Heart Physiology Flashcards
intrinsic conduction
ability to depolarizes and contract on its own
autorhythmic cells
Autorhythmic cells have unstable resting membrane potentials
noncontractile cells in contractile muscle that initiate and propagate impulse
Leaky
Na+ moves in easily to depolarie
Self generate AP
SA node
coronary sinus, in right atrium; main controller “pacemaker”
AV node
in interventricular space, top of septum
Bundle of his
splits to R+L
Bundle branches
in walls
Purkinje fibers
electrical stimulation to muscle tissue in papillary muscle
extrinsic innervation
nervous connection
cardioacceleratory and cardioinhibitory
Cardioacceleratory center
sympathetic; NE causes quicker depolarization; faster heart rate
Cardioinhibitory center
parasympathetic; ACh causes the slower heart rate
vagal tone
reduction of contraction from vagus nerve stimulation
Allows us to increase heart rate
Parasympathetic hyperpolarize SA causing decrease in heart rate from medulla
P wave
SA
depolarization of atria
QRS complex
depolarization of ventricles (masked is the repolarization of atria)
T wave
repolarization of ventricles
what causes lab sound
AV valves close
what causes dup sound
SL valves close
murmur
malfunctioning of the valve
cardiac cycle
Systole and diastole of both atria plus systole and diastole of both ventricles
cardiac output
SV x HR
stroke volume
blood leaving heart per beat
Difference between amount of blood in ventricles before and after systole
End diastolic volume-end systolic volume
cardiac reserve
difference between maximum CO and minimum CO
factors affecting stroke volume
Stretch of cardiac muscle
Contract with more force after stretch
Starling law of the heart
More blood in ventricles= more pressure in contract
preload= blood in ventricles prior to contraction
Contraction strength not due to stretch
NE moves more Ca 2+ into the heart, increases force of contraction
Arterial pressure
After load= artery pressure not as much blood leaves
factors affecting heart rate
Sympathetic nervous system activation
NE
Corresponding increase in contractility
Parasympathetic nervous system activation
ACh
Adrenal medulla production of epinephrine
Thyroid production of thyroxine
Heart rate increases
Gradual and sustained
Blood pressure changes (baroreceptors)
Ionic balances
Age
Heart rate decreases
Sex
Females have higher heart rate
Exercise
Heart rate decreases as you are more efficient (LT)
Temperature
Increase temperature increases heart rate
tachycardia
inability to slow heart rate
bradycardia
abnormally slow heart rate
congestive heart failure
dangerously low CO
Coronary atherosclerosis
blockage in coronary arteries
High blood pressure
less CO, reduces ejection fraction
Myocardial infarctions
heart attack; lose the ability to contract
Dilated cardiomyopathy
flappy, loose ventricle (usually) but can happen in any chamber
Usually due to valve failure
process of fetal heart development
Derived from mesoderm
Originates as two separate endothelial tubes
Tubes fuse into single chambered heart by day 23
Early chambers formed by day 25
D-looping and structural changes divide heart into separate chambers and change orientation by day 46
D looping
rightward circle until its orientation inverted
foramen ovale
connection of two atria through interatrial septum
Shortcut to get O2 blood to body
ductus arteriosus
connection between pulmonary trunk and aorta, becomes ligamentum arteriosum
valve sclerosis
rafi (flaps) of valves accumulate deposits, don’t close as well, leading to leakage
Naturally occurring
decreases cardiac reserve
biggest reason is becoming sedimentary
Fibrosis of myocardium
more sedimentary leads to muscle changes to noncontractile tissue
atherosclerosis
plaque buildup
