Download Chapter 27 Reproductive Endocrinology

Chapter 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
gap junctions
allow ions to pass betw cells
desmosomes
prevents separation of cells
many mitochondria
aerobic respiration
huge O2 requirement
functional syncytium all cells contract simultaneously
autorhythmic cells
cells depolarize without stimulus
cardiac vs skeletal muscle tissue
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cardiac muscle doesn’t fatigue
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long refractory period
more time to make ATP
contraction
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skeletal muscle
motor units
cardiac muscle
entire myocardium
nerve connections
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skeletal
each cell requires a neuron
cardiac
contract without neurons
cardiac muscle contraction - 1
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contracts like skeletal muscle :
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resting membrane potential -90mV
stimulus (+ ions)
• opens fast Na+ channels (voltage-gated)
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depolarization
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repolarization
( -90mV to +30 mV)
• + opens Sarcoplasmic reticulum
• Ca++ stimulates sarcomere to contract
K+ channels (voltage-gated) open
only different :
cardiac muscle contraction - 2
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resting membrane potential
-90mV
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stimulus opens fast Na channels (voltage-gated)
depolarization ( -90mV to +30 mV)
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depolarization opens slow Ca++ channels
cell stays depolarized longer =
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Ca opens SR
plateau
= Calcium stimulated Calcium release
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Ca stimulates sarcomere to contract
decreased K+ permeability
delays repolarization
repolarization
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K+ channels open
Ca – ATPase pump
Ca++ pumped into SR
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Ca pumped out of cell
Na – Ca antiport (20)
cardiac muscle contraction - 3
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much longer contraction in cardiac muscle
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skeletal
2–5 ms
cardiac
300 ms
cardiac depolarized longer
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skeletal
cardiac
Na+ depol
last 1-5 ms
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Ca depol
lasts 150-200ms
long refractory period 250 ms vs skeletal 2-3ms
• prevents summation
• prevents fatigue
• prevents tetany
functional syncytium
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entire atria contract simultaneously
entire ventricles
contract simultaneously
gap junctions
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= electrical synapse
cell stimulates all adjacent cells
heart contracts without nerves
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non-contractile cardiac cells act like neurons
initiate and spread action potential for entire myocardium
autorhythmic
depolarize automatically
conduction pathway
connected autorhythmic cells
autorhythmic cells
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spontaneous depolarization
pacemaker potential
unstable resting potential
hyperpolarized at
- 60 mV
HCN channels (pacemaker channels) = slow Na+ channel
Na+ leaks in
hyperpolar opens HCN channels
threshold
- 40 mV
fast (voltage-gates) Ca++ channel open
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voltage gated K channels open
depolarization
repolarization
hyperpolarization (-60mV) opens HCN channel
rhythm of spontaneous depolarization
intrinsic 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
conduction
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gap junctions spread depolarization along pathway
Ca++ causes threshold in adjacent cells
S-A node
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sino-atrial node
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pacemaker
right atrium
fastest autorhythmic tissue
~ 90+ / min
sets pace for entire myocardium
sinus rhythm
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normal
~ 70 – 75 / min
slowed by P-ANS
vagal tone
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)
only electrical connection from atria to ventricles
R & L bundle branches
Purkinjie fibers
bundle to Purkinjie
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ventricular contraction
contraction begins at apex and moves upward
ANS effects
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S-ANS, epinephrine
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autorhythmic cells
opens HCN channels
 rate
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myocardial cells
open Ca channels
 contractility
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via ß receptors
cAMP
P-ANS
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autorhythmic cells
open K channels
 rate
• via muscarinic receptors
myocardial cells
no effect
ECG
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electrocardiogram
ECG is record of all electrical events 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
entire conduction system
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
S-ANS to myocardium
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increase rate
stronger contract
cardioinhibitory center
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P-ANS to S-A node and A-V node vagal tone
hypothalamus
constant
limbic system
cerebrum
decrease rate
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 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
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atrial systole
ventricular systole
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isovolumetric contraction
no blood movement yet
A-V valves close
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ventricular ejection
ventricle to artery
SL valves open
diastole
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isovolumetric relaxation
SL valves close
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 =
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70 beat / min
70ml x 70 beat/min = 4900 ml/min
~ 5 liters/ min
100ml x 50 beat/min = 5000 ml\min
weak heart requires  HR (more work)
regulation of HR
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positive chronotropic factors
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S-ANS
increase HR
stim Beta receptors
open HCN channels
epinephrine
thyroxine
negative chronotropic factors
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P-ANS
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Beta blockers
decrease HR
stim muscarinic receptors
open K channels = vagal tone
why change HR ?
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to maintain CO
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blood pressure
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 SV
 BP
– baroreceptors
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reflex  HR
to  CO
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 metabolic demand
emotion
danger
exercise

reflex  HR
stroke volume
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EDV end diastolic volume
after filling
ESV end systolic volume
after contraction
SV = EDV - ESV
SV
= 120 ml - 50 ml
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ejection fraction
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70 ml
~ 60 % of EDV
relatively constant, as EDV varies
since  EDV   SV
physics of SV
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What moves blood?
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ΔP
pressure gradient
fluids move from high to low pressure
ventricular P > aortic P
blood moves out
ventricular P = aortic P
blood stops moving
increase vent P
contractility
increase SV
increase aortic P
resistance
decrease SV
regulation of SV
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strength of contraction
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intrinsic control
preload
extrinsic control
contractility
afterload
= EDV
= resistance
intrinsic factors of SV
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Preload
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length-tension relationship
Frank-Starling’s Law of the Heart
• increase stretch  increase contraction
•  EDV   SV
venous return
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amt blood entring heart
skeletal muscle pump
S-ANS
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 due to:
systemic vasoconstriction
due to: exercise
slow HR
very fast HR
blood loss , dehydration
extrinsic factors of SV
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= contractility
positive inotropic factors
• S-ANS ; epinephrine
• thyroxine
• Ca++
• digitalis
 contractility
open Ca channels
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 contractility
negative inotropic factors
• K+
• H+ (pH)
• Calcium channel
blockers
afterload
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afterload
= total peripheral resistance
ventricles pump against resistance in aorta
 BP (aorta) 
 SV
self corrects
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 BP 
 HR
 SV
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 EDV
 contract
myocardial hypertrophy
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systemic hypertension
L ventricle
pulmonary hypertension
R ventricle
cardiac disease
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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
arrhythmia
irregular heart rate
Atherosclerosis
decreased lumen due to plaques
CABG