KIN 292 1nd Edition Lecture 24Outline of Last Lecture I. 13.4- Electrical Activity of the HeartII. 13.5- The Cardiac Cycle Outline of Current Lecture I. 13.6- Cardiac Output and Its ControlCurrent Lecture13.6 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 moreintense. 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 differentThese 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 β1 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 rateFactors Affecting Cardiac Output: Changes in Stroke- Primary factors affecting stroke volumeo Ventricular contractilityo End-diastolic volumeo Afterload = pressure in aorta during ejection ↑ Afterload = ↓ SV ↓ Afterload = ↑ SVo Changes in stroke= how much blood is pumped out per beato More blood in ventricle, the more blood pumped out - Influence of ventricular contractility – force development at a given sarcomere lengtho More forceful contraction will expel more bloodo Controlled by norepi/epi from SNS and adrenal medulla Norepinephrine/epinephrine  1 adrenergic receptors  cAMP second-messenger 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 β-Ar Stimulation- Inotropic (enhances contractility)o ↑ opening of L-type Ca channels = ↑ stimulation to SR Ryanodine receptorso ↑ 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 rateo ↓ Ca sensitivity of troponin- Sympathetic activity- the greater the force, the shorter contraction durationFactors Affecting Cardiac Output: Changes in Stroke Volumeo Influence of end-diastolic volume on stroke volume: Starling's lawo Increased EDV stretches muscle fibers and sarcomereso Sarcomeres closer to optimal lengtho Optimal length → greater strength of contractiono Result → increased SVIncrease venous returnIncrease strength of contractionIncrease stroke volumeFactors Affecting end-diastolic volumeo 1 Filling time – determined primarily by heart rate (next slide)o 2 Lusitropy – sympathetic stimulation enhances both contractility (inotropy) and filling timeo 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 musclebody position blood volumeintrathoracic pressure – Valsalva maneuver can cut off flow1 Filling time – determined by heart rateThe 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 systolico stroke volume plateaus as exercise intensity increases due to increased HR and decreased filling timeo Increased lusitropy and central venous pressure help maintain SV at high