L5/6 Flashcards
autorhythmicity
built-in rhythm of action potentials -> heart contractions
autorhymic fibers function
non-contracting pace maker cells (inititate action potentials)
autorhymic fibers location
- SA node
- AV node
- AV bundle
- right/left bundle branches
- Purkinje fibers
contractile fibers
- delivers action potential via contractions but cannot initiate action potential
- acts as pacemaker conduction system
propagation of cardiac action potential
depolarized SA node -(ap)-> both atria -> atria contraction -(ap)-> AV node -(ap)->AV bundle -(ap)->right & left bundle branches -(ap)-> Purkinje fibers -(ap)-> heart apex -(ap)-> ventircular myocardium -(ap)-> ventricle contraction -(blood)->semilunar valves
peacemaker potential is _mV
-60mV
peacemaker potential reaching threshold
- closed K+ channels & open F-type channels (Na+ permeable) -> almost at threshold
- F-type channels close & T-type voltage-gated Cas2+ channels open -> threshold reached
generation of action potentials in contractile fibers
opening L-type voltage-gated Ca2+ channels -> generates action potential -> causes contractile fibers to enter depolarizing phase
contractile fibers have a potential of _mV
-90mV
contractile fibers depolarizing phase
open fast voltage-gated Na+ channels -> +20mV
contractile fibers initial repolarizing phase
close fast voltage-gated Na+ channel and open fast voltage-gated K+ channels -> decreased from 20mV
contractile fibers plateau phase
close fast voltage-gated K+ channels and partially open slow voltage-gated K+ channels ->constant 10mV
contractile fibers final repolarizing phase
fully open slow voltage-gated K+ channels -> -90mV -> close channels
L-type voltage-gated Ca2+ channels close when
the final repolarizing phase of contractile fibers has been completed (-90mV)
Excitation-Contraction coupling in cardiac muscle
links cardiac action potential to cardiac contraction
calcium-induced calcium release
L-type voltage-gated Ca2+ -> increase extracellular calcium concentration (10% required) -> Ca2+ rleased from SR (other 90% required) -> contraction
graded contractions cardiac muscle
increase or decreasing contraction of syncytium muslce fibers by manipulating how much Ca2+ is in the sarcoplasm
relaxing cardiac muscle after contraction
decrease calcium concentration in the extracellular fluid with Ca2+-ATPase pump
> Ca2+ goes to SR
Cardiac muscle refractory period
-very long because of plateau phase
>helps with proper pumping (heart needs to relax and fill with blood)
ATP production
aerobic respiration
ECG P
atrial depolarization
ECG QRS
ventricular depolarizaiton
ECG T
ventricular repolairzation
ECG P-Q/P-R
atrial ventricular excitation conduction time
ECG S-T
Ventricular contractile fibers depolarize/pleateau phase
ECG Q-T
Ventricular depolarization to repolarization time
increase Q wave
myocardial infraction
increase R wave
enlarged ventricules
flat T wave
decreased O2 (ex: coronory artery disease)
increased T wave
hyperkalemia (high K+ in blood)
systole
phase of contraction
diastole
phase of relaxation
passive ventricular filling
- atria/ventricule(diastole)-(atria fills with blood from veins)-> atrial pressure > ventricular pressure
- AV valves open: atria -(blood)-> ventricules (80% capacity)
- SL valves close
* no muscle contractions * - SA node -(ap)-> atria -> depolaries
atrial contraction
- atrial depolarization -> atrial systole -> contraction -> increased atrial pressure -> opens AV valves
- AV valves add remaining 20% of blood to ventricule
isovolumetric ventricular contraction
- ventricules depolarized -> systole (atrial in diastole)-> increased ventricle pressure -> AV vavles close
- isovolumetric ventricular contraction when AV and SL vavles are closed
ventricular ejection
- left ventricule > aortic pressure/right ventricle>pulmonary trunk -> SL valves open
2a. left ventricle -(70mL blood) -> aorta
2b. right ventricle-(70mL blood) ->pulmonary trunk
EDV
the filled volume of the ventricle prior to contraction
ESV
is the residual volume of blood remaining in the ventricle after ejection
stroke volume
stroke volume = EDV-ESV
volume of blood ejected from each ventricle/contraction
ejection fraction
ejection fraction = SV/EDV x 100%
percentage of the end-diastolic volume that is ejected with each stroke volume
isovolumetric ventricular relaxation
- ventricular repolarization -> diastole -> relexation -> decreased pressure
- vavle cusps collect backflow -> close SL valves
- ventricule pressure < atrial pressure -> A.V valves open -> repeat
Heart beat steps
- passive ventricular filling
- atrial contraction
- ventricular ejection
- isovolumetric ventricular relaxation
lubb & dupp
lubb: AV valves closing (louder)
dupp: SL valves closing
cardiac output
volume of blood ejected from each ventricle/minute
heart rate definition
number of beats per minute
cardiac reserve
maximum cardiac output-cardiac output at rest
stroke volume preload
degree of stretch on heart before it contracts
frank-starling law
increased stretch leads to increased contraction
increased EDV causes
increased filling time and increased venous return
stroke volume contractility definition
forcefulness of contraction of individual ventricular msucle fibers
inotropic effects
alter contractility
>postivie: increases
>negative: decreases
positive inotropic effect mechanisms
- NE + B1-adrenergiic receptor (sarcolemma)
- Gs activates -(stimulates)-> adenylyl cyclase -(produces)-> cAMP
- cAMP + protein kinase -> phosphorylates:
- L-type voltage gated Ca2+ channels -> increased Ca2+ in sacroplasm
- Ca2+ release channels -> release Ca2+ from SR lumen into sacroplasm
- phospholamban -> reuptake Ca2+ to SR lumen after contraction to preserve Ca2+ supply
- myosin heads -> increases rate of crossbridge cycling - increases contractivity
negative inotropic effect mechanisms
decreases Ca2+ in sarcoplasm to decrease contractility
stroke volumme afterload definition
pressure that must be exceed before ejection of blood from ventricles
>must open SL vavles
increased afterload causes
decreased velocity of ventricular muscle fiber shortening
chronotropic effects
+ -> increases heart rate
- -> decreases heart rat
cardiac accelerator nerves and heart rate regulation (ANS)
cardiac accelerator nerves: connect sympathetic NS with SA node, AV node and ventricular myocardium
Vagus X nerves and heart rate regulation (ANS)
connect parasympathetic and heart wall (AV and SA nodes)
NE and increased heart rate via SA node increased ap mechanism
NE + B1-adrenergic receptors in sarcolemma -> Gs -> increased adenyly cyclase -> increased cAMP + F-type NA+ channels -> Na+ enters cell -> depolarziation -> SA node generate action potentials
NE and increased heart rate sympathetic or parasympathetic?
sympathetic
increasing heart rate via increasing action potential conduction (atria->ventricules) mechanism
F-type Na+ channels -> Na+ influx -> depolarize AV node -> fires AP
increasing heart rate via increasing action potential conduction (atria->ventricules) sympathetic or parasympathetic?
sympathetic
increasing heart rate by increasing contractility mechanism
NE + B1-adrenergic receptors -> G protein -> increased Ca2+ -> increased contractility
increasing heart rate by increasing contractility mechanism sympathetic or parasympathetic?
sympathetic
decreasing heart rate via Ach mechanism
Ach + Gi -> decreased cAMP
Ach + Gi -> opens K+Ach channels -> K+ outflux -> hyperpolarizes -> SA node decreases Ap
decreasing heart rate via Ach sympathetic or parasympathetic?
parasympathetic
decreasing heart rate via decreasing conduction (atria -> ventricles) mechanism
K+Ach open -> K+outflow -> hyperpolarizes AV node -> decreases action potentials
decreasing heart rate via decreasing conduction (atria -> ventricles) mechanism sympathetic or parasympathetic?
parasympathetic
heart rate chemical regulation via hormones
E and NE
heart rate chemical regulation via ions
Na+, K+ and Ca2+
heart rate chemical regulation via no ions and no hormones
age, gender, physical fitness and body temperature
