+0
Karma
| Class: | BIOL 2510 - HUMAN ANATOMY AND PHYSIOLOGY II |
| Subject: | Biology |
| University: | Auburn University - Main Campus |
| Term: | Summer 2010 |
INCORRECT
CORRECT

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General Characteristics of blood
|
1.class as a type of connective tissue 2.travels via bld vessels 3.helps maintain homeostasis |
|
Homeostasis (blood)
|
1. bld is a transport mechanism 2. regulate pH (7.35-7.45) 3.helps maintain body temperature (ex.vasodialation) 4. protection -bld contains cells and chemicals of the immune system. 5. clotting formation- bld contains clotting cells and chemicals that prevent excess bld loss. |
|
Composition of blood
(plasma)
|
Liquid portion of blood - 91% H20 and other remaining 9% is plasma proteins. |
|
Plasma Protein
(Albumin)
|
*58% of plasma proteins *regulates the movement of water between tissues spaces and bld vessels by contributing to Plasma Colloid Osmotic Pressure. |
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Plasma Protein
(globulin)
|
*38% of Plasma protein *some act as antibodies -formed in response to antigens(any foreign substance) *some bind to other substances and act as transport molecules |
|
Plasma Protein
(fibrinogen)
|
*4% of plasma protein *contributes to formation of blood clots |
|
Composition of blood
(formed elements)
|
formed elements ( bld cells and platelets) |
|
Hemopoiesis
|
production of formed elements |
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Hemopoeisis
(in embryo/fetus)
|
Takes place in -yolk sac -liver -spleen -lymph nodes -red bone marrow (in almost all forming bone tissue) |
|
Hemopoeisis
(neonatal)
|
takes place in -spleen -lymph nodes -red bone marrow (in almost all bone tissue) |
|
Hemopoeisis
(adults)
|
takes place in -red marrow (only) =sternum =vertebrae =pelvis =proximal end of femur/humerus |
|
Bld cell precusors
|
1.pro-erythrocyte >erythrocyte RBC 2.myeloblasts > basophil WBC 3. >eosinophil WBC 4. > neutrophil WBC 5. lymphoblasts> lymphocyte WBC (BorT) 6. monoblasts > monocyte WBC 7. mega-Karoycyte> platelets (break up product not true cell type |
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Formed Elements
|
RBC- erythrocytes biconcave disks at maturity - no cellular organelles |
|
RBC
|
*main component is Hemoglobin= transports gas and gives red color * other components include lipids , ATP and enzyme Carbonic Anydrase |
|
Fxn of RBC
|
*Transport O2 from lungs > tissues *transport CO2 from tissue>lungs |
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Hemoglobin
|
*protein *made of 4 polypeptide chains("globin") -2 alpha subunits -2 beta subunits =4 heme contain 1 Fe atom each |
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Life history of RBC
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Production=erythropoiesis -stimulated by low plasma O2 levels -regulated by hormone from kidney called erythropoietin -Immature RBC is called reticulocyte |
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Breakdown of Hemoglobin from lysed
RBCs
|
- remanants get trapped in liver and spleen =macrophages enzymatically seperate the 'heme' and 'globin' |
|
globin
|
is broke down into amino acid and they will be used in production for new proteins. -Fe portion of heme is transported to red bone marrow to be recycled into new Hb molecules |
|
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Definition |
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'heme'
|
-pigments of the heme converted into bilirubin, which becomes part of bile secreted by the liver during digestion. |
|
WBC
|
(leukocytes) - have longer life than RBC -lack hemoglobin but have all other cellular organelles |
|
WBC fxn
|
fxn is to protect against invading microorganisms- remove dead cells and debris from circulation |
|
Wbc housed in?
|
lymphatic until infection occurs-released general circulation when needed. |
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Neutrophil
|
=most common WBC =nucleus multi lobed =cytoplasmic granules 'stain purple' with acidic or basic dye =>secrete antibodies lysozyme & defensins ==>fxn in phagocytosis |
|
phagocytosis
|
to engulf solid particles |
|
Eosinophils
|
=1-4% =nucleus is bi-lobed =cytoplasmic granules will stain red/orange w / eosin dye =>secrete toxic chemical specific for parasitic worm infection => secrete chemicals that reduce the severity of an allergic rxn |
|
Basophil
|
=rarest 1/2% =nucleus has to indistinct lobes (not same size) =granules will stain blue with basic dye =>contain histamine,which facilitate an allergic rxn/immune response =>contain heparin, an anti-coagulation(blood thinner) |
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Lymphocyte
|
2nd most common,smallest =large dark nucleus =2x size of RBC *** no granules =play large role in immunity =>B cells- when stimulated by bacteria and toxins they differentiate into plasma cells ==> plasma cells then secret antibodies specific for microorganism => Tcells directly attack virus infected or tumor cells |
|
Monocytes
|
4-8%,largest =distinct kidney shaped nucleus *** no granules =differentiate into macrophages which aid in phagocytosis |
|
Life History of WBC
|
production is called=leukopiesis -takes place in Red bone marrow |
|
Platelets
|
(thrombocytes) structure-cell fragments derived from the breakup of MegaKarocytes -surface has stick glycoproteins,causes them to stick to each other -cytoplasmic granules contain chemicals that facilitate clotting |
Koofers.com
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Hemostasis
|
stopping flow of blood,occurs in 3 phases |
|
1st hemostasis
(vascular spasm)
|
-immediate but temporary closure of damaged B.V. to decrease Blood flow =due to reflexive contraction of smooth muscle w/in vessel wall -triggered by direct injury to vessel =injury causes release of endothelin from endothelial cells. -also be triggered by nervous system local pain receptors are stimulated |
|
2nd hemostasis
(Platelet plug formation)
|
accumulation of platelets at injury site, occurs in 3 steps 1.platelet adhesion 2.platelet release rxn 3.platelet aggregation ***explained in following note cards |
|
Step 1 Platelet plug formation
(platelet adhesion)
|
->injured endothelial cells produce the protein VON Willebrand factor =>adheres the platelets to collagen in B.V. that has been exposed due to injury,uninjured B.V. collagen not exposed |
Koofers.com
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Step 2 Platelet plug formation
(Platelet release rxn)
|
->when platelets bind to collagen , become activated and release chemicals from cytoplasmic granules(not endothel) =>ADP & Thromboxane A2 which recruit more platelets to injury site |
|
Step 3 Platelet plug formation
(Platelet aggregation)
|
->the plasma protein fibrinogen diffuses into area and facilitates binding of platelets together -> PGI2(prostaglandin)-released from damaged endothelial cells limits the aggregation to only the injury area. |
|
3rd Hemostasis
(coagulation)
|
dependent on clotting factors/chemicals in bld. Prothrombin----prothrom activator---> Thrombin fibrinogen----thrombin(activates)--->fibrin |
|
Prothrombin
|
plasma protein made in liver -always around but not active |
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prothrombin activator
|
released by damaged endothelial cells |
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Fibrinogen
|
inactive but always around |
|
fibrin
|
glue that binds platelets |
|
Hemostasis
(Fibrinolysis)
|
endothelial cells around clot released a protein called Tissue Plasminogen Activator Plasminogen----TPA----> plasmin =plasmin hydrolyzes fibrin holding clot together(dissolves) |
Koofers.com
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THE HEART
|
location-thoracic cavity btw lungs -2/3s of the hearts mass is lft of sternum |
|
mediastinum
|
midline partition formed by the heart,trachea, and esophagus |
|
FXNs of HEART
|
-generates Blood pressure(BP) needed to propel bld through B.V. -separates pulmonary circulation(R) from systemic circulation(L) -can change rate and force depending on metabolic needs of tissue |
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Anatomy OF Heart
(pericardial sac)
|
dbl layered closed sac surrounding heart -outermost layer in fibrous pericardium -serous pericardium |
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Fibrous pericardium
|
outermost -tough fibrous connective tissue ,to prevent over distension of the heart and anchor heart w/in mediastinum |
|
Serous pericardium
|
simple squamous epithelium -two layers =perietal pericardium-contact with heart cavity walls =visceral pericardium-covers surface of heart |
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Heart walls
|
3 layers of tissue - epicardium-outer -myocardium-middle layer,thick cardiac muscle cells -endocardium-innermost |
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Heart Chambers
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2 atria and 2 ventricles -tissue separating left atrium from rt atrium is interatrial septum -tissue separating ventricles is interventricular septum |
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Atria
|
auricles on outer heart surface of atria -allows for atria to increase filling capacity -inner post wall is smooth -inner anterior wall is ridged formed of pectinate muscles |
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Atria
|
'receiving chambers' rt. atrium receives de-oxygenated bld from 3veins: =superior vena cavae =inferior vena cavae =coronary sinus |
|
fossa ovalis
|
on the rt. side of the inter atrial septum is a slight oval depression |
|
left atrium
|
receives oxygenated bld from lungs via 4 pulmonary veins |
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Ventricles
|
'distributing chambers' ***know flow |
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Atrioventricular valve
|
-allow bld flow from atria into ventricles -prevents bld from going back into atria b/c (closed) when ventricles contract. ** Tricuspid valve- on rt. side ** Bicuspid valve -on lft. side |
|
Semilunar valves
|
prevent retro grade of bld allow bld to flow from ventricles to aorta and pulmonary trunk. open when ventricles contract. -but valves prevent bld from flowing back into ventricles close when ventricles relax ** pulmonary semilunar valve-btw rt. ventricle and pulmonary trunk ** Aortic semilunar valve- btw left ventricle and aorta |
|
Histology of the HEART
|
-Cardiac muscle is striated muscle with sarcomeres made of actin and myosin |
Koofers.com
|
Intercalated discs
|
cells are electrically coupled by cellular adhesions -areas of low electrical resistance that allow ions to flow quickly from cell to cell =the depolarization current can freely travel over the heart |
|
Cardiac muscle physiology
|
cellular components -contractile cells -conductile cells |
|
contractile cells
|
muscle cells responsible for the actual contraction (ie) muscles that have actin and myosin -makeup 99% of all cardiac cells |
|
conductile cells
|
-self excitable cells that generate their own action potential =** these APs then initiate APs in the contractile cells |
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|
Sinoatrial node
|
- located superiorly in the rt. atrial wall -called heart pacemaker b/c it depolarizes the fastest and starts the sequence of excitation |
|
Internodal pathway
|
connection btwn SA & AV node |
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Atrioventricular node
|
located in the inferior portion of interartrial septum =depolarization is delayed here to give atria time to fully contract and empty blood into ventricles before ventricles are stimulated to contract |
|
Bundle of HIS/AV bundles
|
divides into LF & RT bundle branches at interventricular septum |
Koofers.com
|
PUrkinje Fibers
|
- penetrate heart at apex then wind superiorly toward the base -causes ventricles to contract upwards |
|
EKG
|
displays a summation of all APs traveling through heart at given time. -represents electrical events which are responsible for the mechanical events of systole and diastole |
|
heart sounds
|
1st -"LUBB" -AV valves closing at he start of ventricular systole 2nd -"DUPP"-SL valves closing at the start of ventricular diastole |
|
Tachycardia
|
-increased heart rate -100-250 BPM |
Koofers.com
|
Bradycardia
|
-decreased heart rate -less than 60 BPM |
|
Arythmias
|
change in sequence of excitation |
|
SA nodal block
|
-missing P wave -normal QRS and T wave -lowered heart rate, b/c the AV node is now the pace maker |
|
AV nodal block
|
-blockage of AP through the bundle of HIS -ventricles DO NOT receive all atrial impulses -normal time btw the end of the P wave and the beginning of the QRS is ~ .16 sec ** need to know know 1st degree, 2nd degree, and 3rd degree |
Koofers.com
|
Ventricular fibrillation
|
( V-fib) -very rapid , highly uncoordinated heart contractions -some areas of the ventricles may be contracting while others are relaxing -ventricles are never completely full nor completely empty -results in severe decreases in blood delivery to lungs and tissues; can be fatal in minutes |
|
Cardiac Output
|
CO=the amount of blood pumped by the heart per min -calculated using heart rate and stroke volume = the amount of blood pumped by the heart per beat |
|
Regulation of heart(intrinsic)
|
within the heart -the more the ventricular muscle stretched, the more forceful the next contraction will be -venous return=amt of bld entering the rt atrium via vena cavae -increases stroke volume -increased bld to heart ,the more that will be pumped out (increase in venous return=increased SV=increase in CO) |
|
Extrinsic
|
neural regulation by the autonomic nervous system -vagal center -vasomotor center |
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|
Vagal center
|
-medulla oblongata -parasymp control -rest and relaxation;decreases heart rate |
|
vasomotor center
|
medulla oblongata -sympathetic control -fight or flight; increased HR |
|
Beta Blocker
|
block receptors in the heart to slow down HR |
|
Blood Vessels
|
closed delivery system that begins and ends at the heart |
Koofers.com
|
Tunica Intima
|
innermost layer of endothel cells comes indirect contact with blood |
|
Tunica Media
|
Middle layer composed of smooth muscle and innervated by sympathetic nervous system -vasodilation and constriction |
|
Tunica Adventitia
|
outermost layer that anchors vessels to surrounding structures |
|
Arterial system
|
transport O2 bld from hrt to tissue -Elastic/conducting arteries -muscular/distributing arteries -arterioles |
Koofers.com
|
|
Definition |
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Front |
Back |
|
|---|---|---|
| General Characteristics of blood | 1.class as a type of connective tissue 2.travels via bld vessels 3.helps maintain homeostasis | |
| Homeostasis (blood) | 1. bld is a transport mechanism 2. regulate pH (7.35-7.45) 3.helps maintain body temperature (ex.vasodialation) 4. protection -bld contains cells and chemicals of the immune system. 5. clotting formation- bld contains clotting cells and chemicals that prevent excess bld loss. | |
| Composition of blood (plasma) | Liquid portion of blood - 91% H20 and other remaining 9% is plasma proteins. | |
| Plasma Protein (Albumin) | *58% of plasma proteins *regulates the movement of water between tissues spaces and bld vessels by contributing to Plasma Colloid Osmotic Pressure. | |
| Plasma Protein (globulin) | *38% of Plasma protein *some act as antibodies -formed in response to antigens(any foreign substance) *some bind to other substances and act as transport molecules | |
| Plasma Protein (fibrinogen) | *4% of plasma protein *contributes to formation of blood clots | |
| Composition of blood (formed elements) | formed elements ( bld cells and platelets) | |
| Hemopoiesis | production of formed elements | |
| Hemopoeisis (in embryo/fetus) | Takes place in -yolk sac -liver -spleen -lymph nodes -red bone marrow (in almost all forming bone tissue) | |
| Hemopoeisis (neonatal) | takes place in -spleen -lymph nodes -red bone marrow (in almost all bone tissue) | |
| Hemopoeisis (adults) | takes place in -red marrow (only) =sternum =vertebrae =pelvis =proximal end of femur/humerus | |
| Bld cell precusors | 1.pro-erythrocyte >erythrocyte RBC 2.myeloblasts > basophil WBC 3. >eosinophil WBC 4. > neutrophil WBC 5. lymphoblasts> lymphocyte WBC (BorT) 6. monoblasts > monocyte WBC 7. mega-Karoycyte> platelets (break up product not true cell type | |
| Formed Elements | RBC- erythrocytes biconcave disks at maturity - no cellular organelles | |
| RBC | *main component is Hemoglobin= transports gas and gives red color * other components include lipids , ATP and enzyme Carbonic Anydrase | |
| Fxn of RBC | *Transport O2 from lungs > tissues *transport CO2 from tissue>lungs | |
| Hemoglobin | *protein *made of 4 polypeptide chains("globin") -2 alpha subunits -2 beta subunits =4 heme contain 1 Fe atom each | |
| Life history of RBC | Production=erythropoiesis -stimulated by low plasma O2 levels -regulated by hormone from kidney called erythropoietin -Immature RBC is called reticulocyte | |
| Breakdown of Hemoglobin from lysed RBCs | - remanants get trapped in liver and spleen =macrophages enzymatically seperate the 'heme' and 'globin' | |
| globin | is broke down into amino acid and they will be used in production for new proteins. -Fe portion of heme is transported to red bone marrow to be recycled into new Hb molecules | |
| Definition | ||
| 'heme' | -pigments of the heme converted into bilirubin, which becomes part of bile secreted by the liver during digestion. | |
| WBC | (leukocytes) - have longer life than RBC -lack hemoglobin but have all other cellular organelles | |
| WBC fxn | fxn is to protect against invading microorganisms- remove dead cells and debris from circulation | |
| Wbc housed in? | lymphatic until infection occurs-released general circulation when needed. | |
| Neutrophil | =most common WBC =nucleus multi lobed =cytoplasmic granules 'stain purple' with acidic or basic dye =>secrete antibodies lysozyme & defensins ==>fxn in phagocytosis | |
| phagocytosis | to engulf solid particles | |
| Eosinophils | =1-4% =nucleus is bi-lobed =cytoplasmic granules will stain red/orange w / eosin dye =>secrete toxic chemical specific for parasitic worm infection => secrete chemicals that reduce the severity of an allergic rxn | |
| Basophil | =rarest 1/2% =nucleus has to indistinct lobes (not same size) =granules will stain blue with basic dye =>contain histamine,which facilitate an allergic rxn/immune response =>contain heparin, an anti-coagulation(blood thinner) | |
| Lymphocyte | 2nd most common,smallest =large dark nucleus =2x size of RBC *** no granules =play large role in immunity =>B cells- when stimulated by bacteria and toxins they differentiate into plasma cells ==> plasma cells then secret antibodies specific for microorganism => Tcells directly attack virus infected or tumor cells | |
| Monocytes | 4-8%,largest =distinct kidney shaped nucleus *** no granules =differentiate into macrophages which aid in phagocytosis | |
| Life History of WBC | production is called=leukopiesis -takes place in Red bone marrow | |
| Platelets | (thrombocytes) structure-cell fragments derived from the breakup of MegaKarocytes -surface has stick glycoproteins,causes them to stick to each other -cytoplasmic granules contain chemicals that facilitate clotting | |
| Hemostasis | stopping flow of blood,occurs in 3 phases | |
| 1st hemostasis (vascular spasm) | -immediate but temporary closure of damaged B.V. to decrease Blood flow =due to reflexive contraction of smooth muscle w/in vessel wall -triggered by direct injury to vessel =injury causes release of endothelin from endothelial cells. -also be triggered by nervous system local pain receptors are stimulated | |
| 2nd hemostasis (Platelet plug formation) | accumulation of platelets at injury site, occurs in 3 steps 1.platelet adhesion 2.platelet release rxn 3.platelet aggregation ***explained in following note cards | |
| Step 1 Platelet plug formation (platelet adhesion) | ->injured endothelial cells produce the protein VON Willebrand factor =>adheres the platelets to collagen in B.V. that has been exposed due to injury,uninjured B.V. collagen not exposed | |
| Step 2 Platelet plug formation (Platelet release rxn) | ->when platelets bind to collagen , become activated and release chemicals from cytoplasmic granules(not endothel) =>ADP & Thromboxane A2 which recruit more platelets to injury site | |
| Step 3 Platelet plug formation (Platelet aggregation) | ->the plasma protein fibrinogen diffuses into area and facilitates binding of platelets together -> PGI2(prostaglandin)-released from damaged endothelial cells limits the aggregation to only the injury area. | |
| 3rd Hemostasis (coagulation) | dependent on clotting factors/chemicals in bld. Prothrombin----prothrom activator---> Thrombin fibrinogen----thrombin(activates)--->fibrin | |
| Prothrombin | plasma protein made in liver -always around but not active | |
| prothrombin activator | released by damaged endothelial cells | |
| Fibrinogen | inactive but always around | |
| fibrin | glue that binds platelets | |
| Hemostasis (Fibrinolysis) | endothelial cells around clot released a protein called Tissue Plasminogen Activator Plasminogen----TPA----> plasmin =plasmin hydrolyzes fibrin holding clot together(dissolves) | |
| THE HEART | location-thoracic cavity btw lungs -2/3s of the hearts mass is lft of sternum | |
| mediastinum | midline partition formed by the heart,trachea, and esophagus | |
| FXNs of HEART | -generates Blood pressure(BP) needed to propel bld through B.V. -separates pulmonary circulation(R) from systemic circulation(L) -can change rate and force depending on metabolic needs of tissue | |
| Anatomy OF Heart (pericardial sac) | dbl layered closed sac surrounding heart -outermost layer in fibrous pericardium -serous pericardium | |
| Fibrous pericardium | outermost -tough fibrous connective tissue ,to prevent over distension of the heart and anchor heart w/in mediastinum | |
| Serous pericardium | simple squamous epithelium -two layers =perietal pericardium-contact with heart cavity walls =visceral pericardium-covers surface of heart | |
| Heart walls | 3 layers of tissue - epicardium-outer -myocardium-middle layer,thick cardiac muscle cells -endocardium-innermost | |
| Heart Chambers | 2 atria and 2 ventricles -tissue separating left atrium from rt atrium is interatrial septum -tissue separating ventricles is interventricular septum | |
| Atria | auricles on outer heart surface of atria -allows for atria to increase filling capacity -inner post wall is smooth -inner anterior wall is ridged formed of pectinate muscles | |
| Atria | 'receiving chambers' rt. atrium receives de-oxygenated bld from 3veins: =superior vena cavae =inferior vena cavae =coronary sinus | |
| fossa ovalis | on the rt. side of the inter atrial septum is a slight oval depression | |
| left atrium | receives oxygenated bld from lungs via 4 pulmonary veins | |
| Ventricles | 'distributing chambers' ***know flow | |
| Atrioventricular valve | -allow bld flow from atria into ventricles -prevents bld from going back into atria b/c (closed) when ventricles contract. ** Tricuspid valve- on rt. side ** Bicuspid valve -on lft. side | |
| Semilunar valves | prevent retro grade of bld allow bld to flow from ventricles to aorta and pulmonary trunk. open when ventricles contract. -but valves prevent bld from flowing back into ventricles close when ventricles relax ** pulmonary semilunar valve-btw rt. ventricle and pulmonary trunk ** Aortic semilunar valve- btw left ventricle and aorta | |
| Histology of the HEART | -Cardiac muscle is striated muscle with sarcomeres made of actin and myosin | |
| Intercalated discs | cells are electrically coupled by cellular adhesions -areas of low electrical resistance that allow ions to flow quickly from cell to cell =the depolarization current can freely travel over the heart | |
| Cardiac muscle physiology | cellular components -contractile cells -conductile cells | |
| contractile cells | muscle cells responsible for the actual contraction (ie) muscles that have actin and myosin -makeup 99% of all cardiac cells | |
| conductile cells | -self excitable cells that generate their own action potential =** these APs then initiate APs in the contractile cells | |
| Sinoatrial node | - located superiorly in the rt. atrial wall -called heart pacemaker b/c it depolarizes the fastest and starts the sequence of excitation | |
| Internodal pathway | connection btwn SA & AV node | |
| Atrioventricular node | located in the inferior portion of interartrial septum =depolarization is delayed here to give atria time to fully contract and empty blood into ventricles before ventricles are stimulated to contract | |
| Bundle of HIS/AV bundles | divides into LF & RT bundle branches at interventricular septum | |
| PUrkinje Fibers | - penetrate heart at apex then wind superiorly toward the base -causes ventricles to contract upwards | |
| EKG | displays a summation of all APs traveling through heart at given time. -represents electrical events which are responsible for the mechanical events of systole and diastole | |
| heart sounds | 1st -"LUBB" -AV valves closing at he start of ventricular systole 2nd -"DUPP"-SL valves closing at the start of ventricular diastole | |
| Tachycardia | -increased heart rate -100-250 BPM | |
| Bradycardia | -decreased heart rate -less than 60 BPM | |
| Arythmias | change in sequence of excitation | |
| SA nodal block | -missing P wave -normal QRS and T wave -lowered heart rate, b/c the AV node is now the pace maker | |
| AV nodal block | -blockage of AP through the bundle of HIS -ventricles DO NOT receive all atrial impulses -normal time btw the end of the P wave and the beginning of the QRS is ~ .16 sec ** need to know know 1st degree, 2nd degree, and 3rd degree | |
| Ventricular fibrillation | ( V-fib) -very rapid , highly uncoordinated heart contractions -some areas of the ventricles may be contracting while others are relaxing -ventricles are never completely full nor completely empty -results in severe decreases in blood delivery to lungs and tissues; can be fatal in minutes | |
| Cardiac Output | CO=the amount of blood pumped by the heart per min -calculated using heart rate and stroke volume = the amount of blood pumped by the heart per beat | |
| Regulation of heart(intrinsic) | within the heart -the more the ventricular muscle stretched, the more forceful the next contraction will be -venous return=amt of bld entering the rt atrium via vena cavae -increases stroke volume -increased bld to heart ,the more that will be pumped out (increase in venous return=increased SV=increase in CO) | |
| Extrinsic | neural regulation by the autonomic nervous system -vagal center -vasomotor center | |
| Vagal center | -medulla oblongata -parasymp control -rest and relaxation;decreases heart rate | |
| vasomotor center | medulla oblongata -sympathetic control -fight or flight; increased HR | |
| Beta Blocker | block receptors in the heart to slow down HR | |
| Blood Vessels | closed delivery system that begins and ends at the heart | |
| Tunica Intima | innermost layer of endothel cells comes indirect contact with blood | |
| Tunica Media | Middle layer composed of smooth muscle and innervated by sympathetic nervous system -vasodilation and constriction | |
| Tunica Adventitia | outermost layer that anchors vessels to surrounding structures | |
| Arterial system | transport O2 bld from hrt to tissue -Elastic/conducting arteries -muscular/distributing arteries -arterioles | |
| Definition |
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