Download Ch 18 Cardiac Physiology

Ch 18 Cardiac Physiology
Heart Anatomy
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heart chambers
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R L atrium
R L ventricle
valves
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R atrioventricular valve
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tricuspid
L atrioventricular
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bicuspid = mitral
aortic semilunar valve
pulmonary semilunar valve
other
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interventricular septum
interatrial septum
Heart Anatomy
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blood vessels
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SVC , IVC
into R atrium
pulmonary veins
into L atrium
pulmonary trunk
out of R ventricle
aorta
out of L ventricle
cardiac muscle tissue
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striated (sarcomeres)
short cells , branched
intercalated discs
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specialized connections betw cells
desmosomes
prevents separation of cells
gap junctions
allow ions to pass betw cells
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functional syncytium all cells contract simultaneously
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many mitochondria
aerobic respiration
prevents fatigue
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autorhythmic
contract w/o stim from nerves
cardiac vs skeletal muscle tissue
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cardiac muscle doesn’t fatigue
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long contraction
long refractory period
contraction
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skeletal muscle
motor units
cardiac muscle
entire myocardium
cardiac muscle cells can stimulate adjacent cells to contract
cardiac muscle contraction - 1
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contracts just like skeletal muscle :
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fast Na+ channels (voltage-gated) open
Na+ rushes in
depolarization ( -90mV to +30 mV)
depolarization opens Sarcoplasmic reticulum
Ca++ stimulates sarcomere to contract
only different :
cardiac muscle contraction - 2
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plateau
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delayed repolarization
depolarization opens slow Ca++ channels
Ca++ moves in
inside stays + much longer
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Na depol last 1-5 ms
Ca++ depol lasts 150-200ms
decreased K+ permeability
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repolarization delayed until after plateau
repolarization
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K+ channels open
Ca++ pumped out of cell or into SR
cardiac muscle contraction - 3
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much longer contraction in cardiac muscle
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long refractory period 250 ms vs skeletal 2-3ms
• prevents summation
• prevents fatigue
• prevents tetany
functional syncytium
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all cells contract simultaneously
gap junctions
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+ from adjacent cells
cell stimulates adjacent cells
intrinsic conduction system
initiates impulses
instrinsic conduction system
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non-contractile cardiac cells
act like neurons
initiate and spread action potential for entire myocardium
autorhythmic
autorhythmic cells
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unstable resting potential
pacemaker potential
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spontaneous depolarization
membrane potential
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-60 mV
slow Na channel open
Na+ leaks in
threshold
- 40 mV
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fast Ca channel open
Ca++ rush in = depolarization
repolarization
K+ out
(Na-K pump)
rhythm of spontaneous depolarization
conduction pathway
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Sino-atrial (S-A) node
Atrio-ventricular (A-V) node
A-V bundle (bundle of His)
bundle branches
Purkinjie fibers
gap junctions
spread depolarization along pathway
S-A node
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sino-atrial node
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pacemaker
right atrium
prepotential
~ 90+ / min
fastest autorhythmic tissue
sets pace for entire myocardium
slowed by P-ANS
~ 70 – 75 / min
sinus rhythm
normal
A-V node
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atrio-ventricular node
internodal pathway
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delay ~ 0.1 msec
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50 / min w/o S-A node
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atrioventricular bundle
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from S-A node
atrium contracts
(bundle of His)
“electrical” connection betw atrium and ventricle
R & L bundle branches
Purkinjie fibers
bundle to Purkinjie
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ventricular contraction
plus gap junctions of myocardium
contraction begins at apex and moves upward
ECG
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electrocardiogram
ECG is record of all depolarizations of heart
waves :
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P wave
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atrial depolarization
QRS complex
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ventricular depolarization
T wave
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ventricular repolarization
intervals :
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P-Q interval
begin atrium to begin ventricle
S-T segment
ventricular plateau
Q-T interval
entire ventricular events
R-R interval
1 beat
heart rate
Arrhythmia
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irregular heart beat
bradycardia
slow rate < 60
tachycardia
fast rate
palpitation
brief, temporary arrhythmia
flutter
fast, consistent heart rate > 200
fibrillation
fast, uncoordinated
> 300
ventricles contract w/o filling
> 100
PVC = premature ventricular contraction
occassional, irreg. ventricular contraction
cardiac muscle become conductive
asystole
no contractions
innervation of heart
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vital signs
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what part of brain ?
cardioaccelerator center
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S-ANS to S-A node and pathway
stronger contract
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increase rate
cardioinhibitory center
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P-ANS to S-A node and A-V node weaker contract
decrease rate
modify the rate of depolarization - doesn’t cause pacemaker potential
epinephrine
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S-ANS , hormone
stim ß adrenergic receptors
• cAMP mediated
open Na channels
depolarizes faster
acetylcholine
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P-ANS
open K channels
depolarizes slower
Cardiac cycle
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1 “heartbeat”
all events of blood flow
systole
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contraction
atrial systole
ventricular systole
diastole
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relaxation
atria and ventricles relax
systole + diastole = cardiac cycle
cardiac cycle - basic
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atrial systole
atria contract
ventricular systole
ventricles contract
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(atrial diastole)
diastole
all chambers relax
cardiac cycle - details
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ventricular filling
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passive filling
atrium to ventricle
atrial systole
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ventricular systole
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isovolumetric contraction
A-V valves close
no blood movement yet
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ventricular ejection
SL open
ventricle to artery
diastole
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isovolumetric relaxation
SL valves close
Heart valves
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function :
prevent backflow
open and close by pressure of moving blood
A-V valves
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open :
weight of blood from atria
close : pressure of ventricular contraction
Semilunar valves
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open :
pressure of ventricular contraction
close :
weight of blood in artery (aorta ; pulmonary )
Heart sounds
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closing of valves
1st
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A-V valves close
• forces blood against valves
• ventricular systole
2nd
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Semilunar valves close
• gravity from blood in arteries
• ventricular diastole
heart murmurs
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abnormal heart sounds
abnormal blood flow
defective valves
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mitral stenosis
thickened mitral valve
regurgitation
fail to close
septal defects
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interatrial
patent ductus arteriosus
Cardiac output
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= amt. blood pumped / minute / ventricle
Cardiac output = stroke volume x heart rate
CO = SV x HR
heart rate
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pulse
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beats / min
stroke volume = amount pumped / beat / ventricle
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“resting stroke volume” ~ 70 ml/beat
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stronger heart ( SV )  slower heart rate
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HR
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CO =
70 beat / min
70ml x 70 beat/min = 4900 ml/min
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~ 5 liters/ min
100ml x 50 beat/min = 5000 ml\min
weak heart requires  HR (more work)
stroke volume
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EDV end diastolic volume
after filling
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ESV end systolic volume
after contraction
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SV = EDV - ESV
SV
= 120 ml - 50 ml
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70 ml
factors affecting EDV
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preload
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venous return
Starling’s law of the heart :
increase stretch of cardiac wall  increase force of contraction
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 venous return
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 venous return
slow HR
 BP
exercise (skeletal muscle pump)
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 venous return
very fast HR
blood loss
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contractility
affect Ca++ entry into cells
 contraction (SV)
factors affecting ESV – extrinsic factors
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positive inotropic agents
S-ANS
epinephrine
thyroxine
digitalis
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negative inotropic agents
P-ANS
K+
H+ (pH)
Ca channel blockers
beta blockers
afterload
backpressure from arteries (BP)
factors affecting HR
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chronotropic factors
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increase
S-ANS
epinephrine
thyroxine
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decrease
P-ANS
baroreceptors
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vagal tone
atrial wall
stretch
ANF ; S-ANS
emotion
ANS
MI
myocardial infarction
ischemia
decreased blood supply
infarct
destroyed myocardium
CAD
coronary artery disease
CHF
congestive heart failure
MVP
mitral valve prolapse
Mitral stenosis
decreased size of opening in valve
Angina
brief pain of coronary artery origin
Rheumatic heart disease
Strept infection
cardiac disease
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CABG
arrhythmia
Atherosclerosis
decreased lumen due to plaques