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Complete chapter 18 the heart

by: Delia Navarro

Complete chapter 18 the heart Bio 2313

Marketplace > University of Texas at El Paso > Biology > Bio 2313 > Complete chapter 18 the heart
Delia Navarro
GPA 3.65
Human Anatomy and Physiology II
Zaineb A Al-Dahwi

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Human Anatomy and Physiology II
Zaineb A Al-Dahwi
Class Notes
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This 11 page Class Notes was uploaded by Delia Navarro on Friday October 9, 2015. The Class Notes belongs to Bio 2313 at University of Texas at El Paso taught by Zaineb A Al-Dahwi in Fall 2015. Since its upload, it has received 18 views. For similar materials see Human Anatomy and Physiology II in Biology at University of Texas at El Paso.


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Date Created: 10/09/15
Human Anatomy and Physiology ll Notes September 30 2015 Chapter 18 The Heart Qmparingjkeletal Ml le SM and Cardiac Muscle CM 1 Stride due to arrangement of actin and myosin and arrangement for sarcomeres I band and A band 2 Contracting Differences between Skeletal Muscle and Cardiac Muscle Basic Differences 1 Shorter muscle ber in CM than in SM 2 CM has one nuclei SM has multinuclei with muscle ber 3 SM has no branched muscle cells CM are branched a CM has intercalated disc that contain Desosomes and Gap Junctions protein channels Desmosomes signi cance is they have lateral connections that prevent separation of CM during muscle contraction Gap Junctions connection CM cells mainly allow passage of electrical impulse action potential allowing heart to contract as a single unit Making the heart contract all at once or not at all Major Differences between SM and CM SM does not have gap junctions therefore there electrical impulse is isolated it contracts separately 4 SM have an abundance of t tubules in CM there are much less t tubules due to gap junctions 5 Sarcoplasmic reticulum much less elaborate in CM than the SM much more developed 6 In CM there is an absence of terminal ceternium 7 CM does not have Triade one terminal ceternium ttubules another terminal ceternium 8 CM has a very high number of mitochondria compared to SM the signi cance makes the muscle resistance to fatigue CM very much dependent on oxygen aerobic mechanism Ph sical Differences Similarities Differences Heart is self excitable because they contain what is known as the Pacemakers Pacemakers self excitable cardiac cells that are pace makers make up 1 to 2 and are noncontractile Does not contract all names used for Cardiac muscle cells that do not contract Cardiac Pacemaker Cells lntrinsii Cardiac Conduction System Autorhythmic cells gt 1 of cardiac muscle bers pace makers gt Can generate their own poloriziation provide pace making for the whole heart because of the cells we do not need the nervous system to generate electrical impulse of the heart Heart does not need the nervous system Functional Synsathasium Heart functions as a single unit Contraction of SM is going to be depend on activation Motor unit regroupment of several motor units SM source of calcium totally and completely an internal force from the sarcoplasmic reticulum CM sarcoplasmic reticulum is a partial sure of calcium another source is the extra cellular uid CM is dependent on aerobic mechanism Cardiac muscles cells are known to 1 Generate their own polarization 2 Depolarization is going to be transported through gap juncUons gt Unstable resting membrane potential due to iron channels that are activated at the high depolarized stage 1 Pacemaker potential pre potential Related to instability of resting membrane potential gt This slow depolarization is due to both opening Na channels and closing of k channels Notice that the membrane potential is never a fat line 2 Depolarization Plateau phase The actin potential begins when the pacemaker potential reaches threshold Depolarization is due to Ca channels 3 Repolarization is due to Ca2 channels inactivating and K channels opening This allows K ef ux which brings the membrane potential backs to its most negative voltage Depolarization is not contraction Cardiac Page Maker Cells Intrinsic conduction system Pace Maker of Heart The sinoatrial node node means a collect of cells SA Because it has the fastest rhythm between all others gt An electrical impulse leaves the sinoatrial node into both atrium and ventricles not connected by gap junctions lnternodal Pathway gt Atrioventricular node delay in electrical impulse because there is a contraction of the atrium because the ventricle and atrium cannot contract at the same time 0 Small diameter pace maker signi cance increase residence delaying in electrical impulse because there is a contraction if the atrium Because the ventricles and atrium cannot contract at the same time 0 Due to certain affect it is equal to SA node 75 bpm but because of the vagus nerve known as vagaul Rhythm of SA node natural rhythm 100bpm SA node 75bpm AV node 50bpm AV bundle bundle branches purkinje bers 30bpm Autonomic innervamn of the Heart gt Autonomic nervous system gt The vagus nerve parasympathetic decrease heart rate modi es the heart beat it can increase or decrease but does not generate the depolarization gt Heart beat is generated in the pacemakers Sympathetic and Parasympathetic are connected to the medulla oblongata cardiovascular gt Cardioinhibitory center associated with parasympathetic sending nerve impulse through the vagus nerve gt Vasomotorcenter gt Cardioacceleratory center center that is associated with increasing heart rate and associated with sympathetic system Plateau phase prolonged depolarization is due to Ca2 in ux through sow Ca2 channels this keeps the cell depolarized because few K channels are open due to calcium Repolarization is due to Ca2 channels in activating and K channels opening This allows K ef ux which brings the membrane potential back to its resting voltage Signi cance in prolonging the depolarization prolong the contraction to pump to much blood out Absolute refractory period time period where you cannot stimulate promote a second action optional when the rst one is going on coincides with repoarization and depolarization cannot stimulate another action potential until repoarization is over Almost as long as the contraction is in relaxation because it prevents Tetanic Contractions Tetanic contractions in the heart will keep pumping the blood out being empty an the only time it will have blood is during relaxation non contractile muscles n t have contractions relaxatLJn cycle Electrical Activity of the heart ECG EKGU of all the heart contract cardio ces gt An electrocardiogram tracing electroactivity of heart we look at the pacemakers noncontractile and contractile gt Made up of 3 waves P ORS T P Wave caused by atrial depolarization QRS complex Ventricular both depolarization airway from all ventricles T wave ventricular repolarization going through the ventricle EKG Electical immlse acivity all over the m 2 Typical normal EKG Signi cance of EKG help nd an abnormality represents of both cardiac pace makers non contractile and contractile ST plateau phase of contractile cardiac muscle cells Cardiac Cycle 2 All mechanical events that are associated with blood ow through the heart during one complete heartbeat Mechanical events Contactor systole 0 Relaxation dystole Mainly representing Atrioventricular systole atrioventricular dystole Ventrally systole dystole use cardiac cycle to get the cardiac input Blood ow through heart pressure is the driving force of the blood Blood goes from the arteria of high pressure to low pressure During relaxation we have lling of the blood 7580 is making passively to the ventricle 1St phase Ventricular lling gt Blood returns to the left atrium and it will be the same for both sides left and right gt The valve between the ventricle and the aorta is closed gt P wave id depolarization of the 20 of blood goes from atrium to ventricle Phase 2 Ventricular Systole atria in diastole gt Increase in pressure in going to push the aps a closed position Ventricular systolic atria diastolic lsovolumetric contraction phase the valve between the aorta and ventricle is still closed but contracting gt Not changing its volume drastically increases pressure in ventricle to point it exceeds its pressure inside the aorta During contraction of ventricle Ventricular Ejection Phase gt It pushes the aps open to eject blood out of ventricular to the aorta in depolarization relaxation end of contraction not all the blood will be back in the ventricle lsovolumetric relaxation relaxation of the ventricle almost all of the blood pressure in the ventricle is going to drop becomes less than one aorta causing blood to back ow valve between atrium and vertical stay closed then it opens Cardiac Cycle in the aorta DICROTIC NOTCH point where ventricles start relaxing pressure becomes less than aorta Back Flow occurs Rebounding of the blood that back ew and closed the valve at the base of the aorta Blood Flow through heart is dependent of pressure that goes through a high pressure to low pressure Cardiac Output EDV end diastolic volume collected volume at the end the end of ventricular relaxatioin volume of blood collected at the end of ventricular lling ESV end systolic volume volume of blood that remains after contraction ejection of the ventricle Stroke Volume SV Volume of blood that is ejected by ventricle during ONE HEART BEAT Difference between EDV and ESV Cardiac Cycle One Complete Heartbeat SV Each Beat CO cardiac output One Minute COHRxSV Heart Rate is another word for Beats per minute SVEDV ESV if you decrease the ESV you increase SV and increase CO gt Less amount of blood left in the ventricle decreases the SV increase CO gt The more blood left in the ventricle increases the SV decreases the CO Preload degree to which cardiac muscles cell are stretched before they contract Frank Straling law 2 Higher preload Higher SV 2 Lower Preload Lower SV Factor that stretches the ventricle the lling blood that is lling the ventricle known as Venus Return through the veins Stretching gt VR Venus return TVRHl Hl co Increase of VR leads to Increase of EDV leads to increase of SV leads to increase CO Affect the EDV Volume of VR Ex blood loss decrease blood volume decreasing the volume of blood to the heart Speed of VR Ex exercising blood is pumping returning into the heart faster increasing EDV preload Any factor increasing decreasing speed or volume of VR is going to affect EDV Slow Heart Rate give more time to ll the heart with blood increasing blood volume Factors in uencing EDV are intrinsic Factors in uencing ESV are extrinsic outside the heart gt Contractility of myocardium in uenced by the sympathetic nervous system which is activated in stress 0 Ex ight or ght Nonepiriephirine are binding to receptors that are on the contractile cells gt Activates the heart rate and contractile gt Binds to receptors to activate a single pathway promote increasing of opening calcium membrane in plasma membrane and sarcoplasmic reticulum 0 Increasing force and rate of contraction What is expected More blood is ejected from the ventricle decreased in ESV is an increase in CO Eprnephrine is adrenaline released by adrenaline medulla Negative enotrophic gt Decrease contractility leaving more blood in ventricle Afterload doesn t take place in healthy people occurs in people with high blood pressure Because it exist in the aorta aorta pressure is higher than the ventricle which means the ventricle has a hard time opening the valve at the base leaving more blood in the ventricle increasing ESV decreasing SV decreasing CO Factors Associated with Heart Rate gt Negative decreased heart rate Parasympathetic nervous system in uences sympathetic Activated sympathetic In uences on Heart Rate Increases heart rate Myocardium


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