KIN 292 1nd Edition Lecture 24 Outline of Last Lecture I 13 4 Electrical Activity of the Heart II 13 5 The Cardiac Cycle Outline of Current Lecture I 13 6 Cardiac Output and Its Control Current Lecture 13 6 Cardiac Output and Its Control Cardiac Output Volume of blood pumped by each ventricle per minute Cardiac output CO SV HR Average CO 5 liters min at rest Average blood volume 5 5 liters Control of heart rate and stroke volume Extrinsic and intrinsic regulation Intrinsic autoregulation pacemaker Extrinsic Autonomic nervous system ANS and hormonal adjust intrinsic rate to meet body s needs Two variables Stroke volume Beats per minute Physiology in action CO increases in direct proportion to energy demand exercise intensity O2 uptake by body is related to energy demand and increases as exercise becomes more intense Proper endurance exercise increases maximum CO and VO2max Heart rate also increases in direct proportion to exercise intensity Endurance training lowers HR at submaximal exercise intensities The more times that it beats per minute the more blood that will be pumped For graph yellow couch potato purple athlete Cardiac output will the same across the board the way it lets it in there will be different These notes represent a detailed interpretation of the professor s lecture GradeBuddy is best used as a supplement to your own notes not as a substitute Heart rate determined by SA node firing frequency SA node intrinsic firing rate 100 min No extrinsic control on heart HR 100 SA node under control of ANS and hormones Rest parasympathetic system dominates HR 75 Excitement sympathetic system takes over HR increases Hyperpolarization farther from threshold figure 13 26 Effects of autonomic nervous system and hormones on SA nodal cells Increased sympathetic activity epinephrine binds to 1 receptors in SA node and increases HR Sympathetic Phosphorylation increases open state of If and Ca2 channels Increase rate of spontaneous depolarization Increase heart rate Parasympathetic Increase open state of K channels and closed state of Ca2 channels Decrease rate of spontaneous depolarization and hyperpolarize cell Decrease heart rate Factors Affecting Cardiac Output Changes in Stroke Primary factors affecting stroke volume o Ventricular contractility o End diastolic volume o Afterload pressure in aorta during ejection Afterload SV Afterload SV o Changes in stroke how much blood is pumped out per beat o More blood in ventricle the more blood pumped out Influence of ventricular contractility force development at a given sarcomere length o More forceful contraction will expel more blood o Controlled by norepi epi from SNS and adrenal medulla Norepinephrine epinephrine 1 adrenergic receptors cAMP secondmessenger system 1 Augment open Ca2 channels more open longer 2 Increase Ca2 release from sarcoplasmic reticulum SR 3 Decreases Ca affinity of troponin Book says Increase myosin ATPase rate Not correct 4 Increase Ca2 ATPase activity on SR speeds reuptake The greater the contractility the more force development if at the same starting point 13 27 The effects of sympathetic activity on ventricular contractility Phosphorylation of troponin that requires more calcium Phosphorylate part of calcium ATPase will bring in more calcium faster Summary of Ar Stimulation Inotropic enhances contractility o opening of L type Ca channels stimulation to SR Ryanodine receptors o sensitivity of SR Ryanodine receptors to Ca induced Ca release o SR Ca uptake rate SR Ca content SR Ca release Lusitropic enhances relaxation o SR Ca uptake rate o Ca sensitivity of troponin Sympathetic activity the greater the force the shorter contraction duration Factors Affecting Cardiac Output Changes in Stroke Volume o Influence of end diastolic volume on stroke volume Starling s law o Increased EDV stretches muscle fibers and sarcomeres o Sarcomeres closer to optimal length o Optimal length greater strength of contraction o Result increased SV Increase venous return Increase strength of contraction Increase stroke volume Factors Affecting end diastolic volume o 1 Filling time determined primarily by heart rate next slide o 2 Lusitropy sympathetic stimulation enhances both contractility inotropy and filling time o 3 Compliance diseased hearts may be stiff due to high level of fibrosis connective tissue infarct areas dead tissue etc which would slow rate of filling o 4 Central venous pressure pressure of blood in the large veins leading to the heart Measure of how fast blood is flowing into right atrium Affected by many variables including venous tone stiffness of veins pumping action of skeletal muscle body position blood volume intrathoracic pressure Valsalva maneuver can cut off flow 1 Filling time determined by heart rate The Cardiac Cycle at rest and intense aerobic exercise filling time decreases which affects stroke volume as intensity increases next slide Note also the large change in diastolic period compared to systolic o o stroke volume plateaus as exercise intensity increases due to increased HR and decreased filling time Increased lusitropy and central venous pressure help maintain SV at high intensities