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Clinical Anatomy Tony Serino, Ph.D. .
Mediastinum Clinical Anatomy Tony Serino, Ph.D. .
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Mediastinum: Topic Objectives
Be able to identify and describe the contents of the three major divisions of the mediastinum. Be able to identify normal and pathological variations of the aortic arch and congenital heart defects. Be able to explain differences and similarities between adult and fetal blood flow, and list changes needed at birth. Be able to explain cardiac muscle cell depolarization and relate its significance to heart function. Be able to identify and describe all structures of heart anatomy and their function. Understand coronary circulation and its normal and some pathological variations. Be able to trace the flow of blood through the heart chambers and relate it to valve operation and heart sounds. Be able to identify and trace coronary electrical conduction and its relevance to EKG Be able to explain cardiac rate and force of contraction control Be able to calculate CO and SV Be able to predict effects on heart performance with changes in CO and SV, induced by changes in Starling forces, venous return, BP, and HR
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Mediastinum Superior Anterior Middle Posterior Superior and anterior are continuous with each other; both may be referred to as the superior mediastinum
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Superior Mediastinum Transverse thoracic plane
Aortic arch Great Vessels of the Heart
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Remnant of Ductus arteriosus
Ligamentum arteriosum
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Usual Aortic Arch Pattern
LC RC LS RS BT 65% of all people
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Aortic Arch Variations
left vert. a. 27% one BT with both CC exiting 5% 1.2% two BT
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SVC Vagus Phrenic BC BC SVC
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Pulmonary Arteries and Veins
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Trachea and Primary bronchi
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Structure Order Trachea BC PA Aorta
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Esophagus Function: Deglutition
Two sphincters: upper and lower esophageal sphincters (lower is physiological only) Retropleural position (therefore, covered by adventitia) Mucosa: stratified squamous with many mucus glands (esophageal glands) Muscularis: changes from skeletal to smooth muscle
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Bilobed organ that is largest in children, but begins to regress sharply at the onset of puberty (around age 11) It is the site of T-cell lymphocyte production and produces hormones (such as, thymosin) that modifies their physiology Thymus Gland
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General Circulatory System
Cardiovascular Consists of a closed system of vessels which transport blood Two circuits: Systemic and Pulmonary Arteries move blood away from the heart Veins move blood toward the heart
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Heart Development
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Fetal Circulation
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Selected Heart Defects
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Heart as a Dual Pump Cardiac muscle arranged as whorls that squeeze the blood Twin pumps: systemic and pulmonary Four chambers: 2 atria and 2 ventricles
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Cardiac Muscle Cells
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Cardiac Muscle Depolarization
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Heart: Location
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Heart in Relation to other Organs
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Layers of the Heart and Pericardium
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Heart: Anterior View Transverse Pericardial sinus
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Heart: Posterior View Oblique Pericardial sinus
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Heart: Internal Anatomy
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Differences in Ventricular Wall
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Most Common Coronary Arterial Pattern
Circumflex a. L. Marginal a. Ant. Desc. a. (LAD) Post. Desc. a. R. Marginal a. Fig. 1.51
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Coronary Variation Most people right dominant. 15% LCA dominant
(note: which branch gives rise to posterior descending a.determines dominance) Single CA Circumflex from right aortic sinus (4% have an accessory coronary artery)
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Fig b 12.66b.jpg Angiogram showing coronary blockage (arrow)
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Fig c 12.66c.jpg Angioplasty catheter
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Fig d 12.66d.jpg
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Coronary Veins Fig. 1.52 Ant. Cardiac veins Great Cardiac v.
Coronary sinus Small Cardiac v. Middle Cardiac v. Fig. 1.52
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Major Cardiac Valves
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Heart Valves cusps AV (tricuspid) sinus aortic valve (SL)
Nodule (corpara aranti)
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Heart Murmurs 12.22.jpg
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Diastole: Period of Ventricular Filling
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Systole: Isovolumetric Contraction
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Systole: Ventricular Ejection
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Diastole: Isovolumetric Relaxation
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Conduction System of Heart
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Pacemaker Potential
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ECG and electrical changes
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Normal ECG
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ECG Normal Sinus Rhythm Junctional Rhythm (AV node rhythm)
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Second Degree Heart Block
Ventricular Fibrillation (V-fib)
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Heart Sounds “Lub-dub”
Sound associated with valve closing producing turbulent blood flow
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(ml/min)
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Factors Affecting SV EDV affected by: ESV
Stroke Volume (SV) = End Diastolic Volume – End Systolic Volume (SV = EDV – ESV(ml/beat) ) In a healthy 70-kg man, EDV is approximately 120 mL and ESV is approximately 50 mL, giving a difference of 70 mL for the stroke volume. EDV affected by: Venous return which is dependent on venous tone, skeletal muscle pumps, etc. ESV As the heart fills it is stretched which allows for better overlap of the contractile proteins which will affect the force of contraction and the ESV (Starling’s Law of the Heart –increase preload (ventricular stretch) increases contraction force) Increasing the force of contraction at any EDV will decrease the ESV and increase the SV (sympathetic stimulation and epinephrine)
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Pericardial sac prevents over distension and loss of overlap; decrease performance of myocardium at high EDVs is due to disruption of fibers
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Sympathetic Stimulation
Leads to increase HR Increases in Ca++ release from SR, increase Ca++ through membrane and increase myosin crossbridge cycling Increases force of contraction
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Heart Rate Control Sinus Rhythm = normal SA node control
Autonomic Activity Sympathetic (thoracic trunk) = accelerator (induces tachycardia) Parasympathetic (vagus n.)= brake (induces bradycardia) Hormones epinephrine Drugs -caffeine, nicotine, atropine, etc.
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Cardiac Cycle
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Posterior Mediastinum
Azygous v. Thoracic duct Intercostal a., v., & n. Sympathetic trunk Trachea Vagus n. Thoracic aorta Lung root Phrenic n. Esophagus Hemiazygous v.
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Small Aortic Branches Coronary Bronchial a. Esophageal Intercostals
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Azygous vein Hemiazygous v.
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Nerves of Post. Mediastinum
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Thoracic Duct
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