Figure 22.6

joined by intercalated discs CARDIAC MUSCLE CELLS Branched joined by intercalated discs desmosomes: tightly bind cells & transfer of tension gap junction: electrical synapses that directly transfer electrical activity/AP from one cell to the next Contractile/myocardial Cells => contract and conduct AP’s Conductile/autorhythmic cells => produce and conduct action potentials

AP in SA conductile/nodal/autorhythmic cells VG Na+ channels HCN channels: VG ion channels, open due to hyperpolarization, allow Na+ in VG Ca channels cause depolarization of AP VG K channels cause repolarization

Fig. 13.20 Conduction System

AP/Stimulus begins in SA node Transmitted through conduction system and from cell to cell via gap junctions Both Atria contract, then both ventricles contract

AP in Contractile/Myocardial Cells Plateau cause by slow VG Ca+ channels & Ca+ inflow this prolonged state of depolarization results in long period of refractory. Long refractory prevents heart from entering tetanus (which is a good thing as heart needs to relax to fill)

AP and Excitation-Contraction Coupling in Myocardial cells (contractile cells) AP formation and propagation as in axons and skeletal muscle opening of VG Ca+  Ca+ flows in Ca+ entering cytoplasm causes Ca release channels to open massive Ca release from SR “calcium induced calcium release” actin and mysin interact as in skeletal muscle Extracellular calcium plays bigger role in myocardial contraction than in skeletal muscle fiber contraction Fig. 12.34 8

Fig. 13.10

Table 13.6

Fig. 13.11

the repeating sequence of contraction and relaxation of the heart. Fig. 13.13 Cardiac Cycle: the repeating sequence of contraction and relaxation of the heart. Diastole = relaxation filling Systole = contraction ejection of blood

Fig. 13.14

Isovolumetric contraction Ejection Isovolumetric relaxation Fig. 13.14 Isovolumetric contraction Ejection Isovolumetric relaxation Rapid refilling Atrial contraction

ECG: measures overall electrical activity of the whole heart PR interval: time it takes for depolarization that begins in SA to spread to ventricles Long PR represent damage to atria conductive system or AV note QT interval: time of ventricles to depolairze and repolarize. Can Ax electrolytes imbalance, tissue damage, ischemia

Fig. 13.25

Maintenance of proper blood pressure (BP) is critical for proper CVS function BP is influenced by: cardiac output (CO) heart function peripheral resistance vessel activity and blood characteristics Cardiac Output = Heart Rate (HR) x stroke volume (SV)

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Relationship among factors that determine cardiac output

Heart activity is regulated by Autonomic Nervous System (ANS) Sympathetic Nerves Parasympathetic nerves—vagus nerve Hormones Intrinsic Regulation

Cardiac Control Centers is in medulla Fig. 14.27 Cardiac Control Centers is in medulla influenced by higher brain centers Cardiac centers recieve sensory input from vagus nerve hypoglossal nerve barroreceptors—pressure chemoreceptors—blood chemistry Medulla Signals heart via vagus nerve-parasympathetic sympathetic cardiac nerves

Fig. 14.27

Regulation of Heart Rate Nervous system SD and PD inneration of SA node Endocrine System hormone affects on SA node Intrinsic (autoregulation) stretch of nodal cells directly increases rate of depolarization

Vagus Nerve (parasympathetic) Ach—muscarinic receptors (g-proteins—ion channels) innervates atria/SA node & AV node Sympathetic Nerves (sympathetic) Norepinephrine (NE)—Beta 1 (β1) receptors innervates ventricles sympathetic nervous system also signals the heart via the endocrine system/epinephrine

Autonomic Innervation Parasymphathetic division slows heart rate slows rate of SA node depolarization Sympathetic division increases heart rate speeds up rate of SA node depolarization Heart receives constant input from BOTH systems balance of SD and PD determines if HR goes up or down At rest Parasympathetic signals predominate and this depresses the heart rate below the SA nodes intrinsic rate of ~100 bpm

Nervous Regulation of HR Parasympathic: Ach-muscarinic receptors opens K+ gates slows pacemaker potential decreases HR Sympathetic: NE-- β1 opens Na-Ca+ channels speeds up pacemaker potential increases HR / Natural rate

Interplay between PD and SD activity Increasing PD—slows heart decreasing PD—speeds heart increasing SD—speeds heart decreasing SD—slows heart

Hormones and HR N.E., Epinephrine (E), and Thyroid Hormones delivered through blood can also increase HR increasing levels increase HR decreasing levels decrease HR mechanism similar to nervous system mechanisms (alters rate of pacemaker potential)

Atrial Reflex (SD regulation of heart) Atrial Reflex (Bainbridge reflex) Increased filling of atria (i.e., increased venous return or increased blood volume) stretches atrial wall sensory neurons relay stretch to medulla medulla increase rate of SD signaling of heart (or decreasin PD, literature is unclear) HR increases (in either case).

Intrinsic Regulation (autoregulation) of the Heart Rate Increased filling of atria (i.e., increased venous return or increased blood volume) stretches nodal cells of atrial wall stretching of the cells directly causes their rate of depolarization to increase

Regulation of Stroke Volume Stroke Volume influenced by: ESV EDV SV Preload (directly related to EDV) Afterload (equivalent to peripheral resistance/arterial blood pressure)

EDV: the amount of blood in each ventricle at the end of diastole (i.e., how much blood fills ventricles) ESV: amount of blood in each ventricle at end of systole (how much blood is left after ejection/contraction SV: how much blood is ejected from each ventricle during systole EDV-ESV=SV

Interactions between EDV, Preload, SV and CO Preload: amount of stretching of ventricular wall Caused by filling of ventricle and directly related to EDV ↑ EDV  ↑ Preload ↓ EDV  ↓ Preload EDV is influenced by venous return (rate of blood return to heart through veins) ↑ venous return  ↑ EDV/ Preload ↓ venous return  ↓ EDV/Preload

Interactions between EDV, Preload, SV and CO: Frank-Starling ↑ venous return  ↑ EDV/ Preload  increased ventricular stretching  ↑ ventricular contraction strength  ↑ SV  ↑ CO “more in, more out” intrinsic regulation that makes output match return (also keeps two circuits in synch by making sure amount through systemic circuit keeps pace with amount through pulmonary Increased contraction strength due to lengthening of sarcomeres to a more optimum overlap length  stronger contraction

Fig. 14.3

Contractility: ↑ contractility--↑ SV, ↓ contractility-- ↓ SV Contractility=Increase in contraction strength due to ionotropic effects (i.e., for reasons other than fiber length/overlap) due to Ca+ availability in cytoplasm Causes of Increased Contractility SD fibers to ventricles—NE– Beta 1-- ↑ contractility-- ↑ SV Adrenal medulla—E-- Beta 1(in venricles)-- ↑ contractility-- ↑ SV Although PD technically innervates ventricles their role is negligable Hormones (other than E) Thyroid hormone and glucagon also increase contractility

Topics Related to contractility Beta 1 stimulators or drugs that increase intracellular calcium (like digitalis) increase contractility/CO Beta blockers drugs decrease Ca+, decrease contractility, decrease CO used to treat hypertension Ca+ channels blockers (nifedipine): Ca+, decrease contractility, decrease CO

Afterload and CO Afterload: amount of pressure ventricles need to produce/overcome to eject blood directly related to arterial blood pressure (i.e., peripheral resistance) ↑ afterload  ↓ ejection  ↓ SV  ↓ CO chronic high blood pressure = chronic high afterload causing heart to work excessively hard/stress to maintain CO weakened or diseased heart may be unable to overcome relatively small increases in afterload causing significant problems in maintain CO/BP

~TPR

Table 14.1

Fig. 14.2

Table 14.3

Fig. 14.7

Fig. 14.5 P.R.