control+of+cardiac+output24+canvas.pptx

L03 Control of cardiac output Dr Teresa Thomas [email protected] Learning objectives By the end of this session, you should be able to: Describe the variables that determine cardiac output Describe how heart rate is controlled by the autonomic nervous system Appreciate the role o...

L03 Control of cardiac output Dr Teresa Thomas [email protected] Learning objectives By the end of this session, you should be able to: Describe the variables that determine cardiac output Describe how heart rate is controlled by the autonomic nervous system Appreciate the role of veins in determining cardiac output Describe the intrinsic and extrinsic  ~5L/min CO = HR x SV CO = HR x (EDV – ESV Remember! ) Things to consider: How are these variables controlled at rest? How do they change if CO needs to ↑ or ↓?  1 Control of heart rate CO = HR x SV CO = HR x (EDV – ESV ) Cardiac muscle cells depolarise & contract rhythmically without nerves: myogenic rhythmicity or autorhythmicity ‘Pacemaker’ Sino-atrial (SA) node RA LA RV LV conduction then occurs in a highly coordinated way Yr 2 CPP Autonomic control of the CVS Copyright © Richard E. Klabunde, www.CVphysiology.com, 2009 utonomic control of the heart (antagonistic) Parasympathetic SA (vagus) nerve nod Medulla e Spinal AV Cord nod Sympathetic e ganglion Sympathetic nerve Ventricu lar muscle http://encyclopedia.lubopitko-bg.com/ images/Autonomic%20nervous %20system%20regulation%20of %20the%20heart.jpg  SA node ncreased sympathetic activity increases HR control sympathetic stimulation d& NorA ing t Ad ac at b1 ors t recep threshold increases permeability to Na+ and Ca Positive chronotropic effect reaches threshold quicker – more action potentials/minute * * Year 2 CPP  SA node creased parasympathetic (vagal) activity decreases HR h at Resting HR Ac Parasympathetic stimulation 2 M ept rec or threshold threshold 1. hyperpolarises cell (opens K+ channels) 2. reduces permeability to Na+ and Ca+ (longer to get to threshold) * * Year Negative chronotropic effect 2 CPP  SA node intrinsic rate is 100 action potentials/min so why is resting heart rate 60-70 beats/min? Autonomic control (antagonistic) ‘Pacemaker’ SA node RA LA RV LV ‘Vagal tone predominates’ http://encyclopedia.lubopitko-bg.com/ images/Autonomic%20nervous %20system%20regulation%20of %20the%20heart.jpg CO = HR x SV Remember! CO = HR x (EDV – ESV ) Changing the electrical activity at the SA node is the only way HR can change exerci dru temperat gs se stress ure  2 Control of End Diastolic volume (EDV) CO = HR x SV CO = HR x (EDV – ESV ) Remember from cardiac cycle? Central Venous Pressure (CVP) pressure in the thoracic vena cava near the right atrium cardiac filling (venous return EDV volume of blood in the ventricle at the end of diastole ~120 ml hat determines venous return? To heart To heart Valves prevent backflow (due to gravity) Relaxed Contracted muscle muscle vein Valves open Proximal valve open distal valve closed keletal muscle pump https://basicmedicalkey.com/the-cardiovascular-system-2 hat determines venous return? Pthorax Pthorax ↓ Pright atrium PRA↓ Venous return inspirationexpiration Pabdomen ↑ espiratory pump hat determines venous return? increased total blood volume leads to increases in VR & CVP fluid retention through Renal failure activation of the renin- angiotensin- aldosterone system ased total blood volume leads to decreases in VR & CVP haemorrhage dehydration hat determines venous return? Veins are the capacitance vessels (where 60-80% of total blood volume fou vein shape Volume Stimulation of sympathetic nerves, catecholamines, Ang II Increased Tone (↓Compliance) Adapted from Pocock & Richards, OUP Pressure Venous tone Adapted from Cardiovascular Physiology Concepts (LWW) hat determines venous return? Thorax ↓Vol Lying (supine) Gravity ©1998-2020 Richard E. Klabunde  ↑ ↑ Central Venous Pressure ↑ = EDV – ESV SV (CVP) ↑ cardiac filling (venous return) ↑ EDV ↑S V How does ↑EDV an increase in EDV lead to an increase in SV? unchanged ↑ STROKE VOLUME How does increasing EDV lead to larger SV? Normal resting length Length-tension relationship of skeletal Cardiac muscle muscle  How does increasing EDV lead to larger SV? “Force of ventricular contraction is dependent on the length of ventricular muscle fibres in contraction) diastole.” Starling’s (Force of Law of the Heart Frank-Starling, ventricular function or Starling’s curve 150 300 EDV (ml) (sarcomere DV = PRELOAD on cardiac muscle length) ©1998-2020 Richard E. Klabund How does increasing EDV lead to larger SV? Length-dependent increase in Ca - 2+ sensitivity of contractile apparatus results in greater number of cross- bridges * contraction) (Force of 150 300 * Year 2 EDV (ml) CPP (sarcomere ©1998-2020 Richard E. Klabunde  3 Control of End Systolic volume (ESV) CO = HR x SV CO = HR x (EDV – ESV ) Remember from cardiac cycle? unchanged ↑SV ↓ESV ONTRACTILITY or INOTROPY - n increase in SV at any given EDV contractility 70 norm contractility 120 EDV (ml) Adapted from www.cvphysiology.com/Cardiac%20Function/CF003 ily of Starlings curves – depending on level of contractility contractility contractility 0 150 300 EDV (ml) Adapted from www.cvphysiology.com/Cardiac%20Function/CF003 w can contractility/inotropy be increased? sympathetic nerve activity and/or circulating nor/adrenaline acting at β1 receptors on ventricular cells * NorAd Ad b 1 Ca2+ release Ca2+ influx cross-bridge formation * Year cross-bridge force of contraction 2 ESV formation and SV CPP Afterload also affects SV The load against which the heart must contract to eject the stroke volume For the LEFT ventricle the afterload is the AORTIC PRESSURE (depends on the TPR) 120/80 (systemic resistance high; TPR) Ao 25/10 (pulmonary resistance low) PA LA RA For the RIGHT ventricle the afterload is the PULMONARY PRESSURE LV RV Therefore, LV has thicker muscle than RV Adapted from Cardiovascular Physiology Concepts, Klabunde, Lippincott, Williams & Wilkins Questions? Ask questions anonymousl y on the Week 1 padlet