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January 22nd, 2013 and January 29th.docx

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Health Sciences
Michael Wilkie

BI217 Lecture: The Anatomy and Physiology of the Human Heart Why Do We Need a Circulatory System?  With multicellular organisms – oxygen could not longer diffuse through to all the cells of the body, insufficient for the inner cells  Because of this, it was essential to produce a circulatory system  In Harvey’s equation r squared is the radius  As animals got bigger, the amount of oxygen necessary at the surface increases – to ensure that the innermost cells receive sufficient oxygen Functions of the Cardiovascular System  The typical resting heart beat is roughly 60 beats per minute  In a typical year  5.26x10 min/year  3.2x10 beats per year for the average heart x 70 years = 2.2 – 2.6 billion times in a lifetime  Volume: average cardiac output (sum of the heart rate x the volume of blood pumped per beat) = about 5L of blood per minute  5L x 5.26x10 minutes/year = 2.6 -3.0 million liters of blood pumped per year  2.6 – 3.0 million x 70 years = 184 – 210 million liters of blood per lifetime Anatomy of the Heart  Arteries carry oxygenated blood except for the pulmonary artery (these leave from the heart)  Veins take blood to the heart  The right and left atria contract simultaneously as do the right and left ventricles  The amount pumped from the left and right ventricle should be equal – if not there can be a back up of blood  pulmonary edema, multi-organ failure, and the tissues will be starved of blood (this is often the cause of death for those in high altitudes)  Gas exchange takes place at the level of the capillaries  Left side = systemic circuit  Right side = pulmonary circuit  Coronary arteries and veins are very prominent on the surface of the heart  Left ventricle is much more muscular – greater distance to pump the blood, faces much more resistance to blood flow (must generate a greater force)  Left ventricular hypertrophy  Veins are more floppy looking – they only have a thin layer of muscle surrounding them  Aortic (aneurisms) rupture = instant death (this can increase with cocaine use because of increased blood pressure)  Aorta has a thicker layer of muscle – has many branches (carotid arteries, brachial artery, femoral artery – blood under extreme pressure)  Pericarditis can be caused by streptococci – inflammation of the pericardium can lead to friction rub, where the heart has less room surrounding it  Electrical coupling allows the heart to beat in a coordinated fashion (myocardial infarction would disrupt this – electrical pathways would have to be diverted)  Auto-rhythmic fibers – much smaller, constitute the electrical wiring of the heart, find in the pacemaker of the heart (sino-atrial node)  Contractile fibers – they do all the work, these can get bigger, these are signaled by the auto-rhythmic cells to contract  Gap junctions – electrically coupled because they allow for ions to flow between adjacent cells (or chemical messengers) – therefore electrical currents can move back and forth between adjacent cells  Cardiac muscle allows pumps from the apex to the base (where the aorta and the pulmonary artery leave the heart)  Endocardium lines the internal surface of the heart – it is also what the valves are constructed of (connective tissue)  AV Valves: Tricuspid separates the right atrium and ventricle and bicuspid (mitral) which separates the left atrium from the left ventricle  AV node delays the electrical signaling  Papillary muscles also contract when the ventricles contact to stop the valves from blowing back (act as anchors)  Purpose of valves is to prevent the backflow of blood to maintain cardiac output  Semilunar Valves: Pulmonary and aortic valves Diseases of the Heart  Streptococcal infection can cause rheumatic fever which can lead to tissue damage and scarring  Leaking – could be from calcium deposits or scarring, this can lead to turbulence (aka. Heart murmurs)  Mitral Valve Stenosis (bicuspid valve stenosis)  The left AV valve does not open as much as it should when the valves are suppose to spring open  Narrowing of left AV valve  Can be caused by rheumatic fever which damages tissues throughout the body  Mitral Valve Regurgitation  Blood is going the wrong way – you get a backflow of blood due to leakage in the valve  Can be detected as a heart murmur with a stethoscope  ECG, chest X-rays, and ultrasounds (echocardiogram)  Treatment = valve repair using catheters, or replacement of the valve  Mitral Valve Prolapse  The leaflets or lobes of the valve bulge into the left atrium leading to some leakage or back flow  Difficult to diagnose, probably drops in blood pressure, chest pain, migraines  Signs – clicking sound when listening with a stethoscope, there may also be murmurs as well due to turbulence when the ventricles contract  Could take drugs to slow the heart rate – for example, beta blockers (decrease the work load on the heart)  Aortic Valve Stenosis  Narrowing of the valve – decrease in blood flow through the systemic circuit  May be caused by scar tissue, possibly due to an infection, or build ups of calcium  Diagnosis = echocardiogram, preceded by the detection of a heart murmur, may do cardiac catheterization  Typically seen in the elderly  Aortic Valve Regurgitation  Could be caused by rheumatic fever, or could be congenital  Detected in routine medical exams as a heart murmur  Echocardiogram to confirm the diagnosis  Signs – chest pains, palpitations (noticeable feelings of heart racing)  Treatment – antibiotics if it is due to rheumatic fever, drugs that decrease BP/Digoxin which decreases the strength at which the heart contracts Membrane Transport  Review toolbox on page 100, chapter 4 pages 95-101  Key Definitions – Solute, Solvent (ECF or ICF/cytosol)  If solute concentrations are different between the ICF and ECF – the cell will either swell or shrink  Calcium is incredibly low in the intracellular fluid (this is stored in the sarcoplasmic or endoplasmic reticulum)  important for triggering muscle contraction, and is critically important as a second messenger  Focus of potassium, sodium, calcium, and chloride when looking at the electrochemical properties of cells  Membrane potential is always inside relative to outside – this is pretty much constant across cells because there is a build up of excess anions right next to the plasma membrane  This does not refer to the entire cell  cations must be equal to the number of anions – the charge separation can only occur at the level of the plasma membrane  The driving force (combination of the electrical and chemical gradients) using the Nernst equation  Primary active transport examples – ATPase, Calcium ATPase, Proton pump (H+ ATPase), Sodium-Potassium ATPase  Secondary active transport – antiporter or symporter  Active transport – moves substances from low to high energy  Law of electroneutrality – positive and negative charges have to balance each other (but negative charges tend to collect on the inside of the membrane and positive on the outside due to differences in permeability  when the cell is at rest)  Can use the Nernst potential to predict which way an ion is going to move (in the direction that moves their membrane potential towards the Nernst potential)  Net Driving Force (F )ionE – m ion  Negative F ionindicates inward movement, positive F ionindicates outward movement  Note: membrane must be permeable to that ion  Fig 4-5 – a) some potassium would be leaking out (through potassium leak channels) and at the same time the electrical gradient is drawing some potassium back in  no net gain or loss  F ion= -94 – (-94) = 0  If membrane potential is equal to the Nernst potential, you are not getting any net gain or loss  B) The membrane potential is more positive – the potassium will not be as attracted into the cell so the potassium would move in the direction to drive its Vm in the direction of its Ek  C) The Nernst potential is less than the membrane potential, the potassium will move into the cell to bring the values closer  Against the electrical OR chemical gradients = active transport Chemical and Electrical Properties of the Heart  2 types of heart cells (myocardial arrhythmic cells and myocardial contractile cells)  Contractile cells are signaled by arrhythmic cells  The heart can beat all on its own  SA node – most auto-rhythmic cells (the pacemaker) – connected to the AV node by the intermodal pathways  Signal does not pass into the ventricles because of the fibrous septum – after a few milliseconds it moves into the ventricle and tops off  The ventricles contract simultaneously  Signal goes from the apex to the base  Electrical signaling is always followed by the contraction (ECG represents ONLY electrical activity)  2 types of APs that can take place in the heart:  Pacemaker potential (in autorhythmic cells) – continual depolarization due to funny channels which are permeable to sodium  To accelerate heart rate – open more calcium channels and more funny channels  Cardiac Contractile Cells – stable resting membrane potential  The action potential in these cells is not a spike – but instead a plateau  Resting membrane potential in these cells is -90mV which is almost the exact same as the Nernst value for potassium – this is why it is so dangerous to inject someone with potassium  Fast rectifier K+ channels – open and close really quickly which gives a slight repolarization  Then voltage-gated potassium channels open – moving positive charges back into the cell  Then slow rectifier potassium channels open – potassium leaves down its large EC gradient  Long absolute refractory period – a full action potential has to occur before the second one can  this regulates the maximum tension you can develop in the myocardial cells – cannot get summation taking place but in skeletal muscle cells summation can take place  You do not get summation because the refractory period is very long  During the period of the AP you can no longer stimulate the AP – muscle has to almost completely relax before another signal can commence Excitation-Contraction Coupling in the Heart  Sarcoplasmic-reticulum: huge reservoir of calcium (more in contractile cells than autorhythmic cells)  Adjacent cell gets depolarized – sent through gap junction into adjacent cell  Causes depol towards threshold in the myocardial cell – calcium channels open (acting as an intercellular messenger) – signals calcium induced calcium release (acting on the sarcoplasmic reticulum)  There is a cascade of calcium release – binds to the troponin complex on the actin filaments of the contractile cells – shift in troponin C complex  moves away exposing the actin binding sites  The entire filament sliding theory (actin filaments move in towards the center of the sarcomere) takes place – same as what occurs in the skeletal muscle  Loss of ADP and inorganic phosphate and we get “rowing”  Calcium released is taken up by calcium ATPases and pumped back into the sarcoplasmic reticulum  When calcium is pumped out the cell – troponin releases the calcium bound to it, the fibers undergo relaxation (essential for cardiac output – amount of blood pumped by the heart per unit of time) Electrocardiogram (ECG/EKG)  Invented by Walter Einthoven in the early 1900s (Dutch)  Plasma is a good conductor of electrical current because it contains ions  They now put a series of 12 leads across the chest (more 3-D view of the electrical activity of the heart)  P wave – atrial depolarization (do not say contraction) – but atrial contraction follows  QRS complex – represents ventricular depolarization – followed by ventricular contraction  T wave – ventricular repolarization (returns to resting state)  Between 2 wave forms = segment  An interval includes the wave form
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