Most defects are environmental- maternal infection or maternal exposure to drugs taken during the first 2 months of pregnancy 2 basic kinds of heart birth defects Mixing of oxygen poor systemic blood with oxygenated pulmonary blood; results in poorly oxygenated blood reaching the tissues; septal defects or patent ductus arteriosus Narrowed valves or vessels (stenosis); increases the workload of the heart