Transcript Chapter 20

Chapter 20: The
Cardiovascular System
THE HEART
Heart Anatomy
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Location
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Orientation
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diaphragm, mediastinum, 2/3 left of midline
Apex- points anterior, inferior, left
Base- directed posterior, superior, right
Vessels
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Superior and Inferior Vena Cava
Pulmonary trunk pulmonary arteries(lungs)
Pulmonary veins
Aorta
Pericardium- figure 20.2
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Membrane that surrounds & protects
Confines to position in mediastinum
2 main parts:
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Fibrous pericardium- superficial, anchor
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Tough, inelastic, dense irregular CT
Baglike, open end attached to vessels
Prevents overstretching of heart
Serous pericardium- thinner, delicate
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Forms double layer (pericardial fluid in pericardial cavity reduces friction, allows movement):
 Parietal layer- fused to fibrous
 Visceral layer- inner = EPICARDIUM- adheres tightly to heart
surface
Layers of the heart wall
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Epicardium- thin, transparent, outer
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Myocardium- middle
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Visceral layer of serous pericardium
Smooth slippery outside of heart
Cardiac muscle- striated but involuntary
Bulk of heart
Pumping action
Endocardium- inner
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Thin endothelium over CT
Smooth lining of chambers and valves
Continuous with b.v.
Heart Anatomy fig 20.3-6
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Heart chambers = 4
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2 Atria
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Right- receives blood from vena cavae
Left- receives blood from pulmonary veins
2 Ventricles
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Right- pumps deoxygenated blood to lungs
Left- pumps oxygenated blood to systemic circ
 Myocardium much thicker than right ventricle
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Heart valves = 4
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Atrioventricular valves = tricuspid & bicuspid
Semilunar valves = aortic and pulmonary
Valve function
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When AV valve open:
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Ventricle contracts, pressure  cusps up,  close
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Cusps project into ventricle
Ventricle relaxed  papillary muscle relaxed  chordae
tendineae slack
Blood:  pressure atria   pressure ventricle
Papillary muscles contract  chordae tendineae tighten
SL valves open when pressure in ventricles
exceeds pressure in arteries
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As ventricles relax blood moves back toward heart  SL
valves close
Terms
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Auricles – on anterior surface of atria
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Increases capacity of each atrium so each can
hold a greater volume of blood
Coronary sulcus – separation between
atria and ventricles
 Systole – contraction
 Diastole – relaxation
 Tachycardia – high heart rate, > 100bpm
 Bradycardia – low heart rate, 50 bpm
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Pulmonary and systemic circuits
Coronary circulation (1)
Coronary circulation (2)
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Coronary – “crown,” encircles heart
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 contracts, little blood flows  coronary
artery but as  relaxes, aorta pushes blood
thru coronary arteries
Anastomoses – area where 2 or more
arteries supply the same region
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Provide alternate routes for blood to reach a
particular organ or tissue
Myocardium contains
Provides detours if main route is obstructed
Problems…
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Myocardial ischemia – partial obstruction of blood
flow in coronary arteries
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 blood flow to myocardium
hypoxia may weaken cells w/out killing them
Silent = episodes without pain, dangerous in that no
forewarning to  attack
Angina pectoris – “strangled chest”
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Severe pain usually accompanies myocardial ischemia
Tightness or squeezing sensation
Can occur during exertion when  requires more O2
Pain referred to neck, chin, left arm
Myocardial infarction (MI)
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Heart attack
Complete obstruction of blood flow to coronary
artery
Infarction = death of tissue area due to
interrupted blood supply
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Tissue distal to obstruction dies, replaced by noncontractile scar tissue  loses strength
May also disrupt conduction system and cause sudden
death – ventricular fibrillation – rapid uncoordinated
twitching that disrupts regular rhythm
treatment: injection of clot dissolver, plus
heparin, coronary angioplasty or coronary artery
bypass
Properties of cardiac muscle cells
Shorter than skeletal
 Branching
 Central nucleus, sometimes binucleate
 Intercalated discs- thickenings of
sarcolemma, contain:
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Desmosomes- hold fibers together
Gap junctions- for AP conduction
Mitochondria large & numerous
 Like skeletal- arrangement of proteins
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SR smaller  less intracellular Ca2+
T-tubules wider but less abundant
Functional syncytium
stimulation of individual muscle cell results
in contraction of all muscle cells due to
gap junctions in intercalated discs
 an application of the all-or-none principle
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If stimulus in cardiac muscle is great enough
to initiate contraction of a single cell, the
entire muscular syncytium will undergo
contraction
Contraction physiology
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1% of cardiac fibers become autorhythmic
during embryonic development
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Pacemaker function- set rhythm of electrical
excitation
Conduction system- network of specialized
fibers provide path for excitation to progress
thru heart
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Ensuring coordinated contraction of chambers
 Both atria contract at same time
 Both ventricles contract at same time
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Cardiac AP goes thru following sequence…
Contraction physiology (2)
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Pathway of stimulation
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1. Sinoatrial (SA) node- cells do not have a
stable resting membrane potential
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depolarized spontaneously = pacemaker potential
2. Atrioventricular (AV) node
3. Bundle of His
4. Bundle branches
5. Purkinje fibers
6. Ventricular cells- contraction pushes blood
up to SL valves
Cardiac Action Potentials, 20.11
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Depolarization: Na+ gates open= fast channels
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Rapid depolarization because they open fast
Plateau: opening of slow Ca2+ channels in the
sarcolemma
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More Ca2+ outside cell   cytosol also causing Ca2+
to pour out of SR
 Ca2+  contraction
K+ channels opening but Ca2+ balances it  remains
depolarized for about 0.25 sec
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(in skeletal muscle 0.001 sec, no plateau phase)
Repolarization: K+ outflow restores resting m.p.
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Ca2+ channels also are closing
Cardiac Action Potentials (2)
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Positive inotropic agents  contractility
(substances promote inflow of Ca2+ channels 
strength  contractions
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NE and Epinephrine modify
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Timing
strength of contraction
Do NOT establish a rhythm
Digitalis
 interstitial Ca2+
Negative inotropic agents  contractility
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Ach released by Parasymp NS slows SA node pacing
from 100 to about 75 AP/minute
Also: anoxia, acidosis, some anesthetics,  K+, Ca2+
channel blockers
Long refractory pd- cardiac muscle
Refractory pd- time interval during which
second contraction cannot be triggered
 In cardiac- longer than contraction pd
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Another contraction cannot happen until
relaxation is happening
Tetanus cannot occur
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If tetanus occurred blood flow would cease
Arrhythmias
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Irregular rhythm due to conduction defect
Causes:
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Caffeine, nicotine, alcohol, other drugs, anxiety,
hyperthyroidism, K+ deficiency, & some heart disease
Examples:
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Heart block – AP slowed or blocked (3 types)
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1st °= AP slow thru AV, 2nd °= some AP not thru AV node,
3rd ° = no AP thru AV node
Atrial flutter – rapid atrial contractions
Atrial fibrillation – asynchronous cont- atrial fibers
Ventricular fibrillation– async cont ventricular fibers*
Premature ventricular contraction – ectopic area of high
excitation  abnormal AP (before SA node intends)
Cardiac excitation and the ECG
Electrocardiogram (ECG)
P wave – atrial depolarization  atrial
contraction  ventricular filling
 QRS complex – ventricular depolarization
 ventricular contraction  SL valves
open  blood ejection
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Rt ventriclepulmonary trunk pul arteries
lungs
Left ventricle  aorta  systemic circulation
T wave – ventricular repolarization
Heart sounds
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A. Normal
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First sound – lubb – closure of AV valves
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Second sound – dupp – closure of SL valves
B. Abnormal sounds (murmurs)
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1. stenosis – failure of valve to open
2. insufficiency – failure of valve to close
The Cardiac Cycle
Ventricular filling
 AV open, SL closed
 Isovolumetric contraction
 AV closed, SL closed
 Ventricular ejection
 AV closed, SL open
 Isovolumetric relaxation
 AV closed, SL closed
 Ventricular filling
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Regulation of Cardiac Output
Cardiac output = stroke volume x heart rate
CO = SV x HR
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Stroke volume = ml/ beat
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EDV - ESV
Heart rate = beats/ min
Cardiac output = L/ min
rest = 5.25 L/min (70 mL/beat x 75 bpm)
exercise = 19.5 L/min (130mL/beat x 150bpm)
Regulation of stroke volume
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1. Effect of preload = Frank-Starling Law
of the Heart
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> preload  > force of contraction
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2. Effect of afterload
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rubberband
Pressure rqrd for ejection of blood
3. Effect of contractility-each individual
fiber
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Positive inotropic agents- eg. norepinephrine
Negative inotropic agents - eg. propranolol
Regulation of Heart Rate
1. Normal rate = vagal tone
 2. Regulation
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1. Autonomic Nervous system
2. Chemical
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a. Hormones
b. Ions