# IBHS 527 lecture 6

 The flashcards below were created by user VASUpharm14 on FreezingBlue Flashcards. what is cardiodynamics? 1. cardio: how much blood does the heart eject in 60 seconds?2. dynamic: how does the body increase of decrease this amount?3. what drugs increase of decrease this amount-and how do they do it? cardiac output volume of blood ejected by a heart pump in one minute; amount of blood pumped by each ventricle in one minute use: clinical measure of productivity = heart health*volume ejected by each ventricle is about the same equation of cardiac output C.O. = heart rate (HR) X stroke volume (SV)cardiac output = ? L/min-HR = # of contractions of the heart during one minute *average HR = 75 beats/minute-SV = amount of blood ejected from each ventricle during one beat*average SV = 80 ml/beat=> 6 L/min is cardiac output combined cardiac output L/min for both ventricles*volume ejected by each ventricle is about the same 2 ways to change cardiac output (C.O.) 1. influence the rate of the conduction system (nodes) to change the heart rate2. influence the strength of the contraction system (myocardium) to change the stroke volume heart rate while sleeping 65 beats/min*lower than average of 75 bpm maximum heart rate of person 220 - age = maximum heart rate just increasing heart rate will have what fold increase in cardiac output (C.O.)? ~2.5 x what determines the heart rate? SA nodal cells (top of the heart) regulated by: 1. nervous system (autonomic innervation)2. endocrine system (hormones) what determines the stroke volume? ventricle muscle cells (bottom of the heart)regulated by: 1. cardiovascular system (end-diastolic volume)2. nervous and endo system (end-systolic volume) 3 receptors that detect blood change 1. chemoreceptors2. baroreceptors3. stretch receptors context: 3 receptors that detect blood change chemoreceptors detect gas changes such as O2 and CO2 context: 3 receptors that detect blood change baroreceptors detect changes in blood pressure (BP) and blood volume (BV) context: 3 receptors that detect blood change stretch receptors detect distention of right atrium"Bainbridge reflex" process of regulating cardiac output by Nervous system (autonomic innervation) (1) blood changes detected by receptors (chemo/baro/stretch) --> (2) send action potential (AP) to medulla oblongata --> medulla oblongata sends action potential (AP) to heart --> neurotransmitters are released onto SA node*sympathetic (spinal nerve) = norepinephrine = speed up*parasympathetic (cranial nerve X/vagus nerve) = acetylcholine = slow down process of regulating cardiac output by Endocrine system (hormones) (1) changes in blood detected (chemo/baro) --> (2) send action potential (AP) to medulla oblongata --> medulla oblongata sends action potential (AP) to adrenal medulla --> gland releases epi and norepi --> stimulates SA node*stressful conditions - epistimulation How does ACh decrease the heart rate (HR)? parasympathetic --> ACh release --> bind to muscurinic receptors --> opens K+ channels (inside becomes less positive/more negative and RMP goes from -60 mV to -70 mV and now takes longer to create action potential (AP) --> slower APs => DEC. heart rate (HR) How does NE/E increase the heart rate (HR)? sympathetic --> Norepi/Epi release --> bind to beta-1 adrenergic receptors --> opens Ca2+ channels (inside becomes more positive/less negative and RMP goes from -60 mV to -50 mV and now is quicker to create action potential (AP) --> faster APs => INC. heart rate (HR) process of stroke volume (1) systole (action - squeezing) --> (2) end systolic volume (pause - left over volume in heart) --> (3) diastole (action - distending) --> (4) end diastolic volume (pause - volume gained in heart) equation of stroke volume SV = EDV - ESV*the difference between: -EDV = end-diastolic volume (volume after diastole)-ESV = end-systolic volume (volume after systole) 2 ways to detect ventricle volumes 1. measure via Cardiac Conductance Catheterization (electrical impedance)2. estimate via echocardiogram (ultrasound) 2 ways to change stroke volume 1. change end-diastolic volume (EDV)2. change end-systolic volume (ESV) context: 2 ways to change stroke volume change end-diastolic volume (EDV) 1. INC. stroke volume: INC. EDV (put more in heart- preload) 2 ways: -INC. blood into heart by INC. venous return (INC. BV)-INC. filling time (DEC. HR)2. DEC. stroke volume: opposite of above context: 2 ways to change stroke volume change end-systolic volume (ESV) 1. INC. stroke volume: DEC. blood left in heart 3 ways: -INC. EDV (Frank Starling's law) - more in more out-INC. contractility (Epi, Norepi) with same amount of blood but with INC. calcium release-DEC. afterload (vasodilation = less resistance) positive effectors of the heart increase cardiac output (C.O.)1. increase HR (conduction): -use positive chronotropic agents (affect SA node)2. increase SV (contraction): -use positive inotropic agents (affect myocardial muscle cells)*positive chronotropic/inotropic agents (affect node + muscle cells)1. endogenous/natural: - epi/norepi - binds to beta-1 receptor --> open Ca2+ channels2. exogenous/drugs: - epi pen - beta-1 receptor agonists (like in CHF) negative effectors of the heart decrease cardiac output (C.O.)1. decrease HR (conduction): -use negative chronotropic agents (affect SA node)2. decrease SV (contraction): -use negative inotropic agents (affect myocardial muscle cells) *negative chronotropic/inotropic agents (affect node + muscle cells)1. endogenous/natural: - ACh - binds to muscarinic receptors --> opens K+ channels2. exogenous/drugs: (a) beta-1 receptor antagonists/beta blockersex: - atenolol (Tenormin)- metoprolol (Toprol, Lopressor)(b) calcium channel blockers (with specificity for cardiac calcium channels (cc))ex: - verapamil (Calan SR, Verelan) - high specificity cardiac calcium channels (cc)- diltiazem (Cartia) - medium specificity for cardiac calcium channels (cc) mixed effectors of the heart digoxinfunction: 1. decreases HR (conduction)negative chronotropic agent (affect SA node)-inhibition of the Na+/K+ exchanger-conduction cells can't recover membrane potential as fast 2. increases SV(contraction)positive inotropic agents (affect myocardial muscle cells)-inhibition of the Na+/K+ exchanger-Na+ builds up inside cell --> loss of Na+ gradient-inhibition of Na+/Ca2+ exchanger- calcium builds up inside cell --> more force generation*uses in atrial fibrillation because don't want heart to beat too fast and also to not work too hard-first choice are beta-blockers and calcium channel blockers AuthorVASUpharm14 ID61403 Card SetIBHS 527 lecture 6 DescriptionCardiodynamics. richard. fun stuff Updated2011-01-23T08:27:50Z Show Answers