Exam 2 Objectives PDF

**Structure and Function of the Cardiovascular and Lymphatics System** 1. Detail the anatomy of the heart, including the location of each chamber and surface within the mediastinum. Outline blood flow from the SVC and IVC to the aorta, including chambers, vessels, and valves. a....

**Structure and Function of the Cardiovascular and Lymphatics System** 1. Detail the anatomy of the heart, including the location of each chamber and surface within the mediastinum. Outline blood flow from the SVC and IVC to the aorta, including chambers, vessels, and valves. a. Anterior to descending aorta, esophagus, and major bronchi from **T5-T8** b. Shaped like a blunt cone roughly ⅔ size of clenched fist c. ⅔ to the left of midline d. Projects anterior, superior, and to left e. Heart surfaces i. Sternocostal (anterior): RV, with some LV and RA ii. Diaphragmatic (inferior): LV, with some RV iii. Base (posterior): LA, with some RA 2. State the location where each heart valve is best auscultated. f. **Aortic**: Second intercostal space, R sternal border g. **Pulmonary**: Second intercostal space, L sternal border h. **Mitral**: Apex or PMI; 5th intercostal space, midclavicular line i. **Tricuspid**: Right half of the lower end of the sternum 3. Discuss phases of the cardiac cycle and state which valves are open or closed in each phase. Correlate the waves of the ECG and CVP traces to the events of the cardiac cycle. j. Phases of the Cardiac Cycle iv. **Phase 1**: Atrial systole/ventricular diastole (fast and slow filling) v. **Phase 2**: Isovolumetric ventricular systole (passive); **all 4 valves closed** vi. **Phase 3**: Ventricular ejection (fast and slow ejection); **aortic and pulmonic valves open** vii. **Phase 4**: Isovolumetric ventricular relaxation (S2 heart sound); **aortic and pulmonic valves close** viii. **Phase 5**: Passive ventricular filling; **mitral and tricuspid valves open** k. **Ventricles** as pumps ix. Period of isovolumetric relaxation: **all 4 valves closed** x. Period of active filling 1. Rapid 2. Diastasis (slow filling) 3. Atrial systole (**AV valves open**) xi. Period of isovolumetric contraction: **AV valves close** xii. Period of active ejection (**Semilunar valves open**) 4. Rapid ejection (⅓) 5. Slowed ejection (⅔)  4. List normal cardiac pressures in each chamber. l. RA- Mean: 4 mmHg; range: 0-8 mmHg m. RVESP- Mean: 24 mmHg; range: 15-28 mmHg n. RVEDP- Mean: 4 mmHg; range: 0-8 mmHg o. LA- Mean: 7 mmHg; range: 4-12 mmHg p. LVESP- Mean: 130 mmHg; range: 90-140 mmHg q. LVEDP- Mean: 7 mmHg; range 4-12 mmHg 5. Discuss the layers of the heart wall from the fibrous pericardium to the endocardium. State the function of each layer. Differentiate between atrial, ventricular, and conduction muscle and state the property of each. Discuss how the muscle of the LV differs from that of the RV. r. **Fibrous Pericardium**: heavy connective tissue attached to diaphragm xiii. Fused to connective tissue of great vessels xiv. Protective membrane that prevents overdistension and protects the heart xv. Fibrous skeleton: 6. Surrounds heart valves 7. Annulus of each valve 8. Separates muscle mass of atria and ventricles s. **Serous Pericardium**: thin delicate sac that forms a double layer xvi. Parietal layer (under fibrous pericardium) xvii. Visceral layer (**epicardium**) xviii. Pericardial cavity 9. 10-50 ml fluid (normally 20 mL) 10. Reduces friction 11. Pericarditis and cardiac tamponade t. **Epicardium**: same as serous visceral layer u. **Myocardium** xix. Atrial (contractility) xx. Ventricular (contractility) xxi. Conductive (automaticity): SA node, AV node, Bundle of His, Purkinje fibers xxii. Atria and ventricles separated by fibrous skeleton xxiii. Atrial myocardium is relatively thin xxiv. Myocardium of the LV is 3 x as thick as RV, meaning the RV is more susceptible to ischemia/infarction 12. RV is crescent shaped and moves like a bellow 13. LV requires circumferential shortening to eject against a systemic pressure 4-5 times greater than pulmonary pressure 14. LV is able to maintain stroke volume despite large changes in MAP, but RV decompensates with mild increases in PAP xxv. **Endocardium**: connected to the myocardium by loose connective tissue, blood vessels, terminal conducting branches of nerves 15. Continuous with tunica intima of great vessels 16. Comprised of endothelium and subendothelium 17. Most susceptible to ischemia because the small vessels are exposed to highest pressures (opposes coronary perfusion) 18. Optimal aortic diastolic pressure are critical to perfusing smallest coronary vessels 6. List the common features of the AV valves and semilunar valves. v. **AV valves** xxvi. Cusps: endocardial folds around fibrous tissue xxvii. Annular rings attach to fibrous skeleton xxviii. Free edges attach to chordae tendineae → papillary muscle xxix. Prevents regurgitation from ventricles into atria xxx. Open and close in response to pressure gradients xxxi. Stenotic when less that 1 cm^2^ xxxii. **Tricuspid** 19. RA/RV 20. Anterior, septal, and inferior cusps 21. 7-10 cm ^2^ xxxiii. **Mitral** 22. LA/LV 23. Anterior and posterior leaflets 24. 2-6 cm^2^ w. **Semilunar Valves** xxxiv. **Pulmonary**: separates RV from main pulmonary artery 25. Right, left, and anterior cusps 26. 4 cm^2^ xxxv. **Aortic**: separates LV from ascending aorta 27. Right coronary, left coronary, and noncoronary cusps 28. 3-4 cm^2^ 29. Severe stenosis at \ PVCs) l. Parasympathetic Stimulation lxxxv. **Acetylcholine** 62. Decreases chronotropy (HR) 63. Decreases dromotropy (speed of contraction) 64. Decreases inotropy (force of contraction) 65. Coronary vasodilation lxxxvi. Stimulation from: 66. Chemical (ACH) 67. Strong emotions (vasovagal reflex) 68. Mechanical pressure g. Pressure and volume (valsalva, carotid massage, bainbridge, etc) m. Baroreceptor Reflex (pressure receptors) lxxxvii. Carotid 69. Afferent via **Glossopharyngeal (CN IX)** lxxxviii. Aortic 70. Afferent via **Vagus (CN X)** lxxxix. Both excite the Cardio Inhibitory Center xc. Major role in short-term regulation of BP n. Bainbridge Reflex xci. Sensitive to stretch due to increased volume in right atrium xcii. Opposite effect of carotid and aortic reflex xciii. Increasing stretch sends signals via Vagus nerve 71. Excite Cardio Accelatory Center 72. Inhibits Cardio Inhibitory Center xciv. Increases HR, force of contraction, etc so volume is expelled o. Valsalva Maneuver xcv. Forced expiration against a closed glottis 73. Increases intrathoracic pressure and CVP 74. Decreases venous return xcvi. When glottis opens, venous return increases and causes heart to respond by increased contraction and BP → increased PSNS activity and decreased HR 11. Differentiate between myocyte and nodal action potentials stating their location, ion causing contraction, phases, and correlation to the ECG.  p. Ventricular Myocyte (Fast) xcvii. Located in ventricle and atrial tissue xcviii. Mediated by Na xcix. Phase 0: rapid depolarization (Na in) 75. P wave for atria (PR 0.12-0.2) 76. QRS wave for ventricle (QRS 0.06-0.1) c. Phase 1: initial repolarization (K+ out, Cl- in) ci. Phase 2: plateau (Ca+ in, K+ out) cii. Phase 3: Rapid repolarization (K+ out, Ca+ in briefly) ciii. Phase 4: Resting membrane potential (Na out, remains steady d/t Na/K pump) q. SA Nodal (Slow) civ. Located in the SA or AV node cv. Mediated by Ca cvi. Phase 4: resting membrane potential spontaneously depolarizes (conduction to K slows while Na & Ca start to leak in) cvii. Phase 0: depolarization (Ca in) cviii. Phase 3: repolarization (K out) 12. Discuss the organization of cardiac muscle and detail the structure of a sarcomere, including the actin and myosin filaments. Describe the cross-bridging cycle and excitation contraction coupling. r. Skeletal muscle→ muscle fascicle/fasciculus→ muscle fiber (single muscle cell)→ myofibril→ actin (thin) and myosin (thick) filaments (sarcomere) s. Sarcomere- space b/w each Z-Disc, contain actin and myosin filaments and is the functional unit of contraction cix. I Band: light band extending from Z Disc w/ only Actin filaments 77. **Shortens** during contraction cx. A Band: dark band where actin and myosin overlap 78. **Remains constant** during muscle contraction cxi. H Band/Zone: light area in middle of A band surrounding M line (middle), contains only tails of thick Myosin filament (no heads) 79. **Shortens** during muscle contraction cxii. **A** band is **A**lways same length cxiii. **H** and **I** bands wave **HI** and go up and down cxiv. Myosin length never changes, the actin get pulled in to change the length t. Cross-bridging cycle cxv. Myosin head and arm together are cross-bridges, participate in contraction with actin 80. Troponin I, Troponin T and Tropomyosin on actin filament blocks binding site for myosin head 81. Calcium is released with nerve stimulus, binding to Troponin complex releasing it from actin allowing myosin to bind 82. ATP bound to myosin is hydrolyzed to ADP cocking the myosin head and triggering the power stroke rotating 45 degrees pulling the actin with it 83. If ATP binds again to myosin head, myosin will release the actin bind and return to the relaxed stage u. Excitation contraction coupling cxvi. To spread action potential, it needs to go through T-tubules to communicate with the terminal cisternae of the sarcoplasmic reticulum allowing for release of Ca within the entire muscle fiber cxvii. 2 types of Calcium channels 84. L-type (long) h. Blocked by calcium channel blocking drugs (verapamil, nifedipine, dilt) i. Reduces force of contraction 85. T-type (transient)  13. Define preload, afterload, contractility, and compliance and discuss the impact that each has on cardiac output and stroke volume. Define ejection fraction and list values that correlate with LV function. v. **Preload**: volume inside the ventricle at the end of diastole (LVEDV) cxviii. Determined by: 86. venous return to the ventricle 87. Blood left in the LV at the end of systole w. **Afterload**: Resistance to ejection during systole cxix. Aortic systolic pressure is the most common index of afterload for the LV 88. Decreased afterload = increased force of contraction 89. Increased afterload = decreased force of contraction and increased workload x. **Cardiac output**: HR x SV cxx. Normally 5 L/min in adults cxxi. Affected by preload, afterload, contractility, and heart rate y. **Stroke volume**: amount of blood ejected from the left ventricle during systole cxxii. LVEDV - LVESV cxxiii. Determined by preload, afterload, contractility, and compliance cxxiv. Alterations in nervous system control of ventricles cxxv. Adequacy of myocardial oxygen z. **Ejection fraction**: The fraction of the total volume of blood that is in the ventricle at the end of diastole (EDV) which is ejected during systole (SV) cxxvi. EDV - ESV/EDV cxxvii. 70-80%: **hyperdynamic** cxxviii. 52-72%: **normal** cxxix. 41-51%: **mild dysfunction** cxxx. 30-40%: **moderate dysfunction** cxxxi. \70 years of age; male \ 17. Outline the treatment of heart failure.  18. Discuss the neurohumoral changes associated with the failing heart. x. Increased catecholamines y. Increased angiotensin II, aldosterone z. Increased ADH a. Increased ANP, BNP b. Increased TNF-alpha, IL-6 **Alterations in Cardiovascular Function in Children (1 Question)** 1. **Outline fetal circulation including the role of the foramen ovale, ductus arteriosus, and ductus venosus.** a. **Foramen ovale:** opening between the atria b. **Ductus arteriosus**: joins the pulmonary artery to the aorta c. **Ductus venosus**: connects the inferior vena cava to the umbilical vein 2. **Discuss the changes that occur at birth and postnatal development of the circulation.** d. Receives blood-carrying oxygen and nutrients from the placenta through the umbilical vein e. Blood travels to the liver, where a portion enters the portal and hepatic circulation i. ½ of the flow is diverted away from the liver through the ductus venosus and into the IVC f. **Fetal circulation:** ii. Most of the blood bypasses the lungs by flowing through the ductus arteriosus and into the descending aorta iii. Blood from the descending aorta returns to the placenta through two umbilical arteries that branch from the internal iliac arteries g. **Transitional Circulation:** iv. With clamping of the umbilical cord, SVR increases dramatically and circulatory changes take place after birth v. Gas exchange shifts from the placenta to the lungs vi. Fetal shunts close (ductus venous, foramen ovale, and ductus arteriosus) h. **Postnatal Development and Circulation:** vii. Changes in position of the heart; changes in the size of the right ventricle viii. Decreased PVR, increased SVR -- helps the left ventricular myocardium to become thicker and more dominant, heart ranges from 100-180 bpm ix. Blood flow follows the same pathway as adults 3. **Categorize each congenital heart defect as primarily a lesion that increases pulmonary flow, decreases pulmonary flow, obstructs left or right outflow, or as a mixed lesion. -- do not need to memorize** i. **Prenatal, environmental, and genetic risk factors:** x. Maternal: Rubella, lupus, insulin-dependent diabetes, alcoholism, illicit drug use, age \40, PKU, hypercalcemia j. **Lesions increasing pulmonary blood flow** (defect that shunt from high pressure left side to low pressure right side with pulmonary congestion and cyanosis) xi. Patent ductus arteriosus (PDA) -- xii. Atrial septal defect -- dx by murmur xiii. Ventricular septal defect (VSD) xiv. Atrioventricular canal defect (AVC) k. **Lesions decreasing pulmonary blood flow** (generally complex with right-to-left shunt and cyanosis) xv. Tetralogy of Fallot (TOF) xvi. Tricuspid atresia l. **Obstructive lesions** (right or left-sided outflow tract obstruction that prohibit blood flow out of the heart; no shunting) xvii. Coarctation of the aorta xviii. Aortic stenosis xix. Pulmonary stenosis xx. Hypoplastic left heart syndrome m. **Mixed Lesions** (desaturated blood and saturated blood mix in the chambers or great arteries of the heart) xxi. Transposition of the great veins xxii. Total anomalous pulmonary venous connect (TAPVC) xxiii. Truncus arteriosus xxiv. Hypoplastic left heart syndrome (HLHS) 4. **Discuss Eisenmenger syndrome and list congenital defects that are associated with hypoxia and cyanosis.** n. **Eisenmenger syndrome** -- increased PVR that exceeds or equals vascular resistance, resulting in a reversal of shunting o. **Defects that cause hypoxemia and cyanosis:** xxv. Lesions that cause obstruction and shunting grom the right side of the heart to the left side of the heart, as in tetralogy of Fallot xxvi. Defects involving the mixing of saturated and unsaturated blood, as in the univentricular heart xxvii. Transposition of the great arteries 5. **List the 4 defects in Tetralogy of Fallot and outline the defects in hypoplastic left heart**. p. **Defects of TOF:** xxviii. Large VSD xxix. Overriding aorta straddles the VSD xxx. Pulmonary stenosis xxxi. Right ventricle hypertrophy xxxii. S/S: Cyanosis, hypoxia, clubbing, feeding difficulty, dyspnea, restlessness, squatting. Hypercyanotic spell or "test spell" that occurs with crying and exertion. q. **Hypoplastic left heart** xxxiii. Left sided cardiac structures develop anormally xxxiv. Obstruction to blood from the left ventricular outflow tract xxxv. Left ventricle, aorta, and aortic arch are underdeveloped; mitral atresia or stenosis is observed xxxvi. As the ductus closes, systemic perfusion is decreased, resulting in hypoxemia, acidosis, and shock