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78 Cards in this Set
- Front
- Back
Heart Anatomy |
Fist-sized; Enclosed in pericardium (doubled walled sac) |
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Superficial Fibrous Pericardium |
Protects, anchors, prevents overfilling |
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Deep 2-Layered Serous Pericardium |
Parietal layer lines internal surface of fibrous pericardium; Visceral layer (epicardium) on external surface of heart; Separated by fluid filled pericardial cavity (decreases friction |
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Epicardium |
Visceral layer of serous pericardium |
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Myocardium |
Main wall of heart; Spiral bundles of cardiac muscle cells; Fibrous skeleton of heart anchors cardiac muscle fibers, supports great vessels and valves, limits spread of action potentials to specific paths |
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Endocardium |
Continuous with endothelium
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Ventricles |
Two; Separated by interventricular septum; Anterior and posterior interventricular sulci mark position of septum externally |
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Atria |
Two; Separated internally by interatrial deptum; Coronary sulcus (atrioventricular groove) encircles junction of atria and ventricles; Auricles increase atrial volume |
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Blood Pathway through Heart |
Heart is 2 side-by-side pumps; Circuits are interconnected; Right ventricle is pump for pulmonary circuit; Left ventricle is pump for systemic circuit; Equal volumes of blood are pumped to both circuits |
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Pulmonary Circuit |
Vessels that carry blood to and from lungs, pumped by the right ventricle; Short, low-pressure circulation |
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Systemic Circuit |
Vessels that carry blood to and from all body tissues, pumped by left ventricle; Long pathways cause resistance, high pressure circuit; Left ventricle has more robust walls due to high pressure demands |
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Blood Flow |
RIght atrium to tricuspid valve to right ventricle; to pulmonary semilunar valve to pulmonary trunk to pulmonary arteries to lung; to pulmonary veins to left atrium; to bicuspid valve to left ventricle; to aortic semilunar valve to aorta; to systemic circulation |
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Coronary Circulation |
Function blood supply to heart muscle; Arterial supply varies considerably and contains many anastomoses (junctions) among branches; Collateral routes provide additional routes for blood deliveries |
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Atrioventricular (AV) Valves |
Prevent backflow into atria when ventricles contract; Tricuspid and mitral valve; Chordae tendineas anchor AV valve cusps to papillary muscles |
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Semilunar (SL) Valves |
Prevent backflow into the ventricles when atrias relax; Aortic and pulmonary semilunar valves |
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Cardiac Muscle |
Cells are striated, short, fat, branched, interconnected; Connective tissue matrix (endomysium) connects to fibrous skeleton; T tubules are wide but less numerous - SR is simpler than in skeletal muscle; Numerous large mitochondria (25-35% of cell vol.) |
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Intercalated Discs |
Junctions between cells anchor cardia cells |
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Desmosomes |
Prevent cells from separating during contraction |
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Gap Junctions |
Allow ions to pass, electrically couple adjacent cells |
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Cytoskeletal Cardiac Cell Bands |
Actin - thin filaments; Myosin - thick filaments |
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Cardiac Muscle Contraction |
Depolarization of heart is rhythmic and spontaneous; About 1& of cardiac cells have automaticity (are self-excitable); Gap junctions ensure heart contracts as a unit; Long absolute refractory period (250 ms) - promotes complete relaxation and opportunity for refilling of heart with blood |
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Depolarization |
Opens voltage gated fast Na+ channels in sarcolemma; Reversal of membrane potential form -90 mV to +30 mV; Depolarization wave causes Ca2+ surge which prolongs depolarization |
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Repolarization |
Ca2+ causes EC coupling as Ca2+ binds to toponin; sliding of filaments begins; Repolarization results from inactivation of Ca2 channels and opening of voltage gated K+ channels |
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Intrinsic Cardiac Conduction System |
Network of noncontractile (autorhythmic) cells that initiate and distribute impulses to coordinate depolarization and contraction of heart |
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Autorhythmic Cells |
Populate SA node; Have unstable resting potentials; At threshold, Ca2+ channels open; Ca2+ influx produces rising phase of action potential; Repolarization results from inactivation of Ca2+ channels and opening of voltage gated K+ channels |
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SInoatrial (SA) Node |
Pacemaker; Generates impulses about 75 times/minute (sinus rhythm) |
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Atrioventricular (AV) Node |
Smaller diameter fibers, fewer gap junctions; Delays impulses approximately .1 second; Depolarizes 50 times per minute in absence of SA node input |
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Atrioventriucular Bundle |
Only electrical connection between atria and ventricles |
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Right/Left Bundle Branches |
Two pathways in interventricular septum carry impulses toward apex of heart |
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Purkinje Fibers |
Complete pathway into apex and ventricular walls; AV bundle and Purkinje fibers depolarize only 30 times per minute in absence of AV node input |
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Heart Sequence of Excitation |
SA node to AV node to AV bundle to Right/Left bundle branches to Purkinje fibers |
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Extrinsic Innervation of Heart |
Heartbeat modified by ANS; Cardiac centers are located in medulla oblongata |
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Caridoacceleratory Center |
Innervates SA and AV nodes, heart muscle, and coronary arteries through sympathetic neurons |
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Cardioinhibitory Center |
Inhibits SA and Av nodes through parasympathetic fibers in vagus nerves |
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Electrocardiogram (EKG) |
Composite of all action potentials generated by nodal and contractile cells at a given time |
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P Wave |
Depolarization of SA node |
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QRS Complex |
Ventricular depolarization |
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T Wave |
Ventricular repolarization |
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Heart Sounds |
Two sounds (lub-dup) associated with clsing of heart valves; First sound occurs as AV valves close - signifies beginning of systole; Second sound occurs when SL valves close at beginning of ventricular diastole |
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Heart Murmurs |
Abnormal heart sounds most often indicative of valve problems; Leakage of blood in wrong direction - malformed during embryonic development or disease/mechanical trauma to valve |
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Cardiac Cycle |
All events associated with blood flow through the heart during one complete heartbeat |
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Systole |
Contraction |
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Diastole |
Relaxation |
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Mechanical Events of Cardiac Cycle |
1. Atrial systole and ventricular diastole to 2. Ventricular systole and atrial diastole to 3. Atrial/Ventricular diastole |
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(1) Atrial Systole with Ventricular Diastole |
AV valves open; 80% or more of blood passively flows into ventricles; Atrial systole occurs near end, delivering remaining 20% |
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End Diastolic Volume (EDV) |
Volume of blood in each ventricle immediately before starting ventricular systole, occurs at end of phase 1 of the cardiac mechanical cycle |
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(2) Ventricular Systole with Atrial Diastole |
Atria relax, ventricles begin to contract; Rising ventricular pressure results in closed AV valves; Isovolumetric contraction phase (all valves are closed); IN ejection phase, ventricular pressure exceeds pressure in large arteries, forcing SL valves open |
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End Systolic Volume (ESV) |
Volume of blood remaining in each ventricle at the end of phase 2 of the cardiac mechanical cycle |
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(3) Atrial and Ventricular Diastole |
Isovolumetric relaxation; Ventricles relax; Backflow of blood in aorta and pulmonary trunk closes SL valves and causes dicrotic notch (brief rise in aortic pressure) |
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Cardiac Output (CO) |
Volume of blood pumped by each ventricle in one minute; CO = HR (Heart Rate) x SV (Stroke Volume) |
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Heart Rate (HR) |
number of beats per minute |
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Stroke Volume (SV) |
Volume of blood pumped out by a ventricle with each beat |
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Cardiac Output Statistics |
At rest CO (ml/min) = HR (75 bpm) x SV (70 ml per beat), most adults use 5 to 6 L per circuit; Maximal CO is 4 to 5 times resting CO in nonathletes; Maximal CO may reach 35 L/min in athletes |
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Cardiac Reserve |
Difference between resting and maximal CO |
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Regulation of Stroke Volume |
SV = EDV - ESV; Main factors are preload, contractility, and afterload |
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Preload |
The degree to which cardiac muscle cells can stretch before the contract (Frank Starling law of the heart; Slow heartbeat and exercise increase venous return, which in turn stretches ventricles and increases contraction force |
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Contractility |
Contractile strength at a given muscle length, independent of muscle stretch and EDV |
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Positive Inotropic Agents of Contractility |
Increase contractility (epinephrine and norepinephrine or secondary hormone actions like thyroxine) |
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Negative Inotropic Agents |
Decrease contractility (Acidosis, increased extracellular K+, Calcium channel blockers - propanolol) |
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Afterload |
Pressure that must be overcome for ventricles to eject blood |
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Hypertension |
Increases afterload, resulting in increased ESV and reduced SV; Increases chronic workload of cardiac system; Promotes abnormal ventricular hypertrophy |
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Heart Rate Regulation |
Positive chronotropic factors increase heart rate, negative chronotropic factors decrease heat rate |
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Autonmic Nervous System Regulation |
Sympathetic nervous system activated by emotional/physical stressors; Norephinephrine causes pacemaker to fire more rapidly and increase contractility; Parasympathetic NS opposes sympathetic effects - acetylcholine hyperpolarizes pacemaker cells by opening K+ channels; Heart at rest exhibits vagal tone |
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Atrial (Bainbridge) Reflex |
Sympathetic reflex initiated by increased benous return; Stretch of atrial walls stimulates SA nodes and atrial stretch receptors activating sympathetic reflexes |
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Epinephrine |
Chemical from adrenal medulla that enhances heart rate and contractility |
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Thyroxine |
Increases heart rate and enhances effects of norepinephrine and epinephrine |
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Intra/Extracelluar Ion Concentration |
Ca2+ and K+ concentrations must be maintained for normal heart functions |
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Other Factors for Heart Rate |
Age; Gender; Exercise; Body Temp. |
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Arrhythmmias |
Irregular heart rhythms |
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Fibrilliation |
Rapid, irregular contractions -useless for pumping blood |
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Uncoordinated Atrial/Ventricular Contractions |
Result of defect in intrinsic conduction system |
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Defective SA Node |
Can result in ectopic focus - abnormal pacemaker takes over ; AV node take over - junctional rhythm |
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Defective AV Node |
Can result in heart block; Few or no impulses from SA node reach ventricles |
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Tachycardia |
Abnormall fast heart rate (more than 100 bpm) |
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Bradycardia |
Heart rate slower than 60 bpm - may result in inadequate blood circulation |
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Angina Pectoris |
Thoracic pain caused by fleeting deficiency in blood delivery to myocardium - cells are weakened |
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Myocardial Infarction (Heart Attack) |
Prolonged coronary blockage; Areas of cell death are repaired with noncontractile scar tissue |
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Congestive Heart Failure (CHF) |
Progressive condition where CO is so low that blood circulation is inadequate to meet tissue needs; Caused by coronary atherosclerosis, persistent high blood pressure, multiple myocardial infarcts, dilated cardiomyopathy (DCM) |