CardioVascular - Kin 2230

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Kinesiology 2230A/B
Glen Belfry

Lecture 1 – CardioVascular Cardiac Output (Q) and Ve  There is a linear increase in oxygen consumption as the work rate increases; ventilation increases at the same rate as O2 consumption  Cardiac output or blood flow has a similar profile of O2 consumption; as cardiac output increases, it increases oxygen uptake  However, as a certain work rate is reached (lactic threshold), there is an increase in ventilation (a greater increase in ventilation than O2 consumption)  thus oxygen cannot drive ventilation  Ventilation does not limit maximal exercise; ability to deliver oxygen to tissues is the limiting factor; but cardiac output is limiting for maximal exercise Summary  The total amount of blood volume depends on how big you are but the average is about 5L  On the arterial side of circulation there are resistant vessels (on the venous side, the veins are capacitance vessels) where the blood pressure is going to be based on the diameter of the arterial side of ventilation  If the diameter of the artery is small, there is going to be greater pressure  There is 13% of the 5L in the arterial side of circulation at rest; the heart contains 7% of total blood volume  The blue regions contain the greatest quantity of blood located at rest – on the venous side of the circulation (deoxygenated blood)  When the veins swell up, they are storing blood at rest  The pulmonary circulation which is located on the right side of the heart, it pumps blood to the lungs; while the arteries leave the heart and carry oxygenated blood  The pulmonary arteries carry deoxygenated blood from the heart to the lungs while the pulmonary veins carry oxygenated blood from the lungs to the heart Fick’s Equation  VO = 2R x SV x (a-v O di2ference)  the difference is the amount of oxygen between arteries and veins  Cardiac output is HR x SV  If we can increase the difference, then we can offload more O2 from Hb at the muscle where the aVO will increase Circulation The left side of the heart is thicker than the right because of the extra work the left side has to go to get the blood to all the tissues and organs of the body while the right side only has to pump blood to the lungs. The blood returning from the venous side of circulation (superior and inferior vena cava goes through the right atrium through the right ventricle (deoxygenated blood) and out the right and left pulmonary arteries to the lungs to get oxygenated blood. From the lungs, oxygenated blood comes through the right and left pulmonary veins to the heart, goes through the left ventricle and out the aorta to the tissues. Heart  The heart is a muscle itself that requires oxygen and blood so it has to pump blood to the body as well as itself  The right coronary artery which supplies blood to the right ventricle as well as the 25-35% of the left ventricle  The left coronary artery feeds blood to the left side of the heart  The posterior interventricular artery gets provided with 1/3 of the interventricular system while the anterior interventricular artery gets provided with the remaining 2/3 Initiation of Heart – Contraction & Relaxation o The SA node (cluster of cells within the right atria that will spontaneously depolarize causing an atrial contraction); It will emit an electrical activity on a regular basis that will lead to the contraction of the atria themselves o The AV node is another cluster of cells that is composed of lipids and fat tissue, which slows the electrical movement through the heart tissue  This delay of signal moving into the atria, the atrium can finish contracting before the ventricle can contract  There are also purkingi fibers which accelerate the movements of activity which propagate the electrical activity to begin contraction Phases of a Resting ECG P-Wave: Electrical activity going through the atrial (SA node) PQRST Complex: it is a reflection of depolarizing waves that are moving through the heart; this is helpful because at any given moment in time, the cardiologist can determine where in the heart each particular portion in the wave is actually depolarizing the tissue The amplitude of the wave (P wave) is affected by how much tissue is actually being depolarized There is a delay to allow for the contraction to occur from the AV node  shown by QRS ventricular depolarization  this shows the stats of the AV node T-Wave displays wave of electrical activity that goes through the ventricals to relax heart muscles (repolarization = relaxation of tissues) o The ECG monitors cardiac changes or diagnosis cardiac problems o The P wave represents arterial depolarization and occurs when the electrical impulse travels from the SA node through the atria to the AV node o The QRS complex represents the ventricular depolarization and occurs as the impulse spreads from the AV node to the purkinji fibers and through the ventricles o The T wave represents the ventricular repolarization o Atrial repolarization cannot be seen because it is occurring during the ventricular depolarization (QRS complex) Cardiac Output  Q = HR x SV  VO2 = HR x SV x (a-v O2 diff)  VO2 = Q x (a-v O2 diff) Heart Rate > The sinus rhythm is generated from the SA node > Bradycardia – slow heart rate (clinically less than 60 bpm) > Tachycardia – fast heart rate (clinically over 100 bpm) > Sinus Rhythm – Normal rate (SA node) Stroke Volume  Volume of blood pumped per heart beat  SV = EDV - ESV  EDV: End diastolic volume  volume at the end of filling, end of relaxation period of the heart  ESV: End systolic volume  volume of blood that is still in the heart after it has been contracted Ejection Fraction o How much of total volume (EDV) is being ejected out into the systemic circulation o EF = SV/ EDV x 100 o Echocardiography  it measures blow flow velocity and measures the chamber size and stroke volume through the cardiac cycle Lecture 2 Hypertrophic Myopathy  It is a genetic disorder  Normally, the myocardial cells start to array to the adjacent fibers but in this disorder, instead of longitudinal fibers, there is a disarray of the fibers (myofibrillar disarrays)  Also, a lot less happens (less contraction), so the contraction is going in the disarrayed direction and not in the longitudinal direction where it needs to go  There is also a reduction in the chamber size causing it to pump less blood out and the valves are also reduced due to the hypertrophy of the myocardial tissue  Most common cause of sudden death in the young Stroke Volume  The max HR is 220 – age  If you increase the stroke volume, you are able to increase the oxygen delivery  It refers to the amount of blood ejected from the left ventricle per beat in milliliters  Contractility: the force with which the heart contracts; contractility affects stroke volume  The stroke volume can be increased by sympathetic stimulation and circulating catecholamines (epinephrine and norepinephrine)  There is a direct stimulation in the sympathetic nerve that goes to the heart; there is also a direct stimulation by the nerves which will increase contractility  With the increased contractility, more of EDV is pumped out which will increase EF, however, ESV is reduced o SV is affected by stimulation of sympathetic nerves o Myocardial Force – the force is increased with sympathetic stimulation (dramatically); it greatly reduces the amount of time for that contraction and therefore increasing HR  Stroke volume can also be affected by EDV  As EDV increases, SV increases as well  Effects of sympathetic stimulation: At any given diastolic volume, we see a greater SV (filling is staying the same) so you reduce ESV while maintaining the same EDV – since the contracted force is greater, more blood is pumped out (less ESV is left even though EDV is the same), which increases the stroke volume Factors Affecting EDV Venous Tone: increase in the venomotor tone increases venous return which increases the preload  Increase in the venomotor tone (vasoconstriction of smooth muscle around the veins) which increases the preload  if you push out more blood in the veins, it will increase venous return to the heart  Preload on the heart is the EDV (end diastolic volume)  Ventricular size influences the stroke volume  Distensibility (the elasticity of the heart tissue)  differences in this distensibility will affect SV – how much it can stretch under pressure  Distensibility is related to the left ventricle pressure  Most of the fillings of the ventricles occurs passively – blood is flowing into the heart and into the atria where it keeps going to the right ventricle; when the venous return is increased, the fillings of the ventricles will increase as well Vein Valves: one way  Unlike arteries, veins have valves so that blood will only move in one direction  The top valve opens and the bottom one closes and when the muscle contracts, the blood is able to flow through the opened valve Supine or prone exercise o There is a decreased hydrostatic load where the heart rate is lower and the stroke volume is larger o If you do exercises lying down in either supine or prone position, the vertical distance that the heart has to pump blood is limited; whereas in the upright position there is a decreased hydrostatic load while lying down which makes it easier to pump blood back to your heart in supine position (increase venous return)  If you lie down and then sit then stand, your SV will decrease, therefore you will see an increase in HR due to the decrease in SV o In the upright position, ESV on exercise intensity increasing  ESV is reduced o However, in supine position, there will only be a slight reduction in ESV during the increases in exercise intensity Frank-Starling Mechanism  This mechanism states that the energy of contraction is proportional to the initial length of the cardiac muscle fiber; the greater the length of the myocardial fibers (more they are stretched apart) the greater the force of contraction can be generated (more energy) Lecture 3  Hypoxia, Necrosis (diameter: 2mm x 2mm) Changes in EDV SV = EDV – ESV In the upright position, you see a significant decrease in ESV, therefore there is an increase in EDV. However, in the supine position, a there is a small change in ESV, so the increase in SV you get is by reducing the ESV.  EDV at rest is around 85 ml and ESV is around 30 ml – huge difference at rest; there is a huge change 25% increase in ESV in the supine position, and this is due to the reduction in the hydrostatic pressure  There is less blood returning to the heart when upward that means there is less EDV; there is so much more EDV in supine position that it is advantageous to be in the supine position in SV perspective  For any giver cardiac output, your HR decrease because SV is greater  this is because it is pumping still the same amount of blood but just pumping more blood per beat, hence reducing HR and increasing SV Frank Starling Mechanism o The greater the length of the myocardial fibers, the more they are stretched apart, the greater the force of the contraction o Increase venous return, the more blood returning to the heart, which increases EDV and that increases the filling  therefore it increases the length of the myocardial fibers  greater contraction force EDV – Duration, Heat, Exercise  Prolonged exercise and heat – both lead to cardiovascular drift – in each case there is insufficient venous return and hence a decrease in EDV Several Other Factors affecting Cardiac Output (blood flow) - There is resistance to blood flow – afterload or the load against which the heart has to work - Afterload: the pressure that the LV must generate to eject blood - As the afterload increases, the cardiac output decreases - Preload – same as EDV (volume of blood that heart has to work with) - Afterload – released to resist the blood flow; pressure is required to eject the blood  If there is resistance in the circulation, the afterload will be greater which is problematic because the heart will then have to work harder to maintain the same volume of blood  Afterload is going to be the same during systole (contraction of the heart) and diastole (pumping blood out of heart)  The elasticity of the aorta is what continues to push the blood; if the resistance to blood flow increases, that means the diastolic pressure, pressu
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