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* approximately the size of your fist * Location - Superior surface of diaphragm - Left of the midline - Anterior to the vertebral column - Posterior to the sternum |
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* a double walled sac around the heart composed of: - superficial fibrous pericardium - a deep 2 layer serous pericardium - the parietal layer lines the internal surface of the fibrous pericardium - visceral layer or epicardium lines the surface of the heart - they are separated by the fluid filled pericardial cavity |
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* Protects and anchors heart * prevents overfilling of the heart with blood * allows for the heart to work in a relatively friction-free environment |
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* Epicardium * myocardium * Fibrous skeleton of the heart * endocardium |
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visceral layer of the serous pericardium |
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cardiac muscle layer forming the bulk of the heart |
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Fibrous skeleton of the heart |
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crisscrossing interlacing layer of connective tissue |
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endothelial layer of the inner myocardial surface |
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* receiving chambers of the heart * pectinate muscles mark atrial walls * blood enters right atria from superior and inferior venae cavae * blood enters left atria from pulmonary veins |
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* discharging chambers of the heart * papillary muscles and trabeculae muscles mark vetricular walls * right ventricle pumps blood into the pulmonary trunk * left ventricle pumps blood into the aorta |
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Pathway of blood trough heart and lungs |
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* Right atrium > tricuspid valve > right ventricle * Right ventricle > Pulmonary valve > Pulmonary arteries > Lungs * Lungs > Pulmonary veins > Left atrium * Left atrium > bicuspid/matrovalve > Left ventricle * Left ventricle > Aortic valve > Aorta * Aorta > Systemic circulation |
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* Functional blood supply to the heart muscle itself * collateral routes ensure blood blood delivery to heart even if major vessels are occluded |
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* ensure unidirectional blood flow through the heart |
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Atrioventicular (AV) valve |
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* lie between the atria and the ventricles * prevent backflow into the atria when ventricles contract * chordae tendineae anchor AV valves to papillary muscles |
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prevent backflow of blood into ventricles |
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microscopic anatomy of heart muscle |
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* cardiac muscle is striated, short, fat, branched, and interconnected * intercalated discs anchor cardiac cells together and allow free passage of ions |
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cardiac muscle contraction |
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* stimulated by nerves and is self-excitable * contracts as a unit * has a long absolute refractory period |
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* Sinoatrial (SA) node generates impulses about 75 times a min * SA pace maker of the heart * Atrioventricular (AV) node delays the impulse approximately 0.1 second * impulse passes from atria to ventricles via the atrioventicular bundle |
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*AV bundle splits into 2 pathways in the interventricular septum *bundle branches carry the impulse toward the apex of the heart *purkinje fibers carry the impulse to the heart apex and ventricular walls |
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Extrinsic innervation of the heart |
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*Heart is stimulated by the sympathetic cardioacceleratory center *heart is inhibited by the parasympathetic cardioinhibitory center |
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*electrical activity is recorded by electrocardiogram (ECG) *P wave corresponds to depolarization *T wave corresponds to ventricular repolarization *Atrial repolarization record is masked by the larger QRS complex |
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Sinus Node SN > interatrial tracts > atrium > AV node > bundle of his > bundle branches > purkinje fibers > ventricle |
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congestive heart failure: def |
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Condition in which the pumping of the heart is depressed so that circulation is inadequate to meet tissue needs |
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CHF: right side of the heart failure |
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*Ineffective RV contractility *failure of RV pumping *decreased cardiac output to lungs *Blood backs up into RA + peripheral circulation |
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CHF: left sided heart failure |
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*Ineffective LV contractility *failure of LV pumping *decreased CO to the body *blood backs up into left atrium and lungs *pulmonary congestion, dyspnea, activity intolerance |
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normal beating of the heart |
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rate of more than 100 bpm |
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there is a pause in the rate in the AV node between P-R |
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some QRS complexes are missing |
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PVC: Premature Ventricular Contraction |
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irregular heart beat in which the ventricle contracts prematurely the wave is lower that zero |
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uncoordinated contraction of the cardiac muscle of the ventricles in the heart, making them tremble rather than contract properly |
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No cardiac electrical activity |
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no cardiac electric activity > death |
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*rapid and sometimes irregular heart beat *saw tooth appearance between QRS complexes |
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*The heart's atria quiver instead of beating effectively *Blood isn't pumped completely out of them, so it may pool and clot |
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*associated with closing of heart valves *first sound occurs as AV valves close > beginning of systole *second sound occurs when SL valves close at the beginning of ventricular diastole |
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*all events associated w/ blood flow through the heart |
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contraction of the heart muscle |
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relaxation of heart muscle |
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*ventricular filling > mid-to-late diastole |
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*heart blood pressure is low as blood enters atria and flows into ventricles *AV valves are open, then atrial systole occurs |
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*atria relax *rising ventricular pressure results in closing of AV valves *isovolumetric contraction phase *ventricular ejection phase opens semilunar valves |
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isovolumetric relaxation > early diastole |
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*ventricles relax *backflow of blood in aorta and pulmonary trunk closes semilunar valves |
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brief rise in aortic pressure caused by backflow of blood rebounding off semilunar valves |
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*amount of blood pumped by each ventricle in one min *it is the product of heart rate (HR) and stroke volume (SV) |
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amount of blood pumped out by a ventricle with each beat |
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is the difference between resting and maximal CO |
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factors affecting stroke volume |
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*amount ventricles are stretched by contained blood *Stretch |
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*back pressure exerted by blood in the large arteries leaving the heart *Resistance |
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Frank-Starling law of the heart |
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*Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume *Slow heartbeat and exercise increase venous return to the heart, increasing SV *Blood loss and extremely heart beat decrease SV |
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Extrinsic factors influencing SV |
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*Contractility is the increase in contractile strength,independent of stretch and End Diastolic Volume (EDV) |
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increase in contractility comes from: |
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-Increased sympathetic stimuli -certain hormones -Ca2+ and some drugs |
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-acidosis -increased extracellular K+ -Calcium channel blockers |
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-Positive chronotropic factors > increase heart rate -Negative chronotropic factors decrease heart rate |
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Regulation of heart rate: Autonomic Nervous System |
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-Sympathetic nervous system stimulation is activated by stress, anxiety, excitement, or evercise -Parasympathetic nervous system stimulation is mediated by acetylcholine and opposes the SNS -PNS dominates the autonomic stimulation, slowing heart rate and causing vagal tone |
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Atrial (Bainbridge) reflex |
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-sympathetic reflex initiated by increased blood in the atria -Causes stimulation of the SA node -Increased SNS stimulation |
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Chemical regulation of the heart |
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-hormones epinephrine and thyroxine increase hear rate -intra- and extracellular ion concentrations must be maintained fro normal heart function |
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Congestive Heart Failure CHF causes |
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-Coronary atherosclerosis -persistent high blood pressure -multiple myocardial infarcts -dilated cardiomyopathy DCM |
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