18 The Cardiovascular System: The Heart: Part B.

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Presentation transcript:

18 The Cardiovascular System: The Heart: Part B

Cardiac Muscle Contraction Differences from skeletal muscle: ~1% of cells have automaticity (autorhythmicity) Do not need nervous system stimulation Can depolarize entire heart All cardiomyocytes contract as unit, or none do Action potential and contractile phase last much longer Allow blood ejection from heart © 2013 Pearson Education, Inc.

Cardiac Muscle Contraction Three similarities with skeletal muscle: Depolarization opens few voltage-gated fast Na+ channels in sarcolemma  Reversal of membrane potential from –90 mV to +30 mV Brief; Na channels close rapidly Depolarization wave down T tubules  SR to release Ca2+  Excitation-contraction coupling occurs Ca2+ binds troponin  filaments slide © 2013 Pearson Education, Inc.

Energy Requirements Cardiac muscle Has many mitochondria Great dependence on aerobic respiration Little anaerobic respiration ability Readily switches fuel source for respiration Even uses lactic acid from skeletal muscles © 2013 Pearson Education, Inc.

Homeostatic Imbalance Region of heart muscle is oxygen-starved Ischemic cells (blood deprived)  anaerobic respiration  lactic acid  High H+ concentration  high intracellular Ca2+ concentration  Mitochondrial damage  decreased ATP production  Gap junctions close (usually open)  isolates damaged cells and forces AP to find diff routes to cardiac cells beyond them  fatal arrhythmias © 2013 Pearson Education, Inc.

Heart Physiology: Electrical Events Heart depolarizes and contracts without nervous system stimulation Rhythm can be altered by autonomic nervous system © 2013 Pearson Education, Inc.

Heart Physiology: Setting the Basic Rhythm Coordinated heartbeat is a function of Presence of gap junctions Intrinsic cardiac conduction system Network of noncontractile (autorhythmic) cells Initiate and distribute impulses  coordinated depolarization and contraction of heart © 2013 Pearson Education, Inc.

Heart Physiology: Sequence of Excitation Sinoatrial (SA) node Pacemaker of heart in right atrial wall Depolarizes faster than rest of myocardium Generates impulses about 75X/minute (sinus rhythm) Inherent rate of 100X/minute tempered by extrinsic factors Impulse spreads across atria, and to AV node © 2013 Pearson Education, Inc.

Heart Physiology: Sequence of Excitation Atrioventricular (AV) node In inferior interatrial septum Delays impulses approximately 0.1 second Because fibers are smaller diameter, have fewer gap junctions Allows atrial contraction prior to ventricular contraction Inherent rate of 50X/minute in absence of SA node input © 2013 Pearson Education, Inc.

Heart Physiology: Sequence of Excitation Atrioventricular (AV) bundle (bundle of His) In superior interventricular septum Only electrical connection between atria and ventricles Atria and ventricles not connected via gap junctions © 2013 Pearson Education, Inc.

Heart Physiology: Sequence of Excitation Right and left bundle branches Two pathways in interventricular septum Carry impulses toward apex of heart © 2013 Pearson Education, Inc.

Homeostatic Imbalances Defects in intrinsic conduction system may cause Arrhythmias - irregular heart rhythms Uncoordinated atrial and ventricular contractions Fibrillation - rapid, irregular contractions; useless for pumping blood  circulation ceases  brain death Defibrillation to treat © 2013 Pearson Education, Inc.

Homeostatic Imbalances Defective SA node may cause Ectopic focus - abnormal pacemaker AV node may take over; sets junctional rhythm (40–60 beats/min) Extrasystole (premature contraction) Ectopic focus sets high rate Can be from excessive caffeine or nicotine © 2013 Pearson Education, Inc.

Homeostatic Imbalance To reach ventricles, impulse must pass through AV node Defective AV node may cause Heart block Few (partial) or no (total) impulses reach ventricles Ventricles beat at intrinsic rate – too slow for life Artificial pacemaker to treat © 2013 Pearson Education, Inc.

Extrinsic Innervation of the Heart Heartbeat modified by ANS via cardiac centers in medulla oblongata Sympathetic   rate and force Parasympathetic   rate Cardioacceleratory center – sympathetic – affects SA, AV nodes, heart muscle, coronary arteries Cardioinhibitory center – parasympathetic – inhibits SA and AV nodes via vagus nerves © 2013 Pearson Education, Inc.

Figure 18.16 Autonomic innervation of the heart. The vagus nerve (parasympathetic) decreases heart rate. Dorsal motor nucleus of vagus Cardioinhibitory center Cardioaccele- ratory center Medulla oblongata 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 © 2013 Pearson Education, Inc.

Electrocardiogram (ECG or EKG) Electrocardiography Electrocardiogram (ECG or EKG) Composite of all action potentials generated by nodal and contractile cells at given time Three waves: P wave – depolarization SA node  atria QRS complex - ventricular depolarization and atrial repolarization T wave - ventricular repolarization © 2013 Pearson Education, Inc.

Figure 18.17 An electrocardiogram (ECG) tracing. Sinoatrial node Atrioventricular node QRS complex R Ventricular depolarization Ventricular repolarization Atrial depolarization T P Q S-T Segment P-R Interval S Q-T Interval 0.2 0.4 0.6 0.8 Time (s) © 2013 Pearson Education, Inc.

Figure 18.19 Normal and abnormal ECG tracings. Normal sinus rhythm. Junctional rhythm. The SA node is nonfunctional, P waves are absent, and the AV node paces the heart at 40­–60 beats/min. 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. Ventricular fibrillation. These chaotic, grossly irregular ECG deflections are seen in acute heart attack and electrical shock. © 2013 Pearson Education, Inc.

Electrocardiography P-R interval S-T segment Q-T interval Beginning of atrial excitation to beginning of ventricular excitation S-T segment Entire ventricular myocardium depolarized Q-T interval Beginning of ventricular depolarization through ventricular repolarization © 2013 Pearson Education, Inc.

Two sounds (lub-dup) associated with closing of heart valves Heart Sounds Two sounds (lub-dup) associated with closing of heart valves First as AV valves close; beginning of systole Second as SL valves close; beginning of ventricular diastole Pause indicates heart relaxation Heart murmurs - abnormal heart sounds; usually indicate incompetent or stenotic valves © 2013 Pearson Education, Inc.

heard in 2nd intercostal space at right sternal margin Figure 18.20 Areas of the thoracic surface where the sounds of individual valves can best be detected. 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 © 2013 Pearson Education, Inc.

Mechanical Events: The Cardiac Cycle Blood flow through heart during one complete heartbeat: atrial systole and diastole followed by ventricular systole and diastole Systole—contraction Diastole—relaxation Series of pressure and blood volume changes © 2013 Pearson Education, Inc.

Phases of the Cardiac Cycle 1. Ventricular filling—takes place in mid-to-late diastole AV valves are open; pressure low 80% of blood passively flows into ventricles Atrial systole occurs, delivering remaining 20% End diastolic volume (EDV): volume of blood in each ventricle at end of ventricular diastole © 2013 Pearson Education, Inc.

Phases of the Cardiac Cycle 2. Ventricular systole Atria relax; ventricles begin to contract Rising ventricular pressure  closing of AV valves Isovolumetric contraction phase (all valves are closed) In ejection phase, ventricular pressure exceeds pressure in large arteries, forcing SL valves open End systolic volume (ESV): volume of blood remaining in each ventricle after systole © 2013 Pearson Education, Inc.

Phases of the Cardiac Cycle 3. Isovolumetric relaxation - early diastole Ventricles relax; atria relaxed and filling Backflow of blood in aorta and pulmonary trunk closes SL valves Causes dicrotic notch (brief rise in aortic pressure as blood rebounds off closed valve) Ventricles totally closed chambers When atrial pressure exceeds that in ventricles  AV valves open; cycle begins again at step 1 © 2013 Pearson Education, Inc.

Volume of blood pumped by each ventricle in one minute Cardiac Output (CO) Volume of blood pumped by each ventricle in one minute CO = heart rate (HR) × stroke volume (SV) HR = number of beats per minute SV = volume of blood pumped out by one ventricle with each beat Normal – 5.25 L/min © 2013 Pearson Education, Inc.

Cardiac Output (CO) At rest CO (ml/min) = HR (75 beats/min)  SV (70 ml/beat) = 5.25 L/min CO increases if either/both SV or HR increased Maximal CO is 4–5 times resting CO in nonathletic people Maximal CO may reach 35 L/min in trained athletes Cardiac reserve - difference between resting and maximal CO © 2013 Pearson Education, Inc.

Autonomic Nervous System Regulation Sympathetic nervous system activated by emotional or physical stressors Norepinephrine causes pacemaker to fire more rapidly (and increases contractility) Binds to β1-adrenergic receptors   HR  contractility; faster relaxation Offsets lower EDV due to decreased fill time © 2013 Pearson Education, Inc.

Autonomic Nervous System Regulation Parasympathetic nervous system opposes sympathetic effects Acetylcholine hyperpolarizes pacemaker cells by opening K+ channels  slower HR Little to no effect on contractility © 2013 Pearson Education, Inc.

Chemical Regulation of Heart Rate Hormones Epinephrine from adrenal medulla increases heart rate and contractility Thyroxine increases heart rate; enhances effects of norepinephrine and epinephrine Intra- and extracellular ion concentrations (e.g., Ca2+ and K+) must be maintained for normal heart function © 2013 Pearson Education, Inc.

Homeostatic Imbalance Hypocalcemia  depresses heart Hypercalcemia  increased HR and contractility Hyperkalemia  alters electrical activity  heart block and cardiac arrest Hypokalemia  feeble heartbeat; arrhythmias © 2013 Pearson Education, Inc.

Other Factors that Influence Heart Rate Age Fetus has fastest HR Gender Females faster than males Exercise Increases HR Body temperature Increases with increased temperature © 2013 Pearson Education, Inc.

Homeostatic Imbalances Tachycardia - abnormally fast heart rate (>100 beats/min) If persistent, may lead to fibrillation Bradycardia - heart rate slower than 60 beats/min May result in grossly inadequate blood circulation in nonathletes May be desirable result of endurance training © 2013 Pearson Education, Inc.

Homeostatic Imbalance Congestive heart failure (CHF) Progressive condition; CO is so low that blood circulation inadequate to meet tissue needs Reflects weakened myocardium caused by Coronary atherosclerosis—clogged arteries Persistent high blood pressure Multiple myocardial infarcts Dilated cardiomyopathy (DCM) © 2013 Pearson Education, Inc.

Homeostatic Imbalance Pulmonary congestion Left side fails  blood backs up in lungs Peripheral congestion Right side fails  blood pools in body organs  edema Failure of either side ultimately weakens other Treat by removing fluid, reducing afterload, increasing contractility © 2013 Pearson Education, Inc.

Developmental Aspects of the Heart Fetal heart structures that bypass pulmonary circulation Foramen ovale connects two atria Bypass pulmonary circuit Remnant is fossa ovalis in adult Ductus arteriosus connects pulmonary trunk to aorta (lung bypass) Remnant - ligamentum arteriosum in adult Close at or shortly after birth © 2013 Pearson Education, Inc.

Developmental Aspects of the Heart Congenital heart defects Most common birth defects; treated with surgery Most are one of two types: Mixing of oxygen-poor and oxygen-rich blood, e.g., septal defects, patent ductus arteriosus Narrowed valves or vessels  increased workload on heart, e.g., coarctation of aorta Tetralogy of Fallot Both types of disorders present © 2013 Pearson Education, Inc.

Figure 18.25 Three examples of congenital heart defects. Narrowed aorta Occurs in about 1 in every 500 births Occurs in about 1 in every 1500 births Occurs in about 1 in every 2000 births Ventricular septal defect. The superior part of the inter-ventricular septum fails to form, allowing blood to mix between the two ventricles. More blood is shunted from left to right because the left ventricle is stronger. Coarctation of the aorta. A part of the aorta is narrowed, increasing the workload of the left ventricle. Tetralogy of Fallot. Multiple defects (tetra = four): (1) Pulmonary trunk too narrow and pulmonary valve stenosed, resulting in (2) hypertrophied right ventricle; (3) ventricular septal defect; (4) aorta opens from both ventricles. © 2013 Pearson Education, Inc.

Age-Related Changes Affecting the Heart Atherosclerosis Fatty build-up that clogs coronary arteries Impairs blood and O2 delivery to cells Heart increasingly hypoxic so contracts ineffectively © 2013 Pearson Education, Inc.