Cardiorespiratory System Part I PDF

Cardiorespiratory System: Part I Cardiovascular System Learning Objectives: 1. Describe the components and function of the cardiorespiratory system 2. Discuss cardiac muscle structure and function 3. Explain cardiac muscle cell physiology including action potential generation, action pot...

Cardiorespiratory System: Part I Cardiovascular System Learning Objectives: 1. Describe the components and function of the cardiorespiratory system 2. Discuss cardiac muscle structure and function 3. Explain cardiac muscle cell physiology including action potential generation, action potential propagation, mechanical contraction, and relaxation 4. Summarize what occurs during different parts of the cardiac cycle 5. Discuss the electrophysiology of the heart including how it relates to the cardiac cycle and an ECG reading 6. Discuss measures of cardiac function including cardiac output and ejection fraction 7. Describe how body modifies cardiac function 8. Discuss role of Autonomic Nervous System on cardiac function Components of the Cardiorespiratory System I. Cardiovascular System What’s the difference? Heart Pulmonary vascular system Cardiopulmonary Peripheral/systemic vascular system vs. Cardiovascular II. Pulmonary System vs. Lungs Cardiorespiratory Sites of respiration Terminology: Cardiopulmonary (heart and lungs) Cardiovascular (heart, blood vessels, blood) Cardiorespiratory (cardiovascular, respiration-internal and external) Functions of Cardiorespiratory System I. Transport and delivery III. Protection Transport and exchange of Prevention of blood loss via respiratory gases hemostatic mechanisms Transport and exchange of nutrients Prevention of infection (leukocytes, and waste products lymphatic tissue) Transport of hormones and other chemical messenger II. Homeostatic regulation Fluid balance between fluid compartments Maintain pH Maintain thermal balance Regulate blood pressure Myocardium Forms – R and L atria (thin walls) – 2 ventricles Thick walls LV thicker than RV Inter-ventricular septum – Thick wall Coronary blood supply Right coronary artery Supplies right side of heart Left (main) coronary artery Divides into marginal, posterior Supplies left side of interventricular heart Divides into circumflex, anterior descending Characteristics of Myocardial Cells Highly Oxidative Mitochondria dense Capillary rich Very Highly Fatigue Resistant Slow myosin ATPase Lactase Dehydrogenase (LDH) has high affinity for lactate No muscle bundles or motor units Entire heart – all or none Force controlled by extrinsic factors Cardiac muscle fibers connected by intercalated discs Desmosomes: hold cells together Gap junctions: rapidly conduct action potentials Myocardium Striated Contains actin and myosin in myocardium Requires calcium for contraction Contracts via Sliding Filament Theory Cardiomyocyte Structure Review Sarcomere- functional/contractile unit of the myocyte Repeating sarcomere make up myofibrils Length of one sarcomere is z disc to z disc Made up of actin and myosin proteins Actin – thin filament Myosin – thick filament Titin – stabilizes thick filament to prevent overstretching Striation = visible light and dark bands Interaction between actin and myosin is responsible for muscle contraction via the sliding filament theory Hall, Wooten Excitation Heartbeat when you’re excited about Phys Conduction of cardiac system The heart contracts rhythmically due to self generation of action potentials Autorhythmic Two specialized cell types Contractile – 99% of cardiac muscle cells, do not generate their own AP Autorhythmic – specialized for initiating and conducting AP Pacemaker Activity Cardiac autorhythmic cells do not have a resting membrane potential Membrane potential slowly depolarizes or drifts between action potentials until threshold is reached Pacemaker potential Most important changes in ion movement that give rise to pacemaker potential are 1. Increased inward Na+ current 2. Decreased outward K+ current 3. Increased inward Ca+ current 1. Increased inward Na+ current Initial phase of slow depolarization Caused by net entry of Na+ into cell Voltage gated channels Unique channels open when the potential becomes more negative (hyperpolarizes) Generally at the end of repolarization from previous AP Funny channels or If channels When AP ends these channels open which causes net inward movement of Na+ Moving the potential towards threshold 1 once more 2. Decreased outward K+ current Progressive reduction in the passive outward flux of K+ The K+ channels that were open during the falling phase of previous AP slowly close at negative potentials Slow gradual closing diminishes the outflow of positive K+ So slow outward drift of K+ and slow inward drift of Na+ causes the continued drift towards threshold 2 3. Increased inward Ca+ current In the second half of the pacemaker potential the funny channels close and transient Ca+ channels open before the membrane reaches potential The resultant brief influx of Ca+ further depolarizes the membrane The Ca+ transient channels then close 3 Once threshold is reached the AP rises due to activation of L-type Ca+ channel Longstanding voltage gated calcium channel Large amounts of Ca+ rush into cell Ca+ influx swings the potential in positive direction 4. Repolarization The falling phase is a result of K+ efflux Activation of voltage gated K+ channels open 4 Closure of the L-type Ca+ channels After AP is over low closure of the K+ channels leads to next slow depolarization to threshold Long refractory period The main reason for this is the inactivation, during the plateau phase, of the Na+ channels All double gated Na+ channels are closed Not until the membrane recovers from the inactivation process can the Na+ channels be activated to begin another AP Action Potentials Electrical Conduction in Myocardial Cells Membrane potential of autorhythmic cell Membrane potential of contractile cell Cells of SA node Contractile cell Intercalated disk with gap junctions Depolarizations of autorhythmic cells rapidly spread to adjacent contractile cells through gap junctions. Ca+ induced Ca+ release a) AP carried into interior of cell via T-tubles b) Voltage-sensitive receptors (L- type calcium channels) open to allow Ca2+ entry into the cell c) Ca2+ binds to calcium release channels on the junctional SR d) Causing release of Ca2+ from junctional SR e) Intracellular Ca2+ binds to regulatory protein troponin – leading to cross-bridge formation f) At end of cardiac AP – SR calcium-adenosine triphosphatase (ATPase) pump located on SR, pumps Ca2+ back into SR + sarcoplasmic sodium- 2+ Intrinsic Control of Heart Activity: Cardiac Conduction System Spontaneous rhythmicity: special heart cells generate and spread electrical signal Sinoatrial (SA) node Atrioventricular (AV) node AV bundle (bundle of His) Purkinje Fibers Electrical signal spreads via gap junctions Intrinsic heart rate (HR): 100 beats/min Observed in heart transplant patients (no neural innervation) Extrinsic Control of Heart Activity: Parasympathetic Nervous System Reaches heart via vagus (cranial nerve X) Carries impulses to SA, AV nodes Releases acetylcholine, hyperpolarizes cells Decreases HR, force of contraction Decreases HR below intrinsic HR Intrinsic HR: 100 beats/min Normal resting HR (RHR): 60 to 100 beats/min Elite endurance athlete: 35 beats/min Parasympathetic control of heart Enhanced K+ permeability hyperpolarizes the SA node membrane – RMP now further from threshold Acetylcholine (Ach) depresses inward movement of Na+ and Ca+ through channels Further slowing depolarization to threshold AV node excitability decreases – longer AV nodal delay Again through increasing K+ permeability Atrial contractile cells slower inward current of Ca+, reducing the plateau phase and making contraction weaker No real effect on ventricle Heart is more leaisurly Extrinsic Control of Heart Activity: Sympathetic Nervous System Opposite effects of parasympathetic Carries impulses to SA, AV nodes Releases norepinephrin, facilitates depolarization Increases HR, force of contraction Endocrine system can have similar effect (epinephrine, norepinephrine) Increases HR above intrinsic HR Determines HR during physical, emotional stress Maximum possible HR: 250 beats/min Sympathetic control of heart Biggest thing to occur is greater inward movement of Na+ and Ca+ - swifter drift to threshold Sympathetic stimulation of the AV node reduces AV nodal delay In chambers there is an increase in the permeability of Ca+ through opening of L-type Ca+ channels – more Ca+ means stronger contraction EKG or ECG Electrocardiogram (ECG or EKG) The graphic representation of the heart’s electrical activity Used to evaluate the hearts electrical activity in relation to the clinical situation at hand Able to detect abnormal heart function related to: Cardiac rhythm Electrical conduction Myocardial oxygen supply Tissue damage Does not offer information regarding whether abnormalities are old or new Availability of a prior tracing for comparison ECG Trace Signals picked up from the skin by electrodes – Action Potential! Deflections represent direction of depolarization wave Upward: electrical activity towards a positive lead Downward: electrical activity away from a positive lead ECG Placement Conductivity of the heart is recorded by the use of electrodes placed in specific locations on the body Lead placements allow views of the heart from different angles Standard ECG involves attaching 10 electrodes 4 to each limb plus 6 across the chest ECG Trace Basic pattern of an ECG Electrocardiogram © 2013 Pearson Education, Inc. Abnormal Rhythm Pacemaker cells within the SA node typically regulates the heart rate (60 – 100 bpm) However, pacemaker sites outside of the SA node are also capable of triggering depolarization Referred to as ectopic foci Can occur within the atria or ventricles Slower inherent pacing rate (e.g., atria ~ 60 – 80 bpm; ventricles ~ 20 – 40 bpm) Normally suppressed by the higher rate of the SA node, but may act as a back-up However, may cause arrhythmias Premature Ventricular Contraction (PVC) PVC occurs when a focus in the ventricles generates an action potential before the next SA node potential Could reflect myocardial ischemia and injury Characteristics: Premature: occurs earlier than expected Ectopic: Originates outside SA node Wide QRS complexes: Due to gradual spread of depolarization across the ventricles Compensatory pause: Next normal heart beat arrives after an interval Premature Ventricular Contraction (PVC) CEUFast.com Ventricular Fibrillation Caused by continuous rapid firing of multiple ventricular automaticity foci Uncoordinated contraction of the heart Causes cardiac arrest and sudden cardiac death Myocardial Infarction (MI) Pattern of ST elevation where the QRS complex, ST segment and T wave merge – “tombstone” Myocardial Infarction (MI) meds.queensu.ca Regulation of Cardiovascular Function  Cardiac Cycle: Ventricular Diastole 2/3 of cardiac cycle Relaxation begins Ventricular pressure drops Semilunar valves close (heart sound 2, “dub”) Atrioventricular valves open Fill 70% passively, 30% by atrial contraction At end, blood in ventricle = end- diastolic volume (EDV) Phases of diastole Passive filling ventricular