Module 7 : Cardiac Innervation Flashcards
Cardiac Innervation
How the heart stimulates itself
2 types of cardiac cells in relaxtion and contraction
Conduction cells
Muscle cells/ myocardial cells
Conduction cells
- AKA auto-arrhythmic cells
- capable of initiating impulse
- not completely independent of outside stimulation
- impulse travels via gap junction from cell to cell through heart
- stim occurs and travels from atria to ventricles
- DO NOT CONTAIN MYOFIBRILS
Muscle/myocardial cells
Do work
Contract (actin and myosin)
Must be stimulated in normal rhythm
Present in thinner atrial walls and myocardial layer of the ventricular walls
Cardiac cells function
- work together to form one sequential contraction
Gap junctions
- the conduction cells are joined together by gap junction
- allow passage of electrical impulse from one cell to the next
Anatomy of cardiac cells
- cells have branches
- joined together by INTERCALATED DISCS which contain GAP JUNCTIONS
4 types of cardiac cells
- myocardial/muscle/contractile cells
- conduction cells
- avascular valvular tissue
- endocardial cells
Avascular valvular tissue
- interstitial cells
- less water more collegen
Endocardial cells
- line all of the blood tissue interface including valves fo the heart
- allow blood to easily slide over the surface
- 1mm or less in thickness
- cover all other types of cardiac cells
Myofibril
- make up contractile cells
- contains contractile elements of muscle cells and contain many myofibrils lined up in a row
- several lie on top of each other surround the heart in different directions
- each layer contracts in different directions
Sacromere
- segment of myofibril
Actin and myosin
- within the sarcomeres
- contractile protein
- slide over each other
- 20% more over lap in systole
Actin and myosin - contraction
- actin and myosin slide together and overlap to a greater degree
Actin and myosin - relaxation
- actin and myosin slide apart and overlap only at the ends
Preload effects on actin and myosin
-increased preload stretches the actin and myosin apart
- in normal hear amount of contraction is increased
+ diseased heart may go into failure
After load effects on actin and myosin
- increased after load leads to less overlapping of actin and myosin during peak contraction
- contraction is decreased
Muscle fiber contraction - 2 require stimulation
1) electrical current - pace maker or defibrillator
2) action potential (intrinsic electrical impulse transmitted from another cell or comes from cell itself)
Muscle cells stimulation
- stimulates by impulses from the conduction cells
- can stimulate themselves but at slower heart rate 20-40bpm
Conduction cells contraction ?
Conduction cells DO NOTA contract
- only conduct and generate pulses
- their function is specialized to conducting impulses
Influx
Ions entering the cell through the channels in the membrane
Efflux
Opposite of influx
Exiting cells
Stimulus
Strong electrical signal capable of conducting through the heart (microvolts)
Automaticity
Ability of a cell to PRODUCE their own impulse
+ based on steepness of each cells phase 4 slope
Excitability
- ability of cell to accept an impulse and transmit it to other surrounding cells
Refractory
Ability of a cell to RESPOND to a stimulus
+ based on which stage of action potential the cell is currently in
Electrical mechanical coupling
- muscle fiber contraction requires electrical stimulation
Excitation coupling
- series of events that connects the electrical stimulation to the subsequent mechanical event of contraction
ELECTRICAL BEFORE MECHANICAL ALWAYS
Electrical - action potential
- a wave of electrical discharge (exchange of ions across a cell membranes) that travels along the outer membrane of a cell
- cycle of depolarization/repolarization
- repeated every heart beat
- wave of electrical discharge sent to neighboring cells in heart
Action potential in muscle and conduction cells
- both have action potential but look very different
Auto-rhythmic / conduction cell action potential
- can be self stimulated or stimulated from nearby cells
- impulse or action potential travels all the way to the ‘end’ of the electrical circuit (atria-ventricle)
- heart keeps beating outside body because of this
Action potential ion flux
Stage 1 = sodium rushes into flee
Stage 2 = calcium rushes in
Stage 3/4 = potassium out of cell
Selective permeability
- gate keeper of the cell
- allows certain ions in and out of the cell membrane
The action potential - electrical stages
- sequence of electrical events that must occur every heart beat
\+ stage 0 = depolarization (cell)
\+ stage 1 = early repolarization
\+ stage 2 = plateau - contraction
\+ stage 3 = repolarization
\+ stage 4 = resting statePhase 0
- depolarization of the cell
- DEPOLARIZATION IS NOT CONTRACTION
- cell is stimulated and prepares to contract
- cell fires from threshold to maximal positive state
- cell becomes refractory to all stimulus (cannot respond to another stimulus)
- sodium entering the cell quickly through sodium potassium pump
voltage change in phase 0
(-)90 mV to (+) 40-50 mV
phase 1
- early depolarizing
- very short time interval
- call is refractory (cannot accept another stimulus)
- moves toward a slightly less positive state
- preparing for plateau phase
- potassium chloride leaking out
phase 2
- plateau stage
- EXCITATION COUPLING = actin and myosin reacting to electrical signal leading to contraction
- contraction phase of cell
- cell is still refractory
- calcium is responsible for contraction of cell
phase 3
- repolarization = post contraction
- cell returns to resting state
- all ions return to initial state
- downslope of action potential
resting voltage of cells
(-) 90 mV
phase 4
- upward slope of the stage determines how fast the automaticity rate of the cell is
- once the membrane potential reaches threshold it will depolarize again
steep phase 4
fast intrinsic rate
falt phase 4
slow intrinsic rate
refractory period
- when cell is immune to stimulus
- from onset of depolarization to close to the end of depolarization
- another impulse cannot normally be initiated or transmitted
absolute refractory period
- no external stimuli will make heart beat
- absolut refractory until end of stage 2
relative refractory period
- only a string external stimulus will make the heart beat
- after stage 3
sequence of events (electrical - mechanical)
- electrical events in the heart must occur before mechanical events
cardiac conduction system
- network of specialized cardiac fibres that provide a path for each cycle of cardiac excitation to move through the heart
electrolytes
- importance of electrolyte balance (sodium, calcium, potassium)
- ions are responsible for the action potential and can alter the action potential when there are abnormal levels
not enough electrolytes
- poor function of heart
too much electrolytes
- hyper function of heart
intrinsic innervation
- controls the base heart rate
- controls rates of the individual components of the conduction system (heart rate within heart)
extrinsic innervation
- gives the heart signals to speed up or slow down
- autonomic nervous system
- through sympathetic and para sympathetic nervous system
sympathetic nervous system
- from medulla oblongata to thoracic spine level
- fibres send impulse to heart
+ SA and AV nodes, myocardium - ACCELERATION
parasympathetic nervous system
- DECELERATION
- from medulla to heart via vagus nerve - SA and AV node
sympathetic nervous system on heart
- accelerator
- stimulates in times of stress
+ physical or emotional - releases nor-epinephrine
- increases ion exchange
- increases BOTH HEART RATE AND FORCE OF CONTRACTION
parasympathetic nervous system
- innervates the SA node via vagus nerve
- acts as brake - slows heart down
- stimulated during times of rest
- being fit or beta blockers
- releases acetylcholine
- carotid massage
extrinsic controls - affect what
- heart rate = chronotropy
- contractility = inotropy
- ventricular filling volumes = pre load
- afterload = arterial pressures controlled by baroreceptors in the carotids and aorta
baroreceptors
- pressure sensors in carotid bulb and aortic arch regulate the pressure to protect the brain
- massaging carotid bulb increases pressure to brain to slow HR down
intrinsic conduction pathway
- SA node > LA/RA (internodal tracts) > AV node > bundle of His > right and left bundle branches > purkinjie fibres (LV)
Sinoatrial Node (SA node)
- located near superior wall of RA - near entry of SVC
- pace maker fo heart
- generates pulses 100 times per minute but parasympathetic tone reduces to 60 - 100 bpm
- fastest phase 4 in the heart in action potential
- ability to create pacemaking stimuli is automaticity
SA node > LA/RA internodal pathway > AV node
- impulse travels from SA node through right and left internodal pathway to AV node
- once RA and LA are stimulated they will contract to push blood to ventricles (atrial kick)
AV node location
- located in right side interatrial septum
- above annulus of TV
- near opening of coronary sinus
atrioventricular node (AV node) funtion
- AV groove
- insulates pulse so that it only travels in the pathway of specialized cells
- impulse is delayed to allow for atrial contraction and ventricular filling to occur
- if this sequence malfunctions arrhythmias happen
AV node pulses
- can generate pulses at 40-60 times for second
- ONLY NEEDS TO GENERATE IMPULSES IF SA NODE FAILS
- impulse then travels to AV bundle/bundle of His
junctional rhythm
- the rhythm created when the AV node takes over as pace maker
Bundle of His (AV bundle)
- slightly distal to AV node
- only electrical pathway between atria and ventricles
- sends impulse forward to left and right bundle branches
bundle branches (right and left)
- speed up impulses
- travel along interventricular septum toward apex then turn superiorly toward base on lateral sides of heart
- sometimes path can be blocked LBBB RBBB
- RV septum stimulated first than the Lv septum
- as wave of pulse travels ventricular myocytes depolarize
LBBB or RBBB
- slows conduction through the ventricles and QRS is lengthened
purkinjie fiber location
- branch off of bundle branches
- more elaborate on left side due to thicker muscle
- ## tiny spider webs
purkinjie fibers
- deliver impulse to the individual muscle cell
- long strands of cells
- complete the pathway through the IVS to the apex
- as pathway is completed contraction is completed and ventricle starts to regroup or repolaraize
purkinjie fibres helping AV valves
- aid in the valves function by pulling down on MV and TV when pap muscles are stimulated before rest of the muscle
purkinjie fiber pulse rate
- only generate pulses every 30-40 times per minute
- would need a pacemaker
contraction of ventricles
- ventricular contraction folllows ventricular depolarization
- contraction begins at apex and mover superiorly through base
- post contraction depolarization begins
- REPOLARIZATION CAUSES T WAVE ON ECG
time from impulse formation to repolarization
200 ms
atria and ventricle polarization relationship
as atria are repolarizing the ventricles are depolarizing and vice versa
depolarization wave
- wave of depolarization passes from cell to cell causes all of the cells to depolarize and contract in sequence
- ## atria > ventricles
SA node intrinsic rate
60-100bpm
PACEMAKER NUMBER 1
AV node intrinsic rate
40-60 bpm
PACEMAKER NUMBER 3 BUT ACTIVATES WHEN SA NODE FAILS
bundle of His intrinsic rate
40-60bpm
PACE MAKER NUMBER 4
LV/RV muscle cells
20-30bpm
PACE MAKER NUMBER 6
