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Cheatography

Cardiac Muscle Cheat Sheet (DRAFT) by

npb 101cardiology cheat sheet

This is a draft cheat sheet. It is a work in progress and is not finished yet.

Heart Chambers

 
Left Atria: oxygen- rich blood from pulmonary veins -> left AV valve
Right Atria: oxygen poor blood from vena cavae -> right AV valves
Left Ventricle: oxygen rich blood, from right at--> semilunar valves
Right Ventricle: oxygen poor blood from rigth atrium­-> pulmonary artery

Nodes

SA Node
AV node
Bundle of His
SA node
initiates potential and leads
audtor­hyt­hmi­city: 70 action potentials per minute

AV node
base of right atrium
audtor­hyt­hmi­city: 50 A.P. / minute
follows SA node under normal conditions

Bundle of His
origin: AV node
projects to left and right ventricles

Purkinje Fibers
terminal fibers
extend from Bundle of His
follows faster SA node under normal conditions

Cardiac Cycle

Systole
contra­ction
Diastole
relaxation
End- diastolic volume
volume of blood at end of diastole, max amount that chamber will hold
Isovol­umetric ventri­cular contra­ction
during contra­ction, valves closed, no blood leaves, increase in chamber pressure
Stroke volume
amount of blood pumped out of chamber
Isovol­umetric ventri­cular relaxation
chamber pressure decreases

ACh: Parasy­mpa­thetic release

SA Node
Ach: inc. permea­bility to K+ by delaying inacti­vation of K+ channels -> more hyperp­ola­riz­ation
AV Node
inc permea­bility to K+, reduces excita­bility of node, delays response of input from SA node
Atrial contra­ctile cells
shortens of action potent­ials: reducing Ca2+ permea­bility during plateau
 

Components

Heart
Blood Vessels
Blood

Valves : one way

Right AV Valve
Left AV valve
Aortic/ Pulmonary valve
tricuspid
bicuspic
semilunar

Pathways

Intera­trial
cardiac cells pacemaker activity from right to left atrium
Internodal
cardiac cell pacemaker activity from SA to AV node
AV nodal delay
Slow through AV node due to thickness

Action potential in Contra­ctile cells

Resting potenial
-90mV until excited
Rising phase
rapid, Na+ entry due to opening of fast Na+ channels, close K+ channels
Repola­riz­ation
at peak, open transient K+ efflux, inactivate Na+ channels
Plateu
Slow Ca2+ entry, open of L-type Ca2+ channels, reduce
Falling phase
K+ efflux, open voltag­e-gated K+ channels
Resting Potential
maintained by opening leaky K+ channels

Heart Sounds

Murmer:
turbulent flow of blood through malfun­cti­oning valves
Stenotic valve:
whistling, stiff narrow valve
Insuff­icient valve:
swishing, struct­urally damaged valve
Rheumatic fever:
valvular stenosis, autoimmune disease

Cardiac muscle type

Straited:
striped lines
Involu­ntary
moves by itself

Sarcomere

Z line
sarcomere boundary
A band
thick filament with thin filament overlapp
H zone
where thin filaments don't reach
M line
middle, vertically down A band
I band
remaining thin filament that are not in A band

Muscle

Myofibril:
thin( actin) thick ( myosin), sarcomeres connected together
Sarcomere:
smallest unit of muscle cell,
Myosin:
cytosk­eletal protein
Thin filament
actin, tropom­yosin, troponin
 

Types of Muscle

 
Endoca­rdium - thin/ interior of each chamber
Myocardium - middle layer, thickest, interc­alated disks for connection
Epicardium - thin external membrane with perica­rdial fluid

Pacemaker Activity

 
Open funny channels:
NA+ inward and closes K+ outward
Reaches threshold of -40:
Open L-type Ca2+ and K+ channels

Action potential in Contra­ctile cells

Electrical Activity

 
Autorh­yth­micity- capability to produce own rhythmic electrical activity due to Pacemaker activity
Only 1% of Cardiac cells

Excitation Contra­ction Coupling

Ca2+ entry into cystol
 
T-tubule
contain: dyhyro­pyr­idine recept­ors­-> open Ca2+ into cytosol
#cross­bridges propor­tional to cytosolic Ca2+ concen­tration

Electr­oca­rdi­ogram

P wave
depola­riz­ation of atria
QRS complex
depola­riz­ation of ventricles
T- wave
Repola­riz­ation of ventricles

Cardiac Output

Cardiac Output:
heart rate x stroke volume
Heart rate:
beats per minute, regulated by both parasy­mpa­thetic and sympat­hetic nervous system

Excitation Contra­ction Coupling

ACh
- released by motor neuron axon binds to motor end plate
- results in action potential that propagates to surface membrane and down t-tubule
- triggers Ca2+ release from SR
-Ca2+ released from lateral sacs
- bind to troponin, tropom­yosin moves aside to open actin binding site
- myosin crossb­ridge attach to actin-> bend -> pull actin towards center of sarcomere
- Ca2+ taken up by SR
- tropom­yosin goes back to blocking position.