scit 1408 applied human anatomy and physiology ii - heart chapter 18 b
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SCIT 1408 Applied Human Anatomy and Physiology II - Heart Chapter 18 BTRANSCRIPT
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Heart Physiology: Intrinsic Conduction System Autorhythmic cells:
1% of cardiac cells (SA node, AV node & bundle, right, left bundle branches, Purkinje fibers)
Have unstable resting potentials called pacemaker potentials
Initiate action potentials- whole muscle contracts Due to gap junctions & rapid ion distribution
Use calcium influx (rather than sodium) for rising phase of the action potential
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Heart Physiology: Electrical Events Intrinsic cardiac conduction system
A network of noncontractile (autorhythmic) cells that initiate and distribute impulses to coordinate the depolarization and contraction of the heart
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Autorhythmic cells: Action Potentials
Figure 18.13
Ca2+ influx- action potential
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Contractile Cells: Action Potential
Figure 18.12
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Heart Physiology: Sequence of Excitation 1 Sinoatrial (SA) node – fastest depolarization
Generates impulses about 75 times/min Neural & hormonal influences slow this from
100 to 75/min Sets pace of contraction, rhythm, heart rate
Pacemaker Sinus rhythm
Impulse from SA node thru both atria
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AV node receives impulse via internodal path Inferior part of interatrial septum, above AV valve Delays impulse for 0.1 second Atria complete contraction
Impulse returns to top speed thru bundle of His Only electrical connection between atria &
ventricles is bundle of His
Heart Physiology: Sequence of Excitation 2
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Bundle of His or AV bundle Only electrical connection between the atria and
ventricles
Heart Physiology: Sequence of Excitation 3
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Heart Physiology: Sequence of Excitation 4
4. Right and left bundle branches Two pathways in the interventricular septum that
carry the impulses toward the apex of the heart
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Heart Physiology: Sequence of Excitation 5
5. Purkinje fibers Complete the pathway into the apex and
ventricular walls AV bundle and Purkinje fibers depolarize only
30 times per minute in absence of AV node input
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Cardiac Intrinsic Conduction
Figure 18.14a
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Homeostatic Imbalances1. Dysrhythmias, arrhythmias – abnormal intrinsic conduction
with uncoordinated contraction Cardiogenic shock with dysrhythmia= poor prog.
2. Uncoordinated atrial & ventricular contractions3. Fibrillation- rapid, irregular contractions; no pumping4. Defective SA node may result in
Ectopic focus: abnormal pacemaker takes over If AV node takes over, there will be a junctional rhythm
(40–60 bpm)5. Defective AV node may result in
Partial or total heart block Few or no impulses from SA node reach the ventricles
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Extrinsic (Autonomic) Innervation of the Heart Heart stimulated by
sympathetic NS > rate, > force
Heart inhibited by parasympathetic NS (Vagus nerve)
<rate, < force
Vagal tone- > parasympatheic control; if vagus nerve cut, heart rate = 100/min
Figure 18.15
* cardiac center
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Electrocardiography Electrocardiogram (ECG or EKG): a composite
of all the action potentials generated by nodal and contractile cells at a given time
Three waves
1. P wave: depolarization of SA node
2. QRS complex: ventricular depolarization
3. T wave: ventricular repolarization
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SA node generates impulse;atrial excitation begins
Impulse delayedat AV node
Impulse passes toheart apex; ventricular
excitation begins
Ventricular excitationcomplete
SA node AV node Purkinjefibers
Bundlebranches
Figure 18.17
Heart Excitation Related to ECG
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Atrial depolarization, initiatedby the SA node, causes theP wave.
P
R
T
QS
SA node
AV node
With atrial depolarizationcomplete, the impulse isdelayed at the AV node.
Ventricular depolarizationbegins at apex, causing theQRS complex. Atrialrepolarization occurs.
P
R
T
QS
P
R
T
QS
Ventricular depolarizationis complete.
Ventricular repolarizationbegins at apex, causing theT wave.
Ventricular repolarizationis complete.
P
R
T
QS
P
R
T
QS
P
R
T
QS
Depolarization Repolarization
1
2
3
4
5
6
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Electrocardiography
Figure 18.16
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(a) Normal sinus rhythm.
(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.
(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.
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Heart Sounds Two sounds (lub-dup) associated with closing of
heart valves First sound occurs as AV valves close and signifies
beginning of systole Second sound occurs when SL valves close at the
beginning of ventricular diastole
Heart murmurs: abnormal heart sounds most often indicative of valve problems
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Tricuspid valve sounds typically heard in right sternal margin of 5th intercostal space
Aortic valve sounds heard in 2nd intercostal space atright sternal margin
Pulmonary valvesounds heard in 2ndintercostal space at leftsternal margin
Mitral valve soundsheard over heart apex(in 5th intercostal space)in line with middle ofclavicle
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Cardiac Cycle Cardiac cycle refers to all events associated with
blood flow through the heart Systole – contraction of heart muscle Diastole – relaxation of heart muscle
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Phases of the Cardiac Cycle
1. Ventricular filling – mid-to-late diastole Blood enters atria flows into ventricles SL valves closed AV valves are open Atrial systole at end- remaining 20% blood to
ventricles from atria EDV- End diastolic volume; The vol. of blood in
ventricles just before they contract = max vol they will have
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Phases of the Cardiac Cycle
2. Ventricular systole Atria relax Rising ventricular pressure results in closing of AV
valves Isovolumetric contraction phase – all valves closed Ventricular ejection phase opens semilunar valves (ESV) End systolic volume: volume of blood
remaining in each ventricle
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Phases of the Cardiac Cycle
3. Isovolumetric relaxation – early diastole Ventricles relax Backflow of blood in aorta and pulmonary trunk
closes semilunar valves Dicrotic notch – brief rise in aortic pressure caused
by backflow of blood rebounding off semilunar valves
PLAY InterActive Physiology ®: Cardiac Cycle, pages 3–18
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Cardiac Cycle
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Cardiac Output (CO) and Reserve CO - amt blood pumped by each ventricle/minute
CO = HR X SV
HR - heart beats/minute SV - amt blood pumped out from ventricle/beat Cardiac reserve maximal CO minus resting CO Cardiac Reserve- improves with exercise
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Cardiac Output: Example CO (ml/min) = HR (75 beats/min) x SV (70
ml/beat) CO = 5250 ml/min (5.25 L/min)
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Regulation of Stroke Volume SV = end diastolic volume (EDV) minus end
systolic volume (ESV); how much ventricles can hold minus what is left over after
contraction
EDV = amount of blood collected in a ventricle during diastole
ESV = amount of blood remaining in a ventricle at the end of systole (after contraction)
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Factors Affecting Stroke Volume Preload – amount ventricles are stretched by blood
just before systole (contraction) Contractility – cardiac cell contractile force due to
factors other than EDV Afterload – back pressure exerted by blood in the
large arteries leaving the heart; pressure that ventricles must overcome to open SL valves
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Preload and Afterload
Figure 18.21
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Frank-Starling Law of the Heart Preload, or degree of stretch, of cardiac muscle
cells before they contract is the critical factor controlling stroke volume
Slow heartbeat (>time for ventricular filling) and exercise (>HR) increase venous return to the heart, increasing SV
Blood loss and extremely rapid heartbeat decrease SV
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Regulation of Stroke Volume SV = EDV – ESV Three main factors affect SV
1. Preload – degree of stretch before contracting;
2. Contractility
3. Afterload
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Extrinsic Factors Influencing Stroke Volume Contractility - > contractile strength, independent of stretch
and EDV Increased contractility from:
Increased sympathetic stimuli Hormones (thyroxine, glucagon, and epinephrine) Ca2+ and some drugs
Decrease contractility from: Acidosis Increased extracellular K+
Calcium channel blockers
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Regulation of Heart Rate Positive chronotropic factors > HR Negative chronotropic factors < HR
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GTP GDP
Inactive protein kinase A
Active protein kinase A
ATP cAMP
GTP
SR Ca2+
channel
Ca2+
Ca2+
bindsto
TroponinEnhancedactin-myosininteraction
Extracellular fluid
Cytoplasm
Adenylate cyclaseCa2+
channel
Ca2+1-Adrenergicreceptor
Norepinephrine
Ca2+
uptakepump
Sarcoplasmicreticulum (SR)
Cardiac muscleforce and velocity
1
3
2
Heart Contractilityand Norepinephrine Sympathetic
stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system
Figure 18.22
Basis of Beta blockers/Calcium channel blockers
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Atrial (Bainbridge) Reflex Sympathetic reflex from > blood in the atria Increased blood in atria:
Stimulates SA node Stimulates stretch receptors in atria Together, these stimulate SNS, > HR
Basis of BP control via SNS reflex control of HR
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ESV- end systolic vol
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Chemical Regulation of the Heart Hormones: epinephrine, thyroxine > HR
hyperthroidism
Electrolyte balance required for normal cardiac function
< or > Ca2+ < function < or > K+ life threatening
PLAY InterActive Physiology ®: Cardiac Output, pages 3–9
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Other Factors that Influence Heart Rate Age Gender Exercise Body temperature
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Homeostatic Imbalances Tachycardia: abnormally fast heart rate
(>100 bpm) If persistent, may lead to fibrillation
Bradycardia: heart rate slower than 60 bpm May result in grossly inadequate blood circulation May be desirable result of endurance training
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Congestive Heart Failure (CHF) CO insufficient to supply body; caused by:
Coronary atherosclerosis- < blood to supply heart Persistent high blood pressure- >>hypertrophy Multiple myocardial infarcts Dilated cardiomyopathy (DCM) – over-stretched ventricles
Ca2+ mediated hypertropy; progressive Alcohol, cocaine, chemo, hyperthyroidism,
inflammation Idiopathic
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Left Heart failure Right Heart failure Blood backs up into lungs Right side of heart pumps to
lungs but left cannot eject to body
Pulmonary edema Death
Blood pools in organs Edema in feet, ankles, fingers
Can be caused by lung dysfunction; Cor pulmonale
Failure of either side eventually leads to failure of both sides.
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Developmental Aspects of the Heart Embryonic heart chambers
Sinus venous Atrium Ventricle Bulbus cordis
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Developmental Aspects of the Heart
Figure 18.24
3 wks 1. Sinus venosus
2. Atrium
3. Ventricle
4. Bulbus cordis
4a. Truncus arteriosus
Foramen ovale- septum btwn rt & left atrium
Ductus arteriosus- between pulmonary trunk & aortaBypass pulmonary circulation
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Occurs inabout 1 in every500 births
Occurs inabout 1 in every 1500 births
Narrowedaorta
Occurs inabout 1 in every 2000births
Ventricular septal defect.The superior part of the inter-ventricular septum fails to form; thus, blood mixes between the two ventricles. More blood is shunted from left to right because the left ventricle is stronger.
(a) Coarctation of the aorta. A part of the aorta is narrowed,increasing the workload of the left ventricle.
(b) 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.
(c)
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Age-Related Changes Affecting the Heart Sclerosis and thickening of valve flaps
mitral murmurs
Decline in cardiac reserve Less able to respond to sudden > demand < sympathetic regulation of heart
Fibrosis of cardiac muscle Healthy cardiac cells replaced with fibrous tissue; valves
Atherosclerosis- DIET