* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download Properties of cardiac muscle Properties of Cardiac Muscle
Management of acute coronary syndrome wikipedia , lookup
Coronary artery disease wikipedia , lookup
Artificial heart valve wikipedia , lookup
Heart failure wikipedia , lookup
Cardiac contractility modulation wikipedia , lookup
Lutembacher's syndrome wikipedia , lookup
Cardiac surgery wikipedia , lookup
Hypertrophic cardiomyopathy wikipedia , lookup
Myocardial infarction wikipedia , lookup
Jatene procedure wikipedia , lookup
Mitral insufficiency wikipedia , lookup
Electrocardiography wikipedia , lookup
Quantium Medical Cardiac Output wikipedia , lookup
Dextro-Transposition of the great arteries wikipedia , lookup
Atrial fibrillation wikipedia , lookup
Ventricular fibrillation wikipedia , lookup
Arrhythmogenic right ventricular dysplasia wikipedia , lookup
3/1/2016 Properties of cardiac muscle • Cardiac muscle –Striated –Short –Wide –Branched –Interconnected The Cardiovascular System Part 2 Nucleus Properties of Cardiac Muscle • Skeletal muscle –Striated –Long –Narrow –Cylindrical Intercalated discs Cardiac muscle cell • Cells connected to each other by intercalated discs – Passage of ions between cells – Allows entire heart to work as a syncytium • Numerous large mitochondria Gap junctions –25–35% of cell volume –Increases cell capacity to do what? Desmosomes • Able to utilize many food molecules –Example: lactic acid –Most cells primarily use what? (a) Figure 18.11a Properties of cardiac muscle Cardiac muscle cell Mitochondrion Intercalated disc Nucleus • Some cells are myogenic – Contractile impulse originates in non-contractile pacemaker cells, not in nerve cells • Cardiac control center in medulla can increase or decrease rate through ANS • Primary innervation is inhibitory through vagus nerve T tubule Mitochondrion Sarcoplasmic reticulum Z disc Nucleus Sarcolemma (b) I band A band – Sympathetic or PNS? – Because cells are joined by gap junctions, spontaneous depolarization of pacemaker cells initiates depolarization of contractile cells too I band Figure 18.11b 1 3/1/2016 Action Potential in Myogenic Cells of the Heart Properties of cardiac muscle Threshold Action potential 2 • Heart contracts as a unit or not at all (video) 2 3 – Sodium channels leak slowly in specialized cells • Spontaneous depolarization • Leakage rate sets rhythm 1 – Compare to skeletal muscle 1 Pacemaker potential This slow depolarization is due to both opening of Na+ channels and closing of K+ channels. Notice that the membrane potential is never a flat line. Pacemaker potential 2 Depolarization The action potential begins when the pacemaker potential reaches threshold. Depolarization is due to Ca2+ influx through Ca2+ channels. 1 3 Repolarization is due to Ca2+ channels inactivating and K+ channels opening. This allows K+ efflux, which brings the membrane potential back to its most negative voltage. Figure 18.13 Action Potential of Contractile Cardiac Muscle Cells 2 Tension development (contraction) 3 1 Absolute refractory period Time (ms) Allows sufficient refilling of the heart before the next beat Tension (g) Membrane potential (mV) Action potential Plateau 1 Depolarization is due to Na+ influx through fast voltage-gated Na+ channels. A positive feedback cycle rapidly opens many Na+ channels, reversing the membrane potential. Channel inactivation ends this phase. 2 Plateau phase is due to Ca2+ influx through slow Ca2+ channels. This keeps the cell depolarized because few K+ channels are open. Conduction System of the Heart • Terms – Systole • Contraction of ventricles – Diastole • Relaxation of ventricles 3 Repolarization is due to Ca2+ channels inactivating and K+ channels opening. This allows K+ efflux, which brings the membrane potential back to its resting voltage. Figure 18.12 Conduction System of the Heart Conduction system of the heart • Specialized cardiac cells SA node (pacemaker) – Initiate impulse – Conduct impulse Atrial depolarization and contraction AV node Bundle of His Right and left bundle branches Purkinje fibers Myocardium Contraction of ventricles 2 3/1/2016 Conduction System of the Heart Conduction system of the heart 3. Atrioventricular (AV) bundle (bundle of His) 1. Sinoatrial (SA) node (pacemaker) – Generates impulses about 70-75 times/minute (sinus rhythm) – Depolarizes faster than any other part of the myocardium – Cut the vagus nerve = HR immediately increases by ~25bpm – Only electrical connection between the atria and ventricles 4. Right and left bundle branches – Two pathways in the interventricular septum that carry the impulses toward the apex of the heart 2. Atrioventricular (AV) node – – 5. Purkinje fibers Delays impulses approximately 0.1 second Depolarizes 50 times per minute in absence of SA node input – Superior vena cava Conduction Pathway Complete the pathway into the apex and ventricular walls Conduction System of the heart Right atrium 1 The sinoatrial (SA) node (pacemaker) generates impulses. • Intrinsic innervation • External influences Internodal pathway Left atrium 2 The impulses • Normal: pause (0.1 s) at the atrioventricular (AV) node. 3 The atrioventricular (AV) bundle connects the atria to the ventricles. 4 The bundle branches conduct the impulses through the interventricular septum. – Average = 70 bpm – Range = 60-100 bpm Purkinje fibers Interventricular septum 5 The Purkinje fibers depolarize the contractile cells of both ventricles. (a) Anatomy of the intrinsic conduction system showing the sequence of electrical excitation (Intrinsic Innervation) Figure 18.14a The vagus nerve (parasympathetic) decreases heart rate. Dorsal motor nucleus of vagus Cardioinhibitory center Conduction System of the heart Medulla oblongata Cardioacceleratory center • Sympathetic stimulation – Enhances Ca2+ movement in contractile cells – Increases HR, contractility Sympathetic trunk ganglion Thoracic spinal cord Sympathetic trunk Sympathetic cardiac nerves increase heart rate and force of contraction. • Stroke volume decreases due to less ventricular filling time – Speeds relaxation AV node SA node Parasympathetic fibers Sympathetic fibers Interneurons Figure 18.15 3 3/1/2016 Conduction System of the heart Conduction System of the heart • Parasympathetic stimulation – – – – – Dominant signal under resting conditions Cardiac response mediated by acetylcholine Opens K+ channels, hyperpolarizes cells Decreases HR Innervation of ventricles is sparse = little effect on contractility • Other influences – Blood pressure – Atrial reflex • Increased rate of blood returning to heart -> atrial stretching -> increased HR – Hormonal • Epinephrine, thyroxine = increase HR – – – – – Ion balance Exercise Temperature Exercise Age Homeostatic Imbalances Electrocardiography • A composite of all the action potentials generated by nodal and contractile cells at a given time Defects in the intrinsic conduction system may result in 1. 2. 3. 4. – Represents movement of ions = bioelectricity – Three waves Arrhythmias: irregular heart rhythms Bradycardia < 60 bpm Tachycardia >100 bpm Maximum is about 300 bpm 1. 2. 3. P wave: electrical depolarization of atria QRS complex: ventricular depolarization T wave: ventricular repolarization SA node Depolarization R QRS complex Sinoatrial node T P S 1 Atrial depolarization, initiated by the SA node, causes the P wave. Ventricular depolarization Ventricular repolarization R AV node T P Q Atrial depolarization Repolarization R Q S 4 Ventricular depolarization is complete. R T P T P Q S 2 With atrial depolarization complete, the impulse is delayed at the AV node. Atrioventricular node R Q S 5 Ventricular repolarization begins at apex, causing the T wave. R P-Q Interval S-T Segment T P T P Q-T Interval Q S 3 Ventricular depolarization begins at apex, causing the QRS complex. Atrial repolarization occurs. Figure 18.16 Q S 6 Ventricular repolarization is complete. Figure 18.17 4 3/1/2016 NORMAL HEART RHYTHM ARRHYTHMIAS (b) Junctional rhythm. The SA node is nonfunctional, P waves are absent, and heart is paced by the AV node at 40 - 60 beats/min. (a) Normal sinus rhythm. Figure 18.18 Figure 18.18 ARRHYTHMIAS ARRHYTHMIAS (c) Second-degree heart block. Some P waves are not conducted through the AV node; hence more P than QRS waves are seen. In this tracing, the ratio of P waves to QRS waves is mostly 2:1. (d) Ventricular fibrillation. These chaotic, grossly irregular ECG deflections are seen in acute heart attack and electrical shock. Video Figure 18.18 Figure 18.18 ARRHYTHMIAS ARRHYTHMIAS Atrial fibrillation Normal Atrial fibrillation . Rapid, irregular heartbeat. Note the absence of P waves (which represent depolarization of the top of the heart) Normal Atrial fibrillation 5 3/1/2016 The Cardiac Cycle • All events associated with blood flow through the heart during one complete heartbeat –Systole— ventricular contraction (ejection of blood) –Diastole— ventricular relaxation (receiving of blood) The Cardiac Cycle • Three events 1) Recordable bioelectrical disturbances (EKG) 2) Contraction of cardiac muscle 3) Generation of pressure and volume changes • Blood flows from areas of higher pressure to areas of lower pressure – Valves prevent backflow Left heart The cardiac cycle QRS P Electrocardiogram EKG T 1st Heart sounds P 2nd – Backpressure closes AV valves = isovolumetric contraction – Ventricular pressure becomes greater than aorta & pulmonary artery pressure = semilunar valves open Pressure changes Aorta Left ventricle Atrial systole Left atrium Control of blood flow Ventricular volume (ml) • Ventricular filling → ventricular systole Pressure (mm Hg) Dicrotic notch Changes in volume EDV SV ESV • Portion of ventricular contents ejected Atrioventricular valves Open Aortic and pulmonary valves Closed Phase Contraction 1 Closed Open Open 2a 2b Closed 3 1 Left atrium Right atrium Left ventricle Right ventricle Ventricular filling Atrial contraction 1 Ventricular filling (mid-to-late diastole) Isovolumetric contraction phase 2a Ventricular ejection phase 2b Ventricular systole (atria in diastole) Isovolumetric relaxation 3 Ventricular filling Early diastole Figure 18.20 Heart Sounds • Two sounds associated with closing of heart valves –First sound occurs as AV valves close and signifies beginning of systole = Lub –Second sound occurs when SL valves close at the beginning of ventricular diastole = Dub • Heart murmurs = abnormal heart sounds – Most often indicative of valve problems Aortic valve sounds heard in 2nd intercostal space at right sternal margin Pulmonary valve sounds heard in 2nd intercostal space at left sternal margin Mitral valve sounds heard over heart apex (in 5th intercostal space) in line with middle of clavicle Tricuspid valve sounds typically heard in right sternal margin of 5th intercostal space Figure 18.19 6 3/1/2016 Left heart Heart sounds Heart Sounds QRS P Electrocardiogram P T 1st 2nd Pressure (mm Hg) Dicrotic notch Changes in volume • Mitral stenosis Aorta Left ventricle Atrial systole Ventricular volume (ml) Pressure changes Left atrium EDV SV ESV Atrioventricular valves Open Aortic and pulmonary valves Closed Phase 1 Closed Open Open 2a 2b Closed 3 1 Left atrium Right atrium Left ventricle Right ventricle Ventricular filling Atrial contraction 1 Ventricular filling (mid-to-late diastole) Isovolumetric contraction phase 2a Ventricular ejection phase 2b Ventricular systole (atria in diastole) Isovolumetric relaxation 3 Ventricular filling Early diastole Figure 18.20 Heart sounds • Valvular insufficiency (regurgitation) Cardiac Output (CO) • Definition: volume of blood pumped by each ventricle in one minute – AKA: Minute volume • 2 major factors – Stroke volume (SV) – Heart rate (HR) Heart Sounds • Example: mitral valve prolapse Cardiac output • CO (ml/min) = heart rate (HR) x stroke volume (SV) –HR = number of beats per minute –SV = volume of blood pumped out by a ventricle with each beat (ml/min) 7 3/1/2016 Left heart Cardiac output QRS P Electrocardiogram EKG T 1st Heart sounds P 2nd • Stroke volume – Difference between EDV and ESV Pressure (mm Hg) Dicrotic notch Pressure changes Aorta Left ventricle Atrial systole Left atrium • EDV-ESV=SV Ventricular volume (ml) – Average is about 75 ml Changes in volume EDV SV ESV Atrioventricular valves Open Aortic and pulmonary valves Closed Phase 1 Closed Open Open 2a 2b Closed 3 1 Left atrium Right atrium Left ventricle Right ventricle Ventricular filling Atrial contraction 1 Ventricular filling (mid-to-late diastole) Isovolumetric contraction phase 2a Ventricular ejection phase 2b Ventricular systole (atria in diastole) Isovolumetric relaxation 3 Ventricular filling Early diastole Figure 18.20 Cardiac Output (CO) • At rest –CO (ml/min) = HR (75 beats/min) × SV (70 ml/beat) = 5.25 L/min – Maximal CO is 4–5 times resting CO in nonathletic people – CO may reach 30 L/min in trained athletes – Cardiac reserve Regulation of stroke volume • Stroke volume – Three main factors affect SV • Preload • Contractility • Afterload • Difference between resting and maximal CO Regulation of Stroke Volume Regulation of Stroke Volume • Preload – Frank-Starling law of the heart: the heart can change its CO according to the incoming volume of blood • At rest, cardiac muscle cells are shorter than optimal length • Must be a degree of stretch of cardiac muscle cells before they contract –Slow heartbeat and exercise increase venous return –Increased venous return distends (stretches) the ventricles and increases contraction force 8 3/1/2016 Regulation of Stroke Volume Regulation of Stroke Volume • Contractility • Afterload – Contractile strength at a given muscle length, independent of muscle stretch and EDV – Pressure (resistance) that must be overcome for ventricles to eject blood • Agents increasing contractility • Hypertension increases afterload – Increased Ca2+ influx » Sympathetic stimulation – Results in increased ESV and reduced SV Increase SV Decrease ESV – Hormones » Thyroxin, glucagon, and epinephrine • Agents decreasing contractility – Calcium channel blockers Control of Heart rate Exercise (by skeletal muscle and respiratory pumps; see Chapter 19) • Sympathetic nervous system – Norepinephrine • Increased SA node firing rate • Faster conduction through AV node • Increases excitability of heart by increasing Ca2+ availability Heart rate (allows more time for ventricular filling) Bloodborne epinephrine, thyroxine, excess Ca2+ Venous return Contractility EDV (preload) ESV Exercise, fright, anxiety Sympathetic activity Parasympathetic activity • Parasympathetic nervous system – Vagus nerve Heart rate Stroke volume • Decreases HR Cardiac output Who dominates at rest? Initial stimulus Physiological response Result Figure 18.22 The vagus nerve (parasympathetic) decreases heart rate. Dorsal motor nucleus of vagus Cardioinhibitory center Control of heart rate Medulla oblongata Cardioacceleratory center • Other factors… Sympathetic trunk ganglion Thoracic spinal cord Sympathetic trunk Sympathetic cardiac nerves increase heart rate and force of contraction. AV node SA node Parasympathetic fibers Sympathetic fibers Interneurons Figure 18.15 9 3/1/2016 Cardiac Output Cardiac output Heart rate Stroke volume Usually set by SA node Preload Contractility Afterload Autonomic nervous system (among other things) Rate of venous return Ca2+, hormones Blood pressure 10