19-1 chapter 19 the circulatory system: the heart lecture powerpoint copyright (c) the mcgraw-hill...
TRANSCRIPT
19-1
Chapter 19
The Circulatory System:
The Heart
Lecture PowerPoint
Copyright (c) The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
19-2
Circulatory System: The Heart
• Gross anatomy of the heart
• Overview of cardiovascular system
• Cardiac conduction system and cardiac muscle
• Electrical and contractile activity of heart
• Blood flow, heart sounds, and cardiac cycle
• Cardiac output
19-3
Circulatory System: The Heart
• Circulatory system – heart, blood vessels and blood
• Cardiovascular system – heart, arteries, veins and capillaries
Two major divisions:
• Pulmonary circuit - right side of heart– carries blood to lungs for gas exchange
• Systemic circuit - left side of heart– supplies blood to all organs of the body
19-4
Cardiovascular System Circuit
19-5
Position, Size, and Shape
• Located in mediastinum, between lungs
• Base - broad superior portion of heart
• Apex - inferior end, tilts to the left, tapers to point
• 3.5 in. wide at base, 5 in. from base to apex and 2.5 in. anterior to posterior; weighs 10 oz
19-6
Heart Position
19-7
Pericardium
• Sac which surrounds heart allows heart to beat without friction, room to expand and anchors the heart to surrounding structure.
• Parietal pericardium– outer, tough, fibrous layer of CT
• Pericardial cavity – filled with pericardial fluid
• Visceral pericardium (a.k.a. epicardium of heart wall)– inner, thin, smooth, moist serous layer – covers heart surface
19-8
Pericardium and Heart Wall
Pericardial cavity contains 5-30 ml of pericardial fluid
19-9
Heart Wall• Epicardium:outer (a.k.a. visceral pericardium)
– serous membrane covers heart
• Myocardium: middle– thick muscular layer (cardiac muscle)– fibrous skeleton - network of collagenous and
elastic fibers• provides structural support and attachment for
cardiac muscle• electrical nonconductor, important in coordinating
contractile activity
• Endocardium: inner – lines inner heart
19-10
Heart Chambers• 4 chambers
– right and left atria • two superior,
posterior chambers• receive blood
returning to heart
– right and left ventricles
• two inferior chambers
• pump blood into arteries
• Atrioventricular (coronary) sulcus- groove separates atria, ventricles• Anterior and posterior interventricular sulci - grooves separate
ventricles (next slide)
19-11
External Anatomy - Anterior
19-12
External Anatomy - Posterior
19-13
Heart Chambers - Internal
• Interatrial septum– wall that separates atria
• Pectinate muscles– internal ridges of myocardium in right atrium
and both auricles
• Interventricular septum– wall that separates ventricles
• Trabeculae carneae– internal ridges in both ventricles
19-14
Internal Anatomy - Anterior
19-15
Heart Valvesprevent backflow of blood
• Atrioventricular (AV) valves– right AV valve has 3 cusps (tricuspid valve)– left AV valve has 2 cusps (mitral, bicuspid
valve)– chordae tendineae - cords connect AV valves
to papillary muscles (on floor of ventricles)
• Semilunar valves - control flow into great arteries( pulmonary artery/aorta)– Pulmonary valve: right ventricle into
pulmonary trunk– Aortic valve: from left ventricle into aorta
19-16
Heart Valves
19-17
Heart Valves
19-18
AV Valve Mechanics
• Ventricles relax– pressure drops– Semilunar (pulm valve/aortic valve) valves close– AV (tricuspid/bicuspid) valves open– blood flows from atria to ventricles
• Ventricles contract– AV valves close– pressure rises– semilunar valves open– blood flows into great vessels( pulmonary artery and
aorta)
19-19
Operation of Atrioventricular Valves
19-20
Operation of Semilunar Valves
19-21
Blood Flow Through Heart
19-22
Coronary Circulation(Blood vessels of Heart wall)
• Left coronary artery (LCA)– anterior interventricular branch
• supplies blood to interventricular septum and anterior walls of ventricles
– circumflex branch• passes around left side of heart in coronary sulcus,
supplies left atrium and posterior wall of left ventricle
• Right coronary artery (RCA)– right marginal branch
• supplies lateral R atrium and ventricle
– posterior interventricular branch• supplies posterior walls of ventricles
19-23
Angina and Heart Attack
• Angina pectoris – partial obstruction of coronary blood flow can
cause chest pain – pain caused by ischemia, often activity
dependent
• Myocardial infarction – complete obstruction causes death of cardiac
cells in affected area– pain or pressure in chest that often radiates
down left arm
19-24
Venous Drainage of Heart(venous drainage refers to the route by which blood
leaves an organ)
• 20% drains directly into right atrium and ventricle via small thebesian veins
• 80% returns to right atrium via:– great cardiac vein
• blood from anterior interventricular sulcus
– middle cardiac vein • from posterior sulcus
– left marginal vein– coronary sinus
• collects blood and empties into right atrium
19-25
Coronary Vessels - Anterior
19-26
Coronary Vessels - Posterior
19-27
Nerve Supply to Heart
• Sympathetic nerves from – upper thoracic spinal cord, through
sympathetic chain to cardiac nerves– directly to ventricular myocardium– can raise heart rate to 230 bpm
• Parasympathetic nerves– right vagus nerve to SA node– left vagus nerve to AV node– vagal tone – normally slows heart rate to
70 - 80 bpm
19-28
Cardiac Conduction System(controls the route and timing of electrical conduction so all 4 chambers
are in sync with one another)
• Properties– myogenic - heartbeat originates within heart– autorhythmic – regular, spontaneous
depolarization
• Components– next slide
19-29
Cardiac Conduction System
• SA node: (pacemaker) myocytes in RA which initiates heartbeat and sets heart rate
• AV node: electrical gateway to ventricles
• AV bundle: way out for signals to leave AV node
• Right and left bundle branches: divisions of AV bundle that enter interventricular septum
• Purkinje fibers: distribute electrical excitation
19-30
Cardiac Conduction System
19-31
Structure of Cardiac Muscle• Short, branched cells, one nucleus• Sarcoplasmic reticulum is less developed
than in skeletal muscle, large T-tubules – admit more Ca2+ from ECF
• Intercalated discs join myocytes end to end– mechanical junctions (2 types): tightly join
myocytes1. fascia adherens: actin anchored to plasma
membrane; transmembrane proteins link one cell to the next
2. desmosomes
– electrical junctions - gap junctions which forms channels that allow ions to flow from the cytoplasm from one cell directly into the next
19-32
Structure of Cardiac Muscle Cell
19-33
Cardiac Rhythm
• Systole – ventricular contraction
• Diastole - ventricular relaxation• Sinus rhythm: (normal heartbeat, triggered by the SA
node)
– set by SA node at 60 – 100 bpm– adult at rest is 70 to 80 bpm
• Premature ventricular contraction (PVC): (the following can cause other parts of the conduction system to fire before the SA node does, setting off an extra heartbeat called a PVC)
– Causes: hypoxia, electrolyte imbalance, stimulants, stress, etc.
19-34
Cardiac Rhythm• Ectopic foci – any region of spontaneous firing
other than the SA node (example: if the SA node is damaged)
– nodal rhythm - set by AV node, 40 to 50 bpm • Sufficient to sustain life
– intrinsic ventricular rhythm - 20 to 40 bpm • If neither SA node or AV node are functional• Provides too little flow to the brain to be survivable.
– An artificial pacemaker may be implanted
• Arrhythmia - abnormal cardiac rhythm– One cause of an arrhythmia is:
heart block (failure of conduction system)• bundle branch block• total heart block (damage to AV node)
19-35
Pacemaker Physiology(depolarization of SA Node)
• SA node - no stable resting membrane potential• Pacemaker potential
– gradual depolarization from -60 mV, slow influx of Na+
• Action potential – occurs at threshold of -40 mV– depolarizing phase to 0 mV
• fast Ca2+ channels open, (Ca2+ in)
– repolarizing phase• K+ channels open, (K+ out)• at -60 mV K+ channels close, pacemaker potential starts over
• Each depolarization creates one heartbeat– Each depolarization of the SA node sets off one heartbeat– SA node at rest fires at 0.8 sec, about 75 bpm
19-36
SA Node Potentials
19-37
Impulse Conduction to Myocardium
• SA node signal travels at 1 m/sec through atria• AV node slows signal to 0.05 m/sec
– thin myocytes with fewer gap junctions– delays signal 100 msec, allows ventricles to fill
• AV bundle and purkinje fibers– speeds signal along at 4 m/sec to ventricles
• Ventricular systole begins at apex, progresses up– spiral arrangement of myocytes twists ventricles
slightly
19-38
Contraction of Myocardium• Myocytes have stable resting potential of -90
mV• Depolarization (very brief)
– stimulus opens voltage regulated Na+ gates, (Na+ rushes in) membrane depolarizes rapidly
– action potential peaks at +30 mV – Na+ gates close quickly
• Plateau - 200 to 250 msec, sustains contraction– slow Ca2+ channels open, Ca2+ binds to fast Ca2+
channels on SR, releases Ca2+ into cytosol:
contraction
• Repolarization - Ca2+ channels close, K+ channels open, rapid K+ out returns to resting potential
19-39
Action Potential of Myocyte
1) Na+ gates open
2) Rapid depolarization
3) Na+ gates close
4) Slow Ca2+ channels open
5) Ca2+ channels close, K+ channels open
19-40
Electrocardiogram (ECG)• Composite of all action potentials of nodal and
myocardial cells detected, amplified and recorded by electrodes on arms, legs and chest
19-41
ECG
• P wave– SA node fires, atrial depolarization– atrial systole
• QRS complex– ventricular depolarization– (atrial repolarization and diastole - signal
obscured)
• ST segment - ventricular systole
• T wave– ventricular repolarization
19-42
Normal Electrocardiogram (ECG)
19-43
1) atrial depolarization begins
2) atrial depolarization complete (atria contracted)
3) ventricles begin to depolarize at apex; atria repolarize (atria relaxed)
4) ventricular depolarization complete (ventricles contracted)
5) ventricles begin to repolarize at apex
6) ventricular repolarization complete (ventricles relaxed)
Electrical Activity of Myocardium
19-44
Diagnostic Value of ECG
• Invaluable for diagnosing abnormalities in conduction pathways, MI, heart enlargement and electrolyte and hormone imbalances
19-45
ECGs, Normal and Abnormal
19-46
Heart Sounds
• Auscultation - listening to sounds made by body
• First heart sound (S1), louder and longer “lubb”, occurs with closure of AV (tricuspid/bicuspid) valves
• Second heart sound (S2), softer and sharper “dupp” occurs with closure of semilunar (pulmonary/aortic) valves
• S3 - rarely heard in people > 30
19-47
Phases of Cardiac Cycle(The pressure changes that occur, and how the pressure changes, and
valves govern the flow of blood. Less than 1 second)
• Ventricular filling
• Isovolumetric contraction
• Ventricular ejection
• Isovolumetric relaxation
19-48
Ventricular Filling - 3 phases
1. Rapid ventricular filling • AV valves first open
2. Diastasis • sustained lower pressure, venous return
3. Atrial systole • filling completed
19-49
Isovolumetric Contraction of Ventricles
• Atria repolarize and relax, and remain in diastole for the rest of the cardiac cycle
• Ventricles depolarize
• QRS complex appears in ECG
• Ventricles contract
• Rising pressure closes AV valves - heart sound S1 occurs
• No ejection of blood yet (no change in volume)
19-50
Ventricular Ejection
• Rising pressure opens semilunar valves
• Rapid ejection of blood (at first)
• Reduced ejection of blood (less pressure)
*Stroke volume: amount of blood ejected, 70 ml at rest
*End-systolic volume: amount of blood left in heart
19-51
Ventricles- Isovolumetric Relaxation
• T wave appears in ECG
• Semilunar valves close (sound S2 occurs)
• AV valves remain closed
• Ventricles expand but do not fill (no change in volume)
19-52
Major Events of Cardiac Cycle
• Ventricular filling
• Isovolumetric contraction
• Ventricular ejection
• Isovolumetric relaxation
19-53
Events of the Cardiac Cycle
19-54
Cardiac Output (CO)
• Amount ejected by ventricle in 1 minute
• Cardiac Output = Heart Rate x Stroke Volume– about 4 to 6 L/min at rest– vigorous exercise CO to 21 L/min for fit
person and up to 35 L/min for world class athlete
• Cardiac reserve: difference between a persons maximum and resting CO with fitness, with disease
19-55
Heart Rate
• Pulse = surge of pressure in artery– infants have HR of 120 bpm or more– young adult females avg. 72 - 80 bpm– young adult males avg. 64 to 72 bpm– HR rises again in the elderly
• Tachycardia: resting adult HR above 100– stress, anxiety, drugs, heart disease or
body temp.
• Bradycardia: resting adult HR < 60– in sleep and endurance trained athletes
19-56
Sympathetic Nervous System
• Cardioacceleratory center– stimulates sympathetic cardiac nerves to SA
node, AV node and myocardium– these nerves secrete norepinephrine, which
binds to -adrenergic receptors in the heart(positive chronotropic effect)
– CO peaks at HR of 160 to 180 bpm– Sympathetic n.s. can HR up to 230 bpm,
(limited by refractory period of SA node), but SV and CO (less filling time)
19-57
Parasympathetic Nervous System
• Cardioinhibitory center stimulates vagus nerves
• right vagus nerve - SA node• left vagus nerve - AV node
– secretes ACH (acetylcholine) which binds to muscarinic receptors
• nodal cells hyperpolarized, HR slows
– vagal tone: background firing rate holds HR to sinus rhythm of 70 to 80 bpm
• severed vagus nerves (intrinsic rate-100bpm)• maximum vagal stimulation HR as low as 20 bpm
19-58
Inputs to Cardiac Center
• Higher brain centers affect HR– cerebral cortex, limbic system, hypothalamus
• sensory or emotional stimuli (rollercoaster, IRS audit)
• Proprioceptors – inform cardiac center about changes in
activity, HR before metabolic demands arise
• Baroreceptors signal cardiac center– aorta and internal carotid arteries
• pressure , signal rate drops, cardiac center HR• if pressure , signal rate rises, cardiac center HR
19-59
Inputs to Cardiac Center
• Chemoreceptors– sensitive to blood pH, CO2 and oxygen
– aortic arch, carotid arteries and medulla oblongata
– primarily respiratory control, may influence HR
CO2 (hypercapnia) causes H+ levels, may create acidosis (pH < 7.35)
– Hypercapnia and acidosis stimulates cardiac center to HR