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Cardiovascular System: The Heart. Chapter 18. Heart Anatomy w/Review. Size of a fist In the mediastinum Obliquely situated ___?_____ to the diaphragm ___?_____ to the vertebral column ___?_____ to the sternum Lungs are ___?_____ and slightly obscure it - PowerPoint PPT Presentation
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Cardiovascular System: The Heart
Chapter 18
Heart Anatomy w/Review
• Size of a fist• In the mediastinum– Obliquely situated – ___?_____ to the diaphragm– ___?_____ to the vertebral column– ___?_____ to the sternum
• Lungs are ___?_____ and slightly obscure it
• Base is right and posterior, apex is point
Pericardium
• Serous membrane surrounding the heart• Protects, anchors, and prevents overfilling• Fibrous pericardium, collagen and elastic figure 8’s– Link all parts together while providing additional
support– Limits AP spread
• 2 layers– Parietal layer covers the _____?_____– Visceral layer (epicardium) covers the _____?___
• Pericardial cavity between w/ serous fluid
Heart Wall
• Epicardium (visceral pericardium)– Fatty layer
• Myocardium– Cardiac muscle
• Endocardium– Simple squamous epithelia– Continuous with blood vessels– Forms valves
www.faculty.ccri.edu
Chambers of the Heart
• 2 superior atria– Interatrial septum– Coronary sulcus
• 2 inferior ventricles – Interventricular septum– Anterior and posterior ventricular sulcus
• REMEMBER: directions for specimen/model NOT self
http://www.nku.edu/~dempseyd/HEART_1.htm
Atria of the Heart
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• Receiving chambers• Auricles to increase volume• Pectinate muscles internal, anterior
walls– Fossa ovalis: remnant of fetal opening
• Right entry (O2 poor from systemic)– Superior and inferior venae cavae– Coronary sinus
• Left entry (O2 rich from pulmonary)– Right and left pulmonary veins
Ventricles of the Heart
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• Discharge chambers• Trabeculae carneae, folds of
muscle• Papillary muscles• Right (anterior) exit– Pulmonary trunk• Right and left pulmonary arteries
• Left (posterior) exit– Aorta
Heart Valves
• Keep single directional blood flow• Open/close due to pressure not contraction• Atrioventricular valves (AV)– Right is tricuspid– Left is bicuspid or mitral– Anchored to papillary muscles by chordae tendineae ‘heart strings’
• Semilunar valves (SL)– Aortic– Pulmonary
Valve Function
• AV– Returning blood to atria exerts pressure = valves
open to ventricle– Ventricles contract = increase pressure = valves close– Chordae tendineae and papillary muscles prevent
inward flip• SL– Ventricles contract = increase pressure = valves open– Ventricles relax = blood flows back = close valves
Blood Flow Pathway Overview
Coronary Circulation• Arterial supply in coronary sulcus
– Right coronary splits• Marginal: lateral right myocardium• Posterior interventricular: heart apex and posterior ventricular walls (join for
right atria and ventricle)– Left coronary splits
• Circumflex: left atria and posterior wall of left ventricle• Anterior interventricular: interventricular septum and anterior ventricle walls
(join for right atria and ventricle)– Actually varies between individuals
• Venous supplies join in coronary sinus– Great cardiac in anterior interventricular sulcus– Middle cardiac in posterior interventricular sulcus– Small cardiac w/marginal artery
Cardiac Muscle Anatomy• Intercalated discs – Gap junctions: passage/exchange of ions– Desmosomes: stabilize and maintain structure
• Heart behaves as a single unit• Other characteristics (review)– Nuclei #?– Control?– Structure?
Cardiac Muscle Contraction
• Neural stimulation not needed = autorhythmicity– Can influence pace
• Whole organ (not just motor units) contracts– Signals carried through gap junctions
• Longer absolute refractory period – Regulates contraction rate– Prevents sustained contraction (tetanus)
• Lots of mitochondria– Greater dependence on O2
– Presence of fuel source more important than type
Autorhythmic Cells• Initiate action potentials in the heart• Due to pacemaker potential or unstable resting period
– Basic steps of an AP (review)– Changes
• Continuous depolarization to threshold (no flat line)• Ca 2+ channels open and Ca2+
rushes in• AP NOT triggered by Na+
• Found in specific locations– Sinoatrial and atrioventricular nodes– Right and left bundle branches– Ventricular walls (Pukinje fibers)
Beating to It’s Own Drum
• Sinoatrial (SA) node or ‘pacemaker’– Depolarization rate is fastest– Impulse ~75 times/min
• Atrioventricular (AV) node delays impulse
• Bundle of His electrically connects chambers
• Bundle branches to apex• Pukinje fibers to contractile fibers in
ventricles
Extrinsic Heart Control
• Cardiac centers in medulla• Cardioacceleratroy center– Sympathetic NS– Pre- from T1-T5 up– Post- through cardiac plexus to
SA and AV nodes & arteries• Cardioinhibitory center– Parasympathetic NS– Pre- from vagus to heart– Post- to SA and AV nodes
Electrocardiogram (ECG or EKG)• Records all electrical
autorhythmic cell activity• Distinguishable waves– P wave: SA node depolarizes
atria• Atria contracts• Drop from AV node delay
– QRS complex: ventricle depolarization• Ventricle contracts• Masks atrial repolarization
– T wave: ventricle repolarization
Heart Sounds
• ‘Lub’ when AV valves close– Ventricular systole (contraction)
begins– Bicuspid (mitral) before tricuspid
• ‘Dup’ when SL valves close– Ventricular diastole (relaxation)begins– Aortic before pulmonary
• Listen to 4 regions for differences
Cardiac Cycle
• Ventricular filling– Relaxed chambers creates low pressure allows passive blood flow in– Atria contract, ‘topping off’ ventricles = end diastolic volume (EDV)
• Ventricular systole (contraction)– Ventricles contract increasing pressure (isovolumetric contraction phase)– AV valves close and SL valves open
– End systolic volume (ESV) remains
• Early diastole– Ventricles relax decreasing pressure (isovolumetric relaxation phase)– SL valves close
Cardiac Output (CO)
• Amount of blood pumped by each ventricle– CO (ml/min) = HR (beats/min) x SV (ml/beat)• Stroke volume (SV) is amount of blood per ventricular
contraction
• Variable and increases with demand– Max CO – rest CO = cardiac reserve– Athletes have higher
Regulating Stroke Volume• SV = EDV – ESV
– EDV is amount of blood in ventricle during diastole– ESV is amount of blood in ventricle after systole
• Affecting factors– EDV by preload: degree of cardiac stretch pre-contraction in ventricles
• Slow HR increases volume of return• Exercise increases speed of return
– ESV by contractility: contractile force of cardiac cells• SNS innervation, Ca2+ entry, and hormones increase
– More blood leaves = decrease in ESV• Ca2+ blockers, increased extracellular K+ , and acidosis decrease
– ESV by afterload: pressure needed to eject blood• High BP more difficult to eject blood = increased ESV
Regulating Heart Rate
• ANS– SNS stimulates with stress, excitement, or exercise– PNS stimulates with ACh and opposes SNS
• Majority of autonomic stimuli; slows heart rate
• Chemical controls– Hormones: epinephrine, norepinephrine, and thyroxine
increase– Ions
• Other factors– Temperature– Age and exercise
Homeostatic Imbalances• Pericarditis: inflammation of pericardium roughens serous membrane• Cardiac tamponade: heart is compressed by fluid in pericardial cavity• Angina pectoris: deficient blood flow to myocardium• Myocardial infarction: prolonged coronary blockage; heart attack• Incompetent valves: valves fail to close allowing blood backflow• Stenosis: valves are stiff or obscure opening; heart must work harder• Ischemia: depriving tissue of oxygen• Arrhythmia: uncoordinated atrial/ventricular contractions• Fibrillation: rapid, out of phase contraction• Heart block: AV node damage; ventricles contract on own• Heart murmurs: blood swooshing; valves fail to close• Tachycardia: abnormally fast HR; stress, drugs, or temp cause• Bradycardia: abnormally slow HR; drugs, endurance training, or PNS