Transcript Cardiovascular System: The Heart

Cardiovascular System: The Heart
Chapter 18
Heart Anatomy w/Review
• Size of a fist
• In the mediastinum
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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
http://www.nku.edu/~dempseyd/HEART_1.htm
• REMEMBER: directions for specimen/model
NOT self
Atria of the Heart
• 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
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Ventricles of the Heart
• Discharge chambers
• Trabeculae carneae, folds of
muscle
• Papillary muscles
• Right (anterior) exit
– Pulmonary trunk
• Right and left pulmonary arteries
• Left (posterior) exit
– Aorta
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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
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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