11) 04_Cardiovascular system-CO_AL_PL_2023.pdf

CARDIOVASCULAR SYSTEM Cardiac output & Regulation of the cardiac functions 2024 1 Learning outcomes • Define and calculate cardiac output • Explain preload and afterload • Explain the relationship between the left ventricular volume and pressure by drawing volume-pressure curve • Discuss how left...

CARDIOVASCULAR SYSTEM Cardiac output & Regulation of the cardiac functions 2024 1 Learning outcomes • Define and calculate cardiac output • Explain preload and afterload • Explain the relationship between the left ventricular volume and pressure by drawing volume-pressure curve • Discuss how left ventricular volume-pressure curve is affected with increased preload and afterload 2 • Describe factors affecting heart rate (chronotropic effects) • Describe factors affecting conduction velocity in the heart (dromotropic effects) • Describe factors that are affecting contractility of the heart (inotropic effects) 3 CARDIAC PERFORMANCE • Normally each ventricle has approximately 125 ml at the end of diastole (EDV). • During a systolic contraction, the volume of blood pumped out by each ventricle is called the stroke volume (SV). SV is usually approx. 70 ml/beat. This volume correlated with the force of contraction. • Not all blood in the ventricle is ejected. The volume remaining is called the end-systolic volume (ESV) which is usually 55 ml. Stroke Volume = EDV- ESV 4 a wave - atrial contraction c wave- ventricles begin to contract v wave slow flow of blood into the atria 5 • Cardiac output is the total volume ejected by the ventricle per unit time. (approx. 5 L/min) 6 7 • Ejection fraction is the fraction of the end-diastolic volume ejected in each stroke volume, which is a measure of ventricular efficiency 8 FRANK-STARLING RELATIONSHIP • the volume the ventricle ejected in systole was determined by the end-diastolic volume (volume returned to the heartvenous return). • the principle underlying this relationship is the length-tension relationship in cardiac muscle fibers • Stroke volume and cardiac output are correlated directly with end-diastolic volume 10 Preload: the degree to which cardiac muscle cells are stretched just before they contract. Preload is the critical factor controlling stroke volume. Resting cardiac cells are normally shorter than optimal length, therefore stretching cardiac cells can produce increase in contractile force (Frank- Starling law). • the amount of blood returning to the heart and distending its ventricles à venous return Human Anatomy & Physiology, Cummings, Pearson Education Inc. Afterload - The pressure that must be overcome for the ventricles to eject blood Human Anatomy & Physiology, Cummings, Pearson Education Inc. 12 LEFT VENTRICULAR PRESSURE-VOLUME LOOP Physiology 5th Edition, by Linda S. Costanzo 13 PRESSURE-VOLUME LOOP A = AV valve opens A-B = filling B = End diastolic volume (EDV); AV valves closes B-C = isovolumic contraction C = Aortic valve opens C-D = ejection D = End systolic volume (ESV); Aortic valve closes D-A = isovolumic relaxation EW, net external work. 14 a wave - atrial contraction c wave- ventricles begin to contract v wave slow flow of blood into the atria 15 Increased preload Increased afterload Physiology 5th Edition, by Linda S. Costanzo 16 Regulation of Cardiovascular System 17 Modulation of cardiac activity • Inotropic effects: Any chemical that affects contractility is called an inotropic agent {ino, fiber}, and its influence is called an inotropic effect. • Positive or negative • Sympathetic nervous system has positive inotropic effects on myocard muscle 18 Physiology 5th Edition, by Linda S. Costanzo 19 Heart rate • Chronotropic effects: the effects that change the frequency of the heart beat • Positive or negative • Tachycardia – fast heart rate Usually defined as faster than 100 beats/min (BPM) e.g. increased body temperature, sympathetic nerves • Bradycardia – slow heart rate Usually defined as fewer than 60 beats/min e.g. parasympathetic nerves (vagal stimulation) 21 Autonomic effects on conduction velocity • Dromotropic effects – the effect on conduction velocity • Positive or negative • Stimulation of sympathetic nervous system produces an increase in conduction velocity through the AV node (positive dromotropic effect) • Stimulation of parasympathetic nervous system produces a decrease in conduction velocity through AV node (negative) 22 24 25 Human Physiology: An Integrated Approach 6e Pearson 26 The two types of ACh receptors (cholinergic) Nicotinic* ACh receptors: Always excitatory Muscarinic* ACh receptors: • Can be either inhibitory or excitatory • Depends on the receptor type of the target organ Cells in SA and AV nodes carry inhibitory M2 receptor type • ↑ K+ conductance (G protein mediated - open K+ channels) • ↓ Ca2+conductance (decrease in cAMP) *These are named according the drugs that bind to them and mimic ACh effects 27 Human Physiology: An Integrated Approach 6e Pearson 28 29 Norepinephrine (adrenergic) receptors • Beta (1) receptors – cardiac cells carry β-type adrenergic receptors Ø via G-protein (Gs) β receptor activates adenylate cyclase (AC), which catalyzes the conversion of ATP to cAMP. Ø cAMP activates If channels and protein kinase A (PKA). Ø PKA modulates (by phosphorylating) ion channels, transporters, exchangers, intracellular Ca2+-handling proteins, and the contractile machinery. à increase in heart rate, conduction velocity and contractile force 30 Front. Physiol., 19 October 2011 | doi: 10.3389/fphys.2011.00067 31 Human Physiology: An Integrated Approach 6e Pearson 32 Human Physiology: An Integrated Approach 6e Pearson 33